PREPARED BY MOSES KAZEVU

POLYHYDRAMNIOS AND OLIGOHYDRAMNIOS

POLYHYDRAMNIOS AND
OLIGOHYDRAMIOS
• The amnion is a thin fetal membrane that begins to form 8 days after
conception as a small sac covering the dorsal surface of the embryonic disc.
• The amnion gradually encircles the growing embryo.
• Amniotic fluid fills the amniotic cavity.
• Amniotic fluid is produced almost exclusively from fetal urine (by the fetal
kidneys) from the second trimester onwards, it is swallowed by the fetus.
• The maintenance of amniotic fluid volume is a dynamic process that reflects
a balance between fluid production and absorption.
➢ Fluid production
o Prior to 8 weeks, amniotic fluid is produced by passage of fluid across
the amnion and fetal skin (transudation).
o At 8 weeks the fetus begins to urinate into the amniotic cavity.
o Fetal urine quickly becomes the primary source of amniotic fluid
production.
o Near term, 800-1000ml of fetal urine is produced each day.
o The fetal lungs produce some fluid (300ml/day at term) but much of it
is swallowed before entering the amniotic space.
➢ Fluid absorption
o Prior to 8 weeks’ gestation, transudative amniotic fluid is passively
reabsorbed.
o At 8 weeks’ gestation, the fetus begins to swallow. Fetal swallowing
quickly becomes the primary source of amniotic fluid absorption.
o Near term, 500-1000ml/ day of amniotic fluid is swallowed.
o A lesser amount of amniotic fluid is absorbed through the fetal
membrane and enters the fetal bloodstream. Near term, 250ml of
amniotic fluid is absorbed by this route every day.
o Small quantities of amniotic fluid cross the amnion and enter the
maternal bloodstream (10ml per day near term).
• Amniotic fluid volume is maximal at 34 weeks (750-800ml) and decreases
thereafter to 600ml at 40 weeks. The amount of fluid continues to decrease
beyond 40 weeks.
• Amniotic fluid serves vital functions including:
➢ Protecting the developing baby from pressure or trauma
➢ Protecting the umbilical cord from compression
➢ Allowing limb movement hence normal postural development
➢ Permitting the fetal lungs to expand (pulmonary development) and develop
through breathing.
➢ Lubricating the fetal skin
➢ Preventing maternal chorioamnionitis and fetal infection through its
bacteriostatic properties.
➢ Assisting in fetal temperature control.
• The most common objective approaches in determining Polyhydramnios or
Oligohydramnios is by measuring the amniotic fluid index (AFI) and the
single deepest pocket (SDP)
➢ The AFI measurement is calculated by first dividing the uterus into 4
quadrants using the linea alba for the right and left division and the
umbilicus for the upper and lower quadrant. The maximum vertical
amniotic fluid pocket diameter in each quadrant not containing cord or fetal
extremities is measured in centimeters, the sum of these measurements is
the AFI (normal= 5 – 25cm)

➢ The SDP measurement refers to the vertical dimension of the largest pocket
of amniotic fluid not containing umbilical cord or fetal extremities and it
is measured at a right angle to the uterine contour. The horizontal
component of this vertical dimension must be at least 1cm. (normal= 2 –
8cm)
• An abnormally high level of amniotic fluid, polyhydramnios alerts the
clinician to possible fetal anomalies.
• An inadequate volume of amniotic fluid, oligohydramnios results in poor
development of the lung tissue and can lead to fetal death.

POLYHYDRAMNIOS
• Polyhydramnios or ‘hydramnios’ can be defined as:
➢ Excessive accumulation of amniotic fluid (>2000ml).
➢ Difficulty or inability to palpate fetal parts or fetal position.
➢ Accumulation of amniotic fluid that causes discomfort to the patient.
➢ Amniotic fluid index >25cm (normal 5-25cm)
o Mild if AFI= 24-30cm
o Moderate if AFI= 30.1-34.9 cm
o Severe if AFI ≥35cm
➢ Single deepest pocket >8cm (normal 2.1-8)
o A deepest vertical pocket of 9-12cm has been defined as mild
polyhydramnios.
o A deepest vertical pocket of 12-16 cm has been defined as moderate
polyhydramnios
o A deepest vertical pocket of 16cm or more has been defined as severe
polyhydramnios
• Polyhydramnios is more common in multipara than primigravidae.

PATHOPHYSIOLOGY
• Exact cause is unknown in about 60% of pregnancies.
• It is postulated that it is due to:
➢ Increased production
o Chorioangioma
o Arteriovenous fistula
➢ Decreased/deficient absorption due to:
o Absent fetal swallowing reflex
o Blockage of the fetus’s gastrointestinal tract
• The composition of the amniotic fluid remains normal.

