What Is Basilar Pneumonia?

Lung anatomy illustration Lung anatomy illustration
Interstitial lung disease (ILD) is based on the pathological changes of diffuse lung parenchyma, alveolitis, and interstitial fibrosis, with active dyspnea, X-ray chest radiography showing diffuse shadows, restrictive ventilation disorders, Decreased diffuse function (DLCO) and hypoxemia are the general term for the clinicopathological entities composed of different disease groups with clinical manifestations. ILD is usually not malignant and is not caused by a known infectious pathogen. Mucus and thick sputum may be accompanied by secondary infections, with systemic symptoms such as weight loss, fatigue, anorexia, and joint pain in the extremities, and fever in the acute phase.

Overview of interstitial pneumonia

Lung anatomy illustration
Interstitial pneumonia is inflammation of the interstitial tissue of the lung. Inflammation mainly invades the bronchoalveolar and alveolar walls, especially the connective tissue between the lobules and the alveolar spaces around the blood vessels around the bronchi, and is mostly necrotic.
Interstitial pneumonia is mostly caused by viruses, mainly adenovirus, respiratory syncytial virus, influenza virus, parainfluenza virus, measles virus, etc. Among them, interstitial pneumonia caused by adenovirus and influenza virus is more common and relatively Severe, often with necrotizing bronchitis and bronchial pneumonia, the course of the disease is prone to become chronic pneumonia.
Mycoplasma pneumoniae can also cause interstitial pneumonia. Mycoplasma mainly invades the bronchioles and surrounding bronchi after invasion through the respiratory tract, and can completely recover because there is no destructive disease.

Interstitial pneumonia disease description

Respiratory system anatomy diagram
The term Interstitial lung Disease (ILD) was coined as early as the 18th Aspen Pulmonary Symposium in 1975. After 10 years (1985), the 28th Aspen Pulmonary Symposium discussed ILD again. Although the research on ILD has made great progress in the past ten years, there are still different understandings of its concept and classification, especially the idiopathic pulmonary interstitial fibrosis in ILD (also known as The classification of idiopathic interstitial pneumonia and idiopathic fibrotic alveolitis is more controversial, and no consensus has been reached.
ILD is a group of diseases caused by the alveolar wall as the main lesion. Diffuse pulmonary parenchyma, alveolitis, and interstitial fibrosis are the basic pathological changes. Active dyspnea, X-ray chest X-rays show diffuse shadows, and restrictions. Hypoventilation, reduced diffuse function (DLCO), and hypoxemia are the general term for the clinicopathological entities composed of different disease groups with clinical manifestations. ILD can be acute, subacute, and chronic. In the acute phase, lesions or inflammatory lesions are the main, and in the chronic phase, fibrotic lesions are the main. The lung parenchyma refers to the bronchial and alveolar structures at all levels. Pulmonary interstitial refers to supporting tissues other than the alveolar and terminal bronchial epithelium, including blood vessel and lymphatic tissue. The normal interstitial lung mainly includes two components: cells and extracellular matrix. Cell components account for 75% of the lung interstitial, of which 30% to 40% are mesenchymal cells; the rest are inflammatory cells and immune-active cells.
Mesenchymal cells include: fibroblasts, smooth muscle cells, and perivascular cells. Inflammatory cells and immune cells include: mononuclear macrophages (about 90%) and lymphocytes (about 10%) and a small amount of mast cells. Lymphocytes are mainly T lymphocytes (about 3/4 of the lymphocytes),
lung
A small number (7% to 8%) are B cells, and the rest are non-T and non-B ineffective cells (about 20%). These inflammatory cells, especially monocytes, can produce many chemical mediators or cytokines. The lungs play a major role in the pathogenesis of inflammatory lesions of the lung. The extracellular matrix includes extracellular matrix and connective tissue fiber components. The latter are mainly collagen fibers (about 70%), followed by elastic fibers; the former are mainly basement membrane, some other glycoproteins, laminin, fibronectin, and other matrix proteins or glycoproteins. The space between adjacent alveoli is called the interstitial membrane, and there are capillaries and lymphatic vessels in the cavity. There are endothelial cells on the surface of the pulmonary capillary wall, and the basement membrane is underneath. The connections between the endothelial cells are loose, and there are wide and uneven gaps in the adjacent areas, with an average of 4-5 nm. Inside the plastid cavity. Capillaries are closely attached to the alveolar wall in the interstitial cavity. One side is a thin interstitial cavity to ensure high ventilation efficiency of blood and gas; the other is a thick layer cavity for interstitial fluid storage and blood vessels- Interstitial cavity-regulation of fluid movement between alveoli. The terminal lymph nodes distributed in the interstitial cavity can reach the space of the pulmonary capillary network around the alveoli, attract the water and protein in the interstitial cavity, maintain the water storage in the interstitial cavity, and prevent the interstitial and even alveolar edema. When lung interstitial lesions occur, the number and nature of the above components will change-the activation and participation of inflammatory cells, the destruction of tissue structures, the increase of fibroblasts, the deposition and repair of collagen fibers, etc., together form the tissue of ILD Pathological characteristics. It should be noted that the infiltration of inflammation and the repair of fibers are by no means limited to the interstitial, but can also be seen in the alveoli, alveolar ducts, respiratory and terminal bronchioles.

