Persistent post-surgical pain remains a problem after knee replacement with some studies reporting up to 20% incidence. Pain is usually felt by those who do not operate to be a monolithic entity. All orthopaedic surgeons know that this is not the case. At its most basic level, pain can be divided into two categories, mechanical and non-mechanical.

Mechanical pain is like the pain of a fresh fracture. If the patient does not move, the pain is less. This type of pain is relieved by opiates. Mechanical pain is seen following knee replacement, but is fortunately becoming less frequent. It is caused by a combination of malrotations and maltranslations, often minor, which on their own would not produce problems. The combination of them, however, may produce a knee in which there is overload of the extensor mechanism or of the medial stabilizing structures. If these minor mechanical problems can be identified, then corrective surgery will help.

Non-mechanical pain is present on a constant basis. It is not significantly worsened by activities. Opiates may make the patient feel better, but they do not change the essential nature of the pain. Non-mechanical pain falls into three broad groups, infection, neuropathic and perceived pain. Infection pain is usually relieved by opiates. Since some of this pain is probably due to pressure, its inclusion in the non-mechanical pain group is questionable, but it is better left there so that the surgeon always considers it. Low grade chronic infection can be extremely difficult to diagnose. Loosening of noncemented knee components is so rare that when it is noted radiologically, infection should be very high on the list of suspicions. The name neuropathic pain suggests that we know much more about it than we do in reality. Causalgia or CRPS-type two is rare following knee replacement. CRPS type one or reflex sympathetic dystrophy probably does exist, but it is probably over-diagnosed especially by the author of this abstract. The optimum treatment I have found is lumbar sympathetic blocks. Perceived pain is the largest group. It does not matter what you tell the patient, some believe a new knee should be like a new car, i.e. you step into it and drive away. The fact that they have to work to make it work is horrifying. Some of this pain is actually mechanical, especially in those with no benefits such as hairstylists. Perceived pain is widespread. The classic treatise on this is Dr. Ian McNabb's book “Backache”. It should be studied by all orthopaedic surgeons, who wish to understand pain complaints.

Any experienced knee surgeon will have his list of red flags or caveats. These are often politically incorrect and this information is transferred to young surgeons, usually in dim bars late at night. I will list only a few. If the patient comes in with a form asking for a disability pension on the first visit. If the patient's mother answers the questions. If the patient comes in taking massive doses of opiates. If the patient is referred to you by a surgeon, who does more knee replacements than you do. There is also the recently described Fern Silverman's syndrome.

Persistent post-surgical pain (PPSP) remains a problem after knee replacement with some studies reporting up to 20% incidence. Pain is usually felt by those who do not operate to be a monolithic entity. All orthopaedic surgeons know that this is not the case. At its most basic level, pain can be divided into two categories, mechanical and non-mechanical.

Mechanical pain is like the pain of a fresh fracture. If the patient does not move, the pain is less. This type of pain is relieved by opiates. Mechanical pain is seen following knee replacement, but is becoming less frequent. It is caused by a combination of malrotations and maltranslations, often minor, which on their own would not produce problems. The combination of them, however, may produce a knee in which there is overload of the extensor mechanism or of the medial stabilizing structures. If these minor mechanical problems can be identified, then corrective surgery will help.

Non-mechanical pain is present on a constant basis. It is not significantly worsened by activities. Opiates may make the patient feel better, but they do not change the essential nature of the pain. Non-mechanical pain falls into three broad groups, infection, neuropathic and perceived pain. Infection pain is usually relieved by opiates. Since some of this pain is probably due to pressure, its inclusion in the non-mechanical pain group is questionable, but it is better left there so that the surgeon always considers it. Low grade chronic infection can be extremely difficult to diagnose. Loosening of noncemented knee components is so rare that when it is noted radiologically, infection should be very high on the list of suspicions. The name neuropathic pain suggests that we know much more about it than we do in reality. Causalgia or CRPS-type two is rare following knee replacement. CRPS-type one or reflex sympathetic dystrophy probably does exist, but it is probably over-diagnosed. The optimum treatment I have found is lumbar sympathetic blocks. Lyrica, Gabapentin and Cymbalta may also help. Perceived pain is the largest group. It does not matter what you tell the patient, some believe a new knee should be like a new car, i.e. you step into it and drive away. The fact that they have to work to make it work is horrifying. Perceived pain is widespread. The classic treatise, Dr. Ian McNabb's book “Backache”, should be studied by all who wish to understand pain complaints.

