Eosinophilic pneumonia is diagnosed in one of three circumstances: when a complete blood count reveals increased eosinophils and a chest x-ray or computed tomography (CT) identifies abnormalities in the lung, when a biopsy identifies increased eosinophils in lung tissue, or when increased eosinophils are found in fluid obtained by a bronchoscopy (bronchoalveolar lavage [BAL] fluid). Association with medication or cancer is usually apparent after review of a person's medical history. Specific parasitic infections are diagnosed after examining a person's exposure to common parasites and performing laboratory tests to look for likely causes. If no underlying cause is found, a diagnosis of AEP or CEP is made based upon the following criteria. AEP is most likely with respiratory failure after an acute febrile illness of usually less than one week, changes in multiple areas and fluid in the area surrounding the lungs on a chest x-ray, and greater than 25% eosinophils on a BAL. Other typical laboratory abnormalities include an elevated white blood cell count, erythrocyte sedimentation rate, and immunoglobulin G level. Pulmonary function testing usually reveals a restrictive process with reduced diffusion capacity for carbon monoxide. CEP is most likely when the symptoms have been present for more than a month. Laboratory tests typical of CEP include increased blood eosinophils, a high erythrocyte sedimentation rate, iron deficiency anemia, and increased platelets. A chest x-ray can show abnormalities anywhere, but the most specific finding is increased shadow in the periphery of the lung, away from the heart.

This includes:

- Asthma

- Environmental allergic reaction

- Granulomatosis with polyangiitis (Wegner's syndrome)

- Allergic bronchopulmonary aspergillosis

- Churg-Strauss syndrome

- Loeffler's syndrome

- Acute eosinophilic pneumonia

- Chronic eosinophilic pneumonia (Carrington's disease)

- Polyarteritis nodosa

- Parasitic infections

- Tropical pulmonary eosinophilia

- Tuberculosis

- Fungal infection

- Sarcoidosis

- Drug reaction with eosinophilia and systemic symptoms

- Mastocytosis

- Lymphoproliferative hypereosinophilic syndrome

- Myeloproliferative hypereosinophilic syndrome

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.

A chest radiograph is frequently used in diagnosis. In people with mild disease, imaging is needed only in those with potential complications, those not having improved with treatment, or those in which the cause is uncertain. If a person is sufficiently sick to require hospitalization, a chest radiograph is recommended. Findings do not always match the severity of disease and do not reliably separate between bacterial infection and viral infection.

X-ray presentations of pneumonia may be classified as lobar pneumonia, bronchopneumonia (also known as lobular pneumonia), and interstitial pneumonia. Bacterial, community-acquired pneumonia classically show lung consolidation of one lung segmental lobe, which is known as lobar pneumonia. However, findings may vary, and other patterns are common in other types of pneumonia. Aspiration pneumonia may present with bilateral opacities primarily in the bases of the lungs and on the right side. Radiographs of viral pneumonia may appear normal, appear hyper-inflated, have bilateral patchy areas, or present similar to bacterial pneumonia with lobar consolidation. Radiologic findings may not be present in the early stages of the disease, especially in the presence of dehydration, or may be difficult to be interpreted in the obese or those with a history of lung disease. A CT scan can give additional information in indeterminate cases. Lung ultrasound may also be useful in helping to make the diagnosis.

The fibrosing pattern of NSIP has a five year survival rate of 86% to 92%, while the cellular pattern of NSIP has a 100% five year survival rate. Patients with NSIP(whether cellular or fibrosing), have a better prognosis than those with usual interstitial pneumonia (UIP).

Flavorings-related lung disease can be prevented with the use of engineering controls (e.g. exhaust hoods or closed systems), personal protective equipment, monitoring of potentially affected workers, worker education, and by not using lung-disease-causing flavorings.

The diagnosis can be confirmed by the characteristic appearance of the chest x-ray, which shows widespread pulmonary infiltrates, and an arterial oxygen level (PaO) that is strikingly lower than would be expected from symptoms. Gallium 67 scans are also useful in the diagnosis. They are abnormal in approximately 90% of cases and are often positive before the chest x-ray becomes abnormal. The diagnosis can be definitively confirmed by histological identification of the causative organism in sputum or bronchio-alveolar lavage (lung rinse). Staining with toluidine blue, silver stain, periodic-acid schiff stain, or an immunofluorescence assay will show the characteristic cysts. The cysts resemble crushed ping-pong balls and are present in aggregates of 2 to 8 (and not to be confused with "Histoplasma" or "Cryptococcus", which typically do not form aggregates of spores or cells). A lung biopsy would show thickened alveolar septa with fluffy eosinophilic exudate in the alveoli. Both the thickened septa and the fluffy exudate contribute to dysfunctional diffusion capacity which is characteristic of this pneumonia.

"Pneumocystis" infection can also be diagnosed by immunofluorescent or histochemical staining of the specimen, and more recently by molecular analysis of polymerase chain reaction products comparing DNA samples. Notably, simple molecular detection of "Pneumocystis jirovecii" in lung fluids does not mean that a person has "Pneumocystis" pneumonia or infection by HIV. The fungus appears to be present in healthy individuals in the general population.

Chest radiographs (X-ray photographs) often show a pulmonary infection before physical signs of atypical pneumonia are observable at all.

