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HYDRAMNIOS

(MATERNAL AND CHILD NURSING)


Hydramnios (Polyhydramnios) is a condition in which the amount of the Amniotic Fluid
(AF) is more than 2000ml relatively to the Age of Gestation (AOG). However, to make the
diagnosis more accurate and practical in clinical setting, in ultrasonography, Hydramnios has a
Single Deepest Pocket (SDP) equal or greater than 8cm and an Amniotic Fluid Index (AFI) equal
or greater than 25cm.

Normally, amniotic volume is maintained by a balance of fetal fluid production and fluid
absorption. The amount of AF is regulated by three ways: Fetal Swallowing and Transmembrane
and Intramembrane Net Water Movement. Fetal Swallowing plays the major role in regulating
the amount of AF through its absorption in GI Tract and Respiratory Tract. Transmembrane Net
Water Movement takes place between the amniotic sac and placenta and vice versa while the
Intramembrane Net Water Movement occurs between the Amniotic Fluid to umbilical cord and to
fetus (until fetal skin is keratinized) but both of these are facilitated by diffusion caused by
sudden change of osmolality.

Key point: Fetal urine is the primary source of amniotic fluid with output at term ranging
from 400 to 1,200 ml/day and Fetal swallowing is believed to be the major route of amniotic
fluid resorption.

The following are the causes of excessive amount of AF;

1. MATERNAL CAUSES
1. Maternal Diabetes Mellitus
2. Rh- Isoimmunization
2. FETAL CAUSES
1. Neural Tube Defects (Anencephaly, Spina Bifida)
2. Gastrointestinal Malformation (Esophageal Atresia, Duodenal Atresia)
3. Cleft Lip and Cleft Palate
4. Neck Masses

3. PLACENTAL CAUSE/S
1. Chorioangioma
4. MULTIPLE GESTATION (MONOCHORIONIC DIAMNIOTIC(MCDA) TWIN
PREGNANCY)
1. Twin-to-Twin Transfusion Syndrome (TTTS)

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MATERNAL CAUSES

1. Maternal Diabetes Mellitus

Excessive amount
High Maternal of glucose is Polyuria
Blood Sugar Level filtered in the
kidney and
excreted.
Increased
Fetal amount of
Hyperglycemia amniotic Fluid

A pregnant woman with Diabetes Mellitus has high blood sugar level. Therefore, the
fetus receives excess glucose from the mother through the placenta leading to Fetal
Hyperglycemia. Excessive amount of glucose will be of no use in the fetal body and will be
filtered and excreted by the kidney which causes increased volume of urine produced (polyuria).
Urine is the main contributor to the amount of AF. Increased in urine production also means
increased in AF volume.

2. RH-ISOIMMUNIZATION

Sensitization of the Increased Heart rate caused


During the second pregnancy
Maternal negative by Hypoxia-Stimulated
with the same Rh
Rh blood to Fetal Chemoreceptor and increased
incompatibility in first
positive Rh blood Sympathetic Activity to
pregnancy, the maternal
during the first compensate with anemia.
antibodies will cross through
delivery. placenta and enters the fetal
circulation killing fetal RBCs
resulting to hemolytic anemia Increased blood
flow, thus increasing
renal blood flow and
The sensitization GFR thus increasing
triggers the urine output
formation of Massive death of RBC causes
Maternal anti-Rh insufficiency of O2 in the
antibodies. blood. Increased amount of
amniotic Fluid

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In the first pregnancy of a woman with incompatible Rh group with her baby (negative
Rh mother and Positive Rh fetus), during delivery, the exposure of maternal blood to the fetal
blood will lead to sensitization. Sensitization is a process which an organism became exposed and
sensitive to foreign substance. In this case, the fetal blood will be recognized by the Maternal
body as foreign invaders during the exposure because of the incompatibility of the Rh blood
group. This will trigger the formation of the Maternal Anti-Rh anti-antibodies. The formation of
these antibodies will take longer so it won’t affect the first pregnancy. However, the second
pregnancy with RH incompatibility will be affected. The maternal antibodies will cross the
placenta and will enter the fetal circulation killing fetal RBCs leading to hemolytic anemia. The
massive death of RBC will lead to insufficiency of O2 in the blood. The decreased in O2 will
stimulate hypoxia-stimulated chemoreceptor which increases sympathetic activity of the nervous
system causing increased heart rate to compensate with anemia. Increased Heart Rate also
increases cardiac output and blood flow. Renal blood flow increases as well as the Glomerular
Filtration rate thus increasing urine output and AF volume.

