|Autonomic Dysreflexia: A Clinical Rehabilitation Problem|
|Patricia L. Travers, MS RN||Key
autonomic dysreflexia, hyperreflexia, spinal cord injury
Autonomic dysreflexia, or hyperreflexia, is a life-threatening condition that can occur in a person with a spinal cord injury at or above the T6 level. The classic signs and symptoms are severe hypertension, pounding headache, and diaphoresis. Prevention is the key to avoiding this disease process. This article reviews the pathophysiology, precipitating factors, signs and symptoms, nursing management, and effects of the problem. All healthcare providers must be aware of this condition in order to prevent permanent impairments in clients who may experience it.
Patricia Travers is a nursing coordinator on the medical rehabilitation unit of DeGraff Memorial Hospital, CGF Health System, in North Tonawanda, NY. Address correspondence to Patricia L. Travers, 2880 Albright Road, Ransomville, NY 14131, e-mail email@example.com.
Autonomic dysreflexia, or hyperreflexia, is a life-threatening condition that can occur in a person with a spinal cord injury (SCI) and that requires immediate treatment. An acute episode is characterized by sudden and severe hypertension. This syndrome is more frequently seen in clients with spinal cord lesions at or above T6, but clients with a lesion as low as T8 have been reported to have exhibited it (Lee, Karmakar, Herz, & Sturgill, 1995). The primary cause is a noxious stimulus below the level of the SCI that produces an exaggerated and unopposed sympathetic response (Lee et al.).
Healthcare providers must be aware of this problem and be able to intervene appropriately. With prompt and early intervention, the severity of an episode can be decreased. Inappropriate or delayed treatment can have serious consequences such as apnea, seizures, stroke, retinal hemorrhage, renal failure, subarachnoid hemorrhage, cardiac dysrhythmia, cardiac arrest, or death (Adsit & Bishop, 1995). Autonomic dysreflexia is potentially preventable, and clients should know about it so they can implement preventive measures to safeguard their health.
According to The National Spinal Cord Injury Association (1996), approximately 7,800-12,600 new cases of SCI occur annually in the United States. In 1996, the number of people with an SCI or spinal dysfunction at any given time was assessed to be 250,000-400,000. Estimates are that 8% of people with SCI are institutionalized after they have been discharged from the hospital (The National Spinal Cord Injury Association).
The most common causes of SCI are motor vehicle accidents (45.4%), falls (16.8%), sports injuries (16.3%), and violence (14.6% at some urban centers) (Yarkony & Chen, 1996). The majority (65%) of SCIs occur in people younger than 30 years of age (Spoltore & O’Brien, 1995). Men tend to become injured at a younger age and make up the majority (80%) of the SCI population (Nolan, 1994; Yarkony & Chen).
Autonomic dysreflexia has an incidence rate of 48%-90% in people who are tetraplegic or high paraplegic (Braddom & Rocco, 1991). According to the American Association of Spinal Cord Injury Nurses (AASCIN, 1996), “Age and gender of the individual with SCI do not affect incidence. Episodes of AD [autonomic dysreflexia] are often the most common and unpredictable during the first year following SCI, but can occur at any time throughout the individual’s life” (p. 3). The majority of people who are at risk for autonomic dysreflexia will experience an episode within 6 months of sustaining an SCI (AASCIN).
Autonomic dysreflexia is triggered when a painful stimulus occurs below the level of the SCI. The response is mediated through the nervous system, which includes the central nervous system (CNS) and the peripheral nervous system (PNS). The CNS consists of the “brain and spinal cord with their nerves and end organs that control voluntary acts” (Thomas, 1981, p. C39). The PNS “consists of the 12 pairs of cranial nerves and the spinal and peripheral nerves” (Bates, 1995, p. 491). The PNS also is divided into the somatic nervous system and the autonomic nervous system. The autonomic nervous system is responsible for the signs and symptoms of autonomic dysreflexia. The autonomic nervous system normally maintains body homeostasis via its two branchesÑthe parasympathetic autonomic nervous system (PANS) and the sympathetic autonomic nervous system (SANS). These branches have complementary roles through a negative-feedback system; that is, when one branch is stimulated, the other branch is suppressed (Finocchiaro & Herzfeld, 1990).