Any experienced knee surgeon will have his list of red flags or caveats. I will list only a few. If the patient comes in with a form asking for a disability pension on the first visit. If the patient's mother answers the questions. If the patient comes in taking massive doses of opiates. If the patient is referred to you by a surgeon who does more knee replacements than you do.

There are other issues such as good old fibromyalgia, which appears to have gone the way of the dodo. It has been replaced by something equally silly called central sensitization. The theory of central sensitization is that if one has pain somewhere or other for three months or six months or whatever, there are going to be changes in the brain and spinal cord. It then does not matter what happens to the original pain, i.e. whether or not it goes away, the pain will persist because of the changes in the brain, hence, the title of the pain in the brain syndrome. If this theory was correct, we might as well all go home because we have all been wasting our time for the last 30 years because none of our patients would get any better. After all, all of our patients have had pain for a lot longer than three months, many of them have been involved in trauma and sometimes, compensation is at issue. The pain in the brain theory, therefore, sounds about as realistic as the flat earth society or the treatment of Galileo.

Persistent post-surgical pain (PPSP) remains a problem after knee replacement with some studies reporting up to 20% incidence. At its most basic level, pain can be divided into two categories, mechanical and non-mechanical.

Mechanical pain is like the pain of a fresh fracture. If the patient does not move, the pain is less. This type of pain is relieved by opiates. Mechanical pain is seen following knee replacement, but is fortunately becoming less frequent. It is caused by a combination of malrotations and maltranslations, often minor, which on their own would not produce problems. The combination of them, however, may produce a knee in which there is overload of the extensor mechanism or of the medial stabilizing structures. If these minor mechanical problems can be identified, then corrective surgery will help.

Non-mechanical pain is present on a constant basis. It is not significantly worsened by activities. Opiates may make the patient feel better, but they do not change the essential nature of the pain. Non-mechanical pain falls into three broad groups, infection, neuropathic and perceived pain.

Infection pain is usually relieved by opiates. Since some of this pain is probably due to pressure, its inclusion in the non-mechanical pain group is questionable, but it is better left there so that the surgeon always considers it. Low grade chronic infection can be extremely difficult to diagnose. Loosening of noncemented knee components is so rare that when it is noted radiologically, infection should be very high on the list of suspicions.

The name neurogenic pain suggests that we know much more about it than we do in reality. Causalgia or CRPS-type two is rare following knee replacement. CRPS type one or reflex sympathetic dystrophy probably does exist, but it is probably over-diagnosed especially by the author of this abstract. The optimum treatment I have found is lumbar sympathetic blocks. Lyrica, Gabapentin and Cymbalta may also help.

Perceived pain is the largest group. It does not matter what you tell patient, some believe a new knee should be like a new car, i.e. you step into it and drive away. The fact that they have to work to make it work is horrifying. Some of this pain is actually mechanical, especially in those with no benefits such as hairstylists. Perceived pain is widespread. The classic treatment on this is Dr. Ian McNabb's book “Backache”. It should be studied by all orthopaedic surgeons, who wish to understand pain complaints.

There are other issues such as good old fibromyalgia, which appears to have gone the way of the dodo. It has been replaced by something equally silly called central sensitization. The theory of central sensitization is that if one has pain somewhere or other for three months or six months or whatever, there are going to be changes in the brain and spinal cord. It then does not matter what happens to the original pain, i.e. whether or not it goes away, the pain will persist because of the changes in the brain, hence, the title of the pain in the brain syndrome.

If this theory was correct, we might as well all go home because we have all been wasting our time for the last 30 years because none of our patients would get any better. After all, all of our patients have had pain for a lot longer than three months, many of them have been involved in trauma and sometimes, compensation is at issue. The pain in the brain theory, therefore, sounds about as realistic as the flat earth society or the treatment of Galileo.

