Prompt mobilisation after the Fracture neck of femur surgery is one of the important key performance index (‘KPI caterpillar charts’ 2021) affecting the overall functional outcome and mortality. Better control of peri-operative blood pressure and minimal alteration of renal profile as a result of surgery and anaesthesia may have an implication on early post-operative mobilisation. Aim was to evaluate perioperative blood pressure measurements (duration of fall of systolic BP below the critical level of 90mmHg) and effect on the post-operative renal profile with the newer short acting spinal anaesthetic agent (prilocaine and chlorprocaine) used alongside the commonly used regional nerve block. 20 patients were randomly selected who were given the newer short acting spinal anaesthetic agent along with a regional nerve block between May 2019 and February 2020. Anaesthetic charts were reviewed from all patients for data collection. The assessment criteria for perioperative hypotension: Duration of systolic blood pressure less than 90 mm of Hg and change of pre and post operative renal functions. Only one patient had a significant drop in systolic BP less than 90mmHg (25 minutes). 3 other patients had a momentary fall of systolic BP of less than 5 minutes. None of the above patients had mortality and had negligible change in pre and post op renal function. Only one patient in this cohort had elevation of post-operative creatinine levels but did not have any mortality. Only 1 patient died on day 3 post operatively who had multiple comorbidities and was under evaluation for GI cancer. Even in this patient the peri-operative blood pressure was well maintained (never below 90mmHg systolic) and post-operative renal function was also shown to have improved (309 pre-operatively to 150 post-operatively) in this patient. The use of short-acting spinal anaesthesia has shown to be associated with a better control of blood pressure and end organ perfusion, less adverse effects on renal function leading to early mobilisation and a more favourable patient outcome with reduced mortality, earlier mobilisation, shorter hospital stay and earlier discharge in this elderly patient cohort

Abstract. Objective. To investigate the safety and cost-effectiveness of interscalene brachial plexus block/regional anaesthesia (ISB-RA) in patients undergoing reverse total shoulder replacement. Methods. This retrospective study included 15 patients with symptomatic rotator cuff arthropathy who underwent reverse total shoulder arthroplasty (rTSA) under ISB-RA without general anaesthesia in the beach chair position from 2010 to 2018. The mean patient age was 77 years (range 59–82 years). Patients had associated medical comorbidities: American Society of Anesthesiologists (ASA) grade 2–4. Assessed parameters were: duration of anaesthesia, intra-operative systolic blood pressure variation, sedation and vasopressor use, duration of post-operative recovery, recovery scores, length of stay, and complications. A robust cost analysis was also performed. Results. The mean (range) duration of anaesthesia was 38.66 (20–60) min. Maximum and minimum intra-operative systolic blood pressure ranges were 130–210 and 75–145 mmHg, respectively (mean [range] drop, 74.13 [33–125] mmHg). Mean (range) propofol dose was 1.74 (1–3.0) mg/kg/h. The Median (interquartile range) post-operative recovery time was 30 (20–50) min. The mean (range) postoperative recovery score (local scale, range 5–28 where lower values are superior) was 5.2 (5–8). The mean (range) length of stay was 8 (1–20 days); the two included patients with ASA grade 2 were both discharged within 24 hours. One patient with predisposing history developed pneumonia; however, there were no complications related to ISB-RA. The mean (range) cost per patient was £101.36 (£59.80-£132.20). Conclusions. Our data demonstrate that rTSA under ISB-RA is safe, cost-effective and a potentially viable alternative for patients with multiple comorbidities. Notably, patients with ASA grade 2 who underwent rTSA under ISB-RA had a reduced length of stay and were discharged within 24 hours

