Neurosonology:神経超音波医学
Print ISSN : 0917-074X
ISSN-L : 0917-074X
重症脳障害患者の連続的TCDモニタリングの意義―頭蓋内圧亢進, 脳虚血, 脳機能障害との関連から―
塩貝 敏之野口 明男佐藤 栄志斎藤 勇
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1994 年 7 巻 2 号 p. 104-109

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To clarify the significance of transcranial Doppler (TCD) monitoring for detection of raised intracranial pressure (ICP), cerebral ischemia, and neuronal dysfunction in comatose patients with severe brain damage, vasoreactive correlations during hyperventilation (HV) and changes in cerebral perfusion pressure (CPP) were evaluated by continuous monitoring of TCD in the middle cerebral artery, jugular bulb oxygen saturation (SjO2), end-tidal CO2partial pressure, ICP and CPP, and quantitative EEG (qEEG) . TCD and gEEG (total and spectral power bands) were monitored in a total of 32 cases of severe head injury, CPP in 26, and SjO2in 16 for 7 days (mean) . Peak systolic, mean, and end-diastolic velocity (Vs, Vm, Vd), pulsatility index (PI), resistance index, and cerebrovascular resistance (CVR=CPP/Vm) were evaluated. a) CO2reactivity (ΔVm/ΔCO2, ΔSjO2/ΔCO2) and correlations with ICP and SjO2were compared within ischemic, normal, and hyperemic groups, based on minimal SjO2during HV. b) Effects of CPP changes were correlated with gEEG. a) HV: 1) No significant differences in TCD parameters and ΔVm/ΔCO2were observed among the three groups. However, ΔSjO2/ΔCO2was significantly high in the order of ischemic>normal> hyperemic groups. 2) Close correlations of ICP with Vm and CVR were identified. 3) Significant correlations of SjO2with CVR, Vm, Vs, and PI were observed frequently in the ischemic group. b) CPP: 1) In cases of close correlation between CPP (<60 mmHg) and Vm, there were significant correlations between all gEEG power bands and Vm. 2) Loss of gEEG was observed in four cases of Vm<36 cm/s, Vd=0, and PI>2.74. Continuous TCD monitoring is useful for the early detection of decreased cerebral circulation and increased CVR associated with intracranial hypertension, cerebral ischemia, and neuronal dysfunction, but not always for easy interpretation of the underlying pathophysiology in patients with severe brain damage.

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