decompensated cirrhosis

Decompensation = ascites, variceal bleeding, hepatic encephalopathy, or jaundice. Median survival drops from >12 years (compensated) to ~2 years. On admission: diagnostic paracentesis, sepsis screen, hold nephrotoxins, start lactulose if encephalopathic, and assess transplant candidacy. This note covers ascites, HE, and pulmonary complications. For variceal bleeding and SBP, see dedicated notes. For compensated disease, see cirrhosis.

decompensated cirrhosis admission bundle

diagnostic paracentesis within 6 hr (cell count, albumin, protein, culture in blood culture bottles)
sepsis screen: blood cultures, urinalysis, CXR; empiric antibiotics if infection suspected
hold nephrotoxins: NSAIDs, ACEi/ARBs, aminoglycosides; reassess diuretics
lactulose if any encephalopathy — do not wait for ammonia
calculate MELD 3.0 and Child-Pugh on admission (baseline for trajectory and transplant discussion)
nutrition: 35 kcal/kg/day, protein 1.2–1.5 g/kg/day, late evening snack
alcohol assessment + withdrawal prophylaxis if applicable
VTE prophylaxis: LMWH unless active bleeding or platelets <50 × 10⁹/L
transplant referral if new decompensation and not already listed

defining decompensation

Four cardinal events mark the transition from compensated to decompensated disease:

Ascites — most common first decompensation (~50%)
Variceal haemorrhage — see variceal bleeding
Hepatic encephalopathy
Jaundice (bilirubin >51 µmol/L without an alternative cause)

Each event carries its own mortality trajectory, but the occurrence of any one means CSPH has crossed the threshold where splanchnic haemodynamics can no longer compensate. Further decompensation (ACLF) is covered in the AASLD 2024 ACLF guidance.

scoring

score	components	use
Child-Pugh	albumin, bilirubin, INR, ascites, encephalopathy → A/B/C	prognosis, surgical risk, transplant listing discussions
MELD 3.0	bilirubin, INR, creatinine, sodium, albumin, sex	transplant allocation (replaced MELD-Na); recalibrated to reduce sex-based disparity

MELD 3.0

Adds albumin and a sex-based coefficient. Female patients are no longer systematically disadvantaged in organ allocation. Most Canadian programmes now use MELD 3.0 or a provincial equivalent.

ascites

first presentation

Diagnostic paracentesis — always on first presentation and every hospital admission with ascites. Cell count, albumin, total protein, culture (inoculate blood culture bottles at the bedside).
Serum-ascites albumin gradient (SAAG): ≥11 g/L = portal hypertension. <11 g/L → consider peritoneal carcinomatosis, TB, nephrotic syndrome, pancreatic ascites.

medical management

Sodium restriction: 2 g/day (88 mmol/day) — the backbone of ascites control
Diuretics: spironolactone 100 mg + furosemide 40 mg daily (100:40 ratio), titrate every 3–5 days to a max of 400 mg spironolactone + 160 mg furosemide
Weight loss targets: 0.5 kg/day without peripheral oedema, 1 kg/day with peripheral oedema
Stop diuretics if: Na <120 mmol/L, AKI, refractory HE, or severe muscle cramps unresponsive to dose adjustment

refractory ascites

Ascites unresponsive to maximal diuretics or intolerant of diuretic doses needed for control.

Serial large-volume paracentesis (LVP) q2–3 weeks + albumin 6–8 g per litre removed (when >5 L drained)
TIPS — more effective than serial LVP for recurrence; improves transplant-free survival in selected patients. Contraindicated in Child-Pugh >12, MELD >18 (relative), active HE, right heart failure, or pulmonary hypertension.

albumin after LVP

Albumin replacement after large-volume paracentesis (>5 L) prevents post-paracentesis circulatory dysfunction and reduces mortality. Do not substitute with other plasma expanders — they are inferior.

albumin — what the trials say

ANSWER (2018): long-term albumin 40 g twice weekly in outpatients with uncomplicated ascites reduced mortality and complications — practice-changing in Europe, less adopted in Canada due to cost
ATTIRE (2021): targeting serum albumin ≥30 g/L in hospitalised patients did not improve outcomes and increased adverse events — do not chase a number

hepatic encephalopathy

grading (West Haven)

grade	features
covert (minimal + grade 1)	psychometric testing abnormalities, mild inattention, sleep disturbance
2	disorientation to time, asterixis, lethargy
3	somnolent but rousable, confusion, gross disorientation
4	coma

precipitant search — always

Infection (SBP), GI bleeding, constipation, hyponatraemia, dehydration/over-diuresis, opioids/benzodiazepines, hypokalaemia (drives renal ammoniagenesis), portosystemic shunt (including TIPS).

treatment

Lactulose 15–30 mL PO q1–2h until bowel movement, then titrate to 2–3 soft stools/day. Enemas (300 mL lactulose in 700 mL water) if unable to take PO.
Rifaximin 550 mg PO BID — add for secondary prophylaxis after the second episode of overt HE (Bass, NEJM 2010). Reduces recurrence by ~58%.
Correct the precipitant — this matters as much as lactulose
Do not restrict protein — 1.2–1.5 g/kg/day; protein restriction worsens sarcopenia and outcomes

intubation threshold

Grade 3–4 HE with inability to protect the airway → intubate. Do not delay for ammonia levels — ammonia does not correlate well with grade and should not guide moment-to-moment management.

pulmonary complications

Two distinct entities with opposite physiology — high-yield exam comparison:

feature	hepatopulmonary syndrome (HPS)	portopulmonary hypertension (POPH)
mechanism	intrapulmonary vascular dilatation → shunt	pulmonary arteriolar vasoconstriction/remodelling
gas exchange	hypoxaemia, ↑ A-a gradient	normal gas exchange until late
classic sign	platypnoea-orthodeoxia (worse upright)	exertional dyspnoea, RV failure signs
diagnosis	contrast echo (bubbles in LA within 3–6 cardiac cycles)	echo → RHC (mPAP ≥25 mmHg, PAWP ≤15, PVR >3 WU)
treatment	liver transplant only (no medical Rx); supplemental O₂	PAH-targeted therapy (same agents as group 1 PAH)
transplant	indicated and curative; resolves post-transplant	must treat to lower PVR before transplant; mPAP >45 mmHg = contraindication

screen before transplant listing

Both HPS and POPH are screening indications at transplant assessment. Contrast echocardiography identifies HPS; elevated RVSP on TTE triggers RHC to evaluate for POPH.

common traps

Withholding VTE prophylaxis because the INR is elevated — cirrhotic coagulopathy is rebalanced, not anticoagulated. The INR reflects factor synthesis, not bleeding risk. Cirrhotic patients are at increased VTE risk.
Chasing an ammonia level — ammonia does not guide treatment or predict severity reliably. Treat the clinical picture.
Using albumin to target a serum level — ATTIRE showed this does not improve outcomes. Use albumin for specific indications (LVP, SBP, HRS), not as a number to normalise.
Restricting protein in HE — this worsens sarcopenia and has no evidence of benefit. High protein intake is safe and recommended.
Forgetting SBP prophylaxis — prior SBP or ascitic fluid protein <15 g/L with either Child-Pugh ≥9 or creatinine ≥106 µmol/L → norfloxacin or ciprofloxacin prophylaxis. See spontaneous bacterial peritonitis.
TIPS in the wrong patient — contraindicated in uncontrolled HE, Child-Pugh >12, severe right heart dysfunction, or pulmonary hypertension.