Causes of interstitial pneumonia

Etiology is clear
Inhalation of inorganic dust: silicon dioxide, asbestos, talc, antimony, beryllium, coal, aluminum, tin, iron.
Inhalation of organic dust: mold dust, cane dust, mushroom lung, pigeon feeder disease, cotton dust, synthetic fibers, bakelite radiation damage.
(3) Microbial infections: viruses, bacteria, fungi, pneumocystis carinii, and parasites.
Drugs: cytotoxic chemotherapy drugs, leukoamine, cyclophosphamide.
cancerous lymphangiitis; pulmonary edema.
Inhaled gas: oxygen, sulfur dioxide, chlorine, nitrogen oxide, soot, lipid, mercury vapor
Etiology unknown
Idiopathic pulmonary interstitial fibrosis (also known as cryptogenic fibrotic alveolitis, idiopathic interstitial pneumonia). Acute interstitial pneumonia, desquamative interstitial pneumonia, collagen vascular diseases: systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis, polymyositis-dermatomyositis, Sjogren syndrome, knot Arthritis, histiocytosis, pulmonary hemorrhage-nephritis syndrome, idiopathic pulmonary hemosiderin, Wegener's granulomatosis, chronic eosinophilic pneumonia, alveolar proteinosis, hereditary pulmonary fibrosis, nodules Sclerosis, neurofibromas, pulmonary vascular bed interstitial lung disease, primary pulmonary hypertension, diffuse amyloidosis, occlusive bronchiolitis, and organizing pneumonia. The known etiology accounts for about 35% of all ILDs. Occupational exposure is the most common cause. Among them, inorganic dust is the most common cause, and organic dust is increasing. Organic dust is also called allergic alveolitis, which usually occurs due to a previous history of allergies and when inhaled with foreign protein or polysaccharide. Unexplained ILD accounts for 2/3 of all cases, with idiopathic pulmonary fibrosis, sarcoidosis, and collagen vascular disease being the most common manifestations in the lungs, histiocytosis, pulmonary-renal syndrome, and pulmonary vasculitis. Primary hemosiderinosis followed.

Interstitial pneumonia signs

ILD is usually not malignant and is not caused by a known infectious pathogen. Although the disease has an acute phase, the onset is often insidious and the course of the disease develops chronically. The body initially responds to the lungs and the alveolar wall as an inflammatory reaction, leading to alveolitis, and eventually the inflammation will spread to the adjacent stroma. Interstitial fibrosis will eventually occur in some parts and blood vessels, leading to scarring and destruction of lung tissue, reducing ventilatory function, and inflammation can also affect trachea and capillary bronchi, often with organizing pneumonia, which is also a manifestation of interstitial pneumonia . This group of diseases has many common characteristics, including similar symptoms, X-ray signs, and pulmonary function tests. Mucus and thick sputum may be accompanied by secondary infections, with systemic symptoms such as weight loss, fatigue, anorexia, and joint pain in the extremities, and fever in the acute phase.
Signs: Shortness of breath, cyanosis, Velcro snoring (continuous, high-pitched popping sounds) can be heard in the middle and lower lungs, with clubbing fingers, of which Velcro snoring is the most characteristic.
Classification: The classification of interstitial lung disease is not unified, and can be divided into acute, subacute and chronic according to the severity of the disease.

