Exogenous lipid pneumonia is rare in the general population, but occupational accidents may not be uncommon in fire performers. Diagnosis is usually made on the basis of history of exposure to hydrocarbon fuels, symptoms, and radiological findings. The radiological findings are nonspecific, and the disease presents with variable patterns and distribution. For this reason, lipoid pneumonia may mimic many other diseases, and the diagnosis is often delayed.

Chest X-rays taken shortly after the accident may or may not be abnormal, but typically over time show infiltrates in the lower lobes of the lungs. High-resolution CT will frequently demonstrate abnormalities, including opacities, pleural effusion, consolidation, or pulmonary nodules. Histopathology of lung biopsy or bronchoalveolar lavage may indicate lipid-laden macrophages. Laboratory results may show highly elevated inflammatory markers.

The diagnosis is based upon a history of symptoms after exposure to the allergen and clinical tests. A physician may take blood tests, seeking signs of inflammation, a chest X-ray and lung function tests. The sufferer shows a restrictive loss of lung function.

Precipitating IgG antibodies against fungal or avian antigens can be detected in the laboratory using the traditional Ouchterlony immunodiffusion method wherein 'precipitin' lines form on agar plate. The ImmunoCAP technology has replaced this time consuming, labor-intensive method with their automated CAP assays and FEIA (Fluorescence enzyme immunoassay) that can detect IgG antibodies against Aspergillus fumigatus (Farmer's lung or for ABPA) or avian antigens (Bird Fancier's Lung).

Although overlapping in many cases, hypersensitivity pneumonitis may be distinguished from occupational asthma in that it is not restricted to only occupational exposure, and that asthma generally is classified as a type I hypersensitivity. Unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than bronchi.

The course of treatment of fire breather's pneumonia remains controversial. Administration of bronchodilators, corticosteroids, and prophylactic antibiotics to prevent secondary infection, is a common course of treatment. Some studies suggest that steroids may improve outcomes in severely affected individuals, yet these data are only based on a limited number of patients. The use of gastric decontamination to prevent subsequent pulmonary injury from hydrocarbon ingestion is controversial. It may have potential benefit in large (> 30 cc), intentional ingestion of compounds with systemic toxicity.

Prognosis after peak symptoms is typically good, with most patients making a full recovery in weeks to months.

Lung biopsies can be diagnostic in cases of chronic hypersensitivity pneumonitis, or may help to suggest the diagnosis and trigger or intensify the search for an allergen. The main feature of chronic hypersensitivity pneumonitis on lung biopsies is expansion of the interstitium by lymphocytes accompanied by an occasional multinucleated giant cell or loose granuloma.

When fibrosis develops in chronic hypersensitivity pneumonitis, the differential diagnosis in lung biopsies includes the idiopathic interstitial pneumonias. This group of diseases includes usual interstitial pneumonia, non-specific interstitial pneumonia and cryptogenic organizing pneumonia, among others.

The prognosis of some idiopathic interstitial pneumonias, e.g. idiopathic usual interstitial pneumonia (i.e. idiopathic pulmonary fibrosis), are very poor and the treatments of little help. This contrasts the prognosis (and treatment) for hypersensitivity pneumonitis, which is generally fairly good if the allergen is identified and exposures to it significantly reduced or eliminated. Thus, a lung biopsy, in some cases, may make a decisive difference.

A CT scan of the lungs and histopathology along with a history of working in the flocking industry can diagnose flock worker's lung. A differential diagnosis may also include Sjögren's syndrome and lymphoid interstitial pneumonia. Flock worker's lung may be misdiagnosed as asthma or recurrent pneumonia. Though X-rays may be abnormal, CT scans are more useful as a diagnostic tool in flock worker's lung. Other diagnostic methods may include a transbronchial biopsy or wedge biopsy.