There are two types of pain, mechanical and non-mechanical. Mechanical pain hurts with movement/use, is not constant and is helped by morphine-type products. Non-mechanical pain is different. It is present 24 hours a day, often worse at night, and except for the pain of infection, is not relieved by morphine-type products.

If the cause of mechanical pain can be determined, it can be corrected by an operation. The usual cause of postoperative mechanical knee pain nowadays is multifactorial, i.e. a combination of minor errors, none of which on their own would require revision.

Non-mechanical pain, other than infection, is much more difficult to handle. The commonest cause is not really a pain complaint, it is disappointment due to a failure of expectation. It does not matter how often you tell patients, some patients still think they should step in a drive away. A lot of these failures of expectations become much more realistic by the end of year one.

There are several other categories. Incipient osteoarthritis or sensitive people (The Princess and the Pea). If the pain complaints were severe with minimal arthritis, an operation is not likely to help.

The patient on disability for no clear reason is unlikely to get a good result and Workmen's Compensation Board and motor vehicle accident patients are also a very bad prognostic sign and will often produce the postoperative painful knee. Preoperative use of large doses of morphine is also a very bad sign. It is not clear if it is the morphine, which influences the patient or the patient, who influences the morphine.

There are several pain syndromes, some of which are purely psychiatric such as Conversion Disorders and Somatoform Pain Disorders. Treatment of purely psychiatric conditions should be a referral to a psychiatrist is in order.

Complex regional pain syndrome is an organic pain disorder. Type 2 is causalgia or an actual nerve injury. This is unusual following knee replacement other than the odd drop foot, which even after recovery, leaves an area of dysaethesia on the dorsum of the foot. Type 1 used to be called reflex sympathetic dystrophy. This is not uncommon after total knee replacement. I managed to collect more than 40 cases. One problem is that the diagnosis to some extent is a diagnosis of exclusion. If the diagnosis can be made, then treatment is available including Cymbalta, Lyrica or Gabapentin. I have found most success with lumbar sympathetic blocks, but it is difficult to find someone, who can do these. Some patients have been treated with implantable electrical spinal stimulators with variable results.

The current flavour of the month pain syndrome is called central sensitization. The theory is that if someone has pain for more than six months, then there will be changes in the brain, which will remain after the original pain goes away, hence, the title the pain in the brain syndrome. If this theory were correct, then we as arthroplasty surgeons have been collectively wasting our time for the last 40 years as no patient would have recovered. The likelihood, therefore, of this theory having any basis in reality is pretty remote.

Fortunately, by the end of year one, the vast majority of our knee replacement patients are reasonably content with the procedure.

Introduction and Objective. Malunion after trauma can lead to coronal plane malalignment in the lower limb. The mechanical hypothesis suggests that this alters the load distribution in the knee joint and that that this increased load may predispose to compartmental arthritis. This is generally accepted in the orthopaedic community and serves as the basis guiding deformity correction after malunion as well as congenital or insidious onset malalignment. Much of the literature surrounding the contribution of lower limb alignment to arthritis comes from cohort studies of incident osteoarthritis. There has been a causation dilemma perpetuated in a number of studies - suggesting malalignment does not contribute to, but is instead a consequence of, compartmental arthritis. In this investigation the relationship between compartmental (medial or lateral) arthritis and coronal plane malalignment (varus or valgus) in patients with post traumatic unilateral limb deformity was examined. This represents a specific niche cohort of patients in which worsened compartmental knee arthritis after extra-articular injury must rationally be attributed to malalignment. Materials and Methods. The picture archiving system was searched to identify all 1160 long leg x ray films available at a major metropolitan trauma center over a 12-year period. Images were screened for inclusion and exclusion criteria, namely patients >10 years after traumatic long bone fracture without contralateral injury or arthroplasty to give 39 cases. Alignment was measured according to established surgical standards on long leg films by 3 independent reviewers, and arthritis scores Osteoarthritis Research Society International (OARSI) and Kellegren-Lawrence (KL) were recorded independently for each compartment of both knees. Malalignment was defined conservatively as mechanical axis deviation outside of 0–20 mm medial from centre of the knee, to give 27 patients. Comparison of mean compartmental arthritis score was performed for patients with varus and valgus malalignment, using Analysis of Variance and linear regression. Results. In knees with varus malalignment there was a greater mean arthritis score in the medial compartment compared to the contralateral knee, with OARSI scores 5.69 vs 3.86 (0.32, 3.35 95% CI; p<0.05) and KL 2.92 vs 1.92 (0.38, 1.62; p<0.005). There was a similar trend in valgus knees for the lateral compartment OARSI 2.98 vs 1.84 (CI −0.16, 2.42; p=0.1) and KL 1.76 vs 1.31 (CI −0.12, 1.01; p=0.17), but the evidence was not conclusive. OARSI arthritis score was significantly associated with absolute MAD (0.7/10mm MAD, p<0.0005) and Time (0.6/decade, p=0.01) in a linear regression model. Conclusions. Malalignment in the coronal plane is correlated with worsened arthritis scores in the medial compartment for varus deformity and may similarly result in worsened lateral compartment arthritis in valgus knees. These findings support the mechanical hypothesis that arthritis may be related to altered stress distribution at the knee, larger studies may provide further conclusive evidence

