Intrauterine growth restriction (IUGR) refers to a fetus with an estimated weight less than 10th percentile for gestational age. IUGR can occur due to reduced fetal growth potential from genetic/structural issues or infections, or reduced fetal growth support from maternal/placental factors like malnutrition, hypoxia, or drugs. IUGR increases risks of complications during labor like meconium aspiration or fetal distress. Intrauterine death refers to fetal death after 20 weeks of gestation, which can have unknown causes or be due to maternal/fetal/placental conditions like preeclampsia, infections, or cord accidents. Diagnosis involves assessing fetal movement and heart rate. Management depends on gestational

1. Intrauterine
growth restriction

2. Definition
 Fetus with estimated fetal weight less than 10
percentile for gestational age

3. Aetiology
 On etiological basis IUGR can occur due to
 Reduced fetal growth potential
 Reduced fetal growth support

4. Reduced fetal growth potential occurs in
 Aneuploidies e.g trisomy 18
 Single gene defect e.g seckel’s syndrome
 Structural abnormalities e.g renal agenesis
 Intrauterine infections e.g TORCH

5.  Reduced fetal growth support is due to
 Maternal factors
 Undernourished mother
 Maternal hypoxia (high altitude, cyanotic heart
disease)
 Drugs (alcohol ,cigarettes, cocaine)
 Placental factors
 Reduced uteroplacental perfusion(inadequate
trophopblast invasion, sickle cell disease, multiple
gestations)
 Reduced fetoplacental perfusion(single umblical
artery, TTTS)

6. Risk factors of IUGR
 Multiple gestations
 History of IUGR in previous pregnancies
 Current heavy smokers
 Current drug users
 Pregnancies where SFH is less than expected
 Women with underlying disorders (HTN ,Diabetes,
cyanotic heart disease, Antiphospholipid
syndrome)

8. Classification of IUGR
 Symmetrical
Symmetrically small fetuses are normally associated
with factors that directly impair growth e.g
chromosomal abnormalities and infections
 Asymmetrical
It is associated with uteroplacental insufficiency
which leads to reduced oxygenation to fetus and
impaired excretion of carbon dioxide leads to
hypoxia and growth asymmetry

9.  Fetal brain ,myocardium and adrenals are adequately
perfused so they are spared of impaired growth while
kidneys, skin, liver, limbs do not grow proportionally.
 The result of these circulatory changes is an
asymmetrical fetus with brain sparing ,decrease
abdominal girth and skin thickness
 The vasoconstriction in the fetal kidneys results in
impaired urine formation and oligohydrominias
 Chronic fetal hypoxia leads to fetal acedemia both
metabolic and respiratory which leads to IUD
 IUGR fetuses are at increased risk of asphyxia during
labour due to uterine contraction which further
compromise uteroplacental circulation

10.  Antenatal fetal blood sampling shows
 Decrease glucose ,amino acids, thyroxine and
insulin levels
 Increased levels of corticosteroids and
catecholamines due to asymmetrically increased
perfusion of adrenals
 Increased erythropoetin and reticulocyes (hypoxia)

11. Management
 Detection of IUGR contains two elements
1. Accurate assessment of gestational age
o Crown rump length before 13wks + 6 days
o Head circumference between 13wks-20wks
2. Recognition of fetal smallness
o Ultrasound biometry (biparietal diameter, head
circumference, abdominal circumference and femur
length) serially at interval of 4wks but now it is
performed in high risk pregnancies

12.  USG shows whether the fetus is symmetrical or
asymmetrical
 If symmetrical IUGR with normal volume of
amniotic fluid then amniocentesis and fetal
karyotype should be offered
 Asymmetrical IUGR has relatively decreased
abdominal circumference and oligohydrominias

13.  At present there is no widely accepted treatment is present for
IUGR related to uteroplacental insufficiency
 Smoking alcohol and drug abuse should be stopped
 Nutritional supplementation of mother
 Aspirin in low dose may have a role in high risk pregnancies of
IUGR but it is not established
 When growth restriction is severe and fetus is too immature to
deliver bed rest in hospital is advised in effort to maximize
blood flow to placenta however evidence supporting this is
limited
 If fetures of acidosis and poor biophysical profile is present then
C-section should be performed otherwise wait for gestational
maturity and deliver by normal vaginal delivery
 Nutritional supplementation of mother
 Maintainance of good glycemic control and maintain
hypertension
 and other morbidities

14. Complications
 Perinatal mortality and morbidity of IUGR is 3-20%
more than normal infants
 Antepartum period
 Still births
 Oligohydrominias
 During labour
 High incidence of meconium aspiration
 Fetal distress
 Intrapartum fetal death

15. o Other IU complications include polycythemia ,
metabolic disorders
o Long term complications include
 Hypertension
 Diabetes

16. Intrauterine
death

17. Definition
 In utero death of a fetus after 20 weeks’ gestation
and birth.
 Antenatal demise occurs before labour
 Intrapartal demise occurs after the onset of labour

18. Etiology
 Unknown in 25 – 60% of cases
 Identifiable causes can be attributed to
 Maternal conditions
 Fetal conditions
 Placental conditions

19. Fetal causes
o Chromosomal anomalies
o Birth defects
o Infections
o TORCH

20. placental causes
 Placental abruption
 Cord accidents
 Placental insufficiency
 Placenta previa
 TTTS
 chorioamnionitis

21. Maternal causes
 Antiphospholipid syndrome
 Diabetes
 Hypertension
 Sle
 Trauma
 Abnormal labour
 Post term pregnancy
 thrombophilia
 Sepsis
 Cyanotic heart disease
 Epilepsy
 Severe anemia

22. Diagnosis to confirm IUD
 History and examination
Absence of fetal movements
-Gradual retrogression of the height of the uterus
- Uterine tone is diminished
- Fetal movement are not felt during palpation.
- Fetal heart sound are not audible

23.  Radiography X-ray abdomen
 Spalding sign:it usually appears after 7 days of
IUD.it shows
-overlapping of cranial bones
 USG shows
-Absent fetal movements and fetal heart activity
-oligohydrominias

25. Management
 DIC is the most serious consequence with prolong
fetal demise >2 wks resulting from release of
tissue thromboplastin from deteriorating fetal
organs
 DIC should be ruled out with appropriate labortary
testing.
 Platelet count, d-dimer, fibrinogen ,PT. If DIC is
identified immediate delivery is necessary
 If no DIC then mode of delivery may be as follows

26.  Dilatation and evacuation procedure may be
appropriate in pregnancies of <20 weeks’ gestation
 Induction of labour with oxytocin is appropriate in
pregnancies of >20 weeks
 Cessarean delivery is almost never appropriate for
dead fetus
 Counsel the patient about the loss

27.  Identify cause of death by
 Cervical/placental culture for susoected infection
 Karyotype for aneuploidy
 Maternal blood for Kleihauer-betke (peripheral
smear for suspected fetometernal bleed )