Acute Pancreatitis

1. Definition

Acute pancreatitis is an acute inflammatory condition of the pancreatic parenchyma characterised by abdominal pain and elevated levels of pancreatic enzymes in the blood ^[1][2]. The name itself tells you the condition: "pan" = all, "creas" = flesh (Greek, referring to the fleshy organ), "-itis" = inflammation. So pancreatitis literally means "inflammation of the pancreas."

The key concept is autodigestion — the pancreas, which normally produces powerful digestive enzymes meant for the duodenum, begins digesting itself. This is what distinguishes pancreatitis from other causes of abdominal pain and makes it potentially lethal.

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2. Epidemiology

• Incidence: Approximately 13–45 per 100,000 population per year globally, with incidence rising over recent decades (likely due to increasing obesity, gallstone disease, and alcohol consumption).
• Age: Can occur at any age, but peak incidence is in the 4th–6th decades. Gallstone pancreatitis is more common in older adults (especially women), while alcoholic pancreatitis tends to present in younger men (30s–40s).
• Sex: Gallstone pancreatitis has a female predominance (mirrors gallstone epidemiology — "Fat, Forty, Female, Fertile, Fair"). Alcoholic pancreatitis has a male predominance.
• Hong Kong context: Gallstones are the leading cause. Alcohol is the second most common. Notably, Hong Kong has a relatively high prevalence of hepatobiliary disease including recurrent pyogenic cholangitis (RPC) related to Clonorchis sinensis (liver fluke) infection, which can also cause biliary pancreatitis. Post-ERCP pancreatitis is a recognized iatrogenic cause in tertiary centres performing high volumes of ERCP.
• Mortality:
  • Overall mortality: ~2–5%
  • Mild acute pancreatitis (interstitial/oedematous): < 1% mortality
  • Severe acute pancreatitis (necrotising with organ failure): 15–40% mortality ^[1][3]
  • Since the associated mortality of fulminant acute pancreatitis approaches 40%, early identification of high-risk patients and aggressive supportive care is critical ^[3].

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3. Risk Factors

The classic mnemonic for causes doubles as risk factors. Think "I GET SMASHED":

Risk factors for severe disease (important for prognosis):

• Age > 55
• Obesity (BMI > 30) — predisposes to peripancreatic fat necrosis
• Organ failure at presentation
• Pleural effusion or pulmonary infiltrates
• APACHE II score ≥ 8 at admission ^[3]
• CRP > 150 mg/L at 48 hours ^[2]

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4. Anatomy and Function of the Pancreas

Understanding the anatomy is essential because it explains why pancreatitis causes the clinical features it does (retroperitoneal pain, vascular complications, splenic vein thrombosis, etc.).

4.1 Gross Anatomy

The pancreas is a retroperitoneal organ lying obliquely across the posterior abdominal wall, with the tail higher than the head ^[3].

Four sections (right to left):

4.2 Ductal Anatomy

• Main pancreatic duct (duct of Wirsung): Runs the length of the pancreas, joins the common bile duct (CBD) at the ampulla of Vater (hepatopancreatic ampulla), which opens into the second part of the duodenum at the major duodenal papilla.
• Accessory pancreatic duct (duct of Santorini): Drains the upper head; opens at the minor duodenal papilla.
• The sphincter of Oddi controls flow of bile and pancreatic juice into the duodenum. This is clinically important because:
  • A gallstone impacting at the ampulla obstructs both the CBD and the pancreatic duct → reflux of bile into the pancreatic duct → pancreatitis.
  • Drugs like morphine cause sphincter of Oddi spasm → theoretically worsening obstruction.

Acute biliary pancreatitis occurs when a gallstone (particularly small stones from a gallbladder with multiple small stones) passes through a wide cystic duct and impacts at the common channel (the shared terminal portion of the CBD and pancreatic duct at the ampulla) ^[5]. The stone obstructs outflow → bile reflux into the pancreatic duct → enzyme activation → pancreatitis.

4.3 Vascular Supply

Arterial supply: Dual supply from the coeliac trunk and the superior mesenteric artery (SMA) ^[3]:

• Head: Superior pancreaticoduodenal arteries (from gastroduodenal artery, a branch of the coeliac trunk) and inferior pancreaticoduodenal arteries (from the SMA) — these form anastomotic arcades around the head.
• Body and Tail: Branches of the splenic artery (dorsal pancreatic, great pancreatic/pancreatica magna, caudal pancreatic arteries).

Venous drainage ^[3]:

• Superior and inferior pancreaticoduodenal veins → SMV
• Splenic veins → portal vein
• This is why pancreatitis can cause splenic vein thrombosis (the vein runs along the posterior surface of the pancreas) and portal vein thrombosis.

4.4 Exocrine and Endocrine Function

Normal protective mechanisms against autodigestion:

1. Enzymes are synthesised as inactive zymogens (e.g., trypsinogen, not trypsin)
2. Stored in zymogen granules — physically separated from cytoplasm
3. Pancreatic secretory trypsin inhibitor (PSTI/SPINK1) — a "safety catch" that inhibits any prematurely activated trypsin
4. Enzymes are only activated in the duodenal lumen by enterokinase (which converts trypsinogen → trypsin, and trypsin then activates all other zymogens in a cascade)

Pancreatitis occurs when these protective mechanisms fail.

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5. Aetiology

5.1 Overview — Aetiology of acute pancreatitis [4]

The two dominant causes account for ~90% of cases:

1. Gallstones (55%) ^[4]
2. Chronic alcoholism (35%) ^[4]
3. Miscellaneous causes (10%) ^[4]

A useful mnemonic specifically from senior notes: GAME ID ^[2]:

• G = Gallstone (most common): suspect if history of biliary colic or ↑ALP
• A = Alcohol: suspect if ↑AST
• M = Metabolic: hypertriglyceridaemia / hypercalcaemia
• E = ERCP: reduced by PR NSAID or temporary pancreatic stenting
• I = Idiopathic (10%)
• D = Drugs (NSAIDs, steroids, azathioprine, ACEi, valproate)

5.2 Detailed Aetiology with Pathophysiological Mechanisms

A. Gallstones (Biliary Pancreatitis)

Mechanism: A gallstone (usually small, < 5 mm) migrates from the gallbladder through the cystic duct and impacts at the ampulla of Vater ^[3][5]:

• Transient or persistent obstruction of the common channel → reflux of bile into the pancreatic duct (the "common channel theory")
• Bile activates trypsinogen to trypsin within the pancreatic parenchyma
• Trypsin triggers a cascade of activation of other zymogens → autodigestion
• Additionally, obstruction causes increased intraductal pressure → acinar cell injury

Clinical clues: History of biliary colic, female sex, ↑ALP and bilirubin (cholestatic pattern), gallstones visible on USG.

The slide shows that biliary pancreatitis is facilitated by: wide cystic duct, multiple small stones, a common channel larger than the size of the stone ^[5]. This means small stones can easily traverse the cystic duct but then impact at the narrower ampulla.

B. Alcohol

Mechanism ^[3]:

• Alcohol increases synthesis of digestive enzymes AND lysosomal enzymes (cathepsin B) by pancreatic acinar cells
• Cathepsin B can convert trypsinogen → trypsin within the acinar cell (co-localisation hypothesis)
• Alcohol also causes protein plug formation in small pancreatic ductules → obstruction
• Alcohol is directly toxic to acinar cells, causing oxidative stress and mitochondrial dysfunction
• Usually requires chronic heavy intake (> 4–5 drinks/day for > 5 years), but acute binge can precipitate an acute episode

Clinical clues: History of chronic heavy alcohol use, ↑AST (AST:ALT > 2 is suggestive of alcohol), hepatomegaly, stigmata of chronic liver disease.

C. Metabolic Causes

Hypertriglyceridaemia (TG > 11.3 mmol/L or > 1000 mg/dL):

• Lipase is thought to liberate toxic fatty acids into the pancreatic microcirculation → microcirculatory impairment and ischaemia → acinar cell injury ^[3]
• The free fatty acids are directly cytotoxic to acinar cells and capillary endothelium
• Commonly seen in familial hyperlipoproteinaemia (Types I, IV, V), uncontrolled diabetes, pregnancy, alcohol use, certain drugs (oestrogens, tamoxifen, protease inhibitors)

Hypercalcaemia (most commonly from hyperparathyroidism):

• Ca²⁺ activation of trypsinogen within pancreatic parenchyma ^[3]
• Formation and deposition of calcified stones intraductally in the pancreatic duct → obstruction ^[3]
• Calcium also promotes enzyme secretion and increases duct permeability

D. Post-ERCP Pancreatitis

• Definition: abdominal pain + increase in serum amylase > 3x ULN + requires hospitalisation ^[6]
• Pathogenesis: activation of acinar cells by mechanical, chemical or hydrostatic injury during the procedure ^[6]
• Occurs in approximately 4% of ERCP procedures ^[6]
• Risk factors ^[6]:
  • Patient factors: young female, suspected sphincter of Oddi dysfunction, history of post-ERCP pancreatitis, recurrent pancreatitis
  • Procedural factors: pre-cut sphincterotomy, pancreatic duct injection
• Prevention ^[6]:
  • Pharmacological: PR NSAID (e.g. indomethacin) pre-operatively
  • Mechanical: pancreatic duct stent, guidewire cannulation before contrast injection (by avoiding injection into the pancreatic duct)

E. Drug-Induced Pancreatitis

Mnemonic: "SAND-TV" — Steroids, Azathioprine, NSAIDs, Diuretics (furosemide/thiazides), Trimethoprim-sulfamethoxazole, Valproic acid

Additional drugs ^[3][4]:

• Dipeptidyl peptidase-4 (DPP-4) inhibitors (e.g. sitagliptin — used in diabetes)
• Chemotherapy, anticonvulsants ^[4]
• ACE inhibitors ^[2]

Mechanism varies by drug: direct toxic effect on acinar cells, immunological reaction, increased viscosity of pancreatic juice, or sphincter of Oddi spasm.

F. Infections [3]

Clonorchis sinensis is particularly relevant in Hong Kong — these liver flukes reside in the bile ducts and can cause biliary obstruction → pancreatitis. This overlaps with the aetiology of recurrent pyogenic cholangitis (RPC) ^[7].

