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Cerebral Perfusion Pressure Thresholds for Brain Tissue Hypoxia and Metabolic Crisis After Poor-Grade Subarachnoid Hemorrhage

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Background and Purpose— To identify a minimally acceptable cerebral perfusion pressure threshold above which the risks of brain tissue hypoxia (BTH) and oxidative metabolic crisis are reduced for patients with subarachnoid hemorrhage (SAH). Methods— We studied 30 poor-grade SAH patients who underwent brain multimodality monitoring (3042 hours). Physiological measures were averaged over 60 minutes for each collected microdialysis sample. Metabolic crisis was defined as a lactate/pyruvate ratio >40 with a brain glucose concentration ≤0.7 mmol/L. BTH was defined as P bt O 2 <20 mm Hg. Outcome was assessed at 3 months with the Modified Rankin Scale. Results— Multivariable analyses adjusting for admission Hunt-Hess grade, intraventricular hemorrhage, systemic glucose, and end-tidal CO 2 revealed that cerebral perfusion pressure ≤70 mm Hg was significantly associated with an increased risk of BTH (OR, 2.0; 95% CI, 1.2–3.3; P =0.007) and metabolic crisis (OR, 2.1; 95% CI, 1.2–3.7; P =0.007). Death or severe disability at 3 months was significantly associated with metabolic crisis (OR, 5.4; 95% CI, 1.8–16; P =0.002) and BTH (OR, 5.1; 95% CI, 1.2–23; P =0.03) after adjusting for admission Hunt-Hess grade. Conclusions— Metabolic crisis and BTH are associated with mortality and poor functional recovery after SAH. Cerebral perfusion pressure levels <70 mm Hg was associated with metabolic crisis and BTH, and may increase the risk of secondary brain injury in poor-grade SAH patients.
Title: Cerebral Perfusion Pressure Thresholds for Brain Tissue Hypoxia and Metabolic Crisis After Poor-Grade Subarachnoid Hemorrhage
Description:
Background and Purpose— To identify a minimally acceptable cerebral perfusion pressure threshold above which the risks of brain tissue hypoxia (BTH) and oxidative metabolic crisis are reduced for patients with subarachnoid hemorrhage (SAH).
Methods— We studied 30 poor-grade SAH patients who underwent brain multimodality monitoring (3042 hours).
Physiological measures were averaged over 60 minutes for each collected microdialysis sample.
Metabolic crisis was defined as a lactate/pyruvate ratio >40 with a brain glucose concentration ≤0.
7 mmol/L.
BTH was defined as P bt O 2 <20 mm Hg.
Outcome was assessed at 3 months with the Modified Rankin Scale.
Results— Multivariable analyses adjusting for admission Hunt-Hess grade, intraventricular hemorrhage, systemic glucose, and end-tidal CO 2 revealed that cerebral perfusion pressure ≤70 mm Hg was significantly associated with an increased risk of BTH (OR, 2.
0; 95% CI, 1.
2–3.
3; P =0.
007) and metabolic crisis (OR, 2.
1; 95% CI, 1.
2–3.
7; P =0.
007).
Death or severe disability at 3 months was significantly associated with metabolic crisis (OR, 5.
4; 95% CI, 1.
8–16; P =0.
002) and BTH (OR, 5.
1; 95% CI, 1.
2–23; P =0.
03) after adjusting for admission Hunt-Hess grade.
Conclusions— Metabolic crisis and BTH are associated with mortality and poor functional recovery after SAH.
Cerebral perfusion pressure levels <70 mm Hg was associated with metabolic crisis and BTH, and may increase the risk of secondary brain injury in poor-grade SAH patients.

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