Version 1.0 — Published February 2026
Quick Answer
Cirrhosis complications contribute 3–4 NEET PG questions per paper. Master these 10 high-yield anchors:
- Pathophysiology — fibrosis + nodular regeneration → portal HTN + synthetic dysfunction; decompensation = ascites, variceal bleed, HE, jaundice
- Child-Pugh — 5 variables (bili, alb, INR, ascites, HE) → A (5–6), B (7–9), C (10–15); 1-year survival 100 / 80 / 45%
- MELD-Na — formula from bili, Cr, INR, Na; transplant threshold >=15; used for organ allocation
- Ascites — SAAG >=1.1 = portal HTN (cirrhosis, CHF, Budd-Chiari); <1.1 = TB, malignancy, pancreatic, nephrotic
- SBP — PMN >=250/mm^3; ceftriaxone 2 g/d × 5–7 d + albumin 1.5 g/kg day 1 / 1 g/kg day 3 (Sort NEJM 1999)
- Varices — small + red wale or Child C → NSBB; medium/large → NSBB or EBL (equivalent); carvedilol preferred
- Hepatic encephalopathy — West Haven 1–4; lactulose (2–3 soft stools/day) + rifaximin 550 mg BD (Bass NEJM 2010)
- Hepatorenal syndrome — functional AKI; HRS-AKI (rapid) / HRS-NAKI (chronic); terlipressin + albumin; definitive = transplant
- HCC — surveillance USG ± AFP every 6 months in all cirrhotics; Milan criteria for transplant (1 tumour <=5 cm OR up to 3 each <=3 cm)
- Transplant — MELD >=15, decompensation, FHF (King's College criteria), HCC within Milan; LDLT dominates in India
Cirrhosis is the final common pathway of chronic liver disease, and its complications dominate NEET PG medicine and gastroenterology questions — SAAG cutoffs, SBP diagnosis and prophylaxis, HE grading, HRS vs pre-renal AKI, Milan criteria. This guide walks through pathophysiology, scoring systems, each major complication, and transplant indications. Pair with the medicine subject hub, the medicine high-yield topics overview, and the hepatitis serology and management guide for complete hepatology coverage.
Cirrhosis pathophysiology
Cirrhosis is the end-stage of progressive hepatic fibrosis with nodular regeneration — a histopathological diagnosis characterised by distortion of hepatic architecture that alters blood flow and causes both portal hypertension and hepatocyte synthetic dysfunction.
Core mechanisms:
- Hepatic stellate cell activation — transforms into myofibroblasts that deposit collagen (types I and III)
- Architectural distortion — bridging fibrosis → regenerative nodules → increased intrahepatic resistance
- Portal hypertension — HVPG (hepatic venous pressure gradient) >=5 mmHg; clinically significant when >=10; bleeding risk when >=12
- Synthetic failure — low albumin, prolonged INR, elevated bilirubin
- Hyperdynamic circulation — splanchnic vasodilatation (NO-mediated) → effective hypovolaemia → RAAS + SNS + ADH activation → sodium and water retention
Common Indian aetiologies:
| Cause | Frequency (India) | Key features |
|---|
| Alcohol | ~30% | History, AST:ALT >2:1, GGT elevated, macrocytosis |
| Chronic hepatitis B | ~20–25% | HBsAg +, HBV DNA; vertical transmission common |
| Chronic hepatitis C | ~10–15% | Anti-HCV +, HCV RNA; post-DAA cure rates >95% |
| NAFLD / MASLD | Rising (~20%) | Obesity, diabetes, metabolic syndrome |
| Autoimmune | 5% | ANA, SMA, LKM-1, elevated IgG |
| PBC / PSC | 2–5% | AMA (PBC), p-ANCA + MRCP beading (PSC) |
| Wilson disease | <1% | Low ceruloplasmin, high urinary copper, KF rings |
| Hemochromatosis | <1% | High transferrin saturation, HFE mutations |
| Cryptogenic | ~10% | Often burnt-out NAFLD |
Decompensation = first episode of ascites, variceal bleed, HE, or jaundice (beyond cholestasis baseline). Compensated median survival >12 years; decompensated survival 1.5–2 years untreated.
Child-Pugh and MELD scoring
Child-Pugh and MELD are complementary severity scores — Child-Pugh for bedside stratification and surgical risk, MELD for transplant allocation and 3-month mortality prediction.
