Cardiovascular Dysfunction Presenting as Autonomic Dysreflexia in a Patient with Spinal Cord Injury

Abstract

Autonomic dysreflexia (AD) is a medical emergency that is characterized by hypertension as an autonomic response to noxious stimuli in patients with a history of spinal cord injury at the level of T6 or above. We present the case of a 31-year-old Caucasian male with a history of spinal cord injury at the level of C3-C4, with symptoms described as recurring episodes of hypertension with flushing and sweating above the level of the lesion for the past five to six years. His symptoms are triggered by bowel distention, excitement, a bumpy car ride, or a simple turning of the neck to the left. Physical examination and laboratory studies ruled out other possible differentials (e.g., migraines, pheochromocytoma). As a result, AD was diagnosed.

Autonomic Dysreflexia following Spinal Cord Injury

“…27,31,40,41 The onset of AD is usually provoked by the distension of urinary bladder, genitourinary tract infections, urolithiasis, renal colic, catheterization, urodynamic studies, cystoscopy, sexual stimulation, gynecological problems, vaginal examination, distal bowel or rectal stimulation (enema, mechanical stool removal, fecal impaction), hemorrhoids, gastrointestinal morbidity (pancreatitis, gastroduodenal ulcers, cholelithiasis), tissue damage (bone fracture, decubital necrosis), or skin irritation from tight clothing, sunburn, ingrown toe nails, insect bites, dressing changes, rehabilitation, and physiotherapeutic measures. 17,28,40,42 The compression of surrounding organs by enlarged uterus, as well as labors, delivery, breast-feeding, and changes arising during puerperal period are also strong triggering factors in women with cervical or high-thoracic lesions. 5,7, 40,43,44 Acute Clinical Presentation AD may have an episodic nature or attacks that occur several times a day while persisting from minutes to hours, or even days.…”

“…14 15 27 28 29 30 31 Injuries located below T6 segment less likely cause AD because the intact splanchnic innervation usually ensures the compensatory dilatation of the intraabdominal vascular bed providing the sufficient mass of blood vessels apt to manage arterial hypertension. 6 8 17 A critically increased blood pressure caused by the uncontrolled release of norepinephrine, dopamine-β-hydroxylase, and dopamine 21 27 32 is detected by baroreceptors in the aortic arch, carotid sinus, and coronary arteries, projecting to the nucleus of the solitary tract located in the medulla oblongata. 21 23 This leads to the response of the integration center by a strong vagal reaction.…”

“…Yet, even a significant reduction of heart rate is not able to compensate for the massive splanchnic vasoconstriction. 14 17 Clinical practice shows that frequency, as well as the intensity of AD attacks usually increases over time. 18 29 33 34 This is attributed to the synaptic reorganization of sympathetic preganglionic neurons, primary afferent sprouting, aberrant propriospinal plasticity caudal to the lesion, and peripheral adrenergic hypersensitivity.…”

“…5 13 14 Episode of the high blood pressure might be associated with a high risk of intracranial or retinal hemorrhage, seizures, heart failure, or pulmonary edema. 2 14 15 16 17 This fact represents an emergent situation demanding immediate medical attention. The paucity of familiarity with this clinical entity may cause misdiagnosis, hesitancy, delay in the appropriate management, and thus irreversible harm to the patient.…”

“…The paucity of familiarity with this clinical entity may cause misdiagnosis, hesitancy, delay in the appropriate management, and thus irreversible harm to the patient. 5 17 18 The aforementioned reasons inspired the authors to review literature dealing with current treatment strategies of the serious clinical condition.…”