LAUSR

OBJECTIVE Hyperventilation is a controversial treatment in traumatic brain injury (TBI). Prophylactic severe hyperventilation below 3.3 kPa/25 mm Hg) is generally avoided, due to the risk of cerebral ischemia. Mild hyperventilation (arterial pCO2 within 4.0-4.5 kPa/30-34 mm Hg) in cases of intracranial hypertension is commonly used, but its safety and benefits are not fully elucidated. The aim of this study was to evaluate the use of mild hyperventilation and its relation to, cerebral energy metabolism, pressure autoregulation and clinical outcome in TBI. METHOD This retrospective study was based on 120 patients with severe TBI treated at the neurointensive care unit, Uppsala university hospital, Sweden, 2008-2018. Data from cerebral microdialysis (glucose, pyruvate and lactate), arterial pCO2 and pressure reactivity index (PRx55-15) were analyzed for the first three days post-injury. RESULTS Mild hyperventilation 4.0-4.5 kPa (30-34 mm Hg) was more frequently used early and the patients were gradually normoventilated. Low pCO2 was associated with slightly higher intracranial pressure and slightly lower cerebral perfusion pressure (p-value < 0.01). There was no univariate correlation between low pCO2 and worse cerebral energy metabolism. Multiple linear regression analysis showed that mild hyperventilation was associated with lower PRx55-15 day 2 (p-value = 0.03), suggesting better pressure autoregulation. Younger age and lower ICP were also associated with lower PRx55-15. CONCLUSIONS These findings support the notion that mild hyperventilation is safe and may improve cerebrovascular reactivity.