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The physical space of the MSK Library is scheduled to close to visitors on Friday, May 17, 2024. Please visit this guide for more information.
A wide variety of long-term respiratory complications secondary to COVID-19 have been described ranging from persistent symptoms and radiologically observable changes to impaired respiratory physiology.
Bronchiectasis, which in general carries a poor prognosis, has been reported after severe COVID-19, and could be either due to the disease itself or secondary to superimposed bacterial infection.
Cavitary lung disease is another complication of COVID-19. A study from UAE showed that 7% of patients admitted with COVID-19 pneumonia developed cavitation, most of whom were ICU patients. The cavities were either single or multiple with sizes between 3–10 cm with thick smooth walls and fluid level.
Pneumothorax has been reported in about 1% of hospitalized COVID-19 patients irrespective of whether they were ventilated or not. The overall survival of those who developed pneumothorax was about 63%. Age > 70 carried a poor prognosis. The mechanism for the development of delayed pneumothorax is not fully understood but could be related to damage of the alveolar walls due to the ongoing inflammatory process, or the formation of small alveolar blebs. Vigorous cough may also be a contributing factor. Therefore, physicians should consider the possibility of spontaneous pneumothorax in patients who recovered from COVID-19 pneumonia if their respiratory status deteriorates suddenly. It should be managed according to the established guidelines for secondary spontaneous pneumothorax.
In people recovering from COVID-19, there is evidence of potential long-term pulmonary sequelae and associated lung function impairment. The most severe illness in the context of SARS-CoV-2 infection is acute respiratory distress syndrome (ARDS). In some, the ARDS may result in fibrotic interstitial lung disease.
Several histopathological findings have been identified among COVID-19 autopsy cases, including severe peripheral lung tissue damage tissue. The most commonly reported histological pattern of lung injury was diffuse alveolar damage (DAD) with two identifiable stages; an acute stage, and a more organized stage of lung collapse.
According to a meta-analysis of COVID-19 inpatients, 14.8% developed acute respiratory distress syndrome (ARDS). DAD has long been considered the hallmark histologic finding in acute ARDS. Pulmonary fibrosis (PF) subsequent to ARDS is well-recognized and with the relatively high incidence of ARDS in among COVID-19 patients, it is not surprising there is an increase incidence of pulmonary fibrosis.
It is proposed that a subset of patients post-ARDS develop long-lasting symptoms with decreased lung function, a form of progressive interstitial lung disease (ILD). This post-COVID interstitial lung disease (PC-ILD) is not directly correlated to severity of initial COVID-19 infection. Many patients with only moderate acute infection had a higher burden of respiratory symptoms including cough in the long-term follow up compared to those with severe acute infections.
Pulmonary function abnormalities are seen as early as 2 weeks post-discharge of an acute SARS-CoV-2 infection, with decreased inspiratory vital capacity and forced vital capacity. Several studies have shown persistent lung function abnormalities at 3 and 4 months follow-up. Longitudinal follow-up has shown that lung function impairments improve over time. However, even after a year post-COVID-19, a proportion of patients will continue to have lung function impairment, raising the suspicion of long-term pulmonary complications such as the development of PF.
Persistent symptoms, lung function, and radiological abnormalities have been reported post-COVID-19. Several studies have demonstrated the gradual resolution of these findings over time including improvements in lung function impairment and radiological abnormalities. However, approximately 20-25% of these patients continued to exhibit ongoing radiological abnormalities and lung dysfunction at 12 months post-infection.
There remain several unanswered questions regarding PC-ILD. There is little doubt that a cohort of individuals have residual fibrotic changes at 12 months ranging from 1 to 29% in studies, however, pathologically whether that is related to fibrosis promoted by coronavirus itself or sequelae of severe infection and mechanical ventilation remains to be determined.
Pulmonary fibrosis is a chronic progressive and mostly fatal disease characterized by interstitial collagen deposition with varying degrees of alveolar bronchiolization. There are many causes of pulmonary fibrosis including connective tissue disease (CTD), smoking, drugs, and family history. Idiopathic pulmonary fibrosis (IPF) is a diagnosis of exclusion, perhaps more common among elderly males who are active or former smokers. It is known that viral infection can be a co-factor for IPF pathogenesis. Pulmonary fibrosis has been described in both short and long-term COVID-19 follow-up studies.
For short-term pulmonary fibrosis complicating acute COVID-19, many studies reported this complication in the course of acute COVID-19 and some cases even required immediate lung transplantation. For instance, pulmonary fibrosis described as collagen deposition and loss of lung aeration was the main pathological finding of the lung cryobiopsy performed for patients while on mechanical ventilation and after their death, which correlated with the HRCT signs of lung fibrosis conducted few days before the cryobiopsy.
Pulmonary fibrosis as a long-term complication of COVID-19 has been reported in many studies. One of the noteworthy studies is that by Huang et al. on long-term pulmonary complications among COVID-19 survivors. In their study, the patients were categorized into three groups according to the respiratory support requirement as follows:
Their results showed that 52.6% of the study population had radiological abnormalities 6 months post-COVID-19. These abnormalities decreased significantly on follow-up CT 1-year post-COVID-19; however, they were more likely to persist among patients with severe disease.
These patients particularly had a higher percentage of disease at follow-up 6 months post-COVID-19 than that at the baseline, which speculates the progression of the disease to irreversible fibrosis.
This chronic and mostly irreversible radiological abnormality coincided with functional abnormalities, where almost 39% and 57% of survivors of severe COVID-19 (Scale 5–6) had reduced total lung capacity (TLC) of <80% and reduced diffusion capacity of carbon monoxide (DLCO) of <80%, respectively. This functional reduction persisted during the 12-month follow-up period.