Autonomic dysreflexia (AD), also known as autonomic hyperreflexia or mass reflex, is a condition and medical emergency characterized by uncontrolled hypertension and bradycardia, although tachycardia is known to occur. AD occurs most often in individuals with spinal cord injuries with lesions above the T6 spinal cord level, although it has been reported in patients with lesions as low as T10.
The uncontrolled hypertension in AD may result in mild symptoms, such as discomfort, blurred vision and headache; However, severe hypertension may result in potentially life-threatening complications including seizure, intracranial bleed, or retinal detachment.
AD is triggered by either noxious or non-noxious stimuli, resulting in sympathetic stimulation and hyperactivity. The most common causes include bladder or bowel over-distension, from urinary retention and fecal compaction, respectively. The resulting sympathetic surge transmits through intact peripheral nerves, resulting in systemic vasoconstriction below the level of the spinal cord lesion. The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge originating in the central nervous system to inhibit the sympathetic outflow; however, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion. This results in vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, while there's piloerection, pale and cool skin below the lesion due to the prevailing sympathetic outflow.
Initial treatment involves sitting the patient upright, removing anything constrictive (clothing including), rechecking blood pressure frequently, and then checking for and removing the inciting issue, which may require urinary catheterization or bowel disimpaction. If blood pressure remains elevated (over 150 mmHg) after initial steps, fast-acting short-duration antihypertensives are considered, while other inciting causes must be investigated for the symptoms to resolve.
Prevention of AD involves educating the patient, family and caregivers of the precipitating cause, if known, and how to avoid it, as well as other triggers. Since bladder and bowel are common causes, prevention involves routine bladder and bowel programs and urological follow-up for cystoscopy/urodynamic studies.
Video Autonomic dysreflexia
Signs and symptoms
This condition is distinct and usually episodic, with the people experiencing remarkably high blood pressure (often with systolic readings over 200 mm. Hg), intense headaches, profuse sweating, facial erythema, goosebumps, nasal stuffiness, a "feeling of doom" or apprehension, and blurred vision. An elevation of 40 mm Hg over baseline systolic should be suspicious for dysreflexia.
Complications
Autonomic dysreflexia can become chronic and recurrent, often in response to longstanding medical problems like soft tissue ulcers or hemorrhoids. Long term therapy may include alpha blockers or calcium channel blockers.
Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction or cerebral hemorrhage. Additional organs that may be affected include the kidneys and retinas of the eyes.
Maps Autonomic dysreflexia
Causes
The most common symptoms of autonomic hyperreflexia seen in people with spinal cord injury are loss of bowel and bladder function, resulting in impaction in the case of the bowels and distention in case of the bladder. These are generally found in patients with a spinal cord injury above the T6 (6th thoracic vertebral) level, but can occur in patients with a transection as low as T10 (10th thoracic vertebral) level.
The first episode may occur weeks to years after spinal cord injury takes place, but most people at risk (80%) develop their first episode within the first year after injury. Once a person has their first episode of autonomic dysreflexia, the next 7-10 days are critical because there is a high incidence of recurrence within that time. Some people describe this predisposition as an easily excitable autonomic nervous system.
Another causative factor may be an undetected urinary tract infection. The difficulty in assessing this may be complicated with the usage of indwelling or suprapubic catheters. When a painful stimulus occurs, as when voiding is interrupted or a bowel obstruction occurs, nerve impulses are sent to the brain via the spinal cord. However, in spinal cord transection, these impulses are unable to travel past the injury. This results in a spinal cord reflex to the autonomic nervous system in response to pain. In patients with spinal cord transection, types of stimulation that are tolerated by healthy people create an excessive response from the person's nervous system.
Other causes include medication side effects and various disease processes. The use of stimulants such as cocaine and amphetamines which can result in urinary retention, and the use of CNS depressants and other psychoactive drugs can also lead to urinary retention and constipation thus leading to autonomic dysreflexia when in use over an extended period of time. Guillain-Barré syndrome is a demyelinating disease that can result in peripheral paralysis and can progress to encompass autonomic functions, leading to a loss of normal respiratory, bladder and bowel function resulting in autonomic dysreflexia. Severe head trauma and other brain injuries can instigate autonomic dysreflexia at the central nervous system by interfering with the reception of the signal that brings the urge to void the bladder and bowels and with the voluntary ability to micturate and defecate. Other causal theories for autonomic dysreflexia include noxious stimuli, or painful stimuli arising from the peripheral sensory neurons. These stimuli are interrupted in their journey to the brain due to a transection of the spine result in a paradoxical stimulation of autonomic pathways of the autonomic nervous system.
