1

ABSTRACT

ABSTRACT

Introduction: Reduced amniotic fluid index (AFI) is associated with adverse

effects such as meconium staining, congenital anomalies, growth retardation,

dysmaturity, and fetal asphyxia. However, some studies show that AFI is a poor

predictor of adverse perinatal outcome and should not be the only parameter for

predicting perinatal outcome.

Objectives: To determine the frequency of perinatal outcome in pregnant females

at term having low amniotic fluid index.

Study design: Descriptive, case series study

Settings: Department of Obstetrics & Gynecology, Independent University

Hospital, Faisalabad.

Study duration: 30th August 2019 to 29th March 2020

Materials & Methods: A total of 90 women having singleton pregnancy with

cephalic presentation having 37-40 weeks of gestation with AFI <5cm, 18 to 40

years of age were included. Patients with multiple pregnancy, ruptured membrane,

fetal anomaly, gestational diabetes and Rh incompatibility were excluded.

Cesarean delivery, meconium stained liquor, low birth weight, NICU admission

and APGAR score < 7 at 5 min were assessed by consultant gynecologist.

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Results: Age range in this study was from 20 to 35 years with mean age of 28.92 ±

4.45 years. Majority of the patients 43 (47.77%) were between 31 to 35 years of

age. Mean gestational age was 38.31 ± 1.20 weeks. Mean parity was 2.72 ± 1.02.

In this study, frequency of perinatal outcome in pregnant females at term having

low amniotic fluid index was as follows; cesarean section was found in 60

(66.67%), low birth weight in 58 (64.44%) patients, APGAR score <7 at 5 minutes

in 56 (62.22%), meconium stained liquor in 24 (26.67%) and NICU admission in

17 (18.89%) patients.

Conclusion: This study concluded that proper antenatal monitoring and

management should be done in these high risk patients in order to reduce the

morbidity and mortality of the fetus.

Keywords: low amniotic fluid index, cesarean section, low birth weight.
 3

INTRODUCTION

INTRODUCTION

Amniotic fluid is a clear, slightly yellowish liquid that surrounds the fetus

during pregnancy, contained within amniotic sac and provides supportive

environment for the fetus throughout the pregnancy for normal growth and

development. Amniotic fluid throughout gestation enables normal development of

the fetal respiratory, gastrointestinal and urinary tracts and musculoskeletal system

and allows for continued fetal growth in a non-restricted sterile and thermally

controlled environment. It protects the fetus from trauma and infection through its

dampening and bacteriostatic properties. It prevents compression of the umbilical

cord and placenta and protects the fetus from vascular and nutritional

compromise. 1 There is a gradual increase in volume with advancing gestation until

approximately 31-33 week followed by a significant decrease toward and beyond

the estimated date of confinement. 2

Amniotic fluid assessment is an integral part of the antenatal evaluation of

pregnancies at risk for an adverse pregnancy outcome especially in the third

trimester. Detecting the fetus at risk for in utero damage or death, quantifying, and

balancing the fetal risk against the risk of neonatal complications from immaturity,

and determining the optimal time and mode of intervention is the cornerstone of
 4

modern day obstetrics care and perinatal medicine.3 Assessment of amniotic fluid

volume by ultra sonography is more reliable. 4

Amniotic fluid index (AFI) is the preferred method of amniotic fluid

measurement in pregnancy although single deepest pocket is used in pregnancies.

For measuring AFI the uterus divided into four equal quadrants. AFI is the sum of

deepest pocket from each quadrant. The normal range of AFI is between 5-24 cm

while any value above 24 cm will be considered as Hydraminios and with value

below 5 cm will be indicated as Oligohydraminios. 5

Reduced amniotic fluid index (AFI) is associated with adverse effects such

as meconium staining, congenital anomalies, growth retardation, dysmaturity, and

fetal asphyxia. 3 However, some studies show that AFI is a poor predictor of

adverse perinatal outcome and should not be the only parameter for predicting

perinatal outcome. 6

Amniotic fluid plays a major role in the fetal growth and development. It

provides the fetus with a protective low resistance environment suitable for growth

and development. It provides a cushion against the constricting confines of the

gravid uterus, allowing the fetus room for the movement and growth and

protecting it from external trauma. It helps to maintain the fetal body temperature

and plays a part in the homeostasis of fluid and by permitting extension of the

limbs it prevents joint contractures. It prevents compression of the umbilical cord

and thus protects the fetus from vascular and nutritional compromise. 1,2 The

abnormalities of the fluid volume can thus interfere directly with the fetal
 5

development or may be an indirect sign of underlying disorder such as fetal

hypoxia, neural tube defect or gastrointestinal obstruction. Amniotic fluid index

(AFI) of ≤5 cm defines oligohydramnios. 3

Literature shows variability of perinatal outcome associated with low AFI.

Cesarean delivery was observed in 74%, 7 meconium stained liquor was found in

40.62%, 8 low birth weight was noted in 64%, APGAR score < 7 at 5 min was
6
found in 34% and NICU admission was noted in 92% patients of low AFI. 9 In

other studies, cesarean delivery was observed in 36%, meconium stained liquor

was found in 12%, 10 low birth weight was noted in 32%, 11 APGAR score < 7 at 5
9
min was found in 4% and NICU admission was noted in 3.12% patients of low

AFI. 8

As there is controversy in literature regarding the relation of adverse perinatal

outcome and low AFI. So, I want to conduct this study to assess the exact burden

of adverse perinatal outcome in females having low amniotic fluid index.

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REVIEW OF LITERATURE

REVIEW OF LITERATURE

AMNIOTIC FLUID VOLUME: PHYSIOLOGY AND ASSESSMENT:

Amniotic fluid is vital to the well-being of the fetus. It cushions the fetus from injury,

helps prevent compression of the umbilical cord, and allows room for it to move and

grow. In addition, its bacteriostatic action helps prevent infection of the intra-amniotic

environment. The quantity of amniotic fluid at any time in gestation is the product of

water exchange between the mother, fetus, and placenta, and is maintained within a

relatively narrow range. Disorders of this regulatory process can lead to either

polyhydramnios or oligohydramnios, in which too much or too little fluid exists,

respectively. These disorders may result from abnormal fetal or maternal conditions and,

conversely, may be responsible for alterations of fetal well-being as well. With the advent

of real-time ultrasonography, assessment of amniotic fluid has been possible, resulting in

earlier recognition of abnormal conditions and possible intervention. Because precise

quantification of amniotic fluid volume is not possible with ultrasonography, various

techniques for both qualitative and semiquantitative assessment have been proposed. This

chapter reviews the dynamics of amniotic fluid volume (Figure I), discusses the causality

and perinatal significance of volume disturbances, and reviews the techniques of

 7

ultrasonographic assessment of amniotic fluid volume, as well as their role in the

antenatal testing of high-risk fetuses.12

Figure I: Amniotic fluid dynamics. (Seeds AE: Amniotic fluid physiology. In Sciarra

JJ (ed): Gynecology and Obstetrics, Vol 3. New York, Harper & Row, 1989).
 8

AMNIOTIC FLUID DYNAMICS:

Amniotic Fluid Production:

In the first half of pregnancy, amniotic fluid is derived from fetal and possibly maternal

compartments. Water and solutes freely traverse fetal skin and may diffuse through the

amnion and chorion as well.16 Thus amniotic fluid in early gestation is a dialysate that is

identical to the fetal and maternal plasma, but with a lower protein concentration. Active

secretion of fluid from the amniotic epithelium had been previously suggested to play a

role in early amniotic fluid formation, but this has not been demonstrated.13-15

By the second trimester, the fetal skin becomes keratinized, making it impermeable to

further diffusion. At this time, a fetus contributes to amniotic fluid volume and

composition almost exclusively through urination. Urine has been observed in the fetal

bladder as early as 11 weeks transabdominally and 9 weeks transvaginally. Because fetal

urine is hypotonic (80–140 mOsm/ liter), it results in progressively hypotonic fluid (250–

260 mOsm/liter near term) that contains increasing concentrations of urea, uric acid, and

creatinine as the fetal kidneys mature. By term, a fetus produces on average from 500 to

700 ml/day with a slight decline in hourly fetal urine production after 40 weeks'

gestation.16

Amniotic Fluid Elimination:

 9

Amniotic fluid is eliminated by at least three mechanisms. The primary source of

elimination is through fetal swallowing, which has been observed as early as 16

weeks.17 Studies using radiolabeled red blood cells and radioactive colloid estimate that,

on average, a fetus swallows from 200 to 450 ml/day at term, removing 50% of the

amniotic fluid produced through fetal urination. This fluid is absorbed through the fetal

gastrointestinal system and is either recycled through the kidneys or is transferred to the

maternal compartment through the placenta.

A second, more debatable means of amniotic fluid removal may be by the respiratory

tract. Fetal respiratory activity has been observed as early as 11 weeks' gestation. 18 At

term, inspiratory flow in the fetus is approximately 200 ml/kg/day, up to 600–800

ml/day.19 Because amniotic fluid is more hypotonic than fetal plasma, it is postulated that

exposure of amniotic fluid to the fetal alveolar capillary bed results in net movement of

water from the amniotic cavity into the fetus. Although radioisotopes have been

discovered in fetal lungs after intra-amniotic instillation, this quantity has been small and

inconsistent,12 leading investigators to question the actual contribution of fetal respiration

to amniotic fluid removal. In fact, surface-active phospholipids originating from the fetal

alveoli are found in the amniotic cavity, leading to suggestions that the fetal lungs may

actually be a net contributor to amniotic fluid volume.

Amniotic fluid may also potentially be removed by continuous bulk flow (i.e., via

hydrostatic and oncotic forces). Exchange of fluid may take place at the chorionic plate,

where exposure of the relatively hypotonic amniotic fluid to the fetal surface of the

placenta may lead to net reabsorption of water by the fetus (up to 80 ml/day). Transport

across the amnion may occur through intercellular channels between amniotic epithelial
 10

cells and may be modulated by amniotic fluid prolactin levels. 20 Hebertson and

colleagues provided presumptive evidence for the regulatory role of the amniotic

epithelium in the transport of fluid. They observed ultrastructural changes in the amnion

of pregnancies complicated by disorders of amniotic fluid volume. 21 Whether these

changes reflect a causative role in these disorders or rather a response to long-standing

fluid imbalance remains to be determined.

A final, perhaps underestimated, pathway for volume regulation may occur within the

placenta itself. The large surface area of the fetal capillary/ intervillous interface could

magnify small osmolar gradients between a mother and fetus, resulting in large volumes

of net water transfer.22 Exchange of water at this level would influence fetal intravascular

volume and potentially affect renal blood flow and urine production.

