Reflection is a cognitive process in which new information and experiences are integrated into existing knowledge structures and mental models, resulting in meaningful learning. Reflection often occurs after an experience is over, promoting professional development and lifelong learning. However, a reflective emergency physician (EP) is also able to apply reflection in real time: self-monitoring, coping with the unexpected, and quickly thinking on his or her feet to solve complicated, unique, and challenging clinical problems. Reflection is a skill that can be taught and developed in medical education. Evidence demonstrating the value of teaching reflection is emerging that substantiates longstanding educational theories. While a few educators have started to explore the use of reflection for emergency medicine (EM) learners, the potential for broader application exists. This review summarizes the literature regarding reflection in medical education and provides a basic primer for teaching reflection.

SARS-CoV-2 infection in very preterm pregnancy: Experiences from two cases Dear Editor, We present our experience of managing two cases of SARS-CoV-2 infection in very preterm pregnancy. A 39 year-old primigravida presented with 5 days of dyspnoea, cough and pyrexia at 28 + 4 weeks of gestation. She was Afro-Caribbean, had BMI 42 and type 2 diabetes mellitus. Her respiratory rate was 20 breaths/minute, oxygen saturations (SpO2) 92 % and arterial partial pressure of oxygen (PaO2) was 8.1 mmHg in air. Chest X-ray showed bilateral infiltrates (Fig. 1). SARS-CoV-2 infection causing type 1 respiratory failure was presumed. She received corticosteroids for fetal maturation. After 24 h she deteriorated and was admitted to ICU for high-flow nasal oxygen and then noninvasive ventilation 3 h later. A multidisciplinary (obstetric, anaesthetic and intensivist) decision was made for delivery by caesarean section, to facilitate invasive ventilation of the woman. This followed magnesium sulphate for fetal neuroprotection. Maternal airway pressures and oxygen requirements were high throughout surgery. After surgery she was positioned flat for central venous cannulation and deteriorated acutely post-procedure, with high airway pressures and SpO2 of 35 % despite fractional inspired oxygen (FiO2) of 1.0. Needle chest decompression was performed to exclude iatrogenic tension pneumothorax, although no gas escape was heard, and subsequent ultrasound excluded pneumothorax. Endotracheal tube position was confirmed, air entry was bilateral.

Induction of heat shock proteins (Hsp) 72 and 27 can improve insulin signalling in obesity and type 2 diabetes via inhibition of key stress kinases. In metabolic disease, altered insulin signalling, as illustrated by increased serine phosphorylation of insulin receptor substrate (IRS)-1 (Ser312), is not confined to muscle or liver and can also affect other tissues and cell types, potentially impairing their primary biological function. This study specifically investigated insulin-stimulated glucose metabolism in monocytes and examined the impact of HSP induction on insulin signalling. Control (CG, BMI< 25 kg/m 2 ) or obese (OG, BMI>30 kg/m 2 ) participants were included in the study. Glucose transporter (GLUT)4 expression on monocytes, phosphorylated JNK, IKK-β and IRS-1, as well as Hsp27 and Hsp72, were measured in monocytes under fasting conditions. GLUT4 expression was also measured during an oral glucose tolerance test (OGTT). HSP induction as well as JNK, IKK-β activation and IRS-1 serine phosphorylation was investigated following heat stress. Obese patients showed lower GLUT4 levels on monocytes during the OGTT. pJNK, pIKK-β and pIRS-1 levels were increased in OG with pJNK and pIKK-β levels positively correlated with serine pIRS-1 and negatively with GLUT4 supporting their role in insulin resistance. Heat exposure induced Hsp72 and Hps27, but only in CG for the latter, and decreased pJNK, pIKK-β and pIRS-1. Our results show that induction of Hsp72 and 27 via heat stress is associated with inactivation of stress kinases and reduced serine pIRS-1 in monocytes from obese participants. This indicates that metabolic diseases can also affect monocyte metabolism via cellular stress that can be modulated via HSP induction.

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