Percutaneous Vertebroplasty and Pulmonary Cement Embolism: Results from VERTOS II

Discussion

This study showed that during PV for OVCFs, clinically silent PCE occurs in a quarter of patients. Cement emboli were small and scattered in peripheral portions of the lungs without specific lobar distribution. There were no cement deposits in the heart and large vessels. Cement leakage in the azygos vein was the only risk factor for PCE. Remarkably, the volume of injected cement was not correlated with the occurrence of PCE. After a mean follow-up of almost 2 years, the cement emboli caused no structural parenchymal changes.

In a comparable study with the use of CT to detect PCE, Kim et al¹³ found a similar incidence in 75 patients undergoing PV for OVCFs, with cement leakage to the inferior caval vein as the only relevant risk factor. In studies that used only postprocedural chest radiographs for detection of PCE, the observed incidences were substantially lower.^10,11 This is not surprising because small pulmonary cement deposits easily remain undetected on chest radiographs while they are readily apparent on CT. In 1 study,¹¹ an incidence of 4.6% was reported after retrospectively reviewing postprocedural chest radiographs in 69 VP sessions. In that study, all patients with cement emboli had multiple myeloma and remained asymptomatic. An association was found between PCE and paravertebral venous cement leakage but not between PCE and the number of vertebral bodies treated or the performance of kyphoplasty or vertebroplasty. In another study,¹⁰ the authors also retrospectively reviewed postprocedural chest radiographs, and when PCE was detected, they confirmed it with CT. In that study, 5 of 73 patients (6.8%) had PCE. Four of these patients had osteoporotic compression fractures, and 1 had multiple myeloma. Venous leakage was not recognized during fluoroscopy in patients with PCE.

In the VERTOS II Trial,¹² fluoroscopic venous cement migration to the lungs was detected and reported by the operator in only 1 patient (C.A.H. Klazen, unpublished data, 2010). This patient remained asymptomatic and stopped the trial 3 months later because of unrelated comorbidity. In no patients who were included in the present follow-up study was fluoroscopically visible cement migration toward the lungs reported by the operators. The findings of our study imply that with fluoroscopy, virtually all migration of small cement quantities remains undetected. Thus, when the operator notices cement leakage into anterior venous structures, careful observation of pulmonary symptoms is mandatory. Conversely, when a patient complains of pulmonary symptoms after PV, PCE should be excluded, even though venous cement migration was not seen.

As in previous studies,^9–11 our study showed that cement emboli were scattered in peripheral portions of the lung without specific lobar distribution and no acute inflammatory pulmonary reaction. Our study also indicates that long-term, cement emboli do not cause structural changes of the pulmonary parenchyma. A previous study showed that PCE occurred infrequently and caused no pulmonary reaction on CT after 1 year.⁹

In our study, cement in the azygos vein on postprocedural CT of the treated vertebrae was the only risk factor for PCE. Analogously, other studies^13,14 showed a statistically significant relation between PCE and cement leakage into the inferior caval vein.

Our study has several limitations. Our patient group was relatively small, and not all patients agreed to participate. Results were expressed on a per-patient basis, while some patients had multiple levels treated. Thus, in patients with PCE and multiple treated vertebrae, the level of leakage remained uncertain. However, we used postprocedural CT of the treated levels to indicate the most likely level of the origin of the leakage. Another limitation is that postprocedural chest CT was not routinely performed. Therefore, it is possible that small cement emboli might have been resolved or changed with time or had migrated. In addition, earlier but transient pulmonary changes cannot be excluded. On the other hand, strong points of the study were the use of CT for the detection of PCE and the long follow-up interval, which allowed a reliable assessment of PCE with time.

On the basis of our findings and other studies, in our opinion, standard CT or chest radiography after PV is not warranted in asymptomatic patients, not even when small quantities of cement have been observed migrating toward the lungs. Only in symptomatic patients should CT be performed to guide the appropriate therapy. Because cement emboli remain inert with time, follow-up CT is not necessary.