Michelle Christina Johansen, MD

Gioia LC, Kate M, Choi V, Sivakumar L, Jeerakathil T, Kosior J, et al. Ischemia in Intracerebral Hemorrhage Is Associated With Leukoaraiosis and Hematoma Volume, Not Blood Pressure Reduction. Stroke. 2015

What corresponds to DWI lesions in intracerebral hemorrhage (ICH)? Is this reflective of true ischemic injury? The INTERACT trials refocused the neurointensivist on aggressive blood pressure control as this was shown to correlate with decreased hematoma growth and better functional outcomes. But is there a downside to controlling the blood pressure too aggressively? Does this result in ischemic insult or DWI changes on MRI? 

Dr. Gioia et al., sought to identify the frequency of ischemic lesions in primary ICH patients with the hypothesis that larger hematoma volumes and blood pressure reduction are associated with the presence DWI lesions. 

The Canadian based study retrospectively identified 117 ICH patients who underwent DWI within 14 days of symptom onset. Hematoma/perihematoma edema volumes were measured using planimetric techniques. Perihematoma and remote DWI lesion volumes were measured using apparent diffusion coefficient. The investigators established two thresholds to define the amount of ischemic damage; moderate (<730×10-6mm/s) and severe (<550×10-6mm/s). Acute blood pressure changes over the first 24 hours were calculated using the formula admission systolic blood pressure (SBP) minus nadir SBP. Mean age of the population was 65 and 52% were male. Hypertension was the most common cause indicated in the medical record for ICH (45.7%).

The authors, after controlling for age, baseline NIHSS and perihematoma edema volumes, found that perihematoma DWI lesions were independently associated with larger hematoma volumes. There was no association between changes in blood pressure (maximal systolic blood pressure drop) and the presence of DWI lesions. They did find remote DWI lesions in 17 patients. For the remote lesions, once again no relationship was found with blood pressure, but they did note these patients were more likely to use antiplatelet drugs, have a history of ICH and larger leukoaraiosis (hyperintensity on FLAIR) volumes.

How should the results of this study be applied? The mean time to MRI was 2 days which is a consideration when drawing conclusions between volumes and the presence of DWI lesions. That being said, there was excellent interreliability among the radiologists and they accounted for edema volume which should help mitigate over calculation of hematomal volumes. Blood pressure data was missing in 4 patients with perihematoma DWI lesions in a relatively small cohort of patients (38). Would a larger sample size have led to different results? How does the fact that the majority of patients had lobar ICH affect the data? Thus we are still unable to define the relationship between blood pressure control and patients with cerebral amyloid angiopathy.

Where does the vascular neurologist go from here when faced with perihematoma diffusion restriction after ICH? In ischemic injury, we allow for permissive hypertension to provide critical blood flow to the penumbra yet research supports aggressive blood pressure control for ICH. The authors of this study did not find a relationship between aggressive blood pressure control and ischemia but it cannot be ruled out. In their discussion, they suggest that larger hematomas be treated more conservatively with respect to blood pressure control but appropriately caveat this statement with the need for larger clinical trials. While the answer remains unclear, we must strive to clarify this issue so that our patients can receive the best medical care based on evidence.