Pulmonary ultrasound, performed at the bedside or on the accident scene, is being explored as a diagnosis for pulmonary contusion. Its use is still not widespread, being limited to facilities which are comfortable with its use for other applications, like pneumothorax, airway management, and hemothorax. Accuracy has been found to be comparable to CT scanning.

VALI is most common in patients receiving mechanical ventilation for acute lung injury or acute respiratory distress syndrome (ALI/ARDS).

Possible reasons for predisposition to VALI include:

- An injured lung may be at risk for further injury

- Cyclic atelectasis is particularly common in an injured lung

Chest X-ray is the most common method used for diagnosis, and may be used to confirm a diagnosis already made using clinical signs. Consolidated areas appear white on an X-ray film. Contusion is not typically restricted by the anatomical boundaries of the lobes or segments of the lung. The X-ray appearance of pulmonary contusion is similar to that of aspiration, and the presence of hemothorax or pneumothorax may obscure the contusion on a radiograph. Signs of contusion that progress after 48 hours post-injury are likely to be actually due to aspiration, pneumonia, or ARDS.

Although chest radiography is an important part of the diagnosis, it is often not sensitive enough to detect the condition early after the injury. In a third of cases, pulmonary contusion is not visible on the first chest radiograph performed. It takes an average of six hours for the characteristic white regions to show up on a chest X-ray, and the contusion may not become apparent for 48 hours. When a pulmonary contusion is apparent in an X-ray, it suggests that the trauma to the chest was severe and that a CT scan might reveal other injuries that were missed with X-ray.

Computed tomography (CT, or "CAT scan") is not necessary for the diagnosis of pneumothorax, but it can be useful in particular situations. In some lung diseases, especially emphysema, it is possible for abnormal lung areas such as bullae (large air-filled sacs) to have the same appearance as a pneumothorax on chest X-ray, and it may not be safe to apply any treatment before the distinction is made and before the exact location and size of the pneumothorax is determined. In trauma, where it may not be possible to perform an upright film, chest radiography may miss up to a third of pneumothoraces, while CT remains very sensitive.

A further use of CT is in the identification of underlying lung lesions. In presumed primary pneumothorax, it may help to identify blebs or cystic lesions (in anticipation of treatment, see below), and in secondary pneumothorax it can help to identify most of the causes listed above.

Ultrasound is commonly used in the evaluation of people who have sustained physical trauma, for example with the FAST protocol. Ultrasound may be more sensitive than chest X-rays in the identification of pneumothorax after blunt trauma to the chest. Ultrasound may also provide a rapid diagnosis in other emergency situations, and allow the quantification of the size of the pneumothorax. Several particular features on ultrasonography of the chest can be used to confirm or exclude the diagnosis.

VALI does not need to be distinguished from progressive ALI/ARDS because management is the same in both. Additionally, definitive diagnosis of VALI may not be possible because of lack of sign or symptoms.

Rare cases of BOOP have induced with lobar cicatricial atelectasis.

In rounded atelectasis (Folded lung or Blesovsky syndrome), an outer portion of the lung slowly collapses as a result of scarring and shrinkage of the membrane layers covering the lungs (pleura), which would show as visceral pleural thickening and entrapment of lung tissue. This produces a rounded appearance on x-ray that doctors may mistake for a tumor. Rounded atelectasis is usually a complication of asbestos-induced disease of the pleura, but it may also result from other types of chronic scarring and thickening of the pleura.

The chest x-ray is distinctive with features that appear similar to an extensive pneumonia, with both lungs showing widespread white patches. The white patches may seem to migrate from one area of the lung to another as the disease persists or progresses. Computed tomography (CT) may be used to confirm the diagnosis. Often the findings are typical enough to allow the doctor to make a diagnosis without ordering additional tests. To confirm the diagnosis, a doctor may perform a lung biopsy using a bronchoscope. Many times, a larger specimen is needed and must be removed surgically.

