A 47-year-old Han Chinese male patient presented with a 5-month history of low back pain radiating to the legs, progressive weakness, and hypoesthesia in the lower limbs, accompanied by difficulty walking for 1 month. The patient lived in a pasturing area and worked primarily on herding animals with no history of fever or tuberculosis.
Physical examination revealed a normal tone in both lower limbs. Power examination revealed grade 4 in the right lower limb, accompanied by grade 4 proximal and grade 3 distal to the left lower limb.
Initial laboratory examination results showed that the patient had normal laboratory findings, including complete blood cell count, serum chemistry, and erythrocyte sedimentation rate testing; C-reactive protein (CRP) was 7.93 mg/dL, carcinoembryonic antigen (CEA) was 3.84ng/ml, and a test for mycobacterium tuberculosis was positive.
Imaging examinations include radiography, computed tomography (CT), and magnetic resonance imaging (MRI). Radiography revealed a bone defect in lumbar2 (L2) with the side effect of decreasing the height of vertebral body (Figure-1A and B). Three-dimensional CT scans showed osteolytic destruction of L2 (Figure-1C), and sagittal CT images confirmed osteolytic destruction of L2 and posterior spinous process (Figure-1D). Axial imaging showed the bone destruction of L2 was mainly concentrated in the left posterior part of vertebral body. The left pedicle and lamina were also affected and resulted in bone loss (Figure-1E). As previous examinations showed elevated CEA levels and osteolytic destruction in vertebra, we performed whole-body emission computed tomography (ECT) to exclude the disease of osteosarcoma (Figure-1F). The magnetic resonance imaging (MRI) images revealed multiple cystic components in the sagittal plane of the L2. It presented lobulated, multi-eyed, and honeycomb appearance partially existing in the spinal canal at the posterior edge of L2 in T1-weighted scans (Figure-1G, H), T2-weighted sagittal images showed high intensity cystic component images of L2 and its posterior spinal canal, and multiple scattered large cystic block images were also seen at the posterior margin of lumbar vertebrae1 body with clear boundary between each other accompanied with obvious compression of the dural sac at the corresponding site (Figure-1I, J).
We performed cyst removal through posterior cystectomy and L1-L2 spinal joint fusion under general anesthesia. In general, the patient underwent a posterior midline approach to remove the lesions at the posterior edge of the L1 and L2 vertebral bodies, subtotal L2 vertebral resection and lumbar 1–2 discectomy, subsequently L2 was replaced with a mesh cage. Intraoperative cystic lesions had a white crystal-like appearance (Figure-2A), with white granular tissue infiltrating the entire vertebral body and canal, thus disrupting the integrity of the vertebral body. The pathological results showed a large number of inflammatory cells and macrophage invasion in the vertebral body, consistent with the pathological damage caused by hydatid disease (Figure-2B). Before the end of the operation, the surgical site was irrigated with a hypertonic sodium chloride solution to prevent hydatid recurrence. The patient was postoperatively treated with pharmacotherapy. During the treatment period, hematopoietic and liver enzyme changes were monitored according to the treatment guidelines. The patient had a good recovery state of both lower limb powers, along with no signs of local recurrence at the latest examination one year postoperatively.