IUGR-ETIOLOGY & DIAGNOSIS

Dr.Suman Kumari MS OBGYTATA MAIN HOSPITAL

IntroductionIUGR/FGRA fetus that has not reached its growth potential because of genetic or

envoirnmental factors. Results in

BW < 10%tile as per the customised growth curve.

Inhibition of normal growth potential

implies pathologySGA: BW less than population norms < 10th %-tile usually physiological or constitutional

Cause of concern• Leading contributor - Perinatal mortality rate(50%) at

preterm and 20% at term.

• 40% of all stillbirths are IUGR.

• Perinatal morbidity as well as delayed effects including cerebral palsy(CP) .

Effect of birth weight on Perinatal morbidity and mortality.

The developmental origins of adult disease —Barker’s hypothesis

Growth retardation in utero can Cause hypertension,diabetes ,Cardiac problems in adult life.

Why antenatal diagnosis• Early detection of IUGR categorised the women into high risk

group.• Early identification, further investigation and intervention leads

to significantly improved outcome.

• Depending upon the severity optimal timing of delivery could be decided.

• Antenatal detection of IUGR has better outcome.(Molin J.2005).

• Identification and management lowers this perinatal mortality and morbidity.

Normal Intrauterine Growth

IUGR - Types• Symmetric Stage I growth inhibition

Fewer cells but normal size weight, head, length all < 10th percentile

• Asymmetric Stage II/III growth inhibition

Decrease in cell size, less effect on total cell number weight below 10th percentile,head and length

preserved

Physiology

Pathophysiology• Gas exchange and nutrient delivery to the fetus are not

sufficient - IUGR maternal disease diabetes with vascular disease, hypertension, autoimmune

disease affecting the vessels-- dysfunctional oxygen delivery system

cyanotic heart disease, smoking, hemoglobinopathy--- causing decreased oxygen-carrying capacity

smoking, thrombophilia, various autoimmune diseases-- placental damage

Pre-eclampsia/ HELLP

Diabetes• Diabetes-usually macrosomic.

• IUGR-15-20% when preeclampsia associated with diabetes

without nephropathy .

• IUGR-50% when preeclampsia associated diabetic

nephropathy.

Etiology- Overlapping

Maternal factor• Chronic hypertension• Pregnancy associated hypertension.• Cyanotic heart disease• Class F or higher diabetes• Hemoglobinopathies• Autoimmune disease• Protein-calorie malnutrition• Smoking• Substance abuse

Placenta

• Placental insufficiency– PIH,Preeclampsia,diabetes mellitus.– Chronic hypertension

• Anatomic– abnormal insertion– hemangiomas– infarcts– Abruption– Twin to twin transfusion syndrome.

Fetal factors

• Genetic• Congenital malformations• Genetic/ chromosomal (trisomies, syndromes)• Cardiovascular disease• Congenital infection• Inborn errors of metabolism

Discordant twins

• Growth standards for multiple pregnancies are therebut singleton nomograms are moreused commonly with good accuracy.Discordance >20-25% is significant.

Trisomy 13

Turner syndrome

Toxoplasmosis

Rubella

Uterine factors

• Morphological abnormalities• Fibromyoma

Diagnosis

• History• Physical examination• Biochemical screening in ANC• Ultrasound and Fetal biometry• USG doppler

HISTORY

• Risk factor assessment by history.

• Previous h/o still birth baby have a 50% increase risk of severe

growth restriction in current pregnancy. (Villar J,AJOG 2006)

• h/o dysmorphic feature or chromosomal anomaly .

TORCH” Stigmata

– hepatoslpenomegaly– petechiae/ ecchymoses– blueberry muffin rash– vesicles/ mucocutaneous lesions– chorioretinitis/ cataracts/ salt-pepper retinopathy– PDA– microcephaly/ hydrocephaly• Intracranial calcifications

Physical exam.

• Abdominal exam-detection rate-30 to 50%.• Symphysio fundal height(SFH)-sensitivity is 50%. Uterine fundal height corresponds to week of

gestation between 18 to 36 week. Serial SFH supplemented with anatomic USG- increases the accuracy of diagnosis. Lag of 3 cm-- prompt USG indicated. Unsuitable in case of fibroid uterus,obesity.

Clinical examination

• SFH

Customised growth curve (CGC)

Customised growth curve (CGC)-design to identify fetus <10%tile of their genetic growth potential

Biochemical test in ANC

• Biochemical screening –for at risk pregnancy.

• First trimester-low pregnancy associated plasma

protein –A(PAPP-A) .

• Decrease PAPP-A with increase AFP,inhibin and hCG

suggest IUGR.(Dugoff L,AJOG 2004)

Ultrasound diagnosis

• USG assessment requires three basic steps1. Accurate dating2. Biometric evaluation and3. Assessment of growth.

