Abstract Details

Title Large Bilateral Hemorrhagic Infarctions Secondary to Cerebral Venous Sinus Thrombosis in a Patient with Focal Segmental Glomerulosclerosis: A Case Report

Topic General Neurology

Presentation(s) General Neurology Posters (7:00 AM-5:00 PM)

Poster/Presentation
Number 024

Objective To report a 27 y/o M patient with focal segmental glomerulosclerosis who developed large bilateral hemorrhagic infarctions in the setting of extensive cerebral venous sinus thrombosis with resultant brain death.

Background

Cerebral venous sinus thrombosis in young patients is a potential complication of nephrotic syndrome due to heavy proteinuria and subsequent loss of coagulation proteins (eg, antithrombin III), leading to a hypercoagulable state. The most threatening complication of CVST is hemorrhagic venous infarction, which in turn might result in catastrophic neurological outcomes such as brain death.

Design/Methods Case Report

Results 27 y/o male patient diagnosed with focal segmental glomerulosclerosis 3 months before presenting with moderate-to-severe headache with near-syncope that resolved on its own without immediate sequelae. Three days later he was found unconscious at home, reason for which he was taken to nearest ER and Head CT scan revealed two large frontoparietal hematomas (largest on left side) that correlated with Head venography findings of extensive cerebral venous sinus thrombosis (CVST) of the superior sagittal sinus, extending inferiorly into the torcula and into the left transverse and sigmoid sinuses. After confirming CVST, patient was started on full dose anticoagulation with combination therapy of subcutaneous enoxaparin and warfarin; however, after mild neurological improvement, 5 days later patient developed sudden neurological deterioration secondary to expansion of both hematomas with resultant leftward uncal, transtentorial herniation, and was subsequently declared brain death.

Conclusions

Cerebral venous sinus thrombosis in young patients is a potential complication of nephrotic syndrome due to heavy proteinuria and subsequent loss of coagulation proteins (eg, antithrombin III) leading to decreased inhibition of factor IIa and Xa, and consequently a hypercoagulable state. This in turn might result in catastrophic hemorrhagic infarction which should not delay full anticoagulation, which in the mainstay of therapy to avoid further expansion of hematomas.

Authors/Disclosures
Noelia C. Morales, MD PRESENTER	Dr. Morales has nothing to disclose.
Johnny A. Sanabria Lopez, MD	Dr. Sanabria Lopez has nothing to disclose.
Carmen Serrano, MD, FAAN (University of Puerto Rico, Neurology)	The institution of Dr. Serrano has received research support from Eli Lilly. The institution of Dr. Serrano has received research support from Abbvie.
Jessica Abreu Garcia, MD	Dr. Abreu Garcia has nothing to disclose.
Raymond M. Rivera Vergara, MD	Dr. Rivera Vergara has nothing to disclose.

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