Besides producing insulin, the pancreas secretes digestive enzymes. The enzymes don’t become active until leaving the organ however during pancreatitis inflammation delays release of activated enzymes allowing them to attack pancreatic cells and leak into surrounding tissues. The resulting damage occurs in stages. The stages are less severe and self limiting in mild pancreatitis. Gallstones & chronic alcohol abuse account for 80 to 90% of acute pancreatitis cases also known as interstitial or edematous pancreatitis. Triggers also include drugs such as ACE inhibitors, estrogen, furosemide, procainamide, sulfonamides, tetracycline, thiazide diuretics and salicylates. Other triggers are hypercalcemia, infections, IBD, peptic ulcer disorder and trauma to name a few.
The most common symptom is a sudden onset of sharp, twisting, deep, upper abdominal pain which frequently radiates to the back accompanied by nausea & vomiting. Hypoactive bowel sounds, upper abdominal tenderness, distension and diarrhea are other signs. Serum amylase will be very elevated as well as lipase, AST, BUN, C-reactive protein, direct bilirubin, hematocrit, and WBC count. Patients may undergo an abdominal ULS or CT scan, or endoscopic retrograde cholangiopancreatography.
Treatment includes fluid management, opioid pain management, and reducing stimulation of pancreatic secretions which means no eating and taking proton pump inhibitors. Treatment for mild pancreatitis takes 3 to 7 days and if severe up to 7 weeks. The latter requires nutritional support usually via a feeding tube. There are a host of complications to be alert for if the patient has severe acute pancreatitis.
To read more see January Nursing 2010.