Sedation by intranasal dexmedetomidine at 3 mcg·kg(-1) is associated with acceptable success rate in children undergoing echocardiography with no adverse events in this cohort.

Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) are closely associated with acute and chronic inflammatory processes in hemodialytic patients. However, the mechanisms concerning cytokine production by monocytes during hemodialysis are still conflicting. With the use of the more specific monoclonal antibody ELISA method, contamination detection and crossover protocol of complement-activating and noncomplement-activating hollow fibers, we were able to confirm augmented IL-1β production by zymosan-stimulated monocytes with complement-activating hollow fiber as compared to noncomplement-activating hollow fiber before (1,411.9 ± 143.6 vs. 865.7 ± 149.9 pg/ ml/2 × 10⁶ monocytes, p < 0.01), at the 15th minute (530.6 ± 89.1 vs. 247.3 ± 45.2pg/ml/2 × 10⁶ monocytes, p < 0.01) and at the end of dialysis (1,201.8 ± 135.1 vs. 707.4 ± 109.3 pg/ml/2 × 10⁶ monocytes, p < 0.01). Similar results were observed with TNF-α production. IL-1β as well as TNF-α production decreased significantly at the 15th min of dialysis, thereafter they increased and approached the baseline levels towards the end of hemodialysis with both hollow fibers. Plasma C3a at the 15th minute correlated positively with postdialysis IL-1β and TNF-α production, while plasma C3a did not change in patients dialyzed with noncomplement-activating hollow fiber. Complement activation with complement-activating hollow fiber as well as monocyte-membrane interaction with complement-activating and noncomplement-activating hollow fiber might be involved in the pathogenesis of cytokine production during hemodialysis. Uremic toxin removal as well as stimulation of cytokine production inhibitor might contribute to the decreased cytokine production at the 15th minute of hemodialysis and monocyte-membrane interaction with or without complement activation resulted in augmented cytokine production toward the end of hemodialysis with both hollow fibers. We thus concluded that hollow fiber of bioincompatibility triggered much more cytokine production throughout the dialysis procedure.

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Summary Background Moderate to deep sedation is required for an auditory brainstem response test when high‐intensity stimulation is used. Chloral hydrate is the most commonly used sedative, whereas intranasal dexmedetomidine is increasingly used in pediatric non‐painful procedural sedations. Objective The aim of this study was to compare the sedation success rate after oral chloral hydrate at 50 mg kg−1 and intranasal dexmedetomidine at 3 μg kg−1 plus buccal midazolam at 0.1 mg kg−1 for an auditory brainstem response test. Methods Children who required an auditory brainstem response test were recruited and randomly assigned to receive oral chloral hydrate at 50 mg kg−1 and intranasal placebo, or intranasal dexmedetomidine at 3 μg kg−1 with buccal midazolam 0.1 mg kg−1. The primary outcome was the rate of successful sedation for auditory brainstem response tests. Results Fifty‐seven out of 82 (69.5%) were successfully sedated after chloral hydrate, while 70 out of 78 (89.7%) children were successfully sedated with dexmedetomidine plus midazolam combination, with the odd ratio (95% CI) for successful sedation between dexmedetomidine plus midazolam combination and chloral hydrate estimated to be 3.84 (1.61‐9.16), P = 0.002. Dexmedetomidine plus midazolam was associated with quicker onset with median onset time 15 (IQR 11.0‐19.8) for dexmedetomidine plus midazolam and 20 (IQR 15.0‐27.0) for chloral hydrate respectively, with difference between median (95% CI) of 5 [3‐8], P < 0.0001). The behavior observed during drug administration of intranasal dexmedetomidine and buccal midazolam was better that of the children who had oral chloral hydrate. No children required oxygen therapy or medical intervention for hemodynamic disturbances in this study and the incidence of hypotension and bradycardia was similar. Conclusion Intranasal dexmedetomidine plus buccal midazolam was associated with higher sedation success with deeper level of sedation, with similar discharge time and adverse event rate when compared to chloral hydrate.

Intranasal dexmedetomidine was comparable to oral pentobarbital sedation for TTEcho sedation in infants and did not increase the risk of clinically important adverse events. Intranasal dexmedetomidine appears to be an effective "rescue" sedative for both failed pentobarbital and dexmedetomidine sedation. Dexmedetomidine could be a safer option for repeated sedation in children, but further studies are needed to assess long-term consequence of repeated sedation in this high-risk population.