The infection by the 2019 novel coronavirus affects mainly the respiratory system with a variable clinical presentation, from a flu-like syndrome with mild respiratory symptoms to a viral pneumonia with acute respiratory insufficiency, multiple organ dysfunction and death. Recent studies suggest that patients with SARS-CoV-2 infection may have a hypercoagulable state that could predispose to thrombotic events. We describe a patient with COVID-19 who developed an acute portal vein thrombosis. Case presentationA 27-year-old man from Dominican Republic, with no past medical or surgical history, presented to the emergency department in March 2020, with a three days history of severe colic abdominal pain without nausea, vomiting or diarrhoea. Three weeks before admission he had developed fever and dry cough. In the setting of the COVID-19 pandemic, during those three weeks the patient stayed home self-isolated, with analgesic and antipyretic treatment. In the emergency department, the patient's temperature was 38.8°C, he had sinus tachycardia with 150 beats per minute, blood pressure 100/75 mm Hg, respiratory rate 15 breaths per minute, and oxygen saturation 99% on room air. Physical examination showed an alert young man. Chest auscultation revealed bi-basal crackles. His abdomen was non-distended, with tenderness in the right upper quadrant with negative Murphy's sign. No masses or inguinal hernias were appreciated. No signs of deep vein thrombosis in the lower extremities were found on physical examination. Laboratory findings showed elevated serum aspartate aminotransferase 64 U/L, alanine aminotransferase 111 U/L, lactate dehydrogenase 253 U/L, alkaline phosphatase 148 U/L, total leukocyte count 18 × 10 9 /L (85% neutrophils and 8% lymphocytes), platelets 458 × 10 9 /l, serum fibrinogen > 500 mg/dL (normal range [RN] 150-400), D-dimer using Innovance® D-dimer assay 9.530 μg/L (RN < 500) and C-reactive protein 245 mg/L, while total bilirubin, amylase, lipase, BUN, creatinine clearance, sodium, potassium, calcium, total red blood cell count, haemoglobin, haematocrit, international normalized ratio (INR), activated partial thromboplastin (aPTT) and prothrombin time (PT) were normal. The chest X-ray showed
Background The most susceptible population group to critical and fatal coronavirus disease 2019 (COVID-19) is older adults. In SARS-CoV-2 infection, the host immune response is thought to play a key role in the pathophysiological effects of lung damage. Therefore, corticosteroid therapy could modulate inflammation-mediated pulmonary injury and thereby reduce progression to severe respiratory failure and death. The aim of this study was to analyse the safety and clinical efficacy of corticosteroid therapy in older adults with severe COVID-19 pneumonia. Method We reviewed the clinical records of confirmed COVID-19 patients aged 75 years or older admitted to our hospital over a three months period (March 1, to May 31, 2020). A total of 143 patients were included in the study cohort. From 2 April, 2020, in accordance with World Health Organization (WHO) guidance on COVID-19, our hospital protocol added corticosteroid for COVID-19 treatment. We compared in-hospital mortality among patients with critical COVID-19 who received corticosteroids therapy and those who did not. Results 88 patients (61.5%) were treated with corticosteroids, and 55 patients (38.4%) were not. Both groups were similar in baseline characteristics. The median age was 85 years (IQR, 82–89), and 61.5% (88/143) were male. In-hospital mortality was lower in the corticosteroid group (68.2%) compared with patients in the non-corticosteroid group (81.8%). Treatment with corticosteroids was an independent survival factor (HR=0.61; 95% CI, 0.41–0.93; P=0.006). Conclusions In critically ill older adults with COVID-19 pneumonia, the use of corticosteroid treatment resulted in lower mortality without severe adverse events.
Objectives Several reports had observed a high risk of pulmonary embolism (PE) in patients with coronavirus disease 2019 (COVID‐19), most of them in the intensive care unit. Reported findings indicate that a direct viral‐mediated hyperinflammatory response leads to local thromboinflammation. According to those findings, the incidence of deep venous thrombosis (DVT) in patients with COVID‐19 and PE should be low. The objective of this study was to evaluate the incidence of DVT in patients with COVID‐19 who developed PE. Methods In this prospective observational study, consecutive patients hospitalized in the internal medicine ward with a diagnosis of COVID‐19 who developed PE were screened for DVT in the lower extremities with complete compression ultrasound. Results The study comprised 26 patients. Fifteen patients (57.7%) were male. The median age was 60 years (interquartile range, 54–73 years). Compression ultrasound findings were positive for DVT in 2 patients (7.7%; 95% confidence interval, 3.6%–11.7%). Patients with DVT had central and bilateral PE. In both, venous thromboembolism was diagnosed in the emergency department, so they did not receive previous prophylactic therapy with low‐molecular‐weight heparin. Patients without DVT had higher median d ‐dimer levels: 25,688 μg/dL (interquartile range, 80,000–1210 μg/dL) versus 5310 μg/dL ( P < .05). Conclusions Our study showed a low incidence of DVT in a cohort of patients with COVID‐19 and PE. This observation suggests that PE in these patients could be produced mainly by a local thromboinflammatory syndrome induced by severe acute respiratory syndrome coronavirus 2 infection and not by a thromboembolic event.
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