Pulmonary Embolism in COVID-19 Patients Is Not Related to a Deterioration of Tissue Oxygenation.

Abstract

COVID-19 induces robust systemic inflammation. One of the main complications is the increased coagulation due to endotheliitis. There is an increased incidence of pulmonary embolism (PE) in COVID-19 patients. However, clinical characteristics for a strict analysis are yet to be determined. We evaluated oxygenation and characteristics in patients with COVID-19 PE (CPE). We evaluated 215 COVID-19 patients from 1 January to 30 April 2021. We found 18 patients affected by PE (CPE, 50.0% males, aged 67.00±10.86years). As controls, we used data from patients affected by PE evaluated in our ward between 1 January 2015 and 31 December 2019 (64 patients, 53.1% males, aged 70.88±16.44years). All patients underwent a complete physical examination, pulmonary computerised tomography, laboratory tests, D-dimers and blood gas analysis at the time of diagnosis. There were no differences in laboratory tests nor in D-dimers between the two groups. In the CPE group we found a significantly increased pO2 (92.83±42.52 vs. 76.11±32.58mmHg; p<0.05), difference of oxygen between alveoli and arteries (A-aDO2; 169.3±171.9 vs. 52.97±39.65mmHg; p<0.05), and oxygen saturation % (97.06±2.59 vs. 93.77±5.53%; p<0.05) compared to controls. No difference was found in pCO2 and the ratio between pO2 and percentage of inspired oxygen (P/F). Finally, a significantly decreased urate (3.67±1.49 vs. 5.60±2.10; p<0.05) was found in CPE compared to controls. In CPE, platelets count presents an inverse correlation to P/F (r=-0.389, p=0.02) but a direct correlation to A-aDO2 (r=0.699, p=0.001). No similar findings were present in controls. COVID-19 PE appears to have a different clinical setting. Reduced oxygenation described in PE may not to be considered as a sign of disease. The increased A-aDO2 may indicate that COVID-19 PE involved smaller vessels compared to classical PE. A possible diffuse capillary thrombosis could explain these results.