Autonomic Dysreflexia

Table of Contents  

  Introduction

    When treating patients with spinal cord injuries, healthcare professionals must be aware of possible complications. It is not enough to know the pathology and the treatment of a spinal cord injury. Individuals dealing directly with patients must be cognizant of and able to deal with life-threatening situations brought on by the spinal cord injury, Autonomic Dysreflexia (AD) is such a condition.

    The purpose if this in-service is to explain the pathology, signs, symptoms and treatment protocols for handling a patient experiencing autonomic dysreflexia.

  Pathology

    Autonomic dysreflexia is a sudden and severe rise in blood pressure, this situation is a life-threatening condition that can occur to anyone with a spinal cord injury at the T6 level or above (Paralyzed Veterans of America), although cases have been reported when the injury was as low as T8. It is the body’s response to a noxious stimuli below the level of the injury (Erickson, 1980).

    The pathology of autonomic dysreflexia involves the stimulation of sensory receptors below the level of the spinal cord injury. With an intact central nervous system (CNS) the autonomic nervous system (controlling involuntary body functions) reacts with a reflex arteriolar spasm that increases blood pressure. Typically baroreceptors in cerebral vessels, carotid sinuses, and the aorta sense the hypertension and stimulate a vasodilation (parasympathetic response), and decreased heart rate returning blood pressure and heart rate back to normal levels. Autonomic Dysreflexia occurs when visceral and peripheral vessels don’t dilate because the efferent impulses that cause the vasodilation, and subsequently normalize blood pressure and heart rate, can’t pass through the cord lesion (Spinal Cord Information Station). The signal, which tells the blood vessels to relax, cannot get through the spinal cord because of the injury. Thus the patient develops extremely high blood pressure.

The resolution of AD requires quick and decisive treatment. All health-care providers should be familiar with the diagnosis and treatment of AD. The onset of AD is so rapid and the symptoms are so severe that early recognition is important. In clinics where spinal cord patients are seen recognition of signs and symptoms is even more important.

  Signs and Symptoms

An individual experiencing an episode of autonomic dysreflexia may have one or more of the following signs or symptom. It is important to note that symptoms may be minimal or even absent, despite an elevated blood pressure. Some of the more common symptoms are:

• A sudden and significant increase in both the systolic and diastolic blood pressure above levels usually associated with bradycardia.
• Pounding headache.
• Profuse sweating above the level of the lesion (possibly below), especially in the face, neck, and shoulders.
• Goose bumps above (possibly below) the level of the lesion.
• Flushing of the skin above the level of the lesion (possibly below), especially in the face, neck, and shoulders.
• Blurred vision.
• Appearance of spots in the patient's visual fields.
• Nasal congestion.
• Feelings of apprehension or anxiety over an impending physical problem.
• Cardiac arrhythmia, atrial fibrillation, ventricular contractions, and atrioventricular conduction abnormalities.

  Causes of Autonomic Dysreflexia

    There are many things that can cause noxious stimuli below the level of the injury. The most common causes are distended bladder or bowel, but any stimulation of the skin or pain receptors may also cause this reaction.
 

  What to do

    Prompt treatment for autonomic dysreflexia is essential to avoid permanent damage or even death to the patient. To prevent autonomic dysreflexia, or stop it from progressing, health care workers must understand the underlying causes and their plans for corrective action. Patients experiencing autonomic dysreflexia should never be left alone (Pedretti, 1996).

    The first thing to be done is sit the patient upright (head to 90 degrees), and lower the legs. Next, loosen or take off anything tight (e.g. external catheter tape, elastic hose, bandages, shoes or ankle-foot orthosis (AFOs), and leg-bag straps), followed by examination of the catheter hose for kinks.

More specific procedures include:

1. Check the individual's blood pressure. Elevated blood pressures can be life threatening and need immediate investigation and treatment.

2. If the blood pressure is not elevated, refer the individual to a consultant, if necessary. There may be other medical problems that are causing the signs and symptoms of autonomic dysreflexia.

3. If the blood pressure is elevated and the individual is supine, immediately sit the person up. Performing this maneuver may allow a pooling of blood in the lower extremities and may reduce the blood pressure.

