Acute Encephalopathy in the Neurosciences Intensive Care Unit: Etiologies and Exploratory Descriptive Analysis of Outcome, Length of Stay, and EEG Data
Jaclyn Thoma1, Brianna Sennott1, Asad Rehman1, Sayona John1
1Department of Neurological Sciences, Rush University Medical Center
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 multifactorial (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.