G. Trauma / Iatrogenic

• Blunt abdominal injury (e.g. steering wheel injury in RTA — compresses pancreas against the vertebral column) ^[4]
• Iatrogenic: post-TOCE (transarterial oily chemoembolisation) ^[4], post-surgery (especially gastric/biliary surgery)

H. Tumours [3]

• Pancreatic tumours: Can obstruct the main pancreatic duct
• Periampullary tumours: Obstruct the ampulla (ampullary adenoma/carcinoma, cholangiocarcinoma, duodenal carcinoma)
• Always consider in older patients with "idiopathic" first episode of pancreatitis — do cross-sectional imaging!

I. Autoimmune [2][3]

• Autoimmune pancreatitis (AIP): IgG4-related disease (Type 1) or duct-centric pancreatitis (Type 2)
• SLE, Sjögren's syndrome, Primary biliary cholangitis (PBC)
• Mechanism: immune-mediated ductal and acinar inflammation

J. Anatomical / Congenital

• Pancreas divisum: Most common congenital anomaly of the pancreas ^[2] — failure of fusion of the dorsal and ventral pancreatic buds → the majority of the pancreas drains through the minor papilla (which may be inadequate → recurrent pancreatitis)
• Annular pancreas, choledochal cysts

K. Others [2]

• Pregnancy (related to gallstones and hypertriglyceridaemia)
• Scorpion venom (exotic but board-classic — stimulates pancreatic secretion)

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6. Pathophysiology

This is the heart of understanding the disease. Everything — the clinical features, the complications, the management — makes sense once you understand the pathophysiology.

6.1 The Initiating Event

Activation of pancreatic enzymes → Autodigestion of pancreas → Pancreatic necrosis ^[8]

Step by step:

1. Initiating insult (gallstone obstruction, alcohol toxicity, etc.) → disruption of normal protective mechanisms
2. Unregulated premature activation of pancreatic enzymes, especially trypsin, within pancreatic acinar cells ^[3]
3. Trypsin activates a cascade of other zymogens:
   • Elastase → digests blood vessel walls → haemorrhage
   • Phospholipase A2 → digests cell membranes → cell death
   • Lipase → digests peripancreatic fat → fat necrosis (the chalky white spots you see at surgery)
4. Autodigestion of pancreatic tissues → peripancreatic and pancreatic necrosis ^[3]
5. Autodigestion extends beyond the pancreas into the retroperitoneum, digesting peripancreatic tissues, causing fat necrosis and erosion of blood vessels with haemorrhage ^[3]
6. Entry of enzymes into the bloodstream may cause respiratory and renal injury and other systemic effects ^[3]

6.2 The Inflammatory Cascade (Systemic Events)

NF-κB-dependent inflammatory pathway regulates the synthesis of multiple cytokines and chemokines → recruitment of inflammatory cells (neutrophils, macrophages) → these magnify and propagate systemic inflammation ^[3].

Key mediators:

• Pro-inflammatory cytokines: TNF-α, IL-1, IL-2, IL-6 ^[3]
• Chemokines and anti-inflammatory factors
• Inflammatory cells, once recruited to the pancreas, cause further acinar cell injury → a vicious cycle ^[3]

This cytokine storm is what converts a local pancreatic problem into a systemic disease (SIRS → MODS).

6.3 Progression from Oedematous to Necrotising Pancreatitis

This is a critical teaching point from the lecture slides:

Acute oedematous pancreatitis → Volume depletion → Hypoperfusion of gut and pancreas → Mucosal barrier breakdown → Pancreatic necrosis + Peripancreatic necrosis → Endotoxaemia ^[9]

Reasons for progression ^[10]:

1. Hypoperfusion of pancreas — as the inflammatory oedema and third-spacing cause volume depletion, the pancreas itself becomes ischaemic, converting potentially reversible oedematous pancreatitis into irreversible necrosis
2. Persistent ampullary obstruction by stone — ongoing obstruction prevents resolution and drives continued enzyme activation

Also from the slides, the parallel pathway ^[8]:

Activation of pancreatic enzymes → Autodigestion of pancreas → Pancreatic necrosis (direct enzyme damage pathway)

AND simultaneously:

Occlusion of blood vessels within the pancreas → Hypoperfusion of pancreas → additional ischaemic necrosis ^[8]

Enzyme leakage into retroperitoneum → Peripancreatic necrosis ^[8]

6.4 Why Gut Mucosal Barrier Breakdown Matters

When the gut becomes hypoperfused, the intestinal mucosal barrier breaks down → bacterial translocation (gut bacteria, especially Gram-negatives like E. coli, Klebsiella, enter the bloodstream and reach the necrotic pancreas) → infected pancreatic necrosis → sepsis. This is the main mechanism by which sterile necrosis converts to infected necrosis, and it is the leading cause of late mortality in severe acute pancreatitis.

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7. Classification

7.1 Revised Atlanta Classification (2012) — Morphological Types

Two broad categories based on whether necrosis is present ^[2]:

7.2 Revised Atlanta Classification — Severity Grading [2][3]

This is the most important classification for clinical practice and exams:

Organ failure is defined using the Modified Marshall Scoring System for three organ systems:

• Respiratory: PaO₂/FiO₂ ≤ 300 (= acute lung injury/ARDS)
• Cardiovascular: Systolic BP < 90 mmHg not responsive to fluid resuscitation (= shock)
• Renal: Creatinine ≥ 170 μmol/L (= acute kidney injury)

A score of ≥ 2 in any system = organ failure.

7.3 Scoring Systems for Severity Prediction

A. Ranson's Criteria [2][3]

Mnemonic: 0 hours = "GALAW", 48 hours = "CHOBBS" ^[2]

At admission (0 hours) — GALAW:

At 48 hours — CHOBBS:

Interpretation ^[3]:

• Score < 3: Mortality 0–3% (mild)
• Score ≥ 3: Mortality 11–15% (severe if score ≥ 3) ^[2]
• Score ≥ 6: Mortality ~40%

Limitation: Cannot be fully calculated until 48 hours after admission ^[3]. Validated for alcoholic/gallstone pancreatitis only ^[2].

B. APACHE II Score (Acute Physiology and Chronic Health Examination II) [3]

• 14 parameters: Age, rectal temperature, MAP, HR, RR, GCS, A-a gradient or PaO₂, pH or HCO₃, haematocrit, WBC, serum Na⁺, serum K⁺, creatinine, chronic disease points ^[3]
• Advantage: Can be calculated at admission and updated daily to allow continual reassessment ^[3]
• Disadvantage: Somewhat cumbersome and difficult to calculate, which limits its everyday use ^[3]
• Interpretation ^[3]:
  • Score < 8: Mortality < 4%
  • Score ≥ 8: Mortality 11–18% (indicates severe acute pancreatitis) ^[2]

C. Glasgow (Imrie) Score

• ≥ 3 out of 8 parameters in the first 48 hours indicates severe attack ^[2]
• Parameters (mnemonic "PANCREAS"): PaO₂ < 8 kPa, Age > 55, Neutrophils (WBC) > 15 × 10⁹/L, Calcium < 2 mmol/L, Renal (urea > 16 mmol/L), Enzymes (LDH > 600 U/L), Albumin < 32 g/L, Sugar (glucose > 10 mmol/L)

D. Balthazar CT Severity Index (CTSI)

• Grade of pancreatitis (0–4) + percentage of necrosis (0–6) ^[2]
• Used to correlate CT findings with prognosis
• Higher scores predict morbidity and mortality

E. CRP > 150 mg/L at 48 hours [2]

• Simple, widely available biomarker
• Predicts severe attack ^[2]

F. BISAP Score (Bedside Index for Severity in Acute Pancreatitis)

• 5 parameters (within 24 hours): BUN > 25 mg/dL, Impaired mental status, SIRS, Age > 60, Pleural effusion
• Score ≥ 3: significantly increased mortality
• Advantage: Can be calculated within 24 hours (faster than Ranson's)

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8. Clinical Features

8.1 Symptoms

8.2 Signs

A. General Examination

B. Abdominal Examination

Inspection:

Palpation:

Percussion:

Auscultation:

8.3 Signs Specifically Suggestive of Severe Disease

These should trigger escalation of care:

• Cullen's / Grey Turner's / Fox's signs (retroperitoneal haemorrhage)
• Tachycardia with hypotension (shock)
• Oliguria (AKI)
• Confusion/altered mental status (encephalopathy from hypoxia/hypotension/metabolic derangement)
• Respiratory distress (ARDS)
• Abdominal compartment syndrome (tense distension, oliguria, respiratory failure — from massive retroperitoneal oedema)

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9. Clinical Approach to a Patient with Suspected Acute Pancreatitis

A structured approach on the ward:

Step 1: Recognise the Pattern

• Epigastric pain radiating to back, worse lying flat, better leaning forward, with nausea/vomiting → think pancreatitis
• High level of clinical suspicion ^[11] — the slide emphasises this

Step 2: Confirm the Diagnosis

• Apply the Revised Atlanta diagnostic criteria (2/3) ^[2][3]:
  1. Clinical: typical pain
  2. Biochemical: amylase or lipase ≥ 3× ULN
  3. Imaging: characteristic findings

Step 3: Establish the Aetiology

• History: alcohol, gallstones, recent ERCP, drugs, family history of hyperlipidaemia
• Investigations: LFT pattern (cholestatic = biliary), lipid panel, calcium, USG for gallstones

Step 4: Assess Severity

• Ranson's, APACHE II, Glasgow, BISAP scores
• CRP at 48 hours
• CT abdomen with contrast (ideally at 72–96 hours for necrosis assessment)
• Look for organ failure (Modified Marshall Score)

Step 5: Initiate Management

• (To be covered in detail in the next response)

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10. Summary of Pathophysiology → Clinical Feature Connections

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Active Recall - Acute Pancreatitis (Definition, Epidemiology, Aetiology, Pathophysiology, Classification, Clinical Features)

1. What are the two most common causes of acute pancreatitis and their approximate percentages?

Your answer

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Gallstones (55%) and chronic alcoholism (35%). Together they account for approximately 90% of cases. Miscellaneous causes account for the remaining 10%.

