What happens below the lesion in autonomic dysreflexia?

Autonomic Dysreflexia: Pathophysiology Below the Lesion

Below the lesion in autonomic dysreflexia, there is uncontrolled sympathetic nervous system activation causing widespread vasoconstriction, which contributes to dangerous hypertension and associated symptoms. 1

Pathophysiological Mechanism

• In autonomic dysreflexia, noxious stimuli below the level of injury (typically T6 or above) trigger massive sympathetic discharges from the isolated spinal cord, creating a "sympathetic storm" 2
• The spinal cord injury prevents normal inhibitory signals from higher brain centers from modulating this reflex sympathetic response 3
• Below the level of the lesion, there is:
  • Widespread vasoconstriction in skeletal muscle and splanchnic vascular beds due to uninhibited sympathetic outflow 1, 4
  • Accumulation of substance P, which acts as a modulator initiating strong, slow, and prolonged excitatory sympathetic action 3
  • Decreased levels of inhibitory neurotransmitters including GABA, norepinephrine, and 5-hydroxytryptamine (5-HT) 3
  • Increased sensitivity of peripheral adrenoreceptors (supersensitivity) and possibly increased numbers of spinal alpha adrenoreceptors 3

Clinical Manifestations Below the Lesion

• Vasoconstriction in the lower extremities and splanchnic circulation, contributing to the dangerous elevation in blood pressure 1, 3
• Cold, pale skin below the level of injury due to intense vasoconstriction 1
• Piloerection (goosebumps) below the level of injury 5
• Bladder and bowel distension are common triggers, with sensory impulses traveling via intact peripheral nerves below the lesion 1, 5
• Non-noxious stimuli (not just painful ones) can trigger the response, including:
  • Bladder distension during urodynamic procedures 4
  • Weak electrical stimulation over the abdominal wall 4
  • Vibration of the penis 4
  • Fecal impaction 1

Contrast with Above-Lesion Manifestations

• While below the lesion shows vasoconstriction, above the lesion there is compensatory vasodilation due to intact baroreceptor reflexes attempting to counteract hypertension 1
• This creates a distinct clinical picture:
  • Below lesion: Cold, pale skin with piloerection
  • Above lesion: Flushing, sweating, headache, and nasal congestion 1, 6

Clinical Implications

• Recognition of this pathophysiology is crucial for proper management 5
• The primary goal is to identify and remove the triggering stimulus (most commonly bladder or bowel distension) 1
• Pharmacologic management targets the vasoconstriction with rapid-acting antihypertensives with short half-lives 1
• Common pitfalls in management:
  • Failure to recognize non-noxious stimuli as triggers (contrary to traditional teaching that only noxious stimuli cause autonomic dysreflexia) 4
  • Using beta-blockers like labetalol, which may worsen the condition by blocking vasodilation above the lesion while allowing unopposed alpha-mediated vasoconstriction below 1
  • Inadequate monitoring of blood pressure during procedures in at-risk patients 1

Prevention Strategies

• Regular bladder and bowel management to prevent distension 1
• Education of patients about early recognition of symptoms 1
• Prophylactic measures before procedures that might trigger autonomic dysreflexia 1
• Monitoring of blood pressure during urodynamic testing or cystoscopy in at-risk patients 1

Understanding the pathophysiology below the lesion in autonomic dysreflexia is essential for prompt recognition and effective management of this potentially life-threatening condition.