Chapter 32. Preexisting Spinal Cord Injury

• Spinal cord injury (SCI) is common (˜10,000–11,000 cases per year), occurring usually after trauma
• Degree of dysfunction is directly related to level of injury, especially severe if above T6
• Most common site of injury is lower cervical spine or upper lumbar region:
  • Midthoracic injury less common due to rotational stabilization provided by the rib cage and intercostal muscles
• Pathophysiology:
  • Upregulation of acetylcholine receptors from immobilization causes resistance to nondepolarizing neuromuscular blockers and increased potassium release with depolarizing neuromuscular blockers (e.g., succinylcholine)
  • Sympathetic hyperreflexia:
    • Nociceptive afferent circuits rebranch below the lesion and anastomose with sympathetic efferents, especially between T5 and L2
    • Hyperreflexia mostly if lesion above T6, but possible even around T12
    • Higher risk with:
      • Urological surgery
      • Complete cord section
      • Chronic pain
      • Maximal 1–6 months after injury, but can persist indefinitely
    • Small stimuli can evoke exaggerated, unopposed sympathetic response:
      • Extreme HTN with reflex bradycardia and other dysrhythmias
      • Headache, anxiety
      • Sweating
      • Flushing or pallor
      • Piloerection
    • Complications:
      • Myocardial ischemia
      • Cardiac arrest
      • Pulmonary edema
      • Hemorrhagic CVA
  • Reduced lower limb blood flow, but increased arterial and venous pooling leads to increased risk of thromboembolic disease
  • Spasticity: similar mechanism as hyperreflexia
• Natural history of injury:
  • Acute (<3 weeks from injury):
    • Spinal shock: hypotension and bradycardia
    • Loss of thoracic sympathetic outflow, with vasodilatation and pooling of blood
    • Relative predominance of vagal stimulation to the heart
    • Retention of urine/feces leading to diaphragm elevation, which may impair respiration
    • Hyperesthesia above the lesion
    • Reflexes and flaccid paralysis below the lesion
  • Intermediate (3 days to 6 months):
    • Hyperkalemic response to depolarizing NMB
  • Chronic (after 6 months):
    • Return of muscle tone
    • Positive Babinski sign
    • Hyperreflexia syndrome

NB:

• Creatinine does not correlate with renal function
• Intramuscular injections may have delayed absorption

• Gentle induction for GA (potential for severe hypotension) or neuraxial/regional anesthesia where indicated (less hemodynamic lability, but difficult to assess level; monitor carefully as diagnosis of high/total spinal might be delayed)
• Avoid succinylcholine from 24 hours after injury due to risk of hyperkalemia. Response typically seen if drug is given from 1 week to 6 months after the injury but may be seen before or after that period:
  • If laryngospasm occurs, the benefits of giving a small dose of succinylcholine (20 mg) may outweigh the risk
• Careful padding of pressure points/decubitus ulcers
• Consider ...