Kembara Xtra - Medicine - Hypersensitivity Pneumonitis
Extrinsic allergic alveolitis (EAA) is another name for hypersensitivity pneumonitis (HP). HP is a widespread inflammatory condition of the lung parenchyma brought on by an immune response to antigenic aerosolized particles present in various environments. Classification is based on the relevant time period: - Acute: fever, chills, myalgias, diaphoresis, and nausea; cough and dyspnea are frequent but not always present. occurs between 4 and 12 hours following a strong dose of a provoking substance. Within 12 hours to several days following removal from exposure, symptoms go away. Complete resolution happens in a few of weeks. - Subacute: primarily brought on by repeated low-level antigen exposure, with the potential for a low-grade fever in the first week; cough, dyspnea, exhaustion, anorexia, and weight loss that appear over the course of days to weeks. - Chronic: caused by repeated exposure in either acute or subacute cases; long-lasting and progressive cough; exhaustion; weight loss; may result in fibrosis and respiratory failure. The term "farmer's lung" refers to a type of HP that affects only farmers; the bacterium that causes it can be found in moldy hay or straw. Modern farming techniques have led to new and distinct etiologies for farmer's lung. Epidemiology Not well defined; likely to happen in adults as a result of occupational exposure, however some home environmental exposures are also seen HP is becoming more and more recognized as a significant contributor to fibrotic interstitial lung disease. Incidence 0.9/100,000 Prevalence Farmer exposure ranged from 1 to 19 percent; bird watchers from 6 to 30 percent; and others from 1 to 8 percent. Pathophysiology and Etiology Immunologic reaction types III and IV (hypersensitivity reaction involving immune complexes) are brought on by the binding of inhaled antigens to IgG. T cell-mediated immunological inflammatory response is one example of a cellular response. Workers in agriculture, horticulture, or dairy cattle (1), (2) - Moldy grain, silage, and hay are caused by thermophilic actinomycetes like Faenia rectivirgula. - Thymus vulgaris and Thermoactinomyces sacchari mold on pressed sugar cane - Tobacco plants: Scopulariopsis brevicaulis and Aspergillus sp. Saccharopolyspora rectivirgula, T. vulgaris, and Aspergillus spp. cause worker's lung in the mushroom industry. Thermophilic actinomycetes, T. vulgaris, F. rectivirgula, and Aspergillus sp. cause riddler's lung in the potato industry. - Coffee worker's lung: coffee bean dust Penicillium caseifulvum, Aspergillus clavatus - Cheese washer's lung: - Tea plants: Tea grower's lung Ventilation and water-related contamination: Amoebae, Nematodes, Yeasts, and Bacteria infected humidifiers and air conditioners - Shower without ventilation: Epicoccum nigrum - Cladosporium species, Mycobacterium avium complex, hot-tub lung Aureobasidium sp. causes sauna taker's lung, and Trichosporon cutaneum causes summer-type pneumonitis. - Aerosolized endotoxin and M. avium complex in the swimming pool lifeguard's lung - Cephalosporium and Penicillium spp. in contaminated basement pneumonitis - Handling of birds and poultry - Bird fancier's lung: droppings, feathers, serum proteins - Serum proteins in the lung of poultry workers - Sera for turkey-handling illness - Serum proteins in the canary fancier's lung - Feathers and serum proteins cause duck fever Laboratory worker's lung: proteins, urine, serum, and serum from handling animals used in veterinary medicine - Dried, powdered neurohypophysis is a symptom of pituitary snuff taker's disease. - Furrier's lung: pet fur - Bat serum protein: bat lung - Workers' lung from fish food: fish meal - Coptic lung: mummies wrapped in cloth - Shell of a mollusk Sea snail with pearl oyster shells, HP lung disease: oyster shells Cereal grain, grain dust, and flour: grain measurer's lung - Sitophilus granarius, a cause of Miller's lung Lumber milling, construction, wood stripping, paper, and wallboard manufacturing - Malt worker's disease: Aspergillus fumigatus, Aspergillus clavatus - Wood dust pneumonitis: Alternaria sp., Bacillus subtilis - Trichoderma sp., Pullularia, Graphium, and Aureobasidium pullulans in sequoiosis - Cryptostroma corticale, the cause of maple bark disease - Suberosis: Trogon viridis, Penicillium glabrum; Wood trimmer's disease: Rhizopus sp., Mucor sp.; Wood pulp worker's disease: Penicillium sp. Manufacturing of plastics, paints, electronics, and chemicals Diphenyl diisocyanate and toluene diisocyanate are chemical HPs. B. subtilis enzymes are found in the lungs of detergent workers. Alveolitis caused by the Pauli reagent: sodium diazobenzene sulfate Copper sulfate causes vineyard sprayer's lung. Pyrethrum causes pyrethrum. Bible printer's lung: moldy typesetting water - Epoxy resin lung: phthalic anhydride Pseudomonas fluorescens, an aerosolized metalworking fluid, causes machine operator's lung Cotton mill dust byssinosis in textile workers and nylon, tannic acid, and potato starch lung disease in velvet workers Fusarium species, which produces aflatoxin, infects upholstery fabric. Puffball spores, which cause lycoperdonosis. Genetics No evidence of a distinct genetic tendency, but potential genetic predisposition involving the MHC class II and tumor necrosis factor alpha (TNF-) genes. Risk Elements The chance of acquiring HP increases with contact with organic antigens. Risk may be increased by viral infection at the time of exposure. Compared to smokers, nonsmokers have a higher incidence of HP. Smoking is assumed to provide "protective" effects because nicotine is believed to suppress macrophage activation and lymphocyte proliferation and function. - Smokers' antibodies react less strongly to inhaled antigens. Smokers are more likely to develop chronic disease, and their mortality rate is higher. Prevention