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IM5.15-17 | Liver Disease Management — SDL Guide

Learning Objectives

Describe the management of acute and chronic viral hepatitis including supportive care for HAV/HEV, antiviral indications and agents for HBV (TDF, entecavir) and HCV (DAA therapy, SVR), and emergency management of acute liver failure (NAC, King's College Criteria)
Outline the step-by-step management of each major complication of cirrhosis: ascites (sodium restriction, spironolactone/furosemide, LVP + albumin), SBP (empirical ceftriaxone + albumin, Sort trial protocol, secondary prophylaxis), variceal haemorrhage (terlipressin + antibiotics + EVL within 12h), hepatic encephalopathy (precipitant treatment, lactulose, rifaximin, protein guidelines), HRS (terlipressin + albumin), and HCC (BCLC staging)
Enumerate the indications, schedules, and precautions for hepatitis B vaccination (including neonatal birth dose, healthcare worker vaccination, post-exposure prophylaxis) and hepatitis A vaccination (indications in chronic liver disease patients, travellers, post-exposure)
Identify the indications for liver transplantation: MELD ≥15 for decompensated cirrhosis, Milan criteria for HCC, and King's College Criteria for acute liver failure
Apply the management framework to clinical scenarios involving acute liver disease emergencies

INSTRUCTIONS

This module is organised by complication and management domain. For each complication, learn the pathophysiological rationale first (why does this treatment work?), then the specific protocol (what, at what dose, in what sequence). The clinical scenarios at the end test your ability to execute these protocols under time pressure.

References

Harrison's Principles of Internal Medicine, 21st ed., Ch. 338–340 — Management of Cirrhosis and its Complications (textbook)
Davidson's Principles and Practice of Medicine, 23rd ed., Ch. 22 — Management of Liver Disease (textbook)
API Textbook of Medicine, 10th ed. — Cirrhosis and Portal Hypertension Management (textbook)
EASL Clinical Practice Guidelines: Management of hepatitis B virus infection, 2017 (guideline)
EASL Recommendations on treatment of hepatitis C, 2020 (guideline)
EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis, 2018 (guideline)

Version 2.0 | NMC CBUC 2024

CLINICAL SCENARIO

It is 2 AM on the medical ward. Three patients with liver disease are deteriorating simultaneously. Patient 1: a 42-year-old cirrhotic man vomiting fresh red blood — haematemesis, blood pressure 80/50 mmHg, tachycardia 120/min. Patient 2: a 56-year-old cirrhotic woman with worsening confusion, grade III hepatic encephalopathy, GCS dropping. Patient 3: a 38-year-old with new fever, abdominal pain, and a known large ascites. Each patient is in danger from a different complication of liver disease. You have fifteen minutes before the consultant arrives. What do you do first in each case, and why? The answer requires not a list of complications memorised from a textbook, but a management framework — a set of principles and specific interventions anchored to the pathophysiology of each complication.

WHY THIS MATTERS

Management of liver disease is where the pathophysiological knowledge from the foundations module and the diagnostic skills from the preceding modules translate into direct patient benefit. IM5.15 is a broad, high-yield competency that spans the management of acute hepatitis, chronic viral hepatitis, cirrhosis, portal hypertension and all its complications (ascites, SBP, variceal haemorrhage, HE, HRS), and hepatocellular carcinoma. IM5.16 covers hepatitis vaccination — indications, schedule, and patient counselling. IM5.17 addresses liver transplantation indications. Together they constitute the clinical culmination of the liver disease cluster — the knowledge required to save a patient's life at the bedside.

RECALL

Before proceeding, consolidate three key frameworks from the foundations module. First, the Child-Pugh score (5 parameters: bilirubin, albumin, INR, ascites, encephalopathy; Classes A/B/C = 5–6/7–9/10–15) and MELD score (3 lab values: bilirubin, creatinine, INR — NOT albumin) determine the severity of cirrhosis and guide management decisions including timing of liver transplantation. Second, the pathophysiology of portal hypertension — HVPG ≥12 mmHg drives variceal formation and ascites; splanchnic vasodilatation activates RAAS causing sodium retention; bacterial translocation infects ascitic fluid. Third, hepatic encephalopathy is caused by ammonia accumulation from gut bacterial urease and glutaminase activity; the West-Haven grades I–IV determine treatment intensity; precipitating factors (GI bleed, infection, dehydration, sedatives, constipation) are the first target of management, not ammonia itself.

Clinical Presentations Requiring Management Decisions

Every management decision in liver disease begins with recognising the clinical presentation and placing the patient on the right management pathway. The first step is to distinguish acute from chronic disease, and to identify which complications or disease processes are present — because the management of SBP is fundamentally different from the management of variceal haemorrhage, which is again completely different from the management of chronic viral hepatitis. Miscategorising the presentation — for example, treating ascites conservatively while an occult SBP drives the deterioration — is a common and potentially fatal error.

