Cemented vertebra and adjacent vertebra refractured in a chronic kidney disease-mineral and bone disorder patient: A case report

Abstract

BACKGROUND

Although percutaneous vertebral augmentation (PVA) is a commonly used procedure for treating vertebral compression fracture (VCF), the risk of vertebral refracture should be considered. Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a systemic disease of mineral and bone metabolism. It is associated with an increased risk of fracture. Few studies have reported the use of PVA in patients with CKD-MBD. We herein report a rare case wherein the cemented vertebra and the adjacent vertebra refractured simultaneously in a CKD-MBD patient after PVA.

CASE SUMMARY

A 74-year-old man suffered from low back pain after taking a fall about 3 wk ago. According to physical examination, imaging and laboratory findings, diagnoses of T12 VCF, CKD-MBD, and chronic kidney disease stage 5 were established. He then received percutaneous vertebroplasty at T12 vertebra. Fourteen weeks later, he presented with T12 and L1 vertebral refractures caused by lumbar sprain. Once again, he was given PVA which was optimized for the refractured vertebrae. Although the short-term postoperative effect was satisfactory, he reported chronic low back pain again at the 3-month follow-up.

CONCLUSION

It is necessary that patients with CKD-MBD who have received PVA are aware of the adverse effects of CKD-MBD. It may increase the risk of vertebral refracture. Furthermore, the PVA surgical technique needs to be optimized according to the condition of the patient. The medium- and long-term effects of PVA remain uncertain in patients with CKD-MBD.

Key Words: Chronic kidney disease-mineral and bone disorder; Percutaneous vertebral augmentation; Vertebral compression fracture; Vertebral refracture; Cemented vertebra; Adjacent vertebra; Case report

Core Tip: This is a rare case wherein the cemented vertebra and the adjacent vertebra refractured simultaneously in a chronic kidney disease-mineral and bone disorder (CKD-MBD) patient after percutaneous vertebral augmentation (PVA). He was given PVA once more, which was optimized for the refractured vertebrae. While, the medium- and long-term effects were not satisfactory. It is necessary that patients with CKD-MBD who have received PVA are aware of the adverse effects of CKD-MBD.

INTRODUCTION

Percutaneous vertebral augmentation (PVA), including percutaneous vertebroplasty (PVP) and percutaneous kyphoplasty (PKP), is widely recognized as a suitable procedure for vertebral compression fracture (VCF). However, vertebral refracture is a common concern after PVA. Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a systemic disorder of mineral and bone metabolism caused by CKD and is associated with an increased risk of hip and vertebral fractures[1,2]. The vertebral fracture is relatively common in patients with CKD-MBD. A previous study has shown that PVA can relieve pain and disability in these patients[3], whereas few studies have reported the refracture of the vertebrae. Here, we report a rare case of simultaneous fracture of a cemented vertebra and an adjacent vertebra in a patient with CKD-MBD after PVA.

CASE PRESENTATION

Chief complaints

The patient was a 74-year-old man who experienced persistent low back pain after taking a fall about 3 wk ago.

History of present illness

The patient took a fall 3 wk ago, and then, he suffered from persistent and drastic lower back pain, and he was barely able to stand and walk.

History of past illness

The patient was diagnosed as having CKD stage 5 in 2006, and since then, he has undergone hemodialysis three times a week and was prescribed oral calcium (1000 mg/d) and calcitriol (0.5 μg/d). The causative disease of CKD was not clear. He was diagnosed with urothelium carcinoma in 2012 and received surgical treatment.

Personal and family history

The patient and his family had no history of fragility fracture, and he had no history of chronic low back pain.

Physical examination

Tenderness was found at the thoracolumbar vertebrae, but there were no neurological signs or symptoms. His body mass index was 16.7 kg/m².

Laboratory examinations

Laboratory examination (Table 1) revealed bone metabolism abnormalities in the patient.

Table 1 Results of laboratory examinations for the two admissions.

