Treatment of chronic, stable slipped capital femoral epiphysis via surgical hip dislocation with combined osteochondroplasty and Imhauser osteotomy.

PURPOSE: Treatment of slipped capital femoral epiphysis (SCFE), including the modified Dunn procedure, restores anatomy with significant risk for avascular necrosis (AVN), if performed in the setting of moderate to severe, stable SCFE. The Imhauser osteotomy has been shown to be an effective way to correct residual deformity without the risk of AVN. We sought to evaluate the effectiveness and safety of a combined Imhauser osteotomy and osteochondroplasty, performed via a surgical hip dislocation approach for the acute and delayed treatment of stable SCFE. METHODS: A retrospective review was performed on a series of patients who underwent Imhauser osteotomy and osteochondroplasty via surgical hip dislocation for treatment of chronic, stable SCFE. Patients were divided into acute or delayed treatment groups based on whether osteotomy was performed as the initial slip treatment. RESULTS: In total 19 patients (15 male, four female, average age 13.7 years) were reviewed. Six osteotomies were performed acutely in combination with in situ pinning, 13 were delayed at least six months after in situ pinning (average 21.7 months). Two hips had labral tears that required repair. The mean follow-up was 61 months (23 to 120) (delayed) and 53 months (27 to 61) (acute). The average improvement in slip angle was 40.7° (delayed) and 50.2° (acute) (p = 0.0916), final post-operative slip angle averaged 15.8° (delayed) and 17.8° (acute) (p = 0.544). Femoral neck length and greater trochanteric height were similar between both groups. Average alpha angle at final follow-up measured 55.8° (delayed) and 60.8° (acute) (p = 0.542). No cases of AVN were identified. CONCLUSION: Imhauser osteotomy combined with osteochondroplasty via surgical hip dislocation approach is a safe and effective treatment of moderate to severe, stable SCFE performed in both the acute and delayed setting.

Estimates of injury risks for healthcare personnel working night shifts and long hours.

BACKGROUND: Evidence suggests that working long hours or unconventional shifts (night, evening and rotating shifts) can induce fatigue and stress in healthcare employees that might jeopardise quality of care and patient safety. METHODS: This study is based on a retrospective analysis of 13 years of occupational data from the National Longitudinal Survey of Youth, covering nearly 11,000 American workers. During the study period, 545 injuries were reported by employees in healthcare professions. Cox proportional hazard analyses were used to calculate adjusted hazard ratios comparing the risk of a job-related injury among healthcare workers in various types of demanding schedules to employees working conventional schedules. The analyses were stratified to estimate risks within different occupational classifications and care settings. RESULTS: The greatest injury risks to healthcare workers were in schedules involving overtime or at least 60 h per week. Interestingly, an elevated risk of injury was not observed for healthcare employees working 12 or more hours per day or for those in night, evening or rotating shifts. Among employees working overtime and long-hour (>60 h per week) schedules, those at medical provider offices had a significantly higher risk of injury (HR 2.86) than at hospitals, rehabilitation clinics or long-term care facilities. Support personnel, including aids, attendants, technicians, therapists and dieticians, faced a higher risk of injury than did physicians and nurses. CONCLUSION: Healthcare managers responsible for quality improvement and patient safety programmes should be aware of the possibility for worker fatigue and injury in particular scheduling arrangements.

The impact of overtime and long work hours on occupational injuries and illnesses: new evidence from the United States.

AIMS: To analyse the impact of overtime and extended working hours on the risk of occupational injuries and illnesses among a nationally representative sample of working adults from the United States. METHODS: Responses from 10,793 Americans participating in the National Longitudinal Survey of Youth (NLSY) were used to evaluate workers' job histories, work schedules, and occurrence of occupational injury and illness between 1987 and 2000. A total of 110,236 job records were analysed, encompassing 89,729 person-years of accumulated working time. Aggregated incidence rates in each of five exposure categories were calculated for each NLSY survey period. Multivariate analytical techniques were used to estimate the relative risk of long working hours per day, extended hours per week, long commute times, and overtime schedules on reporting a work related injury or illness, after adjusting for age, gender, occupation, industry, and region. RESULTS: After adjusting for those factors, working in jobs with overtime schedules was associated with a 61% higher injury hazard rate compared to jobs without overtime. Working at least 12 hours per day was associated with a 37% increased hazard rate and working at least 60 hours per week was associated with a 23% increased hazard rate. A strong dose-response effect was observed, with the injury rate (per 100 accumulated worker-years in a particular schedule) increasing in correspondence to the number of hours per day (or per week) in the workers' customary schedule. CONCLUSIONS: Results suggest that job schedules with long working hours are not more risky merely because they are concentrated in inherently hazardous industries or occupations, or because people working long hours spend more total time "at risk" for a work injury. Strategies to prevent work injuries should consider changes in scheduling practices, job redesign, and health protection programmes for people working in jobs involving overtime and extended hours.