2. Explain the pathophysiological mechanism by which gallstones cause acute pancreatitis.

Your answer

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Small gallstone migrates through cystic duct and impacts at the ampulla of Vater, obstructing the common channel. This causes reflux of bile into the pancreatic duct and increased intraductal pressure, leading to premature activation of trypsinogen to trypsin within acinar cells, triggering a cascade of zymogen activation and autodigestion of the pancreas.

3. State the Revised Atlanta diagnostic criteria for acute pancreatitis.

Your answer

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Diagnosis requires 2 out of 3: (1) Typical clinical presentation - acute onset of persistent severe epigastric pain often radiating to back, (2) Serum amylase or lipase at least 3 times the upper limit of normal, (3) Characteristic findings on imaging (USG, CT, or MRI).

4. What is the pathophysiological basis of Cullen's sign and Grey Turner's sign in acute pancreatitis?

Your answer

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Both result from retroperitoneal haemorrhage due to erosion of blood vessels by activated pancreatic elastase. Cullen's sign is periumbilical ecchymosis (blood tracks along the falciform ligament). Grey Turner's sign is flank ecchymosis (blood tracks laterally). Both indicate haemorrhagic or necrotising pancreatitis and are late signs of severity.

5. Using Ranson's criteria, state the parameters assessed at admission (0 hours) using the mnemonic GALAW.

Your answer

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G = Glucose > 11.1 mmol/L, A = Age > 55, L = LDH > 350 U/L, A = AST > 250 U/L, W = WBC > 16 x 10^9/L. Score of 3 or more indicates severe pancreatitis.

6. Explain why acute pancreatitis can cause hypocalcaemia and what clinical sign this manifests as.

Your answer

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Pancreatic lipase causes peripancreatic fat necrosis, releasing fatty acids that bind (precipitate/saponify) with calcium ions, reducing free ionised calcium. Additionally, hypoalbuminaemia from third-spacing reduces total calcium. Clinically manifests as tetany (carpopedal spasm, Chvostek and Trousseau signs).

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References

^[1] General medical knowledge on acute pancreatitis (standard textbook) ^[2] Senior notes: maxim.md (Acute pancreatitis section) ^[3] Senior notes: felixlai.md (Acute pancreatitis section) ^[4] Lecture slides: Acute pancreatitis.pdf (p3 — Aetiology of acute pancreatitis) ^[5] Lecture slides: Acute pancreatitis.pdf (p4 — Acute biliary pancreatitis) ^[6] Senior notes: maxim.md (Post-ERCP pancreatitis section) ^[7] Senior notes: maxim.md (Gallstone pathology section) ^[8] Lecture slides: Acute pancreatitis.pdf (p5 — Activation of pancreatic enzymes pathway) ^[9] Lecture slides: Acute pancreatitis.pdf (p6 — Acute oedematous pancreatitis progression) ^[10] Lecture slides: Acute pancreatitis.pdf (p7 — Reasons for progression to necrotising pancreatitis) ^[11] Lecture slides: Acute pancreatitis.pdf (p8 — Diagnosis of acute pancreatitis clinical features)

Differential Diagnosis of Acute Pancreatitis

The differential diagnosis of acute pancreatitis is essentially the differential of severe acute epigastric pain — and it's a critical list because misdiagnosis can be fatal. The reason the DDx is broad is that the epigastrium is a "crossroads" — it overlays the stomach, duodenum, pancreas, biliary tree, transverse colon, aorta, and even receives referred pain from the heart and lungs. You need a high level of clinical suspicion ^[11] and must systematically exclude dangerous mimics.

The approach to the DDx should be organ-system-based, thinking about what structures lie in the epigastrium and upper abdomen, plus any extra-abdominal causes that can refer pain there.

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Organising Framework

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Detailed Differential Diagnosis

The conditions listed below are taken from the senior notes ^[3][2] and supplemented with additional important mimics. For each, I explain why it mimics pancreatitis and the key distinguishing features.

1. Peptic Ulcer Disease (PUD) [3]

• Why it mimics pancreatitis: Epigastric pain, nausea, vomiting. A posterior duodenal ulcer can even penetrate into the pancreas itself, causing a secondary pancreatitis and elevated amylase.
• Key distinguishing features:
  • PUD pain classically has a relationship with food (gastric ulcer = worsened by eating; duodenal ulcer = relieved by eating, worse on empty stomach — "hunger pain")
  • PUD pain is typically burning and more superficial; pancreatitis pain is deep, boring, and radiates to the back
  • No significant elevation of amylase/lipase to ≥ 3× ULN in uncomplicated PUD
  • Endoscopy (OGD) is diagnostic for PUD

2. Perforated Peptic Ulcer (PPU) [2][12]

• Why it mimics pancreatitis: Sudden severe epigastric pain. Perforated duodenal ulcer fluid can track down the right paracolic gutter and even irritate the pancreas, causing secondary hyperamylasaemia.
• PPU is a key DDx because serum amylase can be elevated (false positive for pancreatitis) ^[2] — gastric/duodenal contents leaking into the peritoneum contain salivary amylase, and peritoneal irritation causes amylase reabsorption.
• Key distinguishing features:
  • PPU causes sudden onset "thunderclap" pain (the moment of perforation), whereas pancreatitis builds up over hours
  • Board-like rigidity and generalised peritonism — PPU causes chemical peritonitis from free gastric acid. In pancreatitis (retroperitoneal), peritoneal signs are often less marked initially.
  • CXR shows free air under the diaphragm (pneumoperitoneum) — this is absent in pancreatitis ^[2]
  • Valentino's sign: gastric contents from a PPU can track down to the RLQ, mimicking appendicitis ^[6]
  • CT abdomen with contrast is indicated when the diagnosis is uncertain (DDx PPU, gangrenous cholecystitis, ischaemic bowel) ^[2]

3. Choledocholithiasis / Acute Cholangitis [3][12]

• Why it mimics pancreatitis: RUQ/epigastric pain, jaundice, deranged LFTs. In fact, gallstone pancreatitis and cholangitis frequently coexist — a stone at the ampulla can cause both simultaneously.
• Key distinguishing features:
  • Charcot's triad (fever + abdominal pain + jaundice) or Reynolds' pentad (+ hypotension + confusion) points towards cholangitis ^[12]
  • Cholangitis presents with a predominantly cholestatic LFT pattern (↑ALP, ↑GGT, ↑conjugated bilirubin) with less dramatic transaminase rise
  • In pancreatitis, amylase/lipase ≥ 3× ULN is the hallmark; in cholangitis, amylase may be mildly elevated but usually < 3× ULN unless there is concurrent pancreatitis
  • USG shows dilated CBD (> 6 mm, or > 10 mm post-cholecystectomy) with possible stone visible
  • Important: if both cholangitis and pancreatitis are present (gallstone pancreatitis with cholangitis), ERCP within 24–72 hours is indicated ^[2]

4. Acute Cholecystitis [3][12]

• Why it mimics pancreatitis: RUQ pain (which can radiate to the epigastrium), fever, nausea/vomiting, leukocytosis, and even mildly elevated amylase.
• Key distinguishing features:
  • Pain is predominantly RUQ, not epigastric. Positive Murphy's sign (inspiratory arrest on palpation of RUQ) — this sign is absent in pancreatitis
  • Biliary colic (gallbladder contraction against an impacted stone) lasts < 6 hours and resolves; cholecystitis pain persists > 6 hours with systemic inflammation ^[12]
  • USG shows gallbladder wall thickening (> 3 mm), pericholecystic fluid, distended gallbladder, and positive sonographic Murphy's sign
  • Amylase/lipase are usually normal or only mildly elevated in isolated cholecystitis

5. Hepatitis [3]

• Why it mimics pancreatitis: Epigastric / RUQ pain, nausea, vomiting, jaundice, malaise. Acute viral hepatitis (especially HAV/HBV/HEV) can present with significant abdominal pain.
• Key distinguishing features:
  • Hepatocellular LFT pattern: massively elevated transaminases (ALT/AST often > 1000 U/L) with bilirubin rise; in pancreatitis, transaminases are only mildly elevated (in gallstone pancreatitis ALT may rise to a few hundred, but not thousands)
  • Viral serology (HBsAg, anti-HAV IgM, anti-HEV IgM) is diagnostic
  • Amylase/lipase are normal in hepatitis
  • Prodromal symptoms (fever, arthralgia, rash in HBV) may precede jaundice

6. Mesenteric Ischaemia [3]

• Why it mimics pancreatitis: Severe epigastric/periumbilical pain, often out of proportion to physical findings (classically "pain out of proportion to exam"), nausea, vomiting, and can cause elevated amylase (from ischaemic bowel releasing amylase).
• Key distinguishing features:
  • Mesenteric ischaemia classically occurs in elderly patients with atrial fibrillation (embolic) or atherosclerotic risk factors (thrombotic), or post-prandially ("intestinal angina" in chronic mesenteric ischaemia)
  • Pain out of proportion to physical examination is the hallmark — the abdomen is initially soft with minimal tenderness despite agonising pain. In pancreatitis, there is usually epigastric tenderness on examination.
  • Metabolic (lactic) acidosis develops early
  • CT angiography shows mesenteric vessel occlusion or bowel wall changes (pneumatosis, portal venous gas)
  • CT abdomen with contrast is indicated when the diagnosis is uncertain (DDx PPU, gangrenous cholecystitis, ischaemic bowel) ^[2]

7. Intestinal Obstruction [3]

• Why it mimics pancreatitis: Abdominal pain, vomiting, distension. Small bowel obstruction can cause a mildly elevated amylase (from mucosal ischaemia and reabsorption).
• Key distinguishing features:
  • Pain in obstruction is classically colicky (comes and goes in waves) — pancreatitis pain is constant
  • Absolute constipation (no flatus, no stool) in complete obstruction — not a feature of pancreatitis
  • High-pitched, tinkling bowel sounds in mechanical obstruction vs hypoactive/absent bowel sounds in pancreatitis (paralytic ileus)
  • AXR shows dilated bowel loops with air-fluid levels in a stepladder pattern; in pancreatitis, you see sentinel loop sign and colonic cut-off sign instead ^[2]

8. Myocardial Infarction (MI) [3]

This is the one you must not miss. It was specifically highlighted with an asterisk in the senior notes ^[3].

