Pancreatitis, inflammation of the pancreas, occurs in acute and chronic forms and may be due to edema, necrosis, or hemorrhage. In men, this disease is commonly associated with alcoholism, trauma, or peptic ulcer and carries a poor prognosis. In women, it's associated with biliary tract disease and has a good prognosis. Mortality in pancreatitis with necrosis and hemorrhage is as high as 60%.
· Biliary tract disease
· Abnormal organ structure
· Metabolic or endocrine disorders, such as high cholesterol levels or overactive thyroid
· Pancreatic cysts or tumors
· Penetrating peptic ulcers
· Blunt trauma, surgical trauma
· Drugs, such as glucocorticoids, sulfonamides, thiazides, hormonal contraceptives, nonsteroidal anti-inflammatory drugs
· Kidney failure or transplantation
· Endoscopic examination of bile ducts and pancreas
Acute pancreatitis occurs in two forms: edematous (interstitial) and necrotizing. Edematous pancreatitis causes fluid accumulation and swelling. Necrotizing pancreatitis causes cell death and tissue damage. In both types, inappropriate activation of enzymes causes tissue damage.
Normally, the acini in the pancreas secrete enzymes in an inactive form. Two theories suggest why enzymes become prematurely activated:
· A toxic agent such as alcohol may alter the way the pancreas secretes enzymes. Alcohol probably increases pancreatic secretion, alters the metabolism of the acinar cells, and encourages duct obstruction by causing pancreatic secretory proteins to precipitate.
· Autodigestion may occur when duodenal contents containing activated enzymes reflux into the pancreatic duct, activating other enzymes and setting up a cycle of more pancreatic damage.
In chronic pancreatitis, persistent inflammation produces irreversible changes in the structure and function of the pancreas. It sometimes follows an episode of acute pancreatitis. Protein precipitates block the pancreatic duct and eventually harden or calcify. Structural changes lead to fibrosis and atrophy of the glands. Growths called pseudocysts contain pancreatic enzymes and tissue debris. An abscess results if pseudocysts become infected.
If pancreatitis damages the islets of Langerhans, diabetes mellitus may result. Sudden severe pancreatitis causes massive hemorrhage and total destruction of the pancreas, manifested as diabetic acidosis, shock, or coma.
Signs and symptoms
· Epigastric pain
· Mottled skin
· Low-grade fever
· Cold, sweaty extremities
· Left pleural effusion
· Basilar crackles
· Abdominal distension
· Weight loss
· Dyspnea, orthopnea
· Cullen's sign
· Turner's sign
· In a severe attack: persistent vomiting, abdominal distention, diminished bowel activity, crackles at lung bases, left pleural effusion
· Extreme malaise (in chronic pancreatitis)
Diagnostic test results
· Serum amylase and lipase levels are elevated.
· Blood and urine glucose tests reveal transient glucose in urine and hyperglycemia. In chronic pancreatitis, serum glucose levels may be transiently elevated.
· White blood cell count is elevated.
· Serum bilirubin levels are elevated in both acute and chronic pancreatitis.
· Blood calcium levels may be decreased.
· Stool analysis shows elevated lipid and trypsin levels in chronic pancreatitis.
· Abdominal and chest X-rays detect pleural effusions and differentiate pancreatitis from diseases that cause similar symptoms; may detect pancreatic calculi.
· Computed tomography scan and ultrasonography show enlarged pancreas with cysts and pseudocysts.
· Endoscopic retrograde cholangiopancreatography identifies ductal system abnormalities, such as calcification or strictures; helps differentiate pancreatitis from other disorders such as pancreatic cancer.
· Nothing by mouth; I.V. fluids, protein, and electrolytes
· Blood transfusions
· Nasogastric suctioning
· Pain medication such as I.V. morphine
· Antacids, histamine antagonists
· Surgical drainage
· Supplemental oxygen, mechanical ventilation
· Laparotomy if biliary tract obstruction causes acute pancreatitis