OBSTETRICS AND

GYNECOLOGICAL NURSING

SEMINAR ON

DISORDERS OF AMNIOTIC FLUID

Submitted to; submitted by;

Mrs Giggy john Aleena Davis
Asst professor II yr MSc nursing
Govt college of nursing Govt college of nursing
Thrisssur Thrisssur
Introduction

Amniotic fluid volume may be higher or lesser than normal in some pregnancies. Women with a
decrease in fluid may not be symptomatic but when there is gross excess of fluid, distension of
abdomen is obvious and other symptoms due to over distension of the abdomen are also evident.
In addition, the underlying cause of gross increase or decrease in fluid can be detrimental to the
fetus.

Normal amniotic fluid

Amniotic fluid surrounds the fetus from early pregnancy.

Production and clearance

Amniotic fluid is produced and reabsorbed continuously. The entire volume of fluid is replaced
several times a day. The major sources of amniotic fluid are fetal urine and fetal lung fluid, and
clearance is by fetal swallowing and by intramembranous transfer to fetal blood. the fluid is in
dynamic equilibrium because net inflow and net clearance are equal. Changes that affect fetal urine
production, lung fluid secretion, and fetal swallowing or an alteration in intramembraneous flow
can affect the AFV drastically.

Normal amniotic fluid volume

The volume of amniotic fluid increases with gestational age and reaches a peak at 34-36 weeks.
Thereafter, it reduces and the rate of reduction is more rapid after 40 weeks.

Amniotic fluid volume increases at high altitudes and with maternal hydration; it decreases with
fluid restriction and dehydration.

Volume of amniotic fluid inflow and clearance/day at term

Production

Fetal urine : 800- 1200 ml

Fetal lung secretion : 170 ml

Oral – nasal secretions : 25 ml

Clearance

Fetal swallowing : 500-1000 ml

Intramembraneous : 200-400 ml

Transmembraneous : 10 ml

Evaluation of amniotic fluid volume

Gross increase or decrease in AFV can be suspected on clinical examination. Accurate methods of
measurement such as dye dilution techniques are not used in routine practice. The most practical
method of assessment is by ultrasonography. Two techniques are commonly used:

 Single deepest pocket (SDP)

 Amniotic fluid index (AFI)

Amniotic fluid index is more commonly used and is more sensitive. The values can be affected by
differences in ultrasound techniques and pressure of transducer on the abdomen.

DISORDERS OF AMNIOTIC FLUID VOLUME

POLYHYDRAMNIOS

Polyhydramnios or hydramnios is defined as a condition in which amniotic fluid is in excessive

amount, i.e. more than 2 liters. But since quantitative assessment of liquor mum: is impractical,
most commonly used definition is by USG assessment, i.e. when amniotic fluid index (AFI) is
more than 25 cm or above or finding a pocket of fluid (SDP Single deepest pocket) more than 8
cm or above in vertical diameter.

INCIDENCE

Poly hydramnios is seen in approximately 0.4 -1.5 % of all pregnancies, being more common in
multiparas than primi-gravida.

GRADES

Mild hydramnios -When single deepest pocket (SDP) is measuring between 8-11 cm in vertical
dimension or AFI of 25 - 30, it is mild hydramnios (80%).
Moderate hydramnios- When SDP measuring between 12-15 cm in vertical dimensions or AFI 30,
it is moderate hydramnios (15%)

Severe hydramnios - When SDP measures 3 16 cm and AFI greater than 35 it is severe hydramnios.

