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Autonomic dysreflexia
Other names	Autonomic hyperreflexia
Specialty	Neurology

Autonomic dysreflexia (AD) is a life-threatening medical emergency characterized by hypertension and cardiac arrhythmias. This condition is sometimes referred to as autonomic hyperreflexia. Most cases of AD occur in individuals with spinal cord injuries. Lesions at or above the T6 spinal cord level are more frequently reported, although there are reports of AD in patients with lesions as low as T10. Guillain–Barré syndrome may also cause autonomic dysreflexia.

Hypertension in AD may result in mild symptoms, such as sweating above the lesion level, goosebumps, blurred vision, or headache. Severe symptoms may result in life-threatening complications including seizure, intracranial bleeds (stroke), myocardial infarction, and retinal detachment.

Both noxious and non-noxious stimuli can trigger AD. The result is stimulation and hyperactivity of the sympathetic nervous system. The noxious stimuli activate a sympathetic surge that travels 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. This surge originates 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 to reduce elevated blood pressure. This can result in bradycardia, tachycardia, vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion. Piloerection and pale, cool skin occur below the lesion due to the prevailing sympathetic outflow.

The most common causes include bladder or bowel over-distension from urinary retention and fecal compaction. Other causes include pressure sores, extreme temperatures, fractures, undetected painful stimuli (such as a pebble in a shoe), sexual activity, and extreme spinal cord pain.

Treating AD immediately involves removing or correcting the noxious stimuli. This entails sitting the patient upright, removing any constrictive clothing (including abdominal binders and support stockings), and rechecking blood pressure often. The inciting issue may require urinary catheterization or bowel disimpaction. If systolic blood pressure remains elevated (over 150 mm Hg) after these steps, fast-acting short-duration antihypertensives are considered, while other inciting causes must be investigated for the symptoms to resolve.

Educating the patient, family, and caregivers about the avoidance of triggers and the cause, if known, is important in the prevention of AD. Since bladder and bowel are common causes, routine bladder and bowel programs and urological follow-up may help reduce the frequency and severity of attacks. These follow-ups may include cystoscopy/urodynamic studies.

Signs and symptoms

This condition is distinct and usually episodic. An elevation of 20 mm Hg over baseline systolic blood pressure, with a potential source below the neurological level of injury, meets the current definition of dysreflexia.

Common presenting symptoms include:

• headache
• diaphoresis
• increased blood pressure
• facial erythema
• goosebumps
• nasal stuffiness
• a "feeling of doom" or apprehension
• blurred vision.

Complications

Autonomic dysreflexia can become chronic and recurrent. This often occurs in response to longstanding medical problems like soft tissue pressure injuries or hemorrhoids.

Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction, or cerebral hemorrhage. Other organs that may be affected include the kidneys and retinas of the eyes. Long-term therapy to decrease blood pressure may include alpha blockers or calcium channel blockers.

Causes

The first episode of autonomic dysreflexia may occur weeks to years after the spinal cord injury takes place. Most people at risk develop their first episode within the first year after the injury.

There are many possible triggers of AD. The most common causative factor is bladder distention. Other causes include urinary tract infections, urinary retention, blocked catheters, constipation, hemorrhoids or fissures, skin damage, fractures, and sexual intercourse. It is important to note that not all noxious stimuli will cause AD. Some otherwise severe noxious stimuli, e.g. broken bones, may not result in AD, and may in fact even go unnoticed. In the absence of clear triggering factors, recurrent episodes of AD can be important signs that there is an underlying pathology in a patient that has not yet been discovered.

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 by 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. This controls vessel diameter and resistance. The adrenal medulla indirectly controls the same action through the release of epinephrine and norepinephrine.

In a patient with a spinal cord lesion, the descending autonomic pathways that are responsible for the supraspinal communication with the SPN are interrupted. This results in decreased sympathetic outflow below the level of the injury. In this circumstance, the SPN is controlled only by spinal influences.

After a spinal injury, the decreased sympathetic outflow causes reduced blood pressure and sympathetic reflex. Eventually, synaptic reorganization and plasticity of the SPN develops into an overly sensitive state. Because of this, there is abnormal reflex activation of SPN due to afferent stimuli. Most commonly, bowel or bladder distension.

Reflex activation then results in systemic vasoconstriction below the spinal cord disruption. This peripheral arterial vasoconstriction and hypertension activates the baroreceptors. There is a resultant parasympathetic surge originating in the central nervous system which inhibits the sympathetic outflow. This 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. Below the lesion, piloerection, paleness, and cool skin occur due to the prevailing sympathetic outflow. This issue is much more prominent for lesions at or above the T6 level. This is because the splanchnic nerves emerge from the T5 level and below.

Diagnosis

AD is diagnosed by documenting an increase in systolic blood pressure greater than 20 to 30 mmHg. The associated symptoms vary from life-threatening to asymptomatic.

Autonomic dysreflexia differs from autonomic instability. Autonomic instability is characterized by modest cardiac and neurological changes that accompany a spinal cord injury. Signs and symptoms include bradycardia, orthostatic hypotension, and ambient temperature intolerance. Because of this more common condition, elevated blood pressure in patients with baseline hypotension may not be recognized unless compared with their baseline levels.

