Definition EFW <10th percentile for gestational age or an AC <10th percentile for gestational age . Fetal cell growth has 3 phases Hyperplasia – till 16weeks, growth rate of 5gm/day Hyperplasia and hypertophy – till 32 weeks , 15gm/day Hypertrophy – after 32 weeks, 30gm/ day (most fetal fat and glycogen accumulate)
Etiologies Maternal - by affecting nutrient and oxygen delivery to the placenta Placental - by affecting nutrient and oxygen transfer across the placenta Fetal - by affecting nutrient uptake or regulation of growth processes (fetal causes)
Fetal factors Teratogenic exposure Fetal infection – TORCH infection Genetic disorders- aneuploidy and syndromes Structural abnormalities Chromosomal abnormalities, congenital malformations, and genetic syndromes have been associated with less than 10% of cases of FGR . Intrauterine infection also accounts for less than 10% of all cases.
Long term Assymetric will have catch up growth after birth Cerebral palsy Increased risk of metabolic syndrome, DM, obesity, hypertension
Amniotic fluid disorder
The main source of amniotic fluid is fetal urine (1 to 1.2l/day). The other source being lung liquid ( fetal sheep 400ml/day)- (50% swallow and 50%to fluid) AF removal – swallowing, intramembranous absorption During the first trimester, AF is isotonic with maternal plasma but contains minimal protein. It is thought that the fluid arises either from a transudate of fetal plasma through non keratinized fetal skin, or maternal plasma across the uterine decidua and/or placenta surface . Thus, fetuses with renal agenesis may demonstrate normal first - trimester AF volumes.
HOW IS IT MEASURED? (TECNIQUES? perpendicular to floor or uterine contour Don’t angle Transverse dimaeter needs to be atleast 1cm better use sdp when afv is decreased and afi when afv is increased
Oligohydraminous rates vary between 1% and 3 %. MVP less than 2 cm or an AFI of 5 cm or less are commonly used as criteria for the diagnosis Fetal Conditions Renal agenesis and Obstructed uropathy - responsible for 51% of oligo in 2 nd trimester Spontaneous rupture of the membranes - 34% in 2 nd trimester Premature rupture of the membranes Abnormal placentation Prolonged pregnancy Severe intrauterine growth restriction – 5% in 2 nd trimester Maternal Conditions Dehydration-hypovolemia Hypertensive disorders Uteroplacental insufficiency Antiphospholipid syndrome TORCH and Parvovirus are ncommon but may occur in 2 nd and 3rd
Oligo is suspected when t present with SGA uterus or PROM When the diagnosis of oligohydramnios is made in the second trimester, perform a targeted ultrasound to help identify a cause After diagnosis on us Look for anomaly Markers of aneuploidy(single UA, echogenic intracardiac focus, choroid plexus cyst, short long bones, echogenic bowels, thick nuchal fold) FGR Placental abnormalities genetic test If fetal anomalies are detected
Amnioinfusion Vesicoamniotic shunt to prevent adverse pulmonary, orthopedic and renal sequele Therapeutic oral hydration
MX Renal causes of oligo – multidisplinary team nds tobe involved () pediatric nephrologist…) Idiopathic oligo has better prognosis Do NST once or twice weekly till birth Monitor growth q 3 to 4weeks Idiopathic oligo terminate 36 – 37+6wks If there is underlyng cause , time of delivery depends on the causes Intrapartum use ctg and consider amnioinfusion for oligo anf variable deceleration
Polyhydraminous The incidence of polyhydramnios is 1% to 2%. MVP of 8 cm and above , whereas others use an AFI of 25 cm or above. Severe polyhydramnios in the second trimester has a significant PMR due to prematurity or aneuploidy. mild (MVP 8 to 11 cm, AFI 24-25 79% of cases), moderate (MVP 12 to 15 cm,AFI 30-34. 16.5%), and severe (MVP ≥16 cm(AFI of 35 or more) 5%). A specific cause was identified in only 16% of the pregnancies with mild, 90% with moderate, and 100% with severe polyhydramnios. even when fetal anomalies and maternal diabetes are excluded, the perinatal morbidity and mortality rates are still increased compared with patients whose AVF is normal.
After dignosis Look for congenital anomaly Check hydrops Do MCA PSV if < 35weeks – look for anemia Amniocentesis for genetic studies (in those with structural diss and may be also in svr poly) Screen for DM
If the underlying cause is known then the management is guided by the causes In severe symptomatic polyhydraminous , management of maternal symptom is the similar to that for patients with idiopathic polyhydraminous Fetal surveilance (Q 2weeks followed by q1 week after 37 weeks for mild to moderate one). Weekly for sever one till birth
Severe abdominal discomfort and shortness of breath- do amnio reduction If preterm labor and uterine irritability (<32wks)- give indomethacine – to relieve uterine contractility and reduce amniotic fluid. Above 32 weeks nifedipine if patient has symptom and periprocedural uterine contraction give indomethacine pre or post procedure for 48hrs Svr symptomatic poly with unsuccessful amnioreduction and >34weeks consider preterm birth and makae shared decision Remove 2 to 2.5l at one time and faster than 1000ml per 20min. Terminate when AFI become 15 to 20cm or MVP <8 Mild to modertae - 39 to 40+6weeks bcs risk of fetal death increase significantly Severe at 37 weeks( prvnt , c ord prolapse and abruption if spontaneous rom occur)