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Sagittal balance is more than just alignment: why PJK remains an unresolved problem

Scoliosis and Spinal Disorders201611:1

https://doi.org/10.1186/s13013-016-0064-0

  • Received: 5 November 2015
  • Accepted: 4 January 2016
  • Published:
Open Peer Review reports

Abstract

Background

The durability of adult spinal deformity surgery remains problematic. Revision rates above 20 % have been reported, with a range of causes including wound infection, nonunion and adjacent level pathology. While some of these complications have been amenable to changes in patient selection or surgical technique, Proximal Junctional Kyphosis (PJK) remains an unresolved challenge. This study examines the contributions of non-mechanical factors to the incidence of postoperative sagittal imbalance and PJK after adult deformity surgery.

Methods

We reviewed a consecutive series of adult spinal deformity patients who required revision for PJK from 2013 to 2015 and examined in their medical records in detail.

Results

Neurologic disorders were identified in 22 (76 %) of the 29 PJK cases reviewed in this series. Neurologic disorders included Parkinson’s disease (1), prior stroke (5), metabolic encephalopathy (2), seizure disorder (1), cervical myelopathy (7), thoracic myelopathy (1), diabetic neuropathy (5) and other neuropathy (4). Other potential comorbidities affecting standing balance included untreated cataracts (9), glaucoma (1) and polymyositis (1). Eight patients were documented to have frequent falls, with twelve cases having a fall right before symptoms related to the PJK were noted.

Conclusion

PJK is an important contributing factor to the substantial and unsustainable rate of revision surgery following adult deformity correction. Multiple efforts to avoid PJK via alterations in surgical technique have been largely unsuccessful. This study suggests that non-mechanical neuromuscular co-morbidities play an important role in post-operative sagittal imbalance and PJK. Recognizing the multi-factorial etiology of PJK may lead to more successful strategies to avoid PJK and improve surgical outcomes.

Keywords

  • Adult spinal deformity
  • Adult scoliosis
  • Proximal junctional kyphosis
  • PJK

Background

Surgical treatment of adult spinal deformity has progressed substantially over the past ten years. There have been significant advances in decision-making, medical management and surgical technique [1, 2]. These improvements in evaluation and treatment have broadened the applicability of adult deformity surgery and lead to more reproducible clinical benefit based upon health related quality of life (HRQOL) scores [3, 4].

Despite these positive developments, the durability of adult spinal deformity surgery remains problematic. Revision rates above 20 % have been reported, with a range of causes including wound infection, nonunion and adjacent level pathology [57]. While some of these complications have been amenable to changes in patient selection or surgical technique, Proximal Junctional Kyphosis (PJK) remains an unresolved challenge.

The initial description of PJK in the pediatric literature was an increased sagittal angulation, without structural failure, at the upper aspect of a fusion construct [8]. At present, the term is applied much more widely to describe any failure or loss of alignment above an instrumented segment [9, 10]. This may result from adjacent level compression fracture, spondylolisthesis or fixation failure [610]. In general, this has been viewed as a consequence of poor bone quality, over-aggressive deformity correction or inadequate fixation.

PJK has been the focus of intense scrutiny, with multiple studies proposing mechanical solutions including adaptations for osteoporotic bone and in particular specific sagittal alignment targets [11, 12]. Unfortunately, none of these mechanical solutions have effectively decreased the rate of PJK. The role of this study is to examine the contributions of non-mechanical factors to the incidence of postoperative sagittal imbalance and PJK after adult deformity surgery.

Methods

After receiving Institutional Review Board Approval, we reviewed a consecutive series of adult spinal deformity patients who required revision for PJK from 2013 to 2015 and examined in their medical records in detail. Standard demographic data including age, gender, smoking status, height and weight were collected. Indications for the index surgery, specifics of the index surgery including upper instrumented vertebra fixation, time to PJK diagnosis, time to PJK surgery, mode of failure. Medical records were extensively evaluated for preoperative comorbidities; specifically for preoperative neurologic disorders and other pathologies that may affect standing balance.

Results

From 2012 to 2014, 245 patients underwent surgical correction of their adult spinal deformity at our institution. A true incidence of PJK will be difficult to determine as (1) some patients presenting at our institution with PJK had their index surgery performed elsewhere and (2) some of the patients who had their index surgery at our institution could have developed PJK and had surgery elsewhere.

