Intrauterine Growth Restriction

Prof. M.C.Bansal

MBBS,MS,MICOG,FICOG

Professor OBGY

Ex-Principal & Controller

Jhalawar Medical College & Hospital

Mahatma Gandhi Medical College, Jaipur.

DefinitionsIUGR: A condition where the fetus

fails to achieve its genetic growth potential and cosequently is at risk of increased perinatal morbidity & mortality.

SGA: Infant with weight < 10th percentile of those born at the same gestational age or > 2 SDs below mean for Gestational Age.

Easiest way to think about these terms are

IUGR: is a term used by Obstetrician to describe a pattern of growth over a period of time.

SGA: is a term used by Pediatrician to describe a single point on a growth curve.

Incidence

3 - 5% of all pregnancies.20 % of stillborns are growth

retarded.1/3 of infants with BW < 2750 gms

are growth retarded and not premature.

Only 20-30% of growth restricted fetuses are small due to pathological restriction of growth.

Perinatal mortality is 8 - 10 times higher for these fetuses.

Normal Intrauterine Growth pattern

Stage I (Hyperplasia) - 4 to 20 weeks - Rapid mitosis - Increase of DNA contentStage II (Hyperplasia &

Hypertrophy) - 20 to 28 weeks - Declining mitosis. - Increase in cell size.

Normal Intrauterine Growth pattern

Stage III ( Hypertrophy) - 28 to 40 weeks - Rapid increase in cell size. - Rapid accumulation of fat,

muscle and connective tissue.

95% of fetal weight gain occurs during last 20 weeks of gestations.

ClassificationBased on evaluation & USG examination

small fetuses are divided into two categaries

Healthy SGA or True IUGR orConstitutionally small Pathologically growth restricted

Type –I Type –IISymmetrical IUGR

Asymmetrical IUGRIntrinsic IUGR Extrinsic

IUGR

Symmetrical IUGR(20-30%)

Patho physiology- Growth inhibition in stage I (hyperplastic stage): - Reuced number of cells in fetus. - Normal cell size.Features-

Uniformally smallPonderal Index(Birth wt /Normal HC/AC-Normal FL/AC-Normal

Symmetrical IUGR

Etiology- Structural Congenital malformation

Chromosomal Intrauterine Infection

-Toxoplasma,Rubella,Cytomegalovirus,Herpes simplex Toxins & Drugs

Neonatal course-Complicated with poor prognosis

Asymmetrical IUGR(70-80%)

Patho physiology Growth Inhibition in Stage II/III (Hyperplasia & Hypertrophy)

-Decrease in cell size and fetal weight

-Less effect on total cell numeric, fetal length, head circumferance.

Features Head > Abdomen(Due to brain

sparing effect) Ponderal Index(Birth wt /-Low HC/AC- Increased FL/AC- Increased

Asymmetrical IUGR

Etiology- Maternal Diseases - Chronic

hypertention Renal diseases

Vasculopathy Placental InsufficiencyNeonatal course- Uncomplicated and good prognosis

Comparison between PFGR and Normal SGA

Normal, Small for gestation Age

Birth weight <10%

Birth weight <2500gms

Normal Ponderal Index

Normal subcutaneous fat

Normal nucleated blood red cells & thrombocytopenia

Uneventful neonatal period usually

Pathological Growth

Restriction

Birth weight usaully <10% but may be <25%

Birth weight usaully <2500gms but may be larger

Low Ponderal Index

Decreased subcutaneous fat

Elevated nucleated blood red cells & thrombocytopenia

Complicated neonatal period

Etiology1) Fetal factors: Genetic Factors:

- Race, ethnicity, nationality- sex ( male weigh 150 -200 gm

more than female )-genetic disorders

( Achondroplasia, Russell - silver syn.)

Chromosomal anomalies: - Chromosomal deletions

- Trisomies 13,18 & 21

Etiology Congenital malformations:

Anencephaly, GI atresia, potter’s syndrome, and pancreatic agenesis.

