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CBF changes and cerebral energy metabolism during hypervolemia, hemodilution, and hypertension therapy in patients with poor-grade subarachnoid hemorrhage.
J Neurosurg. 2020 Jan 10 [Online ahead of print]JN

Abstract

OBJECTIVE

Despite the multifactorial pathogenesis of delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH), augmentation of cerebral blood flow (CBF) is still considered essential in the clinical management of DCI. The aim of this prospective observational study was to investigate cerebral metabolic changes in relation to CBF during therapeutic hypervolemia, hemodilution, and hypertension (HHH) therapy in poor-grade SAH patients with DCI.

METHODS

CBF was assessed by bedside xenon-enhanced CT at days 0-3, 4-7, and 8-12, and the cerebral metabolic state by cerebral microdialysis (CMD), analyzing glucose, lactate, pyruvate, and glutamate hourly. At clinical suspicion of DCI, HHH therapy was instituted for 5 days. CBF measurements and CMD data at baseline and during HHH therapy were required for study inclusion. Non-DCI patients with measurements in corresponding time windows were included as a reference group.

RESULTS

In DCI patients receiving HHH therapy (n = 12), global cortical CBF increased from 30.4 ml/100 g/min (IQR 25.1-33.8 ml/100 g/min) to 38.4 ml/100 g/min (IQR 34.2-46.1 ml/100 g/min; p = 0.006). The energy metabolic CMD parameters stayed statistically unchanged with a lactate/pyruvate (L/P) ratio of 26.9 (IQR 22.9-48.5) at baseline and 31.6 (IQR 22.4-35.7) during HHH. Categorized by energy metabolic patterns during HHH, no patient had severe ischemia, 8 showed derangement corresponding to mitochondrial dysfunction, and 4 were normal. The reference group of non-DCI patients (n = 11) had higher CBF and lower L/P ratios at baseline with no change over time, and the metabolic pattern was normal in all these patients.

CONCLUSIONS

Global and regional CBF improved and the cerebral energy metabolic CMD parameters stayed statistically unchanged during HHH therapy in DCI patients. None of the patients developed metabolic signs of severe ischemia, but a disturbed energy metabolic pattern was a common occurrence, possibly explained by mitochondrial dysfunction despite improved microcirculation.

Authors+Show Affiliations

Departments of1Neuroscience/Neurosurgery and. 2Surgical Sciences/Anesthesia and Intensive Care, Uppsala University, Uppsala, Sweden.Departments of1Neuroscience/Neurosurgery and.Departments of1Neuroscience/Neurosurgery and.Departments of1Neuroscience/Neurosurgery and.Departments of1Neuroscience/Neurosurgery and.Departments of1Neuroscience/Neurosurgery and.Departments of1Neuroscience/Neurosurgery and.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31923897

