Intrauterine growth restriction

Definition Fetus with estimated fetal weight less than 10

percentile for gestational age

Aetiology On etiological basis IUGR can occur due to

Reduced fetal growth potential Reduced fetal growth support

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

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)

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)

Classification of IUGR SymmetricalSymmetrically 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

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

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)

Management Detection of IUGR contains two elements1. Accurate assessment of gestational ageo Crown rump length before 13wks + 6 dayso Head circumference between 13wks-20wks2. Recognition of fetal smallnesso 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

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

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

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

o Other IU complications include polycythemia , metabolic disorders

o Long term complications include Hypertension Diabetes

Intrauterine death

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

Etiology

Unknown in 25 – 60% of cases

Identifiable causes can be attributed to Maternal conditions

Fetal conditions

Placental conditions

Fetal causes o Chromosomal anomalieso Birth defectso Infectionso TORCH

placental causes Placental abruption Cord accidents Placental insufficiency Placenta previa TTTS chorioamnionitis

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

Diagnosis to confirm IUD History and examinationAbsence 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

Radiography X-ray abdomen Spalding sign:it usually appears after 7 days of

IUD.it shows -overlapping of cranial bonesUSG shows-Absent fetal movements and fetal heart activity-oligohydrominias

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

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

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 )

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