FETAL CAUSES

1. Neural Tube Defects: Anencephaly

Transudation of CSF from Increased


Absence of Cranial exposed meninges (area amount of
Vault. cerebrovasculosa) into the amniotic Fluid
AF

During the embryonic stage, the neural folds weren’t able to fully closed leading to
neural tube defects. One example is Anencephaly- the absence of upper portion of brain, skull
and scalp. The Cerebrospinal fluid ,which is initially derived from AF and soon produced by
choroid plexus, can’t be contained due to absence of cranial vault/skull. Also, without skull,
the abnormally formed and highly vascularized meninges, also called area cerebrovasculosa,
is exposed directly to AF. This will lead to transudation of CSF into AF. Transudation is a
process where fluid escapes or leaks slowly from unclosed membrane. CSF will leak
increasing the AF volume.
Decreased Increased
Abnormal Urine
Decreased Water
formation of
in released retention and Output.
the brain thus
of arginine reabsorption
decreasing the
vasopressin in the kidneys
functioning of Increased amount of
4 hypothalamus.
|HYDRAMNIOS amniotic Fluid
Due to malformation of the brain during development, the function of hypothalamus
decreases. Hypothalamus controls the release of arginine vasopressin or also called, Anti-Diuretic
Hormone (ADH) of Posterior Pituitary gland which is responsible for water retention and
reabsorption in the kidneys to regulate body water and electrolyte balance. The released of this
hormone is triggered by decreased blood volume or increased osmolality detected by
osmoreceptor found in hypothalamus. With a decreased functioning of hypothalamus, the
receptor functioning also decreases thus affecting the release of ADH. Less water is retained and
reabsorbed back into the bloodstream resulting to increased urine output and AF volume.

Abnormal
Unequal Increased
formation of the Decreased Fetal production amount
brain thus Swallowing thus and
decreasing the decreasing
of
consumption
functioning of Absorption. amniotic
of AF
primary motor Fluid
cortex and medulla
oblongata.
The primary motor cortex and medulla oblongata are parts of the brain responsible for
swallowing. Therefore, when the brain is malformed, it decreases the function of the swallowing
center thus impairing the normal cycle of fetal swallowing. Fetal Swallowing plays a major role
in regulating the volume of AF by eliminating it through consumption. When fetal swallowing is
impaired, the elimination and production of AF will be unequal. The AF will be continuously
produced in normal manner however the normal amount of AF that should be eliminated will be
reduced leading to increased amount of AF.

1.1 Neural Tube Defects: Spina Bifida

Transudation of the CSF


Unclosed
into the AF from the Increased
section of Spinal
opening of the amount of
Column during
deformed Spinal amniotic Fluid
Development.
Column.

5|HYDRAMNIOS
During the fetal development, the spinal column was unable to fully closed. The
deformed spinal cord also contains CSF produced by choroid plexus. With an opening in the
spinal cord, the CSF will leak directly into the AF thus increasing the AF volume.

2. GI Deformities (Esophageal Atresia, Duodenal Atresia)

Narrowing of
Interruption to Unequal
Gastrointestinal Increased
normal cycle of production and
parts (e.g
fetal consumption of amount of
Esophageal and
swallowing. AF amniotic Fluid
duodenal
atresia)

When parts of GI tract narrowed and weren’t able to form normally (e.g Esophageal and
duodenal atresia), normal fetal swallowing will be interrupted and absorption of AF will be
reduced. Thus, the production and consumption of AF will be unequal. There is more amniotic
fluid produced than the amount consumed increasing the AF volume.

3. Cleft Lip and Cleft Palate

Interruption to Unequal
Increased
normal cycle of production and
amount of
fetal consumption of
Deformed Lips amniotic
swallowing. AF
and Palate Fluid

Both lips and palate help in the mechanical function of swallowing. Thus, its deformities
will affect the normal cycle of fetal swallowing leading to reduce absorption of AF unequal to
production. Therefore, AF volume will increase.

4. Neck Masses

Impaired Unequal
Obstruction to the Fetal production and Increased
airway tubes and/or swallowing consumption of amount of
esophagus due to and AF amniotic
these masses decreased Fluid
Absorption.

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The presence of masses on the fetal neck obstruct the airway tubes and esophagus
causing it to narrow. This will impair the normal cycle of fetal swallowing and will reduce the AF
absorption leading to unequal consumption and production of AF. Therefore, increasing AF
volume.

PLACENTAL CAUSE

1. Chorioangioma

Presence of
small and large Increased Movement of
masses in the Hydrostatic water out from
placenta Pressure intravascular Increased
within the space into the amount of
vessels amniotic fluid amniotic
caused by through the
Fluid
the semipermeable
Obstruction to amniotic cavity.
obstruction
vessels due to
to blood
these masses.
flow.

