Acute & Chronic Pancreatitis

Pancreatitis is inflammation of the pancreas spanning a clinical spectrum from a self-limiting interstitial oedematous attack to lethal necrotising disease and, at the chronic end, irreversible fibrosis with exocrine and endocrine failure. This is among the most heavily examined hepatobiliary topics on NEET PG — Ranson's and Balthazar scoring, the investigation of choice, the surgical drainage procedures, and the named complications recur almost annually.

Definitions & classification

Acute pancreatitis = an acute inflammatory process of the pancreas with variable involvement of peripancreatic tissues and remote organ systems, classically diagnosed when 2 of 3 of the following are present (revised Atlanta 2012):

1. Abdominal pain consistent with acute pancreatitis (epigastric, radiating to back).
2. Serum amylase or lipase ≥ 3× the upper limit of normal.
3. Characteristic imaging findings on contrast-enhanced CT (CECT), MRI or USG.

High-yield: When the clinical picture and enzyme rise already satisfy the diagnosis, CECT is NOT needed to confirm pancreatitis — its main role is staging severity and detecting necrosis, ideally after 72 hours.

The Revised Atlanta Classification (2012) divides acute pancreatitis morphologically and by severity:

Severity grade	Defining feature
Mild	No organ failure, no local/systemic complications
Moderately severe	Transient organ failure (< 48 h) and/or local complications
Severe	Persistent organ failure > 48 h (single or multiple)

Two morphological types: interstitial oedematous pancreatitis (80–90%) and necrotising pancreatitis (10–20%, involving parenchyma and/or peripancreatic tissue).

Chronic pancreatitis = progressive, irreversible inflammatory destruction of pancreatic parenchyma leading to fibrosis, ductal distortion, calcification, and ultimately loss of exocrine (steatorrhoea) and endocrine (diabetes) function.

Etiology

The two commonest causes of acute pancreatitis worldwide are gallstones (≈ 40%) and alcohol (≈ 30%). The classic mnemonic is "I GET SMASHED":

• I – Idiopathic
• G – Gallstones (commonest overall)
• E – Ethanol (alcohol — commonest cause of chronic pancreatitis)
• T – Trauma (and post-ERCP)
• S – Steroids
• M – Mumps / Malignancy / Microbes
• A – Autoimmune (IgG4) / Ascaris
• S – Scorpion sting (Tityus trinitatis — classic exam fact)
• H – Hypercalcaemia / Hypertriglyceridaemia / Hyperparathyroidism
• E – ERCP
• D – Drugs (azathioprine, valproate, thiazides, didanosine, oestrogens)

High-yield: Gallstones are the single most common cause of acute pancreatitis; alcohol is the most common cause of chronic pancreatitis. Hypertriglyceridaemia causes pancreatitis when serum triglycerides exceed ~1000 mg/dL.

In children, the picture differs: trauma, structural anomalies (pancreas divisum, choledochal cyst), and systemic disease dominate. Hereditary pancreatitis is linked to mutations in PRSS1 (cationic trypsinogen — gain of function), SPINK1, and CFTR; PRSS1 carries a markedly raised lifetime risk of pancreatic adenocarcinoma.

Pathophysiology

The central event is premature intra-acinar activation of trypsinogen to trypsin, which then triggers a cascade activating other zymogens (chymotrypsin, elastase, phospholipase A2). Normally trypsin is kept inactive by SPINK1 (pancreatic secretory trypsin inhibitor) and is auto-degraded; when these protective mechanisms are overwhelmed, autodigestion ensues.

Flow of injury:

Acinar injury → co-localisation of zymogen granules with lysosomal hydrolases (cathepsin B) → trypsinogen → trypsin activation → local autodigestion + cytokine release (TNF-α, IL-1, IL-6, IL-8) → capillary leak / SIRS → distant organ injury (ARDS, AKI, shock).

• Gallstone mechanism: a stone impacted at the ampulla obstructs the pancreatic duct (and may cause bile reflux), raising intraductal pressure.
• Alcohol mechanism: increases zymogen secretion, promotes protein plug formation in ducts, and is directly toxic to acinar cells.
• Hypertriglyceridaemia: lipase liberates toxic free fatty acids.

In chronic pancreatitis, repeated injury drives stellate-cell–mediated fibrosis. The SAPE hypothesis (Sentinel Acute Pancreatitis Event) explains progression: an initial acute attack primes the gland, and recurrent insults convert acute injury into chronic fibrosis with ductal protein plugs that calcify into stones.

Clinical features

Acute pancreatitis:

• Severe, constant epigastric pain radiating to the back, often relieved by sitting forward (knee–chest / "prayer" position).
• Nausea, vomiting, low-grade fever.
• Signs of severe disease: tachycardia, hypotension, ecchymotic discolouration —
  • Grey Turner sign – flank bruising
  • Cullen sign – periumbilical bruising
  • Fox sign – inguinal ligament bruising
  • These reflect retroperitoneal haemorrhage and indicate severe necrotising disease (poor prognosis).
• Hypocalcaemia from saponification of calcium with free fatty acids (fat necrosis) — may cause tetany; a marker of severity.

