Update: Microdialysis for Monitoring Cerebral Metabolic Dysfunction after Subarachnoid Hemorrhage

• Published in: Journal of clinical medicine Vol. 10; no. 1; p. 100
• Main Authors: Spencer, Pierce, Jiang, Yinghua, Liu, Ning, Han, Jinrui, Li, Yadan, Vodovoz, Samuel, Dumont, Aaron S, Wang, Xiaoying
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 30-12-2020; MDPI
• Subjects: Apoptosis; Bioenergetics; Clinical medicine; Clinical trials; Energy shortages; Glucose; Hemoglobin; Hemorrhage; Ischemia; Metabolism; Metabolites; Mortality; Patients; Phosphorylation; Review; Smooth muscle; Traumatic brain injury; brain metabolism; cerebral microdialysis; subarachnoid hemorrhage; metabolic dysfunction; brain bioenergetics
• ISSN: 2077-0383; 2077-0383
• DOI: 10.3390/jcm10010100

Cerebral metabolic dysfunction has been shown to extensively mediate the pathophysiology of brain injury after subarachnoid hemorrhage (SAH). The characterization of the alterations of metabolites in the brain can help elucidate pathophysiological changes occurring throughout SAH and the relationship between secondary brain injury and cerebral energy dysfunction after SAH. Cerebral microdialysis (CMD) is a tool that can measure concentrations of multiple bioenergetics metabolites in brain interstitial fluid. This review aims to provide an update on the implication of CMD on the measurement of metabolic dysfunction in the brain after SAH. A literature review was conducted through a general PubMed search with the terms "Subarachnoid Hemorrhage AND Microdialysis" as well as a more targeted search using MeSh with the search terms "Subarachnoid hemorrhage AND Microdialysis AND Metabolism." Both experimental and clinical papers were reviewed. CMD is a suitable tool that has been used for monitoring cerebral metabolic changes in various types of brain injury. Clinically, CMD data have shown the dramatic changes in cerebral metabolism after SAH, including glucose depletion, enhanced glycolysis, and suppressed oxidative phosphorylation. Experimental studies using CMD have demonstrated a similar pattern of cerebral metabolic dysfunction after SAH. The combination of CMD and other monitoring tools has also shown value in further dissecting and distinguishing alterations in different metabolic pathways after brain injury. Despite the lack of a standard procedure as well as the presence of limitations regarding CMD application and data interpretation for both clinical and experimental studies, emerging investigations have suggested that CMD is an effective way to monitor the changes of cerebral metabolic dysfunction after SAH in real-time, and alternatively, the combination of CMD and other monitoring tools might be able to further understand the relationship between cerebral metabolic dysfunction and brain injury after SAH, determine the severity of brain injury and predict the pathological progression and outcomes after SAH. More translational preclinical investigations and clinical validation may help to optimize CMD as a powerful tool in critical care and personalized medicine for patients with SAH.