Acute Pancreatitis Overview

Acute Pancreatitis Overview

• Acute pancreatitis is inflammation of the pancreas, causing autodigestion and severe pain.
• Inflammation ranges from mild edema to severe hemorrhagic necrosis.

Etiology and Pathophysiology

• Most common causes in the US are gallbladder disease (gallstones, more common in women) and chronic alcohol use (more common in men).
• Other causes include drug reactions, pancreatic cancer, and hypertriglyceridemia (serum levels >1000 mg/dL).
• Biliary sludge and microlithiasis (cholesterol crystals and calcium salts) can be present.
• The primary pathogenic mechanism is autodigestion.
• Injury to pancreatic cells or activation of enzymes within the pancreas (rather than the intestines) occurs. Often bile reflux into pancreatic ducts through an open or distended sphincter of Oddi (often from gallstones). This can lead to pancreatic ischemia.
• The mechanism of alcohol-induced pancreatitis is not fully understood, but thought to increase digestive enzyme production.
• Acute pancreatitis can be either mild (edematous or interstitial) or severe (necrotizing).
• Severe pancreatitis carries a high risk of pancreatic necrosis, organ failure, and septic complications, with an overall fatality rate of 9%.

Clinical Manifestations

• Main symptom is severe, deep, piercing abdominal pain (often sudden onset), in the left upper quadrant or mid-epigastric, radiating to the back.
• Worsened by eating, unrelieved by vomiting.
• May be accompanied by flushing, cyanosis, dyspnea, and positions involving trunk flexion to relieve the pain.
• Other symptoms include nausea, vomiting, low-grade fever, leukocytosis, hypotension, tachycardia, and jaundice.
• Abdominal tenderness with muscle guarding, decreased or absent bowel sounds, and paralytic ileus (marked abdominal distention) is common.
• Potential for lung involvement (crackles)
• Intravascular damage from trypsin can cause abdominal wall cyanosis or discoloration (greenish to yellow-brown).
• Bruising on flanks (Grey Turner spots) and periumbilical area (Cullen's sign). These are bloodstained exudate from the pancreas.
• Shock can occur from bleeding, toxemia, or hypovolemia from fluid shifts.

Complications

• Severity depends on the extent of pancreatic destruction.
• Can be life-threatening, but some patients recover completely, others recur, and some develop chronic pancreatitis.
• Local complications:
  • Pseudocysts: Fluid/enzyme collection with a wall, causing abdominal pain and a palpable mass. Often resolve but can rupture.
    • Treatment includes surgical or endoscopic/percutaneous drainage.
  • Abscesses: Infection of a pseudocyst, causing upper abdominal pain, mass, high fever, and leukocytosis.
    • Requires prompt surgical drainage.
• Systemic complications:
  • Cardiovascular and pulmonary issues (pleural effusion, atelectasis, pneumonia, ARDS) are common.
  • Pulmonary complications are from exudate-containing pancreatic enzymes from the peritoneal cavity.
  • Trypsin activation can increase risk for thrombi, emboli, and DIC.
  • Tetany (hypocalcemia) can result from calcium and fatty acids combining during fat necrosis.
  • Abdominal compartment syndrome from intra-abdominal hypertension and edema.

Diagnostic Studies

• Key tests are serum amylase and lipase (often elevated early, high for 24-72 hours). Lipase is a more specific marker.
• Other abnormalities include increased liver enzymes, triglycerides, glucose, and bilirubin; and decreased calcium.
• Imaging: Ultrasound, x-ray, and contrast-enhanced CT scan helpful to diagnose pancreatic issues. CT scan is best for complications like pseudocysts/abscesses. ERCP, EUS, MRCP, and angiography can also be used.

Interprofessional Care

• Goals: Pain relief, prevent/alleviate shock, reduce pancreatic secretions, correct fluid/electrolyte imbalances, prevent/treat infection.
• Initial treatment involves aggressive hydration, pain management, and minimizing pancreatic stimulation.
• Pain management through IV opioids and often an antispasmodic agent.
• Avoid anticholinergics if paralytic ileus is present.
• Reduce pancreatic secretions: NPO, NG suction, drugs to suppress gastric acid.
• Prevent infections, especially in severe necrotizing pancreatitis, with close monitoring and antibiotic therapy if infection occurs.

Treatments (cont'd)

• For gallstone-related pancreatitis : ERCP with sphincterotomy and potentially later cholecystectomy.
• Surgical or endoscopic drainage may be needed for necrotic fluid collections or pseudocysts.

Drug Therapy

• Many drugs are used but no cure exists.

Nutrition Therapy

• Initially, patients are NPO to reduce pancreatic stimulation.
• Enteral nutrition (EN) is started based on severity; parenteral nutrition (PN) is used for those who can't tolerate EN.
• Monitor blood triglyceride levels if IV lipids are administered.
• Transition to small, frequent, high-carbohydrate meals as tolerated, avoiding crash diets.

Nursing Management

• Key assessments: subjective and objective data based on complications and potential issues (detailed in Table 48.21).
• Clinical problems: pain, fluid imbalance, electrolyte imbalance, malnutrition.
• Planning: goals include pain relief, normal fluid/electrolyte balance, minimal complications, and no recurrence.
• Implementation: health promotion that focuses on assessment of risk factors and early intervention; acute care involving vital sign monitoring, assessing fluid/electrolyte balance, addressing potential respiratory complications for severe pancreatitis, and treating complications like hypocalcemia.
• Observation for infections and preventing them including maintaining oral/nasal care (especially when taking anticholinergics).

Ambulatory Care

• Home care, physical therapy, continued infection prevention and complication detection.
• Counseling on abstinence from alcohol and smoking cessation (nicotine stimulates pancreas).
• Patient and caregiver education on the treatment plan, importance of medications, and a low-fat diet with high carbohydrates.
• Recognizing and reporting signs of infection, diabetes, or steatorrhea, and any exogenous enzyme supplementation needs.