Chronic pancreatitis:

• Recurrent or persistent epigastric pain (the dominant symptom).
• Steatorrhoea appears when > 90% of exocrine function is lost (lipase deficiency) — bulky, foul, greasy stools.
• Diabetes mellitus (endocrine failure, "type 3c").
• Weight loss, fat-soluble vitamin (A, D, E, K) deficiency, B12 deficiency.
• The classic triad of chronic pancreatitis = pancreatic calcification + steatorrhoea + diabetes mellitus.

Investigations & investigation of choice

Enzymes:

Enzyme	Notes
Serum amylase	Rises in 6–12 h, falls by 3–5 days; less specific (also rises in parotitis, perforation, ectopic)
Serum lipase	Rises 4–8 h, peaks 24 h, stays elevated 8–14 days; more sensitive AND more specific

High-yield: Lipase is the preferred enzyme for diagnosis — higher specificity and a longer window. The magnitude of enzyme elevation does NOT correlate with severity.

Imaging:

• USG abdomen – first-line to look for gallstones / biliary dilatation (identifies aetiology). Pancreas is often obscured by bowel gas.
• CECT (contrast-enhanced CT) – investigation of choice for assessing severity and necrosis; best done at ≥ 72 h (earlier scans underestimate necrosis). Non-enhancing pancreatic parenchyma = necrosis.
• MRCP – best for ductal anatomy, choledocholithiasis, and pancreatic duct disruption without contrast nephrotoxicity.
• EUS – most sensitive for small stones, microlithiasis and early chronic changes.

For chronic pancreatitis, CT showing pancreatic calcification is pathognomonic; MRCP/ERCP shows the "chain of lakes" / "chain of beads" appearance (alternating dilatation and stricture of the main duct). The secretin-enhanced MRCP and faecal elastase-1 (low) assess function; faecal elastase is the most practical exocrine function test.

Severity scoring

Ranson's criteria (for non-gallstone/general pancreatitis) — 5 on admission, 6 at 48 hours (mnemonic for admission: GA LAW):

On admission	At 48 hours
Glucose > 200 mg/dL	Calcium < 8 mg/dL
Age > 55 years	Haematocrit fall > 10%
LDH > 350 IU/L	Oxygen (PaO₂) < 60 mmHg
AST > 250 IU/L	BUN rise > 5 mg/dL
WBC > 16,000/mm³	Base deficit > 4 mEq/L
	Fluid sequestration > 6 L

High-yield: Ranson's score ≥ 3 = severe pancreatitis. Note that amylase/lipase levels are NOT part of Ranson's criteria. Full Ranson assessment needs 48 hours, which is its main limitation.

Balthazar CT Severity Index (CTSI) combines grade of inflammation (A–E, 0–4 points) with extent of necrosis (0–6 points), max 10:

Necrosis	Points
None	0
< 33%	2
33–50%	4
> 50%	6

CTSI 0–3 mild, 4–6 moderate, 7–10 severe.

Other scores: APACHE II (≥ 8 = severe; usable on day 1), BISAP (BUN > 25, Impaired mental status, SIRS, Age > 60, Pleural effusion — early bedside tool), and a CRP > 150 mg/L at 48 h predicts necrosis.

Management

High-yield: Modern management of acute pancreatitis is supportive — aggressive fluid resuscitation, oxygen, analgesia, and early enteral nutrition. Prophylactic antibiotics are NOT recommended for sterile necrosis.

Stepwise approach:

1. Fluids: early goal-directed crystalloid resuscitation (Ringer's lactate preferred over normal saline — reduces SIRS).
2. Analgesia: opioids; the old dogma against morphine (Oddi spasm) is no longer a contraindication.
3. Nutrition: early enteral feeding (oral/NG/NJ) within 24–72 h is superior to prolonged "nil by mouth"; reduces infective complications and maintains gut barrier. TPN only if enteral route fails.
4. Antibiotics: only for proven infected necrosis or cholangitis. Carbapenems (imipenem/meropenem) penetrate pancreatic tissue best.
5. ERCP + sphincterotomy: indicated urgently (< 24–72 h) in gallstone pancreatitis with concurrent cholangitis or persistent biliary obstruction.
6. Cholecystectomy: in mild gallstone pancreatitis, same admission ("index") laparoscopic cholecystectomy before discharge prevents recurrence. In severe disease, delay until inflammation resolves.

Managing infected necrosis — the "step-up approach" (PANTER trial): percutaneous/endoscopic drainage first → if no improvement, minimally invasive (video-assisted retroperitoneal / endoscopic) necrosectomy, reserving open necrosectomy as last resort. Intervention is ideally delayed ≥ 4 weeks to allow the necrosis to "wall off" (WON).

Chronic pancreatitis:

• Stop alcohol and smoking (smoking is an independent risk factor and accelerator).
• Pancreatic enzyme replacement therapy (PERT) for steatorrhoea; control diabetes.
• Pain control: analgesics, consider coeliac plexus block.
• Surgery / endotherapy for intractable pain or complications.

