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Intra Uterine Growth Retardation

DONE BY RABI’ S. ODWAN Ped. resident 4th year

 Manual of neonatal care 6th edition  NEONATOLOGY: MANAGEMENT, PROCEDURES, ON-CALL

PROBLEMS, DISEASES, AND DRUGS - 5th Ed. LANGE clinical manual
 Intensive Care Nursery House Staff Manual, The Regents

of the University of California
 Article from American Academy of Pediatrics

 -AGA, appropriate for gestational age: Birth weight

is between 10th and 90th percentile for infant’s gestational age (GA). percentile for GA. percentile for GA.

 -LGA, large for gestational age: Birth weight >90th

 - SGA, small for gestational age: Birth weight <10th

Other definitions: are sometimes used for SGA, including <3rd percentile

for GA or more than 2 S.D. below the mean.

 -IUGR vs. SGA: IUGR refers to deviation and reduction

in expected fetal growth pattern. Multiple adverse conditions inhibit normal fetal growth potential. Not all IUGR infants are SGA.

Incidence & Epidemiology .
 About 3-10% of all pregnancies are associated with IUGR,  20% of stillborn infants are growth retarded.  The perinatal mortality rate is 5-20 times higher for

growth-retarded fetuses.
 Term infants with birth weights below the 3rd

percentile have higher morbidity and 10 times higher mortality than appropriate for gestational age infants.

 McIntire DD et al: Birth weight in relation to morbidity and mortality among newborn

infants. NEngl J Med 1999;340:1234.

Uteroplacental insufficiency is the leading

cause of IUGR.
An estimated 10% of cases are secondary to

congenital infection.
 Chromosomal and other genetic disorders

are reported in 5-15% of IUGR infants.
 Intensive Care Nursery House Staff Manual, The Regents of the University of


Fetal weight percentiles throughout gestation

Intrauterine growth retardation (IUGR)

affects 3-10% of pregnancies; 20% of stillborn infants have IUGR.

 Perinatal mortality rates are 4-8 times

higher for growth retarded infants, and morbidity is present in 50% of surviving infants.


the baby's head and body are proportionately small. may occur when the foetus experiences a problem during early development.

baby's brain is disproportionally large when compared to the liver. may occur when the foetus experiences a problem during later development

In a normal infant, the brain weighs about three times more than the liver. In asymmetrical IUGR, the brain can weigh five or six times more than the liver.

Classification of IUGR
 Symmetrical growth restriction: fetus whose

entire body is proportionally small.  Incidence : 20 %  Early gestational growth retardation would be expected to affect the fetus in a symmetric manner, and thus have permanent neurologic consequences for the infant.  Examples of etiologies for symmetric growth retardation include genetic or chromosomal causes, early gestational intrauterine infections (TORCH) and maternal alcohol use.
 Asymmetrical growth restriction: Decrease in

subcutaneous fat and abdominal circumference with relative sparing of head circumference and femur length. Incidence : 80 %

 The foetal growth is dependent on multiple factors.

 IUGR resulting in SGA babies can result from many

factors known and unknown either acting alone or in conjunction or in association.

 In a majority of cases (40%) the cause is unknown–

probably due to placental insufficiency (idiopathic).

1. 2. 3. 4.

Maternal causes. Foetal causes. Placental causes. Idiopathic- In a majority of cases (40%) the cause is unknown– probably due to placental insufficiency.

• Maternal Risk Factors

Has had a previous baby who suffered from IUGR. Extremes of age. Is small in size (Ht & Wt). Has poor weight gain and malnutrition during pregnancy. Is socially deprived. Uses substances (like tobacco, narcotics, alcohol) that can cause abnormal development or birth defects. Has a low total blood volume during early pregnancy.

Is pregnant with more than one baby. High altitude. Drugs like anticoagulants, anticonvulsants. Has a cardio-vascular diseasepreeclampsia, hypertension, cyanotic heart disease, cardiac disease, diabetic vascular lesions. Chronic kidney disease Chronic infection- UTI, Malaria, TB, genital infections Has an antibody problem that can make successful pregnancy difficult (antiphospholipid antibody syndrome, SLE).

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Fetal Risk Factors
 Constitutional  Exposure to an infection-German measles (rubella), cytomegalovirus, herpes simplex, tuberculosis,
syphilis, or toxoplasmosis, TB, Malaria, Parvo virus B19.

 A birth defect (cardiovascular, renal, anencephally, limb defect,


 A chromosome defect- trisomy-18 (Edwards’ syndrome),21(Down’s syndrome), 16, 13, xo (turner’s syndrome).  A primary disorder of bone or cartilage.  A chronic lack of oxygen during development (hypoxia).  Developed outside of the uterus.  Placenta or umbilical cord defects.

Placental Factors
Uteroplacental insufficiency resulting from: Improper / inadequate trophoblastic invasion and placentation in the

first trimester.
 Lateral insertion of placenta.  Reduced maternal blood flow to the placental bed.

Foetoplacetal insufficiency due to-.
 Vascular anomalies of placenta and cord.  Decreased placental functioning mass-.

