Intrauterine Growth Restriction: Recognizing the Risk Factors

July 21, 2011

About 40 years ago, doctors recognized for the first time that the restriction of fetal growth was a phenomenon that not only affected animals, but also human beings.

About 40 years ago, doctors recognized for the first time that the restriction of fetal growth was a phenomenon that not only affected animals, but also human beings.

 

About 40 years ago, doctors recognized for the first time that the restriction of fetal growth was a phenomenon that not only affected animals, but also human beings. In 1961, Warkani and Cabbage informed of weight, longitude and cephalic circumference values in children and they defined retardation of fetal growth. Since then, other researchers into the matter, such as Campbell and Lubchenko, have produced important data on the intrauterine and postnatal growth patterns of different sectors of our populations.

 

 

It is considered that we are in the presence of Intrauterine Growth Restriction (IUGR) when the product of conception presents weight below two standard deviations of the presumably weight for its gestational age or below the tenth percentile of the weight curve. Between 25% and 60% of neonates conventionally diagnosed as small for gestational age had an appropriate growth when factors determining prenatal factors such as ethnic groups, parity, weight and height of the mother are considered. It is a syndrome that corresponds to different, but interrelated causes. It can be classified in different ways: if it is related with the fetus it is of an intrinsic cause and when it depends on the placenta or other maternal factors, the cause is extrinsic.

Among the better known causal factors we can include the following:

Intrinsic causes which include:

1. Genetically small fetus: constitutional factors

-Racial factors

-Karyotype abnormalities

2. Hereditarily small constitution:

-Weight and stature of the parents (mainly of the father)

-Race

3. Developmental abnormalities:

-Trisomies

-Viral infections (rubella and cytomegalovirus)

-Anencephaly and other congenital abnormalities

Extrinsic causes include:

1. Factors conditioned by the same pregnancy:

1.1- Caused by the placenta

- Placental infarctations

- Thrombosis of fetal blood vessels

- Premature fetal separation

- Edema of the placental villi

- Placenta praevia

1.2- Ovulatory causes:

- Multiple gestations (Third trimester restriction of growth due to the mother's inability to provide nutrition to the fetuses)

1.3-Umbilical cord pathologies:

- Single umbilical artery

- Velamentosa insertion of the placenta

1.4- Rh isoimmunization (or incompatibility)

2. Factors attributable to the mother:

- Age - Less than 17 and above 35 years

- Height - Low height (less than 1.50 m)

- Weight - Starting pregnancy underweight and with inadequate gain during the same

- Parity - Mainly when the intergenesic period is lessthan 2 years and in precocious primigravidae.

- Smoking - In active and /or passive smokers.

- Alcohol - Provokes irreversible damage,mental deficiency and malformations have been reported.

- Other drugs - Cytostatic medication, propylthiouracil, heroine, propanolol, anticonvulsivants.

2.2- Social factors:

- Marital status. - Single mothers, unwanted pregnancies.

- Educational level. -Low educational level.

- Family problems.

- Occupation. - Strong physical work and intellectual stress.

- Gender. - Alimentary deficiency with lack of cysteine, trionina, zinc, triptophane.

- Inadequate prenatal care. - inadecuate prenatal attention.

2.3-Environmental factors:

 

- Height

 

- Urban environment

 

- Economic depression

 

- Migration

 

- Culture, etc.

 

2.4-Maternal pathological factors:

 

- Infections. - Rubella, toxoplasmosis, syphilis, herpes simplex, HIV, gonorrhea.

 

- Cardiopathies

 

- Anemias

 

- Hypertension

 

- Diabetes

 

- Urinary infections

 

- Other systemic infections

 

2.5-Uterine factors:

 

- Fibroids or miomas

 

- Synequias

 

- Poor uterine vascularization

 

- Vascular injuries to the uterine arteries

 

2.6-There are no causal factors in 30-40% of the cases.

