Abstract Details

Title Acute Ischemic Leukoencephalopathy Secondary to Circulatory Shock and Metabolic Acidosis

Topic Neuro Trauma and Critical Care

Presentation(s) P8 - Poster Session 8 (11:45 AM-12:45 PM)

Poster/Presentation
Number 1-003

Objective Report the cognitive and functional prognosis of acute ischemic leukoencephalopathy, secondary to circulatory shock.

Background Development of acute ischemic leukoencephalopathy, secondary to circulatory shock, has rarely been reported. Proposed pathogeneses suggest, dysfunctional cerebral autoregulation with pre-existing hypertension, and metabolic imbalances leading to blood-brain barrier disruption, facilitate white matter insults. Data on cognitive and functional improvement for acute ischemic leukoencephalopathy is sparse. Here we present a patient with acute ischemic leukoencephalopathy, who returned to functional and cognitive baseline with supportive management, despite persistent radiological findings.

Design/Methods N/A

Results A 74-year-old male, with past medical history of hypertension, bipolar disorder type 1, and lumbar spondylosis, presented to the emergency room with altered mentation, after deliberate overdose of beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, and non-steroidal anti-inflammatory drugs. His cognitive and hemodynamic status deteriorated, with mean arterial pressure 35 mmHg, requiring intubation and pressor support. Urine output steadily decreased with glomerular filtration rate 53 mL/min/1.73m2, blood urea nitrogen 30 mg/dL, and creatinine 2.03 mg/dL. Arterial blood gas revealed pH 7.05, bicarbonate 18mEq/mL, pCO2 67 mm. Magnetic resonance imaging (MRI) revealed T2-weighted, white matter hyperintensities in bilateral temporal lobes (R>L). Electroencephalogram revealed poorly organized theta activity, with intermixed triphasic waves. Diagnosis of acute ischemic leukoencephalopathy was made after excluding toxic and infectious etiologies. Patient responded to supportive treatment with extubation on day 19. Examination showed Glasgow coma scale 15, with intact cranial nerve and sensorimotor function. Prior to psychiatric facility transfer, MRI at 4-weeks revealed persistent white matter hyperintensities.

Conclusions Acute ischemic leukoencephalopathy, though rare, can occur secondary to hemodynamic instability causing circulatory shock, and concurrent metabolic abnormalities. Interestingly, we observed a lag between clinical and radiological resolution. This case suggests physicians should continue aggressive therapeutic intervention, despite findings of leukoencephalopathy. We also aim to guide physicians in their discussions with families of such patients, regarding prognosis.

Authors/Disclosures
Sharanya Ramakrishnan, MD (Tufts Medical Center) PRESENTER	Dr. Ramakrishnan has nothing to disclose.
	No disclosure on file
Moin Ud Din	Moin Ud Din has nothing to disclose.
Muhammad F. Khan, MD (SUGAR LAND NEUROLOGY AND SLEEP)	Dr. Khan has nothing to disclose.

��ɫ��

��ɫ��