Abstract Details

Title Acute Encephalopathy in the Neurosciences Intensive Care Unit: Etiologies and Exploratory Descriptive Analysis of Outcome, Length of Stay, and EEG Data

Topic Neuro Trauma and Critical Care

Presentation(s) S23 - Neurocritical Care (1:12 PM-1:24 PM)

Poster/Presentation
Number 002

Objective Investigate the complexity of acute encephalopathy (AE) in the neuroscience intensive care unit (NSICU).

Background

AE, a prevalent diagnosis in intensive care, refers to generalized impaired brain function with vast etiological possibilities and no standardized diagnostic nomenclature. This diagnosis is often grouped into generalized categories or called simply delirium which does not fully characterize the complex pathophysiology, and little is understood about the relevance for outcomes and other clinical factors.

Design/Methods This retrospective cohort study included patients diagnosed with acute encephalopathy in Rush University NSICU between 1/1/2020 and 1/1/2022. The electronic medical record was queried for demographics, primary hospital problem, discharge diagnoses, length of stay (LOS), EEG results, discharge disposition and mortality. Etiology of encephalopathy was determined through chart review then categorized based on common determinants. Clinical factors including LOS, outcome/mortality, and EEG data were examined in relation to encephalopathy etiology.

Results 222 unique patients were reviewed (mean age 62.33, 50.45% male). Encephalopathy etiologies were grouped in 8 categories. Majority of cohort had m ultifactorial (79, 35.59%, patients affected by etiologies from at least two categories), neurologic (67, 30.18%), or metabolic (55, 24.77%) etiologies. Remainder separated into toxic (12, 5.41%) or delirium, hepatic, hypertensive, or anoxic (approximately 1% each) etiologies. Patients with multifactorial etiology had longest average LOS, at 16.58 days, followed by neurologic (12.48), and metabolic (10.78). Mortality data showed that 31 patients (13.96%) died, with majority multifactorial or metabolic etiologies. EEG data, available for 144 patients, showed >90% of patients with either multifactorial or metabolic encephalopathies had non-focal slowing consistent with encephalopathy. 74.19% and 55.56% in multifactorial and metabolic groups respectively had non-focal slowing without focal or epileptiform findings.

Conclusions This preliminary review demonstrates the need for a deeper understanding of encephalopathy etiologies, which is clinically relevant for accurate diagnosis and treatment, associated outcomes and clinical factors.

Authors/Disclosures
Jaclyn Thoma PRESENTER	Ms. Thoma has nothing to disclose.
Brianna J. Sennott, MD (Rush University Medical Center)	An immediate family member of Dr. Sennott has received personal compensation for serving as an employee of Abbott Laboratories.
Asad Rehman, DO (Northwest Community Healthcare)	Dr. Rehman has nothing to disclose.
Sayona John, MD, FAAN (Rush University Medical Center)	Dr. John has nothing to disclose.

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