Features of lung impairment due to COVID-19 in patients of the first wave of the pandemic (literature review)

• Published in: Medychni perspektyvy 2022-01, Vol.27 (4), p.20
• Main Authors: Yu.I. Feshchenko, Iashyna, L A, Opimakh, S G, Gumeniuk, G L, Ignatieva, V I, Polianska, M A, Zvol, I V, Moskalenko, S M
• Format: Article
• Language: Ukrainian
• Subjects: COVID-19; Literature reviews; Pandemics; Pneumonia; Pulmonary fibrosis; Respiratory distress syndrome
• ISSN: 2307-0404
• DOI: 10.26641/2307-0404.2022.4.271118

During the COVID-19 pandemic number of patients suffering from symptoms, decreased work ability and the deterioration in quality of life for several weeks and even months after the onset of the disease is increasing. The aim of the literature review is to search and study the existing literature data regarding the lung impairment features in COVID-19, as well as the morphological and pathophysiological prerequisites for the long-term respiratory disorders in patients who have had this disease. The most common complaints of patients after acute COVID-19 are fatigue, dyspnea, cough and chest discomfort. In these cases restrictive pattern in the pulmonary function test, a reduced gas transfer and persistent changes in computed tomography often in the form of fibrosis are observed, less often in the form of bullous-emphysematous changes, bronchiectasis and pleural effusion. The main pathophysiological mechanisms of acute lung impairment in COVID-19 are direct viral toxicity, impaired function of the immune system, hyperinflammatory response, endotheliopathy, microcirculatory disorders and increased blood clotting with small and large vessels thrombosis, which can lead to pneumonia or acute respiratory distress syndrome. After the acute phase of COVID-19 the pathology of the lung can be caused by an immunogenic and hyperinflammatory response, hypercoagulability and lead to pulmonary fibrosis. The possible mechanisms of the pulmonary fibrosis are thrombotic processes, hemosiderosis, necrotic capillaritis, angiogenesis, hypoxia, cytokine storm. Thus abnormal immune response, hyperinflammation, endothelial dysfunction and excessive coagulation not only cause pneumonia or acute respiratory distress syndrome in acute COVID-19, but also may persist for a long time and contribute to pulmonary fibrosis in some patients. The causes of a longer duration and increased severity of the lung impairment in some people compared to others are the subject of current investigations.