AMNIOTIC FLUID

Presenter- Dr Swathi. P.
MS (OBG)
Moderator- Dr Omkar Murthy
SSMC Tumkur
CONTENTS:
Definition
Introduction
Physiology of amniotic fluid
Sonographic Assessment
Abnormalities of amniotic fluid
Uses Diagnostic / Therapeutic
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.
 Introduction:
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 swallowingessential for gastrointestinal tract

development, and fetal breathingnecessary 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.
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 .
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
 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.
 Initially, the cavity is located on the dorsal surface of the embryonic
disk. With the formation of the head, tail and lateral folds, it comes to
surround the fetus.

Its two growing margins finally merge into the body stalk.

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.
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 amniontransmembranous flow,
across the fetal vessels on placental surfaceintramembranous 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.
 This latter observation explains why fetuses with lethal renal
abnormalities may not manifest severe oligohydramnios until after 18
weeks.
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.
 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 daysuch 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/mL, whereas that of amnionic fluid is about 260 mOsm/L.
 This hypotonicity of fetal urineand 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 (Mann, 1996).

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.
 An important third source of amnionic fluid regulation is the respiratory
tract.

Approximately 350 mL of lung fluid is produced daily late in gestation, and

half of this is immediately swallowed.

Last, fetal swallowing is the primary mechanism for amnionic fluid

resorption and averages 500 to 1000 mL per day (Mann, 1996).

Impaired swallowing, secondary to either a central nervous system

abnormality or gastrointestinal tract obstruction, can result in an
impressive degree of hydramnios.
The other pathwaystransmembranous flow and flow across the fetal
skinaccount for a far smaller proportion of fluid transport in the second
half of pregnancy.
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 Production 350
Intramembranous flow across
fetal vessels on the placental surface Resorption 400
Transmembranous flow across
amnionic membrane Resorption Minimal

Adapted from Magann, 2011; Modena, 2004; Moore, 2010.

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
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,
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 (Brace, 1989; Magann, 1997).

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(Modena, 2004). (Williams)
 It measures about:
50 mL at 12 weeks,
400mL at 20 weeks
1 liter at 3638 weeks Thereafter the amount diminishes, till
600800 mL at term
As the pregnancy continues post term, further reduction occurs to
the extent of about 200 mL at 43 weeks.
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.
The osmolality, sodium, urea and creatinine is not significantly
different from the maternal serum.
 The osmolality is lowest at term (250-260mOsml/kg) compared with
fetal blood osmolality of 280mOsml/kg water.

This is a result of extremely hypotonic fetal urine(60-140mOsml/kg

water) in combination of lesser volume of lung fluid.

An osmolarity of 250 mOsmol/L is suggestive of fetal maturity.

The fluid is faintly alkaline with low specific gravity of 1.010. It

becomes highly hypotonic to maternal serum at term pregnancy
 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.
 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. The dark
color is due to frequent presence of old HbA
 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- Its mildly bacteriostatic.

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
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
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
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.
 Magann and colleagues (1997) used dye-dilution measurements and
found that the amnionic fluid volume continues to increase with
advancing gestation.

Specifically, the average fluid volume was approximately 400 mL

between 22 and 30 weeks, doubling thereafter to a mean of 800 mL.

The volume remained at this level until 40 weeks and then declined
by approximately 8 percent per week thereafter
 Although it is considered acceptable for an experienced examiner to
assess the amnionic fluid volume qualitatively, fluid is usually
assessed semiquantitatively (American Institute of Ultrasound in
Medicine, 2013a).

Measurements include either the single deepest vertical fluid pocket

or the sum of the deepest vertical pockets from each of four equal
uterine quadrantsthe amnionic fluid index
 Single Deepest Pocket:

This is also called the maximum vertical pocket.

The ultrasound transducer is held perpendicular to the floor and
parallel to the long axis of the pregnant woman.
In the sagittal plane, the largest vertical pocket of fluid is identified.
The fluid pocket may contain fetal parts or loops of umbilical cord,
but these are not included in the measurement.
The normal range for single deepest pocket that is most commonly
used is 2 to 8 cm, with values above and below this indicating
hydramnios and oligohydramnios, respectively.
 The fetal biophysical profile similarly uses a 2-cm single deepest
vertical pocket threshold to indicate a normal amnionic fluid volume
(American College of Obstetricians and Gynecologists, 2012).

Single vertical pocket-------------------

Measurment of AF
Measurement of AFI- quantitative method of
measurement of amniotic fluid by usg. Single
largest pocket is measured in four quadrants
and added.

Normal range is 5-24 cm

Single deepest pocket
Normal range is 2-8 cm
 Amnionic Fluid Index (AFI) - This was described by Phelan and
coworkers (1987) more than 25 years ago, and it remains one of the
most commonly used methods of amnionic fluid volume assessment.

As with the single deepest fluid pocket measurement, the ultrasound

transducer is held perpendicular to the floor and parallel to the long
axis of the pregnant woman.

The uterus is divided into four equal quadrantsthe right- and left-
upper and lower quadrants, respectively.