• Why it mimics pancreatitis: An inferior MI can present as epigastric pain, nausea, and vomiting — because the inferior surface of the heart (supplied by the RCA) sits on the diaphragm, referring pain to the epigastrium via shared T5–T9 visceral afferents.
• Key distinguishing features:
  • Risk factors for coronary artery disease (smoking, diabetes, hypertension, hyperlipidaemia, family history)
  • Pain is more commonly described as crushing, pressure-like, with radiation to the left arm, jaw, or neck — though atypical presentations (especially in diabetics, elderly, women) may lack these classic features
  • ECG changes (ST elevation/depression, new LBBB, pathological Q waves)
  • Cardiac markers (troponin TnI/TnT) are elevated — this is exactly why troponin ± ECG is part of the workup for acute pancreatitis, to exclude MI as a differential ^[3]
  • Amylase/lipase are normal in MI (unless there is concurrent mesenteric ischaemia from cardiogenic shock)

Cardiac markers ± ECG should be checked in every patient presenting with acute epigastric pain to exclude myocardial infarction (MI) as a differential diagnosis ^[3].

9. Ruptured Abdominal Aortic Aneurysm (rAAA) [2]

• Why it mimics pancreatitis: Severe abdominal/back pain (AAA rupture into the retroperitoneum causes intense back pain, just like pancreatitis). Both conditions can cause Cullen's sign and Grey Turner's sign (both are causes of retroperitoneal haemorrhage) ^[12].
• False positive elevated amylase can occur in ruptured AAA ^[2].
• Key distinguishing features:
  • rAAA presents with the classic triad: abdominal pain + hypotension + pulsatile abdominal mass (though all three are present in only ~50%)
  • Age > 65, male, smoking history, known AAA
  • Haemodynamic instability is typically more dramatic and earlier than in pancreatitis
  • CT angiography is diagnostic (retroperitoneal haematoma, contrast extravasation)

10. Diabetic Ketoacidosis (DKA) [2]

• Why it mimics pancreatitis: DKA commonly presents with abdominal pain, nausea, and vomiting. Additionally, DKA can cause a false positive elevated serum amylase ^[2].
• Key distinguishing features:
  • Known diabetic (or new presentation of T1DM), polyuria, polydipsia, fruity breath (ketone bodies)
  • Blood glucose markedly elevated, ketonaemia/ketonuria, metabolic acidosis with high anion gap
  • Amylase elevation in DKA is usually salivary (not pancreatic) in origin — serum lipase is a better discriminator (normal in DKA, elevated in pancreatitis)
  • Abdominal pain in DKA resolves with correction of ketoacidosis; if pain persists after correction, consider true pancreatitis (which can be precipitated by hypertriglyceridaemia in DKA)

11. Other Important Differentials

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Key Investigations to Differentiate

The differential is narrowed efficiently by a few targeted investigations:

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Life-Threatening Conditions NOT to Miss

From the senior notes, the life-threatening DDx of acute abdomen ^[6] that overlap with pancreatitis presentation:

• Perforated viscus (PPU)
• Ruptured AAA
• Acute mesenteric ischaemia
• Severe pancreatitis (itself)
• Acute MI
• DKA

These require immediate recognition and management. Every patient with acute epigastric pain should have, at minimum: ECG, CXR, amylase/lipase, LFT, troponin, blood glucose, and ABG.

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Summary Table: Key Differentiators at a Glance

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Active Recall - Differential Diagnosis of Acute Pancreatitis

1. Name 6 important differential diagnoses for acute pancreatitis as listed in the senior notes.

Your answer

Grade

Show mark scheme

Peptic ulcer disease, choledocholithiasis/cholangitis/cholecystitis, hepatitis, mesenteric ischaemia, intestinal obstruction, and myocardial infarction. Also accept: PPU, ruptured AAA, DKA.

2. Why must an ECG and troponin be performed in every patient presenting with epigastric pain suspected to be pancreatitis?

Your answer

Grade

Show mark scheme

To exclude acute myocardial infarction (especially inferior MI), which can present with epigastric pain, nausea and vomiting due to shared visceral afferent innervation (T5-T9). The inferior surface of the heart sits on the diaphragm and refers pain to the epigastrium.

3. List 4 conditions that can cause a false positive elevation in serum amylase, mimicking pancreatitis.

Your answer

Grade

Show mark scheme

Perforated peptic ulcer (PPU), ruptured AAA, diabetic ketoacidosis (DKA), and macroamylasaemia. Also accept: intestinal obstruction, bowel ischaemia, acute cholecystitis.

4. How do you distinguish acute pancreatitis from a perforated peptic ulcer at the bedside and on initial investigations?

Your answer

Grade

Show mark scheme

PPU: sudden thunderclap onset, board-like rigidity and generalised peritonism (chemical peritonitis from free acid), absent bowel sounds. Pancreatitis: gradual onset over hours, pain radiates to back, relieved by leaning forward, less marked peritoneal signs (retroperitoneal). Key investigation: erect CXR showing pneumoperitoneum (free air under diaphragm) in PPU but absent in pancreatitis. Serum lipase is more specific for pancreatitis than amylase (amylase can be elevated in both).

5. Why is mesenteric ischaemia a particularly dangerous mimic of acute pancreatitis, and what is its hallmark clinical feature?

Your answer

Grade

Show mark scheme

Dangerous because it can cause elevated amylase (false positive for pancreatitis) from ischaemic bowel, and delayed diagnosis leads to bowel infarction and death. Hallmark: pain out of proportion to physical examination - the patient has agonising pain but the abdomen is initially soft and non-tender. Typically occurs in elderly patients with AF or atherosclerotic risk factors. Diagnosed by CT angiography and elevated lactate.

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References

^[2] Senior notes: maxim.md (Acute pancreatitis section) ^[3] Senior notes: felixlai.md (Acute pancreatitis section) ^[6] Senior notes: maxim.md (Acute abdomen section; Post-ERCP pancreatitis section) ^[11] Lecture slides: Acute pancreatitis.pdf (p8 — Diagnosis of acute pancreatitis) ^[12] Senior notes: felixlai.md (Cholangitis, Cholecystitis, and Ruptured AAA sections)

Diagnostic Criteria

The Revised Atlanta Diagnostic Criteria (2012)

This is the universally accepted standard. The diagnosis of acute pancreatitis requires fulfilment of at least 2 out of 3 criteria ^[2][3]:

Why 2 out of 3? Because:

• If the clinical picture AND biochemistry are both classic (criteria 1 + 2), you do not need imaging to confirm the diagnosis — imaging is then reserved for assessing severity, identifying the aetiology, or detecting complications.
• If one criterion is equivocal (e.g., amylase only mildly raised, or the pain is atypical), imaging becomes essential to confirm the diagnosis.
• In practice, most patients are diagnosed clinically + biochemically, and imaging is added to assess severity rather than to make the diagnosis.

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Diagnostic Algorithm

The following algorithm walks through the clinical decision-making from presentation to severity assessment:

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Investigation Modalities — Detailed Breakdown

I'll walk through each investigation systematically: why we order it, what we're looking for, and how to interpret the results.

A. Baseline Bloods — "The Pancreatitis Panel"

Every patient with suspected acute pancreatitis should have the following ordered immediately ^[2][3]:

CBC, LRFT, CRP, glucose, Ca, cardiac markers ± ECG, pancreatic enzymes ^[2]

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A1. Pancreatic Enzymes (The Diagnostic Markers)

These are the cornerstone of biochemical diagnosis. The word "amylase" comes from Greek amylon = starch; it breaks down starch. "Lipase" from Greek lipos = fat; it breaks down triglycerides.

Serum Amylase [3][2]

Why does amylase rise? When acinar cells are damaged, they release their enzyme contents into the interstitial space → enzymes enter the bloodstream via lymphatics and venous drainage → measurable in serum.

Limitations — false negatives (amylase may NOT reach 3× ULN) ^[3]:

• Alcoholic pancreatitis — chronic alcohol damage to the parenchyma reduces its capacity to produce amylase ("burnt-out" acinar cells)
• Hypertriglyceridaemia-associated pancreatitis — triglycerides interfere with the amylase detection assay (laboratory artefact)
• Delayed presentation — if the patient presents > 3–5 days after onset, serum amylase may have already normalised

False positives (elevated amylase without pancreatitis) ^[2][3]:

• Perforated peptic ulcer (PPU)
• Ruptured AAA
• DKA
• Macroamylasaemia (amylase bound to immunoglobulin → high MW complex → not renally cleared → accumulates in serum)
• Intestinal obstruction, bowel ischaemia
• Acute cholecystitis
• Salivary gland disease (parotitis — remember, salivary glands also produce amylase)

Urine amylase ^[3]:

• Useful when serum amylase is equivocal or in delayed presentation
• Rises within 24–48 hours and persists for up to 1 week even after serum amylase has normalised ^[3]
• Because amylase is renally excreted and has a longer "tail" in the urine

Serum Lipase [3][2]

Why is lipase more specific? Amylase is produced by many tissues (salivary glands, lungs, fallopian tubes, small intestine), so many non-pancreatic conditions raise amylase. Lipase is produced almost exclusively by the pancreas, so its elevation is more reliably pancreatic in origin.

False positives for lipase ^[3]:

• Post-ERCP
• Pancreatic tumours
• Acute cholecystitis (mild elevation, usually < 3× ULN)

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A2. Full Blood Count (CBC with Differentials) [3]

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A3. Liver Function Tests (LFT) [3]

The LFT pattern is crucial for establishing aetiology — specifically, is this biliary pancreatitis?

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A4. Renal Function Tests (RFT) [3]

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A5. Inflammatory Markers [3][13]

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A6. Serum Glucose [3]

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A7. Serum Calcium [3]

Always check corrected calcium (for albumin) or ionised calcium to assess true calcium status.

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A8. Serum Triglycerides

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A9. Cardiac Markers ± ECG [3]

Troponin (TnI, TnT) to exclude myocardial infarction (MI) as a differential diagnosis of epigastric pain ^[3]

This is mandatory in every patient with acute epigastric pain. An inferior MI can perfectly mimic pancreatitis. ECG may show ST changes in MI, or non-specific ST-T changes from the metabolic stress of severe pancreatitis itself.

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A10. Arterial Blood Gas (ABG)

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B. Radiological Investigations

B1. Chest X-Ray (CXR) [2]

Purpose: Rule out perforation (PPU) — look for pneumoperitoneum (free air under diaphragm) — and identify other DDx ^[2].

