AMNIOTIC FLUID

Facilitator
Prof.Ogutu
Group C
Dr. Mokeira Lilian
Dr. Stephen Samba
Dr. Rashid Bunu
Dr. Gideon Kariuki
 Outline
i. Definition of amniotic fluid

ii. Anatomy
• Location of fluid
• Production site

iii. Physiology/ biochemical composition

iv. Function

v. Abnormalities
• Polyhydramnios and oligohydramnios
• Contributing factors
• Maternal and fetal complications

vi. Management

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 Introduction
Definition: Amniotic fluid is the fluid within the amniotic sac which is a fluid
filled extracelomic cavity which eventually becomes amniotic cavity.
Physiology:
It is alkaline with a specific gravity of 0.010.
Compared to the maternal serum it is hypotonic, osmolarity of 250mOsmol/l
at term suggestive of fetal maturity.
Color- it is colorless/ pale straw color .
Deviations from the normal colour has clinical relevance, such as green
indicates fetal distress, dark coloured in concealed accidental hemorrhage,
golden colour in Rh incompatibility.
Volume: 50mls at 12/40, 400mls at 20/40, 1L at 36-38/40, term 600- 800mls,
200mls at 43/40

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 biochemical composition
approximately 98-99% of the amniotic fluid is composed of water, the remainder is
solutes such as Nacl, urea, creatinine, uric acid, glucose, protein, total lipids,
hormones,

its constitutes vary across the gestational age, in early pregnancy it closely
resembles the maternal/fetal serum.

In the second half of the gestation it contains urinary metabolites as urinary

production increases hence decrease in sodium and chloride concentration with
reduced osmolarity.

Near term urea and creatinine concentration increases by 70%, higher than the
maternal serum.

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 Amniotic fluid production
Fetal origin:
i. Fetal urine, its production increases in the second trimester
ii. Fetal lungs contributes 100mls/day
iii. Secretion from the amniotic epithelium in response to the chemical potential gradients-
osmotic/hydrostatic
iv. Fetal oral and nasal cavities
v. Transudation through fetal skin, in early gestation prior to keratinization of the skin
Maternal origin:
vi. Filtrates from the maternal plasma
*The amniotic fluid is primarily cleared by fetal swallowing of about 500-1000mls and
transudation into the maternal circulation.

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 Amniotic fluid circulation

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 Function
The primary function is fetal protection.
During pregnancy
i. It acts as a shock absorber, cushioning the fetus against injury.
ii. Allows room for growth and free movement of the foetus.
iii. In addition, provides nutrition and antimicrobial function.
iv. It maintains temperature
In labour;
v. prevents umbilical cord compression
vi. helps in cervical dilatation
vii. has bactericidal action hence prevents ascending infection to the uterine
cavity

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 Clinical relevance
i. Amniotic fluid analysis provides useful information about the well being
of the fetus and its maturity. Aids in assessment of foetal chromosome
defects, determination of Lecithin/Sphingomyeline ratio, prenatal
diagnosis of neural tube defects .

ii. Assessment of amniotic fluid volume by amniotic fluid index

iii. Induction of labour by the rupture of the membranes with drainage of the
liquor
iv. Induction of abortion by instillation of chemicals

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 Polyhydramnios
This is an excessive volume of amniotic fluid relative to gestational age,
anatomically this is more than 2L clinically causing maternal discomfort.

Sonographically, is when amniotic fluid index is more than 24cm and the
deepest vertical pocket (DVP) is more than 8cm.

It has an incidence of 1-2%of cases. It has been found to be more common in

multiparae.

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 Etiology
Idiopathic 50-60%

Maternal
• Diabetes mellitus-fetal hyperglycemia result in fetal polyuria
• Cardiac or renal disease- placental edema hence increased transudation

Multiple gestation
• More common the monozygotic twins ,affecting the 2 nd sac (increase in renal
perfusion hence more urine production.
• TTTS- the recipient twin develops hydramnios

placenta
• Chorioangioma –tumor growing from a single villus consisting of hyperplasia of
blood vessel and connective tissue results in increase in transudation.

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 Fetal anomalies
CNS abnormalities
• Anencephaly( suppression of fetal antidiuretic hormone, swallowing reflex
absent, transudation from the exposed meninges)
• Open spina bifida – increased transudation from the meninges

GI abnormalities
• Esophageal/duodenal atresia- preventing swallowing of the liquor

Hydrops fetalis
• Rh isoimmunization, non immune hydrops, fetal infection with TORCH

Facial clefts and neck masses

• Interfere with normal swallowing

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 Types
Polyhydramnios is divided into two clinical types depending on the rapidity of
onset.

i. Acute type
ii. Chronic type

Polyhydramnios may also be classified as;

iii. mild: DVP >8cm-11cm,

iv. Moderate: DVP 12-15cm

v. Severe: DVP >16cm

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 Chronic polyhydramnios
Chronic polyhdramnios is the most common, with a gradual onset and more
apparent in the 3rd trimester.
Clinical presentation
The maternal presentation is attributed to the over distended uterus causing
edema of the legs, varicosities of the legs/vulva and hemorrhoids as a
result of inferior vena cava compression.
In addition the diaphragm is elevated causing dysnoea/respiratory distress.
Signs: patient may have dysnoea +/- features of preeclampsia
Abdominal findings: gross abdomen distention, shiny skin, large striae
Fundal height> than period of amenorrhea, abdominal girth>, fluid thrill
present all round the uterus, fetal parts not well defined.
Fetal heart sound not distinct.
Internal exam reveal; the cervix has been pulled up, admit a finger tip and
tense bulging membranes felt.
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 Investigations
Laboratory: Rh/ABO grouping, postprandial sugar +/- glucose tolerance test,
serology for infection, red cell antibody

Imaging: Sonographic diagnosis of congenital malformations, multiple

gestation, determination of the AFI as well as the foetal presentation and
lie.
Amniotic fluid: amniocentesis is a vital diagnostic tool for the foetal well
being. This has enabled assessment of fetal lung maturity, diagnosis of
chromosomal abnormality, neural tube defects, IEM and hematologic
disorders.