The evolution of orthopedic implants has witnessed a great evolution and allowed insights into the various metals and alloys compatible with the human body. However, some recent reports have raised concerns regarding hypersensitivity to several metals used in orthopedic implants. These cases are mostly documented in the field of arthroplasty. Metal ion release following hip or knee arthroplasty is a known phenomenon and associated immune reactions to these metal ions have been implicated in the causation of these hypersensitivity reactions. These reactions frequently lead to poor outcome following these implant surgeries. We here present two rare cases of metal induced hypersensitivity reactions following orthopedic surgeries. We have also reviewed the literature in this context to look into the various causes of metal reactions, types of implant involved in hypersensitivity, methods of testing and management options in these cases

Introduction: Recent cadaveric studies have identified neovascularisation and neoneuralisation as probable mechanisms in the causation of discogenic pain. Calcium pyrophosphate deposits have been observed in discs in several studies. Their significance in the causation of discogenic pain is unclear. Direct correlation between the pain site and histological features can be verified by aware state endoscopic visualisation. Aim and Objectives: The study aims to examine and correlate the presence of neovascularisation, crystalline pyrophosphate deposits in the disc, and discogenic pain by spinal probing and discography under endoscopic visualisation. Material and Methods: Tissue removed from intervertebral discs of 224 patients during surgery was examined directly, and polarised microscopy was used to identify the presence of calcium pyrophosphate and neovascularisation. Their presence was correlated to diagnostic provocative findings of spinal probing and discography and intradiscal distortion during aware state endoscopy. Results: Calcium Pyrophosphate: Twenty out of 224 patients (9%) demonstrated calcium pyrophosphate in the discs. Fourteen had pain reproduced on probing or discography. Thirteen out of 20 patients (65%) had either an annular collection or leak at the index level. 6 had an extradiscal cause of pain. One hundred percent of the patients with annular collections or leaks had pain on spinal probing or discography. Sixteen patients with pyrophosphate deposits did not have neovascularisation. Neovascularisation: Thirty seven out of 224 patients (16.5%) showed neovascularisation in the disc. Four discs had crystalline pyrophosphate deposits. Thirty three out of 37 (90%) had pain on probing and/or discography. Out of four patients who had no pain on probing or discography, two had demonstrated tears during previous discographic procedures which were treated with laser annealing. These patients had disc bulges and compressive radiculopathy. Conclusion: The presence of pyrophosphate in the disc without a tear or leak does not directly render them tender to provocation. The presence of pyrophosphate is not correlated to neovascularisation. Annular tears or leaks are not directly correlated to the presence of pyrophosphates. There is a high correlation between pain provocation and neovascularisation