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B2. Abdominal X-Ray (AXR) [2][3]

AXR is a quick, cheap, widely available initial imaging. It does not diagnose pancreatitis directly, but shows supportive indirect signs and excludes other pathology.

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B3. Ultrasound (USG) Abdomen [2][3]

USG is the first-line imaging in acute pancreatitis — not primarily to diagnose pancreatitis (which is usually biochemically confirmed), but to identify the aetiology (especially gallstones).

Limitations ^[3]:

• Distal (lower end) of CBD may be obscured by bowel gas — the intrapancreatic portion of the CBD sits behind the duodenum and is frequently not visualised
• Cannot clearly delineate extra-pancreatic spread of pancreatic inflammation or identify necrosis within the pancreas — USG lacks the resolution and penetration for this; CT is needed

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B4. CT Abdomen with Contrast — The Gold Standard [3][2][13]

This is the most important imaging modality for acute pancreatitis. Let's break it down comprehensively.

Why CT? CT provides:

1. Diagnostic confirmation when clinical + biochemical criteria are equivocal
2. Severity assessment (necrosis, fluid collections)
3. Complication detection
4. Aetiological clues (gallstones, tumours)
5. Exclusion of other diagnoses

Gold standard for the disease with Sensitivity = 90% and Specificity = 100% ^[3]

Key CT Findings

Why Contrast Is Essential

Contrast is essential to detect the presence of pancreatic necrosis ^[3]

Without IV contrast, you cannot distinguish viable (enhancing) pancreatic tissue from necrotic (non-enhancing) tissue. An unenhanced CT might show a swollen pancreas, but you would miss necrosis entirely — and necrosis is what determines the difference between interstitial oedematous pancreatitis (good prognosis) and necrotising pancreatitis (potentially fatal).

Timing of CT

• CT changes may NOT occur within the first 24 hours of presentation ^[3]
• Best done at 72–96 hours after admission to accurately assess the full extent of necrosis ^[2]
• Earlier CT (within 24–48h) is indicated if:
  • Organ failure is present ^[2]
  • Uncertain diagnosis (DDx PPU, gangrenous cholecystitis, ischaemic bowel) ^[2]
  • Clinical deterioration despite treatment

Balthazar CT Severity Index (CTSI) [3][2][13]

This is a prognostic scale based on CT findings that combines the grade of pancreatitis with the extent of necrosis ^[3]:

Score = Grade of pancreatitis (0–4) + Percentage of necrosis (0–6) ^[2]

Grade of Pancreatitis:

Percentage of Necrosis:

Interpretation ^[3]:

• CTSI 0–3: Low morbidity and mortality
• CTSI 4–6: Moderate morbidity
• CTSI 7–10: Morbidity 92%, mortality 17% ^[3]

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B5. MRI / MRCP [3][13]

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B6. ERCP / MRCP [2]

ERCP and MRCP are not routinely done because the culprit stone usually passes spontaneously ^[2]. However, they are indicated in specific situations:

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C. Severity Assessment Tools — Consolidated

From the lecture slides ^[13]:

Assessment of disease severity involves:

• Clinical scoring systems: Ranson and Glasgow systems (require 48 hours for full assessment), APACHE II and APACHE-O
• Biochemical markers: C-reactive protein, Interleukin-8 or 6, Tumor necrosis factor, Trypsinogen activation peptide (TAP)
• Radiological studies: Dynamic contrast CT scan — pancreatic inflammation and peripancreatic fluid collection (Balthazar system), MRI ^[13]

Modified Marshall Scoring System (for defining organ failure)

This is the scoring system used in the Revised Atlanta Classification to define organ failure:

• A score of ≥ 2 in any organ system = organ failure
• Transient organ failure (resolving within 48 hours) = moderately severe
• Persistent organ failure ( > 48 hours) = severe acute pancreatitis ^[13]

Definition of severe pancreatitis: pancreatitis associated with organ failure and/or local complications e.g. necrosis, abscess formation, or pseudocyst ^[14]

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D. Summary — Diagnostic Investigation Algorithm by Purpose

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Active Recall - Diagnosis of Acute Pancreatitis

1. State the Revised Atlanta diagnostic criteria for acute pancreatitis and explain why imaging is not always needed.

Your answer

Grade

Show mark scheme

Requires 2 out of 3: (1) Typical epigastric pain radiating to back, (2) Serum amylase or lipase at least 3x ULN, (3) Characteristic imaging findings on USG/CT/MRI. If criteria 1 and 2 are clearly met, imaging is not required for diagnosis - it is then used for severity assessment, aetiology, or complications.

2. Compare serum amylase and serum lipase as diagnostic markers for acute pancreatitis. Which is preferred and why?

Your answer

Grade

Show mark scheme

Lipase is preferred. Advantages: (1) More sensitive, especially in alcoholic pancreatitis (chronic acinar damage reduces amylase production). (2) More specific - amylase is produced by many tissues (salivary glands, lungs, bowel). (3) Rises earlier (4-8h vs 6-12h) and lasts longer (8-14 days vs 3-5 days), making it better for delayed presentations. Neither enzyme correlates with disease severity.

3. Why must contrast be given when performing CT abdomen for acute pancreatitis, and what is the optimal timing?

Your answer

Grade

Show mark scheme

Contrast is essential to detect pancreatic necrosis - necrotic tissue has lost its blood supply and appears as hypoenhancing areas, while viable tissue enhances normally. Without contrast, necrosis cannot be distinguished. Optimal timing is 72-96 hours after admission because CT changes may not be present in the first 24 hours and necrosis takes time to fully demarcate. Earlier CT is indicated if there is organ failure or diagnostic uncertainty.

4. Name three characteristic AXR findings in acute pancreatitis and explain the pathophysiological basis of each.

Your answer

Grade

Show mark scheme

(1) Sentinel loop sign - localised ileus of adjacent small bowel due to reflex inhibition of peristalsis by retroperitoneal inflammation. (2) Colonic cut-off sign - paucity of gas distal to splenic flexure due to functional spasm of descending colon from adjacent pancreatic inflammation. (3) Obliteration of psoas outline - retroperitoneal fluid accumulation obscuring the psoas shadow.

5. A patient presents 4 days after onset of epigastric pain. Serum amylase is normal but you still suspect pancreatitis. What should you do and why?

Your answer

Grade

Show mark scheme

Check serum lipase (persists for 8-14 days vs amylase 3-5 days, so still likely elevated at day 4). Check urine amylase (persists for up to 1 week after serum normalises). Also consider CT abdomen with contrast - imaging may confirm the diagnosis when biochemistry is equivocal (the third diagnostic criterion). Amylase can be falsely negative in delayed presentation, alcoholic pancreatitis, and hypertriglyceridaemia-associated pancreatitis.

6. State the Balthazar CT Severity Index scoring system and its prognostic significance.

Your answer

Grade

Show mark scheme

Score = Grade of pancreatitis (0-4: A=normal 0, B=enlargement 1, C=peripancreatic inflammation 2, D=single fluid collection 3, E=multiple collections or retroperitoneal air 4) PLUS percentage of necrosis (0%=0, less than 30%=2, 30-50%=4, more than 50%=6). Total score 0-10. Score 7-10 is associated with morbidity of 92% and mortality of 17%.

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References

^[2] Senior notes: maxim.md (Acute pancreatitis section) ^[3] Senior notes: felixlai.md (Acute pancreatitis section) ^[11] Lecture slides: Acute pancreatitis.pdf (p8 — Diagnosis of acute pancreatitis) ^[13] Lecture slides: Acute pancreatitis.pdf (p10 — Assessment of disease severity) ^[14] Lecture slides: Acute pancreatitis.pdf (p11 — Definition of severe pancreatitis)

Management of Acute Pancreatitis

Overarching Principles

Before diving into specifics, the lecture slides frame two guiding principles beautifully ^[15]:

Aim in treatment of acute pancreatitis:

1. To identify patients with severe pancreatitis to institute directed therapy in the early phase of disease
2. To prevent progression of disease from acute oedematous state to necrotising / haemorrhagic state ^[15]

Everything we do in management serves one of these two goals. The first is about risk stratification (scoring systems, CRP, CT). The second is about maintaining pancreatic perfusion (aggressive fluids) and removing the inciting cause (ERCP for gallstones). If you remember nothing else, remember: fluids prevent necrosis, and necrosis kills.

The management summary from the lecture slides ^[16]:

Summary:

• Conservative management of uncomplicated acute pancreatitis
• Early ERCP and antibiotics to treat acute biliary pancreatitis and cholangitis
• IV carbapenem for necrotising pancreatitis
• Percutaneous / endoscopic / surgical drainage of infected pancreatic necrosis
• Endoscopic or (rarely) open cystogastrostomy for persistent large pseudocysts ^[16]

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Management Algorithm

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1. General Supportive Management (All Patients)

This is the backbone of management — most patients with acute pancreatitis (80% with mild disease) recover with supportive care alone ^[16].

1A. IV Fluid Resuscitation

This is the single most important intervention in acute pancreatitis. Here's why, explained from first principles:

The problem: Pancreatic inflammation → massive third-spacing of fluid into the retroperitoneum, peritoneal cavity, and interstitial spaces (up to > 6 litres in severe cases). This causes intravascular volume depletion → hypoperfusion of the pancreas → ischaemic necrosis (the very thing that converts mild disease into lethal necrotising disease) ^[15].

The solution: Aggressive early fluid resuscitation to maintain intravascular volume and pancreatic perfusion.

1B. Oxygen Supplementation [3]

• Pulse oximetry and ABG monitoring are necessary to assess oxygenation and acid-base status ^[3]
• Supplemental O₂ to maintain SpO₂ > 95%
• Why? Severe pancreatitis causes hypoxaemia through multiple mechanisms: pleural effusions, ARDS, diaphragmatic splinting, atelectasis

1C. Correction of Electrolyte and Glucose Abnormalities [3][2]

• Correct electrolyte and glucose disturbances ^[2]
• Hypocalcaemia: Replete with IV calcium gluconate (monitor ECG — prolonged QTc is dangerous)
• Hypokalaemia/Hypomagnasaemia: Common from vomiting and third-spacing
• Hyperglycaemia: Sliding-scale insulin; avoid over-correction (risk of hypoglycaemia, especially if glucagon-producing α-cells are also damaged)

1D. Nil Per Os (NPO) and Nasogastric Decompression [3]

1E. Nutritional Support [3][2]

This is a paradigm shift in pancreatitis management. The old approach was "rest the pancreas" — starve the patient. This is wrong and harmful.

