Pulmonary laceration may not be visible using chest X-ray because an associated pulmonary contusion or hemorrhage may mask it. As the lung contusion clears (usually within two to four days), lacerations begin to become visible on chest X-ray. CT scanning is more sensitive and better at detecting pulmonary laceration than X-rays are, and often reveals multiple lacerations in cases where chest X-ray showed only a contusion. Before CT scanning was widely available, pulmonary laceration was considered unusual because it was not common to find with X-ray alone. On a CT scan, pulmonary lacerations show up in a contused area of the lung, typically appearing as cavities filled with air or fluid that usually have a round or ovoid shape due to the lung's elasticity.

Hematomas appear on chest radiographs as smooth masses that are round or ovoid in shape. Like lacerations, hematomas may initially be hidden on X-ray by lung contusions, but they become more apparent as the contusion begins to heal. Pneumatoceles have a similar shape to that of hematomas but have thin, smooth walls. Lacerations may be filled completely with blood, completely with air, or partially with both. Lacerations filled with both blood and air display a distinctive air-fluid level. A single laceration may occur by itself, or many may be present, creating an appearance like Swiss cheese in the radiography of the lung.

Pulmonary laceration is usually accompanied by hemoptysis (coughing up blood or of blood-stained sputum).

Thoracoscopy may be used in both diagnosis and treatment of pulmonary laceration.

A healing laceration may resemble a pulmonary nodule on radiographs, but unlike pulmonary nodules, lacerations decrease in size over time on radiographs.

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.

As with other chest injuries such as pulmonary contusion, hemothorax, and pneumothorax, pulmonary laceration can often be treated with just supplemental oxygen, ventilation, and drainage of fluids from the chest cavity. A thoracostomy tube can be used to remove blood and air from the chest cavity. About 5% of cases require surgery, called thoracotomy. Thoracotomy is especially likely to be needed if a lung fails to re-expand; if pneumothorax, bleeding, or coughing up blood persist; or in order to remove clotted blood from a hemothorax. Surgical treatment includes suturing, stapling, oversewing, and wedging out of the laceration. Occasionally, surgeons must perform a lobectomy, in which a lobe of the lung is removed, or a pneumonectomy, in which an entire lung is removed.

Computed tomography (CT scanning) is a more sensitive test for pulmonary contusion, and it can identify abdominal, chest, or other injuries that accompany the contusion. In one study, chest X-ray detected pulmonary contusions in 16.3% of people with serious blunt trauma, while CT detected them in 31.2% of the same people. Unlike X-ray, CT scanning can detect the contusion almost immediately after the injury. However, in both X-ray and CT a contusion may become more visible over the first 24–48 hours after trauma as bleeding and edema into lung tissues progress. CT scanning also helps determine the size of a contusion, which is useful in determining whether a patient needs mechanical ventilation; a larger volume of contused lung on CT scan is associated with an increased likelihood that ventilation will be needed. CT scans also help differentiate between contusion and pulmonary hematoma, which may be difficult to tell apart otherwise. However, pulmonary contusions that are visible on CT but not chest X-ray are usually not severe enough to affect outcome or treatment.

It can be diagnosed with CT scan, angiography, transesophageal echocardiography, or cardiac MRI. Unfortunately, less invasive and expensive testing, such as transthoracic echocardiography and CT scanning are generally less sensitive.

A "Partial anomalous pulmonary venous connection" (or "Partial anomalous pulmonary venous drainage" or "Partial anomalous pulmonary venous return") is a congenital defect where the left atrium is the point of return for the blood from some (but not all) of the pulmonary veins.

It is less severe than total anomalous pulmonary venous connection which is a life-threatening anomaly requiring emergent surgical correction, usually diagnosed in the first few days of life. Partial anomalous venous connection may be diagnosed at any time from birth to old age. The severity of symptoms, and thus the likelihood of diagnosis, varies significantly depending on the amount of blood flow through the anomalous connections. In less severe cases, with smaller amounts of blood flow, diagnosis may be delayed until adulthood, when it can be confused with other causes of pulmonary hypertension. There is also evidence that a significant number of mild cases are never diagnosed, or diagnosed incidentally. It is associated with other vascular anomalies, and some genetic syndromes such as Turner syndrome.

A pulmonary hematoma is a collection of blood within the tissue of the lung. It may result when a pulmonary laceration fills with blood. A lung laceration filled with air is called a pneumatocele. In some cases, both pneumatoceles and hematomas exist in the same injured lung. Pulmonary hematomas take longer to heal than simple pneumatoceles and commonly leave the lungs scarred. A pulmonary contusion is another cause of bleeding within the lung tissue, but these result from microhemorrhages, multiple small bleeds, and the bleeding is not a discrete mass but rather occurs within the lung tissue. An indication of more severe damage to the lung than pulmonary contusion, a hematoma also takes longer to clear. Unlike contusions, hematomas do not usually interfere with gas exchange in the lung, but they do increase the risk of infection and abscess formation.

