Chronic pancreatitis

Pathophysiology/epidemiology

The symptoms of pancreatitis can be associated with pancreatic cell death and/or with ductal fibrosis and calcification and are generally grouped into acute (isolated episodes with serum amylase and lipase elevations) and chronic (identical symptoms that may lack measurable laboratory abnormalities) forms [37-39]. Whereas acute pancreatitis generally resolves without permanent structural abnormalities, most forms of chronic pancreatitis are associated with permanent abnormalities. Acute-on-chronic episodes may occur in a patient with known chronic changes that become coupled to an acute necrotic episode. Alcohol abuse is the primary etiology in 70-80% of cases of chronic pancreatitis in nontropical regions. Only 5-10% of heavy drinkers develop symptomatic chronic pancreatitis, implying that other etiologic factors (e.g. genetic, infectious, nutritional) also contribute to its development. Other potential causes include a pancreas divisum, genetic causes (hereditary type), previous trauma, previous obstructive episodes, hyperparathyroidism, hyper-lipidemia, and ^-antitrypsin deficiency. Like many chronic pain disorders, the magnitude of identifiable pathology does not correlate with reports of pain.

Experimentally, chronic pancreatitis may be induced in animals by the administration of toxins, but attempts to form epidemiologic links in humans to specific toxins, other than alcohol and cigarette smoking [38], have not been successful. However, diets with too much or too little fat and/or protein have also been implicated. In fact, it has been proposed that increases in oxidative stress underlie the patho-physiology of chronic pancreatitis. In this scenario, there would exist periodic bursts of free radical formation producing subsequent injury. A co-morbidity of chronic pancreatitis is cirrhosis of the liver which complements the "cirrhosis" of the pancreas.

Pancreatic fluids have been noted to have altered protein content and to form "sludge" or intraductal "plugs" that calcify into stones with secondary inflammatory and fibrotic reactions. A common consequence of stone formation/fibrosis is intraductal hypertension, which may contribute to the continuous pain that develops in some chronic pancreatitis patients. Unfortunately, relief of ductal obstruction does not invariably result in pain relief.

Evaluation/treatment

The pain of chronic pancreatitis is pain that is typically described as deep, boring and epigastric in location with radiation through to the back. The pain may be episodic in nature but may advance until it is continuous. Exacerbations of pain may be produced by eating, particularly fatty foods. Sitting upright or leaning forward may decrease the pain. It is normally coupled with nausea and vomiting, so dehydration and malnutrition may be the formal indications for medical intervention. It may be possible to palpate an inflammatory mass on physical exam, but abdominal guarding usually precludes such findings. Subjects with alcoholic chronic pancreatitis often have stigmata associated with extensive alcohol use and associated liver failure.

In advanced disease, laboratory tests of pancreatic insufficiency (e.g. steatorrhea) or islet cell loss (e.g. glucose intolerance) may manifest. Elevated serum amy-lase and lipase levels change unreliably in chronic stages of the disease. Diagnostic imaging (radiographs, ultrasound, computed tomography) demonstrating diffuse intraductal calcium deposition will support the diagnosis in 30-90% of cases, depending upon the modality employed. ERCP (endoscopic retrograde cholangiopan-creatography) is the "gold standard" for chronic pancreatitis. Stratification into severity of disease is based on a grading of ductal abnormalities. An incidental finding that is not uncommon during surgical treatment of chronic pancreatitis is evidence of pancreatic cancer.

Some practice guidelines do exist for the treatment of pain due to chronic pancreatitis [39]. Unfortunately, most published treatment options are only validated mainly by case reports and retrospective series. Few studies of chronic pancreatitis pain have employed rigorously controlled methodologies and even fewer have demonstrated robust effects of the studied treatment. A list of potential treatment options is given in Box 15.3. Based on epidemiologic data, abstinence from alcohol is an absolute behavioral alteration that must occur when the etiology of the pancreatitis is alcohol related. An individual who continues to abuse

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