The patient has been brought to the ER in a C-Spine collar.The patient did not lose consciousness. He was wearing his seat belt. What would your approach be? What about the next case? CASE 2:ġ2 year-old passenger seated in the back seat of a vehicle that was hit by another car while changing lanes. The car was spun around and then hit a light pole. Moving her neck to show you that she is okay.No complaints of neck pain or neurologic deficits. Is complaining of left wrist, left ankle and chest wall tenderness.Was wearing her seat-belt & the airbags deployed.In the following cases we will apply the two major CDRs to guide our decision making.Ħ5 year-old F driver rear-end collision on highway at 100 kmh I sometimes show/discuss them with patients so that they understand my thinking process. PEARL: You do not have to memorize CDR’s – know where to look. Fail if doc cannot remember nuances of inclusion/exclusions.Designed by academics and applied by mostly non-academics.Applicability to the patient you are seeing.CDRs allow physicians to make efficient and bias-free clinical decisions.CDRs allow physicians to provide a standardized approach to problems.CDRs are useful where diagnostic uncertainty.2 validated rules exist that can help identify the need for radiography and clear C-Spines safely.ĬDRs usually include a mix of history, physical findings and tests.Persistent medico-legal fear continues to influence our practice.Although there is literature to guide our approach – much of it is confusing and contradictory.A large variation in clearing c-spine practice continues to exist.If you consider just patients going for neck X-Rays, 2.5% will have a CSI.Of these, 1% will end up having a clinically important C-Spine injury.Canadian ER physicians see 200, 000 alert, stable trauma victims per year.Understand when further imaging with CT and MRI may be indicated.Gain an approach to clearing C-Spines in Pediatric Patients.Apply the Canadian C-Spine Rule and NEXUS criteria to aid in the use of clearing C-spines in Adults.I would appreciate some comments – peer review if you will. As a disclaimer, this is my approach based on my clinical experience and from reading the literature – you should discuss this amongst your colleagues and review the literature to see if you reach the same conclusions. Spinal cord ischemia is usually due to small perfusion defects as a result of long period of small collisions with the narrowed canal instead of absence of larger blood supply to the spinal cord 1.I gave a talk the other day on clearing C-Spines, with Prezi linked here. When spinal stenosis is present, either forward (impacting the osteophytes) or backward movement (impacting the hypertrophied ligamentum flavum) of the spine will cause further canal narrowing and compresses the spine, increasing the risk of spinal cord damage, thus causing compressive myelopathy or chronic spinal cord ischemia. Other changes includes facet joint (located between lamina and pedicle) and ligamentum flavum hypertrophy (located on the lamina itself) that also contributes to canal narrowing 1. Uncovertebral joint (that relates laterally to the disc) will also be affected, especially at C5/C6 and C6/C7 levels (most spine movements occur here). However, the "awkward" kyphotic position of the spine gives rise to more stress of the other vertebral levels, resulting in progression of spondylosis to other vertebrae. Osteophytes of the adjacent vertebrae may fuse, slowing the pathologic process and provides stability for the spine. As osteophyte formation increases, it causes the narrowing of spinal canal, compressing the spinal cord, resulting in a condition known as "hyperostotic myelopathy". Disc herniation irritates the posterior adjoining ends of the vertebrae, causing the new bone formation, known as an osteophyte. The bulging disc causes the posterior longitudinal ligament to peel off from the surface of the vertebral body 1. As the disease progresses, the spine is unable to maintain its normal alignment (as in normal lordosis in the cervical and lumbar spine), causing an abnormal kyphotic spine 1.įurther disc desiccation results in disc herniation through the posterior annular tear. Part of the disc bulges posterior to the posterior annulus, as this part of the disc is thinner. Thus, the intervertebral disc becomes easily compressible and the height is reduced. This results in loss of proteoglycan matrix, due to loss of water content and chondroitin sulfate, being replaced by keratin sulfate. Repetitive movements wear down the vertebral body endplates, compromising vascular supply to the central part of the intervertebral disc (made up of the nucleus pulposus and annulus fibrosus). The earliest spondylotic change is disc desiccation. Spondylosis can be divided into static causes (degeneration) or dynamic causes (due to movements) 1.
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