More than 200,000 patients with acute pancreatitis are admitted to U.S. hospitals each year.¹ Eighty percent of these patients suffer from mild disease and demonstrate an overall mortality rate of just 1%. Approximately 20% of patients have severe necrotizing pancreatitis, however, which has a mortality rate of up to 25%.^2,³ The estimated incidence of pancreatitis in the United States is 79.8 per 100,000.⁴ Men are affected more commonly than women, and the condition develops in most patients between 40 and 60 years of age.⁵

Pathophysiology

The pancreas is a retroperitoneal organ with a primary role in digestion; it exhibits both exocrine (i.e., pancreatic enzymes) and endocrine (i.e., insulin and glucagon) functions. Pancreatitis is an inflammatory condition of the pancreas that arises from premature activation of pancreatic enzymes and results in autodigestion of the gland. The exact pathogenesis of this disease is unclear. Both acute and chronic forms exist.

Acute pancreatitis is most often caused by gallstones or alcohol use. Gallstone pancreatitis occurs secondary to obstruction of the common bile or pancreatic duct. Alcohol or its metabolic by-products are thought to act as a direct toxin to the pancreas, and the effects are usually dose dependent. Other less common causes are hyperlipidemia, hypercalcemia, medications, toxins, trauma, surgery, sphincter of Oddi dysfunction, invasive diagnostic procedures (endoscopic retrograde cholangiopancreatography), and hereditary causes. Approximately 20% of cases are idiopathic, with occult microlithiasis thought to be the underlying cause in half of them.⁶ Acute pancreatitis can be classified histologically as edematous or necrotizing, which corresponds to clinically mild or severe disease, respectively. Risk factors for severe disease include older age (>55 years), obesity (body mass index > 30 kg/m²), and pleural effusions or infiltrates (or both).⁷ Pancreatic necrosis (nonviable tissue) is associated with significant morbidity and mortality, especially if infection is present. Complications from pancreatitis include pseudocyst and abscess formation.

Chronic pancreatitis is often a progressive disorder with irreversible lesions, such as glandular fibrosis, distortion of the pancreatic duct, and strictures. Long-standing alcohol abuse is the most common cause of chronic pancreatitis.

Standard definitions and terminology for acute pancreatitis (Table 43.1) have been proposed to establish an exact vocabulary among institutions and within the literature.⁸

Table 43.1 Definitions of Acute Pancreatitis Terminology

Acute pancreatitis	Acute inflammation of the pancreas
Mild acute pancreatitis	Minimal organ dysfunction responsive to fluid administration
Severe acute pancreatitis	One of the following: local complications (pancreatic necrosis, pancreatic pseudocyst, pancreatic abscess), organ failure, ≥3 Ranson criteria, APACHE II score ≥ 8
Acute fluid collections	Fluid collection in or near the pancreas, without a defined wall, occurring early in the course of disease
Acute pseudocyst	Fluid collection containing pancreatic secretions, with a defined wall
Pancreatic necrosis	Nonviable pancreatic tissue diagnosed by contrast-enhanced computed tomography
Pancreatic abscess	Collection of purulent material in or near the pancreas

APACHE II, Acute Physiology and Chronic Health Evaluation, version 2.

Presenting Signs and Symptoms

Classic

Acute pancreatitis is manifested as severe, upper abdominal pain that may radiate to the back. The onset of pain is rapid, typically over a period of an hour or less. The pain is constant and is often worsened by lying flat and partially relieved by sitting up. Nausea and vomiting are typically present. Fever and anorexia may or may not be present. Jaundice is rare. Findings on examination vary with the severity of disease. Abdominal examination usually demonstrates a soft, tender epigastrium without peritoneal signs. Guarding or rebound tenderness suggests more severe disease. Distention may be present secondary to concomitant ileus.

Variations

Painless pancreatitis may be encountered in the postoperative period after major surgery or in association with peritoneal dialysis or legionnaires disease. Though rare, ecchymoses in the flanks (Grey Turner sign) or in the periumbilical area (Cullen sign) from intraabdominal hemorrhage suggest severe disease. Diaphragmatic irritation from an inflamed pancreatic tail may produce hiccups and pleural effusions. Patients with necrotizing pancreatitis may arrive at the emergency department (ED) in shock or coma.

Differential Diagnosis

The differential diagnosis for pancreatitis includes peptic ulcer disease with or without perforation, gastritis, biliary colic, acute cholecystitis, aortic dissection, mesenteric ischemia, myocardial infarction, and renal colic.

Diagnosis

Diagnosis of acute pancreatitis requires two of the following three features: (1) characteristic abdominal pain, (2) elevated serum pancreatic enzymes, and (3) characteristic findings on computed tomography (CT).⁷

Diagnostic Testing

Laboratory Tests

No biochemical marker is considered the “gold standard” for diagnosis or assessment of the severity of acute pancreatitis.⁹ Serum amylase and lipase measurements remain important diagnostic tests for acute pancreatitis. Other useful prognostic tests are a complete blood count; measurements of blood urea nitrogen and serum electrolyte, creatinine, glucose, and triglyceride levels; and liver function tests.

Total serum amylase has a reported sensitivity of 83% and specificity of 88% for acute pancreatitis.¹⁰ Amylase levels rise within 6 to 12 hours of onset and usually remain elevated for 3 to 5 days. A normal amylase value would generally exclude the diagnosis of acute pancreatitis except in cases involving hyperlipidemia, acute exacerbations of chronic pancreatitis, or markedly delayed manifestations (in which case amylase levels may have normalized). Acute pancreatitis should not be excluded on the basis of a normal or mildly elevated amylase value when clinical suspicion of this diagnosis is high. Serum amylase values cannot be used to estimate the severity or determine the cause of acute pancreatitis. Nonpancreatic causes of elevated serum amylase levels are listed in Box 43.1.

The serum lipase level is more sensitive (92%) and specific (96%) than total amylase for acute pancreatitis.¹⁰ Lipase has greater sensitivity in patients with acute alcoholic pancreatitis. It is useful in delayed clinical manifestations because the serum lipase value stays elevated longer than the serum amylase value does. However, serum lipase is not as specific for acute pancreatitis as once thought. The value is elevated in as many disorders as the amylase value (Box 43.2). As with serum amylase values, serum lipase values cannot be used to estimate the severity or determine the cause of acute pancreatitis.