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Trigger finger is a common condition affecting the hand. Therapeutic variability surrounds the management of trigger finger, especially in the mild cases. The aim of this study was to survey secondary care surgeons to describe the current management of trigger fingers. The steering group developed a survey for hand surgeons. Following piloting, the survey was distributed to hand surgeons in the United Kingdom and The Netherlands. A total of 713 plastic surgeons and orthopaedic surgeons were invited to participate in the online survey and 440 (62%) surgeons completed the survey. In both mild and moderate cases of trigger finger, steroid injection was the preferred treatment option. Open surgery was the treatment of choice for severe cases. However, there was variation in delivery of care, including type and dosage of steroid, site of injection, interval between injections, maximum number of injections, type of incision and treatment of patients with diabetes or rheumatoid arthritis. This highlights the need for a better evidence base for the treatment of trigger fingers.

Background Numerous pathologies result in multiple-organ failure, which is thought to be a direct consequence of compromised cellular bioenergetic status. Neither the nature of this phenotype nor its relevance to survival are well understood, limiting the efficacy of modern life-support. Methods To explore the hypothesis that survival from critical illness relates to changes in cellular bioenergetics, we combined assessment of mitochondrial respiration with metabolomic, lipidomic and redox profiling in skeletal muscle and blood, at multiple timepoints, in 21 critically ill patients and 12 reference patients. Results We demonstrate an end-organ cellular phenotype in critical illness, characterized by preserved total energetic capacity, greater coupling efficiency and selectively lower capacity for complex I and fatty acid oxidation (FAO)-supported respiration in skeletal muscle, compared to health. In survivors, complex I capacity at 48 h was 27% lower than in non-survivors (p = 0.01), but tended to increase by day 7, with no such recovery observed in non-survivors. By day 7, survivors’ FAO enzyme activity was double that of non-survivors (p = 0.048), in whom plasma triacylglycerol accumulated. Increases in both cellular oxidative stress and reductive drive were evident in early critical illness compared to health. Initially, non-survivors demonstrated greater plasma total antioxidant capacity but ultimately higher lipid peroxidation compared to survivors. These alterations were mirrored by greater levels of circulating total free thiol and nitrosated species, consistent with greater reductive stress and vascular inflammation, in non-survivors compared to survivors. In contrast, no clear differences in systemic inflammatory markers were observed between the two groups. Conclusion Critical illness is associated with rapid, specific and coordinated alterations in the cellular respiratory machinery, intermediary metabolism and redox response, with different trajectories in survivors and non-survivors. Unravelling the cellular and molecular foundation of human resilience may enable the development of more effective life-support strategies., Graphical abstract Image 1

The syndrome of critical illness is a complex physiological stressor that can be triggered by diverse pathologies. It is widely believed that organ dysfunction and death result from bioenergetic failure caused by inadequate cellular oxygen supply. Teleologically, life has evolved to survive in the face of stressors by undergoing a suite of adaptive changes. Adaptation not only comprises alterations in systemic physiology but also involves molecular reprogramming within cells. The concept of cellular adaptation in critically ill patients is a matter of contention in part because medical interventions mask underlying physiology, creating the artificial construct of “chronic critical illness,” without which death would be imminent. Thus far, the intensive care armamentarium has not targeted cellular metabolism to preserve a temporary equilibrium but instead attempts to normalize global oxygen and substrate delivery. Here, we review adaptations to hypoxia that have been demonstrated in cellular models and in human conditions associated with hypoxia, including the hypobaric hypoxia of high altitude, the intrauterine low-oxygen environment, and adult myocardial hibernation. Common features include upregulation of glycolytic ATP production, enhancement of respiratory efficiency, downregulation of mitochondrial density, and suppression of energy-consuming processes. We argue that these innate cellular adaptations to hypoxia represent potential avenues for intervention that have thus far remained untapped by intensive care medicine.

Delirium is a common and debilitating syndrome in hospitalized patients, and its impact on mortality, morbidity and duration of hospital admission is increasingly apparent. Delirium is a complex phenomenon, for which there is no specific treatment, but research over the last decade has revealed contributing factors, many of which are modifiable, and preventative strategies have demonstrated benefit. This review highlights the importance of reducing the impact of delirium on hospitalized patients, and summarizes the current evidence for strategies to achieve this. Current recommendations focus on the pre-emptive implementation of multi-modal non-pharmacological interventions to reduce the occurrence of delirium in the first place, and routine monitoring using validated tools to identify delirious patients early. Potential therapies for established delirium remain controversial.

