A 36-year-old male patient was admitted to our hospital with paraparesis on both lower extremities that had developed suddenly 2 hours prior to admission. Seven days prior the patient had suffered back pain as a result of a direct fall on the lumbar region, and was diagnosed with a burst fracture with a distraction force on T12 (). The patient underwent an MRI examination on the thoraco-lumbar area on the same day at another hospital (). The MRI showed a collapse of the T12 vertebral body and T12-L1 inter-spinous widening. The lesion was isointense on T1-weighted images and hyperintense on T2-weighted images. A hematoma was detected from the T12 to L2 area. The hematoma displaced the spinal cord and cauda equina (). No neurological deficits were noted. On the same day, the patient underwent in situ posterior pedicle instrumentation on T10-L3 but a laminectomy was not performed. Non-steroidal anti-inflammatory drugs, which influence blood coagulation, were not administered after surgery. A postoperative neurological status was not detected. Three days after surgery, the patient was encouraged to ambulate, and could walk without difficulty.
Fig. 1 T-L spine lateral radiograph. He had been treated for an unstable L1 burst fracture using posterior instrumentation on the T12-L2 and anterior interbody fusion with autoiliac bone graft 3 years ago (A), and one year ago he had the posterior instrument (more ...)
MRI findings on the initial trauma. Isotense on the T1-weighted image (A), hyperintense hematoma on the T2 sagittal and enhanced MRI (B, C), and hematoma compressing the cord on the T1 and T2 axial image (D, E).
Seven days after surgery, the patient suddenly developed weakness and sensory changes in both extremities together with a sharp pain. Consequently, the patient was transferred to the emergency room. In the initial neurological examination performed in the emergency room, the strength of the hip flexion on the right side was trace (1/5) and was zero below the knee (0/5). On the left side, the ankle dorsiflexion was poor (2/5), and was zero below the ankle (0/5). The sensory was decreased to below the L1 dermatome. The knee and ankle jerk were decreased, and the bulvocavenous reflex and anal tone were also decreased.
Medical records revealed that the patient had been treated in our hospital for an unstable L1 burst fracture 3 years prior using posterior instrumentation on T12-L2 and anterior interbody fusion with an autoiliac bone graft. One year ago, the patient had the posterior instrument removed (). No bleeding tendency was noted in the medical history. A laboratory test showed that the blood profile i.e. the platelet count, prothrombin time, activated prothombin time, bleeding time, and coagulation time were within the normal ranges. An MRI performed 6 hours after the development of symptoms in the emergency room showed a heterogeneous isointense lesion on T1-weighted images, and a hematoma that was heterogeneous hypointense on T2-weighted images that had definitely increased in size, as detected on the sagittal plane and axial plane images ().
MRI with neurological deficit 7 days after the spinal trauma and fixation. Heterogeneous hypointense hematoma on the T2-weighted images was noted (A, B), and it was definitely increased on axial plane compared with initial axial images (C).
Twelve hours after the development of symptoms, a partial T12-L3 laminectomy was performed under general anesthesia. The hematoma filled the epidural space completely and ranged from the T12 to L2 level. A hematoma evacuation was performed, and no definite bleeding focus was detected. Two days after surgery, a recovery of neurological function was noted. One year after surgery, the hypoesthesia was below the right L5 dermatome, the ankle dorsiflexion on the right side was good (4/5) but was slightly lower than normal. However, the other neurological functions had returned to normal.