Pancreatitis, acute clinical presentation

Differentiating an episode of acute pancreatitis from chronic pancreatitis maybe difficult because the clinical presentations can be similar. The diagnosis of chronic pancreatitis is made by looking for the effects of chronic pancreatic inflammation and scarring on the pancreas and the patient as a whole. Computed tomography or ERCP will allow visualization of chronic calcified lesions in the pancreas when present.37... 

Amylase enters the blood largely via the lymphatics. An increase in hydrostatic pressure in the pancreatic ducts leads to a fairly prompt rise in the amylase concentration of the blood. Neither an increase in volume flow of pancreatic juice nor stimulation of pancreatic enzyme production will cause an increase in senm enzyme concentration. Elevation of intraductal pressure is the important determinant. Stimulation of flow in the face of obstruction can, however, augment the entry of amylase into the blood, as can disruption of acinar cells and ducts. A functional pancreas must be present for the serum amylase to rise. Serum amylase determination is indicated in acute pancreatitis in patients with acute abdominal pain where the clinical findings are not typical of other diseases such as appendicitis, cholecystitis, peptic ulcer, vascular disease or intestinal obstruction. In acute pancreatitis, the serum amylase starts to rise within a few hours simultaneously with the onset of symptoms and remains elevated for 2 to 3 days after which it returns to normal. The peak level is reached within 24 hours. Absence of increase in serum amylase in first 24 hours after the onset of symptoms is evidence against a diagnosis of acute pancreatitis (76). 

Patients with alcoholic CP usually present with an initial acute attack followed by successive attacks that are slower to resolve. Continued alcohol use leads to chronic abdominal pain and progressive exocrine and endocrine insufficiency. In about 50% of patients, the pain diminishes 5 to 10 years after the onset of symptoms. Steatorrhea, calcification, and diabetes usually develop after 10 to 20 years of heavy ethanol ingestion. Most patients present with varying degrees of pain, malnutrition, and glucose intolerance. The mortality rate of CP is approximately 50% within 20 to 25 years of the diagnosis. About 15% to 20% actually die of complications associated with acute attacks. Most deaths occur as a consequence of malnutrition, infection, or ethanol, narcotic, and tobacco nse. The clinical course of idiopathic CP is more favorable than that of alcoholic pancreatitis. ... 

Frohne et al. (1984) described the clinical course of a man who presented with severe gastroenteritis after ingesting a powder made from jequirity beans. He developed acute pancreatitis, leucocytosis, bloody ascites, increased serum amylase and lipase activities, hypocalcaemia and diabetes mellitus. Moreover, in addition to delirium, hallucinations, reduced consciousness and generalized seizures, he also developed a hemi-paresis. Respiratory depression necessitated ventilation for 10 days but all symptoms improved gradually over the following three weeks. Neurological recovery was complete. 

Once the presence of fasting lipemia has been established, di-ffereyitiation between primary and secondary hyperlipemias can usually be made on the basis of presence or absence of clinical and laboratory findings characteristic of an underlying disease. Plasma lipid and lipoprotein patterns as determined by lipid analyses, ultracentrifugation and electrophoresis are not necessarily diagnostic since similar findings are present in EHL and hyperlipemia of diabetic ketoacidosis, acute pancreatitis, alcoholism, etc. (Schettler 1955, Lees and Fredrickson 1964, Jahnke 1965). 

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