CAUSES

Poly hydramnios can be due to excess production of AF or due to defective absorption. Various
causes are:

1. Idiopathic : In 66 % of cases (two-thirds) the cause is unknown.

2. Fetal causes :

a. Anencephaly .Swallowing is reduced plus increased transudation of CSF into AF due to

absence of cramal vault and increased urination due to inhibition‘of fetal ADH.

b. Spinal deformities like meningocele, meningomyelocele -due to excessive transudation

of fluid from exposed meninges.

c. Facial deformities and neck swellings like -cleft lip, cleft palate, thyroid swelling, cystic
hygroma due to reduce swallowing of AF.

d. Esophageal or duodenal atresia or stenosis due to impaired swallowing

e. Bowel obstruction, congenital diaphragmatic hernia, fetal sacrococcygeal teratoma,

erythroblastosis fetalis, non-immune hydrops, fetal infections like toxoplasma, rubella,
syphilis

f. Multiple pregnancy -due to big placenta

3. Maternal causes:

a. Diabetes: Maternal hyperglycemia leads to fetal hyperglycemia causing fetal diuresis

and hydramnios.

b. Cardiac diseases due to excessive transudation of fluid

c. Renal diseases from large placenta

4. Placental causes:

a. Chorioangioma of placenta : due to excessive transudation of fluid from it.

b. Circumvallate placenta

CLINICAL TYPES

Depending upon rapidity of onset, poly hydramnios can be

(a) Chronic (most common, a problem seen in third trimester) onset is insidious , taking few weeks,
(b) Acute (extremely rare, diagnosed between 20 and 24 weeks)onset is sudden within few days

CLINICAL FEATURES

Symptoms: They are mainly from mechanical causes:

Respiratory

Dyspnoea or orthopnoea and remain in sitting position for easier breathing ' Palpitation

Swelling of legs, vulva and abdominal wall

Varicosities in legs or vulva due to compression of veins by large uterus.

On examination: Abdomen is markedly enlarged with fullness at flanks .Abdominal skin is shiny
and glistening and tensed. Height of uterus is more than the period of amenorrhea. Abdominal
girth is more than the normal. Fetal parts, also the presentation and position are difficult to identify.
Fetal heart sound is not heard distinctly by stethoscope but can be picked up by Doppler USG.

DIAGNOSIS

USG AH more than 25 cm or SDP more than 8 cm

Blood ABC and Rh typing Rh-isoimmunization (hydrops fetalis)

FBS and PPBS to rule out diabetes

COMPLICATIONS

Maternal: There is increased incidence of pre-eclampsia, mal presentation, PROM, pre-term labor,
cord prolapse, increased incidence of operative delivery, retained placenta and PPH, sub-
involution.

Fetal: Prematurity and congenital abnormalities.

MANAGEMENT

Mild poly hydramnios : Commonly found in mid trimester and usually requires no treatment

Severe poly hydramnios : Shift the patient to an equipped hospital.

Supportive therapy with rest in left lateral position with back rest is advisable. ' A careful search
for an anomaly or maternal diabetes has to be looked for.

In severe cases, if the fetus is mature, a planned induction can be done.

If the fetus is pre term but the patient is in distress, amniocentesis and slow release of the AF by
dependent drainage can be done. At a time, not more than 1000-1500 ml is removed. The procedure
will usually have to be repeated , as accumulation is rapid. Another method to relieve symptoms
is the use of indomethacin. This decreases fetal urine production , but the adverse effect is
premature closure of fetal ductus arteriosus. So it should be used with caution.

During labor:

Controlled ARM and slow release of liquor is preferred, because of the dangers of the cord
prolapse and abruption if the membranes rupture spontaneously. Special care is taken to manage
the third stage.

Neonatal care : The neonatologist should carefully evaluate the baby for the presence of congenital
anomalies. Esophageal atresia should be excluded by passing a soft rubber catheter into the
stomach.

In most women with Polyhydramnios, no cause is found ; therefore management is directed at

relieving symptoms and optimizing the time of delivery.
Specific treatment

If an etiological factor is identified, management should address the specific cause. Maternal
diabetes should be well controlled. If the fetal anomaly is incompatible with life, for example,
anencephaly, pregnancy should be terminated. If aneuploidies or other congenital anomalies are
diagnosed, the parents should be counselled and neonatologist and paediatric surgeons consulted.