Pain
Current scientific literature suggests that noxious (painful) stimuli are the primary initiators of AD. (Note: Not all noxious stimuli will cause AD. Some otherwise severe noxious stimuli in normal people, e.g. broken bones, will not result in AD, and may in fact even go unnoticed.) However, different studies have found that activation of pain receptors in muscle and skin below the lesion in spinal cord injured individuals did not trigger AD. These studies suggests that not all noxious stimuli are reliable triggers of AD, and because non-noxious stimuli can also trigger AD, attribution of an episode of AD to noxious stimuli may cause clinicians to overlook underlying non-noxious triggers. As a result, non-noxious trigger factors remain undetected, prolonging an episode of AD. They concluded that when deducing the potential causes of AD it is important to consider non-noxious sources of stimulation in addition to noxious triggers. Current assessment of autonomic dysreflexia in patients with known causative factors include palpation of the bladder and bowel and can also include bladder scan.
Mechanism
Supraspinal vasomotor neurons send projections to the intermediolateral cell column, which is composed of sympathetic preganglionic neurons (SPN) through the T1-L2 segments. The supraspinal neurons act on the SPN and its tonic firing, modulating its action on the peripheral sympathetic chain ganglia and the adrenal medulla. The sympathetic ganglia act directly on the blood vessels they innervate throughout the body, controlling vessel diameter and resistance, while the adrenal medulla indirectly controls the same action through the release of epinephrine and norepinephrine. The descending autonomic pathways, which are responsible for the supraspinal communication with the SPN, are interrupted resulting in decreased sympathetic outflow below the level of the injury. In this circumstance, the SPN is controlled only by spinal influences. The first couple weeks after a spinal injury, the decreased sympathetic outflow causes reduced blood pressure and sympathetic reflex. Eventually, synaptic reorganization and plasticity of SPN develops into an overly sensitive state, which results in abnormal reflex activation of SPN due to afferent stimuli, such as bowel or bladder distension. Reflex activation results in systemic vasoconstriction below the spinal cord disruption. The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge originating in the central nervous system, which inhibits the sympathetic outflow; however, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion. This results in vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, while there's piloerection, pale and cool skin below the lesion due to the prevailing sympathetic outflow.
Diagnosis
The symptoms are usually not subtle, although asymptomatic events have been documented. Autonomic dysreflexia differs from autonomic instability, the various modest cardiac and neurological changes that accompany a spinal cord injury, including bradycardia, orthostatic hypotension, and ambient temperature intolerance. In autonomic dysreflexia, patients will experience hypertension, sweating, spasms (sometimes severe spasms) and erythema (more likely in upper extremities) and may suffer from headaches and blurred vision. Mortality is rare with AD, but morbidity such as stroke, retinal hemorrhage and pulmonary edema if left untreated can be quite severe. Older patients with very incomplete spinal cord injuries and systolic hypertension without symptoms are usually experiencing essential hypertension, not autonomic dysreflexia. Aggressive treatment of these elderly patients with rapidly acting antihypertensive medications can have disastrous results.
Treatment
Proper treatment of autonomic dysreflexia involves administration of anti-hypertensives along with immediate determination and removal of the triggering stimuli. Often, sitting the patient up and dangling legs over the bedside can reduce blood pressures below dangerous levels and provide partial symptom relief. Tight clothing and stockings should be removed. Straight catheterization of the bladder every 4 to 6 hrs, or relief of a blocked urinary catheter tube may resolve the problem. The rectum should be cleared of stool impaction, using anaesthetic lubricating jelly. If the noxious precipitating trigger cannot be identified, drug treatment is needed to decrease elevating intracranial pressure until further studies can identify the cause.
Drug treatment includes the rapidly acting vasodilators, including sublingual nitrates or oral clonidine. Ganglionic blockers are also used to control sympathetic nervous system outflow. Topical nitropaste is a convenient and safe treatment--an inch or two can be applied to the chest wall, and wiped off when blood pressures begin to normalize. Autonomic dysreflexia is abolished temporarily by spinal or general anaesthesia. These treatments are used during obstetric delivery of a woman with autonomic dysreflexia.
Prognosis
The cause of autonomic dysreflexia itself can be life-threatening, and must also be completely investigated and treated appropriately to prevent unnecessary morbidity and mortality.
The Consortium for Spinal Cord Medicine has developed evidence-based clinical practice guidelines for the management of autonomic dysreflexia in adults, children, and pregnant women. There is also a consumer version of this guideline.
See also
- Notable individual with AD - Jeff Erlanger interviewed by Fred Rogers
References
Further reading
Source of the article : Wikipedia