# Hemostasis, Hematoma Expansion, and Outcomes After Intracerebral Hemorrhage

> **NIH NIH R01** · NORTHWESTERN UNIVERSITY · 2021 · $609,173

## Abstract

PROJECT SUMMARY
Intracerebral hemorrhage (ICH) is the most morbid form of stroke and has no treatment approved by the US
Food and Drug Administration. Hematoma expansion (HE), interval growth of the hematoma, is a proximate
cause of worse patient outcomes and death as larger hematomas displace brain tissue; hematomas > 60 mL
reliably lead to disability or death at follow-up. Preventing HE is a promising strategy to improve outcomes for
patients with ICH. Our relative inability to predict HE, however, has impeded the development of effective
treatment strategies for ICH, and several clinical trials have been unsuccessful. Even when HE has been
reduced, our ability to detect a benefit is hampered by relatively insensitive patient outcomes. This proposal will
resolve two roadblocks that prevent the development of effective treatments for ICH, the most morbid form of
stroke.
Three comprehensive stroke centers (two from the Northwestern Medicine system in metropolitan Chicago, IL,
and the University of Texas at Houston) will partner to prospectively enroll patients with ICH, measure
hemostasis, measure HE, and record patient outcomes with state of the art assessments, including the NIH
Patient Reported Outcomes Measurement Information System (PROMIS) and NIH Toolbox.
First, we will determine the mechanisms that lead to HE in acute ICH, broadly grouped into platelet activity,
activation of coagulation, and fibrinolysis. Each can be specifically measured and has specific treatments to
improve it. For example, reduced platelet activity due to aspirin can be reliably improved with desmopressin,
delayed activation of coagulation may be related to hypomagnesemia, and accelerated fibrinolysis may be
reduced with tranexamic acid or aminocaproic acid. Each will be examined for predicting HE; if multiple
pathways are found, we will determine which are most important with machine learning. Once the most
important mechanisms of hemostasis for HE are determined, we will explore if specific therapies improve
platelet activity. It is possible that specific treatments for specific deficits in hemostasis will be more likely to
reduce HE than single therapies applied to ICH patients generally (e.g., Factor VII).
Once hemostatic mechanisms of HE are determine, we will determine the effect of HE on patient outcomes
such as the modified Rankin Scale (mRS, a global ordinal scale), PROMIS, and NIH Toolbox. This will be
crucial to plan for future clinical trials intended to improve patient outcomes through correcting abnormal
hemostasis in acute ICH. Results will apply broadly to other bleeding conditions (e.g., neurotrauma).

## Key facts

- **NIH application ID:** 10133760
- **Project number:** 5R01NS110779-03
- **Recipient organization:** NORTHWESTERN UNIVERSITY
- **Principal Investigator:** ANDREW M NAIDECH
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $609,173
- **Award type:** 5
- **Project period:** 2019-04-01 → 2024-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10133760

## Citation

> US National Institutes of Health, RePORTER application 10133760, Hemostasis, Hematoma Expansion, and Outcomes After Intracerebral Hemorrhage (5R01NS110779-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10133760. Licensed CC0.

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