Twenty-nine cases of PJK requiring revision were identified (Table 1). Of these 9 (31 %) were males and 10 (34 %) were smokers. Mean age was 64.4 years. Mean BMI was 29. kg/m2. Neurologic disorders were identified in 22 (76 %) of the PJK cases reviewed in this series. Neurologic disorders included Parkinson’s disease (1), prior stroke (5), metabolic encephalopathy (2), seizure disorder (1), cervical myelopathy (7), thoracic myelopathy (1), diabetic neuropathy (5) and other neuropathy (4). Other potential comorbidities affecting standing balance included untreated cataracts (9), glaucoma (1) and polymyositis (1) (Table 2). Eight patients were documented to have frequent falls, with twelve cases having a fall right before symptoms related to the PJK were noted. Seventeen cases used an assistive device such as a cane, crutches or a walker and required a wheelchair. One patient had 5 co-morbid conditions affecting standing balance, two had 4 co-morbid conditions, four had 3 co-morbid conditions, nine had 2 co-morbid conditions and ten had only one co-morbid condition (Table 3).
Table 1

Summary of cases

Case. No.

Age/Sex

Smoker

BMI

Indication for Index Surgery

Index Surgery

UIV Fixation

Time to PJK diagnosis

Mode of Failure

PJK surgery

Fall prior

Assistive devise

CCMI

Other co-morbidities

1

68/F

Yes

40.9

Kyphoscoliosis

PSF T10 to Pelvis, TLIF L3-L4

bilateral pedicle screws

8 months

Fracture of T9-T10 with cord compression

T9-T10 laminectomy, extension of fusion T4-T11

No

No

11

None

2

64/M

Yes

19.7

Stenosis

PSF L3 to L5

bilateral pedicle screws

18 months

Fracture of L3

PSO L3, PSF T11 to pelvis

Yes

Cane

11

CVA, Loss of reflexes below knee

3

58/M

No

33.9

Multilevel stenosis

PSF L3 to Pelvis

bilateral pedicle screws

17 months

Fracture of L3

AIF L5-S1, Ponte osteotomies, PSF T10 to pelvis

Yes

No

4

CSM post ACDF

4

63/F

No

25.9

Multilevel stenosis

PSF L2 to L5

bilateral pedicle screws

21 months

Compression of L2 with complete loss of L1-L2 interspace

Extension to T10

No

Wheelchair

10

CVA, Cauda equina requiring emergent decompression, Diabetic neuropathy

5

65/F

Yes

34.9

 

ASF L4-S1, PSF T10 to Pelvis

bilateral pedicle screws

11 months

Compression Fracture T11

Extension of fusion to T3

Yes

Walker

9

Diabetic neuropathy, Frequent falls, post bilateral TKA, ORIF L ankle

6

70/F

No

25.7

Kyphoscoliosis

ASF, PSF T10 to Pelvis

bilateral pedicle screws

12 months

Compression Fracture T9

Extension of fusion to T3

No

Cane

7

Cataracts

       

1 month after 1st PJK

Pull out of claw construct fracturing T4 to T8 laminae

Extension of Fusion T2 to T12

    

7

52/F

Yes

25.6

Degenerative scoliosis, stenosis

PSF, L2 to sacrum

bilateral pedicle screws

64 months

Kyphosis at L1-L2 impingement of screws into disc space

TLIF L1-L2, PSF L1-L2

Yes

Crutches

8

Diabetic neuropathy

8

64/M

No

31.0

Flatback S/P L3-L5 PSF

ASF L5-S1, PSF T9 to Sacrum

bilateral pedicle screws

18 months

T8-T9 Listhesis

Extension of fusion to T2

Yes

Walker

8

CVA, Neuropathy, Cataracts (removed), CSM post laminectomy, Frequent falls, post THA dislocation

9

57/F

No

30.5

Flatback S/P L3-L5 laminectomies

PSF T11 to Pelvis

bilateral pedicle screws

25 months

Compression Fracture T9 - T10

Extension of fusion to T3

No

No

9

TIAs, Diabetic neuropathy, Cataracts, Frequent falls, post bilateral TKA, multiple foot surgeries