Pathophysiology of interstitial pneumonia

Activated macrophages regulate lymphocyte function and secrete inflammatory mediators such as complement components, prostaglandin, collagenase, elastase, neutral protease, plasmin activator, beta glucuronidase, angiogenic factor , Fibroblast growth factor and neutrophil chemokine. Activated T lymphocytes can secrete lymphokines, such as macrophage migration inhibitory factor, leukocyte inhibitory factor, monocyte chemotactic factor, and macrophage activating factor. B lymphocytes can secrete IgG, IgA, and IgM. Neutrophils can secrete collagenase, elastase, neutral protease (Cathepsin G), acid protease (Cathepsin D), -glucuronidase, and inflammatory pathways that activate various body fluids.
Pathological classification
Classified by pathological changes:
Non-inflammatory and non-tumor diseases: such as sarcoidosis and exogenous allergic granulomatous alveolitis.
Granulomatous interstitial lung disease: such as chronic interstitial pulmonary edema, alveolar proteinosis, primary pulmonary hemoxanthinosis, uremia and so on.
Pulmonary-specific inflammation: such as common interstitial pneumonia, occlusive bronchiolitis and organizing pneumonia (BOOP), exogenous irritating smoke, fluid, and other toxic irritating chronic interstitial pneumonia, acute respiratory distress Syndrome (ARDS), idiopathic pulmonary fibrosis, and pulmonary vasculitis.
Inorganic dust inhalation occupational disease.
Hyperplasia and neoplastic lesions: such as primary bronchioalveolar carcinoma induced interstitial lung lesions, diffuse Hodgkin's lymphoma.
Pulmonary interstitial fibrosis and honeycomb lung (end stage lung).
Classified by the type of cell aggregated in the alveolar structure:
Macrophage-lymphocyte-neutrophil type: neutrophil-type alveolitis for short. Macrophages still account for the majority, but neutrophils increase, and they accumulate in the alveolar structure for a long time, which is the most typical feature of this type. Lesions of this type are: idiopathic pulmonary fibrosis (cryptogenic fibrosing alveolitis), familial pulmonary fibrosis, chronic interstitial pulmonary fibrosis associated with collagen vascular diseases, histiocytosis X and asbestos lung.
Macrophage lymphocyte type: referred to as lymphocytic alveolitis. Both macrophages and lymphocytes increased, but lymphocytes increased relatively more than macrophages. Neutrophils do not increase. Sarcoidosis, allergic pneumonia, and beryllium poisoning all belong to this type. Acute alveolitis occurs in the lung parenchymal cells by the direct action of a pathogenic factor, or by the indirect effects of inflammation and the immune cell system. In the stage of alveolitis, if the cause is removed or treated, the lesions can be reversed; when acute alveolitis becomes chronic, neutrophils secrete collagenase and elastase, destroying type I collagen and alveolar walls, and affect the reversibility of the lesion. If the disease develops further, the collagen fibers in the interstitial tissue are disordered, and a large amount of fibrous tissue is seen on the microscopy, the alveolar septum is destroyed, and cystic fibrosis is formed. The damaged alveolar wall cannot be restored; the lesion further develops into complete damage to the alveolar structure, forming extensive cystic fibrosis.
Stage of disease
Phase I
Lung parenchymal cells are damaged and acute alveolitis occurs. Proliferation, recruitment and activation of inflammatory and immune effector cells. In the bronchoalveolar lavage fluid of idiopathic pulmonary fibrosis, an immune complex was confirmed, which can stimulate macrophages to secrete neutrophil chemokines and cause neutrophils to aggregate in the alveolar structure. Activated macrophages and neutrophils are capable of secreting collagenase. Follow-up review of bronchoalveolar lavage for 8 to 24 months, collagenase activity still exists, activated collagenase can destroy interstitial collagen of alveolar structure (in acute pneumonia such as pneumococcal, neutrophils The time is short, so it will not cause progressive and permanent damage to interstitial connective tissue.
Macrophages isolated from bronchoalveolar lavage fluid from idiopathic fibrosis and sarcoidosis were cultured in RPMI-1640-free medium, respectively, and the rate of fibronectin production was 20 times faster than that of normal macrophages. Times and 10 times. Fibronectin has chemotactic effects on lung fibroblasts and plays an important role in the formation of interstitial fibrosis. Sarcoidosis T lymphocytes can secrete lymphokines and cause granuloma formation. In the stage , the lung parenchymal damage is not obvious, and if the stimulus is eliminated, the lesion can be recovered.
Phase II
Alveolar inflammation becomes chronic, and the acellular and cellular components of the alveoli are progressively damaged, causing changes in the number, type, location, and / or differentiation properties of lung parenchymal cells. Type epithelial cells were damaged, and type epithelial cells proliferated and repaired. The evolution from stage to stage is faster or slower, and the elderly can reach several years. Affected by various factors such as the duration of exposure, the effectiveness of the lung defense mechanism, the size of the damage, the integrity of the basement membrane, and the susceptibility of the individual, the destruction of the alveolar structure has gradually become irreversible.
Phase III
It is characterized by a disorder of interstitial collagen, and a large amount of fibrous tissue proliferation can be seen by microscopy. Fibrous tissue proliferation is not simply caused by fibroblast activation, but is caused by various complex factors such as collagen synthesis and various types of cellular abnormalities. The collagen tissue is broken, the alveolar septum is destroyed, and cystic changes are formed. By stage III, most of the alveolar structure was damaged and significantly disturbed, and recovery was impossible.
Stage IV
This disease is advanced. The alveolar structure was completely damaged and replaced by diffuse nonfunctional cystic changes. The basic structure and characteristics of various types of interstitial fibrosis cannot be identified.

Interstitial pneumonia diagnostic test

Interstitial pneumonia diagnosis

The diagnosis can be confirmed based on the patient's medical history, duration of disease, clinical manifestations and X-ray signs, lung function tests, and lung biopsy.

Interstitial pneumonia laboratory test

Blood tests: Inflammatory and immune cell abnormalities in the alveolar structure of interstitial lung disease are not associated with other extrapulmonary lesions. In many patients, the rate of erythrocyte sedimentation, or the increase in blood immunoglobulin, is not closely related to pulmonary fibrosis. Immune complexes are found in the serum of some patients and are produced from the lungs and overflow. Some patients were positive for rheumatoid factor and antinuclear antibodies, and some patients had anti-pulmonary collagen antibodies. Arterial blood gas analysis: due to decreased tidal volume, increased breathing frequency, shallow breathing speed, insufficient alveolar ventilation, resulting in a decrease in ventilation / blood flow ratio, hypoxemia, but normal partial pressure of carbon dioxide in arterial blood. Partial blood oxygen pressure decreased significantly after exercise. Bronchial alveolar perfusion examination: Fiber bronchoscopy was used to insert the left lung tongue lobe or right lung middle lobe, and flushed with saline to obtain the bronchoalveolar lavage fluid. The lavage fluid was used for cytological and acellular determinations. This method has the following advantages:
The cytological examination of the lavage fluid can truly reflect the type and number of inflammatory and effector cells in the alveolar structure of alveolitis.
Diagnosis and differential diagnosis of various interstitial lung diseases. The total number of non-smoking human lavage fluid is (0.2 0.5) × 10E4 / ml. Alveolar macrophages account for 85% 90%, lymphocytes account for about 10%, and neutrophils and eosinophils account for only 1 Below%, the total number of cells is mostly increased by the increase of alveolar macrophages, and changes in cell types have diagnostic significance in ILD.
Such as allergic alveolitis, sarcoidosis, and chronic beryllium lung showed a significant increase in lymphocytes. Increased lymphocytes were also seen with collagen disease with pulmonary interstitial fibrosis. In contrast, neutrophils increase in bacterial pneumonia, airway infections, and ARDS. Increased lymphocytes and granulocytes can occur in obstructive bronchiolitis with organizing pneumonia. B lymphocytes account for 70% to 80% of T lymphocytes and 10% to 20% of B lymphocytes in bronchoalveolar lavage fluid. T lymphocytes increase in sarcoidosis, allergic alveolitis, and chronic beryllium lung in ILD. I have always wanted to explain the activity and prognosis of ILD with the degree of activation of labeled T cell subsets or T cells and B cells. It is only seen that the increase in the number of T cells and activated T cells during sarcoidosis is related to the progress of the disease.
In addition, the increase of activated B cells during idiopathic pulmonary interstitial fibrosis indicates the progression of the disease, and the increase in lymphocytes is better for hormone therapy and the prognosis is also better.

