Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
1.
Adverse Drug Reactions Journal ; 22(6):355-359, 2020.
Article in Chinese | EMBASE | ID: covidwho-2291790

ABSTRACT

Objective: To report the clinical features of pulmonary hypertension diagnosed by echocardiography in 5 patients with novel coronavirus pneumonia (COVID-19) in order to understand the special clinical manifestations of COVID-19 and explore the possible mechanism. Method(s): The echocardiographic data and clinical characteristics of COVID-19 patients complicated with pulmonary hypertension diagnosed by echocardiography in Beijing Ditan Hospital, Capital Medical University were analyzed descriptively from February 5 to March 31, 2020. Result(s): A total of 15 patients with severe and critical COVID-19 patients underwent echocardiography. Of them, 7 patients were diagnosed with pulmonary hypertension, 5 of which were confirmed as complications of COVID-19. Among the 5 patients, 4 were female and 1 was male, aged 62-78 years;4 were with hypertension, 3 were with diabetes, and 1 was with coronary atherosclerotic heart disease. All 5 critically ill patients with COVID-19 were given ventilator-assisted breathing, 2 of which were given extracorporeal membrane oxygenation at the same time. According to echocardiography, the systolic pressure of pulmonary artery in 5 patients was 43-65 mmHg, with an average of 54 mmHg. The severity of pulmonary hypertension was graded as mild in 1 patient and moderate in 4 patients. During the follow-up, pulmonary artery systolic pressure gradually decreased to normal in 4 patients, and then ventilator and ECMO were withdrawn;1 patient died due to respiratory failure and persistent pulmonary hypertension. Conclusion(s): Patients with COVID-19 may be complicated by pulmonary hypertension, which is often found in the critical patients. Echocardiography is an important imagingdiagnostic method for pulmonary hypertension in patients with COVID-19.Copyright © 2020 by the Chinese Medical Association.

2.
European Respiratory Journal Conference: European Respiratory Society International Congress, ERS ; 60(Supplement 66), 2022.
Article in English | EMBASE | ID: covidwho-2273480

ABSTRACT

Introduction: Primitive data suggest prevalence of PH in patients with COVID19 is around 13% but prognosis is unclear. Approximately 0.5-2% of patients develop CTEPH after acute PE and recommendation is to screen them for CTEPH if remains symptomatic at 3/12 after PE. Aim(s): The primary aim of the study was to assess the chances of persistent PH following PE secondary to COVID19 Methods: We conducted a retrospective cohort study at a DGH in the UK. All patients diagnosed with COVID-19 and PE between April, 2020 to October, 2021 were examined. Patients were divided into two groups: . COVID19 and PE with co-morbidities(excluding pre existing PH) . COVID19 and PE without co-morbidities We compared the prevalence of pulmonary hypertension between the two groups on cardiac ECHO (defined as a mean pulmonary arterial pressure >= 25mmHg) at the time of diagnosis of PE and at 3 months following treatment. Result(s): 80 patients were included in the study (49 with co-morbidities & 31 with no co-morbidities). Average age of co-morbidities and no comorbidities groups were 73yrs and 70yrs respectively. Average PaO2/FiO2 ratio for comorbidities and no co-morbidities groups were 170 and 195 respectively. 14 patients (13 with co-morbidities & 1 no co-morbidity) died in total. Results showed that relative risk of persistent PH and subsequent mortality following PE in COVID19 is 4.16 times & 1.32 times more in co-morbidties group as compared to no co-morbidties group respectively (p<0.001) Conclusion(s): Patients with co-morbidities are at high risk of persistent PH and mortality due to PE secondary to COVID19 and should be worked up for CTEPH if PH exist on 3/12 ECHO.

