Covid-19 crisis impact on the next generation of physicians: a survey of 800 medical students.

BACKGROUND: Many initiatives have emerged worldwide to handle the surge of hospitalizations during the SARS-CoV-2 pandemic. In France, the University of Paris North called on its medical students, whose status makes them integral members of the healthcare staff, to volunteer in their capacity of medical students and/or as nurses/nursing aids in understaffed intensive care units and other Covid-19 services. We attempted to evaluate their commitment, whether the pandemic affected their certainty for the medical profession and career choices, and how they scored their sadness and anxiety levels. METHODS: The University of Paris North took a weekly official census of the involvement of 1205 4th-6th year medical students during the first lockdown in France. Six weeks after the lockdown began (May 4th), an e-questionnaire was sent to 2145 2nd-6th year medical students. The survey lasted 4 weeks and documented volunteering by medical students, the association between the pandemic and certainty for their profession, their choice of medical specialty and factors that influenced sadness and anxiety scores. RESULTS: 82% of 4th-6th year medical students volunteered to continue their internship or be reassigned to COVID-19 units. Of 802 2nd-6th year students who completed the e-questionnaire, 742 (93%) volunteered in Covid-19 units, of which half acted as nurses. This engagement reinforced the commitment of 92% of volunteers to become physicians. However, at the peak of the outbreak, 17% had doubts about their ability to be physicians, while 12% reconsidered their choice of future specialty. Finally, 38% of students reported a score of 7/10 or more on the sadness scale, and 43% a score of 7/10 or more for anxiety. Neither study year nor service influenced sadness or anxiety scores. However, gender influenced both, with women scoring significantly higher than men (p < 0.0001). CONCLUSION: Medical students of the University of Paris North who made an early and unconditional commitment to help hospital staff handle the pandemic constituted a powerful healthcare reserve force during the crisis. Although the vast majority remained convinced that they want to become physicians, this experience came at a significant psychological cost, especially for women. Alleviating this cost would improve future crisis responses.

Residual ground glass opacities three months after Covid-19 pneumonia correlate to alteration of respiratory function: The post Covid M3 study.

INTRODUCTION: Lung function in survivors of SARS-Co-V2 pneumonia is poorly known, but concern over the possibility of sequelae exists. METHODS: Retrospective study on survivors with confirmed infection and pneumonia on chest-CT. Correlations between PFT and residual radiologic anomalies at three months taking into account initial clinical and radiological severity and steroid use during acute phase. RESULTS: 137 patients (69 men, median age 59 (Q1 50; Q3 68), BMI 27.5 kg/m2 (25.1; 31.7)) were assessed. Only 32.9% had normal PFT, 75 had altered DLCO. Median (Q1; Q3) values were: VC 79 (66; 92) % pred, FEV1 81 (68; 89), TLC 78 (67; 85), DLCO 60 (44; 72), and KCO 89 (77; 105). Ground glass opacities (GGO) were present in 103 patients (75%), reticulations in 42 (30%), and fibrosis in 18 (13%). There were significantly lower FEV1 (p = 0.0089), FVC (p = 0.0010), TLC (p < 0.0001) and DLCO (p < 0.0001) for patients with GGO, lower TLC (p = 0.0913) and DLCO (p = 0.0181) between patients with reticulations and lower FVC (p = 0.0618), TLC (p = 0.0742) DLCO (p = 0.002) and KCO (p = 0.0114) between patients with fibrosis. Patients with initial ≥50% lung involvement had significantly lower FEV1 (p = 0.0019), FVC (p = 0.0033), TLC (p = 0.0028) and DLCO (p = 0.0003) compared to patients with ≤10%. There was no difference in PFT and residual CT lesions between patients who received steroids and those who did not. CONCLUSION: The majority of patients have altered PFT at three months, even in patients with mild initial disease, with significantly lower function in patients with residual CT lesions. Steroids do not seem to modify functional and radiological recovery. Long-term follow-up is needed.

Alteration of Diffusion Capacity After SARS-CoV-2 Infection: A Pathophysiological Approach.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has affected millions of people worldwide, and pneumonia affects 90% of patients. This raises the possibility of millions of people with altered lung function. Few data exist to date on pulmonary function after SARS-CoV-2 infection, but alteration of diffusion capacity of CO (D LCO) is the most frequently described abnormality. First, we present original data on lung function at 3 months after SARS-CoV-2 infection and discuss the effect of using European Coal and Steel Community (ECSC) or Global Lung Function Initiative (GLI) reference equations to diagnose diffusion capacity. Second, we review existing data on D LCO alteration after SARS-CoV-2 infection and discuss the implication of restrictive disorder in D LCO alteration. Last, we discuss the pathophysiology of D LCO alteration and try to disentangle vascular damage and fibrosis.

