Download Amniotic fluid and it,s abnormality

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts

Miscarriage wikipedia, lookup

Anovulation wikipedia, lookup

Prenatal testing wikipedia, lookup

Cell-free fetal DNA wikipedia, lookup

Transcript
Amniotic fluid and it,s abnormality
The amniotic fluid initially is secreted by the amnion but by the
10th week it,s mainly atransudate of fetal serum via the skin and
umbilical cord ;from 16th wk. the fetal skin becomes
impermeable to water and net increasein amniotic fluid is
through asmall imbalance between the contributions of fluid
through the kidneys and lung fluids and removal by fetal
swallowing.
AF increases progressively:
10 wk.:30 ml
20wk.:300ml
30wk:600ml
38wk:1000ml
But post-term,there is arapid fall in
volume(40wk:800ml,42wk:350ml).
The reason for the late reduction in AF volume has not been
explained.
The function of the amniotic fluid is to :
*Protect the fetus from mechanical injury.
*permit movement of the fetus while preventing limb
contracture.
*It provides an even temperature..
*It is also bacteriostatic,providing some protection against
bacteria.
*prevent adhesions between fetus and amnion .
*permit fetal lung development in which there is two way
movement of fluid into the fetal bronchioles .
Absence of AF in the second trimester is associated with
pulmonary hypoplasia.
*In labor,the even distribution of fluid allows for the force of
uterine contraction to be applied evenly to the cervix when the
presenting part is high.
*The presence of AF provides the ultrasonographer with an
excellent view of the fetus by transmitting sound freely.
*The volume of the AF presents an important indicator of fetal
condition(as in cases with increase or decrease in AF volume)
*It is useful in fetal diagnosis.Access to AF by
amniocentesis,chromosomal
abnormalities,isoimmunization,lung maturity and infection .
Abnormalities of amniotic fluid:
Polyhydramnios;
About 1% of pregnant women have polyhydramnia,most cases
are minor and result from agradual buildup of excess fluid in the
second half of pregnancy. However ,asmall number of women
have arapid buildup of fluid occurring as early as 16 weeks of
gestation that usually results in very early delivery.
The amount of AF in the amniotic cavity is variable dependant
on maternal and fetal factors,the alteration of any factor that
regulate the fetomaternal equilibrium may induce an abnormal
increase in AFvolume,the factors involved in this regulation are
fetal swallowing,micturition,respiratory movements and
uteroplacental blood flow.
Causes of polyhydramnia are ;
*Maternal.
*Fetal.
*Placental.
*Idiopathic.
Maternal causes;15%
1-Rh isoimmunization ;is uncommon now due to the use of
Rh(D)immunoglobulin.
2-Diabetes :form about 14% of cases with polyhydramnia,the
etiology is unknown,fetal hyperglycemia with polyuria and
increased osmolarity of the AFcaused by high glucose
concentration has been proposed
*Placental causes:<1%
1-placental chorioangioma.
2-Circumvallate placenta syndrome.
Fetal causes 18%:
A-multiple pregnancy esp.in monozygotic twins with twin to
twin transfusion syndrome,multiple pregnancy accounts for
4.9% of all cases of polyhydramnia.
B-Fetal infection ,such as with parvovirus B19(which in
childhood commonly causes amild illness called fifth disease)
Rubella,syphilis and toxoplasmosis.
C-Fetal anomalies,12.7% the most common lesions are :
1-Abnormalities of the central nervous system including
anencephaly,hydrocephaly,encephalocele,spina bifida and
microcephaly.
2-Gastrointestinal abnormalities:include esophageal
atresia,annular pancreas,jejunal atresia,diaphragmatic hernia and
duodenal atresia.
3-Genitourinary abnormalities include partial or complete
urinary atresia,most commonly ureteropelvic obstruction.
4-Skeletal malformations:osteogenesis imperfecta and
achondroplasia.
5-Fetal tumors:include cystic congenital adenomatoid
malformation of the lung,sacrococcygeal teratoma.
6-Cardiac abnormalities:severe congenital heart disease and
persistent cardiac arrhythmia.
7-Chromosomal abnormalities:the most frequent are Down
syndrome and trisomies 13 and 18.
8-Genetic syndromes:include hydrocephalus syndrome,multiple
congenital anomalies and myotonia dystrophica.
9-Hematological disorders:homozygous alpha thalassemia and
fetomaternal hemorrhage.
D-Miscellaneous:non immune hydrops fetalis.
*Idiopathic causes:65% most mild cases of polyhydramnios are
idiopathic.
Diagnosis of polyhydramnia:
1-Clinically:
*uterine size larger than expected for gestational age.
*easy ballotment of the fetus.
*difficulty in defining fetal parts.
*faded heart tones.
2-Ultrasound:by finding apocket of fluid measuring 8cm or
more in vertical diameter.
The vertical measurement of the largest single pocket of
amniotic fluid free of fetal parts is used to classify poly
hydramnia into mild(8-11cm),moderate(12-15cm) and
severe(16cm or more).
Another ultrasound definition is by finding an amniotic fluid
index(AFI) greater than 25cm.
AFI:AFvolume is measured with the four quadrant technique
which consist of measuring the largest pool of fluid found in
each of the four quadrants of the uterus,the measurement are
added and the result is the AFI.
Traditionally any volume of AF greater than 2000ml has been
considered as polyhydramnia and there is two types of
polyhydramnia:either acute when it occur before 24wk of
gestation or chronic when the diagnosis is made in the third
trimester.
Complications of polyhydramnios:
Maternal complications include:
1-pregnancy induced hypertention.
2-preterm labor.
3-premature rupture of membrane.
4-respiratory discomfort.
5-Intrapartum complications include placental abruption,cord
prolapse,placental insufficiency and increased incidence of ClS
6-postpartum hemorrhage.
Fetal morbidity and mortality:
The major cause of mortality is congenital abnormality
incompatible with life.
