Abstract TP133: Diabetes/hyperglycemia Is Associated With Poor Six-month Functional Outcomes, But Is Not Associated With The Development Of Microvascular Ischemic Lesions After Intracerebral Hemorrhage
Lusk, JB; Liu, L; Weikel, DP; Li, Y-J; Sekar, P; Demel, SL; Aziz, Y; Woo, D; James, ML
Published in: Stroke
Ischemic lesions seen on diffusion weighted imaging (DWI) are associated with worsened outcomes after intracerebral hemorrhage (ICH) and are thought to arise due to microvascular damage. While hyperglycemia and diabetes mellitus contribute to small vessel disease, it is not known if these factors contribute to the development of DWI lesions and associated outcomes after ICH.
Indicators of diabetes/hyperglycemia will be associated with the development of DWI lesions and poor outcomes after ICH
1123 patients with MRI data from the Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) study were included. Predictors with p<0.15 in univariate analyses were included in initial multivariable logistic regression models. Least absolute shrinkage and selection operator (LASSO) regression was used to identify final models.
In univariate analysis, no measure of diabetes or hyperglycemia (medical history of diabetes, insulin or non-insulin antidiabetic medication use, blood glucose obtained by emergency medical services, blood glucose on admission, fasting blood glucose, or hemoglobin A1c) was associated with the development of DWI lesions (p>0.05). Blood glucose on admission was incorporated into the initial multivariable model (p<0.15). Univariate analysis for poor six-month functional outcome (modified Rankin Score >3) showed that history of diabetes (p<0.001), blood glucose on admission (p=0.002), fasting blood glucose (p=0.049), and use of non-insulin antidiabetic medications (p=0.036) were associated with poor outcomes. Final multivariable logistic regression analyses are shown in Tables 1 and 2.
While diabetes and hyperglycemia are associated with worsened outcomes after ICH, this relationship is unexpectedly not mediated by microinfarcts despite their association with cerebral small vessel disease.
