Опікова енцефалопатія та синдром гіперметаболізму-гіперкатаболізму: чи є взаємозв’язок?

Опікова енцефалопатія є ускладненням тяжкої термічної травми. Значну роль у її розвитку відіграє синдром гіперметаболізму-гіперкатаболізму, який зумовлює порушення пам’яті, мислення, розлади у психоемоційній сфері, розвиток делірію та інсомнії. Ступінь розвитку синдрому гіперметаболізму-гіперкатаболізму залежить від тяжкості термічної травми. Своєчасне призначення додаткового парентерального харчування зменшую прояв синдрому гіперметаболізму-гіперкатаболізму. Aim: To define an influence of hypermetabolism-hypercatabolism syndrome on the burn encephalopathy development on the base of study of metabolic changes on the background of an acute period of burn disease. Materials and methods: there were examined 104 patients separated in 2 groups depending on heaviness of injury. There were defined the levels of cortisol, neurospecific enolase (NSE), glucose and blood protein. There were assessed memory, thinking and psychological state of patients. Results: At admission to hospital the cortisol level in patients of 1 and 2 groups was 270,5±29,2 ng/ml and 330,3±17,4 ng/ml, glucose level - 6,0±0,4 mmol/l and 7,7±0,5 mmol/l in 1 and 2 groups respectively. The protein level of blood maximally decreased at 3 day and was 53,6±1,1 g/l in patients of the 1 group and 48,9±1,1 g/l in patients of the 2 group. An increase of cortisol level depended on heaviness of thermal trauma. There was defined correlation between the levels of cortisol and neuron specific enolase in patients of the 1 group at 3 day (R=0.638, p=0.006), in patients of the 2 group at 7 day (R=0.488, p=0.002). In patients of the 1 group sleep disorder and delirium development did not depended on the level of metabolic changes. At the 7 day there was defined correlative connection between cortisol level and memory (R=-0,681, p=0,071) and thinking (R=-0,520, p=0,038). In patients of the 2 group cortisol level at 1 day determined the memory and thinking disorders to the septic-toxemia stage. Sleep disorder correlated with expressed hypoproteinomia at 3 day (R=-0,483, p=0,001). The delirium development was caused with an increase of blood serum cortisol at 1 day after thermal trauma (R=0,467, p=0,058). Conclusion: The one of mechanisms of nerve tissue injury was the development of metabolic changes caused by stress on the background of heavy thermal trauma. The dynamics of cortisol level to the burn shock stage corresponded with the changes of neurospecific enolase level of blood serum as a marker of the nerve tissue injury