The Good Treatment, the Bad Virus, and the Ugly Inflammation: Pathophysiology of Kidney Involvement During COVID-19.

Kidney involvement is a common complication during SARS-CoV-2 infection. Its association with poor outcomes, especially in critically ill patients, raises issues whether kidney involvement reflects multi-organ damage or if it is a specific feature of the infection. Based on observational studies, autopsy series, and on current understanding of the route of entry of the virus, this review will highlight the different types of kidney involvement during COVID-19 and put them in the perspective of the different pathophysiological hypotheses. Virus entry route through ACE2 ligation and TMPRSS2 coligation allows identifying potential viral targets in the kidney, including tubules, endothelial cells, and glomerulus. While reports have described damages of all these structures and virus kidney tropism has been identified in renal extracts in autopsy series, no direct viral infection has been found in the latter structures thus far on kidney biopsies. Notwithstanding the technical challenge of disclosing viral invasion within tissues and cells, viral direct cytopathogenic effect generally does not appear as the cause of the observed renal damage. Inflammation and altered hemodynamics, described as "viral sepsis," might rather be responsible for organ dysfunction, including kidneys. We shall place these various mechanisms into an integrated vision where the synergy between direct viral pathogenicity and systemic inflammation enhances renal damage. As SARS-CoV-2 inexorably continues its rampant spread, understanding the sequence of events in the kidneys might thus help inform improved therapeutic strategies, including antiviral drugs and immunomodulators.

Controversial Roles of the Renin Angiotensin System and Its Modulators During the COVID-19 Pandemic.

Since December 2019, the coronavirus 2019 (COVID-19) pandemic has rapidly spread and overwhelmed healthcare systems worldwide, urging physicians to understand how to manage this novel infection. Early in the pandemic, more severe forms of COVID-19 have been observed in patients with cardiovascular comorbidities, who are often treated with renin-angiotensin aldosterone system (RAAS)-blockers, such as angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs), but whether these are indeed independent risk factors is unknown. The cellular receptor for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the membrane-bound angiotensin converting enzyme 2 (ACE2), as for SARS-CoV(-1). Experimental data suggest that expression of ACE2 may be increased by RAAS-blockers, raising concerns that these drugs may facilitate viral cell entry. On the other hand, ACE2 is a key counter-regulator of the RAAS, by degrading angiotensin II into angiotensin (1-7), and may thereby mediate beneficial effects in COVID-19. These considerations have raised concerns about the management of these drugs, and early comments shed vivid controversy among physicians. This review will describe the homeostatic balance between ACE-angiotensin II and ACE2-angiotensin (1-7) and summarize the pathophysiological rationale underlying the debated role of the RAAS and its modulators in the context of the pandemic. In addition, we will review available evidence investigating the impact of RAAS blockers on the course and prognosis of COVID-19 and discuss why retrospective observational studies should be interpreted with caution. These considerations highlight the importance of solid evidence-based data in order to guide physicians in the management of RAAS-interfering drugs in the general population as well as in patients with more or less severe forms of SARS-CoV-2 infection.

Association between renin-angiotensin-aldosterone system blockers and outcome in coronavirus disease 2019: analysing in-hospital exposure generates a biased seemingly protective effect of treatment.

OBJECTIVE: The role of renin-angiotensin-aldosterone system (RAAS) blockers during the coronavirus disease 2019 (COVID-19) pandemic is a matter of controversies. Studies based on in-hospital exposure have suggested a beneficial effect of these drugs, unlike those based on chronic exposure. We aimed to analyse RAAS blocker prescription before and during hospital stay in patients with COVID-19, and the corresponding outcomes, to explain these discrepant results. METHODS: In a retrospective cohort study conducted in 347 patients hospitalized for COVID-19 (Bichat Hospital, Paris, France, 23 January-29 April 2020), RAAS blocker exposure, as well as timing and reason for treatment modifications, were collected. The association between exposure and mortality within 30 days of hospital admission was analysed using logistic regression analysis adjusted for age, sex, and comorbidities. RESULTS: Median age was 61 [interquartile range, 51-72] years, 209 (60%) were male, 169 (49%) had a history of treated hypertension, and 117 (34%) received a RAAS blocker prior to hospitalization. RAAS blockers were discontinued within the first 7 days of hospital admission in 33% of previously treated patients (mostly driven by severity of the disease), with a corresponding mortality rate of 33%. Mortality was 8% when treatment was maintained or introduced, and 12% in patients never exposed. Adjusted odds ratios for association between exposure and mortality were 0.62 (95% confidence interval 0.25-1.48) based on chronic exposure and 0.25 (0.09-0.65) based on in-hospital exposure. CONCLUSION: A 'healthy user-sick stopper' bias influences RAAS blocker prescription after hospital admission for COVID-19, and explains the seemingly favourable outcome associated with in-hospital treatment.