Plain chest radiography shows normal lung volumes, with characteristic patchy unilateral or bilateral consolidation. Small nodular opacities occur in up to 50% of patients and large nodules in 15%. On high resolution computed tomography, airspace consolidation with air bronchograms is present in more than 90% of patients, often with a lower zone predominance A subpleural or peribronchiolar distribution is noted in up to 50% of patients. Ground glass appearance or hazy opacities associated with the consolidation are detected in most patients.

Pulmonary physiology is restrictive with a reduced diffusion capacity of the lung for carbon monoxide (DCO). Airflow limitation is uncommon; gas exchange is usually abnormal and mild hypoxemia is common. Bronchoscopy with bronchoalveolar lavage reveals up to 40% lymphocytes, along with more subtle increases in neutrophils and eosinophils. In patients with typical clinical and radiographic features, a transbronchial biopsy that shows the pathologic pattern of organizing pneumonia and lacks features of an alternative diagnosis is adequate to make a tentative diagnosis and start therapy. On surgical lung biopsy, the histopathologic pattern is organizing pneumonia with preserved lung architecture; this pattern is not exclusive to BOOP and must be interpreted in the clinical context.

Histologically, cryptogenic organizing pneumonia is characterized by the presence of polypoid plugs of loose organizing connective tissue (Masson bodies) within alveolar ducts, alveoli, and bronchioles.

Atelectasis may be an acute or chronic condition. In acute atelectasis, the lung has recently collapsed and is primarily notable only for airlessness. In chronic atelectasis, the affected area is often characterized by a complex mixture of airlessness, infection, widening of the bronchi (bronchiectasis), destruction, and scarring (fibrosis).

There is ongoing research on the treatment of ARDS by interferon (IFN) beta-1a to aid in preventing leakage of vascular beds. Traumakine (FP-1201-lyo), is a recombinant human IFN beta-1a drug developed by Faron pharmaceuticals, is undergoing international phase-III clinical trials after an open-label, early-phase trial showed a 81% reduction-in-odds of 28-day mortality in ICU patients with ARDS. The drug is known to function by enhancing lung CD73 expression and increasing production of anti-inflammatory adenosine, such that vascular leaking and escalation of inflammation are reduced.

Radiologic imaging has long been a criterion for diagnosis of ARDS. While original definitions of ARDS specified that correlative chest X-ray findings were required for diagnosis, the diagnostic criteria have been expanded over time to accept CT and ultrasound findings as equally contributory. Generally, radiographic findings of fluid accumulation (pulmonary edema) affecting both lungs and unrelated to increased cardiopulmonary vascular pressure (such as in heart failure) may be suggestive of ARDS.

Ultrasound findings suggestive of ARDS include the following:

- Anterior subpleural consolidations

- Absence or reduction of lung sliding

- “Spared areas” of normal parenchyma

- Pleural line abnormalities (irregular thickened fragmented pleural line)

- Nonhomogeneous distribution of B-lines (a characteristic ultrasound finding suggestive of fluid accumulation in the lungs)

Once a pleural effusion is diagnosed, its cause must be determined. Pleural fluid is drawn out of the pleural space in a process called thoracentesis, and it should be done in almost all patients who have pleural fluid that is at least 10 mm in thickness on CT, ultrasonography, or lateral decubitus X-ray and that is new or of uncertain etiology. In general, the only patients who do not require thoracentesis are those who have heart failure with symmetric pleural effusions and no chest pain or fever; in these patients, diuresis can be tried, and thoracentesis is avoided unless effusions persist for more than 3 days. In a thoracentesis, a needle is inserted through the back of the chest wall in the sixth, seventh, or eighth intercostal space on the midaxillary line, into the pleural space. The use of ultrasound to guide the procedure is now standard of care as it increases accuracy and decreases complications. After removal, the fluid may then be evaluated for:

1. Chemical composition including protein, lactate dehydrogenase (LDH), albumin, amylase, pH, and glucose

2. Gram stain and culture to identify possible bacterial infections

3. White and red blood cell counts and differential white blood cell counts

4. Cytopathology to identify cancer cells, but may also identify some infective organisms

5. Other tests as suggested by the clinical situation – lipids, fungal culture, viral culture, tuberculosis cultures, lupus cell prep, specific immunoglobulins

