Pathology/Pathogenesis
Spinal shock: Refers to the transient loss of all neurological function below the level of the spinal cord injury causing a flaccid paralysis and arreflexia that usually persists for around 2 weeks after the injury. Following resolution, an upper motor neuron deficit develops with exaggerated reflexes and extensor plantar reflexes, due to loss of descending inhibition of spinal cord reflex arcs.
History
The clinical history should include a detailed description of the mechanism of injury as this may inform the nature of the injury to the spinal column (e.g. hyperflexion, hyperextension, axial compression and distraction). The presence of focal neck or back pain may assist in injury localisation. The immediate neurological symptoms should be recorded, and history of a progressive neurological deficit should raise suspicion of an evolving haematoma or severe instability with ongoing cord compromise. The history should include any risk factors identified above that may predispose to traumatic SCI.
Examination
In fully conscious, neurologically intact, non-intoxicated trauma patients, the posterior cervical spine should be palpated for any focal tenderness. If pain free and without high-risk factors for spinal injury (see below), they should be asked to turn their head 45 degrees to each side; if this does not cause significant pain, a fracture can be clinically ruled out.
Log-roll the patient and palpate the spine for any ‘step’ or focal tenderness and look for bruising and also perform a rectal exam to assess anal sphincter contraction. Palpate the abdomen and feel for a full bladder (urinary retention). Perform a full neurological examination including motor and sensory (pain, light touch and proprioception) function, reflexes (tendon jerks initially absent in cord injury) including abdominal and sacral reflexes and observe for any sign of autonomic dysfunction such as incontinence or priapism.
Investigations
The neck should be imaged in any blunt trauma patient with a depressed level of consciousness, abnormal vital signs, neurological symptoms or signs, severe neck pain (>7/10) or tenderness, a low-risk mechanism but restricted/painful movement, or with neck pain or tenderness and a visible injury above the clavicle or severely painful thoracic trauma and a high risk mechanism of injury (fall >1 m or five stairs, axial loading injury (e.g. diving), motor vehicle accident (>60 mph combined speed or rollover), bicycle collision, age >65 years and distracting injury).
Plain X-rays: Should include three views (AP, lateral and open mouth odontoid views) and show 0/C1 and C7/T1 levels (ask for ‘swimmers view’ if cannot see C7/T1). Films of the thoracic and lumbar spine should be used to clear these areas in unconscious/ventilated patients and in those with an abnormal clinical examination including focal tenderness.
CT: Required in any patient with abnormal/inadequate plain films. In the cervical spine, it is the preferred imaging modality in patients with: GCS <13 or intubated, new neurological signs, severe neck pain or known spinal disease (e.g. ankylosing spondylitis and rheumatoid arthritis), and those requiring a CT head.
MRI: Use in patients with suspected cord pathology without history of trauma. In trauma, it should always be used in conjunction with CT and is indicated in any patient with focal neurological signs, those at risk of vertebral artery injury (e.g. posterior circulation syndrome) or those with a normal CT but severe neck pain or restricted movement.
Dynamic plain X-rays: Flexion extension views may be required for patient with possible occult ligamentous instability without significant bony injury.
Bone scan: Can be used to differentiate recent from old injuries.
Management
Fracture: Patients with possible spinal injury are initially managed in the field with immobilisation on a spinal board, hard cervical collar and sandbags either side of the head until significant injury is excluded.