3.
Journal of Clinical Neonatology ; 11(2):65-70, 2022.
Article in English | EMBASE | ID: covidwho-1822508

ABSTRACT

Background: Multisystem inflammatory syndrome in children (MIS-C) is a well-known entity that occurs 3-4 weeks after COVID-19. A similar entity in newborns, known as Multisystem Inflammatory Syndrome in Newborns (MIS-N), is also described. However, the epidemiology, case definition, clinical presentations, and outcomes of MIS-N are still being updated. The presence of SARS CoV 2 antibodies in both the mother and the neonate suggests transplacental transfer of IgG antibodies causing cytokine storm and multisystem inflammatory syndrome in newborns (MIS-N). Aims and Objectives: To investigate the clinical characteristics, laboratory parameters, outcomes, and treatment modalities of neonates with multisystem inflammatory syndrome due to transplacental transfer of SARS CoV 2 antibodies. Materials and Methods: The study included eighteen consecutive neonates who met the MIS-C criteria. Following prior ethical clearance and consent from parents or guardians, socio-demographic data, lab parameters, clinical parameters, and treatment given were documented, tabulated, and analysed. Results: All of the 18 neonates had fever. The most common system involved was the respiratory system (15/18), followed by the cardiovascular system with coronary artery dilatations (10/18) and persistent pulmonary hypertension (4/18). All 17 cases (17/18) responded favourably to intravenous immunoglobulins (2 gm/kg) and intravenous dexamethasone (0.15 mg/kg). D-Dimers decreased significantly after treatment, with a p value of 0.01. One case with more than three systems involved (respiratory, CVS, CNS, and renal involvement) (1/18) resulted in death. Conclusion: A high index of suspicion is warranted in critically ill neonates, especially with fever, multisystem involvement and positive SARS CoV 2 antibodies. Fever may be a soft pointer to the diagnosis as fever is rare in neonates with other illnesses. Followup antibody titres are needed to document if there is any relationship between level of antibodies and disease. Safety of vaccination also needs to be addressed as antibodies are implicated in the etiopathogenesis of MIS-N.

4.
European Heart Journal ; 42(SUPPL 1):1843, 2021.
Article in English | EMBASE | ID: covidwho-1554210

ABSTRACT

Background: Novel coronavirus (COVID-19) has been a world concern since December 2019. The knowledge about vertical transmission and fetal morbidity and mortality from maternal COVID-19 infection is limited.We detected an increase in the number of cases of term and near-term neonates with persistent pulmonary hypertension (PPHN) during the COVID-19 pandemic in 2020. Methods and results: We collected data on all newborns with PPHN born between 2018 and 2020. We excluded premature infants (<34+0 weeks) and infants with other significant pathology or genetic syndromes. Compared to 5 cases of PPHN of 22930 live births in 2018, and 6 cases of PPHN of 22270 live births in 2019 (2-year average 0.02%, 95% CI 0.013%- 0.043%), there were 16 PPHN cases from 22323 live births in 2020 (0.07%, 95% CI 0.044%-0.12%), a 3 fold increase (p<0.01). We report 5 cases of term and near-term neonates born to mothers who had highly suspected (2) and PCR proven (3) COVID-19 infection during the third trimester of pregnancy, who presented with PPHN during COVID-19 pandemic in 2020. All had otherwise unexplained pulmonary hypertension, right ventricular hypertrophy (RVH) and dilatation. Two patients needed endotracheal intubation, one was supported by nasal continuous positive airway pressure (CPAP) without intubation, two needed O2 support by nasal cannula only ant two newborns (one of them was intubated) needed Nitric oxide (NO) as pulmonary vasodilator therapy. No patient required Extracorporeal membrane oxygenation (ECMO) or died, and no prolonged residual cardiovascular or pulmonary morbidity was recorded during a median follow up of 4.8 months (range 4-6 months). Conclusions: The increase in the incidence of PPHN during the COVID- 19 pandemic, and the cases presented, suggest an intrauterine effect of maternal COVID-19 infection on the fetal pulmonary circulation. It is possible that the maternal infection affected the fetal pulmonary vascular resistance, or altered the normal decline in the resistance after birth. The right ventricular hypertrophy and dilatation with reduced function may be secondary to this hypothetical increased afterload or a direct effect of the infection. Further studies are warranted to elucidate the pathogenesis and clinical implications of this phenomenon.

SELECTION OF CITATIONS
SEARCH DETAIL