Interstitial pneumonia auxiliary examination

X-ray chest radiograph
Chest x-ray
One of the commonly used methods for the diagnosis of interstitial lung disease. Early alveolitis showed blurred shadows in the lower lung field and increased density like frosted glass. Because early clinical symptoms are not obvious, patients rarely go to the clinic and are easily ignored. The disease progresses further, and there are reticular shadows or reticular nodules in the field Shadows, nodules ranging in size from 1 to 5 mm. There are cystic changes of various sizes in the later stage, showing honeycomb lungs, reduced lung volume, uplift of the diaphragm muscles, and displacement of interlobular fissures. It is easier to diagnose in the later stages, but it has lost the significance of early diagnosis. About 30% of patients with lung biopsy confirmed interstitial pulmonary fibrosis, but chest X-rays were normal, so X-rays were not sensitive to alveolitis and lacked specificity. Pulmonary CT or high-resolution CT: It can show the morphological structure of lung tissue and interstitial tissue in more detail, which is very valuable for the establishment of early pulmonary fibrosis and honeycomb lung. The characteristics of CT images include nodular shadow and bronchial vascular wall. There are four types of images: regular shadow, linear shadow, and lung field concentration. Nodules can appear in the center of the lobule, around the pleura, around the vein, in the irregular veins of the thin veins and bronchial blood vessel walls. Similarly, the bronchial vessel wall irregularly appears in the center of the lobule, around the bronchial arteries and veins and venules. High-resolution CT images are significantly better than ordinary X-rays in the diagnosis of interstitial lung disease, and are valuable for the early establishment of pulmonary fibrosis and the establishment of honeycomb lungs. In particular, CT images have a unique diagnostic value in determining ILD, which is often dominated by peripheral lesions.

Interstitial pneumonia lung function test

This test is only a functional diagnosis, not a pathological diagnosis. In the early stages, pulmonary function tests can be completely normal, and abnormalities in pulmonary function tests may occur when the disease progresses. The most significant changes in lung function in ILD are abnormal ventilation function and decreased gas exchange function. Ventilation function is mainly restricted ventilation disorder, lung capacity decreases, residual capacity decreases as the disease progresses, and the total lung volume also decreases. At 1s, the ratio of vital capacity (FEV1.0) to forced vital capacity (FVC), that is, the 1s rate, significantly increased, and if it reached 90%, the diagnosis of ILD was supported. Early ILD may have small airway dysfunction, and its V50 and V25 both reduce ILD and form fibrosis, and then increase V50 and V25. In the early stage of ILD, gas exchange dysfunction may also occur. For example, the diffusive function (DLCO) is reduced earlier. Once the interstitial changes are found on the X-ray chest radiograph, the DLCO has decreased by less than 50%. Correlation between lung function changes and lung lesions is extremely poor in patients with mild lesions and better in patients with severe illness. Those with severely impaired lung function must have severe lung disease. Among the various tests of lung function, the volume-pressure curve test and changes in arterial blood oxygen during exercise are only the most sensitive to reflect the severity of pulmonary fibrosis. Pulmonary function tests are very useful for the early diagnosis and prognosis of ILD, especially the dynamic observation of VC, FEV1.0, DLCO and other indicators. As for whether lung function tests can determine the efficacy of hormones or immunosuppressive agents in treating ILD, there are different opinions. It is not enough to evaluate the efficacy based on changes in lung function.

Interstitial pneumonia lung biopsy

Lung biopsy is the best procedure for diagnosing ILD. Lung biopsy is performed when medical history, chest radiographs, lung function tests, bronchoalveolar lavage, and biochemical and infectious disease tests do not give an inferential diagnosis. Lung biopsy is divided into two types: The application of fiberoptic bronchoscopy for lung biopsy has the advantages of simple operation, high safety, can be used as a routine examination, and is convenient for review. Scholars believe that the lung tissue taken by fiberoptic bronchoscopy is too small (<2mm) and it is difficult to see the full picture of the pathological tissue. And the misdiagnosis rate and missed diagnosis rate are high. In order to increase the positive rate, 5 to 6 lung tissues can be taken. Thoracic lung biopsy: 2cm × 2cm of lung tissue is removed, and the type and degree of alveolitis can be observed comprehensively. Although this method is a traumatic examination method, it is undoubtedly necessary to open a chest lung biopsy in terms of establishing diagnosis and avoiding unnecessary various tests and unintended treatments. Foreign scholars report that 90% of cases that can not be diagnosed by fiberoptic bronchoscopy lung biopsy will be confirmed by open chest biopsy. They believe that common interstitial pneumonia and desquamative interstitial disease in idiopathic pulmonary interstitial fibrosis Pneumonia can only be confirmed with a chest lung biopsy. In contrast, few open lung and lung biopsies are performed in China, which is the main reason hindering the improvement of diagnostic levels.

