24 Surgical Failures Mechanisms and Their Treatment

10.1055/b-0039-171420

24 Surgical Failures Mechanisms and Their Treatment

Pierre Roussouly, Hyoungmin Kim, Amer Sebaaly, and Daniel Chopin

Abstract

Several studies have demonstrated a very high level of complication in the surgical treatment of adult spinal deformities. Among them, mechanical failures comprise the bigger share with pseudarthrodesis, proximal junctional kyphosis (PJK), loss of correction, and instrumentation breakage. Recently, numerous authors pointed out the role of the spinopelvic sagittal balance and the correlation between balance restoration and functional quality of life. Strong correlations between pelvic parameters, pelvic incidence (PI), pelvic tilt, and sacral slope, and the spine curvatures, mainly lumbar lordosis (LL), showed a direct relation between PI and LL (PI-LL). Improvement of techniques of osteotomies permitted very strong correction and lordosis restoration. But at the same time, the level of PJK increased dramatically. In this chapter, we describe the various mechanisms of failure based on the effect of a surgical fusion on the spinopelvic alignment. Mechanical compensations described in Chapter 11 may happen with local kyphosis induced by fusion such as adjacent hyperextension of the spine above and below, and/or pelvis retroversion. A primary good reduction may be lost by secondary disk degeneration and collapse inside a fusion area, inducing a delayed kyphosis and loss of balance. Anterior stabilization by interbody cages is required. After these general considerations, the strategy of reduction has to be based on PI value, which is the only signature of the initial status. The Scoliosis Research Society classification considers PI-LL and sagittal vertical axis values to quantify the balance. It generally works well, but two conditions seem to limit this classification: patients with small PI (nonretroverted pelvis) and kyphosis–lordosis interaction based on lordosis length and repartition. In the case of low PI, there is a poor possibility of compensation by pelvic retroversion. The ideal restitution is type 1 or 2 in Roussouly’s classification. The main mistake is correction by an excessively long and curved lordosis (type 3), inducing an anteverted pelvis. Repartition of lordosis is another cause of error when positioning surgical correction up to L4 (L3 pedicle subtraction osteotomy, for instance). Increasing the upper arc of lordosis instead of the lower arc (L4-S1) induces by angle reciprocity an increase of the lower arc of kyphosis and is probably one of the main causes of PJK.

24.1 Introduction

The recent information on sagittal balance has allowed a better understanding of spinopelvic organization. Pelvic and spinal parameters are now quite well-known to the spinal specialists; however, their role (or application) in surgical strategy for treating spinal disorders is still confusing and misunderstood, leading to a common source of serious mistakes. The development of very efficient surgical techniques for correction of spinal alignment, such as posterior column osteotomy or three-column osteotomy (3CO), has allowed dramatic transformation of spinal alignment; at the same time, the need for a better understanding of well-balanced spinal alignment has become more crucial.

Recently, various publications have highlighted poorer clinical outcomes of patients with spinal deformities when the correction was far from an ideal restoration of sagittal balance. ¹ ^, ² ^, ³ Although the mechanism of an unbalanced spine is assessed and understood in a very schematic and simplistic way, such as pelvic retroversion and increasing sagittal vertical axis (SVA), numerous other mechanisms remain unexplained, or are still not found. ⁴

As we have seen in other chapters, understanding of sagittal balance relies on the knowledge of the pelvic parameters pelvic incidence (PI), pelvic tilt (PT), and sacral slope (SS) (PI being a morphometric [or anatomic] parameter, whereas PT and SS are positional parameters), spinal parameters (lordosis and kyphosis), and global balance assessed by C7 or external auditory canal positioning. The strong correlation between PI and SS, as well as SS and spinal lordosis, has simplified our understanding; that is, within the ideal sagittal balance, an adaptable reciprocal value of PI-lumbar lordosis (LL) should be almost constant, so that surgical strategy focuses on restoration of this ideal angular value of LL determined by the individual PI. ⁵ However, things are not that simple, and this simple, clear strategy often results in surgical failures. ⁶ ^, ⁷

As presented in Chapters 6 and 20, we may describe the specific types in different geometries of sagittal alignment in an asymptomatic population as well as its particular degeneration pattern. We could then hypothesize that a different pathological alignment should evolve from a different “normal” or “premorbid” alignment. ⁸ ^, ⁹ By recognizing these particular patterns of pathological alignment and then, within this context, by understanding how PI, their main driver (or a major determinant), is related with responses to other parts affecting whole spinal balance, we can determine the more proper, or ideal, restoration of spinal alignment.