The medical model of history, examination and investigation forms the bedrock of diagnosis and management of all patients. The essence is the recognition of patterns of symptoms and signs. In the modern era there are an increasing number of non-medical resources ranging from web-based information, computer diagnostic aids and non-specialist healthcare professionals to provide a diagnosis and commence management of a wide range of conditions, including knee problems. We analysed the quality and patterns of clinical presentation in order to answer the question how closely clinical symptoms and examination findings correlate to diagnosis based on MRI scan and/or arthroscopic findings. The analysis was a dataset of a consecutive series of patients, aged 18 to 45, with no past history of knee problems or end stage arthritis, presenting to a single specialist triage physiotherapist, working within an integrated knee service, who fully completed a standardised knee assessment proforma of presenting symptoms and signs at a large district general hospital. The study comprises 86 patients and 98 knees. We analysed this data based on diagnostic findings of MRI scan or arthroscopy to provide definitive intra-articular diagnosis. Based on standard textbook descriptions of common presentations, we went on to define the patients' presentation history and examination as typical or atypical, with typical meaning the symptoms and signs correlated with the diagnosis. The null hypothesis is that patients have a high chance of typical presentations for common knee conditions. In the 75% of patients with a significant intra-articular pathology we found the majority had chondral rather than meniscal tears 1.7 to 1. Forty four percent of patients had atypical symptoms and 71% had atypical clinical signs, 30% and only 26% of the cohort had both typical symptoms and signs together, reflecting a surprisingly low positive predictive probability of symptoms and signs in this group of patients, particularly those with chondral lesions which was 44%. In this cohort, 57% of the cohort has 3 or more multiple diagnoses. In the diagnostically normal group, 43% had symptoms and signs typical for a meniscal tear. We conclude that clinical symptoms and signs surprisingly inaccurate in guiding intra-articular pathology within the knee, even in a sub-set considered the easy and accurate to assess. The number of multiple diagnoses and the incidence of false positive results also means that simplistic interpretations of non-definitive diagnoses and linear causation of pain pathways should be treated cautiously

Aims

The Chopart joint complex is a joint between the midfoot and hindfoot. The static and dynamic support system of the joint is critical for maintaining the medial longitudinal arch of the foot. Any dysfunction leads to progressive collapsing flatfoot deformity (PCFD). Often, the tibialis posterior is the primary cause; however, contrary views have also been expressed. The present investigation intends to explore the comprehensive anatomy of the support system of the Chopart joint complex to gain insight into the cause of PCFD.

Objectives. A successful outcome following treatment of nonunion requires the correct identification of all of the underlying cause(s) and addressing them appropriately. The aim of this study was to assess the distribution and frequency of causative factors in a consecutive cohort of nonunion patients in order to optimise the management strategy for individual patients presenting with nonunion. Methods. Causes of the nonunion were divided into four categories: mechanical; infection; dead bone with a gap; and host. Prospective and retrospective data of 100 consecutive patients who had undergone surgery for long bone fracture nonunion were analysed. Results. A total of 31% of patients had a single attributable cause, 55% had two causes, 14% had three causes and 1% had all four. Of those (31%) with only a single attributable cause, half were due to a mechanical factor and a quarter had dead bone with a gap. Mechanical causation was found in 59% of all patients, dead bone and a gap was present in 47%, host factors in 43% and infection was a causative factor in 38% of patients. In all, three of 58 patients (5%) thought to be aseptic and two of nine (22%) suspected of possible infection were found to be infected. A total of 100% of previously treated patients no longer considered to have ongoing infection, had multiple positive microbiology results. Conclusion. Two thirds of patients had multiple contributing factors for their nonunion and 5% had entirely unexpected infection. This study highlights the importance of identifying all of the aetiological factors and routinely testing tissue for infection in treating nonunion. It raises key points regarding the inadequacy of a purely radiographic nonunion classification system and the variety of different definitions for atrophic nonunion in the current mainstream classifications used for nonunion. Cite this article: L. Mills, J. Tsang, G. Hopper, G. Keenan, A. H. R. W. Simpson. The multifactorial aetiology of fracture nonunion and the importance of searching for latent infection. Bone Joint Res 2016;5:512–519. DOI: 10.1302/2046-3758.510.BJR-2016-0138

Aims

The underlying natural history of suspected scaphoid fractures (SSFs) is unclear and assumed poor. There is an urgent requirement to develop the literature around SSFs to quantify the actual prevalence of intervention following SSF. Defining the risk of intervention following SSF may influence the need for widespread surveillance and screening of SSF injuries, and could influence medicolegal actions around missed scaphoid fractures.