Citation

Engquist, Henrik, et al. "CBF Changes and Cerebral Energy Metabolism During Hypervolemia, Hemodilution, and Hypertension Therapy in Patients With Poor-grade Subarachnoid Hemorrhage." Journal of Neurosurgery, 2020, pp. 1-10.
Engquist H, Lewén A, Hillered L, et al. CBF changes and cerebral energy metabolism during hypervolemia, hemodilution, and hypertension therapy in patients with poor-grade subarachnoid hemorrhage. J Neurosurg. 2020.
Engquist, H., Lewén, A., Hillered, L., Ronne-Engström, E., Nilsson, P., Enblad, P., & Rostami, E. (2020). CBF changes and cerebral energy metabolism during hypervolemia, hemodilution, and hypertension therapy in patients with poor-grade subarachnoid hemorrhage. Journal of Neurosurgery, 1-10. https://doi.org/10.3171/2019.11.JNS192759
Engquist H, et al. CBF Changes and Cerebral Energy Metabolism During Hypervolemia, Hemodilution, and Hypertension Therapy in Patients With Poor-grade Subarachnoid Hemorrhage. J Neurosurg. 2020 Jan 10;1-10. PubMed PMID: 31923897.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - CBF changes and cerebral energy metabolism during hypervolemia, hemodilution, and hypertension therapy in patients with poor-grade subarachnoid hemorrhage. AU - Engquist,Henrik, AU - Lewén,Anders, AU - Hillered,Lars, AU - Ronne-Engström,Elisabeth, AU - Nilsson,Pelle, AU - Enblad,Per, AU - Rostami,Elham, Y1 - 2020/01/10/ PY - 2019/10/10/received PY - 2019/11/05/accepted PY - 2020/1/11/entrez PY - 2020/1/11/pubmed PY - 2020/1/11/medline KW - ACA = anterior cerebral artery KW - CBF = cerebral blood flow KW - CMD = cerebral microdialysis KW - CPP = cerebral perfusion pressure KW - DCI = delayed cerebral ischemia KW - GCS = Glasgow Coma Scale KW - HHH = hypervolemia, hemodilution, and hypertension KW - ICP = intracranial pressure KW - L/P = lactate/pyruvate KW - MAP = mean arterial pressure KW - MCA = middle cerebral artery KW - NIC = neurosurgical intensive care KW - PCA = posterior cerebral artery KW - ROI = region of interest KW - SAH = subarachnoid hemorrhage KW - SBP = systolic blood pressure KW - TBI = traumatic brain injury KW - XeCT = xenon-enhanced CT KW - and hemodilution therapy KW - cerebral blood flow KW - cerebral microdialysis KW - delayed cerebral ischemia KW - hypertension KW - hypervolemia KW - rCBF = regional CBF KW - subarachnoid hemorrhage KW - triple-H KW - vascular disorders KW - xenon CT SP - 1 EP - 10 JF - Journal of neurosurgery JO - J. Neurosurg. N2 - OBJECTIVE: Despite the multifactorial pathogenesis of delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH), augmentation of cerebral blood flow (CBF) is still considered essential in the clinical management of DCI. The aim of this prospective observational study was to investigate cerebral metabolic changes in relation to CBF during therapeutic hypervolemia, hemodilution, and hypertension (HHH) therapy in poor-grade SAH patients with DCI. METHODS: CBF was assessed by bedside xenon-enhanced CT at days 0-3, 4-7, and 8-12, and the cerebral metabolic state by cerebral microdialysis (CMD), analyzing glucose, lactate, pyruvate, and glutamate hourly. At clinical suspicion of DCI, HHH therapy was instituted for 5 days. CBF measurements and CMD data at baseline and during HHH therapy were required for study inclusion. Non-DCI patients with measurements in corresponding time windows were included as a reference group. RESULTS: In DCI patients receiving HHH therapy (n = 12), global cortical CBF increased from 30.4 ml/100 g/min (IQR 25.1-33.8 ml/100 g/min) to 38.4 ml/100 g/min (IQR 34.2-46.1 ml/100 g/min; p = 0.006). The energy metabolic CMD parameters stayed statistically unchanged with a lactate/pyruvate (L/P) ratio of 26.9 (IQR 22.9-48.5) at baseline and 31.6 (IQR 22.4-35.7) during HHH. Categorized by energy metabolic patterns during HHH, no patient had severe ischemia, 8 showed derangement corresponding to mitochondrial dysfunction, and 4 were normal. The reference group of non-DCI patients (n = 11) had higher CBF and lower L/P ratios at baseline with no change over time, and the metabolic pattern was normal in all these patients. CONCLUSIONS: Global and regional CBF improved and the cerebral energy metabolic CMD parameters stayed statistically unchanged during HHH therapy in DCI patients. None of the patients developed metabolic signs of severe ischemia, but a disturbed energy metabolic pattern was a common occurrence, possibly explained by mitochondrial dysfunction despite improved microcirculation. SN - 1933-0693 UR - https://www.unboundmedicine.com/medline/citation/31923897/CBF_changes_and_cerebral_energy_metabolism_during_hypervolemia_hemodilution_and_hypertension_therapy_in_patients_with_poor_grade_subarachnoid_hemorrhage_ L2 - https://thejns.org/doi/10.3171/2019.11.JNS192759 DB - PRIME DP - Unbound Medicine ER -
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