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The prognosis for the child depends, of course, upon the degree of development, as well as the pathological condition for which premature delivery is undertaken. Generally speaking, in the case of children born before the thirty-second week, the chances of surviving are very small.
—J. Whitridge Williams (1903)
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At the time of this textbook’s first edition, preterm delivery of a living newborn was frequently followed by neonatal death. Contrast this with today’s technological advances that have advanced the threshold of viability to 22 to 24 weeks’ gestation. Even so, the preterm newborn is susceptible to various serious medical complications both early and later in life (Table 34-1). A less commonly cited cause of morbidity and mortality is congenital malformations, which are much more prevalent in preterm births.
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These complications of prematurity can be placed in perspective in terms of overall neonatal outcomes. In 2009, two thirds of all infant deaths in the United States were in the 12 percent born before 37 weeks (Mathews, 2013). Fortunately, during the past decade, rates of preterm birth have declined from approximately 12 percent in 2007 to 10 percent in 2014. This is in part due to a decline in births to teen mothers (Ferré, 2016).
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RESPIRATORY DISTRESS SYNDROME
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The seminal complication of the preterm newborn is respiratory distress syndrome (RDS). This results from immature lungs that are unable to sustain necessary oxygenation. Resulting hypoxia is an underlying associated cause of neurological damage such as cerebral palsy. In addition, hyperoxia, a side effect of RDS treatment, contributes to morbidities such as bronchopulmonary dysplasia, pulmonary hypertension, necrotizing enterocolitis, periventricular leukomalacia, and retinopathy of prematurity.
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To provide blood gas exchange immediately following delivery, the lungs must rapidly fill with air while being cleared of fluid. Concurrently, pulmonary arterial blood flow must rise remarkably. Although some of the fluid is expressed as the chest is compressed during vaginal delivery, most is absorbed through the pulmonary lymphatics via complex mechanisms described in Chapter 32 (Transition to Air Breathing). Sufficient surfactant, synthesized by type II pneumocytes, is essential to stabilize the air-expanded alveoli. It lowers surface tension and thereby prevents lung collapse during expiration (Chap. 7, Respiratory System). If surfactant is inadequate, hyaline membranes form in the distal bronchioles and alveoli, and RDS develops. Although respiratory distress syndrome is generally a disease of preterm neonates, it does develop in term newborns, especially with sepsis or meconium aspiration. In these cases, surfactant ...