Acute Pancreatitis
Jennifer K. Plichta
Fred A. Luchette
I. DEFINITIONS
A. Clinically acute pancreatitis: Rapid onset of pain associated with alterations in exocrine function and inflammatory changes of the pancreas on imaging studies.
B. Clinically chronic pancreatitis: Repeated episodes of pain associated with diminished exocrine function.
C. Functionally acute pancreatitis: The pancreas was and will be functionally normal before and after the attack.
D. Functionally chronic pancreatitis: The pancreas was functionally abnormal before the attack and may remain abnormal after the attack.
E. Pathologically acute pancreatitis.
1. Mild: predominant tissue changes are inflammatory, with interstitial edema, intrapancreatic or peripancreatic disruption, and associated fat stranding.
2. Severe: predominant tissue changes are necrotic, associated with focal or diffuse acinar cell necrosis, thrombosis of intrapancreatic vessels, intra-parenchymal hemorrhage, and areas of liquefaction.
F. Pathologically chronic pancreatitis: associated with scarring, fibrosis, calcification, and atrophy of acinar tissue.
II. ETIOLOGY
A. Chronic alcohol use.
1. Associated with a mean ethanol consumption of 150 to 175 g/day for 18 years for men and 11 years for women before the first attack.
2. Mechanism for resulting acute or chronic pancreatitis is not clear, although likely multifactorial.
B. Gallstone disease.
1. Along with chronic alcohol use, it accounts for 60% to 80% of patients with acute pancreatitis.
2. Three theories of gallstone pancreatitis:
a. “Common channel”—stones lodge at the ampulla of Vater with a common biliopancreatic channel proximal to the stone-induced obstruction resulting in bile refluxing into the pancreatic duct, triggering pancreatitis.
b. “Duodenal reflux”—an incompetent sphincter of Oddi due to stone passage permits reflux of duodenal juice containing activated digestive enzymes into the pancreatic duct.
c. “Pancreatic duct obstruction”—the only theory currently supported by clinical models; after duct obstruction, lysosomal hydrolases activate digestive enzymes within pancreatic acinar cells, leading to their injury.
C. Drugs.
1. Most commonly seen in patients with immune system abnormalities.
a. Acquired immunodeficiency syndrome (AIDS) patients receiving dideoxyinosine or pentamidine.
b. Transplant or inflammatory bowel disease (IBD) patients receiving azathioprine or mesalazine.
2. Diuretics (thiazides, ethacrynic acid, and furosemide), sulfonamides, and simvastatin also have an association with pancreatitis.
D. Pancreatic duct obstruction.
1. Tumors: duodenal, ampullary, biliary tract, or pancreatic.
2. Inflammatory lesions: peptic ulcer, duodenal Crohn disease, and periampullary diverticulitis.
3. Developmental abnormalities: pancreas divisum and Sphincter of Oddi dysfunction.
4. Other structural abnormalities: choledochocele, pancreatic cysts or pseudocysts, periampullary diverticula, and ductal strictures.
5. Infections: mumps, coxsackievirus, Mycoplasma pneumoniae, ascariasis, and Clonorchis.
E. Miscellaneous causes of acute pancreatitis.
1. Post-procedural: duct exploration, sphincteroplasty, distal gastrectomy, endoscopic retrograde cholangiopancreatography (ERCP), which has been shown to be decreased by the administration of rectal indomethacin, and procedures associated with hypoperfusion or atheroembolism of the pancreatic circulation.
2. Abdominal trauma.
3. Pregnancy.
4. Hereditary (i.e., mutations in PRSS1, SPINK1, CFTR/cystic fibrosis).
5. Hypercalcemia and hypertriglyceridemia.
6. Idiopathic pancreatitis: affects 5% to 10% of population, and possible etiologies include biliary sludge and autoimmune mechanisms.
III. CLINICAL PRESENTATION
A. Symptoms: epigastric pain of rapid onset, pain radiating to the back (often band-like), nausea, vomiting that may result in Mallory-Weiss syndrome, diarrhea, loss of appetite, and fever/chills.
B. Physical examination.
1. Tachycardia, tachypnea, diaphoresis, hyperthermia, delirium, and jaundice (20% incidence).
2. Abdominal tenderness with voluntary or involuntary guarding, rebound, distension, epigastric mass, and diminished or absent bowel sounds.
3. Hemorrhagic complications can produce flank ecchymoses (Grey-Turner sign) or other evidence of retroperitoneal bleeding (Cullen sign, hemorrhagic discoloration of the umbilicus).
IV. DIAGNOSIS
A. Serum lipase.
1. Increases 4 to 8 hours following the onset of symptoms.
2. Normalizes within 7 to 14 days after the treatment.
3. More sensitive and specific than serum amylase.
B. Serum amylase.
1. May be normal in 10% of patients with lethal pancreatitis.
2. Levels increase 2 to 12 hours after attack onset and normalize within 3 to 6 days.
3. May be elevated due to other processes: acute cholecystitis, perforated gastric or duodenal ulcers, bowel obstruction, or salivary gland disease.
C. Routine blood tests.
1. Increased hemoglobin, hematocrit (HCT), blood urea nitrogen (BUN), creatinine, bilirubin, white blood cells (WBCs), glucose, and triglycerides.
2. Decreased calcium, albumin.
3. Severe cases may result in thrombocytopenia, decreased fibrinogen levels, prolonged prothrombin time, and partial thromboplastin time.
4. Other laboratory tests to consider: liver function tests and arterial blood gas analysis.
D. Routine radiography.
1. Chest radiograph: left pleural effusion, basal atelectasis.
