Intrauterine growth restriction

From Wikipedia, the free encyclopedia

Intrauterine growth restriction

Classification and external resources

Micrograph of villitis of unknown etiology, aplacental pathology associated with

IUGR. H&E stain.

ICD-10

P05.9

ICD-9

764.9

DiseasesDB

6895

MedlinePlus

001500

eMedicine

article/261226

MeSH

D005317

Intrauterine growth restriction (IUGR) refers to poor growth of a baby while in the mother's womb during
pregnancy. The causes can be many, but most often involve poor maternal nutrition or lack of adequate oxygen
supply to the fetus.
At least 60% of the 4 million neonatal deaths that occur worldwide every year are associated with low birth
weight (LBW), caused by intrauterine growth restriction (IUGR), preterm delivery, and genetic/chromosomal
abnormalities,[1] demonstrating that under-nutrition is already a leading health problem at birth.
Contents

[hide]

1 Terminology

2 Symmetrical vs. asymmetrical

3 Causes

3.1 Maternal

3.2 Uteroplacental

3.3 Fetal

4 Pathophysiology

5 Outcomes and clinical significance

6 Sheep

7 Notes

8 References

[edit]Terminology

The term IUGR is not synonymous with Small for Gestational Age (SGA). SGA refers to a birth weight that is
below the 10th percentile for gestational age. Not all fetuses with IUGR are classified as SGA, and vice versa.
IUGR is used to describe a pattern of intrauterine fetal growth that deviates from expected norms, whereas
SGA is a category assigned based on birth weight.
[edit]Symmetrical

vs. asymmetrical

There are 2 major categories of IUGR: symmetrical and asymmetrical.

Asymmetrical IUGR is more common. In asymmetrical IUGR, there is restriction of weight followed by length.
The head continues to grow at normal or near-normal rates (head sparing). This is a protective mechanism that
may have evolved to promote brain development. This type of IUGR is most commonly caused
by extrinsic factors that affect the fetus at later gestational ages.

Symmetrical IUGR is less common and is more worrisome. This type of IUGR usually begins early in gestation.
Since most neurons are developed by the 18th week of gestation, the fetus with symmetrical IUGR is more
likely to have permanent neurological sequela.
[edit]Causes
[edit]Maternal

pre-pregnancy weight and nutritional status

poor weight gain during pregnancy

poor nutrition

anemia

alcohol and/or drug use

maternal smoking

recent pregnancy

pre-gestational diabetes

gestational diabetes

pulmonary disease

cardiovascular disease

renal disease

hypertension

[edit]Uteroplacental

preeclampsia

multiple gestation

uterine malformations

[edit]Fetal

chromosomal abnormalities

intrauterine infection

[edit]Pathophysiology

If the cause of IUGR is extrinsic to the fetus (maternal or uteroplacental), transfer of oxygen and nutrients to the
fetus is decreased. This causes a reduction in the fetus stores of glycogen andlipids. This often leads
to hypoglycemia at birth. Polycythemia can occur secondary to increased erythropoietin production caused by
the chronic hypoxemia. Hypothermia, thrombocytopenia,leukopenia, hypocalcemia,
and pulmonary hemorrhage are often results of IUGR.
If the cause of IUGR is intrinsic to the fetus, growth is restricted due to genetic factors or as a sequela of
infection.
[edit]Outcomes

and clinical significance

IUGR affects 3-10% of pregnancies. 20% of stillborn infants have IUGR. Perinatal mortality rates are 4-8 times
higher for infants with IUGR, and morbidity is present in 50% of surviving infants.
[edit]Sheep

