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Orthopaedic Proceedings
Vol. 94-B, Issue SUPP_XXXVII | Pages 60 - 60
1 Sep 2012
Yousri T Yichientsaia A Thyagarajen D Livingstone J Bradley R
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Introduction

Over 300,000 patients present with fragility fractures each year. Following a hip fracture, the 30 days mortality is around 8.3 to 9.3%. Mortality increases to 20–24% after the first year and this risk may persist for at least 5 years. The most significant variables that influence mortality are age, gender, fracture type, prefracture residence, prefracture mobility and ASA scores. Common reported postoperative complications responsible for mortality in hip fracture patients include; heart failure, bronchopneumonia and infections. Most of the studies in the literature focus on management variables influencing mortality rather than the encountered postoperative medical problems leading to death.

The aim of this study is to retrospectively analyze the postoperative medical complications which led to death in a cohort of patients, following a hip fracture.

Methodology

This is a retrospective analysis of a cohort of 82, out of 648, patients with hip fractures who died over a period of 2 years (December 2006–January 2009). Forty nine females and 33 males (ratio 1.5:1) were included in the study with a mean age of 87.8 years (range 59–98 years).

For mortality analysis, patients' co-morbidities and medical events leading to death were categorized according to the involved organ system. This included cardiovascular, respiratory, renal, gastrointestinal, neurological and musculoskeletal systems). The timing and decision of DNAR and palliation was noted for each patient.

The 30 days and the overall mortality were the set outcome measures to be reviewed.


Orthopaedic Proceedings
Vol. 88-B, Issue SUPP_III | Pages 394 - 394
1 Oct 2006
Hamilton S Johnstone A Bradley R
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Introduction: The knee meniscus is prone to injury and has limited intrinsic healing potential despite surgical repair. Methods to enhance fibrochondrocyte function and augment meniscal repair would be invaluable in the treatment of meniscal injuries. Ultraviolet Ozone (UVO) modified surfaces have been characterised chemically and topographically. These surfaces have been shown to promote the function of certain cell types. This study investigated the attachment, proliferation and extracellular matrix production of fibrochondrocytes cultured on UVO modified polystyrene surfaces. Interest was paid to the integrins, a group of transmembrane extracellular matrix attachment glycoproteins. In particular the subunits alpha2 and alpha5, as they specifically bind to the ligands Collagen Type I and Fibronectin, major components in the human meniscus.

Methods: Tissue samples from adult human medial meniscal tears were obtained at knee arthroscopy. Fibrochondrocytes were isolated by standard cell culture techniques and cultured to 100% confluence before seeding onto UVO modified polystyrene surfaces. The untreated polystyrene surfaces of culture dishes were oxidatively modified with an ultraviolet ozone treater. The response of fibrochondrocytes to various surface oxygen concentrations was investigated. Untreated, hydrophobic surfaces acted as controls. Images of cells in culture were obtained with a Leica digital camera mounted on a microscope. Cells were counted at 24, 48, 72 and 96 hours. After 48 and 96 hours of culture standard wet transfer Western Blots were undertaken using antibodies to the alpha2 and aalpha5 integrin subunits (Santa Cruz Biotechnology). To evaluate potential extracellular matrix production total protein assays were undertaken at 1, 2, 3, 4, 6, 8 and 10 days of culture (Bio-Rad Laboratories).

Results: Fibrochondrocytes attached preferentially to the UVO treated surfaces. They proliferated steadily until they reached confluence at 96 hours. Western Blot analysis showed the integrin subunit a5 to be present in the cell lysate after both 48 and 96 hours of culture. The a2 subunit was not detected at these times. There was no increase in total protein concentration on surfaces after fibrochondrocytes had reached confluence. Discussion: UVO modified surfaces promote the attachment and proliferation of human fibrochondrocytes. The alpha2 subunit was not detected in the cell lysate of these surfaces after culture for 96 hours. Whether this is due to defective or absent Collagen Type I at this stage of culture remains to be answered. The presence of the alpha5 subunit suggests that Fibronectin may be involved in the process of fibrochondrocyte attachment to UVO modified polystyrene surfaces. It is suggested that there is little or no extracellular matrix production after 4 days as there is no increase in total surface protein concentration after confluence is reached. The increase in total surface protein concentration up to this point most likely reflects cell proliferation.

Conclusion: Ultraviolet Ozone modified surfaces enhance certain aspects of fibrochondrocyte function and therefore have a potential role in the development of novel therapies for meniscal repair.