Autonomic Dysreflexia

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Introduction

Autonomic dysreflexia is a condition that emerges soon after a Spinal Cord Injury, usually when the damage has occurred at or above the T6 level. It is generally defined as a syndrome in susceptible Spinal Cord injured patients that incorporates a sudden, exaggerated reflexive increase in blood pressure in response to a stimulus, usually bladder or bowel distension, originating below the level of the neurological injury. It is also sometimes known as autonomic hyperreflexia, hypertensive autonomic crisis, sympathetic hyperreflexia, autonomic Spasticity, paroxysmal hypertension, mass reflex, and viscero-autonomic stress syndrome. Guillain–Barré Syndrome may also cause autonomic dysreflexia.

Dysregulation of the Autonomic Nervous System leads to an uncoordinated sympathetic response that may result in a potentially life-threatening hypertensive episode when there is a noxious stimulus below the level of the spinal cord injury. It is usually accompanied by a severe headache, bradycardia, and facial flushing, along with pallor, cold skin, and sweating in the lower part of the body. It is significant because it is a potentially lethal disorder that occurs in about half or more of the potentially susceptible individuals but can usually be easily alleviated by prompt recognition and relatively simple corrective procedures by caregivers.

Pathophysiology

Autonomic Dysreflexia

Etiology

The etiology is a spinal cord injury, almost always at or above the T6 level. Objectively, an episode is defined as an increase in systolic blood pressure of at least 25 mm Hg or more above baseline. A significant episode would usually have a systolic blood pressure of at least 150 mmHg or more than 40mmHg above the patient's baseline. The higher the injury level, the greater the severity of the cardiovascular dysfunction. The severity and frequency of autonomic dysreflexia episodes are also associated with the completeness of the spinal cord injury as well as the level. Patients with a complete spinal cord injury are more than three times more likely to develop autonomic dysreflexia than those with incomplete injuries (91% to 27%).

Although autonomic dysreflexia has been described in the first days or weeks after the original trauma, it generally does not develop until after the period of spinal shock when reflexes have recovered. The earliest reported case appeared on the fourth-day post-injury. Most of the patients (92%) who will ultimately develop autonomic dysreflexia will do so within the first year after their injury.

Clinical Presentation

Acute autonomic dysreflexia is characterised by severe Paroxysmal Hypertension associated with throbbing Headaches, profuse sweating, nasal stuffiness, Piloerection above the level of injury, flushing of the skin above the level of the lesion, bradycardia,cool, pale skin below the level of injury because of severe vasoconstriction, visual disturbances, dizziness and anxiety or feeling of doom, which is sometimes accompanied by cognitive impairment.

The initial presenting symptom is typically a severe headache. The headache is usually sudden, severe, throbbing, and bilateral. It may be frontal, temporal, or occipital. This is caused by significant vasodilation superior to the level of injury. When this cerebral vasodilation is combined with dangerously high blood pressure, a potentially lethal stroke may occur. Symptoms may not necessarily correlate with the severity of the blood pressure elevation.

Hypertension may be asymptomatic or severe enough to cause a hypertensive crisis complicated by pulmonary edema, left ventricular dysfunction, retinal detachment, intracranial hemorrhage, seizures, or death. Patients with T6 level injuries tend to have systolic blood pressures between 90 and 110 mmHg, but readings should be compared with the patient's usual baseline levels. Bradycardia may also range from minor to resulting in cardiac arrest. Tachycardia is less common than bradycardia but may also occur along with cardiac arrhythmias and atrial fibrillation or flutter. If the patient has coronary artery disease, an episode of autonomic dysreflexia may cause a myocardial infarction.

Any patient with paraplegia or quadriplegia who complains of a severe headache or is found unconscious should immediately undergo screening for possible autonomic dysreflexia by checking their blood pressure and comparing it to their baseline level. Systolic blood pressure >150 mmHg or >40 mmHg above baseline should be considered highly suggestive of autonomic dysreflexia and appropriate measures should be taken.

Diagnostic Procedures

The initial presenting complaint is usually a severe headache, typically described as throbbing. Susceptible individuals, usually with spinal cord lesions at or above T6, who complain of a severe headache should immediately have their blood pressure checked. If elevated, a presumptive diagnosis of autonomic dysreflexia can be made.[5] Prompt recognition and correction of the disorder, usually just by irrigating or changing their urinary Foley catheter, can be immediately life-saving. Unfortunately, the vast majority of nurses, emergency room staff, and physiotherapists are unfamiliar with autonomic dysreflexia and are unable to identify or treat it quickly. This is quite problematic as they are often the first healthcare professionals to witness such an event where early recognition and immediate, proper treatment can literally be the difference between life and death.

Fortunately, most episodes are relatively mild and can be managed at home by the patient and their usual caregivers without acute medical intervention. Severe, life-threatening episodes are rarely encountered by most medical personnel except those who work in specialized tertiary care centers. This means that many medical professionals, even emergency personnel, may rarely see this condition acutely in its most severe form and may therefore not be familiar with its early recognition or immediate treatment protocol.

Epidemiology

Autonomic dysreflexia develops in 48% to 70% of patients with a spinal cord injury above the T6 level and is quite unlikely to develop if the injury is below T10. It has also been infrequently reported in non-traumatic spinal cord injury cases, such as radiation myelopathy and cisplatin-induced polyneuropathy.[13]

Patients prone to this disorder will usually have a documented or personal history of prior episodes, but health professionals need to be alert to an initial presentation without any known prior history of autonomic dysreflexia.

Diagnosis

The evaluation includes obtaining a history of previous autonomic dysreflexia episodes with the triggering event if known, monitoring vital signs, and watching for any developing signs and symptoms. The baseline blood pressure should be known and documented for future reference. Many patients with spinal cord injuries will have hypotension. Orthostatic hypotension is found in over 50% of patients with autonomic dysreflexia.

Start by identifying patients at risk (spinal cord injury at or above the T6 level) and recognize the key initial symptom, which is usually a severe headache from cerebral vasodilation. Should this be encountered, the next step would be to check the blood pressure. If elevated above the patient's usual baseline, then the patient is at high risk for an episode of autonomic dysreflexia. A systolic blood pressure >150 mmHg or >40 mmHg above baseline levels should be considered indicative of autonomic dysreflexia.

The likelihood of autonomic dysreflexia is independently predicted by the level of the spinal cord lesion, whether it is complete or incomplete, and the presence of neurogenic detrusor overactivity.

Differential Diagnosis

• Acute glomerulonephritis

• Anxiety

• Cushing's syndrome

• Drug use or overdose (e.g., stimulants, especially alcohol, cocaine, or levothyroxine)

• Hyperaldosteronism

• Hyperthyroidism

• Intracranial hemorrhage

• Ischemic stroke

• Nephritic and nephrotic syndrome

• Polycystic kidney disease

Resources

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