Nonspecific treatment

Idiopathic polyhydramnios is the most common and is managed with measures to relieve
symptoms and prevent complications. Treatment depends on the following:

 Severity of polyhydramnios
 Gestational age
 Symptoms

Mild-to-moderate polyhydramnios

These patients may be followed by serial ultrasonography. The AFI stabilizes or normalizes in
many women. In women with symptomatic moderate polyhydramnios, hospitalization and
indomethacin may occasionally be required.

Severe polyhydramnios

In women with severe polyhydramnios, management depends on gestational age.

Gestational age <34 weeks

 Decompression amniocentesis (amnioreduction) to reduce AFV to normal

 Indomethacin for maintenance of normal AFV
 Betamethasone 12 mg intramuscular every 12 hours x 2 doses to accelerate pulmonary
maturity . Serial monitoring of AFV by ultrasonography
 Deliver as close to term as possible

Gestational age >34 weeks

 Deliver
 Amnioreduction
Amnioreduction

ln moderate to severe Polyhydramnios, removal of amniotic fluid (Amnioreduction) may be

performed for decompression. This is beneficial when the woman is symptomatic, the hydramnios
is severe. Medical therapy with indomethacin is more effective after amnioreduction.

Procedure

 Ultrasonography is performed to locate the placenta and to choose the site of

amniocentesis, avoiding the placenta.
 The selected area of the abdomen is painted and draped.
 Local anesthetic is infiltrated.
 An l8-gauge spinal needle is inserted into the amniotic fluid in the lower quadrants to allow
for decrease in uterine size as the fluid is removed.
 A sterile tubing with a three-way stopcock is attached to the hub of the needle and the other
end of the tube to a vacuum suction bottle or other suction device. It should not be allowed
to drain by gravity alone.
 Fluid can be removed as rapidly as possible. Enough fluid is removed to achieve an SDP
of 8 cm or AFI of 15 cm. However, not more than 5 L is removed at one sitting.
 If the fluid stops draining, the needle tip is adjusted.
 The fetal heartbeat is documented at the end of the procedure.
 Antibiotics and tocolytics are not required.

Amniotic fluid volume should be monitored weekly following amniocentesis. If fluid accumulates
again, the procedure may have to be repeated.

Complications of amniocentesis

 Pre-term labour
 Prelabour rupture of membrane
 Placental abruption
 Intra amniotic infection ( rare)
Medical management

Mild idiopathic polyhydramnios may respond to medical therapy. In moderate to severe

polyhydramnios, amnioreduction is performed before starting medical therapy.

lndomethacin

lndomethacin is a prostaglandin synthetase inhibitor . When administered to mothers, it crosses

the placenta and reduces fetal renal blood flow and urine output and also stimulates fetal
vasopressin secretion. This in turn reduces the AFV since fetal urine production is an important
source of amniotic fluid.

Amniotic fluid volume should be monitored closely since oligohydramnios may develop. Closure
of fetal ductus arteriosus and fetal renal compromise are major side effects. As the risk of these
problems increases dramatically after 32-34 weeks, the drug should not be used beyond 34 weeks’
gestation. Indomethacin is also used as a tocolytic.

 Mechanism of action : Stimulates fetal vasopressin production

Reduces fetal urine production
 Dosage : 25 mg four times daily, oral

Can increase to 2 – 3 mg/kg/day

 Maternal side effects : Nausea , gastritis, vomiting, oligohydramnios

 Fetal complications : closure of ductus arteriosus
 If used for > 48 hours
 Worsens with advanced gestation
 Renal damage and renal failure
 Should not be used after 32- 34 weeks gestation

Sulindac

Sulindac is a non steroidal anti- inflammatory agent. It also reduces the AFV and has less effect
on fetal ductus arteriosus. Its usefulness in polyhydramnios has not been adequately evaluated.
Management of Polyhydramnios