In addition to bulk flow of fluid, which occurs through pathways that are both phasic

(micturition and swallowing) and nonphasic (mediated by hydrostatic and oncotic

gradients), there is also bidirectional flow of water between the amniotic and maternal

compartments.22,23 This process occurs by diffusion, but with no net change in fluid

volume. At term, water may leave the amniotic cavity at a rate of 400–500 ml/hour by

diffusion plus bulk flow.24

NORMAL FLUID VOLUME:

Amniotic fluid volume is most predictable in the first half of pregnancy, when it

correlates with fetal weight. This may relate to the predominant contribution of fetal skin

dialysis to amniotic fluid volume between 8 and 20 weeks. At 12 weeks' gestation, the

average volume is 60 ml.12 By 16 weeks, when genetic amniocentesis is often performed,

 11

the mean volume is 175 ml. 25 From 20 weeks on, there is greater variance of amniotic

fluid volume. Based on numerous studies using dye or para-aminohippurate dilution,

radioactive isotopes, and actual collection of amniotic fluid at amniotomy, it has been

determined that amniotic fluid volume increases steadily throughout pregnancy to a

maximum of 400–1200 ml at 34–38 weeks; however, wide variation does exist. 25-
27
Despite large fluxes of fluid between the various compartments near term (500–700

ml/day through urine; 200–450 ml/day through deglutition), the net increase of amniotic

fluid is only 5–10 ml/day in the third trimester. After 38 weeks, fluid volume declines by

approximately 125 ml/week, to an average volume of 800 ml at 40 weeks. 25-27 After 43

weeks, this volume is reduced to 250 ml. 26 In some instances, this reduction may possibly

reflect a shift of cardiac output away from the kidneys as a result of a relative

uteroplacental insufficiency. Figure 2 provides approximate volumes at various

gestational ages, based on a compilation of 12 published studies of amniotic fluid

volumes.25
 12

Figure II: Amniotic fluid volumes as a function of gestational age. Shaded area

covers 95% confidence interval. (Brace RA, Wolf EJ: Normal amniotic fluid volume

changes throughout pregnancy. Am J Obstet Gynecol 161:382, 1989)

 13

POLYHYDRMANIOS:

Incidence and Origin:

Polyhydramnios, or hydramnios, is defined as an excessive volume of amniotic fluid

relative to the gestational age. Polyhydramnios may be acute or chronic. Acute

polyhydramnios is usually a fulminant second-trimester process, with fluid accumulating

rapidly over a period of a few days. 28 Chronic polyhydramnios has a more gradual onset

and course, often presenting in the third trimester. The incidence varies, depending on

whether the diagnosis is clinical or sonographic. Overall, polyhydramnios complicates

approximately 0.3–1.6% of all pregnancies.28-32 Chronic polyhydramnios is more

frequent, exceeding the incidence of acute polyhydramnios by a 50: 1 ratio.28

Risk factors for polyhydramnios may be broadly divided into maternal, fetal, placental

and idiopathic origins (Table I).

 14

Table I: Risk factors for hydramnios

Maternal conditions Isoimmunization

Diabetes mellitus
Placental conditions Chorioangioma
Circumvallate placenta
Fetal conditions
Multiple gestations Twin-to-twin transfusion syndrome
Gastrointestinal Esophageal atresia, duodenal or jejunal atresia, annular pancreas, midgut
volvulus, diaphragmatic hernia, omphalocele, gastroschisis
CNS lesions Anencephaly, hydrocephalus, encephalocele, spina bifida, microcephaly,
hydranencephaly
Skeletal malformations Arthrogryposis multiplex, osteogenesis imperfecta, thanatophoric dysplasia
Fetal tumors Cystic adenomatoid malformation of the lung, sacrococcygeal teratoma,
cervical teratoma
Cardiac disease Severe congenital heart disease, fetal arrhythmias
Genetic disorders Down syndrome, trisomy 13 and 18, Pena-Shokeir syndrome, multiple
congenital anomalies, myotonia dystrophica
Fetal renal and endocrine Vasopressin insufficiency
disorders
Hematologic disorders Homozygous α-thalassemia, fetomaternal hemorrhage
Intrauterine infections Rubella, syphilis, toxoplasmosis, parvovirus
 15

Miscellaneous Nonimmune hydrops fetalis, fetal retroperitoneal fibrosis

Idiopathic
(Modified from Cardwell MS: Polyhydramnios: A review. Obstet Gynecol Surv 42:612,

1987. Copyright by Williams & Wilkins, 1987)

Diabetes mellitus is the most common maternal factor, occurring in approximately 25%

of cases.28 The exact mechanism for polyhydramnios with diabetes is unclear. It may

represent fetal polyuria secondary to fetal hyperglycemia. However, van Otterlo and

colleagues, measuring fetal urinary output by ultrasonography, found no increase in urine

output in 12 of 13 diabetic pregnancies complicated by polyhydramnios. 15 Alternatively,

fetal glycosuria may lead to an increase in amniotic fluid osmolality, resulting in water

transfer from the fetal compartment to maintain osmolar equilibrium. Pedersen, however,

found no association between amniotic fluid glucose concentration and volume.33

Isoimmunization is another, albeit decreasing, cause of polyhydramnios. The proposed

inciting mechanism is extramedullary hematopoiesis in response to fetal anemia, which

results in portal hypertension and hypoalbuminemia. The decrease in colloid oncotic

pressure, as well as hydrostatic venous engorgement, leads to extravasation of fluid into

the interstitium of the placenta.34 How this extravascular fluid results in hydramnios is

unclear. The extracellular fluid could possibly be transferred across the placenta and

membranes into the amniotic cavity. Alternatively, the interstitial fluid in the placenta
 16

could perhaps interfere with water transfer between the fetal and maternal compartments,

resulting in fetal volume overload, polyuria, and ultimately polyhydramnios.

Fetal conditions have been observed in approximately 20% of polyhydramnios

cases.28 Fetal malformations of the central nervous system (CNS) comprise almost 50%

of fetal anomalies, with anencephaly being the most common. 30 The postulated

mechanisms for polyhydramnios due to CNS malformations include centrally-mediated

reduction in fetal swallowing,35 fetal polyuria resulting from insufficient production of

vasopressin from the fetal pituitary,36 and transudation of fluid across the uncovered

meninges.34 Gastrointestinal anomalies constitute the second leading structural fetal

cause. Any gastrointestinal obstruction proximal to the ligament of Treitz, such as

duodenal or esophageal atresia, may interfere with the effective removal of amniotic fluid

by the alimentary tract.34

Fetal circulatory disturbances account for approximately 7% of fetal anomalies

responsible for hydramnios.30 Structural cardiac malformations and persistent fetal

arrhythmias may result in right and left heart failure. Presumably, the resulting increase

in venous pressure causes an elevation in hydrostatic pressure in the fetal capillaries, with

transudation of fluid into the interstitial space. This mechanism would occur systemically

in the fetus, leading to the characteristic appearance of nonimmune hydrops

(subcutaneous edema, ascites, pleural and pericardial effusions), as well as in the

placenta, resulting in polyhydramnios.

Other circulatory disturbances can also result in polyhydramnios. In twin-to-twin

transfusion syndrome, the recipient twin becomes plethoric and may develop hydramnios,
 17

either through volume overload, increased renal blood flow, and polyuria, 37 or through a

hydropic placenta. The donor twin becomes anemic, often leading to oligohydramnios

and the “stuck twin” syndrome. Placental chorioangiomas and sacrococcygeal teratomas

are other abnormalities in which large arteriovenous shunts may lead to high-output

cardiac failure and ultimately polyhydramnios.38

Inadequate fetal respiratory activity secondary to anomalies may prevent fluid absorption

at the alveolar/capillary interface, leading to polyhydramnios. Examples include

compressing tumors, such as cystic adenomatoid malformations, displaced abdominal

contents, such as congenital diaphragmatic hernia, and thoracic wall abnormalities, such

as thanatophoric dysplasia.

Polyhydramnios not associated with an identifiable cause is labeled “idiopathic” and

accounts for 30–60% of cases.39 Further research is necessary to identify other as yet

undetermined causes. One such possibility is a disorder of intra-amniotic prolactin

regulation by the chorion and decidua. Under normal circumstances, prolactin may be

partially responsible for control of water homeostasis in the intra-amniotic

environment. In vitro studies on human amnion have shown reduced diffusion of water in

response to ovine prolactin administered on the fetal side of the membrane. 20 Hence, an

overproduction of decidual prolactin may impair diffusional flow of water away from the

amniotic compartment, leading to polyhydramnios.

Clinical Presentation:

The maternal signs and symptoms of polyhydramnios are usually caused by the

overdistended uterus and its compressing effect on intrathoracic and intra-abdominal

 18

organs. Elevation of the diaphragm can result in dyspnea and occasionally respiratory

distress.40 Back and abdominal discomfort are also frequent complaints, as are nausea and

vomiting.28 Edema of the lower extremities may result from compression of the inferior

vena cava.

Diagnosis of Polyhydramnios:

The diagnosis of polyhydramnios had formerly been a clinical one, retrospectively based

on the presence of more than 2000 ml of amniotic fluid at the time of delivery or

membrane rupture. Antenatal suspicion was raised by difficulty in palpating fetal parts,

distant fetal heart sounds by unamplified auscultation, a tense uterine wall, and

disproportionate growth of the fundal height. Historically, amniography was used to

qualitatively assess amniotic fluid volume. This method was subsequently supplanted by

static ultrasonographic imaging, which was used to calculate total intrauterine volume

(TIUV). However, inaccuracies in measurement as well as the advent of real-time

ultrasonography led to the abandonment of TIUV. Real-time ultrasonography is now the

primary means of amniotic fluid volume assessment; however, strict ultrasonographic

criteria have never been uniformly adopted. Chamberlain and colleagues arbitrarily

defined polyhydramnios as a fluid pocket of at least 8 cm in vertical and transverse

diameters.41 Using this criterion, the incidence of polyhydramnios in a select high-risk

referral population was 3.2%. Those patients with polyhydramnios had a higher incidence

of major congenital anomalies (4%), macrosomia (33%), and perinatal mortality (3.3%)

compared to a control group with normal amniotic fluid volume. More recently, the

amniotic fluid index (AFI), which is discussed in more detail later in this chapter, has

replaced the largest vertical pocket in many ultrasound units. An AFI of greater than 20
 19

cm was arbitrarily defined as excessive amniotic fluid volume. 42 An alternative to the

semi-quantitative techniques mentioned above is simply the subjective impression of

increased amniotic fluid volume.39 Subjective criteria have included the displacement of

the fetus from the anterior uterine wall by amniotic fluid, as well as the presence of

“floating extremities.”39 Simply put, if there appears to be excessively abundant fluid, it

probably is. Bottoms and colleagues, using subjective criteria, found that the sensitivity

and positive predictive value in detecting infants large for gestational age were similar to

the 8-cm largest vertical pocket rule.43

Perinatal Complications:

The increased perinatal morbidity and mortality associated with polyhydramnios are due

to both an increase in congenital/genetic anomalies and preterm births. Perinatal mortality

used to approach 100% with acute polyhydramnios 28; however, with aggressive repetitive

amniocentesis, survivors have been reported.44,45 Chronic polyhydramnios tends to have a

better prognosis, especially if idiopathic in origin. Perinatal mortality has ranged from

34% to 69% in older studies.32 However, Chamberlain and colleagues quoted a 3.3%

mortality when the diagnosis was made sonographically. 41 Some of the variation in

survival may be a function of diagnostic criteria differences and prenatal therapy, as well

as improved survival of both preterm and anomalous infants.

Polyhydramnios may be complicated by preterm labor in up to 26% and premature

rupture of membranes in up to 19% of cases.30 Both may occur as a result of

overdistention of the uterus. Malpresentations are also encountered more frequently, as a

result of both the abundance of amniotic fluid in which the fetus may maneuver and the
 20

earlier gestational age at the time of delivery. 29 Other intrapartum complications may

include placental abruption due to rapid decompression of the uterus at the time of

rupture of membranes, dysfunctional labor patterns, and postpartum hemorrhage as a

result of uterine atony.32

Clinical Management:

Treatment of polyhydramnios may be medical or surgical or both. The method chosen

will depend on the etiology, severity, clinical symptoms, and gestational age at diagnosis,

as well as the presence and type of associated anomalies.

If the diagnosis is made on the basis of ultrasonographic findings, an attempt should be

made to establish the cause. In cases that are not acute or severe and are not associated

with a fetal malformation, patients should be rescanned periodically to assess the

progression or improvement of the fluid volume. Some reports have documented gradual

resolution of polyhydramnios, either spontaneously or as a result of treating the

underlying cause (e.g., control of hyperglycemia, intrauterine transfusion of the anemic

fetus). These pregnancies progressed uneventfully after resolution of the polyhydramnios,

with no adverse sequelae observed.46

In the absence of rapidly progressive polyhydramnios or maternal symptoms,

management is expectant. If a patient experiences increasing dyspnea, back pain, or

preterm labor, hospitalization for possible tocolysis and amniocentesis should be

considered.