Background. Aseptic loosening of cemented femoral stems results from migration of wear particles along the bone-cement interface, producing a foreign body reaction. After cement insertion, blood back pressure can disrupt the bone-cement interface, enabling this spread of wear particles. Our study investigates whether altering timing and speed of stem insertion can reduce this risk. Methods. We inserted mock “C-Stem” femoral components (De Puy-Synthes), using Smartset HV cement (De Puy-Synthes) into artificial femora, fitted with proximal and distal pressure transducers. Cement insertion began two, three or four minutes after mixing. Cement pressures were then allowed to settle for one minute and the stems were then inserted over durations of 25, 60 or 90 seconds. Results. Quicker insertion led to high peak pressures; however insertion over 90 seconds at 4 and 5 minutes achieved more sustained pressures above blood back pressure. Slower insertion particularly improved proximal pressurisation. Furthermore when the stem was inserted over 90 seconds at 5 minutes then the cement pressures remained high after full insertion of the stem. Conclusions. Commonly, femoral stems are inserted rapidly. Our study demonstrates that by inserting the femoral stem more slowly, cement pressure can be maintained above blood back pressure for longer. We believe that after slower stem insertion, the higher cement viscosity enables the surgeon to maintain cement pressure, via the stem, sufficient to resist blood back pressure without inadvertently over inserting the stem. This safe and simple modification of cementing technique generates higher and more sustained cement pressures. Level of evidence. 3. Disclosures. Depuy-Synthes kindly provided the equipment used in the study. None of the authors received any payment or other benefits

Cardiovascular disease is now the leading cause of morbidity and mortality worldwide. Raised blood pressures (BP) are associated with increased cardiovascular risks such as myocardial infarction, stroke and arteriosclerosis. During surgery the haemodynamic effects of stress are closely monitored and stabilised by the anaesthetist. Although there have been many studies assessing the effects of intraoperative stress on the patient, little is known about the impact on the surgeon. A prospective cohort study was carried out using an ambulatory blood pressure monitor to measure the BP and heart rates (HR) of three consultants and their respective trainees during hallux valgus, hip and knee arthroplasty surgery. Our principle aim was to assess the physiological effects of performing routine operations on the surgeon. We noted if there were any differences in the stress response of the lead surgeon, in comparison to when the same individual was assisting. In addition, we recorded the trainee's BP and HR when they were operating independently. The intraoperative measurements were compared with their baseline readings and their stress response, assessed using the Bruce protocol. Many trends were noted in this pilot study. All of the surgeons had higher BP and HR readings on operating days compared to baseline. The physiological parameters normalised by one hour post-theatre list in all subjects. When the trainer was leading the operation, their BP gradually increased until implant placement, while their trainees remained stable. On the other hand, when the trainee was operating and the trainer assisting, the trainer's BP peaked at the beginning of the procedure, and slowly declined as it progressed. The trainee's BP remained elevated throughout. The highest peaks for trainees were noted during independent operating. We conclude that all surgery is stressful, and that trainees are more likely to be killing themselves than their trainers

Background. Despite the known multifactorial nature of scaphoid wrist fracture non-union, a possible genetic predisposition for the development of this complication remains unknown. This pilot study aimed to address this issue by performing Single Nucleotide Polymorphisms (SNPs) analysis of specific genes known to regulate fracture healing. Materials and Methods. We reviewed 120 patients in a retrospective case-control study from the Hand Surgery Department of Asepeyo Hospital. The case group comprised 60 patients with confirmed scaphoid wrist non-union, diagnosed by Magnetic Resonance Imaging (MRI) and Computed Tomography (CT). The control group comprised 60 patients with scaphoid fracture and complete bone consolidation. Sampling was carried out with a puncture of a finger pad using a sterile, single-use lancet. SNPs were determined by real-time polymerase chain reaction (PCR) using specific, unique probes with the analysis of the melting temperature of hybrids. The X2 test compared genotypes between groups. Multivariate logistic regression analysed the significance of many covariates and the incidence of scaphoid wrist non-union. Results. We found significant differences in subjects who had a smoking habit (p=0.001), high blood pressure (p<0.001), and surgical treatment (p=0.002) in patients with scaphoid non-union. There were more Caucasians (p=0.04) and males (p=0.001) in the case group. Falls were the main mechanism of fracture. The CC genotype in GDF5 (rs143383) was more frequent in patients with scaphoid non-union compared to the controls (p=0.02). CT was prevalent in the controls (p=0.02). T allele in GDF5 was more frequent in patients without non-union (p=0.001). Conclusions. Individuals who were carriers of the CC genotype in GDF5 showed higher susceptibility to suffering scaphoid wrist non-union. Furthermore, being a carrier of CT and T allele suggests that this could be behave as a protection factor against non-union. This is the first clinical study to investigate the potential existence of genetic susceptibility to scaphoid wrist fracture non-union. Level of evidence. Level III, Cross Sectional Study, Epidemiology Study

