Inflammation of the pancreas, or pancreatitis, occurs in acute and chronic forms. It's associated with biliary tract disease, alcoholism, trauma, and certain drugs, and it can be idiopathic. Acute pancreatitis generally resolves clinically and histologically but is serious in nature and has a 10% mortality. Chronic pancreatitis causes irreversible tissue damage and tends to progress to significant loss of pancreatic function.
There are many causes of acute pancreatitis but excess alcohol is one of the most common. This is why doctors use the phrase, 'get smashed' to try and remember them all. The different causes of acute pancreatitis are:
Signs and Symptoms
Commonly, the patient describes intense epigastric pain centered close to the umbilicus and radiating to the back, between the 10th thoracic and 6th lumbar vertebrae. He typically reports that eating fatty foods, consuming alcohol, or lying in a recumbent position aggravates this pain. He may also complain of weight loss with nausea and vomiting.
Investigation may uncover predisposing factors, such as alcoholism, biliary tract disease, and pancreatic disease. Other medical problems, such as peptic ulcer disease and hyperlipidemia, may be discovered.
Assessment of vital signs may reveal decreased blood pressure, tachycardia, and fever. These signs, if present, indicate respiratory complications. Other signs of respiratory complications are dyspnea and orthopnea. Observe the patient for changes in behavior and sensorium; these signs may be related to alcohol withdrawal or may indicate hypoxia or impending shock.
Abdominal inspection may disclose generalized jaundice, Cullen's sign (bluish periumbilical discoloration) and Turner's sign (bluish flank discoloration). Inspection of stools may reveal steatorrhea, a sign of chronic pancreatitis.
During abdominal palpation, you may note tenderness, rigidity, and guarding. If you hear a dull sound while percussing, suspect pancreatic ascites. If bowel sounds are absent or decreased on abdominal ausculation, suspect paralytic ileus.
Elevated serum amylase and lipase levels are the diagnostic hallmarks that confirm acute pancreatitis. Characteristically, serum amylase reaches peak levels 24 hours after onset of pancreatitis, then returns to within 48 to 72 hours, despite continued symptoms. Amylase levels are also dramatically elevated urine, ascites, and pleural fluid. Urine amylase levels and serum lipase levels remain elevated longer than serum amylase levels.
Supportive laboratory studies include elevated white blood cell count and serum bilirubin level. In many patients, hypocalcemia occurs and appears to associated with the severity of the disease. Blood and urine glucose tests may reveal transient glucosuria and hyperglycemia. In chronic pancreatitis, significant laboratory findings include elevations in serum alkaline phosphatase, amylase, and bilirubin levels. Serum glucose levels may be transiently elevated. Stools contain elevated lipid and trypsin levels.
Abdominal and chest X-rays differentiate pancreatitis from other diseases that cause similar symptoms and detect pleural effusions.
Computed tomography scanning and ultrasonography reveal an increased pancreatic diameter. These tests also reveal pancreatic cysts and pseudocysts.
ERCP shows the anatomy of the pancreas. lt's used to identify ductal system abnormalities, such as calcification and strictures, and to differentiate pancreatitis from other disorders such as pancreatic cancer.
The goals of treatment are to maintain circulation and fluid volume, relieve pain, and decrease pancreatic secretions. Emergency treatment for shock (the most common cause of death in early stage pancreatitis) consists of vigorous l.V. replacement of electrolytes and proteins. Metabolic acidosis secondary to hypovolemia and impaired cellular perfusion requires vigorous fluid volume replacement. Blood transfusions may be needed if hemorrhage occurs. Food and fluids are withheld to allow the pancreas to rest and to reduce pancreatic enzyme secretion.
In acute pancreatitis, nasogastric (NG) tube suctioning is usually required to decrease gastric distention and suppress pancreatic secretions. Prescribed medications may include:
When the crisis begins to resolve, oral low-fat, lowprotein feedings are gradually implemented. Alcohol and caffeine are eliminated from the diet. If the crisis occurred during treatment with glucocorticoids, oral contraceptives, or thiazide diuretics, these drugs are discontinued.
Surgery usually isn't indicated in acute pancreatitis. However, if complications occur, such as pancreatic abscess or pseudocyst, surgical drainage may be necessary. If biliary tract obstruction causes acute pancreatitis, a laparotomy may be required.
For chronic pancreatitis, treatment depends on the cause. Nonsurgical measures are appropriate if the patient isn't a suitable candidate for surgery or if he refuses this treatment. Measures to prevent and relieve abdominal pain are similar to those used in acute pancreatitis. Meperidine usually is the drug of choice; however, pentazocine also effectively relieves pain. Treatments for diabetes mellitus may include dietary modification, insulin replacement, or antidiabetic agents. Malabsorption and steatorrhea are treated with pancreatic enzyme replacement.
Surgical intervention relieves abdominal pain, restores pancreatic drainage, and reduces the frequency of acute pancreatic attacks. Surgical drainage is required for an abscess or a pseudocyst. If biliary tract disease is the underlying cause, cholecystectomy or choledochotomy is performed. A sphincterotomy is indicated to enlarge a pancreatic sphincter that has become fibrotic. To relieve obstruction and allow drainage of pancreatic secretions, ancreaticojejunostomy (anastomosis of the jejunum with the opened pancreatic duct) may be required.
Although pancreatitis isn't always preventable, you can take steps to reduce your risk:
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