Flags

Women's Health and Education Center (WHEC)

Obstetrics

Print this ArticleShare this Article

Amniotic Fluid Disorders

WHEC Practice Bulletin and Clinical Management Guidelines for healthcare providers. Educational grant provided by Women's Health and Education Center (WHEC).

For most pregnant women and their health care providers, amniotic fluid (AF) is an unimportant by product of the delivery. With a normal pregnancy, little attention is paid to the AF unless meconium staining occurs in labor. It is only when certain complications of pregnancy present, compromising fetal well-being that any interest is taken in the AF. The conditions of polyhydramnios (too much AF) or oligohydramnios (too little AF) create the greatest concern to patients and health care providers. As an example, with significant oligohydramnios in the second trimester, the perinatal mortality rate (PMR) approaches 90 to 100 percent. Likewise, with marked polyhydramnios in mid-pregnancy, PMR can be higher than 50 percent. Although these two extreme conditions are rare, other less drastic examples are much more common. Efforts to study abnormalities of AF are complicated by the fact that little is known about the processes involved in normal amniotic fluid volume (AFV) regulation. Rarely in modern medical research are the processes that underlie normal physiology so poorly understood. However, many of the disease states associated with the extremes of AFV are better understood than is the normal physiology of AF.

The purpose of this document is to explore what is known about the normal mechanisms affecting the formation and removal of AF, including fetal urination, swallowing, lung liquid, and intramembranous absorption. In addition, the changes in AFV and composition across gestation, in order to help us understand its normal regulation are examined. The various treatment options available for AFV abnormalities are discussed. The goal of this review is to offer the reader a complete understanding of the known mechanisms and functioning of AFV regulation, and their connection with disease states.

Abbreviations:

AF -- Amniotic Fluid
AFV -- Amniotic Fluid Volume
PMR -- Perinatal Mortality Rate
LVP -- Largest Vertical Pocket
AFI -- Amniotic Fluid Index
IUGR -- Intrauterine Growth Restriction
IUFD -- Intrauterine Fetal Death
NICU -- Neonatal Intensive Care Unit
PROM -- Premature Rupture of Membranes
MSAFP -- Maternal Serum Alpha Fetoprotein
MSHCG -- Maternal Serum Human Chorionic Gonadotropin
CNS -- Central Nervous System
TTS -- Twin-to-Twin Transfusion Syndrome

Normal Amniotic Fluid Volume (AFV):

As a result of various limitations, attempts to measure actual AFV are difficult. It is not easy to get near, or into the amniotic compartment. To enter the amniotic cavity, an invasive procedure such as an amniocentesis must be performed. To measure the volume of AF, an inert dye must be injected, which dilutes to fill the amniotic cavity. Follow-up samples of amniotic fluid are then obtained to determine a dilution curve. Obviously, an amniocentesis has a small but real risk of interrupting the pregnancy, and any substance injected into the uterus can cause infection despite every precaution being taken. It can be seen that for each week of gestation, there can be widely varying amounts of AF, which increases with advancing gestational age. The largest variation occurs at 32 to 33 weeks of gestation. At this time, the normal range (5th to 95th percent) is from 400 to 2100 ml. This represents a wide "normal range." One of the most interesting findings is that from 22 weeks through 39 weeks of gestation, the average volume of AF remains unchanged (1, 2). At a time when the fetus weighed, on average, about 500 g at 22 weeks, up to term gestation when it weighed 3,500 g, a 7-fold increase in weight, the mean AFV is almost the same. This would suggest that AFV is being carefully regulated.

