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Occurrence and consequence of late preterm births
(239 to 259 days of gestational age, GA) is a public health problem that
is preventable. These infants account for the bulk of a nation’s preterm
population (of all USA preterm births, 74% are late-preterm), adversely
impact on national breastfeeding rates, increase direct healthcare cost
by need for readmission of infants for severe hyperbilirubinemia and
hypernatremic dehydration, as well as increase the risk for irreversible
brain damage due to kernicterus [1-4].
As a sub-cohort of the preterm population,
late-preterm infants masquerade as term infants (<37
weeks and 0/7 days of GA) on the basis of their relatively mature
appearance, but remain physiologically and metabolically immature [2].
Currently, most late preterm infants are cared for by their mothers and
discharged home with unmonitored home care. Consequently, late-preterm
infants are at higher risk than term infants of developing medical
complications that result in higher rates of mortality and morbidity,
and have higher rates of hospital readmission during the neonatal period
than term infants.
Maturational factors that impact postnatal adaptation
include brain and autonomic nervous system growth and induction of
hepatic metabolic pathways. The brain volume of an infant at 36 weeks GA
is only about 60% of that for a term infant [5]. Reduced number of sulci
and gyri reflect an anatomic in maturity that is defined by the white
matter, myelination and cortical migration of neuronal cells.
Late-preterm infants are also more susceptible to gray matter injury
induced by hypoxia-ischemia than the term infant. Low oromotor tone,
function, and neural maturation also predispose these infants to
dehydration and hyperbilirubinemia that are associated with poor feeding
in the breastfed infant. Breastfeeding of a preterm infant also requires
special coaching of the mother [7]. Decreased maternal breast
stimulation and decreased breast emptying and lead to suboptimal milk
transfer to the baby as well as decreased maternal milk production. This
leads to excessive weight loss and decreased bilirubin excretion leading
to dehydration, slow postnatal weight gain and newborn jaundice.
Jaundice and hyperbilirubinemia occur more commonly and are more
prolonged among late preterm infants than term infants because of
delayed maturation and a lower concentration of uridine
diphospho-glucuronate glucuronosyltransferase and immature
gastrointestinal function. Feeding difficulties that predispose them to
an increase in enterohepatic circulation of bilirubin, decreased stool
frequency, dehydration, and hypernatremia add to the overall bilirubin
load and risk of toxicity.
In a recent commentary, relying on independent
reviews of available evidence, Maisels, et al. [3] recommend a
more structured approach to management and follow-up according to the
predischarge bilirubin, GA, and other clinical risk factors for
hyperbilirubinemia in order to prevent adverse outcomes due to severe
neonatal hyperbilirubinemia. Experience and reports indicate that each
week of GA immaturity is associated with higher incidence of severe
hyperbilirubinemia such that the morbidity rate, due to
hyperbilirubinemia doubles for each week <39 weeks of GA. Current review
supports a pre-discharge bilirubin expressed as a risk zone on an
hour-specific bilirubin nomogram as a simple and accurate means for
determining the risk of developing significant hyperbilirubinemia and
the most accurate risk-assessment strategy incorporates information
about bilirubin values, clinical risk factors and GA [1,3]. The study
reported by Lavanya, et al. [7] validates the predictive
role of bilirubin between 24 to 48 hours age for a select population of
late preterm infants from a single urban birthing facility. However, it
is important not to underestimate the clinical relevance of the
contributory roles of other factors such as race/ethnicity, degree of
immaturity, bruising, blood group incompatibility, G6PD deficiency,
breastfeeding success and infant vulnerabilities to inherent, familial
or genetic co-morbidities. Adverse outcomes among late preterm infants
are thus dependent on patient population mix and clinical practice
patterns.
Competing interests: None stated; Funding:
Nil
References
1. American Academy of Pediatrics, Subcommittee on
Hyperbilirubinemia. Management of Hyperbilirubinemia in the Newborn
Infant 35 or More Weeks Of Gestation. Pediatrics. 2004;114:297–316.
2. Engle WA, Tomashek KM, Wallman C: Committee on
Fetus and Newborn, American Academy of Pediatrics. "Late-preterm"
infants: A population at risk. Pediatrics. 2007;120:1390-1401.
3. Maisels MJ, Bhutani VK, Bogen D, Newman TB, Stark
AR, Watchko JF. Hyperbilirubinemia in the newborn infant > or =35 weeks’
gestation: an update with clarifications. Pediatrics. 2009;124:1193-8.
4. Bhutani VK, Vilms RJ, Hamerman-Johnson L.
Universal bilirubin screening for severe neonatal hyperbilirubinemia. J
Perinatol. 2010;30(Suppl): S6-15.
5. Kinney H C. The near-term (late preterm) human
brain and risk for periventricular leukomalacia: a review. Sem Perinatol.
2006;30:81-8.
6. Walker M. Breastfeeding the late preterm infant. J
Obstet Gynecol Neonatal Nurs. 2008;37:692-701.
7. Lavanya KR, Jaiswal A, Reddy P, Murki S. Predictors
of significant jaundice in late preterm infants. Indian Pediatr.
2012;49:717-20.
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