This is occult pneumonia. In general, occult pneumonia is rather often present in patients with pneumonia and can also be caused by "Streptococcus pneumoniae", as the decrease of occult pneumonia after vaccination of children with a pneumococcal vaccine suggests.

Infiltration commonly begins in the perihilar region (where the bronchus begins) and spreads in a wedge- or fan-shaped fashion toward the periphery of the lung field. The process most often involves the lower lobe, but may affect any lobe or combination of lobes.

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.

Respiratory diseases may be investigated by performing one or more of the following tests

- Biopsy of the lung or pleura

- Blood test

- Bronchoscopy

- Chest x-ray

- Computed tomography scan, including high-resolution computed tomography

- Culture of microorganisms from secretions such as sputum

- Ultrasound scanning can be useful to detect fluid such as pleural effusion

- Pulmonary function test

- Ventilation—perfusion scan

Respiratory disease is a common and significant cause of illness and death around the world. In the US, approximately 1 billion "common colds" occur each year. A study found that in 2010, there were approximately 6.8 million emergency department visits for respiratory disorders in the U.S. for patients under the age of 18. In 2012, respiratory conditions were the most frequent reasons for hospital stays among children.

In the UK, approximately 1 in 7 individuals are affected by some form of chronic lung disease, most commonly chronic obstructive pulmonary disease, which includes asthma, chronic bronchitis and emphysema.

Respiratory diseases (including lung cancer) are responsible for over 10% of hospitalizations and over 16% of deaths in Canada.

In 2011, respiratory disease with ventilator support accounted for 93.3% of ICU utilization in the United States.

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.

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.

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

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.

Investigation is tailored towards the symptoms and signs. A proper and detailed history looking for the occupational exposures, and for signs of conditions listed above is the first and probably the most important part of the workup in patients with interstitial lung disease. Pulmonary function tests usually show a restrictive defect with decreased diffusion capacity (DLCO).

A lung biopsy is required if the clinical history and imaging are not clearly suggestive of a specific diagnosis or malignancy cannot otherwise be ruled out. In cases where a lung biopsy is indicated, a trans-bronchial biopsy is usually unhelpful, and a surgical lung biopsy is often required.

Lung biopsies performed on patients with NSIP reveal two different disease patterns - cellular and fibrosing - which are associated with different prognoses. The cellular pattern displays chronic inflammation with minimal fibrosis. The fibrosing pattern displays interstitial fibrosis with various inflammation levels. Both patterns are uniform and lack the prominent fibroblastic foci that are found in other types of idiopathic interstitial pneumonia.

Bronchiolitis obliterans is often misdiagnosed as asthma, chronic bronchitis, emphysema or pneumonia.

Several tests are often needed to correctly diagnose bronchiolitis obliterans, including chest X-rays, diffusing capacity of the lung tests (DLCO), spirometry, lung volume tests, high-resolution CT (HRCT), and lung biopsy. Diffusing capacity of the lung (DLCO) tests are usually normal; people with early-stage BO are more likely to have normal DLCO. Spirometry tests usually show fixed airway obstructions and sometimes restriction, where the lungs can't expand fully. Lung volume tests may show hyperinflation (excessive air in lungs caused by air trapping). HRCT can also show air trapping when the person being scanned breathes out completely; it can also show thickening in the airway and haziness in the lungs. Transthoracic lung biopsies are preferable for diagnosis of constrictive BO compared to transbronchial biopsies; regardless of the type of biopsy, a diagnosis may only be achieved by examination of multiple samples.

Classification can be complex, and the combined efforts of clinicians, radiologists, and pathologists can help in the generation of a more specific diagnosis.

Idiopathic interstitial pneumonia can be subclassified based on histologic appearance into the following patterns:

Usual interstitial pneumonia is the most common type.

Mycoplasma is found more often in younger than in older people.

Older people are more often infected by Legionella.

UIP may be diagnosed by a radiologist using computed tomography (CT) scan of the chest, or by a pathologist using tissue obtained by a lung biopsy. Radiologically, the main feature required for a confident diagnosis of UIP is honeycomb change in the periphery and the lower portions (bases) of the lungs. The histologic hallmarks of UIP, as seen in lung tissue under a microscope by a pathologist, are interstitial fibrosis in a "patchwork pattern", honeycomb change and fibroblast foci (see images below).

Blood tests can detect bacterial or viral infections, pneumonia, rheumatic fever, a pulmonary embolism, or lupus.

A CT scan provides a computer-generated picture of the lungs that can show pockets of fluid. It also may show signs of pneumonia, a lung abscess, or a tumor.

The major criterion for diagnosis is typically a confirmed surgical biopsy. Minor diagnostic criteria have been proposed for DIPNECH.

- Clinical presentation: woman, between the age of 45 and 67 with cough and/or shortness of breath for 5–10 years

- Pulmonary function: increased residual volume, increased total lung capacity, fixed obstruction, low diffusing capacity of the lung for carbon monoxide that corrects with alveolar volume

- High-resolution CT scan: diffuse pulmonary nodules 4–10 mm, greater than 20 nodules, mosaic attenuation or air trapping in greater than 50% of the lung

- Transbronchial biopsy: proliferation of pulmonary neuroendocrine cells

- Serum markers: elevated serum chromogranin A levels

Table 1: Development of the (histologic) idiopathic interstitial pneumonia classification

Lymphoid interstitial pneumonia was originally included in this category, then excluded, then included again.