First report of lumbar spinal epidural hematoma after pelvic ring fracture.

INTRODUCTION: Spinal epidural hematoma is a rare condition that most commonly occurs as a complication of spinal surgery. For patients with neurological deficits, surgical decompression can generally provide good outcome. CASE: A 56-year-old, otherwise healthy, patient was admitted to the orthopedic emergency department with a pelvic ring fracture. Over the course of 4 days, a lumbar spinal epidural hematoma developed, with the patient complaining of pain radiating to the S1 dermatome and saddle paresthesia. The hematoma was surgically decompressed, and the patient had a complete recovery. DISCUSSION: To our knowledge, this is the first report of a spinal epidural hematoma after pelvic ring fracture. The etiology of spinal epidural hematoma is diverse, but it is most frequently observed after spinal surgery. It has rarely been observed after lumbar spinal fractures, nearly exclusively in patients with ankylosing spondylitis. CONCLUSION: Pelvic ring fracture might result in spinal epidural hematoma. The presence of neurological deficits after such fractures is an indication for lumbosacral MRI. Surgical decompression will generally resolve the neurological symptoms.

Spinal cord injury-induced immune depression syndrome (SCI-IDS).

Infections are among the leading causes of death in spinal cord-injured patients, and are associated with hampered wound healing, prolonged hospitalization and impaired neurological recovery. We have analysed fluctuations of immune cell populations in an experimental rat model of spinal cord injury (SCI) by FACS analysis compared with sham-operated controls to detect the responses specifically induced by SCI. Further, to illustrate the impact of SCI only animals did not receive methylprednisolone in order to exclude confounding iatrogenic factors. Experimental SCI of rats induced a depletion of ED9(+) monocytes (< 45%, P < 0.01), CD3(+) T-lymphocytes (< 35%, P < 0.01), CD45 RA(+) B-lymphocytes (< 25%, P < 0.01), MHC class II(+) (< 40%, P < 0.01) and OX-62(+) dendritic cells (< 50%, P = 0.032) within the first week after SCI. HIS 48(+) granulocytes remained on levels similar to sham-operated controls. Our data suggest that experimental SCI induces early onset of an immune suppression that we refer to as SCI-immune depression syndrome. Iatrogenic application of methylprednisolone in patients suffering may worsen the immune suppression. A deeper understanding of the underlying mechanisms of this novel syndrome might be essential to decrease mortality, costs (time of hospitalization) and to protect the intrinsic neurological recovery potential following SCI.