There has been a clear decline in the volume of oxygen in Earth's atmosphere over the past 20 years. Although the magnitude of this decrease appears small compared to the amount of oxygen in the atmosphere, it is difficult to predict how this process may evolve, due to the brevity of the collected records. A recently proposed model predicts a non-linear decay, which would result in an increasingly rapid fall-off in atmospheric oxygen concentration, with potentially devastating consequences for human health. We discuss the impact that global deoxygenation, over hundreds of generations, might have on human physiology. Exploring the changes between different native high-altitude populations provides a paradigm of how humans might tolerate worsening hypoxia over time. Using this model of atmospheric change, we predict that humans may continue to survive in an unprotected atmosphere for ~3600 years. Accordingly, without dramatic changes to the way in which we interact with our planet, humans may lose their dominance on Earth during the next few millennia.

Time of day is a critical factor for most biological functions, but concepts from the field of chronobiology have yet to be fully translated to clinical practice. Circadian rhythms, generated internally and synchronised to the external environment, promote function and support survival in almost every living species. Fetal circadian rhythms can be observed in utero from 30 weeks gestation, coupled to the maternal rhythm, but synchronise to the external environment only after birth. Important cues for synchronisation include the light/dark cycle, the timing of feeding, and exposure to melatonin in breast milk. Disruption to these cues may occur during admission to the neonatal intensive care unit. This can impair the development of circadian rhythms, and influence survival and function in the neonatal period, with a potential to impact health and well-being throughout adult life. Here we outline the rationale and evidence to support a chronobiological approach to neonatal care.

Purpose To investigate whether palmaris longus interposition or flexor carpi radialis ligament reconstruction and tendon interposition improve the outcome of trapezial excision for the treatment of basal joint arthritis after a minimum follow-up of 5 years. Methods We randomized 174 thumbs with trapeziometacarpal osteoarthritis into 3 groups to undergo simple trapeziectomy, trapeziectomy with palmaris longus interposition, or trapeziectomy with ligament reconstruction and tendon interposition using 50% of the flexor carpi radialis tendon. A K-wire was passed across the trapezial void and retained for 4 weeks, and a thumb spica was used for 6 weeks in all 3 groups. We reviewed 153 thumbs after a minimum of 5 years (median, 6 y; range, 5–18 y) after surgery with subjective and objective assessments of thumb pain, function, and strength. Results There was no difference in the pain relief achieved in the 3 treatment groups, with good results in 120 (78%) patients. Grip strength and key and tip pinch strengths did not differ among the 3 groups and range of movement of the thumb was similar. Few complications persisted after 5 years, and these were distributed evenly among the 3 groups. Compared with the results at 1 year in the same group of patients, the good pain relief achieved was maintained in the longer term, irrespective of the type of surgery. While improvements in grip strength achieved at 1 year after surgery were preserved, the key and tip pinch strengths deteriorated with time, but the type of surgery did not influence this. Conclusions The outcomes of these 3 variations of trapeziectomy were similar after a minimum follow-up of 5 years. There appears to be no benefit to tendon interposition or ligament reconstruction in the longer term. Type of study/level of evidence Therapeutic I.

What you need to know ### Sources and selection criteria We selected published guidance on sleep and shift work from the National Institute for Health and Care Excellence (NICE) and the Royal Colleges of Physicians and Anaesthetists. We then searched PubMed and Cochrane databases (to May 2017) for observational studies, randomised controlled studies, meta-analyses, and systematic and narrative reviews relating to the health consequences of shift work and for each proposed sleep intervention given in table 1. Priority was given to randomised controlled trials and meta-analyses, but given the interdisciplinary nature of sleep and shift work, and the overall quality of evidence, we also considered observational studies and grey literature from aviation and heavy industries, as well as published expert opinion. Night shift work occurs during the period of the sleep-wake cycle (“circadian phase”) programmed for sleep. Alertness, cognitive function, psychomotor coordination, and mood all reach their lowest point between 3 and 5 am1 After the shift, workers must rest during the circadian phase least conducive to sleeping,2 which compounds fatigue and can lead to chronic sleep disturbance.3 A recent systematic review linked night shift work with an increased risk of sleep loss, occupational accidents, obesity and weight gain, type 2 diabetes, coronary heart disease, and breast, prostate, and colorectal cancers.4 In a 2017 survey of 2231 UK trainee anaesthetists, more than 70% reported that fatigue affected their physical and psychological wellbeing. Fifty seven per cent described an accident or near-miss travelling home from night shifts.5 Performance on night shift declines with …