Acute life-threatening cardiac tamponade in a mechanically ventilated patient with COVID-19 pneumonia

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has recently evolved as a pandemic disease. Although the respiratory system is predominantly affected, cardiovascular complications have been frequently identified, including acute myocarditis, myocardial infarction, acute heart failure, arrhythmias and venous thromboembolic events. Pericardial disease has been rarely reported. We present a case of acute life-threatening cardiac tamponade caused by a small pericardial effusion in a mechanically ventilated patient with severe COVID-19 associated pneumonia. The patient presented acute circulatory collapse with hemodynamic features of cardiogenic or obstructive shock. Bedside echocardiography permitted prompt diagnosis and life-saving pericardiocentesis. Further investigation revealed no other apparent cause of pericardial effusion except for SARS-CoV-2 infection. Cardiac tamponade may complicate COVID-19 and should be included in the differential diagnosis of acute hemodynamic deterioration in mechanically ventilated COVID-19 patients

Low T3 Syndrome in severely ill patients with COVID-19 infection

Introduction The coronavirus disease (COVID-19) is an infectious disease, caused by the SARS-CoV-2 virus, which causes severe respiratory disease. Critical ill patients often experience a condition known as Low T3 Syndrome (LT3S). Previous studies showed an association between low FT3 levels and mortality among patients with COVID-19. Moreover, thyroid hormones might be altered by cigarette consumption. Τhe aim of this study was to investigate the association of LT3S with mortality and the severity and risk of intubation in critically ill patients with COVID-19 infection, and to explore whether this association is confounded by smoking. Methods A total of 105 critically ill patients aged ≥18 years, with laboratoryconfirmed (RT-PCR) COVID-19 were enrolled. The study was conducted between January 2021 and October 2021 in the Intensive Care Unit of the 1st Department Respiratory Medicine in ‘Sotiria’ Hospital and laboratory data and clinical information were retrieved retrospectively from the electronic patients record. LT3S was defined as serum levels of FT3 <2.3 pg/mL with low or normal TSH levels. Patients were divided into two groups according to serum FT3 values: group with LT3S and group without LT3S. Mortality in the ICU was the primary outcome of the study, while the risk of intubation was a secondary outcome. Results In all, 43 out of the 105 included patients were diagnosed with LT3S. Patients in the LT3S group were older than those with non LT3S [median (IQR): 62 (13.7) vs 52.8 (15.5), p=0.011]. Non-statistically significantly higher mortality rate, SOFA and APACHE II scores were observed in the LT3S group compared to no LT3S group (p=0.080, p=0.311 and p=0.079, respectively). Moreover, LT3S was not associated with high risk of intubation (HR=1.32; 95% CI: 0.78–2.22). Twenty-five patients (58.1%) in the LT3S group were never smokers, versus 41 (66.1%) patients in the non LT3S group. Never smokers with LT3S had significantly higher mortality rate than never smokers without LT3S (40% vs 17.1%, p=0.039), and LT3S in the never smoking subgroup was associated with an increased risk of intubation (HR=2.21; 95% CI: 1.18–4.16). Conclusions LT3S was found to be associated with mortality of patients with critical COVID-19 among never smokers but not among ex-smokers or active smokers. This finding may denote that smoking may act as a confounder of the association between LT3S and mortality. Further investigation is needed to demonstrate the impact of LT3S in critically ill patients with COVID-19 infection, as well as the role of smoking in the development of the syndrome

Cutaneous Vasculopathy in a COVID-19 Critically Ill Patient: A Histologic, Immunohistochemical, and Electron Microscopy Study

We describe a critically ill, SARS-CoV-2 positive patient with respiratory failure and thrombotic/livedoid skin lesions, appearing during the course of the disease. The biopsy of the lesions revealed an occlusive, pauci-inflammatory vasculopathy of the cutaneous small vessels characterized by complement and fibrinogen deposition on vascular walls, pointing to a thrombotic vasculopathy. Transmission electron microscopy of the affected skin failed to reveal any viral inclusions. Clinical evaluation and laboratory findings ruled out systemic coagulopathies and disseminated intravascular coagulation, drug-induced skin reaction, and common viral rashes. Our hypothesis is that the, herein evidenced, microvascular occlusive injury might constitute a significant pathologic mechanism in COVID-19, being a common denominator between cutaneous and pulmonary manifestations