The SANS is associated with the flight-or-fight response, causing dilation of the pupils, increased heart rate, vasoconstriction, decreased peristalsis and tone of the gut, release of epinephrine and norepinephrine, as well as other effects. The effects of PANS stimulation are the opposite of the SANS; for the most part, these are constriction of the pupil, decreased heart rate, as well as increased peristalsis and tone of the gut (Finocchiaro & Herzfeld, 1990; Lombardo, 1986).
The PANS and SANS exit at different sites in the CNS (see Figure 1). The PANS exits via the midbrain, pons, medulla (cranial nerves [CN] III, VII, IX, and X), and the sacral level of the spinal cord. The SANS exits via the thoracic and lumbar segments of the spinal cord (Tortora & Anagnostakos, 1981). There is a major sympathetic output (called the splanchnic outflow) between T5 and L2 (Dunn, 1991). Being aware of the different exit sites can help nurses understand the pathophysiology of autonomic dysreflexia.
In a client with a high-level SCI, intact lower motor neurons sense the painful stimuli below the level of injury and transmit the message up the spinal cord (see Figure 2). At the level of the SCI, the pain signal is interrupted and prevented from being transmitted to the cerebral cortex. The site of the SCI also interrupts the two branches of the autonomic nervous system and disconnects the feedback loop, causing the two branches to function independently (Finocchiaro & Herzfeld, 1990).
The ascending information reaches the major splanchnic sympathetic outflow (T5-T6) and stimulates a sympathetic response. The sympathetic response causes vasoconstriction, resulting in hypertension, pounding headache, visual changes, anxiety, pallor, and gooseflesh below the level of injury. This hypertension stimulates the baroreceptors in the carotid sinuses and aortic arch. The PANS is unable to counteract these effects through the injured spinal cord, however. Instead, the PANS attempts to maintain homeostasis by slowing down the heart rate. The brainstem stimulates the heart, through the vagus nerve, causing bradycardia and vasodilation above the level of injury. The PANS impulses are unable to descend past the lesion, and therefore no changes occur below the level of injury (Dunn, 1991; Finocchiaro & Herzfeld, 1990; Lee et al., 1995).
Precipitating factors: Noxious stimuli that can trigger autonomic dysreflexia are painful or uncomfortable sensations below the level of the SCI. The client is unable to detect these sensations, however, because of the disruption of the nerves in the spinal cord. Any stimulus that would normally cause pain can cause an episode of autonomic dysreflexia in clients who are at high risk for this condition. Figure 3 lists potential causes of the noxious sensory input.
Signs and symptoms: Clients experiencing autonomic dysreflexia may exhibit the signs and symptoms listed in Figure 4.
Most cases of autonomic dysreflexia can be managed through nursing interventions administered by a healthcare provider or caregiver (Dunn, 1991). Treatment of this syndrome consists of discovering and removing the noxious stimulus. It is imperative to differentiate autonomic dysreflexia from hypertension because the stimulus causing the autonomic dysreflexia must be resolved in order to stabilize the client’s blood pressure.
Immediate interventions: The first intervention for autonomic dysreflexia is to raise the head of the client’s bed, lower the client’s legs, and loosen all constrictive clothing, appliances, and vascular support. The rationale is to lower the blood pressure through venous pooling. The client’s blood pressure should be monitored every 2-3 minutes. If the client’s blood pressure is more than or close to double his or her baseline level, the nurse should contact a physician immediately (Rancho Los Amigos Medical Center, 1993).