10

60/M

Yes

19.3

Kyphoscoliosis

ASF L4-S1, PSF T10 to Pelvis

bilateral pedicle screws

82 months

Fracture of T9, T8-T9 spondylolisthesis

PSF T4 to T12

Yes

Walker

9

CVA, Sensory neuropathy, Glaucoma, Frequent falls, post multiple revisions of bilateral TKA

       

14 months after 1st PJK

Pull out of claw construct fracturing T3 lamina

Extension of Fusion T1 to T10

    

11

58/M

No

34.7

Degenerative scoliosis, stenosis

PSF T10 to Pelvis, TLIF L5-S1

bilateral pedicle screws

1 month

T9-T10 Listhesis

PSF T4 to T10

Yes

No

6

DTs, Neuropathy, Frequent falls, alcoholic, had DTs after index surgery

12

75/F

No

29.0

Degenerative scoliosis S/P L2-L3 PDSF

PSF T10 to Pelvis, TLIF L5-S1

bilateral pedicle screws

27 months

Screw pull out

Extension to T4

Yes

No

5

None

13

62/F

Yes

30.0

Flatback deformity S/P L2-LS1 PDSF

PSF L2 to S1

bilateral pedicle screws

12 months

Fracture L1

Extension to T10

No

Cane

6

Tremors, Multiple foot surgeries

       

38 months after 1st PJK

T9-T10 fracture with erosion of screws into disc

Removal of instrumentation, PSF T4 to L2

    

14

69/F

Yes

26.5

Adjacent segment degeneration S/P L3 to L5 PSF

Extension of fusion L1 to S1

bilateral pedicle screws

1 month

L1-L2 listhesis

Extension from T10 to S1

No

No

7

None

15

57/F

No

40.8

Degenerative scoliosis, stenosis

PSF L2 to S1

bilateral pedicle screws

92 months

L1-L2 listhesis

Extension from T10 to S1

No

Cane

5

Parkinson's disease

16

63/F

No

23.2

Adjacent segment stenosis S/P L1 to S1 PSDF

PSF T9 to L3

bilateral pedicle screws

7 months

Posterior lysis of T9 and T10

Removal of instrumentation, PSF T4 to L3

Yes

Cane

8

Cataract, CSM post C3 to T1 ACDF

17

73/F

No

36.4

Scoliosis

PSF T6 to Sacrum

bilateral hooks

80 months

Fracture T6

Removal of instrumentation, PSF T3 to L1

No

No

9

Cataract

18

61/M

Yes

32.5

Scoliosis

PSF T8 to Sacrum

bilateral pedicle screws

11 months

Fracture T8

Removal of instrumentation, PSF T4 to Pelvis

No

Walker

7

Polymyositis

19

72/M

No

36.8

Scoliosis

PSF T11 to L3

bilateral pedicle screws

23 months

T10-T11 listhesis

Removal of instrumentation, PSF T8 to T11

No

Walker

6

CSM post laminoplasty, Frequent falls

       

41 months after 1st PJK

T7-T8 listhesis

Removal of instrumentation T9-L1, PSF T2 to T9

    

20

78/F

No

39.9

Scoliosis

PSF L1 to S1

bilateral pedicle screws

14 months

Fracture T12

Extension of Fusion to T8

No

No

7

Metabolic encephalopathy, Cataract

21

71/F

Yes

26.5

Degenerative Scoliosis

PSF L2-L3

bilateral pedicle screws

45 months

L1-L2 collapse and localized scoliosis

Extension to T10

No

Cane

10

Cataract (removed), Cervical osteomyelitis with cord compromise

22

75/F

No

30.4

Scoliosis

PSF T4 to Pelvis

bilateral hooks

2 months

Hook pull-out with T4-T6 laminar fractures

Extension to T2

No

No

10

Cataract

23

69/M

No

27.4

Post-laminectomy instability

ASF L3 to S1, PSF L2 to S1

bilateral pedicle screws

1 month

Compression Fracture of L2 with screw pullout

Removal of instrumentation, PSF T10 to L1

No

No

6

Diabetic neuropathy

24

55/F

No

38.0

Adjacent segment stenosis S/P L2 to S1 PSDF

PSF T10 to Pelvis, TLIF L2-L3, L5-S1

bilateral pedicle screws

9 months

Compression Fracture T10

Extension to T3

Yes

No

8

CSM post ACDF

25

70/F

No

35.5

Stenosis

PDSF L2-L5

bilateral pedicle screws

10 months

Compression of L2

PSF T10 to Pelvis

Yes

Cane

7

Metabolic encephalopathy, Cataract, Frequent falls

       