Medical management, including salt restriction, diuretics, and intra-amniotic vasopressin

has not proved beneficial.34 Indomethacin has been suggested as a therapeutic modality to
 21

reduce the amniotic fluid volume, because it has been observed to decrease urinary output

in neonates being treated for patent ductus arteriosus. A reduction in amniotic fluid has

been observed in one series of eight patients with hydramnios treated with indomethacin,

as documented by decreasing fundal height measurements and largest vertical fluid

pocket by ultrasonography.47 This observation further confirms the important contribution

of fetal urination in overall amniotic fluid dynamics. Although case reports and early

studies suggested the therapeutic benefit of indomethacin in the treatment of

polyhydramnios, it is not typically used in the third trimester, due to its recognized affects

of in-utero narrowing of the fetal ductus arteriosus, which can result in pulmonary

hypertension postnatally.48

Therapeutic amniocentesis, or amnioreduction, is an effective modality for acute

decompression of the tense and distended uterine cavity. It is typically performed for

relief of maternal symptoms or preterm labor. It should be performed under ultrasonic

guidance to avoid fetal contact, using a long 20 gauge amniocentesis needle which is

often connected via plastic tubing to a suction bottle. Amnioreduction is usually

accomplished over 30–45 minutes, although no ideal time period for drainage has been

established. During this time, uterine contractions may occur, which can be

uncomfortable for the patient. Typically, these contractions will abate spontaneously

within 24 hours after the procedure has been completed. The quantity of amniotic fluid

that should be removed has also not been established and may be dependent on

gestational age, severity, and rapidity of reaccumulation. Volumes aspirated in various

reports have ranged from 200 to 4000 ml.44,45 There has been concern that too rapid or too

extensive a decompression could result in placental separation. 44,45 Amniocentesis may

 22

need to be repeated initally 2–3 times in the first week, followed by weekly

amnioreduction or as clinically indicated. Periodic evaluation of maternal electrolytes and

serum protein may need to be assessed if frequent amniocenteses are required 28 although

no studies have demonstrated the efficacy of such surveillance.

OLIGOHYDRAMNIOS:

The amniotic fluid that bathes the fetus is necessary for its proper growth and

development. It cushions the fetus from physical trauma, permits fetal lung growth, and

provides a barrier against infection. Normal amniotic fluid volume varies. The average

volume increases with gestational age, peaking at 800-1000 mL, which coincides with

36-37 weeks' gestation. An abnormally high level of amniotic fluid, polyhydramnios,

alerts the clinician to possible fetal anomalies. Inadequate volume of amniotic

fluid, oligohydramnios, results in poor development of the lung tissue and can lead to

fetal death.

In pregnancies affected by polyhydramnios, approximately 20% of neonates are born

with a congenital anomaly of some type; therefore, the delivery of these newborns in a

tertiary care setting is preferred. This article presents the causes, outcomes, and

treatments of polyhydramnios and oligohydramnios, as well as their effects on the

developing fetus and neonate.

PATHOPHYSIOLOGY:

Rupture of the membranes is the most common cause of oligohydramnios. However,

because the amniotic fluid is primarily fetal urine in the latter half of the pregnancy, the

absence of fetal urine production or a blockage in the fetus' urinary tract can also result in

oligohydramnios. Fetal swallowing, which occurs physiologically, reduces the amount of

 23

fluid, and an absence of swallowing or a blockage of the fetus' GI tract can lead to

polyhydramnios.

EPIDEMIOLOGY:

Oligohydramnios occurs in 4% of pregnancies, and polyhydramnios occurs in 1% of

pregnancies.

Mortality/Morbidity:

See the list below:

 Chamberlin used ultrasonography to evaluate the perinatal mortality rate (PMR) in

7562 patients with high-risk pregnancies.49 The PMR of patients with normal fluid

volumes was 1.97 deaths per 1000 patients. The PMR increased to 4.12 deaths per

1000 patients with polyhydramnios and 56.5 deaths per 1000 patients with

oligohydramnios.

 Preterm labor and delivery occurs in approximately 26% of mothers with

polyhydramnios. Other complications include premature rupture of the membranes

(PROM), abruptio placenta, malpresentation, cesarean delivery, and postpartum

hemorrhage.50

 Studies show an increased risk of associated fetal anomalies in more severe forms

of polyhydramnios. In a series in 1990, 20% of cases of polyhydramnios involved

associated fetal anomalies, including problems of the GI system (40%), CNS

(26%), cardiovascular system (22%), or genitourinary system (13%). 51 Among these

cases of polyhydramnios, multiple gestations occurred in 7.5%, 5% were due to

maternal diabetes, and the remaining 8.5% were due to other causes. However, at

least 50% of the patients had no associated risk factors.

 24

 The mortality rate in oligohydramnios is high. The lack of amniotic fluid allows

compression of the fetal abdomen, which limits movement of its diaphragm. In

addition to chest wall fixation, the lack of amniotic fluid flowing in and out of the

fetal lung leads to pulmonary hypoplasia. Oligohydramnios is also associated with

meconium staining of the amniotic fluid, fetal heart conduction abnormalities,

umbilical cord compression, poor tolerance of labor, lower Apgar scores, and fetal

acidosis. In cases of intrauterine growth restriction (IUGR), the degree of

oligohydramnios is often proportional to growth restriction, is frequently reflective

of the extent of placental dysfunction, and is associated with a corresponding

increase in the PMR.

 In twin gestation with twin-to-twin transfusion, polyhydramnios may occur in the

recipient twin, and oligohydramnios may occur in the donor. This complication is

associated with high morbidity and mortality rates.

Age:

No age variables are recognized.

PRESENTATION:

Physical:

See the list below:

 Amniotic fluid:

o The volume of the amniotic fluid is evaluated by visually dividing the

mother's abdomen into 4 quadrants. The largest vertical pocket of fluid is

measured in centimeters. The total volume is calculated by multiplying this

value by 4.
 25

o Polyhydramnios is usually defined as an amniotic fluid index (AFI) of more

than 24 cm or a single pocket of fluid at least 8 cm in depth that results in an

amniotic fluid volume of more than 2000 mL.52

o Oligohydramnios is sonographically defined as an AFI less than 7 cm or the

absence of a fluid pocket 2-3 cm in depth.

 Oligohydramnios:

o When the oligohydramnios is associated with renal agenesis or dysgenesis,

symptoms include a marked deformation of the fetus due to of intrauterine

constraint (Potter syndrome).

o Obstructive uropathies cause similar deformations, including external

compression with a flattened facies and epicanthal folds, hypertelorism, low-

set ears, a mongoloid slant of the palpebral fissure, a crease below the lower

lip, and micrognathia. Thoracic compression may also occur.

o Oligohydramnios adversely affects fetal lung development, resulting in

pulmonary hypoplasia that typically leads to death from severe respiratory

insufficiency. Other fetal deformations include bowed legs, clubbed feet, a

single umbilical artery, GI atresias, and a narrow chest secondary to external

compression. Infants are typically small for their stated gestational age

(SGA).53 When an abdominal mass is found on examination of the infant in

this clinical setting, it often represents multicystic-dysplastic kidney, enlarged

urinary bladder, or prune-belly syndrome.

 26

CAUSES:

Causes include the following:

 Fetal urinary tract anomalies, such as renal agenesis, polycystic kidneys, or any

urinary obstructive lesion (eg, posterior urethral valves)

 PROM and chronic leakage of the amniotic fluid

o Chorioamnionitis is an additional important maternal complication from

oligohydramnios due to rupture of the membranes, which has an incidence of

21-74%.

o The earlier chorioamnionitis occurs in pregnancy, the greater the fetal risk of

bronchopulmonary dysplasia (BPD), neurologic complications, pulmonary

hypoplasia, and, in severe cases, respiratory failure in the neonate.

 Placental insufficiency, as seen in pregnancy-induced hypertension (PIH), maternal

diabetes, or postmaturity syndrome when the pregnancy extends beyond 42 weeks'

gestation

 Maternal use of prostaglandin synthase inhibitors or ACE inhibitors

WORKUP:

Laboratory Studies:

If premature delivery is anticipated with either oligohydramnios or polyhydramnios, the

amniotic fluid lamellar body count, lecithin-sphingomyelin (L:S) ratio, and

phosphatidylglycerol (PG) concentration are helpful in determining the maturity of the

fetal lungs and, therefore, in assessing the likelihood of respiratory distress syndrome.

o Test for systemic lupus erythematosus, which causes immune-mediated

infarcts in the placenta and placental insufficiency.

 27

o Evaluate for PIH and hemolysis, elevated liver enzymes, and low platelet

count (HELLP) syndrome. Test for elevated blood pressure, proteinuria,

elevated uric acid, increased liver function test results, and low platelet count.

Imaging Studies:

Ultrasonography:

The diagnosis is confirmed by means of ultrasonography (see the images below).

Oligohydramnios may be discovered incidentally during routine ultrasonography and

noted during antepartum surveillance for other conditions. The diagnosis may be

prompted by a lag in sequential fundal height measurements (size less than that expected

for the dates) or by fetal parts that are easily palpated through the maternal abdomen.54

During ultrasonography of the fetal anatomy, normal-appearing fetal kidneys and fluid-

filled bladder may be observed to rule out renal agenesis, cystic dysplasia, and ureteral

obstruction. Check fetal growth to rule out intrauterine growth restriction (IUGR) leading

to oliguria.
 28

Figure III: Sonogram obtained before second-trimester amnioinfusion. This fetus

has bilaterally absent kidneys consistent with a diagnosis of Potter syndrome. The

cystic structures in the renal fossae are most likely the adrenal glands.
 29

Figure IV: Sonogram obtained after second-trimester amnioinfusion. This fetus has

bilaterally absent kidneys consistent with a diagnosis of Potter syndrome. The cystic

structures in the renal fossae are most likely the adrenal glands.
 30

Although ultrasonography has provided a means of assessing the volume of amniotic

fluid, a consensus of criteria for sonographic diagnosis of oligohydramnios has not been

achieved. In early reports, amniotic fluid volume was assessed subjectively, allowing for

differences according to gestational age. Subsequent investigators attempted to quantify

amniotic fluid volume by various techniques.

Subjective Ultrasonographic Evaluation of Amniotic Fluid Volume:

Crowley used subjective criteria to evaluate amniotic fluid volume in pregnancies after

42 weeks, looking for the presence or absence of anechoic space between fetal limbs and

uterine wall, as well as between limbs and the fetal trunk. Philipson and colleagues used

the subjective criteria of paucity of amniotic fluid, crowding of the fetal parts, and “poor

fluid/fetal interspace.” Projecting these criteria to a theoretical study population in

predicting small for gestational age (SGA) infants, the sensitivity was 15.5% and positive

predictive value was 39.6%. Bottoms and associates subsequently compared a five-tiered

subjective evaluation (oligohydramnios, decreased, normal, increased, hydramnios) to an

objective measurement of maximum vertical pocket diameter, the latter measured with

the transducer held at right angles to the sagittal plane of the maternal abdomen. Using

SGA infants as an abnormal end point, the sensitivity and positive predictive values were

similar between the two techniques (32% vs.31%, and 83% vs. 82%, respectively).