Purpose. In patients with multiple trauma delayed fracture healing is often diagnosed, but the pathomechanisms are not well known yet. The purpose of the study is to evaluate the effect of a severe hemorrhagic shock on fracture healing in a murine model. Methods. 10 male C57BL/6N mice per group (Fx, TH, THFx, Sham) and point in time were used. The Fx-group received an osteotomy after implantation of a fixateur extern. The TH-group got a pressure controlled hemorrhagic shock with a mean arterial blood pressure of 35 mmHg over 90 minutes. Resuscitation with 4 times the shed blood volume of Ringer solution was performed. The THFx group got both. Sham-animals received the implantation of a catheter and a fixateur extern but no blood loss or osteotomy. After 1, 2, 3, 4 or 6 weeks the animals were sacrificed. For the biomechanics the bones were analyzed via X-ray, µCT and underwent a 3-point bending test. The nondecalcified histology based on slices of Technovit 9100. The signaling pathway was analyzed via RT. 2. Profiler™ PCR Array Mouse Osteoporosis, Western Blot and Quantikine ELISA for RankL and OPG. Statistical significance was set at p < 0.05. Comparisons between groups were performed using the Mann–Whitney U (Fx vs. THFx) or Kruskal-Wallis Test (other groups). Results. The experiment showed that after 1 week the bones of the Fx- and THFx-mice were macroscopically instable. After 2 weeks the Fx-group showed macroscopically a stable bridging whereas the bones of the THFx-group were partly not stable bridged. 3 weeks after surgery the bones of both groups were stable bridged. Analysis via µCT showed that trauma hemorrhage leads to decreased density of the bone and callus and also to increased share of callus per bone volume after 2 weeks. The 3-point-bending test showed that the maximum bending moment is decreased in the group THFx compared to Fx after 2 weeks. The studies of the histology showed after 2 weeks a decrease in bone and cartilage after trauma-hemorrhage by optical analysis of photographs of the slices. The analyses of the signaling pathway pointed to an involvement of the RankL/Opg and IL6 pathway. Conclusion. A hemorrhagic shock has a negative effect on fracture healing in terms of reduced density of the bone and callus, increased share of callus per bone volume, decreased maximum bending moment, reduced mineralization of the callus and leads to changes in the RankL/Opg and IL6 pathways