It is NO longer acceptable to "rest the pancreas" by avoiding enteral nutrition ^[3]

Why enteral feeding is critical:

• Early enteral feeding is associated with lower rates of infection, surgical intervention, and length of stay ^[3]
• Delay in enteral feeding may contribute to the development of intestinal ileus and feeding intolerance ^[3]
• Enteral nutrition maintains gut mucosal barrier integrity → prevents bacterial translocation → reduces risk of infected necrosis (recall the pathophysiology: gut barrier breakdown → bacterial translocation → infected necrosis → sepsis → death)

Route of enteral feeding:

Parenteral nutrition (TPN):

• Should only be considered if the enteral route is not available, not tolerated, or caloric requirements cannot be met ^[3]
• TPN has higher infection rates (line sepsis) and does not maintain gut mucosal barrier
• In the slides for severe pancreatitis: Nutritional support (TPN + early enteral feeding) ^[17] — meaning TPN is a supplement, not a replacement

Recommended nutrient requirements in severe AP ^[3]:

1F. Monitoring [2]

• Monitor vitals, I/O, RFT, Ca, glucose ± ABG ^[2]
• Frequency: Vitals Q1–4H depending on severity; bloods at least daily initially
• Serial CRP (48-hour value is prognostic)
• Ranson's parameters at 48 hours

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2. Medical Treatment

2A. Analgesia

Pain control is essential — pancreatitis is excruciatingly painful, and uncontrolled pain causes tachycardia, hypertension, and splanchnic vasoconstriction (worsening pancreatic perfusion).

2B. PPI (Proton Pump Inhibitor) [2]

• PPI for prophylaxis of acute stress ulcer ^[2]
• Why? Critically ill patients are at high risk of stress-related mucosal disease (Curling's ulcer in burns, Cushing's ulcer in raised ICP). In pancreatitis, haemodynamic instability and SIRS increase gastric acid-related mucosal injury risk. Omeprazole or pantoprazole IV covers this.

2C. Antibiotics

This is one of the most commonly tested and nuanced topics in pancreatitis management.

The key principle: Prophylactic antibiotics are generally NOT recommended ^[3][2][16]

Why not? Most pancreatitis is a sterile inflammatory process. Routine antibiotics:

• Do not reduce mortality or infected necrosis in uncomplicated pancreatitis (multiple RCTs and meta-analyses)
• Promote antibiotic resistance and Clostridioides difficile infection
• May give a false sense of security

When ARE antibiotics indicated? ^[3][2]

Why carbapenems specifically?

• "Carba-" = carbapenem nucleus; "penem" = β-lactam subclass. These are the broadest-spectrum β-lactams, covering Gram-positives, Gram-negatives (including ESBL-producers), and anaerobes.
• Crucially, they achieve therapeutic concentrations in necrotic pancreatic tissue — most other antibiotics cannot penetrate avascular necrotic debris effectively.

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3. Management of Biliary Pancreatitis

Biliary pancreatitis has specific additional management steps because the cause is treatable — remove the gallstones, and you prevent recurrence.

3A. ERCP — Acute Phase

Emergency ERCP for biliary pancreatitis ^[17]

Treatment protocol of acute biliary pancreatitis: Emergency ERCP ± EPT (endoscopic papillotomy/sphincterotomy) → Elective cholecystectomy ^[18]

Decision tree for suspected CBD stones ^[3]:

• Clinical suspicion of CBD stone is high → ERCP
• Clinical suspicion is moderate → MRCP or EUS to exclude CBD stones before proceeding to cholecystectomy
• Clinical suspicion is low → Cholecystectomy with intraoperative cholangiogram (IOC) during the procedure

3B. PTBD (Percutaneous Transhepatic Biliary Drainage) [3][2]

• Decompress and drain the biliary system in biliary pancreatitis ^[3]
• Indicated in patients who are unable to perform ERCP ^[3] — e.g. post-Billroth II gastrectomy (the duodenum is not accessible endoscopically), failed ERCP, unstable patient
• Alternative: PTBD to decompress biliary tract if unfit for ERCP ^[2]

3C. Exploration of Common Bile Duct (ECBD) [3]

• Open surgical drainage — rarely performed nowadays ^[3]
• Last resort when ERCP and PTBD are both impossible

3D. Cholecystectomy — Definitive Prevention [3][2][18]

After resolving the acute episode, the gallbladder must be removed to prevent recurrence (recurrence rate without cholecystectomy is ~30–40% within 6 weeks).

Elective cholecystectomy — laparoscopic or open ^[18]

Intraoperative cholangiography (IOC) is performed during cholecystectomy to rule out persistent choledocholithiasis ^[3].

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4. Management of Severe Pancreatitis

Principles of management of severe pancreatitis ^[17]:

• Close monitoring (haemodynamic, urine output)
• Fluid resuscitation
• Cardiovascular support
• Renal support
• Mechanical ventilation
• Prophylactic potent antibiotic
• Emergency ERCP for biliary pancreatitis
• Nutritional support (TPN + early enteral feeding) ^[17]

4A. ICU Admission [2]

Consult ICU for organ support ^[2]:

4B. Indications for Surgery in Severe Pancreatitis [2]

Surgery indicated if:

• Infected pancreatic necrosis
• Progressive clinical deterioration despite maximal conservative and ICU management ^[2]

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5. Management of Infected Pancreatic Necrosis — The Step-Up Approach

This is one of the most important modern concepts in pancreatitis surgery. The key principle is minimise surgical aggression — infected necrosis is managed with a graduated ("step-up") approach rather than rushing to open necrosectomy.

The Step-Up Approach [3][2][19]

Definitive treatment for infected pancreatic necrosis ^[19]:

• Radiologically-guided drainage → Dilatation of tract and video-assisted retroperitoneal debridement (VARD)
• Endoscopic ultrasound drainage → Stent insertion ± endoscopic debridement
• Necrosectomy (surgical debridement) — Open (standard) or minimally invasive approaches (for selected cases) ^[19]

Step 1: Antibiotics ^[3]

• Empirical antibiotics that penetrate pancreatic necrosis ^[3]
• Carbapenem monotherapy (imipenem/meropenem) OR Ceftazidime/Cefepime/Fluoroquinolone + Metronidazole ^[3]

Step 2: Drainage ^[3]

• Percutaneous catheter drainage or endoscopic drainage is used as the first step to stabilise the patient's overall clinical status ^[3]
• Drainage "buys time" and allows the lesion to become more walled off and safer to treat ^[3]
• Primary percutaneous catheter drainage may be the only intervention required in 1/3 to 1/2 of patients ^[3]

Step 3: Delayed necrosectomy ^[3]

• Resection of necrosis by minimally-invasive or endoscopic means is performed as a second procedure 3–4 weeks later if necessary ^[3]
• Should be delayed to at least 3–4 weeks after onset ^[3] — why?
  • Allow sequestration and demarcation of the necrosis — necrotic tissue separates from viable tissue over time, making debridement easier and safer
  • Reduce risk of bleeding, disseminated infection, and collateral damage to adjacent organs ^[3]
  • Continued conservative treatment allows a minimally invasive debridement to be performed at a later date ^[3]
• Minimally invasive preferred: endoscopic or percutaneous > open ^[2]
• Open necrosectomy is reserved for patients who fail to improve with less invasive approaches ^[3]

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6. Management of Pancreatic Fluid Collections

This follows the Revised Atlanta classification timeline (< 4 weeks vs ≥ 4 weeks) and whether necrosis is present:

6A. Acute Peripancreatic Fluid Collection (APFC) [3]

• Resolve spontaneously within 7–10 days without the need for drainage ^[3]
• Management: observation and serial imaging
• No intervention needed unless they become infected (rare)

6B. Pancreatic Pseudocyst [3][20]

Treatment strategy for pancreatic pseudocyst ^[20]:

• Observe
• If cyst > 5 cm by 6 weeks → internal drainage
• If cyst develops complication (e.g. bleeding, rupture, infection, obstruction) → external drainage ^[20]

6C. Walled-Off Necrosis (WON) [2][19]

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7. Management of Pseudoaneurysm [3]

This deserves special mention because of a critical safety rule:

• Angiography is the definitive diagnostic test and has been used increasingly to manage pseudoaneurysms by embolisation with radiological coils ^[3]
• Pseudoaneurysms are an ABSOLUTE contraindication to endoscopic drainage unless arterial embolisation is performed first ^[3]
• Why? Severe and fatal haemorrhage can occur following endoscopic drainage in patients with an unsuspected pseudoaneurysm ^[3]

Before draining ANY pancreatic fluid collection, always consider whether a pseudoaneurysm might be present. If the Hb is dropping, the collection is expanding, or there's unexplained GI bleeding — do angiography FIRST.

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8. Prevention of Recurrence [3]

8A. Treatment of Underlying Risk Factors [3]

• Hypertriglyceridaemia: Fibrates, dietary modification, insulin infusion in acute setting
• Hypercalcaemia: Treat underlying hyperparathyroidism (parathyroidectomy)
• Alcohol: Absolute abstinence counselling
• Offending drugs: Discontinue causative medications

8B. Gallstone Pancreatitis — Preventing Recurrence [3]

Already covered above — the critical point is:

• ERCP for CBD stones (if present)
• Cholecystectomy during index admission (mild) or after recovery (severe) ^[3]
• IOC to rule out residual CBD stones ^[3]

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Summary Table — Management by Severity

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Active Recall - Management of Acute Pancreatitis

1. What is the fluid of choice for resuscitation in acute pancreatitis and why? What is the target urine output?

Your answer

Grade

Show mark scheme

Lactated Ringer's solution — superior to normal saline in reducing SIRS because it is more physiological (buffered, lower chloride, avoids hyperchloraemic metabolic acidosis). Target urine output: at least 0.5 mL/kg/hr (minimum adequate renal perfusion); 1.0 mL/kg/hr is optimal.

