Moderate hypocapnia for intracranial pressure control after traumatic brain injury: a common practice requiring further investigations

Hypocapnia and hyperventilation are often considered as secondary insults to the brain. After traumatic brain injury (TBI), hypocapnia induces vasoconstriction, increases cerebral oxygen extraction fraction, and decreases cerebral blood flow and volume and intracranial pressure (ICP) [1‐3]. Increases in brain extracellular glutamate and lactate concentrations in tissue adjacent to cerebral contusions or underlying subdural hematomas have been observed after 30 min of hyperventilation (PaCO₂ around 25 mmHg), particularly in the first 24–36 h after injury, suggesting deleterious metabolic effects of profound hypocapnia in vulnerable regions [4]. Thirty years ago, a good quality randomized controlled trial, even if performed in a relatively small groups, comparing the effects of severe and prolonged hypocapnia (25 ± 2 mmHg) to normocapnia (35 ± 2 mmHg) for a period of 5 days after severe TBI, found a worse neurological outcome in the hyperventilation group at 3 and 6 months, but not at 12 months [5]. The effect of moderate hypocapnia remains, however, controversial as the balance between potential negative metabolic effects and better ICP control may be considered. Some guidelines suggest that moderate hypocapnia could be used as a second-tier therapy [6]; others suggest that hyperventilation can be recommended only as a temporizing measure for the reduction of elevated ICP [7], and that hyperventilation should be avoided during the first 24 h after injury [7, 8]. …