Intra-uterine growth restriction ( IUGR )

Definition :
- Is defined as failure of the fetus to achieve its genetic growth potential .
This usually results in a fetus that is small for gestational age ( SGA ) , and babies born below a particular centile weight for gestation ( e.g. below the 3rd or 5th centiled are frequently classified as IUGR .
- The terms SGA and IUGR are not synonymous .
- The term SGA : implies that the fetus or neonate is below a certain defined centile of weight or size for a particular gestational age , and some SGA fetuses are constitutionally small due to normal genetic influences .
- IUGR indicates that modify pathological process is operating to modify the intrinsic growth potential of the fetus by reducing the its growth rate .

Incidence :

3% if the 3rd or 5% if the 5th centile is chosen .

A etiology :

There are many causes IUGR , They best grouped into two main categories .
I Factors that directly affect the intrinsic growth potential of the fetus .
1. Chromosomal defects : e.g. trisomy 18 , triploidy .
2. Single gene effects e.g. seckel's syndrome .
3. Structural abnormalities , e.g. renal agenesis and an anencephaly .
4. Infections , e.g. cytomegalovirus , rubella .
Protozoal infection , such as toxoplasmosis .
II External influences that affect fetal growth can be
subdivided into :

1. Maternal Factors :

a. Maternal under-nutrition is go bally the major cause of IUGR , e.g. poverty , eating disorders .
b. maternal chronic respiratory disease . or at high altitude , will reduce fetal Po2 levels and fetal metabolism .
C. Drugs : Smoking C carboxy hemoglobin in maternal circulation , alcohol , herion , cocaine and marijuana .

2. Placental Factors :

a. Reduced utero placental perfusion , e.g. In adequate trophoblast invasion , anti phospholipids syndrome , sever diabetes mellitus , sickle-cell disease and multiple gestation .
b. Reduced feto-placental perfusion e.g. single umbilical antery , twin-twin transfusion syndrome in monochromic twinning .


Intrauterine growth restriction fetuses are frequently described as symmetrical or asymmetrical in terms of their body proportions . Symmetrically small fetuses are usually associated with factors that directly impair the intrauterine growth potential of the fetus . While asymmetrical growth restriction is classically associated with uteroplacental insufficiency . The cause of fetal asymmetry follows upon the reduced oxygen transfer to the fetus and impaired excretion of carbon dioxide by the placenta . The resulting fall in Po2 and rise in Pco2 in the blood will induce a chemoreceptor response in the fetal carotid bodies , with resulting vasodilatation in the fetal brain , myocardium and adrenal glands and vasoconstriction in the kidneys , splanchnic vessels , limps and subcutaneous tissues . The liver circulation is also severely reduced .
The result of all these circulatory changes is an asymmetrical fetus with relative brain sparing , reduced abdominal girth and skin thickness .
The vasoconstriction in the fetal kidneys results in impaired urine production and oligohydrambios .
Antenatal fetal blood sampling has shown reduced levels of nutrients such as glucose and amino acids ( especially essential amino acids ) and of hormones such as thyroxine and insulin . There are increased levels of corticosteroids and catecholamines , which reflect the increased perfusion of the adrenal gland . Haematological changes also reflect the chronic hypoxia , with increased levels of erythropoietin and nucleated red blood cells .
The fetal hypoxia eventually leads to fetal acidaemia , both respiratory and metabolic , which if prolonged can lead to intrauterine death if the fetus is not removed from its hostile environment . IUGR fetuses are especially at risk from profound asphyxia in labour due to the further compromise of the uteroplacental circulation caused by the uterine contractions .

Investigation :

The prediction and detection of the IUGR fetus are the principal aims of antenatal care , and the earlier the diagnosis is made , the better the chance of improving the outlook for the fetus .
The detection of an SGA infant contains two elements : First the accurate assessment of gestational age , and second the recognition of fetal smallness .
If there is any discrepancy between the assessments made at 12 weeks and 20 weeks , the prediction from the earlier measurement should be accepted . The most precise method of detecting fetal smallness is by ultrasound biometry , in particular , measurement of the biparietal diameter , head circumference , abdominal circumference and femur length .
Serial ultrasound biometry is usually performed on the following groups .
The next step is to establish whether this represents IUGR or whether the fetus is small normal .
A careful ultrasound scan of the fetal anatomy should be made to detect whether there are any fetal abnormalities to explain fetal smallness that may have been missed on the second trimester scan .
If the anatomy is normal , if the fetal head femur are disproportionately small or if there is an increased amount of amniotic fluid , this would raise the suspicion of a fetal genetic defect and , under these circumstances , an amniocentesis and rapid fetal karyotype should be offered .
Features suspicious of uterplacental insufficiency be an asymmetrical fetus with a relatively small abdominal circumference , olighydramnios and a high umbilical artery resistance .

Management :

At present , there are no widely accepted treatments available for growth restriction related to placental dysfunction . Obvious adverse factors such as smoking , alcohol and drug abuse should be stopped and the health of the woman should be maximized ( optimize control of diabetes , thyroid dysfunction , etc ) .
When growth restriction is severe , and the fetus is considered too immature to be delivered , bed rest in hospital is usually advised in an effort to maximize placental blood flow . Thereby reducing the morbidity associated with prematurity .
Timing delivery to maximize gestation without the baby dying in utero involves intensive fetal surveillance .
In brief , serial ultrasound scans are performed to establish that some fetal growth is maintained ; cessation of fetal growth may be an indication in itself for delivery . However , fetal biometry cannot give meaningful estimates of growth rate at intervals of less than 2 weeks .
Dynamic tests of fetal well-being such as Doppler ultrasound and fetal cardiotocography are now the principal means of determining fetal well-being . Absence of blood flow in the umbilical artery during fetal cardiac diastole or reversed flow ( i.e. back towards the heart ) requires delivery in the near future , as it reflects high placental resistance and is usually a pre-terminal event .
No effective drug therapy for IUGR has yet been found . Small studies have suggested that aspirin , nitric oxide donors or anti-oxidants may be helpful in some cases . These drugs may act by reducing platelet activation in the uteroplacental circulation , or may be acting directly as vasodilators .

Prognosis :

The Main danger to the baby is intrauterine death , due either to failure in making the diagnosis or to excessive delay prior to delivery . Some babies will suffer morbidity , or die , as a result of premature delivery .
Most infants with IUGR secondary to placental insufficiency show catch-up growth after delivery , when feeding can be optimized . Where IUGR is related to a congenital infection , or chromosomal anomaly , subsequent development of the child will be determined by the precise abnormality present .
A link between IUGR and the adult incidence of both hypertension and diabetes has now been established .


The student :

- Should be known the significance of intrauterine growth restriction which is a major cause of neonatal morbidity and mortality .

- Should be differentiated between SGA and IUGR fetuses .

- Should known the aetiology and types of the IUGR fetuses .

- Should known the pathophysiology of the IUGR .

- How can investigate them & how can manage them appropriately to prevent intrauterine fetal death improve fetal and neonatal outcome .



رفعت المحاضرة من قبل: Mubark Wilkins
المشاهدات: لقد قام 8 أعضاء و 84 زائراً بقراءة هذه المحاضرة

تسجيل دخول

عبر الحساب الاعتيادي
الرجاء كتابة البريد الالكتروني بشكل صحيح
الرجاء كتابة كلمة المرور
لست عضواً في موقع محاضراتي؟
اضغط هنا للتسجيل