Acute Pancreatitis
Acute pancreatitis is an inflammation of the pancreas, ranging from mild oedema to extensive haemorrhage, resulting from various insults to the pancreas. It is defined by a discrete episode of abdominal pain and serum enzyme elevations. The structure and function of the pancreas usually return to normal after an acute attack. Chronic pancreatitis occurs when there is persistent cellular damage to the pancreas.
Pathophysiology and Etiology Acute Pancreatitis
1. Excessive alcohol consumption is the most common cause.
2. Also commonly caused by biliary tract disease, such as cholelithiasis, acute and chronic cholecystitis.
3. Less common causes are bacterial or viral infection, blunt abdominal trauma, peptic ulcer disease, ischemic vascular disease, hyperlipidemia, and hypercalcemia; the use of corticosteroids, thiazide diuretics, and oral contraceptives; surgery on or near the pancreas or after instrumentation of the pancreatic duct by ERCP; tumours of the pancreas or ampulla; and a low incidence of hereditary pancreatitis.
4. Mortality is high (10%) because of shock, anoxia, hypotension, or multiple organ dysfunction.
5. Attacks may resolve with complete recovery, may recur without permanent damage, or may progress to chronic pancreatitis.
6. Autodigestion of all or part of the pancreas is involved, but the exact mechanism is not completely understood.
Clinical Manifestations of Acute Pancreatitis
(Depends on severity of pancreatic damage.)
1. Abdominal pain, usually constant, mid epigastric or periumbilical, radiating to the back or flank. The patient assumes a fetal position or leans forward while sitting (known as “proning”) to relieve pressure of the inflamed pancreas on celiac plexus nerves. Pain can be mild to incapacitating.
2. Nausea and vomiting.
3. Fever.
4. Involuntary abdominal guarding, epigastric tenderness to deep palpation, and reduced or absent bowel sounds.
5. Dry mucous membranes; hypotension; cold, clammy skin; cyanosis; and tachycardia, which may reflect mild to moderate dehydration from vomiting or capillary leak syndrome (third space loss).
6. Shock may be the presenting manifestation in severe episodes, with respiratory distress and acute renal failure.
7. Purplish discolouration of the flanks (Turner’s sign) or of the periumbilical area (Cullen’s sign) occurs in extensive hemorrhagic necrosis of the pancreas.
Diagnostic Evaluation of Acute Pancreatitis
1. Serum amylase, lipase, glucose, bilirubin, alkaline phosphatase, lactate dehydrogenase, AST, ALT, potassium, and cholesterol may be elevated.
2. Serum albumin, calcium, sodium, magnesium, and, possibly, potassium may be low due to dehydration, vomiting, and the binding of calcium in areas of fat necrosis.
3. Abdominal x-ray to detect an ileus or isolated loop of small bowel overlying pancreas. Pancreatic calcifications or gallstones may suggest an alcohol or biliary aetiology.
4. CT scan is the most definitive study for determining pancreatic changes.
5. Chest x-ray for detection of pulmonary complications. Pleural effusions are common, especially on the left, but maybe bilateral.
Management of Acute Pancreatitis
Depending on severity of episode, management focuses on alleviation of symptoms and support of the patient to prevent complications.
1. Restoration of circulating blood volume with IV crystalloid or colloid solutions or blood products.
2. Maintenance of adequate oxygenation is reduced by pain, anxiety, acidosis, abdominal pressure, or pleural effusions.
3. Pain control to alleviate pain and anxiety, which increases pancreatic secretions.
4. Rest of the GI tract.
a. Withhold oral feedings to decrease pancreatic secretions.
b. NG intubation and suction to relieve gastric stasis, distention, and ileus, if needed.
5. Maintenance of alkaline gastric pH with PPI or H2--receptor antagonists and antacids to suppress acid drive of pancreatic secretions and to prevent stress ulcer complications of acute illness.
6. Nutrition provided or treatment of malnutrition with parenteral feedings, as needed.
7. Pharmacotherapy.
a. Electrolyte replacements, as needed.
b. Sodium bicarbonate to reverse metabolic acidosis.
c. Insulin to treat hyperglycemia.
d. Antibiotic therapy for documented infection or sepsis.
8. Surgical intervention if complications occur.
a. Incision and drainage of infection and pseudocysts.
b. Debridement or pancreatectomy to remove necrotic pancreatic tissue.
c. Cholecystectomy for gallstone pancreatitis.
Complications of Acute Pancreatitis
1. Pancreatic ascites, abscess, or pseudocyst.
2. Pulmonary infiltrates, pleural effusion, acute respiratory distress syndrome.
3. Hemorrhage with hypovolemic shock.
4. Acute renal failure.
5. Sepsis and multiple-organ dysfunction syndrome.
Nursing Assessment of Acute Pancreatitis
1. Obtain history of gallbladder disease, alcohol use, or precipitating factors.
2. Assess GI distress, including nausea and vomiting, diarrhoea, and passage of stools containing fat.
3. Assess characteristics of abdominal pain.
4. Assess nutritional and fluid status.
5. Assess respiratory rate and pattern and breath sounds.
Nursing Diagnoses of Acute Pancreatitis
Acute Pain related to the disease process.
Deficient Fluid Volume related to vomiting, self-restricted intake, fever, and fluid shifts.
Ineffective Breathing Patterns related to severe pain and pulmonary complications.
Nursing Interventions of Acute Pancreatitis
Controlling Pain
1. Administer opioid analgesics, as ordered, to control pain.
2. Assist the patient to a comfortable position.
3. Maintain NPO status to decrease pancreatic enzyme secretion.
4. Maintain patency of NG suction to remove gastric secretions and to relieve abdominal distention, if indicated.
5. Provide frequent oral hygiene and care.
6. Administer antacids, PPI or H2-receptor antagonists, as prescribed.
7. Report increase in severity of pain, which may indicate haemorrhage of the pancreas, rupture of a pseudocyst, or inadequate dosage of the analgesic.
Restoring Adequate Fluid Balance
1. Monitor and record vital signs, skin colour, and temperature.
2. Monitor intake and output and weigh daily.
3. Evaluate laboratory data for haemoglobin, hematocrit, albumin, calcium, potassium, sodium, and magnesium levels and administer replacements, as prescribed.
4. Observe and measure abdominal girth if pancreatic ascites is suspected.
5. Report trends in falling BP or urine output or rising pulse because this may indicate hypovolemia and shock or renal failure.
Improving Respiratory Function
1. Assess respiratory rate and rhythm, effort, oxygen saturation, and breath sounds frequently.
2. Position in upright or semi-Fowler’s position to enhance diaphragmatic excursion.
3. Administer oxygen supplementation, as prescribed, to maintain adequate oxygen levels.
4. Report signs of respiratory distress immediately.
5. Instruct the patient in coughing and deep breathing to improve respiratory function.
Patient Education and Health Maintenance
1. Instruct the patient to gradually resume a low-fat diet.
2. Instruct the patient to increase activity gradually, providing for daily rest periods.
3. Reinforce information about the disease process and precipitating factors. Stress that subsequent bouts of acute pancreatitis may destroy the pancreas, cause additional complications, and lead to chronic pancreatitis.
4. If pancreatitis is a result of alcohol abuse, the patient needs to be reminded of the importance of eliminating all alcohol; advice about Alcoholics Anonymous or other substance abuse counselling.
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