From the Guidelines
Autonomic dysreflexia in quadriplegia due to spinal cord injuries is a life-threatening condition triggered by a noxious stimulus below the level of injury, resulting in an exaggerated sympathetic nervous system response, which can be managed by immediately identifying and removing the triggering stimulus and using pharmacologic management as needed, as recommended by the AUA/SUFU guideline 1. The pathophysiology of autonomic dysreflexia involves a complex interplay between the sympathetic and parasympathetic nervous systems. When a noxious stimulus, such as bladder distension or bowel impaction, occurs below the level of injury, it activates sensory neurons that send signals to the spinal cord. However, due to the injury, these signals cannot reach the brain, and instead, trigger a massive sympathetic discharge, causing severe vasoconstriction below the level of injury, resulting in sudden hypertension. Key features of autonomic dysreflexia include:
- Sudden onset of hypertension, often with systolic blood pressure greater than 150 mm Hg and/or 20 mm Hg above baseline
- Classic symptoms such as flushing, sweating, headache, blurry vision, and a sense of impending doom
- Bradycardia, as the body attempts to counteract the hypertension
- Nasal congestion The AUA/SUFU guideline recommends that clinicians should immediately initiate pharmacologic management and escalate care in patients with ongoing and persistent autonomic dysreflexia following bladder drainage, particularly in those with systolic blood pressure greater than 150 mm Hg and/or 20 mm Hg above baseline who exhibit persistent classic symptoms 1. In terms of management, it is essential to:
- Identify and remove the triggering stimulus, often by checking for bladder distension, bowel impaction, or skin irritation
- Place the person in an upright position to reduce blood pressure
- Use rapid-acting antihypertensives, such as nifedipine 10mg or nitrates, if hypertension persists Prevention of autonomic dysreflexia focuses on regular bladder and bowel care, skin checks, and avoiding triggers, as the condition occurs due to the disruption of the autonomic nervous system's normal regulatory mechanisms by the spinal cord injury, allowing uncontrolled sympathetic responses below the injury level without the usual inhibitory control from higher brain centers.
From the Research
Pathophysiology of Autonomic Dysreflexia
The pathophysiology of autonomic dysreflexia in quadriplegia due to spinal cord injuries (SCI) involves an uncontrolled sympathetic discharge in response to noxious stimuli below the level of the spinal cord injury 2, 3, 4, 5, 6. This occurs because the spinal cord lesion is above the major sympathetic outflow tract, typically at or above the T6 level, resulting in the absence of higher control over reflex sympathetic activity 6.
Causes and Triggers
The most common causes of autonomic dysreflexia are:
- Bladder distention 3, 4, 6
- Fecal impaction 3
- Urological, gastrointestinal, or gynecological problems or manipulations 2
- Other noxious stimuli below the level of the spinal cord injury 4, 6
Mechanisms
The mechanisms underlying autonomic dysreflexia include:
- Reflex sympathetic activity resulting in life-threatening hypertension 6
- Supersensitivity and possibly increased numbers of spinal alpha adrenoreceptors and peripheral microvascular adrenoreceptors 6
- Accumulation of substance P below the lesion, which acts as a modulator initiating the sympathetic event 6
- Absence of gamma amino benzoic acid (GABA), norepinephrine (NE), and 5-hydroxytryptamine (5-HT) below the lesion, which are inhibitory neurotransmitters 6
- Resetting of the baroreceptors at a lower level, which plays an important role in maintaining and accentuating the biochemical changes 6
Clinical Presentation
The clinical presentation of autonomic dysreflexia includes: