Recent advances in combat casualty care have enabled survival following battlefield injuries that would have been lethal in past conflicts. While some injuries remain beyond our current capability to treat, they have the potential to be future ‘unexpected’ survivors. The greatest threat to deployed coalition troops currently and for the foreseeable future is the improvised explosive device (IED) Therefore, the aim of this study was to conduct an analysis of causes of death and injury patterns in recent explosive blast fatalities in order to focus research and mitigation strategies, to further improve survival rates. Since November 2007, UK Armed Forces personnel killed whilst deployed on combat operations undergo both a post mortem computed tomography (PMCT) scan and an autopsy. With the permission of the coroners, we analysed casualties with PMCTs between November 2007 and July 2010. Injury data were analysed by a pathology-forensic radiology-orthopaedic multidisciplinary team. Cause of death was attributed to the injuries with the highest AIS scores contributing to the NISS score. Injuries with an AIS < 4 were excluded. During the study period 227 PMCT scans were performed; 211 were suitable for inclusion, containing 145 fatalities due to explosive blast from IEDs. These formed the study group. 24 cases had such severe injuries (disruptions) that further study was inappropriate. Of the remaining 121, 79 were dismounted, and 42 were mounted (in vehicles). Leading causes of death were head CNS injury (47.6%), followed by intra-cavity haemorrhage (21.7%) in the mounted group, and extremity haemorrhage (42.6%), junctional haemorrhage (22.2%) and head CNS injury (18.7%) in the dismounted group. The severity of head trauma in both mounted and dismounted IED fatalites would indicate that prevention and mitigation of these injuries is likely to be the most effective strategy to decrease their resultant mortality. Two thirds of dismounted fatalities have haemorrhage implicated as a cause of death that may have been amenable to prehospital treatment strategies. One fifth of mounted fatalites have haemorrhagic trauma which currently could only be addressed surgically. Maintaining the drive to improve all haemostatic techniques for combat casualties from point of wounding to definitive surgical proximal control alongside development and application of novel haemostatics could yield a significant survival benefit

Aim: We have previously shown that long-term survival after hip fracture is highly dependent on age at the time of fracture and that fracture risk is similarly age-dependent. It has been suggested that the excess mortality occurs mainly during the first years after fracture, while mortality in a remaining life-time perspective is not well studied. The aim of this study was to evaluate short- and long-term mortality in relation to cause of death in a cohort of patients with hip fracture in comparison with the back-ground population. Methods: All adult patients suffering a hip fracture due to low energy trauma 1984–1985 in Malmö, Sweden were identified; 1029 cases (766 women, 263 men). The cases were compared with two age- and gender matched controls from the same background population, all alive and living in the catchment area when the hip fracture occurred. Date of death and cause of death were available through the national database, EPIC. Cases and controls were followed until death or up to 22 years. Results: The median survival was 4.4 yrs (+/− 0.2 [CI 95% 4.0–4.8]) in hip fracture patients and 7.7 yrs (+/− 0.2 [CI 95% 7.3–8.1]) in controls, equal to a median loss of 3.3 yrs. Mortality rate continued to be elevated for approximately 10 yrs, thereafter observed mortality approached expected mortality. Mean survival was 2.9 years shorter in fracture cases compared to controls (6.4 yrs (+/− 0.2 [CI 95% 6.0–6.8]) versus 9.4 yrs (+/− 0.2 [CI 95% 9.1–9.7])). Ischemic heart failure was the major underlying cause of death (25%) both among cases and controls. Conclusion: In hip fracture patients, excess mortality is evident both in the short- and long-term with an increased risk beyond 10 yrs. Nevertheless, the major causes of death were similar to that of controls

Introduction. Neck of femur (NoF) fractures have an inherent 6.5% 30-day mortality as per National hip fracture database(2019). Several studies have demonstrated a higher mortality rate in covid positive NoFs but have been unable to demonstrate whether there are risk factors that contribute to the risk of mortality in this patient group or whether COVID is solely responsible for the higher mortality. Aims. To assess risk factors that are concurrently present in a fracture NoF cohort that may contribute to higher mortality in COVID positive patients. Methods. A cross sectional, retrospective study was performed for a period of 1 year starting from 1st March 2020. All surgically treated neck of femur fracture patients having an isolated intra/extracapsular fracture were included in the study. Data fields recorded- patient demographics, date and time of admission, ward discharge, surgery, mode of surgery (fixation/arthroplasty), prehospital AMTS score, residential status and mobility, ASA grade as per anaesthetist's records, date of death (if deceased), cause of death (as per death certificate/ postmortem / coroner's report). Analysis of mortality was carried out by creating a matched comparison group for each risk factor as well as some combinations. Results. 344 patients were surgically treated for a neck of femur fracture in our DGH during the period of 1st March 2020 to 28th February 2021. 46 patients did not receive a COVID swab (reasons unknown) and were excluded from the study. 35 patients had a COVID-19 RT PCR positive test during their hospital stay and 264 patients remained negative. There were 12 deaths in COVID positive patients (34%) and 53 deaths in COVID negative patients (20%) within the time frame of the study. For each risk factor matched group COVID was seen to confer higher mortality in general. There was no mortality in ASA 1 or 2 patients. Mortality rates in matched groups for age and ASA revealed 23.8% mortality in COVID positive as opposed to 17.3% in COVID negative for ASA 3 and 33.3% mortality in COVID positive vs. 28% in ASA 4. 11 out of the 12 COVID positive patients who died had an AMTS score >6. No correlation was seen between COVID positive deaths and preinjury residential status, type of fracture or surgery offered, or preinjury mobility. The average length of hospital stay was much higher for COVID positive patients (19.5days) as compared to 9.5 days for COVID negative patients. Conclusion. Matched group analysis show that there is a 37.5% increase in COVID positive neck of femur fracture mortality in ASA 3 patients, the same number falls to 17.8% for ASA 4 patients. These figures are much lower compared to other studies in the UK. There is a need to understand the real cause of death in this subset and to improve death certification so that we can differentiate between patients whose mortality is ‘due to’ or ‘With’ COVID

Venous thromboembolism (VTE) is a preventable cause of morbidity and mortality in patients undergoing elective hip arthroplasty surgery. The balance of post-operative VTE prophylaxis and risk of post-operative haemorrhage remains at the forefront of surgeon's mind. The National Institute for Clinical Excellence (NICE) has altered their prophylaxis guidance in the setting of total hip arthroplasty (THA). The aim of this study was to present the VTE incidence in 8,890 patients who underwent total hip arthroplasty between January 1997 and March 2018 with Aspirin as the primary agent for pharmacological thromboprophylaxis. Analysis of prospective data collection from consecutive patients undergoing THA was performed with the incidence of deep vein thrombosis (DVT) and pulmonary embolism (PE) occurring within 6 months of the index operation as the primary outcome measure. 90-day all-cause mortality of this cohort of patients was also analysed. 8890 patients were reviewed. This included 7235 primary, 224 complex primary and 1431 revision cases. The incidence of DVT was 0.64% after elective THA and the incidence of PE was 0.54%. There was no difference in the incidence between primary and revision cases. The 90-day all-cause mortality was 0.88%. Cardiovascular and respiratory disease were the main causes of death following surgery. Only 0.03% of deaths (n= 3) within 90 days of index surgery were due to VTE. Our results support the use of aspirin as an effective form of prophylaxis against VTE following THA. It is not associated with an increased incidence in symptomatic DVT, PE or death compared to other published studies. The fact that it is inexpensive, readily available, requires no monitoring and does not pose an increased risk of bleeding are other attractive advantages of using aspirin for VTE prophylaxis

Aims. Pigment epithelium-derived factor (PEDF) is known to induce several types of tissue regeneration by activating tissue-specific stem cells. Here, we investigated the therapeutic potential of PEDF 29-mer peptide in the damaged articular cartilage (AC) in rat osteoarthritis (OA). Methods. Mesenchymal stem/stromal cells (MSCs) were isolated from rat bone marrow (BM) and used to evaluate the impact of 29-mer on chondrogenic differentiation of BM-MSCs in culture. Knee OA was induced in rats by a single intra-articular injection of monosodium iodoacetate (MIA) in the right knees (set to day 0). The 29-mer dissolved in 5% hyaluronic acid (HA) was intra-articularly injected into right knees at day 8 and 12 after MIA injection. Subsequently, the therapeutic effect of the 29-mer/HA on OA was evaluated by the Osteoarthritis Research Society International (OARSI) histopathological scoring system and changes in hind paw weight distribution, respectively. The regeneration of chondrocytes in damaged AC was detected by dual-immunostaining of 5-bromo-2'-deoxyuridine (BrdU) and chondrogenic markers. Results. The 29-mer promoted expansion and chondrogenic differentiation of BM-MSCs cultured in different defined media. MIA injection caused chondrocyte death throughout the AC, with cartilage degeneration thereafter. The 29-mer/HA treatment induced extensive chondrocyte regeneration in the damaged AC and suppressed MIA-induced synovitis, accompanied by the recovery of cartilage matrix. Pharmacological inhibitors of PEDF receptor (PEDFR) and signal transducer and activator of transcription 3 (STAT3) signalling substantially blocked the chondrogenic promoting activity of 29-mer on the cultured BM-MSCs and injured AC. Conclusion. The 29-mer/HA formulation effectively induces chondrocyte regeneration and formation of cartilage matrix in the damaged AC. Cite this article: Bone Joint Res 2024;13(4):137–148

Aims. Traumatic central cord syndrome (CCS) typically follows a hyperextension injury and results in a motor impairment affecting the upper limbs more than the lower limbs, with occasional sensory impairment and urinary retention seen. Current evidence on mortality and long-term outcomes is limited. The primary aim of this study is to assess the five-year mortality of CCS, and to determine any difference in mortality between management groups or age. Patients and Methods. Patients ≥18 years with traumatic CCS between January 2012 and December 2017 in Wales were identified. Patient demographics and injury, management and outcome data was collected. Statistical analysis was performed to assess mortality and between group differences. Results. 65 patients were identified (66.2% male, mean age 63.9 years). At five-years follow-up, 32.3% (n=21) of CCS patients were dead. 6 (9.2%) patients had died within 31 days of their injury. 69.2% (n=45) of patients were managed conservatively and there was no significant difference (p=0.062) in age between conservatively and surgically managed patients. Kaplan-Meier analysis revealed no significant difference in mortality between patients managed conservatively compared to those managed surgically (log rank test, p=0.819). However, there was a significant difference (p=0.001) in mortality between the different age groups (<50 years vs 50–70 years vs >70 years). At five-years follow up, 55.6% of the patient group aged >70 years at time of injury were dead. Respiratory failure was the most common cause of death (n=9, 42.9%). Conclusion. Almost one third of patients with traumatic CCS in Wales were dead at five years following their injury. Management type did not significantly affect mortality, however age at time of injury did. Further work assessing the long-term functional outcomes of surviving patients is needed, to allow more reliable prognostic information and functional recovery predictions to be given

Two-stage exchange arthroplasty is traditionally used to treat periprosthetic hip infection. Nevertheless, particularly in high-risk patients, there has been increased attention towards alternatives such as 1.5-stage exchange arthroplasty which takes place in one surgery. Therefore, we sought to compare (1) operative time, length-of-stay (LOS), transfusions, (2) causative organism identification and polymicrobial infection rates, (3) re-revision rates and re-revision reasons, (4) mortality, and determine (5) independent predictors of re-revision. Retrospective chart review of 71 patients who underwent either 1.5- (n=38) or 2-stage (n=33) exchange hip arthroplasty at a single institution (03/2019-05/2023). Demographics, surgical, inpatient, and infection characteristics were noted. Main outcomes evaluated were re-revision rates, re-revision reasons, mortality, and cause of death. Independent predictors of re-revision were assessed utilizing logistic regression. Mean follow: 675 days (range, 23–1,715). Demographics were not significantly different except for a higher proportion of 1.5-stage patients classified as American-Society-of-Anesthesiologists (ASA) status 3 or 4 (84.2 vs. 48.5%, p=0.002). Length of follow-up was significantly longer in the 2-stage group (924.4 vs. 458 days, p<0.001) as well as operative time (506 vs. 271 minutes, p<0.001). In the 1.5-stage group, there was a higher proportion of polymicrobial infections (23.7 vs. 3.0%, p=0.016), re-revision rates (28.9 vs. 9.1%, p=0.042) and periprosthetic infections as a cause of revision (90.9 vs. 0%, p=0.007). Mortality rates were not significantly different, and no patient died for causes related to infection. Type of surgery (1.5-stage vs. 2-stage) was the only independent predictor of re-revision (odds-ratio 4.0, 95% confidence-interval 1.02–16.16, p=0.046). Our data suggests that patients who undergo 1.5-stage exchange arthroplasty have a significantly higher re-revision rate (mostly due to infection) when compared to 2-stage patients. We acknowledge potential benefits of the 1.5-stage strategy, especially in high-risk patients since it involves single surgery. However, higher re-revision rates must be considered when counseling patients

Background. Serious traumatic injury is a leading cause of death and disability globally, with the majority of survivors developing chronic pain. Methods. The aims of this study were to describe early predictors of poor long-term outcome for post-trauma pain. We conducted a prospective observational study, recruiting patients admitted to a Major Trauma Centre hospital in England within 14 days of their injuries, and followed them for 12 months. We defined a poor outcome as Chronic Pain Grade ≥ II and measured this at both 6-months and 12-months. A broad range of candidate predictors were used, including surrogates for pain mechanisms, quantitative sensory testing, and psychosocial factors. Univariate models were used to identify the strongest predictors of poor outcome, which were entered into multivariate models. Results. 124 eligible participants were recruited. At 6-months, 19 (23.2%) of 82 respondents reported a good outcome, whereas at 12-months 27 (61.4%) of 44 respondents reported a good outcome. The multivariate model for 6-months produced odds ratios for a unit increase in: number of fractures, 3.179 (0.52 to 19.61); average pain intensity, 1.611 (0.96 to 2.7); pain extent, 1.138 (0.92 to 1.41) and post-traumatic stress symptoms, 1.044 (0.10 to 1.10). At 12-months, equivalent values were: number of fractures, 1.653 (0.77 to 3.55); average pain intensity, 0.967 (0.67 to 1.40); pain extent, 1.062 (0.92 to 1.23) and post-traumatic stress symptoms, 1.025 (0.99 to 1.07). Conclusion. A poor long-term pain outcome from musculoskeletal traumatic injuries can be predicted by measures recorded within days of injury. Conflicts of interest: No conflicts of interest. Sources of funding: This study was funded by the National Institute for Health Research (NIHR) Surgical Reconstruction and Microbiology Research Centre (SRMRC)

Abstract. Introduction. Ultrasonic cutting in surgery has great potential. However, a key limitation is heat created by friction between the bone and the blade. Bone has poor thermal conductivity which hinders the dissipation of heat, causing cell death near the cut site In addition, ultrasonic vibration may create microcracks. It was hypothesised that these effects on bone would vary with the frequency and displacement of the ultrasonically powered blade. Therefore varying frequencies and displacements of the tip of the blade were studied to find the combination with fewest microcracks and lowest temperature rise at the bone-tool interface. Aim. To explore the effect of different frequencies and tip displacements of ultrasonic cutting devices on the amount of thermal and mechanical damage. Methods. In vitro tests were conducted on fresh rat femoral shafts using two different frequencies; 20kHz and 35kHz.Two displacement amplitudes of two different frequencies were used: 23.9 μm (p-p) and 7.5 μm (p-p) both at 20kHz and 18.7 μm (p-p) and 27 μm (p-p) both at 35kHz and. Cooling was used to emulate clinical conditions. Histological examination (H & E and TUNEL) was performed to identify live and dead cells. Further rat femoral shafts (n=6) were exposed to the same number of cuts by each tool to identify any micro-damage induced by different electrical currents using Micro-CT and confocal Laser scanning microscope. All experimental data were expressed as mean ± standard deviation. Statistical analysis was performed using one-way ANOVA, followed by Post Hoc multiple comparisons test. Differences between groups were considered statistically significant at p < 0.05. Results. The cut site at 7.5 μm (p-p) in 20kHz displayed only indentation instead of a cut, and was excluded. Histological examination revealed a high incidence of cell death at the cutting edge, in both frequencies. At 35kHz and 27 μm (p-p) some charring was evident, while at 20kHz and 23.9 μm (p-p) more irregularities were seen on the surface of the cut indicating instability during cutting when this setting was used. In contrast, the 35kHz at 18.7 μm (p-p) resulted in a smoother cutting surface. The highest cell death percentage ranged from 25% (at 35kHz, 18.7 μm (p-p)) to 44 % (at 35kHz, 27 μm (p-p)). Most of the tool's effect was located within 25 µm of the cut surface. There was a significant decrease to < 5 % at 200 µm. No cell death was found over 200 µm from the cut surface in both frequencies (35 kHz and 20 kHz). No significant difference in total percentage cell death was found between cutting at 35kHz and 18.7 μm (p-p) and at 20kHz and 23.9 μm (p-p). No microcracks were detected along the depth of the cut site at either frequency. Conclusion. Of the 2 ultrasonic cutting frequencies tested, the combination of the higher vibration frequency (35kHz) and the lower displacement amplitude (18.7 μm (p-p) demonstrated least damage to the bone tissue. No microcracks were displayed when using either of the ultrasonic cutting frequencies. Declaration of Interest. (b) declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported:I declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project

Aims. Thromboprophylaxis following Total Hip Replacement (THR) surgery remains controversial, balancing VTE prevention against wound leakage and subsequent deep infection. We analysed the 90 day cause of death post THR in our institution after the implementation of new thromboprophylactic policy of low dose aspirin for low risk patients, as part of a multimodal regime. Those at high risk were anticoagulated. Patients and methods. The PAS database was used to identify patients undergoing primary THR between January 2012 and June 2017 at The Royal Derby Hospital, and all deaths within 90 days. Trauma cases were excluded. Case note review and Coroner's verdict were utilised to ascertain cause of death. Results were compared to a previous study at the same institution prior to the introduction of the new policy, where thromboprophylaxis was decided upon by surgeon preference for either LMWH, aspirin or warfarin. Results. During this period 4021 THRs were performed. The rate of mortality was 0.22% at 90 days. This compares to 0.58% in the previous study with the only other factor changing being the rapidity of post op mobilization. Of the 9 deaths, only one was due to fatal pulmonary embolism. None of the deaths were at high risk of VTE. This compared to 5 fatal pulmonary embolism deaths in1838 patients in the previous study in the LMWH group. The leading causes of death were heart failure and lower respiratory tract infection. Conclusion. Our institution reports a similar 90 day (0.22%) mortality using aspirin to that in the last 5 years on the NJR (0.3%) in which over 80% use LMWH. We confirm that fatal PE following elective THR with a multi-modal prophylaxis regime is rare. Changing to low dose aspirin in low risk patients is a safe option

