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Autonomic Dysreflexia in Spinal Cord Injury
Autonomic Dysreflexia in Spinal Cord Injury
Autonomic Dysreflexia in Spinal Cord Injury
Autonomic dysreflexia (AD) is a syndrome of massive imbalanced reflex sympathetic discharge occurring in patients with spinal cord injury (SCI) above the splanchnic sympathetic outflow (T5-T6). Anthony Bowlby first recognized this syndrome in 1890 when he described profuse sweating and erythematous rash of the head and neck initiated by bladder catheterization in an 18-year-old patient with SCI. Guttmann and Whitteridge completed a full description of the syndrome in 1947. This condition represents a medical emergency, so recognizing and treating the earliest signs and symptoms efficiently can avoid dangerous sequelae of elevated blood pressure. SCI patients, caregivers, and medical professionals must be knowledgeable about this syndrome and its management.
Etiology
Autonomic dysreflexia (AD) occurs after the phase of spinal shock in which reflexes return. Individuals with injury above the major splanchnic outflow may develop AD. Below the injury, intact peripheral sensory nerves transmit impulses that ascend in the spinothalamic and posterior columns to stimulate sympathetic neurons located in the intermediolateral gray matter of the spinal cord. The inhibitory outflow above the SCI from cerebral vasomotor centers is increased, but it is unable to pass below the block of the SCI. This large sympathetic outflow causes release of various neurotransmitters (norepinephrine, dopamine-b-hydroxylase, dopamine), causing piloerection, skin pallor, and severe vasoconstriction in arterial vasculature.[3] The result is sudden elevation in blood pressure and vasodilation above the level of injury. Patients commonly have a headache caused by vasodilation of pain-sensitive intracranial vessels. Vasomotor brainstem reflexes attempt to lower blood pressure by increasing parasympathetic stimulation to the heart through the vagus nerve to cause compensatory bradycardia. The fact that this reflex action cannot compensate for severe vasoconstriction is explained by the Poiseuille formula, which demonstrates that pressure in a tube is affected to the fourth power by a change in radius (vasoconstriction); the pressure is affected only linearly by a change in flow rate (bradycardia). Parasympathetic nerves prevail above the level of injury, which may be characterized by profuse sweating and vasodilation with skin flushing. Cameron and colleagues found that site-directed genetic manipulation of fiber sprouting in the spinal dorsal horns in a cord compression rat model could alter the extent of hyperreflexia after bowel distention, indicating that endogenous spinal cord circuitry/neural sprouting plays a role in the pathophysiology of AD.[4]
Episodes of AD can be triggered by many potential causes.[5] Essentially any painful, irritating, or even strong stimulus below the level of the injury can cause an episode of AD. Although the list is not comprehensive, the following events or conditions all can cause episodes of AD:
Bladder distention Urinary tract infection Cystoscopy Urodynamics[6] Detrusor-sphincter dyssynergia[7] Epididymitis or scrotal compression Bowel distention Bowel impaction Gallstones Gastric ulcers or gastritis Invasive testing Hemorrhoids Gastrocolic irritation Appendicitis or other abdominal pathology trauma Menstruation Pregnancy - Especially labor and delivery Vaginitis Sexual intercourse Ejaculation Deep vein thrombosis Pulmonary emboli Pressure ulcers Ingrown toenail Burns or sunburn Blisters
Insect bites Contact with hard or sharp objects Temperature fluctuations Constrictive clothing, shoes, or appliances Heterotopic bone Fractures or other trauma Surgical or diagnostic procedures Pain
Good bladder and bowel care (ie, preventing fecal impaction, bladder distention) are mainstays in preventing episodes of autonomic dysreflexia.
History
The patient with autonomic dysreflexia (AD) generally gives a history of blurry vision, headaches, and a sense of anxiety. Feelings of apprehension or anxiety over an impending physical problem commonly are exhibited.
Physical Examination
A patient with AD may have 1 or more of the following findings on physical examination:
Sudden, significant rise in systolic and diastolic blood pressure Profuse sweating above the level of lesion - Especially in the face, neck, and shoulders; rarely occurs below the level of the lesion because of sympathetic cholinergic activity Goose bumps above, or possibly below, the level of the lesion Flushing of the skin above the level of the lesion - Especially in the face, neck, and shoulders; this is a frequent symptom Blurred vision Spots in the patient's visual field Nasal congestion A common symptom
With regard to the first item above, the sudden rise in blood pressure in AD is usually associated with bradycardia. Normal systolic blood pressure for SCI above T6 is 90-110 mm Hg; blood pressure 20-40 mm Hg above the reference range for such patients may be a sign of AD. However, patients with AD may display no symptoms, despite elevated blood pressure. Differentials for AD include essential hypertension and pheochromocytoma.
degree of autonomic dysreflexia, as well as of vesicoureteral reflux, hydronephrosis, and urinary tract infection.