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Extract from:
Respiratory Morbidity and Lung Function in Preterm Infants of 32 to 36 Weeks' Gestational Age.
Colin AA, McEvoy C, Castile RG.
Pediatrics. 2010 Jun 7. PubMed
06/07/2010

Respiratory morbidity and lung function in preterm infants of 32-36 weeks’ gestational age

This systematic review summarizes the evidence supporting respiratory system vulnerability in infants aged 34 to 36 weeks’ GA and discusses the developmental and physiologic principles that underlie this vulnerability.

Normal lung development follows a series of orchestrated events. Premature birth interrupts normal in utero lung development, which results in significant alterations in lung function and physiology. Increasingly, there are reports documenting the broad range of complications experienced by infants aged 34 to 36 weeks’ gestational age (GA). This systematic review summarizes the evidence supporting the vulnerability of the respiratory system in infants aged 32 to 36 weeks’ gestational age (GA) and discusses the developmental and physiologic principles that underlie this vulnerability.
Of the 24 studies identified, 16 were retrospective population-based cohort studies; 8 studies were observational.
Overall, the evidence presented in the reviewed articles demonstrates that the respiratory vulnerability of preterm infants born at 32 to 36 weeks’ GA, usually considered to be at low risk for subsequent respiratory problems, is more similar to that of very preterm infants (<32 weeks’ GA) than that of term infants. Therefore, these infants carry a high risk of developing medical complications that result in higher rates of respiratory morbidity and mortality compared with term infants. In detail, they present higher rates of hospital readmission shortly after discharge and during the following 6 months, longer hospital stays, and increased health care use compared with term infants.
Infants born at 30 to 34 weeks’ GA without clinical lung disease have altered lung function that persists throughout infancy. Moreover, the observation of a direct association between premature birth and reduced forced expiratory flows suggests that interruption of lung development is an important determinant of the subsequent increase in respiratory morbidity. These deficits seem to persist until early adulthood and, if associated with lower respiratory illnesses, may increase the risk of chronic obstructive pulmonary disease later in life.
One of the consequences of altered lung development in preterm infants is their increased vulnerability to infections by respiratory syncytial virus (RSV). The reviewed studies have suggested that preterm birth at 33 to 35 weeks’ GA significantly increases the risk for severe outcomes among infants who are hospitalized for RSV. Of note, RSV hospitalization in healthy premature infants (32 to 35 weeks’ GA) is associated with a significant increase in subsequent health care resource use. It has been suggested that the pathogenesis of viral lower respiratory tract infection could be related to the failure to develop an adaptive cytotoxic T-lymphocyte response and that clearance of the virus depends on inefficient innate immune responses mediated by macrophages and neutrophils. These factors may be more pronounced in premature infants.
The above-described findings should be considered by health-care providers when making decisions regarding delivery of late-preterm infants and by clinicians involved in the care of young patients. However, further research efforts are needed to shed new light on the vulnerability of lungs in preterm infants.

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