The document discusses amniotic fluid disorders. It provides information on: 1. The normal functions and composition of amniotic fluid, which cushions the fetus and allows for growth and development. 2. Clinical conditions related to abnormal amniotic fluid levels, including polyhydramnios (excess fluid) and oligohydramnios (low fluid). 3. Causes, diagnosis, and management of polyhydramnios and oligohydramnios. Polyhydramnios can be caused by fetal anomalies or diabetes and managed with bed rest or induction. Oligohydramnios can affect lung development and be caused by renal issues.

1. AMNIOTIC FLUID DISORDERS
Dr. Abdela Kumbi,MD,Obstetricianand Gynecologist

2. Amnionic Fluid
 In early pregnancy, amnionic fluid is an ultrafiltrate of maternal plasma.
 In second trimester, it consists largely of extracellular fluid that diffuses through the fetal skin
 After 20 weeks, however, the cornification of fetal skin prevents this diffusion, and amnionic
fluid is composed largely offetal urine.
 The fetal kidneys start producing urine at 12 weeks, and by 18 weeks they are producing 7 to
14 mL per day.
 Pulmonary fluid contributes a small proportion of the amnionic volume, and fluid filtering
through the placenta accounts for the rest.
 The volume increases by 10 mL per week at 8 weeks and increases up to 60 mL per week at 21
weeks, then declines gradually back to a steady state by 33 weeks.

3. Function of amniotic fluid
 Protecting the fetus: The fluid cushions the baby from outside pressures, acting as a shock
absorber.
 Temperature control: The fluid insulates the baby, keeping it warm and maintaining a regular
temperature.
 Infection control: The amniotic fluid containsantibodies.
 Lung and digestive system development
 Allow room for fetal growth, movement and development
 Lubrication Amniotic fluid prevents parts of the body such as the fingers and toes from
growing together; webbing can occur if amnioticfluid levelsare low.
 Umbilical cord support: prevent compression ofcord
 Ingestion into GIT→ growth and maturation.
 Aids dilatation of the cervix during labour.

4. Clinical importance of AF
 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).

5. Volume and composition
 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 intoAF.
 Fetal respiratory tract secretes 250ml/dayinto AF.
 Fluid transfers across the placenta.
 Fetal oro-nasal secretions.

6. Amniotic fluid
 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….

7. Amniotic fluid volume
 Amniotic fluid volume :
 About 500 mls enter and leave the amnioticsac each hour.
 Gradual increase up to 36 weeks to around 600 to 1000 ml then decrease.
 The normal range is wide but the approximate volumes are: - 500 ml at 18 weeks - 800 ml
at 34 weeks. - 600 ml at term.
 Amniotic fluid volume assessment:
 Amniotic fluid index (AFI):
 It is a total of the deepest vertical pool DVPs in each four quadrants of the uterus.
 It is a more sensitive indicator of AFV throughout pregnancy.
 AFI ranges between 8 and 24 cm
 largest vertical pocket of amniotic fluid: normal range is 2 to 8 cm

8. Polyhydramnios (Hydramnios)
 Definition:
 Polyhydramnios is defined asa state where liquor amnii exceeds2,000 mL
 Amniotic fluid index (AFI) is more than 24 cm (more than 95th centile for gestational age)
 Deepest vertical pocket (DVP) is more than 8 cm.
 Incidence:
 Varies from 1–2% of cases
 Hydramnios sufficient to produce clinical symptoms probably occurs in 1 in 1,000
pregnancies

9. Classificationof Polyhydramnios
 Clinical type of polyhydramnios:
 Acute polyhyramnios
 Chronic polyhydramnios
 Types based on Ultrasound:
 Mild hydramnios:
 Defined as pockets measuring 8 to 11 cm in vertical dimensionwas
 Present in 80 percent ofcases with excessive fluid.
 Moderate hydramnios:
 defined as a pocket containing only small parts and measuring 12 to 15 cm deep
 Present in 15 percent
 Severe hydramnios: Present in 5 percent
 Defined by a free-floatingfetus found in pockets of fluid of 16 cm or greater.

