Editing Intrauterine growth restriction (section)

==Outcomes==

=== Postnatal complications ===

After correcting for several factors such as low gestational parental weight, it is estimated that only around 3% of pregnancies are affected by true IUGR. 20% of [[stillbirth|stillborn]] infants exhibit IUGR. Perinatal [[mortality rate]]s are 4-8 times higher for infants with IUGR, and [[morbidity]] is present in 50% of surviving infants.<ref>{{Cite book|last=Carlo L. Acerini|url=https://www.worldcat.org/oclc/1223311499|title=Oxford Handbook of Paediatrics|date=2013|others=Robert J. McClure, Robert C. Tasker|publisher=OUP Oxford |isbn=9780191015885|oclc=1223311499}}</ref> Common causes of mortality in fetuses/infants with IUGR include: [[Placental insufficiency|severe placental insufficiency]] and chronic hypoxia, [[congenital malformations]], [[congenital infection]]s, [[placental abruption]], cord accidents, [[Umbilical cord prolapse|cord prolapse]], [[Placental infarction|placental infarcts]], and [[Postpartum depression|severe perinatal depression]].<ref name=":4" />

IUGR is more common in preterm infants than in full term (37–40 weeks gestation) infants, and its frequency decreases with increasing gestational age. Relative to premature infants who do not exhibit IUGR, premature infants with IUGR are more likely to have adverse neonatal outcomes, including [[Infant respiratory distress syndrome|respiratory distress syndrome]], [[intraventricular hemorrhage]], and [[necrotizing enterocolitis]]. This association with prematurity suggests utility of screening for IUGR as a potential risk factor for preterm labor.<ref>{{Cite journal|last1=Gilbert|first1=William M.|last2=Danielsen|first2=Beate|date=2003|title=Pregnancy outcomes associated with intrauterine growth restriction|url=https://linkinghub.elsevier.com/retrieve/pii/S0002937803003387|journal=American Journal of Obstetrics and Gynecology|volume=188|issue=6|pages=1596–1601|doi=10.1067/mob.2003.384|pmid=12824998|issn=0002-9378}}</ref>

Feeding intolerance, [[hypothermia]], [[hypoglycemia]], and [[hyperglycemia]] are all common in infants in the postnatal period, indicating the need to closely manage these patients' temperature and nutrition.<ref>{{Cite journal|last1=Hoe|first1=Francis M.|last2=Thornton|first2=Paul S.|last3=Wanner|first3=Laura A.|last4=Steinkrauss|first4=Linda|last5=Simmons|first5=Rebecca A.|last6=Stanley|first6=Charles A.|date=February 2006|title=Clinical features and insulin regulation in infants with a syndrome of prolonged neonatal hyperinsulinism|url=https://linkinghub.elsevier.com/retrieve/pii/S0022347605009832|journal=The Journal of Pediatrics|language=en|volume=148|issue=2|pages=207–212|doi=10.1016/j.jpeds.2005.10.002|pmid=16492430}}</ref> Furthermore, rapid metabolic and physiologic changes in the first few days after birth can yield susceptibility to [[hypocalcemia]], [[polycythemia]], immunologic compromise, and [[renal dysfunction]].<ref>{{Cite journal|last1=Hyman|first1=Sharon J.|last2=Novoa|first2=Yeray|last3=Holzman|first3=Ian|date=October 2011|title=Perinatal Endocrinology: Common Endocrine Disorders in the Sick and Premature Newborn|url=https://linkinghub.elsevier.com/retrieve/pii/S0031395511000897|journal=Pediatric Clinics of North America|language=en|volume=58|issue=5|pages=1083–1098|doi=10.1016/j.pcl.2011.07.003|pmid=21981950}}</ref><ref>{{Cite journal|last1=Mukhopadhyay|first1=Dhriti|last2=Weaver|first2=Laura|last3=Tobin|first3=Richard|last4=Henderson|first4=Stephanie|last5=Beeram|first5=Madhava|last6=Newell-Rogers|first6=M. Karen|last7=Perger|first7=Lena|date=May 2014|title=Intrauterine growth restriction and prematurity influence regulatory T cell development in newborns|url=https://doi.org/10.1016/j.jpedsurg.2014.02.055|journal=Journal of Pediatric Surgery|volume=49|issue=5|pages=727–732|doi=10.1016/j.jpedsurg.2014.02.055|pmid=24851757|issn=0022-3468}}</ref>

=== Long-term consequences ===
According to the theory of [[thrifty phenotype]], intrauterine growth restriction triggers [[epigenetic]] responses in the fetus that are otherwise activated in times of chronic food shortage. If the offspring actually develops in an environment where food is readily accessible, it may be more prone to metabolic disorders, such as [[obesity]] and [[Diabetes mellitus type 2|type II diabetes]].<ref>{{cite book|title=Fetal and infant origins of adult disease|publisher=British Medical Journal|year=1992|isbn=978-0-7279-0743-1|editor=Barker, D. J. P.|location=London}}</ref>

