OVERVIEW
Allergic pneumonitis (exogenous allergic alveolitis) is a group of diffuse interstitial granulomatous lung diseases caused by repeated inhalation of various antigenic organic dusts and low-molecular-weight chemicals in susceptible people. Farmer’s lung caused by repeated inhalation of hay containing thermophilic actinomycetes is a representative of this. Allergic pneumonia is associated with seasonal atmospheric pollution, indoor microbial pollution, and the patient must first be removed from the pathogenic environment.
Causes
Allergic pneumonia is a group of non-asthmatic allergic lung diseases caused by different allergens, with a low incidence in children. Allergens are organic dust particles containing fungal spores, bacterial products, animal proteins or insect antigens.
Symptoms
After inhalation of allergens, a small number of children have prodromal symptoms such as wheezing and runny nose, and start to have symptoms 3-6 hours later, which are fever, dry cough, shortness of breath, chest pain and hypoxia, cyanosis of lips and fingers and toes, etc. The above symptoms reach the peak in 6-8 hours, and the symptoms basically disappear in 24 hours. Lung signs during an attack are different from those of an asthma attack, and there are mostly no wheezing sounds, and wet rales are mainly heard.
In the acute form, the onset of symptoms usually occurs 4-8 hours after exposure to the antigen, with fever, chills, cough and dyspnea, as well as anorexia, nausea and vomiting. The lungs are auscultated with fine to medium inspiratory phase wet rales, and rales are uncommon. Symptoms usually improve within a few hours after removal of the antigen, but full recovery takes several weeks, and repeated episodes can lead to pulmonary fibrosis. In subacute cases, the onset may be insidious, with cough and dyspnea lasting days to weeks, and hospitalization is required for progressive disease. In chronic cases, dyspnea, cough, fatigue, and weight loss can be progressive after activity for months to years. The disease may progress to respiratory failure.
Examination
1. Imaging
Chest X-ray may be normal or there may be diffuse interstitial fibrosis. Bilateral plaques or nodular infiltrates are often present, and bronchopulmonary texture is thickened, or small adenoidal changes are present, suggesting pulmonary edema. Rarely, hilar lymph node enlargement and pleural effusion are seen.CT, especially high-resolution CT, is of high value in determining the type and extent of the lesion.
(1) CT manifestations of acute hypersensitivity pneumonitis: glassy changes in both lungs; extensive patchy, flocculent or flocculent pulmonary solid shadows in both lungs, with blurred edges, uneven density and distribution, more common in the middle and lower lungs, and the location of foci changes greatly in a short period of time, and they have a wandering nature. The pathology of acute hypersensitivity pneumonitis imaging is based on diffuse pulmonary congestion and edema caused by infiltration of neutrophils and eosinophils in the lung parenchyma and inflammation of small blood vessels, as well as exudation of proteinaceous fluid in the alveoli.
(2) CT manifestations of subacute hypersensitivity pneumonitis: diffusely distributed centrally located nodular shadows in the lobules with indistinct margins; patchy ground-glass shadows; gas trapping and cystic changes. Pathologic basis of imaging manifestations of subacute hypersensitivity pneumonitis: centrilobular nodular shadow is a manifestation of cellular fine bronchiolitis; ground-glass shadow is a manifestation of the presence of diffuse lymphocytic interstitial pneumonitis; gas trapping sign and pulmonary cystic changes are the result of inflammation and obstruction of fine bronchioles. Lobule-centered nodular shadows and ground-glass changes are the characteristic changes of allergic pneumonia, while lobule-centered nodular shadows are the characteristic changes of subacute allergic pneumonia.
(3) CT manifestations of chronic hypersensitivity pneumonitis can be seen as lattice-like, honeycomb-like fibrous cord shadow, which is interstitial fibrosis; in some cases, atelectasis, emphysema and pleural thickening can be seen.
2. Lung function
Lung function is mostly restrictive, with reduced lung volume, decreased carbon monoxide diffusion, abnormal ventilation/blood flow ratio and hypoxemia. Airway obstruction is uncommon in acute cases, but can occur in chronic cases. Eosinophils are not abnormal.
3. Bronchoscopy
Bronchoalveolar lavage is a sensitive method of determining the presence or absence of alveolitis. Lymphocytes, especially T-cells, are usually seen, with a predominance of CD8+ (cytotoxicity suppressor) T-cell subsets. Transbronchoscopic biopsy is of very limited value and can lead to misdiagnosis due to too few specimens.
Diagnosis
The presence of serum antibodies is neither sensitive nor specific, although in the past, a positive serum precipitating antibody was considered sufficient for a definitive diagnosis. Diagnosis is based on a history of environmental exposure, relevant clinical features, chest X-ray and spirometry, and fiberoptic bronchoscopy. A history of exposure may provide clues (e.g., a person exposed to the antigen at work may be asymptomatic, or symptoms may reappear 48 hours after re-exposure). A history of exposure to the causative antigen is not easy to detect, especially in “air-conditioned lung” (humidifier lung). Environmental investigations by specialists in difficult cases can help in diagnosis. Lung biopsy may be performed in patients in whom it is difficult to draw conclusions or in whom there is no history of environmental exposure.