Aims

The aims of this study were to describe the demographic, socioeconomic, and educational factors associated with core surgical trainees (CSTs) who apply to and receive offers for higher surgical training (ST3) posts in Trauma & Orthopaedics (T&O).

Aims

The volume of ambulatory total hip arthroplasty (THA) procedures is increasing due to the emphasis on value-based care. The purpose of the study is to identify the causes for failed same-day discharge (SDD) and perioperative factors leading to failed SDD.

The purpose of our study is to assess the degenerative changes in the motion segments above a L5S1 spondylolytic spondylolisthesis, and to analyse the factors that contribute towards a retro-listhesis in the segment immediately above the slip. Prospective radiographic case series. 38 patients with a symptomatic L5S1 spondylolytic spondylolisthesis, with a mean age of 52.8 yrs (95% CI 47.2 – 58.4). 55.3% (n = 21) were females and 44.7% (n = 17) males. 58% (22) had grade 1 and 42% (16) grade 2 slips. Plain radiographs: Lumbar lordosis, slip angle, sacral slope, grade of the slip, and retro-listhesis at L45. MRI scans: facet angles at L34 and L45, facet degenerative score at L34 and L45 (cartilage and sclerosis), disc degenerative score at L45 and L5S1 (Pfirrmann). The Pfirmann disc score for L45 was 2.75 and L5S1 4.4 (p < 0.0001); the mean facet angle at L34 50.9° and L45 57.9° (p = 0.001) and the facet score at L34 was 8 and at L45 was 10.5 (p = 0.0001). 29% (11) demonstrated a retrolithesis at L45. Analysing the effect of these factors on the causation of retro-listhesis at L45 (table) the slip angle and L45 disc degenerative score were the only factors that predicted a retro-listhesis. There is a cascade of degenerative changes involving both the disc and the facet joints at the levels above a spondylolytic spondylolisthesis. The degenerative changes at the L45 disc and a higher slip angle predict a retro-listhesis at the level above the slip

Slipped Capital Femoral Epiphysis (SCFE) is a common paediatric disorder with documented racial predilection. No data exists regarding the Australian indigenous and Australian non-indigenous populations. This study provides a comprehensive demographic and epidemiologic analysis of SCFE in South Australia, with emphasis on establishing associations between increasing obesity and incidence. A demographic review of all cases of SCFE managed in South Australian public hospitals between 1988 and 2007 was performed. Clinical presentation, surgical management and complication profile information was collected. Given that obesity is implicated in the biomechanical causation of SCFE due to increased shearing forces, particular emphasis was placed on gathering weight, race, gender and age data. A profile of the incidence and nature of SCFE was generated. Comparisons were then drawn between this profile and existing epidemiologic percentile data of weight, age and gender in South Australia. A rising prevalence of obesity in South Australia corresponded with a rising incidence of SCFE. However, this relationship was not linear as the incidence of SCFE has doubled in the last 20 years and the average weight of SCFE patients has increased markedly. The indigenous population was found to have higher rates of obesity than the non- indigenous population in South Australia. The indigenous population also has a relative risk of developing a SCFE of over three times the non-indigenous population. The overall rate of complications in South Australian public hospitals was low, with avascular necrosis being recognised in our profile. The rise in incidence of SCFE in South Australia; especially noticeable in the indigenous population is associated with an increasing prevalence of obesity. The considerable morbidity associated with SCFE was confirmed in our analysis and further highlights the importance of public health initiatives to tackle obesity in our community

