Natural course of perihemorrhagic edema after intracerebral hemorrhage.

BACKGROUND AND PURPOSE: There is only limited knowledge on the time course of perihemorrhagic edema (PHE) after intracerebral hemorrhage (ICH). We aimed to investigate the chronological PHE course and its relation to in-hospital mortality in a large retrospective ICH cohort. METHODS: Patients with supratentorial ICH treated at our institution between 2006 and 2009, who had received at least 3 CT scans in the course of conservative treatment, were included in the present analysis. PHE at Days 1, 2, 3, 4 to 6, 7 to 11, 12 to 16, 17 to 21, and >22 was assessed using a threshold based semiautomatic volumetric algorithm. A chart review was performed to achieve data on duration of stay, ventilation, treatment with external ventricular drains, and in-hospital mortality. RESULTS: Two hundred nineteen patients aged 69.9±10.5 years with deep (n=103) or lobar (n=116) ICH were included in the study. Mean ICH volume was 35.7±31.5 mL. Mean absolute PHE volume significantly increased from initially 32.6±29.9 mL to 63.7±46.7 mL at Days 7 to 11. No significant changes were observed at later time points. ICH volume was strongly correlated with absolute PHE volume (ρ=0.8, P<0.001) and inversely correlated with relative PHE (ρ=-0.4 to -0.5, P<0.001). Increase in absolute PHE between Days 1 and 3 was significantly predictive for in-hospital mortality (P=0.014, ExpB=1.04). CONCLUSIONS: PHE develops early after ICH and doubles within the first 7 to 11 days after the initial bleeding event. This additional mass effect may contribute to secondary clinical deterioration and mortality, especially in larger ICH. Because of its inverse correlation with ICH volume, relative PHE may not be suitable for analyses considering the clinical impact of PHE.

Effects of continuous hypertonic saline infusion on perihemorrhagic edema evolution.

BACKGROUND AND PURPOSE: Mass effect of hematoma and the associated perihematomal edema are commonly responsible for neurological deterioration after intracerebral hemorrhage. Efficacy of surgical and medical therapy is limited. We studied the effect of early continuous hypertonic saline infusion on development of perihematomal edema after severe spontaneous supratentorial hemorrhage. METHODS: Patients with spontaneous lobar and basal ganglia/thalamic bleeding >30 mL (n=26) were treated with early (<72 hours) continuous hypertonic saline infusion (3%) to achieve sodium of 145 to 155 mmol/L and osmolality of 310 to 320 mOsmol/kg. Evolution of absolute edema volume and relative edema volume (ratio absolute edema volume/initial hematoma volume) was assessed on repeated cranial CT and compared to historical patients (n=64) identified on database with hematoma >30 mL. RESULTS: In the treatment group, absolute edema volume was significant smaller between day 8 and day 14 (P(absolute edema volume)= 0.04) and relative edema volume was significant smaller between day 2 and day 14 (P(relative edema volume)=0.02). Intracranial pressure crisis (>20 mm Hg for >20 minutes or new anisocoria) occurred less frequently in the treatment group (12 versus 56; P=0.048). In-hospital mortality was 3 (11.5%) in the hypertonic saline group and 16 (25%) in the control group (P=0.078). Side effects theoretically associated with hypertonic saline including cardiac arrhythmia and acute heart and renal failure occurred in both groups to a similar extent. CONCLUSIONS: Early and continuous infusion of hypertonic saline in patients with severe spontaneous intracerebral hemorrhage was feasible and safe. The beneficial effect of this treatment regimen on edema evolution and outcome has to be demonstrated in a controlled trial.

Early continuous hypertonic saline infusion in patients with severe cerebrovascular disease.

OBJECTIVE: To study the safety and the effects of early continuous hypertonic saline infusion in patients with cerebral edema and underlying cerebrovascular disease. DESIGN: Retrospective analysis. SETTING: University medical center. PATIENTS: Neurologic intensive care unit population with mixed cerebrovascular diseases. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Between May 2008 and December 2009, 100 patients with severe intracerebral hemorrhage, cerebral ischemia, or aneurysmal subarachnoid hemorrhage and signs of intracranial hypertension received within ≤72 hrs after symptom onset a continuous infusion of hypertonic saline (3%, target sodium 145-155 mmol/L, target osmolality 310-320 mOsm/kg) over 13 (4-23) days. We analyzed the frequency of episodes with elevated intracranial pressure (new anisocoria or intracranial pressure >20 mm Hg for ≥20 mins), inhospital mortality, and the occurrence of adverse effects theoretically associated with hypertonic saline. The findings were compared with those of a historical control group (n = 115, 2007-2008) with equal underlying disease. In the treatment group, fewer episodes of critically elevated intracranial pressure (92 vs. 167, p = .027) in fewer patients (50 of 100 = 50.0% vs. 69 of 115 = 60.0% patients, p = .091) were observed, and inhospital mortality was significantly decreased (17.0% vs. 29.6%, p = .037). Adverse events, including cardiac arrhythmia, heart, liver or renal dysfunction, or pulmonary edema, occurred in both groups to a similar extent. CONCLUSIONS: Early and continuous infusion of hypertonic saline in patients with severe cerebrovascular disease and impending intracranial hypertension is safe and might reduce the frequency of intracranial pressure crises and mortality rate. A randomized controlled trial is warranted to confirm our findings and to evaluate the effects of hypertonic saline on functional outcomes.