Discussion:
COVID-19 infection has a wide spectrum of clinical course and can involve various organs. Lungs are the most common organs involved. Presenting complains include a dry cough, fever, myalgias, headache, dyspnea, sore throat, diarrhea, vomiting, ageusia and anosmia [7]. Most cases of COVID-19 infection are mild to moderate, whereas around 20 % progress to severe and critical illness. The long-term Respiratory sequelae of COVID 19 infection remains unclear, and may depend on disease presentation [8].
The greater part of research related to SARS-CoV-2 focuses on the management. To date, the treatment is largely supportive. Many drugs have been and are being investigated for this purpose, including hydroxychloroquine, Interleukin-6 pathway inhibitors such as tocilizumab, convalescent plasma, remdesivir and dexamethasone [2, 3, 9-11]. Among all the tested treatment modalities, the most promising results are from remdesivir and dexamethasone, as the preliminary reports show a reduction in hospital stay from the former and a reduced mortality by the latter.
The RECOVERY trial is investigating the role of dexamethasone in SARS-CoV-2 infection. Initial results show a decreased 28-day mortality in the treatment arm. However, this effect is seen only in the subset of patients requiring invasive and non-invasive mechanical ventilation [3]. Consequently, current guidelines recommend the use of dexamethasone only in moderate to severely ill patients [12].
In some patients, a second phase of dyspnea is seen after an interval asymptomatic recovery phase in patients successfully treated for COVID-19 pneumonia or ARDS. We propose two possible mechanisms behind this, post-infection fibrotic changes in the lungs or a continued subclinical infective process which becomes symptomatic again after some time. Fibrotic lung changes are reported in survivors with COVID-19 pneumonia and abnormalities in lung function have been detected in COVID-19 patients shortly after the discharge from the hospital [6, 13] . Our patient suffered from ongoing lung damage despite viral clearance and symptomatic recovery. This resulted in chronic lung changes as the pulmonary function test revealed a restrictive pattern with decreased diffusion capacity.
Pulmonary fibrosis usually occurs secondary to dysregulated healing process. Chronic inflammation can lead to fibrosis. The changes in the cellular and molecular environment in the lung tissue secondary to viral infection as in COVID are the key factors behind the fibrosis [14].
The ongoing damage takes place in the tissues secondary to the inflammation leading to an over expression of inflammatory cytokines, including transforming growth factor-1 , tumor necrosis factor-a (TNF-a), interleukin-1, and interleukin-6 (IL-6 ). This in turn stimulates the proliferation of type 2 alveolar cell and increase in fibroblast recruitment [15, 16]. Eventually, the cascade can lead to an increase the production and deposition of extracellular matrix (ECM), impairing gas exchange and hence leading to hypoxemia [16].
The long-term reversible and irreversible respiratory sequelae of COVID-19- remain obscure, as does the patient population at a high risk to develop them. Our patient had an excellent recovery with steroids. Authors are of the view that a large scale randomized controlled trial is required to establish the efficacy of steroids in post-COVID-19 recurrent dyspnea.