Episode 84: Acute liver failure with Sergio Navarrete

We discuss assessment, monitoring, medical stabilization, and when to consider transplant of the patient with acute liver failure. We are joined by Dr. Sergio Navarrete, anesthesiologist and intensivist with fellowship training in transplant anesthesia. Learn more at the Intensive Care Academy! Find us on Patreon here! Buy your merch here! Takeaway lessons * Transaminases rising into the many hundreds or thousands (especially with pre-existing liver disease), or a MELD in the low teens (from baseline normal) should raise concern for a concerning degree of liver injury, usually due to shock liver, congestion, or infection. This should also prompt consideration for transplant evaluation, and usually a phone call to your transplant center. * Reversible causes, such as acetaminophen toxicity or portal vein thrombosis, must be ruled out. * Optimization of perfusion should include not only the left-sided systemic circulation, but also the right-sided system and venous congestion; congestive hepatopathy (from volume overload or RV failure) can absolutely cause severe liver injury. Echo, potentially with tools like VEXUS scoring, can be a great help here. * N-acetylcysteine has a clear indication for treating acetaminophen poisoning, but not much data for other causes of liver failure. However, many clinicians believe it may provide some benefit, and there is probably no harm—other than administering a fair amount of volume. * Hypoglycemia and hypothermia are both relatively late and ominous findings in the ALF patient (put them on a dextrose infusion and hourly glucose checks). Transaminase levels reflect hepatocyte injury but not liver function. Synthetic function as measured by INR or fibrinogen are helpful. Bilirubin is usually too slow and non-specific to be actionable. Trend this stuff every 6 hours or so. * Mental status is a key monitoring tool as a marker of cerebral edema. The clinical exam, ammonia level, potentially serial CT scans, and maybe invasive ICP monitoring (Sergio prefers a bolt over EVD) may all be needed in high-risk cases. * The highest risk patients for cerebral edema are those with truly acute/hyperacute liver failure. Trend ammonia, which has some correlation with herniation risk, but the neuro exam is more useful. Neurosonography could be used as well. * Lactulose should be used, and in extremis hyperosmolar therapy considered, although data for this is less clear than in other neurologic emergencies. * Liver ischemia and death will reliably cause a systemic inflammatory state with resulting distributive shock; this can persist even after transplant, due to persistent elements of the dying liver. Treat this like any SIRS/distributive shock state. * Bleeding and clotting can both occur; numbers usually suggest coagulopathy, but hemostatic rebalancing is often present, at least until something perturbs the balance (e.g. a procedure). Labs like the INR are a marker of disease severity, not bleeding risk. Fibrinogen is a little better, but TEG is probably the most useful marker of bleeding status, as many of these people are actually hypercoagulable. * Some would use CRRT relatively early in a liver failure patient; Sergio would not. However, he would consider it in the volume overloaded patient to manage congestion (if diuresis proved inadequate). * Liver-specific extracorporeal organ support us...