4. Loosen any clothing or constrictive devices. Performing this maneuver may allow a pooling of blood in the abdomen and lower extremities and may reduce the blood pressure.

5. Monitor the blood pressure and pulse frequently. Blood pressures have the potential of fluctuating quickly during an AD episode. Therefore, pressures need to be monitored every few minutes (every 2 to 5 minutes is commonly cited), until the individual is stabilized.

6. Quickly survey the individual for the instigating causes, beginning with the urinary system. As stated earlier, the most common causes of autonomic dysreflexia involve the urinary bladder.

7. If an indwelling urinary catheter is not in place, catheterize the individual.

8. Prior to inserting the catheter, instill 2 percent lidocaine jelly (if readily available) into the urethra and wait several minutes. Catheterization can exacerbate autonomic dysreflexia. The lidocaine jelly may decrease the sensory input and relax the sphincter to facilitate catheterization.

9. If the individual has an indwelling urinary catheter, check the system along its entire length for kinks, folds, constrictions, or obstructions and for correct placement of the indwelling catheter. If a problem is found, correct it immediately.

10. If the catheter appears to be blocked, gently irrigate the bladder with a small amount of fluid, such as normal saline at body temperature. Avoid manually compressing or tapping on the bladder. Using a larger volume or of a cold solution might irritate the bladder and exacerbate autonomic dysreflexia. If a lidocaine solution is readily available, irrigation with it may be beneficial by decreasing sensory input from the bladder. Bladder pressure or tapping may also increase sensory input and exacerbate autonomic dysreflexia.

11. If the catheter is draining and the blood pressure remains elevated, proceed with step 16, fecal impaction.

12. If the catheter is not draining and the blood pressure remains elevated, remove and replace the catheter. Irrigating and changing the catheter should be done as quickly as possible. Pharmacological management may become necessary if the blood pressure remains elevated and/or if catheter replacement is difficult.

13. Prior to replacing the catheter, instill 2 percent lidocaine jelly (if readily available) into the urethra and wait several minutes. Catheterization can exacerbate autonomic dysreflexia. The lidocaine jelly may decrease the sensory input and relax the sphincter to facilitate catheterization.

14. If the catheter cannot be replaced, consider attempting to pass a coude catheter, or consult a urologist. A coude catheter may be useful if there is an associated bladder neck obstruction.

15. Monitor the individual's blood pressure during bladder drainage. Sudden decompression of a large volume of urine might produce hypotension.

16. If acute symptoms of autonomic dysreflexia persist, including a sustained elevated blood pressure, suspect fecal impaction. Fecal impaction is the second most common cause of autonomic dysreflexia (PVA, 1997).

17. If the elevated blood pressure is at or above 150 mm Hg systolic, consider pharmacological management to reduce the systolic blood pressure without causing hypotension prior to checking for fecal impaction. If the blood pressure remains elevated but is less than 150 mm Hg systolic, proceed to step 20. Opinion varied on whether the next step should be investigating other causes (e.g., fecal impaction) or initiating pharmacological management. The control of hypertension may need to be addressed prior to digital stimulation or other diagnostic maneuvers, which may exacerbate autonomic dysreflexia.
[There are no studies showing the exact pressure at which the blood pressure becomes dangerous. For this guideline, the panel decided to adopt 150 mm Hg systolic BP as the value at which pharmacological treatment should be considered. A person with an injury at or above T6 would be expected to have a baseline BP between 90 and 110 mm Hg.]

18. Use an antihypertensive agent with rapid onset and short duration while the causes of autonomic dysreflexia are being investigated.

19. Monitor the individual for symptomatic hypotension. Treat severe (symptomatic) hypotension by laying down the individual and elevating the legs.

20. If fecal impaction is suspected, check the rectum for stool, using the following procedure. With a gloved hand, instill a topical anesthetic agent such as 2 percent lidocaine jelly generously into the rectum. Wait approximately 5 minutes for sensation in the area to decrease. Then, with a gloved hand, insert a lubricated finger into the rectum and check for the presence of stool. If present, gently remove, if possible. If autonomic dysreflexia becomes worse, stop the manual evacuation. Instill additional topical anesthetic and recheck the rectum for the presence of stool after approximately 20 minutes. A rectal examination may exacerbate autonomic dysreflexia, thus instillation of a local anesthetic agent may decrease the occurrence of autonomic dysreflexia during the exam.

