The acute stage of lung infection in COVID-19 presents with ground glass opacities whereas the late-stage manifest as crazy pavy patterns and subpleural peripheral fibrotic bands. Some COVID-19 infection leading to progressive fibrotic lung disease was also reported in the literature. Anti-fibrotic drugs like pirfenidone and nintedanib in some cases had been proven to be beneficial [5]. The pathogenesis of post-viral pulmonary fibrosis is most likely due to the release of matrix metalloproteinase causing epithelial and endothelial injury [6]. Vascular endothelial growth factor, interleukin-6, and TNF- alpha are also being implicated in pulmonary fibrosis [7]. There are many etiologies for lung fibrosis; one of the causes is interstitial lung disease (ILD).
ILD is a heterogeneous group of disorders that are classified into four types: (a) ILD with a known cause like rheumatoid arthritis, asbestosis, connective tissue disorders, and hypersensitive pneumonitis; (b) idiopathic interstitial pneumonia (IIP) like idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia (NSIP), respiratory bronchiolitis associated ILD (RB-ILD), desquamative interstitial pneumonia (DIP), and acute interstitial pneumonia; (c) granulomatous ILD—sarcoidosis and silicosis; and (d) others include Langerhans cell histiocytosis (LCH) and lymphangioleiomyomatosis [8]. The common patterns of findings in ILD include a combination of reticulation, ground-glass opacities, honeycombing, traction bronchiectasis, nodules, and thickening of interlobular septa [9].
The most common idiopathic interstitial pneumonia includes usual interstitial pneumonia (UIP) and NSIP. UIP has typical findings of reticulation, bilateral subpleural symmetrical basal distribution of honeycombing [10]. The key finding in NSIP includes bilateral symmetrical ground-glass opacities in lower lobe predominance with subpleural sparing. Overtime, GGO can be replaced by reticulation [11]. The cardinal features of RB-ILD include centrilobular nodules, GGO, and smooth thickening of interlobular septa, distributed in the upper lobes. The imaging features of desquamative interstitial pneumonia are GGO in the mid and lower zones [8]. Smoking-related ILD includes RB-ILD, LCH, DIP, and combined pulmonary fibrosis with emphysema (CPFE). CPFE is characterized by the co-existence of UIP/NSIP with emphysema in smokers. The emphysematous changes in CPFE are often predominant in the upper zone.
The co-existence of interstitial lung disease and COVID-19 has been reported, and it has been postulated that patients with COVID-19 have an increased risk for developing interstitial lung disease [12]. In patients with preexisting ILD, COVID-19 infection has led to acute exacerbation of underlying ILD. The criteria for ILD exacerbation include subacute worsening of dyspnea and hypoxemia, new pulmonary infiltrates on imaging, and absence of pulmonary emboli, cardiac failure, and other non-pulmonary causes. Surgeries, aspiration of gastric contents, infection, and other factors have also been postulated for ILD exacerbation [13].
ILD renders the host susceptible to viral infection, although the exact etiology is unknown [14]. ILD exacerbation has the worst prognosis [15]. Patients with ILD exacerbation are treated with corticosteroids/other immunosuppressants. It was presumed that if the steroid is given to patients with COVID-19, it decreases the resistance against the virus [13]. To date, there are no clear data to support this fact. A recent study postulated that steroids were likely to be safe and beneficial in patients with severe respiratory disease [16]. In a case-control study by Esposito et al., patients with ILD in advanced age has increased the odds of the worse outcome in COVID-19 patients with underlying ILD [17].