Assessment: Bladder. The first area the nurse should assess is the client’s bladder. The nurse should check the bladder for distention; if distention is present, the client should be catheterized using 2% lidocaine jelly as a lubricant. Neither the Valsalva nor the CredŽ maneuver should be attempted to empty the client’s bladder because these could increase the severity of the syndrome. If the client has an indwelling catheter, the nurse should ensure the catheter’s patency and ability to provide adequate drainage. If the client’s indwelling catheter needs to be irrigated, a minimum of 60 cc of a 2% lidocaine solution should be used to prevent further bladder distention or irritation. Lidocaine can be used to relieve and prevent bladder spasms. If the client’s indwelling catheter is plugged and must be changed, lidocaine jelly should be used as a lubricant (Dunn, 1991). If these measures do not relieve the symptoms, the nurse must continue searching for the cause of the autonomic dysreflexia.
Bowel. The bowel is the second most likely cause of autonomic dysreflexia. The nurse should insert 30 g of dibucaine into the client’s rectum and allow it to numb the rectal mucosa (this should take about 5 minutes). Then the nurse should assess the client for a fecal impaction. Any stool in the rectum should be carefully removed. The nurse should check the client’s rectum again 20 minutes after the impaction has been removed (again using dibucaine) (Dunn, 1991; Lee et al., 1995; Rancho Los Amigos Medical Center, 1993). The nurse should continue the assessment if the cause of autonomic dysreflexia has not been located.
Skin. The third most likely cause is pressure on the skin. The nurse should reposition the client and check for pressure areas (Lee et al., 1995).
Other interventions: When the cause (bowel, bladder, or skin) of autonomic dysreflexia is not readily identifiable, the nurse should notify the physician immediately and continue to assess the client for the precipitating factor. At this point, the nurse should be prepared to give antihypertensive medication (Dunn, 1991). The most common medication is 10 mg of nifedipine (Procardia) given sublingually (the capsule should be pierced and the contents squeezed under the client’s tongue, then the client should swallow the capsule). Rapid results are usually obtained, although it may be necessary to administer another dose in the same manner 30-60 minutes later (Braddom & Rocco, 1991).
Once the noxious stimulus has been identified and removed (if possible), the client must be monitored for rebound hypotension. This condition can occur especially when antihypertensive medications have been used. Clients who are at risk for autonomic dysreflexia can be placed on a maintenance dose of antihypertensive medication when the noxious stimulus cannot be entirely removed (e.g., a fracture, pressure ulcer, postoperative pain) (Dunn, 1991). When a client has a history of autonomic dysreflexia, spinal anesthesia should be considered if there is a need for surgery or any major invasive testing (Chui & Bhatt, 1983).
Female clients who are at high risk of experiencing autonomic dysreflexia and are contemplating pregnancy should find an obstetrician who is familiar with the special needs of a pregnant client who has an SCI because the elevated blood pressure associated with autonomic dysreflexia could be mistaken for pregnancy-induced hypertension (eclampsia) (Dunn, 1991). According to Finocchiaro and Herzfeld (1990), “The wrong treatment can be as dangerous as either disorder to the mother and child” (p. 59).
Related nursing diagnoses: The North American Nursing Diagnosis Association (NANDA) nursing diagnoses associated with autonomic dysreflexia are dysreflexia and knowledge deficit.
Effects of the problem
Autonomic dysreflexia can have devastating, even fatal, effects on the client, ranging from apnea to death (Dunn, 1991); however, when treated quickly and appropriately, the client will often have no long-term consequences. Therefore, education of clients, caregivers, and healthcare providers is imperative. This syndrome occurs suddenly and addressing it must supersede whatever else the client is doing.
According to Dunn (1991), “The patient [and caregiver] must be taught that proper care in carrying out health maintenance regimens, such as good bowel and bladder care, prevention of pressure sores, avoiding falls, burns or other injury, and selection of proper shoes and clothing can prevent many AD [autonomic dysreflexia] episodes” (p. 62). Clients and their caregivers must be aware of this syndrome and be able to identify an episode early and initiate treatment (Dunn). Clients at high risk for autonomic dysreflexia should be taught the benefits of carrying an identification card, such as the one distributed by the Eastern Paralyzed Veterans of America (1995). This card defines autonomic dysreflexia and lists the signs and symptoms, possible causes, home interventions, and medical interventions (McCourt, 1993).