In sheep, intrauterine growth restriction can be caused by heat stress in early to mid pregnancy. The effect is
attributed to reduced placental development causing reduced fetal growth. [2][3][4]Hormonal effects appear
implicated in the reduced placental development. [4] Although early reduction of placental development is not
accompanied by concurrent reduction of fetal growth;[2] it tends to limit fetal growth later in gestation. Normally,
ovine placental mass increases until about day 70 of gestation, [5] but high demand on the placenta for fetal
growth occurs later. (For example, research results suggest that a normal average singleton Suffolk x Targhee
sheep fetus has a mass of about 0.15 kg at day 70, and growth rates of about 31 g/day at day 80, 129 g/day at
day 120 and 199 g/day at day 140 of gestation, reaching a mass of about 6.21 kg at day 140, a few days
before parturition.[6])
In adolescent ewes (i.e. ewe hoggets), overfeeding during pregnancy can also cause intrauterine growth
restriction, by altering nutrient partitioning between dam and conceptus. [7][8] Fetal growth restriction in
adolescent ewes overnourished during early to mid pregnancy is not avoided by switching to lower nutrient
intake after day 90 of gestation; whereas such switching at day 50 does result in greater placental growth and
enhanced pregnancy outcome.[8] Practical implications include the importance of estimating a threshold for
"overnutrition" in management of pregnant ewe hoggets. In a study of Romney and Coopworth ewe hoggets
bred to Perendale rams, feeding to approximate a conceptus-free live mass gain of 0.15 kg/day (i.e. in addition

to conceptus mass), commencing 13 days after the midpoint of a synchronized breeding period, yielded no
reduction in lamb birth mass, where compared with feeding treatments yielding conceptus-free live mass gains
of about 0 and 0.075 kg/day.[9]
In both of the above models of IUGR in sheep, the absolute magnitude of uterine blood flow is reduced.
[8]

Evidence of substantial reduction of placental glucose transport capacity has been observed in pregnant

ewes that had been heat-stressed during placental development. [10][11]

[edit]Notes

1.

^ Lawn 2005

2.

^ a b Vatnick, I., G. Ignotz, B. W. McBride and A. W. Bell. 1991. Effect of heat stress on ovine placental growth in
early pregnancy. J. Devel. Physiol. 16: 163-166.

3.

^ Bell, A. W., B. W. McBride. R. Slepetis, R. J. Early and W. B. Currie. 1989. Chronic heat stress and prenatal
development in sheep. I. Conceptus growth and maternal plasma hormones and metabolites. J. Anim. Sci. 67: 32893299.

4.

^ a b Regnault, T. R. H., R. J. Orbus, F. C. Battaglia, R. B. Wilkening and R. V. Anthony. 1999. Altered arterial
concentrations of placental hormones during maximal placental growth in a model of placental insufficiency. J.
Endocrinol. 162: 433-442.

5.

^ Ehrhardt, R. A. and A. W. Bella. 1995. Growth and metabolism of the ovine placenta during mid-gestation.
Placenta 16: 727-741.

6.

^ Rattray, P. V., W. N. Garrett, N. E. East and N. Hinman. 1974. Growth, development and composition of the
ovine conceptus and mammary gland during pregnancy. J. Anim. Sci. 38: 613-626.

7.

^ Wallace, J. M. 2000. Nutrient partitioning during pregnancy: adverse gestational outcome in overnourished
adolescent dams. Proc. Nutr. Soc. 59: 107-117.

8.

^ a b c Wallace, J. M., T. R. H. Regnault, S. W. Limesand, W. W. Hay Jr. and R. V. Anthony. 2005. Investigating
the causes of low birth weights in contrasting ovine paradigms. J. Physiol. 565: 19-26.

9.

^ Morris, S. T., P. R. Kenyon and D. M. West. 2005. Effect of hogget nutrition in pregancy on lamb birthweight
and survival to weaning. N. Z. J. Agr. Res. 48: 165-175.

10.

^ Bell, A. W., R. B. Wilkening and G. Meschia. 1987. Some aspects of placental function in chronically heatstressed ewes. J. Dev. Physiol 9: 17-29.

11.

^ Thureen, P. J., K. A. Trembler, G. Meschia, E. L. Makowski and R. B. Wilkening. 1992. Placental glucose
transport in heat-induced fetal growth retardation. Am. J. Physiol. Regul. Integr. Comp. Physiol. 263: R578-R585.

[edit]References

Lawn, JE (2005) "4 million neonatal deaths: when? Where? Why?" Lancet.

http://en.wikipedia.org/wiki/Intrauterine_growth_restriction#Symmetrical_vs._asym
metrical