1. What Is Necrotising Pancreatitis?

Pathophysiology

• Haemorrhage and oedema
• Microthrombus formation in the pancreatic microcirculation
• Hypoperfusion and necrosis of pancreatic parenchyma and peripancreatic fat

The failure of the pancreatic microcirculation — a hallmark feature — distinguishes necrotising pancreatitis from interstitial oedematous pancreatitis, where the blood supply is maintained. — Schwartz's Principles of Surgery, 11th Ed.

Three Anatomical Patterns (Revised Atlanta Classification 2012)

Extrapancreatic fat necrosis alone fulfils the criteria for NP but carries a better prognosis than cases with parenchymal necrosis. — Grainger & Allison's Diagnostic Radiology

2. The Classification Landscape — NP vs ANC vs WON

Full Comparison Table

The Distinction From Pseudocyst

3. When to Suspect Necrotising Pancreatitis

Clinical Red Flags

• Acute pancreatitis with persisting or worsening pain despite initial management
• SIRS criteria (≥2 of): temperature <36°C or >38°C, HR >90, RR >20 or PaCO₂ <32 mmHg, WBC >12,000 or <4,000/µL
• Hemoconcentration — haematocrit >44% (marker of third-space loss)
• Elevated admission BUN >20 mg/dL
• BISAP score ≥3: BUN >25, Impaired mental status, SIRS, Age >60, Pleural effusion
• APACHE II ≥8 at 24 h

• Age >60 years
• Obesity (BMI >30)
• Significant comorbidities (Charlson comorbidity index)
• Hypertriglyceridaemia-induced pancreatitis

• No clinical improvement after 48–72 hours of aggressive supportive care
• Rising or persistently elevated CRP >150 mg/L
• Development of organ failure — renal (creatinine >2.0 mg/dL), respiratory (PaO₂ <60), cardiovascular (SBP <90, HR >130)
• Fever spike after initial defervescence → raises concern for infected necrosis
• Gas bubbles on CT within a peripancreatic collection → strongly suggests infected necrosis
• Deteriorating haemodynamics despite fluid resuscitation

1. First 1–2 weeks: Dominated by SIRS and multi-organ dysfunction (early phase mortality)
2. Weeks 2–4 and beyond: Dominated by infectious complications — infected necrosis accounts for ~80% of deaths from acute pancreatitis

4. Diagnosis

Step 1 — Confirm Acute Pancreatitis

1. Abdominal pain characteristic of acute pancreatitis (epigastric, radiating to back)
2. Serum lipase or amylase >3× upper limit of normal
3. Characteristic imaging findings

Step 2 — Identify Necrosis (CECT)

• Timing: Not recommended in the first 24–48 hours (early CT underestimates necrosis extent). Optimal window is 48–72 hours after onset, or earlier if diagnosis is unclear.
• Key finding: Non-enhancing pancreatic parenchyma — necrotic tissue fails to take up IV contrast, appearing as a dark hypodense area against enhancing viable pancreas.
• ANC appearance: Heterogeneous, mixed-density collection (fluid + solid debris), no wall
• WON appearance: Heterogeneous collection with a thick, well-defined, enhancing rim; may have loculations
• Infected necrosis: Gas bubbles within the collection (pathognomonic); also rim-enhancement

CECT showing extensive hypoenhancing necrosis (asterisk) of the pancreatic body and tail, with residual enhancing parenchyma at the pancreatic head (arrow). — Current Surgical Therapy, 14th Ed.

Infected necrotising pancreatitis: gas foci within the collection + rim-enhancement + percutaneous drain in situ. — Current Surgical Therapy, 14th Ed.

MRI / MRCP

• Superior to CT for characterising solid debris within collections (distinguishing pseudocyst from WON)
• Can identify disconnected pancreatic duct (critical for surgical planning)
• Preferred in patients with renal impairment (no gadolinium needed for necrosis assessment)
• Detects choledocholithiasis without radiation

EUS (Endoscopic Ultrasound)

• Best for confirming WON location relative to stomach/duodenum before endoscopic drainage
• Allows aspiration for Gram stain and culture if infection is suspected but CT equivocal

Fine-Needle Aspiration (FNA)

• Image-guided FNA for Gram stain/culture when infected necrosis is suspected but CT is equivocal
• Risk: may introduce infection into a sterile collection — weigh this carefully
• Less commonly needed since gas on CT is sufficient evidence of infection

Laboratory Markers

Severity Scoring Systems

Scoring systems should augment clinical judgment, but not replace it. — Schwartz's Principles of Surgery, 11th Ed.

