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Complications and Comorbidities> Gastrointestinal>
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Pancreatitis

Reza Alavi, M.D. and Jeanne Clark, M.D.
02-10-2010

DEFINITION

  • Refers to inflammation of the pancreas.
  • Common etiologies of acute pancreatitis include: gallstones, alcohol, hypercalcemia, drugs, infections, trauma.

EPIDEMIOLOGY

  • The annual incidence of acute pancreatitis ranges from 4.9 to 35 per 100,000 population. People with type 2 diabetes have almost a three-fold greater risk of acute pancreatitis compared to those without diabetes (Vege).
  • Drug- induced pancreatitis is generally extremely uncommon with diabetes medications (Balani).
  • Extreme hypertriglyceridemia, >1000 mg/dl (chylomicronemia),can cause chronic pancreatitis.
  • Other etiologies include cystic fibrosis, autoimmune disorders, pancreatic anomalies (e.g. pancreas divisum).
  • During acute pancreatitis, one-half of patients have glucose intolerance, but few require insulin administration (Gorelick).
  • In chronic pancreatitis, up to one-half have reported overt diabetes (Wakasugi), up to an incidence of 70% when pancreatic calcification is present (Gorelick).
  • Overall, mortality in hospitalized patients with acute pancreatitis is ~ 10 % (range 2 - 22%). Mortality rates unaffected by diabetes status (Cavallini). 

DIAGNOSIS

  • Serum amylase rises within 6 - 12 hours of onset, usually to >3 times the upper limit of normal (more sensitive test).
  • Serum lipase is a more specific test.
  • Serial measurements do NOT predict prognosis or alter management.
  • White blood cell count is usually elevated even in the absence of infection.
  • Always check serum electrolytes, especially calcium.
  • Consider toxicology screen, lipid profile, blood cultures to evaluate for secondary etiologies.
  • Pancreas-dedicated CT scan with oral and iv contrast is the most important imaging test, looking for pancreatic necrosis.
  • Abdominal plain films help to exclude other causes of abdominal pain such as obstruction and bowel perforation.
  • Abdominal ultrasound can show a diffusely enlarged, hypoechoic pancreas and can also detect gallstones in the gallbladder.

SIGNS AND SYMPTOMS

  • Upper abdominal pain
  • Nausea and vomiting
  • Fever and tachycardia
  • Abdominal distention, epigastric tenderness  and guarding
  • Shallow respirations due to diaphragmatic irritation
  • Vasodilatory shock in severe acute pancreatitis without sepsis

CLINICAL TREATMENT

  • ICU monitoring for severe pancreatitis including pancreatic necrosis, organ failure, or pleural effusion at admission; high severity of disease score (i.e. APACHE-II).
  • Fluid resuscitation with 250-300cc/hr of isotonic saline for 24-48 hours if the cardiac status permits (Tenner)
  • Correction of electrolyte and metabolic abnormalities. 
  • Supplemental oxygen to keep pulse oxygen levels above 95%
  • Pain management: Meperidine usually favored over morphine because morphine increases  sphincter of Oddi pressure, but no clinical evidence that morphine actually aggravates or causes pancreatitis or cholecystitis.
  • Nutritional support if likely to remain fasting for >7 days. Nasojejunal tube feeding (using an elemental or semi-elemental formula) is preferred to parenteral nutrition.
  • Prophylactic antibiotics to prevent pancreatic infection is NOT routinely recommended (Banks), although imipenem/meropenem may help if >30 percent pancreatic necrosis. (Villatoro)
  • ERCP indicated for the clearance of bile duct stones in severe pancreatitis or cholangitis, if poor candidate for cholecystectomy, or post-cholecystectomy in those with persistent biliary obstruction.
  • Surgical treatment may be required in patients with intractable pain from chronic pancreatitis.

FOLLOW UP

  • After necrotizing pancreatitis, high prevalence of IGT due to both loss of beta-cell function and insulin resistance.
  • Perform cholecystectomy after recovery in patients with gallstone pancreatitis, within 7 days after recovery in mild pancreatitis, and 3-4 weeks after in severe necrotizing pancreatitis.
  • Exocrine pancreatic insufficiency can be common in chronic pancreatitis and both type 1 and type 2 diabetes.
  • Exocrine pancreatic insufficiency is treated with low-fat diet and administration of exogenous pancreatic enzymes.

EXPERT COMMENTS

  • Glucose intolerance occurs frequently in chronic pancreatitis, but overt diabetes usually occurs late in the course of disease.
  • Diabetes is more common with chronic calcifying disease, particularly early calcifications.
  • Diabetes in patients with chronic pancreatitis usually requires insulin treatment, and has increased risk of hypoglycemia (presumably both alpha and beta cell damage).
  • Although preliminary reports suggesting exenatide, sitagliptin, and sitagliptin/metformin increase the risk of drug-induced pancreatitis, the data are inconclusive at this point (Drucker).

REFERENCES

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