Aims. This retrospective study aimed to determine the causes of in-hospital death after Neck of Femur (NOF) fracture in Southampton General Hospital (SGH) over a 6 year period, comparing the clinical cause of death with findings at post-mortem. A previous study showed discrepancies between pre-mortem clinical diagnosis and autopsy findings after in-hospital deaths in SGH. Methods. The study included all patients who died in SGH after NOF fracture from 2007–2013. Case notes were reviewed to determine the pre-mortem clinical diagnosis and compared with the autopsy findings to analyse major and minor discrepancies. Data were also analysed from the period 1997–2003 in order to compare the causes of death. Results. 43 cases were referred for autopsy after NOF fracture during the 6 year study period, of which 39 cases (90.1%) were available for analysis. There was complete agreement between pre-mortem clinical diagnosis and autopsy findings in 64.1% of cases. Major discrepancies were found in 35.9% of cases and minor discrepancies in 23.1% of cases. Causes of death due to bronchopneumonia and pulmonary embolism had decreased significantly during the recent 6 year period when compared with the previous study period. No pulmonary emboli were identified as the primary causes of death between 2007 and 2013. Conclusion. Deaths due to pulmonary emboli after NOF have declined significantly. The reasons for this are unclear and are the subject of an ongoing study which will be discussed. Discrepancies between pre- and post-mortem diagnoses highlight the importance of autopsy findings. The current study revealed a similar rate of major discrepancies compared to the previous study

Aims. Staphylococcus aureus is a major cause of septic arthritis, and in vitro studies suggest α haemolysin (Hla) is responsible for chondrocyte death. We used an in vivo murine joint model to compare inoculation with wild type S. aureus 8325-4 with a Hla-deficient strain DU1090 on chondrocyte viability, tissue histology, and joint biomechanics. The aim was to compare the actions of S. aureus Hla alone with those of the animal’s immune response to infection. Methods. Adult male C57Bl/6 mice (n = 75) were randomized into three groups to receive 1.0 to 1.4 × 10. 7. colony-forming units (CFUs)/ml of 8325-4, DU1090, or saline into the right stifle joint. Chondrocyte death was assessed by confocal microscopy. Histological changes to inoculated joints were graded for inflammatory responses along with gait, weight changes, and limb swelling. Results. Chondrocyte death was greater with 8325-4 (96.2% (SD 5.5%); p < 0.001) than DU1090 (28.9% (SD 16.0%); p = 0.009) and both were higher than controls (3.8% (SD 1.2%)). Histology revealed cartilage/bone damage with 8325-4 or DU1090 compared to controls (p = 0.010). Both infected groups lost weight (p = 0.006 for both) and experienced limb swelling (p = 0.043 and p = 0.018, respectively). Joints inoculated with bacteria showed significant alterations in gait cycle with a decreased stance phase, increased swing phase, and a corresponding decrease in swing speed. Conclusion. Murine joints inoculated with Hla-producing 8325-4 experienced significantly more chondrocyte death than those with DU1090, which lack the toxin. This was despite similar immune responses, indicating that Hla was the major cause of chondrocyte death. Hla-deficient DU1090 also elevated chondrocyte death compared to controls, suggesting a smaller additional deleterious role of the immune system on cartilage. Cite this article: Bone Joint Res 2022;11(9):669–678

Hip and knee arthroplasties are very common operations in the UK with over 70000 hip and over 80000 knee arthroplasties taking place in England and Wales in 2011. Fortunately mortality following these operations is rare. However it remains important to understand the incidence and causes of death, in order to manage risk where possible and to inform the consent process. This study aimed to evaluate the incidence and causes of death within 30 days after undergoing hip or knee arthroplasty in our unit and to highlight possible risk factors. We looked at 30 day mortality in all patients undergoing hip or knee arthroplasty in our institution between 2005 and 2011. Data on post-operative deaths was derived from the Scottish Arthroplasty Project and correlated with procedural and demographic data from our hospital Patient Administration System (PAS). The notes of all patients who had died within a period of 30 days post-operatively were reviewed to collect data on co-morbid conditions, pre-operative investigations, post-operative thromboprophylaxis and cause of death. All primary and revision knee and hip arthroplasties including bilateral procedures were included. Arthroplasty for trauma was excluded. A total of 12,243 patients underwent hip or knee arthroplasty within the study period. 59% were female and the mean age was 68 (range 21–91). During this time period the standard protocol was to use aspirin for thromboprophylaxis. Eleven patients died following surgery giving a mortality rate of 0.09%. The most common cause of death was myocardial infarction (7/11 patients). Our finding of a mortality rate of 0.09% is similar or lower to those found in previous studies. To our knowledge this is the first series of this size looking at mortality from hip and knee arthroplasty within a single centre in the UK

