Abstract Details

Title Acute Wernicke’s Encephalopathy after Hemorrhagic Shock in a Non-alcoholic Patient

Topic General Neurology

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

Poster/Presentation
Number 066

Objective To describe a non-classical case of Wernicke's Encephalopathy.

Background

Wernicke’s Encephalopathy (WE) is an acute neurological disease resulting from thiamine deficiency mainly related to alcoholism. Severe thiamine deficiency is an emerging problem in non-alcoholic patients. We present a unique case of WE that developed in a non-alcoholic patient after she developed hemorrhagic shock.

Design/Methods

Case Report

Results 34-year-old, right-handed woman with history of malignant uterine perivascular epithelioid cell tumors (PEComa), LLE deep venous thrombosis (DVT), chronic kidney disease and bilateral percutaneous nephrostomy tubes (PCNT), and chronic anemia who was admitted to the hospital for replacement of PCNTs. Hospital course was complicated by E. cloacae urosepsis, lactic acidosis and hemorrhagic shock. Patient had a hemoglobin of 6.7 and became acutely hypotensive and tachycardic. She was started on vasopressors and required massive transfusion protocol along with embolization of the left ovarian and internal iliac arteries to control bleeding. Within 10 days, she developed new bilateral horizontal nystagmus, intermittent dizziness lasting seconds, persistent N/V and hiccups. MRI of the brain was done that showed new FLAIR symmetrical hyperintensity in the mammillary bodies, dorsal medulla andthe medial aspect of thalami consistent with WE. Of note, patient had MRI done 10 days prior due to acute encephalopathy but no acute ischemia or intracranial metastatic disease was present. She was started on high-dose IV thiamine (500 mg three times daily for 2 days followed by 250 mg daily while inpatient followed by oral treatment with 200 mg daily on discharge). Also, the patient’s thiamine level returned low at 42 (ref: 66-200 nmol/L). Patient’snystagmus improved after starting IV thiamine and eventually resolved.

Conclusions

Despite advances in imaging techniques, WE remains a clinical diagnosis with mortality rate exceeding 17%. WE is a reversible neurological disorder and supplementation should be started as soon as clinical suspicion exists.

Authors/Disclosures
Maryum Shoukat, MD PRESENTER	Dr. Shoukat has nothing to disclose.
Sama Astani, MD	Dr. Astani has nothing to disclose.
Temitope A. Lawal, MD (Neurology, ECU health)	Dr. Lawal has nothing to disclose.
Danny Samkutty, MD (OU Health)	Dr. Samkutty has nothing to disclose.

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