Autonomic Dysreflexia

Introduction

• AD is a syndrome that occurs after SCI, characterized by an uncoordinated autonomic response above and below the level of injury.¹
• Approximately 85% of patients with lesions at or above the T6 level exhibit this reflex, while it is rare in injuries below T10.
• The reflex is most common in chronic SCI patients but has been seen in acute SCI.^2-3
• Those with complete SCI are more likely to exhibit AD than those with incomplete injuries.
• AD is potentially life-threatening as it can lead to complications such as myocardial infarction, seizures, and stroke.^3-5

Pathophysiology

• Stimulation below the level of SCI initiates afferent impulses that enter the spinal cord and activate the sympathetic nervous system, leading to vasoconstriction below the SCI.¹
• In a neurologically intact individual, increased sympathetic activity and vasoconstriction would activate descending inhibitory signals to counteract the rise in blood pressure, resulting in a slowed heartrate and vasodilation.¹
• In AD, the increased sympathetic activity is uninhibited, leading to diffuse vasoconstriction and hypertension, followed by a compensatory parasympathetic response that results in bradycardia and vasodilation above the level of the SCI.^1-2

Clinical Presentation

• The hallmarking clinical findings of AD are severe hypertension (often >200 mmHg systolic) and reflex bradycardia.^3-4 Additional signs and symptoms include:
  • Severe headache
  • Facial flushing above the level of injury
  • Diaphoresis above the level of injury
  • Dry and pale skin below the level of injury
  • Blurred vision
  • Nasal congestion
• Untreated episodes may lead to seizures, intracranial hemorrhage, cardiac arrhythmias, or death.^3-5

Preoperative Assessment

• The level and completeness of SCI should be determined, along with any history of prior AD episodes and their triggers (bladder, bowel, sensory stimuli).^1-2
  Bladder/bowel preparation is essential: empty the bladder (avoid overdistension) and manage constipation.³
• Clinicians should review medications (e.g., anticholinergics, vasodilators) and consider pharmacologic prophylaxis (e.g., nifedipine, nitrates).^2-3
• The need for invasive monitoring (arterial line) should be assessed in patients who are at high risk of developing AD.

Intraoperative Considerations

• Management begins with efforts to prevent the onset of AD.³
  • Ensure appropriate depth of anesthesia to blunt afferent stimuli.
  • Implement neuraxial and regional techniques when appropriate.
• Management of an episode of AD^1-2,5
  • First-line management involves removing the inciting stimulus
  • Deepen anesthetic
  • Use short-acting antihypertensives (e.g., nitroglycerin, sodium nitroprusside) for rapid management of critical hypertension
  • Consider placement of an arterial line if AD does not resolve quickly

Postoperative Management

• It is essential to understand that AD may first manifest postoperatively when the effects of anesthetic agents subside.^1-2
• Blood pressure and heart rate should be monitored closely in the recovery period.
• Bladder and bowel vigilance should be continued postoperatively.
• Availability of rescue medications should be ensured in the postanesthesia care unit and ward settings.
• Ongoing education should be ensured for all staff members, with participation in postoperative patient care.
• Clinicians should document and communicate intraoperative AD episode for continuity of care.