	Serum calcium (mmol/L)	Serum phosphorus (mmol/L)	Parathyroid hormone (pg/mL)	Vitamin D (ng/mL)	Alkaline phosphatase (U/L)
1st admission	2.45	2.74	562.2	9.25	53
2nd admission	2.16	1.71	557.4	8.57	60

Imaging examinations

The computed tomography (CT) and magnetic resonance imaging revealed T12 VCF (Figure 1A-C). The L1-L4 bone mineral density (BMD) was 0.922 (T score: -1.3), and the femoral neck BMD was 0.579 (T score: -3.1).

Figure 1 Pre- and post-operative images of T12 vertebral compression fracture. A: preoperative sagittal computed tomography; B: preoperative T1-weighted magnetic resonance imaging (MRI); C: preoperative T2-weighted fat-suppressed MRI; D: postoperative anteroposterior radiograph; E: postoperative lateral radiograph. Orange arrow: The intravertebral cleft in the vertebra.

FINAL DIAGNOSIS

According to the history, physical examination, laboratory and imaging examinations, he was diagnosed as having T12 VCF, CKD-MBD, and CKD stage 5. The secondary causes like hyperparathyroidism, osteomalacia, and malignant tumors were excluded.

TREATMENT

He underwent hemodialysis and was prescribed oral medicine as usual. After full preoperative testing and preparation, the patient received T12 PVP (left pedicle approach, cement injection: 3 mL). Typically, the standard procedures of PVP and PKP are the surgical treatment for VCF in patients with CKD-MBD. However, in this case, to fill the intravertebral cleft (IVC; Figure 1, orange arrow) with cement, we penetrated the cleft as precisely as possible during the operation. Postoperatively, the X-ray (Figure 1D and E) revealed that the IVC was filled with the cement without any leakage.

OUTCOME AND FOLLOW-UP

The pain was alleviated significantly on the first postoperative day: The visual analog scale (VAS) score had decreased from 9 to 2, the Oswestry disability index (ODI) score had decreased from 72.5 to 47.5, and he was discharged 3 d later.

During 14^th week postoperatively, low back pain occurred again after a lumbar sprain, but he showed no neurological signs or symptoms. CT and bone scan showed T12 and L1 VCFs (Figure 2A-C, thin arrow), the IVC around the injected cement (Figure 2, orange arrow), and the rupture of the posterior vertebral wall (Figure 2, white arrow). The results of the laboratory examination were similar to the previous findings (Table 1). This time, he was diagnosed as having L1 VCF, T12 cemented vertebral refracture, CKD-MBD, and CKD stage 5. After clinical assessment and discussion, we decided to operate again with a further optimized and improved method.

Figure 2 Cemented vertebral refracture and adjacent vertebral refracture after percutaneous vertebral augmentation. A: preoperative sagittal computed tomography (CT); B: preoperative axial CT; C: bone scan; D: postoperative anteroposterior radiograph; E: postoperative lateral radiograph. Orange arrow: the intravertebral cleft in the vertebra; White arrow: the rupture of the posterior vertebral wall; Thin arrow: The fracture of T12 and L1 vertebrae; Bold arrow: Cement leakage in T12 vertebra.

L1 PKP (left pedicle approach, cement injection: 4 mL) was performed as usual, whereas the T12 vertebra was punctured bilaterally (PVP, cement injection: 4 mL). On the left side, a hole in the previous bone cement was drilled using a fine drill, and then, the newly mixed bone cement was injected into the hole and vertebra. The procedure was as usual on the right side. The postoperative X-ray (Figure 2D and E) showed a little cement leakage (Figure 2, bold arrow) in the T12 segment. No neurological signs or symptoms were identified postoperatively. The next day, he could stand and walk with a brace. The VAS score had decreased from 9 to 3, and the ODI score had decreased from 95 to 57.5. He was satisfied with the treatment and discharged 4 d later.

At 1-month follow-up, the VAS score was 2 and ODI was 27.5. The patient complained of chronic low back pain at the 3-month telephonic follow-up, and his VAS score and ODI were found to be 5 and 47.5, respectively. However, owing to loss of follow-up, his imaging examination scheduled to be done at 3-month follow-up could not be performed.