67Ga Interstitial pneumonia 67Ga nuclide scan

67Ga does not accumulate in normal tissues and organs, but accumulates in chronic inflammatory tissues. It has high sensitivity but low specificity. The 67Ga index is the percentage of total lung area that 67Ga accumulates in the lung. > 50U means positive. 70% of idiopathic pulmonary fibrosis has a 67Ga index> 50U.

Interstitial pneumonia epidemiology

The disease is mostly sporadic, and is seen in all age groups, aged 40 to 70 years old. The incidence of ILD in the United States is 20 / 100,000 to 40 / 100,000. According to the US Centers for Disease Control, fibrosis (collagen vascular disease, collagen vascular disease, Radiation pneumonia and asbestos death), the number of males increased from 48.6 / 100,000 (1979) to 50.9 / 100,000 (1991), and the number of women increased from 21.4 / 100,000 to 27.2 / 100,000. The number of ILD reports is increasing and the incidence rate is increasing. It is also growing.
The incidence of idiopathic pulmonary interstitial fibrosis is unknown. It has been reported from 1990 to 1994 that the incidence rate is 3 / 100,000 to 6 / 100,000. There are more men than women in this disease. Surveys conducted in New Mexico in 1994 show that the incidence of idiopathic pulmonary fibrosis is 20.2 / 100,000 in men and 13.2 / 100,000 in women. Most of them are middle-aged, usually between 40 and 70 years old. The mean age at diagnosis was 66 years, and the incidence increased with age. The prevalence rate in the age group of 35 to 44 years is 2.7 / 100,000; the prevalence rate in those over 75 years of age increases to 175 / 100,000. There is no obvious difference in geographical distribution and no obvious racial tendency, but the mortality rate seems to be higher in whites than in blacks, and the reasons are unclear. Mortality increases with age.
ILD of unknown cause cannot be prevented. But smokers have an increased risk of developing idiopathic pulmonary fibrosis, and the risk increases with the increase in smokers. The prevention of ILD with a known cause should be for all types of personnel in large dusty working environments, and long-term exposure to irritating gases such as chlorine, ammonia, carbon dioxide, formaldehyde and various types of acid mist, radiation damage, and bird breeding Crowds and other people shall be monitored, and lung function measurement, blood gas analysis, and regular X-ray examinations shall be performed regularly to detect diseases early and diagnose and treat in time. In addition, inhalation of various microorganisms, particles, heteroprotein allergens and harmful irritating gases in the air can also cause lung damage.

Interstitial pneumonia treatment options

Interventional Interstitial Pneumonia

Idiopathic pulmonary interstitial fibrosis is a progressive disease. The natural course of untreated patients averages 2 to 4 years, and it can be extended to about 6 years after application of adrenal corticosteroids. Regardless of whether it is early or late, treatment should be carried out immediately to improve the absorption of emerging alveolitis, and some fibrosis can also be improved and prevent the development of the disease. The first choice is corticosteroids, followed by immunosuppressants and traditional Chinese medicine. Adrenocortical hormones can regulate the inflammation and immune processes, reduce the content of immune complexes, inhibit the proliferation of alveolar macrophages and the function of T lymphocyte factors, and apply in the stage of alveolitis and cell exudation, which can make some patients' X-rays of the lungs Shadow absorption improved, clinical symptoms improved significantly, and lung function improved. If treatment is started at the late stage of extensive interstitial fibrosis and the honeycomb lung phase, clinical symptoms can also be improved to varying degrees, but there is no significant improvement in lung shadows and lung function. The regular starting dose of chronic is 40 ~ 60mg / d of prednisone, which is divided into 3 ~ 4 times. When the condition is stable, the X-ray shadow can no longer be absorbed and it can be gradually reduced. After 4 to 8 weeks, it is reduced by 5mg each time. When it is reduced to 20mg / d, it is reduced by 2.5mg every week, and the maintenance of 10mg / d should be shorter than 1 year. If the disease relapses during the reduction, the dose should be increased again to control the disease, which is still effective. The course of treatment can be extended to two years, and can be used for life if needed. Care should be taken to detect the side effects of the drug, to achieve the best results with the smallest dose possible and the least side effects. When applying glucocorticoids, attention should be paid to opportunistic bacterial infections, pay attention to the recurrence of tuberculosis, and if necessary, combine antituberculosis drugs. Long-term application of glucocorticoids should pay attention to fungal infections. If the disease progresses dangerously or acutely, glucocorticoid shock therapy, such as methylprednisolone (methylprednisone) 500mg / d, can be used for 3 to 5 days, and then change to oral after the condition is stable. Finally, find the optimal maintenance amount based on individual differences to avoid recurrence. Those who cannot accept hormones and cannot tolerate hormones for special reasons can switch to immunosuppressive agents, or reduce the amount of corticosteroids and add immunosuppressive agents. Traditional Chinese medicines such as ligustrazine, Acanthopanax senticosus and Salvia miltiorrhiza have the effects of promoting blood circulation and removing blood stasis, and have a certain effect of preventing interstitial fibrosis. Indirectly, it suppresses humoral immunity and has a certain effect on the prevention of pulmonary interstitial fibrosis. It can be used as an important auxiliary drug.
Penicillamine, hormones, and hormones alone for treating pulmonary interstitial fibrosis have no significant difference in efficacy, but the side effects of the penicillamine + hormone group are significantly less than those of the hormone group alone, but penicillamine should be used before penicillamine Try, pay attention to its side effects, the main side effects are gastrointestinal reactions and allergic reactions. Anti-cytokine therapy, which is still in the experimental research stage, is inconclusive. Other symptomatic treatments include correcting hypoxia, improving cardiopulmonary function, and controlling bacterial infections. Lung transplantation technology has been implemented in some advanced countries and has received certain effects. The one-year survival rate for single lung transplantation is 73.1%, the three-year survival rate is 62.7%, the one-year lung transplantation survival rate is 70%, and the three-year survival rate is 55. %.