A pleural effusion appears as an area of whiteness on a standard posteroanterior chest X-ray. Normally, the space between the visceral pleura and the parietal pleura cannot be seen. A pleural effusion infiltrates the space between these layers. Because the pleural effusion has a density similar to water, it can be seen on radiographs. Since the effusion has greater density than the rest of the lung, it gravitates towards the lower portions of the pleural cavity. The pleural effusion behaves according to basic fluid dynamics, conforming to the shape of pleural space, which is determined by the lung and chest wall. If the pleural space contains both air and fluid, then an air-fluid level that is horizontal will be present, instead of conforming to the lung space. Chest radiographs in the lateral decubitus position (with the patient lying on the side of the pleural effusion) are more sensitive and can detect as little as 50 mL of fluid. At least 300 mL of fluid must be present before upright chest X-rays can detect a pleural effusion (e.g., blunted costophrenic angles).

Chest computed tomography is more accurate for diagnosis and may be obtained to better characterize the presence, size, and characteristics of a pleural effusion. Lung ultrasound, nearly as accurate as CT and more accurate than chest X-ray, is increasingly being used at the point of care to diagnose pleural effusions, with the advantage that it is a safe, dynamic, and repeatable imaging modality. To increase diagnostic accuracy of detection of pleural effusion sonographically, markers such as boomerang and VIP signs can be utilized.

Rapid diagnosis and treatment are important in the care of TBI; if the injury is not diagnosed shortly after the injury, the risk of complications is higher. Bronchoscopy is the most effective method to diagnose, locate, and determine the severity of TBI, and it is usually the only method that allows a definitive diagnosis. Diagnosis with a flexible bronchoscope, which allows the injury to be visualized directly, is the fastest and most reliable technique. In people with TBI, bronchoscopy may reveal that the airway is torn, or that the airways are blocked by blood, or that a bronchus has collapsed, obscuring more distal (lower) bronchi from view.

Chest x-ray is the initial imaging technique used to diagnose TBI. The film may not have any signs in an otherwise asymptomatic patient. Indications of TBI seen on radiographs include deformity in the trachea or a defect in the tracheal wall. Radiography may also show cervical emphysema, air in the tissues of the neck. X-rays may also show accompanying injuries and signs such as fractures and subcutaneous emphysema. If subcutaneous emphysema occurs and the hyoid bone appears in an X-ray to be sitting unusually high in the throat, it may be an indication that the trachea has been severed. TBI is also suspected if an endotracheal tube appears in an X-ray to be out of place, or if its cuff appears to be more full than normal or to protrude through a tear in the airway. If a bronchus is torn all the way around, the lung may collapse outward toward the chest wall (rather than inward, as it usually does in pneumothorax) because it loses the attachment to the bronchus which normally holds it toward the center. In a person lying face-up, the lung collapses toward the diaphragm and the back. This sign, described in 1969, is called fallen lung sign and is pathognomonic of TBI (that is, it is diagnostic for TBI because it does not occur in other conditions); however it occurs only rarely. In as many as one in five cases, people with blunt trauma and TBI have no signs of the injury on chest X-ray. CT scanning detects over 90% of TBI resulting from blunt trauma, but neither X-ray nor CT are a replacement for bronchoscopy.

At least 30% of TBI are not discovered at first; this number may be as high as 50%. In about 10% of cases, TBI has no specific signs either clinically or on chest radiography, and its detection may be further complicated by concurrent injuries, since TBI tends to occur after high-energy accidents. Weeks or months may go by before the injury is diagnosed, even though the injury is better known than it was in the past.

The rate of BPD varies among institutions, which may reflect neonatal risk factors, care practices (e.g., target levels for acceptable oxygen saturation), and differences in the clinical definitions of BPD.

Vehicle occupants who wear seat belts have a lower incidence of TBI after a motor vehicle accident. However, if the strap is situated across the front of the neck (instead of the chest), this increases the risk of tracheal injury. Design of medical instruments can be modified to prevent iatrogenic TBI, and medical practitioners can use techniques that reduce the risk of injury with procedures such as tracheotomy.