There is no one single test for confirming that breathlessness is caused by pulmonary edema; indeed, in many cases, the cause of shortness of breath is probably multifactorial.

Low oxygen saturation and disturbed arterial blood gas readings support the proposed diagnosis by suggesting a pulmonary shunt. Chest X-ray will show fluid in the alveolar walls, Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern, upper lobe diversion (increased blood flow to the superior parts of the lung), and possibly pleural effusions. In contrast, patchy alveolar infiltrates are more typically associated with noncardiogenic edema

Lung ultrasound, employed by a healthcare provider at the point of care, is also a useful tool to diagnose pulmonary edema; not only is it accurate, but it may quantify the degree of lung water, track changes over time, and differentiate between cardiogenic and non-cardiogenic edema.

Especially in the case of cardiogenic pulmonary edema, urgent echocardiography may strengthen the diagnosis by demonstrating impaired left ventricular function, high central venous pressures and high pulmonary artery pressures.

Blood tests are performed for electrolytes (sodium, potassium) and markers of renal function (creatinine, urea). Liver enzymes, inflammatory markers (usually C-reactive protein) and a complete blood count as well as coagulation studies (PT, aPTT) are also typically requested. B-type natriuretic peptide (BNP) is available in many hospitals, sometimes even as a point-of-care test. Low levels of BNP (<100 pg/ml) suggest a cardiac cause is unlikely.

Pulmonary veno-occlusive disease can only be well diagnosed with a lung biopsy. CT scans may show characteristic findings such as ground-glass opacities in centrilobular distribution, and mediastinal lymphadenopathy, but these findings are non-specific and may be seen in other conditions. However, pulmonary hypertension (revealed via physical examination), in the presence of pleural effusion (done via CT scan) usually indicates a diagnosis of pulmonary veno-occlusive disease. The prognosis indicates usually a 2-year (24 month) life expectancy after diagnosis.

For people considered likely to have PAH based on the above tests, the specific associated condition is then determined based on the physical examination, medical/family history and further specific diagnostic tests (for example, serological tests to detect underlying connective tissue disease, HIV infection or hepatitis, ultrasonography to confirm the presence of portal hypertension, echocardiography/cardiac magnetic resonance imaging for congenital heart disease, laboratory tests for schistosomiasis, and high resolution CT for PVOD and pulmonary capillary hemangiomatosis). Routine lung biopsy is discouraged in patients with PAH, because of the risk to the patient and because the findings are unlikely to alter the diagnosis and treatment.

Although pulmonary arterial pressure (PAP) can be estimated on the basis of echocardiography, pressure measurements with a Swan-Ganz catheter inserted through the right side of the heart provide the most definite assessment.[42] Pulmonary hypertension is defined as a mean PAP of at least 25 mm Hg (3300 Pa) at rest, and PAH is defined as precapillary pulmonary hypertension (i.e. mean PAP ≥ 25 mm Hg with pulmonary arterial occlusion pressure [PAOP] ≤ 15 mm Hg and pulmonary vascular resistance [PVR] > 3 Wood Units). PAOP and PVR cannot be measured directly with echocardiography. Therefore, diagnosis of PAH requires right-sided cardiac catheterization. A Swan-Ganz catheter can also measure the cardiac output; this can be used to calculate the cardiac index, which is far more important in measuring disease severity than the pulmonary arterial pressure.

"Mean" PAP (mPAP) should not be confused with systolic PAP (sPAP), which is often reported on echocardiogram reports. A systolic pressure of 40 mm Hg typically implies a mean pressure of more than 25 mm Hg. Roughly, mPAP = 0.61•sPAP + 2.

The prevalence of pulmonary interstitial emphysema widely varies with the population studied. In a 1987 study 3% of infants admitted to the neonatal intensive care unit (NICU) developed pulmonary interstitial emphysema.

In those with underlying heart disease, effective control of congestive symptoms prevents pulmonary edema.

Dexamethasone is in widespread use for the prevention of high altitude pulmonary edema. Sildenafil is used as a preventive treatment for altitude-induced pulmonary edema and pulmonary hypertension, the mechanism of action is via phosphodiesterase inhibition which raises cGMP, resulting in pulmonary arterial vasodilation and inhibition of smooth muscle cell proliferation. While this effect has only recently been discovered, sildenafil is already becoming an accepted treatment for this condition, in particular in situations where the standard treatment of rapid descent has been delayed for some reason.

Studies reflecting international frequency demonstrated that 2-3% of all infants in NICUs develop pulmonary interstitial emphysema. When limiting the population studied to premature infants, this frequency increases to 20-30%, with the highest frequencies occurring in infants weighing fewer than 1000 g.

