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To advance the understanding of AD among wound care practitioners, the authors review the literature and describe the clinical presentation to recognize the most common presenting phenomena, delineate a protocol to guide management, and conclude with a discussion of potential preventative measures.

Case Report and Methods

  A 57-year-old man with C5 tetraplegia was being followed by the plastic surgery service for management of a Stage IV sacral pressure ulcer, complicated by devitalized and macerated wound edges. Sharp debridement and excision of this tissue was planned, under local anesthesia in the minor procedures room, to promote further wound healing. As scalpel debridement and excision of the circumferential edges of a 5 cm x 2.5 cm wound began, the patient reported a sense of uneasiness and a headache. At that time, debridement was stopped and additional 1% lidocaine was injected at the site. After allowing time for local anesthesia to take effect, sharp debridement continued. Immediately, the patient began to sweat, his face appeared flushed, and he became hypertensive with a BP elevation to 210/180 from 105/67 before the procedure. The treatment team, now suspecting AD, initiated the institution’s (James A. Haley Veterans Hospital) AD protocol (Figure 1). The procedure ceased, the head of the bed was elevated, his clothes were loosened and his catheter was inspected for kinks or obstructions to rule out a bladder etiology. Despite the previous interventions, the patient’s BP remained elevated (200/170). Accordingly, 1-in of 2% nitroglycerin ointment was applied. His BP remained elevated (> 150 mmHg systolic) 5 minutes later, thus a 10 mg oral dose of nifedipine was administered. His BP then began to return to baseline and stabilized at 110/55 15 minutes later. He was inspected for bowel triggers (eg, fecal impaction), and other possible cutaneous triggers (eg, paronychia), with none detected. The episode was documented and the patient’s history was reviewed. It was known that the patient had a history of AD associated with bladder distension and bowel manipulation; however, there was no history of AD associated with pressure ulcers. The patient was followed over the next 2 years and his wound required 4 further procedures—3 involving sharp debridement and 1 involving surgical debridement with flap closure. All of these procedures were performed under general anesthesia, and the patient did not experience another AD episode.

Discussion

  Pathogenesis. To appreciate the clinical presentation of AD and the relationship to surgical procedures, it is paramount to understand the pathogenesis of AD. Autonomic dysreflexia develops following SCI from dysfunctional sympathetic regulation, spinal cord reorganization, and an abnormal disconnect between the parasympathetic and sympathetic autonomic nervous systems (ANS).³ Sensory stimuli are carried by primary afferent fibers to the dorsal grey matter (DGM) of spinal cord segments.