USG1. Accurate assessment of the gestational age is most important

before diagnosing IUGR.

• 1ST trimester USG can confirm the date with margin of 1 wk.

• TCD-most effective ,for dating in second and third trimester and being normal in 75% of 73 previously dated IUGR fetuses.

• serial measurement are nessessary to depict actual growth lag.• Interval between growth scan should be atleast 2 wk.

Parameters

2.Parameters to assess biometric growth are- Biparietal diameter(BPD) Head circumference(HC) Abdominal circumference(AC) Femur length.(FL)To estimate fetal weight(EFW)-sensitivity 89%,specificity-91% HC/AC ratio,FL/AC ratio

Abdominal circumference(AC)

Most accurate measurement to predict IUGR.

Cut off-below the 10TH %tile.

Sensitivity 74-94% ,specificity-50%

Should increase by atleast 10 mm / 2 week.

So SFH measurment and biometry scan are basically surveillance test,require serial monitoring.

USG • For fetal anatomy (anomaly scan) At 18 -20 wk gestation. Risk factors are- Asymmetry of parameters Short femur Bowel echogenisity Oligohydraminous• Placental mlorphology• Amniotic fluid volume.(AFI)-when oligohydraminous AFI<5cm at

37 wk-suspected IUGR.• Polyhydraminous with suspected IUGR s/o fetal cause.

Doppler velocimetry.

• Purpose to dectect IUGR fetus at risk of hypoxia

• Not to be used as routine screening method.

• Used only when USG picks up IUGR.

Umbilical artery doppler

• Umblical artey doppler is the standard test ,to detect Placental insufficiency(m.c cause of IUGR)

• Diffrentiate between SGA and IUGR.• Progression is from normal end-diastolic velocity

(EDV)---- to decreased,---- to absent to ------reverse EDV.

• Absent or reversed end-diastolic velocities are mostly S/O early-onset IUGR.

• These patterns seen to be present approx. 1 week before the acute deterioration.(Ferrazzi E,2002)

• The normal umbilical artery flow --marked positive end-diastolic velocity (A). • Moderate abnormalities in the villous vascular structure raise the blood flow

resistance and are associated with a decline in end-diastolic velocities (B). • When a significant proportion of the villous vascular tree is abnormal (50-70%),

end-diastolic velocities may be absent (C) or even reversed (D). • Depending on the magnitude of placental blood flow resistance and the fetal

cardiac function, reversal of end-diastolic velocities may be minimal (D), moderate (E), or severe (F).

Uterine artery doppler

• By 20 weeks, low-impedance waveform and no diastolic

notch.

• If still high impedance and diastolic notch, high risk of

IUGR and/or preeclampsia.

• As screening test, 82% sensitivity, 38% specificity

(Bewley, 1991)

• Value in high-risk patients only

Flow velocity waveforms obtained from the uterine artery• (A) high-volume diastolic

flow –normal• placental vascular

resistance is associated with a decline in diastolic velocities and a subsequent rise in the Dopplerindex (B).

• Persistence of an early diastolic notch is evidence of increased spiral artery blood flow resistance. (C)

“notching” (D).

Ductus venosus doppler

• Normal is forward flow during atrial contraction.

• IUGR causes peripheral resistance and eventually heart failure

with no forward flow.

• When back pressure reaches umbilical vein, normally minimally

pulsatile waveform becomes pulsatile as sign of imminent

demise.

In the ductus venosus blood flow is always antegrade throughout the cardiac cycle under normal circumstances. Pulsatility is less pronounced in waveform patterns obtained at the inlet (A) versus the outlet (B). With impaired cardiac forward function there is a decline in forward flow during atrial systole (C). If progressive atrial forward flow may be lost (D) or reversed (E, F).

Middle cerebral artery doppler

• In normal fetus –increase in middle cerebral artery resistance

as shown by resistance indices.

• When there is hypoxia,or stress,fetus show redistribution of

blood flow preferentially to brain and heart(brain sparing).

• doppler showing decrease in middle cerebral artery

resistance.

MCA doppler cont....

• Up to 20% of SGA fetuses have reduced resistance in the

middle cerebral artery (MCA),

• This sign is associated with poorer perinatal outcome

• suboptimal neurodevelopmental development at 2 years of

age.

A, Color Doppler assessment of the MCA at the level of the circle of Willis. B, Normal and abnormal(high diastolic velocities and decreased pulsatility index) C,

Diagnostic algorythm

History s/o –IUGR

Usg for dating

Biochemical markers serial SFH and biometric assessment

Umblical artery doppler Ut. artery doppler

MCA/DV doppler