Spinal cord injury (SCI) is a devastating disorder for which the identification of exacerbating factors is urgently needed. Although age, blood pressure and infection are each considered to be prognostic factors in patients with SCI, exacerbating factors that are amenable to treatment remain to be elucidated. Microglial cells, the resident immune cell in the CNS, form the first line of defense after being stimulated by exposure to invading pathogens or tissue injury. Immediately after SCI, activated microglia enhance and propagate the subsequent inflammatory response by expressing cytokines, such as TNF-α, IL-6 and IL-1β. Recently, we demonstrated that the activation of microglia is associated with the neuropathological outcomes of SCI. Although the precise mechanisms of microglial activation remain elusive, several basic research studies have reported that hyperglycemia is involved in the activation of resident monocytic cells, including microglia. Because microglial activation is associated with secondary injury after SCI, we hypothesized that hyperglycemia may also influence the pathophysiology of SCI by altering microglial responses. The mice were anesthetized with pentobarbital (75 mg/kg i.p.) and were subjected to a contusion injury (70 kdyn) at the 10th thoracic level using an Infinite Horizons Impactor (Precision Systems Instrumentation). For flow cytometry, the samples were stained with the antibodiesand analyzed using a FACS Aria II flow cytometer and the FACSDiva software program (BD Biosciences). We retrospectively identified 528 SCI patients admitted to the Department of Orthopaedic Surgery at the Spinal Injuries Center (Fukuoka, Japan) between June 2005 and May 2011. The patients' data were obtained from their charts. We demonstrate that transient hyperglycemia during acute SCI is a detrimental factor that impairs functional improvement in mice and human patients after acute SCI. Under hyperglycemic conditions, both in vivo and in vitro, inflammation was enhanced through promotion of the nuclear translocation of the nuclear factor kB (NF-kB) transcription factor in microglial cells. During acute SCI, hyperglycemic mice exhibited progressive neural damage, with more severe motor deficits than those observed in normoglycemic mice. Consistent with the animal study findings, a Pearson χ2 analysis of data for 528 patients with SCI indicated that hyperglycemia on admission (glucose concentration ≥126 mg/dl) was a significant risk predictor of poor functional outcome. Moreover, a multiple linear regression analysis showed hyperglycemia at admission to be a powerful independent risk factor for a poor motor outcome, even after excluding patients with diabetes mellitus with chronic hyperglycemia (regression coefficient, −1.37; 95% confidence interval, −2.65 to −0.10; P < 0.05). Manipulating blood glucose during acute SCI in hyperglycemic mice rescued the exacerbation of pathophysiology and improved motor functional outcomes. Our findings suggest that hyperglycemia during acute SCI may be a useful prognostic factor with a negative impact on motor function, highlighting the importance of achieving tight glycemic control after central nervous system injury

Significance. Acute compartment syndrome (ACS) occurs after muscle injury and is characterised by increased pressure in the muscle compartment that can result in devastating complications if not diagnosed and treated appropriately. ACS is currently confirmed by repeated needle sticks to measure the compartment pressure using a hand-held compartment pressure monitor. This approach is often not reproducible and is not appropriate for continuous monitoring. To address the shortcomings of currently available technology we are developing an implantable micro-device that will measure compartment pressure directly and continuously over the 24 hours critical period following injury using a radio frequency identification (RFID) platform integrated with a MEMS capacitive pressure sensor. Methods. The prototype implantable device measuring 3mmx3mm consists of a capacitive pressure sensor, a sensor readout circuitry, an antenna and a radio frequency reader. A prototype sensor was packaged in Silicone gel (MED-6640, Nusil Technology LLC) for ex vivo and in vivo testing in three compartment models. First, it was tested ex vivo in an airtight vessel using a blood pressure monitor to pump air and increase the pressure inside the vessel. Second, it was implanted in a muscle compartment of a fresh porcine hind limb and an infusion pump with normal saline was used to raise the tissue pressure. Third, it was implanted in the posterior thigh muscle of a rat where the pressure was increased by applying a tourniquet around the thigh. The readings were compared with those from a hand-held Stryker Intra-compartmental Pressure Monitor System used in the trauma room. Results. The sensor reading from the radio frequency reader software interface in all three models showed good linearity against the pressure applied to the compartment. Conclusion. The successful completion of this project will lead to the development of an implantable miniaturised wireless pressure sensor microsystem capable of measuring tissue compartment pressures in the critical period after traumatic injury and reduce the incidence of serious complications such as severe pain, paralysis, sensory deficits, muscle necrosis and permanent disability