The six most common presentations requiring specific management decisions in liver disease are: (1) Acute viral hepatitis — newly elevated transaminases + jaundice + prodrome; (2) Acute liver failure — coagulopathy + encephalopathy within 26 weeks, no prior liver disease; (3) Decompensated cirrhosis with ascites — new or worsening abdominal distension + shifting dullness + fluid thrill; (4) Spontaneous bacterial peritonitis — fever + abdominal pain/tenderness + deteriorating encephalopathy in a cirrhotic with ascites; (5) Acute variceal haemorrhage — haematemesis + melaena + haemodynamic instability in a cirrhotic; (6) Hepatic encephalopathy — confusion + altered GCS + asterixis + precipitating factor in a cirrhotic. The clinical recognition pattern for each presentation is the gateway to the management algorithm that follows.

Aetiology-Directed Management: Viral Hepatitis

The management of acute and chronic viral hepatitis is directly linked to the aetiology — which virus, which phase of infection, and whether the disease is acute or chronic. This is the pathophysiological basis of treatment selection: HAV and HEV are self-limiting infections where the immune response reliably clears the virus, making supportive care the only intervention required; HBV and HCV have mechanisms that allow viral persistence (HBV integrates into the host genome and forms cccDNA; HCV escapes immune surveillance via hypervariable envelope proteins), requiring specific antiviral therapy to prevent progression to cirrhosis and hepatocellular carcinoma. The failure to apply this aetiology-directed framework leads to both under-treatment (not starting TDF in a patient with active HBV replication and fibrosis) and over-treatment (unnecessary antiviral therapy in acute self-limiting hepatitis). Understanding WHY a treatment works — not just what it is — is the foundation of safe prescribing in hepatology.

The aetiology-treatment map is:
- HAV/HEV (self-limiting): supportive care only; vaccination prevents HAV; HEV in pregnancy is an exception (high mortality — monitor closely, consider ribavirin in severe cases)
- Acute HBV: supportive care for most; antiviral (TDF or entecavir) for severe acute HBV (INR >1.5 or hospitalised)
- Chronic HBV with replication + fibrosis: TDF 300 mg/day or entecavir 0.5 mg/day, lifelong
- Chronic HCV: pan-genotypic DAA (sofosbuvir/velpatasvir 12 weeks), achieves SVR >95% = functional cure
- Alcoholic hepatitis: steroids (prednisolone 40 mg/day × 28 days) for severe cases (Maddrey's Discriminant Function ≥32 or MELD ≥21); pentoxifylline is no longer recommended (STOPAH trial showed no survival benefit); alcohol abstinence is mandatory

Diagnostic Thresholds That Trigger Treatment

A critical set of diagnostic thresholds in liver disease directly triggers specific management — knowing the threshold IS the management decision, because treatment must begin as soon as the threshold is crossed. Waiting for confirmation or delaying treatment beyond the threshold has documented mortality consequences. This is what distinguishes a physician who manages liver disease well from one who is merely informed about it. The thresholds are precise, evidence-based, and must be applied without equivocation.

The key management-triggering thresholds:

SBP threshold: Ascitic fluid PMN ≥ 250 cells/mm³ → begin ceftriaxone + albumin immediately, before culture results. The evidence for this threshold is strong — treating at 250/mm³ prevents the 20–30% death rate of untreated SBP. Do NOT wait for culture positivity (30% of SBP cases are culture-negative).

Variceal haemorrhage threshold: Active haematemesis/melaena + haemodynamic instability in a cirrhotic → begin terlipressin + ceftriaxone immediately, before endoscopic confirmation. The combination of vasoactive drug + antibiotics from the time of presentation saves lives regardless of whether the bleeding is subsequently confirmed to be variceal at endoscopy.

HRS diagnostic algorithm threshold: Creatinine rising in a cirrhotic with ascites → (1) exclude obstructive uropathy + parenchymal renal disease + nephrotoxins, (2) albumin challenge 1 g/kg/day × 2 days, (3) if no improvement: HRS confirmed → terlipressin + albumin infusion.

HBV antiviral threshold: HBV DNA elevated (typically >2,000 IU/mL) + ALT elevated (>1× ULN persistently) + fibrosis ≥F2 → begin TDF or entecavir. The HBV DNA alone is insufficient (immune-tolerant phase has high DNA but no fibrosis — treatment not indicated at this stage).

Liver transplant listing thresholds: MELD ≥15 (chronic liver disease listing), King's College Criteria met (ALF urgent listing), within Milan criteria (HCC listing + MELD exception points). These thresholds are not soft guides — they are the decision point at which the physician initiates a transplant referral.