Targeted temperature control in improving cerebral metabolism in patients with severe traumatic brain injury associated with the development of hyperthermia

Background. Severe traumatic brain injury (TBI) remains one of the leading causes of mortality and disability among the working-age population. Preventing and treating secondary brain damage is a priority in intensive care. Therefore, temperature control and cerebral metabolism monitoring are essential components of intensive care for patients with severe TBI. Objective: to study the state of cerebral metabolism in patients with severe TBI associated with central hyperthermia by investigating the relationship between core body temperature and jugular lactate levels under targeted temperature control. Materials and methods. The study included 60 patients with severe TBI and associated hyperthermia who were treated in an intensive care unit. They were divided into two groups: the control one (n = 30) received standard antipyretic therapy, while the study group (n = 30) underwent targeted temperature control using the Blanketrol II hypothermia system. Core body temperature was measured using an esophageal probe, and jugular lactate levels were determined with a biochemical analyzer. Statistical analysis was conducted using standard methods in Jupyter Notebook (https://jupyter.org). Results. On the first day of the study, the median temperature in both groups exceeded 38.3 °C and was significantly higher in the study group (p = 0.008). From the third day, the median temperature in the controlled normothermia group was significantly lower (p < 0.001) at 37.8 °C. By the seventh day, it stabilized within target values, whereas in the control group, the temperature remained elevated and was significantly higher (p = 0.005). Jugular lactate dynamics had a similar trend: in the study group, significantly higher levels (p = 0.019) were observed on the first day, while on the third day, median levels were significantly lower — 2.3 mmol/L compared to 3.2 mmol/L in the control group (p = 0.004). A significant (p < 0.001) difference between groups persisted until the sixth day, with higher levels in the control group. There was a strong positive correlation (p < 0.001) between core body temperature and jugular lactate levels (rs = 0.83), with a significant (p < 0.001) difference between groups: rs = 0.93 in the study group vs. rs = 0.71 in the control one. Conclusions. The use of targeted temperature control technology in patients with severe TBI associated with hyperthermia allows for the effective reduction of body temperature and its maintenance within normal values, as well as a decrease in jugular lactate levels compared to baseline, which indicates an improvement in cerebral metabolism. The results of the study confirm the need to introduce temperature control methods into the routine practice of intensive care in severe TBI.