Pulmonary edema is a consequence of a disease process rather than a primary pathology. Pulmonary edema can be classified into cardiogenic and noncardiogenic based on the cause of the edema. In non-cardiogenic pulmonary edema, the main pathology is a direct or indirect insult to the pulmonary capillary membrane which results in an increased permeability of the endothelial cell layer.
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Noncardiogenic Pulmonary Edema

Image: “Initial Chest x-ray showing pulmonary infiltrates in the right lung especially in the right mid and lower lung zones indicative of pulmonary edema.” by Shrestha P, Pun M, Basnyat B. License: CC BY 2.0


Etiology of Non-Cardiogenic Pulmonary Edema

Many conditions can cause non-cardiogenic pulmonary edema. They all share a similar pathogenic mechanism when they cause pulmonary edema, namely, pulmonary capillary increased permeability. The most common causes of non-cardiogenic pulmonary edema encountered in the emergency department are:

  • Drowning
  • Fluid overload
  • Aspiration injury
  • Allergic reactions
  • Adult respiratory distress syndrome

Neurogenic pulmonary edema is another possible etiology of pulmonary edema in a patient with acute spinal cord injury. The main mechanism behind pulmonary edema is thought to involve an abnormal sympathetic nervous system regulation.

Patients with non-cardiogenic pulmonary edema frequency have pulmonary hemorrhage as well. This is especially true in case of acute glomerulonephritis-associated pulmonary syndromes such as Goodpasture’s disease or Wegener granulomatosis.

In conditions where vasculitis is not a major issue, the main mechanism behind pulmonary hemorrhage is thought to be related to acute pulmonary vasoconstriction and impaired pulmonary blood flow which is followed by pulmonary microvascular injury. Pulmonary microvascular injury is believed to be the main pathology behind pulmonary edema in patients with etiologies other than glomerulonephritis.

The main mechanisms of pulmonary edema in these etiologies are elevated intravascular pressure and increased pulmonary capillary leak. Patients with conditions associated with increased intravascular pressure in the pulmonary capillary bed might develop mechanical injuries to their pulmonary capillaries which render the capillaries leakier.

Gadolinium-enhanced MRI can be used to assess the degree of leakage from pulmonary capillaries, however this is no longer recommended mainly because Gadolinium-based contrasts have been found to be associated with an increased risk of causing non-cardiogenic pulmonary edema themselves.

Imaging Modalities in Non-Cardiogenic Pulmonary Edema

Plain chest radiography

The initial imaging modality of choice in a patient with pulmonary symptoms suggestive of pulmonary edema is a chest x-ray. These patients are usually very ill. Therefore, portable chest x-ray is the imaging modality of choice for the initial evaluation.

The combination of the clinical history, physical examination findings and radiographic features are usually enough to reach a diagnosis and determine the etiology of pulmonary edema.

Unfortunately, portable anteroposterior images of the chest using conventional x-ray are of low quality. Sometimes, it is impossible to differentiate between lung parenchymal diseases and pulmonary edema with this imaging technique.

Main radiographic features of non-cardiogenic pulmonary edema

The heart shadow is usually normal in non-cardiogenic pulmonary edema. Pleural effusions are common with non-cardiogenic pulmonary edema. Septal lines which indicate interstitial edema are rarely seen in non-cardiogenic pulmonary edema compared to cardiogenic pulmonary edema.

While cardiogenic pulmonary edema tends to present as diffuse infiltrates on chest radiography, non-cardiogenic edema typically is localized to the periphery when the etiology is lung-related. Nephrogenic pulmonary edema is described as having a bat-wing distribution. Air bronchograms point towards a lung injury as the most likely mechanism behind non-cardiogenic pulmonary edema.

Acute respiratory distress syndrome usually resembles cardiogenic pulmonary edema on chest radiography in the initial stage. One to two days after the onset of ARDS symptoms, the picture becomes quite different from your typical cardiogenic pulmonary edema. The picture becomes more of widespread and uniform infiltrates.

Substantial improvement of pulmonary edema within 24 hours after the initiation of treatment is characteristic of cardiogenic pulmonary edema. Patients with non-cardiogenic pulmonary edema typically have a slower response to treatment.

Degree of confidence in plain chest radiography in non-cardiogenic pulmonary edema

The main advantage of plain chest radiography is its universal availability. Additionally, the adequate and systematic examination of a chest radiography in a patient with pulmonary edema is usually sufficient in identifying the etiology.

In a recent study to compare the accuracy of chest radiography in the differentiation between cardiac, renal, and capillary permeability induced pulmonary edema, the authors concluded that chest radiography is most accurate for the diagnosis of capillary permeability edema. Capillary permeability edema is caused by near-drowning and acute respiratory distress syndrome among other causes.

In a patient with known history of congestive heart failure, a portable radiographic evaluation of the chest should not be relied upon for the differentiation between cardiogenic and non-cardiogenic pulmonary edema. While the treating physician might conclude that the cause of pulmonary edema in the patient is cardiogenic, up to 90 % of the cases were later found to have some sort of acute respiratory failure as the main cause of their pulmonary edema.

Computed Tomography in Non-Cardiogenic Pulmonary Edema

Patients with non-cardiogenic pulmonary edema are usually too sick to be transferred for a computed tomography scan. If a computed tomography scan is obtained, the features of non-cardiogenic pulmonary edema are widespread airspace consolidation in the dependent lung regions. Bilateral lung opacities are the main finding in patients with acute respiratory distress syndrome on computed tomography.

These opacities might be patchy, homogenous, mixed, or less likely ground glass in appearance. Air bronchograms are commonly seen on computed tomography scans of the lungs in patients with non-cardiogenic pulmonary edema. Most of these abnormalities are found in the basal regions of the lungs in an ambulatory patient.

Small pleural effusions are commonly identified on computed tomography scans of patients with pulmonary edema due to acute respiratory distress syndrome. Up to 50 % of the patients had a pleural effusion on their computed tomography scan. Fortunately, these pleural effusions were not found to be correlated with prognosis.

The main advantage of computed tomography in the evaluation of a patient with non-cardiogenic pulmonary edema due to acute respiratory distress syndrome is the exclusion of lung cysts. Lung cysts are common in patients with this disease and are associated with an increased mortality.

The detection of such cysts, which are usually multiple in number, allows for adequate management. In a recent series of 15 acute respiratory distress syndrome patients, computed tomography scans of the chest identified large and multiple lung cysts in five patients.

The management plan was changed in these five patients. Because of this added benefit, some experts are advocating the idea that computed tomography scans should be used more often if possible in patients with acute respiratory distress syndrome.

Ultrasonography in Non-Cardiogenic Pulmonary Edema

Ultrasonography is useless in the identification of non-cardiogenic pulmonary edema or in providing any information about the most likely etiology. However, ultrasonography might be useful in the evaluation of small pleural effusions and in the exclusion of cardiogenic causes of pulmonary edema.

Nuclear Imaging in Non-Cardiogenic Pulmonary Edema

Patients with non-cardiogenic pulmonary edema typically have concurrent pulmonary hemorrhage. The sequestration of neutrophils within the alveoli can be detected with FDG-PET (Fluorodeoxyglucose positron emission tomography) scans of the lungs.

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