Child-Pugh score (original CTP / Child-Turcotte-Pugh):
| Variable | 1 point | 2 points | 3 points |
|---|
| Bilirubin (mg/dL) | <2 | 2–3 | >3 |
| Albumin (g/dL) | >3.5 | 2.8–3.5 | <2.8 |
| INR | <1.7 | 1.7–2.3 | >2.3 |
| Ascites | None | Mild (controlled with diuretics) | Moderate/severe (refractory) |
| Encephalopathy | None | Grade 1–2 | Grade 3–4 |
- Class A: 5–6 points — 1-year survival ~100%
- Class B: 7–9 points — ~80%
- Class C: 10–15 points — ~45%
Mnemonic — "Pour Another Beer At Eleven": PT (INR), Albumin, Bilirubin, Ascites, Encephalopathy.
MELD (Model for End-stage Liver Disease):
- Formula: 3.78 × ln(bilirubin) + 11.2 × ln(INR) + 9.57 × ln(creatinine) + 6.43
- Range 6–40
- MELD-Na adds sodium (lower Na → higher score)
- MELD 3.0 (2023) adds female sex and albumin
- Predicts 3-month mortality
- Transplant listing threshold: MELD >=15 (below this, transplant mortality exceeds natural history)
NEET PG differentiator:
- Child-Pugh → severity class, peri-operative risk, bedside use
- MELD → organ allocation, prognostication, RCT endpoint
Ascites and spontaneous bacterial peritonitis
Ascites is the most common decompensation event in cirrhosis — SAAG-based classification and stepwise sodium restriction / diuretics / paracentesis guide management, and SBP must be excluded at every paracentesis.
Ascites workup — diagnostic paracentesis in every new ascites:
| Test | Purpose |
|---|
| Cell count and differential | SBP diagnosis (PMN >=250/mm^3) |
| Albumin | SAAG calculation |
| Total protein | <1 g/dL → high SBP risk → prophylaxis |
| Culture | Direct bedside inoculation into blood culture bottles (higher yield) |
| Amylase | Pancreatic ascites |
| Cytology | Malignancy |
| ADA, AFB | Peritoneal TB (sensitivity modest) |
| Glucose, LDH | Secondary peritonitis workup |
SAAG interpretation:
| SAAG >=1.1 g/dL (portal HTN) | SAAG <1.1 g/dL (non-portal HTN) |
|---|
| Cirrhosis | Peritoneal TB |
| Alcoholic hepatitis | Peritoneal carcinomatosis |
| Cardiac failure | Pancreatic ascites |
| Budd-Chiari syndrome | Nephrotic syndrome |
| Massive liver metastases | Serositis (SLE) |
| Veno-occlusive disease | Biliary ascites |
Ascites management (non-refractory):
- Sodium restriction — <2 g Na (88 mmol) per day
- Spironolactone 100 mg/day + furosemide 40 mg/day (100:40 ratio maintains normokalaemia); titrate every 3–5 days up to 400:160
- Goal — 0.5 kg/day weight loss without edema; 1 kg/day if pedal edema present
- Fluid restriction only if Na <125 mmol/L
- Abstain from alcohol
Refractory ascites (failure despite maximal diuretics or diuretic-induced complications):
- Large-volume paracentesis (LVP) + albumin (8 g per L removed beyond 5 L) to prevent post-paracentesis circulatory dysfunction
- TIPS in suitable candidates
- Consider transplant referral
Spontaneous bacterial peritonitis (SBP):
| Parameter | Detail |
|---|
| Diagnosis | Ascitic fluid PMN >=250 cells/mm^3 regardless of culture; "culture-negative neutrocytic ascites" treated the same |
| Classic triad | Fever, abdominal pain, worsening HE (but ~33% asymptomatic) |
| Common organisms | E. coli (most common), Klebsiella, Streptococcus |
| Initial empirical | Ceftriaxone 2 g IV daily or cefotaxime 2 g IV every 8 h × 5–7 days |
| Albumin | 1.5 g/kg day 1 + 1 g/kg day 3 → reduces HRS and mortality (Sort NEJM 1999) |
| Prophylaxis | Primary in ascitic protein <1.5 g/dL + advanced liver disease; during GI bleed (ceftriaxone 1 g daily × 7 d); secondary lifelong after first SBP (norfloxacin 400 mg/day or ciprofloxacin) |
| Secondary peritonitis | Polymicrobial + protein >1, glucose <50, LDH higher than serum; CT to exclude perforation |
Varices and portal hypertension prophylaxis
Esophageal and gastric varices are the most feared complication of portal hypertension — primary prophylaxis prevents first bleed and secondary prophylaxis prevents rebleeding.
