Summary

Acute Pancreatitis is an acute inflammatory condition of the pancreas caused by the intracellular activation of digestive enzymes (trypsinogen -> trypsin), leading to autodigestion, local inflammation, and potentially a systemic inflammatory response (SIRS). The clinical spectrum ranges from mild, self-limiting inflammation (Interstitial Edematous Pancreatitis) to fulminant multi-organ failure and death (Necrotizing Pancreatitis).

Key Facts

• Definition: requires 2 of 3 criteria (Revised Atlanta Classification):
  1. Pain: Typical upper abdominal pain (epigastric, radiating to back).
  2. Enzymes: Amylase or Lipase > 3x Upper Limit of Normal (ULN).
  3. Images: Characteristic findings on CECT (Contrast Enhanced CT) or MRI.
• Top Causes: Gallstones (40-50%) and Alcohol (25-30%) account for the vast majority.
• Mortality:
  • Mild: <1%.
  • Severe (Persistent Organ Failure): 20-40%.
  • Infected Necrosis: >50% if untreated.

Clinical Pearls

Amylase vs Lipase: Amylase rises quickly (hrs) but normalizes in 3-5 days. Lipase rises later and stays elevated for 2 weeks. Lipase is more specific for pancreas. (Amylase leaks in perf DU, ovarian cysts, salivary stones).

Pain Relief: Traditionally, Morphine was avoided due to "Sphincter of Oddi spasm" theory. Modern evidence shows this is clinically irrelevant. Give Morphine or Fentanyl. Do not undertreat pain.

The "Sentinel Loop": A localized ileus (dilated loop of small bowel) near the pancreas on X-ray, paralyzed by the inflammation.

The classic mnemonic for causes.

Gallstones: To ERCP or Not?

• Scenario A: Pancreatitis + Cholangitis (Fever/Jaundice/Rigors).
  • Action: Urgent ERCP (<24h) to clear the duct. This is sepsis control.
• Scenario B: Pancreatitis + Biliary Obstruction (Bilirubin high) but no sepsis.
  • Action: Early ERCP (<72h).
• Scenario C: Pancreatitis + Gallstones but LFTs normal.
  • Action: No ERCP. The stone has likely passed. Proceed to Cholecystectomy.

The Scorpion Story

A tropical pearl.

• Culprit: Tityus trinitatis (Trinidad).
• Venom: Neurotoxin causes massive acetylcholine release from post-ganglionic parasympathetic neurons.
• Result: Hypersecretion of "enzyme-rich" pancreatic fluid against a spastic Sphincter of Oddi.
• Clinical: Severe pain + Sialorrhea (drooling) + Bradycardia.

Drug-Induced Pancreatitis (DIP)

Classification by Badalov et al.

Autoimmune Pancreatitis (IgG4 Disease)

The "Sausage Pancreas".

• Feature: Diffuse enlargement of the pancreas (featureless rim). Often mimics Pancreatic Cancer (painless jaundice).
• Types:
  • Type 1: Systemic IgG4 disease (Sjogren's, Retroperitoneal fibrosis).
  • Type 2: Pancreas specific. Associated with IBD.
• Treatment: Steroids (Prednisolone). Spectacular response ("Melting like ice").

Predicting who will die is crucial for ICU triage.

BISAP Score (Bedside Index for Severity in Acute Pancreatitis)

Simpler than APACHE, more accurate than Ranson. Score 0-5. Mortality increases with score.

HAPS (Harmless Acute Pancreatitis Score)

Who can go home safely?

• Absence of tenderness + Normal Hct + Normal Creatinine.
• PPV: 98% for a non-severe course. These patients can often be managed on the ward (or even home).

The Modified Glasgow Score (Imrie)

Mnemonic: PANCREAS. Score >= 3 indicates Severe Pancreatitis. Measured at 48 hours.

Ranson's Criteria (The Classic)

Historical significance, but requires 48h wait.

At Admission (0 Hours)

• Age > 55
• WCC > 16
• Glucose > 11 mmol/L
• LDH > 350
• AST > 250

At 48 Hours

• Hct drop > 10%
• BUN rise > 1.8 mmol/L
• Calcium < 2.0 mmol/L
• PaO2 < 60 mmHg
• Base Deficit > 4
• Fluid Sequestration > 6L

Score >= 3 = Severe Pancreatitis.

"Score Wars": Which one to use?

• Ranson: Too slow (needs 48h). Historic interest mainly.
• APACHE II: Gold standard for research (ICU data), but too complex for ward use.
• Glasgow: Excellent Negative Predictive Value. Specific for alcohol/gallstone pancreatitis.
• BISAP: Best bedside tool for the first 24h. Use this on admission.

Revised Atlanta Classification (2012)

The modern global standard for definitions.

1. Mild: No Organ Failure. No local complications. Discharged < 1 week.
2. Moderate: Transient Organ Failure (<48h) OR Local complications (Fluid colection).
3. Severe: Persistent Organ Failure (>48h). Mortality high.

