gms | German Medical Science

Objective: Deep sedation (DS) in patients with severe acute brain injury has been used in the early phase following hospital admission in order to improve cerebral tolerance to ischemia and to limit supply/demand mismatch in conditions of impaired autoregulation. However, DS can also reduce cerebral blood flow by lowering mean arterial pressure, thus leading to secondary brain tissue hypoxia/ischemia. Patients with high grade aneurysmal subarachnoid hemorrhage (aSAH) often undergo DS as part of their treatment, sometimes with the goal of preventing delayed cerebral ischemia (DCI). The goal of this study was to establish whether or not DS has a protective effect against DCI.

Methods: We conducted a retrospective analysis of patients admitted to our center between January 2012 and September 2015 with aSAH. The use of DS was assessed, as well as its duration, medications used, and indication for DS. Furthermore, the incidence of DCI was determined. Bivariate correlation analysis was performed using Spearman’s rho. Additionally, ordinal regression was conducted to account for other variables such as age and Hunt and Hess Grade at presentation that could possibly predict the incidence of DCI. For statistical analysis, IBM® SPSS® Statistics Version 21 was used.

Results: A total of 170 patients were included in our analysis. Of these, 82/170 (48.2%) underwent DS. The mean duration of DS was 10 days (range: 2-21 days). All the patients (82/82, 100%) underwent DS with midazolam and ketamine, while 36/82 (44%) and 41/82 (50%) additionally received propofol and sufentanyl, respectively. The most common indication for DS was a high grade at presentation with clinical and imaging findings suggestive of severe acute brain injury/edema (62/82, 75.6%). Other indications included brain edema with elevated intracranial pressure developed over the course of the hospital admission (14/82, 17.1%) and flow accelerations on transcranial Doppler (6/82, 7.3%). DCI occurred in 54/82 (65.9%) of the patients with DS. Correlation analysis showed a statistically significant correlation between DS and DCI (Spearman’s rho=0.306, p<0.01). The ordinal regression also revealed DS as a statistically significant predictor of DCI (p=0.03), assuming Hunt and Hess Grade and age were kept constant.

Conclusion: Our analysis shows that DS does not reduce the incidence of DCI. In fact, DS appears to predict a higher incidence of DCI in patients with aSAH, probably due to the changes in cerebral perfusion pressure. Prospective studies need to assess the role of DS in aSAH and its influence on DCI, as it might be more deleterious that previously assumed.