Screening:
- Endoscopy at diagnosis of cirrhosis in all patients
- Baveno VII: in compensated cirrhosis with LSM (liver stiffness measurement) <20 kPa AND platelets >150,000, screening endoscopy can be deferred (very low varices risk)
- Repeat every 1–3 years depending on findings and liver disease activity
Varices classification:
- Small <5 mm, medium/large >=5 mm
- Red wale signs, cherry-red spots = high bleeding risk
- Gastric: Sarin GOV1/GOV2/IGV1/IGV2; IGV1 highest rebleeding
Primary prophylaxis:
| Finding | Intervention |
|---|
| No varices | Repeat endoscopy in 2–3 years; treat underlying cause |
| Small varices, no red signs, Child A | No prophylaxis; repeat in 1–2 years |
| Small varices with red signs OR Child C | NSBB (propranolol / carvedilol / nadolol) |
| Medium/large varices | NSBB OR EBL (equivalent efficacy) |
| Compensated cirrhosis + CSPH (HVPG >=10) | Carvedilol (preferred) even without varices (PREDESCI trial — reduced decompensation) |
NSBB dosing and target:
- Propranolol 20 mg BD → titrate to HR 55–60 or maximum tolerated
- Nadolol 40 mg OD
- Carvedilol 6.25–12.5 mg/day — preferred (alpha-1 blockade adds portal pressure reduction)
- Goal HVPG reduction >20% from baseline OR HVPG <12 mmHg
Acute variceal bleed management (detailed in the upper GI bleed guide):
- Resuscitation with restrictive transfusion (Hb 7–9)
- Octreotide or terlipressin
- Ceftriaxone prophylaxis
- EBL within 12 h
- Early TIPS within 72 h in Child C (≤13) or Child B with active bleeding
Secondary prophylaxis:
- NSBB + EBL combination
- TIPS if recurrent bleed despite above
- Transplant evaluation
Hepatic encephalopathy
Hepatic encephalopathy (HE) is a spectrum of neuropsychiatric manifestations in liver failure caused by accumulation of gut-derived toxins (predominantly ammonia) that bypass hepatic detoxification — graded by West Haven criteria and managed by addressing precipitants and gut-luminal ammonia.
West Haven grading:
| Grade | Consciousness | Cognitive | Neurological |
|---|
| Minimal (covert) | Normal | Subtle psychometric deficits only | No asterixis |
| Grade 1 | Mild lack of awareness | Euphoria / anxiety, shortened attention | Tremor, incoordination |
| Grade 2 | Lethargy | Disoriented to time, obvious personality change, inappropriate behavior | Asterixis, slurred speech |
| Grade 3 | Somnolent but arousable | Gross disorientation, bizarre behavior | Muscular rigidity, hyperreflexia, clonus |
| Grade 4 | Coma | Unresponsive | Decerebrate posturing |
Precipitants (most common — check all before adding drugs):
| Category | Example |
|---|
| Infection | SBP, UTI, pneumonia, cellulitis |
| GI bleed | Variceal or non-variceal (protein load) |
| Constipation | Reduced ammonia clearance |
| Electrolyte | Hypokalaemia, hyponatraemia, alkalosis |
| Drugs | Benzodiazepines, opioids, diuretics |
| Dehydration | Over-diuresis, diarrhea |
| Dietary | High protein load |
| Portosystemic shunt | Spontaneous or iatrogenic (TIPS) |
| HCC / vascular thrombosis | Portal vein thrombosis |
Treatment:
| Step | Intervention |
|---|
| 1. Identify and treat precipitant | Mandatory first step |
| 2. Lactulose | 30–45 mL PO TID titrated to 2–3 soft stools/day; 300 mL in 700 mL water per retention enema in coma |
| 3. Rifaximin | 550 mg BD — reduces recurrence by 58% (Bass NEJM 2010); preferred secondary prophylaxis |
| 4. L-ornithine-L-aspartate (LOLA) | IV / oral — enhances urea cycle; useful adjunct |
| 5. Zinc replacement | 220 mg BD — often deficient; cofactor for OTC |
| 6. Avoid protein restriction | Counterproductive — maintain 1.2–1.5 g/kg/day protein; vegetable and dairy protein preferred |
| 7. Branched-chain amino acids (BCAAs) | In refractory HE |
| 8. Transplant | Definitive for recurrent/refractory HE |
Do not routinely use: neomycin (nephrotoxic / ototoxic), metronidazole (neuropathy), benzodiazepine antagonist flumazenil (only if benzodiazepine precipitant identified).
