Systemic Hyperthermia in Traumatic Brain Injury—Relation to Intracranial Pressure Dynamics, Cerebral Energy Metabolism, and Clinical Outcome

Abstract

Background: Systemic hyperthermia is common after traumatic brain injury (TBI) and may induce secondary brain injury, although the pathophysiology is not fully understood. In this study, our aim was to determine the incidence and temporal course of hyperthermia after TBI and its relation to intracranial pressure dynamics, cerebral metabolism, and clinical outcomes.Materials and Methods: This retrospective study included 115 TBI patients. Data from systemic physiology (body temperature, blood pressure, and arterial glucose), intracranial pressure dynamics (intracranial pressure, cerebral perfusion pressure, compliance, and pressure reactivity), and cerebral microdialysis (glucose, pyruvate, lactate, glycerol, glutamate, and urea) were analyzed during the first 10 days after injury.Results: Overall, 6% of patients did not have hyperthermia (T > 38°C) during the first 10 days after injury, whereas 20% had hyperthermia for > 50% of the time. Hyperthermia increased from 21% ( ± 27%) of monitoring time on day 1 to 36% ( ± 29%) on days 6 to 10 after injury. In univariate analyses, higher body temperature was not associated with higher intracranial pressure nor lower cerebral perfusion pressure, but was associated with lower cerebral glucose concentration (P = 0.001) and higher percentage of lactate-pyruvate ratio > 25 (P = 0.02) on days 6 to 10 after injury. Higher body temperature and lower arterial glucose concentration were associated with lower cerebral glucose in a multiple linear regression analysis (P = 0.02 for both). There was no association between hyperthermia and worse clinical outcomes. Conclusion:Hyperthermia was most common between days 6 and 10 following TBI, and associated with disturbances in cerebral energy metabolism but not worse clinical outcome.

Fine Tuning of Traumatic Brain Injury Management in Neurointensive Care—Indicative Observations and Future Perspectives

“…Furthermore, lactate is a cerebral vasodilator and higher systemic levels may increase CBF ( 55 ). However, we have found that a higher arterial lactate is independently associated with a higher PRx ( 33 ), and it is possible that the corresponding increase in CBF ( 55 ) represents dysregulated hyperemia. This calls for caution in clinical TBI trials on lactate-based fluids as a way of increasing the delivery of an alternative energy fuel to the brain due to the possible negative effect of lactate on pressure autoregulation.…”

“…This calls for caution in clinical TBI trials on lactate-based fluids as a way of increasing the delivery of an alternative energy fuel to the brain due to the possible negative effect of lactate on pressure autoregulation. Hyperthermia could induce cerebral vasodilation, and some findings support an association between a higher body temperature and a higher PRx ( 56 ), whereas other studies have found no such association ( 33 ). Arterial hypoxia also leads to cerebral vasodilation in order to increase CBF to maintain normal brain tissue oxygenation ( 57 ), whereas higher oxygen levels may increase the cerebrovascular tone.…”

“…However, even if brain tissue oxygenation and the level of energy metabolites are at adequate levels, cerebral energy failure may still occur due to mitochondrial dysfunction ( 26 – 28 ). In addition, mechanisms such as seizures and hyperthermia increase energy consumption and may be detrimental if the compensatory cerebral energy reserve is compromised ( 29 – 33 ).…”

“…The arterial glucose level and CBF determine cerebral glucose delivery, but the cerebral glucose level also depends on the cerebral energy metabolic rate. Arterial and cerebral glucose are normally correlated, but this association may be disturbed after TBI ( 33 , 54 , 82 – 84 ) as the CBF and cerebral energy metabolic rate could have greater influence on cerebral glucose levels. The immediate effects of TBI include a sympathetic stress response that, among other things, gives rise to a surge in arterial glucose ( 85 ).…”

“…An increased consumption of lactate as an energy fuel may, in turn, spare cerebral glucose ( 55 , 102 , 103 ). Higher lactate decreases the cerebrovascular tone, induces vasodilation, and increases CBF ( 55 , 104 ), but possibly at the expense of a worsened pressure autoregulation ( 33 ). Exogenous, hypertonic lactate may exert anti-edematous effects and alleviate intracranial hypertension ( 102 ).…”