Complete spinal cord injury

Complete spinal cord injury is the complete sensory and motor loss below the site of spinal cord injury following acute or chronic destruction, compression, or ischemia of the spinal cord. Initially, this may manifest as spinal shock, which is an acute physiological loss or depression of spinal cord function. It manifests as a flaccid areflexic paralysis below the level of the injury with autonomic features (e.g., hypotension, bradycardia). After some days to weeks the spinal shock wears off and a complete spinal cord injury may remain which manifests with spastic paresis, hyperreflexia, and continued sensory loss. Acute stabilization, a thorough neurological examination, and imaging is required for adequate diagnosis. Treatment involves acute care (e.g., analgesia, urinary catheterization) and definitive treatment (bracing or surgery). Symptomatic treatment, assistant devices, and physical therapy can improve mobility and quality of daily life. Less than five percent of cases fully recover after complete spinal cord injury. Autonomic dysreflexia is a long-term complication from thoracic spinal cord injury, leading to life-threatening episodes with cardiovascular instability.

• Definition: acute loss or depression of spinal cord function; (loss of all sensorimotor functions below the level of injury) and reflexes following a spinal cord injury
• Etiology
  • Mainly traumatic (e.g., motor vehicle accidents, severe sports injury, knife/gunshot wounds)
  • Less commonly: nontraumatic (e.g., malignancy, inflammation, infection, disk degeneration, hemorrhage, infarction)
• Pathophysiology
  • Neuronal damage → loss of intracellular potassium into the extracellular space → hyperpolarization of neurons → poor axonal transmission and reflex depression
  • Potassium levels between intracellular and extracellular space eventually normalize → reversal of spinal shock
• Clinical features
  • Flaccid areflexic paralysis
    • Paraplegia, tetraplegia if the cervical cord is involved
    • Areflexia: absence of the proprioceptive and polysynaptic reflexes (e.g., abdominal reflex)
    • Bilateral diaphragm paralysis: impaired breathing
  • Anesthesia: below the level of the lesion
  • Autonomic dysfunction
    • Neurogenic shock: hypotension and bradycardia
    • Loss of bladder control: urine retention, bladder distention, and dribbling incontinence
    • Loss of bowel control: paralytic ileus, fecal incontinence
    • Absent bulbocavernosus reflex: fecal incontinence
    • Male patients: priapism may occur
• Diagnostics and treatment: See ”Evaluation and diagnosis of spinal cord injuries“ below.
• Prognosis
  • Symptoms are usually reversible but during the acute phase the outcome (e.g., remaining disabilities) is difficult to predict.
  • Prognosis is poor if transition to complete spinal cord injury occurs (see below).
  • Prognosis is better if transition to incomplete spinal cord syndrome occurs.

References:^[1]

• Definition: damage to the spinal cord resulting in complete bilateral loss of communication between the nerve fibers above and below the lesion
• Epidemiology: ∼ 33% of annual spinal cord injuries in the US ^[2]
• Etiology
  • Trauma (complete spinal cord transection)
  • Nontraumatic causes include spinal tumors, multiple sclerosis, myelitis, infarction (e.g., spinal artery), compression (e.g., hematoma)
• Clinical features
  • Symptoms classically occur 6–8 weeks after spinal shock has worn off
  • Bilaterally absent sensory and motor function below the lesion (including lowest sacral segments S4–S5)
    • Impaired sensation (i.e., to pain, position, etc.)
    • Muscle hypertonia with spastic paresis
      • Hyperreflexia
      • Inexhaustible clonus (e.g., ankle clonus)
      • Bilateral diaphragm paralysis: impaired breathing, coughing, and sneezing
      • Absent anal reflex
    • Pathological reflexes, e.g., positive Babinski reflex
    • Neurogenic bladder: involuntary urination caused by contractions
      • Usually results from spinal cord damage above T12
      • Uncoordinated bladder contraction and urinary sphincter relaxation (detrusor-sphincter dyssynergia) causes frequent urination with a sudden urge to urinate, urine leakage, nocturia, and/or incomplete bladder emptying (due to sphincter spasms)
    • Neurogenic bowel: constipation/bowel impaction, bowel incontinence, diarrhea
    • In men: erectile dysfunction can occur
    • Autonomic dysreflexia in spinal cord injuries at T6 or above (see section below)
• Diagnostics
  • Stabilizing patient
    • ABCDE approach in the field
    • Stabilize spine to avoid further damage to the spine from movement during care and transport.
      • Log-rolling of patient
      • Backboard for transfer
      • Rigid cervical collar
  • Neurological exam
    • Examine for neurological damage (e.g., determine motor and sensory function, examine bulbocavernosus reflex)
    • Determine level of injury
    • Determine extent of injury (complete or incomplete)
    • Exclude associated injuries
  • Imaging
    • Complete spinal imaging (cervical, thoracic, lumbar): plain x-rays or CT if available
      • CT is better than x-ray in patients with additional head injury
      • CT is superior to MRI for imaging fractures of the vertebrae
    • MRI: can provide further information on the extent of ligamentous/disc injuries, spinal cord pathology, or epidural hematoma
• Treatment
  • Acute management
    • Analgesia and intensive medical care
    • Insert urinary catheter
    • VTE prophylaxis (e.g., heparin)
  • Definitive management
    • Bracing (e.g., in gunshot wounds) or surgical repair (e.g., decompression and stabilization of spine fracture)
    • C1–C4 tetraplegia
      • Phrenic nerve pacemakers may be indicated
      • Tracheostomy and/or ventilator may be needed
  • Rehabilitation (multidisciplinary care)
    • Walking aids in the case of paresis
    • Physical therapy, occupational therapy, and psychotherapy
    • In the case of immobility:
      • Pressure ulcer prophylaxis
      • Osteoporosis prophylaxis
      • Treatment of pneumonia and urinary tract infections

