Spinal Trauma

Essentials of Diagnosis

• History of trauma

• Development of an acute neurologic deficit

• Signs of myelopathy on examination

General Considerations

• Although spinal cord damage may result from whiplash injury, severe injury usually relates to fracture-dislocation causing compression or deformity of the cord either in the cervical or in the lower thoracic and upper lumbar regions

• Extreme hypotension following injury may also lead to cord infarction

Symptoms and Signs

Total cord transection

• Immediate flaccid paralysis and loss of sensation below the level of the lesion

• Reflex activity is lost for a variable period; urinary and fecal retention

• As reflex function returns, spastic paraplegia or quadriplegia develops, with hyperreflexia and extensor plantar responses

• A flaccid atrophic (lower motor neuron) paralysis may be found depending on the segments of the cord affected

• The bladder and bowels regain some reflex function, permitting urine and feces to be expelled at intervals

• As spasticity increases, flexor or extensor spasms (or both) of the legs become troublesome, especially if bed sores or a urinary tract infection develops

• Paraplegia with the legs in flexion or extension may eventually result

Lesser degrees of injury

• Mild limb weakness, distal sensory disturbance, or both

• Sphincter function may be impaired, urinary urgency and urge incontinence being especially common

• A unilateral cord lesion leads to an ipsilateral motor disturbance with accompanying impairment of proprioception and contralateral loss of pain and temperature appreciation below the lesion (Brown-Séquard syndrome)

• A central cord syndrome may lead to a lower motor neuron deficit at the level of the lesion and loss of pain and temperature appreciation below it, with sparing of posterior column functions

• With more extensive involvement, posterior column sensation may also be impaired and pyramidal weakness develops

• A radicular deficit may occur at the level of the injury—or, if the cauda equina is involved, there may be evidence of disturbed function in several lumbosacral roots

Differential Diagnosis

• The history of the preceding trauma distinguishes the disorder from other causes of nontraumatic myelopathy

Diagnostic Procedures

• Obtain history of trauma

Medications

• Early treatment with high doses of corticosteroids (eg, methylprednisolone, 30 mg/kg by intravenous bolus, followed by 5.4 mg/kg/h for 23 hours)

  • Can improve neurologic recovery if commenced within 8 hours after injury

  • However, evidence is limited and some neurosurgical guidelines do not recommend their use

Surgery

• If there is cord compression, early decompressive laminectomy and fusion (within 24 hours)

Therapeutic Procedures

• Immobilization

• Anatomic realignment of the spinal cord by traction and other orthopedic procedures is important

Follow-Up

• Subsequent care of the residual neurologic deficit—paraplegia or quadriplegia—requires treatment of spasticity and care of the skin, bladder, and bowels

Complications

• Pressure injuries (formerly pressure ulcers)

• Urinary tract infection

• Renal calculi

• Depression

• Pneumonia

When to Refer

• All patients with focal neurologic deficits

When to Admit

• Patients with neurologic deficits

• Patients with spinal cord injury, compression, or acute epidural or subdural hematoma

• Patients with vertebral fracture-dislocation likely to compress the cord