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1. Optimal Cerebral Perfusion Pressure During Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Author

Weiss, M., Weiss, M., Albanna, W., Conzen, C., Megjhani, M., Tas, J., Seyfried, K., Kastenholz, N., Veldeman, M., Schmidt, T.P., Schulze-Steinen, H., Wiesmann, M., Clusmann, H., Park, S., Aries, M., Schubert, G.A., Weiss, M., Weiss, M., Albanna, W., Conzen, C., Megjhani, M., Tas, J., Seyfried, K., Kastenholz, N., Veldeman, M., Schmidt, T.P., Schulze-Steinen, H., Wiesmann, M., Clusmann, H., Park, S., Aries, M., and Schubert, G.A.

Abstract

OBJECTIVES: The recommendation of induced hypertension for delayed cerebral ischemia treatment after aneurysmal subarachnoid hemorrhage has been challenged recently and ideal pressure targets are missing. A new concept advocates an individual cerebral perfusion pressure where cerebral autoregulation functions best to ensure optimal global perfusion. We characterized optimal cerebral perfusion pressure at time of delayed cerebral ischemia and tested the conformity of induced hypertension with this target value. DESIGN: Retrospective analysis of prospectively collected data. SETTING: University hospital neurocritical care unit. PATIENTS: Thirty-nine aneurysmal subarachnoid hemorrhage patients with invasive neuromonitoring (20 with delayed cerebral ischemia, 19 without delayed cerebral ischemia). INTERVENTIONS: Induced hypertension greater than 180 mm Hg systolic blood pressure. MEASUREMENTS AND MAIN RESULTS: Changepoint analysis was used to calculate significant changes in cerebral perfusion pressure, optimal cerebral perfusion pressure, and the difference of cerebral perfusion pressure and optimal cerebral perfusion pressure 48 hours before delayed cerebral ischemia diagnosis. Optimal cerebral perfusion pressure increased 30 hours before the onset of delayed cerebral ischemia from 82.8 +/- 12.5 to 86.3 +/- 11.4 mm Hg (p < 0.05). Three hours before delayed cerebral ischemia, a changepoint was also found in the difference of cerebral perfusion pressure and optimal cerebral perfusion pressure (decrease from -0.2 +/- 11.2 to -7.7 +/- 7.6 mm Hg; p < 0.05) with a corresponding increase in pressure reactivity index (0.09 +/- 0.33 to 0.19 +/- 0.37; p < 0.05). Cerebral perfusion pressure at time of delayed cerebral ischemia was lower than in patients without delayed cerebral ischemia in a comparable time frame (cerebral perfusion pressure delayed cerebral ischemia 81.4 +/- 8.3 mm Hg, no delayed cerebral ischemia 90.4 +/- 10.5 mm Hg; p < 0.05). Inducing hypertensio

Published
2022

2. Optimal Cerebral Perfusion Pressure During Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Author

Weiss, M., Albanna, W., Conzen, C., Megjhani, M., Tas, J., Seyfried, K., Kastenholz, N., Veldeman, M., Schmidt, T.P., Schulze-Steinen, H., Wiesmann, M., Clusmann, H., Park, S., Aries, M., Schubert, G.A., Weiss, M., Albanna, W., Conzen, C., Megjhani, M., Tas, J., Seyfried, K., Kastenholz, N., Veldeman, M., Schmidt, T.P., Schulze-Steinen, H., Wiesmann, M., Clusmann, H., Park, S., Aries, M., and Schubert, G.A.

Abstract

OBJECTIVES: The recommendation of induced hypertension for delayed cerebral ischemia treatment after aneurysmal subarachnoid hemorrhage has been challenged recently and ideal pressure targets are missing. A new concept advocates an individual cerebral perfusion pressure where cerebral autoregulation functions best to ensure optimal global perfusion. We characterized optimal cerebral perfusion pressure at time of delayed cerebral ischemia and tested the conformity of induced hypertension with this target value. DESIGN: Retrospective analysis of prospectively collected data. SETTING: University hospital neurocritical care unit. PATIENTS: Thirty-nine aneurysmal subarachnoid hemorrhage patients with invasive neuromonitoring (20 with delayed cerebral ischemia, 19 without delayed cerebral ischemia). INTERVENTIONS: Induced hypertension greater than 180 mm Hg systolic blood pressure. MEASUREMENTS AND MAIN RESULTS: Changepoint analysis was used to calculate significant changes in cerebral perfusion pressure, optimal cerebral perfusion pressure, and the difference of cerebral perfusion pressure and optimal cerebral perfusion pressure 48 hours before delayed cerebral ischemia diagnosis. Optimal cerebral perfusion pressure increased 30 hours before the onset of delayed cerebral ischemia from 82.8 +/- 12.5 to 86.3 +/- 11.4 mm Hg (p < 0.05). Three hours before delayed cerebral ischemia, a changepoint was also found in the difference of cerebral perfusion pressure and optimal cerebral perfusion pressure (decrease from -0.2 +/- 11.2 to -7.7 +/- 7.6 mm Hg; p < 0.05) with a corresponding increase in pressure reactivity index (0.09 +/- 0.33 to 0.19 +/- 0.37; p < 0.05). Cerebral perfusion pressure at time of delayed cerebral ischemia was lower than in patients without delayed cerebral ischemia in a comparable time frame (cerebral perfusion pressure delayed cerebral ischemia 81.4 +/- 8.3 mm Hg, no delayed cerebral ischemia 90.4 +/- 10.5 mm Hg; p < 0.05). Inducing hypertensio

Published
2022

3. Invasive Multimodal Neuromonitoring in Aneurysmal Subarachnoid Hemorrhage A Systematic Review

Author

Veldeman, M., Veldeman, M., Albanna, W., Weiss, M., Park, S., Hoellig, A., Clusmann, H., Helbok, R., Temel, Y., Schubert, G.A., Veldeman, M., Veldeman, M., Albanna, W., Weiss, M., Park, S., Hoellig, A., Clusmann, H., Helbok, R., Temel, Y., and Schubert, G.A.

