Pancreatitis
Pancreatitis: Excerpt from Handbook of Diseases
Pancreatitis, inflammation of the pancreas, occurs in acute and chronic forms. With pancreatitis, the enzymes that the pancreas normally excretes digest pancreatic tissue (autodigestion). Acute pancreatitis can range from mild self-limiting episodes of abdominal discomfort to severe systemic illness associated with fluid sequestration, metabolic disorder, hypotension, sepsis, and death. Life-threatening illness is associated with pancreatic hemorrhage or necrosis in about 10% of patients.
In 90% of patients with acute pancreatitis, the disease occurs as a mild, self-limiting illness and requires only simple supportive care. In the remaining 10% of patients, the disease can evolve into a severe form with significant complications, a lengthy duration, and a significant mortality rate. Complications include heart and kidney failure and adult respiratory distress syndrome.
Causes
The most common causes of pancreatitis are biliary tract disease and alcoholism; however, it can also result from pancreatic cancer, trauma, or certain drugs, such as glucocorticoids, sulfonamides, chlorothiazide, azathioprine, excessive use of acetaminophen, and hormonal contraceptives.
This disease may also develop as a complication of peptic ulcer, mumps, or hypothermia. Rarer causes are stenosis or obstruction of the sphincter of Oddi, hypercalcemia, duodenal obstruction, hyperlipemia, ischemia from vasculitis or vascular disease, viral infections, mycoplasmal pneumonia, scorpion venom, and pregnancy. The disease may also be familial or idiopathic.
AGE ALERT: In children, pancreatitis may coincide with abdominal trauma, cystic fibrosis, hemolytic uremic syndrome, Kawasaki disease, mumps, Reye’s syndrome, viral illness, or medications the child may be taking.
Pancreatitis may also develop in a patient after surgery. This occurrence has the highest morbidity and mortality. Whatever the cause, complications from acute pancreatitis are possible.
CLINICAL TIP: Determining the cause of pancreatitis is useful for managing and predicting complications.
Signs and symptoms
In many patients, the first and only symptom of mild pancreatitis is steady epigastric pain centered close to the umbilicus. Examination of the abdomen reveals muscle guarding or tenderness. If there’s seepage of bloody exudate from the pancreas, periumbilical bruising (Cullen’s sign) and bruising of the flanks (Turner’s syndrome) may occur. The pain usually begins as a gradually increasing midepigastric pain reaching its maximum intensity several hours after the beginning of the illness. With pancreatitis resulting from alcohol ingestion, the pain begins 12 to 48 hours after an episode of binge drinking. Nausea and vomiting commonly accompany the abdominal pain. However, a severe attack causes extreme pain, persistent vomiting, abdominal rigidity, diminished bowel activity (suggesting peritonitis), right or left pleural effusion, or elevation of the left half of the diaphragm.
Severe pancreatitis may produce extreme malaise and restlessness, mottled skin, tachycardia, and diaphoresis. Hypotension, hypovolemia, hypoperfusion, sepsis, and shock may ensue. Pulmonary complications, secondary pancreatic infections (such as pancreatic abscess or infected pancreatic necrosis) and, later, pancreatic pseudocyst may also occur. The proximity of the inflamed pancreas to the bowel may cause ileus. Renal failure may occur because of severe hypovolemia.
If pancreatitis damages the islets of Langerhans, complications may include diabetes mellitus and enzyme deficiency. (See Chronic pancreatitis, page 602.)
Fulminant pancreatitis causes massive hemorrhage and total destruction of the pancreas, resulting in diabetic acidosis, shock, or coma.
Diagnosis
Clinical presentation and combined laboratory and radiographic findings form the basis for diagnosis. A thorough patient history (especially for alcoholism) and physical examination are the first steps in diagnosis; however, the retroperitoneal position of the pancreas makes physical assessment difficult.
Dramatically elevated serum amylase levels —in many patients over 500 U/L — confirm pancreatitis and rule out perforated peptic ulcer, acute cholecystitis, appendicitis, and bowel infarction or obstruction. Persistent elevation of serum amylase levels may indicate pancreatic necrosis, pseudocyst, or abscess.
Similarly, dramatically elevated amylase levels are also found in urine, ascites, or pleural fluid. Characteristically, amylase levels return to normal within 48 hours after the onset of pancreatitis, despite continuing symptoms. Laboratory values that support the diagnosis include:
❑ increased serum lipase levels, which rise more slowly than serum amylase levels
❑ white blood cell counts that range from 8,000 to 20,000/µl, with increased polymorphonuclear leukocyte counts
❑ elevated glucose levels — as high as 500 to 900 mg/dl — indicating hyperglycemia.
