Abstract
Introduction Cement leakage into adjacent structures is the main complication during vertebroplasty. The majority of these leaks are asymptomatic, but pulmonary cement embolism has been reported to cause cardiovascular disturbances and even death (1,2). Furthermore, the use of calcium phosphate (CaP) cements for vertebroplasty may aggravate cardiovascular deterioration in the event of cement embolism by stimulating coagulation [3].
The cardiovascular effects of pulmonary cement embolism were investigated using an animal model.
Methods In 18 skeletally mature sheep, 2.0ml cement was injected into the pulmonary trunk during general anaesthesia (approved by Animal Ethics Committee). Three different cements were used: 1) PMMA (Simplex P, Stryker); 2) PMMA with 10% hydroxyapatite (PMMA & HA) (Vertecem, Synthes); 3) Experimental injectable CaP cement (Synthes). The following cardiovascular parameters were recorded continuously (endpoint: 60min post-injection): arterial, central venous, pulmonary arterial pressures and cardiac output. Blood gases and coagulation parameters (antithrombin, D-dimer, prothrombin fragments I & II) were measured pre-injection, 10, 30 and 60min post-injection. Postmortem, lungs were removed intact and submitted to computer tomography (CT) imaging.
Results There were no fatalities. After 1min, mean pulmonary arterial pressure had increased by 9%, 14% and 21% from pre-injection value in the PMMA, PMMA & HA and CaP group respectively. Differences in pulmonary arterial pressure between the three material groups were not statistically significant. Pulmonary arterial pressure stayed elevated for the duration of the experiment (i.e. 60min post-injection). There were no other significant changes in cardiovascular, blood gas or coagulation parameters from pre- to post-injection values. Three dimensional reconstructions of the CT images showed a tendency of the CaP cement to break up into multiple smaller pieces whereas the two other cements did not.
Discussion Cement embolism led to mild pulmonary hypertension in all material groups. Present results are in contrast to earlier reports (pig model) of fulminant cardiovascular deterioration after CaP cement embolism (3). Present changes were not as severe and there was no evidence of thromboembolism. This discrepancy may have been due to differences in the cement formulations or the animal model.
Pulmonary hypertension was more severe in the CaP cement group. This may have been due to the disintegration of the CaP cement resulting in blockage of more pulmonary vessels compared to the PMMA cements.
The abstracts were prepared by Assoc Prof Bruce McPhee. Correspondence should be addressed to him at the Division of Orthopaedics, The University of Queensland, Clinical Sciences Building, Royal Brisbane Hospital, Herston, Brisbane, 4029, Australia.
References
1 Chen HL, Wong CS, Ho ST, et al. Anesth Analg2002; 95:1060–2. Google Scholar
2 Stricker K, Orler R, Yen K, et al. Anesth Analg2004; 8:1184–6. Google Scholar
3 Bernards CM, Chapman J, Mirza S. ORS2004; #0254. Google Scholar
