Targeted temperature management and PbtO2 in traumatic brain injury

Targeted Temperature Management (TTM) to normothermia is widely used in traumatic brain injury (TBI). We investigated the effects to of TTM to normothermia patients with TBI (GCS≤12) monitored with multimodality monitoring, to better understand the physiological consequences of this intervention. In TBI patients cooled to normothermia and in which brain oxygenation deteriorates, are there changes in physiological parameters which are pertinent to brain oxygenation? 102 TBI patients with continuous recordings of intracranial pressure (ICP) and brain oxygen tension (PbtO2) were studied retrospectively. Non-continuous arterial carbon dioxide (PaCO2) and oxygen (PaO2) tensions, and core body temperature (Tc) were added. PaO2 and PaCO2 were also corrected for Tc. Transitions from elevated Tc to normothermia were identified in 39 patients. The 8 h pre and post the transition to normothermia were compared. Data is given as median [IQR] or mean (SD). Overall, normothermia reduced ICP (12 [9–18] −11 [8–17] mmHg, p < 0.009) and Tcore (38.3 [0.3]-36.9 [0.4] oC, p < 0.001), but not PbtO2 (23.3 [16.6]-24.4 [17.2–28.7] mmHg, NS). Normothermia was associated with a fall in PbtO2 in 18 patients (24.5 [9.3] −20.8 [7.6] mmHg). Only in those with a fall in PbtO2 with cooling did ICP (15 [10.8–18.5] −12 [7.8–17.3] mmHg, p = 0.002), and temperature corrected PaCO2 (5.3 [0.5]- 4.9 [0.8] kPa, p = 0.001) decrease. A reduction in PbtO2 was only present in the subgroup of patients with a fall in temperature corrected PaCO2 with cooling. This suggests that even modest temperature changes could result in occult hyperventilation in some patients. pH stat correction of ventilation may be an important factor to consider in future TTM protocols.