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Lung fibrosis in patients recovering from COVID-19 poses higher risk, needs prolonged oxygen supplement
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  • Lung fibrosis in patients recovering from COVID-19 poses higher risk, needs prolonged oxygen supplement

Lung fibrosis in patients recovering from COVID-19 poses higher risk, needs prolonged oxygen supplement

Myupchar • December 21, 2020, 12:49:20 IST
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Immune hyper reaction, referred to as cytokine storm, due to uncontrolled release of an excessive amount of cytokines, has been reported as a major contributor to multi-organ dysfunction in SARS-CoV-2 infection.

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Lung fibrosis in patients recovering from COVID-19 poses higher risk, needs prolonged oxygen supplement

It is coming to a year since the first case of COVID-19 was detected and a worrying trend among recovered COVID-19 patients is being noticed. Some of them are returning to the hospital with post-COVID 19 lung fibrosis. Lung fibrosis refers to scarring of the lung tissue and is associated with permanent pulmonary architectural distortion and irreversible lung dysfunction. Generally, pulmonary fibrosis occurs due to severe lung injury, secondary to respiratory infections, chronic granulomatous diseases, medications and connective tissue disorders. Available clinical, radiographic and autopsy data has indicated that pulmonary fibrosis is central to severe acute respiratory distress syndrome (SARS) and Middle Eastern Respiratory Syndrome (MERS) pathology and current evidence suggests that pulmonary fibrosis could also complicate infection by SARS-CoV-2. Lung fibrosis in COVID-19 Fibrosis could be viewed as a consequence of a disordered wound healing process. Various mechanisms of lung injury in SARS-CoV-2 infected patients have been described, with both viral and immune-mediated mechanisms being implicated. An initial phase of lung injury is followed by acute inflammation as well as an attempt at repair. This process can result in the restoration of normal pulmonary architecture or it may lead to pulmonary fibrosis with architectural distortion and irreversible lung damage. Immune hyper reaction, referred to as cytokine storm, due to uncontrolled release of an excessive amount of cytokines, has been reported as a major contributor to multi-organ dysfunction in SARS-CoV-2 infection. Certain risk factors have been identified as predisposing for lung fibrosis post-SARS-CoV-2 infection. These include advanced age, history of smoking, severe illness, prolonged ICU stay and mechanical ventilation. Mechanical ventilation poses an additional risk of ventilator-induced lung injury (VILI), which can result in lung fibrosis. Elevated serum lactic acid dehydrogenase (LDH) levels during illness correlate to post COVID 19 sequelae (leftover complication or condition from a sickness). Serum LDH level has been used as a marker of disease severity following acute lung injuries and is an indicator of pulmonary tissue destruction. The mechanisms by which SARS-CoV-2 infection causes lung fibrosis are not fully understood but transforming growth factor-b (TGF-b) and angiotensin-converting enzyme 2 (ACE2)-mediated lung fibrosis are among the most documented ones. Long term effects A substantial proportion of patients who develop ARDS will experience residual long-term impairment of lung function and HRCT (high-resolution computed tomography) evidence of pulmonary fibrosis. These patients end up with permanent lung damage of varying degrees and might require home oxygen supplementation for a prolonged duration, even after recovering from COVID 19 infection. 
Hence, the role of anti-inflammatory drugs in the treatment of moderate to severe infections cannot be negated, especially in patients requiring oxygen support, where the use of steroids has shown definite mortality benefit. The role of available anti-fibrotic therapies like pirfenidone and nintedanib (which are used for the treatment of idiopathic pulmonary fibrosis) to prevent or reduce post-COVID fibrosis, is under evaluation. They aid broad anti-fibrotic activity, regardless of aetiology, and these drugs might have a role in attenuating pro-fibrotic pathways in SARS-CoV-2 infection. The burden of fibrotic lung disease following SARS-CoV-2 infection is likely to be high; therefore, given the scale of the pandemic, the global burden of fibrotic lung disease will probably increase considerably in the coming times. This article was written by Dr Richa Sareen, Consultant, Pulmonology and Critical Care Medicine, Fortis Hospital, Vasant Kunj, New Delhi.  For more information, read our article on COVID-19 and permanent lung damage. Health articles in Firstpost are written by myUpchar.com, India’s first and biggest resource for verified medical information. At myUpchar, researchers and journalists work with doctors to bring you information on all things health.

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COVID 19 SARS CoV 2 lung fibrosis Cytokine storm lactic acid dehydrogenase
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