Cirrhosis & compensated ESLD
Compensated vs decompensated (ascites, variceal bleed, HE, jaundice). Decompensation jumps mortality.
Compensated vs decompensated
Cirrhosis is irreversible fibrosis plus regenerative nodules that scramble architecture and blood flow (). Compensated: no ascites, HE, jaundice, or bleed — nonbleeding varices are allowed, and patients may feel fine. Decompensated: ascites, HE, jaundice, SBP, variceal bleed, HRS, or hepatopulmonary syndrome. ESLD is the pathophysiologic state of failed function.
- Symptoms: fatigue, jaundice, pruritus, nausea, anorexia, distention, GIB, confusion, cramps.
- Exam: low BP, splenomegaly, caput, ascites (+LR 7.3), jaundice, spiders (+LR 4.3), gynecomastia, testicular atrophy, palmar erythema, asterixis, Terry nails, Dupuytren.
- Labs: ↑ Tbili, ↑ INR, ↓ albumin, ↓ Na, platelets <160 (+LR 6.3); AST/ALT/ALP/GGT may be high or normal.
- Imaging: Doppler RUQUS for morphology, ascites, vessels, biliary tree, HCC. Elastography for stiffness. Biopsy is gold standard but uncommon — uncertainty, or transjugular when you also want HVPG ().
Etiology: globally MASLD 54%, HBV 29%, HCV 9%, ALD 2% () — ALD is a much larger slice in the US. Also iron, Wilson, A1AT, CF, AIH, PBC, PSC, celiac, right-heart / Budd-Chiari / VOD, schisto, amiodarone, MTX.
Child-Pugh at the bedside, MELD on the list
Class A 5–6, B 7–9, C 10–15. Compensated (usually A): median survival ~12 y, 1-year survival >95%, 5–10% decompensate per year. Decompensated (B/C): median ~2 y, 1-year survival 40–80%.
| Child-Pugh points | 1 | 2 | 3 |
|---|---|---|---|
| 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 / diuretic-controlled | Refractory |
| HE | None | Grade 1–2 | Grade 3–4 |
- MELD-Na predicts 90-day mortality and still drives allocation: bilirubin, INR, creatinine, sodium.
- MELD 3.0 adds female sex and albumin (to correct waitlist disparity), interactions (bili×Na, albumin×Cr), and caps creatinine at 3 ().
- <5
Normal
Hepatic venous pressure gradient between portal vein and IVC.
- ≥6
Portal hypertension
The number that starts the pathophysiology.
- ≥10
Clinically significant portal HTN
Varices, decompensation risk. Also diagnosed by varices on EGD, collaterals/ascites, or LSM ≥25 kPa (or 20–24.9 with platelets <150, or 15–19.9 with platelets <110).
- ≥12
Variceal-bleed territory
This is why we band and beta-block.
Complications to name on every admission
- Portal hypertension package: esophageal varices, portal hypertensive gastropathy, hypersplenism, ascites, SBP, HRS, hepatic hydrothorax, hepatopulmonary syndrome, portopulmonary hypertension, cirrhotic cardiomyopathy.
- Immune dysfunction — bacterial and fungal infection is a leading killer. Every decompensation has a trigger: infection, bleed, alcohol, PVT, HCC, drugs, surgery.
- Endocrine: hypoglycemia, thyroid, hypogonadism, hyperestrinism.
- Acute PVT: start LMWH unless bleeding risk is prohibitive, then DOAC or warfarin ≥6 months (AGA: ).
- Frailty / sarcopenia predicts decompensation, admission, and death ().
VIBES — a systematic pass
V
Volume
Ascites, edema, hydrothorax, HRS. Na <2 g/d; fluid 1.5 L if Na <125. Diuretic response, LVP history, TIPS candidacy.
I
Infection
Prior SBP, primary vs secondary prophylaxis, current treatment. Tap on arrival.
B
Bleeding
Varices, gastropathy, coagulopathy. Carvedilol 6.25–12.5 mg/d preferred NSBB. Acute bleed: PPI, octreotide, EGD, SBP prophylaxis.
E
Encephalopathy
Grade, precipitant, lactulose goal (3–4 BMs or mental-status improvement), rifaximin.
S
Screening / surgery (transplant)
HAV/HBV, influenza, pneumococcal, COVID vaccines. Alcohol off. No NSAIDs. HCC US ± AFP q6 months. Listed or not, MELD, Milan if HCC.
Also record etiology, compensated vs not, the decompensation trigger, Child-Pugh, and MELD 3.0. Acetaminophen ≤2 g/day is the preferred analgesic. Avoid raw shellfish and indicationless PPIs.