Infants with IUGR may continue to show signs of abnormal growth throughout childhood. Infants with asymmetric IUGR (head-sparing) typically have more robust [[Compensatory growth (organism)|catch-up postnatal growth]], as compared with infants with symmetric IUGR, who may remain small throughout life. The majority of [[catch-up growth]] occurs in the first 6 months of life, but can continue throughout the first two years. Approximately 10% of infants who are small for gestational age due to IUGR will still have short stature in late childhood.<ref>{{Cite journal|last1=Karlberg|first1=J.|last2=Albertsson-Wikland|first2=K.|date=1995|title=Growth in Full- Term Small-for-Gestational-Age Infants: From Birth to Final Height|journal=Pediatric Research|language=en|volume=38|issue=5|pages=733–739|doi=10.1203/00006450-199511000-00017|pmid=8552442|issn=1530-0447|doi-access=free}}</ref>

Infants with IUGR are also at elevated risk for neurodevelopmental abnormalities, including motor delay and [[cognitive impairments]]. Low [[IQ]] in adulthood may occur in up to one third of infants born small for gestational age due to IUGR. Infants who fail to display adequate catch-up growth in the first few years of life may exhibit worse outcomes.<ref>{{Cite journal|last1=Løhaugen|first1=Gro C.C.|last2=Østgård|first2=Heidi Furre|last3=Andreassen|first3=Silje|last4=Jacobsen|first4=Geir W.|last5=Vik|first5=Torstein|last6=Brubakk|first6=Ann-Mari|last7=Skranes|first7=Jon|last8=Martinussen|first8=Marit|date=2013|title=Small for Gestational Age and Intrauterine Growth Restriction Decreases Cognitive Function in Young Adults|url=https://doi.org/10.1016/j.jpeds.2013.01.060|journal=The Journal of Pediatrics|volume=163|issue=2|pages=447–453.e1|doi=10.1016/j.jpeds.2013.01.060|pmid=23453550|issn=0022-3476}}</ref><ref>{{Cite journal|last1=Lundgren|first1=Ester Maria|last2=Cnattingius|first2=Sven|last3=Jonsson|first3=Björn|last4=Tuvemo|first4=Torsten|date=2001|title=Intellectual and Psychological Performance in Males Born Small for Gestational Age With and Without Catch-Up Growth|journal=Pediatric Research|language=en|volume=50|issue=1|pages=91–96|doi=10.1203/00006450-200107000-00017|pmid=11420424|issn=1530-0447|doi-access=free}}</ref>

Catch-up growth can alter fat distribution in children diagnosed with IUGR as infants and increase risk of [[metabolic syndrome]].<ref>{{Cite journal|last1=McMillen|first1=I. C.|last2=Muhlhausler|first2=B. S.|last3=Duffield|first3=J. A.|last4=Yuen|first4=B. S. J.|date=2004|title=Prenatal programming of postnatal obesity: fetal nutrition and the regulation of leptin synthesis and secretion before birth|url=https://www.cambridge.org/core/product/identifier/S0029665104000552/type/journal_article|journal=Proceedings of the Nutrition Society|language=en|volume=63|issue=3|pages=405–412|doi=10.1079/PNS2004370|pmid=15373950|issn=0029-6651|hdl=2440/3152|s2cid=29901966|hdl-access=free}}</ref> Infants with IUGR may be susceptible to long-term dysfunction of several endocrine processes, including [[Growth hormone|growth hormone signaling]], the [[Hypothalamic–pituitary–adrenal axis|hypothalamic-pituitary-adrenal axis]], and [[puberty]].<ref>{{Cite journal|author1-link=Simon Langley-Evans|last1=Langley-Evans|first1=Simon C.|last2=Gardner|first2=David S.|last3=Jackson|first3=Alan A.|date=1996-06-01|title=Maternal Protein Restriction Influences the Programming of the Rat Hypothalamic-Pituitary-Adrenal Axis|journal=The Journal of Nutrition|volume=126|issue=6|pages=1578–1585|doi=10.1093/jn/126.6.1578|pmid=8648431|issn=0022-3166|doi-access=free}}</ref> [[Renal dysfunction]], disrupted lung development, and [[Bone metabolism|impaired bone metabolism]] are also associated with IUGR.<ref>{{Cite journal|last1=Bacchetta|first1=Justine|last2=Harambat|first2=Jérôme|last3=Dubourg|first3=Laurence|last4=Guy|first4=Brigitte|last5=Liutkus|first5=Aurélia|last6=Canterino|first6=Isabelle|last7=Kassaï|first7=Behrouz|last8=Putet|first8=Guy|last9=Cochat|first9=Pierre|date=2009|title=Both extrauterine and intrauterine growth restriction impair renal function in children born very preterm|journal=Kidney International|volume=76|issue=4|pages=445–452|doi=10.1038/ki.2009.201|pmid=19516242|issn=0085-2538|doi-access=free}}</ref>