Abstract
Autonomic hyperreflexia is a clinical syndrome occurring in patients with spinal cord injuries, typically at or above the T6 level. Episodes occur when a noxious stimulus below the spinal cord injury level activates the sympathetic nervous system, which is unopposed by the parasympathetic nervous system because of the spinal cord lesion. The unopposed sympathetic activation can cause extensive vasoconstriction below the level of the lesion, resulting in elevations in blood pressure with potential life-threatening sequelae. Recognition of the risks and triggers of autonomic hyperreflexia with appropriate interventions are essential steps in the prevention of these hypertensive crises. Special care should be taken to ensure proper anesthetic depth is achieved in surgical patients and that analgesia is adequate in the perioperative period, even in patients with little or no sensation below the level of the spinal cord lesion. Vigilance for signs and symptoms of autonomic hyperreflexia episodes and availability of appropriate medications for prompt treatment are paramount for good outcomes.
Keywords
autonomic dysreflexia, autonomic hyperreflexia, autonomic nervous system, hypertension, spinal cord injury
Case Synopsis
A 34-year-old male veteran who sustained a complete spinal cord injury at C5 during combat 10 years ago underwent a cystoscopy with ureteral stent placement under conscious sedation. During the procedure the patient became hypertensive to 260/120 mm Hg and bradycardic with a heart rate of 42 beats per minute. He complained of headaches and blurred vision and started becoming agitated and confused.
Acknowledgment
The authors wish to thank Dr. C. Lee Parmley and Dr. Steven J. Allen for their contributions to the previous edition of this chapter.
Problem Analysis
Definition
Autonomic hyperreflexia, also known as autonomic dysreflexia, is a clinical syndrome associated with cervical and thoracic spinal cord injuries (SCIs). Autonomic hyperreflexia episodes are usually characterized by an acute, and often dramatic, increase in blood pressure in association with a stimulus below the level of the spinal cord lesion. This elevation in blood pressure can be accompanied by bradycardia or (more rarely) tachycardia. The clinical criteria for an autonomic hyperreflexia episode includes an increase from baseline systolic blood pressure of at least 20% associated with at least one of the following symptoms: sweating, chills, goose bumps, flushing, or headache. Intensity of an autonomic hyperreflexia episode can vary from asymptomatic to a life-threating hypertensive emergency. During an episode of autonomic hyperreflexia, an offending stimulus below the level of the spinal cord lesion leads to sympathetic nervous system activation that is no longer opposed by inhibitory descending parasympathetic pathways, as occurs in patients without SCI. This sympathetic activation below the SCI lesion leads to extensive vasoconstriction of the peripheral circulation and of the splanchnic vasculature that accounts for the majority of the vascular capacitance in humans. It also causes mild to malignant elevations in blood pressure.
An autonomic hyperreflexia episode can be triggered by activation of pain fibers below the level of the spinal cord lesion whether the patient has sensation or not. Such stimuli can include distention or contraction of hollow organs such as bowel or bladder, with bladder distention being the most common cause of autonomic hyperreflexia episodes overall. Gastroesophageal reflux, gastritis, gallstones, fecal impaction, hemorrhoids, obstruction or manipulation of indwelling urinary catheters, urologic procedures, pregnancy, childbirth, and surgical procedures have all been implicated in triggering autonomic hyperreflexia. Other triggering events can include spasms, temperature alterations, sexual intercourse, bone fractures, or hip dislocation.
Recognition
Increased muscle tone, spasms, and pilomotor erection indicative of increased sympathetic activity may be observed below the SCI level. Above the spinal cord lesion, patients can have flushing and sweating of the skin, nasal congestion, headache, and bradycardia or other arrhythmias. These symptoms are caused by the activation of the parasympathetic nervous system after baroreceptors in the aortic arch or carotid sinus that are cephalad to the SCI lesion sense a rise in blood pressure. The parasympathetic system then counteracts the sympathetic-driven vasoconstriction below the SCI level by causing vasodilation above this level. Symptoms of an episode of autonomic hyperreflexia can range from asymptomatic to severe. More ominous symptoms and signs may include dyspnea and chest pain from the acute left ventricular afterload, as well as blurred vision, headaches, and confusion signaling that the upper limit of cerebral autoregulation has been surpassed and that the cerebral vasculature can no longer compensate for this acute rise in blood pressure ( Box 85.1 ).
Signs Below the Spinal Cord Injury Level
Pilomotor erection
Blanching
Spasms
Signs and Symptoms Above the Spinal Cord Injury Level and Sequelae
Nausea
Sweating
Chills
Headache
Nasal congestion
Flushing
Dyspnea
Confusion
Blurred vision
Chest pain
Hypertension (systolic blood pressure >20% from baseline)
Bradycardia
Tachycardia
Arrhythmias
Asystole
Conduction
Ischemic electrocardiogram changes
Seizures
Hypertensive encephalopathy
Hemorrhagic or ischemic stroke
Myocardial infarction
Acute left ventricular failure
Pulmonary edema
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