The document discusses amniotic fluid, which surrounds and protects the fetus during pregnancy. It defines amniotic fluid and describes its physiology, development, composition, volume regulation, and diagnostic/therapeutic uses. Amniotic fluid serves several roles, including allowing fetal movement and development of organ systems. Its volume is regulated through pathways like fetal urination, lung fluid production, and transfer across membranes. Abnormalities in volume can indicate fetal or placental issues and affect pregnancy outcomes.

1. AMNIOTIC FLUID

2. CONTENTS
•Definition
•Introduction
•Physiology of amniotic fluid
•Sonographic Assessment
•Abnormalities of amniotic
fluid
•Uses – Diagnostic /
Therapeutic

3. Definition
•Amniotic fluid is a clear, yellowish liquid that
surrounds and protects the unborn baby (fetus)
during pregnancy. It is contained in the amniotic
sac.

4. • Amniotic fluid serves several roles during pregnancy.
• It creates a physical space for fetal movement, which is necessary for
normal musculoskeletal development.
• It permits fetal swallowing—essential for gastrointestinal tract
development and fetal breathing—necessary for lung development.
• Amniotic fluid guards against umbilical cord compression and
protects the fetus from trauma.
• It even has bacteriostatic properties.
• Amnionic fluid volume abnormalities may reflect a problem with fluid
production or its circulation, such as underlying fetal or placental
pathology.
• These volume extremes may be associated with increased risks for
adverse pregnancy outcome.

5. DEVELOPMENT
•Along with the changes in the trophoblast, on the 8th day, the
embryoblast differentiates into bilaminar germ disc which consists of
dorsal ectodermal layer of tall columnar cells and ventral endodermal
layer of flattened polyhedral cells.
•The bilaminar germ disc is connected with the trophoblast by
mesenchymal condensation, called connecting stalk or body stalk
which later on forms the umbilical cord .

6. Two cavities appear one on each side of the germ disc.
1) On 12th postovulatory day, a fluid filled space appears between the
ectodermal layer and the cytotrophoblast which is called amniotic
cavity.
•Its floor is formed by the ectoderm and the rest of its wall by
primitive mesenchyme.
2) The yolk sac appear on the ventral aspect of the bilaminar disk and
is lined externally by the primitive mesenchyme and internally by the
migrating endodermal cells from the endodermal layer of the germ
disc

8. • Amniogenic cells line the inner surface of trophoblast
• Derived from fetal ectoderm of the embryonic disc
• Fluid accumulates slowly at first, but ultimately the fluid-filled cavity
becomes large enough to obliterate the chorionic cavity;the amnion and the
chorion come in loose contact by their mesenchymal layers.

9. • Initially, the cavity is located on the dorsal surface of the embryonic
disk. Which surrounds the fetus.
• Thus, the liquor amnii surrounds the fetus everywhere except
at its attachment with the body stalk.
• The amnion is firmly attached to the umbilical cord up to its point
of insertion to the placenta, but everywhere it can be separated
from the underlying chorion.

10. Physiology of amniotic fluid
• The maintenance of amniotic fluid is a dynamic process throughout pregnancy,
with differing origins for the amniotic fluid at advancing gestational age.
• Early in pregnancy, the amnionic cavity is filled with fluid that is similar in
composition to extracellular fluid.
• During the first half of pregnancy, transfer of water and other small molecules
takes place across the amnion—transmembranous flow, across the fetal vessels
on placental surface—intramembranous flow and across fetal skin.
• Fetal urine production begins between 8 and 11 weeks, but it does not become
a major component of amnionic fluid until the second trimester.

11. • Water transport across the fetal skin continues until keratinization occurs at
22 to 25 weeks.
• This explains why extremely preterm infants can
experience significant fluid loss across their skin.

12. • With advancing gestation, four pathways play a major role in
amnionic fluid volume regulation
• First, fetal urination is the primary amnionic fluid source by the
second half of pregnancy.
• By term, fetal urine production may exceed 1 liter per day—such
that the entire amnionic fluid volume is recirculated on a daily
basis.
• Fetal urine osmolality is significantly hypotonic to that of
maternal and fetal plasma and similar to that of amnionic fluid.
• Specifically, the osmolality of maternal and fetal plasma is
approximately 280 mOsm/L, whereas that of amnionic fluid is
about 260 mOsm/L.

13. •This hypotonicity of fetal urine—and thus of amnionic
fluid— accounts for significant intramembranous fluid
transfer across and into fetal vessels on the placental
surface and thus into the fetus.
•This transfer reaches 400 mL per day and is a second
regulator of fluid volume.
•In the setting of maternal dehydration, the resultant
increase in maternal osmolality favors fluid transfer
from the fetus to the mother, and then from the amnionic
fluid compartment into the fetus.

