OBJECTIVE This study seeks to evaluate the efficacy and safety of intranasal (IN) dexmedetomidine as a sedative medication for non-invasive procedural sedation. METHODS Subjects 6 months to 18 years of age undergoing non-invasive elective procedures were included. Dexmedetomidine (3 mcg/kg) was administered IN 40 minutes before the scheduled procedure time. The IN dexmedetomidine cohort was matched and compared to a cohort of 690 subjects who underwent sedation for similar procedures without the use of dexmedetomidine to evaluate for observed events/interventions and procedural times. RESULTS One hundred (92%) of the 109 included subjects were successfully sedated with IN dexmedetomidine. There were no significant differences in the rate of observed events/interventions in comparison to the non-dexmedetomidine cohort. However, the IN dexmedetomidine group had a longer postprocedure sleep time when compared to the non-dexmedetomidine cohort (p < 0.001), which had a significant effect on recovery time (p = 0.024). Also, the dexmedetomidine cohort had longer procedure time and total admit time (p < 0.001 and p = 0.037, respectively). CONCLUSIONS IN dexmedetomidine may be used for non-invasive pediatric procedural sedation. Subjects receiving IN dexmedetomidine had a similar rate of observed events/interventions as the subjects receiving non-dexmedetomidine sedation, with the exception of sleeping time. Also, patients sedated with IN dexmedetomidine had longer time to discharge, procedure time, and total admit time in comparison to other forms of sedation.
Motor vehicle accident is the most common cause of blunt cardiac injury (BCI) in children (85.3%) due to the height of the child in relation to proper restraints and the compliant pediatric rib cage (J Trauma. 1996;40:200-202). Trauma to the chest wall may lead to injury of the myocardium, resulting in myocardial contusion, ventricular septal defect (VSD), ventricular free wall rupture, or valve compromise (J Trauma. 1996;40; 200-202; Heart Lung. 2012;41:200-202; J Inj Violence Res. 2012;4:98-100). There are several proposed mechanisms for the formation of VSD after blunt chest trauma including rupture of ischemic myocardium related to the initial trauma and reopening of a spontaneously closed congenital VSD. Also, chest trauma during isovolumetric contraction of the ventricles may generate enough intraventricular force to cause myocardial rupture (J Trauma. 1996;40:200-202; J Inj Violence Res. 2012;4:98-100; Korean J Pediatr. 2011;54:86-89; Ann Thorac Surg. 2012;94:1714-1716; J Emerg Trauma Shock. 2012;5:184-187). Previous case reports highlight the formation of a true VSD after BCI and the requirement of emergent repair (J Emerg Trauma Shock. 2012;5:184-187; Am Heart J. 1996;131:1039-1041; Korean Circ J. 2011;41:625-628; Ann Thorac Surg 2013;96:297-298; Kardiol Pol. 2013;71:992; Chin Med J. 2013;126:1592-1593). Reported is a case of a 6-year-old girl who developed an interventricular septal pseudoaneurysm after a motor vehicle accident of pedestrian versus car. On the day of presentation, she developed bradycardia after emergent surgical repair for abdominal trauma that required cardiopulmonary resuscitation including 5 minutes of chest compressions. At the time of resuscitation, an emergent transthoracic echocardiogram noted an interventricular pseudoaneurysm. She has been followed with serial transthoracic echocardiograms and has not required surgical intervention. We discuss the risk factors, prevalence, and diagnostic studies and recommended treatment options for structural heart disease after BCI.
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