Hepatorenal syndrome and AKI in cirrhosis
Hepatorenal syndrome (HRS) is a functional pre-renal AKI occurring in advanced cirrhosis — driven by splanchnic vasodilatation and renal vasoconstriction — and is diagnosed by exclusion after excluding structural, pre-renal volume-responsive, and nephrotoxic causes.
Diagnostic criteria (ICA-AKI 2015, updated 2023):
- Cirrhosis with ascites
- AKI per ICA (rise in Cr >=0.3 mg/dL within 48 h or >=50% within 7 days)
- No response to 2 days of diuretic withdrawal + albumin 1 g/kg/day
- No shock
- No recent nephrotoxins (NSAIDs, aminoglycosides, contrast)
- No structural renal disease (proteinuria <500 mg/day, no haematuria, normal USG)
Two clinical patterns:
| Feature | HRS-AKI (type 1) | HRS-NAKI (type 2) |
|---|
| Onset | Rapid (<2 weeks) | Gradual (months) |
| Creatinine | Doubling to >2.5 mg/dL | Slow rise |
| Precipitant | SBP, GI bleed, LVP without albumin, alcoholic hepatitis | Progressive; often refractory ascites |
| Median survival untreated | ~2 weeks | ~6 months |
Treatment:
| Intervention | Dose |
|---|
| Terlipressin | 1–2 mg IV every 4–6 h (up to 12 mg/day) — drug of choice |
| Noradrenaline (ICU alternative) | 0.5–3 mg/h titrated |
| Midodrine + octreotide (when terlipressin unavailable) | Midodrine 7.5–15 mg TID; octreotide 100–200 mcg SC TID |
| Albumin | 1 g/kg day 1 (max 100 g) → 20–40 g/day |
| RRT | Bridge to transplant; not curative |
| TIPS | Select HRS-NAKI (type 2) cases |
| Liver transplant | Definitive — combined liver-kidney transplant if AKI >4 weeks or baseline CKD |
CONFIRM trial (NEJM 2021): terlipressin + albumin achieved reversal in 32% vs 17% placebo in HRS-AKI.
Hepatopulmonary syndrome
Hepatopulmonary syndrome (HPS) is defined by the triad of liver disease, pulmonary vascular dilatation (intrapulmonary right-to-left shunt), and arterial hypoxemia — and liver transplantation is the only definitive therapy.
Definition (triad):
- Chronic liver disease (usually cirrhosis, rarely non-cirrhotic portal hypertension)
- Pulmonary vascular dilatation — confirmed by contrast echo or macroaggregated albumin scan
- Arterial hypoxemia — PaO2 <80 mmHg or A-a gradient >=15 mmHg on room air (age-adjusted >=20 if >64 years)
Clinical features:
- Platypnea — dyspnea on sitting up
- Orthodeoxia — desaturation >=5% or PaO2 drop >=4 mmHg on sitting up
- Clubbing, cyanosis, spider naevi
- Reason: dilated vessels are predominantly basal — when upright, more blood flows through shunt
Diagnosis:
- Contrast-enhanced transthoracic echocardiography (bubble study) — agitated saline bubbles in LA >3 beats after RA (intrapulmonary shunt) — vs immediately in intracardiac shunt
- Macroaggregated albumin lung scan — quantifies shunt fraction
- ABG on room air — PaO2 and A-a gradient
Severity by PaO2:
- Mild: >=80 mmHg
- Moderate: 60–79
- Severe: 50–59
- Very severe: <50
Treatment:
- Supplemental O2 (symptomatic)
- Liver transplantation — reverses HPS in >80% (MELD exception points granted for severe HPS to prioritise)
- No effective pharmacotherapy — pentoxifylline, garlic, somatostatin have limited evidence
Differentiate from portopulmonary hypertension (POPH):
| Feature | HPS | POPH |
|---|
| Lesion | Pulmonary vascular dilatation | Pulmonary vascular constriction / arteriopathy |
| PAP | Normal or low | Elevated (mPAP >25) |
| PaO2 | Low | Near-normal |
| Treatment | O2 + transplant | PAH therapy (endothelin antagonists, PDE-5i); transplant if mPAP <35 after therapy |
Hepatocellular carcinoma surveillance
HCC is the leading cause of death in compensated cirrhosis — and universal surveillance with 6-monthly ultrasound (with or without AFP) is the highest-impact intervention after treating the underlying liver disease.
