Treating intracranial hypertension in traumatic brain injury: keep it cool!

Abstract

Stocchetti et al. [1] have reported their experience with currently available “second tier” therapeutic options for the treatment of refractory intracranial hypertension in patients with traumatic brain injury (TBI) in three Italian neurotrauma centres. The authors discuss three options to control intracranial pressure: profound hyperventilation, barbiturate coma and decompressive craniectomy. These options were used alone or in combination. We were surprised that fever management and mild therapeutic hypothermia were not discussed or even mentioned (other than as a potential source of complications) in this article. Various research groups (including one of the centres involved in the present study) have reported that development of fever following TBI is closely linked to intracranial hypertension [2–5]; this would suggest that fever management should be one of the first steps in controlling intracranial hypertension, but this is not mentioned in the article of Stocchetti et al. Further, it has been conclusively demonstrated (in 14 studies enrolling >1,500 patients) that ICP can be significantly decreased by induction of mild hypothermia [5–10]. Moreover, although the results from studies using hypothermia to improve outcome following severe TBI have been conflicting, the preponderance of evidence strongly suggests that prolonged (3–5 days) cooling can significantly improve neurological outcome in patients with intracranial hypertension [5–10]. None of the therapeutic options discussed by Stocchetti et al. has so far been shown to improve neurological outcome; studies using barbiturate coma [11–13] or hyperventilation [14–15] in patients with refractory intracranial hypertension reported decreases in ICP but no benefits in outcome. Decompressive craniotomy has shown promise in one small study in 27 paediatric patients [16], but has not yet been well studied in adults [17]. Two RCTs addressing this issue are currently in process [18–19]. Hypothermia does not decrease cerebral blood flow without reducing metabolism and oxygen demand, as is the case with hyperventilation [20], and, when used judiciously, tends to cause no hypotension and less myocardial dysfunction than barbiturates. The evidence regarding improved neurological outcome in TBI associated with hypothermia can certainly be debated; but the evidence is (at the very least!) as strong and as favourable as for barbiturates and hyperventilation. Therefore, induced hypothermia should be regarded as one of the “second tier” therapies in refractory intracranial hypertension, and as such deserves to be mentioned as a feasible option in the otherwise excellent discussion by Stocchetti et al.