The AFI is the sum of the single deepest pocket from each quadrant.
 A fluid pocket may contain fetal parts or umbilical cord loops, but
these are not included in the measurement.

Color Doppler is generally used to verify that no umbilical cord is

included in the measurement.

This may result in greater consistency and in reduction of

intraobserver variation(Callen, 2008; Hill, 2003).

It has been reported, however, that color Doppler use results in a

lower AFI measurement, thus potentially leading to overdiagnosis of
oligohydramnios(Magann, 2001).
Measurement of amniotic fluid volume
Amniotic fluid index
Oligohydroamnios:
This is an abnormally decreased amount of amnionic fluid.
Oligohydramnios complicates approximately 1 to 2 percent of
pregnancies (Casey, 2000; Petrozella, 2011).
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 or on a single deepest pocket of amnionic fluid 2 cm
(American College of Obstetricians and Gynecologists, 2012).
 The diagnosis also may be based on an AFI below the 5th or 2.5th
percentile determined by a gestational-age-specific nomogram. Or, it
may be based on subjective assessment of decreased amnionic fluid
volume.

In the Moore nomogram, a threshold of 5 cm is below the 2.5th

percentile throughout the second and third trimesters

When evaluating twin pregnancies for twintwin transfusion

syndrome, a single deepest pocket 2 cm is used to define
oligohydramnios (Society for Maternal-Fetal Medicine, 2013).
Causes:
1- Preterm premature rapture of membrane: perhaps the most common
causes of oligohydramnios is PPROM.
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.
 Fetal chromosomal anomalies
Intrauterine infections
Drugs- PG inhibitors, ACE inhibitors
IUGR associated with placental insufficency
Amnion nodosum-failure of secretion by the cells of the amnion
Oligohydramnios-causes
Fetal Maternal
Chromosomal anomalies Uteroplacental insufficiency
Congenital abnormalities Hypertension
Growth restriction Pre-ecclampsia
Demise Diabetes
Post-term pregnancy Iatrogenic
Ruptured membranes PG synthesis inhibitors
Placental ACE inhibitors
Abruption Idiopathic
TTTS
Early-Onset Oligohydramnios:
When amnionic fluid volume is abnormally decreased from the early
second trimester, it may reflect a fetal abnormality that precludes
normal urination, or it may represent a placental abnormality severe
enough to impair perfusion.

In either circumstance, the prognosis is poor.

Second-trimester rupture of the fetal membranes may result in

oligohydramniosand should be excluded.
Oligohydramnios after Midpregnancy:
When amnionic fluid volume becomes abnormally decreased in the late
second or in the third trimester, it more likely is associated with fetal-
growth restriction, a placental abnormality, or a maternal complication
such as preeclampsia or vascular disease.

Underlying etiology is often presumed to be uteroplacental insufficiency,

which can impair fetal growth and reduce fetal urine output.

Investigation of third-trimester oligohydramnios generally includes

evaluation for membrane rupture and sonography to assess growth.
Post term:
Trimmer and coworkers (1990) sonographically measured hourly fetal
urine production using sequential bladder volume measurements in 38
pregnancies of 42 weeks.

Diminished urine production was found to be associated with

oligohydramnios.

They hypothesized that decreased fetal urine flow was likely the result of
preexisting oligohydramnios that limited fetal swallowing.

Oz and associates (2002), using Doppler waveforms, concluded that fetal

renal blood flow is reduced in those postterm pregnancies complicated by
oligohydramnios.
Congenital Anomalies:
Decreased amnionic fluid volume beginning early in gestation are
secondary to genitourinary anomalies.

Anomalies of other organ systems, aneuploidy, and other genetic

syndromes also have the potential to cause oligohydramnios
indirectly, either from fetal decompensation, fetalgrowth restriction,
or an accompanying placental abnormality.

Overall, approximately 3 percent of newborns with congenital

anomalies have oligohydramnios found during prenatal sonography
(Martinez-Frias, 1999).
Congenital anomalies associated with oligohydramnios
Amnionic band syndrome Cystic hygroma
Cardiac Diaphragmatic hernia
Fallots tetralogy Genitourinary
Septal defects Renal dysgenesis/aplasia
CNS Urethral obstruction
Holoprosencephaly Bladder exystrophy
Meningocele Meckel gruber syndrome
Encephalocele Uretro-pelvic junction obstruction
microcephaly Prune belly syndrome
Cloacal dysgenesis Hypothyroidism
Chromosomal Skeletal
Triploidy TRAP sequence
Trisomy 18 TTTS
Turner syndrome
 Selected renal abnormalities that lead to absent fetal urine production
include :
Bilateral renal agenesis
Bilateral multicystic dysplastic kidney,
unilateral renal agenesis with contralateral multicystic dysplastic kidney,
Infantile form of autosomal recessive polycystic kidney disease.
Fetal bladder outlet obstruction
-- Posterior urethral valves,
-- urethral atresia or stenosis, or the megacystis
Microcolon intestinal hypoperistalsis syndrome.
Complex fetal genitourinary abnormalities such as persistent cloaca and
sirenomelia
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 (Fanos, 2011).
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, subsequently, 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,

 Vascular tone is an essential target of the paracrine and endocrine
regulations during pregnancy.

