Pulmonary Edema

Pathology and Pathogenesis

Pulmonary edema can result from hemodynamic disturbances or from direct increases in capillary permeability due to alveolar microvascular injury. In hemodynamic cause of pulmonary edema (left-sided heart failure), it is characterized by heavy, wet lungs, due to fluid accumulation initially in basal regions (dependent edema). Histologically, alveolar capillaries are engorged and granular pink precipitate in alveolar spaces is seen. In long-standing cases of pulmonary congestion (mitral stenosis), many hemosiderin-laden macrophages appear in the alveolar spaces and the soggy lungs become firm and brown [5].

Symptoms and Signs

The clinical manifestations of pulmonary edema vary with its severity. Initial symptoms are dyspnea, cough, and tachypnea. Patients can complain of mild pedal edema during the day and paroxysmal nocturnal dyspnea. Wheezing may be heard. Once alveolar flooding has occurred, patients have severe dyspnea, tachypnea, and cough with frothy or bloodtinged sputum. Crackles and rhonchi are heard over the chest. Cheyne–Stokes respiration is common in severe congestive heart failure.

CT Findings

The thin-section CT (TSCT) findings of pulmonary interstitial edema consist of thickening of the interlobular septa,

interlobular fissures, and the peribronchovascular connective tissue (peribronchial cuffing) [6, 7] (Fig. 16.2). The interlobular septal thickening is smooth and uniform, except for a focal nodular appearance due to prominent septal veins. Another common finding is the areas of GGO. These opacities can be diffuse or patchy in distribution and usually involve mainly the perihilar and the dependent lung regions. In cases of alveolar edema, areas of GGO and consolidation involving mainly the perihilar and dependent lung regions are seen on TSCT [6].

CT-Pathology Comparisons

The earliest manifestation of hydrostatic pulmonary edema is the expansion of connective tissue spaces around conducting airways, their accompanying vessels, and the interlobular septa. Accumulation of fluid within peribronchovascular interstitial tissue and interlobular septa results in peribronchial cuffing and thickening of interlobular septa [8]. Because the pleural connective tissue is in continuity with that of the interlobular septa, accumulation of fluid in the interlobular septa is often associated with thickening of the interlobular fissures. The areas of GGO seen in pulmonary interstitial edema are related to the presence of thickened alveolar walls. If alveoli are filled with fluid, airspace edema appears as areas of GGO and consolidation.

Patient Prognosis

Treatment of pulmonary edema requires adequate life support followed by specific therapy directed at the factors leading to pulmonary edema. Oxygen supplementation and lung-protective mechanical ventilation may be necessary.