Interstitial pneumonia medication

Western medicine treatment
IPF is a continuously developing disease. The principle of treatment is mainly to actively control and reverse alveolitis, thereby preventing the development of irreversible pulmonary fibrosis. However, there is no effective treatment so far. Glucocorticoids are still the drug of choice, followed by immunosuppressants.
The usual starting dose of chronic corticosteroids is prednisone 30-40 mg / day, which is divided into 3 to 4 times. When the condition is stable, the X-ray shadow can no longer be absorbed and can be gradually reduced. It will be reduced by 5mg each time after 4 to 6 weeks, and reduced to 20mg / day, 2.5mg each time. If the patient's illness is unstable, the reduction is more It should be slow, even reduced by only 1mg at a time. The maintenance amount is not less than 10mg / day, and the course of treatment should not be less than 1 year. If the condition is repeated during the reduction, the dose should be increased again to control the condition, which is still effective. If you need it, you can take it for life. After the start of treatment, the majority of patients have improved or significantly improved their clinical symptoms in a short period of time, but the lung X-ray shadows have not changed significantly. If it is acute or has developed into a severe hypoxic phase, the hormone should be started from a large dose in order to quickly reverse the condition. Prednisone 60 80mg / day, divided into 3 to 4 applications. If the condition is dangerous, use shock therapy immediately. Intravenous injection of methylprednisolone 500-1000mg / day for 3 to 5 days. If the condition is stable, change to oral. Finally, find the optimal maintenance amount based on individual differences to avoid recurrence. .
Immunosuppressive corticosteroids are not effective, you can switch to immunosuppressive drugs or combination drugs, but the effect is yet to be determined.
Azathioprine: the drug of choice, the dose is 100mg / day, once a day orally, with little side effects.
Cyclophosphamide: 100 mg / day orally. Less effective than azathioprine. Its side effects, such as bone marrow suppression, should be closely observed.
(3) Tripterygium glycosides: it has exact anti-inflammatory and immunosuppressive effects. Combined application with hormones or immunosuppressants can reduce the dose of the two drugs and increase the efficacy. The dose is 10-20 mg, 3 times a day, orally.
For symptomatic treatment, if secondary infection occurs, antibiotics should be selected according to the type of bacteria; hypoxemia can be given low-flow oxygen inhalation.
Chinese medicine treatment
Interstitial pneumonia belongs to the category of "pulmonary paralysis". The lung is evil, the Qi and blood are not accessible, and the collaterals and blood stasis are obstructed. There is a clinical evolution process from lung to the lungs. The pulmonary fibrosis has a long course of disease. Can be a "pulmonary dysentery". Some scholars believe that both "pulmonary paralysis" and "pulmonary dysentery" can be used as their disease names, both of which reflect the characteristics of the pathogenesis at different stages of the development and development of the disease course. Primary, secondary, and priority, so as to determine the ownership of the disease name.
When choosing Chinese medicine treatment for interstitial pneumonia, we should focus on the overall adjustment and give individualized dialectical treatment. There is no fixed prescription that can "generate" the disease.
Interstitial pneumonia life considerations:
Ensure adequate rest, keep warm, avoid cold, and prevent various infections. Pay attention to climate change, especially in the winter and spring seasons, when the temperature changes drastically, add and remove clothing in time to avoid exacerbating the illness after the cold.
Have a comfortable living environment. The room should be quiet, clean and hygienic. The air should be fresh, moist, and circulating. Avoid irritating factors with strong smells such as smoke, perfume, and air fresheners. Also avoid inhaling air that is too cold, dry, or humid.
In terms of diet, the diet should be light and digestible, mainly liquid or semi-liquid, eat more fruits and vegetables, drink plenty of water, and avoid eating pungent, sour, hemp, spicy, fried food, eggs, fish, shrimp, etc. Foods that can easily induce asthma. Do not eat irritating food. In general, the characteristics of the diet should be: the diet must be diversified, properly matched, nutritious, proportionate, and suitable for digestion and absorption.
The spirit should be pleasant and optimistic to prevent mental stimulation and mental stress. This requires you to have an open and cheerful attitude towards life, that is, to maintain a happy spirit, you must cultivate the "satisfaction and constant joy" of thinking, but the excessive pursuit of fame and enjoyment must be experienced "more than less than more than" It makes sense to feel life and psychological satisfaction. Keep your spirits up and enjoy your daily routine.
Keep away from exogenous allergens, such as: some flowers (especially those who are allergic to pollen), bedding, pillows, birds, animals (pets or experimental breeders) filled with allergic items such as feathers or old cotton wool, wood (Sequoia dust, cork processing), sucrose processing, mushroom farming, cheese, wine processing, moldy straw exposure, water sources (hot water pipes, air conditioners, humidifiers, saunas) and agricultural pesticides or herbicides.

