Cirrhosis Health Maintenance & Extrahepatic Complications

Preventive care and nutrition

Vaccination. Check anti-HAV IgG and hepatitis B serologies (HBsAg, anti-HBs, anti-HBc), and vaccinate every patient who is not immune. Acute hepatitis A or B in a cirrhotic liver can precipitate acute-on-chronic liver failure. Cirrhosis blunts the response to hepatitis B vaccine, so confirm anti-HBs after the series. Pneumococcal conjugate vaccine and yearly inactivated influenza vaccine are also indicated, because infection often triggers decompensation.

Alcohol. Complete abstinence is the most effective intervention in alcohol-associated cirrhosis. It lowers portal pressure, reduces decompensation and death, and can restore a compensated state. Any patient with cirrhosis should avoid alcohol. For alcohol use disorder, add baclofen or acamprosate to counseling. Avoid disulfiram, which is hepatotoxic, and avoid naltrexone in decompensated disease.

Nutrition. The cirrhotic liver stores little glycogen, so even an overnight fast forces the body to break down fat and muscle ("accelerated starvation"). Prescribe about 35 kcal/kg/day and 1.2–1.5 g/kg/day of protein, given as small frequent meals with a late-evening snack that combines carbohydrate and protein. Once ascites is present, limit sodium to about 2 g/day.

Never restrict protein, even during hepatic encephalopathy. Restriction speeds muscle loss, and skeletal muscle helps clear ammonia by converting it to glutamine.

Sarcopenia and bone. Sarcopenia is often hidden by obesity or fluid. It independently predicts decompensation, infection, and death both before and after transplant. Screen with grip strength, chair stands, or CT muscle area at L3, and treat with nutrition plus resistance exercise. Osteoporosis is common, especially with PBC or PSC, alcohol, or glucocorticoid use. Obtain DEXA, replace vitamin D and calcium, and give a bisphosphonate when indicated.

Safe prescribing

Analgesia. Acetaminophen is the preferred analgesic. It is capped at 2 g/day because glutathione stores are low, and at that dose it does not worsen liver function.

Why NSAIDs are dangerous. In cirrhosis, renal perfusion depends on vasodilatory prostaglandins that counter high angiotensin II, norepinephrine, and ADH. NSAIDs, including COX-2 inhibitors, block those prostaglandins. The result is AKI, sodium retention, hyponatremia, and diuretic-resistant ascites. Platelet inhibition and mucosal injury add GI bleeding.

Coagulation: rebalanced hemostasis

Both sides fall. The liver makes the procoagulant factors (fibrinogen and factors II, V, VII, IX, X, XI) and also the natural anticoagulants (protein C, protein S, antithrombin). Cirrhosis lowers both. Factor VIII and von Willebrand factor rise, which partly offsets the thrombocytopenia caused by splenic sequestration and low thrombopoietin. The result is a fragile balance that can tip toward bleeding or toward clotting.

The INR misleads. The INR was designed to monitor warfarin and captures only procoagulant factors. An elevated INR therefore does not mean the patient is anticoagulated. Patients with cirrhosis develop DVT, PE, and portal vein thrombosis. Inpatients need standard pharmacologic VTE prophylaxis unless they are bleeding or have another contraindication.

Do not give FFP (or prophylactic platelets) to correct numbers before paracentesis, thoracentesis, or endoscopy. FFP barely moves the INR, adds volume that raises portal pressure, and carries a risk of TACO and TRALI. Viscoelastic tests (TEG, ROTEM) reflect overall clotting better, and vitamin K corrects only a true deficiency (cholestasis, poor intake, antibiotics).

Dilutional hyponatremia

Mechanism. Nitric oxide–mediated splanchnic vasodilation lowers effective arterial volume. That triggers nonosmotic ADH release together with RAAS and sympathetic activation. The kidneys retain more water than sodium, producing hypervolemic hyponatremia with edema and ascites. A sodium below 130 mEq/L marks advanced disease and is linked to more encephalopathy, hepatorenal syndrome, and death. This is why sodium was added to MELD.

Malnutrition, alcohol use, and hypokalemia put cirrhotic patients at high risk of osmotic demyelination, so correct slowly. Tolvaptan carries an FDA warning against use in liver disease because it is hepatotoxic.

Pulmonary complications

Hepatic hydrothorax. Negative intrathoracic pressure pulls ascitic fluid through small diaphragmatic defects. This produces a transudative effusion that is right-sided in about 85% of cases, sometimes without obvious ascites. Tap it to exclude other causes and spontaneous bacterial empyema, the pleural counterpart of SBP. Treat it as you would ascites: sodium restriction and diuretics, therapeutic thoracentesis, TIPS if refractory, and transplant.

Never place a chest tube. Continuous drainage of liters of protein-rich fluid causes AKI, electrolyte loss, infection, and high mortality.

Hepatopulmonary syndrome (HPS). Excess nitric oxide dilates pulmonary capillaries, mainly at the lung bases, so blood crosses the lung without being fully oxygenated. Standing sends more flow to the bases, which causes platypnea and orthodeoxia that ease when the patient lies down. Clubbing, cyanosis, and spider angiomas are other clues. Diagnosis requires two findings:

• an A-a gradient ≥15 mmHg (≥20 after age 64)
• intrapulmonary dilatation on agitated-saline echo: bubbles reach the left heart after at least 3 cardiac cycles; earlier bubbles suggest an intracardiac shunt such as a PFO

Oxygen is supportive, and transplant is the only cure. A PaO₂ <60 mmHg earns MELD exception points.

Portopulmonary hypertension (POPH). The pulmonary arteries constrict and remodel, causing pulmonary arterial hypertension with exertional dyspnea, a loud P2, and right heart failure. Echo screens transplant candidates, and right heart catheterization confirms the diagnosis: raised mPAP and PVR with a wedge pressure ≤15 mmHg. Treat with pulmonary vasodilators (PDE-5 inhibitors, endothelin receptor antagonists, prostacyclins), withdraw nonselective beta-blockers, and avoid TIPS. An mPAP ≥35 mmHg sharply raises transplant mortality unless therapy lowers it.

Surgical risk and transplant referral

Operative risk. Anesthesia and surgery reduce hepatic blood flow and can precipitate decompensation. Child-Pugh class and MELD both predict perioperative death. Class A patients usually tolerate surgery and class B patients need optimization first. Class C, a high MELD, or acute alcoholic or viral hepatitis rules out elective operations.

Transplant referral. Refer at the first decompensation (ascites, variceal hemorrhage, encephalopathy, or jaundice), when MELD reaches 15, or when HCC is diagnosed. At about MELD 15, transplant begins to improve survival. MELD combines bilirubin, INR, creatinine, and sodium, and MELD 3.0 adds albumin and sex. It estimates 90-day mortality and is used to allocate organs.