Cytotoxic Edema and Adverse Clinical Outcomes in Patients with Intracerebral Hemorrhage

BACKGROUND: Cytotoxic edema (CE) is an important form of perihematomal edema (PHE), which is a surrogate marker of secondary injury after intracerebral hemorrhage (ICH). However, knowledge about CE after ICH is insufficient. Whether CE has adverse effects on clinical outcomes of patients with ICH remains unknown. Therefore, we aimed to investigate the temporal pattern of CE and its association with clinical outcomes in patients with ICH. METHODS: Data were derived from a randomized controlled study (comparing the deproteinized calf blood extract with placebo in patients with ICH). Intervention in this original study did not show any impact on hematoma and PHE volume, presence of CE, or clinical outcomes. We conducted our analysis in 20 patients who underwent magnetic resonance imaging with diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) images at day 3 and within 7–12 days after symptom onset. CE was defined as an elevated DWI b1000 signal and an ADC value reduced by > 10% compared with the mirror area of interest in the perihematomal region. The modified Rankin Scale (mRS), National Institutes of Health Stroke Scale (NIHSS), and Barthel Index (BI) were performed face to face at 30-day and 90-day follow-ups after ICH onset to assess the clinical outcomes of the patients. RESULTS: CE was detected in nearly two thirds of patients with ICH in our study and seemed to be reversible. CE within 7–12 days, rather than at day 3 after symptom onset, was associated with poor clinical outcome (mRS 3–6) at the 30-day follow-up (P = 0.020). In addition, compared with those without CE, patients with CE within 7–12 days had more severe neurological impairment measured by NIHSS score (P = 0.024) and worse daily life quality measured by BI (P = 0.004) at both the 30- and 90-day follow-ups. CONCLUSIONS: CE appears in the acute phase of ICH and might be reversible. CE within 7–12 days post ICH was related to poor outcomes, which provides a novel therapeutic target for ICH intervention. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12028-022-01603-2.