Neurotoxin quinolinic acid is selectively elevated in spinal cords of rats with experimental allergic encephalomyelitis.

Experimental allergic encephalomyelitis (EAE) is an autoimmune, animal model of multiple sclerosis (MS) in which demyelination and paralysis are evident. Quinolinic acid (QUIN) is a neurotoxin and endogenous N-methyl-D-aspartate receptor agonist formed from tryptophan. The role of neurotoxins in general and QUIN in particular in EAE or MS is unknown. Lewis rats inoculated with myelin basic protein developed signs of EAE by day 12, were killed, and their tissues assayed for QUIN by gas chromatography with mass spectrometry. QUIN levels were significantly elevated in the more caudal regions of the spinal cords of animals with EAE. Brain, serum, and liver levels of QUIN were not altered. In a similar manner, QUIN in mylin basic protein-injected, asymptomatic animals was not different from control animals. The time course for QUIN was similar to the neurological signs of the disorder; however, the initial elevation in QUIN occurred before the appearance of behavioral signs. Last, treatment with the glucocorticoid dexamethasone prevented both the signs of EAE and the elevation in spinal cord QUIN. It is not known whether QUIN contributes to the paralysis in EAE. However, if QUIN is pathogenic in EAE this finding could have therapeutic implications for MS.

A radiometric assay for kynurenine 3-hydroxylase based on the release of 3H2O during hydroxylation of L-[3,5-3H]kynurenine.

A rapid and sensitive assay for kynurenine 3-hydroxylase (KH) has been developed. This radiometric assay is based on the enzymatic synthesis of tritiated water from L-[3,5-3H]kynurenine during the hydroxylation reaction. Radiolabeled water is quantified following selective adsorption of the isotopic substrate and its metabolite with activated charcoal. The assay is suitable for detecting 0.1 pmol enzyme activity per minute per milligram protein in tissues displaying low levels of the enzyme. The amount of water produced in the reaction, as calculated from the tritium released, was stoichiometric with the 3-hydroxykynurenine product detected by HPLC. Rat liver KH was characterized by cofactor specificity and kinetic parameters. NADPH was preferred over NADH as coreductant in the reaction. Tetrahydrobiopterin was not a cofactor. The tissue distribution of KH activity in the rat suggested that the majority of active enzyme is located in liver and kidney. Detectable amounts were found in several other tissues, including brain which had low but significant levels of activity in every region assayed.

Different pharmacological anatomy in the paraventricular hypothalamic nucleus, supraoptic nucleus, and suprachiasmatic nucleus of rats: quantitative autoradiography on angiotensin II receptor binding sites.

Angiotensin II (AII) and vasopressin (VP) play important roles in cardiovascular function. Using 125I-[Sar1,Ile8]-angiotensin II (125I-SI-AII), a potent AII antagonist, AII receptor binding sites were autoradiographically localized in three VP-producing areas of the hypothalamus and compared in hypertensive and normotensive rats. Within three major VP-producing areas, AII receptor binding was highest in the paraventricular hypothalamic nucleus and lowest in the supraoptic nucleus, suggesting that a differential AII regulation of separate VP systems exists in the brainstem. No statistical difference in 125I-SI-AII receptor binding was found between WKY and SHR rats in each of the three major VP-producing nuclei studied. These results are consistent with a role of AII receptors in a subtle and complicated regulation of VP in cardiovascular function.

High-performance liquid chromatographic analysis of 'specifically bound' label after [125I]angiotensin II binding to rat brain membranes.

The combined hypothalamus-thalamus-septum and anteroventral third ventricular region (HTSA) of the rat was examined for [125I]angiotensin II ([125I]AII) binding using two protocols: one that preserved synaptosomal structure and a second that did not. Although maximum binding (Bmax) and dissociation constants (Kd) were similar in both preparations, high-performance liquid chromatographic analyses revealed that [125I]AII made up the majority of specifically bound label in the synaptosome preserved preparation while [125I]tyrosine ([125I]Tyr) represented most of the specifically bound label in the disrupted preparation. These results indicate that [125I]Tyr accumulation occurred subsequent to binding and degradation of [125I]AII and are consistent with the notion that rapid internalization of the receptor-[125I]AII complex occurs in those preparations where the synaptosomal structure remains intact.