Symptoms of complete spinal cord injury classically occur 6–8 weeks after acute spinal cord injury (spinal shock) and include spastic paralysis, hyperreflexia, and presence of pathological reflexes (e.g., plantar reflex) below the site of injury.

If spinal injury is suspected (e.g., previous trauma to the neck or back), the patient's spine should be stabilized and the patient should be moved with extreme caution to avoid further damage to the spine!

A complete spinal cord injury above C4 represents a life-threatening situation due to the risk of diaphragmatic paralysis.

References:^[1][3]

• Description
  • A clinical syndrome involving a sudden onset of excessively high blood pressure caused by an imbalanced autonomic reflex response
  • Considered a medical emergency
• Etiology: autonomic hyperreflexia develops in individuals with spinal cord injury who are exposed to stimuli affecting the body below the level of injury ^[4]
  • Spinal cord injury
    • Usually at the level of T6 or higher
    • Causes predisposition for episodes of life-threatening autonomic dysfunction
  • Episode provoking stimulus: can initiate a cascade of imbalanced autonomic reflexes and is located below the level of the lesion
    • Cutaneous (e.g., skin infection, traumatic injury, pressure ulcer)
    • Visceral
      • Bladder (e.g., distended bladder, UTI)
      • Genital (e.g., childbirth, sexual intercourse)
      • Intestinal (e.g., bowel obstruction, constipation)
• Pathophysiology ^[4]
  • Development of the predisposition: damage to descending spinal cord fibers → loss of modulating signaling from the brain → lack of inhibition of spinal cord reflexes → excessive sympathetic reflex response to stimuli below the lesion → life-threatening overactivation of the autonomic nervous system (sympathetic and parasympathetic)
  • Development of a hypertensive emergency: stimulus (below the lesion) → uninhibited sympathetic activation → hypertension (through vasoconstriction and tachycardia) → parasympathetic activation (by carotid sinus baroreceptor) → vasodilation in the area above the lesion; and decrease in heart rate → bradycardia, heart block, and hypertensive emergency
• Clinical features ^[5]
  • Hypertension
  • Throbbing headache
  • Diaphoresis
  • Dilated pupils
  • Guttmann sign: a clinical feature in high spinal cord lesions that manifests with nasal congestion due to sympathetic overactivity
    • Caused by facial vasodilation
    • Often accompanied by flushing, sweating, piloerection, mydriasis, hypertension, and bradycardia
  • Flushing (above the lesion)
  • Paleness (below the lesion)
  • Bradycardia (and AV block) or tachycardia
  • Anxiety
• Management ^[4]
  • Prevention of hypertensive episodes
    • Bladder voiding
      • Monitor urinary output
      • Assess urine retention (e.g., with bedside ultrasound)
      • Provide urinary catheter care (e.g., regular catheterization, examination for signs of infection, application of local anesthetics with catheter insertion)
    • Bowel movement
      • Monitor frequency of defecation
      • Assess for distension, bowel sounds, and masses
      • Release stool impaction (e.g., enema, manual disimpaction)
    • Skin protection
      • Regular skin assessment
      • Frequent position changes
      • Avoid localized pressure (e.g., from clothing or bedding)
  • Detection and treatment of hypertensive episodes
    • Regular assessment for clinical features
    • Monitor blood pressure
    • Position patient in 90° upper body elevation
    • Investigate and eliminate responsible stimulus
    • Antihypertensive treatment (e.g., nitroprusside, nifedipine)
• Complications ^[6]
  • Intracerebral hemorrhage
  • Seizures
  • Death

Autonomic dysreflexia is a medical emergency!

Patients with spinal cord injuries at T6 or above are at the highest risk for autonomic dysreflexia.

The most common stimuli for autonomic dysreflexia are bladder irritation (e.g., distended bladder, UTI), bowel irritation (bowel obstruction, constipation), and breakdown of skin (e.g., cutaneous lesions).