The lowering of arteriolar tonicity precedes blood volume expansion

and seems to be the primary step in the physiological hemodynamic
modifications.

Poor placentation may be expressed in the persistence of high

impedance in the uteroplacental circulation
-assessed by the second trimester Doppler in the uterine vessels,
represents a powerful predisposing factor to
IUGR
Oligohydramnios
Preeclampsia
 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, after Dr. Edith Potter, who described it in
1946.

When this constellation stems from another etiology of decreased

amnionic fluid volume, it is generally called Potter sequence.
Normal-sized lungs (top) are shown in comparison
with hypoplastic lungs (bottom) of fetuses at the same gestational
age. (From Newbould, 1994, with permission)
 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 oligohydramniosthe chronic abruption-oligohydramnios
sequenceit commonly also causes growth restriction.

The prognosis for this constellation is similarly poor.

 Borderline Oligohydramnios
The term borderline AFI or borderline oligohydramnios is somewhat
controversial. It usually refers to AFIs between 5 and 8 cm (Baron,
1995; Magann, 2011; Petrozella, 2011).
Through the mid-third trimester, an AFI value of 8 cm is below the
5th percentile on the Moore nomogram
Petrozella and colleagues (2011) found that pregnancies between 24
and 34 weeks with an AFI between 5 and 8 cm were not more likely
than those with an AFI above 8 cm to be complicated by maternal
hypertension, stillbirth, or neonatal death
Pregnancy Outcomes
Casey and colleagues (2000) found that an AFI 5 cm complicated 2
percent of pregnancies higher rates of fetal stillbirth, growth
restriction, nonreassuring heart rate pattern, and meconium
aspiration syndrome were noted.

Petrozella and associates(2011) similarly reported that with an AFI 5

cm identified between 24 and 34 weeks, there was increased risk for
stillbirth, spontaneous or medically indicated preterm birth, heart
rate pattern abnormalities, and growth restriction.
 Chauhan and coworkers (1999) found that women with
oligohydramnios had a twofold increased risk for cesarean delivery
for fetal distress and a fivefold risk for an Apgar score < 7 at 5
minutes compared with pregnancies with normal AFI.
Diagnosis:
1) Uterine size is much smaller than the period of amenorrhea
2) Less fetal movements
3) The uterus is full of fetus because of scanty liquor
4) Malpresentation (breech) is common
5) Evidences of intrauterine growth retardation of the fetus
6) Sonographic diagnosis is made when largest liquor pool is less
than 2 cm. Ultrasound visualization is done following
amnioinfusion of 300 ml of warm saline solution
7) Visualization of normal filling and emptying of fetal bladder
essentially rules out urinary tract abnormality.
8) Oligohydramnios with fetal symmetric growth restriction is
associated with increased chromosomal abnormalities.
 Dr Mona Shroff *
www.obgyntoday.info
Management
ADEQUATE REST decreases dehydration
HYDRATION Oral/IV Hypotonic fluids(2 Lit/d)
temperory increase
helpful during labour,prior
to ECV, USG
SERIAL USG Monitor growth,AFI,BPP
INDUCTION OF LABOUR/ LSCS
Lung maturity attained
Lethal malformation
Fetal jeopardy
Sev IUGR
Severe oligo
DDAVP: ? Research settings

AMNIOINFUSION
INDICATIONS
1.Diagnostic
2.Prophylactic
3.Therapeutic

*
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
Many different amnioinfusion protocols have been reported, but
most include a 500- to 800-mL bolus of warmed normal saline
followed by a continuous infusion of approximately 3 Ml per minute
(Owen, 1990; Pressman, 1996).

In another study, Rinehart and colleagues (2000) randomly gave a

500-mL bolus of normal saline at room temperature alone or 500-mL
bolus plus continuous infusion of 3 mL per minute.
Prophylactic Amnioinfusion for Variable
Decelerations:
Hofmeyr and Lawrie (2012) used the Cochrane Database to
specifically analyze the effects of amnioinfusion in the management
of fetal heart rate patterns associated with umbilical cord
compression.
Nineteen suitable studies were identified, most with fewer than 200
participants.
It was concluded that amnioinfusion appeared to be useful in
reducing the occurrence of variable decelerations, improving
neonatal outcome, and reducing cesarean delivery rates.
The American College of Obstetricians and Gynecologists (2013a)
recommends consideration of amnioinfusion with persistent variable
decelerations.
Prophylactic Amnioinfusion for Oligohydramnios
Amnioinfusion in women with oligohydramnios has been used
prophylactically to avoid intrapartum fetal heart rate patterns from
cord occlusion.
Nageotte and coworkers (1991) found that this resulted in
significantly decreased frequency and severity of variable
decelerations in labor.
However, the cesarean delivery rate or condition of term infants was
not improved. In a randomized investigation, Macri and colleagues
(1992) studied prophylactic amnioinfusion in 170 term and postterm
pregnancies complicated by both thick meconiu and
oligohydramnios.
Amnioinfusion significantly reduced cesarean delivery rates for fetal
distress and meconium aspiration syndrome. In contrast, Ogundipe
and associates (1994) randomly assigned 116 term pregnancies with
an amnionic fluid index < 5 cm to receive prophylactic amnioinfusion
or standard obstetrical care.
There were no significant differences in overall cesarean delivery
rates, delivery rates for fetal distress, or umbilical cord acid-base
studies.
Amnioinfusion for Meconium-Stained Amnionic Fluid

