Pancreatitis
Inflammation of the pancreas from premature activation of digestive enzymes within the gland, causing autodigestion.
Acute pancreatitis is most commonly caused by gallstones or alcohol (together accounting for the large majority of cases), with other causes including hypertriglyceridemia (typically above 11.3 mmol/L), post-ERCP, drugs (azathioprine, thiazides, valproate, GLP-1 agonists, among others), trauma, and, rarely, autoimmune or hereditary pancreatitis.
Chronic pancreatitis represents irreversible fibrosis and progressive exocrine and endocrine dysfunction, most commonly from long-term alcohol use, with recurrent acute pancreatitis, autoimmune pancreatitis, and cystic fibrosis among other causes.
Acute: severe, constant epigastric pain radiating to the back, often relieved by sitting forward, associated with nausea and vomiting.
Examination may show epigastric tenderness, guarding, reduced bowel sounds, and, in severe hemorrhagic pancreatitis, Cullen's sign (periumbilical bruising) or Grey Turner's sign (flank bruising), both uncommon but indicative of severe disease. Systemic features in severe disease include fever, tachycardia, hypotension, and hypoxia reflecting SIRS or evolving organ dysfunction.
Chronic: recurrent or persistent epigastric pain (though a subset of patients become pain free as the gland burns out), steatorrhea and weight loss from exocrine insufficiency, and diabetes mellitus from endocrine insufficiency as islet cell mass is progressively lost.
Acute pancreatitis diagnosis requires two of three: characteristic abdominal pain, serum lipase or amylase greater than three times the upper limit of normal (lipase preferred, more sensitive and specific and remains elevated longer than amylase), and characteristic findings on cross sectional imaging.
Severity assessment uses scoring systems such as the Glasgow Imrie or APACHE II criteria, alongside CRP (a level above 150 mg/L at 48 hours predicts severe disease) and hematocrit trend.
Abdominal ultrasound identifies gallstones as the underlying cause. Contrast enhanced CT is reserved for diagnostic uncertainty or to assess complications (necrosis, pseudocyst, abscess), ideally performed after 72 hours if necrosis is being assessed, since early imaging can underestimate necrotic extent.
Triglycerides, calcium, and a thorough medication history complete the etiological workup when gallstones and alcohol are absent.
Chronic pancreatitis diagnosis uses CT or MRI showing pancreatic calcification, duct dilatation, and atrophy; endoscopic ultrasound for early or equivocal changes; fecal elastase to confirm exocrine insufficiency; and formal assessment for diabetes.
Differentials include perforated peptic ulcer, mesenteric ischemia, biliary colic, cholecystitis, and myocardial infarction (particularly inferior MI, which can mimic epigastric pain).
Acute pancreatitis:
Aggressive IV fluid resuscitation with crystalloid, guided by urine output and hemodynamic response, is the cornerstone of early management. Analgesia should be given generously, typically with opioids.
Early enteral nutrition (oral or nasogastric feeding as tolerated, started within 24 to 72 hours) is preferred over prolonged fasting, since it reduces infectious complications and mortality compared with nil by mouth strategies.
Antibiotics are not given prophylactically and are reserved for confirmed infected necrosis or another proven source of infection.
Gallstone pancreatitis requires cholecystectomy during the same admission for mild disease, or once inflammation has settled for severe disease, to prevent recurrence; ERCP with sphincterotomy is indicated urgently if there is concurrent cholangitis or persistent biliary obstruction.
Severe pancreatitis with organ dysfunction requires ICU or HDU level care. Local complications such as infected pancreatic necrosis are managed with a step up approach, starting with percutaneous or endoscopic drainage before progressing to necrosectomy if needed, since early surgical intervention carries higher mortality than a delayed, minimally invasive strategy.
Chronic pancreatitis:
Alcohol cessation and smoking cessation are essential to slow progression. Analgesia follows a stepwise approach, escalating from simple analgesics to neuropathic agents and, in refractory cases, to endoscopic or surgical intervention (duct decompression, celiac plexus block, or resection).
Pancreatic enzyme replacement therapy is given with meals for exocrine insufficiency, titrated to control steatorrhea and support weight.
Diabetes arising from endocrine insufficiency is managed per standard diabetes principles, though patients are often more prone to hypoglycemia given concurrent glucagon deficiency.
Fat soluble vitamin deficiency (A, D, E, K) should be screened for and replaced.
Referral: hepatobiliary or pancreatic surgery for gallstone pancreatitis requiring cholecystectomy, necrotizing pancreatitis requiring drainage, or chronic pancreatitis requiring duct decompression; gastroenterology for ERCP and ongoing chronic pancreatitis management.