Mild to moderate
Severe polyhydramnios
polyhydramnios

Monitor NST, BPP

< 34 weeks >34 weeks
Medical management as
required

Medical management Confirm pulmonary

Deliver at term
decompression by maturity
amniocentesis
Monitor NST, BPP

Deliver
Deliver at 37 weeks

Confirm vertex
presentaion

Amniocentsis or
controlled
amniotomy

Augment with oxytocin if required prophylactic oxytocin 10-20 units IV

infusion in third stage
NURSING MANAGEMENT

Assessment includes :

Maternal respiratory condition, fetal condition by electronic fetal monitoring, abdominal girth
assessment to assess the uterine height, abdominal pain, edema, varicosities of vulva and lower
extremities

I. Ineffective breathing pattern related to pressure on the diaphragm as evidenced by

respiratory rate 26/ min.

Goal

The woman will experience reduction in respiratory discomfort as evidenced by normal RR

Intervention

Administer oxygen 8-10L/ min (to reduce discomfort) Provide adequate rest and comfort

Maintain intake -out put chart (to compare with clinical condition)

2. Fear related to fetal outcome as evidenced by facial expression

Goal

The woman will express feelings of fear and loss and will cope with the present situation.

Intervention

Assess the emotional state.

Note the cultural beliefs and expectations (personal expectations may affect the response)

Note the previous life experiences, coping skills, noting strengths and weakness (useful in dealing
with the present situation)

Make time to listen to client (will help in expressing their feelings)

Be honest in answering questions and providing information (develops sense of trust in nurse client
relationship)

Provide an open, non-judgmental environment (promotes free expression of feelings)

OLIGOHYDRAMNIOS

It is a condition in which the amount of amniotic fluid is reduced to less than 200ml at term.
Sonographically, it is defined as when the AFI is less than 5 cm or SDP is less than 2 cm.

INCIDENCE

It is seen in approximately 4 % of all pregnancies.

ETIOLOGY

l. Maternal:

a. Preterm premature rupture of membranes

b. Utero-placental insufficiency

 Preeclampsia
 Pregestational diabetes

c. Post term pregnancy

d. placental abruption

e. dehydration

2. Fetal

a. chromosomal or structural anomalies

b. IUGR. IUD

c. Renal agenesis

d. Obstructive uropathy

e. Twin to Twin transfusion

3. Drugs like PG inhibitors, ACE inhibitors.

4. Placental :

amnion nodosum ( failure of secretion by cells of amnion)

Abruption

5. Idiopathic

First trimester: oligohydramnios or reduced gestational sac fluid may occur but the etiology is
usually unknown. The criterion for the diagnosis is a difference of < 5 mm between the men
gestational sac size and the crown rump length. Reduced fluid prior to 10 weeks is generally
associated with a poor outcome.

Second trimester : the common cause of oligohydramnios are chromosomal and congenital
anomalies, rupture of membranes, placental abruption and fetal growth restriction.
Oligohydramnios may also be idiopathic. An elevated maternal serum alpha fetoprotein in
association with oligohydramnios carries a poor prognosis.

Third trimester : oligohydramnios is usually due to fetal growth restriction, placental

insufficiency, prelabour rupture of membranes, or post maturity.

DIAGNOSIS

History

When reduced AFV is suspected clinically, history of rupture of membranes, watery discharge,
uterine contraction, hypertension, and history suggestive of antiphospholipid antibody syndrome
should be asked for.

Physical examination

Blood pressure should be checked to exclude hypertension/ preeclampsia. Obstetric examination

reveals; Uterine size is smaller than the period of amenorrhea. Uterus is full of fetus because of
scanty liquor

Decreased fetal movements

Mal-presentations

IUGR

USG -AFI less than 5 cm or SDP less than 2 cm

Speculum examination may reveal watery or blood stained discharge in the presence of ruptured
membranes.

