Hepatocellular Carcinoma (HCC)

Stage the liver, not just the tumor - Child-Pugh from albumin, bilirubin, INR, ascites, and encephalopathy; MELD if transplant is on the table. That score, not the imaging, predicts how the patient handles a laparotomy.

Check the paraneoplastic labs - Glucose, hematocrit, and calcium. HCC can present with hypoglycemia, erythrocytosis, or hypercalcemia, and each of the three will bite you intraoperatively if you find it late.

Coagulation and blood availability - INR and platelet count. Synthetic failure and hypersplenism stack on each other, so type and cross early and place an arterial line for anything with resection-level blood loss.

Varices are the hemorrhage you can cause - Blunt the hypertensive response to laryngoscopy and avoid straining on extubation. Both raise portal pressure in a patient with known esophageal varices.

Ascites changes the airway plan - Raised intra-abdominal pressure plus a distended abdomen means treat as full stomach. Drainage during the case drops preload sharply — replace volume as it comes off.

Protect hepatic oxygen delivery - Anesthesia and surgery drop hepatic blood flow by as much as 30-40%. Add hypotension and the result is ischemia-reperfusion injury on a liver with no reserve.

Drug choices - Reduce doses of hepatically cleared agents. Acetaminophen deserves particular caution in liver disease, and volatile agents are among the drugs implicated in postoperative hepatic dysfunction.

Watch the kidneys - Creatinine and urine output. Hepatorenal failure is the companion organ failure in advanced disease, and it often declares itself in the first postoperative days.

Expect postoperative jaundice - Hyperbilirubinemia is the most frequent sign of postoperative liver dysfunction and is usually multifactorial: hemolysis from transfused blood, hepatocellular ischemia, and biliary injury all contribute. Rising bilirubin with a rising INR is the pattern that signals real trouble.

Hepatocellular carcinoma (HCC) is the primary malignancy of hepatocytes and accounts for more than 90% of primary liver tumors. It is fundamentally a disease of cirrhosis: 80-90% of cases arise in a cirrhotic liver, with an annual incidence of 2-4% in that population.

Chronic hepatitis B and C drive more than 70% of cases worldwide. Alcohol, NASH/NAFLD, aflatoxin exposure, iron overload, glycogen storage disease, Wilson disease, and alpha-1 antitrypsin deficiency account for most of the rest.

What matters at the board is usually not the tumor but the liver it grew in — synthetic failure, portal hypertension with varices and ascites, encephalopathy, and hepatorenal physiology set the ceiling on what the patient tolerates. HCC also throws paraneoplastic curveballs: hypoglycemia, erythrocytosis, hypercalcemia, and severe watery diarrhea.