eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury
Autonomic Dysreflexia in Spinal Cord Injury: Treatment & Medication
Updated: Jul 2, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Rehabilitation Program
Physical Therapy
Physical therapists who treat SCI patients need to have a good understanding of autonomic dysreflexia (AD) and be familiar with the signs and symptoms of this potentially life-threatening condition.3 When completing physical therapy sessions, the therapist needs to monitor the urinary catheter for any blockage or twisting. If the patient becomes hypertensive during therapy, he/she should be placed in an upright position immediately, rather than remain in a supine or reclining position. The therapist needs to complete careful inspection to identify the source of painful stimuli (eg, catheter, restrictive clothing, leg bag straps, abdominal supports, orthoses).4
A less common cause of AD during physical therapy sessions may originate with muscle stretching, either from range of motion or passive stretching. If the patient develops AD, the physical therapist needs to treat it as a medical emergency and be familiar with established protocols for medical management within his/her particular setting. The individual therapy session then must be discontinued to allow the patient to stabilize and recover.
Occupational Therapy
Occupational therapy is another discipline involved extensively in the rehabilitation of individuals with SCI. The occupational therapist also must be familiar with the signs and symptoms of autonomic dysreflexia (AD) and be able to respond quickly if the condition develops during a therapy session.3 The occupational therapist performs extensive training in the performance of activities of daily living with patients who have sustained SCI. Activities of daily living include proper bowel and bladder management, which can help prevent the occurrence of AD. The occupational therapist may be involved in establishing a regular bowel program and also may complete patient and family/caregiver education on this aspect of care. The occupational and physical therapists should educate the patient and family members about AD and ensure that they are familiar with prevention strategies, signs and symptoms, and proper management of the condition.
Speech Therapy
Generally, the treatment provided by the speech therapist is not associated with any painful stimuli below the lesion that may precipitate an autonomic dysreflexia response; however, as health care providers involved in the care of individuals with SCI, the speech therapist must be familiar with the manifestations of this potential life-threatening complication.3
Recreational Therapy
Recreational therapists also are important members of the rehabilitation team, as they help patients with SCI to become involved in recreational and social activities. As members of the SCI team, they also must be knowledgeable about autonomic dysreflexia and know how to respond appropriately if the patient develops symptoms during a recreational therapy session.3
Medical Issues/Complications
Complications associated with autonomic dysreflexia result directly from sustained, severe peripheral hypertension and include retinal/cerebral hemorrhage, myocardial infarction, and seizures.
Consultations
If the cause of the autonomic dysreflexia episode is not found and blood pressure remains elevated, recommend that the patient go to the nearest emergency department for close monitoring and further investigation of the possible cause. Consult an intensive care specialist for ICU monitoring and treatment of the hypertension.
Medication
Check the patient's blood pressure. If blood pressure is elevated and the person is supine, have the person sit up immediately and loosen any clothing or constrictive devices. Sitting leads to pooling of blood in the lower extremities and may reduce blood pressure. Monitor blood pressure and pulse every 2-5 minutes until they have stabilized; blood pressures can fluctuate quickly during an AD episode from impaired autonomic regulation. Survey the person for instigating causes, beginning with the urinary system, the most common cause of autonomic dysreflexia (AD).6
- If an indwelling urinary catheter is not in place, catheterize the patient.
- 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 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.
- If the catheter is draining and blood pressure remains elevated, suspect fecal impaction, the second most common cause of AD, and check the rectum for stool using lidocaine jelly as lubricant.
- Use an antihypertensive agent with rapid onset and short duration while the causes of AD are being investigated.
- The most commonly used agents are nifedipine and nitrates (eg, nitroglycerine paste). Nifedipine should be in the immediate release form; bite-and-swallow is the preferred method of administration, not sublingual. Other agents used are mecamylamine, diazoxide, and phenoxybenzamine.
- Use antihypertensives with extreme caution in older persons or people with coronary artery disease.
- Monitor the individual's symptoms and blood pressure for at least 2 hours after resolution of the AD episode to ensure that elevation of blood pressure does not recur. AD may resolve because of medication, not because of resolution of the underlying cause.
- If there is poor response to treatment and/or if the cause of the AD has not been identified, send the patient to ER for monitoring, maintenance of pharmacologic control of blood pressure, and investigation of other possible causes of the AD.
- Document the episode.