Similarly, Goldstein and Filly also demonstrated good correlation between subjective and

objective evaluations of amniotic fluid volume.55

 31

Semi-Quantitative Ultrasonographic Assessment of Amniotic Fluid Volume:

In 1981, the concept of the "1 cm rule" was introduced in a selected high-risk patient

population.33 Subjects included were those with suspected fetal growth restriction (FGR)

based on fundal height measurements. Volume was arbitrarily classified as decreased if

the largest fluid pocket measured less than 1 cm in broadest dimension. Of these subjects,

24% were found to have decreased amniotic fluid volume, and 90% of these were

delivered of babies that were found to be SGA. Conversely, 84% of SGA infants were

observed to have had decreased fluid. However, subsequent studies were less optimistic,

showing both a lower prevalence and sensitivity of' oligohydramnios as a predictor of

IUGR.56

The 1 cm rule was re-evaluated in 1984. Amniotic fluid volume was recorded in all

patients referred for a biophysical profile by measuring the vertical and transverse

dimension of the largest amniotic fluid pocket, with the transducer oriented perpendicular

to the contour of the uterus. Vertical diameters less than 1 cm were classified as

decreased, 1–2 cm as marginal, and greater than 2 cm to less than 8 cm as normal. It was

found that 0.9% had decreased and 2% had marginal amniotic fluid. As a result of

improved sensitivity in detecting FGR by including the marginal category (5.5% for

decreased, 13.2% for decreased plus marginal groups), it was suggested that the 1 cm rule

might be too stringent. Subsequently, the amniotic fluid component of the biophysical

profile was modified to a 2 cm cutoff in two perpendicular planes.

In addition to the 2 cm rule, other objective techniques of amniotic fluid volume have

been evaluated. Patterson and colleagues measured the vertical and two horizontal
 32

dimensions of the largest fluid pocket and calculated a mean value of the three

dimensions.56 Only pockets that were free of umbilical cord and extremities were

included. By using a receiver operating characteristic curve, a statistical tool that is

employed to maximize sensitivity and specificity, a cutoff of 3.2 cm was established.

Using this value, 15% of a study population “at risk for fetal malnutrition” was abnormal.

The 3.2-cm cutoff was 40% sensitive and 91% specific, with a 50% positive predictive

value and 86% negative predictive value for detecting SGA infants. Observed differences

in average fluid volume were more likely to be due to true differences between patients

and not due to measurement error; measurement of the average dimension of the largest

amniotic fluid pocket had an interpatient variability that was fourfold higher than the

intraobserver variability. In contrast, use of maximum vertical diameter had an

intraobserver variability that was higher than the interpatient variability. The authors

concluded that average amniotic fluid volume was more reproducible than the largest

vertical diameter and would be a superior screening test to identify malnourished fetuses.

In 1987, Phelan and colleagues introduced the four-quadrant technique of amniotic fluid

volume assessment. Using 353 gravidas at 36–42 weeks who were referred for an

external cephalic version or postdate pregnancy from 36 to 42 weeks, the largest vertical

diameter in each quadrant was measured and summed. For all measurement, the

transducer was held in a sagittal plane perpendicular to the floor. This number, in

centimeters, was termed the amniotic fluid index (AFI). Between 36 and 40 weeks, the

average AFI was 12.4 ± 4.6 cm. Whereas two standard deviations below and above the

mean would have resulted in statistical cutoffs of 3.7 and 22.1 cm, respectively, the

authors used threshold values of 5 cm to arbitrarily define decreased amniotic fluid and
 33

20 cm for excessive fluid. Further investigation by these authors demonstrated a

significant increase in meconium-stained fluid, cesarean section, and low Apgar scores in

subjects with AFI less than 5 cm.57

Moore and Cayle subsequently assessed the amniotic fluid index in 791 normal

pregnancies between 16 and 42 weeks. Since significant differences were observed

between the preterm, term, and postdates pregnancies, a finding that is consistent with

physiologic fluid changes that occur throughout gestation, the data was stratified by week

of gestation. The mean AFI value at each week of pregnancy, as well as the 90–95%

confidence intervals, was calculated (Table II). This study demonstrated the importance

of establishing gestation-specific norms for the AFI, rather than a single cutoff value.

Interestingly, the 2.5th percentile AFI value at each gestational age was greater than the 5

cm threshold established by Phelan. Therefore, the use of the 2.5th percentile cutoff

would result in a more frequent diagnosis of oligohydramnios.

 34

Table II: Amniotic fluid index values in normal pregnancy (in mm)

Amniotic fluid index percentile values

Week 2.5th 5th 50th 95th 97.5th n

16 73 79 121 185 201 32

17 77 83 127 194 211 26

18 80 87 133 202 220 17

19 83 90 137 207 225 14

20 86 93 141 212 230 25

21 88 95 143 214 233 14

22 89 97 145 216 235 14

23 90 98 146 218 237 14

24 90 98 147 219 238 23

25 89 97 147 221 240 12

26 89 97 147 223 242 11

27 85 95 146 226 245 17

28 86 94 146 228 249 25

29 84 92 145 231 254 12

30 82 90 145 234 258 17

31 79 88 144 238 263 26

 35

Amniotic fluid index percentile values

Week 2.5th 5th 50th 95th 97.5th n

32 77 86 144 242 269 25

33 74 83 143 245 274 30

34 72 81 142 248 278 31

35 70 79 140 249 279 27

36 68 77 138 249 279 39

37 66 75 135 244 275 36

38 65 73 132 239 269 27

39 64 72 127 226 255 12

40 63 71 123 214 240 64

41 63 70 116 194 216 162

42 63 69 110 175 192 30

(Moore TR, Cayle JE: The amniotic fluid index in normal human pregnancy. Am J

Obstet Gynecol 162:1168, 1990)

 36

Comparison of Ultrasonographic Assessment of Amniotic Fluid Volume:

To date, no single method to assess amniotic fluid volume has proved to be the most

valuable clinically. Difficulty in comparing fluid assessment methods arises from

differences in the population tested, the abnormal end point chosen, and the variety of

ultrasonographic criteria. The 2 cm rule traditionally had been most widely used,

predominantly as a component of the biophysical profile. Recently, however, the

amniotic fluid index has appeared with increasing frequency in the literature and in

clinical practice. The AFI, by measuring all four quadrants, would appear to more

accurately assess serial changes in fluid volume over time, compared to a single vertical

pocket, which might be subject to greater variation due to fetal positioning. Additionally,

by using gestation-specific norms, the AFI may more accurately reflect abnormalities in

fluid volume compared to the 2 cm rule. However, the AFI has not been evaluated as

extensively in identifying the fetus at risk for IUGR, cord compression, and abnormal

perinatal outcome. By comparison, the use of subjective criteria, which may be less

dependent on fetal positioning in serial testing, relies more on a gestalt of fluid volume

than on any one measurement value. As a result, the experience of the examiner may be

more critical in determining if the amniotic fluid is appropriate for the gestational age, as

the same subjectively normal amniotic fluid volume at 42 weeks might be decreased for

34 weeks. Additionally, subjective criteria may vary from individual to individual,

making interobserver communication and statistical comparisons more difficult to

express. At the author's institution, the amniotic fluid volume is initially assessed
 37

subjectively. If it is normal, no AFI or largest vertical pocket is measured. However, if

the fluid subjectively appears decreased, an AFI is calculated.

The variability in definitions of ultrasound-based oligohydramnios was highlighted in a

clinical commentary by Magann and colleagues, which included a plea for future studies

that correlate amniotic fluid volume assessment to clinically relevant perinatal

outcomes.58 Fischer and colleagues assessed postdate women and compared various

ultrasound criteria for oligohydramnios with a composite perinatal outcome. 62 The largest

pocket in each quadrant was measured in two perpendicular planes. Indices evaluated

included the largest vertical pocket, largest transverse pocket, AFI, largest pocket product

(vertical x transverse), sum of all pocket measurements, and the sum of the pocket

products. They found that the largest vertical pocket, the AFI, and the sum of all pockets

were significantly different between the normal and abnormal perinatal outcome

groups. Using receiver operating characteristic curves to establish optimal threshold

values, a vertical pocket of 2.7 was ideal in identifying abnormal perinatal outcome. No

optimal AFI cutoff based could be established based on the ROC curve.

Chauhan and colleagues performed a prospective randomized clinical trial comparing the

AFI to the largest vertical pocket.59 They randomly assigned 1080 high risk gravidas to be

followed with weekly nonstress tests and either an AFI or largest vertical pocket. They

defined oligohydramnios as either an AFI of 5 cm or less, or the absence of a fluid pocket

measuring at least 2 x 1 cm. Women followed by the AFI was significantly more likely to

be diagnosed with oligohydramnios than those in the largest vertical pocket group (17%

vs. 10%, p = 0.002). However, there was no difference between the two fluid assessment

techniques with regards to cesarean delivery for non-reassuring fetal heart rate testing,
 38

Apgar score, umbilical artery pH <7.1, or admission to the neonatal intensive care unit.

The authors concluded that using the AFI increases the number of interventions for

oligohydramnios without improving perinatal outcome. They also observed that both

techniques of amniotic fluid assessment are poor diagnostic tests for predicting adverse

perinatal outcome.

Inconsistencies in Ultrasonographic Assessment of Amniotic Fluid Volume:

Difficulties arise when comparing various criteria for oligohydramnios. One variable not

often addressed in studies is the inclusion or exclusion of fluid pockets that contain loops

of umbilical cord. With oligohydramnios, the umbilical cord makes up an increased

proportion of fluid pockets. Some studies excluded any pocket that contained cord, while

others measured the dimensions of fluid that surrounded cord.

A frequently overlooked but critically important issue is that of transducer positioning. In

some reports, the transducer was held at right angles to the uterine contour, whereas in

others the plane of the ultrasound was perpendicular to the floor or sagittal plane of the

abdomen.60 Many studies did not indicate how the transducer was oriented. Orientation is

critical in evaluating vertical diameter. If the transducer is held perpendicular to the

uterine contour, a view from the lateral aspect of the uterus might falsely create a vertical

pocket on the ultrasonography screen. For the sake of consistency, it is recommended that

the transducer be oriented longitudinally and perpendicular to the plane of the floor (the

plane in which the fluid has layered), thereby minimizing differences if the subject is

laterally displaced.

Sterile speculum examination:

 39

Sterile speculum examination may be performed to check for range of motion (ROM).

Amniotic fluid may pool in the vagina, and an arborization or ferning pattern may be

observed when dried posterior vault fluid is examined microscopically. Cervical mucous

may cause false-positive results, as can semen and blood. Nitrazine paper turns blue. The

amniotic fluid is more basic (pH 6.5-7.0) than normal vaginal discharge (pH 4.5).

Measurement of amniotic fluid volume:

Initial studies to objectively measure amniotic fluid volume (AFV) involved dye dilution

techniques. The techniques were accurate, although they required amniocentesis, an

invasive procedure that increased the risk of perinatal morbidity.

The routine use of ultrasonography has created a safe, reliable, and repeatable method of

measuring AFV. Early methods of assessing AFV with ultrasonography involved

nonquantitative assessments, including sonographers' subjective impression of AFV.

Subjective oligohydramnios criteria have included the following:

 The absence of fluid pockets throughout the uterine cavity

 Crowding of the fetal limbs

 The absence of pockets surrounding the fetal legs

 Overlapping of the fetal ribs (in severe cases)

The 2 most commonly used objective methods of determining AFV include measurement

of the single deepest pocket (SDP) and the summation of the SDPs in each quadrant, or

the amniotic fluid index (AFI). These tests are routinely performed with the patient in the

supine or semi-Fowler position, although studies have demonstrated accuracy in the

lateral decubitus position as well.61,62

 40

The ultrasound transducer is held along the maternal longitudinal axis and maintained

perpendicular to the floor while the SDP of the amniotic fluid is measured. Pockets

should be free of fetal limbs and the umbilical cord, although some authors allow for a

single loop of cord to be within the fluid pocket. AFV may be artificially increased if the

transducer is not maintained perpendicular to the floor. Excessive pressure on the

maternal abdomen with the transducer may lead to an artificially reduced measurement

(see the image below).

Figure V: Amniotic fluid index (AFI) measurement technique.

 41

Phelan et al described the AFI as a quantitative measurement to predict a poor pregnancy

outcome and the success of external cephalic versions. The pregnant abdomen is divided

into 4 quadrants by using the umbilicus as a reference point to divide the uterus into

upper and lower halves and by using the linea nigra to divide the uterus into left and right

halves. The 4 measurements are summed to obtain the AFI in centimeters.