Surveillance:
- Ultrasound abdomen every 6 months in all cirrhotics and high-risk hepatitis B carriers (Asian men >=40, Asian women >=50, family history, cirrhosis)
- AFP — add-on, increases sensitivity from 63% to 78% (AASLD now permits but does not mandate)
- If USG positive → 4-phase multiphase CT or MRI with contrast
Diagnosis (non-invasive imaging criteria, LI-RADS):
- Cirrhotic liver + nodule >=1 cm with arterial phase hyperenhancement + portal venous or delayed phase washout + capsule / threshold growth = HCC (no biopsy needed)
- Biopsy reserved for atypical lesions
Staging — BCLC (Barcelona Clinic Liver Cancer):
| Stage | Tumour | Liver function | ECOG | Treatment | 5-yr survival |
|---|
| 0 (very early) | Single <2 cm | Child A | 0 | Ablation / resection | >70% |
| A (early) | Single or up to 3 <=3 cm | Child A–B | 0 | Resection, ablation, transplant | 50–70% |
| B (intermediate) | Multinodular | Child A–B | 0 | TACE (transarterial chemoembolisation) | 30–50% |
| C (advanced) | Vascular invasion / extrahepatic spread | Child A–B | 1–2 | Systemic — atezolizumab + bevacizumab (first-line IMbrave150), sorafenib, lenvatinib | ~2 years median |
| D (terminal) | Any | Child C | 3–4 | Best supportive care | <3 months |
Milan criteria for transplant eligibility in HCC:
- Single tumour <=5 cm OR
- Up to 3 tumours each <=3 cm
- No macrovascular invasion
- No extrahepatic spread
- → Post-transplant 5-year survival ~70–80% (Mazzaferro NEJM 1996)
UCSF criteria (expanded): single <=6.5 cm OR up to 3 each <=4.5 cm with total <=8 cm — similar outcomes.
Down-staging via TACE / ablation can bring initially outside-Milan HCC into Milan for transplant.
Liver transplantation — indications and contraindications
Liver transplantation is the definitive therapy for end-stage liver disease — organ allocation uses MELD in most systems and the key exam distinction is between adult living-donor liver transplant (LDLT, dominant in India) and deceased donor liver transplant (DDLT).
Indications:
| Category | Examples |
|---|
| Chronic liver disease | Decompensated cirrhosis (MELD >=15), refractory ascites, recurrent variceal bleed, recurrent HE, HRS, HPS |
| Acute liver failure | Fulminant hepatic failure meeting King's College Criteria |
| Hepatocellular carcinoma | Within Milan / UCSF criteria |
| Metabolic | Wilson disease with liver failure or progressive disease, hemochromatosis, alpha-1 antitrypsin deficiency, tyrosinaemia |
| Cholestatic | PBC (bilirubin >6), PSC with cholangiocarcinoma surveillance |
| Miscellaneous | Polycystic liver, Budd-Chiari, familial amyloid polyneuropathy |
King's College Criteria for acute liver failure (transplant listing):
Paracetamol-induced:
- Arterial pH <7.3 after resuscitation, OR
- All three: INR >6.5, Cr >3.4 mg/dL, grade 3–4 HE
Non-paracetamol:
- INR >6.5, OR
- Any three of: age <10 or >40, aetiology (non-A non-B hepatitis, halothane, idiosyncratic), jaundice-to-encephalopathy >7 days, INR >3.5, bilirubin >17.6 mg/dL
Contraindications:
| Absolute | Relative |
|---|
| Active extrahepatic malignancy | Ongoing alcohol/substance use (most programmes require 6 months abstinence) |
| Uncontrolled sepsis | Age >70 (centre-dependent) |
| Advanced cardiopulmonary disease (severe PAH, uncontrolled CAD) | HIV with uncontrolled viremia / low CD4 |
| Persistent non-compliance | Severe obesity (BMI >40) |
| Brain death / anoxic brain injury | Psychosocial / support issues |
LDLT in India:
- Dominant modality due to limited deceased donor supply
- Right lobe for adult recipients; left lateral segment for paediatric
- Donor safety is paramount (mortality ~0.2–0.5%)
Post-transplant immunosuppression: calcineurin inhibitor (tacrolimus > cyclosporine) + mycophenolate ± steroids; complications include CNI nephrotoxicity, PTLD, infections, recurrence of disease.
