Treatment of Strokes

Browne, Thomas R.; Poskanzer, David C.

doi:10.1056/nejm196909112811105

Cited by 55 publications

(3 citation statements)

References 57 publications

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“…Experimental studies showed clinical worsening in animals after early anticoagulant treatment (10,11,30) and autopsy studies showed a high incidence of HI after embolic cerebral events (7,8,9). Because of these findings, some authors rejected early anticoagulant treatment since they feared cerebral hemorrhage (25,28,31,32,33,34,35). Recent studies, however, have shown that early anticoagulation in cases with embolic stroke can safely be applied, provided general contraindications are absent and cerebral hemorrhage and HI are excluded by CT (17,18,19,26,29).…”

Section: Discussionmentioning

confidence: 99%

CT-detected hemorrhagic infarction; relation with the size of the infarct, and the presence of midline shift

Lodder

2009

Acta Neurologica Scandinavica

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The incidence of mass effect indicated by midline shift, and the incidence of hemorrhagic infarction were studied in 952 consecutive CT scans with supratentorial infarcts. Hemorrhagic infarction was found in 5.1 % indicating that the incidence of hemorrhagic infarction during life is far less than was suggested from pathological studies. Midline shift was found in 3.6% and, accordingly, the chance of finding a hemorrhagic infarct with mass effect indicated by a shift of the midline would be 0.2% if these 2 phenomena were not related. However, this incidence appeared to be 12 times higher, indicating they are closely related. In addition, the incidence of hemorrhagic infarcts and midline shift were both related to large infarcts with bad outcome. Cardiac emboli were not more prevalent in patients with hemorrhagic infarcts than in a control series, indicating that cardiac emboli do not produce hemorrhagic infarction more often than other causes of cerebral infarction, and that cardiac embolic cause cannot be inferred from hemorrhagic infarction on CT. This probably also applies to carotid emboli. When anticoagulation is considered in patients with cerebral infarction, CT-confirmed hemorrhagic infarction and shift of midline structures as well as decreased consciousness are contraindications to such treatment. In their absence, and in the absence of general contraindications, anticoagulant treatment can safely be started.

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Section: Discussionmentioning

confidence: 99%

CT-detected hemorrhagic infarction; relation with the size of the infarct, and the presence of midline shift

Lodder

2009

Acta Neurologica Scandinavica

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“…Millikan (1979) recommended immediate intravenous heparin in the face of minimal deficit but a three to five day delay if the deficit is judged severe. Brown and Poskanzer (1969) advocated anticoagulation as soon as the diagnosis of cerebral embolism is established or at least within forty-eight hours. Easton and Sherman (1980) in their recent review of cerebral embolism supported the view of Marshall (1976) in namely immediate therapy so long as the CSF is clear and the clinical deficit is not severe.…”

Section: Therapeutic Considerationsmentioning

confidence: 99%

Anticoagulation in Cerebral Embolism

Bass

1983

Can. j. neurol. sci.

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SUMMARY:A case of presumed anticoagulant induced hemorrhage into infarction is presented along with a retrospective study of 110 cases of cerebral embolus.An accurate recommendation for the timing of anticoagulation following cerebral embolism hinges on balancing the risk of hemorrhage into infarction against the benefits of early treatment attributed to preventing recurrent embolism. It is felt that the present literature, concepts of pathogenesis and experimental data provide insufficient information to make absolute clinical decisions. The available evidence implies that the risk of further embolic events is three to four times that of hemorrhage into infarction, yet additional randomized prospective studies and better experimental models are needed to establish a valid treatment plan. It may be possible to distinguish separate mechanisms underlying early diffuse hemorrhage into infarction from sudden delayed massive hematoma formation.

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“…Potential therapy modalities include microsurgical embolectomy- Chou (1963), Ya~argil et al (1970), Piscal (1973, Jacobson et al (1962), and Khodadad (]973) or revascularization -Crowell etal. (1973), hypothermia, pressor agents- Browne (1969) corticoids, Patten et al (1971) hyperventilation- Soloway et al (1968), Cooper et al (1970) and barbiturates-Smith et al (1974), but there are no clinical or experimental guidelines as to their use and timing at present.…”

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confidence: 99%

Experimental middle cerebral artery microsurgical embolectomy

et al. 1976

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The canine middle cerebral has been embolized using the method of Molinari. Microsurgical embolectomies were done at two hours and six hours post-embolism. Animals done at two hours remained virtually intact neurologically, and hence fared better than control dogs whose embolus remained in place. Animals done six hours post embolism had increased neurologic morbidity and mortality as compared to the controls. Pathologic study revealed hemorrhagic infarctions in 50% of the animals done six hours post embolism.

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Treatment of Strokes

Cited by 55 publications

References 57 publications

CT-detected hemorrhagic infarction; relation with the size of the infarct, and the presence of midline shift

CT-detected hemorrhagic infarction; relation with the size of the infarct, and the presence of midline shift

Anticoagulation in Cerebral Embolism

Experimental middle cerebral artery microsurgical embolectomy

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