Introduction. The interstitial fluid of bone fluid flow is supplied by flowing blood. Blood flow is determined by three kinds of muscles: cardiac, smooth, and skeletal. Cardiac muscle establishes baseline blood pressure. Smooth muscle controls vessel diameter and skeletal muscle creates intermittent intravascular pressure pulses. For the tibia the relevant skeletal muscle is the gastrocnemius which functions as a muscle pump. This study tested the hypotheses: 1) skeletal muscle-caused pressure pulses increase cortical blood flow, 2) extravasation of vascular fluid and, consequently, interstitial bone fluid flow are enhanced by resultant increased microvascular pressure and 3) bone healing is enhanced by increased bone fluid flow. Methods. Eighteen skeletally mature female New Zealand white rabbits were implanted with bone chamber windows (BCIs) as described previously. The windows were exposed at three weeks and observed weekly until Week 10 using intravital microscopy. During observation, the subject was suspended in prone position in a mesh fabric torso sling jacket so as to eliminate gravity-based reaction forces. Electrodes of a transcutaneous electrical nerve stimulator (TENS) were gel-glued at each rabbits gastroc-soleus position; but activated only in the 11 experimentals. A 4Hz 2.8 ± 1.3V impulse was delivered for 60 minutes. Still and video images were obtained at 0, 2, and 60 minutes following injection of 1μm fluorescent microspheres. Each such injection was followed by injection of 70 kD FITC- or RITC-dextran to define vascularity and capillary filtration. Additional still images were obtained at 5, 30, and 55 minutes. Muscle contraction forces during TENS were obtained acutely following the Week 10 observation with a Futek force transducer cell through an attached nylon suture. Bone mineral density was obtained at Week 3 and Week 10 with a Stratec pQCT and associated software. Data were analyzed statistically using a Wilcoxon signed rank test. Results. All three hypotheses were supported statistically by the data. The average force produced by TENS stimulated gastrocnemius contraction was 18.98 ± 9.42 N/kg muscle. This produced a microstrain of 192μe in bone around the BCI. Bloodflow results are shown in the figure. On average, flow decreased in controls by 12.6% and increased in experimentals by about 2%. Capillary filtration in experimentals was about 34.6% higher than controls after 60 minutes of TENS. Bone formation rate was 62.5% higher with TENS. Conclusion. In order to understand the role of fluid flows in bone physiology, we need to know the how and where of movement. These results suggest the part played by skeletal muscle in bone fluid movement cannot be ignored. As with many evolutionary adaptations, the muscle pump's hydrodynamic contribution to bone may be redundant and merely serve as a backup to percolation from poroelastic deformation. On the other hand, it may be crucial in disuse osteoporosis instigating conditions such as microgravity. The measured increases in capillary filtration and blood flow suggest that intravascular pressure which drives the former and resultant percolation has been increased by the muscle pump. It follows that fluid shear on cortical bone cells also increased. The challenge now is to obtain local flow measurements that would tell us how much

Objectives

We studied subchondral intraosseous pressure (IOP) in an animal model during loading, and with vascular occlusion. We explored bone compartmentalization by saline injection.

Objectives

We aimed to examine the characteristics of deep venous flow in the leg in a cast and the effects of a wearable neuromuscular stimulator (geko; FirstKind Ltd) and also to explore the participants’ tolerance of the stimulator.

Objectives

To assess the sensitivity and specificity of self-reported osteoporosis compared with dual energy X-ray absorptiometry (DXA) defined osteoporosis, and to describe medication use among participants with the condition.

The stress response to trauma is the summation of the physiological response to the injury (the ‘first hit’) and by the response to any on-going physiological disturbance or subsequent trauma surgery (the ‘second hit’).

Our animal model was developed in order to allow the study of each of these components of the stress response to major trauma. High-energy, comminuted fracture of the long bones and severe soft-tissue injuries in this model resulted in a significant tropotropic (depressor) cardiovascular response, transcardiac embolism of medullary contents and activation of the coagulation system. Subsequent stabilisation of the fractures using intramedullary nails did not significantly exacerbate any of these responses.

