• J Neurosurg Anesthesiol · Sep 1990

    Transcranial Doppler sonography as a supplement in the detection of cerebral circulatory arrest.

    • C Werner, E Kochs, M Rau, and J Schulte Esch.
    • Department of Anesthesiology, University Hospital Eppendorf, Hamburg, West Germany.
    • J Neurosurg Anesthesiol. 1990 Sep 1;2(3):159-65.

    AbstractThe effects of compromised cerebral hemodynamics on intracranial blood flow velocity patterns (BFV) were studied by noninvasive transcranial Doppler sonography (TCD). Pulsatility index (PI) as an estimation of peripheral cerebral vascular resistance was additionally analyzed. TCD patterns were determined in 19 mechanically ventilated brain dead patients (group A) and 8 resuscitated or severely head injured patients (group B) with intermittent elevated intracranial pressure (ICP). Group A and B TCD data were compared to control measurements obtained in 20 healthy volunteers (group C). Normal TCD recordings (group C) were characterized by anterograde Doppler wave-forms with a predominantly high diastolic flow pattern and PI values of <1. In brain dead patients (group A), flow velocity profiles were significantly decreased. The flow curve consisted of low systolic anterograde spikes, while early diastolic flow components of low amplitudes revealed retrograde phases with a late diastolic zero flow. In some cases, total diastolic circulatory arrest was obtained. PI in brain dead patients was increased by a factor of 10 and was infinite in situations of zero net flow. The low systolic spikes and retrograde diastolic flow may be explained by the effects of reduced intracranial compliance due to increased intracranial pressure (ICP). The detection of bidirectional signals, indicating anterograde and retrograde movements of the blood column or low systolic spikes without diastolic signals, seems to be specific for the condition of brain death. Insonation of the basilar artery should be performed in order to exclude preserved perfusion of infratentorial brain regions during supratentorial circulatory arrest and vice versa. In group B patients, episodes of increased ICP predominantly affected the diastolic flow velocity component. In these patients, resistive Doppler signals with normal or reduced systolic peaks and decreased diastolic flow velocities were expressed as increases in PI. Noninvasive transcranial Doppler sonography appears to confirm cerebral circulatory arrest. Additionally, TCD may be of value for the early detection of impaired cerebral hemodynamics due to changes in intracranial compliance.

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