Interstitial Lung disease (ILD) is also called diffuse lung disease, interstitial pneumonia, and pulmonary fibrosis, depending on the extent of the lesions. It is a group of diseases with diffuse exudation, infiltration, and fibrosis of the interstitial lung as the main lesions, including more than 100 species. Since the 1980s, many authors have put together a large group of diseases with predominantly interstitial lesions for multifaceted studies. It is considered that it is not an independent disease, but a group of diseases with many etiologies, pathogenesis, pathological changes, natural evolution, treatment and prognosis are not identical, while the clinical manifestations, X-ray changes and lung function damage are very similar, and the etiological diagnosis is difficult, we call this group of diseases collectively as interstitial lung disease.
First, the etiology: the cause is clear and the cause is not known two major categories.
(a) The cause is clear 35%, may have.
1, inhalation of inorganic dust: silica, asbestos, talc, antimony, aluminum, coal, beryllium (occupational disease, silicosis, coal pneumoconiosis).
2, inhalation of organic dust: mold grass dust, cane dust, cotton dust, mushroom millers lung, bird feeders lung, varicella lung (allergic pneumonia, eosinophilic lung infiltration)
3.Radiation damage
4, infection: viruses, bacteria, fungi, parasites (Pneumocystis carinii pneumonia)
5.Inhaled gas: sulfur dioxide, high pus oxygen, chlorine, nitrogen oxide, soot, lipids, mercury vapor, chemical dust, synthetic fiber, electric end, etc.
6.Drugs: Ketomycin, cyclophosphamide, methotrexate (MTX), self-extinguishing, amiodarone, bleomycin, etc.
(ii) 65% of the cases with unknown causes.
1, idiopathic pulmonary interstitial fibrosis (IPF), also known as common interstitial pneumonia (UIP).
2, connective tissue disease caused by interstitial fibrosis: (rheumatoid arthritis, polymyositis, dermatomyositis, progressive systemic sclerosis, systemic lupus erythematosus)
3.Nodular disease
4, histiocytosis
5, pulmonary-renal syndrome.
6, Idiopathic pulmonary ferritin-containing hyperplasia
7, Wegener’s granulomatosis
8, chronic eosinophilic pneumonia
9, diffuse amyloidosis
10, alveolar proteinosis
Bronchoalveolar carcinoma
II. Diagnosis.
(a) Medical history: The medical history of ILD patients is quite important and can suggest the cause of the disease. Ask for the history of occupational exposure, history of living environment (unit and home), history of medication use, and genetic history.
(B) The main clinical manifestations: most of the disease is insidious, progressive aggravation, the main manifestations are
1. Progressive shortness of breath, dyspnea, and reduced tolerance to activities.
2. A few have dry cough or a small amount of white sputum or white foamy sputum.
3.Late stage of hypoxemia, cyanosis, and type I respiratory failure.
4.There are fine wet rales in the lower lateral chest of both lungs and the lung bases, and the velcro sounds are mostly absent in inspiration.
5, respiratory acceleration > 24 times/min, respiratory movement is reduced.
6.Some patients (30%~50%) have rod-shaped toes (mainly seen in idiopathic interstitial pulmonary fibrosis).
7.The end stage shows respiratory failure and pulmonary heart disease.
III. Laboratory tests.
(A) General examination: WBC count or classification suggests the presence of infection. Immunochemical abnormalities suggest a possible etiologic diagnosis (IgA.M.G.E; a1, g globulin, complement, ANA profile, RF, CRP, ESR).
Tumor markers are excluded.
(ii) X-ray features.
1.Grinded glass-like changes
2. Grid-like changes
3, mesh-like nodules or nodules with small shadow changes
4.Honeycomb lung
The above changes often coexist, and are accompanied by a reduction in lung volume. Chest film changes and lesions are not necessarily parallel, about 5-10% of pathological diagnosis and normal chest film, about 10% have symptoms without pathological changes.
(D) Pulmonary function test: It has important value for diagnosis and determination of efficacy.
The main manifestations are restrictive performance usually air dysfunction and reduced diffusion function.
Bronchoscopy is important for diagnosis, and lung tissue is obtained through bronchoscopy for pathological examination, and lung cell lavage fluid examination is of considerable importance for etiological diagnosis and treatment prognosis.
Arterial blood gas analysis: hypoxia, decreased partial pressure of oxygen.
(E) Treatment: firstly, find the etiology of the disease and provide targeted treatment according to the etiology. Etiological diagnosis is difficult. Early on, it is often misdiagnosed as bronchitis and pneumonia, and failure to get effective treatment delays the condition and makes future treatment and prognosis difficult. The treatment of the disease varies depending on the patient’s etiology, condition, physical status, and severity. Patients with similar manifestations are recommended to go to a hospital with the conditions to have an early diagnosis and receive appropriate treatment.
To summarize the characteristics of this disease: 1, progressive dyspnea, hypoxemia; 2, HRCT is very helpful for the diagnosis of this disease, manifested as: diffuse ground glass shadows, lattice-like fibrous strip-like shadows, patchy shadows, nodular shadows and honeycomb shadows in both lungs; 3, lung function is manifested as restrictive ventilation impairment, diffusion function is reduced; 4, lung biopsy pathology or lung cell lavage fluid analysis is very helpful for the diagnosis, treatment and prognosis of this disease. 4, lung biopsy pathology or lung cell lavage fluid analysis is of great help in the diagnosis, treatment and prognosis of the disease.
The number of patients suffering from this disease is increasing day by day, and if there is a lack of understanding of it, it is often misdiagnosed as chronic bronchitis and obstructive emphysema, bronchial asthma, the disease is diagnosed early and seize the time for effective treatment, most of the patients can improve or be cured, on the contrary, the prognosis will be very poor if the treatment is mistaken and develops into pulmonary fibrosis.