We have compared the energy expenditure during walking in three patients, aged between 51 and 55 years, with unilateral disarticulation of the hip when using the mechanical-controlled stance-phase control knee (Otto Bock 3R15) and the microprocessor-controlled pneumatic swing-phase control knee (Intelligent Prosthesis, IP). All had an endoskeletal hip disarticulation prosthesis with an Otto Bock 7E7 hip and a single-axis foot. The energy expenditure was measured when walking at speeds of 30, 50, and 70 m/min.

Two patients showed a decreased uptake of oxygen (energy expenditure per unit time, ml/kg/min) of between 10.3% and 39.6% when using the IP compared with the Otto Bock 3R15 at the same speeds. One did not show any significant difference in the uptake of oxygen at 30 m/min, but at 50 and 70 m/min, a decrease in uptake of between 10.5% and 11.6% was found when using the IP. The use of the IP decreased the energy expenditure of walking in these patients.

The re-establishment of vascularity is an early event in fracture healing; upregulation of angiogenesis may therefore promote the formation of bone. We have investigated the capacity of vascular endothelial growth factor (VEGF) to stimulate the formation of bone in an experimental atrophic nonunion model.

Three groups of eight rabbits underwent a standard nonunion operation. This was followed by interfragmentary deposition of 100 μg VEGF, carrier alone or autograft.

After seven weeks, torsional failure tests and callus size confirmed that VEGF-treated osteotomies had united whereas the carrier-treated osteotomies failed to unite. The biomechanical properties of the groups treated with VEGF and autograft were identical. There was no difference in bone blood flow.

We considered that VEGF stimulated the formation of competent bone in an environment deprived of its normal vascularisation and osteoprogenitor cell supply. It could be used to enhance the healing of fractures predisposed to nonunion.

Ovine articular chondrocytes were isolated from cartilage biopsy and culture expanded in vitro. Approximately 30 million cells per ml of cultured chondrocytes were incorporated with autologous plasma-derived fibrin to form a three-dimensional construct. Full-thickness punch hole defects were created in the lateral and medial femoral condyles. The defects were implanted with either an autologous ‘chondrocyte-fibrin’ construct (ACFC), autologous chondrocytes (ACI) or fibrin blanks (AF) as controls. Animals were killed after 12 weeks. The gross appearance of the treated defects was inspected and photographed. The repaired tissues were studied histologically and by scanning electron microscopy analysis.

All defects were assessed using the International Cartilage Repair Society (ICRS) classification. Those treated with ACFC, ACI and AF exhibited median scores which correspond to a nearly-normal appearance. On the basis of the modified O’Driscoll histological scoring scale, ACFC implantation significantly enhanced cartilage repair compared to ACI and AF. Using scanning electron microscopy, ACFC and ACI showed characteristic organisation of chondrocytes and matrices, which were relatively similar to the surrounding adjacent cartilage.

Implantation of ACFC resulted in superior hyaline-like cartilage regeneration when compared with ACI. If this result is applicable to humans, a better outcome would be obtained than by using conventional ACI.

This study explored the relationship between the initial stability of the femoral component and penetration of cement into the graft bed following impaction allografting.

Impaction allografting was carried out in human cadaveric femurs. In one group the cement was pressurised conventionally but in the other it was not pressurised. Migration and micromotion of the implant were measured under simulated walking loads. The specimens were then cross-sectioned and penetration of the cement measured.

Around the distal half of the implant we found approximately 70% and 40% of contact of the cement with the endosteum in the pressure and no-pressure groups, respectively. The distal migration/micromotion, and valgus/varus migration were significantly higher in the no-pressure group than in that subjected to pressure. These motion components correlated negatively with the mean area of cement and its contact with the endosteum.

The presence of cement at the endosteum appears to play an important role in the initial stability of the implant following impaction allografting.