Pancreatitis — Symptoms, Causes & Treatment | MyMedicPlus

Pancreatitis is inflammation of the pancreas — a dual-function glandular organ situated in the retroperitoneum behind the stomach, secreting digestive enzymes (exocrine function: amylase, lipase, trypsinogen, chymotrypsinogen) via the pancreatic duct into the duodenum, and producing hormones (endocrine function: insulin and glucagon from the islets of Langerhans). In pancreatitis, premature activation of pancreatic digestive enzymes within the pancreatic acinar cells — normally only activated after reaching the duodenum — causes autodigestion of pancreatic tissue and surrounding structures, triggering a local and systemic inflammatory cascade. Pancreatitis is classified as acute (AP) or chronic (CP). Acute pancreatitis is a sudden inflammatory condition presenting with severe abdominal pain, elevated serum amylase or lipase, and radiological evidence of pancreatic inflammation; it occurs at an incidence of 30-40 per 100,000 per year. Most episodes of AP (80%) are mild and self-limiting — resolving within 3-5 days with supportive care — but 20% develop severe AP with systemic complications including acute respiratory distress syndrome (ARDS), acute kidney injury (AKI), sepsis, and multi-organ failure; mortality from severe AP is 15-30%. Chronic pancreatitis is a progressive fibroinflammatory disease of the pancreas characterised by recurrent episodes of inflammation causing irreversible structural damage — ductal strictures, pancreatic stones (calcifications), fibrosis, and progressive loss of both exocrine (malabsorption, steatorrhoea) and endocrine (type 3c pancreatogenic diabetes) function. The most common causes are gallstones (AP — 40-50%) and chronic alcohol consumption (AP and CP — 30-40%).

Gallstones are the leading cause of acute pancreatitis (40-50%), particularly small gallstones (microlithiasis, sludge) passing through the common bile duct and temporarily obstructing the ampulla of Vater — causing bile and pancreatic juice backflow or ductal hypertension that triggers premature enzyme activation. Alcohol excess (30-40% of AP, and the most common cause of CP): repeated alcohol and its metabolites (acetaldehyde, fatty acid ethyl esters) cause oxidative stress in acinar cells, premature zymogen activation, and stellate cell activation driving fibrosis in CP; heavy drinking (above 5 drinks/day for more than 5 years) is typically required for CP development. Hypertriglyceridaemia: serum triglycerides above 11 mmol/L (1000 mg/dL) cause pancreatitis through fatty acid-mediated oxidative injury and microvascular thrombosis in the pancreatic circulation — accounts for 2-5% of AP cases; severe familial hypertriglyceridaemia (Fredrickson Type I, IV, V) and secondary causes (uncontrolled diabetes, hypothyroidism, nephrotic syndrome, medications including isotretinoin, tamoxifen, propofol). Drug-induced pancreatitis (2-5%): azathioprine, 6-mercaptopurine, valproic acid, tetracyclines, mesalazine, pentamidine, and SGLT-2 inhibitors (GLP-1 analogues have been studied extensively with no confirmed association). Post-ERCP pancreatitis (PEP — 3-5% of procedures, more common after pancreatic sphincterotomy — the most common complication of ERCP; risk reduced by rectal indomethacin prophylaxis). Autoimmune pancreatitis (AIP): Type 1 AIP is an IgG4-related disease causing pancreatic mass lesion and bile duct stricture, mimicking pancreatic cancer; Type 2 AIP is associated with IBD; both respond dramatically to corticosteroids. Genetic causes: PRSS1 mutations (cationic trypsinogen — hereditary pancreatitis, autosomal dominant, high penetrance — recurrent AP from childhood, very high risk of pancreatic cancer); SPINK1 mutations (serine protease inhibitor Kazal type 1 — reduces trypsin inhibition, risk modifier); CFTR mutations (cystic fibrosis gene — idiopathic CP). Anatomical: pancreas divisum (most common pancreatic anatomical variant — dorsal duct draining via the minor papilla, causing ductal hypertension in susceptible individuals); annular pancreas. Hypercalcaemia (primary hyperparathyroidism — calcium activates trypsinogen prematurely). Idiopathic (10-20% of AP after thorough investigation).

