Nutritional Support in Critical Condition Caused by Acute Cerebral Insufficiency

V.I. Chernii, S.Ye. Kugler, T.V. Chernii

Abstract


Hypermetabolism in traumatic brain injury (TBI) is caused by massive hormonal response to stress. Hyperglycemia in acute lesions of the brain (without the presence of diabetes) is considered as a factor that enhances the damaging processes like intracellular acidosis, accumulation of extracellular glutamate, the formation of cerebral edema, a breakthrough of blood-brain barrier, hemorrhagic transformation of cerebral infarction. The predominance of anaerobic glycolysis in TBI reduces the macroergic phosphate (phosphocreatine concentration of ATP) and increases AMP. Lactic acidosis with increased lactate in the brain tissue and cerebral spinal fluid develops. Glucose intolerance during TBI promotes to violation of its metabolism. In patients with severe TBI glucose level ore than 11 mmol/l is associated with poor outcome. Intensive monitoring of blood glucose levels and maintaining normoglycemia can be effective neuroprotective intervention. Despite the violation of energy and plastic substrates utilization in acute period, artificial nutrition is one of the tenets of intensive care. Early nutritional support is important for patients with traumatic brain injury, which is associated with the development hypercatabolism syndrome with significant demand for calories and proteins in these patients. Neurointensive care patients need a special type of nutritional support in connection with the intensification of catabolism and prolonged fasting. Enteral or mixed enteral and parenteral administration of formulas (if enteral nutrition does not provide more than 60 % as needed) is recommended. Summarizing the mentioned above, it should be noted that the problem of adequate correction of hypermetabolism-hypercatabolism syndrome in patients with acute cerebral insufficiency of different genesis requires further study.


Keywords


stroke; traumatic brain injury; hyperglycemia; parenteral nutrition

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DOI: https://doi.org/10.22141/2224-0586.5.68.2015.78516

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