Cirrhosis

Altered drug handling - Reduced metabolism and protein binding prolong many drugs, so titrate carefully and expect delayed offset. A larger volume of distribution can raise the initial dose while clearance stays slow.

Rebalanced coagulation - Reduced clotting factors and platelets coexist with reduced anticoagulants, so the standard PT/INR overstates bleeding risk. Use viscoelastic testing where available and treat targeted deficits, not the number alone.

Full stomach and aspiration - Ascites raises intra-abdominal pressure and delays gastric emptying; consider a rapid-sequence induction and aspiration precautions.

Hemodynamics - The hyperdynamic, low-resistance circulation tolerates hypovolemia poorly and may need vasopressor support; watch for cirrhotic cardiomyopathy under stress.

Protect the kidneys - Hepatorenal physiology makes these kidneys fragile — maintain perfusion, avoid nephrotoxins, and manage volume carefully around any ascites drainage.

Encephalopathy and emergence - Sensitivity to sedatives and slow clearance prolong emergence; minimize long-acting sedation and avoid precipitants of encephalopathy.

Cirrhosis is end-stage hepatic fibrosis: chronic injury (alcohol, viral hepatitis, non-alcoholic steatohepatitis) replaces functional liver with scar and regenerative nodules, distorting architecture and blood flow.

The result is portal hypertension (varices, ascites, splenomegaly) plus failing synthetic and metabolic function — reduced clotting factors and albumin, impaired drug metabolism, encephalopathy, and a hyperdynamic circulation with high output and low systemic vascular resistance. Advanced disease brings hepatorenal and hepatopulmonary syndromes and cirrhotic cardiomyopathy. Severity scores (Child-Pugh, MELD) predict a perioperative risk that is substantial, because nearly every anesthetic variable is altered.