Satisfaction and functional outcome with "self-care" for the management of fifth metacarpal fractures.

BACKGROUND: Fifth metacarpal fractures are common and comprise a significant proportion of traditional orthopaedic fracture clinic workload. We reviewed the functional outcome and the satisfaction of patients managed with a new protocol that promoted "self-care" and resulted in the discharge of most of these patients from the emergency department with no further follow-up. METHODS: A retrospective study was performed of patients discharged with a fifth metacarpal fracture between April 2012 to October 2012. A postal questionnaire was sent to each patient, followed by a telephone call. Patient-reported outcome measures (EQ-5D, QuickDASH) and patient satisfaction were assessed. Of the 167 patients eligible for the study, 5 were excluded. Of the remaining 162, 64 were uncontactable or declined to participate. The mean follow-up time was 21.6 months (SD 1.9, range 18.1 to 24.7). RESULTS: The median EQ-5D health index score was 0.87 (IQR 0.74 to 1.00), and the median QuickDASH score was 2.3 (IQR 0 to 6.8). Seventy-nine (80.6 %) patients were satisfied with the outcome of their injury, while 83 (84.9 %) reported being satisfied with the process. There was no difference between those with a fracture or those without a fracture in EQ-5D (p = 0.307) or QuickDASH (p = 0.820). CONCLUSION: Fifth metacarpal fractures can be managed effectively through an Emergency Department protocol without any formal orthopaedic follow-up. This pathway lead to excellent patient-reported outcome measures and patient satisfaction. This protocol has reduced unnecessary hospital attendances for patients and increased the time available for clinicians to deal with more challenging injuries.

Influence of skin incision position on physiological and biochemical changes in tissue after primary total knee replacement - a prospective randomised controlled trial.

BACKGROUND: Influence of skin incision position on physiological and biochemical changes in tissue after primary total knee replacement. A prospective randomised controlled trial. The blood supply to the skin covering the anterior knee has been shown to arise predominantly from blood vessels on the medial side of the knee. Skin incisions for primary Total Knee Replacement (TKR) positioned medially therefore risk creating a large lateral skin flap that may be poorly perfused. Poorly perfused skin is likely to result in hypoxia at the wound edges and consequently may lead to delayed wound healing and complications. METHODS: We have carried out a randomised controlled trial (n = 20) to compare blood flow on both the medial and lateral sides of two commonly used skin incisions in TKR (midline and paramedian). We have also assessed interstitial biochemistry (glucose, pyruvate and lactate levels) in the presumed at risk lateral skin flap of both incision types. RESULTS: In both incision types tissue hyper-perfusion occurs post-operatively and is maintained for at least 3 days. We found no significant difference between blood flow between the two incision types on the medial side of the incision at either day 1 (p = 0.885) or day 3 post-op (p = 0.269), or, on the lateral side of the incision (p = 0.885 at day 1, p = 0.532 at day 3). Glucose levels are maintained post-operatively in the at risk lateral flap with only minimal changes. Lactate levels rise post-operatively and remain elevated for at least 24 hours. However, the levels did not reach levels suggestive of critical ischaemia in either incision group and no significant difference was observed between incision types. CONCLUSION: We conclude that the use of a paramedian incision results in only minimal biochemical changes, which are unlikely to alter wound healing. TRIAL REGISTRATIONS: ISRCTN06592799 .

Electromagnetic navigation in total knee arthroplasty-a single center, randomized, single-blind study comparing the results with conventional techniques.

We report on the results of a randomized study (n=200) to compare total knee arthroplasty performed using conventional instrumentation or electromagnetic computer assisted surgical technique. 92% of navigated and 85% of conventional knees were implanted within ±3° from neutral mechanical alignment; there was no statistically significant difference between these proportions. There was also no difference in femoral or tibial rotation assessed by CT scan. At 1year follow up there was no statistical difference between the two groups in American Knee Society Score, Oxford Knee Scores, patient satisfaction, quality of life, hospital length of stay, complication rates or other adverse events. Tourniquet time in the navigated group was longer. Proving value for navigation in total knee arthroplasty surgery remains a challenge.

Functional outcome and satisfaction with a "self-care" protocol for the management of mallet finger injuries: a case-series.