Measurements of Amniotic Fluid Volume (AFV):

Measuring true AFV is not only difficult but clinically impractical as well. Initial clinical assessments of AFV were through Leopold's abdominal measurements, or measurement of the fundal height of the pregnant uterus. If the maternal uterus was large for gestational age, and the fetus could not be easily palpated, or was ballotable, it was believed that AFV was increased. More commonly, the diagnosis of polyhydramnios was made at the time of delivery when large volumes of AF rained down on the delivery room floor. The diagnosis of oligohydramnios considered when the fundal height was small for gestational age or the fetus could be easily palpated. Clearly, palpation as a method for determining AFV has its place, but the advent of ultrasound has afforded us the ability of looking, non-invasively, into the human uterus to examine both the fetus and AFV. Early ultrasound estimations of AFV were made by measuring the largest vertical pocket (LVP) of AF. Other researchers have examined the LVP, and then considered the horizontal plain, if the LVP was less than 1 cm. Many studies have found that with the LVP of AF less than 1 cm or 0.5 cm, respectively, perinatal morbidity and the PMR were increased (2, 14). These lower values of the LVP certainly identified at-risk fetuses, but the sensitivity for identifying the majority of pregnancy complications associated with oligohydramnios, was not as strong, causing others to choose higher values as a cutoff point.

As the quality of ultrasound improved, investigators expanded their measurements to include the LVP in each of the four quadrants of the uterus throughout gestation. The uterus at any gestational age beyond 20 weeks is divided into four equal quadrants. The deepest clear pocket of AF is then measured, making sure that the ultrasound transducer is perpendicular to the floor. This four-quadrant measurement is termed the amniotic fluid index (AFI). The 5th and 95th percentile of the AFI varies for each gestational age, suggesting that what may be normal for one gestational age period, may be abnormal for another. The 95th percentile for 35 to 36 weeks of gestation is a value of 24.9 cm, whereas the 95th percentile for 41 weeks of gestation is 19.4 cm. The variation in the AFI at the 5th percentile is less than that of the 95th percentile, but it still varies by as much as 2.5 cm. The investigators reported the inter-observer variation to be 3.1% and 6.7 %, which is acceptable for this commonly, performed procedure. Comparing the ultrasound estimation of the AFV by the AFI with the actual measured volume demonstrates very similar-appearing curves. Several authors have attempted to compare estimates of AFV by ultrasound (the LVP and the AFI) with actual measurement by the dye dilution technique, and report that the AFI does not predict actual AFV that well (2). The researchers went on to conclude that the difference between actual volume and estimated volume by the AFI should not change clinical practice.

Measurement of the AFI can also vary widely depending upon the technique used. It is reported that increase of the AFI (13%) by using low pressure with the ultrasound transducer on the maternal abdomen, as compared with moderate pressure, or decrease the AFI (21%) with high pressure on the maternal abdomen. Clearly technique is important to prevent overestimating or underestimating the ultrasound measurement of the AFI (3). For many years, investigators have tried, with mixed success, to demonstrate the utility and applicability of ultrasound estimation of AFV in relation to perinatal outcome. With the LVP smaller than 1 cm, there is a marked increase in perinatal morbidity and mortality, which persist even after correcting for birth defects. Despite overwhelming evidence that any ultrasound method for predicting AFV is poor at best, clinical practice continues to include the use of weekly or biweekly AFV estimation by ultrasound.

Amniotic Fluid Formation:

Fetal urine: The main source of AF is fetal urination. In the human, the fetal kidneys begin to make urine before the end of the first trimester, and production of urine continues from this point, ever increasing, until term gestation. Many different animal models have been used to study fetal urine production, with the fetal sheep being the most common. The fetal sheep provides an excellent model for comparative human study owing to its similar fetal weight at term, its sufficient size allowing catheter placement, and the fact that the sheep fetus has a low risk of premature labor after catheter placement. In the fetal sheep, urine production has been reported to be approximately 200 to 1200 ml/day in the last third of pregnancy (5). Efforts to measure human fetal urine production have been accomplished by ultrasound measuring the change in fetal bladder volume over time. The three dimensions of the fetal bladder measured every 15 minutes and reported a human fetal urine production rate of 230 ml/day at 36 weeks of gestation, which increased to 655 ml/day at term. The human fetal urine production rate can be seen to be approximately 1000 to 1200/ ml/ day at term, suggesting that the entire AFV is replaced more frequently than every 24 hours (3).