The test is reproducible, with interobserver and intraobserver variations of about 10-15%

or 1-2 cm in pregnancies with normal AFVs. The margin of error is less in patients with

decreased amounts of amniotic fluid.

Oligohydramnios has been defined as an AFI less than 5 cm, although 8 cm has

occasionally been used as a cut-off threshold. Because the AFV depends on the

gestational age, oligohydramnios has been defined as an AFI less than the fifth percentile

(corresponding to an AFI of < 6.8 cm at term).

Oligohydramnios has been defined as an SDP less than 2 cm. Perinatal morbidity rates

have been shown to increase sharply with SDPs below this value. Some have suggested

that an SDP of 2.5-3.0 cm is a better lower limit for separating normal SDPs from those

consistent with oligohydramnios.

Many studies have shown that the SDP and the AFI methods have equal diagnostic

accuracies. The SDP technique may be a better means of assessing the AFV in twin

gestations and in pregnancies at an early gestational age. Some study results have shown

that the AFI has greater sensitivity and a higher predictive value than the SDP in
 42

diagnosing abnormally high and low AFVs. Most obstetricians prefer to assess a broader

area of the uterine cavity by using the AFI because the single measurement of the SDP

does not allow for an asymmetric fetal position in the uterus.

According to a survey of members of the Society of Maternal-Fetal Medicine, deepest

vertical pocket is considered to be the most accurate method of evaluating amniotic fluid

in the second trimester, and amniotic fluid index is considered to be the most accurate

method of evaluating fluid in the third trimester. Over 50% of respondents felt that

oligohydramnios is overdiagnosed when using amniotic fluid index compared with

deepest vertical pocket.63-68

Other examinations:

MRI and 3-dimensional (3D) ultrasonography are newer (and more expensive) modalities

for accurately assessing the AFV.68-74

Fetal MRI can complement ultrasonography by providing better visualization in the fetus

when ultrasound may be limited, in cases such as severe maternal obesity. Although MRI

may offer a larger field of view and better tissue contrast and not be limited by

shadowing from osseous structures, it has a limited resolution when compared with

ultrasonography and is less readily available and is more expensive.75

In 35 women with healthy singleton pregnancies, rapid MRI-based projection

hydrography (PH) measurement was found to be a better predictor of amniotic fluid

volume than ultrasonography (in utero at 28-32 weeks’ gestation). For the ultrasound

measurements, single deepest vertical pocket (SDVP) measurement related most closely

to amniotic fluid volume, with amniotic fluid index (AFI) demonstrating a weaker
 43

relationship. Manual multisection planimetry (MSP)-based measurement of AFV was

used as a proxy reference standard.74

Amniotic wrinkle:

Finberg reported a possible pitfall in the sonographic analysis of amniotic fluid in twin

pregnancies, the "amniotic wrinkle," which may give the misleading impression of

adequate amniotic fluid for both twins when one twin actually has little to none.

The author reevaluated sonograms of twin pregnancies in which an initial sonographer's

assessment was adequate fluid for each twin but which the author's own imaging

assessment on the same day showed oligohydramnios in one twin.

He found either of the following may occur when oligohydramnios of one twin is present:

 The intertwin membrane may fold in on itself, creating an amniotic wrinkle (a short

linear structure that extends perpendicularly away from the twin with decreased

amniotic fluid in toward the amniotic space of the other twin)

 An intrauterine sling or "cocoon" may be present, in which a fetus appears to be

suspended within the amniotic space of the other twin may be present

Finberg recommended showing the intertwin membrane in all images used to document

each twin's amniotic fluid, with additional right-angle images to identify amniotic

wrinkles.76

Other Tests:

See the list below:

 Testing of the infant is recommended, depending on the results of postnatal

evaluation of the infant. Such evaluation may include chromosome testing, testing
 44

for evidence of congenital infection, ultrasonography of the genitourinary tract, and

appropriate radiologic evaluation of the GI tract. ECG and echocardiography may

also be indicated.

Procedures:

See the list below:

o The transabdominal instillation of indigo carmine may be used to evaluate for

PROM.

o The transcervical instillation of isotonic sodium chloride solution (ie,

amnioinfusion) at the time of delivery reduces the risk of cord compression,

fetal distress and meconium dilution. It also reduces the potential need for

cesarean delivery.

Histologic Findings:

See the list below:

 Examination of the placenta may be helpful in determining the cause of the

polyhydramnios or oligohydramnios.

TREATMENT:

Medical Care:

The first step is identifying the etiology of the abnormal volume of amniotic fluid.

Medical care includes the use of steroids to enhance fetal lung maturity if preterm

delivery is anticipated.

o Maternal bed rest and hydration promote the production of amniotic fluid by

increasing the maternal intravascular space. Bed rest may also help when PIH

is present, allowing prolongation of the pregnancy.

 45

o Studies show that oral hydration, by having the women drink 2 liters of water,

increases the AFI by 30%.

o In singleton pregnancies where oligohydramnios is present without maternal

and fetal complications, evidence exists that either oral or intravenous

maternal hydration (1500-2500ml/day) is associated with a 20-30%

improvement in AFI and a reduction in cesarean delivery. Further studies are

necessary to determine if a corresponding improvement in fetal and neonatal

wellbeing can be substantiated with such "forced hydration" therapy.56

Consultations:

See the list below:

 A specialist in maternal-fetal medicine should be consulted when significant

oligohydramnios or polyhydramnios is present, especially when the condition is

unexplained, involves hydrops fetalis, or is associated with congenital

malformations.

 Genetic counseling may be helpful in cases in which congenital anomalies are

identified.

 Consult a neonatologist, pediatric surgeon, pediatric cardiologist, pediatric

nephrologist, or other genetics specialists as required to care for the infant.

Diet:

See the list below:

 In cases of polyhydramnios in which maternal diabetes is suspected, perform a

glucose tolerance test. If the test results are positive, treat the mother with an

American Diabetes Association (ADA) diet. Insulin is rarely needed.

 46

MEDICATION SUMMARY:

Most cases of polyhydramnios respond in the first week of treatment with

indomethacin.58,59 The approach appears to be highly effective (90-100% in some studies),

provided that the cause is not hydrocephalus or a neuromuscular disorder that alters fetal

swallowing.

Prostaglandin inhibitors:

When administered to pregnant women with polyhydramnios, these drugs can reduce

fetal urinary flow, decreasing the volume of amniotic fluid.

Indomethacin (Indocin):

Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and

glucuronide conjugation; inhibits prostaglandin synthesis.

Clinical Significance of Oligohydramnios:

The literature suggests that oligohydramnios does increase the risk in a fetus with no

major anomalies. However, the clinical significance of oligohydramnios differs between

studies, depending on criteria used and end points evaluated. Overall, decreased amniotic

fluid is associated with a higher incidence of SGA infants (less than the 10th percentile

for gestational age), postmaturity syndrome, variable and late decelerations in labor,

cesarean section for nonreassuring fetal heart rate tracing, lower umbilical artery pH,

lower Apgar scores, and higher perinatal mortality. Second-trimester oligohydramnios is

 47

especially associated with adverse perinatal outcomes, as a result of both pulmonary

hypoplasia and lethal congenital anomalies.77

The relative degree to which the increased morbidity results from either the underlying

condition producing the oligohydramnios or from a direct effect of the reduced fluid (i.e.,

umbilical cord compression) has not been determined. However, there is some suggestion

that part of the risk of cord compression may be reversible, as indicated by studies in

which fluid was removed versus those in which fluid was replaced (amnioinfusion) to

determine clinical effect. Gabbe and colleagues noted that removal of amniotic fluid from

the amniotic cavity of fetal monkeys resulted in variable decelerations secondary to cord

compression. This pattern resolved after amnioinfusion. Confirmation of this finding in

humans has been demonstrated by Miyazaki and associates, who observed a significant

diminution of intrapartum variable decelerations in 5 1% of patients treated by

amnioinfusion through an intrauterine pressure catheter. Nageotte and co-workers

observed a significantly lower rate of variable decelerations and higher cord pH values in

patients who had PROM and underwent prophylactic amnioinfusion.78

Pulmonary hypoplasia, as measured by low wet lung weights, low lung DNA content,

and low radial alveolar counts, can occur after PROM and oligohydramnios in the very

preterm gestation (<24 weeks). It may result from limitation of lung expansion secondary

to prolonged external compression, inhibition of fetal respiratory movements, and lack of

fluid circulation into the terminal alveoli, which may require growth factors contained in

amniotic fluid that are critical for alveolar development. 79 In one study of PROM in

which pulmonary hypoplasia was observed, the majority of cases were less than 26 weeks

at the time of membrane rupture, suggesting that the developing terminal air sacs are
 48

more susceptible to the damaging effects of oligohydramnios. Further, prolonged

oligohydramnios increases the risk of Potter's sequence, which, in addition to pulmonary

hypoplasia, includes fetal skeletal and facial deformities due to prolonged external

compression.

FOLLOW UP:

Further Inpatient Care:

See the list below:

o Consider hospitalizing and thoroughly evaluating the mother in cases

diagnosed after 26-33 weeks' gestation.

o If the fetus does not have an anomaly, delivery should be performed if the

biophysical profile is non-reassuring.

o The instillation of isotonic sodium chloride solution in the second trimester

may be of benefit in some patients. Use transabdominal amnioinfusion to

instill 400-600 mL, which may improve visualization for ultrasonography and

increase volume of the amniotic fluid.

o In cases associated with post-maturity, review pregnancy dating. If the

gestation is truly longer than term, deliver the fetus by means of either

induction or cesarean delivery.

o If meconium is present during labor, administer amnioinfusion therapy to

reduce the potential for fetal distress and prenatal aspiration.

COMPLICATIONS:

See the list below:

 49

o The primary complications are those related to fetal distress before or during

labor.

o The risk of fetal infection is increased in the presence of prolonged rupture of

the membranes.

PROGNOSIS:

See the list below:

o In renal agenesis, the mortality rate is 100%.

o Milder forms of renal dysplasia or obstructive uropathy can be associated with

mild-to-severe degree of pulmonary hypoplasia and long-term renal failure.

o In cases of pulmonary hypoplasia, the effectiveness of many treatments such

as the administration of surfactant, high frequency ventilation, and nitric oxide

has not been established. The prognosis in these cases is related to the volume

of amniotic fluid and the gestational age at which oligohydramnios develops.

 50

OBJECTIVES

OBJECTIVES & OPERATIONAL DEFINITIONS

OBJECTIVES:

The objective of the study was:

 “To determine the frequency of perinatal outcome in pregnant females at

term having low amniotic fluid index.”

OPERATIONAL DEFINITIONS:

Low amniotic fluid index:

Amniotic fluid index < 5 cm on ultrasound was said to be low amniotic

fluid index.

Pregnant females at term:

Females having 37- 40 weeks of gestation on ultrasound.

Perinatal outcome:

It was assessed in terms of

Cesarean section:

Cesarean section is a surgical procedure in which fetus was delivered

 51

through an incision in the mother’s abdomen and uterus.

Meconium stained liquor:

After artificial rupture of membrane, light to dark green or brown color of

amniotic fluid was said to have meconium stained liquor.

Low birth weight:

It was the weight of baby < 2.5 kg at birth.

NICU admission:

It was the admission of baby to neonatal intensive care unit within 24 hours

of birth.

APGAR score < 7 at 5 min:

It was assessed after 5 minutes of birth as follows:

Indicator 0 point 1 point 2 point

A Activity Absent Flexed arms & legs Active
(muscle tone)
P Pulse Absent Below 100 bpm Over 100 bpm
G Grimace Floppy Minimal response to Prompt
(reflex stimulation response to
irritability) stimulation
A Appearance Blue, pale Pink body, blue Pink
(skin color) extremities
R Respiration Absent Slow and irregular Vigorous cry
 52

MATERIALS AND METHODS

MATERIALS & METHODS

STUDY DESIGN:

Descriptive, case series study.

