Autonomic dysreflexia
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| Autonomic dysreflexia | |
|---|---|
| Classification and external resources | |
| ICD-9 | 337.3 |
| DiseasesDB | 1155 |
| MedlinePlus | 001431 |
| eMedicine | article/322809 |
| MeSH | D020211 |
Autonomic dysreflexia, "AD" also known as "autonomic hyperreflexia or Hyperreflexia, is a potentially life threatening condition which can be considered a medical emergency requiring immediate attention. AD occurs most often in spinal cord-injured individuals with spinal lesions above the (T6) spinal cord level. Acute AD is a reaction of the autonomic (involuntary) nervous system to overstimulation. It is characterised by severe paroxysmal hypertension (episodic high blood pressure) associated with throbbing headaches, profuse sweating, nasal stuffiness, flushing of the skin above the level of the lesion, bradycardia, apprehension and anxiety, which is sometimes accompanied by cognitive impairment. [1]The sympathetic discharge that occurs is usually 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).
Contents
Causes
The most common causes of autonomic hyperreflexia in patients 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. 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.[2] 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 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 psychotropic and 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-Barre syndrome a demyelinating disease that can result in peripheral paralysis can progress to encompass autonomic functions leading to a loss of normal respiratory, bladder and bowel function, thus resulting in autonomic dysreflexia. Severe head trauma, and other brain injuries[3] 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 volutary abiliity 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.
Controversy Over Peripherally Noxious Causes of Autonomic Dysreflexia
Current scientific literature suggests that noxious (painful) stimuli are the primary initiators of AD. 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. [4] [5]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 causitive factors include palpation of the bladder and bowel and can also include bladder scan.
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, 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 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.
Onset
The risk is greatest with cervical spinal cord lesions and is rare with lesions below T6 Thoracic vertebrae. 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 hemorrhage.
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
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<references />, or <references group="..." />- Karlsson AK. Autonomic dysreflexia. Spinal Cord 1999; 37: 383–391.
- 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
- [1] 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.
- [2] Consortium for Spinal Cord Medicine (2001) Autonomic Dysreflexia: What you should know. Paralyzed Veterans of America, Washington, DC.
- ↑ Khastgir J, Drake MJ, Abrams P (2007). "Recognition and effective management of autonomic dysreflexia in spinal cord injuries". Expet Opin Pharmacother. 8 (7): 945–956. doi:10.1517/14656566.8.7.945. PMID 17472540.
- ↑ University Hospital Balgrist, Zurich, Switzerland - Sacral posterior rhizotomy suppressing autonomic hyper-reflexia in patients with spinal cord injury, UJUS 2009, Retrieved 4 Apr. 2010
- ↑ http://www.nlm.nih.gov/medlineplus/ency/article/001431.htm
- ↑ Burton AR, Brown R, Macefield VG? (2008). "Selective activation of muscle and skin nociceptors does not trigger exaggerated sympathetic responses in spinal-injured subjects". Spinal Cord. 46: 660–665. PMID 18427566. Text "doi:10.1038/sc.2008.33 " ignored (help)
- ↑ Marsh DR, Weaver LC? (2004). "Autonomic dysreflexia, induced by noxious or innocuous stimulation, does not depend on changes in dorsal horn substance p". Journal of Neurotrauma. 21 (6): 817–828. PMID 15253807. Text "doi:10.1089/0897715041269605 " ignored (help)
