Our results demonstrated that IVCF could prevent BCIS effectively, suggesting that PE might be the leading cause of the constellation of symptoms of BCIS.
The most constant manifestations of BCIS include hypotension, oxygen desaturation and pulmonary hypertension. These symptoms were all induced in the present CI model, which suggests that a reliable BCIS model was established for the following experiments. Zhou et al. established BCIS model with dogs, in a recent study (13). Blood pressure (BP) and partial pressure of oxygen (PaO2) were both decreased in their models, which were consistent with our findings. However, partial pressure of carbon dioxide went down and arterial pH went up in our models, which were opposite to what was found in Zhou’s models. They used mechanical ventilation during their anesthesia and this might be the reason why their animals did not show respiratory alkalosis (13).
The mechanism suggested to cause these symptoms mainly involves four theories: the toxic effects of methyl methacrylate monomers, allergic responses, humoral factors, like cytokines and complement components, and PE induced by high temperature and pressure in the medullary cavity (14-18). The leading cause of BCIS symptoms was commonly recognized as the PE. The emboli are composed of bone marrow, fat, bone particles and gas, which enter the inferior vena cava via injured veinlets, after pressurizing the medullary cavity (19-24). The emboli then enter the right heart chambers and pulmonary arteries, where pulmonary artery resistance increases and blood flow is reduced. Consequently, oxygen exchange is reduced, blood desaturates in oxygen, and BP decreases, as a result of hypoxia-induced cardiac depression. A previous study has proved that the peak pressure in the medullary cavity was positively relevant to the number of emboli (12, 25). They inserted bone wax instead of bone cement, into the medullary cavity, and the embolism and cardiovascular responses were aggravated after pressurizing. In this study, we gradually pressurized the medullary cavity to model BCIS. With the pressure increasing, the hypotension, oxygen desaturation and PE were aggravated.
The IVCF is applied in patients who are at high risk of developing PE, secondary to venous thromboembolism venous thromboembolism (VTE). We hypothesized that the use of IVCF could decrease the incidence of BCIS, since PE is also considered to be the major factor behind the development of BCIS. In the CI model group, using echocardiography, emboli inside the right heart chambers was observed when cement was inserted to the cavity, in the CI group. The removed embolus was dotted first and became snowflake-like later, which is consistent with another study that demonstrated the development of PE (26). No significant embolus was observed during osteotomy and reaming, in this study, which is in contrast to another clinical investigations that showed obvious embolism during drilling in femur and acetabular bones (27). However, no significant image of embolus was detected throughout the procedure in the IVCF group, even when the pressure in the medullary cavity was raised to 300 mmHg. Fat could be stained by oil red, which was used to detect fat component in sheep lungs. The findings from fat staining assay, performed during the autopsy of sacrificed sheep, were consistent with echocardiography, revealing the inhibitive effects of IVCF on PE.
In respect to the components of the emboli in BCIS, bone marrow, fat, bone debris, methyl methacrylate methyl methacrylate (MMA) particles were detected in lungs of dead patients (28-30). The IVCF was supposed to inhibit PE in BCIS, and the influences of IVCF on manifestations, other than pulmonary embolism, were also investigated, as a part of this study. The pressure in the medullary cavity was raised to 150 mmHg, 5 min after bone cement insertion, and 300 mmHg at 10 min after insertion. Arterial BP decreased continuously after cement insertion, in BCIS group, while there was no statistically significant drop in IVCF group. Pulse pressure was concomitantly investigated. Pulse pressure dropped very fast after cement insertion, showing a tendency of shock, while IVCF impeded such tendency. These results suggest IVCF could inhibit hypotension during BCIS.
Simultaneously, there was a preventive effect of IVCF on oxygen desaturation during the development of BCIS. The PaO2 decreased the moment cement was implanted, and respiratory failure type I occurred 20 min after cement implantation, in BCIS group. However, IVCF implanting partially slowed down the rate of PaO2 decrease. Although PaO2 dropped in the IVCF group, as well, it did not reach respiratory failure and kept stable 10 min after insertion. The results suggest that the PaO2 decrease was partially caused by PE in BCIS. Besides, pH and PaCO2 were investigated in the present study. The IVCF also showed preventive effects against the devastating changes of pH and PaCO2.
In conclusion, this study had successfully recreated a BCIS model, which was then used to study the effect of IVCF in preventing BCIS. The IVCF was found to successfully prevent the development of BCIS. The results from this study suggest that there may be a role of IVCF in high-risk patients, in whom cemented arthroplasties are performed.
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