The burst fracture is a comminuted fracture of the vertebral body caused by axial loading or vertical compression. With vertical compression forces, there is increase in intradiscal pressure with subsequent herniation through the endplate of the adjacent vertebral body, causing the body to explode from within outward and resulting in disbursement of the bony fragments in all directions. Retropulsed fragments are characteristically seen narrowing B spinal canal frequently associated with spinal cord, conus medullaris, or cauda equina injury (Fig. 20).
The simple wedge compression fracture is the result of a hyperflexion mechanism of injury. These are stable injuries because the middle and posterior column remain intact. There is loss of vertebral body height anteriorly, resulting in anterior wedging or depression of the superior end plate, and intact posterior elements.
Osteoporotic compression fractures are seen in patients with a diminished bone mass, commonly found in the elderly (primary osteoporosis). Other common causes of generalized osteoporosis (secondary osteoporosis) include alcoholism, smoking, poor nutrition, drugs, and hormonal and congenital disorders. Pathologic compression fractures are fractures secondary to weakened bone due to neoplastic infiltration with primary or secondary malignancies. Most of these fractures are the manifestation of metastatic disease. MRI has proven helpful in the differentiation between benign and pathologic compression fractures. Chronic benign osteoporotic compression deformities are characterized by isointense marrow signal relative to marrow of normal vertebrae on all pulse sequences. Acute, subacute, and pathologic compression deformities show similar signal characteristics on MRI, with decreased T1 signal and increased T2 signal relative to normal bone marrow. Nonspecific findings have been
described to help differentiate benign from pathologic compression fractures. Total vertebral body marrow replacement is usually seen with pathologic fractures while benign deformities may show areas of preserved normal marrow. In osteoporotic compressions, the marrow edema eventually resolves. A short-term follow-up study may be useful in this differentiation. Other features that suggest malignant involvement include signal abnormality extending to the pedicle, cortical destruction, abnormal marrow signal in nonfractured vertebrae, and paraspinal soft tissue masses. Increased signal on diffusion-weighted imaging with evidence of restricted diffusion have been described in recent studies of pathologic
compression fractures, whereas benign fractures demonstrates low signal intensity utilizing this technique. Diffuse vertebral body enhancement and bone marrow enhancement greater than normal marrow following the administration of gadolinium are other characteristics suggestive of malignant marrow replacement. Increased Tl signal or preservation of normal marrow signal on T1W and T2W images are characteristics of benign compression deformities.
Patients with vertebral body compression fractures may undergo percutaneous vertebroplasty. Vertebroplasty involves a transpedicular injection of polymethylmethacrylate (PMMA) into the vertebral body. The injected PMMA is dark on Tl- and T2-weighted images and may show a thin rim of enhancement with contrast (Fig. 21).
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