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 Complications
During pregnancy:
• Preeclampsia
• Malpresentation- more room for free movement
• Premature rupture of membranes –over distention of the uterus
• Preterm labour
• Accidental hemorrhage –rapid uterine decompression during rupture of
membranes

During labour
• Cord prolapse
• Increased operative delivery
• Retained placenta/PPH/shock- uterine atony
• Early rupture of membranes
• Uterine inertia

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 • Subinvolution
Cont’
• Increased puerperal morbidities – operative delivery and blood loss

Increased perinatal mortality

• prematurity, congenital malformations , hydrops, accidental hemorrhage

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 Management
Management of polyhydramnios is executed according to underlying cause as well as degree of
severity.
The principles of its management involve identifying the cause, relief of the symptoms,
prevention of complications and their mitigation.
Mild polyhydramnios is managed with bed rest, the excess liquor is expected to diminish as
pregnancy advances.
Severe polyhydramnios requires an admission to identify the underlying cause, management
of underlying medical disease/ complications.
Supportive therapy should be instituted such as bed rest
Use of sulindac 200mg bd (it reduces fetal urine output) .
Indomethacin 2.2-3mg/kg/day

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 Cont’
Further management
is dependent on:
• response to treatment
• period of gestation
• presence of foetal malformation
• associated complicating factors

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 Management
During labour:
Usual management of labour should be followed. After rupture of membranes,
an internal examination ought to be done to exclude cord prolapse and
incase of uterine inertia, oxytocin infusion is started.

To avert PPH, methergine 0.2mg should be give after the delivery of the
anterior shoulder.

The delivered baby should be examined for any congenital abnormalities.

Look out for retained placenta, postpartum hemorrhage and shock.

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 Acute polyhydramnios
Acute polyhydramnios is a rare type, amniotic fluid accumulation is sudden and
usually occur in the 2nd trimester. Usually associated with monozygotic twins with
TTT or chorioangioma of the placenta.

Symptoms: abdominal pain nausea, vomiting

Signs: the patient is sick looking with an gross abdominal distention which is tense
and shiny.

The abdomen is tense, fundal height is more than the period of amenorrhea, fetal
parts are not felt and fetal heart sounds are present

Internal examination reveal that the cervix is pulled up +/- dilatation of the os with
bulging membranes.

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 Management

Spontaneous abortion commonly occur.

Repetitive amnioreduction is done in case of severe TTT.

Laser ablation may cure the cause of TTTS.

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 Oligohydramnios
Oligohydramnios is the deficit of amniotic fluid to the extent of < 200mls at
term.

Sonographically it is defined as when AFI <5cm or when the maximum

vertical pocket amniotic fluid is <2cm

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 Etiology
Fetal conditions Maternal conditions

• Renal agenesis • Hypertensive disorders

• Obstructive uropathy • Uteroplacental insufficiency
• Fetal chromosomal anomalies • Dehydration
• Spontaneous rupture of • Idiopathic
membranes
• Intrauterine infection
• Drugs-ACEI, PG inhibitors
• Post maturity
• IUGR
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 Diagnosis

The fundal height is smaller than period of amenorrhea, there uterus is full of

the fetus, malpresentation, commonly breech presentation and evidence of

IUGR

Sonographic features- largest liquor pool is less than 2cm, absent normal

filling and emptying of fetal bladder

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 complications

fetal maternal

• abortion deformities • Prolonged labor

• fetal hypoplasia • Increased operative interference
• cord compression • Maternal mortality
• increased fetal mortality

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 Management
In the event of fetal congenital malformation, patient ought to be referred to a
fetal medicine unit.

Use of amniopatch/ amniogel- form a thick gel around amniotic sac to seal
any point of leakage.

Induce labour in cases of severe oligohydramnios, IUGR, severe malformation

and if lung maturity has been attained.

Oligohydramnios in the 3rd trimester with a normal foetus may be managed

conservatively

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 Cont’
Amnion infusion indicated for diagnostic and therapeutic purposes.
These includes:
 Attempts to dilute/wash out meconium

 Prophylaxis in oligohydramnios
 Treatment of variable deceleration

Various amnion infusion protocols reported, mostly include 500-

800mls bolus of warm normal saline followed by continuous
infusion of approximately 3ml/min (Owen, 1990; pressman 1996)

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 References
• https://www.glowm.com/section-view/heading/amniotic-fluid-physiology-
and-assessment/item/208#r18
• DC Dutta’s textbook of obstetrics, 9th edition, pages 200,34

• Harman, C. R. (2008). Amniotic Fluid Abnormalities. In Seminars in

Perinatology (Vol. 32, Issue 4, pp. 288–294).
https://doi.org/10.1053/j.semperi.2008.04.012
• Lotgering, F. K., & Wallenburg, H. C. S. (1986). Mechanisms of
Production and Clearance of Amniotic Fluid.

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