Alcoholic Liver Disease (ALD)

Stage the disease before you plan - Baseline PT/INR, platelet count, bilirubin, albumin, and creatinine. Those values feed the MELD score and the discriminant function used to grade alcoholic hepatitis, and they tell you whether you are dealing with reversible steatosis or established cirrhosis.

Cardiac evaluation - Echo for left ventricular dilation and systolic dysfunction: alcoholic cardiomyopathy accounts for about 10% of dilated cardiomyopathies and tracks with roughly 80 g/day for five years or more. Add an ECG for QT prolongation, since cirrhotic cardiomyopathy occurs in up to half of cirrhotics and only shows itself under stress, which is exactly what surgery supplies.

Coagulopathy and neuraxial - Hypersplenism causes thrombocytopenia and the failing liver drops factors V and VII. Portal hypertension also engorges the epidural veins and raises the chance of a bloody tap. Get a platelet count and INR and correct before the block, not after.

Varices - Avoid the pressure swings that rupture them. The hypertensive response to laryngoscopy and straining at extubation both raise portal pressure. Treat hypotension with volume first rather than a vasoconstrictor that produces a sudden pressure spike.

Ascites means full stomach - Ascites and splenomegaly raise intra-abdominal pressure on top of everything else keeping the stomach full. Plan an RSI, and preload before the abdomen is opened or ascitic fluid is drained because decompression drops the pressure fast.

Know what precipitates encephalopathy - Hypotension, GI bleeding, hypoxia, hypokalemia, hyponatremia, alkalosis, sedatives, diuretics, and the stress of surgery itself. Most of that list sits under your control.

Drug handling - Deranged hepatic function alters both metabolism and excretion. Titrate to effect and expect prolonged action and slower emergence.

Withdrawal is a perioperative event - Symptoms start 6 to 24 hours after the last drink, and delirium tremens is fatal in roughly 15% of untreated cases versus about 1% treated. Document the time of the last drink. Lorazepam and oxazepam are the preferred benzodiazepines in liver disease.

Glucose - Alcohol suppresses gluconeogenesis and these patients are often several days into poor intake. Check a glucose and a gas: alcoholic ketoacidosis presents with tachycardia, tachypnea, dehydration, agitation, and abdominal pain, with beta-hydroxybutyrate as the dominant ketoacid.

Renal function - Hepatorenal syndrome shows as worsening azotemia, hyponatremia, progressive oliguria, and hypotension, and it is a leading cause of death in alcoholic hepatitis. Avoiding hypotension is the lever you actually hold intraoperatively.

Infection - Alcoholic hepatitis patients are prone to infection, more so on steroids, and infection predicts acute kidney injury and multiorgan dysfunction. Strict aseptic technique for lines and blocks.

Alcoholic liver disease (ALD) runs from steatosis through alcoholic hepatitis to cirrhosis. Alcohol dehydrogenase converts ethanol to acetaldehyde and aldehyde dehydrogenase converts that to acetate; the resulting rise in the NADH/NAD ratio pushes fatty acids into triglyceride and stops lipolysis, so fat accumulates in hepatocytes. Continued drinking recruits interleukins and neutrophils, producing ballooned hepatocytes containing Mallory-Denk bodies, which is alcoholic hepatitis. Ongoing injury lays down perivenular and sinusoidal collagen in a chicken-wire pattern around regenerative nodules, which is irreversible cirrhosis.

Steatosis occurs in 90% of people drinking over 60 g/day, and cirrhosis in 30% of those drinking over 40 g/day long term. The perioperative problems are the consequences: portal hypertension, coagulopathy, cardiomyopathy, and withdrawal.