An abdominal computed tomography scan with contrast is the most sensitive noninvasive test used to confirm the diagnosis of pancreatitis; however, abdominal ultrasound and abdominal magnetic resonance imaging also show pancreatic inflammation. Other tests that may show alterations include aspartate aminotransferase, carcinoembryonic antigen, fecal fat test, ionized calcium, lactate dehyrogenase (LD), LD isoenzymes, serum magnesium, and trypsinogen.
Treatment
The goal of therapy is to maintain circulation and fluid volume. Treatment measures must also relieve pain and decrease pancreatic secretions. In 90% of patients with acute pancreatitis, the disease occurs as a mild self-limiting illness and requires only simple supportive care alone. In the remaining 10% of patients, the disease can evolve into a severe form of acute pancreatitis with significant complications, a lengthy duration of illness and, for many, death.
Emergency measures
Emergency treatment of shock (which is the most common cause of death in early-stage pancreatitis) consists of vigorous I.V. replacement of electrolytes and proteins. The patient receives nothing by mouth, a nasogastric tube is inserted for abdominal distention, and an anticholinergic may be administered.
Metabolic acidosis that develops secondary to hypovolemia and impaired cellular perfusion requires vigorous fluid volume replacement.
Drug treatment may include morphine sulfate for pain, diazepam for restlessness and agitation, and antibiotics for documented bacterial infections.
Specific metabolic complications — such as hypokalemia, hypocalcemia, hemorrhage, and coagulopathy — must be treated with appropriate replacement products, such as potassium chloride, I.V. calcium gluconate or chloride, red blood cells, and fresh frozen plasma. Hyperglycemia and glycosuria are manifestations of altered carbohydrate metabolism. Treatment consists of careful titration of glucose and insulin to maintain a euglycemic state.
CLINICAL TIP: Treating the underlying condition may prevent recurrent attacks.
After the emergency
After the emergency phase, continuing I.V. therapy should provide adequate electrolytes and protein solutions. If the patient is unable to resume oral feedings, total parenteral nutrition may be necessary. Nonstimulating enteral feedings may be safer because of the decreased risk of infection and maintenance of normal physiology.
Surgery for acute pancreatitis is reserved for treating specific complications and correcting anatomic problems. Surgery is usually required for patients with necrotizing pancreatitis to debride devitalized tissue and to provide external drainage. Debridement, usually at 24- to 48-hour intervals, until the necrotic tissue is replaced by a granulating wound, is commonly required.
Special considerations
❑ Acute pancreatitis is a life-threatening emergency. Provide meticulous supportive care, and continuously monitor the patient.
❑ Monitor the patient vital signs and pulmonary artery pressure closely.
❑ Monitor the patient fluid intake and output and electrolyte levels.
❑ Assess the patient for crackles, rhon-chi, decreased breath sounds, or respiratory failure.
❑ Observe the patient for signs of calcium deficiency, such as tetany, carpopedal spasm, cramps, and seizures.
CLINICAL TIP: Serum calcium levels decrease in acute pancreatitis, possibly from fat necrosis, resulting in a binding of calcium with free fatty acids. Muscle twitching, tremors, and irritability are signs of decreased calcium levels.
❑ Administer analgesics, as needed, to relieve the patient’s pain and anxiety.
❑ Observe the patient for adverse reactions to antibiotics: nephrotoxicity with aminoglycosides, pseudomembranous enterocolitis with clindamycin, and blood dyscrasias with chloramphenicol.
❑ Monitor the patient for complications due to total parenteral nutrition, such as sepsis, hypokalemia, overhydration, and metabolic acidosis.
❑ Observe the patient for signs of sepsis, such as fever, cardiac irregularities, changes in arterial blood gas measurements, and deep respirations.
Pictures
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
More About Acute Pancreatitis
More Medical Textbooks Online about Acute Pancreatitis
Review other book chapters online related to Acute Pancreatitis:
Medical Books Excerpts
- Diabetes Mellitus
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
|
|
More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
|
|
» Next page: Diabetes mellitus (Handbook of Diseases)
Rate This Website
What do you think about the features of this website?
Take our user survey and have your say:
Website User Survey
Medical Tools & Articles:
Next articles:
Tools & Services:
Medical Articles:
Forums & Message Boards
- Ask or answer a question at the Boards:
