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  • 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

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  • Cervical cord injury
  • Early intubation with in-line stabilization
  • Respiratory muscle involvement
  • Diaphragm involved at C5 or above SCI
  • Atelectasis/pneumonia
  • Impaired handling of secretions
  • Pulmonary function tests (FEV1/FVC)
  • ABG
  • Chest x-ray
  • Myocardial conduction abnormalities
  • Hypotension (orthostatic)
  • Baseline BP may run lower than normal
  • Electrocardiogram
  • Invasive BP monitoring
  • Status of renal function
  • Urinary tract infections
  • Intravascular volume status
  • Bladder function
  • BUN, Cr
  • Electrolyte status
  • Bowel function
  • Full stomach from GI atony (mostly if cervical lesion)
  • Na+, K+
  • RSI
  • Mental status
  • Deficits (level of SCI)
  • Autonomic hyperreflexia
  • Review imaging
  • Bone fractures
  • Decubitus ulcers
  • Physical examination



  • 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 invasive ...

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