In addition, physiological shunt studies with infusions of bubbles during echocardiography suggest the presence of prominent intrapulmonary shunting during exercise in older subjects, including survivors of BPD ( 11). Studies in infants have shown decreased lung diffusion capacity for carbon monoxide (D l CO) even in patients with relatively mild BPD ( 5), and decreased D l CO can persist into adulthood ( 5). Although several mechanisms contribute to abnormal lung function and gas exchange, an increased susceptibility for profound hypoxemia with infections, stress, or activity may also be related to impaired lung surface area due to decreased vascular and alveolar growth ( 6– 9).Īlthough PH is often associated with severe BPD ( 10), many late signs of disease and hypoxemia cannot be adequately explained on a physiologic basis by elevated pulmonary artery pressure alone. Decreased lung vascular growth also leads to late cardiopulmonary abnormalities, such as hypoxemia with acute respiratory infections, exercise intolerance, recurrent edema, and progression of pulmonary hypertension. In addition to PH, the reduced alveolar-capillary surface area with decreased arterial number further contributes to the need for prolonged oxygen and ventilator therapy due to abnormal gas exchange with marked hypoxemia ( 5). The distal pulmonary arterioles often appear reduced in number and abnormally distributed within the lung parenchyma ( 3).Ĭhanges in vascular growth and structure contribute to pulmonary hypertension (PH), which is associated with high morbidity and mortality in infants with BPD ( 4).
With premature birth and related lung injury, the normal sequence of lung development is disrupted, resulting in the histologic pattern of alveolar simplification (larger but fewer alveoli with decreased septation) and impaired or “dysmorphic” vascular growth. Despite marked advances in perinatal care, including antenatal steroids, surfactant therapy, improved respiratory care, and others, BPD remains one of the major sequelae of prematurity, leading to prolonged oxygen or ventilator dependency, recurrent respiratory exacerbations, and related problems ( 2). We propose that persistence or expansion of these vessels after premature birth provides the anatomic basis for intrapulmonary shunt and hypoxemia in neonates with severe bronchopulmonary dysplasia and may play a significant role in the morbidity and mortality of BPD.īronchopulmonary dysplasia (BPD) is the chronic lung disease of infancy that occurs in premature infants after oxygen and ventilator therapy for acute respiratory disease at birth ( 1). These prominent vessels appear similar to “misaligned pulmonary veins” described in the lethal form of congenital lung disorder, alveolar capillary dysplasia.Ĭonclusions: We found striking histological evidence of precapillary arteriovenous anastomotic vessels in the lungs of infants with severe bronchopulmonary dysplasia. Measurements and Main Results: We report histologic evidence of intrapulmonary vessels that bridge pulmonary arteries and veins in the distal lungs of infants dying with severe BPD. Methods: We collected lung tissues from fatal BPD cases and performed histology, immunohistochemistry, and high-precision three-dimensional reconstruction techniques. Objectives: We sought to find histologic evidence of intrapulmonary anastomotic vessels in lungs of patients who died of severe BPD. Preacinar anatomic and functional communications between systemic and pulmonary vascular systems has been established in fetal lungs, but whether increased intrapulmonary anastomotic vessels or their failure to regress after birth contributes to hypoxemia in preterm infants with BPD is unknown. Despite improvement in current therapies, the clinical course of infants with BPD is often characterized by marked hypoxemia that can become refractory to therapy.
Rationale: Bronchopulmonary dysplasia (BPD) is the chronic lung disease of infancy that occurs in premature infants after oxygen and ventilator therapy for acute respiratory disease at birth.
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