Hepatitis C (HCV)

Stage the liver, not the serology - A patient cured by direct-acting antivirals with normal synthetic function is a different case from one with decompensated cirrhosis. Get albumin, bilirubin, INR, and platelet count, and look for ascites and encephalopathy — those are the Child-Pugh parameters; MELD adds creatinine. Everything else in the plan follows from where that lands.

Coagulopathy is synthetic, not dilutional - Chronic parenchymal liver disease impairs synthesis of factors I, II, V, VII, and X, and hypersplenism drops the platelet count on top of that. Draw a day-of INR and platelet count rather than trusting a clinic value, and have plasma and platelets available for anything beyond minor surgery.

Think twice before neuraxial in portal hypertension - Portal hypertension engorges the epidural veins and raises the risk of a bloody tap, in a patient who is often already coagulopathic and thrombocytopenic. Check INR and platelet count before committing. If you proceed, the left lateral decubitus position carries less bloody-tap risk than sitting.

Varices bleed with straining - Laryngoscopy, coughing, and straining on emergence all raise portal pressure; diaphragmatic contraction alone can triple it. Blunt the hypertensive response to intubation and extubate smoothly. In an actively bleeding patient, fluid is a safer first-line treatment for hypotension than a vasoconstrictor, which spikes pressure and can re-open a variceal bleed.

Drug handling is unpredictable - Deranged hepatic function alters both metabolism and excretion of what you give. Titrate to effect rather than to weight, favor agents you can watch work, and expect prolonged effect from anything the liver clears.

Protect against encephalopathy - Hepatic encephalopathy is precipitated by hypotension, GI bleeding, hypoxia, hypokalemia, hyponatremia, alkalosis, sedatives, diuretics, and the stress of surgery itself. Correcting the potassium and avoiding a long hypotensive stretch does more for the postoperative mental status than any drug choice you make at induction.

Hepatorenal syndrome - Worsening azotemia, hyponatremia, progressive oliguria, and hypotension in a cirrhotic patient is hepatorenal failure until proven otherwise. Severe GI bleeding and any period of marked hypotension precipitate it, so treat a low blood pressure as a renal event and not just a number on the monitor.

Ascites raises aspiration risk - A tense abdomen raises intra-abdominal pressure and pushes gastric contents up, which is why cirrhotic patients with ascites and a full stomach are managed as high-aspiration-risk. Plan an RSI, and expect preload to fall when the surgeon decompresses the abdomen.

Look for the extrahepatic disease - HCV is the leading cause of mixed cryoglobulinemia: 20% to 50% of patients carry serum cryoglobulins and up to a third of those develop clinical vasculitis. Membranoproliferative glomerulonephritis is the usual renal lesion — a creatinine and a urinalysis looking for proteinuria and hematuria will find it. Porphyria cutanea tarda, lichen planus, insulin resistance, and B-cell lymphoproliferative disease travel with HCV as well.

Cryoglobulins precipitate when cold - Cryoglobulins come out of solution below 37 °C and re-dissolve on warming. In a patient with known cryoglobulinemic vasculitis, forced-air warming and fluid warmers go on from the start, not after the temperature drops.

Check a glucose - Insulin resistance travels with chronic HCV and is itself one of the factors that accelerates fibrosis. Run point-of-care glucose intraoperatively rather than assuming a non-diabetic label holds.

Occupational exposure - HCV, not HIV, is the main bloodborne concern after a needlestick today. Epidemiologic studies put seroconversion after an HCV needlestick near 1.8%, and more than 75% of adults who seroconvert go on to chronic infection. There is no post-exposure prophylaxis for HCV: report the stick, get baseline and follow-up serology, and treat early if you convert.

Hepatitis C virus (HCV) is an enveloped, positive-strand RNA flavivirus and the most common blood-borne pathogen, infecting roughly 58 million people worldwide. It spreads mainly through injection drug use, contaminated blood, and percutaneous injury; sexual and perinatal transmission happen but are uncommon. What separates HCV from the other hepatitis viruses is chronicity — 80% to 85% of people who become acutely infected never clear the virus. The virus itself is not cytopathic; the host inflammatory response drives fibrogenesis, and alcohol, HIV or hepatitis B coinfection, obesity, insulin resistance, and fatty liver all accelerate it.

Ten to twenty percent of those who reach cirrhosis decompensate within five years into portal hypertension, esophageal varices, ascites, coagulopathy, encephalopathy, or hepatocellular carcinoma. That end-stage liver physiology, not the viremia, is what you are anesthetizing. Direct-acting antivirals, available since 2011, now cure most patients — so the diagnosis on the chart tells you much less than the liver's current synthetic function does.