Pierce and associates (2000) summarized the results of 13

prospective trials of intrapartum amnioinfusion in 1924 women with
moderate to thick meconium-stained fluid.
Infants born to women treated by amnioinfusion were significantly
less likely to have meconium below the vocal cords and were less
likely to develop meconium aspiration syndrome than infants born to
women not undergoing amnioinfusion.
The cesarean delivery rate was also lower in the amnioinfusion
group.
Last, Fraser and colleagues (2005) randomized amnioinfusion in 1998
women with thick meconium staining of the amnionic fluid in labor
and found no benefits.

Because of these findings, the American College of Obstetricians and

Gynecologists (2012a, 2013c) does not recommend amnioinfusion to
dilute meconium-stained amnionic fluid.

According to Xu and coworkers (2007), in areas lacking continuous

monitoring, amnioinfusion may be used to lower the incidence of
meconium aspiration syndrome.
Hofmeyr GJ. Prophylactic versus therapeutic amnioinfusion
for oligohydramnios in labour. Cochrane Database of
Systematic Reviews 1996,Issue concludes

There appears to be no advantage of prophylactic

amnioinfusion over therapeutic amnioinfusion carried out
only when fetal heart rate decelerations or thick meconium-
staining of the liquor occur.
Complications Associated with Amnioinfusion
from a Survey of 186 Obstetrical Units
Uterine hypertonus -------------------------------27 (14)
Abnormal fetal heart rate tracing ---------------17 (9)
Chorioamnionitis---------------------------------------7 (4)
Cord prolapse-------------------------------------------5 (2)
Uterine rupture---------------------------------------- 4 (2)
Maternal cardiac or respiratory-compromise---3 (2)
Placental abruption-----------------------------------2 (1)
Maternal death----------------------------------------2 (1)
 Oral hydration + DDAVP : Prevents diuresis

Results in maternal plasma hypotonicity -fetal plasma

hypotonicityincreased fetal urine productionreduced
fetal swallowingincreased AFI
TREATMENT ACC. TO CAUSE

Drug induced OMIT DRUG

PROM INDUCTION
PPROM Antibiotics,steroid Induction
FETAL SURGERY
VESICO AMNIOTIC SHUNT-PUV
Laser photocoagulation for TTTS
 Posterior urethral valves
Sonographic findings:
Keyhole sign
 Posterior urethral valves
Management:
Karyotyping
Perform serial bladder drainage every 3-4 days
Use sample of 3rd drainage
Isotonic urine indicate poor function
 Posterior urethral valves
Good prognostic biochemical markers:
Na < 100meq/L
Cl < 90meq/L
Osmolarity <210mOsm/L
B2 microglobulin < 4mg/L
Ca < 8mg/dl
Indication for vesico amniotic shunts
*
 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.

Palmer RM, Ashton DS, Moncada S. Vascular endothelial cells synthesize nitric oxide from L-arginine.
Nature 1999;333:664-6.
Act by
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.

Rytlewski et al. studied the influence of oral supplementation with low dose of ARG on
biophysical profile,
Oligohydramnios,
feto-placental circulation and
neonatal outcome in preeclampsia.
This was a randomized, placebo-controlled, double-blind, clinical trial.
Oral therapy with 3 g of Arginine daily or placebo was given as a supplement to standard
therapy.
The results
-L arginine treatment accelerated fetal weight gain and
-improved biophysical profile.
Starting from the 3rd week of therapy,
- the umbilical artery pulsatility indices values were significantly lower in the ARG group.
-Neonates in this group revealed higher Apgar scores.
 The authors 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.
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 single deepest pocket 8 9.9 c.m./ AFI is 25 to 29.9 cm
2- Moderate : single deepest pocket 10 -11.9 c.m./ 30 to 34.9 cm
3- Severe : single deepest pocket 12 c.m./ 35 cm or more

Incidence : 1 2 % of all pregnancies.

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.
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
Hydramnios is often a component of hydrops fetalis, and several of
the above etiologiesselected anomalies, infections, and
alloimmunizationmay result in a hydropic fetus and placenta.

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.
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(Dashe, 2000;
Spellacy, 1973; Weiss, 1985).

Such findings support the hypothesis that maternal hyperglycemia

causes fetal hyperglycemia, with resulting fetal osmotic diuresis into
the amnionic fluid compartment.
Congenital Anomalies
Severe central nervous system abnormalities, such as anencephaly,
hydranencephaly, or holoprosencephaly, 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 tractesophageal or

duodenal atresiais often associated with hydramnios.
Other obstructive causes include clefts, micrognathia, congenital
high-airway obstruction sequence, and fetal neck masses.

Severe fetal thoracic abnormalities, such as diaphragmatic hernia,

cystic adenomatoid malformation, and pulmonary sequestration,
may be associated with hydramnios due to mediastinal shift and
impaired swallowing, occasionally with development of hydrops.