Questions you may be concerned about
Diagnostic Criteria for Allergic Pneumonia
Allergic pneumonia is also known as exogenous allergic alveolitis, and its main diagnostic criteria include a clear history of antigen exposure, clinical symptoms and signs, imaging examination, alveolar lavage fluid examination, and pathologic histologic examination.
1. A clear history of antigen exposure before the onset of the disease, such as a history of working in a textile factory and bird feeding. This is very important for the diagnosis of hypersensitivity pneumonitis.
2. Typical clinical symptoms and signs, such as chills and fever, cough, dyspnea, generalized discomfort with chest tightness. End-inspiratory Velcro sounds can be heard on auscultation at the base of the lungs, and some of them have pestle-shaped fingers.
3. Imaging examination, chest high-resolution CT, can be seen in the center of the fine bronchial nodules, patches of ground-glass shadows or with solid changes, gas trapping the formation of mosaic signs and other characteristic manifestations.
4. Alveolar lavage fluid is dominated by lymphocytes, which can make a clear diagnosis.
5. Histopathologic examination can further support the diagnosis, and usually does not require open lung biopsy.
The diagnosis can be made by combining the above patient history, typical signs and symptoms, and relevant laboratory, imaging, and histopathologic examinations.
Patients with exogenous allergic alveolitis need to seek medical attention and standardized treatment by a physician to avoid delays.
Differential diagnosis
1. Viral pneumonia
The first attack of allergic pneumonitis is easily confused with viral pneumonia, with symptoms appearing several hours after exposure to the antigen: fever, dry cough, dyspnea, chest pain and cyanosis. A small number of atopic patients may have a rapid-onset allergic reaction such as wheezing and runny nose after exposure to the antigen, followed by a type III reaction manifesting as hypersensitivity pneumonitis 4-6 hours later. Physical examination of the lungs has wet rales, mostly without wheezing, without solidification or airway obstruction.X-ray chest radiograph shows diffuse interstitial infiltration, and millet or small nodular shadows, which are more obvious in the middle and bottom of the lungs, and later expand into patchy dense shadows.
In acute exacerbation, the peripheral blood picture shows an elevated white blood cell count (15-25) × 109/L (15,000-25,000/mm3) with neutrophil elevation, but mostly without eosinophil elevation, and elevated gammaglobulin up to 20-30 g/L (2-3 g/dl) with elevated IgG, IgM, and IgA; serum complement is normal, and rheumatoid factor may be positive. Pulmonary function tests show restrictive ventilation disorders with decreased lung volume, decreased diffusion function, local ventilation-blood flow disproportion, no obvious airway obstruction and increased vascular resistance.
2. Psittacosis, viral pneumonia and other infectious pneumonias
Allergic pneumonia can be differentiated from psittacosis, viral pneumonia and other infectious pneumonias by culture and serologic tests. Idiopathic fibrosis (HammanRich syndrome, cryptogenic fibrosing alveolitis, endogenous allergic alveolitis) is difficult to distinguish from hypersensitivity pneumonitis when the typical history of exposure prior to the acute exacerbation cannot be determined because of the similarity of the clinical features, X-rays, and pulmonary function tests. Variants of adult bronchiectasis (e.g., obstructive bronchiectasis with opportunistic pneumonia) can resemble restrictive (interstitial) disease and are difficult to differentiate between the two when there is no relevant history or when autopsy lung biopsy does not reveal typical changes.
Evidence of autoimmunity (positive antinuclear DNA antibodies or latex fixation tests, or collagenous vascular disease) indicates idiopathic or secondary common interstitial pneumonia. Chronic eosinophilic pneumonia is often associated with peripheral blood eosinophilia. Nodular disease often causes enlarged hilar and paratracheal lymph nodes and may involve other organs. Pulmonary vasculitis granulomatosa syndrome (Wegener’s granulomatosis), lymphomatoid granulomatosis, and allergic granulomatosis (ChurgStrauss syndrome) are often associated with upper respiratory and renal disease. Bronchial asthma and allergic bronchopulmonary aspergillosis have eosinophilia and obstructive rather than restrictive lung function abnormalities.
Treatment.
Early diagnosis and avoidance of exposure to antigens are key to treatment, and removal of sensitizing antigens from the patient’s exposure environment is critical for both treatment and prevention. Pharmacologic therapy is an important adjunct in only some cases.
Glucocorticoid therapy relieves and eliminates symptoms during acute exacerbations and prevents permanent damage such as bronchiectasis, irreversible airway obstruction, and pulmonary fibrosis. Hormone therapy is not necessary for patients with mild lung function impairment who can recover on their own by avoiding antigenic exposure. Prednisone may be used in more severe cases. Lung function should be dynamically observed during the first four weeks of treatment, and the dosage of hormones should be gradually reduced until discontinued after the objective indicators improve.
Cytotoxic drugs such as cyclophosphamide, cyclosporine and azathioprine can be used for refractory and progressive hypersensitivity pneumonitis, but their efficacy has not been adequately studied.