34 research outputs found

    Midwives' experiences of personal pregnanacy related loss

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    The aim of the study was to explore the experiences of midwives who were having problems with any aspect of reproduction, and relate this to their approach and attitude to their work with pregnant and childbearing women, and to their colleagues. The study used a grounded theory approach. Data were obtained from written narrative accounts from 40 participants and from 10 follow up, in-depths, semi-structured interviews. Data were analysed using a constant comparative technique producing categories and the core category of the thesis. The findings suggested that pregnancy related losses, including infertility, miscarriage, termination of pregnancy, stillbirth and neonatal death, influenced the participants' personal and professional relationships. In common with nonmidwives in similar situations, some midwives found it difficult being with pregnant women or babies, although most differentiated between longing for their own baby, and envy of any other baby. Some found difficulty working in particular areas, for example labour ward, although there seemed to be no link between the type of loss, and problematic areas. Most participants spoke of their love for midwifery, and their determination to continue despite difficulties. At work, participants valued practical and emotional support. Some participants suggested that their experiences had increased their practical knowledge and understanding. Some had improved support systems for clients and for colleagues. Many participants mentioned the therapeutic value of involvement in the study. The implications of the study were that the midwives could not avoid evidence of others' fertility in their work. How they addressed this influenced their approach to work, and some recommendations are made, based on the findings. These relate to potentially supportive management and teaching strategies, and to further research and awareness raising which might help midwives and others in similar occupations following personal experience of pregnancy related loss.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

    Genetic mechanisms of critical illness in COVID-19.

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    Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

    Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

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    IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

    Death from paracetamol overdose despite appropriate treatment with n‐acetylcysteine

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    A case of death from severe paracetamol poisoning which presented early and received appropriate treatment according to evidence‐based guidelines is presented here. It is very rare for patients to die from paracetamol poisoning when they receive N‐acetylcysteine (NAC) within 8 h of ingestion. The patient had a marked lactic acidosis on presentation to hospital. This case demonstrates that a patient can die from paracetamol poisoning despite early and appropriate treatment, and raises the question whether lactic acidosis in a patient following paracetamol overdose should prompt the initiation of NAC treatment while awaiting paracetamol levels
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