Fetal Cardiovascular anomalies Congenital Infections:

mainly TORCH infections. Inborn error of metabolism:

- Transient neonatal diabetes- Galactosemia - PKU

Etiology2) Maternal Factors:Decrease Uteroplacental blood

flow:- Pre eclampsia / eclampsia- chronic renovascular disease- Chronic hypertension

Maternal malnutritionMultiple pregnancyDrugs

- Cigarettes, alcohol, heroin, cocaine

- Teratogens, antimetabolites and therapeutic agents such as trimethadione, warfarin, phenytoin

Etiology Maternal hypoxemia

- Hemoglobinopathies - High altitudes

• Others- Short stature- Younger or older age (<15 and >45)- Low socioeconomic class- Primiparity- Grand multiparity- Low pregnancy weight- Previous h/o preterm IUGR baby

- Chronic illness ( DM, renal failure, cyanotic heart

disease etc.)

Etiology

3) Placental Factors: Placental insufficiency ( most imp in 3rd

trimester) Anatomic problems:

– Multiple infarcts– Aberrant cord insertions– Umbilical vascular thrombosis &

hemangiomas– Premature placental separation– Small Placenta

Diagnosis

Clinical Biophysical Biochemical Ultrasonography MSAFP & hCG in 2nd trimester Erythropoietin level in cord blood is high in IUGR

Diagnosis- ClinicallyMaternal weight gain- Stationary or falling during second half

of pregnancy

Palpation of uterus- Symphysio Fundal Height-Normally

increases by 1 cm per week between 14 – 32 wks

- A lag in fundal height of 4 wks s/o moderate IUGR and over 6 wks s/o severe IUGR Abdominal girth – stationary or

decreasing Liquour volume - less

ComplicationsFETAL Antepartum-

OligohydroamniosFetal distressFetal death

Intrapartum-Fetal AcidosisFetal Hypoxia

MATERNAL-Per se fetal growth restriction does not cause any harm to mother.But underlying disease progress like pre-

eclampsia, heart diseases, malnutrition may be life threatening.

A woman with a growth restricted infant , risk of having another is two fold.

PreventionStrategies include

– prenatal care modalities for high risk screening

– protein/energy supplementation– vitamin/mineral supplementation – fish oil supplementation– prevention and treatment of

Hypertensive disordersInfectionAnemia

PreventionStrong evidence of benefit only for

the following interventions: – balanced protein/energy

supplementation & maternal volume expansion

– strategies to reduce maternal smoking

– antibiotic administration to prevent urinary tract infections and

– antimalarial prophylaxis.

Few statistically significant reductions in the risk of IUGR have been demonstrated with other interventions.

Antenatal Fetal Surveillance

The purpose is to identify further progression of the disease process that would jeopardize the foetus to a point that it would be better to be delivered than to remain in utero.

There are four testing modalities which are helpful –Daily fetal movement count,Non-Stress Test, Amniotic Fluid Index, Doppler of the Umbilical Artery & Biophysical Profile, each of which addresses different aspects of surveillance.

Combination of tests are better than an isolated test.

Some more complex protocols have been also proposed like—

Kramer & Weiner suggested that UmA doppler is more reliable because severely abnormal doppler findings can precede an abnormal FHR by several weeks.

Harman & Baschat suggested a different strategy which includes multiple venous & arterial doppler and Biophycal profile

MANAGEMENT Suspect IUGR clinically

Confirm IUGR & Type of IUGR

Symmetrical Asymmetrical-Screening for TORCH Management depends upon-USG to r/o cong.malformation -Complicating factor-Fetal blood sampling to r/o -Previous obs history- Chromosomal abnormality -Gestational Age Abnormality+ No abnormality -Neonatal facilityTermination Mx acco.to GA -Degree of IUGR

Treatment

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

TreatmentAlthough there are many causes of IUGR,

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

When blood flow is improved, the delivery of oxygen and other nutrients to the foetus occurs. If the foetus is lacking in these substances, their increased availability may result in improved growth and development.

Treatment

1.Maternal Bed RestThis is the initial approach for the treatment of IUGR. Adequate bed rest in left lateral position results in increased blood flow to the uterus & placenta.

Treatment

Treatment 2. Aspirin Therapy(1- 2mg/kg/day) The use of aspirin to treat fetuses 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).

The Maternal-Fetal Medicine Network randomized 3135 women to receive 60mg/d aspirin or placebo and found no significant difference in incidence of IUGR

Aspirin Therapy(1-2mg/kg/day)

However it is benificial in cases with history of thrombotic disease, hypertension, pre-eclampsia.