There is evidence to show that steroids given to babies less than 8 days old can prevent bronchopulmonary dysplasia. However, the risks of treatment may outweigh the benefits.

It is unclear if starting steroids more than 7 days after birth is harmful or beneficial. It is thus recommended that they only be used in those who cannot be taken off of a ventilator.

Alveolar disease is visible on chest radiography as small, ill-defined nodules of homogeneous density centered on the acini or bronchioles. The nodules coalesce early in the course of disease, such that the nodules may only be seen as soft fluffy edges in the periphery.

When the nodules are centered on the hilar regions, the chest x-ray may develop what is called the "butterfly," or "batwing" appearance. The nodules may also have a segmental or lobar distribution. Air alveolograms and air bronchograms can also be seen.

These findings appear soon after the onset of symptoms and change rapidly thereafter.

A segmental or lobar pattern may be apparent after aspiration pneumonia, atelectasis, lung contusion, localized pulmonary edema, obstructive pneumonia, pneumonia, pulmonary embolism with infarction, or tuberculosis.

Benign asbestos pleural effusion is an exudative pleural effusion (a buildup of fluid between the two pleural layers) following asbestos exposure. It is relatively uncommon and the earliest manifestation of disease following asbestos exposure, usually occurring within 10 years from exposure. Effusions may be asymptomatic but rarely, they can cause pain, fever, and breathlessness. Effusions usually last for 3–4 months and then resolve completely. They can also progress to diffuse pleural thickening. Diagnosis relies on a compatible history of asbestos exposure and exclusion of other probable causes.

Alveolar lung diseases, are a group of diseases that mainly affect the alveoli of the lungs.

Asbestos can cause lung cancer that is identical to lung cancer from other causes. Exposure to asbestos is associated with all major histological types of lung carcinoma (adenocarcinoma, squamous cell carcinoma, large-cell carcinoma and small-cell carcinoma). The latency period between exposure and development of lung cancer is 20 to 30 years. It is estimated that 3%-8% of all lung cancers are related to asbestos. The risk of developing lung cancer depends on the level, duration, and frequency of asbestos exposure (cumulative exposure). Smoking and individual susceptibility are other contributing factors towards lung cancer. Smokers who have been exposed to asbestos are at far greater risk of lung cancer. Smoking and asbestos exposure have a multiplicative (synergistic) effect on the risk of lung cancer. Symptoms include chronic cough, chest pain, breathlessness, haemoptysis (coughing up blood), wheezing or hoarseness of the voice, weight loss and fatigue. Treatment involves surgical removal of the cancer, chemotherapy, radiotherapy, or a combination of these (multimodality treatment). Prognosis is generally poor unless the cancer is detected in its early stages. Out of all patients diagnosed with lung cancer, only 15% survive for five years after diagnosis.

High risk infants may be identified by fetal tachycardia, bradycardia or absence of fetal accelerations upon CTG in utero, at birth the infant may look cachexic and show signs of yellowish meconium staining on skin, nail and the umbillical cord, these infants usually progress onto Infant Respiratory distress syndrome within 4 hours. Investigations which can confirm the diagnosis are fetal chest x-ray, which will show hyperinflation, diaphragmatic flattening, cardiomegaly, patchy atelectasis and consolidation, and ABG samples, which will show decreased oxygen levels.

The mortality rate of meconium-stained infants is considerably higher than that of non-stained infants; meconium aspiration used to account for a significant proportion of neonatal deaths. Residual lung problems are rare but include symptomatic cough, wheezing, and persistent hyperinflation for up to five to ten years. The ultimate prognosis depends on the extent of CNS injury from asphyxia and the presence of associated problems such as pulmonary hypertension. Fifty percent of newborns affected by meconium aspiration would die fifteen years ago; however, today the percent has dropped to about twenty.

Baylor College of Medicine in Houston, Texas has conducted ACD research since 2001.