14. •An important third source of amnionic fluid regulation is
the respiratory tract.
•Approximately 350 mL of lung fluid is produced daily late
in gestation
•The other pathways—transmembranous flow and flow
across the fetal skin—account for a far smaller proportion
of fluid transport in the second half of pregnancy.

15. Amnionic Fluid Volume Regulation in Late
Pregnancy
• Pathway Effect
onVolume
Approximate Daily
Volume
(mL)
• Fetal urination Production 1000
• Fetal swallowing Resorption 750
• Fetal lung fluid secretion
• Intramembranous flow across
Production 350
fetal vessels on the placental
surface
• Transmembranous flow across
Resorption 400
amnionic membrane Resorption Minimal

17. Intermembranous & transmembranous
pathways
▪As a further pathway, rapid movements of both water and
solute occur between amniotic fluid and fetal blood
within the placenta and membranes; this is referred to as
the intramembranous pathway.
▪Movement of water and solute between amniotic fluid
and maternal blood within the wall of the uterus is an
exchange through the transmembranous pathway

18. Regulatory mechanisms act at three levels
•Placental control of water and solute transfer.
• Regulation of inflows and outflows from the fetus: fetal urine
flow and composition are modulated by vasopressin,
aldosterone, and angiotensin II in much the same way as they in
adults.
• Maternal effect on fetal fluid balance: during pregnancy, there is
a strong relationship between maternal plasma volume and
AFV,

19. Normal amnionic fluid volume
• Amnionic fluid volume increases from approximately 30 mL at 10
weeks to 200 mL by 16 weeks and reaches 800 mL by the mid-third
trimester.
• A full-term fetus contains roughly 2800 mL of water, and the placenta
another 400 mL, such that the term uterus holds nearly 4 liters of water

20. Characteristics of amniotic fluid
• Water content and osmolality: at first trimester, amniotic fluid
has an electrolyte composition and osmolality similar to that of
fetal and maternal blood.
• As fetal urine begins to enter the amniotic cavity, amniotic
fluid osmolality decreases compared with fetal blood.
• At term it contains 99% water.

21. • The fluid is faintly alkaline with low specific gravity of
1.010. It becomes highly hypotonic to maternal serum at
term pregnancy

22. • Colour: In early pregnancy, it is colorless but near term it becomes
pale straw colored due to the presence of exfoliated lanugo and
epidermal cells from the fetal skin.
• It may look turbid due to the presence of vernix caseosa.
• Abnormal color: has got clinical significance
• Meconium stained (green) is suggestive of fetal distress in
presentations other than the breech or transverse.
• Depending upon the degree and duration of the distress, it may be
thin or thick or pea souped (thick with flakes).
• Thick with presence of flakes suggests chronic fetal distress.

23. •Golden color in Rh incompatibility is due to excessive
hemolysis of the fetal RBC and production of excess
bilirubin.
•Greenish yellow (saffron) in post maturity.
•Dark colored in concealed accidental hemorrhage
is due to contamination of blood.
•Dark brown (tobacco juice) amniotic fluid is found in
IUD.

24. Constituents of the fluid: In early pregnancy , amniotic fluid is
an ultra filtrate of maternal plasma.
By the beginning of second trimester , it consist largely of
extracellular fluid which diffuse through the fetal skin and therefore
reflects the composition of fetal plasma it contains:
a- Organic, inorganic and cellular constituent.
b- It contains traces of steroid and non-steroid hormones.
c- It’s mildly bacteriostatic.

25. Composition
Organic constituents -
• Proteins-0.3 mg/dl
• Glucose- 20mg/dl
• Urea- 30 mg/dl
• Non protein nitrogen-30mg/dl
• Uric acid – 4 mg/dl
• Creatinine -2 mg/dl
• Lipids- 50 mg/ dl
• Hormones- insulin,prolactin, renin
Inorganic constituents - Na, K,Cl
Suspended particles - Lanugo,Desqamated fetal skin cells,vernix
caseosa,shedded amniotic cells, cells from the respiratory tract, GIT
Genitourinary tract

26. Function of amniotic fluid
During pregnancy:
• Act as a shock absorber to protect the fetus from external
injury
• Maintains the fetal temprature
• Allows free movement and growth of fetus
• Prevents adhesion formation between the fetal parts and the
amniotic sac
• Has some nutritive value because of small amount of
protein and salt content

27. During Labour:
• It forms hydrostatic wedge to help dilatation of cervix
• During uterine contractions , the amniotic fluid in the intact
membranes prevents interference with placental circulation
• Provides pool for the fetus to excrete urine
• Protect the fetus from the ascending infections by its bactercidal
action

28. Measurement
• From a practical standpoint, the actual volume of amnionic fluid is rarely
measured outside of the research setting.
• That said, direct measurement and dye-dilution methods of fluid quantification
have contributed to an understanding of normal physiology.
• These measurements have further been used to validate sonographic fluid
assessment techniques.
• The dye-dilution method involves injection of a small quantity of a dye such as
aminohippurate into the amnionic cavity under sonographic guidance.
• The amnionic fluid is then sampled to determine the dye concentration and hence
to calculate the fluid volume in which it was diluted.

