Hepatocellular carcinoma
2–4%/year in cirrhosis. Screen US ± AFP q6 months. Diagnose with multiphase CT/MRI (LI-RADS); biopsy if atypical.
Screen, then LI-RADS — do not ‘follow in a year’
HCC risk 2–4%/year in cirrhosis. May be silent, may decompensate, or may declare with pain, early satiety, a mass (: ). Primary prevention: HBV vaccine, treat HBV/HCV, lifestyle, coffee.
- Screen all etiologies of cirrhosis except Child C patients who are not transplant candidates (they will not live long enough to benefit).
- Also screen noncirrhotic HBV: men >40 / women >50 from endemic countries, African / African-American >30, family HCC, or PAGE-B ≥10.
- Tool: RUQUS ± AFP every 6 months. If ultrasound is limited (ascites, body habitus), use multiphase CT or contrast MRI.
- Lesion <1 cm: repeat US + AFP in 3–6 months. Lesion ≥1 cm, AFP ≥20, or rising AFP: multiphase CT/MRI and LI-RADS.
BCLC stage and Milan criteria
Barcelona Clinic Liver Cancer staging uses size, number, nodes, portal-vein invasion, extrahepatic disease, Child-Pugh, and performance status. Anything beyond BCLC 0 needs a noncontrast chest CT for metastases. Discuss at tumor board.
| BCLC | Typical survival | Move |
|---|---|---|
| 0–A early | >5 | Resection if Child A and T1–T2 ± adjuvant immunotherapy. Ablation. Transplant if unresectable but within Milan |
| B intermediate | >2.5 | TACE / TARE, radiation, locoregional therapy to downstage toward Milan |
| C advanced | >2 | Systemic: atezolizumab–bevacizumab or durvalumab–tremelimumab (assess variceal risk before bevacizumab) |
| D terminal | ~3 months | Palliation |
One lesion
≤5 cm, no vascular invasion, no extrahepatic disease.
Up to three lesions
Each ≤3 cm, same caveats.
Outside Milan
Locoregional therapy to downstage, then list if they come into criteria. Inside Milan: locoregional therapy as a .
LI-RADS 5 on an adequate multiphase study in a high-risk patient is diagnostic — treat without biopsy. Arterial hyperenhancement + washout + capsule. Ruptured HCC: and a bloody tap; embolize.
Hepatic hydrothorax and infected pleural space
~4–12% of cirrhosis. Ascites tracks through diaphragmatic defects into the negative-pressure thorax — can occur with little abdominal fluid. Right 75%, left 15%, bilateral 10% (: ; Medicine 2014;93:135).
- Exclude other effusions: thoracentesis + chest CT, abdominal US, TTE; radioisotope if still unclear.
- First-line: diuretics and 2 g Na. Therapeutic thoracentesis for dyspnea. Refractory: serial taps, TIPS, pleurodesis, repair, or transplant.
- Chest tubes raise mortality (~2.5%) and complication rates — do not place one for hydrothorax ().
- Spontaneous bacterial empyema (~15%; 40% without concurrent SBP): >250 PMN + culture or >500 PMN without culture, no pneumonia. Treat like SBP ().
Pulmonary and cardiac cousins of portal hypertension
Hepatopulmonary syndrome ()
- Intrapulmonary vascular dilatations → V/Q mismatch and diffusion limitation, possibly NO-driven. Basal shunting → platypnea and orthodeoxia (PaO2 down ≥4 mmHg or 3–5% upright), clubbing, cyanosis, telangiectasias.
- If SpO2 <96%: A-a gradient ≥15 (≥20 if age ≥65) or PaO2 <80 → bubble echo with late (3–6 cycle) left-heart bubbles (early = PFO). 99mTc-MAA if intrinsic lung disease muddies the echo. ↓ DLCO. Angiography only if severe hypoxemia ignores 100% oxygen and there is an embolizable target.
- No drug therapy. Oxygen to SpO2 >88%. Transplant can reverse severe HPS (PaO2 <60) — MELD exception.
Portopulmonary hypertension
- Group 1 PAH in portal hypertension; women 3×; autoimmune liver disease raises risk. Screen with TTE (PASP >30 has excellent NPV). euvolemic RHC: mPAP ≥20, PCWP <15, PVR >3 WU. Mild 25–35, moderate 35–44, severe ≥45.
- Epoprostenol, bosentan, sildenafil, iloprost may help. Transplant can improve moderate disease (MELD exception). Beta-blockers and TIPS can harm. mPAP ≥35 raises operative risk; ≥50 is a transplant contraindication (EASL: ).
Cirrhotic cardiomyopathy (: )
Up to 50% of transplant candidates. Blunted contractile reserve, diastolic dysfunction, long QTc, chronotropic incompetence — without known heart disease. Often subclinical until infection, LVP, TIPS, transplant, terlipressin, or albumin overload unmasks it. Echo with stress testing; treat like other HF; transplant can recover the phenotype.