21. Monitor the individual's symptoms and blood pressure for at least 2 hours after resolution of the autonomic dysreflexia episode to make sure that it does not recur. The hypertension and symptoms may have resolved because of the medication rather than the treatment of the cause. Symptoms managed by pharmacological treatment may begin to reverse themselves within this time frame.

22. If there is poor response to the treatment specified above and/or if the cause of the autonomic dysreflexia has not been identified, strongly consider admitting the individual to the hospital to be monitored, to maintain pharmacological control of the blood pressure, and to investigate other causes of the autonomic dysreflexia. Because of the loss of sensation, individuals with spinal cord injury can have significant pathology with minimal symptoms. These may include problems such as acute abdominal pathology, long bone fractures, and ingrown toenails (Braddom and Rocco, 1991); therefore other causes of autonomic dysreflexia also should be investigated.

23. Document the episode in the individual's medical record. This record should include the presenting signs and symptoms and their course, treatment instituted, recordings of blood pressure and pulse, and response to treatment. It is important to note that pregnant woman should be referred to a doctor immediately.

  Implications for Occupational Therapists

   Health professionals who frequently deal with spinal cord injured patients must be aware of related conditions. The seriousness of autonomic dysreflexia can not be exaggerated.

    Occupational therapists have two distinct areas of concern regarding autonomic dysreflexia. The first concern is the ability to recognize the signs, and know immediate care procedures. The second concern is of educating the patient and his family or primary caretakers. It is necessary to inquire about the patient’s familiarity with and ability to recognize the signs of an autonomic dysreflexia episode. If not, they should be referred to their physician or appropriate healthcare professional for further education.

    Among the long range goals of occupational therapy in the treatment of a person with a spinal cord injury, is helping individuals to achieve the maximum level of self-care independence possible, and resume meaningful life roles (Pedretti, 1981). It is clear that the occupational therapist must be thoroughly mindful of autonomic dysreflexia, its etiology, signs, symptoms, and treatment for the purpose of accomplishing this goal.

  Terminology  

*alternative names for autonomic dysreflexia

  References

Internet Resources

• Arkansas Spinal Cord Commission
• (501) 296-1788
• The National Spinal Cord Injury Association
• (800) 962-9629.
  www.spinalcord.org/resource/factshts/fact17.html

• The Paralyzed Veterans of America
• (888) 860-7244.
  Call for a free patient booklet entitled, "Autonomic Dysreflexia: What You Should Know."
  www.pva.org/index.htm

• University of Alabama at Birmingham Spinal Cord Injury Network
• www.spinalcord.uab.edu

• The National Spinal Cord Injury Association
• www.spinalcord.org/resource/factshts/fact17.html

Selected Journal Articles

• Abouleish, E. I., Hanley, E. S., and Palmer, S.M. (1989). Can epidural fentanyl control autonomic hyperreflexia in a quadriplegic partient? Current Research in Anesthesia and Analgesia 68 523 - 26.

• Black, J. (1988). Autonomic dysreflexia/hyperreflexia in spinal cord injury. ALAA J 8 12.

• Braddom, R.L., and Rocco, J. F. (1991). Autonomic dysreflexia: A survey of current treatment. American Journal of Physical Medicine and Rehabilitation 70 234 - 41.

• Guttmann, F.L., and Whitteridge, D. (1947). Effects of bladder distention on autonomic mechanisms after spinal cord injuries. Journal of the Brain 70 361 - 404.

• Lindan, R., Joiner, E. and Freehafer, A.A.(1980). Incidence and clinical features of autonomic dysreflexia in patients with spinal cord injury. Paraplegia 18 285 - 92.

• Rossier, A. B., Ziegler, W. H. and Duchosal P. W. (1971). Sexual function and autonomic dysreflexia. Paraplegia 9 51 - 63.