RESUMO
BACKGROUND Coronavirus Disease 2019 (COVID-19) has been associated with a hypercoagulability state. Clinical presentation can range from asymptomatic to severe illness and mortality. Thrombotic complications in COVID-19 have been associated with mortality. The incidence of systemic hypercoagulation in COVID-19 is associated with the process of severe inflammation. The majority of severely ill patients have developed coagulopathy, and this condition is associated with poor outcomes. CASE REPORT A 72-year-old man presented with respiratory symptoms and was diagnosed with a COVID-19 infection. He presented with tachypnea, tachycardia, increased blood pressure, and 74% peripheral oxygen saturation under 15 L/min oxygen per non-rebreather mask. Initial laboratory test results showed severe hypoxemia as per blood gas analysis (pH 7.42, pCO2 23 mmHg, pO2 43 mmHg, HCO3 15 mmol/L, base deficit -9 mmol/L), with increased procalcitonin, high-sensitivity C-reactive protein, D-dimer, fibrinogen, creatine kinase myocardial band, and Troponin I. He subsequently developed thrombosis of the pulmonary arteries and multiple branches of the pulmonary vein despite therapeutic anticoagulation. We initiated heparin therapy (average dose 25 191 units per day, mean activated partial thromboplastin time, 64.35 seconds). Radiological investigations revealed multiple thromboses on pulmonary arteries and pulmonary veins, as well as multiple locations of brain infarction. Rescue thrombolytic therapy was given, but unfortunately, the patient died due to multiple end-organ failures. CONCLUSIONS Controlling coagulopathy, and thrombolytic therapy type and timing, are critical issues, and new strategies must be sought to lower its morbidity and mortality rates further.