 Small placenta, abruptio placenta, placenta previa, post term


A. Establishing gestational age.

Determining the correct gestational age is imperative.
B. Fetal assessment C. Neonatal assessment

B. Fetal assessment
1. Clinical diagnosis. The patient's history

will raise the index of suspicion regarding suboptimal growth.

Ultrasonography. The following anthropomorphic measurements are used in combination to predict growth impairment with a high degree of accuracy.

a. Biparietal diameter (BPD). 

When serial measurements of BPD are less than optimal, 50-80% of infants will have subnormal birth weights.

b. Abdominal circumference.  The liver is the first organ to suffer the effects of growth retardation. Reduced abdominal circumference is the earliest sign of asymmetric growth retardation and diminished glycogen storage.

c. Ratio of head circumference to abdominal
 This ratio normally changes as pregnancy progresses.  In the second trimester, the head circumference is

greater than the abdominal circumference.  At about 32-36 weeks' gestation, the ratio is 1:1, and after 36 weeks the abdominal measurements become larger. Persistence of a head-abdomen ratio >=1 late in gestation is predictive of asymmetric IUGR.

d. Femur length.
 Serial measurements of femur length are as effective as

head measurements for detecting symmetric IUGR.

e. Placental morphology and amniotic fluid assessment
 For example, placental aging with oligohydramnios

suggests IUGR and fetal jeopardy, whereas normal placental morphology with a normal amount of amniotic fluid suggests a constitutionally small fetus.

4. Doppler velocity waveform:
 Decreased maternal arcuate arterial waveform velocities

indicate decreased uteroplacental perfusion.  Fetal Doppler arterial waveform velocities indicate chronic fetal distress and hypoxia.  Greatest risk is associated with absent or reversed diastolic flow in umbilical arteries.

C. Neonatal assessment
1. Reduced birth weight for gestational age is the simplest

method of diagnosing IUGR

Physical appearance. infections are excluded, the remaining group of IUGR infants have characteristic physical appearance.

 When infants with congenital malformation syndromes and

 These infants in general are thin, with loose, peeling skin

because of loss of subcutaneous tissue, a scaphoid abdomen, and a disproportionately large head.
3. A ponderal index below the 10th percentile helps to identify

neonates with IUGR, especially those with birth weight <2500 g.
4. Ballard score. Gestational age can also be assessed by means

of the Ballard scoring system.

Pathological examination of the placenta

for infarction or congenital infection may be helpful
Serological screening for congenital

infection is not indicated unless Hx or examination suggests infection as possible cause

Outcome &Long term Prognosis
 -Perinatal mortality:  for IUGR infants is 5-20 times greater than for AGA, mainly due to intrauterine death, perinatal asphyxia, and congenital anomalies.  Neurologic morbidity:  is 5-10 times higher than for AGA infants, especially for infants with ↓ head circumference at birth.
 Early identification and treatment of hypoglycemia and

polycythemia improves outcome. infectious causes of IUGR.

 Neurologic abnormalities are usual with genetic and

 Institute for Child Neurology and Neurology Unit, Dana

Children’s Hospital, Souraski Medical Center, University of Tel Aviv, Tel Aviv, Israel; Psychology Department, Developmental Neuropsychological Laboratory, Gonda (Goldschmied) Multidisciplinary Brain Research Center, Bar-Ilan University, Ramat Gan, Israel

OBJECTIVE.  The aim was to evaluate the effect of late-onset

intrauterine growth restriction on the neuropsychological profile and on academic achievements at 9 years of age using a largescale prospective paradigm.

 123 infants diagnosed with late-onset intrauterine growth

restriction were followed up yearly for 9 years. They were matched with 63 children for gestation age and multiple socioeconomic factors and evaluated by an extensive neuropsychological battery to assess intelligence quotient, academic achievements, learning and memory, visuomotor skills, visuospatial integration, attention, language, executive functions, and creativity.

 Children with intrauterine growth restriction had lower

intelligence quotient and more frequent neuropsychological difficulties. Difficulties in executive functioning, inflexibility-creativity, and language, indicative of frontal lobe dysfunction, were typically affected by intrauterine growth restriction and were rarely identified in the control group. Learning difficulties accompanied by lower academic achievements were more prevalent in the intrauterine growth restriction group, particularly when anthropometric catch-up was incomplete.

 Maternal-Fetal Medicine

Neonatology Departments, Hospital Clinic CIBER-ER, University of Barcelona, Barcelona, Spain Fetal and Perinatal Research Group, August Pi i Sunyer Institute for Biomedical Research, Barcelona, Spain Department of Clinical and Health Psychology, Autonomous University of Barcelona, Barcelona, Spain

OBJECTIVE:  The goal was to evaluate the

neurobehavioral outcomes of term, smallfor-gestational age (SGA) newborns with normal placental function.

 A cohort of consecutive term SGA newborns with normal prenatal umbilical artery Doppler ultrasound findings was created and compared with a group of term infants with size appropriate for gestational age, who were sampled from our general neonatal population.

