Nonalcoholic Fatty Liver Disease (NAFLD)

Most of these patients are pre-cirrhotic - Isolated steatosis and early NASH do not cause hepatic synthetic failure. Bilirubin, albumin and INR are typically normal and aminotransferases only mildly elevated, two to five times normal with ALT above AST in about a 2:1 ratio. Plan a normal anesthetic and treat the metabolic comorbidities as the real risk.

Find the fibrosis that changes the plan - Hypoalbuminemia, hyperbilirubinemia, thrombocytopenia or a prolonged prothrombin time mean synthetic dysfunction, and that puts you in cirrhosis territory rather than NAFLD territory. The FIB-4 index, the NAFLD Fibrosis Score and elastography are the non-invasive routes to a fibrosis stage if the workup is already in the chart. Note that the AST:ALT ratio flips to AST above ALT once advanced fibrosis or cirrhosis has developed.

Cardiac risk drives the outcome - Cardiovascular disease, not liver disease, is the most common cause of death in NAFLD. Work up the same metabolic syndrome that produced the fatty liver — a systems-based history and physical plus a baseline ECG, looking for coronary disease, heart failure, hypertension and dyslipidemia.

Airway exam and rapid desaturation - NAFLD travels with obesity, and obesity significantly reduces functional residual capacity, so desaturation after induction comes fast. Do a detailed airway exam including neck circumference at the level of the thyroid cartilage and thyromental and sternomental distances. Ramp the patient so the external auditory meatus sits level with the sternum, or use 25 degrees of reverse Trendelenburg, and run apneic oxygenation at 15 L/min through a nasal cannula or nasopharyngeal airway to buy safe apneic time.

Ask about the sleep study - Obstructive sleep apnea is one of the recognized extrahepatic complications of NAFLD. Get the sleep study result and home CPAP settings rather than a yes/no snoring question, and bring the machine to the PACU.

Protective ventilation - Tidal volumes of 6 to 8 mL/kg ideal body weight, low to moderate PEEP, and FiO2 titrated to a saturation of 92% to 95%. PEEP counters the atelectasis that comes with reduced total lung capacity, vital capacity and FRC.

End-tidal CO2 underreads - The expired-to-arterial CO2 gradient is wider than in lean patients and CO2 production is higher because oxygen consumption is higher. If the ventilator settings matter, get an arterial blood gas rather than trusting the capnograph number.

Blood pressure is harder to measure - Noninvasive cuff pressures are less accurate in obesity. Forearm readings perform better than upper arm or lower leg, and wrist readings correlate best with radial arterial line values.

Glycemic control - About three-quarters of patients with insulin resistance or type 2 diabetes have fatty liver, and 30% to 50% of diabetics have NAFLD. Check a preoperative glucose and a basic metabolic panel, and keep checking intraoperatively in anyone on insulin.

Renal function - Chronic kidney disease is another extrahepatic complication of NAFLD. Look at the creatinine before dosing renally cleared drugs.

Do not hold the statin - Statins should not be withheld in NAFLD just because the liver biochemistries are abnormal. The cardiovascular risk is the thing most likely to kill this patient.

Extubation and PACU - Extubate ramped or at 25 degrees reverse Trendelenburg after confirming adequate tidal volumes, and have an oral airway or nasal trumpet ready if obstruction develops. Watch the PACU for recurrent respiratory events — apnea, bradypnea, pain-sedation mismatch, CO2 retention, desaturation. Postoperative pulmonary complications lengthen PACU time and hospital stay and carry mortality; persistent events are grounds for admission.

Assume it in bariatric cases - Over 95% of patients undergoing bariatric surgery have biopsy-proven NAFLD at the time of surgery. It is often simply undocumented.

Nonalcoholic fatty liver disease (NAFLD) is fat in at least 5% of hepatocytes with no secondary cause — no significant alcohol intake (more than 20 g/day in men, 10 g/day in women), no steatogenic drug, no hereditary disorder. Nonalcoholic fatty liver is steatosis alone and is reversible if the insult is removed; nonalcoholic steatohepatitis (NASH) adds lobular inflammation and hepatocyte ballooning and can progress to fibrosis, cirrhosis and hepatocellular carcinoma.

Insulin resistance drives it. Adipocyte lipolysis floods the liver with free fatty acids while hyperinsulinemia keeps de novo lipogenesis running; lipotoxic metabolites then generate oxidative stress, hepatocyte injury and stellate-cell fibrosis. Roughly 25% to 30% of US adults have NAFLD, rising to 80% to 90% of obese adults. What matters at the board is usually not the liver but the company it keeps — metabolic syndrome, and cardiovascular disease, which is the leading cause of death in NAFLD.