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| title | chunk | source | category | tags | date_saved | instance |
|---|---|---|---|---|---|---|
| Autonomic dysreflexia | 2/3 | https://en.wikipedia.org/wiki/Autonomic_dysreflexia | reference | science, encyclopedia | 2026-05-05T07:26:24.727358+00:00 | kb-cron |
The autonomic nervous system comprises the sympathetic, parasympathetic, and enteric nervous systems. The mechanism of autonomic dysreflexia has to do with the relationship of the sympathetic and parasympathetic systems. Supraspinal vasomotor neurons send projections to the intermediolateral cell column, which is composed of sympathetic preganglionic neurons (SPN) through the T1-L2 segments of the spinal cord. 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 and there is a heightened sympathetic response. 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 == Autonomic dysreflexia 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. An essential step to diagnosing AD is careful monitoring of blood pressure and other vital sign changes. Having knowledge of the patient's baseline blood pressure can be helpful in diagnosing AD. Especially in cases of patients with baseline hypotension since the condition 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.
=== Differential Diagnoses === Other diagnoses that should be considered due to similar presentation include:
Intracranial hemorrhage Ischemic stroke Hyperthyroidism Anxiety Essential hypertension Drug overdose
== Treatment == Initial management of autonomic dysreflexia 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 stimuli cannot be identified or the systolic blood pressure remains above 150 mmHg, then 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 will include antihypertensive medications. 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. 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. 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. Patients with AD should have a card or file about their medical history in case they have an episode in public. This will help the individuals responding to the episode manage the situation by looking for common triggers. Patients with history of AD should also carry their medications for easy access in emergency scenarios.
== Prognosis == The prognosis of autonomic dysreflexia is generally good, given that the trigger is identified and managed. Attacks can be prevented by recognizing and avoiding triggering stimuli. 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.