Skip to main content

Autonomic Dysreflexia in Spinal Cord Injury

NULL

You have just been dispatched to the home of a 40-year-old male, who is complaining of a sudden onset of a severe headache, blurred vision and diaphoresis. Upon arrival, you find the patient lying on the couch. His initial blood pressure is 220/140 and his heart rate is 125 bpm. As you continue to assess the patient, you notice a wheelchair in the corner. The patient verifies that it is his chair, reporting that he suffered a spinal cord injury approximately eight months ago. His level of injury is T-6. How does this new information change your plan of care?

While his initial complaints may be a cardiac event, a migraine headache or even a stroke, the pre-existing spinal cord injury should refocus your areas of concern and initial care of this patient. The patient may be experiencing the medical emergency known as autonomic dysreflexia. Simple interventions may easily correct some of his presenting symptoms and prevent further injury to the patient.

Autonomic Dysreflexia

Autonomic dysreflexia is an exaggerated response of the nervous system, which may include an increase in blood pressure. It occurs in response to a noxious stimuli arising from a source below the level of a spinal cord injury and may occur after spinal shock resolves. The normal sympathetic response to a painful stimulus is not balanced, because descending impulses are blocked by the spinal cord injury (SCI).1

The most common cause of noxious stimuli is distension of the hollow viscera, such as the urinary bladder or bowel. These account for approximately 80% of autonomic dysreflexia cases.1 The SCI patient often has an indwelling urinary catheter, and simple kinks in the tubing or plugs in the catheter can trigger autonomic dysreflexia. Thus, when caring for a SCI patient, always ensure catheter patency (by making sure the catheter is not kinked or pulled too tight, and that it is actually draining urine). For those patients who self-catheterize, it may be appropriate to have the patient catheterize himself at home, prior to transport. After assuring catheter patency, or a decompressed bladder, assess for signs of a urinary tract infection, such as dark, cloudy urine or sediment in the catheter tubing.

Careful physical exam of the SCI patient is imperative during this crisis. Correction of any noxious stimulus will often reduce both the blood pressure and headache without pharmaceutical intervention. Other causative agents usually not considered in medical emergencies include tight clothing, ingrown toenails and constipation.2 Occasionally, the cause may not be readily found. In those instances, your care is focused on blood pressure control, which should be monitored every 3–5 minutes. Assisting the patient to a sitting position may help lower the blood pressure through lower-extremity vascular pooling. Loosening all restrictive garments (shirts, belts, slacks, straps and even shoes) may also reduce the stimulus.

Notifying the receiving facility is imperative, as pharmaceutical interventions may possibly veer from standard protocol. While your current EMS protocol may not include nifedipine, there is still research indicating its use. Nifedipine 10 mg orally (instruct the patient to bite the capsule, then swallow it) can be used for blood pressure readings of 180 mmHg systolic.1,3 Additional medications that may be used in the prehospital phase of care include nitroglycerin sublingual (1/150) or topical paste (1/2 inch), clonidine 0.1–0.2 mg p.o., and hydralazine 10–20 mg IM/IV.4 Upon arrival at the hospital, the patient may be given sodium nitroprusside in an attempt to reduce the blood pressure to 90–100 mmHg systolic.1

Once the symptoms are resolved, have patients and their family members try to determine the causative factors involved in this episode. They should also receive extensive education about early recognition and treatment of A.D. Finally, encourage the patient to carry some type of medic alert identification. It is estimated that approximately 85% of spinal cord injury patients at level T-6 will suffer at least one episode of autonomic dysreflexia. Knowledgeable, educated patients and healthcare providers will be able to treat this medical emergency quickly and efficiently, while minimizing the associated risks.

Pathophysiology of Autonomic Dysreflexia

Spinal cord injury is a disease of young adults. An estimated 11,000 cases occur each year, with the number of living persons afflicted with the injury at approximately 183,000–230,000.2 Fifty-five percent of injuries occur in the 16–30-year-old age group; males sustain spinal cord injuries at a rate four times higher than females. The most frequent cause of SCI is motor vehicle accidents, followed by falls, violence, sports injuries and other types of injuries, including suicide attempts and occupational injuries. Both alcohol and drugs have been cited as contributing factors in SCI.2

The spinal column begins at the base of the skull and ends at the coccyx, or tailbone. Approximately 32–33 individual vertebral bodies make up the spinal column: 7 cervical, 12 thoracic, 5 lumbar, 5 fused sacral and 3-4 fused coccygeal vertebrae. The intervertebral disks and the supporting ligaments assist the vertebral column in supporting and protecting the spinal cord. Injuries to the vertebral column can include fractures, dislocations and subluxations (partial dislocations). The level at which the injury occurs affects body functions and determines the degree of impairment.

