title: Decreased perihematomal edema in thrombolysis-related intracerebral hemorrhage compared with spontaneous intracerebral hemorrhage.
abstract: OBJECTIVE
  Intracerebral hemorrhage (ICH) is a highly morbid disease process. Perihematomal edema is reported to contribute to clinical deterioration and death. Recent experimental observations indicate that clotting of the intrahematomal blood is the essential prerequisite for hyperacute perihematomal edema formation rather than blood-brain barrier disruption.
  
  
  METHODS
  We compared a series of patients with spontaneous ICH (SICH) to a series of patients with thrombolysis-related ICH (TICH). All patients were imaged within 3 hours of clinical onset. We reviewed relevant neuroimaging features, emphasizing and quantifying perihematomal edema. We then analyzed clinical and radiological differences between the 2 ICH types and determined whether these factors were associated with perihematomal edema.
  
  
  RESULTS
  TICHs contained visible perihematomal edema less than half as often as SICHs (31% versus 69%, P<0.001) and had both lower absolute edema volumes (0 cc [25th, 75th percentiles: 0, 6] versus 6 cc [0, 13], P<0.0001) and relative edema volumes (0.16 [0.10, 0.33] versus 0.55 [0.40, 0.83], P<0.0001). Compared with SICHs, TICHs were 3 times larger in volume (median [25th, 75th percentiles] volume 69 cc [30, 106] versus 21 cc [8, 45], P<0.0001), 4 times more frequently lobar in location (62% versus 15%, P<0.001), 80 times more frequently contained blood-fluid level(s) (86% versus 1%, P<0.001), and were more frequently multifocal (22% versus 0%, P<0.001).
  
  
  CONCLUSIONS
  The striking qualitative and quantitative lack of perihematomal edema observed in the thrombolysis-related ICHs compared with the SICHs provides the first substantial, although indirect, human evidence that intrahematomal blood clotting is a plausible pathogenetic factor in hyperacute perihematomal edema formation.
authors.affiliation: Department of Neurology, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA. jgebel@stroke.upmc.edu
authors.forename: J M
authors.initials: JM
authors.lastname: Gebel
authors.forename: T G
authors.initials: TG
authors.lastname: Brott
authors.forename: C A
authors.initials: CA
authors.lastname: Sila
authors.forename: T A
authors.initials: TA
authors.lastname: Tomsick
authors.forename: E
authors.initials: E
authors.lastname: Jauch
authors.forename: S
authors.initials: S
authors.lastname: Salisbury
authors.forename: J
authors.initials: J
authors.lastname: Khoury
authors.forename: R
authors.initials: R
authors.lastname: Miller
authors.forename: A
authors.initials: A
authors.lastname: Pancioli
authors.forename: J E
authors.initials: JE
authors.lastname: Duldner
authors.forename: E J
authors.initials: EJ
authors.lastname: Topol
authors.forename: J P
authors.initials: JP
authors.lastname: Broderick
mesh_terms: D000368:Aged; D002543:Cerebral Hemorrhage / Q000139:chemically induced* / Q000150:complications* / Q000000981:diagnostic imaging / Q000188:drug therapy; D004487:Edema / Q000000981:diagnostic imaging / Q000209:etiology*; D005260:Female; D005343:Fibrinolytic Agents / Q000009:adverse effects* / Q000627:therapeutic use; D006406:Hematoma / Q000150:complications* / Q000000981:diagnostic imaging / Q000188:drug therapy; D006801:Humans; D008297:Male; D008875:Middle Aged; D016032:Randomized Controlled Trials as Topic; D014057:Tomography, X-Ray Computed
chemical_list: D005343:Fibrinolytic Agents