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Emergency and Acute Medicine – Pancreatitis (Don’t-Miss Points Included)
Pancreatitis is inflammation of the pancreas caused by premature activation, liberation, and autodigestion of the gland by pancreatic enzymes. Acute pancreatitis results in temporary impairment of exocrine and endocrine function that usually resolves over weeks to months, whereas chronic pancreatitis leads to progressive and irreversible glandular destruction with steatorrhea, malabsorption, diabetes, and chronic pain. A pancreatic pseudocyst is a common complication, defined as a pancreatic enzyme–rich fluid collection surrounded by fibrous tissue without epithelial lining, typically forming 4–6 weeks after acute pancreatitis.
The two most common causes of acute pancreatitis—gallstones and alcohol abuse—account for 75–80% of cases and must always be considered first. Chronic pancreatitis is most commonly due to long-term alcohol abuse (70–80%). Other important etiologies include pancreatic duct obstruction, ischemia, medications, infections, metabolic disorders (hypercalcemia, hyperlipidemia), trauma, post-ERCP injury, penetrating peptic ulcer disease, hereditary causes, and rare toxins (e.g., scorpion venom). In children, pancreatitis is most often caused by viral illness, trauma, or medications. Pancreatic pseudocysts occur in 5–16% of acute pancreatitis and up to 40% of chronic pancreatitis, and rupture or hemorrhage is life-threatening.
Severe epigastric pain radiating to the back is the hallmark symptom and is present in nearly all patients. Pain is often worse when supine and may improve with leaning forward. Nausea and vomiting occur in most cases, with low-grade fever, hypotension, and jaundice being common associated findings. Decreased or absent bowel sounds are typical. Cullen sign (periumbilical ecchymosis) and Grey Turner sign (flank ecchymosis) are rare but ominous indicators of hemorrhagic pancreatitis. Respiratory complications are common and include pleural effusions (especially left-sided), atelectasis, pulmonary edema, and hypoxemia. Cardiovascular instability may progress to shock, while neurologic findings range from irritability to confusion and coma. Significant GI bleeding is uncommon and suggests an alternative diagnosis.
Diagnosis relies on clinical presentation supported by laboratory testing. Serum lipase is the most reliable diagnostic test, rising within 4-8 hours of symptom onset and remaining elevated longer than amylase. Amylase may be elevated earlier but is less specific and may be normal in severe disease. Additional lab abnormalities include leukocytosis, hemoconcentration (hematocrit >47% suggests risk of necrosis), electrolyte abnormalities, hyperglycemia, hypocalcemia (marker of severe disease), hypomagnesemia (especially in alcohol use), and abnormal liver enzymes suggesting biliary pancreatitis. Ranson criteria must be assessed, as a score ≥3 indicates severe disease with increased mortality. Arterial blood gases are required in hypoxic or toxic patients.
Imaging is guided by clinical severity. Ultrasound is essential when gallstones are suspected. CT abdomen with contrast is indicated for severe pancreatitis, diagnostic uncertainty, suspected necrosis, hemorrhage, or pseudocyst, and should not be performed routinely in mild cases. Chest radiographs may reveal pleural effusions or atelectasis. ERCP is indicated urgently only in severe pancreatitis with cholangitis or persistent biliary obstruction.
Initial management must not be delayed. Aggressive IV fluid resuscitation is critical and lifesaving, often requiring 5–6 liters in the first 24 hours, with close monitoring of vitals, urine output, and electrolytes. Supplemental oxygen and cardiac monitoring are mandatory. Early and adequate opioid analgesia is essential; morphine or hydromorphone are appropriate. Antiemetics should be administered promptly. Nasogastric suction is not routinely indicated but may help in severe disease or intractable vomiting. Antibiotics are NOT indicated unless infected pancreatic necrosis is confirmed—routine prophylaxis increases resistance without benefit. Correct electrolyte abnormalities promptly, especially hypocalcemia, hypokalemia, and hypomagnesemia.
Patients with significant pain, vomiting, hypoxia, systemic instability, or laboratory evidence of severe disease require hospital admission. ICU admission is mandatory for necrotizing or hemorrhagic pancreatitis. Discharge is appropriate only for mild acute pancreatitis when the patient tolerates oral intake, has controlled pain, and no biliary obstruction. Chronic pancreatitis patients may be discharged if pain is minimal and oral intake is adequate. All discharged patients require close follow-up within 24–48 hours.
Critical Don’t-Miss Pearls
- Gallstones and alcohol cause 75–80% of acute pancreatitis—always rule them out first
- Lipase > amylase for diagnosis; normal amylase does NOT exclude pancreatitis
- Early aggressive IV fluids reduce necrosis and mortality
- Ranson score ≥3 = severe disease
- Do NOT give antibiotics unless infected necrosis is proven
- NG tubes are not routine
- CT early only if diagnosis is unclear or disease is severe
- Ruptured or hemorrhagic pseudocyst = surgical emergency
- Hypocalcemia and rising hematocrit are markers of severe disease
Pancreatitis is common, potentially lethal, and time-sensitive—early recognition, aggressive resuscitation, and avoidance of common pitfalls are critical to survival.
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