A) Epidemiology
In the UK in 2000, the general population numbered almost 59 million. In one year, 666 new cases were admitted to a spinal injury centre as a result of a traumatic injury. This doesn't include those purely treated at general district hospitals but one would estimate this number to be very low as almost all patients who sustain a cord injury even if they have a stabilisation procedure performed locally will eventually referred for rehabilitation.
If you look at the breakdown of the causes of traumatic cord injury then about 41% were as a result of various falls, 37% of injuries were from road traffic accidents and about 11% were sports related injuries. Other causes included lifting or collision injuries and assault with sharp trauma. Falling from a height and falling downstairs were the commonest type of fall injury. Road traffic accidents mostly involved motorbikes and four wheeled vehicles. Sports injury breakdown showed diving to be the predominant mechanism followed by rugby and horse riding.
More recent statistics from a single spinal injury centre (Duke of Cornwall, Salisbury) confirmed the frequency of the various causes of traumatic injury. In addition, their statistics showed two to three people a day become paralysed from cord injury, 80% of injured patients are male, and that currently 40,000 people are living with paralysis secondary to cord injury. In terms of the types of cord injuries sustained about 45% were incomplete and so 55% were complete. About 50% of all spinal cord injuries result in quadriplegia, although interestingly 92% cord injuries from sports injury also result in quadriplegia.
Comparing all these statistics with those from the United States show the figures to be generally similar.
B) Pathophysiology
There are three phases of spinal cord injury response that occur after injury: the acute, secondary, and chronic injury processes.
1) Acute phase
This encompasses the moment of injury and extends for the first few days; a variety of processes begin. Upon initial injury, there is immediate mechanical damage to neural and other soft tissue, including endothelial cells of the blood vessels in the vicinity. Cell death, results from these mechanical and ischaemic insults is instantaneous. Then the injured nerve cells respond with an injury-induced barrage of nerve action potentials and concurrent electrolytic shifts, principally involving Na+, K+ and Ca2+ which cause failure in normal neural function and spinal shock, which lasts for about 24-48 hours. Haemorrhage, localised oedema, thrombosis, vasospasm, mechanical damage (both from direct trauma and vertebral or disc displacement), and loss of vasculature autoregulation are the major processes in this phase which compound the cord injury.
2) Secondary phase
Extracellular concentrations of glutamate and other excitatory amino acids reach toxic concentrations as a result of cell lysis from mechanical injury. In addition, lipid peroxidation and free-radical production also occur as a result of glutamate receptor-activated mediated pathways. Apoptosis, programmable cell death, occurs. There is increased expression of glial fibrillary acidic protein (GFAP) and astrocytic proliferation.
As part of an inflammatory response to inflammation, neutrophils and lymphocytes invade the spinal tissue from the circulation reaching peak numbers within 48 hours. These invading inflammatory cells increase the local concentrations of cytokines and chemokines and inhibitory factors and barriers to regeneration are expressed around the injured location. The injury therefore grows in size from the initial core of cell death with cells at risk of dying in the immediate region, to a larger area of cell death.
3) Chronic phase
Over a time course of days to years, apoptosis continues proximally and distally. Scarring and tethering of the cord occurs in the penetrating injuries. Demyelination results in conduction deficit. A cyst can form within the cord and can enlarge (syrinx). Lacerated axons exhibit regenerative and sprouting responses but go no farther than 1mm. Neural circuits are altered due to changes in inhibitory and excitatory input and permanent hyperexcitability develops, which results in chronic pain syndromes in a majority of cord injured patients.
C) Clinical Examination and Investigation
There are three aspects to the initial examination and investigation.
1) ATLS with spine protection
As mentioned earlier, roads traffic accidents and falls are common causes of traumatic cord injury so these patients may also have other life threatening injuries. These other injuries must be sought out and treated before treatment of the cord injury can be considered. These patients when they arrive in hospital should be subjected to ATLS guidelines. In line immobilisation and protection of the spine should be maintained during the entire resuscitation process. The entire spine should be immobilised on a long board with padding and a semi rigid collar should be applied to the neck. At this stage protection is primary and detection is secondary.
2) Suspect Injury
The mechanism of action is key to suspecting an injury. All the common mechanism have been mentioned earlier with RTA's and falls being the commonest but don't forget the sport injuries. Other clinical pointers are the unconscious patient and patients who present with spine pain or tenderness and those who have a neurological deficit.
3) Diagnose Injury
A full neurological examination should be carried out and documented. This should also be repeated to detect any improvement or deterioration subsequently. The ASIA (American Spinal Injury Association) chart is now the standard form on which all neurological examination should be recorded. This removes the ambiguity at some levels regarding the precise innervations of muscles and boundaries of sensory regions.
Imaging should include plain radiographs, CT and MRI scanning to assess an injury. There are clear guidelines issued by BOAST (British Orthopaedic Association for Standards in Trauma) on the type and extent of imaging required to clear a patient of spinal injury. The salient points from the guidelines are:
i) If it