Progression of Mass Effect After Intracerebral Hemorrhage

Abstract

Background and Purpose-While the evolution of mass effect after cerebral infarction is well characterized, similar data regarding intracerebral hemorrhage (ICH) are scant. Our goal was to determine the time course and cause for progression of mass effect after ICH. Methods-Patients with spontaneous supratentorial ICH who underwent Ն2 CT scans were identified in our prospectively collected database. CT lesion size and midline shift of the pineal and septum pellucidum were retrospectively measured and correlated with clinical and CT characteristics. Causes for increased midline shift were determined by 2 independent observers. Results-Seventy-six patients underwent 235 scans (3.1Ϯ1.3 per patient). Initial CT was obtained within 24 hours of ICH in 66. Twenty-five scans were repeated on day 1, 80 on days 2 through 7, 31 on days 8 through 14, and 24 Ͼ14 days after ICH. Midline shift was present on 88% of the initial scans. There were 17 instances of midline shift progression: 10 occurred early (0.2 to 1.7 days) and were associated with hematoma enlargement, and 7 occurred late (9 to 21 days) and were associated with edema progression. Progression of mass effect due to edema occurred with larger hemorrhages (PϽ0.05). Of 65 scans repeated for clinical deterioration, only 10 were associated with increased mass effect. Conclusions-Progression of mass effect after ICH occurred at 2 distinct time points: within 2 days, associated with hematoma enlargement, and in the second and third weeks, associated with increase in edema. The clinical significance of later-developing edema is unclear.

Decompressive Hemicraniectomy in Hypertensive Basal Ganglia Hemorrhages

“…Subsequently, osmotically active proteins in the hematoma cause edema formation in the surrounding tissue, with approximately 75% of patients experiencing an increase in perihematomal edema within the first 24 hours. 8,17 Rather counter intuitively, surgical clot evacuation may in some cases also contribute to ICP elevation, as it bears the potential to induce edema formation through tissue manipulation and/or venous interruption. 5,10 Although the topic of clot evacuation in ICH has gained increased attention in recent years 11,14 following a relatively silent period after the 1961 landmark paper by McKissock et al, 13 the role of decompressive craniectomy in large ICHs has only scarcely been explored.…”

Stereotactic fibrinolysis of spontaneous intracerebral hematoma using infusion of recombinant tissue plasminogen activator

“…We know from the literature that during the early period after the ictus, intracerebral hematomas may cause neurological deterioration as a result of an increasing mass effect caused by surrounding edema, and this can last up to 4 weeks 19,20 . The good outcome in these patients could be explained due the fact that admission and diagnosis took about 4 hours.…”

Therapeutic Hypothermia in Acute Stroke

“…[63] After the acute phase of ICH, high morbidity and mortality are essentially caused by the evolution of a peri-hemorrhagic, space-occupying edema associated with gradually increasing ICP. [64] Although the natural course of edema formation is still not fully understood, edema mostly increases during the first week and reaches its maximum during the second week after bleeding onset. [65,66] Animal studies have suggested that hypothermia may have a neuroprotective role after ICH in reducing edema formation by various mechanisms.…”