The following are precautionary measures that can be taken to avoid the spread of bagassosis:

1. Dust control-prevention /suppression of dust such as wet process, enclosed apparatus, exhaust ventilation etc. should be used

2. Personal protection- masks/ respirators

3. Medical control- initial medical examination & periodical checkups of workers

4. Bagasse control- keep moisture content above 20% and spray bagasse with 2% propionic acid

General treatment principles are removal from exposure, protection of the airway (i.e., preemptive intubation), and treatment of hypoxemia. Concomitant airway injury with acute bronchospasm often warrants treatment with bronchodilators because of the airway obstruction.

A beneficial role for corticosteroids has not been established by controlled trials in humans. Despite the lack of controlled evidence of efficacy, anecdotal reports of benefits from systemic corticosteroid use continue to appear.

Prophylactic antibiotic drugs have not proved to be efficacious in toxic lung injury. Antibiotics should be reserved for those patients with clinical evidence of infection.

Chest x-rays of affected individuals typically reveal nonspecific alveolar opacities. Diagnosis is generally made by surgical or endoscopic biopsy of the lung, revealing the distinctive pathologic finding. The current gold standard of PAP diagnosis involves histopathological examination of alveolar specimens obtained from bronchoalveolar lavage and transbronchial lung biopsy.

Microscopically, the distal air spaces are filled with a granular, eosinophilic material that is positive with the PAS stain and the PAS diastase stain. The main histomorphologic differential diagnosis is pulmonary edema, which does not have dense bodies.

An ELISA to measure antibodies against GM-CSF has been validated for routine clinical diagnosis of autoimmune PAP.

For some types of chILD and few forms adult ILD genetic causes have been identified. These may be identified by blood tests. For a limited number of cases this is a definite advantage, as a precise molecular diagnosis can be done; frequently then there is no need for a lung biopsy. Testing is available for

Endogenous lipoid pneumonia and non-specific interstitial pneumonitis has been seen prior to the development of pulmonary alveolar proteinosis in a child.

Chest radiography is usually the first test to detect interstitial lung diseases, but the chest radiograph can be normal in up to 10% of patients, especially early on the disease process.

High resolution CT of the chest is the preferred modality, and differs from routine CT of the chest. Conventional (regular) CT chest examines 7–10 mm slices obtained

at 10 mm intervals; high resolution CT examines 1-1.5 mm slices at 10 mm

intervals using a high spatial frequency reconstruction algorithm. The HRCT therefore provides approximately 10 times more resolution than the conventional CT chest, allowing the HRCT to elicit details that cannot otherwise be visualized.

Radiologic appearance alone however is not adequate and should be interpreted in the clinical context, keeping in mind the temporal profile of the disease process.

Interstitial lung diseases can be classified according to radiologic patterns.

Flock worker's lung can be prevented with engineering controls that protect workers from inhaling flock. Engineering controls to prevent inhalation of flock can include using guillotine cutters rather than rotary cutters, and ensuring that blades are sharp, since dull blades shear off more respirable particles. Flocking plants have also implemented medical surveillance programs for workers to diagnose cases at an earlier stage. Another technique for preventing flock worker's lung is cleaning the workplace with alternatives to compressed air in order to avoid resuspending particulates in the air.

Rapid progression from initial symptoms to respiratory failure is a key feature. An x-ray that shows ARDS is necessary for diagnosis (fluid in the small air sacs (alveoli) in both lungs). In addition, a biopsy of the lung that shows organizing diffuse alveolar damage is required for diagnosis. Other diagnostic tests are useful in excluding other similar conditions, but history, x-ray, and biopsy are essential. These other tests may include basic blood work, blood cultures, and bronchoalveolar lavage.

The clinical picture is similar to ARDS, but AIP differs from ARDS in that the cause for AIP is not known.

Physical examination may sometimes reveal low blood pressure, high heart rate, or low oxygen saturation. The respiratory rate may be faster than normal, and this may occur a day or two before other signs. Examination of the chest may be normal, but it may show decreased chest expansion on the affected side. Harsh breath sounds from the larger airways that are transmitted through the inflamed lung are termed bronchial breathing and are heard on auscultation with a stethoscope. Crackles (rales) may be heard over the affected area during inspiration. Percussion may be dulled over the affected lung, and increased, rather than decreased, vocal resonance distinguishes pneumonia from a pleural effusion.