ASSOCIATED FACTORS
• Associated factors can be classified as:
➢ Fetal
➢ Placental
➢ Maternal
FETAL
• Fetal anomalies (20%)
➢ Structural and chromosomal abnormalities (aneuploidy, Trisomy 21,
Trisomy 18 and Trisomy 13)
o Anecephaly (50%)-due to (a) transudation from the exposed meninges
(b) absence of fetal swallowing reflex and (c) possible suppression of
fetal ADH leading to excessive urination.
o Open spin bifida (transudation of fluid from meninges)
o Esophageal atresia (usually associated with tracheoesophageal fistula),
tracheal agenesis, duodenal atresia and other intestinal atresia.
o Facial cleft and neck masses (obstruction)
➢ CNS abnormalities (e.g. anencephaly) & neuromuscular diseases that
cause swallowing dysfunction.
• Fetal akinesia syndrome with absence of swallowing
• Hydrops fetalis (Rhesus isoimmunization), cardiothoracic anomalies and fetal
cirrhosis are also associated with hydramnios.
• Idiopathic
PLACENTAL
• Angioma of placenta (chorioangioma)- resulting in hyperplasia of the blood
vessels of the placenta.
• Arterio-venous fistula
MATERNAL
• Multiple pregnancy (twin-to-twin transfusion syndrome), monozygotic twins
have an increased amniotic fluid in the recipient twin and decreased amniotic
fluid in the donor.
• Maternal medical conditions: diabetes mellitus (in DM there is hyperglycemia
in the fetus which results in polyuria and polyhydramnios), hypertension in
pregnancy or renal disease may lead to edema of the placenta leading to
increase in transudation, TORCH infection.
PREPARED BY MOSES KAZEVU

CLINICAL PRESENTATION
• Presentation can be acute with rapid onset or chronic with gradual onset.
➢ Acute (extremely rare): painful with tense uterus and edematous abdominal
wall, primiparous, pre-eclampsia, often early (22-32 weeks’ gestation but
usually it occurs before 20 weeks)
o It is associated with monozygotic twins with TTS or chorioangioma of
the placenta.
o Features of an acute abdomen predominate- abdominal pain, nausea and
vomiting.
o Signs:
▪ Patient is ill looking
▪ Absent features of shock
▪ Edema of legs or presence of other associated features of pre-
eclampsia
▪ Abdomen is hugely enlarged more than the period of amenorrhea:
the wall is tense with shiny skin
▪ Fluid thrill is present
▪ Fetal parts cannot be felt nor is the fetal heart sound audible
▪ Internal examination reveals- taking up the cervix or even dilation
of the os through which the bulged membranes are felt.
▪ Sonography may show multiple fetuses or at times fetal
abnormalities.
o Treatment: most often, spontaneous abortion occurs. In case with severe
TTTS, repetitive amnioreduction until the AFI is normal, may improve
the perinatal outcome. Laser ablation may cure the cause of TTTS
whereas amnioreduction only treats the symptoms
 ➢ Chronic (most common): slower insidious onset taking few weeks,
uncomfortable rather than painful, it is common in the lasts weeks of
pregnancy.
• History:
➢ Tenseness and swelling of the abdomen.
➢ Unable to lie comfortably in any position (discomfort/abdominal pain)
➢ Palpitations
➢ Dyspnea, indigestion, piles, varicose veins or varicosities in the vulva,
edema of legs,
➢ Decreased sensation of fetal movement
• Examination:
➢ On inspection:
o Markedly distended abdomen (abdomen looks globular with fullness at
the flanks)
o Tense skin, shiny with Stria gravidarum
➢ On palpation
o Very tense cystic uterus bigger than maturity (like a balloon filled with
water)
o Abnormal girth of the abdomen round the umbilicus.
o Increased symphysio-fundal height- Large for dates ≥3cm
o Difficult to feel any fetal part
o Fluid thrill is positive
➢ On auscultation: fetal heart sound is not heard distinctly, although its
presence can be picked up by Doppler ultrasound.
➢ Vaginal examination: cervix is effaced into the uterus. The cervix is pulled
up, may be partially taken up or at times, dilated to admit a finger tip
through which tense bulged membranes can be felt
➢ Stigmata of TORCH infections.
➢ Presence of pre-eclampsia (edema, hypertension and proteinuria)
• May also present with signs and symptoms of underlying cause e.g.
hypertension, hyperglycemia, rhesus negative etc.