A common fetal renal anomaly, ureteropelvic junction obstruction,

may at times result in paradoxical hydramnios.
And although rare, tumors such as fetal sacrococcygeal teratoma,
fetal mesoblastic nephroma, and large placental chorioangiomas are
frequently accompanied by abnormally increased amnionic fluid
volume.

If a fetal abnormality is encountered concurrent with hydramnios,

amniocentesis should be considered, because the aneuploidy risk is
significantly increased(Dashe, 2002; Pri-Paz, 2012).
Hydramnios is generally defined in multifetal gestations as a single
deepest amnionic fluid pocket measuring 8 cm or more.
It may be further characterized as moderate if the single deepest
pocket is at least 10 cm and severe if this pocket is at least 12 cm.
In monochorionic pregnancies, hydramnios of one sac and
oligohydramnios of the other are diagnostic criteria for twintwin
transfusion syndrome,
Polyhydramnios causes:
Maternal hyperglycemia
GIT anomalies(obstructive)
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 pseudohyperaldosteronism
Fetal bartter
Nephrogenic diabetes insipidus
Placental chorioangioma
Maternal substance abuse
CLINICAL TYPES:
Depending on the rapidity of onset, hydramnios may be:
(a) Chronic (mostcommon) 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.

Acute Polyhydramnios: Onset is acute usually occurs before 20 weeks of
pregnancy and presents usually with symptoms and labour starts before 28
weeks of pregnancy.
It may present as
Acute abdomen - abdominal pain, nausea, vomiting
Breathlessness which increases on lying down position
Palpitation
Oedema of legs, varicosities in legs, vulva and hemorroids
Signs:
Patient looks ill, with out features of shock
Oedema of legs with signs of PIH
Abdomen unduly enlarged with shiny skin
Fluid thrill may be present
Internal examination shows taking up of cervix or even dilatation with bulging
membranes
Chronic Polyhydramnios: More common than acute 10% more common
Since accumulation of liquor is gradual and so patient may be symptomatic or
asymptomatic.
Symptoms are mainly due to mechanical causes
Dyspnoea is more in supine position
Palpitation
Oedema
Oliguria may result from ureteral obstruction by enlarged uterus
Pre-eclampsia 25 %( oedema, hypertension and proteinuria)
Signs GPE
Patient may be dyspnoic at rest
Pedal Oedema
Evidence of PIH
Abdominal examination
Inspection
Abdomen is markedly enlarged globular with fullness in flanks
Skin over the abdomen is tense shiny with large striae
Palpation:
Height of uterus is more than the corresponding periods of
Amenorrhoea
Abdominal girth is more
Fetal parts cannot be well defined external ballotment is more easily
elicited
Malpresentations are more common and presenting part is usually
high up
Fluid thrill is present
Auscultation
Fetal heart sounds are not heard distinctly
Internal examination :
Cervix is pulled up
May be sometimes dilated and admits tip of finger through which
bag of membranes which is tense is felt.
At times patient may present with complications like
Pre ecclampsia
PROM
Preterm labour
Placental abruption
Cord prolapse
 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.
Sonogram of severe hydramnios at 35 weeks in a
pregnancy complicated by fetal aqueductal stenosis. This
pocket
of amnionic fluid measures more than 15 cm, and the amnionic
fluid index measured nearly 50 cm
Management:
Routine OBH

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%

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 amniocentesistermed
amnioreductionmay 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.
The goal is to restore amnionic fluid volume to upper normal range
Hydramnios severe enough to necessitate amnioreduction almost
invariably has an underlying etiology, and subsequent
amnioreduction procedures may be required as often as weekly or
even semiweekly.

Importantly, amnioreduction is typically performed later in gestation

and carries additional risks of membrane rupture, preterm labor or its
exacerbation, and placental abruption.
Amnioreduction:
Indomethacin:
2.2-3 mg/kg/day (75 mg twice daily/25 mg every 6 hours).
It has been found to decrease amniotic fluid as it reduces fetal urine
output.
determine the effect
a-) maternal symptoms and uterine contractions;
b) weekly measurement of fundal height and abdominal girth at the
level of the umbilicus and serial ultrasound (to monitor foetal growth
and amniotic fluid); and
c) prolongation of pregnancy.
Complication:
With chronic hydramnios, fluid accumulates gradually, and a woman
may tolerate excessive abdominal distention with relatively little
discomfort.

Acute hydramnios, however, tends to develop earlier in pregnancy. It

may result in preterm labor before 28 weeks or in symptoms that
become so debilitating as to necessitate intervention.
Symptoms may arise from pressure exerted within the overdistended
uterus and upon adjacent organs.

When distention is excessive, the mother may suffer dyspnea and

orthopnea to such a degree that she may be able to breathe
comfortably only when upright

Edema may develop as a consequence of major venous system

compression by the enlarged uterus, and it tends to be most
pronounced in the lower extremities, vulva, and abdominal wall.
Rarely, oliguria may result from ureteral obstruction by the enlarged
uterus.

