SEH usually occurs immediately after spinal trauma or surgery4. However, Kummell disease with huge SEH is a unique complication, which has been rarely reported since it was first reported in 20085. It occurs more commonly in the conservative treatment of thoracolumbar osteoporotic vertebral compression fracture with or without neurological deficits6.
The pathogenesis and natural course of Kummell disease associated with SEH is still unclear. Several hypotheses have been used to explain it. One hypothesis7 is that there is a connection between the intravertebral cleft and epidural space in Kummell disease, so that during weight bearing by nonunion or re-fracture with dynamic mobility, the fluid including hemorrhage may be under pressure and pushed into the epidural space, resulting in SEH. Another theory8 is that local pooling of thin-walled epidural venous plexus may be ruptured due to a brief increase in venous pressure caused by nonunion or dynamic re-fracture. In our case, the patient suffered from the aggravation of low back pain caused by minor trauma again and MRI suggested evidence of re-fracture, so we believe that the formation of SEH may be caused by re-fracture.
Whether the patients of Kummell disease with SEH have neurological deficits remains to be elucidated. Kummell disease is a nonunion of fractures characterized by pseudoarthrosis and vacuum cleft9. We believe that whether the patient has neurological deficits may be related to the segment of Kummell disease, the size of the hematoma and the relative position of the hematoma to the conus medulla.
The treatment of Kummell disease with SEH depends on the following factors: the patient's general ability to withstand surgery, the presence of severe back pain, kyphosis, and the presence of neurological deficits. For patients of Kummell disease with huge SEH when their neurological intact, or the whole body is unable to tolerate surgery such as hematoma removal, percutaneous vertebroplasty, as a minimally invasive treatment, not only can effectively alleviate pain, restore vertebral body height, reconstruction of spinal stability10, but also fill the vacuum cleft with bone cement, thus blocking the connection between the vacuum cleft and the epidural space, helps to spontaneous absorption of the hematoma. For patients with neurological deficits, the prognosis is related to the degree of preoperative neurological impairment and the time to operation11. Therefore, timely and adequate decompression is the key to achieve great surgical results. Kim et al 12adopted anterior thoracolumbar vertebrae resection and bone grafting, and posterior bone cement enhanced screw fixation to increase spinal stability. Oda et al 5performed vertebroplasty combined with posterior decompression, which provided satisfactory vertebral reconstruction and posterior decompression through a single posterior approach. In this case, the patient had no neurological deficits, and we performed percutaneous vertebroplasty. The patient recovered well immediately and the reexamination 1 week after operation showed that the hematoma almost completely subsided.