30. Oligohydroamnios
• This is an abnormally decreased amount of amnionic fluid.
• Oligohydramnios complicates approximately 1 to 2 percent
of pregnancies.
• Oligohydramnios is a cause for concern. When no measurable
pocket of amnionic fluid is identified, the term anhydramnios may
be used.
• The sonographic diagnosis of oligohydramnios is usually based
on an AFI ≤ 5 cm

31. Causes
1- Preterm premature rapture of membrane
2- Post maturity.
3- Placental insufficiency or intrauterine growth restriction.
4- Fetal causes: a reduction in the production of amniotic fluid in the second and
third trimester is mediated primarily through a reduced or absent fetal urine
output.
• This is in turn is the consequence of an abnormality in fetal urinary tract like:
• - Renal agenesis.
• - Bladder outlet obstruction.
• - Renal dysplasia
• - Polycystic or multicystic kidney disease.

32. •Fetal chromosomal anomalies
•Intrauterine infections

33. Medication
• Oligohydramnios has been associated with exposure to drugs that
block the renin-angiotensin system.
• These include angiotensin-converting enzyme (ACE) inhibitors and
nonsteroidal antiinflammatory drugs (NSAIDs). When taken in the
second, third trimester, ACE inhibitors and angiotensin-receptor
blockers may create fetal hypotension, renal hypoperfusion.
• NSAIDs have been associated with decreased fetal urine production. In
neonates, their use may result in acute and chronic renal insufficiency.

34. Oligohydramnios complication
▪ Midtrimester PROM often leads to pulmonary hypoplasia, fetal
compression syndrome and amniotic band syndrome.
▪ Oligohydramnios is a frequent finding in pregnancies involving IUGR and is
most likely secondary to decreased fetal blood volume, renal blood flow and fetal
urine output.
▪ AFV is an important predictor of fetal well-being in pregnancies
beyond 40 weeks gestation
▪ AFV is a predictor of the fetal tolerance of labor

35. • If there is bilateral renal agenesis, no urine is produced, and the
resulting anhydramnios leads to limb contractures, a distinctively
compressed face and death from pulmonary hypoplasia
• When this combination of abnormalities results from renal agenesis, it is
called Potter syndrome.
• When this constellation stems from another etiology of decreased
amnionic fluid volume, it is generally called Potter sequence.

36. Pulmonary Hypoplasia
• When decreased amnionic fluid is first identified before the midsecond
trimester, particularly before 20 to 22 weeks, pulmonary hypoplasia is a
significant concern.
• The underlying etiology is a major factor in the prognosis for such
pregnancies.
• Severe oligohydramnios secondary to a renal abnormality generally has a
lethal prognosis.
• If a placental hematoma or chronic abruption is severe enough to result in
oligohydramnios—the chronic abruption-oligohydramnios sequence—it
commonly also causes growth restriction.
• The prognosis for this constellation is similarly poor.

37. Management
●Adequate rest – decreases dehydration
●Hydration– Oral/IV Hypotonic fluids(2
Lit/d) temporary increase helpful during
labour

38. AMNIOINFUSION
•Transvaginal amnioinfusion has been extended into three clinical areas.
•These include:
(1) treatment of variable or prolonged decelerations,
(2) prophylaxis for women with oligohydramnios, as with prolonged ruptured
membranes and
(3) attempts to dilute or wash out thick meconium

39. L – Arginine
•L-arginine is a versatile amino acid with a wide range of biological
functions.
•It serves as a precursor not only to proteins but also nitric oxide which has
been identified as endothelium- derived relaxing factor.

40. •L-arginine increases uteroplacental blood flow through nitric oxide mediated
dilatation of vessels thereby increasing the supply of nutrients to the fetus aiding
its growth.
•L-Arginine improves uteroplacental blood flow to overcome placental
ischemia by increasing Nitric oxide.
•This results in vasodilation of uterine arteries.

42. Oral therapy with 3 g of Arginine daily was given as a supplement to standard therapy.
•The results
-L arginine treatment accelerated fetal weight gain and
-improved biophysical profile.
It was concluded that supplementary treatment with oral ARG seems to be
 promising in improving
- foetal well-being
-neonatal outcome
- prolonging pregnancy complicated with pre-eclampsia & Oligohydramnios.