10. Etiologyof polyhydramnios
 Fetal anomalies:are associated with polyhydramnios in about 20% cases.
 Anencephaly:
 In about 50% cases
 The causes of excessive production of liquor amnii may be due to:
 Transudationfrom the exposed meninges
 Absence of fetal swallowing reflex and
 Possible suppression of fetal antidiuretic hormone leadingto excessiveurination.
 Open spina bifida: increasedtransudation from the meninges.
 Esophageal orduodenal atresia:preventingswallowing of the liquor.
 Facial clefts and neck masses:by interfering normal swallowing.
 Hydrops fetalis due to Rhesus isoimmunization, nonimmune hydrops, cardiothoracic
anomalies, fetal cirrhosisand fetal infections with TORCH and parvovirusB19 infection
are often associated with hydramnios.
 Aneuploidy and genetic syndromes

11. Etiologyof polyhydramnios
 Placenta:
 Chorioangioma of the placenta: Tumor growing from a single villus consisting of
hyperplasia of blood vessels and connective tissue results in increased transudation.
 Multiple pregnancy:
 10 times more common than its overall incidence.
 More common in monozygotic twins
 Maternal:
 Diabetes: in about 30% cases
 It is presumed that a raised maternal blood sugar → raised fetal blood sugar → fetal
diuresis → hydramnios.
 Cardiac or renal disease: may lead to edema of the placenta leading to increase in
transudation.
 Idiopathic: 50–60%

12. Chronic polyhydramnios
 Gradual accumulationof liquor
 Symptoms:
 The patient may suffer from dyspnea or even remain in the sitting position for easier
breathing.
 Palpitation
 Edema of the legs, varicosities in the legs or vulva and hemorrhoids.
 Signs:
 The patient may be in a dyspneic state in the lying down position.
 Evidence of preeclampsia (edema, hypertension and proteinuria)may be present.

13. Chronic polyhydramnios
 Abdominal examination:
 Abdomen is markedly enlarged, looks globular with fullness at the flanks.
 The skin is tense, shiny with large striae.
 Height of the uterus is more than the period of amenorrhea.
 Girth of the abdomen round the umbilicusis more than normal
 Fluid thrill can be elicited inall directions over the uterus.
 Fetal parts cannot be well-defined; so also the presentation or the position. External
ballottement canbe elicited more easily
 Fetal heart sound is not heard distinctly
 GUS: The cervix is pulled up, may be partially taken up or at times, dilated, to admit a
fingertipthrough which tense bulged membranes can be felt.

14. Chronic polyhdramnios
 Investigation:
 Sonography:
 largest vertical pocket more than 8 cm
 Amniotic fluid index (AFI) is more than 25 cm
 To exclude multiple fetuses
 To note the lie and presentation of the fetus
 To diagnose any fetal congenital malformation.
 Blood: ABO and Rh grouping: Rhesus isoimmunization may cause hydrops fetalis and
fetal ascites.
 Postprandial sugar and if necessary glucosetolerance test.
 Amniotic fluid: Estimation of alpha fetoprotein which is markedly elevated in the presence
of a fetus with an open neural tube defect.

15. Differential diagnosisof polyhydramnios
 Twins pregnancy
 Abdomen is markedly enlarged
 Multiple palpable fetal parts
 Fluid thrill absent
 Sonography confirms the diagnosis.
 Pregnancy with huge ovarian cyst
 The gravid uterus can be felt separatefrom the cyst
 Abdomen sonography
 Maternal ascites: Presence of shifting dullness
 Resonance on the midline
 Sonography helps to excludepregnancy.
 Fetal Macrosomia

16. Complicationof polyhydramnios
 Maternal:
 During pregnancy:
 Preeclampsia(25%)
 Malpresentationand persistence of floatinghead
 Premature rupture of the membranes
 Preterm labor eitherspontaneous or induced
 Accidental hemorrhage due to decreasein the surface area of the emptying uterus
beneath theplacenta, followingsudden escape of liquor amnii.
 During labor: Early rupture of the membranes
 Cord prolapse
 Increasedoperativedeliverydue to malpresentation
 Uterine inertia and Retained placenta, postpartum hemorrhage and shock.

17. Complicationof polyhydramnios
 Puerperium:
 Subinvolution
 Increased puerperal morbidity due to infection resulting from increased operative
interference and blood loss.
 Fetal:
 There is increased perinatal mortality to the extent of about 50% due to prematurity and
congenital abnormality (40%). Other contributing factors are cord prolapse, hydrops
fetalis, effects of increased operative delivery and accidental hemorrhage.

18. Management of polyhydramnios
 Mild polyhydramnios: (DVP: 8–11 cm): It is commonly found in midtrimester and
usually requires no treatment, except extra bed rest for a few days.
 Severe polyhydramnios:DVP: ≥16 cm):
 To relieve the symptoms
 To find out the cause and treat associated condition like preeclampsia or diabetes
on the usual line.
 Supportive therapy includes bed rest, if necessary, with a back rest Sulindac (COX-
2 inhibitor), 200 mg every 12 hours, (under supervision) has been found to be most
effective in unexplained cases. It has been found to decrease amniotic fluid as it
reduces fetal urine output.

