With input from Dr Monica Vasudev

1253:  

IMA-CMAAO Webinar on “Post-COVID pulmonary fibrosis”

19^th December, 2020, 4-5pm

Participants: Dr KK Aggarwal, President CMAAO, Dr RV Asokan, Hony Secretary General IMA, Dr Jayakrishnan Alapet, Dr Brijendra Prakash, Dr T Narasinga Reddy, Dr S Sharma

Faculty:  Dr Rajesh Chawla, Senior Consultant, Respiratory Medicine and Critical Care, Indraprastha Apollo Hospitals, Delhi, Past President, ISCCM 

• COVID-19 leads to a wide spectrum of respiratory diseases with a very high incidence of ARDS.
• Patients with idiopathic pulmonary fibrosis are at higher risk of severe COVID-19 as risk factors are common for both.
• Post-COVID fibrosis is likely to be a substantial problem given the magnitude of the pandemic.
• Giving high FiO2 or HFNC oxygen or noninvasive ventilation has definitely led to increase in fibrosis. Avoiding use of high FiO2 has enabled early extubation and patients do not develop fibrosis.
• Duration of disease determines the incidence of fibrosis.
• In patients with ARDS, the incidence of fibrosis is 4% with disease duration less than 1 week; the incidence increases to 61% with a disease duration of greater than 3 weeks (Lancet Respir Med. 2013).
• The pathological feature of ARDS is diffuse alveolar damage. There is an initial acute inflammatory exudative phase followed by an organizing phase and then fibrotic phase.
• Analysis has shown that 47% of COVID-19 patients had impaired gas transfer and about 25% had reduced total lung capacity. More than one-third of recovered patients develop fibrotic abnormalities.
• Cytokine storm may initiate and promote pulmonary fibrosis. VEGF and cytokines such as IL-6 and TNF-α are also involved in the fibrotic process.
• Diffuse alveolar damage, which is the defining feature of ARDS, has been the characteristic histological feature in fatal COVID-19 cases.
• COVID-induced ARDS is different from the classical ARDS. CT findings in many COVID cases are also not suggestive of classical ARDS.
• Pathological findings point to alveolar epithelial cells being the site of injury, and not the endothelial cells.
• Predictive risk factors for pulmonary fibrosis are age, severity of illness, length of ICU stay and mechanical ventilation (ventilation-induced lung injury), smoking and chronic alcoholism.
• Lung fibrosis is seen more often in persons with advanced age.
• Presence of comorbidities and lab findings of lymphopenia, leukocytosis and high LDH correlate with increased disease severity. Serum LDH is a predictor of destruction of lung tissue.
• Smokers are 1.4 times more likely to have severe symptoms of COVID-19, 2.4 times more likely to need ICU admission and mechanical ventilation.
• Severe the disease, more are the chances of developing pulmonary fibrosis.
• Damage to the lung tissue by COVID-19 could be reversible for the common COVID-19 patients. It has been shown that lung lesions of almost 65% discharged patients were fully absorbed after a follow-up of 4 weeks.
• Pulmonary function tests show reduced FEV1 and FVC (restrictive defect), reduced lung volume and decreased diffusion capacity.
• IL-6 is generally considered to be pro-fibrotic.
• Prolonged low dose steroids may prevent lung remodeling in survivors, although risk-benefit ratio should be evaluated before use.
• Pirfenidone has anti-fibrotic, anti-oxidative and anti-inflammatory effects.
• Nintedanib confers a theoretically increased risk of bleeding when co-administered with full-dose anticoagulation.
• Antifibrotic therapies might have potential as novel therapeutics for severe COVID-19.
• Pirfenidone and nintedanib are available only as oral formulations and so cannot be used in patients who are intubated or mechanically ventilated.
• Pirfenidone should be avoided if eGFR is less than 30 ml/min per 1.73 m2. Both pirfenidone and nintedanib can cause hepatotoxicity.
• The existing antifibrotic therapies do not address the immune dysregulation or attenuate the prothrombotic state.

Dr KK Aggarwal

President CMAAO, HCFI and Past National President IMA