Chorioangioma is characterized by hypo or hyperechoic masses in the placenta. These


masses can cause vessel obstruction depending on its location on the placenta. Commonly. The
large masses located in the fetal side of the placenta contributes to the development of
hydramnios. With the masses obstructing the vessels, the capillary hydrostatic pressure inside the
intravascular space increases. The increasing pressure will cause the movement of water and
other small molecules out of the intravascular space through the semipermeable amniotic cavity
leading to increased AF volume.

MULTIPLE GESTATION (MCDA Twin Pregnancy)

1. Twin-to-Twin Transfusion Syndrome The recipient twin has


Changes in increased blood flow, thus
Higher in number and/or larger
Expression of increasing renal blood flow
in diameter Arterio-Venous
Growth Factors and GFR.
Anastomoses in the placenta
and Receptors in resulting to inability of the
Endothelial Cells Arterio-Arterial and Veno-
during Renal Hypertrophy and Polyuria
Venous Anastomoses to
Vasculogenesis compensate with the abnormal
and increased of blood flow from the
Angiogenesis. donor twin to the recipient twin. Increased amount of Amniotic Fluid
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In MCDA, the twins have connected vessels in the placenta called anastomoses which
varies in sizes and diameter. Both Arterio-Arterial and veno-venous Anastomoses has bi-
directional flow depending on the pressure inside these vessels while Arterio-venous
Anastomoses has unidirectional flow (from artery to vein only). AA AND VV Anastomoses
compensate with AV anastomoses, maintaining the balanced flow of blood from one twin to
another. These vascular connections play the key role in developing Twin-to-twin Transfusion
Syndrome (TTTS). TTTS only affects the twin pregnancy with fetuses with different amniotic sac
but sharing with one placenta (Monochorionic Diamniotic). This happens when there is changes
in expression of growth factors (GF) and receptors in endothelial cells during Vasculogenesis
(forming large network of blood vessels esp. Arteries and Veins) and angiogenesis (formation of
capillary network) affecting the shared placental vessels’ sizes and diameter. With higher in
number and/or larger in diameter AV anastomoses, the AA AND VV anastomoses weren’t able
to compensate with blood flow between the twins. One of the twins become the donor twin and
the other one becomes the recipient twin. There is increased blood flow to the recipient twin thus
increasing renal blood flow and GFR causing renal hypertrophy and polyuria. AF volume
increases.

SIGNS AND SYMPTOMS OF POLYHDRAMNIOS

Polyhydramnios symptoms result from pressure being exerted within the uterus and on
nearby organs. Mild polyhydramnios may cause few signs or symptoms. Severe polyhydramnios
may cause:

 Shortness of breath or the inability to breathe


 Uterine discomfort or contractions
 Fetal malposition, such as breech presentation
 Uterus is excessively enlarged
 Difficult to feel the fetal parts

TREATMENT
1. Amnioreduction
The rationale behind amnioreduction is thus to restore normal amniotic
pressure by draining a large amount of amniotic fluid volume in order to reduce

8|HYDRAMNIOS
maternal discomfort, improve uteroplacental perfusion, and prolong pregnancy
by limiting the risk of preterm labor and rupture of the membranes.

2. Pharmacological Treatment
a. Prostaglandin Synthetase Inhibitor
Prostaglandin synthetase inhibitors stimulate fetal secretion of arginine
vasopressin, resulting in vasopressin-induced antidiuresis. Reduced renal
blood flow reduces fetal urine production. These substances can also
inhibit fetal lung liquid production or increase reabsorption rates.
b. Sulindac
Sulindac is a non-steroidal anti-inflammatory drug; use of sulindac can
also lead to a reduction of amniotic fluid volume.

COMPLICATION
 Preterm contractions and possibly preterm labor
 Premature rupture of membranes
 Fetal malposition
 Maternal respiratory compromise
 Umbilical cord prolapse
 Uterine atony
 Abruptio placentae
 Fetal death (risk is increased even when polyhydramnios is idiopathic)

Risks tend to be proportional to the degree of fluid accumulation and vary with the cause.
Other problems (eg, low Apgar score, fetal distress, nuchal cord, malpresentation requiring
cesarean delivery) may occur.

NURSING INTERVENTION
 Mild to moderate degrees usually does not require treatment.
 Hospitalization if symptoms are severe dyspnea, abdominal pain and difficult ambulation.
 Maintain bed rest with sedation to make the situation endurable.
 Monitor the patient for signs and symptoms of premature labor.
 Monitor maternal vital signs and fetal heart rate frequently; report changes immediately.

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 Prepare the patient for amniocentesis and possible labor induction, as appropriate; keep in
mind that amniocentesis for fluid removals is only temporary and may need to be done
repeatedly.

10 | H Y D R A M N I O S

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