Jae Hyun Kim1,*, Yoon Hee Choo2,*, Moinay Kim1, Hanwool Jeon1, Hee-Won Jung3, Eun Jin Ha4, JIWOONG OH5, Youngbo Shim6, Seung Bin Kim7, Han-Gil Jung7, So Hee Park8, Jung Ook Kim9, Junhyung Kim10, Hyeseon Kim11, Seungjoo Lee,1
Abstract
Neuro-critically ill patients face unique challenges in nutritional support due to varying metabolic and energy demands arising from clinical situations such as elevated intracranial pressure, trauma, stroke, epilepsy, targeted temperature management (TTM), and pharmacological interventions. Despite these challenges, there is a lack of systematic reviews addressing their specific needs. This study conducts a systematic review and narrative synthesis of the existing literature on nutritional support for neuro-critical patients, focusing on amino acids that act as neurotransmitters or their precursors. We examined nutritional requirements and timing in patients with stroke and traumatic brain injury, as well as energy and metabolic demands during TTM, a common therapeutic intervention in neuro-critical care. Our review aims to clarify uncertainties surrounding amino acid provision in neuro-critical patients and provide up-to-date recommendations on nutritional support for those with elevated intracranial pressure and undergoing TTM, serving as a foundation for future research and evidence-based guideline development. Key findings include the potential benefits of branched-chain amino acids (BCAAs) in neuro-critical care, the roles of methionine and serine, the significance of arginine in vascular constriction, the controversial role of glutamate in nutrition, and the potential benefits of selenium supplementation. We also discussed special considerations in nutritional support for neuro-critical patients, such as changes in energy demand, the influence of sedation on energy demand, and metabolism changes during TTM. Our review highlights the need for a better understanding of the unique metabolic requirements of neuro-critical patients and the development of evidence-based guidelines for optimal nutritional support in this population.
Fig. 3.
Mechanisms of neuronal damage in traumatic brain injury and the involvement of essential amino acid metabolism. This figure illustrates the interconnected mechanisms contributing to neuronal damage following brain injury and the role of essential amino acid metabolism. (A) Sequential events in the cascade include: 1) brain injury triggering glutamate release, which leads to calcium overload, followed by activation of calcium-regulated proteins such as calpain and calcineurin, ultimately resulting in proteolysis and neuronal degeneration; 2) calcium overload causing oxidative stress and lipid peroxidation of proteins and DNA, which contribute to neuronal degeneration; 3) calcium overload inducing mitochondrial dysfunction, followed by MTP opening, cytochrome C release, apoptosis, and neuronal degeneration. (B) The metabolism of branched-chain amino acids (BCAAs) involves their conversion to branched-chain keto acids by the branched-chain dehydrogenase complex, and the subsequent formation of ketone bodies, which play a role in the overall mechanism of neuronal damage.
서울아산병원 이승주교수님 연구실 202410 작성
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