Episode 39: Liver Transplant with Dr. Steve Frank

In this episode, episode 39, I interview Dr. Steve Frank, Professor of Anesthesia and Critical Care Medicine at Johns Hopkins, Medical Director of Blood Management for Johns Hopkins Health System and Chief of Adult Anesthesiology about anesthesia for liver transplants.

8 Replies to “Episode 39: Liver Transplant with Dr. Steve Frank”

  1. Hey Dr Volpaw,
    Sorry this isn’t too related to this podcast, but seeing more and more on the central venous/arterial pCO2 difference. My search basically yield “a Difference of co2 between central vein and artery more than 6 suggestive of poor perfusion.” Is this similar to the concept of o2 extraction? Are you using this value clinically?

    1. Hi Josh,

      There is some early, retrospective evidence that this may be useful in guiding resuscitation and maybe aiding in prognosis but I think it’s definitely too early to tell how useful it is. We are not using it here at all as far as I know. But definitely something to keep our eyes on moving forward and see where it goes. Thanks!


  2. What is the rationale behind using both plasma-based coagulation assays (PT, aPTT, INR) and whole blood assays such as TEG or ROTEM? Couldn’t a patient have an INR of 2 and be thrombophilic? You would only see this on a whole blood assay. Not to mention that plasma-based studies tell you nothing about fibrinolysis while whole blood assay do. Availability of whole blood assays seems to be a non-issue anymore so I don’t see why we don’t use these exclusively. Thoughts?

    1. Hi Sean, great question. You can make a good argument that the only coagulation related lab that you may want in addition to a TEG or ROTEM is fibrinogen. If your MA is low it could be due to platelets (low number or dysfunction) or from low fibrinogen. If you get a fibrinogen level and it is normal it helps you know that platelets are probably the issue. Some institutions can run a FIBTEM that will help differentiate between platelet related and fibrinogen related causes of a low MA but not everyone has that option. Apart from that, though, you are right, you could probably save some money by just sending a TEG or ROTEM and not PT, apTT, INR.


  3. If I remember correctly, you discuss prophylactic fuerosemide for reprofusion acidosis associated hyperkalemia. What is the efficacy of this? A majority of K is intracellular, so does ridding of the little extra cellular K that we have at normal acid base balance really save the day?

    1. Hi Chris,

      Good question. Remember that the body will try it’s best to maintain extracellular K at normal levels for a given pH. When we give Lasix and it lowers K, it has lowered total body K, not just extracellular K, because the body will shift K out of cells as soon as the extracellular level dips, then that will dip, more will shift out, etc, until both intra and extra cellular K have reached a new equilibrium at a lower level. I hope that helps!

  4. I’m a little bit confused by a statement Dr. Frank made around 32:14. He says that the coagulation studies get worse really fast during the anhepatic phase, and that indicates how even a sick liver still makes clotting factors. You seemed to agree. Can you explain this to me?

    1. Hi Tameka,

      What we mean is that even in a patient with a very sick liver, they still have some clotting factors being made. So when you take out that liver, they now have NO liver, and are making NO clotting factors, and their coagulation studies get worse. So Dr. Frank was using this to show that even a sick liver is better than no liver at all.


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