Autonomous dysfutia ( AD ), also known as autonomic hyperreflexia or reflex mass , is a medical emergency and condition characterized by uncontrolled hypertension and bradycardia, although tachycardia is known to occur. DA is most common in individuals with spinal cord injury with lesions above the T6 spinal level, although it has been reported in patients with lesions as low as T10.
Uncontrolled hypertension in AD can cause mild symptoms, such as discomfort, blurred vision and headaches; However, severe hypertension can lead to potentially life-threatening complications including seizures, intracranial bleeding, or retinal release.
AD is triggered by dangerous or non-harmful stimuli, resulting in sympathetic and hyperactive stimulation. The most common causes include bladder or bowel movements, from urinary retention and fecal compaction, respectively. The resulting sympathetic wave transmits through peripheral nerves intact, resulting in systemic vasoconstriction below the level of the spinal cord lesion. Arterial vasoconstriction and peripheral hypertension activate baroreceptors, producing parasympathetic waves derived from the central nervous system to inhibit sympathetic flow; however, parasympathetic signals can not transmit below the level of the spinal cord lesions. This causes vasodilation, flushing, pupil constriction and nasal congestion over the spinal lesions, while there is a piloerection, pale and cold skin beneath the lesions due to existing sympathetic flow.
Initial care involves sitting upright patients, removing anything constrictive (including clothing), re-checking blood pressure frequently, and then checking and removing instigating problems, which may require urinary catheterization or bowel implantation. If the blood pressure remains high (more than 150 mmHg) after the initial step, rapid short-acting antihypertensive is considered, while other instigating causes should be investigated for symptoms to resolve.
AD Prevention involves educating the patient, family and carer causing the cause, if known, and how to avoid it, as well as other triggers. Because the bladder and bowel are a common cause, prevention involves bladder and bowel programs routine and urological follow up for cystoscopy/urodynamic studies.
Video Autonomic dysreflexia
Signs and symptoms
This condition is different and usually episodic, with people who have very high blood pressure (often with systolic readings over 200 mm Hg), intense headaches, excessive sweating, facial erythema, goose bumps, stuffy noses, "doomsets" or fear, and blurred vision. An increase of 40 mm Hg over the initial systolic should be suspicious for dysreflexia.
Complications
Autonomic dyslexesis may become chronic and recurrent, often in response to long-standing medical problems such as soft tissue ulcers or hemorrhoids. Long-term therapy may include alpha blockers or calcium channel blockers.
Complications of severe acute hypertension may include seizures, pulmonary edema, myocardial infarction or cerebral hemorrhage. Additional organs that may be affected include kidney and eye retina.
Maps Autonomic dysreflexia
Cause
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 intestinal cases and distension in the case of the bladder. It is commonly found in patients with spinal cord injury above T6 (thoracic vertebral 6), but may occur in patients with transection as low as T10 (10th thoracic vertebral).
The first episode can occur week after year after a spinal cord injury occurs, but most people at risk (80%) develop their first episode within the first year after injury. Once a person experiences the 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 excited autonomic nervous system.
Another possible cause is an undetectable urinary tract infection. Difficulties in assessing this may be complicated by the use of catheters in the body or suprapubic. When painful stimuli occur, such as when urination is stopped or intestinal obstruction occurs, nerve impulses are sent to the brain through the spinal cord. However, in spinal cord transections, these impulses can not travel through injury. It produces a spinal cord reflex to the autonomic nervous system in response to pain. In patients with spinal cord transfers, the type of stimulation tolerated by a healthy person creates an exaggerated response from the person's nervous system.
Other causes include drug side effects and various disease processes. The use of stimulants such as cocaine and amphetamines that can cause urinary retention, and the use of CNS depressants and other psychoactive drugs may also cause urinary retention and constipation resulting in autonomic dysfunction when used for long periods of time. Guillain-BarrÃÆ'Â © Syndrome is a demyelinating disease that can cause peripheral paralysis and may develop to include autonomic functions, leading to loss of normal respiratory, bladder and bowel function resulting in autonomic disrefllexia. Severe head trauma and other brain injuries can trigger autonomic dysrhythmias in the central nervous system by interfering with the reception of signals that encourage emptying of the bladder and intestines and with the voluntary ability to urinate and defecate. Other causal theories for autonomic dysreflexia include harmful stimuli, or painful stimuli arising from peripheral sensory neurons. These stimuli are impaired in their journey to the brain due to the transection of the spinal results in the paradoxical stimulation of the autonomic pathways of the autonomic nervous system.
