Amnionic fluid

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 Tm
• 98-percent is water.
• A full-term fetus contains roughly 2800 mL of water,
• the placenta & another 400 mL, such that the term
uterus holds nearly 4 liters of water
• Abnormally decreased fluid volume is termed
oligohydramnios, whereas
• abnormally increased flid volume is termed
hydramnios or polyhydramnios.
physiology
 Early in pregnancy, the amnionic cavity is filed with fluid that is similar in
composition to extracellular fluid
 During the fist 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.
 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.
extremely preterm infants can experience significant fluid loss across their skin.
 Physiology
• with advancing gestation, four pathways play a major role in
amnionic fluid volume regulation
1) 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 re
circulated on a daily basis
2) second regulator of fluid volume is intramembranous fluid
transfer across and into fetal vessels on the placental surface,
– The hypotonicity of fetal urine is allowed for this process and
accounts for 400 mL/day
 Physioloy …
 3) The third source of amnionic fluid regulation is the
respiratory tract.
 350 mL of lung fluid is produced daily late in gestation,
 half of this is immediately swallowed.
 4) Last, fetal swallowing is the primary mechanism for
amnionic fluid resorption and
Averages 500 to 1000 mL per day
Impaired swallowing, secondary to either a central nervous
system abnormality or gastrointestinal tract obstruction, can
result in an impressive degree of hydramnios.
Measurement
• From a practical standpoint, the actual volume of amnionic
fluid is rarely measured outside of the research setting.
• There was considerable variation at each week of
gestation, particularly in the mid-third trimester.
• At this time, the 5th percentile was 300 mL, and
the 95th percentile approximated 2000 mL.
• Specifially, the average fluid volume was about 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
 Sonographic Assessment
• Amnionic flid volume evaluation is a component
of every standard sonogram performed in the
second or third trimester
• Volume is typically assessed semi-
quantitatively,
• Either a single pocket or the amnionic fluid index—AFI
• A qualitative or subjective estimate acceptable
if performed by an experienced examiner
Single Deepest Pocket
 Also called the maximum vertical pocket.
 Using the ultrasound; the sagittal plane, the largest
vertical pocket of fluid is identified.
• Thenormal 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.
Amnionic Fluid Index (AFI)
• Remains one of the most commonly used
• The uterus is divided into four equal quadrants—
– the right- and left-upper and lower quadrants,.
• The AFI is the sum of the single deepest pocket from each
quadrant
• Has intraobserver variability 1cm and the interobserver
variability about 2 cm.
• Approximately three times the single deepest
pocket of fluid encountered
• The normal range for AFI that is most commonly used is 5
to 24 cm,
• Values above and below this indicating hydramniosand
oligohydramnios, respectively
1. HYDRAMNIOS /polyhydramnios
HYDRAMNIOS…

Is an abnormally increased amnionic fluid volume,

complicates 1-2 %of px
suspected if the uterine size exceeds that of the
expected for GA
The uterus may feel tense, and palpating fetal
small parts or auscultating fetal heart tones may
be difficult.
HYDRAMNIOS…
• categorized according to degree.
– 70%== As mild if the AFI is 25 to 29.9 cm, or single pocket of
8 to 9.9 cm
– 20%== moderate if AFI is 30 to 34.9 cm or single pocket 10
to 11.9 cm,
– 15%== severe AFI 35 cm or more ≥ 12 cm
• In general, severe hydramnios is far more likely to have
an underlying etiology and
• to have consequences for the pregnancy than mild
hydramnios—which is frequently idiopathic and benign
 Etiology
 Common underlying causes of hydramnios include
fetal congenital anomalies in approximately 15 percent
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
pathophysiology in such cases is complex but is frequently
related to a high cardiac-output state.
Severe fetal anemia is the classic example
1. 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.
2. Congenital Anomalies

• Various anomalies may be found in the setting of hydramnios, and some are more characteristically
linked with it than others.

–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 tract—

•esophageal or duodenal atresia—is often associated with hydramnios

 3.Idiopathic Hydramnios
When there is no obvious cause of hydramnios it is considered
idiopathic
this accounts for up to 70 percent of cases
 Pregnancies with idiopathic hydramnios have been reported to
have at least twice the likelihood of infant birthweight
exceeding 4000 g
– A rationale for this association is that larger
infants have higher urine output, by virtue of their increased
volume of distribution, and fetal urine is the largest contributor to
amnionic fluid volume.
Mild, idiopathic hydramnios is most commonly a benign
finding, and associated pregnancy outcomes are usually good
Complications
• Unless hydramnios is severe or develops rapidly, maternal
symptoms are infrequent.

• 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.
 Pregnancy Outcomes
•
Some outcomes that have been reported to be increased
with hydramnios include cesarean delivery rate, birthweight
> 4000 g, and importantly, perinatal mortality rate. Th cesarean delivery rate is increased
approximately threefold when
hydramnios has been identifid, and the perinatal mortality
rate rises approximately fourfold

found that
pregnancies with severe hydramnios were at particular risk, but
reported no perinatal deaths with idiopathic hydramnios.

