Introduction
In Victoria, most spinal cord injuries (SCI) result in permanent neurological disability for patients. Australian data collected from 2006–07 indicated that 52% per cent of injuries were related to transport accidents and 29% were as a result of falls. These two mechanisms alone accounted for more than three-‐quarters of all traumatic SCI.2.
Presentations of SCI have a bimodal distribution. Cases related to trauma in younger adults often involve higher velocity injury in a healthy spine. Injuries to the older adult often appear in later life with other causes, which may be associated with a lower velocity injury in a vulnerable spine. These may be a result of a pathological vertebral fracture, a first sign of malignancy and/or result from seemingly insignificant injury presentation.3
Damage to the spinal cord may cause irreversible injury with the outcome of either temporary or permanent neurological deficit.4 The natural progression of SCI, in particular rising spinal cord oedema, may lead to an exacerbation of symptoms in the hours following an accident. Early care of SCI can have a significant effect on the long-term outcomes for these patients, with safe and appropriate transport to definitive care facilities a vital process.5 ,6 Emergent surgical fixation, where indicated, and stabilisation of the spinal injury may provide the best outcome for patients and is the first stage of recovery.
Injuries to the spinal cord may be classified as: complete (with no neurological connection between the cortex of the brain and the lowest sacral spinal cord segment) and incomplete injury (with some connection maintained). The American Spinal Injury Association (ASIA) Standards for Classification of Neurological Injury include documentation of incomplete and/or motor preservation and identification of unilateral deficits.7
Click to enlarge
Following a traumatic injury, the spinal cord becomes oedematous and, with limited capacity for swelling inside the vertebral column, normal neurological function rapidly becomes compromised. This may affect about two nerve exit levels of the spinal cord above the level of initial injury. As resolution of swelling occurs over time, there may be recovery at the level of SCI but not always recovery in the long tracts below.
Importantly, SCI trauma patients may present with an amalgamation of motor and sensory neurological deficits, which may be unilateral or bilateral, affecting upper and/or lower body regions. Conscious patients may describe various perceptions such as numbness, burning pain or absence of feeling or movement. The emerging and frequently ascending nature of spinal injury signs and symptoms indicate a need for exacting and ongoing assessment, as well as monitoring and management of the SCI trauma patient. Two important outcomes of a SCI are neurogenic shock and spinal shock.
Neurogenic shock is seen in SCI affecting the sixth thoracic vertebrae or above, typically occurring within 30 minutes of cord damage and lasting six to eight weeks following injury. It is a result of the loss of vasomotor and sympathetic nervous system tone or function. Its critical features are hypotension, bradycardia and poikilothermia.
Spinal shock is a combination of loss of and decreased reflexes and autonomic dysfunction that accompanies SCI. Skeletal and smooth muscles are therefore flaccid from hours to weeks.8
All patients with spinal trauma must receive a rapid and systematic primary and secondary survey. The main goals are to ensure understanding of injury mechanisms and pattern optimum management in the emergency setting, including prevention of secondary insults, and activation of the retrieval network, with timely transfer to an appropriate trauma facility.