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COMMENTARY |
Kennedy Center, Section of Developmental and Behavioral Pediatrics, Institute of Molecular Pediatrics Sciences, University of Chicago, Comer and LaRabida Children’s Hospitals, Chicago, Illinois
Abbreviations: CP, cerebral palsy • IVH, intraventricular hemorrhage • ELBW, extremely low birth weight • ROP, retinopathy of prematurity
Among the 500000 infants born prematurely in 2003 in the United States, 79000 were born very prematurely.1–3 These very premature infants, defined as having been born before 32 weeks’ completed gestation, have benefited from collaborative and regional efforts of obstetrics and neonatology. In particular, among infants of extreme prematurity (defined as <28 weeks’ completed gestation), optimizing the intrauterine environment of high-risk pregnancies while concurrently using knowledge from developmental biology and multicenter translational trials has resulted in more aggressive management of respiratory, cardiac, nutritional, metabolic, and infectious-disease complications. This strategy has resulted in significant advances in survival but has come with increasing concern that current management is unable to significantly reduce the high rates of both neurosensory disability (ie, cerebral palsy [CP], blindness, and deafness) and developmental cognitive disability (Bayley mental developmental index of <70) among extremely preterm infants, especially those born between 22 and 26 weeks’ gestation.4–6 Schmidt et al7 successfully reduced rates of severe intraventricular hemorrhage (IVH) by the use of prophylactic indomethacin in extremely low birth weight (ELBW) infants. However, despite this neuroprotection, rates of death and neurodisability were not significantly different among the survivors. In a secondary analysis, 3 neonatal complications (chronic lung disease, severe retinopathy of prematurity [ROP], and sonographic parenchymal brain injury) significantly predicted short-term neurosensory and neurodevelopmental disability.8 Among the children with parenchymal brain injury (IVH grades III–IV, ventriculomegaly, and/or cystic periventricular leukomalacia), >1 (36%) in 3 had one of the CP syndromes. Among those with severe ROP, almost 1 (24%) in 4 had CP. Among those with chronic lung disease, defined as supplemental oxygen use at 36 weeks’ postmenstrual age, >1 (17%) in 6 had CP. Of most concern was that almost 9 (88%) of 10 of infants with all 3 conditions had outcomes of either death or recognized neurodisability in early childhood.
It is with this concern about the increasing rates of child neurodisability among those at the limits of viability that the article by Tommiska et al9 (in this issue of Pediatrics) is a substantial contribution. In the study they examined the outcomes of 1040 ELBW infants born in Finland in the latter part of the past decade. All infants with a birth weight of <1000 g (ELBW) were included in this study, and both perinatal and follow-up data were uniformly collected through an ELBW national registry. In addition, neurodevelopmental outcomes at 3 years of age were available through registries for children with CP and visual disability. Thus, this study meets the highest quality of epidemiologic investigations. These strengths include a very large cohort of ELBW pregnancies (with 75% having accurate early sonographic dating of gestational age before the end of the 20th gestational week), meticulous monitoring of intrauterine growth with concurrent use of up-to-date national standards, comprehensive obstetric and neonatal management data, quality improvement initiatives to lessen regional variation, and follow-up data in a country with both universal health insurance and comprehensive early childhood developmental and disability supports. In essence, this research was performed under the best possible circumstances and reflects the best outcomes using current technologies.
What were some of the findings?
6 days (median: 0.5 days) in era 1 and 5 days (median: 1 day) in era 2. Despite aggressive treatment, there are continued high rates of neonatal deaths and high rates of neonatal morbidities at <26 weeks’ gestation. Mikkola et al10 previously examined the 5-year outcome of these 206 Finnish survivors of <1000 g from era 1 of the Tommiska et al study. At 5 years of age, 14% had CP, 9% had cognitive disability, 4% had hearing disability, and 2.6% had visual disability. Marlow et al11 demonstrated that high rates of neurodisability in early childhood are the harbingers of school-age disability. In addition, even among children who escape major neurodevelopmental disability in early childhood, a very large number (>50%) struggle in school performance and have difficulty with academic competitiveness.12,13 Most importantly, there is increased recognition in the United States of increasing rates of early childhood cognitive disability that is occurring in an era of scarce resources for community health, early childhood, and education.
With current technologies, health professionals can increasingly recognize both our limited knowledge in preventing all degrees of prematurity as well as our inability to substantially decrease major neuromotor and neurosensory disability. However, this is only the tip of the iceberg of concerns that the current generation of survivors may not be able to enter school healthy and ready to learn. It is for this reason that explicit comprehensive strategies of neuroprotection that address both white matter injury and gray matter dysfunction are required. Unraveling the complex mechanisms involved in these structural markers are crucial for preventing disorders of movement, perception, attention, and cognition.14–16 Two additional themes for enhancing developmental outcomes include prevention of severe ROP and increased attention to mechanisms that underlie ototoxicity.17 Most importantly, because of fragmentation in the accessibility of quality childhood experiences for all children, but especially for those living in poverty, eliminating missed opportunities involving critical postnatal developmental experiences is essential. Thus, our efforts require a threefold approach of reducing short-term neurodevelopmental disability, minimizing missed opportunities to optimize developmental functioning, and comprehensive supports to families who are most vulnerable. This approach will ensure not only that our technologies address the limits of viability but also that we systematically begin a multipoint approach to address our current limits of neuroprotection across all degrees of prematurity. We will know when we have succeeded when all NICU graduates have ongoing academic, vocational, and employment successes.
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ACKNOWLEDGMENTS |
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Jen Park was invaluable in editing and technical assistance.
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FOOTNOTES |
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Address correspondence to Michael E. Msall, MD, Kennedy Center, Section of Developmental and Behavioral Pediatrics, Institute of Molecular Pediatrics Sciences, Pritzker School of Medicine, University of Chicago, 5841 South Maryland Ave, MC09000, Chicago, IL 60637. E-mail: mmsall{at}peds.bsd.uchicago.edu
The author has indicated he has no financial relationships relevant to this article to disclose.
Opinions expressed in these commentaries are those of the authors and not necessarily those of the American Academy of Pediatrics or its Committees.
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REFERENCES |
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This article has been cited by other articles:
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  C. Limperopoulos, H. Bassan, N. R. Sullivan, J. S. Soul, R. L. Robertson Jr, M. Moore, S. A. Ringer, J. J. Volpe, and A. J. du Plessis Positive Screening for Autism in Ex-preterm Infants: Prevalence and Risk Factors Pediatrics, April 1, 2008; 121(4): 758 - 765. [Abstract] [Full Text] [PDF]
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