Sources and references
- Harrison's Principles of Internal Medicine, 21st Edition (Loscalzo et al., 2022) — Chapters on cirrhosis and its complications.
- Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th Edition (Feldman, Friedman, Brandt, Eds., 2020).
- European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol 2018; 69:406-460.
- Biggins SW et al. Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 AASLD Practice Guidance. Hepatology 2021; 74:1014-1048.
- de Franchis R et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022; 76:959-974.
- Bass NM et al. Rifaximin treatment in hepatic encephalopathy. N Engl J Med 2010; 362:1071-1081.
- Sort P et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med 1999; 341:403-409.
- Mazzaferro V et al. Liver transplantation for the treatment of small hepatocellular carcinomas in patients with cirrhosis. N Engl J Med 1996; 334:693-699.
Frequently asked questions
How many liver cirrhosis questions appear in NEET PG?
Liver cirrhosis and its complications contribute 3-4 direct questions per NEET PG paper across medicine, gastroenterology and critical care. The most tested subtopics are SAAG-based ascites classification, Child-Pugh vs MELD scoring, spontaneous bacterial peritonitis diagnosis and treatment, hepatic encephalopathy grading, hepatorenal syndrome types, varices prophylaxis, and HCC surveillance per Milan criteria based on 2019-2025 pattern analysis.
What is the SAAG and how is it used?
SAAG (Serum-Ascites Albumin Gradient) equals serum albumin minus ascitic fluid albumin. SAAG greater than or equal to 1.1 g/dL indicates portal hypertensive ascites (cirrhosis, heart failure, Budd-Chiari, massive liver metastases) with 97 percent accuracy. SAAG less than 1.1 g/dL indicates non-portal hypertensive ascites (peritoneal TB, peritoneal carcinomatosis, pancreatic ascites, nephrotic syndrome). SAAG replaced the old transudate-exudate classification because it is physiology-based and more accurate.
How is spontaneous bacterial peritonitis diagnosed and treated?
SBP is diagnosed by ascitic fluid PMN count greater than or equal to 250 cells/mm3 regardless of culture. Classic triad is fever, abdominal pain, worsening encephalopathy in a cirrhotic with ascites — but up to a third are asymptomatic. Treat with IV third-generation cephalosporin (ceftriaxone 2 g daily or cefotaxime 2 g every 8 h) for 5-7 days. Add albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 to prevent hepatorenal syndrome (reduces mortality per Sort NEJM 1999). Secondary prophylaxis with norfloxacin 400 mg daily or ciprofloxacin 500 mg daily is lifelong after first episode.
What is Child-Pugh and MELD scoring?
Child-Pugh assesses cirrhosis severity using 5 variables — bilirubin, albumin, INR, ascites, encephalopathy — each scored 1-3 for total 5-15. Class A (5-6, 1-year survival 100 percent), Class B (7-9, 80 percent), Class C (10-15, 45 percent). MELD uses bilirubin, creatinine, INR, sodium (MELD-Na) in a mathematical formula for 3-month mortality prediction and organ allocation for liver transplant. MELD greater than or equal to 15 is the transplant threshold; MELD greater than 40 caps the score. MELD is objective and preferred for transplant listing; Child-Pugh is used for severity stratification and peri-operative risk.
What are the hepatorenal syndrome types?