44. Polyhydramnios
Definition :
It means excessive amniotic fluid, more than 2 liters. By ultrasound the
vertical diameter of the largest pocket of amniotic fluid measure 8 cm or
more, or the amniotic fluid index (AFI) is 25 cm or more.
It can be classified into :
1 Mild
2 Moderate
3 Severe
Incidence : 1 – 2 % of all pregnancies.

45. •Mild hydramnios is the most common, comprising approximately two
thirds of cases.
•Moderate hydramnios accounts for about 20 percent, and severe
hydramnios approximately 15 percent.

46. •Common underlying causes of hydramnios include fetal congenital anomalies
in approximately 15 percent and diabetes in 15 to 20 percent
•Congenital infection and red blood cell alloimmunization are less frequent
reasons.
•Infections that may present with hydramnios include
cytomegalovirus, toxoplasmosis, syphilis and parvovirus

47. •The underlying pathophysiology in such cases is complex but is
frequently related to a high cardiac-output state.
•Severe fetal anemia is the classic example. Because the etiologies of
hydramnios are so varied, hydramnios treatment also varies and is
tailored in most cases to the underlying cause.

48. Diabetes Mellitus
•The amnionic fluid glucose concentration is higher in diabetic women than
in those without diabetes, and the amnionic fluid index may correlate with
the amnionic fluid glucose concentration.
•Such findings support the hypothesis that maternal hyperglycemia causes
fetal hyperglycemia, with resulting fetal osmotic diuresis into the amnionic
fluid compartment.

49. Congenital Anomalies
•Severe central nervous system abnormalities, can result in hydramnios
due to impaired fetal swallowing.
•Fetal neuromuscular disorders such as myotonic dystrophy also may lead
to excessive amnionic fluid.
•Obstruction of the fetal upper gastrointestinal tract—esophageal or
duodenal atresia—is often associated with hydramnios.

50. Polyhydramnios causes
▪ Maternal
hyperglycemia
▪ GIT
anomalies(obstructi
ve)
▫ Esophageal atresia
▫ Tracheoesophageal
fistula
▫ Duodenal atresia
▪ Nonimmune
hydrops
▪ CNS anomalies
▫ Anencephaly
▫ Open spina bifida
▪ Thoracic
malformations
▫ Diaphragmatic
hernia
▪ Congenital
infections
▫ Syphilis, hepatitis
▪ Chromosomal
anomalies
▪ High output Cardiac
failure
▫ Fetal anemia
▫ Sacrococcygeal
teratoma
▫ chorioangioma
▪ Fetal polyuria
▫ Fetal
pseudohyperaldosteronis
m
▫ Fetal bartter
▫ Nephrogenic diabetes
insipidus
▪ Placental
chorioangioma
▪ Maternal substance
abuse

51. CLINICAL TYPES
Depending on the rapidity of onset, hydramnios may be:
(a) Chronic (most common) — onset is insidious taking few weeks.
(b) Acute (extremely rare) — onset is sudden, within few days or may appear
acutely on pre-existing chronic variety.
•The chronic variety is 10 times commoner than the acute one.

52. ▪ The diagnostic approach to polyhydramnios consists of
(1)physical examination of the mother with an investigation for
diabetes mellitus, diabetes insipidus and Rh isoimmunization;
(2)sonographic confirmation of polyhydramnios and assessment of the
fetus;
(3) fetal karyotyping; and
(4) maternal serologic testing for syphilis.

53. Management
•Routine health care
•History suggestive of Rh iso- immunization such as still birth, fetal hydrops,
jaundice in new born requiring exchange transfusion etc.
•History suggestive of DM – Previous big baby fetal death at 35 weeks, classical
symptoms of DM like polyurea, polydypsia, polyphagia
•History of Drug intake especially in First trimester
•History of Previous fetal anomalies like Anencephaly-risk of recurrence is 2%

54. •Management
•As noted previously, hydramnios etiologies are varied and treatment is
directed in most situations to the underlying cause.
•Occasionally, severe hydramnios may result in early preterm labor or the
development of maternal respiratory compromise.
•In such cases, large-volume amniocentesis—termed amnioreduction—may be
needed.
•However, either an evacuated container bottle or a larger syringe is
connected to the needle via sterile intravenous tubing with a stopcock.
•In general, approximately 1000 to 1500 mL of fluid is slowly
withdrawn during approximately 30 minutes, depending on the severity
of hydramnios and gestational age.

55. •Importantly, amnioreduction is typically performed later in gestation
and carries additional risks of membrane rupture, preterm labor or its
exacerbation and placental abruption.

56. Amniotic fluid testing
 Chromosome and DNA analysis
 Biochemistry
 Fetal infections
 Rh disease and other alloimmunisation
 Lung maturity
 Chorioamnionitis
 Obstetric cholestasis
 Fetal therapy-decompression
severe oligohydramnios
multifetal pregnancy
reduction throxine therapy