Introduction. Reaming of the canal is an important step in the debridement phase of treating intramedullary infections. Numerous techniques of radical canal debridement have been successfully reported. The use of the Reamer-Irrigation-Aspiration system (RIA-Synthes) is currently expanding to include this clinical scenario. Materials and methods. Prospective collection of data related to infected cases treated with the use of the RIA in a tertiary referral centre referring to a 3 year period. Peri-operative details, microbiology results, and follow-up outcome over a minimum period of 12 months post-surgery are reported. Results. Twenty patients (13 men), with average age 44.8 years (18–75), suffering from 7 tibial and 13 femoral infections represent the study cohort. There were 19 surgical-site-infections, and 1 spontaneous haematogenous infection in non-previously operated extremity. The canal was stabilised using an antibiotic-loaded-cement-nail in 18 cases. The antibiotic nail was subsequently removed after 6–8 weeks. The most commonly isolated organism was staphylococcus aureus. There were followed-up regularly (2,6, 12 weeks, and then at 6 months and 12, 24, 36 months). At 6 months follow up (range 12–43 months) no recurrence was observed. Two patients died during the course of the study. One patient at the day after surgery due to septic shock, and another one at 2 years due to irrelevant causation. Another patient had a below knee amputation after debriding of the canal for pan-medullary osteomyelitis. However, there was no recurrence in the stump at the latest follow up after 1 year. Conclusion. The usage of this new device shows promising results in the treatment of intramedullary osteomyelitis. Reaming under simultaneous irrigation and suction appears to be an effective and safe alternative for debridement of the intra medullary infections of femur and tibia. Long term follow up is essential, as post traumatic osteomyelitis can occur at any time after surgical treatment although the majority of recurrences are seen within 2 years

Cerebral micro emboli have been noted to occur during both total hip and knee arthroplasty. These micro emboli have been implicated in the causation of postoperative cognitive impairment. The aim of this study was to determine whether cerebral micro emboli occur during hip fracture surgery. 28 patients undergoing hip fracture surgery had transcranial doppler assessment of the middle cerebral artery to detect cerebral micro emboli. Micro embolic signals (MESs) were recorded during the operative procedure. Successful monitoring was carried out in 26 patients. MES were recorded in 16 out of 26 patients. 12 out of 16 patients who had MESs had undergone a cemented hemiarthroplasty; the remainder had a sliding hip screw for an extracapsular hip fracture. 75% (9/12) of patients who had a cemented hemiarthroplasty had the majority of MESs after reaming and cementing. MESs in the patients who had a sliding hip screw occurred throughout the operative procedure. Conclusion: Cerebral micro emboli do occur during hip fracture surgery. These emboli may be responsible for the cognitive dysfunction that occurs in this susceptible group of patients

Purpose: Subacromial impingement syndrome is a painful condition which occurs during overhead activities as the rotator cuff is compressed between the greater tuberosity and the acromion. Unrecognized secondary causes of impingement syndrome may lead to treatment failure. Posterior capsular tightness, believed to alter shoulder joint kinematics, is often cited as a secondary cause but scientific evidence is lacking. The objective of this study was to evaluate the effect of posterior capsular tightness on pressure in the subacromial space. Method: Ten fresh-frozen cadaver shoulder specimens were mounted on a custom testing apparatus. With the scapula fixed, the deltoid and cuff muscles were loaded statically with a constant ratio to elevate the humerus in the scapular plane under physiologic loading conditions. For each treatment (intact capsule, 1cm and 2cm plication), pressure in the subacromial space and glenohumeral kinematics were recorded during elevation. The treatment order was randomly assigned to each specimen. Peak pressure and translation of the humeral head center were compared using a repeated measures ANOVA. Results: Peak subacromial pressures (mean±sd) were similar between treatment groups: 345±152 kPa, 410±213 kPa and 330±164 kPa for the intact, 1cm and 2cm plication respectively (p> 0.05). No significant differences were found for superior or antero-posterior translations of the humeral head at the peak pressure position (p> 0.05). Conclusion: Posterior capsular tightness, as a sole variable, did not contribute significantly to increased pressure in the subacromial space or to increased anterior or superior humeral head translation during abduction. Clinically, posterior capsular tightness may occur in association with impingement syndrome but may not play a significant role in causation