**2.3 Type 3: endplate failure**

This is one of the most common forms of ASD and it occurs when the most cranial instrumented vertebral body collapses (**Figures 5** and **6**). It can occur with posterior or anterior/lateral implants and its causes can be classified as:


**Figure 3.** *Type 2 (adjacent bone failure).*

*An Anatomical and Pathological Classification of Thoracolumbar Adjacent Segment Disease DOI: http://dx.doi.org/10.5772/intechopen.89960*

### **Figure 4.**

*A lateral standing full spine x-ray of a patient who had undergone an L2-S1 fusion with a failure to correct sagittal balance who developed an adjacent compression fracture of L1 that accentuated the spinal imbalance and over a 6-year period, despite attempted compensation with pelvic retrolisthesis and thoracic hypokyphosis, they developed a progressive anterolisthesis of T11/12 causing thoracic myelopathy.*

**Figure 5.** *Type 3 failure (endplate failure).*

### **Figure 6.**

*Lateral standing X-rays of an obese osteoporotic patient who had previously undergone an L4/5 circumferential fusion complicated by global sagittal imbalance, pedicle screw malposition causing right L5 radiculopathy and dysfunction as well as progressive type 4d ASD of L3/4 causing critical central stenosis (a). They underwent revision of their instrumentation with L3-S2 fusion and correction of their sagittal balance, supplemented with cranial vertebroplasty (b). However, the patient developed type 3d ASD (c).*

Most are thought to occur because of poor bone stock and therefore mimic osteoporotic compression fractures. However, end-plate devascularisation, either from a direct injury to the end arteries of the endplate by subcortical screws or by damage of the nutrient vessels to the endplate by anterior dissection can occur [17]. Similarly, with interbody devices the excessive load induced by rigid constructs can surpass the endplates' biomechanical tolerance and induce fracture.

Treatment depends on the severity of symptoms and the degree of compression of the vertebrae. In asymptomatic patients bracing to prevent further compression and bone supplementation may need to be considered if there is poor bone stock. In symptomatic patients amendable to operative intervention, treatment should consist of:

3a. Treat as osteoporotic compression fractures. Bone supplementation ± bracing. If metalware protrudes into the adjacent IVD consider deformity correction with increased fixation.

3b. Bracing. If metalware protrudes into adjacent IVD consider deformity correction. While the cause is endplate vascular compromise, there is to date no evidence that changing the surgical technique for the extension of fusion will reduce the risk, however surgeons should consider avoidance of cranial endplate compromise if possible (e.g. cortical trajectory screws, sublaminar bands or hooks).

3c. Deformity correction with extension of fusion and avoidance of a rigid interbody device at the most cranial fusion level.

3d. Treat as osteoporotic compression fractures. Bone supplementation ± bracing. If metalware protrudes into adjacent IVD consider deformity correction with extension of fusion and avoidance of both cranial endplate compromise and a rigid interbody device at the most cranial fusion level.

*An Anatomical and Pathological Classification of Thoracolumbar Adjacent Segment Disease DOI: http://dx.doi.org/10.5772/intechopen.89960*
