The document outlines various aspects of fetal assessment, including screening for malformations, assessments of fetal well-being, and amniotic fluid measurements. It discusses maternal and placental causes of complications, risks associated with abnormalities, and potential treatments for managing conditions like hydramnios and fetal distress. Key interventions include ultrasound diagnostics, amniocentesis, and medication to adjust amniotic fluid levels.

4. • Screening for fetal malformation (serum α-fetoprotien).
• Assessment of fetal well-being (amniotic fluid index).
• Assessment of fetal lung maturity (L/S ratio).
• Diagnosis and follow up of labour.
• Diagnosis of PROM (ferning test).
PROM: Premature rupture of membranes

6. • From 20 weeks up to term (mainly fetal urine)
• At 18th week, the fetus voids 7-14ml/day; at term fetal
kidneys secretes 600-700ml of urine/day into AF.
- Fetal respiratory tract secretes 250ml/day into AF.
- Fluid transfers across the placenta.
- Fetal oro-nasal secretions.
• Secretion is controlled by:
- Fetal swallowing at term removes 500ml/day.
- Reabsorption into maternal plasma (osmotic gradient).
• AF constituents:
- urea, creatinine & uric acid + desquamated fetal
cells, vernix, lanugo hair & others→ hypo-osmolar amniotic
fluid

8. • Clinical assessment is unreliable.
• Objective assessment depends on U/S to
measure:
Deepest vertical pool (DVP) &
Amniotic fluid index (AFI)

13. • Fundal height < gestational age
• Decreased fetal movement
• Fetal Heart Rate tracing abnormality
• Diagnosis: Ultrasound

14. 2. Maternal causes:
• Uteroplacental insufficiency.
• Preeclampsia.
3. Placental causes:
• twin-twin transfusion.
4. Drug causes:
Prostaglandin synthase inhibitor as NSAID.
5. Idiopathic

15. • In early pregnancy:
• Amniotic adhesions or bands→ amputation/death.
• Pressure deformities (club feet).
• Pulmonary hypoplasia:
- Thoracic compression.
- No breathing movement.
- No amniotic fluid retain.
 Flattened face.
 Postural deformities.

16. • In late pregnancy:
• Fetal growth restriction.
• Placental abruption.
• Preterm labour.
• Fetal distress.
• Fetal death.
• Meconium aspiration.
• Labour induction/CS.

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20. The endothelium (inner lining) of blood vessels uses
nitric oxide to relax smooth muscle, thus resulting in
vasodilation and increasing blood flow

21. NO causes vasodilation &
increasing blood flow

30. • Fetal malformation: • Hydrops fetalis: congestive
- GIT: esophageal/duodenal heart failure, severe
atresia, tracheoesophageal anaemia or hypoproteinemia
fistula. → placental transudation
- CNS: anencephaly
(↓swallowing, exposed • Diabetes mellitus (osmotic
meninges, no antidiuretic diuresis).
hormone).
• Twin-twin transfusion → • Idiopathic.
fetal polyuria.

31. • Fetal prognosis worsens with more severe
hydramnios and congenital anomalies
• 15-20% fetal malformations
• Preterm delivery
• Suspect diabetes
• Prolapse of cord
• Abruption

32. • Dyspnea
• Venous Stasis
• Placental abruption
• Uterine dysfunction
• Post-partum hemorrhage
• Abnormal presentation -- C/S

33. • Minor degrees: no treatment.
• Bed rest, diuretics, water and salt restriction: ineffective.
• Hospitalization: dyspnea, abdominal pain or difficult
ambulation.
• Indomethacin therapy: .
- impairs lung liquid production/enhances absorption.
- ↓fluid movement across fetal membranes.
* Complications: premature closure of ductus
arteriosus, impairment of renal function, and cerebral
vasoconstriction.
• Amniocentesis: to relieve maternal distress and to test for fetal
lung maturity. Complications: ruptured
membrane, chorioamnionitis, placental abruption, preterm
labour.