19. Management of polyhydramnios
 Further management depends on:
 Response to treatment and Period of gestation
 Presence of fetal malformation
 Associated complicating factors
 Uncomplicatedpolyhdramnios:
 The pregnancy is to be continuedawaiting spontaneousdelivery at term.
 Pregnancy less than 37 weeks(with maternal distress):
 An attempt is made to relieve the distress with a hope of continuation of pregnancy by
amniocentesis (amnio reduction.
 Slow decompression is done at the rate of about 500 mL per hour and the amount of
fluid to be removed should be sufficient enough to relievethe mechanical distress.
 Normally amniodrainage is stopped when the AFI is less than 25 cm.
 Pregnancy more than 37 weeks: Induction of labor is done

20. Management of polyhydramnios
 Polyhydramnios with congenital fetalabnormality:
 Termination to be done irrespectiveof duration of pregnancy.
 Amniocentesis is done to drain good amount of liquor.
 Induction by vaginal PGE2 gel insertion followed by low rupture of membranes is done
and oxytocin infusion may be started.

21. Acute polyhydramnios
 The onset is acute and the fluid accumulateswithin a few days.
 It usuallyoccurs before 20 weeks of pregnancy.
 It is usually associated with monozygotictwins with TTTS or chorioangioma of the placenta.
 Clinical features:
 Abdominal pain, nausea and vomiting.
 The patient looks ill
 Absence of featuresof shock
 Edema of the legs or presence ofother associatedfeaturesof preeclampsia
 Abdomen is hugely enlargedmore than the period of amenorrhea;the wall is tense with
shiny skin
 Fluid thrill is present
 Fetal parts cannot be felt nor is the fetal heart sound audible

22. Acute polyhydramnios
 Investigation: Sonography shows multiple fetuses or at times fetal abnormalities.
 Treatment:
 Most often, spontaneousabortion occurs.
 Severe TTTS, repetitive amnioreduction until the AFI is normal, may improve the
perinatal outcome.
 Laser ablation may cure the cause of TTTS whereas amnioreduction only treats the
symptoms

23. Oligohydramnios
 Definition:
 A condition where the liquor amnii is deficient in amount to the extent of less than 200 mL
at term.
 It is defined when the maximum vertical pocket of liquor is less than <2 cm
 When amniotic fluid index (AFI) is less than 5 cm (less than 5 percentile).
 Absence of any measurable pocket of amniotic fluid is defined as Anhydramnios.
 Incidence: between 1 to 3 percent.

24. Etiology
 Fetal conditions:
 Fetal chromosomal or structural anomalies
 Renal agenesis
 Obstructed uropathy
 Spontaneousrupture of the membrane
 Intrauterine infection
 Drugs: PG inhibitors, ACE inhibitors
 Postmaturity
 IUGR
 Amnion nodosum (failure of secretionby the cells of the amnion covering theplacenta).

25. Etiology
 Maternal conditions:
 Hypertensivedisorders
 Uteroplacental insufficiency
 Dehydration
 Idiopathic.

26. Diagnosis
 Uterine size is much smaller than the period of amenorrhea
 Less fetal movements
 The uterus is “full of fetus” because of scanty liquor
 Malpresentation(breech) is common
 Evidencesof intrauterine growth retardation ofthe fetus
 Sonographic diagnosisis made when largest liquor pool is less than 2 cm.
 Ultrasound visualization is done following amnioinfusion of300
 mL of warm saline solution
 Visualization of normal filling and emptying of fetal bladder essentially rules out urinary tract
abnormality.
 Oligohydramnioswith fetal symmetric growth restriction is
 associatedwith increased chromosomal abnormality

27. Complications
 Fetal:
 Abortion
 Deformity due to intra-amniotic adhesions or due to compression which includes alteration
in shape of the skull, wry neck, club foot, or even amputation ofthe limb
 Fetal pulmonary hypoplasia
 Cord compression
 High fetal mortality
 Maternal:
 Prolonged labor due to inertia
 Increasedoperativeinterference due to malpresentation.
 Increasedmaternal morbidity.

28. Treatment
 When decision for delivery is made, it should be done irrespective of the period of gestation.
 Isolated oligohydramnios in the third trimester with a normal fetus may be managed
conservatively.
 Oral administration of water increases amniotic fluid volume.
 In labor, cord compression is common.
 Amnioinfusion (prophylactic or therapeutic) for meconium liquor is found to improve neonatal
outcome.

29. Thank You