A Case of Meningoencephalitis Presenting with Pseudo-subarachnoid Hemorrhage (pSAH) and Vasculopathy
Chetna Dengri1, Saira Afzal1, Efrain Salgado1, Mubashir Pervez2
1Cleveland Clinic Florida, 2Cleveland Clinic
Background:
pSAH appears as hyperdensity in the subarachnoid space on CT without corresponding MRI evidence of blood seen with diffuse cerebral edema. Literature suggests it may result from blood-brain barrier disruption and contrast extravasation, the link to infectious causes is not widely recognized.
Results:
37-year-old woman with history significant for alcoholic liver cirrhosis, recent liver transplant, hypothyroidism, hemophagocytic lymphohistiocytoses syndrome transferred from outside hospital with loss of consciousness with 2-day history of altered mental status. CT brain with and without contrast was performed a few hours at outside hospital showing bilateral cerebral hypodensity along with left MCA stenosis. CT Brain without contrast obtained at our hospital showed similar hypodensity but was remarkable for bilateral frontoparietal & sylvian fissure subarachnoid hyperdensity, concerning for a possible SAH or pSAH in setting of contrast extravasation. CTA head was negative for intracranial aneurysms but demonstrated mild/moderate narrowing of the left middle cerebral artery M1 & M3 segments concerning for vasospasm or vasculitis. Patient was intubated for airway protection for multiple generalized tonic- clonic seizures. Cerebral angiogram was deferred due to worsening hemodynamic instability. MRI Brain with and without contrast showed multiple areas of evolving acute/subacute ischemic infarctions in the supra and infratentorial brain and nonspecific leptomeningeal enhancement. Patient was started on empiric coverage for meningitis & lumbar puncture was performed. CSF (cerebrospinal fluid) was remarkable for high protein (88), neutrophilic predominant pleocytosis (95%), no xanthochromia, negative cultures. Hospital course was complicated with hypoxic respiratory failure & septic shock. CT Chest demonstrated nodular opacity in the right upper lobe. CMV PCR & AFB cultures were positive in blood. Bronchoalveolar lavage was positive for mycobacterium. The family decided to proceed with comfort care.
Conclusions:
pSAH may be an early sign of vasculopathy caused by aggressive opportunistic infection in an immunocompromised patient requiring a thorough workup and early broad spectrum antibiotics.
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