History

 Watery / blood stained vaginal discharge

 Hypertension
 Preeclampsia
 Pregestational hypertension
 Antiphospholipid antibody syndrome
 Family history
o Congenital anomalies
o Chromosomal abnormalities
 Medications
o ACE inhibitors
o Prostaglandin synthetase
 Physical examination
o Blood pressure
o Uterine size less than gestational age
o Reduced amniotic fluid on palpation
 Speculum examination
o Watery / blood stained discharge
o Pooling of fluid in the posterior fornix

INVESTIGATIONS

Ultrasonography should be performed to confirm the diagnosis and to estimate AFI. If

oligohydramnios is confirmed, target ultrasonography is recommended to detect fetal anomalies
such as renal agenesis, polycystic kidneys, outflow obstruction, markers of chromosomal
abnormalities, and fetal growth restriction. Doppler ultrasonography of renal arteries may confirm
renal agenesis. Fetal MRI can also be used to confirm diagnosis. If structural anomalies are
detected, fetal blood sampling and karyotyping are recommended. The placenta should be
localised and abruption should be ruled out.

If there is history of watery vaginal discharge, rupture of membrane must first be excluded by
speculum examination. If there is no obvious watery discharge, microscopic examination of
vaginal swab for ferning or detection of vaginal PH of > 7.5 by nitrazine test will confirm rupture
of membranes.

COMPLICATIONS

Fetal: Abortion, deformities (due to intra-amniotic adhesions or bands ) like amputation of digits,
club foot, alteration in shape of skull, Potter facies (low set ears, epicanthal folds, receding
mandible and flattened nose), pulmonary hypoplasia, cord compression

Due to etiological factors ;

 Congenital anomalies
 Chromosomal anomalies
 Fetal growth restriction
 IUD
 Intrauterine infection following ROM
 Prematurity

Due to reduced AFV

 Skeletal deformities
 Contractures
 Amniotic bands and auto amputations
 Pulmonary hypoplasia
 Umbilical cord compression
 Meconium aspiration
 Fetal herat rate abnormalities
 Low apgar scores
 Intrapartum death
Maternal : Prolonged labor, increased chance of operative delivery, chorioamnionitis.

If lethal anomalies like bilateral renal agenesis are diagnosed, the parents must be counseled and
the option of termination can be given.

In case of correctable anomalies like posterior urethral valves, the option for early neonatal
correction can be given.

In case of IUGR , ante partum fetal surveillance and proper timing of delivery is essential.

Intra partum : Cesarean section may have to be done in many cases especially when the fetus is
compromised. If vaginal delivery is possible , CTG monitoring is essential. The presence of
meconium staining of AF is an indication for amnio-infusion in labor. Amnioinfusion is carried
out using NS which has been warmed to the body temperature. This is extremely useful to prevent
meconium aspiration syndrome

MANAGEMENT

Management depends on the gestational age at diagnosis , the causes of oligohydramnios and fetal
prognosis.

First trimester : If reduced gestational sac fluid is found in the first trimester, the woman should
be counselled regarding the risk of spontaneous miscarriage. Follow up with serial
ultrasonography.

Second trimester : Since prognosis is poor in second trimester oligohydramnios, counselling is

important. The underlying cause should be determined. Amnioinfusion may be required to
visualize the fetus on ultrasonography and perform proper evaluation. Termination of pregnancy
is recommended, if the fetal anomalies is lethal. Follow up with serial ultrasonography is
recommended for others.

Third semester

Management depends upon on the cause of oligohydramnios

 Post term pregnancy with reduced AFI should be delivered

 If the fetus is growth restricted, management should be directed toward the underlying
maternal condition. The fetus should be monitored by serial ultrasonography combined
 with umbilical and middle cerebral artery Doppler. Delivery should be dictated by fetal
condition.
 Women with preterm prelabor rupture of membrane should be managed conservatively till
34 weeks with close monitoring and delivered if leakage of fluid persists.
 Women with idiopathic oligohydramnios should be observed and monitored by non stress
test, serial ultrasonography, and biophysical profile.

