Appearing and disappearing right-heart thrombus: A case reporto in COVID- 19 patient

Aims: Venous thromboembolism represents frequent complication of patients with severe COVID-19 disease. Several reports about atypical thrombosis are described, rarely it has been described a right venticular thrombus during the course of infection. We report a case of right endoventricular thrombosis in a patient with SARSCov- 2 pneumonia. Methods and results: A 58-year-old man was admitted to our ward for severe respiratory failure in interstitial pneumonia. The nasopharyngeal swab for COVID-19 resulted positive. Steroids and prophylaxis with LMWHwere started, associated to CPAP to maintain good gas exchange. During hospitalization a venous ECD was performed with evidence of left popliteal thrombosis despite the therapy. D-Dimer was 44±3 ng/ml. A new onset AF was documented at the telemetry, without troponin elevation. A cardiac ultrasound was performed showing a right endoventricular lesion of 1.8 cm adhering to the free wall of the right ventricle. A CT-pulmonary angiogram (CTPA) resulted negative for pulmonary embolism and confirmed suspected right ventricular thrombus. Treatment with fondaparinux 7.5mg was started. After 10 days, cardiac ultrasound shown complete resolution of thrombosis, and CT confirmed the disappearing of the mass. Dabigatran 150 mg twice/day was started. Patient clinically improved and he was discharged after 20 days of hospitalization. Conclusions: SARS-CoV-2 infection may cause inflammation with cytokine storm and hypercoagulability leading to venous thromboembolism. Atypical thrombus formation was reported, including right-ventricle free wall. Early caridac ultrasound was critical to make diagnosis and starting prompt treatment, therefore routine cardiac ultrasound is mandatory in severe COVID-19 patients.

Fever, anemia, thrombocytopenia, kidney failure and neurological changes: Acquired thrombotic thrombocytopenic purpura (aTTP) in a CoViD-19 patient

Background: The association between CoViD-19 and thrombotic complication such as pulmonary embolism or deep vein thrombosis, is well known. However, SARS-CoV-2 infection may cause also thrombotic microangiopathy with significant clinical pictures. We report a case of a patient with CoViD-19 infection, thrombocytopenia, hemolitic anemia and neurological manifestation. Description of the case: A 70-year-old patient was admitted to the hospital for CoViD-19 pneumonia needing non-invasive ventilation. After 15 days he developed severe diffuse weakness and altered mental status with episodes of hyperkinetic delirium. A head CT scan and brain MRI performed were negative for lesions. On blood examination elevated creatinine (2.9 mg/dL), anemia (Hb 8,3g/dL) and thrombocytopenia (76∗103mmc) were present. The study for the hemolysis revealed total bilirubin 2.46 mg/dL, haptoglobin non detectable, direct and indirect Coombs test negatives and elevated presence of schistocytes >100/1000 blood cells. The ADAMTS-13 was negative. During the hospitalization platelet count drop to 16∗103mmc and patient developed a right ileopsoas hematoma. The patient died before the treatment started. Conclusions: Acquired thrombotic thrombocytopenic purpura represent a fearsome CoViD-19 complication with unfavorable outcome. The early recognition may be associated with a better prognosis. The presence of thrombotic microangiopathy on blood tests and Moskowitz's pentad in the clinic should rise the suspicion: the first step in diagnosing aPTT is to suspect it.

Severe bacterial complications of COVID-19 pneumonia treated with corticosteroids: description of two cases

Background: SARS-CoV-2 infection, in the most severe cases, can cause bilateral pneumonia and respiratory failure. In these cases, therapy is based on the use of antiviral drugs, immunosuppressants (in order to reduce the cytokine-mediated inflammatory response),oxygen and sometimes non-invasive mechanical ventilation (NIV).We describe 2 cases of severe bacterial infections probably favored by the immunosuppressive therapy. Description of the cases: A 63-year-old man with no history of significant medical conditions and an 86-year-old man with history of ischemic heart disease treated with PTCA+DES, were both hospitalized for severe bilateral SARS-CoV-2 pneumonia and treated with NIV associated with high-dose steroids (Dexamethasone 8 mg IV per day). After the resolution of the pulmonary infection, the first one developed a Pneumocystis jirovecii pneumonia with the need for re-hospitalization and treatment with trimethoprim-sulfamethoxazole;the second one developed a methicillin-resistant Staphylococcus aureus (MRSA) endocarditis with infarct lesions caused by septic emboli in brain and splenic area, with subsequent clinical aggravation and death. Conclusions: The SARS-CoV-2 pneumonia treatment is based on combined use of NIV and anti-inflammatory, antiviral and immunosuppresive drugs: it is important to minimize duration of treatment because it may lead to the development of serious complications like septic states (even by opportunistic pathogens) that are lifethreatening for the patients.

In transit thrombosis in CoViD-19 patient

Background: Venous thromboembolism represents frequent complication of patients with severe CoViD-19 disease. The occurrence of venous thromboembolism is mainly in typical district, however several reports about atypical thrombosis are described. We report a case of isolated right endoventricular thrombosis in a patient with SARS-CoV-2 infection. Case Report: A 60-year-old man was admitted to our ward for severe respiratory failure in interstitial pneumonia. The nasopharyngeal swab for CoViD-19 resulted positive. Prophylaxis with LMWH were started associated to CPAP to maintain good gas exchange. During hospitalization a new onset AF was documented at the telemetry and an echocardiogram was performed showing a right endoventricular lesion of 1.8 cm adhering to the free wall. A CTpulmonary angiogram (CTPA) resulted negative for pulmonary embolism. Doppler ultrasound showed left popliteal thrombosis. A treatment with fondaparinux was started. After 10 days, an echocardiogram was repeated showing complete resolution of thrombosis. Another CTPA confirmed the absence of pulmonary embolism. The patient clinically improved and he was discharged with dabigatran. Conclusions: SARS-CoV-2 infection may cause hypercoagulability and inflammation leading to venous thromboembolism and this seems to be related with worse outcome of these patients. For this reason, to monitor the venous thrombosis complication is an important step in the assessment of patients with CoViD-19.