Surgical procedures for chronic pancreatitis (high-yield):

Procedure	Indication / principle
Puestow (modified) – lateral pancreaticojejunostomy	Dilated main duct (> 7 mm) — longitudinal drainage
Frey procedure	Duct drainage + local resection of pancreatic head
Beger procedure	Duodenum-preserving pancreatic head resection
Whipple (pancreaticoduodenectomy)	Head-dominant disease / suspected malignancy
Distal pancreatectomy	Disease confined to body/tail

High-yield: The (modified) Puestow procedure = lateral pancreaticojejunostomy is the answer for a chronically dilated pancreatic duct ("chain of lakes"). It drains rather than resects.

Complications

Local (acute):

• Acute peripancreatic fluid collection (< 4 weeks, no wall) → may resolve or evolve into a pseudocyst (> 4 weeks, fibrous wall, no epithelial lining; contains amylase-rich fluid).
• Acute necrotic collection → walled-off necrosis (WON) after 4 weeks.
• Pancreatic abscess (infected collection), haemorrhage, splenic/portal vein thrombosis, pseudoaneurysm (classically splenic artery), pancreatic ascites, colonic necrosis.

High-yield: A pseudocyst has NO epithelial lining (hence "pseudo"), takes > 4 weeks to mature, and is the commonest cystic complication. Intervene only if symptomatic, infected, > 6 cm, or persistent — by endoscopic cystogastrostomy (preferred), surgical drainage, or percutaneous drainage.

Systemic (acute): ARDS (most common pulmonary), AKI, shock, DIC, hypocalcaemia, hyperglycaemia, purtscher retinopathy, and metabolic disturbances. Persistent organ failure > 48 h defines severe disease and drives mortality.

Chronic: pseudocyst, common bile duct/duodenal obstruction, splenic vein thrombosis with sinistral (left-sided) portal hypertension and gastric varices, pancreatic ascites, and markedly increased risk of pancreatic adenocarcinoma.

Key differentials

• Perforated peptic ulcer — also raises amylase, free air on erect X-ray.
• Acute cholecystitis / cholangitis — RUQ pain, Murphy sign, Charcot triad.
• Mesenteric ischaemia — pain out of proportion, lactic acidosis, AF.
• Ruptured/dissecting aortic aneurysm — tearing back pain, pulsatile mass.
• Inferior MI — always ECG epigastric pain in older patients.
• Diabetic ketoacidosis — can itself raise amylase and mimic an abdomen.

Recently asked / exam angle

• Investigation of choice for severity / necrosis = CECT abdomen (done after 72 h); USG is first-line to find gallstones.
• Most specific enzyme = lipase; magnitude does not predict severity.
• Ranson's criteria — repeatedly tested on which parameter is/ is not included (amylase is NOT; glucose, age, LDH, AST, WBC are admission criteria).
• Scorpion sting (Tityus trinitatis) as a cause — single-best-answer favourite.
• Grey Turner / Cullen / Fox signs matched to anatomical site of bruising.
• Puestow = lateral pancreaticojejunostomy for a dilated duct — classic surgery one-liner.
• Pseudocyst: no epithelial lining, > 4 weeks, drainage of choice = endoscopic cystogastrostomy.
• Step-up approach / delayed necrosectomy (≥ 4 weeks) — PANTER trial concept.
• Hypertriglyceridaemia > 1000 mg/dL and hypercalcaemia as metabolic causes.
• Chain of lakes / chain of beads on MRCP = chronic pancreatitis.
• PRSS1 mutation in hereditary pancreatitis and its cancer link.
• Type 3c diabetes arising from chronic pancreatitis.

Rapid revision

1. Diagnose acute pancreatitis on 2 of 3 (pain, enzymes ≥ 3× ULN, imaging).
2. Gallstones = commonest acute cause; alcohol = commonest chronic cause.
3. Lipase is more sensitive and specific than amylase and stays up longer.
4. CECT at ≥ 72 h is the investigation of choice for necrosis and staging (Balthazar/CTSI).
5. Ranson's = 5 on admission (GA LAW) + 6 at 48 h; amylase is not a criterion; ≥ 3 = severe.
6. Grey Turner (flank), Cullen (umbilical), Fox (inguinal) signs = retroperitoneal bleed, severe disease.
7. Hypocalcaemia from fat saponification is a marker of severity.
8. Cornerstones of treatment: Ringer's lactate, oxygen, analgesia, early enteral nutrition; no prophylactic antibiotics for sterile necrosis.
9. Urgent ERCP only if gallstone pancreatitis has cholangitis/biliary obstruction; index cholecystectomy in mild gallstone disease.
10. Infected necrosis → step-up approach, necrosectomy delayed ≥ 4 weeks (walled-off necrosis).
11. Pseudocyst: no epithelial lining, > 4 weeks, drain by cystogastrostomy if symptomatic/large/infected.
12. Chronic pancreatitis triad = calcification + steatorrhoea + diabetes; Puestow (lateral pancreaticojejunostomy) drains a dilated duct.