Hemorrhagic transformation in cerebral embolism.

Abstract

We studied the mechanism of hemorrhagic infarction after acute cerebral embolism in 160 patients by brain computed tomography and angiography. Hemorrhagic infarction during the month after the embolic event was evident in 65 patients (40.6%). Initial angiography a median of 1.5 (range 1-60) days after the event revealed occlusion of the cerebral arteries in 117 of 142 patients (82.4%), and reopening of the vessels was observed in 56 (94.9%) of 59 patients who had follow-up angiography a median of 20 (range 3-47) days after the event. The incidence of hemorrhagic infarction was higher in patients ^70 years old (31 of 61, 50.8%) than in those aged 50-69 years (27 of 72, 37.5%) or <50 years (seven of 27, 25.9%) (2=70 vs. <50, /><0.05). In patients with moderate or large infarcts, hemorrhagic infarction developed in 50.0% or 51.5%, respectively, while in those with small infarcts it developed in only 2.9% (p<0.05). No correlation was found between hemorrhagic infarction and history of hypertension or blood pressure during the acute stage of stroke. Thrombolytk and/or anticoagulant therapy did not affect the incidence of hemorrhagic infarction (40.0% with vs. 40.7% without therapy) but tended to cause massive hematoma. Our results indicate that hemorrhagic transformation in cerebral embolism is caused not only by reopening of the occluded vessels but also by other factors such as age and size of the infarct. Hypertension per se seems to be less important for hemorrhagic infarction. Anticoagulants and/or thrombolytk agents should be carefully administered i n the elderly and i n patients with large infarcts. (Stroke 1989;20:598-603)

Outcome Evaluation of Intra-arterial Infusion of Urokinase for Acute Ischemic Stroke

“…In our series, the incidence of hemorrhage was 29%, including five patients (10%) with parenchymal hematoma; this was similar to the rate seen in other series in which thrombolytic therapy was employed (5,12), and in series involving spontaneous hemorrhagic transformation of the infarction (16,17). The frequency of hemorrhage was unrelated to the presence or absence of recanalization.…”

Haemorrhagic transformation in ischaemic stroke is more frequent than clinically suspected – A neuropathological study

“…Okada et al examined 160 acute ischaemic stroke patients. Their CT based results showed all together 40.6% HT, from which 15.4% could be seen in the first 1-4 days, 67.7% in the first 10 days and 100% within the first 30 days and they haven't detected any new HTs after the first month [20]. Hornig et al evaluated 65 patients' data.…”

“…The distribution of haemorrhagic transformation in our material was the following: HI1 26.5%, HI2 29.4%, PH1 29.4% and PH2 14.7% (Table 2). Okada et al defined four types of HT: spotty and scattered petechial haemorrhage, along the cortical margin of the ischaemic lesion (56.9%), diffuse haemorrhage (18.5%), small (< 3 cm in diameter) (13.8%) and massive (> 3 cm in diameter) (10.8%) haematoma [20]. Fiorelli et al examined the subtypes and frequency of HT after iv.…”

Therapeutic interventions in acute stroke.

“…Open doseranging studies include the NIH tPA Study (Brott et al, 1990) Haemorrhagic transformation is a potential complication of thrombolytic treatment. This must be viewed in the light of the natural incidence of haemorrhagic transformation, which ranges from 10-43% depending on the circumstances and which increases as the time elapsed from stroke progresses (Fisher et al, 1984;Hornig et al, 1986;Lodder, 1984;Okada et al, 1989). The rate of intracerebral haemorrhage in 46,092 patients with myocardial infarction who were randomised in the ISIS-3 trial was only 0.3-0.7%, streptokinase causing significantly less haemorrhage than tPA or APSAC.…”