Management of Pancreatitis

James M. Richter

The primary physician encounters pancreatitis in three forms that lend themselves to ambulatory management: (a) the recovery phase of acute pancreatitis, (b) chronic or chronic relapsing pancreatitis presenting as recurrent abdominal pain, and (c) pancreatic insufficiency, with steatorrhea and weight loss. The primary physician must be able to distinguish acute pancreatitis from other causes of acute upper abdominal pain (see Chapter 58), distinguish chronic abdominal pain due to pancreatitis from that due to pancreatic carcinoma and other important etiologies (see Chapters 58 and 76), and recognize and manage pancreatic insufficiency and other causes of steatorrhea (see Chapter 64). The objectives of management include relief of pain, removal of precipitants, and assurance of adequate nutrition.

PATHOPHYSIOLOGY, CLINICAL PRESENTATION, AND COURSE (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15 and 16)

Pathophysiology

In the United States, most cases of pancreatitis are a result of excess ethanol ingestion or biliary tract disease, chiefly among middle-aged alcoholic men and elderly women with gallstones, respectively. Autoimmune disease, penetrating duodenal ulcer, trauma, hypercalcemia, hypertriglyceridemia, vascular insufficiency, tumor, heredity, ampullary stenosis, and drugs such as thiazide diuretics, glucocorticosteroids, azathioprine, and sulfasalazine are also associated with pancreatitis. Often, a specific cause of pancreatitis is not found. In patients with AIDS, the risk of acute pancreatitis increases by 35 to 500 times, due in part to some of the drugs used to treat the condition and to increased risk of infection. Mutations in the cystic fibrosis gene are found in persons with chronic pancreatitis, suggesting a genetic predisposition.

The manifestations of acute pancreatic disease are produced by inflammatory breakdown of pancreatic architecture, with release of digestive enzymes into the interstitium of the gland, leading to autolysis. Chronic pancreatitis is characterized by recurrences of acute inflammation and the adverse consequences of destruction, scarring, and distortion of the pancreatic ductal and glandular tissue (e.g., pseudocyst formation and pancreatic insufficiency).

Clinical Presentation and Course

Acute Pancreatitis

Typically, acute pancreatitis produces constant epigastric, periumbilical, or left or right upper abdominal pain radiating to the back, often increased by food and decreased by upright posture. Vomiting can be persistent. Examination reveals abdominal tenderness and may include decreased bowel sounds, distention, and fever. The clinical presentation in HIV-infected patients is similar to that in immunocompetent patients but is often obscured by concurrent illnesses.

The course of acute pancreatitis depends on the severity of the disease and the underlying etiology. Patients with HIV infection or frank AIDS have particularly poor prognoses. In a patient recovering from acute pancreatitis, symptoms, principally pain, are reliable indicators of disease activity. There are grading systems that predict very severe disease but none that predict mild disease appropriate for ambulatory management. Elevated enzymes in an otherwise asymptomatic patient are usually of no significance. The serum amylase routinely falls to normal within several days but may remain elevated for weeks after an uncomplicated illness. In other instances, persistently elevated enzymes in an asymptomatic person may be a clue to the presence of a silent pseudocyst. Pseudocysts most often arise with severe pancreatitis, mostly in those with alcohol-induced disease or AIDS. Spontaneous resolution occurs over 3 months in about 50% of patients; those with persistent lesions greater than 5 cm usually require drainage.

Chronic Pancreatitis

Chronic pancreatitis characteristically presents and proceeds as bouts of mild to severe recurrent epigastric pain, often occurring in alcoholic patients after years of excessive drinking. Sometimes chronic pancreatitis is heralded by a severe attack of acute pancreatitis. At other times, there may be mild pain or simply the painless insidious onset of exocrine insufficiency and diabetes. The pain of chronic pancreatitis is not entirely constant and often varies in intensity over days to weeks. There may be exacerbations of pain, nausea, and vomiting after eating or drinking alcohol.

The clinical course of chronic pancreatitis is variable and depends on elimination of precipitating factors. Gallstones, particularly common bile duct stones, should be promptly removed, either surgically or endoscopically. Successful and early removal greatly reduces the risk of recurrent or chronic pancreatitis. With recurrent disease, pancreatic insufficiency may gradually develop over years, manifested by weight loss and steatorrhea. Although mild glucose intolerance may occur early in the disease process, the onset of clinical diabetes is a late complication and a sign of advanced disease. There appears to be an increased risk of pancreatic cancer.

Pancreatic Insufficiency

Patients with pancreatic exocrine insufficiency complain of weight loss and frequent greasy bowel movements (i.e., steatorrhea). Weight loss is often striking but nonspecific in these
patients, who tend to substitute alcohol for other forms of nourishment. Steatorrhea is a late development, not seen until more than 80% of pancreatic exocrine function has been lost.

DIAGNOSIS (4,11,13,14,16, 17, 18, 19, 20, 21, 22, 23, 24 and 25)

Acute Pancreatitis

The diagnosis of acute pancreatitis is supported by increases in the serum amylase and serum lipase. The serum amylase is elevated principally in pancreatic disease but may also be high in renal insufficiency, salivary gland disease, biliary tract obstruction, aortic dissection, and such other intraabdominal conditions as perforated peptic ulcer, mesenteric infarction, and small-bowel obstruction without detectable pancreatitis. Patients with AIDS may have hyperamylasemia from salivary gland pathology or macroamylasemia. Macroamylasemia is also seen in connective tissue diseases, lymphoma, and liver disease. The serum lipase is more specific but less sensitive and is a good confirmatory test.

Improved rapid screening methods for diagnosis acute pancreatitis continue to be sought. Trypsinogen-2 dipstick testing of the urine is being studied as a means of quickly ruling out acute pancreatitis in the urgent care/emergency room setting. The qualitative version of the test has a sensitivity of 94% and a specificity of 95% for acute pancreatitis. When applied to patients with acute abdominal pain, a negative result effectively rules out acute pancreatitis; a positive result needs confirmation because the test has a 5% false-positive rate.

The serum amylase is the best initial diagnostic study. At times, ultrasonography can be used for diagnostic purposes; it shows edema of the gland and any biliary tract pathology. Contrast-enhanced computed tomography (CT) of the abdomen also can be used to detect such findings and provide an estimate of severity. Intraglandular necrosis, surrounding edema, and fluid collections can also be detected. The test is considered the gold standard for severe cases of acute pancreatitis but is less sensitive for mild disease. Endoscopic ultrasonography and magnetic resonance cholangiopancreatography (MRCP) are emerging technologies for pancreatic and biliary tree imaging. They provide enhanced sensitivity and specificity compared to transabdominal ultrasound for detection of gallstones and pancreatic pathology because they are not affected by overlying bowel gas. Unlike CT, they require no iodinated dye load. They are worth considering in persons who appear to have “idiopathic” disease after standard diagnostic testing and imaging. If a mass is palpable or pain recurs, it should be investigated, starting with ultrasonography or CT scan of the upper abdomen, examining for pseudocyst and other pathology.

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