SURGICAL OUTCOME IN ANKYLOSING SPONDYLITIS PATIENTS WITH ANDERSSON’ S LESION AND NEUROLOGICAL DEFICIT.

Abstract

Introduction: Pseudoarthrosis in Ankylosing spondylitis is often misdiagnosed as infection. It is a slow progressing lesion resulting in a kyphosis and slow onset weakness of the lower limbs. We are presenting our strategy and experience in treating 9 patients with such a lesion.

Method: 9 patients age range from 40–55 years who presented with pseudoarthrosis of the ankylosed spine underwent back-front surgery during 2001–204. 6 patients had dorsal spine lesion, 2 had dorso-lumbar junctional lesion and 1 had cervico-dorsal junctional lesion. 8/9 patients had insidious onset with progressive weakness of both lower limb. 1 patient had an acute onset with deformity. 7/9 patients had neurodeficit (Frankel C) 1/9 had complete paraplegia. All patients underwent posterior kyphosis correction and decompression of the spinal cord. During posterior decompression 8/9 patients had an incidental dural tear due to adherence fractured lamina. The dura was repaired primarily or patch graft. 5/9 patients had single stage back and front surgery. The rest of the patients had staged surgery. The front surgery was excision of the tough fibrotic psuedoarthosis and reconstruction using strut graft/cage.

Results: Average duration of surgery was 4 ½ hours (3 ½ to 6 hours). Blood loss was 800 ml (600–1300 ml). All patients required blood transfusion. Primary dural repair was done in 7/8 cases, patch graft in 3/8 cases, ceiling with fusion glue and fat graft in 1 patient. 5 patients who had less that 1000 ml blood loss during posterior surgery had same stage anterior reconstruction. Rest of the patient had 2 staged surgery. 4/9 patients had previous THR B/L. All patients showed rapid improvement in the neurological status and at 3 months follow up all were Frankel E.

Conclusion: The surgical outcome of the ankylosing spondylitis patients with Andersson lesion with neurological deficit is encouraging. Excision of the pseudoarthroses anteriorly and posterior spinal stabilization resulted in full recovery of the deficit. However there were difficulties encountered during the posterior decompression due to adhesions of the posterior elements to the dura.