Tasty Morsels of Critical Care 019 | Liver Transplant Part 2

14 Jan

Welcome back to the tasty morsels of critical care podcast.

Welcome back to what I hope will be the final little segment (boom boom) on liver transplant. Part 1 lives here. Though at this stage I certainly can’t rule out an ongoing process somewhat akin to the great Douglas Adams’ increasingly inaccurately named Hitch Hiker’s Guide to the Galaxy trilogy that ended up at 5 parts.

Two things worth knowing about and easily mixed up are

  1. hepatopulmonary syndrome
  2. portopulmonary hypertension

First off hepatopulmonary syndrome. This can be found in ~20% of cirrhotics and the key clinical finding is hypoxia that gets better when lying flat, otherwise known as platypnea-orthodeoxia which is probably more common in ASDs but hepatopulmonary syndrome is definitely on the list. In this scenario there is abnormal pulmonary vascular dilation allowing blood to shunt right to left within the lungs. The pathogenesis is unclear but nitric oxide plays a role. It is fairly easily diagnosed with echo and agitated saline where the bubbles can be seen to enter the LA within a few cycles following injection. Remember that agitated saline should NOT opacify any left sided structures under normal circumstances.

The presence of HPS is seen by some as an indication for transplant and also is a poor prognostic marker for transplant. Good news is that HPS typically resolves with transplant

This can be contrasted with portopulmonary hypertension where the combo of pulmonary hypertension and increased pulmonary vascular resistance is a very bad sign. To be clear – simply having pulmonary hypertension at echo or right heart cath is common in cirrhotics and they usually do well. But the combo of increased pressure AND resistance AND failure to respond to pulmonary vasodilators is a bad thing. In this scenario transplant does not always fix the problem.

Briefly let’s mention the infectious issues.

We all get excited about CMV but in reality this is not often an ICU issue in the post transplant period and comes later on often at the 3-4 week mark. It is particularly important where the graft is CMV +ve in a recipient who has no sign of previous CMV. Along with PJP we can prophylax against these relatively well and they don’t tend to cause us trouble in the immediate post op period.

The killers in the ICU are going to be bacterial and these days it’s going to be gram +ve causing the damage rather than gram -ve. Invasive fungal disease can be a big issue and echinocandins and amphotericin have been commonly used. Expect high rates of MDROs given that most chronic liver disease patients are frequent flyers to hospitals and frequent receivers of broad spectrum antibiotics. An alphabet soup of VRE and ESBL is often plastered in multicoloured stickers over the front of their charts.

Final point on immunosuppression. Expect some steroids to be given and a tacrolimus chaser it often withheld a few days due to the joys of basilixmab allowing a delayed introduction and less chance of renal injury. Note the absence of the antimetabolite agent that is more commonly present in combo with tacrolimus in the heart and lung transplant population.

References:

LITFL PPH

Deranged Physiology

Oh’s Manual Chapter 103

 

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