PANCREATITIS

Etiologies

Acute pancreatitis refers to inflammation of the pancreas.† This results clinically in severe epigastric pain that often radiates to the back and elevated pancreatic enzymes.† There is often an associated ileus (sentinel ileus) noted on abdominal radiography.† Severe disease may have associated pancreatic fat necrosis and parenchymal hemorrhage.† There are many potential etiologies, the most common being gallstone pancreatitis, alcohol induced, and hypertriglyceridemia. Other etiologies include but are not limited to post ERCP, traumatic pancreatitis and idiopathic pancreatitis.† Most patients require only supportive care and correction of the underlying etiology; however, some patients suffer grave complications.† Cullenís sign refers to periumbilical ecchymosis and is often associated with hemorrhagic pancreatitis, however, this sign may also be seen with ruptured ectopic pregnancy, ruptured aortic aneurysm, ruptured spleen, ruptured common bile duct, perforated duodenal ulcer, hepatocellular carcinoma, hepatic lymphoma, metastatic thyroid cancer, and percutaneous liver biopsy.

†The diagnosis of pancreatitis is established by finding an elevation in the urine or plasma amylase or the plasma lipase in patients who present with typical symptoms.† The serum amylase returns to normal levels within 5 to 10 days.† The serum amylase is not specific being elevated with multiple other conditions to include common bile duct obstruction, mesenteric ischemia, intestinal perforation, parotitis, ruptured ectopic pregnancies, and renal failure.† Lipase is more specific for pancreatitis; however, it may be elevated with underlying intestinal ischemia or perforation.† If the diagnosis is still in question after serologic or urinary testing, then contrast-enhanced abdominal CT scanning should be performed.† If the CT scan is normal, then the diagnosis of pancreatitis is unlikely as even mild disease will cause radiographic abnormalities.

††Once the diagnosis is established, the next step is to determine the etiology.† Gallstone pancreatitis is the most likely etiology if there is sonographic evidence of gallstones.† Gallstone pancreatitis is also the most likely etiology if the AST or ALT levels are more than three times the normal value or if there is associated hyperbilirubinemia even in the absence of sonographic evidence of gallstones as the stones may have already passed through the bile duct.† An alcohol level and serum triglyceride level should be determined when the etiology is not secondary to gallstone disease. Common bile duct stones may develop years after a cholecystectomy and may cause pancreatitis.

†Most cases resolve without complication and require only conservative treatment with aggressive intravenous fluids, pain control and keeping the patient from eating.† However, acute episodes may be complicated by multiorgan failure (especially pulmonary failure) infection/sepsis, and necrosis.† During the first week of illness, pulmonary failure and shock are the most dreaded complication.† All patients should be monitored for signs of tachypnea (if present monitor for hypoxia with ABG testing), hypotension and oliguria, and if present, transfer to an intensive care unit and aggressive treatment for pulmonary failure and shock are indicated.† Associated hematologic abnormalities include leukocytosis (when noted early in the disease course may be an indicator of a more severe form of disease), red cell fragmentation, burr cell formation, increased reticulocyte counts, and rarely TTP or HUS.

†††† Different rating systems have been developed to predict the severity of an acute attack of pancreatitis to include Ranson criteria, Glasgow criteria, BISAP, and the APACHE II scoring system.† After the first week of illness, the most common cause of death is pancreatic sepsis, which is usually secondary to infected necrosis.† The use of prophylactic antibiotics in patients with pancreatitis is controversial.† Choices for prophylactic antibiotic coverage include imipenem (500 mg IV TID for 1-2 weeks) or a combination of ciprofloxacin (400 mg IV Q 12 hours) plus metronidazole (500 mg IV Q 8 hours) for 1 to 2 weeks.† Another controversial issue in the management of pancreatitis is whether patients with gallstone pancreatitis should undergo emergent endoscopic removal of impacted gallstones acutely.

†††† As stated above, most patients improve with only supportive therapy.† Serial labs (amylase or lipase) are not required to monitor the patient.† Resolution of pain is the endpoint at which bowel rest can be discontinued.† The patient should be monitored while a diet is reintroduced, and if there is no further pain, the patient may be discharged.

†††† Patients who do not improve following conservative therapy should undergo dual-phase, contrast-enhanced, pancreatic-protocol CT scanning (the procedure may need to be repeated even if patients who underwent scanning on admission had a normal scan).† If pancreatic necrosis is appreciated (as evidenced by portions of the pancreatic parenchyma not turning opaque during the arterial phase of contrast injection), the next step is to determine if it is sterile or infected.† Fever and leukocytosis are inadequate parameters to establish if the necrotic material is infected.† CT guided fine-needle aspiration (FNA) for culture is required.† If the material is infected, surgical debridement is prudent.† Another option is to monitor the patient in the ICU with the patient on broad-spectrum antibiotics (imipenem-cilastin combination or cirpofloxacin plus metronidazole).† If the patient does not improve after 10 to 14 days, then CT guided FNA for culture and gram staining should be performed.† Again, if there is evidence of infection, surgery is indicated.† If there is no evidence of infection, continued supportive care in the ICU setting with weekly serial FNAs should be considered.† In some cases pseudocysts will be detected on CT scanning.† Many will resolve without treatment within 6 weeks.† Therefore, observation is all that is required in patients with asymptomatic pseudocysts. Early ERCP with sphincterotomy should be considered in severe cases due to ongoing retained biliary stones or if there are indications of retained stones (rising bilirubin and alkaline phosphatase values with a dilated bile duct on ultrasonography). Patients with pancreatitis due to bile stones should have a consultation with a surgeon to arrange an appropriate future date for laparoscopic cholecystectomy.

†††† When mild pancreatitis is secondary to cholelithiasis many physicians request ERCP to reverse the underlying pathology and thus prevent a prolonged hospitalization; however, this is not the most prudent course in all cases.† The majority of gallstones which cause pancreatitis are usually less than 5 mm in diameter and thus generally pass spontaneously.† Therefore, ERCP is unnecessary, adds to the cost of the hospital course, and increases the possibility for complications without adding to the treatment of the underlying disease.† Once these patients stabilize, they can be referred for laparoscopic cholecytectomy with intraoperative cholangiography (IOC).† If IOC detects common bile duct stones (choledocholithiasis), then postoperative ERCP may be performed in order to retract these stones if necessary. 

†††† Chronic pancreatitis refers to the condition which results from chronic pancreatic inflammation with resultant abdominal pain, diarrhea (secondary to steatorrhea), weight loss, and possibly diabetes mellitus.† Potential complications include pseudocyst formation, common bile duct obstruction, duodenal obstruction, pancreatic duct fistula, splenic vein thrombosis, and pancreatic carcinoma.† Chronic alcoholism is a common etiology.† Abdominal radiographs are helpful to establish the diagnosis.† Pancreatic calcifications noted on plain or CT abdominal radiographs establishes the diagnosis in symptomatic patients, but these findings are often lacking.

†††† Therapy for this condition is with exogenous pancreatic enzyme supplementation.† The endpoint of therapy is to reduce the amount of steatorrhea/diarrhea and weight gain.† This may require high doses of enzyme supplementation.† Gastric acid inactivates exogenous lipase; therefore, short-acting formulations should be administered with concomitant acid suppression therapy (H2 blockers or proton pump inhibitors).† Abdominal pain is a common complication and may be managed with analgesics (NSAIDs, acetaminophen, or narcotics).† All patients should be questioned regarding continued alcohol use and counseled to abstain.