PubMed · 10507329
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A S Greenwald. 1999. Current concepts in joint replacement.. https://doi.org/10.3928/0147-7447-19990901-03
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Orthopedic wear debris has been thought to be an important factor associated with osteolysis and loosening of total joint arthroplasties. Previous in vitro studies have reported that particles of wear debris induce the release of pro-inflammatory cytokines and other inflammatory mediators from macrophages and other cells. Several recent investigations, however, have suggested that the wear particles themselves may not be primarily responsible for the inflammatory cellular responses, but that the observed cytokine release in vitro may be caused by endotoxin adsorbed to commercially available particle preparations. The intracellular pathways involved in macrophage signal transduction also are poorly understood. The purposes of this study are to use isolated orthopedic wear debris particles to evaluate pro-inflammatory cytokine release and nuclear factor kappa B (NFkappaB) activation from macrophages. Cells from human monocyte/macrophage cell line (THP-1) were differentiated and incubated with particles of debris that had been isolated from a failed human total hip arthroplasty. The titanium-alloy particles did not evoke release of TNF-alpha or IL-1beta whereas lipopolysaccharide (LPS) or LPS-treated debris particles induced both TNF-alpha and IL-1beta. LPS-treated particles, but not particles alone, stimulated NFkappaB activation. Our results suggest that at the concentrations tested in this study, endotoxin-free wear debris particles may not themselves initiate inflammatory cellular responses in differentiated THP-1 cells. It is unclear whether adsorbed endotoxin is clinically associated with osteolysis and/or loosening in total joint arthroplasties, but several factors, including adsorbed endotoxin, need to be investigated to explore the cellular responses responsible for osteolysis and/or loosening.
BACKGROUND: Erythrocyte salvage, the collection of a patient's blood shed from the surgical wound, is one aspect of blood management. Previous investigators have examined salvaged blood for content; however, to our knowledge, none have examined the viability of erythrocytes after exposure to the chemical and thermal reactions produced by motorized instruments and polymethylmethacrylate during surgery. The purpose of this study was to determine the viability of salvaged erythrocytes from patients undergoing primary total joint arthroplasty with cement. METHODS: Erythrocyte viability studies were performed on specimens from three subjects with use of a double isotope-labeling technique employing chromium-51 and technetium-99m. With use of a fresh blood specimen obtained prior to surgery and a specimen of salvaged blood that had been recycled, washed, and filtered with use of the Cell Saver, the viability of the Cell-Saver-processed erythrocytes, labeled with chromium-51, was calculated on the basis of the technetium-99m-labeled red blood-cell mass. RESULTS: The mean erythrocyte viability (and standard deviation) in blood salvaged with use of the Cell Saver was 88.0% +/- 3.8%. The standard of the American Association of Blood Banks for minimum erythrocyte viability in adequately cross-matched allogeneic blood or predeposited autologous blood is 70%. CONCLUSIONS: The high rate of viability of the erythrocytes in this study shows that the Cell Saver is a valuable adjunct to other blood management techniques for patients having total joint arthroplasty. We believe that the very high mean rate of erythrocyte viability and the extremely small standard deviation in our three subjects, as compared with the standards of the American Association of Blood Banks, made additional study subjects unnecessary.
The epidemiology and economics of venous thromboembolism (VTE) associated with hip and knee arthroplasty and surgical repair of hip fracture are reviewed. In the 1960s and 1970s, prior to the widespread use of prophylaxis, the risk of VTE following major orthopedic surgery was substantial. The risk of fatal pulmonary embolism (PE) following hip fracture repair may have been as high as 7.5%. With improvements in surgical and anesthetic techniques and the use of anticoagulant prophylaxis, these risks have decreased significantly for most patients. Current risks after hip and knee arthroplasty appear to be about 2.5% for deep vein thrombosis, 1% for nonfatal PE, and a few tenths of 1% for fatal PE over a three-month period following surgery. Because of the traumatic nature of the injury, delays in getting to surgery, and their more advanced age and poorer overall health, hip fracture patients appear to have a greater risk of postoperative VTE, but data are lacking for a reliable estimate of current risk. The cost of VTE after major orthopedic surgery includes initial therapy (the chief component), follow-up care, and the expected costs of major hemorrhage (due to anticoagulation), recurrent VTE, and postthrombotic syndrome. The total cost per patient of such care is approximately $11,600. The risk of VTE after surgery to replace hip and knee joints and repair hip fracture is far lower today than in the 1960s and 1970s, but the cost of treating VTE remains high: an estimated $11,600 per patient, including hospitalization costs.