Maternal complications such as these are typically associated with

severe hydramnios from an underlying etiology.
Maternal complications: associated with hydramnios include
placental abruption, uterine dysfunction, and postpartum
hemorrhage.

Placental abruption is fortunately infrequent. It may result from the

rapid decompression of an overdistended uterus that follows fetal-
membrane rupture or therapeutic amnioreduction.

With prematurely ruptured membranes, a placental abruption

occasionally occurs days or weeks after amniorrhexis.

Uterine dysfunction consequent to overdistention may lead to

postpartum atony and, in turn, postpartum hemorrhage.
Complication :

I. Maternal :
A) During Pregnancy :
1- Abortion (as a result of overdistension of the uterus).
2- Preterm labour.
3- Premature rupture of membranes.
4- Cord prolapse.
5- Placental abruption.
6- Malpresentation.
7- Nonengagement of the presenting part.
8- Pressure symptoms : as dyspnea, palpitation and edema
of lower limbs.
B) During Labour :
1- Premature rupture of membranes.
2- Prolapse of arm, cord or both.
3- Abruptio placentae due to rapid escape of liquor with premature separation
of the placenta.
4- Splanchnic shock occurs if the fluid escapes rapidly, so the pressure exerted
by the uterus on the splanchnic vessels drops suddenly leading to pooling of
blood in the splanchnic area and shock.
5- Postpartum hemorrhage due to :
- Uterine atony due to overdistension of the uterus.
-Retained placenta.
-Prolonged labour.

C) During Purperium : The uterus may take a longer time to involute

(subinvolution).
 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
AMNIOCENTESIS
Usually performed between 16-20 weeks of gestation.
Procedure performed using ultrasound guidance and sterile
technique.
Typically performed by two operators.
The main operator performs the invasive procedure while the
assistant performs the ultrasound examination and guides the
needle insertion.
Pre procedure ultrasound examination is performed to identify
the placental location and fetal position in an attempt to avoid
both during the needle insertion.
 The desired area of the maternal abdomen is cleaned, sterilized
and draped with sterile drapes.

Ultrasound probe covered by sterile sleeve an continuous

ultrasound guidance is provided during the procedure.

Ultrasound probe held vertically and the desired target is

centered on the screen.

Needle guide is attached to the probe laterally , which provides

a needle track ,at a 45 angle to the horizontal plane.
Alternative :
Free hand needle insertion can be done , the needle is inserted 3 cm
lateral to the probe, in the same plane and at 45 angle.

The guide increases the ease of needle insertion & reduces the risks
of failed attempts and complications.
5 inch length 22 gauge spinal needle is used.
Rarely 7 inch length needle is used in obese patients.
 Amniotic sac is entered and fluid is aspirated using sterile syringes.
The first 1-2ml of the amniotic fluid may be contaminated by
maternal cells and can be discarded.
Fluid subsequently aspirated can be sent for fetal chromosomal
analysis after tissue culture or direct fluorescent insitu hybridization
techniques.
Amount required for chromosomal analysis : 15-20 ml.
 Pregnancy loss rate : 1 in 200

Complications :

Infection
Inadvertent trauma to the fetus or placenta
Leakage of amniotic fluid
Miscarriage.
Feto maternal hemorrhage,
Isoimmunization may occur in Rh negative women and it
should be covered by prophylactic antiD in non sensitized
women.
Early amniocentesis:
12-14 WEEKS
Done in order to obtain the results earlier in gestation
Increase in risk of talipes equinovarus.
For patients desiring earlier diagnosis , transabdominal CVS should
be preferred over early amniocentesis.
Amniotic fluid testing
Testing amniotic fluid for AFP and AChE can predict open neural tube
defects more accurately than maternal serum screening.

Patient with unexplained high maternal serum AFP levels and normal
ultrasonography findings should be offered amniotic fluid testing.

Any patient who has had a child with a neural tube defect has 3%
to5% risk for recurrence and also should be offered amniotic fluid
AFP testing

Any elevation of AFP in amniotic fluid should lead to AChE analysis

Amniotic fluid testing
Testing should be performed at or before 16 weeks gestation.
Determination of fetal karyotype is also reasonable.
Amniocentesis role in Rh disease and alloimmunisation

Amniocentesis and estimation of bilirubin in the amniotic fluid by

spectrophotometry are indicated in
(1) Antibody titer rises more than 1: 8 to determine whether the
particular baby will be affected or not;
(2) Previous history of severely affected baby;
(3) Father is heterozygous to determine whether the particular baby
will be affected or not. As such, if Rh antibodies are found in the
current pregnancy, it is an essential procedure to guide the
management.
Selection of time
(1) No history of previously affected babyIt is done at 3032
weeks and a second test should be repeated after 34 weeks;
(2) Positive history of previously affected babyIt should be done
atleast 10 weeks prior to the date of previous stillbirth or other
hemolytic manifestations on the baby.
However, it is useless to perform prior to 20 weeks.
Inference:
The optical density of the liquor containing the bilirubin pigment, is
observed at 250700 nm wave length.
The optical density difference at 450 nm wave length gives the
prediction of the severity of fetal hemolysis.
In presence of bilirubin, there is a deviation bulge peaking at 450
nm wave length.
The bigger the deviation bulge, the more severe is the affection of
the baby. For any given period of gestation, the height of the
spectrophotometric deviation bulge at OD450 falls within one of
the three zones when plotted in Lileys chart.
Spectrophotometric analysis of amniotic fluid Plotting of the deviation bulge in Lileys
showing optical density difference at 450 nm wave length with prediction
deviation bulge in Rh hemolytic disease chart at different periods of gestation
Predictions:
Lileys zone I (low zone): The fetus is unlikely to be affected and the
pregnancy can be continued to term.

