Cor Pulmonale and Pulmonary Edema in Children Secondary to Chronic Upper Airway Obstruction
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TL;DR
Four cases of children with cardiovascular disease secondary to chronic upper airway obstruction will be described, and somnoence was marked to such a degree that the child fell asleep during an examination by the physician.
Abstract
Symptoms other than acute respiratory obstruction are rarely attributed to enlargement of the tonsils and adenoids (3). That large tonsils and adenoids can lead to chronic obstruction, hypoxia, hypercapnia, pulmonary hypertension, cor pulmonale, and pulmonary edema has only recently been recognized. Four cases of children with cardiovascular disease secondary to chronic upper airway obstruction will be described. Case Material In each of the 4 patients, difficult, stertorous breathing was noted by the parents in the first few months of life. The supine position accentuated the difficulty. Respiratory infections were frequent, often associated with acute episodes of severe respiratory distress and cyanosis. Lethargy was frequent. In one patient, somnoence was marked to such a degree that the child fell asleep during an examination by the physician. In none of the patients was dubbing present. Each child developed slowly, with the weight falling below the tenth percentile. On physical examination during the acute episodes, a low grade fever was usually present. Tachycardia and tachypnea were marked. The large tonsils and adenoids were obvious clinically and radiographically (Fig. 1). Cardiac murmurs were not significant. The liver was enlarged 3 to 4 cm below the right costal margin in each patient. Periorbital and pedal edema and ascites were present in only one patient. Right atrial and right ventricular enlargement were present electrocardiographically in all. In each child, the heart was large radiographically. Pulmonary edema was present during severe exacerbations of the symptoms in all four patients (Figs. 2–4), and in one instance there was an associated pneumonia. The patients were treated with digitalis, antibiotics, mist, and oxygen. Improvement occurred over three to four days. Cardiac catheterization was performed in 3 of the 4 cases, and blood gas studies were obtained in all 4 (Tables I and II). The catheterization data revealed elevation of the right ventricular and pulmonary artery pressures. There were wide fluctuations in pulmonary artery and right atrial pressures with respiration. Arterial blood samples showed a decreased pO2, a low pH, an elevation of the pCO2, and arterial unsaturation. These values improved with an airway in place. No intracardiac defects were found. Tonsillectomy and adenoidectomy were performed in each patient. Clinical improvement was prompt and marked with easy, quiet breathing and no recurrence of the acute episodes. Lethargy and somnolence cleared. A rapid increase in weight occurred. Radiographically, the lung fields became clear. The heart size decreased but did not assume a normal size in any case. Repeat electrocardiograms were normal.