Regardless of the cause of misalignment—natural degeneration, trauma, iatrogenic, etc.—a local hyperkyphosis or hypolordosis is the main culprit of sagittal misalignment and they induce two means of compensation: (1) hyperextension (to decrease kyphosis or to increase lordosis) of the flexible spine above and below the kyphotic area, and (2) retroversion of the pelvis around the femoral heads (FHs). This last mechanism is dependent on PI: a very small range of adaptation with small PI and a higher range of adaptation in higher PI.

Recent identification of a new type of sagittal alignment, anteverted type 3 or, type 3 with anteverted pelvis, in an asymptomatic population allowed our understanding of the mechanisms of adaptive positioning of the pelvis in the case of hyperlordosis by inducing an increasing SS and decreasing PT (to values less than 0). ⁸ This very anteverted unbalanced situation may occur in the case of hypercorrection of the lordosis.

In this chapter, we will analyze the occurrence of simple deleterious compensation in response to PI and, in more complicated cases, the association of several mechanisms inducing the most common sagittal balance-related complication after surgery, proximal junctional kyphosis (PJK).

24.2 Compensation to Spinal Imbalance

In Chapter 11, mechanisms of compensation for a loss of balance either by decreasing lordosis or by increasing kyphosis depend on spinal flexibility and muscular contraction. When the spine is flexible, the part of the spine above and below the deformity area compensates using hyperextension. When the spine is rigid, pelvic retroversion is engaged to compensate.

24.2.1 Compensation by Extension

Short Fusion for Local Degeneration

As this mechanism needs a flexible spine, this method of compensation is found typically in younger patients with local degeneration like one level diskopathy, with or without stenosis and/or previous disk herniation, without multiple levels of degeneration.

When local fusion is done with insufficient lordosis, extension of the flexible spine above and below the fusion area is the common rule. In types 3 and 4, lordosis is mainly located in the lower arc between the apex and S1 plateau. In other words, the extension with sufficient lordosis between L4 and S1 has to be maintained in the case of local fusion. The classical situation is the fusion between L4 and L5 or L4 and S1—for local degenerative L4-L5 spondylolisthesis—with insufficient lordosis. This induces an adjacent compensation by L3-L4 hyperextension (i.e., the first nonfused level). Various technical errors are involved in this problem. The rod bending must be done according to the curve restoration. A polyaxial system often fails to maintain an adequate degree of lordosis and only fixes the motion segment, frequently in an improper angle rather than correcting the deformity. In addition, especially in cases with posterior lumbar interbody fusion/transforaminal lumbar interbody fusion, using a nonlordotic cage or with a cage placed too posteriorly (near to the posterior longitudinal ligament), sufficient extension, or lordosis, is limited by the tension of the anterior longitudinal ligament, which interferes with posterior closing (Fig. 24‑1).

**Fig. 24.1** When introduced by the posterior approach as in posterior lumbar interbody fusion, the tension of the anterior longitudinal ligament may impede lordosis restoration.

The first step of compensation by adjacent-level hyperextension is a forward opening at the junctional disk level, followed by posterior facet subluxation and, in addition, a true retrolisthesis. Of course, this situation is painful and may induce back and even radicular pain (Fig. 24‑2). One treatment option is to extend the fusion to the adjacent level and to stabilize the junctional disk. But, from a sagittal balance point of view, this is not enough because this leaves the previously fused distal levels in insufficient lordosis and restoring the lordosis angle is performed only by increasing the proximal lordosis (upper angle). If the apex of LL is above the level where it should exist naturally, it is known to be related to a higher risk of PJK occurrence. ⁶ In our opinion, it is necessary to restore the distal lordosis (lower angle) where the previous fusion was performed, and to extend the fusion on this physiologically restored alignment.

**Fig. 24.2** **(a)** L4-L5 degenerative listhesis previously treated by posterior fusion with posterior lumbar interbody fusion L4-L5; the local lack of lordosis induces a compensation by hyperextension of the adjacent level L3-L4. **(b)** Extension of fusion to L3 maintaining the hyperextension restored enough but not harmonious lordosis.