SETTING:

Department of Obstetrics & Gynecology, Independent University

Hospital, Faisalabad.

DURATION OF STUDY:

30 th August 2019 to 29 th March 2020.

SAMPLE SIZE:

By using WHO sample size calculator

6
P = 34%

Absolute precision required = 10%

Confidence level = 95%

Sample size = 90

SAMPLE TECHNIQUE:
 53

Non-probability, consecutive sampling.

SAMPLE SELECTION:

a. Inclusion Criteria:

 Females age ranges from 20-35 years.

 Females having singleton pregnancy with cephalic presentation having 37-40

weeks of gestation.

 Females having AFI < 5 cm.

 Females having intact membrane.

b. Exclusion Criteria:

Females having

 Ruptured membranes

 Fetal anamoly

 Gestational diabetes

 Rh incompatibility

 Multiple pregnancies.

DATA COLLECTION PROCEDURE:

After taking approval from hospital ethical committee, patients coming

through OPD fulfilling the inclusion criteria were enrolled and informed consent

was taken. Cesarean delivery, meconium stained liquor, low birth weight, NICU

admission and APGAR score < 7 at 5 min were assessed by consultant

gynecologist. All the information was collected on a specially designed proforma

(attached) by me.
 54

STATISTICAL ANALYSIS:

The data was entered and analyzed in SPSS version 22. Descriptive

statistics including mean and standard deviation of numerical values like age,

parity and gestational age were calculated. Frequency and percentage were

calculated for all qualitative variables like cesarean delivery, meconium stained

liquor, low birth weight, NICU admission and APGAR score < 7 at 5 min.

Effect modifiers like age, parity and gestational age were controlled by

stratification. Post stratification chi-square test was applied. P-value ≤ 0.05 was

considered significant.
 55

RESULTS

Age range in this study was from 20 to 35 years with mean age of 28.92 ±

4.45 years. Majority of the patients 43 (47.77%) were between 31 to 35 years of

age as shown in Table III. Mean gestational age was 38.31 ± 1.20 weeks (Table

IV). Mean parity was 2.72 ± 1.02 (Table V).

In this study, frequency of perinatal outcome in pregnant females at term

having low amniotic fluid index was as follows; cesarean section was found in 60

(66.67%), low birth weight in 58 (64.44%) patients, APGAR score <7 at 5 minutes

in 56 (62.22%), meconium stained liquor in 24 (26.67%) and NICU admission in

17 (18.89%) patients as shown in Table VI.

Stratification of the cesarean section, APGAR score <7 at 5 minutes,

meconium stained liquor and NICU admission with respect to age is shown in

Table VII, VIII, IX, X & XI respectively. Stratification of the cesarean section,

APGAR score <7 at 5 minutes, meconium stained liquor and NICU admission with

respect to gestational age is shown in Table XII, XIII, XIV, XV & XVI

respectively. Stratification of the cesarean section, APGAR score <7 at 5 minutes,

meconium stained liquor and NICU admission with respect to parity is shown in

Table XVII, XVIII, XIX, XX & XXI respectively.

 56

Table-III: Age distribution of patients (n=90).

Age (in years) No. of Patients %age

20-25 24 26.67

26-30 23 25.56

31-35 43 47.77

 Mean ± SD = 28.92 ± 4.45 years

 57

Table-IV: Distribution of patients according to gestational age (n=90).

Gestational age (weeks) No. of Patients %age

37-38 weeks 53 58.89

39-40 weeks 37 41.11

Mean ± SD 38.31 ± 1.20

 58

Table-V: Distribution of patients according to Parity (n=90).

Parity No. of Patients %age

0-2 72 80.0

3-5 18 20.0
 59

Table VI: Frequency of perinatal outcome in pregnant females at term having

low amniotic fluid index

Frequency (%)

Fetomaternal outcome yes no

Cesarean section 60 (66.67%) 30 (33.33%)

Low birth weight 58 (64.44%) 32 (35.56%)

APGAR score <7 at 5 minutes 56 (62.22%) 34 (37.78%)

NICU admission 17 (18.89%) 73 (81.11%)

Meconium stained liquor 24 (26.67%) 66 (73.33%)

 60

Table VII: Stratification of the cesarean section with respect to age.

Cesarean section
P-value
Age (in years) Yes No

20-25 14 10

0.335
26-30 18 05

31-35 28 15
 61

Table VIII: Stratification of the low birth weight with respect to age.

Low birth weight

P-value
Age (in years) Yes No

20-25 16 08

0.654
26-30 13 10

31-35 29 14
 62

Table IX: Stratification of the APGAR score < 7 at 5 min with respect to age.

APGAR score < 7 at 5 min

P-value
Age (in years) Yes No

20-25 13 11

0.018
26-30 20 03

31-35 23 20
 63

Table X: Stratification of the meconium stained liquor with respect to age.

meconium stained liquor

P-value
Age (in years) Yes No

20-25 03 21

0.183
26-30 07 16

31-35 14 29
 64

Table XI: Stratification of the NICU admission with respect to age.

NICU admission
P-value
Age (in years) Yes No

20-25 02 22

0.103
26-30 03 20

31-35 12 31
 65

Table XII: Stratification of the cesarean section with respect to gestational

age.

Cesarean section
P-value
GA (weeks) Yes No

37-38 37 16 0.449

39-40 23 14
 66

Table XIII: Stratification of the low birth weight with respect to gestational
age.

Low birth weight

P-value
GA (weeks) Yes No

37-38 33 20 0.605

39-40 25 12
 67

Table XIV: Stratification of the APGAR score <7 at 5 min with respect to
gestational age.

APGAR score <7 at 5 min

P-value
GA (weeks) Yes No

37-38 34 19 0.651

39-40 22 15
 68

Table XV: Stratification of the meconium stained liquor with respect to

gestational age.

meconium stained liquor

P-value
GA (weeks) Yes No

37-38 13 40 0.583

39-40 11 26
 69

Table XVI: Stratification of the NICU admission with respect to gestational

age.

NICU admission
P-value
GA (weeks) Yes No

37-38 11 42 0.588

39-40 06 31
 70

Table XVII: Stratification of the cesarean section with respect to parity.

Cesarean section
P-value
Parity Yes No

0-3 49 24 0.849

4-5 11 06
 71

Table XVIII: Stratification of the low birth weight with respect to parity.

Low birth weight

P-value
Parity Yes No

0-3 44 28 0.186

4-5 14 04
 72

Table XIX: Stratification of the APGAR score <7 at 5 min with respect to
parity.

APGAR score <7 at 5 min

P-value
Parity Yes No

0-3 45 27 0.913

4-5 11 07
 73

Table XX: Stratification of the meconium stained liquor with respect to

parity.

meconium stained liquor

P-value
Parity Yes No

0-3 18 54 0.475

4-5 06 12
 74

Table XXI: Stratification of the NICU admission with respect to parity.

NICU admission
P-value
Parity Yes No

0-3 15 57 0.346

4-5 02 16
 75

DISCUSSION

DISCUSSION

Amniotic fluid assessment is an essential part of evaluation of fetus health

in terms of fetal distress, meconium aspiration, caesarean and fetal mortality. 80 The

assessment of amniotic fluid volume is very crucial for the survival of the fetus

and the Amniotic Fluid Index (AFI) is the most common way for the estimation of

amniotic fluid volume which is performed by ultrasound method. 81,82 Studies have

revealed that AFI is an accurate criterion for estimating adequate placental

function. 83 Amniotic fluid volume varies with gestational age, rising to a plateau

between 22-39 weeks of gestation and reaching 700 and 800 ml, which correspond

to an AFI of 14-15 cm. 84,85 Any decrease or increase in the volume of amniotic

fluid leads to pregnancy complications. 80

In spite of different views on borderline AFI in different studies, there are,

also, different views about its function and influence on maternal and fetal

complications and medical care for fetus health. In most reported studies, the

pregnancies with borderline AFI of 5-10 cm have shown outcomes such as non-

reactive non-stress tests, fetal heart rate (FHR) deceleration, meconium aspiration,

immediate caesarean delivery, low Apgar score, LBW, NICU admission and SGA
 76

in comparison with control subjects with normal amniotic fluid level (8.1-18

cm). 86-94 Also the low amniotic index may increase the operative delivery rate. 81

Also, according to Luo et al the pregnancy outcomes of a borderline versus

normal AFI suggested no difference in the incidence of fetal distress or neonatal

mortality, but the rate of caesarean delivery in borderline AFI was reported higher

than the rate in normal cases. They evaluated 196 trails of labor with a borderline

AFI (5.1-8) and 200 women with normal AFI (8.1-18). 95 Meanwhile, in another

study, oligohydramniosis was shown to be associated with pregnancy

complications but the diminished amniotic fluid volume doesn't seem to have any

noticeable effect on anticipating the outcomes. 96

In my study, frequency of perinatal outcome in pregnant females at term

having low amniotic fluid index was as follows; cesarean section was found in 60

(66.67%), low birth weight in 58 (64.44%) patients, APGAR score <7 at 5 minutes

in 56 (62.22%), meconium stained liquor in 24 (26.67%) and NICU admission in

17 (18.89%) patients. In a study 81 , the caesarean section rate in oligohydramnios

was 68% as compared to 28% in the control group. The incidence of meconium

stained liquor in the oligohydramnios group was 32%, compared with 18% in the

control group, apgar score <7 at 5 minutes was 14% versus 4% and NICU

admission was 14% versus 4%. 97 In another study, the caesarean section rate in

oligohydramnios was 27% as compared to 13% in the control group. The incidence

of meconium stained liquor in the oligohydramnios group was 42%, compared

with 16% in the control group, apgar score <7 at 5 minutes was 16% versus 3%

and NICU admission was 16% versus 3%. 98

 77

Study by Casey B et al 99 found that, there was increased rate of induction of

labour (42%) and caesarean section (32%) in oligohydramnios cases. Jun Zhang et

al 100 found that, the overall caesarean delivery rates were similar between women

with oligohydramnios and the controls (24% vs. 19%). Golan A et al 101 et al. found

that, the caesarean section was performed in 35.2% of pregnancies.

Oligohydramnios is associated with increased maternal and foetal morbidities. The

perinatal morbidity and mortality is due to foetal distress, low APGAR scores and

meconium aspiration syndrome in the foetus. 102-104

In a case control prospective comparative study 105 performed on 200

randomly selected low risk pregnant patients at term, the results showed that

increased number of LSCS in cases that is 35 while only 10 in control and almost

equal incidences of MSL and FD in both the groups, while in cases 17 women

were planned for elective LSCS for various indications in expectation of better

fetal outcome. There was significant low APGAR score in babies of cases, but

clinically we refute this. In this study almost double the no. of babies in cases was

IUGR or FGR. 105

Literature shows variability of perinatal outcome associated with low AFI.

