HIV/HCV coinfection & decompensated liver failure

Thanks to Dan for presenting a very interesting patient with decompensated liver failure in the context of HIV/HCV coinfection and concurrent alcoholism. We covered a few different topic areas today:

1. The importance of recognizing the broader context of a patient's life and thus the illness with which they are presenting to you. Dr. Hwang did a great job of highlighting this fact, and acknowledging the importance of the social determinants of health in a patient's illness. Here's a very interesting systematic review to come out of SMH on the positive impact of housing status in HIV patients on patient outcomes including medication adherence, health behaviours, and utilization of services. Note the authorship!

2. We also discussed the approach to a patient with decompensated liver failure and management principles. Decompensated liver disease is a constellation of clinical findings that can include all or some of: encephalopathy, coagulopathy, renal failure, rising LFTs, worsening ascites, and jaundice. Whenever someone presents to you in this way, it is important to ask WHY they are decompensating. You must rule out spontaneous bacterial peritonitis (done by doing a paracentesis and sending fluid for cell count/diff and C&S, with a neutrophil count of >250 suggesting SBP), as well as rule out UGIB. Other causes include medication/diet nonadherence, constipation, portal vein thrombosis, other infection, and development of a hepatoma (AKA hepatocellular carcinoma). I really like table 5 in the Lancet article for a list of cirrhosis complications and their management.

3. Lastly, we discussed the management of ascites. Here's a NEJM review on this topic, as well as an image I really like on paracentesis. Key principles include:

a. Mechanism of ascites: cirrhosis leads to hepatic resistance to portal flow, which ultimately causes portal hypertension, formation of collaterals, and shunting of blood systemically. As this develops, local vasodilator production (Nitric Oxide mostly) leads to splanchnic vasodilation and the 'transudate' that is ascites.

b. Management must include consideration of liver transplantation - at least consider whether they are a candidate, as patients with ascites have poor prognosis in the absence of transplantation.

c. Ongoing management requires a low Na diet, diuresis (typically with spironolactone starting at 100mg OD and furosemide starting at 40mg OD, with particular caution around the risk of inducing prerenal failure). Florence Wong, another SMH staff, has a great practical article on how to titrate your diuretics to 24h urine collection: Hope you find this information useful! Have a great evening and enjoy the sunshine (with sunscreen :)).