 

From the point of view of their pathogenesis, two fundamental processes can be identified:

 

a) Reduction of the growth potential with basic circumstances that act through intrinsic mechanisms, dependent on the fetus and that cause a symmetrical restriction, originating from the inhibition of mitosis thus reducing all diameters and the longitude.

 

b) Fetal malnutrition created by extrinsic mechanisms and that gives place to symmetrical reduction and an asymmetric restriction.

 

In the symmetry of extrinsic origin, it is provoked by an intense deterioration and prolongation in the delivery of nutrients. In the asymmetry of this same origin, the cause is generally an uteroplacental dysfunction provoked by the vascular lesions that reduce the nutrition flow creating a visceral wastage with relative preservation of fetal length and circumference, since neuronal cells have their biggest growth rate at 22 weeks and the fat cells at 34-35 weeks.

 

Several researchers point out that IUGR contributes especially to the overalls perinatal morbidity and mortality when it is associated to preterm gestation; an incidence of 10% to 13% in relation to low birth weight, with high neonatal morbidity, especially of the cardiovascular and nervous apparatus.

 

The placenta is an organ with the functions of respiration and nutrition, amongst others, for the exchange between mother and fetus. This exchange exerts a major influence on fetal development and weight. The transplacental changes depend primarily on the uterine modifications and the flow of blood in the umbilical cord. When there is an increment in uterine vascular resistance and the flow of uterine blood decreases, this can be a predictive risk factor and can be associated to the delayed fetal growth. These changes depend on the vascularization and angiogenesis of the placenta. Other important factors include fibroblastosis and angiopoyetin, which plays the more important role in the placental vascularization. Recent studies suggest that these angiogenetic factors interact with local vasodilatation, due to the presence of nitric oxide in blood, influencing the transportation of nutrients to the fetus. As a consequence of faulty transportation, restriction in fetal growth results.

The lack of increase in maternal weight during the second trimester of pregnancy correlates in an especially intense way with a reduction of fetal weight. As such, a marked limitation of body weight increase should not be encouraged during the second half of gestation, as less than 1500 Kcal / day affects fetal growth.

Preeclampsia and the restriction of birth weight are associated to a poor placental perfusion that may be accompanied by the compensatory presence of vasoactive substances in the feto-placental circulation. This situation creates chronic hypoxia with the increment of Cyclic Guanosine Monophosphate that produces the feto-placental vasoconstriction. It is suggested that these situations give place to an asymmetric fetus with a high prenatal mortality and complications like Preeclampsia-Eclampsia, HELLP Syndrome in as much as 70% and Gestational Diabetes in as much as 10% of women with growth restricted fetuses. These pathologies are responsible for the placental insufficiency as well as placental infarctations. Other authors give value to the anemia, pointing out that the anemia induces fetal distress, which in turn stimulates the. The elevated concentrations of the corticotropic hormone represents a high risk, not only of preterm labor but also of Intrauterine Growth Restriction, Pregnancy Induced Hypertension and Premature Rupture of Membranes increasing the production of fetal cortisol that inhibits the longitudinal development of the fetus. Iron deficiency increases the oxidative damage of the erythrocytes and the feto-placental unit, a defect that can be corrected by the administration of parenteral iron supplement that improves the concentration of red blood cells.

Small placentas are generally described, with increase in the thickness of the placental villi; this is associated with the increment in the umbilical artery resistance index according to the Doppler velocimetry. Some authors have analysed fetal growth by ultrasound, pointing out that the prolonged effect of the abnormal fluid flow through the umbilical artery is associated to the restriction of the fetal weight, postnatal intellect, as well as neurological and social development.

Many of these risk factors of IUGR are preventable but only if they are recognized and precocious administration of adequate prenatal care is applied. Clinical and ultrasonographic measurements of fetal biometry are increasingly becoming indispensable in predicting IUGR. These are the first steps towards the delivery of a healthy baby and a guarantee for a happy motherhood.

Please send correspondence to:

Dr. John Essien, Calle Horca, Entre San Ramón y Primera, Camagüey, C.P. 70100, Cuba
E-mail: johnessien@medscape.com