DISCUSSION

Cemented vertebral refracture rarely co-occurs with the adjacent vertebral refracture after PVA in patients with CKD-MBD. The incidence rate of cemented vertebral refracture is reportedly 0.56%–12.5%[4], and its risk factors include age, low BMD, the IVC, high anterior vertebral height restoration, high Cobb angle restoration, and low cement dose in the previous operation[5]. Furthermore, the rate of adjacent vertebral refracture is reportedly 9.9%–16.2%[6-9], and its risk factors include intradiscal cement leakage[6], low BMD, female[10], exceeded cement injection[10], preoperative segmental kyphosis >30°[8], and rheumatoid arthritis and cardiovascular disease[8]. Few studies have reported simultaneous refracture of cemented vertebrae and adjacent vertebrae.

In this case, low BMD and low cement dose in the previous operation may be the factors related to the dual refracture. The minimum volume of cement recommended in the thoracolumbar vertebra is 4–6 mL[11]; however, only 3 mL of the cement was injected in the first operation. In our patient, abnormalities in bone turnover and mineralization caused by CKD-MBD led to low BMD, and we believe this was the most predominant factor resulting in T12 and L1 vertebra refracture. Previous studies have reported that the IVC is the presentation of ischemic vertebral osteonecrosis complicated with fracture nonunion and pseudoarthrosis[12], the histomorphological feature of which is delayed callus mineralization[13].

In the T12 vertebra, IVCs were found both times he was admitted to the hospital. For the first visit at the 3rd week after injury, the abnormality in mineralization and the fracture nonunion caused the formation of the IVC, and its imaging findings were typical[13,14]. At the time of refracture, the IVC formed around the cement again because of abnormal bone mineralization. A large IVC reduced or nullified the strengthening effect of the cement, and the cement even made the vertebra more unstable, thus leading to a fracture even after a minor traumatic injury.

For the L1 vertebra, the low BMD and biomechanical changes of the adjacent vertebra[15] together resulted in the refracture. Thus, the refractures of the vertebrae in this case were both related to the abnormal bone mineralization and low BMD caused by CKD-MBD.

The distribution of cement and filling with cement in the IVC may reportedly influence the clinical outcome[16,17]. In the first operation, we did our best to ensure that the IVC was full of cement and there was sufficient cement distribution. According to the CT findings (Figure 2A and B) acquired after the refracture, although the IVC was completely filled with the cement, the cement was not distributed well. Meanwhile, a larger IVC formed in T12 vertebra, which was accompanied by rupture of the posterior vertebral wall. The surgical technique was optimized to bond the old and the new cement with each other; the IVC was filled with the cement, and more cement was injected into the vertebra. In this way, cement was diffusely distributed, and the stability of the vertebra was enhanced.

The findings of Mo et al[18] and Li et al[19] establish that cement distribution is associated with the degree of postoperative pain relief. Based on their findings, our patient should have experienced a satisfactory treatment effect; however, he presented with low back pain at 3 months postoperatively. We speculated that the increased stiffness of the cemented vertebrae led to a minimal fracture in the osteoporotic adjacent vertebrae. This implies that medium- and long-term efficacy of PVA may be uncertain in patients with CKD-MBD. Unfortunately, we could not find results of long-term follow-up of these patients in the literature.

Taken together, we consider the following factors to have contributed to the refractures: low BMD, abnormal bone turnover, and abnormal bone mineralization caused by CKD-MBD. These led to the formation of IVCs and may explain why the efficacy was not satisfactory at the last follow-up. The limitation of the case was that bone turnover markers were not tested at the time of admission.

CONCLUSION

For the PVA treatment in patients with CKD-MBD, it is necessary to be aware of the adverse effects of CKD-MBD. It may increase the risk of vertebral refracture. PVA surgical technique needed to be optimized according to the condition of the patient. The medium- and long-term treatment effects of PVA may still be uncertain in patients with CKD-MBD.