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Original Articles| Volume 12, ISSUE 2, P88-92, March 2003

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Transcranial doppler monitoring and clinical decision-making after subarachnoid hemorrhage

  • Matthew J. McGirt
    Affiliations
    From the *School of Medicine, †‡Department of Medicine (Neurology), ‡Duke Center for Cerebrovascular Disease, and the ‡Center for Clinical Health Policy Research, Duke University, and the ‡Durham VA Medical Center, Durham, NC
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  • Robert P. Blessing
    Affiliations
    From the *School of Medicine, †‡Department of Medicine (Neurology), ‡Duke Center for Cerebrovascular Disease, and the ‡Center for Clinical Health Policy Research, Duke University, and the ‡Durham VA Medical Center, Durham, NC
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  • Larry B. Goldstein
    Affiliations
    From the *School of Medicine, †‡Department of Medicine (Neurology), ‡Duke Center for Cerebrovascular Disease, and the ‡Center for Clinical Health Policy Research, Duke University, and the ‡Durham VA Medical Center, Durham, NC
    Search for articles by this author

      Abstract

      Our objective was to examine the impact of transcranial Doppler ultrasound (TCD) vasospasm monitoring on clinical decision-making following subarachnoid hemorrhage (SAH). The records of 50 randomly selected patients undergoing serial TCD monitoring following SAH were reviewed. Dates and results of TCDs and cerebral angiograms, the use of hypertensive hemodilution (HH) therapy, and the development of new neurological deficits were recorded. The independent effects of TCD-defined vasospasm and new neurological deficits on patient management were determined with multiple logistical regression. Results were validated in a second randomly selected, 50 patient cohort. Mild or moderate TCD-defined vasospasm developed in 76% of patients 5.8 ± 0.5 days after SAH; 38% developed severe TCD-defined vasospasm after 7.9 ± 0.7 days. Focal neurological deficits occurred in 50% after 5.7 ± 0.6 days with TCD abnormalities preceding the deficit by 2.5 ± 0.7 days in 64%. TCD-defined vasospasm or a new neurological deficit explained 60% of the variance in the use of HH therapy (P =.005). New neurological deficits increased the odds of HH therapy 33-fold (P =.004) whereas there was no independent effect of TCD-defined vasospasm. These variables explained 64% of the variance in the performance of angiography (P =.0002). An abnormal TCD did not increase the odds of angiography whereas its use increased 28-fold (P =.01) after a neurological deficit developed. These results were confirmed in an independent cohort. We concluded that TCD-defined vasospasm did not independently influence the use of HH therapy or angiography with both decisions associated with the development of new neurological deficits. As TCD-defined vasospasm preceded the neurological deficit in 64%, earlier intervention might reduce the incidence of vasospasm-related stroke in institutions with similar practice patterns. Copyright © 2003 by National Stroke Association

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