The diagnosis can be confirmed by lung biopsy. A videoscopic assisted thoracoscopic wedge biopsy (VATS) under general anesthesia may be necessary to obtain enough tissue to make an accurate diagnosis. This kind of biopsy involves placement of several tubes through the chest wall, one of which is used to cut off a piece of lung to send for evaluation. The removed tissue is examined histopathologically by microscopy to confirm the presence and pattern of fibrosis as well as presence of other features that may indicate a specific cause e.g. specific types of mineral dust or possible response to therapy e.g. a pattern of so-called non-specific interstitial fibrosis.

Misdiagnosis is common because, while overall pulmonary fibrosis is not rare, each individual type of pulmonary fibrosis is uncommon and the evaluation of patients with these diseases is complex and requires a multidisciplinary approach. Terminology has been standardized but difficulties still exist in their application. Even experts may disagree with the classification of some cases.

On spirometry, as a restrictive lung disease, both the FEV1 (forced expiratory volume in 1 second) and FVC (forced vital capacity) are reduced so the FEV1/FVC ratio is normal or even increased in contrast to obstructive lung disease where this ratio is reduced. The values for residual volume and total lung capacity are generally decreased in restrictive lung disease.

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

Treatments for primary pulmonary hypertension such as prostacyclins and endothelin receptor antagonists can be fatal in people with PVOD due to the development of severe pulmonary edema, and worsening symptoms after initiation of these medications may be a clue to the diagnosis of pulmonary veno occlusive disease.

The definitive therapy is lung transplantation, though transplant rejection is always a possibility, in this measures must be taken in terms of appropriate treatment and medication.

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.

Hypoxia caused by pulmonary fibrosis can lead to pulmonary hypertension, which, in turn, can lead to heart failure of the right ventricle. Hypoxia can be prevented with oxygen supplementation.

Pulmonary fibrosis may also result in an increased risk for pulmonary emboli, which can be prevented by anticoagulants.

The diagnosis of pulmonary heart disease is not easy as both lung and heart disease can produce similar symptoms. Therefore, the differential diagnosis should assess:

Among the investigations available to determine cor pulmonale are:

- Chest x-ray – right ventricular hypertrophy, right atrial dilatation, prominent pulmonary artery

- ECG – right ventricular hypertrophy, dysrhythmia, P pulmonale (characteristic peaked P wave)

- Thrombophilia screen- to detect chronic venous thromboembolism (proteins C and S, antithrombin III, homocysteine levels)

Lung symptoms in a patient who is taking a medicinal drug that can cause pulmonary toxicity should not automatically lead to a diagnosis of "pulmonary toxicity due to the medicinal drug", because some patients can have another (i.e., simultaneous) lung disease, e.g. an infection of the lungs "not" related to the medicinal drugs the patient is taking. But if the patient is taking such a medicinal drug, this should not be overlooked. Diagnostic care should be executed. The correct diagnosis is an exclusion diagnosis and can require some tests.

Diagnosis is confirmed with CT, or bedside ultrasound for less stable patients. Exploratory laparotomy is rarely used, though it may be of benefit in patients with particularly severe hemorrhage. A set of CT scan grading criteria was created to identify the need for intervention (surgery or embolization) in patients with splenic injury. The criteria were established using 20 CT scans from a database of hemodynamically stable patients with blunt splenic injury. These criteria were then validated in 56 consecutive patients retrospectively and appear to reliably predict the need for invasive management in patients with blunt injury to the spleen (sensitivity of 100%, specificity 88%, overall accuracy was 93%).

The study suggested that the following three CT findings correlate with the need for intervention:

1. Devascularization or laceration involving 50% or more of the splenic parenchyma

2. Contrast blush greater than one centimeter in diameter (from active extravasation of IV contrast or pseudoaneurysm formation)

3. A large hemoperitoneum.

Side effects on the lungs can be very varied, and can include signs and symptoms that are either clinical, or radiological (i.e., seen on chest X-ray or CT), or both. They can include lung inflammation (pneumonitis), secondary (in this context, indirectly caused) lung infection (pneumonia), lung fibrosis, organising pneumonia (bronchiolitis obliterans organising pneumonia, BOOP), ARDS (acute respiratory distress syndrome), solitary pulmonary mass (even including lung cancer in some cases, mainly in cases of asbestos-related lung disease, but today this is very rare, because asbestos is now completely prohibited by law in most countries), or pulmonary nodule. The diagnosis should be made by a specialist, if possible.

In treating pulmonary insufficiency, it should be determined if pulmonary hypertension is causing the problem to therefore begin the most appropriate therapy as soon as possible (primary pulmonary hypertension or secondary pulmonary hypertension due to thromboembolism). Furthermore, pulmonary insufficiency is generally treated by addressing the underlying condition, in certain cases, the pulmonary valve may be surgically replaced.

To treat a septal haematoma it is incised & drained to prevent avascular necrosis of the septal hyaline cartilage which depends on diffusion of nutrients from its attached nasal mucosa. Small hematomas can be aspirated with a wide-bore needle. Large hematomas are drained by an incision parallel to nasal floor. Systemic antibiotics are given after the incision and drainage to prevent local infection.