Pathology

Pulmonary congestion/pulmonary edema

 

The capillary bed in the lungs has a surface of between 70 and 140 m2. The endothelial cells in the pulmonary capillaries are permeable to water, but impermeable to proteins and other large- molecule fluids. The alveolar epithelium on the other hand is almost impermeable to water as well.

In normal lungs, a continuous stream of fluid flows from the capillary bed to the alveolar interstitium. In the interstitium there are a number of lymph vessels which remove superfluous fluid.

Pulmonary congestion and pulmonary edema arise when the amount of extravascular fluid in the lungs increases. The major causes of this are shown in the following table.

Causes of extravascular fluid in the lungs
Increased hydrostatic pressure
Increased capillary permeability
Over-hydration
Pulmonary infiltration
Pulmonary vein occlusion
Pulmonary embolism
Reduced osmotic pressure
Transfusion reaction
Reduced production of plasma proteins
ARDS (Adult Respiratory Distress Syndrome)

These changes are usually symmetrical, but asymmetrical pulmonary congestion/pulmonary edema may also occur. The most frequent causes of asymmetrical distribution are shown in the following Table.

Causes of asymmetrical congestion/edema
Gravitational (lying preferentially on one side)
Emphysema (unilateral)
Unilateral venous occlusion
Occlusion of a pulmonary artery
Bronchial occlusion
Thrombosis/ embolism
Lymphatic obstruction
After removal of pneumothorax or pleural effusion

Pulmonary congestion and edema develop in two stages. Initially, interstitial edema occurs with collection of fluid in the interalveolar septa and Kerley B lines appear. Kerley B lines are seen as 3-6 mm long horizontal lines in the lateral basal segments of the lung, near the chest wall (on the frontal film). They develop when the pressure in the interstitium exceeds about 18-20 mm Hg. At this stage, the patient usually becomes dyspnoeic with tachypnoea, but with minimal changes in the arterial blood gases.

Further progression of congestion and edema produces fluid in the alveoli. This reduces the alveolar surface for the exchange of gases. At this stage, the chest film shows a combination of alveolar and interstitial opacities.

Cardiogenic congestion/edema

The first radiological sign of interstitial edema is blurred outlines of the pulmonary arteries. The blurring is observed first and most readily in the hilar regions. In addition, the basal segments of the lung often seem rather blurred. At the same time, a redistribution of flow occurs with equivalent or larger diameter of the arteries of the upper lobe compared to lower lobe vessels (antler sign). When fluid collects in the interlobular and interalveolar septa, the so-called A and B lines (Kerley A/Kerley B) are formed. When the congestive changes progress, alveolar edema with fluid in the alveoli develops. This produces diffuse lung opacities without air bronchogram. The edema fluid usually develops symmetrically and collects mainly in the lowest parts of the lungs (Fig. 69). However, asymmetrical distribution of edema is not unusual, and is most often related to the patient's position in bed (lying on right or left side). The fact that the opacities in edema tend to be most pronounced in the lowest lung

Figure 69. Enlarged heart with congestive changes in both lungs. Bilateral pleural fluid.

Figure 70. Pulmonary congestion/edema with congestive changes chiefly in the hilar regions. Relatively sharply defined opacities (Bat-wing).

segments, and are symmetrical, may be used in the differential diagnosis between congestion/edema and pneumonia.

In same cases the congestive changes/edema are limited to the hilar regions (Fig. 70). The peripheral borders of these opacities may be sharply defined (Bat-wing). These opacities were previously regarded as characteristic of uremia, but may equally often be seen in heart failure.

In most cases of pulmonary congestion/edema, the heart will be enlarged (Fig. 71), but with acute pump failure of the left ventricle (for example as a result of acute myocardial infarct or rupture of papillary

Figure 71. Heart failure with considerably enlarged heart (cor bovinum) with congestive changes in both lungs.

Figure 72. Near drowning - pronounced pulmonary congestion (edema with extensive alveolar opacities caused by large collections of fluid in the alveoli).

muscles), there may be pronounced congestive changes without simultaneous heart enlargement.

Non-cardiogenic congestion/edema

Drowning
Congestion/edema changes are seen in patients who have almost drowned (Fig. 72). Diffuse alveolar opacities caused by edema fluid can be seen on the chest radiograph. In addition, there is usually aspiration of water and stomach contents. Increased capillary permeability also leads to interalveolar collection of edema fluid that is rich in protein,

Figure 73. Pulmonary congestion in a patient with reticular opacities in both lungs. which may in turn lead to formation of hyaline membranes.

lnhalation of gases
The most common gases are nitrogen, phosporus, sulphur dioxide, ammonia, chlorine, and ordinary smoke (in connection with fires). Congestion/edema usually occurs as a result of a direct effect of the gases on the endothelial cells in the alveoli. The accompanying edema is usually fairly pronounced with diffuse blurring of the affected lung segment. The size of the heart is always normal.

Renal failure
Pulmonary congestion/edema is frequently seen in patients with both acute and chronic renal failure, and is a common cause of death in patients with acute nephritis (Fig. 73). However, the most frequent cause of the development of pulmonary congestion/edema in these patients is failure of the left side of the heart.

Sepsis
Pulmonary congestion/edema is frequently seen in patients with sepsis. The primary cause is probably the release of vasoactive substances that affect the permeability of the capillaries/alveoli. It is not possible to make a radiological differentiation between this type of pulmonary congestion and that seen in heart failure. However, the size of the heart will be normal unless there is a simultaneous involvement of the heart.

ARDS (AduIt Respiratory Distress Syndrome)
Pulmonary congestion is always seen in patients with ARDS (see this section).

 

Alf Kolbenstvedt, Arnulf Skjennald and Charles B. Higgins