You arrive to see the patient. You ask the resident how long their exam has been like this-- since admission, it seems. She hasn't had any pharmacologic dilation of her pupils. No nebulized treatments, but she's been intubated anyway, so a little less likely for something to have leaked out. On your exam, you identify bilateral non-reactive pupils, both 7mm in diameter. Corneal reflex is intact. Oculocephalic reflex is intact. Cough and gag reflexes are intact. There's no extremity movement in response to noxious stimuli. She does not overbreathe the ventilator.
You review her medication list. She's currently on IV vancomycin, cefepime, metronidazole, and voriconazole. Her labs are notable for WBC 10.7, Hb 7, Plt 180, Na 142, K 3.6, HCO3 15, Cr 2.41. You look through her imaging and realize that the MICU had already obtained an MRI of her brain, with and without contrast. You review the images yourself. It was normal. No concerning mass lesions with edema, nor any leptomeningeal enhancement. Radiology agrees with you.
There's no clear big bad structural etiology causing the fixed and dilated pupils. They've already gotten the MRI that would show you the parenchyma with higher resolution. That leaves something infiltrative. You didn't see any leptomeningeal enhancement around the brainstem. (In what other areas should you pay especially close attention to identify leptomeningeal disease? The cerebellar folia, cranial nerves, convexity sulci.)
So where does that leave us? Something bad must have happened (or is happening still). You might think about whether or not they had a cardiac arrest. History was not supportive of this, either at the OSH or even here. There weren't any findings of cerebral ischemia on the MRI, though you suppose that the sensitivity for that might not be great anyway. You can't blame these findings on his renal dysfunction either.
But wait. We haven't actually ruled out anything infiltrative. We need to remind ourselves that there are plenty of pathologies that will come with normal neuroimaging. That might very well be the case here. What could the cause be? We need to go back and re-formulate the case. This patient has Crohn's disease and takes several immunosuppressants, and is currently being treated for septic shock. Time course is more on the acute side, possibly subacute if the actual presumed onset is incorrect (they were admitted for a week at the OSH before even coming here). So it's important to think of infectious etiologies in particular. You note that at least her blood cultures haven't been too concerning (the CONS positivity in one bottle looks to be just a contaminant). With an active GI problem with a mucosal barrier that's very much disrupted, gut pathogens such as Staphylococcus (e.g. aureus), Streptococcus (e.g. anginosus), Bacteroides, and E. coli are important to consider. Could she have developed a bacterial meningitis? With the active immunosuppression, more atypical infections should also be on the list. Pathogens like Candida and Cryptococcus are known to affect the CNS.
With the time course given, you don't suspect etiologies such as autoimmune encephalitis. Patients on anti-TNF alpha drugs such as infliximab can get central and/or peripheral demyelination, but you didn't see CNS demyelination on her MRI, and that wouldn't explain her exam anyway.
Other than infiltrative processes discussed above, is there anything else that could cause the fixed and dilated pupils and depressed mental status?
There's no clear big bad structural etiology causing the fixed and dilated pupils. They've already gotten the MRI that would show you the parenchyma with higher resolution. That leaves something infiltrative. You didn't see any leptomeningeal enhancement around the brainstem. (In what other areas should you pay especially close attention to identify leptomeningeal disease? The cerebellar folia, cranial nerves, convexity sulci.)
So where does that leave us? Something bad must have happened (or is happening still). You might think about whether or not they had a cardiac arrest. History was not supportive of this, either at the OSH or even here. There weren't any findings of cerebral ischemia on the MRI, though you suppose that the sensitivity for that might not be great anyway. You can't blame these findings on his renal dysfunction either.
With the lack of any clear large structural problem, you don't see a role for any acute neurosurgical intervention. You might recommend cEEG but otherwise defer further care to neurology.
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