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Year : 2021  |  Volume : 1  |  Issue : 2  |  Page : 37

Long-term impact of COVID-19 on lung health and function

Department of Pulmonary Medicine DM Wayanad Institute of Medical Sciences, Wayanad, Kerala, India

Date of Submission18-May-2021
Date of Decision23-May-2021
Date of Acceptance23-May-2021
Date of Web Publication21-Jun-2021

Correspondence Address:
Prof. Ravindran Chetambath
Navaneeth, Sarovaram-Biopark Road, Calicut, Kerala - 673 020
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jalh.jalh_11_21

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How to cite this article:
Chetambath R. Long-term impact of COVID-19 on lung health and function. J Adv Lung Health 2021;1:37

How to cite this URL:
Chetambath R. Long-term impact of COVID-19 on lung health and function. J Adv Lung Health [serial online] 2021 [cited 2021 Oct 21];1:37. Available from: http://www.jalh.com/text.asp?2021/1/2/37/318908

As chest physicians, preservation of lung function and health is our top priority. Traditionally, tobacco smoking has been regarded as the worst enemy to lungs. Clinicians' perspectives have taken a sidewise turn in the last year and a half with our conventional thinking process on lung protection strategies taking a backward step. This is mainly attributed to the onset of coronavirus disease-2019 (COVID-19) pandemic. It is uniformly agreed upon that COVID-19 primarily and predominantly affects the upper and lower respiratory tract before attacking other organs in the body. Hence, major concerns for practitioners would be COVID pneumonia, acute respiratory distress syndrome (ARDS), and pulmonary vascular thrombosis. With the passage of time and accumulation of evidence, the long-term pulmonary sequelae of COVID-19 are being increasingly appreciated.

Most people, who have pneumonia due to COVID-19, recover completely within a few weeks. While the vast majority is left behind with no residual lung damage, considering the sheer number of COVID-19 victims, it is likely that a substantial number will be left with residual lung fibrosis. Our past experience has taught us that a sizeable proportion (about 25%) of patients who developed ARDS in the pre-COVID era, irrespective of etiology, are left behind with functional and structural pulmonary sequalae.

Prospective data on COVID-19 patients tend to suggest that the lung changes gradually stabilize and resolve to a significant extent over time with progressive fibrosis being a rarity. In general, the extent of abnormalities persisting on follow-up high-resolution computed tomography (HRCT) scans and severity of functional limitation correlates with the severity of COVID disease. However, it may be noteworthy that some people who had mild versions of the disease continue to experience symptoms after their initial recovery. These patients who had mild upper respiratory infection during COVID positivity present with extensive lung lesions after 4–8 weeks of COVID negativity with the ground-glass opacities giving way to peripheral honeycombing. Whether this represents a progressive self-perpetuating fibrotic process triggered by COVID-19 infection or unmasking of an otherwise quiescent fibrotic lung disease is unclear, and clear-cut scientific explanation is lacking at this moment of time. We recently encountered a young patient who presented with breathlessness after 4 months of COVID negativity. He had minimal symptoms only during the active phase of disease. HRCT at 4 months showed multiple areas of ground-glass shadows and subpleural fibrosis with a reported radiological severity score of 11/25.

Post-COVID lung fibrosis is an already recognized entity, and treatment protocols have been devised. Patchy ground glassing suggests acute inflammation, and areas of organizing pneumonia are a subacute process. How can we attribute acute inflammation in a patient who had COVID infection 4 months back? This clinical scenario is seen in many patients 8–12 weeks after COVID negativity. Is this a slow resolving inflammation or a granulomatous inflammation? Delayed symptoms, delayed lung involvement, and radiological lesions resembling acute inflammation are all seen as manifestations of SARS-CoV-2 infection. Can we include this in post-COVID-19 syndrome or “long COVID-19.” These health issues are generally considered to be effects of COVID-19 that persist for more than 4 weeks after a diagnosis of COVID-19 virus. Following SARS-CoV-2 pneumonitis, cohorts of patients are left with both radiological inflammatory lung disease and persistent physiological and functional deficit. Early treatment with corticosteroids was well tolerated and associated with rapid and significant improvement. Are these principles extrapolatable to COVID-19? Probably, we need more insight into the pathogenesis of COVID lung lesions to categorize and manage these patients effectively.

Editorial Team

Journal of Advanced Lung Health


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