2. Why should morphine be avoided in acute pancreatitis, and what analgesics are preferred?

Your answer

Grade

Show mark scheme

Morphine causes sphincter of Oddi spasm, which theoretically worsens pancreatic duct obstruction and exacerbates pancreatitis. Preferred analgesics: tramadol or pethidine (meperidine). NSAIDs should also be avoided as they can worsen pancreatitis. Paracetamol can be used as adjunctive analgesia.

3. State the indications for antibiotics in acute pancreatitis, and name the antibiotic of choice for infected pancreatic necrosis.

Your answer

Grade

Show mark scheme

Prophylactic antibiotics are NOT recommended. Indications: (1) Concurrent cholangitis — IV Augmentin, (2) Infected pancreatic necrosis — IV carbapenem (imipenem or meropenem), (3) SIRS with evidence suggesting infection. Carbapenems are chosen because they penetrate necrotic pancreatic tissue effectively and cover enteric Gram-negatives.

4. Describe the step-up approach for infected pancreatic necrosis.

Your answer

Grade

Show mark scheme

Step 1: IV antibiotics (carbapenem monotherapy or ceftazidime/fluoroquinolone + metronidazole). Step 2: Percutaneous catheter drainage or EUS-guided endoscopic drainage to stabilise and buy time (sufficient in one-third to one-half of patients). Step 3: Delayed necrosectomy at 3-4 weeks if no improvement — minimally invasive methods preferred (endoscopic, VARD, percutaneous) over open surgery. Delay allows necrosis to demarcate and wall off, reducing surgical morbidity.

5. In gallstone pancreatitis, when should ERCP be performed and when should cholecystectomy be performed?

Your answer

Grade

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ERCP: within 24-72 hours if there is concurrent cholangitis, jaundice, or evidence of persistent CBD stone obstruction. NOT indicated without CBD obstruction. Cholecystectomy: in mild pancreatitis, perform during the same index hospitalisation (within 1 week of recovery). In severe necrotising pancreatitis, delay until inflammation subsides and fluid collections resolve (interval cholecystectomy, typically 6+ weeks).

6. Why is a pseudoaneurysm an absolute contraindication to endoscopic drainage of a pancreatic fluid collection?

Your answer

Grade

Show mark scheme

Pseudoaneurysms form when pancreatic enzymes (especially elastase) erode into arterial walls (commonly GDA, splenic, left gastric arteries). If endoscopic drainage is performed without first embolising the pseudoaneurysm, the drainage procedure can rupture it, causing severe and fatal haemorrhage. Management: angiographic embolisation with coils FIRST, then drainage can proceed safely.

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References

^[2] Senior notes: maxim.md (Acute pancreatitis section) ^[3] Senior notes: felixlai.md (Acute pancreatitis section) ^[15] Lecture slides: Acute pancreatitis.pdf (p9 — Aim in treatment of acute pancreatitis) ^[16] Lecture slides: Acute pancreatitis.pdf (p50 — Summary) ^[17] Lecture slides: Acute pancreatitis.pdf (p12 — Principles of management of severe pancreatitis) ^[18] Lecture slides: Acute pancreatitis.pdf (p16 — Treatment protocol of acute biliary pancreatitis) ^[19] Lecture slides: Acute pancreatitis.pdf (p24 — Definitive treatment for infected pancreatic necrosis) ^[20] Lecture slides: Acute pancreatitis.pdf (p44/p49 — Treatment strategy for pancreatic pseudocyst)

Complications of Acute Pancreatitis

Overview — The Natural History

The lecture slide gives a powerful snapshot of the clinical course ^[21]:

Clinical course of acute pancreatitis (per 100 patients):

• 70 patients with uneventful recovery (Mild pancreatitis)
• 30 patients with complications
  • 20 patients with prolonged hospital stay
  • 10 patients died (Severe pancreatitis) ^[21]

So roughly 30% of patients develop complications, and the overall mortality is about 10%. This frames everything that follows — complications are common and can be lethal.

Definition of severe pancreatitis: pancreatitis associated with organ failure and/or local complications e.g. necrosis, abscess formation, or pseudocyst ^[14]

Complications are broadly divided into local (things happening in and around the pancreas) and systemic (distant organ effects driven by the cytokine storm). I will explain each from first principles, connecting back to the pathophysiology.

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A. Local Complications

These arise because the pancreas sits in the retroperitoneum surrounded by vital structures (duodenum, CBD, splenic vessels, portal vein, SMA/SMV, colon, stomach). When autodigestion extends beyond the pancreas, it damages everything in its path.

Local complications of acute pancreatitis ^[22]:

1. Pancreatic and/or peripancreatic necrosis and haemorrhage
2. Pancreatic abscess
3. Pseudocyst
4. Gastric fistula
5. Colonic fistula
6. Duodenal fistula
7. Duodenal obstruction
8. Splenic vein thrombosis → left-sided portal hypertension
9. SMV or SMA thrombosis → bowel infarction ^[22]

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A1. Pancreatic Fluid Collections (Revised Atlanta Classification)

This is one of the most commonly tested topics. The key organising principle is a 2 × 2 matrix — based on (1) whether necrosis is present and (2) whether it's early (< 4 weeks) or late (≥ 4 weeks) ^[2][3]:

Acute Peripancreatic Fluid Collection (APFC) [3]

• Timeline: Early complication developing < 4 weeks after onset ^[3]
• What it is: Enzyme-rich fluid that leaks from the inflamed pancreas into the peripancreatic spaces
• Key feature: Does NOT have a well-defined wall — the fluid simply collects in anatomical spaces (lesser sac, anterior pararenal space) ^[3]
• Imaging: Anechoic collection on USG; fluid-density collection without a capsule on CT
• Clinical significance: Usually remains asymptomatic and resolves spontaneously without the need for drainage ^[3]
• Management: Observation — resolves within 7–10 days ^[3]

Why does it resolve? The inflammatory exudate is reabsorbed by the peritoneum and lymphatics as the acute inflammation settles. Intervention would introduce infection risk into a sterile, self-resolving process.

Pancreatic Pseudocyst [3][2][20]

"Pseudo" = false (Greek) — this is a "false cyst" because it lacks an epithelial lining (true cysts are lined by epithelium). It's walled by inflammatory fibrosis instead.

• Timeline: Late complication developing > 4 weeks after onset ^[3]
• Definition: Encapsulated collection of fluid with a well-defined inflammatory wall (without epithelial cells), usually outside the pancreas, with minimal or no necrosis ^[3]
• Pathophysiology: Pancreatic ductal disruption (partial or complete) → pancreatic juice leaks into the peripancreatic space → over weeks, the body walls off this fluid with granulation tissue and fibrosis → a defined "pseudocyst" forms
• Risk factors: Chronic pancreatitis > acute pancreatitis ^[2] — because ductal disruption is more common with chronic duct damage
• Clinical features ^[2]:
  • Persistent epigastric pain — the collection causes pressure on surrounding structures
  • Mass effect: gastric outlet obstruction (GOO — the pseudocyst compresses the stomach/duodenum), obstructive jaundice (compresses the CBD)
  • Palpable epigastric mass on examination
• Investigations:
  • Amylase persistently elevated ^[2] — because the pseudocyst communicates with the pancreatic duct, so enzyme-rich fluid continuously leaks
  • CT abdomen with contrast: well-defined, homogeneous, fluid-density collection with a distinct enhancing wall; NO solid component (unlike WON)
• Management ^[3][20]:
  • Observe — watchful waiting for 6 weeks to allow the wall to "mature" (thicken and become strong enough to hold sutures/stents). 50% resolve spontaneously ^[2].
  • If cyst > 5 cm by 6 weeks → internal drainage ^[20]:
    • Cystogastrostomy (endoscopic or operative) — creates an opening between the pseudocyst and the stomach ^[20]
    • Cystoduodenostomy (operative) ^[20]
    • Cystojejunostomy (operative) — Roux-en-Y ^[20]
    • EUS-guided cystogastrostomy is first-line ^[2]
  • If cyst develops complications (e.g. bleeding, rupture, infection, obstruction) → external drainage ^[20]

Acute Necrotic Collection (ANC) [3]

• Timeline: Early complication developing < 4 weeks ^[3]
• Definition: Collection containing variable amounts of both fluid and necrosis associated with necrotising pancreatitis, with no defined wall ^[3]
• Content: Mix of semisolid and solid material — non-viable pancreatic parenchyma ^[2]
• Key feature: Necrosis can involve the pancreatic parenchyma or the peripancreatic tissues ^[3]
• Imaging: Heterogeneous collection on CT (mixture of fluid and non-enhancing solid tissue); no capsule
• Management: Usually conservative unless infected (see step-up approach in management section)

Walled-Off Necrosis (WON) [3][2]

• Timeline: Late complication developing > 4 weeks ^[3]
• Definition: Mature and encapsulated collection of pancreatic or peripancreatic necrosis that has developed a well-defined inflammatory wall ^[3]
• Key feature: Contains solid necrotic debris within a wall — this is what distinguishes it from a pseudocyst
• Clinical features ^[2]:
  • Mass effect: palpable mass, GOO, obstructive jaundice ^[2]
• Imaging: CT abdomen with contrast — well-defined wall, can be intra-pancreatic or extra-pancreatic ^[2]; heterogeneous content (solid + liquid)
• Management ^[2]:
  • EUS/ERCP-guided transmural drainage ± necrosectomy (first-line) ^[2]
  • Percutaneous drainage (higher recurrence rate, risk of pancreatocutaneous fistula) ^[2]
  • Surgical debridement (open/lap) with external/internal drainage ^[2]

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A2. Pancreatic Necrosis (Necrotising Pancreatitis) [3]

This is the most feared local complication and the main driver of mortality.

• Definition: Inflammation associated with pancreatic parenchymal necrosis or peripancreatic necrosis ^[3]
• Pathophysiology: Two mechanisms converge:
  1. Autodigestion — activated enzymes (trypsin, elastase, lipase) directly destroy pancreatic tissue ^[3]
  2. Hypoperfusion — volume depletion → pancreatic ischaemia → infarction. Reasons for progression: hypoperfusion of pancreas + persistent ampullary obstruction by stone ^[10]
• Diagnosis: Contrast-enhanced CT — necrotic areas show hypoenhancement (they have lost their blood supply and cannot take up contrast) ^[2]. Gas within necrotic areas on CT is suggestive of infected necrosis ^[3].

