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From the Cleveland Clinic Foundation (Ohio) (J.M.G., C.A.S., J.W.,
E.J.T.); the University of Maryland Medical Center, Baltimore (M.A.S.); Duke
University Medical Center, Durham, NC (C.B.G., K.W.M., C.L.G., R.M.C.); Green
Lane Hospital, Auckland, New Zealand (H.D.W.); the University of
Massachusetts, Worcester, Mass (J.M.G.); and the University of Washington,
Seattle, Wash (W.D.W.).
Correspondence to Cathy A. Sila, MD, Department of Neurology (S-91), Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195.
Background and Purpose—Intracranial
hemorrhage (ICH) is a serious complication of
thrombolytic therapy. We systematically reviewed the
radiographic features of 244 cases of
symptomatic ICH complicating thrombolysis
for acute myocardial infarction in the Global Utilization of
Streptokinase and Tissue Plasminogen Activator
for Occluded Coronary Arteries (GUSTO-1) trial, correlated
these observations with clinical data, and speculated on
hemorrhage pathogenesis.
Methods—CT scans from 244 patients suffering
symptomatic ICH were systematically reviewed for selected
radiographic features, including ICH type, location,
hematoma characteristics, mass effect features, hydrocephalus, and
preexisting lesions. Hematoma volume was estimated by computer-assisted
volumetric analysis. Data from this analysis were
correlated with clinical data including hypertension, anticoagulation,
age, thrombolytic regimen, and ICH timing.
Results—Most hemorrhages were large (median [25th, 75th
percentile] volume, 72 mL [39, 118]), solitary (66%), lobar (77%),
confluent (80%), and intraparenchymal (82%) with a blood/fluid level
(82%) and little edema (median [25th, 75th percentile] volume, 9 mL
[5, 16]). Hydrocephalus (P<.001), any one mass effect
feature (P<.001), intraventricular
hemorrhage (P=.022), mottled hematoma appearance
(P=.050), and hematoma blood/fluid level
(P<.001) were associated with higher hemorrhage
volume in the radiographic analysis, as were older
age (P=.005), treatment with combined streptokinase and
tissue plasminogen activator
(P=.034), and hemorrhage onset 8 to13 hours
after treatment (P=.008) in the clinical
analysis. Subdural hemorrhage was a high-volume
subgroup whose risk increased with antecedent trauma
(P=.026) or syncope (P=.006). Deep
intraparenchymal hemorrhage was associated with hypertension
(P=.016), and multifocal ICH occurred significantly
earlier after treatment (P=.002).
Conclusions—Although the majority of
postthrombolytic ICH are large, solitary, and
supratentorial, the spectrum is diverse. Features
of mass effect reflected the large volumes, and hematoma
characteristics of mottling and blood/fluid levels were frequent.
Thrombolysis-related coagulopathy and age appear to be the
most important identifiable factors in the genesis of
postthrombolytic ICH, but the hemorrhage
subtype seen may reflect an interaction with other factors such as
hypertension, ICH timing, antecedent head trauma, and syncope.
© 1998 American Heart Association, Inc.
Original Contributions
Thrombolysis-Related Intracranial Hemorrhage
A Radiographic Analysis of 244 Cases From the GUSTO-1 Trial With Clinical Correlation
Key Words: cerebral hemorrhage • myocardial infarction • thrombolytic therapy
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