Overpowering the crankshaft mechanism. The effect of posterior spinal fusion with and without stiff transpedicular fixation on anterior spinal column growth in immature canines.

STUDY DESIGN

This experimental study was designed to test the hypothesis that posterior spinal fusion and internal fixation, using a stiff transpedicular construct, would withstand additional anterior column growth without the need for an anterior procedure and would prevent the development of deformity secondary to asymmetric growth of the anterior column in the immature canine model.

OBJECTIVES

This model revealed that a mechanical epiphysiodesis of the anterior spinal column can be created through a posterior approach in an immature growing animal using a stiff transpedicular construct. These results were correlated to the crankshaft mechanism clinically to provide a possible rationale for transpedicular posterior spinal instrumentation and fusion, without a concomitant anterior procedure, in immature patients.

SUMMARY OF BACKGROUND DATA

All operative immature canines underwent posterior fusion of L1-L5 vertebral bodies with autogenous iliac crest bone graft. Instrumented canines underwent the additional placement of transpedicular screws at L1, L3, and L5 as well as 3/16-inch rods and a transverse connector. Previous studies have revealed that continued anterior spinal column growth after posterior arthrodesis causes a resultant deformity in quadrupeds. No previous study has assessed whether a transpedicular construct can overpower the anterior spinal growth plate in an immature growing model.

METHODS

Twenty-five skeletally immature canines were randomized into four groups: control, fusion only, screw and fusion, and instrumentation and fusion. Disc space growth, vertebral body growth, and sagittal plane angulation were the variables analyzed. Management response variables were visualized graphically and radiographically.

RESULTS

Posterior tethering and anterior column growth occurred in the noninstrumented fusion groups, producing substantial lordosis. Anterior column growth was arrested in the instrumented canines as demonstrated by decreased vertebral body length, disc space narrowing, and, most importantly, prevention of lordosis.

CONCLUSIONS

The present study confirmed that in immature canines anterior column growth continues after posterior fusion without instrumentation. The magnitude of this growth, combined with a posterior tether, is sufficient to cause significant lordosis. The results are the first to document that a stiff posterior spinal instrumentation system is sufficient to overpower the residual anterior growth centers, even in the presence of a posterior tether (fusion mass). This technique creates a mechanical epiphysiodesis evidenced by arresting vertebral body length, narrowing disc space, and preventing lordosis, thus thwarting the deformity-producing mechanism without an additional anterior procedure.