MANAGEMENT
PRINCIPLES
• Relieving the discomfort of the mother (if necessary by amnio-drainage)
• Establish the cause (hence determining the fetal prognosis)
• Treatment and management of complications
INVESTIGATIONS
• Ultrasound (Diagnostic)
 ➢ Confirm diagnosis: the deepest column >8cm
➢ Amniotic fluid index >25cm
➢ Note: Fetal lie and presentation
➢ Note any fetal anomalies and malformations specially of the CNS, GIT and
musculoskeletal
• Blood:
➢ ABO and Rhesus determination (if not done): Rh isoimmunization may
cause hydrops fetalis and fetal ascites.
➢ Postprandial sugar and if necessary glucose tolerance test
• Oral glucose tolerance test
• Supportive: FBC, U&Es, Creatinine and liver enzymes
• Amniotic fluid: estimation of alpha fetoprotein which is markedly elevated in
the presence of a fetus with an open neural tube defect.
DIFFERENTIAL DIAGNOSIS
• Twins:
➢ Abdomen is markedly enlarged
➢ Too many fetal parts
➢ Fluid thrill absent
➢ Straight X-ray or sonography confirms the diagnosis
• Pregnancy with huge ovarian cyst:
➢ Gravid uterus can be felt separate from the cyst
➢ Internal examination shows the cervix to be pushed down into the pelvis.
In hydramnios the lower segment has to rid above the pelvic brim so that
the cervix is drawn up.
➢ X-ray of abdomen or sonography is helpful
• Maternal ascites:
➢ Shifting dullness
➢ Resonance on the midline due to floating gut whereas in hydramnios it
becomes dull
➢ Internal examination and palpation of the normal size uterus, if possible
can give the clue
➢ Erect X-ray of the abdomen or sonography helps to exclude pregnancy
MANAGEMENT
• Dependent on cause.
• For treatable etiologies treat the cause.
• Mild polyhydramnios is commonly found in mid-trimester and usually does
not require treatment except extra bed rest for a few days. The excess liquor
is expected to diminish as pregnancy advances.
• Severe polyhydramnios should be treated in a hospital equipped to deal with
“high risk” patients.
• Supportive therapy:
➢ Bed rest, if necessary with a back rest and treatment of associated
conditions like pre-eclampsia or diabetes.
➢ The use of diuretic is of little value.
➢ Indomethacin given orally to the mother (25mg every 6 hours) has found
to decrease amniotic fluid as it reduces fetal urine output
• Uncomplicated cases:
➢ Pregnancy <37 weeks
o Outpatient ultrasound for growth and AFI every 2 weeks
o Monitor for preterm labor or maternal symptoms of dyspnea and
abdominal pain
o If there are no congenital anomalies wait for term to reach and induce
labor. During induction perform artificial rupture of membranes
(AROM)
o If the baby is preterm with no congenital anomalies give steroids
(Dexamethasone 6mg IM every 12 hours x 4 doses) if 26-34 weeks
gestation.
o Indomethacin 25mg OD for 1 week if <32 weeks gestation and
moderate/severe polyhydramnios or maternal symptoms
▪ Indomethacin is believed to decrease amniotic fluid volume and
prevent premature labor.
▪ US-guided amnioreduction if maternal symptoms are present despite
indomethacin.
▪ Note: Indomethacin may close the ductus arteriosus.
▪ Amniocentesis (amnio reduction): slow decompression is done at
the rate of about 500ml per hour and the amount of fluid to be
removed should be sufficient enough to relieve the mechanical
distress. Ordinarily it should not exceed 1-1.5 liter. Because of slow
decompression, chance of accidental hemorrhage is less but
amniotic fluid may reaccumulate for which the procedure may have
to be repeated. Amniotic fluid can be tested for fetal lung maturity.
➢ Pregnancy >37 weeks: induction of labor is done. Amniocentesis is done
and a good amount of liquor is drawn. Check the favorable lie and
presentation of the fetus and then a stabilizing oxytocin infusion is started.
Low rupture of the membranes is done when the lie becomes stable and the
presenting part gets fixed to the pelvis. This will minimize sudden
decompression with separation of the placenta, change in lie of the fetus
and cord prolapse.
• For congenital anomalies or idiopathic:
➢ If congenital anomalies are present or there is fetal/maternal compromise
deliver regardless of the gestational age. Amniocentesis is done to drain
god amount of liquor. Thereafter induction by vaginal PGE 2 gel insertion
followed by low rupture of membranes is done. If accidentally, low rupture
of the membranes occurs, escape, of gush of liquor should be immediately
controlled by placing the palm over the introitus to avoid accidental
hemorrhage. The lie should be checked and if found longitudinal, oxytocin
infusion may be started.
• During labor:
➢ Usual management for twin pregnancy.
➢ Internal examination should be done soon after the rupture of membranes
to exclude cord prolapse. If the uterine contractions become sluggish
oxytocin infusion is started, if not contraindicated.
➢ To prevent postpartum hemorrhage, intravenous methergine 0.2mg should
be given with delivery of the anterior shoulder.
➢ One must remain vigilant following the birth of the baby for retained
placenta, postpartum hemorrhage and shock.
➢ The baby should be thoroughly examined for any congenital anomaly.
COMPLICATIONS
MATERNAL
• Perinatal:
➢ Pre-eclampsia
➢ PROM and PPROM
➢ Pre-term labor: either spontaneous or induced
➢ Malpresentation and persistence of floating head
➢ Placenta abruption
• Intrapartum:
➢ Cord prolapse
➢ Uterine inertia
➢ Increased operative delivery due to malpresentation
➢ Retained placenta
• Postnatal
➢ Postpartum hemorrhage (due to uterine atony) and shock
➢ Subinvolution
➢ Increased puerperal morbidity due to infection resulting from increased
operative interference and blood loss
FETAL
• Prematurity and death due to prematurity.
• Cord prolapse
• Hydrops fetalis
• Effects of increased operative delivery and accidental hemorrhage
OLIGOHYDRAMNIOS
• Oligohydramnios is defined as:
➢ A lack of amniotic fluid (<200ml at term)
➢ Amniotic fluid index <5 (normal 5-25cm)
➢ Single deepest pocket <2cm (normal 2.1-8cm)
• Any of the above parameters are considered abnormal at gestational age from
28-40 weeks.