CRP (The Simple Predictor)

• A CRP > 150 mg/L at 48 hours is a strong predictor of severe necrotizing pancreatitis.

Signs

• Tachycardia/Hypotension: Third space fluid loss (Pancreatic Burn).
• Abdominal Tenderness: Epigastric guarding.
• Jaundice: Suggests Gallstone obstruction (Cholangitis).
• Ileus: Absent bowel sounds.

The "Hemorrhagic Signs" (Rare <1%)

Signs of retroperitoneal hemorrhage digesting fascial planes.

• Grey-Turner's Sign: Flank bruising (Blood tracks via Pararenal space).
• Cullen's Sign: Periumbilical bruising (Blood tracks via Falciform ligament).
• Fox's Sign: Bruising over inguinal ligament.

Pancreatic Ascites (Internal Fistula)

The "Leaky Duct".

• Mechanism: Disruption of the main pancreatic duct leaks amylase-rich fluid into the peritoneum.
• Presentation: Progressive painless distension. High amylase in ascitic fluid (>10,000).
• Treatment:
  1. Conservative: NBM, TPN, Octreotide (Somatostatin analogue to dry up secretions).
  2. Endoscopic: ERCP + Stent across the leak.

Local Complications Timeline

Revised Atlanta Classification Definitions.

1. < 4 Weeks:
   • APFC: Acute Peripancreatic Fluid Collection. (Sterile fluid). -> Leave alone.
   • ANC: Acute Necrotic Collection. (Solid/Liquid mix). -> Leave alone.
2. > 4 Weeks (Encapsulated):
   • Pseudocyst: Fluid wall. -> Drain if symptomatic.
   • Walled-Off Necrosis (WON): Encapsulated dead tissue. -> Debride if infected.

The Infected Necrosis Timeline

When to panic.

Vascular Complications

The pancreas sits on top of major vessels.

1. Splenic Vein Thrombosis:
   • Incidence: 10-20% of severe pancreatitis.
   • Mechanism: Inflammation causes clot in the splenic vein running behind the pancreas.
   • Result: Gastric Varices (Isolated). The spleen engorges and drains retrogradely via the short gastric veins.
   • Treatment: Splenectomy (only if bleeding varices). Anticoagulation is controversial.
2. Pseudoaneurysm:
   • Erosion of the Splenic or Gastroduodenal artery.
   • Presentation: Sudden massive GI bleed (Hemosuccus Pancreaticus).
   • Treatment: Angio-embolization.

Abdominal Compartment Syndrome (ACS)

The silent killer in the ICU.

• Pathology: Massive fluid resuscitation + Ileus + Ascites = Increased Intra-Abdominal Pressure (IAP).
• Effect:
  • Renal: Veins compressed -> Anuria / AKI.
  • Respiratory: Diaphragm pushed up -> High peak airway pressures / Hypoxia.
  • Cardiac: Decreased venous return.
• Diagnosis: Measure Bladder Pressure. (>20 mmHg + Organ Failure = ACS).
• Treatment: Nasogastric decompression, Paralysis, Diuretics, Paracentesis. Laparostomy (Open Abdomen) is the nuclear option.

Infected Necrosis: The "Step-Up Approach"

Don't just cut it open.

• Scenario: Patient deteriorates 3 weeks later (Gas in pancreas on CT).
• The "PANTER" Trial: Open necrosectomy has high mortality.
• Protocol:
  1. Antibiotics: Meropenem.
  2. Percutaneous Drain: IR puts a drain into the collection.
  3. VARD: Video-Assisted Retroperitoneal Debridement (upsize drain track to laparoscope).
  4. Open Surgery: Last resort.

Gallstone Pancreatitis: The "Golden Window"

• The Protocol: Cholecystectomy should be performed during the index admission (once acute inflammation settles, typically Day 5-7).
• Delayed Surgery Risk: Waiting 6 weeks allows a 20-30% recurrence rate.
• Surgical Nuance:
  • Difficult GB: The gallbladder is often inflamed/adherent. Higher conversion rate to Open Cholecystectomy.
  • Intra-operative Cholangiogram (IOC): Mandatory to check if stones remain in the duct.

Alcohol

• Counseling: Strict abstinence. Smoking cessation (Smoking accelerates Chronic Pancreatitis).
• Relapse Prevention: Naltrexone/Acamprosate referral.

Metabolic Control

• Triglycerides: Start Fibrates (Gemfibrozil) if TG > 5. Avoid Statins initially (less effective for TG).

Q: Can I ever drink alcohol again? A: If alcohol was the cause, the answer is usually "No". The pancreas is permanently sensitized. Even one drink can trigger a relapse.

Q: Do I need digestive enzymes? A: Usually no. But if the pancreas was severely damaged (necrosis), you might develop Exocrine Insufficiency (steatorrhea). We test this with "Fecal Elastase".

Q: Why is my calcium low? A: The fat necrosis in your belly "soaps up" the calcium from the blood. We will replace it via IV.