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.
Anzeige
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
Clinical characteristics | |||
Age, years | 53 [35–68] | ||
Male | 84 (83.2) | ||
Neuro-psychiatric comorbidities | 24 (23.8) | ||
- Preesistent psychosis | 12 (11.9) | ||
- Preesistent dementia | 5 (5) | ||
- Preesistent epilepsy | 7 (6.9) | ||
Traumatic brain injury (TBI) | 78 (77.2) | ||
- Isolated traumatic brain injury | 14 (13.8) | ||
- Polytrauma with traumatic brain injury | 64 (63.4) | ||
Non-traumatic brain injury | 23 (22.8) | ||
ISS at admission (TBI only) | 23 [17–29] | ||
Head-AIS at admission (TBI only) | 3 [2–4] | ||
GCS at admission* | 10 [7–14] | ||
SAPS II at Dex-LS start | 34 [26–44] | ||
SOFA at Dex-LS start | 4 [3–7] | ||
MV at admission | 91 (90.1) | ||
MV at Dex-LS start | 80 (79.2) | ||
ICU LOS pre-Dex-LS, days | 4 [2–8] | ||
ICU LOS post-Dex-LS, days | 8 [3–15] | ||
ICU mortality | 4 (4) | ||
Hospital mortality | 8 (7.9) | ||
Hours of MV# | 39 [12–72] | ||
MV in assisted mode# | 71 (88.8) | ||
MV in assisted mode, hours# | 24 [6–48] | ||
Successful weaning# | 56 (70) | ||
Successful weaning in pts with previous weaning failure## | 16 (57.1) | ||
Spontaneous breathing, hours# | 25 [0–72] | ||
Analgosedation details | |||
RASS | 0 [− 1/0] | ||
Propofol co-infusion | 35 (34.7) | ||
Midazolam co-infusion | 0 | ||
Remifentanil co-infusion | 59 (58.4) | ||
Other opioids co-infusion** | 15 (14.9) | ||
Antipsychotic drugs co-administration*** | 40 (39.6) | ||
Dex length of infusion, hours | 64 [33–120] | ||
Dex start dosage, μg/kg/h | 0.7 [0.5–0.9] | ||
Dex median dosage, μg/kg/h | 0.6 [0.5–0.9] | ||
Dex maximum dosage, μg/kg/h | 0.9 [0.6–1.2] | ||
Dex dosage at suspension, μg/kg/h | 0.5 [0.3–0.8] | ||
Hemodynamic parameters and adverse events (n = 101) | |||
Pre-Dex infusion### | Dex-LS | P value | |
RASS | − 2 [− 3/0] | 0 [− 1/0] | < 0.001 |
HR, bpm | 78 [70–89] | 80 [66–91] | 0.165 |
SAP, mmHg | 133 [124–146] | 139 [126–150] | 0.136 |
DAP, mmHg | 65 [56–72] | 69 [62–78] | < 0.001 |
MAP, mmHg | 85 [78–98] | 90 [84–99] | 0.039 |
Bradycardia | 2 (2) | 23 (22.8) | < 0.001 |
- Bradycardia in pts receiving remifentanil co-infusion^ | – | 12 (20.3) | – |
- Dex median dosage in pts with bradycardia, μg/kg/h^^ | – | 0.6 [0.4–0.9] | – |
Arterial hypotension requiring vasopressors | 42 (41.6) | 27 (26.7) | 0.037 |
Seizures | 3 (3) | 3 (3) | 1 |
ICP, mmHg* | 9 [8–14] | 8 [7–10] | 0.164 |
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].
Anzeige
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.
Supplementary information
Supplementary information accompanies this paper at https://doi.org/10.1186/s13054-019-2637-9.
Acknowledgements
Not applicable.
Ethics approval and consent to participate
The study was approved by the ethics committee of the Catholic University of the Sacred Heart (Prot. UCSC34998/18). Due to its observational, non-interventional design, informed consent was waived.
Consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing interests.
Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.