Case-Based Modules > Case 4 > Stage 4

The repeat non-contrast head CT looks completely stable. No new abnormalities. You look through to see what was happening in those days where you weren't following the patient. Neurology had put the patient on cEEG, with the report shown below. The patient isn't on any antiseizure medication. They had also recommended an LP. No opening pressure was documented, but the CSF studies are notable for WBC 250 (60% lymphocytes), RBC 10, protein 180, glucose 50. The remainder of the CSF studies are pending.

cEEG Findings (Days 2-3):

  • Abnormal in wakefulness and sleep
  • Diffusely slow, disorganized background
  • No sleep architecture
  • Abundant delta slowing that was at times rhythmic (GRDA), with frequency 0.5-1Hz
  • No epileptiform abnormalities
  • No clinical events captured
What do you make of the CSF studies?

Abnormal, for sure. Not a florid pleocytosis (in the 1000s range), but they're immunosuppressed, so who knows. The pattern of mild-moderate lymphocyte-predominant pleocytosis with elevated protein and somewhat lower glucose is very concerning for fungal infection moreso than bacterial. For this patient, something like Cryptococcus definitely rises up in the differential diagnosis. A result on that CrAg would be very helpful now. Would this explain the original reason for consultation-- the fixed and dilated pupils with depressed mental status?


What do you think is happening?

Shoot. The same thing happened again! Except we have more data from tests, and we still don't have a unifying answer. Or do we?

There is clearly something very wrong with this patient neurologically (and also just systemically from a MICU perspective). Take a step back and think about this again: what has been happening to the patient? She's had some episodic fixed and dilated pupils in the setting of immunocompromise and septic shock. Neuroimaging and neurophysiology studies haven't shown anything specific, but her CSF studies raise concern for an atypical infection. Since there isn't anything large that's structurally causing the encephalopathy and pupillary findings, our most likely etiology with the clinical history and CSF studies is this atypical infection coating the cranial nerves. But what else could this process-- of leptomeningeal spread-- do from a physiologic standpoint to the brain that could also cause episodic signs/symptoms?


What do you do now?

Go back