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Hydramnios: (Maternal and Child Nursing)
Hydramnios: (Maternal and Child Nursing)
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.
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)
2|HYDRAMNIOS
MATERNAL CAUSES
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
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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
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.
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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.
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.
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.
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:
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
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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.
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