Acute pancreatitis: the cardinal presenting symptom is sudden-onset severe epigastric pain — classically constant, boring, or band-like in quality, radiating to the back (50-70% of patients) from the retroperitoneal location, reaching maximum intensity within 30-60 minutes, and typically persisting for hours to days without the colicky waxing-waning character of renal or biliary colic. Pain is often partially relieved by leaning forward (reduces pressure on the pancreas) and worsened by lying flat or eating. Nausea and vomiting: present in 90% of AP — typically severe, frequent, and not relieved by vomiting (in contrast to biliary colic where vomiting may temporarily relieve colicky pain). Abdominal examination: upper abdominal tenderness with guarding (voluntary and involuntary); peritonism suggests severe AP with peripancreatic necrosis or perforation; abdominal distension from ileus (absent bowel sounds); a palpable epigastric mass suggests pseudocyst or walled-off necrosis in late AP. Rarely: Cullen's sign (periumbilical ecchymosis — bluish discolouration from haemoperitoneum in haemorrhagic pancreatitis) and Grey-Turner's sign (flank ecchymosis from retroperitoneal haemorrhage tracking to the flank) — both indicate severe haemorrhagic pancreatitis and carry very poor prognosis. Systemic features of severe AP: fever and tachycardia from systemic inflammatory response; respiratory distress from early ARDS (bilateral pulmonary infiltrates, hypoxaemia); oliguria from intravascular depletion and AKI; cardiovascular compromise (hypotension, shock). Chronic pancreatitis: chronic or recurrent epigastric and back pain (the dominant and most disabling symptom — often described as constant, aching, and weight-bearing; present in 80-90%); steatorrhoea (fatty, oily, floating, foul-smelling stools from exocrine insufficiency — develops when less than 10% of pancreatic exocrine function remains; causing fat-soluble vitamin malabsorption — vitamins A, D, E, K, B12); weight loss; and pancreatogenic (type 3c) diabetes mellitus.

Acute pancreatitis diagnosis requires 2 of 3 criteria: (1) characteristic abdominal pain; (2) serum amylase or lipase elevated above 3 times the upper limit of normal; (3) CT imaging characteristic of acute pancreatitis — according to the Revised Atlanta Classification. Serum lipase: more sensitive (90%) and specific (93%) than amylase for AP, remains elevated for 7-14 days (compared to amylase which normalises within 3-5 days); preferred biochemical marker. Serum amylase: elevated 3-5x ULN — also elevated in salivary gland disease, bowel ischaemia, and renal failure (reduced clearance); may be normal in AP from alcoholic or hypertriglyceridaemia pancreatitis. Liver function tests (LFTs): ALT above 3x ULN within 48 hours of onset strongly suggests gallstone aetiology. Serum triglycerides: measured in all AP without gallstone cause — levels above 11 mmol/L confirm hypertriglyceridaemic pancreatitis. CRP at 48 hours: the most validated biochemical severity marker — CRP above 150 mg/L at 48 hours predicts severe AP. Haematocrit, creatinine, urea, and blood glucose: organ dysfunction markers. CT abdomen and pelvis with IV contrast (CECT): not required for initial diagnosis of mild AP (clinical and biochemical diagnosis sufficient) — indicated when diagnosis is uncertain, clinical deterioration occurs, or to assess complications; the CT Severity Index (CTSI) grades AP from 0-10 based on pancreatic inflammation, peripancreatic fat inflammation, and necrosis extent; CECT at 72-96 hours maximises necrosis detection. MRI/MRCP: superior to CT for characterising pancreatic parenchyma, bile duct stones (cholecystocholedocholithiasis), and pancreatic duct anatomy — preferred in young patients to avoid radiation and for gallstone assessment. Abdominal ultrasound: first-line for gallstone detection (sensitivity 95% for gallbladder stones; lower for CBD stones) and bile duct dilation. ERCP: therapeutic, not diagnostic — for gallstone removal from the CBD in AP with cholangitis or persistent CBD obstruction. Chronic pancreatitis: secretin-stimulated MRCP for ductal anatomy; EUS for early fibrosis detection (most sensitive); CECT/MRI for parenchymal changes, ductal dilation, and calcifications; faecal elastase-1 (below 100 mcg/g confirms exocrine insufficiency); 72-hour faecal fat collection.