Sterile vs Infected Necrosis

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A3. Peripancreatic Vascular Complications

The pancreas is surrounded by major vessels (splenic artery/vein, GDA, SMA/SMV, portal vein). Inflammation and enzyme leakage erode into these structures.

Splanchnic Venous Thrombosis [3][22]

• Vessels affected: Splenic vein, portal vein, or superior mesenteric vein (SMV) ^[3]
• Mechanism: Inflammatory phlebitis — the inflamed pancreas directly irritates the adjacent vein wall → endothelial injury → thrombosis (Virchow's triad: endothelial damage + stasis from compression + hypercoagulability from inflammation)
• Consequences:
  • Splenic vein thrombosis → left-sided (sinistral) portal hypertension ^[22] — this is a classic exam point. The splenic vein drains into the portal vein; when it's occluded, blood backs up through the short gastric veins → gastric fundal varices (NOT oesophageal varices, because the portal vein itself may be patent). Isolated gastric varices in a non-cirrhotic patient should prompt you to think of splenic vein thrombosis from pancreatitis.
  • SMV or SMA thrombosis → bowel infarction ^[22] — compromise of bowel perfusion → mesenteric ischaemia → gangrene
  • Portal vein thrombosis → hepatic decompensation ^[3]
• Management: Treatment should focus on the underlying pancreatitis as effective treatment may result in spontaneous resolution of thrombosis ^[3]. Anticoagulation is considered on a case-by-case basis (risk of haemorrhage in necrotic pancreatitis vs risk of bowel infarction from clot propagation).

Pseudoaneurysm [3][2]

"Pseudo" = false; "aneurysm" = dilation of a blood vessel. A pseudoaneurysm is NOT a true aneurysm (which involves all three vessel wall layers). It's a contained rupture — pancreatic enzymes (especially elastase) erode through the arterial wall, and blood is contained only by the adventitia and surrounding tissues.

• Frequency: Rare but serious complication, most common in patients with necrotising pancreatitis ^[3]
• Arteries commonly involved: Gastroduodenal artery (GDA), left gastric artery, and splenic artery ^[3] — these arteries run in close proximity to the pancreas
  • Pancreatic pseudo-aneurysm: erosion into artery (especially GDA) ^[2]
• Danger: Rupture is a life-threatening emergency ^[3] — massive intra-abdominal or GI haemorrhage
• Three clinical features suggesting pseudoaneurysm ^[3]:
  1. Unexplained GI bleeding
  2. Drop in haemoglobin (Hb) or haematocrit
  3. Sudden expansion of a pancreatic fluid collection
• Diagnosis and Management: Angiography is the first step — both diagnostic and therapeutic ^[3] (can embolise with radiological coils)
• Critical safety rule: Pseudoaneurysms are an ABSOLUTE contraindication to endoscopic drainage unless arterial embolisation is performed first ^[3] — Severe and fatal haemorrhage can occur following endoscopic drainage in patients with an unsuspected pseudoaneurysm ^[3]

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A4. Fistulae [22]

Activated enzymes erode through the walls of adjacent hollow viscera:

These are uncommon but severe complications, usually associated with necrotising pancreatitis. Management is typically conservative initially (NPO, TPN, drainage), with surgery reserved for failures.

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A5. Duodenal Obstruction [22]

• Duodenal obstruction ^[22] — the inflamed/necrotic pancreatic head or a pseudocyst compresses the duodenum (C-loop), causing gastric outlet obstruction
• Symptoms: persistent vomiting, inability to tolerate oral intake, gastric distension
• Management: NG decompression, treat underlying pancreatitis, endoscopic duodenal stenting if persistent, surgical bypass (gastrojejunostomy) rarely needed

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A6. Pancreatic Duct Disruption and Pancreatic Ascites

• Mechanism: Complete disruption of the main pancreatic duct (from necrosis or trauma) → pancreatic juice leaks freely into the peritoneal cavity → pancreatic ascites
• Clinical features: Progressive abdominal distension, shifting dullness
• Diagnosis: Ascitic fluid amylase is massively elevated (typically > 1000 U/L); protein is usually > 25 g/L (exudative)
• Management: ERCP with pancreatic duct stenting to bridge the disruption; surgical repair if ERCP fails

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A7. Pancreatic Exocrine and Endocrine Insufficiency [2]

When significant pancreatic parenchyma is destroyed:

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B. Systemic Complications

Systemic complications are driven by the cytokine storm — the same NF-κB-dependent inflammatory cascade (TNF-α, IL-1, IL-6) that we discussed in pathophysiology. These cytokines enter the bloodstream and cause distant organ injury.

Systemic Complications of acute pancreatitis ^[23]:

1. Heart failure
2. Respiratory failure
3. Renal failure
4. Cholestasis
5. DIC
6. Hyperglycaemia
7. Hypocalcaemia ^[23]

Let me explain each from first principles:

Additional systemic complications ^[3]:

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C. Organ Failure and SIRS [3]

Systemic inflammatory response syndrome (SIRS) — Pancreatic inflammation results in activation of a cytokine cascade that manifests clinically as SIRS ^[3]

The connection from local pancreatic inflammation to systemic organ failure:

Organ failure may present as shock, acute respiratory failure, and renal failure ^[3]

The Modified Marshall Score defines organ failure (score ≥ 2 in any system):

• Respiratory: PaO₂/FiO₂ ≤ 300
• Cardiovascular: SBP < 90 mmHg not responding to fluids
• Renal: Creatinine ≥ 170 μmol/L

Persistent organ failure ( > 48 hours) = severe pancreatitis = 15–40% mortality.

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D. Temporal Framework of Complications

Understanding the timeline helps predict what complication to expect and when:

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E. Long-Term Sequelae

Even after recovery from acute pancreatitis, patients are at risk of:

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Active Recall - Complications of Acute Pancreatitis

1. Draw out the Revised Atlanta classification for pancreatic fluid collections as a 2x2 table. Name each entity and state the key distinguishing feature between a pseudocyst and walled-off necrosis.

Your answer

Grade

Show mark scheme

Rows: less than 4 weeks vs 4 or more weeks. Columns: no necrosis (interstitial oedematous) vs necrosis present (necrotising). Less than 4 weeks, no necrosis = APFC; less than 4 weeks, necrosis = ANC; 4 or more weeks, no necrosis = pseudocyst; 4 or more weeks, necrosis = WON. Key distinction: pseudocyst contains purely liquid (no solid necrotic debris) whereas WON contains solid necrotic material within an inflammatory wall. This matters because WON may require necrosectomy in addition to drainage.

2. Explain why splenic vein thrombosis in pancreatitis causes isolated gastric varices rather than oesophageal varices.

Your answer

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The splenic vein runs along the posterior surface of the pancreas and is vulnerable to inflammatory thrombosis. When occluded, blood from the spleen cannot drain normally into the portal vein. It reroutes through the short gastric veins into the gastric fundal venous plexus, causing isolated gastric fundal varices. The portal vein itself remains patent, so there is no portal hypertension in the liver or oesophageal venous system. This is called left-sided (sinistral) portal hypertension.

3. List the 7 systemic complications of acute pancreatitis from the lecture slides and explain the pathophysiology of hypocalcaemia.

Your answer

Grade

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Seven systemic complications: (1) Heart failure, (2) Respiratory failure, (3) Renal failure, (4) Cholestasis, (5) DIC, (6) Hyperglycaemia, (7) Hypocalcaemia. Hypocalcaemia mechanism: pancreatic lipase causes peripancreatic fat necrosis, releasing fatty acids that bind (saponify/precipitate with) ionised calcium to form insoluble calcium soaps. Additionally, hypoalbuminaemia from third-spacing reduces total calcium. May also involve decreased PTH response.

4. A patient with necrotising pancreatitis develops unexplained GI bleeding and a sudden drop in haemoglobin. What complication should you suspect, how do you diagnose it, and what is the critical management caveat?

Your answer

Grade

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Suspect pseudoaneurysm (most commonly GDA, splenic, or left gastric artery). Diagnose with angiography (both diagnostic and therapeutic — can embolise with coils). Critical caveat: pseudoaneurysm is an ABSOLUTE contraindication to endoscopic drainage of any adjacent pancreatic fluid collection until arterial embolisation is performed first, because drainage can rupture the pseudoaneurysm causing fatal haemorrhage.

5. Explain the two peaks of mortality in acute pancreatitis and how they differ in mechanism and management.

Your answer

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Early peak (week 1): driven by SIRS and multi-organ failure from the cytokine storm (TNF-alpha, IL-6). This is sterile inflammation — antibiotics do NOT help. Management: aggressive fluid resuscitation, organ support in ICU. Late peak (weeks 2-6): driven by infected pancreatic necrosis from bacterial translocation (gut mucosal barrier breakdown from hypoperfusion allows enteric organisms to colonise necrotic tissue). Management: IV carbapenems, step-up approach (drainage then delayed necrosectomy).

6. What is abdominal compartment syndrome in the context of acute pancreatitis, and how is it diagnosed?

Your answer

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Massive retroperitoneal oedema, ascites, and paralytic ileus cause markedly elevated intra-abdominal pressure (IAP). Defined as IAP greater than 20 mmHg with new organ failure. Diagnosed by measuring IAP via bladder pressure (Foley catheter transducer). Consequences: compression of IVC (reduced venous return, shock), renal veins (AKI), diaphragm (respiratory failure). May require decompressive laparotomy.

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References

^[2] Senior notes: maxim.md (Acute pancreatitis section) ^[3] Senior notes: felixlai.md (Acute pancreatitis section) ^[9] Lecture slides: Acute pancreatitis.pdf (p6 — Acute oedematous pancreatitis progression) ^[10] Lecture slides: Acute pancreatitis.pdf (p7 — Reasons for progression to necrotising pancreatitis) ^[14] Lecture slides: Acute pancreatitis.pdf (p11 — Definition of severe pancreatitis) ^[20] Lecture slides: Acute pancreatitis.pdf (p44/p49 — Treatment strategy for pancreatic pseudocyst) ^[21] Lecture slides: Acute pancreatitis.pdf (p2 — Clinical course of acute pancreatitis) ^[22] Lecture slides: Acute pancreatitis.pdf (p18 — Local complications of acute pancreatitis) ^[23] Lecture slides: Acute pancreatitis.pdf (p19 — Systemic complications of acute pancreatitis)