Treatment is with corticosteroids and possibly intravenous immunoglobulins.

Aspiration pneumonia is typically diagnosed by a combination of clinical circumstances (a debilitated or neurologically impaired person), radiologic findings (an infiltrate in the proper location), and sometimes with the help of microbiologic cultures. Some cases of aspiration pneumonia are caused by aspiration of food particles or other particulate substances like pill fragments; these can be diagnosed by pathologists on lung biopsy specimens.

Pneumonia is typically diagnosed based on a combination of physical signs and a chest X-ray. However, the underlying cause can be difficult to confirm, as there is no definitive test able to distinguish between bacterial and non-bacterial origin.

The World Health Organization has defined pneumonia in children clinically based on either a cough or difficulty breathing and a rapid respiratory rate, chest indrawing, or a decreased level of consciousness. A rapid respiratory rate is defined as greater than 60 breaths per minute in children under 2 months old, greater than 50 breaths per minute in children 2 months to 1 year old, or greater than 40 breaths per minute in children 1 to 5 years old. In children, low oxygen levels and lower chest indrawing are more sensitive than hearing chest crackles with a stethoscope or increased respiratory rate. Grunting and nasal flaring may be other useful signs in children less than five years old.

In general, in adults, investigations are not needed in mild cases. There is a very low risk of pneumonia if all vital signs and auscultation are normal. In persons requiring hospitalization, pulse oximetry, chest radiography and blood tests—including a complete blood count, serum electrolytes, C-reactive protein level, and possibly liver function tests—are recommended. Procalcitonin may help determine the cause and support who should receive antibiotics.

The diagnosis of influenza-like illness can be made based on the signs and symptoms; however, confirmation of an influenza infection requires testing. Thus, treatment is frequently based on the presence of influenza in the community or a rapid influenza test.

Pulmonary aspiration resulting in pneumonia, in some patients, particularly those with physical limitations, can be fatal.

Bronchoalveolar lavage (BAL) is a well-tolerated diagnostic procedure in ILD. BAL cytology analyses (differential cell counts) should be considered in the evaluation of patients with IPF at the discretion of the treating physician based on availability and experience at their institution. BAL may reveal alternative specific diagnoses: malignancy, infections, eosinophilic pneumonia, histiocytosis X, or alveolar proteinosis. In the evaluation of patients with suspected IPF, the most important application of BAL is in the exclusion of other diagnoses. Prominent lymphocytosis (>30%) generally allows excluding a diagnosis of IPF.

BFL symptoms improve in the absence of the bird proteins which caused the disease. Therefore, it is advisable to remove all birds, bedding and pillows containing feathers from the house as well as washing all soft furnishings, walls, ceilings and furniture. Certain small mammals kept as pets have the same or similar proteins in their fur and feces and so should be removed. Peak flow measurements will indicate a lung condition however a spirometric test on lung capacity and patients ability to move air in and out of the lungs plus in more advanced cases an X-ray test or CT scan is available to confirm whether someone has the disease or not. Steroid inhalers similar to those used for asthma are effective or in cases where the patient finds inhaling difficult high dosages of steroids combined with bone density protecting drugs are used to treat a person with BFL, reducing the inflammation and hopefully preventing scarring. Recovery varies from patient to patient depending on what stage the condition was at when the patient consulted the doctor, the speed of diagnosis and application of the appropriate treatment to prevent residual damage to the lungs and many make a full recovery. However, BFL may reoccur when in contact with birds or other allergens.

Diagnosis of occupational asthma uses several techniques.

A non-specific bronchial hyperreactivity test can be used to help diagnose occupational asthma. It involves testing with methacholine, after which the forced expiratory volume in 1 second (FEV) of the patient is measured. This test is often used for measuring the intensity of a person's asthma and to confirm that the person needs to be treated for asthma.