Lileys zone II (mid zone): Repeat amniocentesis by 2 weeks

value upward cordocentesis hematocrit < 30% intrauterine
transfusion to raise haematocrit 4045%. Preterm delivery may be
needed after 34 weeks.

Lileys zone III (High zone): The fetus is severely affected and death
is imminent. Pregnancy > 34 weeks delivery.
Pregnancy <34 weeks cordocentesis hematocrit < 30%
intrauterine transfusion to raise hematocrit 4045%. Preterm
delivery may be needed after 34 weeks.
Advantages:
Spectrophotometric analysis when plotted in relation to the Lileys
zone can predict with fair degree of accuracy, the degree of
hemolytic process in the fetus.
This can give indications when to terminate the pregnancy and when
to give intrauterine fetal transfusion.
Assessment of fetal anemia is more accurate by fetal umbilical cord
blood sampling
Cordocentesis also helps to detect fetal blood type, hematocrit, DCT
and total bilirubin level.
Fetal hematocrit value <15 percent is associated with hydrops.
Tests for Lung Maturity

1. Lecithin/ sphingomyelin ratio

a. Method:____________________________
b. Principles: Lecithin is produced at a relatively low and constant rate until the 35th week of gestation
while sphingomyelin is produced at a constant rate after about 26 week gestation and therefore conserve
as a control on which to base the rise in lecithin. Prior to 35 week gestation, L/S ratio is 1.6 and rises
to >2.0 when lecithin production increases.

2. Amniostat-FLM

a. Method:________________________
b. Principle: the test uses antisera for phosphatidly glycerol and is affectected by specimen contamination with blood and
meconium.
3. Foam stability index

a. method:_____________________________
b. Principle: a semiquatitative measure of the amount of surfactant is done by adding 0.5 mL of amniotic fluid to increasing
amounts of 95% ethanol (0.42 mL to 0.55 mL in 0.01-mL increments), shaken for 15 seconds, and allowed to sit undisturbed
for 15 minutes. If a sufficient amount of phospholipid is present, a continuous line of bubbles will be observed even in the
presence of alcohol, an anti-foaming agent.

4. Microviscosity

a. Method:______________________
b. Principle: Phospholipids decrease the microviscosity of amniotic fluid and the change is detected by determining the
surfactant to albumin ratio (mg/g) based on the polarization of a fluorescent dye that combines (internal standard,
decreased fluorescence lifetime and high polarization).
5. Lamellar body count

a. Method:___________________________
b. Principle: Lamellar bodies (lamellated phospholipids that represent a storage from of surfactants secreted by the type
II pneumocytes of the fetal lung)range in size from 1.7 to 7.3 fL, and therefore can be counted using the platelet
channel of hematology analyzers.

6. Optical density at 650 nm

a. Method:_________________________
b. Principle : the increase in OD of the amniotic fluid caused by the presence of lamella bodies in determined by
centrifuging the specimen at 2000 g for 10 min and reading the absorbance at 650 nm.
 Table 24. Tests for fetal lung maturity
Normal values Significance

L/S ratio 2.0 FLM

Amniostat-FLM Positive FLM/phosphotidyl glycerol

Foams Stability index 47 FLM

Microviscosity 55 mg/ g FLM

Lamellar body count 32,00/ mL FLM

OD at 650 nm 0.150 FLM

Bilirubin scan A 450 less .025 HDN

Alpha Fetoprotein Less than 2.0 Neural tube disorder

MoM
Test for Fetal Distress

1. Bilirubin assay

a. Method: _____________________
b. Principle: the optical density of amniotic fluid is normally highest at 365 nm and decreases linearly to 550 nm
except when bilirubin is present where a rise in OD is seen at 450 nm. The 450 is then plotted on a liley graph
to determine the severity of HDN and the need for interventions.

2. Alpha fetoprotein

a. Method:_________________
b. Principle: The Test is based on the measurement of the neural tube defects using an automated
immunoassay method: results are reported in terms of multiples of the median with a value >2 MoM
considered abnormal
3. Acetylcholinesterase

a. Method: ____________________
b. Principle: Ache is an enzyme derived primarily from the neural tissue and is normally absent in amniotic
fluid. Its presence in amniotic fluid in conjunction with elevated AFP values is highly diagnostic of NTDs.
Other Tests

1. Differentiation of amniotic fluid from maternal urine

Creatinine is 3.5 mg/ dL and urea is 30 mg/dL in amniotic

fluid, whereas high as 10 mg/ dL creatinine and 300 mg/dL
urea may be found in urine

