Jae Hyun Kim 1, Heewon Jeong 2, Yoon-Hee Choo 3, Moinay Kim 1, Eun Jin Ha 4, Jiwoong Oh 5, Youngbo Shim 6, Seung Bin Kim 7, Han-Gil Jung 8, So Hee Park 9, Jung Ook Kim 10, Junhyung Kim 11, Hye Seon Kim 12, Seungjoo Lee 1
Abstract
Mannitol, derived from mannose sugar, is crucial in treating patients with elevated intracranial pressure (ICP). Its dehydrating properties at the cellular and tissue levels increase plasma osmotic pressure, which is studied for its potential to reduce ICP through osmotic diuresis. While clinical guidelines support mannitol use in these cases, the best approach for its application continues to be debated. Important aspects needing further investigation include: 1) bolus administration versus continuous infusion, 2) ICP-based dosing versus scheduled bolus, 3) identifying the optimal infusion rate, 4) determining the appropriate dosage, 5) establishing fluid replacement plans for urinary loss, and 6) selecting monitoring techniques and thresholds to assess effectiveness and ensure safety. Due to the lack of adequate high-quality prospective research data, a comprehensive review of recent studies and clinical trials is crucial. This assessment aims to bridge the knowledge gap, improve understanding of effective mannitol use in elevated ICP patients, and provide insights for future research. In conclusion, this review aspires to contribute to the ongoing discourse on mannitol application. By integrating the latest findings, this review will offer valuable insights into the function of mannitol in decreasing ICP, thereby informing better therapeutic approaches and enhancing patient outcomes.
Keywords: Hypertonic solutions; Intracranial pressure; Mannitol; Osmolar concentration.
FIGURE 2. Mannitol metabolism and its influence on the glycolytic pathway.
This figure presents an overview of the metabolic pathway of mannitol and its interaction with the glycolytic pathway. Mannitol is primarily metabolized in the liver by the enzyme mannitol dehydrogenase, converting it to fructose. The fructose can then enter the glycolytic pathway through phosphorylation by fructokinase, yielding fructose-1-phosphate, which is subsequently cleaved by aldolase B to produce DHAP and glyceraldehyde. Both DHAP and glyceraldehyde can be further metabolized through the glycolytic pathway, ultimately generating energy in the form of ATP. This figure highlights the interplay between mannitol metabolism and the glycolytic pathway, demonstrating the broader metabolic implications of mannitol administration in neurosurgical applications.
DHAP: dihydroxyacetone phosphate, FBP: fructose 1,6-bisphosphate, GAP: glyceraldehyde 3-phosphate, NAD: nicotinamide adenine dinucleotide, NADH: nicotinamide adenine dinucleotide hydride, ATP: adenosine triphosphate, CoA: co-enzyme A.
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