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Published on: August 30, 2020
Cerebrovascular carbon dioxide reactivity and delayed cerebral ischemia after subarachnoid hemorrhage
Emmanuel Carrera1, Pedro Kurtz, Neeraj Badjatia
1Division of Neurocritical Care, Department of Neurology, Columbia University Medical Center, New York, New York 10032, USA.
Insights
Impaired cerebrovascular reactivity (CVR) after subarachnoid hemorrhage (SAH) is common, especially in poor-grade patients. Progressive CVR loss predicts delayed cerebral ischemia (DCI), while normal CVR indicates a low risk.
Area of Science:
- Neuroscience
- Neurology
- Critical Care Medicine
Background:
- Subarachnoid hemorrhage (SAH) poses significant risks, including delayed cerebral ischemia (DCI).
- Cerebrovascular reactivity (CVR) is crucial for maintaining cerebral blood flow.
- Predicting DCI is vital for timely intervention in SAH patients.
Purpose of the Study:
- To identify predictors of impaired CVR following SAH.
- To assess the predictive value of CVR for the development of DCI.
- To understand the temporal changes in CVR after SAH.
Main Methods:
- Prospective observational study involving 34 acute SAH patients.
- CVR measured using middle cerebral artery blood flow velocity response to CO2 challenge in three periods post-SAH.
- Normal CVR defined as >2% increase in mean blood flow velocity per 1-mm Hg increase in PCO2.
Main Results:
- DCI occurred in 29% of patients.
- Impaired CVR was more frequent in patients with poor clinical grades.
- Patients who developed DCI showed progressively lower CVR in later periods (P < .001).
- A decrease in CVR between early periods and a high Hunt-Hess score independently predicted DCI.
Conclusions:
- Impaired CVR is common after SAH, particularly in those with poor clinical grades.
- Progressive loss of CVR is a significant predictor of DCI.
- Persistently normal CVR suggests a low risk of DCI.
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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