9. Autonomic Hyperreflexia
Definition
Autonomic hyperreflexia is an imbalanced reflex sympathetic discharge that occurs in patients with spinal cord injury (SCI) higher than the level of splanchnic sympathetic outflow. Autonomic hyperreflexia is also known as autonomic dysreflexia (AD).
Incidence
Approximately 65% to 85% of patients with SCI above the T 7 level experience autonomic hyperreflexia. Prevalence rates vary, with the incidence occurring in 48% to 90% of the patients with an injury above T 6. Because the male to female ratio of SCI is 4:1, that same ratio applies to the incidence of autonomic hyperreflexia.
Etiology
Autonomic hyperreflexia is typically seen after the post-injury period of spinal shock has “run its course” and some reflexes have returned. These intact peripheral sensory nerves transmit to the spinothalamic and posterior columns, which then return impulses via the sympathetic neurons located in the intermediolateral gray matter. The inhibitory mechanisms above the SCI are not transmittable past the level of the SCI; thus the sympathetic stimulation is unopposed and can produce serious vasoconstriction, bradycardia, and other symptoms. The box on p. 37 lists stimuli that produce or trigger an episode of autonomic hyperreflexia.
Signs and Symptoms
• Bradycardia
• Cardiac dysrhythmias
• Cerebral hemorrhage
• Convulsions
• Erythematous rash
• Headache
• Hypertension
• Nasal congestion
• Piloerection below the level of the lesion
• Profuse sweating
• Pulmonary edema
• Vasoconstriction below the lesion level
• Vasodilation above the lesion level
• Vision changes
Stimuli/Triggers of Autonomic Hyperreflexia
• Abdominal pathology/trauma
• Appendicitis
• Bladder distention
• Blister
• Burns/sunburn
• Constrictive clothes, shoes, appliances
• Contact with hard or sharp objects
• Cystoscopy
• Deep vein thrombosis
• Detrusor-sphincter dyssynergia
• Ejaculation
• Epididymitis
• Fractures
• Gallstones
• Gastric ulcers
• Gastritis
• Gastrocolic irritation
• Hemorrhoids
• Heterotropic bone
• Ingrown toenail
• Insect bites
• Intestinal distention
• Invasive testing
• Menstruation
• Pain
• Pregnancy: labor and delivery
• Pressure ulcers
• Pulmonary emboli
• Scrotal compression
• Sexual intercourse
• Surgical incision (skin)
• Surgical or diagnostic procedures
• Temperature fluctuations
• Urinary tract infection
• Urodynamics
• Uterine contractions
• Vaginitis
Medical Management
Onset of autonomic hyperreflexia is a medical emergency. Medical management begins with thoroughly educating the patient, family, and/or caregivers to recognize the signs and symptoms of autonomic hyperreflexia and to initiate appropriate treatment measures as quickly and efficiently as possible to prevent dangerous sequelae. The initial treatment measure is removal of the causative stimulus, if at all possible. Symptoms that persist despite stimulus removal require pharmacologic intervention, the main form of which is reduction of the hypertension that has been precipitated.
Complications
If left untreated, the sustained peripheral hypertension can culminate in serious sequelae, such as retinal hemorrhage, myocardial infarction, cerebral hemorrhage, seizures, hypertensive crisis, stroke, and death.
Anesthesia Implications
Because this unregulated sympathetic response to stimulation occurs rapidly, the primary concern of the anesthetist is to provide adequate depth of anesthesia. Essentially any method of anesthesia is acceptable—general, regional, or local infiltration—provided the depth of anesthesia ameliorates the reflexive response to surgical stimulation. General anesthesia is the easiest method of achieving a depth adequate to prevent reflexive response to stimulation. Epidural or subarachnoid anesthesia is an appropriate anesthetic choice. However, it can be difficult for the following reasons: (1) determination of the level of anesthesia is inexact, at best; and (2) technical difficulties arise because of vertebral deformities, osteoporosis, and positioning. Regional anesthesia is capable of blocking the afferent pathways to prevent the sympathetic discharge, but once “set,” the level or depth cannot be changed. General anesthesia is the only technique whereby the depth can be deepened to thwart the onset of unopposed sympathetic response to surgical stimulation; epidural anesthesia levels (if obtained at all) can be adjusted, but in a much more limited manner.
