The place of dexmedetomidine light sedation in patients with acute brain injury

To the Editor,

An individualized titration of sedative and analgesic drugs is pivotal in the late phase management of acute brain injury (ABI) patients, when weaning from mechanical ventilation (MV) needs to be implemented [1]. Due to its pharmacologic profile, dexmedetomidine (Dex) represents a drug of choice in such setting. Nevertheless, its use in ABI patients has been recently debated mainly as a consequence of its hemodynamic effects [2, 3]. The present study aimed to evaluate clinical outcomes and safety profile of Dex administration in this patients’ category.

We retrospectively analysed prospectively collected data on the main clinical features and adverse events observed during light sedation with dexmedetomidine (Dex-LS) in ICU patients with ABI. Light sedation was defined by the maintenance of a Richmond Agitation and Sedation Scale (RASS) score between 1 and − 2. The rate of potential side effects during Dex-LS was compared with the 6-h period before Dex initiation (see Additional file 1 for further details).

The main clinical and analgosedation characteristics of the 101 included patients are listed in Table 1. Traumatic ABI (77.2%) was the main admission diagnosis, and haemorrhage (59.4% of the cohort) was the most common admission feature (see Additional file 1: Table S1). Out of 101 patients, 80 were mechanically ventilated during Dex-LS. In most cases, dexmedetomidine was administered in association with other sedatives, opioids or antipsycotic drugs, for a median duration and dosage of 64 h and 0.6 μg/kg/h, respectively.

Table 1 Features of 101 patients undergoing Dex-LS

Dexmedetomidine has been administered safely in our population of ABI patients. Dex infusion rate and duration were comparable with those previously described [2, 3]. The rate of systemic arterial hypotension was consistent with available findings [2, 3] and lower compared with the pre-infusion period. The 23% rate of bradycardia takes place in the wide range of occurrence reported in ABI patients [2]. Nevertheless, bradycardia never imposed dexmedetomidine interruption. These findings should be interpreted in the light of the relatively young age and low severity scores of our population, where Dex was frequently co-infused with other sedatives or opioids. Neither seizure rate nor intracranial pressure increased during Dex-LS, supporting the clinical absence of Dex impact on cerebral physiology [4].

During Dex-LS, the majority of patients were weaned from MV, including more than half who previously failed a weaning attempt. These observations are in line with the available evidence comparing Dex sedation with midazolam and propofol use, even though in ICU patients without ABI [5].

In conclusion, despite the intrinsic limitations of our retrospective design lacking a control group, this study suggests that when used to target light sedation in our cohort of ABI patients, dexmedetomidine was safe and enabled the weaning from MV and the maintenance of spontaneous breathing.