Interstitial pneumonia

Glucocorticoid treatment, prednisone (prednisone) 40 to 60 mg / d, and gradually reduce the dose 4 to 8 weeks when the condition is stable, 5 mg each time to 20 mg / d, 2.5 mg each week, reduced To 10mg / d, maintenance should not be shorter than 1 year.

Interstitial pneumonia rehabilitation

The rehabilitation of patients with pulmonary interstitial fibrosis is also very important, including:
Nutritional support therapy: With the progress of the disease, the hypoxia condition further worsens, the patient's activity is significantly reduced, and the muscle tissue is significantly atrophied, coupled with repeated infections, loss of appetite, often accompanied by progressive weight loss, and finally leads to respiratory muscle failure , Aggravated the condition and even died. Therefore, nutritional support therapy is particularly important. The purpose is to provide patients with reasonable nutrition, ensure the metabolism of the body's cells, maintain the structure of organs and tissues, participate in the regulation of the body's physiological and immune functions and tissue repair, and promote patient recovery.
Oxygen therapy: An oxygen cylinder or a small oxygen generator should be provided at home to relieve the symptoms of dyspnea at any time.
Exercise: Those with a mild condition are most suitable for applying rehabilitation treatment such as medical sports, which has a better effect, can significantly improve lung function and conscious symptoms, and prevent further development of lesions. Those with more severe conditions can exercise with caution to adapt to daily minor activities.
Prevention of infection: increase or decrease clothes according to climate change. Immunosuppressants can be applied to improve the body's immunity.
Life care:
Remedy
From the point of view of Chinese medicine, it should be asked to ask Wenqin's four consultations, and the incompleteness of the four consultations can only be symptomatic treatment. From the theoretical perspective of Chinese medicine, it can be considered to be lung and kidney yin deficiency. Pulmonary phlegm.
Take 30 grams of Polygonatum glutinosa, cooked Rehmannia glutinosa, asparagus, asparagus, almonds, 15 grams each of licorice root, raw gypsum (fried first), Zhimu, yam, red rattan, Maichuan achyranthes, whole buckwheat, scutellaria baicalensis, ground bone, purple 10 grams of grass each. Decoction. 1 dose daily, 7 consecutive doses, if effective, you can continue to take, while taking Liu Wei Di Huang Wan, 30 capsules (water pills) each time, 2 times daily, 1- 3 months, it can be relieved.
If you have heart symptoms, you can use Danshen drip pills.
Medicated diet
According to pathological anatomy, pneumonia can be divided into lobar pneumonia, bronchial pneumonia, and interstitial pneumonia. The main clinical manifestations are cough, sputum, wheezing, chest tightness, etc., and appropriate medicated diet can be selected as auxiliary treatment.
Here are some unilateral and compound recipes for your choice.
Unilateral
Among the traditional Chinese medicine for colds and bronchitis, chrysanthemums that can evacuate wind-heat, light tempeh, etc. can be applied to those who have lung-heat syndrome in the early stage of pneumonia; crickets, lilies that can clear the heat, reduce sputum, or nourish the lungs, Pear, coriander, honey, etc., can also be used in patients with pneumonia syndrome who have lung fever or lung yin.
garlic
Take 5% garlic juice. Take 20 ml each time, 4 times a day; or 10% garlic syrup, 15-20 ml each time, once every 4 hours.
The active ingredient allicin in this recipe has a strong antibacterial effect, so garlic juice and garlic syrup can be used to treat pneumonia.
Purslane
Use 50 grams of japonica rice and 30 grams of purslane.Boil them for porridge and take 1--2 times a day, which can be used as an adjuvant treatment for pneumonia.
In this recipe, the whole grass of the annual herb purslane is a kind of edible wild vegetable that has heat-clearing, cooling-blood, detoxifying effects, and inhibits a variety of bacteria.
Compound
The initial evidence of pneumonia belongs to those who suffer from wind-heat and lung-loss, can refer to the medicated diet compound of wind-heat type cold or wind-heat type acute bronchitis. With the further development of pneumonia, when the symptoms of lung-heat fever are present, sputum fever Bronchitis medicated diet. For patients with both Qi and Yin injuries during pneumonia recovery, you can refer to the medicated diet for chronic bronchitis of lung deficiency type. Here are a few recipes:
Compound Yinju Tea
Take 30 grams of reed root (double for fresh ones), 21 grams of honeysuckle, 9 grams of chrysanthemum and mulberry leaves, 6 grams of almonds, decoction, remove residue, and add 30 grams of honey.
This prescription is applicable to those who have been diagnosed with wind-heat fever and lungs since the beginning of pneumonia.
Reed bamboo shoots porridge
Use 60 grams of reed root (double for fresh ones), fry in water, filter the juice to remove the residue, add 50 grams of japonica rice and an appropriate amount of water. Cook together for porridge, add 30 grams of bamboo leaches, 15 grams of rock sugar, and serve after cooking a little 1 to 2 times a day. Pneumonia syndrome is a person with strong lung fever, and this porridge can be taken.
This prescription can be used as adjuvant treatment. [1]

Prognosis prevention of interstitial pneumonia

Prognosis of interstitial pneumonia

For the prognosis of interstitial fibrosis, most of them have a poor prognosis. The length of the disease depends on the progress of the disease, and the death in the acute phase can be as short as two weeks. The slower development can be more than 20 years. Since the application of glucocorticoids, immunosuppressants and Chinese medicine, the course of disease has been significantly prolonged. But most patients eventually die of respiratory failure. Very few patients are stable and have a long-term remission after treatment.

