Interstitial lung disease (ILD) is a broad term encompassing various conditions characterized by inflammation or fibrosis within the lung interstitial space. The primary consequence of ILD is impaired gas exchange, which leads to progressive symptoms such as dyspnea, dry cough, shortness of breath, and fatigue, ultimately resulting in respiratory failure and death. In the early stages, ILD is often associated with excess conditions, closely related to external pathogens invading the lung and local qi stagnation with blood stasis. Lung qi stagnation is the core pathological mechanism. In the middle and late stages, due to stagnation of qi, blood stasis, phlegm-dampness, and heat, the lung collaterals become obstructed, leading to lung atrophy with dysfunction, with qi deficiency and insufficient function as the core pathological mechanisms. Professor Zhang Hongchun emphasizes the "excess-deficiency" nature of ILD. He advocates for recognizing, diagnosing, and treating the disease from both the excess and deficiency perspectives, adjusting treatment based on the disease course and pathology. In the early stage of ILD, the condition is primarily one of "lung qi stagnation with obstruction of the collaterals" , and treatment focuses on dispersing stagnation, expelling pathogens, and resolving blockages. In the later stages, the disease is more often characterized by "lung deficiency with collateral atrophy" , and treatment should focus on tonifying the lungs, unblocking the collaterals, and promoting recovery of lung function. This paper discusses the treatment of ILD based on the principles of "lung qi stagnation with obstruction of the collaterals" and "lung deficiency with collateral atrophy" through clinical cases.

interstitial lung disease;pulmonary fibrosis;clinical experience;lung impediment;lung atrophy