5 months after 1st PJK

Compression Fracture T9

Extension to T2

    

26

62/F

No

21.4

Adjacent segment stenosis S/P L3 to L5 PSDF

ASF L2 to L5, Extension of fusion to T10

bilateral hooks

3 months

Fracture T10

Extension to T2

No

Cane

No

CSM post ACDF, Neuropathy, Frequent falls

27

73/F

No

20.6

Scoliosis

PSF T10 to Pelvis

bilateral pedicle screws

4 months

T10 compression fracture

PSF T7 to T12

Yes

Walker

Yes

Mild cognitive impairment, Benign thoracic tumor S/P excision

28

65/F

No

21.1

Scoliosis

PSF T11 to S1

bilateral pedicle screws

22 months

T10-T11 listhesis, nonunion L5-S1

AIF L3 to S1, PSF T10 to Pelvis

No

No

No

Seizures, Eye surgery

29

33/M

Yes

26.7

Scoliosis

PSF L1 TO L4

bilateral pedicle screws

22 months

Compression of T12

Removal of instrumentation, PSF T10 to Pelvis

No

Cane

No

Chronic dropfoot

PSDF posterior spinal decompression and fusion, PSF posterior spinal fusion, ASF anterior spinal fusion, TLIF transforaminal lumbar interbody fusion, CVA cerebrovascular accident, CSM cervical spondylotic myelopathy, ACDF anterior cervical discectomy and fusion, TKA total knee arthroplasty, ORIF open reduction internal fixation, THA total hip arthroplasty, DT delirium tremens

Table 2

Frequency of co-morbid conditions that can affect balance

Co-morbid condition

Frequency

Prior stroke

5

Metabolic encephalopathy

2

Parkinson's disease

1

Seizures

1

Polymyositis

1

Diabetic Neuropathy

5

Neuropathy

4

Cataract

9

Glaucoma

1

Myelopathy

8

Frequent falls

8

Table 3

Number of co-morbid conditions that can affect balance

 

Frequency

None

3

One

10

Two

9

Three

4

Four

2

Five

1

Discussion

Proximal Junctional Kyphosis was first identified in 1999 [8], and was initially described as a radiographic finding with limited clinical relevance [13, 14]. This sanguine assessment was short lived, as subsequent reports have documented the frequent need for revision surgery [5, 6] as well as the occurrence of catastrophic failures, termed Proximal Junctional Failure (PJF) [9, 10, 15, 16]. The reported increase in PJK was coincident with several major changes in treatment paradigm. Adult deformity surgery became more common in older patients, and more aggressive correction was undertaken using osteotomies and rigid instrumentation. Studies have highlighted these factors and examined their etiologic role in PJK and PJF [10, 17, 18].

Deformity surgeons clearly recognize PJK and PJF as important challenges, but often regard these complications as mechanical problems for which there should be a straight forward mechanical solutions. As osteoporosis is commonly identified as an etiology of PJK, surgeons have pursued options to offset poor bone quality. Strategies have included prophylactic medical treatment of low bone density, strengthening proximal instrumented and adjacent vertebral levels with cement injection. Other strategies have included decreasing rod rigidity, and softening the transition to unfused levels using hooks rather than screws [11, 19, 20]. Another major focus has been on selection of fusion levels and restoration of sagittal alignment [12, 18, 21, 22]. Studies have advocated both more aggressive and less aggressive deformity correction. Maruo et al. report that restoration of normal sagittal alignment protected against PJK, and that greater than 30-degree increase in lumbar lordosis was a significant risk factor for PJK. [18] As increase in lumbar lordosis is generally the mechanism by which normal sagittal alignment is restored, these observations appear contradictory.

