Anemia of Prematurity - Portal Neonatal

Plenat et al described two topographic varieties of air leak, intrapulmonary pneumatosis and
intrapleural pneumatosis. In the intrapulmonary type, which is more common in premature infants,
the air remains trapped inside the lung and frequently appears on the surface of the lung, bulging
under the pleura in the area of interlobular septa. This phenomenon develops with high frequency on
the costal surface and the anterior and inferior edges but can involve all of the pulmonary areas. In
the intrapleural variety, which is more common in more mature infants with compliant lungs, the
abnormal air pockets are confined to the visceral pleura, often affecting the mediastinal pleura. The
air of PIE may be located inside the pulmonary lymphatic network.
The extent of PIE can vary. It can present as an isolated interstitial bubble, several slits, lesions
involving the entire portion of one lung, or diffuse involvement of both lungs. PIE does not localize
preferentially in any one of the 5 pulmonary lodes.
PIE compresses adjacent functional lung tissue and vascular structures and hinders both ventilation
and pulmonary blood flow, resulting in impedance of oxygenation, ventilation, and blood pressure.
This further compromises the already critically ill infant with a significant increase in mortality and
morbidity. PIE can regress completely or decompress into adjacent spaces causing
pneumomediastinum, pneumothorax, pneumopericardium, pneumoperitoneum, or subcutaneous
emphysema.
Frequency:
• In the US: The prevalence of PIE varies widely with the population studied. In a study by
Gaylord et al, PIE developed in 3% of infants admitted to the neonatal intensive care unit
(NICU). No specific data are available on the prevalence of PIE in the postsurfactant era;
reported incidence of PIE in published clinical trials can be useful. In a randomized trial of
surfactant replacement therapy at birth, in premature infants of 25-29 weeks' gestation,
Kendig et al found PIE in 8 of 31 (26%) control neonates and 5 of 34 (15%) surfactanttreated
neonates.
Another randomized controlled trial of prophylaxis versus treatment with bovine surfactant in
neonates of less than 30 weeks' gestation included 2 of 62 (3%) early surfactant-treated, 5 of
60 (8%) late surfactant-treated, and 15 of 60 (25%) control neonates with PIE. Kattwinkel et
al compared prophylactic surfactant administration versus the early treatment of RDS with
calf lung surfactant in neonates of 29-32 weeks' gestation. Three of 627 neonates in the
prophylaxis group and 3 of 621 neonates in the early treatment group developed PIE. This
information suggests a higher incidence of PIE in more immature infants.
• Internationally: Studies reflecting international frequency demonstrated that 2-3% of all
infants in NICUs develop PIE. When limiting the population studied to premature infants, this
frequency increases to 20-30%, with the highest frequencies occurring in infants weighing
fewer than 1000 g. In another study of low birth weight infants, the incidence of PIE was 42%
in infants with birth weight of 500-799 g, 29% in those with birth weight of 800-899 g, and
20% in those with birth weight of 900-999 g. Minimal information is available about the
prevalence of PIE in the postsurfactant era. In a recent prospective multicenter trial
comparing early high-frequency oscillatory ventilation (HFOV) and conventional ventilation in
preterm infants of fewer than 30 weeks' gestation with RDS, 15 of 139 (11%) infants in the
high-frequency group and 15 of 134 (11%) infants in the conventional group developed PIE.
Mortality/Morbidity: The mortality rate associated with PIE is reported to be as high as 53-67%.
Lower mortality rates of 24% and 39% reported in other studies could result from differences in
population selection. Morisot et al reported an 80% mortality rate with PIE in infants with birth weight
of fewer than 1600 g and severe RDS. The early appearance of PIE (