Cesarean delivery was observed in 74%, 7 meconium stained liquor was found in

40.62%, 8 low birth weight was noted in 64%, APGAR score < 7 at 5 min was
6
found in 34% and NICU admission was noted in 92% patients of low AFI. 9 In

other studies, cesarean delivery was observed in 36%, meconium stained liquor

was found in 12%, 10 low birth weight was noted in 32%, 11 APGAR score < 7 at 5
 78

9
min was found in 4% and NICU admission was noted in 3.12% patients of low

AFI. 8

In the study by Magann et al. meconium stained amniotic fluid was not

different between the groups. 106 In study by Nargis et al meconium stained liquor

was seen in 44% of the women with low AFI (<5 cm) as compared to present study

where 12% had meconium stained liquor. 107 Ahmad et al 108 also found no

difference in the low Apgar score at 5 minutes in the two groups. Ahmad et al

observed that oligohydroamnios group when compared with control group had

significantly lower birth weight babies and they were delivered at a significant

earlier gestation due to iatrogenic preterm delivery via induction of labor or

caesarean sections as compared to control group. 108

In a prospective comparative study 109 included a total of 100 women with

singleton term pregnancy with cephalic presentation, divided into two groups of 50

each. Women in Group 1 had amniotic fluid index <5 cm and in Group 2, had AFI

from 6-20 cm. An AFI <5 cm was associated with significant high rate of

induction of labor (p<0.001), caesarean section (p=0.04) and fetal distress

(p<0.05). Meconium-stained liquor (p=0.76), Apgar score less than seven at 5

minutes (p=0.307), low birth weight (p=0.130) or NICU admission (p=1) were

comparable in the two groups. 109

Another study 110 showed significantly higher rate (65.5%) of low birth

weight resulting from the low AFI. The APGAR score less than 7 in 5 minute was

significantly higher in severe oligohydramnios group and majority of the neonate

experienced complications like RDS (13%), meconeum aspiration (21%) with

 79

admission in neonatal ward (54%). Low AFI has poorer prognosis to some extent

with maternal as well as fetal outcome. It is responsible for a significantly higher

rate of caesarean section & also associated with low birth rate along with low

APGAR score and increase in neonatal complications. 110

 80

CONCLUSION

CONCLUSION

 This study concluded that frequency of perinatal outcome in pregnant

females at term having low amniotic fluid index was as follows; cesarean

section was found in 66.67%, low birth weight in 64.44% patients, APGAR

score <7 at 5 minutes in 62.22%, meconium stained liquor in 26.67% and

NICU admission in 18.89% patients. So, we recommend that proper

antenatal monitoring and management should be done in these high risk

patients in order to reduce the morbidity and mortality of the fetus.

 81

REFERENCES

REFERENCES

1. Rathod S, Samal SK. Evaluation of maternal and perinatal outcomes of induction

in borderline oligohydramnios at term. J Clin Diagn Res. 2017;11(9):QC05-7.

2. Rezaie Kahkhaie K, Keikha F, Rezaie Keikhaie K, Abdollahimohammad A,

Salehin S. Perinatal outcome after diagnosis of oligohydramnios at term. Iran Red

Crescent Med J. 2014;16(5):e11772.

3. Madaan S, Mendiratta SL, Jain PK, Mittal M. Amniotic fluid index and its

correlation with fetal growthand perinatal outcome. J Fetal Med. 2015;2(2):61-7.

4. Gaikwad PR, Oswal MS, Gandhewar MR, Bhatiyani BR. Perinatal outcome in

oligohydramnios and borderline amniotic fluid index: a comparative study. Int J

Repord Contracept Obstet Gynecol. 2016;5:1964-8.

5. Jamal A, Kazemi M, Marsoosi V, Eslamian L. Adverse Perinatal outcomes in

borderline amniotic fluid index. Int J Repord Biomed (Yazd). 2016;14:705-8.

6. Bachhav AA, Waikar M. Low amniotic fluid index at term as a predictor of

adverse perinatal outcome. J Obstet Gynaecol India. 2014;64(2):120-3.

7. Thobbi VA, Sabahath S. A study of perinatal outcome in patients with low

amniotic fluid index (AFI). Al Ameen J Med Sci. 2017;10(2):119-23.

8. Rosati P, Guariglia L, Cavaliere AF, Ciliberti P, Buongiorno S, Ciardulli A, et al.

 82

A comparison between amniotic fluid index and the single deepest vertical pocket

technique in predicting adverse outcome in prolonged pregnancy. J Prenat Med.

2015;9(1-2):12-5.

9. Bhagat M, Chawla I. Correlation of amniotic fluid index with perinatal outcome. J

Obstet Gynaecol India. 2014;64:32-5.

10. Singhal SR, Gupta R, Sen J. Low amniotic fluid index as a predictor of adverse

perinatal outcome – an Indian perspective. Clinics Mother Child Health.

2015;12:201.

11. Panda S, Jayalakshmi M, Kumari GS, Mahalakshami G, Srujan Y, Anusha V.

Oligoamnios and perinatal outcome. J Obstet Gynaecol India. 2017;67:104-8.

12. Sari AE, Tanziha I. Effect of Water Intake on Sprague-Dawley Rat Off

Spring's Linear Growth. Pak J Nutr. 2015 Jul 1;14(7):436.

13. Nicksa GA, David CY, Kalish BT, Klein JD, Turner CG, Zurakowski D, et

al. Serial amnioinfusions prevent fetal pulmonary hypoplasia in a large

animal model of oligohydramnios. J Pediatr Surg. 2011;46(1):67-71.

14. Kahkhaie KR, Keikha F, Keikhaie KR, Abdollahimohammad A, Salehin S.

Perinatal Outcome After Diagnosis of Oligohydramnious at term. Iran Red

Crescent Med J.2014 May; 16(5): e11772.

15. Siraj A, Baqai S, Naseer S, Raja A. The effect of oligohydramnios on

perinatal outcome. Pak Armed Forces Med J 2016; 66(3):333-36.

16. Pritchard JA. Fetal swallowing and amniotic fluid volume. Obstet Gynecol

1996;28: 606.
 83

17. Boddy K, Dawes GS: Fetal breathing. Br Med Bull 1975;31: 3.

18. Duenhoelter JH, Pritchard JA. Fetal respiration: Quantitative measurements

of amniotic fluid inspired near term by human and rhesus fetuses. Am J

Obstet Gynecol 1976;125: 306.

19. Leontic EA, Schruefer JJ, Andreassen B et al. Further evidence for the role

of prolactin on human fetoplacental osmoregulation. Am J Obstet Gynecol

1979;133: 435.

20. Hebertson RM, Hammond ME, Bryson MJ. Amniotic epithelial

ultrastructure in normal, polyhydramnic, and oligohydramnic pregnancies.

Obstet Gynecol 1986;68: 74.

21. Seeds AE. Current concepts of amniotic fluid dynamics. Am J Obstet

Gynecol 1980;138: 575.

22. Wallenburg HCS. The amniotic fluid. I. Water and electrolyte homeostasis.

J Perinat Med 1977;5: 193.

23. Gillibrand PN. The rate of water transfer from the amniotic sac with

advancing pregnancy. J Obstet Gynaecol Br Commonw 1969;76: 530.

24. Brace RA, Wolf EJ. Normal amniotic fluid volume changes throughout

pregnancy. Am J Obstet Gynecol 1989;161: 382.

25. Elliott PM, Inman WHW. Volume of liquor amnii in normal and abnormal

pregnancy. Lancet 1961;2: 835.

 84

26. Queenan JT, Thompson W, Whitfield CR. Amniotic fluid volumes in

normal pregnancies. Am J Obstet Gynecol 1972;114: 34.

27. Queenan JT, Gadow EC. Polyhydramnios: Chronic versus acute. Am J

Obstet Gynecol 1970;108: 349.

28. Zamah NM, Gillieson MS, Waiters JH. Sonographic detection of

polyhydramnios: A five-year experience. Am J Obstet Gynecol 1982;143:

523.

29. Jacoby HE, Charles D. Clinical conditions associated with hydramnios. Am

J Obstet Gynecol 1966;94: 910.

30. Murray SR: Hydramnios. A study of 846 cases. Am J Obstet Gynecol

1964;88: 65.

31. Barry AP. Hydramnios. Obstet Gynecol 1998;11: 667.

32. Pedersen J. Glucose content of the amniotic fluid in diabetic pregnancies.

Acta Endocrinol 1954;15: 342.

33. Wallenburg HCS, Wladimiroff JW. The amniotic fluid. II. Polyhydramnios

and oligohydramnios. J Perinat Med 1997;6: 233.

34. Pritchard JA. Deglutition by normal and anencephalic fetuses. Obstet

Gynecol 1965;25: 289.

35. Benirschke K, McKay DG. The antidiuretic hormone in fetus and infant.

Obstet Gynecol 1953;1: 638.

 85

36. Kirshon B. Fetal urine output in hydramnios. Obstet Gynecol 1989;73: 240.

37. Cousins L, Benirschke K, Porreco R. Placentomegaly due to fetal

congestive failure in a pregnancy with a sacrococcygeal teratoma. J Reprod

Med 1980;25: 142.

38. Alexander ES, Spitz HB, Clark RA. Sonography of polyhydramnios. AJR

1982;138: 343.

39. Queenan JT. Recurrent acute polyhydramnios. Am J Obstet Gynecol

1970;106: 625.

40. Chamberlain PF, Manning FA, Morrison I. Ultra-sound evaluation of

amniotic fluid volume. II. The relationship of increased amniotic fluid

volume to perinatal outcome. Am J Obstet Gynecol 1984;150: 250.

41. Phelan JP, Smith CV, Broussard P. Amniotic fluid volume assessment with

the four-quadrant technique at 36–42 weeks’ gestation. J Reprod Med

1987;32: 540.

42. Bottoms SF, Welch RA, Zador IE. Limitations of using maximum vertical

pocket and other sonographic evaluations of amniotic fluid volume to

predict fetal growth: Technical or physiologic? Am J Obstet Gynecol

1986;155: 154.

43. Denehy TR, Hollander DI, Dembner A. Acute polyhydramnios. Int J

Gynecol Obstet 1989;28: 181.

 86

44. Pitkin RM. Acute polyhydramnios recurrent in successive pregnancies.

Obstet Gynecol 1976;48: 42S.

45. Hill LM. Resolving polyhydramnios: A sign of improved fetal status. Am J

Perinatol 1988;5: 61.

46. Cabrol D, Landesman R, Muller J. Treatment of polyhydramnios with

prostaglandin synthetase inhibitor (indomethacin). Am J Obstet Gynecol

1987;157: 422.

47. Moise KJ, Huhta JC, Sharif DS. Indomethacin in the treatment of premature

labor: Effects on the fetal ductus arteriosus. N Engl J Med 1988;319: 327.

48. Chamberlain PF, Manning FA, Morrison I, et al. Ultrasound evaluation of

amniotic fluid volume. II. The relationship of increased amniotic fluid volume to

perinatal outcome. Am J Obstet Gynecol. 1984 Oct 1. 150(3):250-4.

49. Rosenberg VA, Buhimschi IA, Dulay AT, Abdel-Razeq SS, Oliver EA, Duzyj

CM, et al. Modulation of Amniotic Fluid Activin-A and Inhibin-A in Women

With Preterm Premature Rupture of the Membranes and Infection-Induced

Preterm Birth. Am J Reprod Immunol. 2011 Oct 13.

50. Ben-Chetrit A, Hochner-Celnikier D, Ron M, Yagel S. Hydramnios in the third

trimester of pregnancy: a change in the distribution of accompanying fetal

anomalies as a result of early ultrasonographic prenatal diagnosis. Am J Obstet

Gynecol. 1990 May. 162(5):1344-5.

51. Phelan JP, Smith CV, Broussard P, Small M. Amniotic fluid volume assessment

with the four-quadrant technique at 36-42 weeks' gestation. J Reprod Med. 1987
 87

Jul. 32(7):540-2.

52. Dasari P, Niveditta G, Raghavan S. The maximal vertical pocket and amniotic

fluid index in predicting fetal distress in prolonged pregnancy. Int J Gynaecol

Obstet. 2007 Feb. 96(2):89-93.

53. Fok WY, Chan LY, Lau TK. The influence of fetal position on amniotic fluid

index and single deepest pocket. Ultrasound Obstet Gynecol. 2006 Aug.

28(2):162-5.

54. Johnson JM, Chauhan SP, Ennen CS, Niederhauser A, Magann EF. A comparison

of 3 criteria of oligohydramnios in identifying peripartum complications: a

secondary analysis. Am J Obstet Gynecol. 2007 Aug. 197(2):207.e1-7; discussion

207.e7-8.

55. Moore TR, Cayle JE. The amniotic fluid index in normal human pregnancy. Am J

Obstet Gynecol. 1990 May. 162(5):1168-73.