Interstitial pneumonia prevention

Pneumonia prevention
ILD of unknown cause cannot be prevented. But smokers have an increased risk of developing idiopathic pulmonary fibrosis, and the risk increases with the increase in smokers. The prevention of ILD with a known cause should be for all types of personnel in large dusty working environments, and long-term exposure to irritating gases such as chlorine, ammonia, carbon dioxide, formaldehyde and various types of acid mist, radiation damage, and bird breeding Crowds and other people shall be monitored, and lung function measurement, blood gas analysis, and regular X-ray examinations shall be performed regularly to detect diseases early and diagnose and treat in time.
In addition, inhalation of various microorganisms, particles, heteroprotein allergens and harmful irritating gases in the air can also cause lung damage. Through clinical observation, the onset of ILD is sometimes very slow. Clinically, patients who have been exposed to dust or poisons when they are young and who have obvious symptoms until old age are often encountered. For these elderly patients, due to their low immune function and nutritional status Poor and the existence of heart, lung, kidney and other basic diseases, it is very difficult to treat, and the mortality rate is very high.
Elderly people with less physical activity may conceal symptoms such as breathing difficulties and shortness of breath caused by the disease. Therefore, the high-risk group of the disease should assume the health function on the basis of the family and the community, and regularly carry out health education and health consultation.

Interstitial pneumonia diet conditioning

Celery bream carp: 250 grams of carp, 50 grams of fresh celery, starch, ginger, garlic, soy sauce, sugar, vinegar, refined salt, monosodium glutamate, rice wine, sour pepper, vegetable oil. Cut the carp into shreds, cut the celery into sections, and mix the soy sauce, sugar, vinegar, monosodium glutamate, rice wine, salt, and starch into the soup. Set the wok on the high heat, heat the oil to 50% heat, let the mermaid shred, loosen the remaining oil, put the ginger and sour pepper. Stir-fry the celery section, then cook in the tartar sauce, put in the bright oil, and bring it to the pan. Carp has the effects of clearing heat and detoxifying, diuretic swelling, cough and lowering qi; celery has the effects of clearing liver and clearing heat, expelling wind and dampness, and nourishing qi and energy. Common carp and celery, suitable for adjuvant treatment of acute and chronic pneumonia.
Shredded rabbit meat and mushrooms: 100 grams of cooked rabbit meat, 50 grams of mushrooms, 25 grams of light white, chili oil, soy sauce, vinegar, sugar, sesame oil, sesame sauce, pepper powder, MSG amount. Shred the cooked rabbit meat and green onions separately and cook the mushrooms. Shallots, mushrooms at the bottom, rabbit silk cover surface, and served in the dish. Use soy sauce to disperse the sesame sauce in portions, mix the sesame oil into a flavor sauce, and drizzle it with rabbit silk. Free meat has the effects of clearing heat and detoxifying, nourishing qi and strengthening the spleen, removing dampness and cooling blood, and facilitating the convenience. Mushrooms have the effects of detoxifying and moisturizing, nourishing spleen, nourishing spleen, and dampening diarrhea. Rabbit meat with mushrooms is suitable for the treatment of acute pneumonia.
Quail Lily Soup: 1 quail, 25 grams of lily, ginger, spring onion, monosodium glutamate, fine salt. After the quail is killed, remove its hair, remove its feet, remove its internal organs, and wash it in boiling water. Remove the cut pieces. Wash the lily petals and wash them for future use. Wash the ginger and shallots, smash the ginger, and cut the shallots into sections. Place the pot on a hot fire, pour an appropriate amount of water, add the quail, boil, boil the lilies, ginger pieces, and spring onions, and simmer over low heat until the quail is cooked. Add salt and MSG for a few minutes. Edible. Quail meat has the effects of nourishing the five internal organs, nourishing the liver and clearing the lungs, clearing away heat and dampness, eliminating diarrhea, and reducing diarrhea; lily has the effects of nourishing the lungs and relieving cough, nourishing yin and clearing heat, and soothing the mind and soothing. The two are the same food, suitable for acute and chronic pneumonia.
Lean meat cabbage soup: 100 grams each of lean meat and cabbage heart, ginger, garlic, salt, monosodium glutamate, and a little chicken oil. Shred lean meat, wash and shred cabbage, put in boiling water, remove when fresh, rinse with clear water, filter and dry the water for later use; place on a hot fire, sauté chicken oil and let it mature Garlic, stir-fry golden brown, add lean meat and stir-fry, add fine salt, cook with soup, boil cabbage heart, add MSG and serve. Lean meat has the functions of tonifying qi, invigorating the intestines and moisturizing the intestines; Chinese cabbage is flat and sweet, and has the functions of clearing heat and detoxifying, resolving phlegm and relieving cough, and removing troubles and laxatives. Lean meat and cabbage together, suitable for acute and chronic pneumonia.

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