Morbidity usually is associated with minor abnormalities and
with prematurity and its complications.
Management:
1-U\S examination to detect congenital and placental
abnormalities and to confirm gestational age.
2-Fetal karyotyping using amniocentesis,cordocentesis or
placental biopsy.
3-Fetal swallowing studies are also indicated..
4-Basic laboratory studies include maternal antibody
screen,diabetic screening and TORCH serology.If these
evaluations are negative ,the case should be considered as
idiopathic.
5-serial amniotic fluid decompression is the treatment of choice
relieves maternal discomfort and also reduces excessive
intrauterine pressure that can induce preterm labor.
6-Prostaglandin synthetase inhibitors(Indomethacine) have been
proven in reducing the amount of amniotic fluid,it probably acts
by decreasing the fetal urinary output or by increasing the
reabsorption of fluid via the lung .the dose is 2.2mg/kg/day
orally every 6 hr.this treatment should be suspended at 32wk of
gestation to avoid neonatal hemodynamic complications.
This drug may cause fetal ductal constriction and close
monitoring by serial fetal echocardiographic studies is
necessary.
7-Prenatal therapy:the aim is to reduce the risk of very
premature delivery,treatment will depend on the diagnosis and
will include better glycemic control of maternal
D.M,antiarrhythmic medication for fetal hydrops due to
dysrrhythmias,thoracoamniotic shunt for fetal pulmonary cysts
or pleural effusions.
In twin to twin transfusion syndrome ,presenting with acute
polyhydramnia at 18-22wks of gestation endoscopic laser
occlusion of placental anastomoses or serial amniodrainage may
be carried out.
Oligohydramnios;
About 4% of pregnant women have oligohydramnios,it can
develop at any time during pregnancy,although it is most
common in the last trimester,some 12% of women whose
pregnancies last about 2wks beyond their due dates(42wks
gestation) develop oligohydramnios.
Defined asAFI of less than 5cm in severe cases and less than 10
cm in mild cases.
Causes:
1-postterm pregnancy.
2-PROM
3-maternal health condition such as chronic hypertension,severe
PET,SLE and chronic renal disease
4-fetal congenital abnormalities,such as renal
agenesis,obstructive uropathy,multicystic,dysplastic
kidney,skeletal dysplasia,congenital heart block and multiple
anomalies.
5-certain medications,like angiotensin converting enzyme
inhibitors(captopril) used to treat hypertension,can damage the
fetal kidneys and cause severe oligo hydramnios and fetal death.
6-leaking fluid following amniocentesis and chorionic villi
sampling.
7-uteroplacental insufficiency.
Diagnosis:
1-Largest single pocket of AF being 1cm or less.
2-AFI of 5 cm.
4-in uteroplacental insufficiency,Doppler blood flow studies
will often demonstrate high impedence to flow in the placental
circulation and redistribution in the fetal circulation.
5-In the remaining cases,intraamniotic instillation of normal
saline may help improve ultrasonographic examination and lead
to the diagnosis of fetal abnormalities like renal agenesis.
Risk of oligohydramnios:
Oligohydramnios is more likely to have serious consequences if
it occur in the first half of pregnancy than if it occur in the last
trimester,these consequences include;
*Birth defect:too little amniotic fluid early in pregnancy can
lead to compression of fetal organs,resulting in lung and limb
defects.
*Miscarriage.
*Premature birth.
*Stillbirth.
When oligo hydramnia occurs in the 2nd half of pregnancy,it
may be associated with poor fetal growth.Near term it may
increase the risk of complication of labor and delivery,including
compression of the umbilical cord.This can deprive the baby of
oxygen ,sometimes resulting in stillbirth,women with
oligohydramnios are more likely than un affected women to
need c/s.
Treatment:
Women with normal pregnancies who develop oligohydramnios
near term need no treatment and their babies are likely to be
born healthy,they need weekly or more frequent u/s examination
to see if the level of amniotic fluid is decreasing to adangerous
point that necessate termination of pregnancy.
Nearly half the cases of oligohydramnios resolves themselves
without treatment.
Tests of fetal well being such as non stress test,if the test show
that the baby is having difficulties ,then delivery help to prevent
serious problems.
Afetus with poor growth whose mother has oligohydramnios is
at high risk of complication such as asphyxia before and during
birth,mothers with these conditions are monitored very
closely,they sometimes need to be hospitalized.
If awoman has severe oligohydramnios near the time of
delivery,infusing salty water through the cervix into the
uterus(amnioinfusion) may help to reduce complications during
labor and delivery and reduce the need for c/s.
Some studies suggest that women with oligohydramnia can help
increase their level of amniotic fluid by drinking extra water.
Prognosis:
The prognosis of patients with oligohydramnios in the 2nd
trimester is poor because the 2 most common causes,PROM and
fetal congenital anomally are not amenable to successful
treatment.Also pulmonary hypoplasia occurs frequently in
fetuses deprived of amniotic fluid for several weeks.
The best outcomes are obtained in fetuses with severe IUGR
that occasionally can be saved by early delivery and intensive
neonatal care.
Pulmonary hypoplasia is alethal neonatal condition
characterized by small anatomically immature lungs,pulmonary
hypertension and surfactant deficiency,it affects fetuses with
prolonged oligohydramnios before 28wks.
The option of termination of pregnancy should be offered to
patients with lethal fetal abnormalities or PROM before 20wks.
One exception is those patients with PROM following
amniocentesis or CVS in whom recovery is the rule.
For patient with PROM after fetal viability ,the management
will be according to gestational age.