PATHOPHYSIOLOGY
• Due to either:
➢ Excessive absorption
➢ Reduced production
ASSOCIATED FACTORS
• Fetal: POTTER SEQUENCE
➢ PROM (most common cause) P-Pulmonary hypoplasia
➢ Structural and chromosomal defects
O-oligohydramnios
➢ Bilateral renal agenesis (Potter
sequence/syndrome: bilateral renal agenesis=> T-twist skin (wrinkled skin)
decreased urine production =>
T-twist face (facial deformities)
oligohydramnios=> pulmonary hypoplasia and
structural abnormalities) E-extremities (limb deformities)
➢ Fetal obstructive uropathy: e.g. posterior urethral
R-renal agenesis
valves in males
➢ Intrauterine infection
➢ Drugs e.g. enalapril (inhibit breakdown of bradykinins and this affects the
kidneys), PG inhibitors
➢ Post-maturity
➢ IUGR
• Placental: amnion nodosum (these are nodules on the fetal surface of the
amnion and is frequently present in oligohydramnios, the nodules are
composed of squamous cell aggregates derived from the vernix caseosa on the
fetal skin): failure of secretion by the cells of the amnio covering the placenta
• Maternal:
➢ Hypertensive disorders
➢ Uteroplacental insufficiency
➢ Dehydration
➢ Idiopathic
CLINICAL PRESENTATION
• History:
➢ May be associated with draining
➢ Maternal hypertension
➢ Fetal renal anomalies
• Examination
➢ Fundal height smaller than expected by dates (small for dates)-early sign.
➢ Easily palpable fetal parts (Uterus is “Full of fetus”)-Late sign
➢ Less fetal movements
➢ Malpresentation (breech is common)
➢ Evidence of intrauterine growth restriction

INVESTIGATIONS
• Ultrasound (diagnostic)
➢ Confirm diagnosis: the deepest column <2cm or the amniotic fluid index
<5cm
➢ Fetal position
➢ Fetal anomalies
➢ Evidence of intrauterine growth restriction
• Amniocentesis if GI anomalies (Send for chromosomal defects)
• Supportive: FBC, U&Es, creatinine and LFTs.

MANAGEMENT
• At term: induction of labor
• Transfusion of amniotic fluid (transcervical amnioinfusion)
• For preterm <37weeks
➢ Give the mother dexamethasone (6mg IM every 12 hours x 4 doses)
➢ Encourage hydration: Oral administration of water increases amniotic fluid
➢ Monitor fetus
• For intrauterine growth restriction perform a C-section (note:
oligohydramnios is not an indication for C-section only when associated with
IUGR).
• If there are any anomalies deliver despite the gestational age.

COMPLICATIONS
• Fetal:
➢ Deformities due to intramniotic adhesions e.g. club foot (talipes), altered
skull shapes, wry neck, amputations, dislocations
➢ Pulmonary hypoplasia (may be the cause or effect)
➢ Cord compression
➢ Fetal death
• Maternal
➢ Prolonged labor due to inertia
➢ Preterm labor
➢ Malpresentation and increased operative delivery