ICU Transfer II

I also had a patient who hovered in and out of the ICU. He was a patient with end stage renal disease, dialysis dependent, first admitted with a surprising transaminitis, peaking in the AST/ALT range of the 3000s. Few things give a transaminitis this high: shock liver from hypotension, toxins such as acetaminophen or mushrooms, and acute viral hepatitis (though at UCSF, I saw a Wilson's disease that mounted impressive enzymes). His viral panel was negative and acetaminophen levels were undetectable, but we still started him on an N-acetylcysteine protocol. Shock liver was not too high on our differential because he was fairly hypertensive. But with supportive care, he was transferred out of the ICU, and by chance, onto my medicine service. I only kept him a day on my medicine service. He actually looked pretty good and we sent him home.

He came back the next day with a fever at dialysis. Bounce backs are embarrassing events; we want to make sure people are safe before we send them home. But I scoured his chart and his history and I couldn't find any signs that he would return to the hospital. At dialysis, he had a fever and a bit of confusion so they readmitted him to the hospital. His blood cultures grew out Staph aureus, a sticky bug that can cause infection of the heart valves. Unfortunately, the echocardiogram was equivocal because there was heavy calcification of the patient's valves. We decided to empirically treat him as if he had endocarditis.

Usually, these patients are quick: put in a long term access PICC line, then find a nursing facility to take them. But this patient kept getting sicker; he would spike fevers, and then his labs started becoming inexplicably bizarre. He began showing an indirect bilirubinemia without evidence of hemolysis. Not only that, but with a bilirubin of 8 or 9, I did not find any icterus or jaundice on exam. If I looked in the right light, there might be a yellow tinge, but I really had to squint to get that. None of his other liver function enzymes budged.

Then, his INR - a sign of synthetic liver function - started shooting up dramatically. Within 3 days, it went from INR of 1.5 to 7. I've never seen something like that happen. Sometimes for patients with clots or atrial fibrillation, we purposely want to raise the INR. But invariably in those circumstances, the INR waffles excruciatingly slowly; it might take a week to get from INR 1 to 2.5. What's even more bizarre, we gave the patient a touch of vitamin K and his INR dropped from 7 back to 2 within 2 days. Strange, strange.

In the end, a CT abdomen/pelvis identified lesions in the liver concerning for abscess. We needed interventional radiology to drain it, but I had so much trouble getting him down for the procedure because he was hemodynamically tenuous. Despite being hypertensive on his first ICU admission, he was now hypotensive to the 100s/50s and tachycardic to the 120s (my EKG read was atrial flutter with variable block). He was definitely showing SIRS physiology which was concerning because he could have been septic - severely infected. A repeat CT showed more abscesses despite the antibiotics he was getting for his endocarditis. To my chagrin, he eventually bought himself an ICU bed again, but I have not been able to follow up to see how he has been doing.