Growth of Lung Parenchyma in Infants and Toddlers with Chronic Lung Disease of Infancy

Abstract

Rationale:The clinical pathology describing infants with chronic lung disease of infancy (CLDI) has been limited and obtained primarily from infants with severe lung disease, who either died or required lung biopsy. As lung tissue from clinically stable outpatients is not available, physiological measurements offer the potential to increase our understanding of the pulmonary pathophysiology of this disease. Objectives: We hypothesized that if premature birth and the development of CLDI result in disruption of alveolar development, then infants and toddlers with CLDI would have a lower pulmonary diffusing capacity relative to their alveolar volume compared with full-term control subjects. Methods: We measured pulmonary diffusing capacity and alveolar volume, using a single breath-hold maneuver at elevated lung volume. Subjects with chronic lung disease of infancy (23-29 wk of gestation; n 5 39) were compared with full-term control subjects (n 5 61) at corrected ages of 11.6 (4.8-17.0) and 13.6 (3.2-33) months, respectively. Measurements and Main Results: Alveolar volume and pulmonary diffusing capacity increased with increasing body length for both groups. After adjusting for body length, subjects with CLDI had significantly lower pulmonary diffusing capacity (2.88 vs. 3.23 ml/ min/mm Hg; P 5 0.0004), but no difference in volume (545 vs. 555 ml; P 5 0.58). Conclusions: Infants and toddlers with CLDI have decreased pulmonary diffusing capacity, but normal alveolar volume. These physiological findings are consistent with the morphometric data obtained from subjects with severe lung disease, which suggests an impairment of alveolar development after very premature birth.

Membrane and capillary components of lung diffusion and pro-angiogenic cells in infants

“…Flow was measured by a pneumotachometer (Hans Rudolph, Shawnee, KS, USA) and gas concentrations were measured using a mass spectrometer (Perkin Elmer MGA-1100, Waltham, MA, USA). Measurements were obtained in replicate using a normoxic test gas (0.3% C 18 O, 4% SF 6 , 4% He, 21% O 2 and balance N 2 ). Prior to obtaining measurements of DLCO using the hyperoxic test gas (0.3% C 18 O, 4% SF 6 , 4% He and balance O 2 ), subjects breathed 90% oxygen for several breaths.…”

Impact of bronchopulmonary dysplasia on pulmonary function during childhood: a systematic review

“…The remaining ten reviewed studies performed pulmonary function testing in one single moment (transversal). [17][18][19][20][21][22][29][30][31][32] therapy Evidence Data base) and Medline (Medical Literature Analysis and Retrieval System Online via Ovid. The publications were selected until the date of online searching, i.e., September 2016, regardless of the language.…”

“…Currently, pulmonary function testing in early childhood, i.e., the time period ranging from 0 to 6 years including infants and preschoolers, can be performed by examinations, such as rapid chest compression, single breath occlusion, plethysmography and helium dilution 6 . Studies indicate that infants with BPD show compromised pulmonary function in the first years of life, with significant expiratory flow limitation, namely, forced expiratory volume in one second (FEV1), mean forced expiratory flow (FEF25-75%), as well as reduced pulmonary compliance, increased pulmonary resistance, higher respiratory rate, reduced functional residual capacity (FRC) and residual volume [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24] . These results are characteristics of ventilatory and functional changes, the knowledge of which may provide a better understanding of the disease and, consequently, improve treatment and preventive strategies to manage the disease.…”

The Robyn Barst Memorial Lecture: Differences between the Fetal, Newborn, and Adult Pulmonary Circulations: Relevance for Age‐Specific Therapies (2013 Grover Conference Series)

“…[82][83][84][85] Although long-term studies of BPD have primarily focused on late abnormalities of airway function, PVD can also persist into childhood and adult life. 79,[86][87][88][89] Tepper and colleagues 88 have reported that infants with even mild BPD have decreased diffusion capacity when corrected for lung volume, in comparison with age-matched term controls, suggesting that BPD infants may have decreased alveolar surface area available for gas exchange. These differences in diffusion capacity for carbon monoxide were also found to persist in children at 11 years of age who had been born extremely preterm, and striking decreases in diffusion capacity can persist in adult survivors of BPD.…”