A Taiwanese study indicated that in patients with SCI who have detrusor sphincter dyssynergia, using a combination of fluoroscopy and electromyography to localize the external urethral sphincter, with a Foley catheter employed to visualize vesicourethral anatomy, makes transperineal injection of botulinum toxin type A into the external urethral sphincter safe, accurate, and easy to perform.5 Such injections have been shown to reduce the occurrence and degree of autonomic dysreflexia, as well as of vesicoureteral reflux, hydronephrosis, and urinary tract infection.
Antihypertensives
Antihypertensive agents with rapid onset and short duration are administered while the causes of autonomic dysreflexia (AD) are investigated if BP is at or above 150 mm Hg systolic. Patients who have experienced episodes of AD are treated with antihypertensives prior to procedures known to cause their AD episodes.
Nifedipine (Procardia)
Calcium ion influx inhibitor (slow-channel blocker or calcium ion antagonist); inhibits transmembrane influx of calcium ions into cardiac and smooth muscle. Reduces arterial pressure at rest and at a given level of exercise by dilating peripheral arterioles and reducing the total peripheral resistance (afterload).
Adult
10 mg cap PO initially; bite and swallow
Pediatric
Not recommended
Concomitant administration with beta-blocking agents usually well tolerated; may increase likelihood of congestive heart failure, severe hypotension, or exacerbation of angina; concomitant administration with nitrates safe, but no controlled studies evaluate antianginal effectiveness
Isolated reports of patients with elevated digoxin levels; possible interaction between digoxin and nifedipine; monitor digoxin levels when initiating, adjusting, and discontinuing
Rare reports of interaction between quinidine and nifedipine with a decreased plasma level of quinidine
Rare reports of increased prothrombin time in patients taking Coumadin anticoagulants and nifedipine; relationship uncertain
Significant increase in peak plasma levels (80%) and area-under-the-curve (74%) after 1 week of cimetidine at 1000 mg/d and nifedipine at 40 mg/d
Smaller nonsignificant increases with ranitidine; effect possibly mediated by known inhibition of cimetidine on hepatic cytochrome P-450, enzyme system probably responsible for first-pass metabolism
Cautious titration advised if nifedipine therapy initiated in patient receiving cimetidine
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Decreases peripheral vascular resistance; careful monitoring of BP advised during initial administration and titration
Mild-to-moderate peripheral edema seen in 1/10 patients, associated with arterial vasodilation, not from left ventricular dysfunction
Occasional significant elevations of enzymes (eg, alkaline phosphatase, CPK, LDH, SGOT, SGPT); rarely associated with clinical symptoms; cholestasis with or without jaundice reported; allergic hepatitis; decreases platelet aggregation in vitro; moderate but statistically significant decrease in platelet aggregation and increase in bleeding time in some patients; probably function of inhibition of calcium transport across platelet membrane; no clinical significance demonstrated for these findings; positive direct Coombs test with or without hemolytic anemia reported but causal relationship not determined
Nitroglycerine (Depo-Nit, Nitrostat, Nitrol, Nitro-Bid)
Principal pharmacologic action of nitroglycerin is relaxation of vascular smooth muscle, producing vasodilator effect on both peripheral arteries and veins with more prominent effects on the latter. Dilation of postcapillary vessels, including large veins, promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end-diastolic pressure (preload). Arteriolar relaxation reduces systemic vascular resistance and arterial pressure (after-load).
Adult
0.4 mg per metered spray for SL use or 2% nitroglycerine ointment
Start with 0.5-in strip to chest wall and titrate as necessary; alternatively, 0.15-0.6 mg tab SL or 5 mcg/min IV
Pediatric
Not established
Alcohol may enhance sensitivity to hypotensive effects of nitrates (acts directly on vascular muscle); other agents that depend on vascular smooth muscle as final common path may have decreased or increased effect depending upon agent; symptomatic orthostatic hypotension reported when calcium channel blockers and oral controlled-release nitroglycerin concomitantly administered; dose adjustments sometimes necessary
Documented hypersensitivity; concurrent use of sildenafil (Viagra)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in severe hypotension, particularly with upright posture, possible; use with caution in subjects with volume depletion from diuretic therapy or with low systolic blood pressure; paradoxic bradycardia and increased angina pectoris from nitroglycerin-induced hypotension; may aggravate angina caused by hypertrophic cardiomyopathy; tolerance and cross-tolerance to other nitrates possible; tolerance to vascular and antianginal effects of nitrates demonstrated in clinical trials, occupational exposure, and tissue experiments in laboratory; tolerance in industrial workers demonstrated; physical dependence occurs since chest pain, acute myocardial infarction, and sudden death occur in industrial workers during withdrawal
Phenoxybenzamine hydrochloride (Dibenzyline)
Long-acting, adrenergic, alpha-receptor blocking agent that can produce and maintain chemical sympathectomy by oral administration; increases blood flow to skin, mucosae, and abdominal viscera and lowers supine and erect blood pressures.
