Pancreatitis — Acute vs Chronic

Pancreatitis is autodigestion: pancreatic enzymes (trypsin, lipase) activate inside the gland instead of the duodenum, causing inflammation and tissue destruction. The two leading causes are gallstones (biliary obstruction triggers enzyme backup) and chronic alcohol use (direct toxic injury to acinar cells). Acute pancreatitis presents with sudden, severe epigastric pain radiating straight through to the back, often after a fatty meal or binge drinking. The client assumes a fetal position for relief. Cullen's sign (periumbilical ecchymosis) and Grey Turner's sign (flank ecchymosis) indicate hemorrhagic pancreatitis. Serum lipase is the most specific diagnostic marker — elevated more than three times the upper limit of normal is highly indicative. Serum amylase rises early but is less specific. Monitor for third-spacing: fluid shifts into the retroperitoneal space cause hypovolemia, tachycardia, and hypotension. Monitor serum calcium — hypocalcemia occurs from fat saponification and signals worsening disease. Aggressive IV fluid resuscitation is the priority intervention. The pancreas is rested — NPO status, NG tube if vomiting is severe, and pain management (typically IV hydromorphone or morphine; morphine was historically avoided due to theoretical sphincter of Oddi spasm but is now considered acceptable per current guidelines; meperidine is no longer preferred). Chronic pancreatitis results from repeated injury, causing irreversible fibrosis, calcification, and progressive loss of exocrine and endocrine function. These clients develop steatorrhea (fatty, foul-smelling stools) from fat malabsorption and eventually secondary diabetes mellitus from islet cell destruction. They require lifelong pancreatic enzyme replacement (pancrelipase) taken with every meal and snack — swallow capsules whole, do not crush. Alcohol cessation is essential to slow disease progression.