LAUSR

To the Editor, In this journal Hou et al. recently reported their experience on clinical aggravation in COVID-19 patients [1]. Patients with disease progression were more likely to have various complications and cardiac complications in particular. In addition, ARDS, secondary infection, sepsis and septic shock, kidney injury, and liver injury were also related to disease progression. We here describe three cases of pulmonary artery thromboembolism with a positive lupus anticoagulant detection, discovered late in the course of COVID-19 and discuss potential implications for early screening and thrombosis prophylaxis strategies. A 56-year-old man without known comorbidities or thromboembolic risk factors presented to the emergency department with non-productive cough and high fever for 10 days and dyspnoea for mild efforts, severe asthenia and occasional episodes of diarrhoea for 5 days. A nasopharyngeal swab for SARS-CoV-2 resulted positive. On admission, oxygen saturation was 96% in ambient air and arterial blood gas test was as follows: PaO2 84mmHg, PaCO2 30.5mmHg, pH 7.49, PaO2/FiO2 400mmHg. Blood test results are reported in Table 1. A chest X-ray showed bilateral interstitial pneumonia and parenchymal hypodiaphania in the middle-basal right lung. A high-resolution computed tomography showed bilateral ground glass opacities associated to interstitial thickening. After clinical improvement and in the presence of two negative swabs for SARS-CoV 2, on day 10 from hospitalisation (day 20 from disease onset) the patient presented an acute onset of intercostal pain exacerbated by cough, fever and worsening dyspnoea. Based on impaired arterial blood gas oxygen therapy was started and a contrast enhanced chest CT scan was obtained, showing opacification defects suggestive of pulmonary artery thromboembolism (Figure 1). The patient underwent blood tests and examination for underlying factors predisposing to thrombophilia, showing platelet count within normal range, increased Ddimer (8892 ng/ml, rr < 500), prolonged aPTT (46.9 s, rr 20–38) and a positive Lupus Anticoagulant. PaO2/FiO2 at the onset of symptoms was 367mmHg. A venous doppler ultrasound of lower limbs was negative for deep venous thrombosis. Low-molecular-weight heparin was initiated as twice daily subcutaneous injections of 100 IU/kg (1mg/kg). Gradually, the patient’s symptoms improved and arterial blood gas values in ambient air showed pH 7.46, pO2 95.7mmHg, pCO2 35.2mmHg, PaO2/FiO2 456mmHg. A second patient was an obese, otherwise healthy 45years-old man of Argentinean origin, admitted to the emergency department complaining of fever and nonproductive cough for 7 days and recent onset of worsening dyspnoea. Oxygen saturation in ambient air was 89% and arterial blood gas (FiO2 28%) showed: PaO2 83mmHg, PaCO2 35mmHg, pH 7.43, PaO2/FiO2 296mmHg. A chest X-ray demonstrated bilateral interstitial pneumonia. A diagnosis of SARS-CoV-2 infection was made by nasopharyngeal swab. Then, due to the worsening of the clinical condition, the patient underwent non-invasive mechanical ventilation for three days, followed by High Flow Nasal Cannula oxygen therapy. A contrast-enhanced chest CT scan was obtained on day 16 after the onset of symptoms, showing signs of pulmonary thromboembolism (Figure 1). Coagulation tests and investigations for thrombophilia were performed showing an elevated platelet count (629,000/mm, rr 150.000–450.000) and D-dimer (3943 ng/ml, rr < 500), an