ABSTRACT
INTRODUCTION: Autonomic dysreflexia (AD) is a well-established association of high spinal cord injury (SCI), particularly in those occurring above T6. When a noxious stimulus is encountered, the body responds by stimulating an increase in blood pressure, which is then countered by vasodilation. In patients with autonomic dysreflexia, the patient is unable to vasodilate below the level of spinal injury due to interruption of the autonomic innervation below the injury. This then leads to persistently elevated blood pressure causing uncoordinated autonomic responses such as headache, flushing, sweating, and even hypertensive crisis. The noxious stimulus most commonly reported is bladder or bowel distention [1]. This potential trigger is especially important since many patients with SCI require catheterization and repeated urodynamic testing, both of which predispose them to bladder distention. In response to an incident during which a patient developed severe hypertension during UDS, institutional concern was raised about the potential risk of AD in other patients with SCI ≥ T8 and other severe neurological disease undergoing urodynamic testing, and a protocol was initiated in 2007 for monitoring for AD during UDS. Although no long-term complication was encountered in this incident, the need for improvement in our understanding of the detection and treatment of AD during urodynamic testing was highlighted. However, due to the potential of UDS to trigger AD and possible subsequent severe cardiovascular crisis, a protocol was established at our institution. Because of reports documenting episodes of AD for patients with severe, non-SCI neurologic disease and the unknown risk, these patients also were historically monitored at our institution as well. OBJECTIVE: Autonomic dysreflexia (AD) is an uncoordinated autonomic response seen in patients with spinal cord injury (SCI). AD is often triggered by bladder distention, which may occur during urodynamic studies (UDS), and has potentially life-threatening consequences. Our purpose is to determine the prevalence and associated factors of AD in children undergoing UDS with either SCI or other neurological disease. METHODS: We identified 13 pediatric patients with SCI at the eighth thoracic vertebrae or above (SCI ≥ T8) or other severe neurological disorder with urodynamic evaluations between 2007 and 2011 at our institution. We retrospectively reviewed these patients for age, gender, bladder volume, bladder compliance, detrusor instability, symptoms of AD, blood pressure, and urinary infection. RESULTS: There were a total of 13 patients with SCI ≥ T8 (9), transverse myelitis (2), and encephalomyelitis (2). There were a total of 41 urodynamic studies with an average of 3.2 studies per patient. One adolescent with C1/2 injury and a prepubertal child with T2/3 injury developed AD. AD was not observed in non-SCI patients. The patients who developed AD had multiple subsequent episodes with follow up UDS. No statistical associations were found for the variables evaluated. No major complications occurred, and AD was successfully managed conservatively. CONCLUSIONS: With appropriate monitoring and education, AD is easily recognized and managed conservatively. We found an increased risk of patients developing subsequent AD episodes after an initial episode. Patients who did not have autonomic dysreflexia during initial UDS did not experience autonomic dysreflexia on subsequent UDS. We did not observe autonomic dysreflexia occurring in children with transverse myelitis or encephalomyelitis.
