Chronic Viral Hepatitis

Stage the liver, don't just name the virus - Child-Turcotte-Pugh uses serum albumin, bilirubin, PT, ascites, and encephalopathy; MELD uses bilirubin, creatinine, and INR. A well-compensated carrier and a decompensated cirrhotic share a diagnosis and nothing else.

Coagulation workup - the liver makes the clotting factors, so check PT/INR, aPTT, and a platelet count. Thrombocytopenia here is usually splenic sequestration from portal hypertension, not a marrow problem.

Neuraxial needs a hard look - a raised INR plus hypersplenic thrombocytopenia is the common picture in advanced disease, and portal hypertension engorges the extradural veins, making a bloody tap more likely. Get the numbers and correct them before you go near the back.

Drug handling changes - a diseased liver metabolizes and excretes drugs abnormally. Titrate to effect rather than dosing by the book, and expect prolonged action.

Don't tip them into encephalopathy - infection, GI bleeding, sedating drugs, and alkalosis all aggravate hepatic encephalopathy. Go light on sedatives and expect a slow wake-up.

Look for varices - once portal hypertension is established, gastroesophageal varices are on the table. Ask about hematemesis, prior banding, and beta blocker therapy.

Ascites is a fluid and pressure problem - manage volume deliberately, follow electrolytes closely, and remember that a tense abdomen plus organomegaly raises intra-abdominal pressure and aspiration risk.

Watch the kidneys - hepatorenal syndrome follows systemic hypotension and renal vasoconstriction, so track creatinine and urine output and defend perfusion pressure.

Hypoxemia has a hepatic differential - hepatopulmonary syndrome, portopulmonary hypertension, and hepatic hydrothorax all present as a low resting saturation with V/Q mismatch and reduced diffusion. A room-air saturation before the case is worth the thirty seconds.

Protect yourself - healthcare workers are a named risk group for HBV, transmitted percutaneously or by mucosal contact with infected fluids. Standard precautions and sharps discipline, every case, no exceptions.

Chronic viral hepatitis is persistent hepatic inflammation from hepatitis B (HBV), C (HCV), or D (HDV) — and, in immunocompromised patients, hepatitis E (HEV). Infection is called chronic once it persists beyond six months. Most of the liver injury comes from the host immune response against infected hepatocytes rather than from any direct cytopathic effect of the virus. HBV spreads by percutaneous inoculation or mucosal exposure to infected body fluids; 80% to 85% of people acutely infected with HCV fail to clear the virus and go on to chronic infection. HDV coinfection or superinfection accelerates the march to cirrhosis in chronic HBV.

What matters at the board is where on that march the patient sits. Ongoing inflammation drives fibrosis, cirrhosis, portal hypertension, and hepatocellular carcinoma — and with them the synthetic failure, thrombocytopenia, ascites, encephalopathy, renal, and pulmonary problems that reshape the anesthetic.