The pathologic spectrum of acute pancreatitis varies from interstitial pancreatitis, which is usually a mild and self-limited disorder, to necrotizing pancreatitis, in which the degree of pancreatic necrosis correlates with the severity of the attack and its systemic manifestations.
Most common causes in the United States are cholelithiasis and alcohol. Others are listed in Table 162-1.
TABLE 162-1 CAUSES OF ACUTE PANCREATITIS
Can vary from mild abdominal pain to shock. Common symptoms: (1) steady, boring midepigastric pain radiating to the back that is frequently increased in the supine position; (2) nausea, vomiting.
Physical exam: (1) low-grade fever, tachycardia, hypotension; (2) erythematous skin nodules due to subcutaneous fat necrosis; (3) basilar rales, pleural effusion (often on the left); (4) abdominal tenderness and rigidity, diminished bowel sounds, palpable upper abdominal mass; (5) Cullen’s sign: blue discoloration in the periumbilical area due to hemoperitoneum; (6) Turner’s sign: blue-red-purple or green-brown discoloration of the flanks due to tissue catabolism of hemoglobin.
1. Serum amylase: Large elevations (>3 × normal) virtually assure the diagnosis if salivary gland disease and intestinal perforation/infarction are excluded. However, normal serum amylase does not exclude the diagnosis of acute pancreatitis, and the degree of elevation does not predict severity of pancreatitis. Amylase levels typically return to normal in 48–72 h.
2. Urinary amylase–creatinine clearance ratio: no more sensitive or specific than blood amylase levels.
3. Serum lipase level: increases in parallel with amylase level and measurement of both tests increases the diagnostic yield.
4. Other tests: Hypocalcemia occurs in ~25% of pts. Leukocytosis (15,000–20,000/μL) occurs frequently. Hypertriglyceridemia occurs in 15–20% of cases and can cause a spuriously normal serum amylase level. Hyperglycemia is common. Serum bilirubin, alkaline phosphatase, and aspartame aminotransferase can be transiently elevated. Hypoalbuminemia and marked elevations of serum lactic dehydrogenase(LDH) are associated with an increased mortality rate. Hypoxemia is present in 25% of pts. Arterial may spuriously elevate serum amylase.
1. Abdominal radiographs are abnormal in 30–50% of pts but are not specific for pancreatitis. Common findings include total or partial ileus (“sentinel loop”) and the “colon cut-off sign,” which results from isolated distention of the transverse colon. Useful for excluding diagnoses such as intestinal perforation with free air.
2. Ultrasound often fails to visualize the pancreas because of overlying intestinal gas but may detect gallstones, pseudocysts, mass lesions, or edema or enlargement of the pancreas.
3. CT can confirm the clinical impression of acute pancreatitis. It can also be helpful in indicating the severity of acute pancreatitis via the CT severity index (CTSI—see Table 313-3, p. 2637, HPIM-18), assessing the risk of morbidity and mortality and in evaluating the complications of acute pancreatitis.
Intestinal perforation (especially peptic ulcer), cholecystitis, acute intestinal obstruction, mesenteric ischemia, renal colic, myocardial ischemia, aortic dissection, connective tissue disorders, pneumonia, and diabetic ketoacidosis.
TREATMENT Acute Pancreatitis
Most (90%) cases subside over a period of 3–7 days. Conventional measures: (1) analgesics, such as meperidine; (2) IV fluids and colloids; (3) no oral alimentation. The benefit of antibiotic prophylaxis in necrotizing acute pancreatitis remains controversial. Current recommendation is use of an antibiotic such as imipenem-cilastatin, 500 mg tid for 2 weeks. Not effective: cimetidine (or related agents), H2blockers, protease inhibitors, glucocorticoids, nasogastric suction, glucagon, peritoneal lavage, and anticholinergic medications. Precipitating factors (alcohol, medications) must be eliminated. In mild or moderate pancreatitis, a clear liquid diet can usually be started after 3–6 days. pts with severe gallstone-induced pancreatitis often benefit from early (<3 days) papillotomy.
It is important to identify pts who are at risk of poor outcome. Risk factors and markers of severe acute pancreatitis are listed in Table 162-2. Fulminant pancreatitis requires aggressive fluid support and meticulous management. Mortality is largely due to infection.
TABLE 162-2 SEVERE ACUTE PANCREATITIS
Shock, GI bleeding, common duct obstruction, ileus, splenic infarction or rupture, disseminated intravascular coagulation, subcutaneous fat necrosis, acute respiratory distress syndrome, pleural effusion, acute renal failure, sudden blindness.
