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]

Causes of autonomic dysreflexia

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.

Treatment of High Blood Pressure

Check the patient's blood pressure. If the blood pressure is elevated and the person is supine, have the person sit up immediately and loosen any clothing or constrictive devices. Sitting leads to pooling of blood in the lower extremities and may reduce blood pressure. Monitor blood pressure and pulse every 2-5 minutes until the patient has stabilized; impaired autonomic regulation can cause blood pressure to fluctuate quickly during an episode of autonomic dysreflexia (AD). Survey the person for instigating causes, beginning with the urinary system, the most common cause of AD.[8, 6] If an indwelling urinary catheter is not in place, catheterize the patient. If the individual has an indwelling urinary catheter, check the system along its entire length for kinks, folds, constrictions, or obstructions and for correct placement. If the catheter appears to be blocked, gently irrigate the bladder with a small amount of fluid, such as normal saline at body temperature. Avoid manually compressing or tapping on the bladder. If the catheter is draining and blood pressure remains elevated, suspect fecal impaction, the second most common cause of AD, and check the rectum for stool, using lidocaine jelly as lubricant. Use an antihypertensive agent with rapid onset and short duration while the causes of AD are being investigated if the blood pressure is at or above 150 mm Hg systolic. The most commonly used agents are nifedipine and nitrates (eg, nitroglycerine paste). Nifedipine should be in the immediate release form; bite and swallow is the preferred method of administering the drug, not sublingual administration. Other agents used are mecamylamine, diazoxide, and phenoxybenzamine. Use antihypertensives with extreme caution in older persons or in people with coronary artery disease. Monitor the individual's symptoms and blood pressure for at least 2 hours after resolution of the AD episode to ensure that elevation of blood pressure does not recur. AD may resolve because of medication, not because of resolution of the underlying cause. If there is poor response to treatment and/or if the cause of the AD has not been identified, send the patient to the emergency room (ER) for monitoring, maintenance of pharmacologic control of blood pressure, and investigation of other possible causes of the AD. Remember to document the episode of AD. Patients who have previously experienced episodes of AD are treated with antihypertensives prior to procedures known to cause their episodes. A Taiwanese study indicated that in patients with SCI who have detrusor sphincter dyssynergia, using a combination of fluoroscopy and electromyography to localize the external urethral sphincter, with a Foley catheter employed to visualize vesicourethral anatomy, makes transperineal injection of botulinum toxin type A into the external urethral sphincter safe, accurate, and easy to perform.[7] Such injections have been shown to reduce the occurrence and

degree of autonomic dysreflexia, as well as of vesicoureteral reflux, hydronephrosis, and urinary tract infection.