Publications

We designed, implemented and evaluated a near-peer simulation training programme teaching diagnostic and therapeutic abdominal paracentesis to core medical trainees (CMTs). We taught diagnostic and therapeutic abdominal paracentesis to 77 north-west London CMTs over 8 training days over 4 years, 2015 to 2019. The programme was optimised by use of plan, do, study, act (PDSA) cycles and the content was evaluated by anonymous pre- and post-course questionnaires.

• Globally, coal workers pneumoconiosis, silicosis, and asbestosis remain the most important pneumoconioses.
• Idiopathic pulmonary fibrosis (IPF) and asbestosis can be challenging to differentiate clinically, and there is clear evidence for an occupational contribution to IPF.
• Bacterial contamination of metal working fluid has recently emerged as an important cause of occupational hypersensitivity pneumonitis.

The General Medical Council (GMC) national trainee survey (NTS) monitors junior doctor training experience annually, which is then used by organisations such as Health Education England to inform quality management. Its validity as an assessment of the learning environment to drive improvement is frequently questioned; currently there are no published evidence-based studies to demonstrate its impact. To explore the effects of the GMC survey, we carried out a retrospective cohort study using publicly available GMC NTS survey data.

Rationale: Chronic hypersensitivity pneumonitis (CHP) is a condition that arises after repeated exposure and sensitization to inhaled antigens. The lung microbiome is increasingly implicated in respiratory disease, but, to date, no study has investigated the composition of microbial communities in the lower airways in CHP.

Objectives: To characterize and compare the airway microbiome in subjects with CHP, subjects with idiopathic pulmonary fibrosis (IPF), and control subjects.

When we conceived of the theme of ‘learning well’ for the June 2020 issue of FHJ, it is safe to say that the world was a different place. Our thinking around how to utilise education as a method of promoting improved self-care, wellbeing and belonging within a stretched healthcare system was based on current cultural philosophies of civility, preventing moral injury and burnout, and ensuring that healthcare professionals could be empowered – through autonomy and competence – to learn without blame from even the most challenging of situations.

Tuberculous pericarditis is a severe form of extrapulmonary tuberculosis and is the commonest cause of pericardial effusion in high incidence settings. Mortality ranges between 8 and 34%, and it is the leading cause of pericardial constriction in Africa and Asia. Current understanding of the disease is based on models derived from studies performed in the 1940–50s. This review summarises recent advances in the histology, microbiology and immunology of tuberculous pericarditis, with special focus on the effect of Human Immunodeficiency Virus (HIV) and the determinants of constriction.

Introduction Many patients with chronic obstructive pulmonary disease (COPD) experience a sustained worsening in symptoms termed an acute exacerbation (AECOPD). AECOPDs impact on patients’ quality of life and lung function, are costly to health services and are an important topic for research. Electronic health records (EHR) are increasingly being used to study AECOPD, requiring accurate detection of AECOPD in EHRs to ensure generalisable results.

We are delighted to introduce an issue of FHJ in which we have focused our minds, and hopefully those of our readers, on the ever-present activity of all clinicians (and humans) – learning. This is such a wide topic, so we have considered a number of different dimensions with the confidence that these will stimulate interest, debate and discussion. Firstly, we have considered the important issue of learning to speak up in our workplaces.

In their published article, Alif et al report the findings from a carefully conducted longitudinal study showing the effects of occupational exposures on lung function decline between the ages of 45 and 50 years.