Acute pancreatitis management: supportive care is the cornerstone of treatment for the majority of AP cases. Fluid resuscitation: aggressive early intravenous fluid replacement (Ringer's lactate preferred over normal saline — reduces systemic acidosis; 250-500mL/hour in the first 12-24 hours), guided by clinical response (heart rate, blood pressure, urine output) and reassessed hourly; over-resuscitation carries risks (abdominal compartment syndrome, pulmonary oedema); goal-directed fluid therapy targeting urine output above 0.5mL/kg/hour. Analgesia: opioid analgesia is required for severe AP pain — IV morphine or fentanyl titrated to pain control; epidural analgesia for refractory severe pain; NSAIDs may provide adjunctive benefit but avoided in AKI. Nutritional support: early enteral nutrition (within 24-48 hours) via nasogastric (NG) tube or nasojejunal (NJ) tube — superior to total parenteral nutrition (TPN) in reducing infections, organ failure, and mortality (PYTHON trial and NEJM meta-analyses); NJ feeding bypasses the pancreatic stimulatory effect of food in the stomach; TPN reserved for those unable to tolerate enteral nutrition. Antibiotic therapy: not recommended for prophylaxis or for uncomplicated AP — used only for confirmed secondary infection (infected necrosis — fever, elevated CRP, CT evidence of gas in peripancreatic collections); carbapenem (meropenem 1g TDS) for infected pancreatic necrosis pending culture sensitivities. Endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy: indicated within 24 hours for AP with concurrent cholangitis (fever, jaundice, sepsis from CBD stone obstruction) — ERCP removes the obstructing CBD stone and decompresses the biliary system. Cholecystectomy: definitive treatment to prevent recurrent gallstone AP — should be performed within 2 weeks for mild AP during the same hospitalisation or within 4-6 weeks for moderate-severe AP after resolution. Interventional management of complications: infected pancreatic necrosis — step-up approach: percutaneous CT-guided drainage first, followed by minimally invasive (retroperitoneal) necrosectomy if drainage insufficient; endoscopic transluminal drainage/necrosectomy via EUS guidance for walled-off necrosis. Chronic pancreatitis management: pain management (gabapentin, pregabalin, tricyclic antidepressants, and specialist pain team involvement; consider endoscopic (ESWL + ERCP) or surgical duct drainage — Frey procedure or Berne modification — for ductal obstruction causing pain in pancreatic duct dilation above 5mm); pancreatic exocrine insufficiency (PEI) management with pancreatic enzyme replacement therapy (PERT — high-lipase pancrelipase capsules, e.g., Creon 25000-50000 units lipase with each meal and 10000-25000 units with snacks — taken with meals, not before); fat-soluble vitamin supplementation (A, D, E, K); pancreatogenic diabetes managed with insulin (type 3c diabetes has low glucagon reserve — hypoglycaemia risk; metformin generally safe); absolute alcohol abstinence.

Acute pancreatitis complications are classified as local and systemic. Local pancreatic complications: acute fluid collections (peripancreatic fluid accumulation in the first 4 weeks — most resolve spontaneously); acute necrotic collection (contains necrotic pancreatic tissue and fluid — may become infected causing infected necrosis, requiring drainage and necrosectomy); walled-off necrosis (WON — encapsulated collection containing necrotic tissue, developing after 4 weeks, managed endoscopically or surgically when symptomatic or infected); pancreatic pseudocyst (encapsulated fluid collection containing enzyme-rich pancreatic juice, arising from pancreatic duct disruption — may cause pain, early satiety, and biliary or gastric outlet obstruction; managed by endoscopic transmural drainage via EUS guidance). Infected pancreatic necrosis: the most feared local complication, developing in 20-30% of necrotising pancreatitis — characterised by bacterial contamination of necrotic tissue (CT gas, fever, deteriorating clinical course) requiring antibiotics and step-up drainage/necrosectomy; carries 30-40% mortality. Systemic complications of severe AP: acute respiratory distress syndrome (ARDS) — bilateral pulmonary infiltrates from cytokine-mediated increased permeability pulmonary oedema, requiring mechanical ventilation (ICU); acute kidney injury (AKI) — from intravascular depletion, renal vasoconstriction, and direct tubular toxicity; cardiovascular failure (hypotension, myocardial depression); coagulopathy (DIC). Recurrent AP leading to CP: 20-30% of patients with a first episode of AP develop chronic pancreatitis over 10 years, with risk highest in alcoholic aetiology. Chronic pancreatitis complications: pancreatic exocrine insufficiency causing malabsorption and malnutrition (fat-soluble vitamin deficiencies — osteoporosis from vitamin D deficiency); pancreatogenic diabetes mellitus (type 3c) — present in 50-80% of advanced CP, brittle (alternating hyper and hypoglycaemia due to combined insulin and glucagon deficiency); pancreatic cancer risk (20-year cumulative risk of 4-5% in hereditary pancreatitis; 1.5-2x increased risk in alcoholic CP).

