Case #05 Discussion:

Impression

Pulmonary edema with pleural effusions consistent with congestive heart failure.

Discussion

There are two main types of pulmonary edema: cardiogenic and noncardiogenic. Increased capillary hydrostatic pressure is the principal mechanism in cardiogenic edema. The chest radiograph provides an estimate of the severity of pulmonary edema. The chest radiograph is normal when the pulmonary capillary wedge pressure is less than 12 mm Hg. When the pulmonary capillary wedge pressure increases to 12 - 18 mm Hg, a cephalized pattern of pulmonary vascular redistribution occurs where the lower lobe vessels constrict and the upper lobe vessels become larger in diameter than the lower lobe vessels. As the pulmonary capillary wedge pressure continues to increase, peribronchial cuffing (haziness around the pulmonary hila) and blurring of the pulmonary vessel margins is noted The edema may also flow peripherally to cause thickening of the interlobular septa, manifested on chest radiographs as septal (Kerley) lines.

Radiographic features of congestive heart failure include a widened vascular pedicle, cardiomegaly, septal lines, pleural effusions, and a predominantly basilar and perihilar distribution of edema. In the absence of cardiomegaly, it is unlikely the edema is the result of congestive heart failure, unless the patient is suffering from acute myocardial infarction, arrhythmia, or fluid overload.

Fluid overload secondary to either excessive saline infusion or renal failure with salt and water retention may produce pulmonary edema due to increased hydrostatic pressure and decreased colloid osmotic pressure. Fluid overload may sometimes be distinguished from cardiogenic edema on the basis of a more central (perihilar) radio-density pattern. However, the distinction is often dependent on clinical presentation as vascular engorgement and cardiac dilation are often present in both cardiogenic edema and fluid overload.

Noncardiogenic causes of pulmonary edema generally produce edema on the basis of increased capillary permeability. These include inhaled substances, e.g. smoke inhalation, nitrogen dioxide in silo-filler's disease, fluid aspiration, and near drowning. Circulating toxins also produce pulmonary edema, such as fat embolism from a recent fracture or amniotic fluid embolism in a recently postpartum woman. The chest radiograph in patients with increased capillary permeability is more likely to reveal a patchy, peripheral pattern of pulmonary edema in the presence of a normal vascular pedicle and cardiac silhouette. Air bronchograms may be present. Pleural effusions and septal lines are uncommon.

The most common causes of pleural effusion are shown below, in descending order.

• Heart Failure
• Bacterial Pneumonia
• Viral Pneumonia
• Metastatic Malignancy
  • Lung
  • Breast
  • Other
• Pulmonary Embolism
• Cirrhosis with Ascites
• Lymphoma
• Gastrointestinal Disease
• Collagen Vascular Disease
• Tuberculosis
• Asbestos Exposure
• Mesothelioma

Heart failure is the most common cause, where effusion develops in up to 75% of cases. The effusion is usually bilateral, but when unilateral it is more often on the right. Both left and right ventricular failure can result in pleural effusion. In left heart failure, the elevated hydrostatic pressure in the pulmonary veins slows the absorption of pleural fluid. In right heart failure, the elevated systemic vein pressure increases pleural fluid formation and decreases lymphatic drainage.

A related cause of pleural effusion is constrictive pericarditis. The effusion is generally bilateral; when unilateral, it is almost always on the right.