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Index: WOUNDS. 2012;24(6):160–167.

  Abstract: Autonomic dysreflexia (AD) is an acute, life-threatening syndrome of uncontrolled sympathetic discharge that occurs in patients with spinal cord injury at T6 or higher. Despite a high incidence in tetraplegics, the condition is under-recognized, putting both the practitioner and patient at risk. This report presents a case of AD triggered by debridement of a pressure ulcer. To advance the understanding among wound care practitioners, the authors review the literature, describe the common clinical presentations and scenarios leading to AD, delineate a protocol to guide management, and conclude with a discussion of potential preventative measures.

Introduction

  Traumatic spinal cord injury (SCI) affects 200,000 people in the United States, with an average rate of 10,000 new cases developing each year.¹ While both the severity of neurological injury and the existence of comorbid diseases are predictors of long-term mortality in patients with SCI, secondary complications of SCI are also associated with adverse outcomes.² Autonomic dysreflexia (AD) and pressure ulcers are of particular importance because of the high incidence rates and fatalities attributed to each.

  Autonomic dysreflexia is an acute, life-threatening syndrome of uncontrolled sympathetic discharge that occurs, in response to stimuli, in patients with SCI above the splanchnic outflow tract (level T6). Clinically, AD is characterized by a sudden elevation in blood pressure (BP) of at least 20 mmHg above baseline, and one of the following signs/symptoms: bradycardia, headache, flushing, and/or profuse sweating above the lesion level.^3,4 Left untreated, the sympathetic surges can progress to hypertensive crises with serious sequelae, including intracranial or retinal hemorrhage, seizures, myocardial infarction, arrhythmias, and death.^3,5-9The reported incidence of AD varies greatly, but is as high as 91% in patients with complete tetraplegia.¹⁰ Despite this high incidence, AD is an often unrecognized phenomenon.¹¹ The paroxysmal hypertensive episodes of AD occur in response to a variety of organic and iatrogenic stimuli below the level of SCI. Although bladder and bowel etiologies are most commonly reported,^12-16 integumentary system deficits, such as pressure ulcers and their management, might also prompt a dysreflexic reaction.^5,16-19

  Pressure ulcers occur in 23% to 40% of patients with SCI during acute rehabilitation,^20,21 and then recur in 35%–80% of patients,^22-24 contributing significantly to increased morbidity and diminished quality of life.²⁵ In concert with the patient’s primary care physician, the wound care team plays an integral role in the evaluation and management of pressure ulcers. The approach to treatment varies depending on ulcer stage and risk factors for poor wound healing. It often involves a spectrum from removal of devitalized tissue by bedside debridement to surgical closure with flap reconstruction.²⁶ These procedures induce strong stimuli beneath the level of SCI, and therefore, might trigger AD.

  This report presents a case of AD triggered by sharp debridement of a pressure ulcer.