Type:
Educational Exhibit
Keywords:
Trauma, Education and training, Arthritides, Safety, Diagnostic procedure, Conventional radiography, MR, CT, Musculoskeletal spine
Authors:
C. Sayer1, G. Price1, F. Cuthbert2, E. Sellon1; 1Brighton/UK, 25BE/UK
DOI:
10.1594/ecr2013/C-1078
Background
Ankylosing spondylitis (AS) is a well recognised clinical entity. It was previously thought of as a variant of rheumatoid arthritis (RA) until around 1960 and termed ‘rheumatoid spondylitis’. In 1973,
the association with human leukocyte antigen (HLA)-B27 gene was discovered,
thus establishing the genetic background of AS,
and in 1976 a unifying concept for the ‘seronegative spondylarthritides’ was proposed.
The prevalence today is 0.5 – 1.9%.
Bone formation is typical for AS and distinguishes AS from RA in which bone destruction prevails. The radiographic findings may take 10 years or more to develop (although early inflammatory changes on MRI can be appreciated as Romanus and Andersson lesions). The process of enthesitis,
spondylitis and sacroilitis may lead to eventual ankylosis.
This is characterised by intra and extra-osseous bone formation (sclerosis,
syndesmophytes) ossification of ligamentous structures,
intervertebral discs and fusion of the sacroiliac joints.
In AS there is altered spinal biomechanics.
Due to multilevel bony fusion,
long lever arms develop in the spinal column on which forces can act during even minor trauma.
Fractures are characterised by their unusual location (e.g.
at the cervical spine and dens).
These are usually trans-discal extension injuries through syndesmophytes involving the posterior elements resulting in three-column unstable spinal injuries.
Falls are the most frequent cause of trauma in AS patients and around 65% of fractures result from minor trauma. Cooper et al present a population based study of fractures in AS. 39% result from a fall from ground level and there is a high incidence of spinal cord injury (58-70%).
The clinical outcome was worse compared with general spine trauma population with13.9% (vs 0.08%) having secondary neurological deterioration following admission. There is a 17.7% mortality following injury (>3 months) (vs 0.4%) in AS.
Westerveld et al looked at 345 AS patients with spinal fractures.
Low energy trauma was responsible for 65.8% of these.
There was a delay in diagnosis > 24hrs in 17.1%.
52.7% of the time this was due ‘doctors delay’,
for example,
failure to obtain imaging,
dismissal of ‘minor trauma’ and back pain,
or incorrect interpretation of plain radiography.
The remaining 47.3% was the result of a patient delay in presentation. They found that neurological impairment was present at presentation in 68.2% but there was secondary neurological deterioration in 13.9%.
Thumbikat et al looked at all spinal cord injury patients with AS over 10 years at a spinal cord unit in Sheffield,
UK.
The majority sustained injuries as the result of a fall from standing.
They found that 12 out of 18 patients were able to walk following injury but subsequently underwent secondary neurological deterioration.
This was the result of the correction of pre-existing kyphosis (most common) and poor transfers and positioning e.g.
in scanner gantry. On the basis of their findings they made recommendations for transferring and stabilising these patients in neutral flexion and having a low threshold for use of CT and MRI.