No effect on parasympathetic system.
Adult
Adjust dose to fit needs of each patient
Slowly increase dose until desired effect obtained or side effects from blockade problematic
Observe patient on each level before instituting increase
Dosage should provide symptomatic relief and/or objective improvement, but not to where side effects from blockage are troublesome
Initially, administer 10 mg of Dibenzyline (phenoxybenzamine hydrochloride) PO bid; increase dose qod, usually to 20-40 mg 2 or 3 times/d, until an optimal dosage is obtained, as judged by blood pressure control
Pediatric
Not established
Alpha-adrenergic blockade leaves beta-adrenergic receptors unopposed; compounds stimulating both types of receptors associated with exaggerated hypotensive response and tachycardia; caution in patients with marked cerebral or coronary arteriosclerosis or renal damage; may aggravate symptoms of respiratory infections; may interact with compounds that stimulate alpha-adrenergic and beta-adrenergic receptors (eg, epinephrine) to produce exaggerated hypotensive response and tachycardia; blocks hyperthermia production by levarterenol and hypothermia production by reserpine
Documented hypersensitivity; those to whom a fall in blood pressure would be undesirable
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cerebral or coronary arteriosclerosis and renal impairment; can worsen symptoms of respiratory tract infections
Adverse effects include postural hypotension, tachycardia, inhibition of ejaculation, nasal congestion, miosis, gastrointestinal irritation, drowsiness, fatigue
Mecamylamine (Inversine)
Potent oral secondary amine, antihypertensive agent, and ganglion blocker.
Produces smooth and predictable reduction of blood pressure with small oral dose.
Antihypertensive effect predominantly orthostatic, but supine blood pressure also significantly reduced.
Used for management of moderately severe-to-severe essential hypertension and in uncomplicated cases of malignant hypertension.
Adult
2.5 mg PO prn
Pediatric
Not established
Antibiotics and sulfonamides; may be potentiated by anesthesia, other antihypertensive drugs, and alcohol
Documented hypersensitivity; coronary insufficiency, pyloric stenosis, glaucoma, uremia, recent myocardial infarction, unreliable/uncooperative patients
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in impaired renal function, previous CNS abnormalities, prostatic hypertrophy, bladder obstruction, patients receiving sulfonamides or antibiotics that cause neuromuscular blockade; adverse effects include dizziness, lightheadedness (getting up slowly is advised)
Interstitial pulmonary edema and fibrosis, urinary retention, impotence, decreased libido, weakness, fatigue, sedation, marked cerebral and coronary arteriosclerosis, recent cerebral accident may occur
No restriction of sodium intake necessary, but adjustment of dosage of ganglion blocker if necessary
Caution in prostatic hypertrophy, bladder neck obstruction, and urethral stricture
Frequent loose bowel movements with abdominal distention and decreased borborygmi are first signs of paralytic ileus (discontinue immediately and take remedial steps)
Diazoxide (Hyperstat)
Nondiuretic benzothiadiazine antihypertensive agent; achieves prompt reduction of blood pressure by relaxing smooth muscle in peripheral arterioles; cardiac output increases as blood pressure is reduced.