The findings of the present study suggest that our failure to control the rate of PJK may be related in part to the narrow focus on mechanical factors. This study demonstrates that 76 % of patients with PJK after spinal deformity correction have co-morbidities that adversely affect standing balance, regardless of alignment. These include neuromuscular disease, history of cerebral vascular accident, cervical myelopathy and neuropathy. All of these conditions may contribute to an inability to rebalance through unfused segments after deformity correction. This phenomenon is clearly recognized with substantial neurologic impairment such as patients with Parkinson’s disease [23], but has not been clearly defined in those patients with less severe neurologic impairment.

Beyond potential neurogenic causes of standing imbalance, other factors such as visual impairment, vestibular dysfunction and severe muscular deconditioning also impact balance and gait [24, 25]. Visual impairment was noted in 40 % of PJK cases and more than a single potentially relevant co-morbidity was noted in more than 66 % of cases. While these findings do not implicate neuromuscular disease as the direct cause of PJK, they certainly suggest a multi-factorial etiology.

The mechanisms by which these non-mechanical risk factors contribute to PJK are not well defined, and probably do not represent a unique common pathway. In some instances, such as patients with neuropathy or central neurologic deterioration, an impaired feedback loop may limit the ability to compensate appropriately after mechanical realignment. In essence, the patient’s brain does not properly register the “improved alignment” as determined by radiographic assessment. In other cases, lack of appropriate sensory feedback may result in accelerated proximal segment degeneration, akin to the appearance of a Charcot joint. In patients with severe deconditioning, muscular support may be inadequate regardless of mechanical alignment.

It is not completely clear how best to apply these observations in clinical practice. Our case series methodology cannot provide a relative risk assessment for any of the individual co-morbid conditions, and to-date no diagnostic test has been developed to quantify a global risk for post-operative standing imbalance or PJK. It is also unknown as to whether these risks can be modified by pre-operative interventions such as balance training, in the same way that treatment of osteoporosis is thought to reduce the risk of post-operative vertebral fracture or screw pull-out.

Weaknesses of this study include firstly the case series methodology. As some of the patients had their index procedure elsewhere, we do not have an accurate denominator to assess the incidence of PJK in the primary cohort. This series is also relatively small, so that the relative risk of the various co-morbidities cannot be effectively compared. Despite these weaknesses, this study clearly supports the role of concomitant neuromuscular disease in the development of post-op standing imbalance and PJK. The data does not provide a specific threshold at which surgery should be withheld, but certainly emphasizes the importance of including an assessment of associated neuromuscular disease in pre-operative planning and shared decision-making.

Spine surgeons have devoted a great deal of time and effort to defining optimal sagittal alignment, but sagittal balance is more than just alignment. Dubousset outlined the many interactive systems that contribute to ambulation and stated, “good alignment is preferable in order to obtain a good balance, but it is not sufficient” [26]. Understanding and avoiding PJK requires that we move beyond the one-dimensional view that finding an ideal sagittal alignment, softening the transition at the proximal aspect of the instrumented segment, or improving the adjacent bone strength will solve the problem of PJK. Thinking about PJK more broadly is a step in the right direction.

Conclusions

PJK is an important contributing factor to the substantial and unsustainable rate of revision surgery following adult deformity correction. Multiple efforts to avoid PJK via alterations in surgical technique have been largely unsuccessful. This study suggests that non-mechanical neuromuscular co-morbidities play an important role in post-operative sagittal imbalance and PJK. Recognizing the multi-factorial etiology of PJK may lead to more successful strategies to avoid PJK and improve surgical outcomes.

Declarations

Acknowledgments

No other person aside from the authors made substantial contributions to conception, design, acquisition of data, or analysis and interpretation of data, or was involved in drafting the manuscript or revising it critically for important intellectual content. No funding was received for the design, in the collection, analysis, and interpretation of data; in the writing of the manuscript; and in the decision to submit the manuscript for publication. No language editor or scientific (medical) writer was involved in the preparation of the manuscript.

Disclaimer

The views expressed in this presentation are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States government.

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Norton Leatherman Spine Center, 210 East Gray Street, Suite 900, Louisville, Kentucky 40202, USA

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