Clinical Presentation

Radiography

The chest radiographic findings of hydrostatic pulmonary edema are detailed in Box 100-1. These findings are all more reliably distinguishable on posteroanterior (PA) and lateral chest radiographs than on portable radiographs, but commonly patients with the greatest likelihood of hydrostatic pulmonary edema will be imaged using an anteroposterior technique (AP). AP techniques can make the diagnosis of hydrostatic pulmonary edema difficult because heart magnification, resulting from the considerably shorter focus-film distance as well as projectional magnification, can render determination of cardiac size unreliable, particularly in patients with low lung volumes. Additionally, pulmonary vascular congestion is difficult to determine accurately in nonerect patients because upper lobe vessels frequently normally appear larger than lower lobe vessels for patients imaged in a supine or semierect position. Furthermore, azygos vein dilation, often considered an indicator of elevated right atrial pressure, is a common and potentially normal finding on supine radiographs. Finally, pleural effusions often appear only as hazy attenuation projecting over lungs in patients imaged in a supine or semierect position. However, this appearance is not specific for pleural effusion and can be seen with extensive posterior atelectasis because anterior aerated lung superimposes on the increased opacity of the posteriorly located atelectatic lung. This pattern is often seen in severely ill patients and patients in the intensive care unit, which is the same patient population at risk for hydrostatic pulmonary edema.

BOX 100-1

Thoracic Imaging Findings in Hydrostatic Pulmonary Edema

CHEST RADIOGRAPHY

Cardiomegaly

Pulmonary venous enlargement

Widened vascular pedicle

Azygos vein distention

Interstitial edema

Vascular indistinctness

Interlobular septal thickening

Peribronchial cuffing

Subpleural edema

Pleural effusion

THORACIC CT

Cardiomegaly

Pulmonary venous enlargement

Vascular engorgement

Bronchial wall thickening

Ground-glass opacity

Centrilobular nodules, often with ground-glass attenuation

Smooth interlobular septal thickening

Pleural effusions, fissure thickening pericardial effusion

The first chest radiographic signs of pulmonary venous hypertension include pulmonary vascular redistribution, appearing as equalization of the size of the upper and lower lobe vessels, which progresses to the upper lobe vessels becoming larger than those in the lower lobes (a reversal of the normal situation). In the acute setting, this phenomenon is seen with left atrial (wedge) pressures in the range of 12 to 19 mm Hg.² In chronically compensated patients, such as those with mitral stenosis, upper and lower lobe vascular equalization and reversal will occur with left atrial pressures between 15 to 25 mm Hg.² As the physiologic derangements worsen, pulmonary venous hypertension progresses to frank interstitial pulmonary edema, with the development of interlobular septal thickening, often referred to as Kerley A and B lines (Fig. 100-1A), perihilar indistinctness and vascular haze (see Fig. 100-1B), peribronchial cuffing (see Fig. 100-1C), and subpleural edema (see later).² Findings of interstitial edema usually are apparent on the chest radiograph, with left atrial pressures of 20 to 25 mm Hg in the acutely ill patient and 25 to 30 mm Hg in chronically compensated patients.² At higher left atrial pressures, frank alveolar edema occurs, with spillage of fluid into the air spaces. In these patients, the chest radiograph will show an air space consolidation pattern (see Fig. 100-1D) and acinar nodules,² often superimposed on findings of interstitial edema. The relationship between left atrial (pulmonary capillary wedge) pressure and radiographic findings is not precise, and the radiographic findings often lag behind the physiological changes. Furthermore, stepwise progression through these phases is not always seen, and some imaging findings of hydrostatic edema may be present in the absence of others.

FIGURE 100-1 Chest radiographic findings of interstitial (A-C) and alveolar (D) edema. A, Interlobular septal thickening. B, Perihilar “haze.” C, Peribronchial cuffing (arrow). D, Consolidation (alveolar edema).

CT

On thoracic CT, findings of hydrostatic pulmonary edema include those seen on chest radiographs, such as cardiomegaly, vascular engorgement, and pleural effusions. Findings of interstitial edema (see later), are also apparent and are more readily appreciable with thoracic CT, particularly high-resolution CT (HRCT), than with chest radiography. Bronchial wall thickening, smooth interlobular septal thickening (Fig. 100-2), and ground-glass opacity (often with hazy, poorly defined centrilobular nodules) are highly suggestive of hydrostatic pulmonary edema.