Treatment3.Hyperoxygenation

Fetal oxygenation is crucial for fetal growth .

A positive response to maternal oxygen therapy found by decreased resistance in placental circulation is marker of good prognosis and lack of response is an indication of poor outcome.

(Bilardo et al 1991)

Treatment Other forms of treatment that have

been studied are maternal hyperalimantation by aminoacids,nutritional supplementation, zinc supplementation, fish oil and hormones.

Maternal volume expansion may be helpful in improving placental perfusion.

Limited studies are available regarding the use of these modalities in the treatment of IUGR.

Judge Optimum Time Of Delivery

RISK OF PREMATURITY

Difficult extra uterine existence

RISK OF IUD

Hostile intra uterine environment

Management according to Gestational Age

Less than 24 weeks of gestational ageAntenatal surveillance with Umbilical &

Ductus venosus doppler study is reliable.

٠ If UmA diastolic flow +nt ٠ If UmA –RDF٠ DV – Uninterrupted ٠ DV– Interrupted forward flow forward flow

Fetal Acidosis& HypoxiaExpectant Management Imminent Fetal Death

Termination

Less than 24 weeks of gestational age

There is no evidence that corticosteroids accelerate the fetal pulmonary maturity or prevent the development of Intraventricular haemorrhage.

On the other hand, there is evidence that the use of steroids in severe IUGR may cause hemodynamic decompensation

(Simchen et al 2004).

26 to 34 weeks Gestational Age

Antenatal surveillance with NST and Umbilical A, Middle cerebral A, Ductus venosus doppler.

1. NST-Reactive UmA Doppler-Reassuring Repeat in 1wk UmA Doppler-Non reassuring Ductus venosus Doppler Reassuring--Repeat in 1wk Non reassuring—Deliver

2. NST-Non reactive UmA Doppler—follow as above Or Biophysical profile ≥8 UmA doppler ≤4 Deliver 6 Repeat in 6-24hrs wait till ≥36wks

Deliver

34 to 37 weeks Gestational Age

Antenatal surveillance with FHR monitoring by NST and Color doppler velocimery.1. Both the tests reassuring Repeat in 1 wk Test for lung maturity Immature Mature Repeat in 1 wk Deliver

2.Either test non reassuring Deliver

Delivery of Pathological Growth Restricted Fetus

The full term fetus has a large capacity

to tolerate the hypoxic stress of labour

which is substantially reduced in PGRF

due to marked depletion of energy

stores in liver & subcutaneous tissue.

Thus, intrapartum asphyxia is the

major cause of perinatal morbidity &

mortality in PGRF

Therefore, when umbilical doppler shows Absent flow or Reverse flow

Fetal aciosis & hypoxia is more common

Delivery by cesarean section is indicated

Now ,the question is how to deliver the PGRF with lesser degrees of doppler or FHR abnormalities.

Skinner et al (1998) and Li et al (2003)

Conclusion- Vaginal delivery is not contraindicated in patients with resistance in UmA velocimetry but cesarean delivery should be anticipated in a large number of them. Indications for LSCS in IUGR pregnancies1. Established fetal acidosis2. Absent or Reverse flow in UmA doppler3. Unfavourable cervix

Precautions to be taken during delivery Delivery should be in an equipped institution

with Intensive intranatal monitoring & neonatal intensive care facilities.

Continous FHR monitoring Amnioinfusion in early stage of labour if

amniotic fluid volume is decreased. Second stage of labour requires special

attention. Second stage should not be prolonged > 2

hrs in nulliparous and 1 hr in multiparous . Placenta needs careful examination as in

many cases it will provide evidence about the etiology of the problem (Rayburn et al 1989).

AmnioinfusionAmnioinfusion refers to the instillation

of fluid into the amniotic cavity. This procedure is typically performed

during labor through an intrauterine pressure catheter introduced transcervically after rupture of the fetal membranes.

Alternatively, fluid can be infused through a needle transabdominally, the reverse process of amniocentesis.

Randomised trial of amnioinfusion during labour with meconium

stained amniotic fluid(BJOG Jan 2002)

Conclusion- Amnioinfusion in an under resourced labour ward decreases caesarean section rates and fetal morbidity

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