Post-COVID-19 Pulmonary Fibrosis: Facts-Challenges and Futures: A Narrative Review

Abstract

Patients with coronavirus disease 2019 (COVID-19) usually suffer from post-acute sequelae of coronavirus disease 2019 (PASC). Pulmonary fibrosis (PF) has the most significant long-term impact on patients' respiratory health, called post-COVID-19 pulmonary fibrosis (PC19-PF). PC19- PF can be caused by acute respiratory distress syndrome (ARDS) or pneumonia due to COVID-19. The risk factors of PC19-PF, such as older age, chronic comorbidities, the use of mechanical ventilation during the acute phase, and female sex, should be considered. Individuals with COVID-19 pneumonia symptoms lasting at least 12 weeks following diagnosis, including cough, dyspnea, exertional dyspnea, and poor saturation, accounted for nearly all disease occurrences. PC19-PF is characterized by persistent fibrotic tomographic sequelae associated with functional impairment throughout follow-up. Thus, clinical examination, radiology, pulmonary function tests, and pathological findings should be done to diagnose PC19-PF patients. PFT indicated persistent limitations in diffusion capacity and restrictive physiology, despite the absence of previous testing and inconsistency in the timeliness of assessments following acute illness. It has been hypothesized that PC19-PF patients may benefit from idiopathic pulmonary fibrosis treatment to prevent continued infection-related disorders, enhance the healing phase, and manage fibroproliferative processes. Immunomodulatory agents might reduce inflammation and the length of mechanical ventilation during the acute phase of COVID-19 infection, and the risk of the PC19-PF stage. Pulmonary rehabilitation, incorporating exercise training, physical education, and behavioral modifications, can improve the physical and psychological conditions of patients with PC19-PF.

Keywords: Antifibrotic treatment; COVID-19; Post-COVID-19 pulmonary fibrosis (PC19-PF); Post-acute sequelae of coronavirus disease 2019 (PASC); Pulmonary fibrosis (PF).

Fig. 1

Process of post-COVID pulmonary fibrosis and risk factors. ACE-2 angiotensin-converting enzyme, DAMP damage-associated molecular patterns, ANG II angiotensin II, EGF epidermal growth factor, PDGF platelet derived growth factor, TGF-β tumor growth factor β

Fig. 2

Pathophysiological mechanisms of post-COVID pulmonary fibrosis. ACE-2 angiotensin-converting enzyme, ECM extracellular matrix, MoAM monocyte-derived alveolar macrophages

Fig. 3

Chest CT scan of patient with post-COVID-19 pulmonary fibrosis demonstrating diffuse ground-glass opacities and consolidations, predominantly in lower lung lobes