Abstract

Background and Purpose: Aneurysmal subarachnoid hemorrhage is a devastating disease leaving surviving patients often severely disabled. Delayed cerebral ischemia (DCI) has been identified as one of the main contributors to poor clinical outcome after subarachnoid hemorrhage. The objective of this review is to summarize existing clinical evidence assessing the diagnostic value of invasive neuromonitoring (INM) in detecting DCI and provide an update of evidence since the 2014 consensus statement on multimodality monitoring in neurocritical care. Methods: Three invasive monitoring techniques were targeted in the data collection process: brain tissue oxygen tension (p(ti)O(2)), cerebral microdialysis, and electrocorticography. Prospective and retrospective studies as well as case series (>= 10 patients) were included as long as monitoring was used to detect DCI or guide DCI treatment. Results: Forty-seven studies reporting INM in the context of DCI were included (p(ti)O(2): N=21; cerebral microdialysis: N=22; electrocorticography: N=4). Changes in brain oxygen tension are associated with angiographic vasospasm or reduction in regional cerebral blood flow. Metabolic monitoring with trend analysis of the lactate to pyruvate ratio using cerebral microdialysis, identifies patients at risk for DCI. Clusters of cortical spreading depolarizations are associated with clinical neurological worsening and cerebral infarction in selected patients receiving electrocorticography monitoring. Conclusions: Data supports the use of INM for the detection of DCI in selected patients. Generalizability to all subarachnoid hemorrhage patients is limited by design bias of available studies and lack of randomized trials. Continuous data recording with trend analysis and the combination of INM modalities can provide tailored treatment support in patients at high risk for DCI. Future trials should test interventions triggered by INM in relation to cerebral infarctions.

Published
2021

14. Optimal cerebral perfusion pressure for DCI after aneurysmal subarachnoid hemorrhage - a prospective observational study in the context of induced hypertension

Author

Weiss, M., Albanna, W., Conzen, C., Tas, J., Seyfried, K., Kastenholz, N., Veldeman, M., Schmidt, T., Schulze-Steinen, H., Wiesmann, M., Clusmann, H., Park, S., Aries, M. J.H., Schubert, G. A., Weiss, M., Albanna, W., Conzen, C., Tas, J., Seyfried, K., Kastenholz, N., Veldeman, M., Schmidt, T., Schulze-Steinen, H., Wiesmann, M., Clusmann, H., Park, S., Aries, M. J.H., and Schubert, G. A.

Published
2021

15. Invasive Multimodal Neuromonitoring in Aneurysmal Subarachnoid Hemorrhage A Systematic Review

Author

Veldeman, M., Albanna, W., Weiss, M., Park, S., Hoellig, A., Clusmann, H., Helbok, R., Temel, Y., Schubert, G.A., Veldeman, M., Albanna, W., Weiss, M., Park, S., Hoellig, A., Clusmann, H., Helbok, R., Temel, Y., and Schubert, G.A.

Abstract

Background and Purpose: Aneurysmal subarachnoid hemorrhage is a devastating disease leaving surviving patients often severely disabled. Delayed cerebral ischemia (DCI) has been identified as one of the main contributors to poor clinical outcome after subarachnoid hemorrhage. The objective of this review is to summarize existing clinical evidence assessing the diagnostic value of invasive neuromonitoring (INM) in detecting DCI and provide an update of evidence since the 2014 consensus statement on multimodality monitoring in neurocritical care. Methods: Three invasive monitoring techniques were targeted in the data collection process: brain tissue oxygen tension (p(ti)O(2)), cerebral microdialysis, and electrocorticography. Prospective and retrospective studies as well as case series (>= 10 patients) were included as long as monitoring was used to detect DCI or guide DCI treatment. Results: Forty-seven studies reporting INM in the context of DCI were included (p(ti)O(2): N=21; cerebral microdialysis: N=22; electrocorticography: N=4). Changes in brain oxygen tension are associated with angiographic vasospasm or reduction in regional cerebral blood flow. Metabolic monitoring with trend analysis of the lactate to pyruvate ratio using cerebral microdialysis, identifies patients at risk for DCI. Clusters of cortical spreading depolarizations are associated with clinical neurological worsening and cerebral infarction in selected patients receiving electrocorticography monitoring. Conclusions: Data supports the use of INM for the detection of DCI in selected patients. Generalizability to all subarachnoid hemorrhage patients is limited by design bias of available studies and lack of randomized trials. Continuous data recording with trend analysis and the combination of INM modalities can provide tailored treatment support in patients at high risk for DCI. Future trials should test interventions triggered by INM in relation to cerebral infarctions.

Published
2021

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