56. Peipert JF, Donnenfeld AE. Oligohydramnios: a review. Obstet Gynecol Surv.

1991 Jun. 46(6):325-39.

57. Sherer DM. A review of amniotic fluid dynamics and the enigma of isolated

oligohydramnios. Am J Perinatol. 2002 Jul. 19(5):253-66.

58. Lee SE, Romero R, Lee SM, Yoon BH. Amniotic fluid volume in intra-amniotic

inflammation with and without culture-proven amniotic fluid infection in preterm

premature rupture of membranes. J Perinat Med. 2010. 38(1):39-44.

59. Ross MG, Beall MH, Christenson PD. Amniotic fluid volume and perinatal

outcome. Am J Obstet Gynecol. 2007 Mar. 196(3):e17.

60. Petrozella LN, Dashe JS, McIntire DD, Leveno KJ. Clinical significance of
 88

borderline amniotic fluid index and oligohydramnios in preterm

pregnancy. Obstet Gynecol. 2011 Feb. 117(2 Pt 1):338-42.

61. Patrelli TS, Gizzo S, Cosmi E, Carpano MG, Di Gangi S, Pedrazzi G, et al.

Maternal hydration therapy improves the quantity of amniotic fluid and the

pregnancy outcome in third-trimester isolated oligohydramnios: a controlled

randomized institutional trial. J Ultrasound Med. 2012 Feb. 31(2):239-44.

62. Chamberlain PF, Manning FA, Morrison I, et al. Ultrasound evaluation of

amniotic fluid volume. I. The relationship of marginal and decreased amniotic

fluid volumes to perinatal outcome. Am J Obstet Gynecol. 1984 Oct 1.

150(3):245-9.

63. Jaba B, Mohiuddin AS, Dey SN, Khan NA, Talukder SI. Ultrasonographic

determination of amniotic fluid volume in normal pregnancy. Mymensingh Med

J. 2005 Jul. 14(2):121-4.

64. Magann EF, Chauhan SP, Barrilleaux PS, Whitworth NS, McCurley S, Martin

JN. Ultrasound estimate of amniotic fluid volume: color Doppler overdiagnosis of

oligohydramnios. Obstet Gynecol. 2001 Jul. 98(1):71-4.

65. Moore TR. Sonographic screening for oligohydramnios: does it decrease or

increase morbidity?. Obstet Gynecol. 2004 Jul. 104(1):3-4.

66. Zlatnik MG, Olson G, Bukowski R, Saade GR. Amniotic fluid index measured

with the aid of color flow Doppler. J Matern Fetal Neonatal Med. 2003 Apr.

13(4):242-5.

67. Vink J, Hickey K, Ghidini A, Deering S, Mora A, Poggi S. Earlier gestational age

at ultrasound evaluation predicts adverse neonatal outcomes in the preterm

 89

appropriate-for-gestational-age fetus with idiopathic oligohydramnios. Am J

Perinatol. 2009 Jan. 26(1):21-5.

68. Brace RA, Resnik R. Dynamics and disorders of amniotic fluid. Creasy RK,

Resnik R, eds. Maternal-Fetal Medicine. 4th ed. 1999. 632-43.

69. Fanaroff AA, Martin RJ. Diseases of the fetus and infant. Neonatal-Perinatal

Medicine. 6th ed. 1997. 315-9.

70. Kilpatrick SE. Histologic prognostication in soft tissue sarcomas: grading versus

subtyping or both? A comprehensive review of the literature with proposed

practical guidelines. Ann Diagn Pathol. 1999 Feb. 3(1):48-61.

71. Macri CJ, Schrimmer DB, Leung A, et al. Prophylactic amnioinfusion improves

outcome of pregnancy complicated by thick meconium and oligohydramnios. Am

J Obstet Gynecol. 1992 Jul. 167(1):117-21.

72. Morales WJ, Talley T. Premature rupture of membranes at Am J Obstet Gynecol.

1993 Feb. 168(2):503-7.

73. Phelan JP, Ahn MO, Smith CV, et al. Amniotic fluid index measurements during

pregnancy. J Reprod Med. 1987 Aug. 32(8):601-4.

74. Pitt C, Sanchez-Ramos L, Kaunitz AM, Gaudier F. Prophylactic amnioinfusion

for intrapartum oligohydramnios: a meta- analysis of randomized controlled

trials. Obstet Gynecol. 2000 Nov. 96(5 Pt 2):861-6.

75. Rib DM, Sherer DM, Woods JR Jr. Maternal and neonatal outcome associated

with prolonged premature rupture of membranes below 26 weeks' gestation. Am J

Perinatol. 1993 Sep. 10(5):369-73.

76. Schumacher B, Moise KJ Jr. Fetal transfusion for red blood cell alloimmunization
 90

in pregnancy. Obstet Gynecol. 1996 Jul. 88(1):137-50.

77. Vergani P, Ghidini A, Locatelli A, et al. Risk factors for pulmonary hypoplasia in

second-trimester premature rupture of membranes. Am J Obstet Gynecol. 1994

May. 170(5 Pt 1):1359-64.

78. Xiao ZH, Andre P, Lacaze-Masmonteil T, et al. Outcome of premature infants

delivered after prolonged premature rupture of membranes before 25 weeks of

gestation. Eur J Obstet Gynecol Reprod Biol. 2000 May. 90(1):67-71.

79. Regnault TR, Friedman JE, Wilkening RB, Anthony RV, Hay WW, Jr.

Fetoplacental transport and utiliza-tion of amino acids in IUGR – a review.

Placenta. 2005 Apr; 26 Suppl A: S52-62.

80. 2Ali HS. Assessment of amniotic fluid index in normal pregnancy at a

tertiary care hospital setting. J Ayub Med Coll Abbottabad. 2009;21:149–

151.

81. Karim R, Jabeen S, Pervaiz F, Wahab S, Yasmeen S, Raees M. Decreased

amniotic fluid index and adverse pregnancy outcome at term. JPMI.

2010;4:307–311.

82. Voxman EG, Tran S, Wing DA. Low amniotic fluid index as a predictor of

adverse perinatal outcome. J Perinatol. 2002;22:282–185.

83. Pankaj D, Purvi P, Anjali G. Decrease of amniotic fluid index in low- risk

pregnancy. Any significance? J Obstet Gynecol Ind. 2004;54:464–466.

84. Magann EF, Chauhan SP, Bofill JA, Martin JN Jr. Comparability of the
 91

amniotic fluid index and single deepest pocket measurements in clinical

practice. Aust N Z J Obstet Gynaecol. 2003;43:75–77.

85. Anderson D, Yang Q, Hohimer A, Faber J, Gi Raud G, Davi SL. Int r

amembranous absorption rate is unaffected by changes in amniotic fluid

composition. Am J Physiol Renal Physiol. 2005;288:964–968.

86. Phelan JP, Smith CV, Broussard P, Small M. Amniotic fluid volume

assessment with the four-quadrant technique at 36-42 weeks’ gestation. J

Reprod Med. 1987;32:540–542.

87. Rutherford SE, Phelan JP, Smith CV, Jacobs N. The 4 quadrant assessment

of amniotic fluid volume: An adjunct to antepartum fetal heart rate testing.

Obstet Gynecol. 1987;70:353–356.

88. Kwon JY, Kwon HS, Kim YH, Park YW. Abnormal Doppler velocimetry is

related to adverse pregnancy outcome for borderline amniotic fluid index in

the third trimester. J Obstet Gynecol Res. 2006;32:545–549.

89. Haas DM, Magann EF. External cephalic version with an amniotic fluid

index <or =10: a systematic review. J Matern Fetal Neonatal Med.

2005;18:249–252.

90. Gumus II, Koktener A, Turhan NO. Perinatal outcome of pregnancies with

borderline amniotic fluid index. Arch Gynecol Obstet. 2007;276:17–19.

91. Banks EH, Miller DA. Perinatal risks associated with borderline amniotic
 92

fluid index. Am J Obstet Gynecol. 1999;180:1461–1463.

92. Baron C, Morgan MA, Garite TJ. The impact of amniotic fluid volume

assessed intrapartum on perinatal outcome. Am J Obstet Gynecol.

1995;173:167–174.

93. Akhter H, Guha K, Daisy KP. Amniotic Fluid Index in High Risk

Pregnancies and Pregnancy Outcome. Dinajpur Med Col J. 2010;3:1–5.

94. Petrozella LN, Dashe JS, McIntire DD, Leveno KJ. Clinical significance of

borderline amniotic fluid index and oligohydramnios in preterm pregnancy.

Obstet Gynecol. 2011;117:338–342.

95. Luo X, Huang Y, Liang R. [Analysis of 196 cases of trial of labor with

borderline oligohydramnios assessed by ultrasound. Zhonghua Fu Chan

KeZaZhi. 1988;33:585–587.

96. Locatelli A, Zagarella A, Toso L, Assi F, Ghidini A, Biffi A. Serial

assessment of amniotic fluid index in uncomplicated term pregnancies:

prognostic value of amniotic fluid reduction. J Matern Fetal Neonatal Med.

2004;15:233–236.

97. Sowmya K. Effect of isolated oligohydramnios in otherwise normal term

pregnancy. Int J Biomed Res. 2015;5(2):98-101.

98. Al-Bayatti MM. Amniotic fluid index as a predictor of perinatal outcome in

patients with prolonged pregnancy. Iraqi J Comm Med. 2008;3:216-9.

99. Casey Brian M, Donald D. McIntire. Pregnancy outcomes after antepartum

 93

diagnosis of oligohydramnios at or beyond 34 weeks’ gestation. Am J

Obstet Gynaecol. 2000 Apr;182(4):909-12.

100. Zhang J, Troendle J. Isolated oligohydramnios is not associated with

adverse perinatal outcome. Int J Gynaecol Obstet. 2004 Mar;3:220-5.

101. Golan A, Lin G. Oligohydramnios – maternal complications and

fetal outcome in 145 cases. Gynaecol Obstet Invest. 1994;37(2):91-5.

102. Ekin A, Gezer C, Taner CE, Ozeren M. Perinatal outcomes in

pregnancies with oligohydramnios after preterm premature rupture of

membranes. J Matern Foetal Neonatal Med. 2015;28(16):1918–22.

103. Naveiro-Fuentes M, Puertas Prieto A, Ruíz RS, Carrillo Badillo MP,

Ventoso FM, Gallo Vallejo JL. Perinatal outcomes with isolated

oligohydramnios at term pregnancy. J Perinat Med. 2016;44(7):793–98.

104. Leibovitch L, Kuint J, Rosenfeld E, Schushan-Eisen I, Weissmann-

Brenner A, Maayan-Metzger A. Short term outcome among term singleton

infants with intrapartum oligohydramnios. Acta Paediatr. 2012;101(7):727–

30.

105. Mathuriya G, Verma M, Rajpoot S. Comparative study of maternal

and fetal outcome between low and normal amniotic fluid index at term. Int

J Reprod Contracept Obstet Gynecol. 2017;6:640-4.

106. Magann EF, Chauhan SP, Martin JN. Oligohydroamnios at term and
 94

pregnancy outcome. Foetal Matern Med Review 2001;12:209-227.

107. Nargis N, Begum F. Oligohydramnios at third trimester and perinatal

outcome. Bangla J Med Sci 2012;11:33-36.

108. Ahmad H, Munim S. Isolated oligohydramnios is not an indicator for

adverse perinatal outcome. J Pak Med Assoc 2009;59: 691-694.

109. Singhal SR, Gupta R, Sen J. Low Amniotic Fluid Index as a

Predictor of Adverse Perinatal Outcome – An Indian Perspective. Clinics

Mother Child Health 2015;12:201.

110. Fahmida M, Rumana N, Rumana A, Tahmina B, Kayum A,

Mohshina A, et al. Low amniotic uid index and the materno-fetal out come

in 3rd trimester of pregnancy. Bangladesh Med J. 2015 Jan; 44 (1): 16-20.