Fracture Treatment

Spine fractures occur in younger patients and frequently at the thoracolumbar (TL) level. ¹⁰ With increased local kyphosis, there is a compensatory increase of lordosis by extension in the lumbar area. If the surgical reduction does not address the traumatic kyphosis correctly, the compensatory lumbar extension exceeds the physiologic range of intervertebral motion and generates pain, usually arising from increased pressure on facet joints. The lumbar ability for extension may allow a local compensation for a slightly increased kyphosis. This is the case in types 3 and 4 spines where lumbar flexibility is better than in type 2. In type 2, a traumatic kyphosis in the TL junction area turns the spinal alignment into the pattern of type 1, with distal hyperlordosis, on a spine that is not adapted for such hyperextension. In type 1, a fracture commonly occurs in the TL area because of the characteristic TL kyphosis, and the compensatory lordosis of the distal lumbosacral area easily exceeds the segmental extension capacity as it has already greatly increased.

24.2.2 Compensation by Simple Retroversion

When the spine is rigid as after a long fusion, and when the sagittal balance reduction is insufficient, the main mechanism of compensation is by pelvic retroversion (increasing PT). This mechanism depends on both the individual value of PI and the ability of the hips for extension. The greater the PI, the greater the possibility of PT compensation. But when PT increases, the hips are more extended. When the PT needs to be increased more than the range of hip extension, femoral shaft tilting (with knee flexion) occurs, allowing the additional pelvic retroversion. There are two steps of PT compensation: (1) pure hip extension with vertical femurs, and (2) hip extension and femur tilting with knee flexion. Even if efficient in restoring overall balance, the retroversion mechanism is uneconomical. First, to maintain the retroverted pelvis, gluteal and hamstring muscle overuse is necessary, thus inducing posterior thigh pain from muscle fatigue. In addition, when walking, at the time of the posterior step with the hip limited in extension, the pelvis has to follow the femoral forward tilt, inducing a global forward tilt of the trunk. Incidentally, even if the patient with a retroverted pelvis seems quite balanced in the standing position, when walking, the forward unbalance emerges dramatically (Fig. 24‑3). In some patients with a great ability of hip extension, pelvic retroversion may be quite well accepted without trouble walking. Of course, the mechanism of knee flexion and femoral tilting used in severe unbalance remains a very bad situation with limited walking. Frequently, there are no complaints of pain in such patients; they just feel tired and limited when walking. The Oswestry Disability Index questionnaire based on lumbar pain is completely inadequate to assess unbalance with a pelvic retroversion compensation.

**Fig. 24.3** Compared effect of pelvic retroversion: in a standing stable position, the balance seems correct, but when walking, the hip extension is overpassed in the posterior gait and induces an anterior pelvic tilt with forward trunk unbalance.

Restoring a standard lordosis by osteotomies can be considered the better plan for decreasing PT. In severe unbalance, many authors have integrated the femoral shaft tilting in correction planning. Le Huec et al ¹¹ have described the full balance integrated technique, which includes the angle of femoral tilting in the strategy of 3CO calculation. However, if PT reduction is included in the preoperative planning, when reducing PT, the femoral tilt angle is automatically reduced because it is a part of PT.

With a small PI, this compensatory mechanism by pelvic retroversion is poor. This is the reason why an equivalent quantity of kyphosis seems more unbalanced with a greater SVA (and C7 tilt) in small PI compared with higher PI. Nonetheless, with a small PI, less lordosis is required to correct sagittal imbalance with 3CO than in cases with higher PI. In simple terms, it is easier to restore good balance in severe sagittal imbalance with low PI than in the same case with high PI.

Many controversies appear in the literature regarding the best level for 3CO. van Royen et al ¹² demonstrated geometrically that the more distal the osteotomy site, the more efficient it was (Fig. 24‑4). Because of an easier approach with fewer complications, Schwab defended the level L3 as the most appropriate for LL restoration. ¹³ If the overall LL angle is the only concern, regardless of the level of osteotomy placement and the location of the new apex of lordosis, this assertion can be right and, in this context, the surgical strategy will focus simply on the target lordosis angle. However, unfortunately, things are not so simple. We have seen in Chapter 6 that by lordosis segmentation, dividing the spinal lordosis into two arcs of circles, in higher angulated curves, the lower arc (between L4 and S1) concentrates the bigger part of the angle. Physiologically, if the lordosis is lost in this area, it is necessary to restore it by treating the same area; an L4–3CO is expected to restore alignment much closer to normal than L3. Recently, Obeid et al published a description for a 3CO at L5 with promising results. ¹⁴ Sebaaly et al showed, in a recent publication, that a higher level of a postosteotomy apex of lordosis was one of the most reliable negative factors in PJK occurrence ⁶ ^, ¹⁵ (Fig. 24‑5).