Atypical Pulmonary Patterns of Congestive Failure in Chronic Lung Disease

THE ROENTGENOGRAPHIC features of left-sided cardiac failure and pulmonary edema are well documented. The basic pattern of gross intra-alveolar pulmonary edema is well known from the earlier literature: large, homogeneous, confluent, amorphous, ill-defined radiopacities radiating symmetrically from the perihilar areas of the lung (1–3). Later authors noted several variations of this classical pattern, including miliary (4, 5), reticular (6), focal, asymmetric, and even totally unilateral forms (7). Interstitial edema has been recognized as an early stage of pulmonary edema since the 1950's (8), so that by now the pathological and roentgenographic division of pulmonary edema into interstitial and intra-alveolar typesis fully accepted (9–11). Almost a decade later, the radiographic features of an even earlier stage of congestive failure were identified. At first, increased vascular dilatations in the upper zones and hilar areas, as compared to relatively constricted lower vessels, were observed in association with the chronic hemodynamic disturbances of mitral stenosis (12–15). Soon, however, the same pattern was observed and accepted as radiographic evidence of early left ventricular decompensation, irrespective of the underlying cause (16–18). Finally, well-defined elevations of pulmonary venous pressure were shown to be associated with radiographically recognizable cardiac failure patterns of increasing hemodynamic severity (19, 20). Researchers have tried to correlate underlying pathology with particular patterns. The “butterfly” or “bat wing” arrangement of acute edema, frequently found in uremic patients, was often called “uremic edema” (21, 22), but it soon became apparent that this pattern occurs in pulmonary edema of any etiology and is by no means specific for renal disease (23, 24). Lobar or unilateral edema has been ascribed to the patient's position and gravity (20, 25). More recently, localized pulmonary edema has been associated with defective lymph drainage in the areas of previous pulmonary disease, while the “butterfly” pattern has been attributed to the difference of ventilation, circulation, and lymph flow between the medulla and cortex of the lung (26, 27). Beyond these few concepts, little is understood about the basic physiopathogenesis underlying each observed pattern of failure. For this reason, our interest was aroused by the observation of a high frequency of atypical failure patterns in patients with chronic lung disease. The prognosis in heart failure and pulmonary edema with chronic pulmonary disease is notoriously poor (28–30). Only by prompt diagnosis and vigorous therapy can a strikingly better prognosis be achieved (31).