**2.5 Type 5: facet failure**

This form of ASD occurs when the facets joints fail, usually through hypermobility in the early stages and degeneration in the later stages (**Figures 9** and **10**). Hypermobility may occur in anterior procedures due to excessive stretch from oversized interbody devices, but this affects the motion segment that is fused and is therefore rarely a symptomatic problem once fusion occurs, but may cause longterm symptoms in disc arthroplasty.

**Figure 9.** *Type 5 failure (facet failure).*

### **Figure 10.**

*Sagittal (a) and axial (b) MRI of a patient with a previous L3–5 postero-lateral fusion with left facet dysfunction causing a dynamic rotational deformity and unilateral retrolisthesis of L2/3 causing foraminal stenosis.*

Type 5 failure is therefore predominantly seen with posterior instrumentation. The cause of type 5 failure is usually multifactorial and is classified as follows:


To understand type 5 failure, one needs to appreciate the anatomy of the posterior spine. The extensor musculature acts to lordose the spine and is a dynamic control of spinal posture. It is innervated by posterior branches of the dorsal ramus, which run with the posterior vascular supply of these muscles, adjacent to the pars and is therefore at risk with the lateral dissection necessary for posterolateral fusion and standard pedicle screw insertion.

The extensor ligaments, namely the interspinous and supraspinous ligaments, and ligamentum flavum act as static restraints to kyphosis. In contrast, the intertransverse ligaments predominantly restrain lateral flexion. The facet capsule restrains excessive motion of the facet joint, particularly kyphosis. The facet joint itself is innervated and supplied by nerves and vessels that run with the dorsal muscular supply and are therefore at risk during posterolateral fusion and the dissection necessary for the insertion of standard pedicle screws.

We believe extensor mechanism dysfunction is caused by dysfunction of the dynamic or static restraints to segmental kyphosis. Dynamic restraint damage is caused by direct posterior musculature trauma and/or denervation and devascularisation of the paraspinal musculature most commonly induced by multi segment posterior dissection. This causes extension weakness, which results in adjacent segment kyphosis with load. Static restraint dysfunction is caused by transection of the cranial inter- and supraspinous ligaments or most cranial spinous process during the index procedure. The adjacent segment then relies on the ligamentum flavum and facet joint capsules as static restraints. Thus, adjacent flavectomy or direct capsular injury further disables the static restraints. Damage to the adjacent intertransverse ligaments is rarer, because the ligaments at risk are usually incorporated into the fusion, and the lateral IVD capsule offers significant restraint to lateral flexion. However, if a cranial transverse process fracture occurs the adjacent intertransverse ligament is affected and that increases the load on the lateral IVD capsule and may predispose to coronal failure.

Malalignment, particularly sagittal imbalance, puts excessive strain on both the dynamic and static restrains. This is particularly important if there is already dysfunction of the extensor mechanism, as the additional load induced by malalignment needs to be compensated for by the extensor mechanism.

The facet joints themselves are also commonly injured with posterior instrumentation. This is caused by the dissection necessary to insert posterior instrumentation, particularly standard pedicle screws through a midline approach, which involves far lateral dissection with stripping of the soft tissue from the posterior facet capsule and exposure of the pedicle entry point, which damages the neurovascular supply of the facet joints and extensor musculature.

Percutaneous insertion of the most cranial posterior implants is therefore preferable if possible, because this limits the degree of dissection necessary for insertion of the metalware, reducing the risk of neurovascular injury to the extensor mechanism and facet joints.

Metalware impingement on the adjacent facets is also common with pedicle screws, with estimates of up to 60% of pedicle screws breaching the facet [18–20]. Furthermore, even without facet joint breach, impingement can occur of the adjacent inferior articular process on the pedicle screw or rod with spinal extension, driving the adjacent level into kyphosis.

The treatment of asymptomatic patients or those not amenable to operative intervention remains non-operative. However, the treatment of symptomatic patients amendable to operative intervention is as follows:

5a. Single level extension of fusion, with protection of the extensor mechanism. This may involve the use of interbody fusion from anterior or lateral approaches, or a posterior approach with cortical trajectory screws or percutaneous insertion of cranial pedicle screws, with protection of the ligamentous restraints to kyphosis.

5b. Deformity correction and extension of fusion.

5c. Single level extension of fusion, with protection of the adjacent facet, often with anterior or lateral approaches, or a posterior approach with cortical trajectory screws or percutaneous insertion of pedicle screws.

5d. Dependent on facet function


5e. Deformity correction with extension of fusion and avoidance of extensor mechanism and adjacent facet injury.

This classification broadly classifies ASD into anatomical and pathological groups, in order to further our understanding of its aetiology and treatment. However, as with any classification, it has limitations. Some patients with ASD fit more than one category and others fail in an atypical way. In such cases, the causes may be multifactorial and therefore the treatment may differ from those proposed in this classification system. Clinicians should be aware of these nuances and treat patients accordingly.

Understanding this anatomical and pathological based classification system allows treating clinicians to limit the modifiable risk factors for ASD after thoracolumbar fusion. By optimising bone quality preoperatively, the surgeon reduces the risk of bone failure, such as type 1a, 1c, 2a, 2c, 3a and 3d. In addition, ensuring spinal alignment and balance, reduces the risks of all failure mechanisms. Furthermore, ensuring adequate fixation at the time of operative intervention surgeons will reduce the risk of type 1b and 1c failure. However, this must be achieved without complete rigidity, which imparts excessive load through the cranial endplate and adjacent IVD motion to type 3c and type 4 failure. In addition, posterior dissection should be limited to avoid type 5a, 5c and 5e failure and the most cranial implants should avoid damage of the cranial endplate causing type 3b failure and the adjacent facet causing type 5d failure. Abiding by these principals reduces the risk of ASD, but does not prevent ASD because there remain non-modifiable risk factors for the condition.

Similarly, if ASD does develop, the clinician should critically appraise the causes of the failure, to ensure that optimal treatment is provided. In the setting of bone failure, bone supplementation should be provided, however, these alone fail to resolve the problem and therefore bracing or further surgical intervention is necessary. In all revision procedures, spinal alignment and balance should be considered. Abiding by the same principals as discussed above, clinicians will reduce the risk of recurrence.

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

Lastly, this classification is the first to describe the pathophysiology of ASD and therefore provides a framework on which further work can expand the prevention and treatment of this increasingly common condition.

In conclusion, this anatomical and pathological based classification system allows treating clinicians to limit the modifiable risk factors for ASD, understand the causes of ASD and offer a treatment algorithm for ASD. Furthermore, understanding this classification and the causes of failure allows clinicians to not only diagnose and treat ASD, but also offers a clearer understanding of what modifiable factors should be addressed during the index procedure. In addition, it illustrates that new technologies to eliminate modifiable risk factors are necessary, which should stimulate research and industry to find solutions to this common problem.