Specific measures to increase AFV

Maternal hydration

Review of randomized trials has shown that oral hydration with 1500-2000ml of fluid per day
increases AFV. This is particularly useful in women with dehydration and in summer months.
Intravenous infusion of hypotonic fluid has also been found to be useful but the effects is similar
to oral hydration

Amnioinfusion

Amnioinfusion refers to the instillation of fluid into the amniotic cavity, either addominally or
transcervical amnioinfusion is usually performed. Abdominal amnioinfusion is performed in
second trimester;

 to facilitate visualization of anomalies on ultrasonography

 rarely in preterm prelabour rupture of membranes, after the leak is sealed.

Procedure

 ultrasonography is performed to localise the placenta and identify a pocket of amniotic

fluid
 the abdomen is painted and draped
 a 20 g needle is inserted, taking care to avoid fetal parts
 the needle is connected to sterile tubing, a three way stopcock, and a 50 ml syringe
 normal saline is injected under ultrasound guidance till normal AFV is achieved.
 Antibiotic are not recommended. Anti D globulin must be administered to Rh negative
women
 In women with preterm prelabour rupture of membranes, if the leakage stops spontaneously.
Pulmonary hypoplasia can be prevented and outcome improved with amnioinfusion.

Timing of delivery

When an etiological factor is detected, timing of delivery is guided by the specific condition such
as preeclamsia , growth restriction or fetal anomaly. Pregnancies with idiopathic oligohydramnios
are delivered at 38 weeks or when there is non reassuring fetal status.

Management of labor

Close monitoring is essential in labor. Electronic fetal monitoring is recommended. Membranes

should be ruptured when the women enters active phase of labour, to look for meconium. If
meconium staining and / or fetal heart rate decelerations are present transcervical amnioinfusion
should be considerd. If fetal heart rate abnormalities persist, immediate caesarean section is
indicated.
 Management of oligohydramnios

Second Third trimester

First trimester
trimester

Counsel
Counsel Post Growth
PROM idiopathic
Excludes term restriction
Serial scans
anomalies

Exclude PPROM

Serial scans
Maternal hydration
Consider
Serial NST/ BPP
amnioinfusion

Leakage Fetal
38 weeks
persists or compromise

>/= weeks

Deliver
Nursing management

If the fetus has been diagnosed with a congenital anomaly, psychological support is needed to
assist the family. Explain the procedure to the couple , if needed.

Nursing diagnoses includes:

1. Risk for impaired gas exchange related to cord compression secondary to oligohydramnios

Goal The woman will verbalize understanding of the causative factors and appropriate
interventions

Intervention

Assess Vital signs every 15 minutes (provides baseline on maternal blood loss)

Maintain bed rest (reduce fatigue and improve strength)

Monitor for DFMC and frequent NST (to identify signs of fetal distress)

Position mother on her left side (to provide placental perfusion)

Increase intake of fluids

Monitor uterine contractions and HR by external monitor (gives the information on fetal status)

Administer oxygen as indicated (provides fetal oxygenation

2. Fear related to unknown outcome of pregnancy.

Goal: The woman will express feelings of fear and loss and will cope with the present situation.
Intervention

Assess the emotional state. Note the cultural beliefs and expectations (personal expectations may
affect the response)

Note the previous life experiences, coping skills, noting strengths and weakness (useful in dealing
with the present situation) Make time to listen to client (will help in expressing their feelings)

Be honest in answering questions and providing information (develops sense of trust in nurse client
relationship)
Provide an open, non-judgmental environment (promotes free expression of feelings)

Amniotic Fluid Embolism

Historical/Clinical Background

Amniotic fluid embolism is a rare obstetrical complication that carries a significant probability of
maternal and/or fetal death. Maternal presentation classically includes early postpartum onset of
cardiorespiratory arrest and somatic hemorrhage. 89

Clinical Evaluation

The clinical diagnosis is usually based on presentation, although definitive diagnosis requires
pathologic confirmation. Because signs and symptoms of amniotic fluid embolism are severe and
develop rapidly, and other disorders can mimic amniotic fluid embolism clinically, prompt
treatment and successful outcome remain elusive in many cases.

