Autonomic Dysreflexia



Autonomic dysreflexia (AD) is a medical emergency characterized by a sudden and uncontrolled sympathetic response in patients with spinal cord injury (SCI) at T6 and above. It is secondary to a noxious stimulus below the SCI; prominent signs include an acute elevation in blood pressure (BP) and bradycardia.



  • Men 4 times more than women
  • Males represent 80% of SCI worldwide.
  • Affects patients with both complete and incomplete SCI; symptoms less severe with incomplete SCI
  • Often manifests in the first 3 to 6 months after SCI and as late as 12 years following the event
  • Incidence within the first month is 5.7%; can occur just 4 days following SCI
  • In chronic stage of SCI at T6 and above, the incidence is 48–90%.
  • Frequency varies from daily to once in a few years.

Pediatric Considerations

  • For children, AD is defined as an increase in BP 15 mm Hg above baseline.
  • For adolescents, AD is defined as an increase in BP 15 to 20 mm Hg above baseline.
  • BPs >140 mm Hg in an adolescent, 130 mm Hg in children 6 to 12 years old, or 120 mm Hg in children <5 years old warrant antihypertensive medications.
  • Give guidelines, baseline BP, and description of AD to the child’s pediatrician and school.

Pregnancy Considerations

  • AD occurs during labor in 2/3 of pregnancies of patients with SCI at T6 or above.
  • Can also occur antepartum or postpartum
  • Epidural block is effective treatment or prophylaxis for AD during labor.
  • Consult OB-GYN for:
    • Life-threatening AD
    • First episode of AD
    • AD in the 3rd trimester
    • Vaginal bleeding or suspected labor
    • Persistent symptoms despite treatment
    • Guidance in choosing antihypertensive therapy


  • 91% of tetraplegic patients with complete SCI present with AD versus 27% of patients with incomplete lesions.
  • Children and adolescents with SCI: 16%

Etiology and Pathophysiology

  • Normal regulation of the sympathetic system is modulated by input from higher centers. After SCI, that input is lost leading to a disconnection between the sympathetic and parasympathetic nervous systems.
  • Noxious stimulus below the SCI spurs impulses transmitted via the intact peripheral nerves to the sympathetic neurons of the thoracic spinal cord. Unopposed sympathetic outflow causes a massive release of catecholamines, resulting in severe vasoconstriction below the lesion and a sudden elevation of BP.
  • Simultaneously, baroreceptors in the brain, carotid sinus, and aorta detect the rising BP and attempt to trigger visceral and peripheral vasodilatation, but the impulses cannot pass through the SCI. The parasympathetic response is limited to vagal slowing of the heart rate (HR) and vasodilatation above the SCI.
  • SCI below T6 rarely causes AD because the intact greater splanchnic nerve is able to respond with a compensatory dilation of the splanchnic vasculature.

Risk Factors

  • SCI at or above T6
  • Any noxious stimulus below the lesion can cause AD.
  • Urologic stimuli: bladder distention, urinary tract infection, cystoscopy, transurethral litholapaxy, and extracorporeal shock-wave lithotripsy (most common precipitants)
  • Anorectal stimuli: fecal impaction, rectal exam, enema (second most common precipitants)
  • Competitive athletes may induce AD (e.g., by clamping Foley) to enhance performance with resultant increased peak HR, BP, norepinephrine levels, and O2 uptake compare with nonboosted athletes.

General Prevention

  • Good bladder and bowel care
  • Anesthetic lubricants for urethral catheterization
  • Nerve blocks for procedures below the SCI even if the patient does not feel pain
  • Topical lidocaine might not reduce occurrence of AD with anal procedures; consider intersphincteric anal block.
  • Patient and provider education

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