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Chest Imaging

Pulmonary oedema

abnormal accumulation of fluid in the interstitial compartment of the lung with or without associated air-space filling. The oedema is due to changes in hydrostatic forces in the capillaries, to increased capillary permeability or to impaired lymphatic drainage. Transudative pulmonary oedema is due to increased hydrostatic pressure or, rarely, due to decreased oncotic pressure across a functioning capillary membrane. Hydrostatic pulmonary oedema can result from cardiogenic or noncardiogenic (renal failure, fluid overload) causes. Cardiogenic pulmonary oedema is a consequence of elevated left-sided pressure which may result from left ventricular dysfunction, mitral valve disease, left atrial disease or, rarely, pulmonary venous obstruction. Milne has emphasized that the term "left heart failure" is preferable to "congestive heart failure" since the latter term has been used to describe right heart failure too (congested liver or neck veins). Left heart failure contrasts with exudative pulmonary oedema which is due to endothelial injury causing increased capillary permeability for both fluid and protein. The latter, characteristic of ARDS, is discussed elsewhere (see adult respiratory distress syndrome).

The radiographic changes of hydrostatic oedema are quite characteristic. In the normal adult, the lower lobe pulmonary vessels are larger than the upper lobe vessels due to gravitational forces. As the left-sided pressure increases, the blood is diverted to the upper lobes. This results in "cephalization" with the upper lobe vessels becoming larger than the lower lobe vessels. A great aid in evaluating cephalization is the end-on appearance of the paired pulmonary artery and bronchus of the anterior segments of the upper lobes. These are normally equal in diameter but in left heart failure, the artery enlarges relative to the bronchus. Since they are in the same plane, magnification is not an issue.

As left heart pressure increases, fluid enters the peribronchovascular interstitium. The pulmonary vessellung interface becomes oedematous resulting in unsharp vessel margins and peribronchial thickening or "cuffing" of the bronchi viewed on end. As the interstitium becomes oedematous, the interlobular septa become prominent and the markings indistinct. Kerley B, A, and C lines, seen in a minority of patients, are suggestive of, but not specific for, left heart failure. Severe interstitial oedema causes a ground-glass appearance in the perihilar areas and in the lower lungs. As the hydrostatic pressure increases further, symmetrical central and lower lung alveolar oedema is seen. The periphery of the lung tends to be spared. Air bronchograms are much more common in exudative than transudative oedema (Fig.1).

Cardiomegaly is frequent with chronic left ventricular dysfunction but is often absent atrial disease, mitral stenosis, acute myocardial infarction, acute arrhythmia or pulmonary veno-occlusive disease. The fissures may thicken due to subpleural oedema or fluid in the pleural space. Left heart failure is the leading cause of pleural pseudotumours. Mild to moderate pleural effusions are frequent in the more severe stages of left heart failure with a slight predominance to the right.

In recent years, the CT appearance of pulmonary oedema due to left heart failure has been reported. The signs are similar to the radiographic signs, ranging from enlarged and redistributed vessels, to peribronchial cuffing, to thickened interlobular septum, to diffuse ground-glass or alveolar consolidation showing a gravity-dependent distribution (Fig.2). Mediastinal lymph nodes may enlarge and the mediastinal fat may become oedematous. Pleural effusions are more easily seen on CT than on the radiograph.

In acute left heart failure, the radiograph may not reflect the severity of the heart dysfunction both at onset and during resolution. After an ac to lymphatic drainage by tumour or radiation.

Ipsilateral decreased oedema is seen where there is diminished blood flow to one lung, protecting that lung from pulmonary oedema. Conditions include:

  • decreased pulmonary artery blood flow (pulmonary embolus, hypoplastic pulmonary artery, etc.);

  • asymmetrical emphysema or constrictive bronchiolitis (Swyer James syndrome); and

    • unilateral impaired ventilation (fibrothorax, chest wall abnormality) causing hypoxic vasoconstriction.

    In patients with mitral valve insufficiency (see mitral regurgitation), pulmonary oedema may also be asymmetrical, predominantly in the right upper lobe. In ventricular systole, regurgitant blood flow across the open mitral valve impinges upon the orifice of the right upper lobe pulmonary vein. This raises the pulmonary venous pressure and may cause a localized increase in oedema.

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    Fig.1

    Acute heart failure. The heart is 1 cm larger than it was a month earlier but still relatively normal in size. The upper lobe pulmonary vessels are enlarged and indistinct. Peribronchial cuffing is seen in the anterior segmental bronchus of the left upper lobe. There is a moderate right pleural effusion with pseudotumours in the major and minor fissures. There is a moderate subpulmonary effusion on the left. (Reprinted from: Goodman LR. Felson's Principles of Chest Roentgenology, 2nd edition, WB Saunders, Philadelphia, 1998.)
    Pulmonary oedema, Fig.1 (a)
    Pulmonary oedema, Fig.1 (b)
    Pulmonary oedema, Fig.2 (a)
    Pulmonary oedema, Fig.2 (b)