1. Sterile or infected pancreatic necrosis—necrosis may become secondarily infected in 40–60% of pts, typically within 1–2 weeks after the onset of pancreatitis. Most frequent organisms: gram-negative bacteria of alimentary origin, but intraabdominal Candida infection increasing in frequency. Necrosis can be visualized by contrast-enhanced dynamic CT, with infection diagnosed by CT-guided needle aspiration. Laparotomy with removal of necrotic material and adequate drainage should be considered for pts with sterile acute necrotic pancreatitis, if pt continues to deteriorate despite conventional therapy. Infected pancreatic necrosis requires aggressive surgical debridement and antibiotics.
2. Pancreatic pseudocysts develop over 1–4 weeks in 15% of pts. Abdominal pain is the usual complaint, and a tender upper abdominal mass may be present. Can be detected by abdominal ultrasound or CT. In pts who are stable and uncomplicated, treatment is supportive; pseudocysts that are >5 cm in diameter and persist for >6 weeks should be considered for drainage. In pts with an expanding pseudocyst or one complicated by hemorrhage, rupture, or abscess, surgery should be performed.
3. Pancreatic abscess—ill-defined liquid collection of pus that evolves over 4–6 weeks. Can be treated surgically or in selected cases by percutaneous drainage.
4. Pancreatic ascites and pleural effusions are usually due to disruption of the main pancreatic duct. Treatment involves nasogastric suction and parenteral alimentation for 2–3 weeks. If medical management fails, pancreatography followed by surgery should be performed.
Chronic pancreatitis may occur as recurrent episodes of acute inflammation superimposed upon a previously injured pancreas or as chronic damage with pain and malabsorption.
Chronic alcoholism is most frequent cause of pancreatic exocrine insufficiency in U.S. adults; in 25% of adults, etiology is unknown. Other causes are listed in Table 162-3.
TABLE 162-3 CHRONIC PANCREATITIS AND PANCREATIC EXOCRINE INSUFFICIENCY: TIGAR-O CLASSIFICATION SYSTEM
SYMPTOMS AND SIGNS
Pain is cardinal symptom. Weight loss, steatorrhea, and other signs and symptoms of malabsorption common. Physical exam often unremarkable.
No specific laboratory test for chronic pancreatitis. Serum amylase and lipase levels are often normal. Serum bilirubin and alkaline phosphatase may be elevated. Steatorrhea (fecal fat concentration ≥9.5%) late in the course. The bentiromide test, a simple, effective test of pancreatic exocrine function, may be helpful. D-Xylose urinary excretion test is usually normal. Impaired glucose tolerance is present in >50% of pts. Secretin stimulation test is a relatively sensitive test for pancreatic exocrine deficiency.
Plain films of the abdomen reveal pancreatic calcifications in 30–60%. Ultrasound and CT scans may show dilation of the pancreatic duct. ERCP and endoscopic ultrasound (EUS) provide information about the main pancreatic and smaller ducts.
Important to distinguish from pancreatic carcinoma; may require radio-graphically guided biopsy.
TREATMENT Chronic Pancreatitis
Aimed at controlling pain and malabsorption. Intermittent attacks treated like acute pancreatitis. Alcohol and large, fatty meals must be avoided. Narcotics for severe pain, but subsequent addiction is common. pts unable to maintain adequate hydration should be hospitalized, while those with milder symptoms can be managed on an ambulatory basis. Surgery may control pain if there is a ductal stricture. Subtotal pancreatectomy may also control pain but at the cost of exocrine insufficiency and diabetes. Malabsorption is managed with a low-fat diet and pancreatic enzyme replacement. Because pancreatic enzymes are inactivated by acid, agents that reduce acid production (e.g., omeprazole or sodium bicarbonate) may improve their efficacy (but should not be given with enteric-coated preparations). Insulin may be necessary to control serum glucose.
Vitamin B12 malabsorption in 40% of alcohol-induced and all cystic fibrosis cases. Impaired glucose tolerance. Nondiabetic retinopathy due to vitamin A and/or zinc deficiency. GI bleeding, icterus, effusions, subcutaneous fat necrosis, and bone pain occasionally occur. Increased risk for pancreatic carcinoma. Narcotic addiction common.
For a more detailed discussion, see Greenberger NJ, Conwell DL, Banks PA: Approach to the Patient With Pancreatic Disease, Chap. 312, p. 2629; Greenberger NJ, Conwell DL, Wu BU, Banks PA: Acute and Chronic Pancreatitis, Chap. 313, p. 2634, in HPIM-18.