 RESULTS:  A total of 202 newborns (102 SGA and 100 appropriate

for gestational age) were included. All of the neurobehavioral areas studied were poorer in the SGA group, with significance for attention, habituation, motor, social-interactive, and regulation of state.
 CONCLUSION: Term SGA newborns with no signs of

placental insufficiency had poorer neurobehavioral competencies, which suggests delayed neurologic maturation.

 Retarded growth:  With placental causes of IUGR, catch-up

growth occurs after birth, but these patients usually remain smaller than expected.
 Fetal “programming” of

cardiovascular disease:  Recent studies implicate IUGR with adult onset of hypertension, coronary heart disease, hypercholesterolemia, and diabetes. These studies suggest that IUGR

A. Hypoxia:
1. Perinatal asphyxia. IUGR infants frequently have
birth asphyxia because they tolerate the stress of labor poorly. IUGR accounts for a large proportion of stillborn infants with hypoxia in utero.


Persistent pulmonary hypertension (persistent fetal circulation).
Several reports suggest accelerated fetal pulmonary maturation in association with IUGR secondary to chronic intrauterine stress.


Respiratory distress syndrome.

4. Meconium aspiration. Postterm IUGR infants are at
risk for meconium aspiration.

B. Hypothermia.
 Thermoregulation is compromised in IUGR

infants because of diminished subcutaneous fat insulation. Infants with IUGR secondary to fetal malnutrition late in gestation tend to be scrawny as a result of loss of subcutaneous fat. They tend to be more alert than their premature counterparts.



1. Hypoglycemia.
 Carbohydrate metabolism is seriously disturbed, and

  

IUGR infants are highly susceptible to hypoglycemia as a consequence of diminished glycogen reserves and decreased capacity for gluconeogenesis. Oxidation of free fatty acids and triglycerides is reduced in IUGR infants, which limits alternate fuel sources. Hyperinsulinism, excess sensitivity to insulin deficient catecholamine release during hypoglycemia suggest abnormality of counterregulatory hormone mechanisms during periods of hypoglycemia in IUGR infants. Hypothermia may potentiate the problem of hypoglycemia.

2. Hyperglycemia. Very low birth weight infants have low insulin secretion, resulting in hyperglycemia.

D. Hematologic disorders:
 Hyperviscosity and polycythemia may result from

increased erythropoietin levels secondary to fetal hypoxia associated with IUGR.  Thrombocytopenia,  neutropenia, and altered coagulation profile are also seen in IUGR infants.  Polycythemia may also contribute to hypoglycemia and lead to cerebral injury.

E. Altered immunity.  IUGR infants have decreased IgG levels.  In addition, the thymus is reduced in size by 50% and peripheral blood lymphocytes are decreased.


IUGR has many causes, therefore, there is not one treatment that always works.

 Although there are many causes of IUGR, the treatment

consists of either delivery or remaining in utero and improving blood flow to the uterus.

 If IUGR is caused by a problem with the placenta and the

baby is otherwise healthy, early diagnosis and treatment of the problem may reduce the chance of a serious outcome.

 There is no treatment that improves foetal growth, but IUGR

babies who are at or near term have the best outcome if delivered promptly.

Treatment  Maternal bed rest
This is the initial approach for the treatment of IUGR. The benefit of bed rest is that it results in increased blood flow to the uterus. Studies have shown, however, that in most cases bed rest at home is just as effective as bed rest in the hospital environment.

Treatment  Aspirin Therapy
 The use of aspirin to treat foetuses with IUGR is still controversial.  If aspirin is used, it may be advantageous if given to patients before 20 weeks of gestation. It is minimal to limited benefit if given at the time of diagnosis (third trimester).  At the present time it is not recommended as a form of prevention for low risk patients.

Treatment  Other Forms of Treatment
 Other forms of treatment that have been studied are nutritional supplementation, zinc supplementation, fish oil, hormones and oxygen therapy.  Limited studies are available regarding the use of these modalities in the treatment of IUGR.

 A. History of risk factors.  The presence of maternal risk factors should alert the obstetrician to the likelihood of fetal growth retardation. Ultrasonography confirms the diagnosis. Correctable causes of impaired fetal growth warrant immediate attention.  B. Delivery and resuscitation.
 Appropriate timing of delivery is important. Delivery is usually

undertaken when the lungs are mature or when biophysical data obtained by monitoring reveal fetal distress.  Labor is particularly stressful to IUGR fetuses. Skilled resuscitation should be available because birth asphyxia is common.

 C. Prevention of heat loss. Meticulous care

should be taken to prevent heat loss

D. Hypoglycemia.  Close monitoring of blood glucose levels is

essential for all IUGR infants. Hypoglycemia should be treated promptly with parenteral dextrose and early feeding
E. Hematologic disorders. A central

hematocrit reading should be obtained to detect polycythemia.

F. Congenital infection.  IUGR infants should be examined for

congenital malformations or signs of congenital infections.  Many intrauterine infections are clinically silent, and screening for these should be done routinely in IUGR infants.
G. Genetic anomalies. Screening for

genetic anomalies should be done as indicated by the physical examination.