3.3 Acute & Chronic Viral Hepatitis & Pancreatitis

Acute & Chronic Viral Hepatitis & Pancreatitis

Gastroenterology questions in UPSC CMS frequently test viral hepatitis serology profiles, transmission routes, acute pancreatitis diagnostic guidelines (Revised Atlanta criteria), early resuscitation protocols, and chronic pancreatitis complications.

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Viral Hepatitis: Etiology & Serology

Viral hepatitis is caused by primary hepatotropic viruses: Hepatitis A (HAV), B (HBV), C (HCV), D (HDV), and E (HEV).

Viral Transmission & Chronicity Risk

• Enteric Transmission (Fecal-Oral):
  • HAV: Single-stranded RNA virus. Causes self-limiting acute hepatitis; never causes chronic disease.
  • HEV: Single-stranded RNA virus. Usually self-limiting, but causes fulminant hepatic failure with high mortality (20–25%) in pregnant females in their 3rd trimester.
• Parenteral / Sexual / Perinatal Transmission:
  • HBV: Partially double-stranded DNA virus (Hepadnaviridae). Risk of chronicity depends on age at acquisition: perinatal transmission $\rightarrow 90%$ chronicity risk; adult transmission $\rightarrow <5%$ chronicity risk.
  • HCV: Single-stranded RNA virus (Flaviviridae). High rate of chronicity (75–85%). Treated curatively with Direct-Acting Antivirals (DAAs, e.g., Sofosbuvir/Velpatasvir for 12 weeks with $>95%$ Sustained Virologic Response [SVR]).
  • HDV: Defective delta RNA virus requiring HBsAg coat for virion assembly and infectivity. Co-infection (simultaneous HBV+HDV) vs. Superinfection (HDV added to chronic HBV; carries high risk of rapid cirrhosis).

Serological Markers of Hepatitis B Virus

Diagnostic Profiles Matrix for HBV

• Acute Infection: HBsAg (+), IgM anti-HBc (+), Anti-HBs (-), HBeAg (+).
• Window Period: HBsAg (-), Anti-HBs (-), IgM anti-HBc (+).
• Chronic Infection (High Replication): HBsAg (+) $>6$ months, IgG anti-HBc (+), HBeAg (+), Anti-HBs (-).
• Resolved Past Infection: HBsAg (-), Anti-HBs (+), IgG anti-HBc (+).
• Vaccination Immunity: HBsAg (-), Anti-HBs (+), IgG anti-HBc (-).

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Acute Pancreatitis

Acute pancreatitis is an acute inflammatory process of the pancreas resulting from premature intra-acinar enzyme activation.

Etiology

• Gallstones (40%): Most common cause overall (biliary pancreatitis due to ampullary obstruction).
• Alcohol (30%): Second most common cause.
• Hypertriglyceridemia: Serum triglycerides $>1000\text{ mg/dL}$ ($11.3\text{ mmol/L}$).
• Post-ERCP: Occurs in 3–10% of diagnostic/therapeutic procedures.
• Hypercalcemia, Trauma, Drugs: (Azathioprine, Furosemide, Valproate, Sulfonamides).

Diagnostic Criteria (Revised Atlanta Criteria 2012)

Requires at least 2 of the following 3 criteria:

1. Abdominal pain: Severe, sharp epigastric pain radiating directly to the back, characteristically partially relieved by sitting upright and leaning forward (Mohammedan posture).
2. Biochemical markers: Serum Lipase or Amylase elevated $>3$ times the upper limit of normal (ULN). Serum lipase is more specific, rises earlier, and remains elevated longer (8–14 days) than amylase.
3. Imaging: Contrast-enhanced computed tomography (CECT), MRI, or transabdominal ultrasound demonstrating findings characteristic of acute pancreatitis.

CECT Timing: Early CECT within 24–48 hours of onset is inaccurate for assessing pancreatic necrosis. Optimal timing for CECT abdomen is 72 hours post-symptom onset.

Physical Examination Signs

• Cullen Sign: Periumbilical blue-purple ecchymosis (indicates hemoperitoneum from necrotizing pancreatitis).
• Grey Turner Sign: Flank ecchymosis (indicates retroperitoneal hemorrhage).
• Fox Sign: Ecchymosis over the anteromedial thigh near the inguinal ligament.

Management Protocols

• Fluid Resuscitation: Immediate goal-directed crystalloid administration (Lactated Ringer's preferred over Normal Saline to decrease systemic inflammation and hyperchloremic acidosis) at $200–500\text{ mL/hr}$ or $5–10\text{ mL/kg/hr}$. Monitor urine output ($>0.5\text{ mL/kg/hr}$) and hematocrit reduction.
• Nutritional Support: Early oral feeding with low-fat solid diet as tolerated. If oral route failed, enteral tube feeding (nasogastric or nasojejunal) is superior to total parenteral nutrition (TPN) by preserving gut mucosal barrier integrity.
• Antibiotics Rule: Prophylactic antibiotics are NOT recommended in acute pancreatitis regardless of severity or sterile necrosis. Antibiotics are indicated only for confirmed infected pancreatic necrosis (diagnosed via CT-guided fine-needle aspiration showing bacteria/fungi or gas bubbles on CECT).

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Chronic Pancreatitis

Progressive, irreversible inflammatory and fibrotic disease of the pancreas leading to permanent destruction of exocrine and endocrine parenchyma.

Classic Clinical Triad

1. Pancreatic Calcifications: Visualized on abdominal radiograph or CECT (pathognomonic).
2. Steatorrhea: Exocrine insufficiency occurring when $>90%$ of lipase-secreting capacity is destroyed (bulky, foul-smelling, oily stools).
3. Diabetes Mellitus: Endocrine insufficiency from islet cell loss (Pancreatogenic / Type 3c Diabetes).

Diagnostic Tests & Management

• Fecal Elastase-1: Most sensitive non-invasive test for exocrine pancreatic insufficiency ($<200\text{ }\mu\text{g/g}$ indicates insufficiency; $<100\text{ }\mu\text{g/g}$ severe).
• Treatment: Pancreatic Enzyme Replacement Therapy (PERT: enteric-coated lipase/protease/amylase microtablets taken during meals), alcohol/smoking cessation, low-fat frequent meals, and insulin for Type 3c diabetes.