What is pancreatitis?

Pancreatitis is inflammation of the pancreas — occurring in two forms: acute pancreatitis (sudden onset, usually resolving with treatment; gallstones and alcohol account for approximately 80% of cases; ranges from mild and self-limiting to severe necrotising pancreatitis with 25-30% mortality) and chronic pancreatitis (irreversible scarring causing progressive loss of digestive enzyme production — exocrine insufficiency — and insulin production — type 3c diabetes).

How is acute pancreatitis managed?

Modern management: IV fluids: Lactated Ringer's (preferred — WATERFALL 2022 showed superiority over normal saline for reducing SIRS and severity). Pain control: opioids appropriate (contrary to old teaching, morphine does not worsen pancreatitis). Early oral nutrition: within 24-48 hours as tolerated — reduces complications vs prolonged fasting. Antibiotics: NOT routinely — only for confirmed infected necrosis. Urgent ERCP: for biliary pancreatitis with cholangitis or persistent obstruction.

What is necrotising pancreatitis?

Necrotising pancreatitis: necrosis of pancreatic tissue in 10-20% of cases. Sterile necrosis: managed conservatively — antibiotics and drainage do not improve outcomes. Infected necrosis (fever + gas on CT, or culture-positive FNA): step-up approach — (1) CT-guided percutaneous catheter drainage → (2) endoscopic transluminal necrosectomy → (3) open surgery only if steps 1-2 fail (PANTER trial, NEJM 2010: step-up reduced major complications 43%). Timing: drainage deferred until walled-off necrosis forms (≥4 weeks) when feasible.

What is chronic pancreatitis and how is exocrine insufficiency managed?

Chronic pancreatitis causes irreversible pancreatic fibrosis — most commonly from alcohol (adults) or hereditary mutations (PRSS1, CFTR, SPINK1 — children/young adults). Exocrine pancreatic insufficiency (EPI): steatorrhoea (fatty, greasy, floating stools); weight loss; fat-soluble vitamin deficiency. Treatment: PERT — high-dose enteric-coated pancreatic enzymes (minimum 25,000-40,000 PhEur lipase units per main meal + 10,000-20,000 per snack) taken with every meal and snack. Type 3c diabetes: careful insulin therapy — hypoglycaemia-prone due to glucagon co-deficiency.

How does GMJ News cover pancreatitis?

GMJ News covers Atlanta Classification, gallstone + alcohol aetiology, WATERFALL trial, early oral feeding, BISAP severity score, step-up approach for infected necrosis, ERCP indications, hypertriglyceridaemia pancreatitis, autoimmune pancreatitis, PERT for EPI, type 3c diabetes, and chronic pancreatitis management.

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Pancreatitis

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Pancreatitis — inflammation of the pancreas — occurs in two major clinical forms: acute pancreatitis (the most common GI emergency requiring hospitalisation in many HICs, with gallstones and alcohol together responsible for approximately 80% of cases) and chronic pancreatitis (progressive irreversible fibrosis causing exocrine insufficiency, endocrine failure and intractable pain), with acute pancreatitis carrying a mortality of <1% in mild disease but exceeding 25-30% in infected necrotising pancreatitis — the most severe form (WHO). The most important clinical advances: early oral feeding (shown to reduce complications vs prolonged NPO); Lactated Ringer’s solution superior to normal saline for initial resuscitation (WATERFALL trial, NEJM 2022); and the step-up approach for infected pancreatic necrosis — catheter drainage before endoscopic necrosectomy before surgery — which has transformed the mortality of this condition.

Key messages

Gallstones + alcohol = ~80% of acute pancreatitis

Gallstones (biliary pancreatitis, 40-45%) and alcohol (35-40%) account for approximately 80% of acute pancreatitis cases. Gallstone migration lodges at the ampulla of Vater → ductal obstruction → premature trypsinogen activation → autodigestion. Other causes: hypertriglyceridaemia (>11 mmol/L); ERCP-induced; drugs (azathioprine, valproate, thiazides); autoimmune (IgG4-related); hereditary (PRSS1, CFTR mutations).

Lactated Ringer's preferred over normal saline — WATERFALL NEJM 2022

WATERFALL trial (NEJM 2022): 434 patients randomised to LR vs NS. LR significantly reduced moderately severe or severe pancreatitis (8.8% vs 16.0%) and SIRS. LR is buffered, calcium-containing — reduces the chloride-driven inflammatory cascade. LR is now the first-choice resuscitation fluid for acute pancreatitis.

Early oral feeding within 24-48 hours — the paradigm shift

Historical practice: prolonged NPO and nasojejunal tube feeding. Evidence: multiple RCTs and Cochrane review show early oral feeding (clear liquids → soft low-fat diet within 24-48 hours) reduces complications, hospital stay and the need for NJ tube feeding. NICE and IAP-APA guidelines: start oral nutrition as soon as tolerated, regardless of serum lipase/amylase levels.