Fetal Lungs: Although rarely even contemplated by the practicing clinician, fetal lung liquid plays an important role in AF formation. For years, it was presumed that there was actual movement of AF into the fetal lungs under normal conditions; however, recent data offer no support of this concept. In fact, there is normally an outward rather than inward movement of fluid from the lungs. Throughout gestation, the fetal lungs produce fluid that exits in the trachea and is either swallowed, or leaves the mouth, and enters the amniotic compartment. Although never directly measured in humans, lung liquid values from the fetal sheep have provided some valuable data. In the fetal sheep, the lungs have been reported to produce volumes of up to 400 ml/day, with 50% being swallowed and 50% exiting via the mouth (5). In humans, we know that fetal lung liquid enters the amniotic compartment owing to the presence of surfactant within the AF, both near and at term, as measured by amniocentesis for lung maturity. During normal fetal life, the fetus performs breathing movements that provide a "to-and-fro" movement of AF into and out of the trachea, upper lungs and mouth. Although AF may move back and forth, there is a net outward movement of fetal lung liquid. Clearly, the fetal lungs provide a volume of liquid to the AF, which adds to that of the fetal urine (4).

Amniotic Fluid Removal:

Fetal Swallowing: In the humans, fetal swallowing begins early in gestation. In the fetal sheep, swallowing has mostly been measured in the latter half of pregnancy and appears to increase with increasing gestational age. The studies have reported that the ovine fetus swallows in episodes lasting 2 minutes and at volumes of 100 to 300 ml/kg/day. In the term ovine fetus, that volume represents a daily swallowing rate of 350 to 1,000 ml/day for a 3.5 kg fetus. This is obviously more than the adult sheep, which drinks 40 to 60 ml/kg daily. Many different techniques have been used to determine swallowing rates in the animal model, including repetitive sampling of injected dye and actual flow probe measurements (5). For obvious reasons, actual measurement of human fetal swallowing is much more difficult. In spite of this limitation, early studies in humans in the 1960s used fetuses that underwent injection of substances into the amniotic compartment to measure swallowing. Initial work was done in normal and anencephalic fetuses. Human fetal swallowing was studied by injecting radioactive chromium--labeled erythrocytes and hypaque into the amniotic compartment, and swallowing rates of 72 to 262 ml/kg/day were found. Clearly, fetal swallowing could not remove the entire volume of fluids entering the amniotic compartment from fetal urine production and lung liquid, and therefore, other mechanisms for AF removal must occur.

Intramembranous Absorption: One major stumbling block to the understanding of AFV regulation was the discrepancy between fetal urine and lung liquid production, and its removal by swallowing. If the measurements and estimates of AF production and removal were accurate, there would be at least 500 to 750 ml/day entering the amniotic compartment, without leaving, which would result in acute polyhydramnios. This does not occur under normal conditions, clearly demonstrating the presence of other mechanisms that remove AF in order to maintain a normal volume. A second route for AF removal has been suggested, namely the intramembranous pathway. This process describes the movement of water and solutes between the amniotic compartment and the fetal blood, which circulates through the fetal surface of the placenta. The large osmotic gradient between AF and fetal blood provides a substantial driving force for the movement of AF into the fetal blood. This intramembranous absorption has been described in detail in the fetal sheep and also demonstrated to be present in the rhesus monkey fetus (5). Several anecdotal studies suggest that intramembranous absorption also occurs in humans. In a study, injection of labeled amino acids into the amniotic compartments of women, who were shortly thereafter delivered by cesarean section were measured. The groups found high levels of the amino acids concentrated in the placenta within 45 minutes of injection. They concluded that the amino acids had to be absorbed by some route other than swallowing in order to explain the rapid absorption into the fetal circulation within the placenta (1, 2). Intramembranous absorption could easily explain this movement. This route of absorption is now being actively investigated, and researchers have noted that 200 to 500 ml/day leaves the amniotic compartment under normal physiologic conditions.

With the identification of intramembranous absorption as a significant route for the removal of amniotic water and solutes, it appears that all routes of entry and removal from the amniotic compartment have possibly been identified, and the equation of input and outflow has finally been balanced. Recent work on the mechanisms associated with intramembranous absorption should help clarify in our understanding of the normal physiology associated with AFV regulation.