Introduction The 2002 NCEPOD report recommended that autopsies should be the subject of a formal external audit process. It is thought that a post mortem would improve the understanding of the pathological events leading up to the death of a patient. The aims of this study were to find out the number of post mortems requested for patients with hip fracture and to establish the cause of death of all hip fracture patients as documented on the death certificate by medical practitioners and the coroner. Patients and Methods A retrospective review of all hip fracture deaths in the year 2000 was performed. The number of cases referred to the coroner for a post mortem and the given verdict was documented. Data regarding the cause of death (as per part 1a on the death certificate) recorded by the medical practitioner and the coroner was established. Results 83 patients with a hip fracture died in hospital in 2000 (mean age 83.6 years, range 58–97 years). There were 30 male and 53 female deaths. 37 patients (44.6%) were referred to the coroner for a post mortem examination. The common causes of death documented by the medical practitioner were: Bronchopneumonia; 27.9%, Congestive cardiac failure; 11.6%, Left ventricular failure; 9.3%, Cerebrovascular accident; 14%, and Carcinomatosis; 4.6%. The common causes of death documented by the coroner were: Bronchopneumonia; 35.1%, Congestive cardiac failure; 16.2%, Left ventricular failure; 10.8%, Cerebrovascular accident; 2.7%, carcinomatosis; 8.1%, and Pulmonary embolism; 8.1%. Conclusion Approximately 45% of hip fracture deaths are referred to the coroner. Apart from PE, the cause of death documented by medical practitioners and the coroner was no different in terms of frequency and spectrum. Cardiac and respiratory causes account for nearly 2/3 of hospital hip fracture deaths. Resources need to be targeted accordingly in an attempt to improve in hospital morbidity and mortality

Introduction. Cancellous and cortical bone used as a delivery vehicle for antibiotics. Recent studies with cancellous bone as an antibiotic carrier in vitro and in vivo showed high initial peak concentrations of antibiotics in the surrounding medium. However, high concentrations of antibiotics can substantially reduce osteoblast replication and even cause cell death. Objectives. To determine whether impregnation with gentamycine impair the incorporation of bone allografts, as compared to allografts without antibiotic. Materials and method. Seventy two healthy rabbits (24 rabbits in each group) were used for this study. Bone defects (3-mm diameter, 10-mm depth) were created in the femur. Human femoral head prepared according to the Marburg bone bank system was used as bone allograft. In the experimental groups, in 1 group - the defects were filled with bone allografts, in 2 group – Perforated Gentamycin-impregnated bone allografts. The control group did not receive any filling. The animals were killed after 14, 30 and 60 days. Evaluations consisted of X-ray plain radiography, histology at 14-, 30- and 60-days post-surgery. Results. Active osteoblast activity and active formation of new bones were detected around the defect area in all groups, but the amount of new bone formation was greater in the experimental groups than the control group. We found no statistically significant differences in the rate of bone formation between 1 and 2 groups at 14, 30 and 60 days in any of the parameters studied. X-ray results showed no significant difference in bony callus formation around allografts in 1 and 2 groups. In contrast, no significant callus formation was observed in the control group. Conclusion. The use of gentamycin-impregnated bone allografts may be of value in procedures performed at the site of osteomyelitis which require a second stage reconstruction with impacted bone grafting techniques

Abstract. Objective. The preparation of host degenerate cartilage for repair typically requires cutting and/or scraping to remove the damaged tissue. This can lead to mechanical injury and cartilage cell (chondrocytes) death, potentially limiting the integration of repair material. This study evaluated cell death at the site of cutting injury and determined whether raising the osmotic pressure (hyper-osmolarity) prior to injury could be chondroprotective. Methods. Ex vivo human femoral head cartilage was obtained from 13 patients (5 males and 8 females: 71.8 years old) with Ethical Permission and Patient consent. Cartilage wells were created using 3 or 5mm biopsy punches. Cell death at the wounded edge of the host cartilage and the edge of the extracted explants were assessed by quantifying the percentage of cell death (PCD) and measuring the width of the cell death zone at identified regions of interest (ROI) using the confocal laser scanning microscopy and image analysis software. To assess the chondroprotective effect of hyper-osmolarity, cartilage specimens were incubated in 340 or 600mOsm media, five minutes prior to injury to allow the chondrocytes to respond to the altered osmolarity. Wounded cartilage explants and cartilage wells were then cultured for a further 150 minutes following injury. Results. In 340mOsm media, the PCD around the 3mm cartilage wells was significantly less compared to the corresponding explants (20.05±10.24% vs 35.25±4.86%; P=0.0003). When using the 5mm biopsy punch, the PCD at the wound edges was significantly lower when compared to the 3mm cartilage wells (13.33±7.80% vs 20.05±10.24%; P=0.0121) at the same osmolarity. The width of the cell death zone for the well edges for both 3 and 5mm punches was significantly narrower when compared to their corresponding harvested cartilage explants in 340mOsm media (P<0.0001; P=0.0218, respectively). Exposing cartilage to raised osmolarity (600mOsm) prior to injury significantly reduced the PCD for cartilage wells produced by the 3mm biopsy punches (from 20.05±10.24% to 12.24±6.00%; P=0.0025). In addition, the zone of cell death was marginally reduced at the edges of the 5mm cartilage wells (19.25±15.78mm to 12.72±9.09mm; P=0.0499). Conclusions. The choice of biopsy punch and the osmolarity of the incubation medium prior to cartilage injury markedly affected the extent of chondrocyte death both at the edges of the cartilage wells and the explants. The smaller biopsy punch caused more chondrocyte death in the native cartilage wells compared to the larger punch, but this could be compensated for by the chondroprotective effect of raising the osmotic pressure. In general, there was less cell death at the wounded edges of the cartilage wells, compared to the explants. These results suggest that there is scope for further optimising the cutting implements used to create the cartilage wells and protecting chondrocytes by hyper-osmolarity in order to minimize cell death at cut edges and potentially enhance integration between cartilage repair material and host cartilage. Declaration of Interest. (b) declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported:I declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project