BISAP score — rapid severity prediction

BISAP score (5 parameters): BUN >25 mg/dL; Impaired mental status; SIRS criteria met; Age >60; Pleural effusion. Score ≥3 = high risk for mortality and severe disease. Necrotising pancreatitis (10-20% of cases): mortality 25-30%. Infected necrosis: step-up approach (catheter → endoscopic → surgical).

Step-up approach for infected pancreatic necrosis

PANTER trial (NEJM 2010): step-up approach (CT-guided percutaneous catheter drainage → endoscopic transluminal necrosectomy → open surgery only if preceding steps fail) reduced major complications by 43% vs primary open necrosectomy. Sterile necrosis: manage conservatively — do not drain without clinical indication.

Chronic pancreatitis — PERT for exocrine insufficiency

Chronic pancreatitis → exocrine pancreatic insufficiency (EPI): malabsorption of fat, protein, fat-soluble vitamins → steatorrhoea. Treatment: pancreatic enzyme replacement therapy (PERT): high-dose enteric-coated microsphere preparations (minimum 25,000-40,000 PhEur lipase units per main meal + 10,000-20,000 per snack). Also: type 3c diabetes (beta-cell destruction — brittle, hypoglycaemia-prone); alcohol and tobacco cessation.

Key statistics

~80%

of acute pancreatitis caused by gallstones (40-45%) and alcohol (35-40%)

IAP-APA

WATERFALL 2022

LR reduces severe pancreatitis vs normal saline (NEJM 2022)

NEJM 2022

25-30%

mortality in infected necrotising pancreatitis

IAP-APA

PANTER 2010

step-up approach cut complications 43% vs primary open necrosectomy (NEJM 2010)

NEJM 2010

24-48 hours

target for starting early oral feeding in mild-moderate acute pancreatitis

NICE/IAP-APA

25,000 PhEur

minimum lipase units per main meal with PERT for EPI

ESPEN/IAP-APA

Acute pancreatitis severity distribution and mortality (Atlanta Classification)

Source: IAP-APA/Atlanta Classification. 80-90% mild and self-limiting; 10-20% severe with high mortality.

Glossary of key terms

Revised Atlanta Classification 2012
IAP-APAInternational standard for acute pancreatitis severity: Mild: no organ failure; no local or systemic complications. Moderately severe: transient organ failure (<48h) and/or local complications (peripancreatic fluid, pseudocyst, acute necrotic collection, walled-off necrosis). Severe: persistent organ failure (>48h) — respiratory (PaO2/FiO2 <300), renal (creatinine >170), cardiovascular (SBP <90).

Walled-off necrosis (WON)
Radiology/GIMature encapsulated necrotic collection — develops ≥4 weeks after necrotising pancreatitis. Distinguished from pseudocyst (fluid only). WON requires drainage if: infected (fever + gas on CT); symptomatic (pain, biliary/gastric outlet obstruction). EUS-guided transluminal drainage + lumen-apposing metal stent (LAMS) + direct endoscopic necrosectomy: preferred minimally invasive approach.

ERCP in gallstone pancreatitis
NICE/IAP-APAUrgent ERCP (within 24-48 hours) is indicated for gallstone pancreatitis with: concurrent cholangitis; persistent biliary obstruction. NOT indicated for uncomplicated gallstone pancreatitis without biliary obstruction — multiple RCTs show no benefit, risk of ERCP complications. After recovery: laparoscopic cholecystectomy during same admission or within 2 weeks.

Hypertriglyceridaemia pancreatitis
EndocrinologyTriglycerides >11.3 mmol/L cause pancreatitis via toxic free fatty acid release from TG hydrolysis. Management: insulin infusion ± plasmapheresis (rapid TG removal). Causes: familial hypertriglyceridaemia; secondary (uncontrolled diabetes, alcohol, hypothyroidism, drugs). After acute episode: fibrates + dietary fat restriction + omega-3 for long-term control.

Autoimmune pancreatitis (AIP)
Gastroenterology/IgG4Immune-mediated pancreatitis — Type 1 AIP (IgG4-related): elevated serum IgG4; diffuse sausage pancreas on imaging; dramatic response to prednisolone (30-40mg) — the hallmark. Can mimic pancreatic cancer. Type 2: no IgG4; IBD associated. Always consider AIP before pancreatic surgery — steroid trial appropriate when AIP is suspected.

Type 3c diabetes
Endocrinology/PancreatitisDiabetes from pancreatic disease: reduced insulin AND glucagon secretion → brittle diabetes with hypoglycaemia unawareness. Occurs after necrotising pancreatitis, chronic pancreatitis, pancreatectomy or pancreatic cancer. Often accompanied by exocrine insufficiency (requiring PERT). Management differs from T1/T2DM — particularly careful insulin titration.