Clinical Correlates/Outcome

Amniotic fluid embolism-associated maternal and perinatal mortality remain high (case fatality
rates of 19% and 38% in two recent studies, respectively). In survivors, morbidity is predominantly
neurologic: permanent maternal neurologic deficits and neonatal asphyxia, the latter with its
attendant long-term deficit risks

Diagnostic Criteria

In cases of maternal death, postmortem pulmonary examination reveals diagnostic plugs of fetal
skin cells (“squames”), maternal neutrophils, and fibrin within alveolar capillaries and small
arterioles. In women who survive, if hysterectomy is performed, amniotic fluid elements (squames
with or without lanugo hairs) may also be found in myometrial vessels. There is no specific
microscopic placental pathology in amniotic fluid embolism.
Differential Diagnosis and Potential Pitfalls

Maternal mortality due to amniotic fluid embolism can overlap clinically with other causes of
cardiorespiratory collapse, most notably hypovolemic shock secondary to postpartum hemorrhage,
anesthetic accident, pulmonary thromboembolism, septic shock, and anaphylactic shock. 89
Consequent clinical manifestations may therefore also overlap, including DIC and refractory
hypotension. Pathologically, findings common to these conditions can include widespread visceral
hemorrhage and early ischemic myocardial infarction. However, only amniotic fluid embolism
will manifest the characteristic intravascular elements within small pulmonary vessels and within
myometrial vasculature. Too, fibrin microthrombi should be absent in other viscera, unless perhaps
profound and prolonged DIC has supervened before death.

Am J Obstet Gynecol. 1996 May;174(5):1608-13.

Treatment of oligohydramnios with maternal 1-deamino-[8-D-arginine] vasopressin-

induced plasma hypoosmolality.

Ross MG1, Cedars L, Nijland MJ, Ogundipe A.

Author information
Abstract
OBJECTIVE:

Maternal 1-deamino-[8-D-arginine] vasopressin (a selective antidiuretic agonist) and oral water

loading decrease maternal and fetal plasma osmolality and markedly increase fetal urine flow in
sheep. We hypothesized that a titrated reduction in maternal plasma osmolality would increase
human amniotic fluid volume.

STUDY DESIGN:

Pregnant women (n = 5) with oligohydramnios at term were administered oral water loading (20
ml/kg) and intravenous 1-deamino-[8-D-arginine] vasopressin (2 micrograms) to induce
antidiuresis. Maternal plasma and urine osmolality and urine production were measured hourly,
and water replacement was titrated for 8 hours to reduce plasma osmolality by 15 to 20 mOsm/kg.
The amniotic fluid index determined by ultrasonography was measured at baseline, 8 hours, and
24 hours. A control group of pregnant women (n = 5) with oligohydramnios at term was observed
for 8 hours with maintenance intravenous hydration.
RESULTS:

In 1-deamino-[8-D-arginine] vasopressin-treated women, maternal urine flow increased with oral

water loading, decreased with 1-deamino-[8-D-arginine] vasopressin administration, and remained
reduced for 8 hours. Maternal plasma osmolality significantly decreased (285 +/- 4 to 265 +/- 4
mOsm/kg) and the amniotic fluid index significantly increased (4.1 +/- 0.6 to 8.2 +/- 1.5 cm) at 8
hours. Although maternal urine osmolality returned to basal values at 24 hours, plasma osmolality
was reduced and the amniotic fluid index remained significantly increased (8.2 +/- 1.3 cm). There
was no change in the amniotic fluid index (4.3 +/- 0.4 to 4.7 +/- 0.7 cm) in control patients observed
with maintenance intravenous hydration.