Incomplete spinal cord injuries occur when the patient still has residual function more than three segments below the level of injury. Complete spinal cord injuries imply there is no motor or sensory function more than three levels below the level of injury. Complete cord injuries can result from severance of the cord, disruption of nerve fibers themselves or interruption of the blood supply to the affected segment.

Functional abilities after a SCI are subject to several degrees of altered reflex activity based on the level of cord injury and the extent of damage. Thoracic injuries (T-1 through T-12), for example, allow full upper extremity control with limited to full control of intercostal and trunk muscle and balance. Individuals with a spinal cord injury at the thoracic level T-6 or above are generally at risk of developing autonomic dysreflexia.

Individuals with injuries above the major splanchnic outflow, which is T-6 through L-2, have the potential for developing autonomic dysreflexia. Intact sensory nerves below the level of the injury transmit impulses to the spinal cord, which ascends in the spinothalamic and posterior columns. Sympathetic neurons in the intermediolateral gray matter are stimulated by these ascending impulses. Sympathetic inhibitory impulses that originate above T-6 are blocked due to injury. Therefore, below the injury, there is a relatively unopposed sympathetic outflow with a release of norepinephrine, dopamine-beta-hydroxylase and dopamine. The release of these chemicals may cause skin pallor, severe vasoconstriction and a sudden increase in blood pressure. The elevated blood pressure may cause a severe headache.5

The human body has several compensatory mechanisms in place that attempt to correct the symptoms. There is an increase in parasympathetic stimulation to the heart via the vagus nerve, which may cause bradycardia. The bradycardia, however, cannot compensate for the severe vasoconstriction. There is also an increase in the sympathetic inhibitory outflow from the vasomotor centers above the spinal cord injury. Unfortunately, these impulses cannot pass below the injury site. This may result in profuse sweating and vasodilation, with skin flushing above the injury site.

When a noxious stimulus occurs, a reflex is initiated that causes the blood vessels to constrict and raise the blood pressure. A noxious stimulus, as discussed earlier, may mean many different things, including fecal impactions, ingrown toenails, bladder distension and even pressure sores. In an intact spinal cord, this same stimulus also sets in motion another set of reflexes that moderate the constriction of blood vessels.

In someone with a spinal cord injury at the level of T-6 or above, the signal that tells the blood vessels to relax cannot get through because of the injury. Nerves at the T-6 level also control the bloodflow to and from the gut, which is a large reservoir of blood. This may result in a dangerous increase in blood pressure.6

The first episode of autonomic dysreflexia usually occurs within four to six months after a spinal cord injury; however, it may occur as early as two months or as late as 10 to 12 years after the injury.7 The frequency of occurrence varies greatly among individuals. Autonomic dysreflexia may occur from several times a day to once in several years.

Treatment

Autonomic dysreflexia is considered a serious emergency. Elevated blood pressures require immediate and aggressive treatment. Identifying the cause of hypertension is the first priority. Since the typical resting blood pressure for a quadriplegic is 90/60, a blood pressure of 120/80 could suggest dysreflexia. Blood pressures should be monitored every five minutes to watch for improvements. After successful reduction of the blood pressure, continue to monitor the patient for two hours after resolution of AD. The hypertension and symptoms may have resolved due to medication, but symptoms may resume as the medication wears off.

Conclusion

For purposes of reducing the recurrence of autonomic dysreflexia, the episode should be well documented in the prehospital medical record. The record should contain the presenting symptoms, required treatment, blood pressure readings and the response to treatment. In addition, upon discharge from the treatment facility, the patient should be given extensive education on possible precipitating events, treatment options and early recognition of symptoms. Finally, all discharge instructions should also contain written descriptions of treatments that can be referred to in an emergency situation.

References

1. Medical Care of Persons with Spinal Cord Injury. Department of Veteran Affairs Employee Education System, 2001.

2. Porth CM. Pathophysiology Concepts of Altered Health States, 6th Ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2002.

3. Dirksen SR, Lewis SM, Heitkemper MM. Clinical Companion to Medical Surgical Nursing, 3rd Ed. St. Louis, MO: Mosby, 2004.

4. Cody T, Zieroff V. Autonomic Dysreflexia, Retrieved June 28, 2004, from http://www.northeastrehab.com/articles/dysreflexia.html.

5. Acute Management of Autonomic Dysreflexia [brochure].Consortium for Spinal Cord Medicine, 1997.

6. National Spinal Cord Injury Association Resource Center. March 3, 1996. Factsheet #17: What is autonomic dysreflexia? Retrieved February 2, 2004, from http://makoa.org/nscia/fact17.html.

7. Spinal Cord Injury Information Network. October 3 1995. Autonomic Dysreflexia–Fact Sheet #25. Retrieved February 26, 2004, from www.spinalcord.uab.edu.

8. Allen B. How to Treat Autonomic Dysreflexia. Retrieved March 4, 2004, from www.geocities.com/budallen98_98spinal_cord.html.

Back to Top