Autonomic dysreflexia
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| Autonomic dysreflexia | |
|---|---|
| Specialty | Neurology  |
Autonomic dysreflexia, "AD" or "autonomic hyperreflexia" is a condition characterized by a massive sympathetic discharge that can occur in association with spinal cord injury (SCI) or disease (e.g. multiple sclerosis). AD is believed to be triggered by afferent stimuli (nerve signals that send messages back to the spinal cord and brain) which originate below the level of the spinal cord lesion. It is believed that these afferent stimuli trigger and maintain an increase in blood pressure via a sympathetically mediated vasoconstriction in muscle, skin and splanchnic (gut) vascular beds (Karlsson, 1999). AD is considered as a medical emergency.
Causes
The most common cause of autonomic hyperreflexia is spinal cord injury. This is generallay in patients with a spinal cord injury above the T5 level, but can occur in patients with a transection as low as T10 level. When a painful stimulus 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 sympathetic nervous system in response to pain. In this condition, 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, use of illegal stimulants such as cocaine and amphetamines, Guillain-Barre syndrome (a severe form of paralysis that can lead to respiratory failure), subarachnoid hemorrhage (a form of brain bleeding), severe head trauma, and other brain injuries[1]
Controversy over causes of AD
Current dogma in scientific literature states that noxious (painful) stimuli are the primary initiators of AD. However, a study has found that activation of pain receptors in muscle and skin below lesion in spinal cord injured individuals did not trigger AD (Burton et al. 2008). This study suggests that not all noxious stimuli may be reliable triggers of AD. Since non-noxious stimuli can also trigger AD (Marsh & Weaver 2004), (Burton et al. 2008) suggests that attribution of an episode of AD to assumed noxious stimuli may allow clinicians to overlook underlying non-noxious trigger factors. This may allow underlying non-noxious trigger factors to remain undetected, hence 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.
Diagnosis
The diagnosis is usually not subtle, although asymptomatic events have been documented. Autonomic dysreflexia differs from autonomic instability, a term used to describe the variety of 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, bradycardia, sweating 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 hemmhorage 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.
Onset
The risk is greatest with cervical spinal cord lesions and is rare with lesions below T6[1]. It has rarely been reported in spinal cord lesions as low as T10. 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.
Symptoms
This condition is distinct and usually episodic, with the patient experiencing remarkably high blood pressure (often with systolic readings over 200 mm. Hg), intense headaches, profuse sweating, facial erythema, goosebumps, nasal stuffiness, and a "feeling of doom". An elevation of 40 mm. Hg. over baseline systolic should be suspicious for dysreflexia.
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. Catheterization of the bladder, 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. 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 treatment are used during obstetric delivery of a woman with autonomic 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 haemorrhage.
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.
References
- Karlsson AK. Autonomic dysreflexia. Spinal Cord 1999; 37: 383–391.
- Burton AR et al. Selective activation of muscle and skin nociceptors does not trigger exaggerated sympathetic responses in spinal-injured subjects. Spinal Cord 2008; Apr 22
- Marsh DR, Weaver LC. Autonomic dysreflexia, induced by noxious or innocuous stimulation, does not depend on changes in dorsal horn substance p. J Neurotrauma 2004; 21: 817–828.
- Allman (2005) Emergencies in Anaesthesia, ISBN 0-19-852099-9, 18
- Spinal Cord Medicine: Principles and Practice (2002) Lin VWH, Cardenas DD, Cutter NC, Frost FS, Hammond MC. Demos Medical Publishing
- [2] Consortium for Spinal Cord Medicine (2001)Acute Management of Autonomic Dysreflexia: Individuals with spinal cord injury presenting to health-care facilities. Paralyzed Veterans of America, Washington, DC.
- [3] Consortium for Spinal Cord Medicine (2001) Autonomic Dysreflexia: What you should know. Paralyzed Veterans of America, Washington, DC.
- http://www.nlm.nih.gov/medlineplus/ency/article/001431.htm