Can antithrombotic treatment be used in a patient with liver failure? If yes, when is it recommended?
Mark Crowther, MD: The problem with liver failure is twofold. The first is, the liver metabolizes many of the drugs that we use. If the liver is not working properly, you cannot predict very accurately the pharmacokinetics of a drug. But that requires very serious liver failure and there are relatively few patients with very serious liver failure.
The second thing is that liver failure predisposes patients to bleeding, because they have things like esophageal varices, varices elsewhere, or gastritis.
The short answer to the question is, of course you can anticoagulate anyone, but again it comes back to the risk-benefit discussion. If you have a patient who has got severe hepatic insufficiency with an elevated international normalized ratio (INR) and partial thromboplastin time (PTT), but they had pulmonary embolism 3 day ago, most of us would be comfortable anticoagulating that patient because what is more likely to kill them than anything else is the pulmonary embolism. Many of us would use therapeutic-dose low-molecular-weight heparin in that patient because it does not require monitoring, and we have a pretty good sensation of what the dose should be.
If the patient has, for example, atrial fibrillation, lowish CHADS2 score, and an INR of 2.6, many of us would not anticoagulate that patient because our perception is that, first of all, we would not want to use warfarin in that patient because they have already got an elevated INR. We do not have good-quality data for low-molecular-weight heparin to prevent stroke or systemic embolization in atrial fibrillation, and the patient has an enhanced risk of bleeding. So in that particular circumstance the risk-benefit ratio of treatment would not be as clear as it would be with a recent episode of deep vein thrombosis.