Gallstone pancreatitis prevention: prompt cholecystectomy after a first episode of gallstone AP is the most effective preventive measure — reducing recurrent AP risk from 30% to below 2% at 1 year; guidelines recommend cholecystectomy within 2 weeks for mild AP; patients unfit for surgery should have endoscopic sphincterotomy (breaks the gallbladder-duct functional connection preventing future stone passage into the duct). Ursodeoxycholic acid (UDCA) for gallstone dissolution in patients unfit for surgery. Alcohol cessation: alcohol abstinence is the single most important intervention in alcoholic pancreatitis — reducing subsequent pain episodes, hospital admissions, and risk of CP development; brief motivational intervention plus referral to alcohol dependency services at the time of hospitalisation for acute alcoholic pancreatitis. Hypertriglyceridaemia management: strict dietary fat restriction (below 20g/day); triglyceride-lowering medications (fibrates — gemfibrozil, fenofibrate; omega-3 fatty acids); alcohol abstinence; tight glycaemic control (hyperglycaemia massively amplifies triglycerides); emergency plasmapheresis for very severe acute hypertriglyceridaemia-induced AP. Post-ERCP pancreatitis prevention: rectal indomethacin (100mg suppository) immediately post-ERCP reduces PEP risk by 50% in high-risk patients — routine in most centres; pancreatic duct stent placement to protect the duct during complex procedures. Drug-induced pancreatitis: identify and discontinue causative medication; use alternative drug class where possible. Pancreatic cancer surveillance in hereditary pancreatitis (PRSS1 mutation): annual EUS and MRI/MRCP from age 40 (or 20 years after first AP episode) — hereditary pancreatitis carries 50-fold increased pancreatic cancer risk. Recurrent idiopathic pancreatitis: thorough aetiological workup (genetic panel: PRSS1, SPINK1, CFTR; EUS for microlithiasis and early CP changes; MRCP for pancreas divisum) before labelling as truly idiopathic.

Call emergency services (999/112) or go to A&E immediately for: sudden onset severe epigastric pain radiating to the back — this is the classic presentation of acute pancreatitis and requires immediate hospital assessment (IV fluid resuscitation, analgesia, and blood tests), as severity ranges from mild to life-threatening; pain associated with fever and jaundice (yellow skin and eyes) — suggests cholangitis from an obstructing bile duct stone and requires urgent ERCP within 24 hours; any severe abdominal pain in someone with known gallstones or a history of heavy alcohol use; and signs of shock (pallor, cold sweaty skin, very rapid pulse, faintness) with abdominal pain — possible haemorrhagic pancreatitis or bowel perforation requiring emergency surgery. Seek same-day or urgent GP assessment for: a known pancreatitis patient with increasing or worsening abdominal pain after discharge (possible pseudocyst formation, recurrence, or infected necrosis); new fever in a recovering pancreatitis patient (infected necrosis typically develops 1-3 weeks post-onset — requires urgent CT and medical review); and unexplained weight loss with steatorrhoea (fatty, oily stools) and back pain in a patient with a history of heavy alcohol use (possible chronic pancreatitis with exocrine insufficiency). Do not delay seeking help for severe abdominal pain — untreated severe acute pancreatitis has a 30% mortality, but with early appropriate care, most patients make a full recovery.