2. Determination of fetal age

AF creatinine level ranges from 1.5 to 2.0 mg/ dL prior to 36

weeks gestation and rises above 2.0 mg/dL thereafter,
providing a means of determining fetal age as >36 weeks

3. Kleihauer-Betke test

used to determine the source of the blood (maternal or

fetal) in a bloody specimen for further case management.
THANK YOU!!!
THANK YOU
ARM
AMNIOTIC FLUID EMBOLISM
DIAGNOSTIC USES
Amniocentesis :
Transabdominal withdrawal o f amnionic fluid remains the most
common procedure used to diagnose fetal aneuploidy and other
genetic conditions.
It is generally performed between 15 and 20 weeks gestation but
may be performed later as well.
The indication is usually to assess fetal karyotype, although use of
FISH and array-based comparative genomic hybridization studies
have increased considerably.
 Because the amniocytes must be cultured before fetal karyotype can
be assessed, the time needed for karyotyping is 7 to 10 days.
Outside the context of prenatal genetic analysis, amnionic fluid
occasionally may be removed in large amounts therapeutically to
relieve symptomatic hydramnios .
 Technique: Amniocentesis is performed using aseptic technique,
under direct sonographic guidance, using a 20- to 22-gauge spinal
needle.
A standard spinal needle is approximately 9 cm long, and depending
on patient habitus, a longer needle may be required. The needle is
directed into a clear pocket of amnionic fluid, while avoiding the fetus
and umbilical cord and ideally without traversing the placenta.
Efforts are made to puncture the chorioamnion rather than to tent
it away from the underlying uterine wall. (Mujezinovic, 2011).
AF and Respiratory distress syndrome (RDS)
AF and Respiratory distress syndrome (RDS)

Respiratory distress syndrome (RDS) was associated with a

significant mortality rate approaching approximately 30%.

In the 1950s, it was discovered that the resistance of

pulmonary alveoli to collapse during expiration was mainly
caused by the presence of a surface tension-lowering
material lining the alveolus (surfactant).

As the lungs develop, significant quantities of surfactant are

washed out of the fetal lung and accumulate in the amniotic
fluid.
AF and Respiratory distress syndrome (RDS)

All of the available biochemical tests for fetal lung maturity rely on
the amniotic fluid content of surfactant .

Adult mature surfactant is approximately 80% phospholipids, about

10% protein, and about 10% neutral lipids (primarily cholesterol).

The major species of phospholipid in surfactant is

phosphatidylcholine (also referred to as lecithin), which accounts
for 80% of the total phospholipid.
L/S ratio test
The L/S ratio test remains one of the most commonly used tests,
and one of the standardized tests against which all other tests are
compared.

With a L/S ratio of 1.5-1.9, approximately 50% of infants will

develop RDS. Below a ratio of 1.5, the risk of subsequent RDS
increases to 73%.

One of the major disadvantages of the L/S ratio is the inability to

use this test in the setting of contaminated amniotic fluid. Both
blood and meconium staining of amniotic fluid have been found to
interfere with L/S ratio determinations.
PG determinations:

It is found that the false-positive rate for PG determination was

1.8%. This rate is significantly lower than the false-positive rate
they found for the L/S ratio(5%).

PG performs much better than the L/S ratio in predicting babies

who will develop RDS. Finally, PG determinations accurately predict
pulmonary maturity and give a better indication of pulmonary
immaturity than does the L/S ratio.
Saturated Phosphatidylcholine
Saturated Phosphatidylcholine has been found to predict pulmonary
maturity

Respiratory distress syndrome was correctly predicted 55.5% of the

time by L/S ratio and 82% of the time by SPC.

Pulmonary immaturity = an SPC <500 g/dl

In addition, the SPC was found to be valid in the presence of blood

and meconium, whereas the L/S ratio was not.
Shake test
This test use the principle that when ethanol is added to amniotic
fluid, the nonsurfactant foam causing substances in amniotic fluid
are removed.

Any stable foam layer that persists after shaking is due to the
presence of surfactant in a critical concentration.

When serial dilutions of ethanol are used, the surfactant can be

quantified.

It is found that the shake test was comparable to the L/S ratio and
had a high predictive value for RDS when applied to
uncontaminated amniotic fluid.
Tap Test
The tap test examines the ability of surfactant within amniotic fluid
to break down bubbles within an ether layer.

The test is performed on 1 ml of amniotic fluid mixed with a drop of

6N hydrochloric acid and 1.5 ml of diethylether.

The tube is tapped 4 times and examined for the presence of bubbles
within the ether layer.
In mature samples, the bubbles quickly breakdown, whereas in
immature amniotic fluid specimens more than 5 bubbles persist in
the ether layer.
This rapid test was comparable with the phospholipid profile.
Visual Inspection

The basis is whether or not newspaper could be read through the

amniotic fluid sample, that is, was the fluid too turbid to read text
through.

With clear fluid (readable newsprint) the sensitivity of an immature

result is 98%.
Optical Density at 650 nm
With a OD 650 value of 0.15 or greater, the L/S ratio was always
greater than 2.0

When the OD 650 was less than 0.15, only 6% of L/S ratios were
greater than 2