Autonomic dysreflexia can occur anytime after spinal shock has been resolved and can occur anytime after discharge (Spoltore & O’Brien, 1995). Clients may seek medical help in small community emergency rooms during an acute episode; therefore, it is important that all healthcare professionals, not just those who work with clients with SCI, become aware of this disease process. Dunn (1991) said, “The nurse who is educated about AD [autonomic dysreflexia] can act as the patient’s advocate in assuring that proper preventive measures are taken and that any needed treatment is given without delay according to accepted protocols” (p. 63).
Adsit, P.A., & Bishop, C. (1995). Autonomic dysreflexia: Don’t let it be a surprise. Orthopaedic Nursing, 14(3), 17-20.
American Association of Spinal Cord Injury Nurses (AASCIN). (1996). Clinical practice guideline: Autonomic dysreflexia. Jackson Heights, NY: Author.
Bates, B. (1995). The nervous system. In D.L. Hilton, S.M. Keneally, B. Ryalls, & M. Norris (Eds.), A guide to physical examination and history taking (6th ed., pp. 491-554). Philadelphia: J.B. Lippincott.
Braddom, R.L., & Rocco, J.F. (1991). Autonomic dysreflexia: A survey of current treatment. American Journal of Physical Medicine & Rehabilitation, 70, 234-241.
Chui, L., & Bhatt, K. (1983). Autonomic dysreflexia. Rehabilitation Nursing, 8(2), 16-19.
Dunn, K.L. (1991). Autonomic dysreflexia: A nursing challenge in the care of the patient with a spinal cord injury. Journal of Cardiovascular Nursing, 15(4), 57-64.
Eastern Paralyzed Veterans of America. (1995). Medical alert for autonomic dysreflexia [Brochure]. Washington, DC: Author.
Finocchiaro, D.N., & Herzfeld, S.T. (1990). Understanding autonomic dysreflexia. American Journal of Nursing, 90(9), 56-59.
Lee, B.Y., Karmakar, M.G., Herz, B.L., & Sturgill, R.A. (1995). Autonomic dysreflexia revisited. The Journal of Spinal Cord Medicine, 18(2), 75-87.
Lombardo, M.C. (1986). Neurologic disorders. In S.A. Price & L.M. Wilson (Eds.), Pathophysiology: Clinical concepts of disease processes (3rd ed., pp. 711-832). New York: McGraw-Hill.
McCourt, A.E. (Ed.). (1993). The specialty practice of rehabilitation nursing: A core curriculum (3rd ed.). Skokie, IL: Rehabilitation Nursing Foundation.
The National Spinal Cord Injury Association. (1996). Factsheet #2: Spinal cord injury statistics [On-line]. Available: http://www.spinalcord.org/resource/factshts/factO2/html
Nolan, S. (1994). Current trends in the management of acute spinal cord injury. Critical Care Nurse Quarterly, 17(1), 64-78.
Rancho Los Amigos Medical Center. (1993). Management of autonomic dysreflexia [Algorithm]. Downey, CA: Author.
Spoltore, T.A., & O’Brien, A.M. (1995). Rehabilitation of the spinal cord injured patient. Orthopaedic Nursing, 14(3), 7-16.
Thomas, C.L. (Ed.). (1981). Taber’s cyclopedic medical dictionary (14th ed.). Philadelphia: F.A. Davis.
Tortora, G.J., & Anagnostakos, N.P. (1981). Control systems of the human body. In S.P. Heckel, A. Torbert, & D. Nickol (Eds.), Principles of anatomy and physiology (3rd ed., pp. 278-437). New York: Harper & Row.
Yarkony, G.M., & Chen, D. (1996). Rehabilitation of patients with spinal cord injuries. In R.L. Braddom (Ed.), Physical medicine and rehabilitation (pp. 1149-1179). Philadelphia: W.B. Saunders.
The author gratefully acknowledges Sharon S. Dittmar, PhD RN, for her editorial guidance during the preparation of this manuscript.