Avoiding offending antigens and/or wearing protective gear Constrictive bronchiolitis is a condition that is related. Diagnoses The most popular yet unreliable diagnostic criteria are: (i) a history, physical examination, and pulmonary function tests (PFTs) showing diffusion or restriction illness. The most frequently affected lung parameter, DLco, may be normal in up to 22% of patients, (ii) radiologic imaging consent with interstitial lung disease, (iii) exposure to a known cause, (iv) evidence of sensitization in BAL fluids (serum precipitins and/or lymphocytosis), and (v) exposure to a recognized cause ● There are six important predictors: exposure to a known antigen, precipitation of positive antibodies (if known), recurring symptom episodes, inspiratory crackles, symptoms 4 to 8 hours after exposure, and weight loss. Acute form: appears 4–12 hours after exposure. Chest tightness, cough, dyspnea without wheezing, fever, chills, diaphoresis, headache, nausea, and malaise. Symptoms can continue for hours or days. Sequela (previous subacute, chronic): occurs over days, weeks, or months and includes a progressive or gradual productive cough, exhaustion, anorexia, and weight loss that may result in respiratory failure. Symptomatic relief when not at work or home clinical assessment Sequela or chronic symptoms include inspiratory crackles, increasing hypoxia, weight loss, diffuse rales, clubbing, and occasionally wheezing. Acute symptoms include fever, tachypnea, and diffuse fine rales. Differential Diagnosis Acute: acute infectious pneumonia caused by Pneumocystis jiroveci pneumonia, mycoplasma, influenza (or other viral pneumonia), aspiration, and asthma Chronic conditions include P. jiroveci pneumonia, sarcoidosis, chronic bronchitis, chronic obstructive lung disease, tuberculosis, collagen vascular disease, and idiopathic pulmonary fibrosis. The majority of cases are covered by the following antigens: pigeon and parakeet sera, dove feather, Aspergillus sp., Penicillium, S. rectivirgula, and Thalassomonas viridans PFTs: The typical profile is a restrictive pattern with low diffusing capacity; could also have an obstructive pattern BAL with serum precipitins and lymphocytosis (greater than 10) Positive antigen-specific inhalation challenge testing involves re-exposure to the environment and an in-hospital challenge to the suspected antigen, but it is not standardized. Chest x-ray (CXR): used to obviate the presence of other diseases - Acute: interstitial pattern in various lung field distributions, ground-glass infiltrates, nodular or striated patchy opacities. Up to 20% might be typical. - Sequela/chronic: emphysematous alterations, upper lobe fibrosis, nodular or groundglass opacities, volume loss Chest CT scan; non-HP-specific patterns: - Acute: air trapping, ground-glass opacities, and poorly defined centrilobular nodules on expiratory imaging.- Chronic: honeycombing, fibrosis, ground-glass attenuation, irregular opacities, bronchiectasis, decrease of lung volume Usually begin with CXR; may move to HRCT depending on results. High-resolution CT (HRCT) mid-to-upper zone predominance of centrilobular ground glass or nodular opacities with evidence of air trapping Diagnostic techniques and other lung biopsies: Transbronchial: Shows extensive foam cells, peribronchial fibrosis, and tiny, poorly formed noncaseating granulomas close to respiratory or terminal bronchioles. Open lung biopsy yields the most information when the disease is advanced; it displays different organizing pneumonia patterns, centrilobular and perilobular fibrosis, and multinucleated giant cells with clefts. Caution Farmers' HP must be recognized from organic dust toxic syndrome (ODTS), which causes feverish, toxic reactions to inhaled dusts. Farmers get nonimmunologic responses 30–50% more frequently than HP. ODTS is connected to a day of extremely high exposure. The patient should be kept fully away from repeated exposure to the causing antigen, with the exception of cases of acute pneumonitis and hospitalization for workup (BAL, lung biopsy). The best treatment for disease is provided by this action. First Line of Medicine Avoiding the offending antigen is the main treatment, which causes the condition to regress. Corticosteroids assist manage exacerbation symptoms, but they have no lasting positive effects. Prednisone: 20 to 50 mg daily; first treatment, 1 to 2 weeks with taper; for patients with severe symptoms Next Line Patients with wheezing and chest tightness may have symptomatic relief from bronchodilators and inhaled corticosteroids. In more severe situations, oxygen might be required. When medical treatment is ineffective for serious instances, lung transplantation may be the only option. Referral Advisory for a pulmonologist or immunologist Admission Supportive care, when required, to sustain breathing and oxygenation Changes in mental status, oxygen need, and unstable breathing Requirement for invasive testing (lung biopsy) Patient Follow-Up Monitoring Depending on the severity and course, the initial follow-up should be weekly to monthly. Serial CXR, PFTs, and circulating antibody levels should be performed after therapy. Education of Patients Keep in mind that prolonged exposure can cause acute symptoms to disappear (the patient may stop being aware of the connection between exposure and symptoms). Fibrosis is a factor that indicates a poor prognosis. Acute: If the offending antigen is removed early in the course of the disease, there is a good chance that the pathologic findings will be reversed. Sequela/chronic: Corticosteroids have been shown to temporarily enhance lung function but have no discernible effect on the long-term prognosis. Progressive interstitial fibrosis with eventual respiratory failure is a complication. Cor pulmonale and failure of the right heart
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