BACKGROUND: Mallet finger injuries are usually successfully treated non-operatively with a splint. Most patients are reviewed at least twice in a clinic after the initial presentation in A&E. A new protocol promoting "self-care" was introduced at our institution. Patients were provided with structured verbal and written information, and given access to a telephone helpline. METHODS: A prospective electronic patient record was used to identify all patients who presented to the emergency department with a mallet finger with a minimum six month follow-up. A satisfaction and patient reported outcome measure was administered via a postal questionnaire. The response rate was 36/47 (77%). RESULTS: The median QuickDASH score was 2.3 (IQR 0 to 4.6). All patients were satisfied with the treatment plan provided. Nine used the helpline and all were satisfied with information given. Although 13 patients reported some extensor lag, or bump, they had no functional limitation. Seven patients were reviewed by the general practitioner or other clinicians during their treatment period for issues such a skin care, splint size changes or sickness certification. Five were subsequently reviewed at the end of their treatment period in a clinic at their request, or their general practitioner, but did not require further surgical intervention. CONCLUSIONS: Self-care for mallet finger injuries, with adequate patient information and telephone back-up, leads to acceptable functional results and satisfaction. LEVEL OF EVIDENCE: III.

Predisposition to accelerated Alzheimer-related changes in the brains of human immunodeficiency virus negative opiate abusers.

Cognitive impairment is a recognized effect of drug misuse, including the use of opiates. The pathological basis for this is unknown but the temporal and frontal cortices have been implicated. We have shown previously that deposits of hyperphosphorylated tau in drug user brains exceed those seen in age-matched controls. The present quantitative study of hyperphosphorylated tau and beta amyloid in drug user brains allows comparison with the related pathology in Alzheimer's disease. Brains were obtained from the Edinburgh Medical Research Council Brain Banks, comprising 39 human immunodeficiency virus negative drug users, five subjects with Alzheimer's disease and 37 age-matched, cognitively normal controls, all legally and ethically approved for research. Hyperphosphorylated tau positive (AT8, AT100) neuropil threads were significantly increased in the frontal and temporal cortex, and in the locus coeruleus, of drug users aged > 30 years (all P = 0.04). Under the age of 30 years, drug users showed a similar increase in neuropil threads compared with controls, but this reached significance only in the frontal cortex (P = 0.03). Immunopositivity for both three- and four-repeat tau was present in drug user brains. There was a direct relationship between the numbers of neuropil threads and of neurofibrillary tangles: neurofibrillary tangles were sparse in brains that had neuropil thread counts below 200 cm(2). Hyperphosphorylated tau positive neuropil threads increased at a faster rate in drug users than in controls and the levels of the phosphorylating enzyme, GSK-3, was raised in drug user brains. Beta amyloid (AB4, AB42 and 4G8) was raised in drug user brains (mainly as shadow plaques) but not significantly different from controls and there was no correlation between high beta amyloid and hyperphosphorylated tau in individual cases. Hyperphosphorylated tau levels correlated significantly (P = 0.038) with microglial activation in drug users but not in controls. The levels of hyperphosphorylated tau in drug users fell far short of those seen in Alzheimer's disease but overlapped with those in elderly controls. We conclude that drug users show early Alzheimer's disease-related brain pathology that may be the basis for cognitive impairment and that neuroinflammation is an early accompanying feature. This provides an opportunity to study the pathogenesis of tau pathology in the human brain.

Impact of HIV on regional & cellular organisation of the brain.

There are many excellent reviews of HIV infection of the nervous system. However these all assume that the reader has a working knowledge of the structure and cellular architecture of the brain. It may be that specialised brain vocabulary represents an unwelcome hurdle for those scientists with expert knowledge of the effects of HIV in other cell systems and who wish to extend that interest to the brain. This review provides an introduction to the component structures and cells of the brain and an overview of their involvement in HIV/AIDS. HIV infection leads to death through its capacity to progressively devastate the immune system. Current anti-HIV therapy has achieved considerable success in halting and partially reversing this process. In the absence of treatment, the breakdown of immunity is marked by declining CD4 counts and increasing vulnerability to opportunistic infections. In parallel with these effects on the lymphoid system, the nervous system is frequently the site of an initially stealthy infection which leads ultimately to symptomatic disease in a significant proportion of HIV infected individuals. The most feared manifestation of central nervous system (CNS) involvement is dementia. Unfortunately, serial CD4 counts and measurement of blood viral load do not serve to identify or monitor early infection of brain tissue. Since effective anti-HIV therapy has not achieved eradication of virus from lymphoid tissues, and anti-HIV drugs do not enter the nervous system easily, it is hardly surprising that HIV infection of the nervous system continues to cause clinical problems. Even in treatment-compliant patients, a measurable degree of cognitive impairment may develop, signalling previous or present HIV-related brain injury. The cause of HIV associated dementia and cognitive disability remains poorly understood. Perhaps most significantly, the long-term consequences of clinically occult brain infection are unknown and will require further investigation.

