MANAGEMENT OF MILD AND SEVERE ALCOHOLIC PANCREATITIS

The mechanism by which the heavy consumption of ethanol leads to attacks of pancreatitis is not clear. The administration of ethanol t o human subjects and experimental animals has been reported to produce the following physiologic, biochemical, and ultrastructural changes in the pancreas: (a) substantial inhibition of volume, concentration, and output of bicarbonate, lipase, and chymotrypsin; (b) a concomitant direct effect on the sphincter of Oddi that would increase sphincteric resistance with resultant increase in intrapancreatic ductal pressure; (c) ductal metaplasia; (d) decreased protein synthesis; (e) inhibition of uptake of 32P into pancreatic phospholipids; (f) increased cellular autophagia; (9) accumulation of lipid droplets in acinar cells; (h) cytoplasmic degradation of acinar, centroacinar, and duct cells; (i) mitochrondrial swelling and reduction of their inner membranes; 6 ) impairment of Na+-dependent uptake of lysine, proline, and methionine by pancreatic slices from alcohol-treated mice in virro; and (k) precipitation of protein plugs in the pancreatic duct system.’-3 In spite of these observations, many of them made in experimental animals, the mode of production of alcoholic pancreatitis is still debatable and requires further investigation. Classically, alcohol-induced pancreatitis has been classified pathologically as interstitial (edematous) and hemorrhagic. Clinically, it may be classified as acute, or acute recurrent and chronic, o r chronic recurrent with a varying spectrum of severity from mild to very severe. In general, mild pancreatitis is characterized by nausea, vomiting, abdominal pain, frequently gradual in onset and mild to moderate in severity, low-grade fever, and tachycardia. The majority of the patients are moderately heavy drinkers, and the clue to the alcohol etiology is provided by the characteristic time relationship between a night’s overindulgence and the onset of pain some 24 to 48 hours later.4 On the other hand, severe pancreatitis is a disease of multiple organ involvement. The characteristic findings in the severe form are: (a) presence of incipient or actual shock, (b) depressed serum calcium, (c) evidence of respiratory insufficiency, (d) pleural effusion, (e) significant hyperglycemia, (f) marked hemoconcentration, and (g) failure to respond to initial treatment.