CONCLUSIONS:

Maternal 1-deamino-[8-D-arginine] vasopressin and oral water administration can reduce and
stabilize plasma osmolality and increase amniotic fluid volume. 1-Deamino-[8-D-arginine]
vasopressin therapy has potential for the prevention and treatment of oligohydramnios.

Polyhydramnios: Causes, Diagnosis and Therapy

A.
Hamza,1 D. Herr,1 E. F. Solomayer,2 and G. Meyberg-Solomayer1
Potential Future Experimental Therapies

As fetal urine production constitutes the main source of amniotic fluid and changes in urine
production can significantly change the dynamics of amniotic fluid volumes, the effect of intra-
amniotic administration of arginine vasopressin was investigated. Arginine vasopressin is
absorbed into fetal plasma from the intra-amniotic fluid. The effects of a V2 receptor agonist,
deamino(D-Arg8)-vasopressin, on fetal plasma arginine vasopressin immunoreactivity, fetal urine
production and swallowing was investigated in 6 individual ovine pregnancies. It was
demonstrated that intra-amniotic administration of deamino(D-Arg8)-vasopressin resulted in
persistent fetal antidiuresis with no cardiovascular effects and no changes in fetal swallowing.
Even though the data do not permit a general conclusion to be drawn, these results indicate this
could be a potential therapy for polyhydramnios 63.

Another potential therapy is based on mRNA expression in chorion and amnion cells of aquaporin
(AQP) 1, 8 und 9 in amniotic fluid, which is increased in polyhydramnios. Aquaporins are water
channel proteins which regulate the flow of water across cellular membranes. AQP1 expression
could represent a compensatory response to polyhydramnios. The effect of reducing this protein
on polyhydramnios requires further study 64, 65. The efficacy and safety of these experimental
therapeutic approaches should be investigated in prospective randomized studies.

Go to:

Monitoring of Pregnancies with Polyhydramnios

In view of the increased perinatal mortality and morbidity associated with pregnancies with
polyhydramnios, careful monitoring is recommended 46.
Expectant management vs. intervention

There are no prospective randomized studies comparing expectant management to active

intervention in idiopathic polyhydramnios 1. Intervention is generally recommended in cases with
severe maternal discomfort or obstetric complications, e.g. premature labor.

Delivery

Fetal head presentation should be checked several times during labor, as fetal position change to
breech presentation or transverse lie can occur intrapartum.

Spontaneous rupture of membranes can lead to acute uterine decompression with the risk of cord
prolapse or placental abruption. Artificial rupture of membranes should therefore only be done
under controlled conditions.

Although polyhydramnios does not constitute a contraindication for the application of oxytocin or
prostaglandins, these substances should be administered with care. There is an increased risk of
atonic bleeding and amniotic-fluid embolism postpartum 57, 67.

CONCLUSION

Amniotic fluid is an important part of pregnancy and fetal development. This watery fluid is inside
a casing called the amniotic membrane (or sac) and fluid surrounds the fetus throughout pregnancy.
Amniotic fluid helps protect and cushion the fetus and plays an important role in the development
of many of the fetal organs including the lungs, kidneys, and gastrointestinal tract. Fluid is
produced by the fetal lungs and kidneys. It is taken up with fetal swallowing and sent across the
placenta to the mother's circulation. Too much or too little amniotic fluid is associated with
abnormalities in development and pregnancy complications. Differences in the amount of fluid
may be the cause or the result of the problem.
REFERENCE

Dutta D C Konar H. textbook of obstetrics newdelhi, india

Lowdermilk, Perry, Bobak. Maternity Nursing. Mosby, Inc.

S Balakrishnan Textbook Of Obstetrics, Paras Medical Publisher (2007)

https://www.ncbi.nlm.nih.gov/pubmed/9065138

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3857760/

https://www.sciencedirect.com/topics/neuroscience/amniotic-fluid

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964358/