Adult
1-3 mg/kg IV to maximum dose of 150 mg in single injection; repeat at 5-15 min intervals until reduction of BP is satisfactory (eg, diastolic pressure <100 mm Hg)
Pediatric
Administer as in adults
Highly bound to serum protein, can be expected to displace other substances also bound to protein (eg, bilirubin or coumarin and derivatives, resulting in higher blood levels of these substances)
Hypotension may result when administered to patients who have received other antihypertensive medication within 6 h
Excessive hypotension in 1 patient after concomitant administration with hydralazine and methyldopa may occur
Maternal hypotension and fetal bradycardia occurred in patient in labor who received reserpine and hydralazine prior to administration
Neonatal hyperglycemia following intrapartum administration after injection also reported; should not be administered IV within 6 h of administration of hydralazine, reserpine, alphaprodine, methyldopa, beta-blockers, prazosin, minoxidil, nitrites
Concomitant administration with thiazides or other commonly used diuretics may potentiate hyperuricemic and antihypertensive effects
Hyperglycemic and hyperuricemic effects of diazoxide preclude proper assessment of metabolic states
Increased renin secretion, IgG concentrations, decreased cortisol secretion noted
Inhibits glucagon-stimulated insulin release and causes false-negative insulin response to glucagon
Increased serum free fatty acids and decreased plasma insulin levels in rat, dog, monkey
Documented hypersensitivity; aortic coarctation, pheochromocytoma, arteriovenous shunts, and aortic aneurysm; compensatory hypertension (eg, that associated with aortic coarctation or arteriovenous shunt)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Transient hyperglycemia in most patients usually requires treatment only in patients with diabetes mellitus; responds to usual management measures, including insulin
Monitor blood glucose levels, especially in patients with diabetes and in those requiring multiple injections
Cataracts observed in animals receiving repeated daily doses of intravenous diazoxide
May precipitate edema and congestive heart failure if injected frequently
Increased volume of extracellular fluid may cause treatment failure in nonresponsive patients because of increased extracellular fluid
Increase in fluid volume responds to diuretics if renal function adequate
Concurrent administration of thiazide diuretics may potentiate antihypertensive and hyperuricemic actions of diazoxide (see Interactions above)
Should be administered only into peripheral vein
Alkalinity of solution irritates tissue, so avoid extravascular injection or leakage
SC administration produces inflammation and pain without subsequent necrosis; if leakage into subcutaneous tissue occurs, area should be treated with warm compresses and rest
More on Autonomic Dysreflexia in Spinal Cord Injury |
| Overview: Autonomic Dysreflexia in Spinal Cord Injury |
| Differential Diagnoses & Workup: Autonomic Dysreflexia in Spinal Cord Injury |
 Treatment & Medication: Autonomic Dysreflexia in Spinal Cord Injury |
| Follow-up: Autonomic Dysreflexia in Spinal Cord Injury |
| Multimedia: Autonomic Dysreflexia in Spinal Cord Injury |
| References |
| Further Reading |
| « Previous Page | Next Page » |
References
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Krassioukov A, Warburton DE, Teasell R, et al. A systematic review of the management of autonomic dysreflexia after spinal cord injury. Arch Phys Med Rehabil. Apr 2009;90(4):682-95. [Medline].
Tsai SJ, Ying TH, Huang YH, et al. Transperineal injection of botulinum toxin A for treatment of detrusor sphincter dyssynergia: localization with combined fluoroscopic and electromyographic guidance. Arch Phys Med Rehabil. May 2009;90(5):832-6. [Medline].
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Vaidyanathan S, Soni BM, Sett P, et al. Pathophysiology of autonomic dysreflexia: long-term treatment with terazosin in adult and paediatric spinal cord injury patients manifesting recurrent dysreflexic episodes. Spinal Cord. Nov 1998;36(11):761-70. [Medline].
Further Reading
Related eMedicine topics:
Athletes With Disabilities
Cardiovascular Concerns in Spinal Cord Injury
Neurogenic Bladder
Post Head Injury Autonomic Complications
Posttraumatic Syringomyelia
Spinal Cord Trauma and Related Diseases
Clinical guidelines:
Acute management of autonomic dysreflexia: individuals with spinal cord injury presenting to health-care facilities. Consortium for Spinal Cord Medicine - Private Nonprofit Organization
Paralyzed Veterans of America - Private Nonprofit Organization. 1997 Feb (updated 2001 Jul; reviewed 2006). 29 pages. NGC:002190
Clinical trials:
Prazosin Vibrostimulation Autonomic Dysreflexia and Spinal Cord Injury Study
Keywords
autonomic dysreflexia, dysreflexia, hyperreflexia, spinal cord injury, SCI, autonomic nervous system, sympathetic nervous system, parasympathetic nervous system, parasympathetic, spinal cord injuries, autonomic disorders, autonomic hyperreflexia, paroxysmal hypertension, hypertensive autonomic crisis, visceroautonomic stress syndrome, autonomic spasticity, sympathetic hyperreflexia, mass reflex