The goal of this study was to identify the effect of mismatches in the subchondral bone surface at the native:graft interface on cartilage tissue deformation in human patellar osteochondral allografts (OCA). Hypothesis: large mismatches in the subchondral bone surface will result in higher stresses in the overlying and surrounding cartilage, potentially increasing the risk of graft failure. Nano-CT scans of ten 16mm diameter cadaveric patellar OCA transplants were used to develop simplified and 3D finite element (FE) models to quantify the effect of mismatches in the subchondral bone surface. The simplified model consisted of a cylindrical plug with a 16 mm diameter (graft) and a washer with a 16 mm inner diameter and 36 mm outer diameter (surrounding native cartilage). The thickness of the graft cartilage was varied from 0.33x the thickness of native cartilage (proud graft subchondral bone) to 3x the thickness of native cartilage (sunken graft subchondral bone; Fig. 1). The thickness of the native cartilage was set to 2 mm. The surface of the cartilage in the graft was matched to the surrounding native cartilage. A 1 MPa pressure was applied to the fixed patellar cartilage surface. Scans were segmented using Dragonfly and meshed using HyperMesh. FE simulations were conducted in Abaqus 2019. The simplified model demonstrated that a high stress region occurred in the cartilage at the sharp bony edge between the graft and native subchondral bone, localized to the region with thinner cartilage. A 20% increase in applied pressure occurs up to 50μm away from the graft edge (primarily in the graft cartilage) for grafts with proud subchondral bone but varies little based on the graft cartilage thickness. For grafts with sunken subchondral bone, the size of the high stress region decreases as the difference between graft cartilage and native cartilage thickness decreases (Fig. 2-4), with a 200 μm high stress region occurring when graft cartilage was 3x thicker than native cartilage (i.e., greater graft cartilage thickness produces larger areas of stress in the surrounding native cartilage). The 3D models reproduced the key features demonstrated in the simplified model. Larger differences between native and graft cartilage thickness cause larger high stress regions. Differences between the 3D and simplified models are caused by heterogeneous cartilage surface curvature and thickness. Simplified and 3D FE analysis confirmed our hypothesis that greater cartilage thickness mismatches resulted in higher cartilage stresses for sunken subchondral bone. Unexpectedly, cartilage stresses were independent of the cartilage thickness mismatch for proud subchondral bone. These FE findings did not account for tissue remodeling, patient variability in tissue mechanical properties, or complex tissue loading. In vivo experiments with full-thickness strain measurements should be conducted to confirm these findings. Mismatches in the subchondral bone can therefore produce stress increases large enough to cause local chondrocyte death near the subchondral surface. These stress increases can be reduced by (a) reducing the difference in thickness between graft and native cartilage or (b) using a graft with cartilage that is thinner than the native cartilage. For any figures or tables, please contact the authors directly

Distracted driving is now the number one cause of death among teenagers in the United States of America according to the National Highway Traffic Safety Administration. However, the risks and consequences of driving while distracted spans all ages, gender, and ethnicity. The Distractions on the Road: Injury eValuation in Surgery And FracturE Clinics (DRIVSAFE) Study aimed to examine the prevalence of distracted driving among patients attending hospital-based orthopaedic surgery fracture clinics. We further aimed to explore factors associated with distracted driving. In a large, multi-center prospective observational study, we recruited 1378 adult patients with injuries treated across four clinics (Hamilton, Ontario, Toronto, Ontario, Calgary, Alberta, Halifax, Nova Scotia) across Canada. Eligible patients included those who held a valid driver's license and were able to communicate and understand written english. Patients were administered questions about distracted driving. Data were analyzed with descriptive statistics. Patients average age was 45.8 years old (range 16 – 87), 54.3% male, and 44.6% female (1.1% not disclosed). Of 1361 patients, 1358 self-reported distracted driving (99.8%). Common sources of distractions included talking to passengers (98.7%), outer-vehicle distractions (95.5%), eating/drinking (90.4%), music listening/adjusting the radio (97.6%/93.8%), singing (83.2%), accepting phone calls (65.6%) and daydreaming (61.2%). Seventy-nine patients (6.3%), reported having been stopped by police for using a handheld device in the past. Among 113 drivers who disclosed the cause of their injury as a motor vehicle crash (MVC), 20 of them (17%) acknowledged being distracted at the time of the crash. Of the participants surveyed, 729 reported that during their lifetime they had been the driver in a MVC, with 226 (31.1%) acknowledging they were distracted at the time of the crash. Approximately, 1 in 6 participants in this study had a MVC where they reported to be distracted. Despite the overwhelming knowledge that distracted driving is dangerous and the recognition by participants that it can be dangerous, a staggering amount of drivers engage in distracted driving on a fairly routine basis. This study demonstrates an ongoing need for research and driver education to reduce distracted driving and its devastating consequences