FIGURE 100-2 Interstitial pulmonary edema—interlobular septal thickening. This axial CT scan shows a pronounced linear pattern in the apices.

Interstitial Edema

The findings of interstitial edema on chest radiography (see Box 100-1) are usually readily visible with CT scanning and, in addition to the findings noted, ground-glass opacity and centrilobular nodules are frequently present in patients with hydrostatic pulmonary edema.

Interlobular Septal Thickening (Kerley A and B lines)

Both Kerley A and B lines represent thickened interlobular septae. Kerley B lines are horizontal linear opacities, 1 to 2 cm in length, in contact with the pleural surface. Kerley B lines are most readily visible in the inferior and lateral aspects of the thorax, near the lateral costophrenic sulcus (see Fig. 100-1A). The regular appearance of Kerley B lines in the lung bases is the result of the regular organization of pulmonary lobules at the lung bases.

Kerley A lines also represent interlobular septal thickening but are relatively uncommon compared with Kerley B lines. Kerley A lines are obliquely oriented linear opacities several centimeters long, radiating outward from the central or perihilar lung. Kerley A lines have a somewhat different appearance from Kerley B lines because of the different organization of secondary lobules within the central lung.

The interlobular septal thickening resulting from hydrostatic pulmonary edema is readily visualized on thoracic CT, especially HRCT. Interlobular septal thickening in patients with hydrostatic pulmonary edema is smooth and often most readily visualized in the lung bases and in the pulmonary apices (Fig. 100-2). Poorly defined, ground-glass attenuation centrilobular nodules or lobular ground-glass opacity often coexists.

Vascular Indistinctness and Perihilar Haze

In patients with pulmonary venous hypertension and interstitial edema, fluid transudating from the vessels surrounds the vessels and blurs their margin on chest radiographs, rendering the vascular margins indistinct. Pulmonary vascular indistinctness is frequently most visible in the lower lobes and may be present before Kerley lines are apparent.

Perihilar haze is a term occasionally used to refer to poor definition of and slightly increased opacity surrounding the perihilar vessels; it manifests as perihilar vascular indistinctness with a hazy or ground-glass appearance (see Fig. 100-1B). Although not always easily recognizable, perihilar haze can be a useful finding that suggests hydrostatic pulmonary edema in patients with lower lobe atelectasis.

Peribronchial Cuffing

Peribronchial cuffing represents bronchial wall thickening, possibly accompanied by a variable amount of peribronchial interstitial fluid. Peribronchial cuffing is most readily recognizable in the central and perihilar regions of lung, when bronchi are seen in cross section (see Fig. 100-1C). Peribronchial cuffing may also be seen as a tram-track appearance when bronchi are visualized in longitudinal section. Peribronchial cuffing may also appear as nonspecific thickening of the interstitium radiating outward from the hilum. On thoracic CT, peribronchial thickening or cuffing usually appears as bronchial wall thickening. Peribronchial cuffing may represent a finding of interstitial edema in the proper clinical setting, but is not specific for that diagnosis; peribronchial inflammation or tumor may also produce this finding.

Subpleural Edema

The subpleural interstitium is contiguous with the peribronchovascular interstitium through the peripheral centrilobular interstitium and interlobular septa. When fluid accumulates within interlobular septa, this fluid may track into the subpleural interstitium, creating thickening of this compartment as well. On chest radiography and thoracic CT, subpleural edema appears as fissural thickening.

Ground-Glass Opacity

An abnormal increase in lung water may produce an overall increase in haziness in the pulmonary parenchyma, often with decreased lung volumes because of diminished pulmonary compliance. This haziness may create the appearance of ground-glass opacity (increased attenuation without obscuration of the underlying vascular bundles) on chest radiographs, although this finding is usually difficult to appreciate. However, ground-glass opacity caused by interstitial edema is readily recognizable on HRCT, and may occasionally appear as centrilobular nodules.

Air Space (Alveolar) Edema

As factors producing interstitial edema progress, eventually interstitial fluid will begin to accumulate within the air spaces, producing air space edema. Because the edema fluid replaces air within the alveoli, air space edema represents a form of air space consolidation and appears as a confluent opacity (see Fig. 100-1D), which may be accompanied by air space or acinar nodules.