After the resolution of spinal shock, the return of normal reflexes may be hyperactive and exaggerated. Injury above T6 causes reflex stimulation of sympathetic nervous system and result in major uncompensated cardiovascular reactions. The sensory receptors below the level of injury are stimulated with a reflex arteriolar vasoconstriction that increases blood pressure. However, due to the spinal cord injury, the parasympathetic nervous system is unable to counteract the sympathetic nervous system's response.
Autonomic dysreflexia may cause episodic high blood pressure known as paroxysmal hypertension. After the resolution of spinal cord injury, the arteriolar reflex is activated and causes vasoconstriction that increases blood pressure. The patient's systolic blood pressure may read as high as 300 mm Hg. Monitor the patient's blood pressure frequently during the episode.
After spinal cord injury, increased blood pressure stimulates the parasympathetic nervous system and results in decreased heart rate. Autonomic dysreflexia may cause bradycardia and decrease the heart rate to 30-40 beats/minute.
Since there is an increased in warm blood circulating in the area, the patient with autonomic dysreflexia may experience diaphoresis above the level of injury.
The patient with autonomic dysreflexia may experience flushing of the skin above the level of injury due to the increased amount of blood in the area.
Autonomic dysreflexia may cause pilomotor spasms that cause goosebumps. In addition, the patient may experience erection of body hair known as piloerection.
Since autonomic dysreflexia increases the amount of fluid circulating above the level of injury, the patient may experience nasal congestion.
The patient with autonomic dysreflexia may experience a throbbing headache. This is caused by an increase of blood being shunted to above the level of the injury. If the patient with spinal cord injury complains of a headache, measuring the blood pressure is critical in helping to determine the presence of autonomic dysreflexia.
Immediately elevate the patient's head of the bed or place them in an upright sitting position to help decrease the elevated blood pressure. Determine the noxious stimuli causing the autonomic dysreflexia and alert the medical team.
Removing the noxious stimuli will help resolve autonomic dysreflexia. Common causes include a distended bladder or impacted rectum. Immediate catheterization may be necessary to relieve bladder distention. If the patient already has an inserted Foley catheter, assess for kinks, folds, or plugs in the tubing. Stool impaction may require applying anesthetic lubricating ointment to decrease rectal stimulation before performing a digital rectal examination. Other causes include stimulation of sensory receptors, skin, or pain receptors. If the cause is skin stimulation, loosening the patient's constrictive clothing and tight shoes will also help relieve symptoms. If symptoms remain after removing the noxious stimuli, an alpha-adrenergic blocker or arteriolar vasodilator may be administered to help stabilize vital signs.
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