ABSTRACT
Objective: To analyze the diagnostic accuracy of lung ultrasonography (LUS) and high-resolution computed tomography (HRCT), to detect COVID-19. Materials and Methods: This study recruited all patients admitted to the emergency medicine unit, due to a suspected COVID-19 infection, during the first wave of the COVID-19 pandemic. These patients also who underwent a standardized LUS examination and a chest HRCT. The signs detected by both LUS and HRCT were reported, as well as the sensitivity, specificity, positive predictive value, and negative predictive value for LUS and HRCT. Results: This cohort included 159 patients, 101 (63%) were diagnosed with COVID-19. COVID-19 patients showed more often confluent subpleural consolidations and parenchymal consolidations in lower lung regions of LUS. They also had "ground glass” opacities and "crazy paving” on HRCT, while pleural effusion and pulmonary consolidations were more common in non-COVID-19 patients. LUS had a sensitivity of 0.97 (95% CI 0.92–0.99) and a specificity of 0.24 (95% CI 0.07–0.5) for COVID-19 lung infections. HRCT abnormalities resulted in a 0.98 sensitivity (95% CI 0.92–0.99) and 0.1 specificity (95% CI 0.04–0.23) for COVID-19 lung infections. Conclusion: In this cohort, LUS proved to be a noninvasive, diagnostic tool with high sensitivity for lung abnormalities that were likewise detected by HRCT. Furthermore, LUS, despite its lower specificity, has a high sensitivity for COVID-19, which could prove to be as effective as HRCT in excluding a COVID-19 lung infection.
ABSTRACT
SARS-CoV-2 infection is characterized by extremely heterogeneous features, going from cases with few symptoms to severe respiratory failures. Chest Computed Tomography (CT) is currently the gold-standard imaging method, although burdened by the risk of exposure to ionizing radiation and management / organizational concerns. In particular, the critical patient undergoing ventilation (invasive or not) seems to be difficult to monitor by repeated CT scan over time. We report the case of a 55-year-old male patient subjected to Continuous Positive Airway Pressure (CPAP) and prone positioning, in which the use of ultrasound monitoring allowed to verify the effectiveness of the pressure support used in recruiting previously atelectasis lung areas. Lung ultrasound can guide pulmonary recruitment and pronation maneuvers in patients undergoing non-invasive ventilation. Ultrasound can identify atelectatic lung areas, which demonstrate an alveolar re-expansion following the setting of high PEEP values, as underlined by the reappearance of pleural/air interface.
ABSTRACT
Background: Thromboembolic disease is strongly associated with,or even an integral part of, COVID-19 pneumonia. Indeed, endothelial/microvascular damage to pulmonary capillaries seemsto be the main trigger of the pneumonia. Description of case: A 51-year-old man was referred to our emergency department for vomiting, fever and loss of appetite for aweek, cough and atypical chest pain towards the top of his sternum. Blood gas analysis revealed: pH 7.4, pCO2 40 mmHg, pO273.9 mmHg, P/F 352, and alveolar-arterial gradient 26 (expectedvalue for age: 17). Lung ultrasound showed minimum pleural effusion in the right basal field, while a round pleural-based consolidation was present with some B lines in the right field. A chest CTscan was therefore performed and showed filling defects compatible with non-occlusive bilateral thromboembolism. The nasopharyngeal swab was positive for SARS-CoV-2 infection. The echocolor Doppler did not reveal any venous thrombosis in the limbs. Conclusions: The final diagnosis was bilateral pulmonary embolismin a patient positive for COVID-19. Reports in the literature haveshown that thromboembolic disease is strongly associated with, oreven an integral part of, COVID-19 pneumonia. Indeed, endothelial/microvascular damage to pulmonary capillaries seems to bethe main trigger for pneumonia. Virus binding to pneumocytes viathe ACE-2 receptor causes pneumocytic damage with activation ofthe inflammatory response and release of prothrombotic factors.