Key result
A decrease in cerebrovascular reactivity between days 0-3 and 4-7 independently predicted delayed cerebral ischemia (P=0.03) in patients with acute subarachnoid hemorrhage.
Why the study?
Does impaired cerebrovascular reactivity to carbon dioxide challenge predict delayed cerebral ischemia in patients with acute subarachnoid hemorrhage?
Observational (n=34)
No
Does impaired cerebrovascular reactivity to carbon dioxide challenge predict delayed cerebral ischemia in patients with acute subarachnoid hemorrhage?
p-value: p=0.03
Progressive loss of normal cerebrovascular reactivity to carbon dioxide challenge identifies patients at high risk for delayed cerebral ischemia after subarachnoid hemorrhage.
May support early risk stratification for delayed cerebral ischemia after subarachnoid hemorrhage; leaves open whether reactivity monitoring improves outcomes.
OBJECTIVE: To determine the predictors of impaired cerebrovascular reactivity (CVR) and the value of CVR in predicting delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH). DESIGN: Prospective observational study. We evaluated CVR during the following intervals: period 1, SAH days 0 to 3; period 2, SAH days 4 to 7; and period 3, SAH days 8 to 10. Normal CVR was defined as an increase in mean blood flow velocity of at least 2% per 1-mm Hg increase in PCO(2). SETTING: Neurointensive care unit of the Columbia Presbyterian Medical Center. PATIENTS: Thirty-four consecutive patients with acute SAH who underwent measurement of changes in the middle cerebral artery mean blood flow velocity after carbon dioxide challenge. MAIN OUTCOME MEASURE: Occurrence of DCI. RESULTS: Delayed cerebral ischemia occurred in 10 patients (29%). Impaired CVR was more frequent in patients with a poor clinical grade on admission and at the time of examination. During period 1, there was only a trend toward lower CVR in patients who later developed DCI (1.1% vs 1.9% per 1-mm Hg increase in PCO(2); P = .07). However, those who developed DCI had progressively lower CVR during periods 2 (0.7%/mm Hg vs 2.1%/mm Hg; P < .001) and 3 (0.6%/mm Hg vs 2.4%/mm Hg; P < .001). Independent predictors of DCI included a decrease in CVR between periods 1 and 2 (P = .03) and a poor Hunt-Hess score (P = .04). Impaired CVR at any point had a sensitivity for subsequent DCI of 91% and a specificity of 49%. CONCLUSIONS: Impaired CVR in response to carbon dioxide challenge is frequent after SAH, particularly in patients with a poor clinical grade. Progressive loss of normal CVR identifies patients at high risk for DCI, and persistently normal reactivity implies a low risk.
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Carrera et al. (2010) conducted an observational in Acute subarachnoid hemorrhage (n=34). Decrease in cerebrovascular reactivity (CVR) vs. Normal or persistently normal CVR was evaluated on Occurrence of delayed cerebral ischemia (DCI) (p=0.03). A decrease in cerebrovascular reactivity between days 0-3 and 4-7 independently predicted delayed cerebral ischemia (P=0.03) in patients with acute subarachnoid hemorrhage.
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