Venous thromboembolism (VTE) is the second most common complication and pulmonary embolism (PE) is the fourth most common cause of death after a hip fracture. Despite thromboprophylaxis, deep vein thrombosis (DVT) is detected in up to 45% of hip fracture patients. Thrombelastography (TEG) is a whole-blood, point of care test capable of providing clinicians with a global assessment of the clotting process, from fibrin formation to clot lysis. Maximal amplitude (mA) from TEG analysis is a measure of clot strength. Elevated admission mA values of >65mm and >72mm have been determined to be independent predictors of in-hospital PE. The coagulation index (CI) is calculated based on TEG parameters and defines hypercoagulable state as CI >3. This study aimed to use serial TEG analysis to determine the duration of hypercoagulable state after hip fracture. A prospective cohort of hip fracture patients >50 years of age amenable to surgical treatment (AO 31A1–A3 & 31B1–B3) were enrolled at a Level I trauma centre. Serial TEG analysis (TEG 6S) was performed every 24-hours from admission until 5-days post-operatively and at 2- and 6-week follow-up visits. All patients received a minimum of 28 days of thromboprophylaxis. Descriptive statistics and single sample t-tests were used for comparison of mA to the 65mm threshold. Thirty-five patients (26 female) with a median age of 83 (range = 71–86) years were included. On admission, 31.4% and 82.9% of patients were hypercoagulable based on mA >65mm and CI, respectively. At 2 weeks, all patients remained hypercoagulable, however, mA >72mm showed that 16 patients (47.1%) were at even higher risk for VTE. At 6-weeks, 65.7% and 97.1% of patients were hypercoagulable based on mA >65mm and CI, respectively. When compared with the mA >65mm threshold, patients were hypocoagulable at the time of admission (mA = 62.2 (±6.3), p = 0.011), but became significantly more hypercoagulable at 2-weeks (mA = 71.6 (±2.6), p < 0 .001), followed by continued hypercoagulability at 6-weeks, however not significantly elevated above the 65mm threshold (mA = 66.2 (±3.8), p = 0.058). One patient developed a symptomatic DVT at 2-weeks and had a mA = 72.9 and a CI of 5.9. This is the first study to demonstrate that >50% of hip fracture patients remain hypercoagulable 6 weeks post fracture despite thromboprophylaxis, and there are individual hypercoagulable responses. This is critical, as guidelines only recommend 28 to 35 days of thromboprophylaxis in this high-risk population. Previously determined mA thresholds may be a more sensitive test for risk-stratifying patients' VTE risk than the CI threshold. Additionally, assessing ΔmA using serial TEG may better predict VTE risk

Objectives. Staphylococcus aureus (S. aureus) is the most commonly implicated organism in septic arthritis, a condition that may be highly destructive to articular cartilage. Previous studies investigating laboratory and clinical strains of S. aureus have demonstrated that potent toxins induced significant chondrocyte death, although the precise toxin or toxins that were involved was unknown. In this study, we used isogenic S. aureus mutants to assess the influence of alpha (Hla)-, beta (Hlb)-, and gamma (Hlg)-haemolysins, toxins considered important for the destruction of host tissue, on in situ bovine chondrocyte viability. Methods. Bovine cartilage explants were cultured with isogenic S. aureus mutants and/or their culture supernatants. Chondrocyte viability was then assessed within defined regions of interest in the axial and coronal plane following live- and dead-cell imaging using the fluorescent probes 5-chloromethylfluorescein diacetate and propidium iodide, respectively, and confocal laser-scanning microscopy. Results. Hla-producing mutants caused substantial chondrocyte death compared with the toxin-deficient control (Hla-Hlb-Hlg-), whilst mutants producing Hlb and Hlg in the absence of Hla induced minimal chondrocyte death. Coronal studies established that Hla-induced chondrocyte death started in the superficial zone of cartilage and spread to deeper layers, whereas Hlb and Hlg toxins were without significant effect. Conclusion. This study identified Hla as a highly potent S. aureus toxin that caused rapid chondrocyte death in bovine cartilage, with other toxins or metabolic products produced by the bacteria playing a minor role. The identification of Hla in mediating chondrocyte death may assist in the development of therapeutic strategies aimed at reducing the extent of cartilage damage during and after an episode of septic arthritis. Cite this article: I. D. M. Smith, K. M. Milto, C. J. Doherty, S. G. B. Amyes, A. H. R. W. Simpson, A. C. Hall. A potential key role for alpha-haemolysin of Staphylococcus aureus in mediating chondrocyte death in septic arthritis. Bone Joint Res 2018;7:457–467. DOI: 10.1302/2046-3758.77.BJR-2017-0165.R1