Accelerated Tau deposition in the brains of individuals infected with human immunodeficiency virus-1 before and after the advent of highly active anti-retroviral therapy.

This study aims to investigate the influence of human immunodeficiency virus (HIV) infection on the neurodegenerative processes normally associated with ageing. We have looked for evidence of beta amyloid and hyperphosphorylated Tau deposition in HIV-infected subjects before and after the advent of highly active anti-retroviral therapy (HAART). In addition we have looked for evidence of axonal damage. We have compared these HIV-positive cases with age-matched controls and with older non-demented controls. We find no evidence of significant premature beta amyloid deposition in HIV-infected cases; however, we do observe elevated levels of hyperphosphorylated Tau in the hippocampus of many HIV-infected subjects, compared with age-matched controls. The greatest levels of hyperphosphorylated Tau are noted in HAART-treated subjects. Axonal damage marked by expression of beta amyloid pre-cursor protein (BAPP) was highly variable in all groups including control subjects. We surmise that HIV infection and/or the use of anti-retroviral therapy may predispose to accelerated neuroageing in the form of hyperphosphorylated Tau deposition in the hippocampus. Within the age groups studied these significant neuropathological changes remained subclinical and were not yet associated with cognitive impairment.

Neurobiology of multiple insults: HIV-1-associated brain disorders in those who use illicit drugs.

Despite two decades of research, certain aspects of HIV-related central nervous system (CNS) disease remain poorly understood. HIV targets microglia and macrophages within the CNS and enters the brain compartment early. However, HIV is there held in check apparently until the onset of significant immune compromise, when viral replication, microglial activation, neuronal damage, and cognitive impairment are likely to ensue. Illicit drug abuse continues to be a significant risk factor for HIV transmission worldwide. Whether HIV-related CNS disease is more prevalent or more severe in this risk group has long been debated. Drugs of abuse can of themselves cause immune suppression, blood-brain barrier breakdown, microglial activation, and neuronal injury. This review presents evidence that HIV associated CNS disorders are indeed accentuated in drug abusers. However, the advent of effective therapy has added a new dimension, which must be taken into consideration. Treated individuals are surviving much longer and HIV encephalitis and HIV-associated dementia have become much less common. However, more subtle forms of CNS damage are emerging. Examination of the brains of individuals who have been treated long term with highly active antiretroviral therapy (HAART) reveals a surprising degree of microglial activation, comparable at times to that seen formerly in milder cases of HIV encephalitis. In addition, these individuals show evidence of increased deposition of neurodegenerative proteins, particularly hyperphosphorylated tau. Similar observations have been made in young opiate abusers who are HIV negative. Taken together, these results suggest that neuroinflammation and neurodegeneration, which are clinically silent at present, may cause problems in the future in HAART-treated subjects.

Effects of human immunodeficiency virus encephalitis and drug abuse on the B lymphocyte population of the brain.

We aimed to assess the effects of human immunodeficiency virus (HIV) encephalitis (HIVE) on the B-lymphocyte population of the brain. We also tested the effects of intravenous opiate drug abuse because this is a major risk factor for infection, with known immunosuppressive properties. Immunohistochemistry was used to identify B lymphocytes in the brains of clinically well-characterized HIV-negative drug abusers, individuals with HIVE, and, for comparison, HIV-negative individuals with encephalitis. Perivascular and parenchymal B lymphocytes were studied in 11 regions of each brain. We found that despite a small apparent rise, the abuse of opiate drugs had no significant effect on the B-lymphocyte population of the brain. Individuals with HIVE were found to have a greater number of B lymphocytes in brain tissue than individuals with acquired immunodeficiency syndrome (AIDS) who had no central nervous system (CNS) pathology. However, in comparison to nonimmunocompromised individuals with encephalitis, the B-lymphocyte population of HIVE brains was greatly reduced. We suggest that this latter finding may be linked to declining CD4 T-lymphocyte levels in end-stage AIDS, and that CD4 T lymphocytes may be required for efficient entry of B lymphocytes to the CNS. The brain B-lymphocyte population correlated well with CD4 T-lymphocyte level in the blood, in cases with viral encephalitis. These findings suggest that systemic immune competence is required to mount a full B-lymphocyte response to viral CNS infections. Furthermore, we suggest that CD4 T lymphocytes may play a key role in the humoral immune response to viral infection of the brain.