Pain
The current scientific literature shows that harmful stimuli (painful) are the main initiators of the army. (Note: Not all harmful stimuli will cause AD Some other harmful stimuli in normal people, such as fractures, will not produce AD, and may even be unknown.) However, different studies have found that activation of pain receptors in muscle and the skin beneath the lesion on the spinal cord of the injured person does not precipitate AD. These studies show that not all harmful stimuli are reliable AD triggers, and since non-harmful stimuli can also trigger AD, attribution of AD episodes to harmful stimuli may cause physicians to ignore non-harmful triggers. As a result, the harmless trigger factor remains undetected, extending the AD episode. They conclude that when it comes to the potential causes of AD, it is important to consider non-hazardous sources of stimulation other than harmful triggers. Current assessment of autonomic dysreflexia in patients with known causes factors includes palpation of the bladder and bowel and may also include bladder scans.
Mechanism
The supraspinal vasomotor neuromes send projection to intermediolateral cell columns, composed of sympathetic preganglionic neurons (SPNs) through the T1-L2 segment. Supraspinal neurons work on the SPN and its tonic shoots, modulating its action on the peripheral sympathetic tissue ganglia and the adrenal medulla. The sympathetic ganglia act directly on the blood vessels they are preserved throughout the body, controlling the diameter and resistance of the blood vessels, while the adrenal medulla indirectly controls the same action through the release of epinephrine and norepinephrine. The decreased autonomic route, responsible for supraspinal communication with the NES, is disrupted resulting in a decrease in sympathetic flow below the injury rate. Under these circumstances, the NES is controlled only by the influence of the spine. The first few weeks after spinal cord injury, decreased sympathetic flow leads to decreased blood pressure and sympathetic reflexes. Finally, the synaptic reorganization and SPN plasticity develop into an overly sensitive state, resulting in an abnormal SPN reflex activation due to afferent stimuli, such as bowel distension or bladder. The result of reflex activation in systemic vasoconstriction under spinal cord disturbance. Peripheral arterial vasoconstriction and hypertension activate baroreceptors, producing parasympathetic waves derived from the central nervous system, which inhibit sympathetic flow; however, parasympathetic signals can not transmit below the level of the spinal cord lesions. This causes vasodilation, flushing, pupil constriction and nasal congestion over the spinal lesions, while there is a piloerection, pale and cold skin beneath the lesions due to existing sympathetic flow.
Diagnosis
Symptoms are usually not smooth, although asymptomatic events have been documented. Autonomic dysreflexia differs from autonomic instability, a variety of simple cardiac and neurologic changes that accompany spinal cord injuries, including bradycardia, orthostatic hypotension, and environmental temperature intolerance. In autonomic dysreflexia, the patient will develop hypertension, sweating, seizures (sometimes severe seizures) and erythema (more likely in the upper limb) and may suffer from headaches and blurred vision. Mortality is rare in DA, but morbidity such as stroke, retinal hemorrhage and pulmonary edema if left untreated can be severe. Older patients with very incomplete spinal cord injuries and symptomless systolic hypertension usually develop essential hypertension, not autonomic disrefleksia. Aggressive treatment in these elderly patients with fast-acting antihypertensive drugs can have poor results.
Treatment
Proper treatment of autonomic dysreflexia involves administration of anti-hypertension along with the immediate determination and removal of stimulating stimuli. Often, sitting the patient and dangle the legs on the bed can reduce blood pressure below dangerous levels and provide partial symptomatic relief. Tight clothes and stockings should be removed. Direct bladder catheterization every 4 to 6 hours, or eliminating blocked urinary catheter can solve the problem. The rectum should be cleaned of impaction stool, using anesthetic lubricating jelly. If a dangerous trigger trigger can not be identified, drug therapy is needed to reduce the increase in intracranial pressure until further research can identify the cause.
Drug treatments include fast-acting vasodilators, including sublingual nitrate or oral clonidine. Ganglionic blockers are also used to control the outflow of the sympathetic nervous system. Topical nitropaste is a comfortable and safe treatment - one or two inches can be applied to the chest wall, and removed when blood pressure begins to normalize. Autonomic dysreflexia is temporarily removed by spinal or general anesthesia. This treatment is used during the delivery of obstetric women with autonomic dysreflexia.
Prognosis
The cause of autonomic dysreflexia itself can be life-threatening, and should also be thoroughly 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 disrefleksia in adults, children, and pregnant women. There are also consumer versions of these guidelines.
See also
- Leading individual with AD - Jeff Erlanger interviewed by Fred Rogers
References
Further reading
Source of the article : Wikipedia
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