Hepatorenal syndrome (HRS) is a functional pre-renal AKI in advanced cirrhosis with no structural kidney disease. HRS type 1 (now HRS-AKI) is rapid — doubling of creatinine to greater than 2.5 mg/dL in less than 2 weeks, often precipitated by SBP or large-volume paracentesis without albumin; median survival 2 weeks untreated. HRS type 2 (now HRS-NAKI) is chronic — gradual rise in creatinine with refractory ascites; median survival 6 months. Treat with terlipressin (2-12 mg/day) plus albumin (1 g/kg day 1 then 20-40 g/day); noradrenaline plus albumin if ICU. Definitive therapy is liver transplantation.
How is hepatic encephalopathy graded and treated?
West Haven grading. Grade 1: trivial lack of awareness, euphoria, shortened attention. Grade 2: lethargy, disorientation in time, obvious personality change, asterixis. Grade 3: somnolent but arousable, gross disorientation. Grade 4: coma. Treatment starts with identifying and treating precipitants (infection, GI bleed, constipation, electrolyte imbalance, sedatives, dehydration). Lactulose 30-45 mL TID titrated to 2-3 soft stools/day is first-line. Add rifaximin 550 mg BD for secondary prophylaxis (Bass NEJM 2010 — 58 percent relative risk reduction). Restrict protein only in refractory cases; high-protein diet is otherwise preferred.
What is the Milan criteria for HCC?
Milan criteria defines patients with hepatocellular carcinoma (HCC) eligible for liver transplantation — single tumor less than or equal to 5 cm, OR up to 3 tumors each less than or equal to 3 cm, no vascular invasion, no extrahepatic spread. Post-transplant 5-year survival within Milan is 70-80 percent (Mazzaferro NEJM 1996). UCSF criteria expanded this to single tumor less than or equal to 6.5 cm or 3 tumors less than or equal to 4.5 cm each with total less than or equal to 8 cm. BCLC staging guides overall HCC management — BCLC A (very early/early — resection, ablation, transplant), BCLC B (intermediate — TACE), BCLC C (advanced — systemic — atezolizumab + bevacizumab, sorafenib), BCLC D (terminal — best supportive care).
How are esophageal varices prevented from bleeding?
All cirrhotics should have screening endoscopy at diagnosis. Small varices (less than 5 mm) without red wale signs — no prophylaxis, repeat endoscopy in 1-2 years. Small varices with red wale signs or Child C — non-selective beta-blocker (NSBB — propranolol or carvedilol). Medium/large varices (greater than 5 mm) — NSBB OR endoscopic band ligation (equivalent efficacy). Carvedilol is preferred NSBB in compensated cirrhosis with clinically significant portal hypertension (HVPG greater than or equal to 10). Goal HVPG reduction is greater than 20 percent or less than 12 mmHg — if not achievable, EBL is added.
What is hepatopulmonary syndrome?
Hepatopulmonary syndrome (HPS) is defined by the triad of liver disease, pulmonary vascular dilatation, and arterial hypoxemia (PaO2 less than 80 mmHg or alveolar-arterial gradient greater than or equal to 15 mmHg). Clinical hallmark is platypnea-orthodeoxia — dyspnea and desaturation on sitting up, improving on lying down — due to preferential perfusion of dilated basal vessels. Diagnosis is by contrast-enhanced transthoracic echocardiography showing delayed (3-6 beats) passage of bubbles into left atrium. Treatment is supplemental oxygen and liver transplantation (reverses HPS in most); pentoxifylline has limited evidence.
When is liver transplantation indicated?
Liver transplantation is indicated for end-stage liver disease with MELD greater than or equal to 15 (survival benefit), decompensated cirrhosis (ascites, variceal bleed, encephalopathy, HRS, HPS), fulminant hepatic failure (King College criteria), and HCC within Milan criteria. Contraindications include active extrahepatic malignancy, uncontrolled sepsis, advanced cardiopulmonary disease, ongoing substance use (relative — many programs require 6 months abstinence), and inability to comply with immunosuppression. In India, living donor liver transplant (LDLT) dominates due to limited deceased donor supply.
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This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
Written by: NEETPGAI Editorial Team
Reviewed by: Pending SME Review
Last reviewed: February 2026
This article is reviewed by qualified medical professionals for clinical accuracy and exam relevance. For corrections or updates, contact the editorial team.