Considering that uterine distention from hydramnios

may result in uterine size approaching that of a term gestation, preterm delivery is a logical concern.
Somewhat surprisingly, studies of idiopathic hydramnios have generally found
no association with preterm birth
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.
• such cases, large-volume amniocentesis—termed
amnioreductionn
• Approximately 1000 to 1500 mL of fluid is slowly withdrawn during
approximately 30 minutes,
• 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
2. OLIGOHYDRAMNIOS
• Ths is an abnormally decreased amount of amnionic
fluid
• Oligohydramnios complicates approximately 1 to 2
percent of pregnancies
• Unlike hydramnios, which is often mild and confers
a benign prognosis in the absence of an underlying
etiology, oligohydramnios is a cause
for concern.
• When no measurable pocket of amnionic flid is
identifid, the term anhydramnios may be used.
OLIGOHYDRAMNIOS…
• The sonographic diagnosis of oligohydramnios is
usually based on an AFI ≤ 5 cm or

• on a single deepest pocket of amnionic flid ≤ 2 cm

• The diagnosis also may be based on an AFI below

the 5th or 2.5th percentile determined by a
gestational-age-specifi nomogram.
Early-Onset Oligohydramnios
• When amnionic flid volume is abnormally decreased from
the early second trimester, it may reflct 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 oligohydramnios—and should be excluded
• More commonly, membrane rupture presents with fluid
leakage, vaginal bleeding, or uterine contractions.
• With early-onset oligohydramnios, targeted sonography
should be offred to assess for fetal abnormalities.
Oligohydramnios after Midpregnancy
• When amnionic flid 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 In such
cases, the underlying etiology is often presumed to be uteroplacental
insuffiency,
• which can impair fetal growth and reduce fetal urine output
• Exposure to selected medications has also been linked with
oligohydramnios as discussed subsequently
• Investigation of third-trimester oligohydramnios generally includes
evaluation for membrane rupture
and sonography to assess growth
• Umbilical artery Doppler studies may be performed if growth restriction is
identifid
Congenital Anomalies
• By approximately 18 weeks, the fetal kidneys are the main
contributor to amnionic fluid volume.
• most cases of severely decreased amnionic fulid
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, fetal growth restriction, or an
accompanying placental abnormality.
• Overall, approximately 3 percent of newborns with congenital
anomalies have oligohydramnios found during prenatal
sonography
 Congenital Anomalies
• 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, and
• the infantile form of autosomal recessive polycystic kidney disease
• If no amnionic fluid is visible beyond the mid-second
trimester due to a genitourinary etiology, the prognosis is
extremely poor unless fetal therapy is an option.
Medication
• Oligohydramnios has been associated with exposure to drugs
that block the renin-angiotensin system
• Thse include angiotensin-converting enzyme (ACE) inhibitors and
nonsteroidal antiinflmmatory drugs (NSAIDs)
• When taken in the second or third trimester, ACE inhibitors and
angiotensin-receptor blockers may create fetal hypotension,
• renal hypoperfusion, and renal ischemia, with subsequent anuric renal
failure
• These adverse outcomes appear to be more prevalent following exposure
to angiotensin-receptor blockers,
• but both medication types are contraindicated in pregnancy
• NSAIDs have been associated with fetal ductus arteriosus constriction and
with decreased fetal urine production.
–In neonates, their use may result in acute and chronic renal insuffiency
Pregnancy Outcomes
• Oligohydramnios is associated with increased risk of adverse
pregnancy outcomes
• Newborns from pregnancies with oligohydramnios were more
likely than those with AFIs > 5 cm to have malformations.
• Even in the absence of malformations, higher rates of fetal
stillbirth, growth restriction, nonreassuring heart rate pattern,
and meconium aspiration syndrome were noted.
• women with oligohydramnios had a two fold increased risk
for cesarean delivery for fetal distress and
• Afive fold risk for an Apgar score < 7 at 5 minutes compared with
pregnancies with normal AFI.
Management
• As with hydramnios, management targets the underlying etiology when
feasible
• Initially, an evaluation for fetal anomalies and growth is essential
• In a pregnancy complicated by oligohydramnios and fetal-growth
restriction, close fetal surveillance is important because of associated
morbidity and mortality
• oligohydramnios detected before 36 weeks in the presence of normal
fetal anatomy and growth may be managed expectantly in conjunction
with increased fetal surveillance.
• Amnioinfusion be used intrapartum in the setting of variable fetal heart
rate decelerations.
• It is not considered treatment for oligohydramnios perse, although the
decelerations are presumed secondar to umbilical cord compression
resulting from lack of amnionic fluid
• Amnioinfusion is not the standard of care for other etiologies of
oligohydramnios and is not generally recommended
• TNX