Apart from the increased blood pressure, additional symptoms help differentiate AD from other conditions. These include sweating, spasms, erythema (more likely in upper extremities), headaches, and blurred vision. Older patients with very incomplete spinal cord injuries and systolic hypertension may be experiencing essential hypertension, not autonomic dysreflexia, if they lack additional symptoms.

Treatment

Initial management of AD includes measuring and monitoring blood pressure and sitting the patient upright to attempt to lower their blood pressure. It is also important to search for and correct the triggering stimuli. Tight clothing and pressure stockings should be removed. Catheterization of the bladder should be performed as well as evaluation for possible urinary tract infection (UTI). Indwelling catheters should be checked for obstruction. Relief of a blocked urinary catheter tube may resolve the problem. A rectal examination can be performed to clear the rectum of any possible stool impaction. If the noxious precipitating trigger cannot be identified, prompt pharmacologic treatment may be needed. In this situation, the aim is to decrease the elevated intracranial pressure until further studies can identify the cause.

Pharmacologic treatment includes rapidly acting vasodilators. Options include sublingual or topical nitrates as well as oral hydralazine or clonidine. Ganglionic blockers can also be used to control sympathetic nervous system outflow. Epidural anesthesia has been demonstrated to be effective in reducing AD in women in labor. However, there is less evidence for its use in reducing AD during general surgical procedures.

Prognosis

Mortality is rare with AD, but morbidities such as stroke, retinal hemorrhage, and pulmonary edema if left untreated can be quite severe. The cause of autonomic dysreflexia itself can be life-threatening. There must be proper investigation and appropriate treatment of the inciting cause to prevent unnecessary morbidity and mortality.

Attacks can be prevented by recognizing and avoiding triggering stimuli. Because bladder distension is a common trigger of AD, botulinum toxin used to treat bladder dysfunction in SCI patients may be effective in reducing attacks. Prophylactic use of medications has also been reported to prevent attacks. Some examples include nifedipine, prazosin, and terazosin. If the episode of AD is triggered by bowel or bladder irritants, topical analgesics such as lidocaine and bupivacaine are commonly used. Yet, their effectiveness in reducing AD remains inconclusive.

References

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4. "Autonomic dysreflexia". Medline. NIH. Retrieved 19 March 2019.
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6. ^ Daroff RB, Jankovic J, Mazziotta JC, Pomeroy SL, Bradley WG (2016). Bradley's neurology in clinical practice (Seventh ed.). London: Elsevier. ISBN 978-0-323-28783-8. OCLC 932031625.
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17. Marsh DR, Weaver LC (June 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. doi:10.1089/0897715041269605. PMID 15253807.
18. ^ Wan D, Krassioukov AV (January 2014). "Life-threatening outcomes associated with autonomic dysreflexia: a clinical review". The Journal of Spinal Cord Medicine. 37 (1): 2–10. doi:10.1179/2045772313Y.0000000098. PMC 4066548. PMID 24090418.
19. Vaidyanathan, Subramanian; Soni, Bakul M.; Mansour, Paul; Oo, Tun (2017-11-02). "Fatal collapse due to autonomic dysreflexia during manual self-evacuation of bowel in a tetraplegic patient living alone: lessons to learn". International Medical Case Reports Journal. 10: 361–365. doi:10.2147/IMCRJ.S135586. PMC 5679675. PMID 29138603.
20. Solinsky R, Bunnell AE, Linsenmeyer TA, Svircev JN, Engle A, Burns SP (October 2017). "Pharmacodynamics and effectiveness of topical nitroglycerin at lowering blood pressure during autonomic dysreflexia". Spinal Cord. 55 (10): 911–914. doi:10.1038/sc.2017.58. PMID 28585557.
21. Petsas, Anna; Drake, Jeremy. "Perioperative management for patients with a chronic spinal cord injury". academic.oup.com. Retrieved 2023-10-26.
22. Gray, Katherine; Sheehan, Whitley; McCracken, Laura; Krogh, Klaus; Sachdeva, Rahul; Krassioukov, Andrei V. (12 August 2022). "Are local analgesics effective in reducing autonomic dysreflexia in individuals with spinal cord injury? A systematic review". Spinal Cord. 61 (1): 1–7. doi:10.1038/s41393-022-00840-8. ISSN 1476-5624. PMID 35962043.

Further reading

• Allman KG, McIndoe A, Wilson IH (2005). Emergencies in anaesthesia. Oxford: Oxford University Press. p. 18. ISBN 978-0-19-852099-3.
• Lin VWH, Cardenas DD, Cutter NC, Frost FS, Hammond MC (2010). Spinal Cord Medicine: Principles and Practice (2nd ed.). Demos Medical Publishing. ISBN 978-1-933864-19-8.
• Consortium for Spinal Cord Medicine (2001). "Acute Management of Autonomic Dysreflexia: Individuals with Spinal Cord Injury Presenting to Health-Care Facilities" (PDF) (2nd ed.). Washington DC: Paralyzed Veterans of America. Archived from the original (PDF) on 2018-04-07. Retrieved 2018-04-07.
• Vallès M, Benito J, Portell E, Vidal J (December 2005). "Cerebral hemorrhage due to autonomic dysreflexia in a spinal cord injury patient". Spinal Cord. 43 (12): 738–740. doi:10.1038/sj.sc.3101780. PMID 16010281.

External links

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• Peripheral nervous system disorders