Acute Pancreatitis
GENERAL PRINCIPLES
Definition
Acute pancreatitis consists of inflammation of the pancreas and peripancreatic tissue from activation of potent pancreatic enzymes within the pancreas, particularly trypsin.
Etiology
The most common causes are alcohol and gallstone disease, accounting for 75%-80% of all cases. Less common causes include abdominal trauma, hypercalcemia, hypertriglyceridemia, and a variety of drugs. Post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis occurs in 5%-10% of patients undergoing ERCP; prophylaxis with rectal NSAIDs or placement of prophylactic pancreatic duct stents can help prevent post-ERCP pancreatitis.86
DIAGNOSIS
Clinical Presentation
Typical symptoms consist of acute onset of epigastric abdominal pain radiating to the back, nausea, and vomiting often exacerbated by food intake. Systemic manifestations can include fever, shortness of breath, altered mental status, anemia, electrolyte imbalances, and shock.
Diagnostic Testing
LABORATORIES
• Acute pancreatitis is diagnosed in the presence of two of the following three findings: (1) characteristic upper abdominal pain radiating to the back; (2) serum lipase or amylase greater than 3x the upper limit of normal; or (3) characteristic imaging findings. Serum lipase is more specific and sensitive than serum amylase, although both are usually elevated beyond 3? the upper limits of normal. These values do not correlate with severity or outcome of pancreatitis. Patients with renal insufficiency may have elevated enzymes at baseline from impaired clearance.87 There is no utility in tracking serum levels over time.
• Hepatic function testing may identify biliary obstruction as a possible etiology, and a lipid panel may suggest hypertriglyceridemia as the cause of acute pancreatitis.
IMAGING
• Dual-phase (pancreas protocol) CT scan is useful in the initial evaluation of severe acute pancreatitis but should be reserved for patients in whom the diagnosis is unclear, who fail to improve clinically within 48-72 hours, or in whom complications are suspected.88 CT scan early in presentation may underestimate the severity of acute pancreatitis.
• MRI with gadolinium can also be used with at least similar efficacy, especially when CT is contraindicated. Magnetic resonance cholangiopancreatography (MRCP) is useful to detect a biliary source for pancreatitis before ERCP is performed.88
TREATMENT
• Aggressive goal-directed volume repletion with IV fluids must be undertaken, with careful monitoring of fluid balance, urine output, serum electrolytes (including calcium and glucose), and awareness of the potential for significant fluid sequestration within the abdomen. Intensive care unit monitoring may be necessary. The use of Ringer's lactate at a dose of 20 mL/kg bolus followed by 3 mL/kg/h has shown improved outcomes within 36 hours.89 Ringer's lactate may be the preferred fluid, as it improved inflammatory markers compared to normal saline; however, no difference in outcomes has been demonstrated. Fluid status should be reassessed frequently, as overresuscitation may lead to poor outcomes.89
• Early enteral nutrition may improve clinical outcomes. In general, patients should be allowed to eat within 24 hours. If they are unable to meet their nutritional needs by 72 hours, an NG or nasoenteric feeding tube can be placed. A clinical trial showed no benefit to early (within 24 hours) tube feeding compared to on demand feeding.90
Medications
• Narcotic analgesics are usually necessary for pain relief.
• Routine use of antibiotics is not recommended in the absence of documented infection.88
Other Nonoperative Therapies
Urgent ERCP and biliary sphincterotomy within 72 hours of presentation can improve the outcome of severe gallstone pancreatitis in the presence of cholangitis.88 There is no benefit to urgent ERCP in the absence of cholangitis.91
Surgical Management
Cholecystectomy is recommended during the index hospitalization in acute gallstone pancreatitis.88
Complications
• Necrotizing pancreatitis represents a severe form of acute pancreatitis, usually identified on dynamic dual-phase CT with IV contrast.
Increasing abdominal pain, fever, marked leukocytosis, and bacteremia suggest infected pancreatic necrosis that requires broad-spectrum antibiotics and drainage. CT-guided percutaneous aspiration for Gram stain and culture can confirm the diagnosis of infected necrosis. Carbapenems or a combination of a fluoroquinolone and metronidazole has good penetration into necrotic tissue.• The presence of pseudocysts is suggested by persistent pain or high amylase levels. Complications include infection, hemorrhage, rupture (pancreatic ascites), and obstruction of adjacent structures. Asymptomatic pseudocysts can be followed clinically with serial imaging studies to resolution. Decompression of symptomatic or infected pseudocysts can be performed by percutaneous, endoscopic, or surgical techniques. Noninvasive approaches should be used before surgery.92
• Infection: Potential sources of fever include pancreatic necrosis, abscess, infected pseudocysts, cholangitis, and aspiration pneumonia. Cultures should be obtained, and broad-spectrum antimicrobials appropriate for bowel flora should only be used when there is a high clinical suspicion for infection.
• Pulmonary complications: Atelectasis, pleural effusion, pneumonia, and acute respiratory distress syndrome can develop in severely ill patients (see Chapter 10, Pulmonary Diseases).
• Renal failure can result from intravascular volume depletion or acute tubular necrosis.
• GI bleeding can result from stress gastritis, pseudoaneurysm rupture, or gastric varices from splenic vein thrombosis.
• Other complications: Metabolic complications include hypocalcemia, hypomagnesemia, and hyperglycemia.