Here are the labs and question again:

Direct bilirubin – 5.8

Your job:

construct a differential diagnosis and make your best guess for the correct answer.  We do know the answer.

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I will write this answer at the 3rd year medical student level, with apologies to anyone who thinks I have become pedantic.  I do know that many students and residents read this blog and like these cases.

As you can see, I have constructed my grid for liver tests into 3 categories.  The first category represents cellular destruction.  This patient has markedly elevated AST and ALT, therefore, the patient has significant cellular destruction – or hepatitis.  I will discuss that differential soon.

The patient has minimal elevation of alk phos, but a high total bilirubin.  The minimal alk phos could represent obstruction, but my experience suggests that for obstruction to cause cellular destruction, I would see a much higher alk phos.  Most cellular destruction causes local swelling and thus some increase in alk phos.  I suspect the patient does have some intrahepatitic ductal obstruction with swelling, and thus the elevated bilirubin.  Elevated bilirubin occurs commonly with significant acute cellular destruction.

The normal albumin and INR make a diagnosis of cirrhosis unlikely.  Despite the cellular destruction, the liver’s factory functions are still intact.

What could cause such acute cellular destruction?  When I first heard this presentation at morning report I assumed viral hepatitis.  Medications could do this, but I knew that the patient was not taking any medications (even for his seizures.)  Hypotension could do this – shock liver – but the patient had not had any known hypotensive episodes.

So I assumed a viral etiology.  The most likely candidates would be A, B or C.  I have seen EBV and CMV present like this.

Our patient had positive IgM antibodies for hepatitis C, confirming the diagnosis of acute hepatitis C.

Congratulations to Grant for guessing the right answer.