Benjamin G. Goss

Influence of Bone Marrow Fat Embolism on Coagulation Activation in an Ovine Model of Vertebroplasty

BACKGROUND Intraoperative cardiovascular deterioration as a result of pulmonary embolization of bone marrow fat is a potentially serious complication during vertebroplasty. The release of fatty material and thromboplastin from the bone marrow cavity during vertebroplasty may activate the coagulation cascade resulting in thrombogenesis, and pharmacological prophylaxis may therefore prevent cardiovascular complications. Thus, the effects of bone marrow fat embolism on coagulation activation during vertebroplasty were investigated with use of an animal model. METHODS Polymethylmethacrylate was injected into three lumbar vertebrae of six sheep in order to force bone marrow fat into the circulation. Invasive blood pressures and heart rate were recorded continuously until sixty minutes after the last injection. Cardiac output, arterial and mixed venous blood gas parameters, and coagulation parameters were measured at selected time-points. Postmortem lung biopsy specimens were assessed for the presence of intravascular fat. RESULTS Embolization of bone marrow fat resulted in a sudden and dramatic increase in mean pulmonary arterial pressure and a decrease in mean arterial blood pressure. There were no significant changes in any coagulation parameter from before the injection to after the injection. Intravascular fat and bone marrow cells were present in all lung lobes. CONCLUSIONS Injection of polymethylmethacrylate into vertebral bodies caused embolization of bone marrow fat with subsequent transient cardiovascular deterioration, but no changes in coagulation parameters were observed. Thromboembolism did not contribute to the observed cardiovascular changes.

Modelling of infectious spreading in heterogeneous polymer oxidation I. Development of a stochastic model

The heterogeneous features of the oxidation of polypropylene in the amorphous region are consistent with infectious spreading from a small number of sites, such as catalyst residues. A stochastic model was developed for demonstrating the spatial and temporal development of oxidation from these sites. In this model, the probability of passing the infection from one site to an adjacent site could be used in place of conventional rate constants. The probability of spreading was assumed to be temperature dependent, and modelled with Arrhenius behaviour. Each site was given a predefined lifetime such that the maximum probability of spreading coincided with the maximum rate of oxidation at a particular site. This has enabled visualisation of the spatial development of oxidation within the amorphous region. The epidemiological fractions corresponding to the remaining (unoxidised) polymer, the dead (oxidised) polymer and the infectious (oxidising) polymer, were calculated and used to test the limitations of the simple epidemiological model.

Chemiluminescence as a Probe of Polymer Oxidation

Many oxidation reactions of organic materials, including polymers, are accompanied by the emission of weak chemiluminescence (CL). From a study of the mechanism of this weak CL, it is shown that the time development of the CL intensity may provide the kinetics of the oxidation reaction and is thus a sensitive probe of the degradation of the material. The intensity of emission reflects the concentration of peroxidic species in the material. Whereas the kinetics of the oxidation may be described by a series of elementary, homogeneous free radical reactions, the use of imaging techniques has shown that the oxidation of polymers such as polypropylene is highly heterogeneous. A model that describes the oxidation as spreading through the material as an infection from a number of initiating sites is able to rationalize these observations and provide a new approach to the prediction of the useful lifetime of a polymeric material.

Sildenafil prevents cardiovascular changes after bone marrow fat embolization in sheep

Background:Sudden, intraoperative cardiovascular deterioration as a result of pulmonary embolization of bone marrow fat is a potentially fatal complication during total hip and knee arthroplasty, intramedullary nailing, and spine surgery. Anesthetic management is challenging in the presence of increased right ventricular afterload due to pulmonary hypertension. Selective pulmonary vasodilation may be an appropriate prophylactic or therapeutic measure. The effect of sildenafil (phosphodiesterase inhibitor) on cardiovascular deterioration after bone marrow fat embolization was therefore investigated. Methods:Bone cement (polymethylmethacrylate) was injected into three lumbar vertebrae in 12 sheep. Invasive blood pressures and heart rate were recorded continuously until 60 min after the last injection. Cardiac output and arterial and mixed venous blood gas variables were measured at selected time points. Before the first cement injection, 6 animals received a bolus injection (0.7 mg/kg) of sildenafil, with continuous infusion (0.2 mg · kg−1 · h−1) thereafter. Postmortem lung and kidney biopsies were taken for semiquantitative analysis of intravascular fat. Results:Fat embolism was associated with a transient increase (21 ± 7mmHg) in pulmonary arterial pressure. A transient decrease in arterial blood pressure and temporary increases in central venous pressure and dead space were also observed. No significant changes in any cardiovascular variable were observed after fat embolism in the sildenafil group. There was significantly (P < 0.05) less intravascular fat in the lungs of the sildenafil (median count of 5 emboli per microscopic view) compared with the control group (median count of 1). Conclusions:Administration of sildenafil prevented the acute cardiovascular complications after bone marrow fat embolism in sheep.

Plasma levels of endothelin-1 after a pulmonary embolism of bone marrow fat

Background:  During orthopedic surgery, embolization of bone marrow fat can lead to potentially fatal, intra‐operative cardiovascular deterioration. Vasoactive mediators may also be released from the bone marrow and contribute to these changes. Increased plasma levels of endothelin‐1 (ET‐1) have been observed after pulmonary air and thrombo‐embolism. The role of ET‐1 in the development of acute cardiovascular deterioration as a result of bone marrow fat embolization during vertebroplasty was therefore investigated.