5. Management

A. Immediate Supportive Care (First 24–72 Hours)

1. IV fluid resuscitation — the single most important early intervention
   • Lactated Ringer's is preferred over normal saline (lowers CRP, reduces systemic inflammation)
   • Initial strategy: ~10–15 mL/kg bolus, followed by 1.5–2 mL/kg/h; titrate to urine output >0.5 mL/kg/h
   • Recent RCT evidence: overly aggressive hydration (>20 mL/kg) risks fluid overload without improved outcomes
   • Monitor: hematocrit and BUN every 8–12 h; rising BUN = inadequate resuscitation and higher mortality
2. Analgesia — IV opioid analgesics for pain control
3. NPO initially — to minimise pancreatic stimulation
4. Supplemental oxygen and monitoring
5. Early enteral nutrition (within 24–48 h if tolerated)
   • Strongly preferred over TPN; maintains gut barrier, reduces infectious complications
   • Nasojejunal (NJ) or nasogastric (NG) feeding both acceptable
   • TPN only if enteral route not tolerated
6. Antibiotics: Do NOT use prophylactic antibiotics routinely in sterile necrosis
   • Current guidelines recommend against routine prophylactic carbapenem use
   • Antibiotics indicated ONLY when infected necrosis is confirmed (clinical + radiological)
   • Use carbapenems, fluoroquinolones, or metronidazole (good pancreatic tissue penetration)
7. ICU admission for persistent organ failure, haemodynamic instability
8. Transfer to tertiary centre early for severe/complicated cases

B. Management of Infected Necrosis

The Step-Up Approach (Current Standard of Care)

Treatment algorithm for pancreatic necrosis — Current Surgical Therapy, 14th Ed.

Step 1 — Percutaneous Catheter Drainage (PCD)

• First-line intervention for infected/symptomatic necrosis
• Performed by interventional radiology under CT/US guidance
• Retroperitoneal access preferred (left flank) to allow potential VARD if needed
• Serial catheter upsizing + irrigation with saline or H₂O₂ for thick debris
• Up to 50% of patients treated with PCD alone — obviating need for further surgery
• Disadvantage: risk of pancreaticocutaneous fistula, especially if communicating with pancreatic duct

Step 2 — Endoscopic Transluminal Drainage + Necrosectomy (for WON only)

• Best for mature WON (≥4 weeks) within 2 cm of stomach or duodenum
• EGD + EUS to confirm location → needle puncture → balloon dilation of cystgastrotomy → placement of pigtail stents or lumen-apposing metal stent (LAMS)
• Nasocystic catheter for irrigation
• Direct endoscopic necrosectomy: endoscope inserted into cavity; mechanical debridement
• Requires multiple sessions (typically 3–5); specialist centre
• PENGUIN trial: endoscopic necrosectomy had fewer major complications, less organ failure, fewer fistulas than open surgery
• Operative debridement avoided in ~2/3 of patients

Step 3 — Surgical Necrosectomy

• Reserved for failures of percutaneous and endoscopic approaches
• Options: video-assisted retroperitoneal debridement (VARD), minimally invasive retroperitoneal pancreatic necrosectomy (MIRPN), or open necrosectomy
• Open necrosectomy now last resort due to high mortality historically (~45% vs 8.3% with conservative/minimally invasive approach)

6. Complications to Monitor

7. Quick Reference Summary

Acute Pancreatitis
       │
       ├── Interstitial Oedematous Pancreatitis (90–95%)
       │         │
       │         ├── <4 wks → APFC (Acute Peripancreatic Fluid Collection)
       │         └── >4 wks → Pseudocyst (pure fluid, thin wall)
       │
       └── NECROTISING PANCREATITIS (5–10%)
                 │
                 ├── <4 wks → ANC (Acute Necrotic Collection)
                 │         • Heterogeneous, NO wall, fluid + solid debris
                 │         • May be sterile or infected
                 │
                 └── >4 wks → WON (Walled-Off Necrosis)
                           • Heterogeneous, THICK WALL, fluid + solid debris
                           • May be sterile or infected
                           • Target for endoscopic/percutaneous drainage

Recent Evidence (2025)

• Current Surgical Therapy, 14th Edition — Local Complications of Acute Pancreatitis
• Schwartz's Principles of Surgery, 11th Edition — Management of Acute Pancreatitis
• Harrison's Principles of Internal Medicine, 22nd Edition (2025)
• Grainger & Allison's Diagnostic Radiology — Necrotising Pancreatitis
• Rosen's Emergency Medicine — Necrotizing Pancreatitis
• 2012 Revised Atlanta Classification (Banks PA et al., Gut 2013;62:102–111)Here is a comprehensive breakdown of everything you asked about:

Key Takeaways

The Core Distinction: NP vs ANC vs WON

When to Suspect NP

• Acute pancreatitis that does not improve in 48–72 hours
• Persistent SIRS, haemoconcentration (Hct >44%), rising BUN
• BISAP ≥3 or APACHE II ≥8
• Late deterioration or new fever → think infected necrosis (responsible for ~80% of deaths)
• Gas bubbles in a collection on CT = infected until proven otherwise

Diagnosis

• CECT at 48–72 h is gold standard — non-enhancing parenchyma = necrosis
• MRI/MRCP preferred if renal impairment or when characterising solid debris
• EUS to confirm WON position before endoscopic drainage
• FNA only if CT equivocal for infection (risk of seeding sterile necrosis)

Management

1. Supportive care: Lactated Ringer's IV fluid resuscitation, early enteral nutrition within 24–48 h, analgesia, ICU
2. No prophylactic antibiotics in sterile necrosis
3. Infected necrosis: delay intervention to ≥4 weeks if possible (let it wall off), then step-up approach:
   • Percutaneous catheter drainage first (~50% cured here alone)
   • Endoscopic transluminal drainage + necrosectomy for mature WON near stomach/duodenum
   • Surgical necrosectomy only as last resort