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DR.HAJRA HUMA
TMO GYNAE-B UNIT
HMC
Amniotic Fluid:
Surround fetus after first few weeks of
gestation.
Protection
Antibacterial properties
Reservoir for water and nutrients.
Normal development of fetal lung,
musculoskeletal system,GI system.
Sources of AF
:
In early gestation:
derived directly from mother amnion, fetal
surface of placenta and fetal body surface.
In mid gestation:
fetal urine and fetal lung
Near Term:
fetal urine and fetal lung liquid.
Fetal swallowing
Feta urine
(800-1200ml/day)
(500-1000ml/day)
Intramembranous flow
(200-400ml/day)
Transmembranous flow (100ml/day)
AF volume
From 10wks (20ml) - 28wks (770ml) increases
dramatically.
After 28 wks until 39weeks little changes .
After 39wks decreases dramatically.
Average AFV in 3rd trimester is 700-800ml
Normal range at 32 weeks is v wide (<2000ml
or >500ml)
Evaluation of AFV
Physical examination:
Examination of fluid compartments.
Dye dilution test (invasive technique).
Ultrasonography (SDP , AFI)
quadrants of abdomen.
Pockets measured perpendicular to floor with patient
supine without containing small parts or umblical cord.
AFI: is sum of all these four quadrants measurements.
SDP: is single largest measurement obtained.
ABNORMALITIES:
POLYHYDROMNIOS
Definition:
AFI of 25cm or greater.
OR
SDP of more than 8cm.
The 95th percentile for the maximum AF
volume in normal pregnancy is about 2200ml and the
95th percentile of AFI at maximum fluid volume for
normal gestation is between 18cm to 20cm.
Occurance: 1% to 3% of pregnancies.
Classification
Mild:
ETIOLOGY
Obstetrics
Complication
Rare
Complication
1)TTT syndrome
1)Maternal
alloimunization
1)CNS
abnormalities
(anencephaly)
1)Inherited
Disorder of renal
function
2)Maternal
diabetes
2)Fetal
infections
(Parvovirus
B19 & Cong:
syphilis
infection)
2)Myotonic
dystrophy
a) Barter
syndrome
b) Perlmans synd
c) Beckwith synd
d) Overgrowth
synd
3)Esophageal
blockade
2)Fetal or
placental tumours
4)High gut
obstruction
5)Thoracic tumours
(diaphragmatic
hernia)
6)Cystic
adenomatoid
Complications
Maternal Complication:
1.
2.
3.
4.
5.
6.
7.
8.
9.
Fetal complications:
5.
Fetal macrosomia
Preterm labour(10%-20%)
Fetal malpresentation
Fetal death(3%-5%)
Fetal anomalies
6.
1.
2.
3.
4.
Management Options
DIAGNOSTIC WORKUP:
Detailed History:
- drug exposure
-maternal DM
INVESTIGATIONS:
1.
2.
GTT
3.
4.
5.
Karyotyping
6.
Patient Counselling:
Prognosis depends on severity & etiology.
Best prognosis with mild and idiopathic .
pregnancy with severe polyhydromnios increased risk of preterm
delivery, perinatal mortality.
Treatment:
Mainly to relieve symptoms and to prolong gestation.
Mildly symptomatic: Expectantly managed with no evidence for use
SPECIFIC TREATMENT
1. Standard
2. Experimental
Sulinadac:
-NSAIDs
-decreases AF
-less potential to constrict ductus
arteriosis
(<
indomethacin)
Other Therapies:
-Intraamniotic DDAVP
-modulation of Amniotic
membrane water channels
(aquaporin)
INDOMETHACIN:
Mech: Increases water reabsorbtion in renal tubules by
inhibiton
of PGs.
Dose:
Duration:
stopped if oligohydromnios or signs of ductal constriction
otherwise can be continued untill 32-34wks.
A/E:
closure or constriction ofductus arteriosis
development of oligohydromnios
tricuspid regurge
Rt ventricular dysfunction
Stop or discontinue treatment if AFI<8cm.
Amnioreduction
Standard Amnioreduction :
fluid removed at rate of 45-90ml/min
Aggressive Amnioreduction:
fluid removed more rapidly
Complications:
Both associated with similar rates(4%-15%)
PROM
Infections
Placental abrubtion
Fetal death
Fetal Surgery:
No intervention is specifically targeted to
polyhydromnios with the exception of:
fetal laser ablation of vascular anastomosis in
patients with TTTS
Indirect therapy i.e shunting of intrathoracic
cystic leisions
Fetal surgery for thoracic leisions of teratomas
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