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Abstract Details

Exploring the Role of Perihematomal Edema in Delirium after Intracerebral Hemorrhage
Neuro Trauma and Critical Care
P6 - Poster Session 6 (5:30 PM-6:30 PM)
1-002
Delirium is common in patients with ICH and is often associated with devastating consequences. Although some acute ICH features are delirium risk factors, the role of downstream inflammation and perihematomal edema (PHE) in delirium pathogenesis is unclear.
To explore the potential role of perihematomal edema (PHE) and neuroinflammation in delirium after intracerebral hemorrhage (ICH). 
Using data from a single-center ICH registry, we identified consecutive patients with acute ICH who received magnetic resonance imaging (MRI) scans, with each patient classified as delirious or non-delirious during their hospitalization using DSM-5 criteria. We analyzed de-identified T2-FLAIR MRIs using semi-automated software and performed blinded volumetric measurements of each hematoma and adjacent PHE. We then determined associations between PHE volume and incident delirium using multivariable regression models adjusted for age and ICH features, while also using interaction terms to account for the day of MRI acquisition and interaction between PHE and ICH size. 
Of 188 ICH patients, 79 (42%) experienced delirium during their hospitalization; median hospital day of MRI was 3 (IQR 1-4). Compared with non-delirious patients, those with delirium had more PHE (mean 52.4 [SD 41.4] vs. 21.0 [18.7] cm3) at the time of their MRI, while also having larger hematomas (mean 37.9 [SD 32.2] vs. 13.8 [21.6] cm3). In multivariable models accounting for age, ICH features, and MRI timing, PHE was independently associated with delirium (OR 1.38 per 10 cc, 95% CI 1.08-1.76). There was not a significant interaction between PHE volume and MRI timing (p=0.27), nor between ICH and PHE volume (p=0.79), suggesting that the effect of PHE on delirium did not depend on timing of measurement or ICH size.
PHE is independently associated with delirium in ICH patients, suggesting that downstream neuroinflammation may play a role in delirium pathogenesis.
Authors/Disclosures
Jesse Menville
PRESENTER
Ms. Menville has nothing to disclose.
Nathaniel Rex Mr. Rex has received research support from NIH Heart, Lung, Blood Institute (NHLBI) .
No disclosure on file
No disclosure on file
No disclosure on file
No disclosure on file
No disclosure on file
Karen L. Furie, MD (RIH/Alpert Medical School of Brown Univ) The institution of Dr. Furie has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Janssen/BMS. Dr. Furie has received personal compensation in the range of $50,000-$99,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for BMJ/JNNP. The institution of Dr. Furie has received research support from NINDS.
No disclosure on file
Jesse Menville Ms. Menville has nothing to disclose.