Other non specific tests could require the patient to run for a few minutes at a continuous pace. In this case, the individual’s peak expiratory flow rate (PEFR) is measured, showing how fast a person can exhale. PEFR can also be measured at work to see if there is a difference from the PEFR in a controlled environment. Measuring PEFR at work is a highly reliable test for occupational asthma.

A skin prick test is usually performed on the inner forearm where a grid is marked and a drop of the allergens to be tested are placed on the arm in the grid. Once this has been done, the skin is pricked through the drop using a lancet. Reactions, if any, occur within 10 to 15 minutes and these results can then be analyzed.

Immunoglobulin E is an antibody found in human blood and is effective against toxins. Since it can also trigger allergic reactions to specific allergens like pollen, the IgE test is performed to evaluate whether the subject is allergic to these substances.

A spirometer is a device used to measure timed expired and inspired volumes, and can be used to help diagnose occupational asthma.

Specific inhalation challenges test for reactions to substances found in the workplace. One method is a whole body sealed chamber where the patient is exposed to articles that are present in their workplace. This method has the advantage of being able to assess, albeit highly subjectively, ocular and nasal symptoms as well as a reduction in FEV. Another test requires the patient to breathe aerosols of the suspected asthmagens through an oro-facial mask. These asthmagens are aerosolized using closed circuit chambers, and the quantities and concentrations administered are minute and extremely stable, to minimize the risk of exaggerated responses.

The only prevention for FLD is ventilating the work areas putting workers at risk and using face masks to filter out the antigens attempting to enter the lungs through the air.

Prevention of occupational asthma can be accomplished through better education of workers, management, unions and medical professionals. This will enable them to identify the risk factors and put in place preventive measures, including respiratory protection and exposure limits.

The lungs are normally protected against aspiration by a series of "protective reflexes" such as coughing and swallowing. Significant aspiration can only occur if the protective reflexes are absent or severely diminished (in neurological disease, coma, drug overdose, sedation or general anesthesia). In intensive care, sitting patients up reduces the risk of pulmonary aspiration and ventilator-associated pneumonia.

Measures to prevent aspiration depend on the situation and the patient. In patients at imminent risk of aspiration, tracheal intubation by a trained health professional provides the best protection. A simpler intervention that can be implemented is to lay the patient on their side in the recovery position (as taught in first aid and CPR classes), so that any vomitus produced by the patient will drain out their mouth instead of back down their pharynx. Some anesthetists will use sodium citrate to neutralize the stomach's low pH and metoclopramide or domperidone (pro-kinetic agents) to empty the stomach.

People with chronic neurological disorders, for example, after a stroke, are less likely to aspirate thickened fluids.

The location of abscesses caused by aspiration depends on the position one is in. If one is sitting or standing up, the aspirate ends up in the posterior basal segment of the right lower lobe. If one is on one's back, it goes to the superior segment of the right lower lobe. If one is lying on the right side, it goes to the posterior segment of the right upper lobe, or the posterior basal segment of the right upper lobe. If one is lying on the left, it goes to the lingula.

According to the updated 2011 guidelines, in the absence of a typical UIP pattern on HRCT, a surgical lung biopsy is required for confident diagnosis.

Histologic specimens for the diagnosis of IPF must be taken at least in three different places and be large enough that the pathologist can comment on the underlying lung architecture. Small biopsies, such as those obtained via transbronchial lung biopsy (performed during bronchoscopy) are usually not sufficient for this purpose. Hence, larger biopsies obtained surgically via a thoracotomy or thoracoscopy are usually necessary.

Lung tissue from people with IPF usually show a characteristic histopathologic UIP pattern and is therefore the pathologic counterpart of IPF. Although a pathologic diagnosis of UIP often corresponds to a clinical diagnosis of IPF, a UIP histologic pattern can be seen in other diseases as well, and fibrosis of known origin (rheumatic diseases for example). There are four key features of UIP including interstitial fibrosis in a ‘patchwork pattern’, interstitial scarring, honeycomb changes and fibroblast foci.

Fibroblastic foci are dense collections of myofibroblasts and scar tissue and, together with honeycombing, are the main pathological findings that allow a diagnosis of UIP.