Last Updated: May 24, 2001

Background: 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.

Pathophysiology: This phenomenon 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. 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. This reflex action cannot compensate for severe vasoconstriction, explained by the Poiseuille formula, where pressure in a tube is affected to the fourth power by change in radius (vasoconstriction) and only linearly by 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.

Frequency:

In the US: Incidence reported in the literature varies; however, generally reported figures suggest incidence in 48-90% of all individuals who are injured at T6 and above. Some incidence has been reported in SCI as low as T10. AD occurs during labor in approximately two thirds of pregnant women with SCI above the level of T6. The occurrence of AD increases as the patient evolves out of spinal shock. With the return of Sacral reflexes, the possibility of AD increases.

Mortality/Morbidity: Morbidity is associated with the hypertension, which can cause retinal/cerebral hemorrhage, myocardial infarction, or seizures. Mortality is rare.

Sex: The male-to-female ratio for sustaining SCI is 4:1; therefore, AD is primarily a male phenomenon.

Age: No specific relationship has been documented between AD and age.

History: The patient 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: A patient may have one or more of the following findings on physical examination:

• A sudden significant rise in both systolic and diastolic blood pressures, usually associated with bradycardia, can appear. 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.
• Profuse sweating above the level of Lesion, especially in the face, neck, and shoulders, may be noted, but it rarely occurs below the level of the lesion because of sympathetic cholinergic activity.
• Goose bumps above, or possibly below, the level of the lesion may be observed.
• Flushing of the skin above the level of the lesion, especially in the face, neck, and shoulders, frequently is noted.
• The patient may report blurred vision.
• Appearance of spots in the patient's visual fields may be noted.
• Nasal congestion is common.
• No symptoms may be observed, despite elevated blood pressure.

Causes: Episodes of AD can be triggered by many potential causes. 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 distension
• Urinary Tract Infection
• Cystoscopy
• Urodynamics
• Detrusor-sphincter dyssynergia
• Epididymitis or scrotal compression
• Bowel distension
• 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

Other Problems to be Considered:

Essential hypertension
Pheochromocytoma