Management of thoracic spinal cord injury in a professional American football athlete: illustrative case

Abstract

Background: A case of catastrophic thoracic spinal cord injury (SCI) sustained by a professional American football player with severe scoliosis is presented.

Observations: A 25-year-old professional football player sustained an axial loading injury while tackling. Examination revealed a T8 American Spinal Injury Association Impairment Scale grade A complete SCI. Methylprednisolone and hypothermia protocols were initiated. Computed tomography scan of the thoracic spine demonstrated T8 and T9 facet fractures on the left at the apex of a 42° idiopathic scoliotic deformity. Magnetic resonance imaging (MRI) demonstrated T2 spinal cord hyperintensity at T9. He regained trace movement of his right lower extremity over 12 hours, which was absent on posttrauma day 2. Repeat MRI revealed interval cord compression and worsening of T2 signal change at T7-T8 secondary to hematoma. Urgent decompression and fusion from T8 to T10 were performed. Additional treatment included high-dose omega-3 fatty acids and hyperbaric oxygen therapy. A 2-month inpatient spinal cord rehabilitation program was followed by prolonged outpatient physical therapy. He currently can run and jump with minimal residual distal left lower limb spasticity.

Lessons: This is the first known football-related thoracic SCI with idiopathic scoliosis. Aggressive medical and surgical intervention with intensive rehabilitation formed the treatment protocol, with a favorable outcome achieved.

Keywords: football; hyperbaric oxygen therapy; hypothermia; rehabilitation; spinal cord injury; sports medicine; steroids.

FIG. 1.

Initial computed tomography scan obtained at presentation. Axial (left) and sagittal reconstruction (right) views demonstrate T8 and T9 facet fractures on the right.

FIG. 2.

Left: Axial T2 MRI immediately after injury. Right: After neurological deterioration on postinjury day 2, a repeat MRI performed 48 hours after injury demonstrated interval development of epidural hematoma and thickening of the ligamentum flavum with new spinal cord compression and worsened spinal cord edema.

FIG. 3.

Left: Standing posteroanterior long-cassette spine radiograph at 3 months after injury demonstrating the construct at T8-T10 and 45° idiopathic thoracic dextroscoliosis. Right: Standing posteroanterior long-cassette spine radiograph at 6 months after injury revealed that the thoracic Cobb angle increased to 55°, concerning for interval development of neuromuscular scoliosis. Focused rehabilitation on core and paraspinal musculature was associated with no further change in patient’s curve in the ensuing 2 years.

FIG. 4.

Medical illustration depicting the mechanism of injury. An axial loading force vector at the crown of the helmet during a head-first tackle is transmitted through the spinal column, exiting at the apex of the thoracic scoliosis. The concavity of the apex at T9 was the site of load failure. Also in scoliosis, the spinal cord lies eccentric in the canal toward the concavity. Over the first 48 hours after, an epidural hematoma developed, causing spinal cord compression and worsening neurological insult, which led to surgical intervention.