Oligohydramnios

The incidence of oligohydramnios varies depending on which definition is used, with a general reporting rate between 1 and 3%. When women undergoing antepartum testing for high-risk pregnancy conditions are examined, the incidence of oligohydramnios is much higher (19 to 20%), as would be expected. This is primarily due to the underlying maternal or fetal indication for the antepartum testing. Three studies have reported actual measured AFV but have reported somewhat different values for oligohydramnios: less than 318 ml; less than 500 ml; and less than 200 ml (4, 6). With the advent of ultrasound estimation of AFV, multiple thresholds have been reported. It has been reported in number of studies a 50-fold increase in PMR for pregnancies with a LVP of less than 1 cm. These reports were instrumental in raising concern about the risk of stillbirth and neonatal mortality in the presence of oligohydramnios. A second, less-often reported finding of that study was that 40% of the cases with oligohydramnios also had other confounding factors such as intrauterine growth restriction (IUGR), maternal hypertensive disorders, and congenital malformations. Clearly, oligohydramnios in the presence of IUGR, or preeclampsia, has markedly worse perinatal outcomes, but what are the risks in the cases of isolated oligohydramnios? Other investigators have reported that oligohydramnios in the prolonged pregnancy has an increased risk of meconium staining of the AF, fetal distress in labor, and low 1-minute Apgar scores. A common clinical finding is the existence of a low AFI in an otherwise normal pregnancy, when an ultrasound is obtained for some other reason. Because the diagnosis of oligohydramnios has been associated with poor perinatal outcomes, many women, who are at or near term are sent to labor and delivery to be considered for induction, solely due to the low AFI. Frequently, their cervical examination is unfavorable for induction, and in spite of this, an induction is attempted. This can often result in a cesarean delivery for failed induction. Although the evidence for induction in the prolonged pregnancy is solid, the term or preterm patient with isolated oligohydramnios may not need immediate delivery.

Women at greater than 34 weeks' gestation with an AFI less than 5 cm, have been found to have increase in intrauterine fetal death (IUFD), admissions to the neonatal intensive care unit (NICU), neonatal death, low birth weight, and meconium aspiration syndrome as compared with women with an AFI greater than 5 cm. If the birth defects and IUGR are removed, there is no difference in admissions to the NICU, neonatal death, or respiratory distress syndrome. This suggests that the IUGR and birth defects contributed to the increased morbidity and mortality, and not the oligohydramnios itself (6). There is increasing evidence that patients with isolated oligohydramnios with a normally grown fetus, good fetal movement, and an unfavorable cervix may be candidates for observation or possible therapeutic intervention, or both, to increase the AF level.

It has been clearly established that when the AFV is greatly decreased, especially in midpregnancy, the perinatal mortality rate approaches 100%. The cause of the decrease or absence of AF largely determines the perinatal outcome. With renal agenesis, virtually 100% of newborns die due to pulmonary hypoplasia. AF is required during certain periods of early and mid-gestation for fetal lung development, and without it, the lungs do not develop. If premature rupture of the membranes (PROM) results in a loss of all AF, perinatal outcome will vary based on during which period of gestation the membrane rupture occurred, and whether or not intraamniotic infection was the cause of the membrane rupture. Oligohydramnios can occur with hypertensive disorders or the antiphospholipid syndrome. In these cases, if the fetus is large enough for survival outside of the uterus, there may be little impact on perinatal outcome other than the consequences of prematurity.

Fetal and Maternal Causes of Oligohydramnios:

Fetal conditions: renal agenesis; obstructed uropathy; spontaneous rupture of the membranes (SROM); premature rupture of the membranes (PROM); abnormal placentation—elevated MSAFP/MSHCG; and postdate pregnancy.

Maternal conditions: dehydration-hypovolemia; hypertensive disorders; uteroplacental insufficiency; antiphospholipid syndrome; and idiopathic. (MSAFP: maternal serum alpha fetoprotein; MSHCG: maternal serum human chorionic gonadotropin)

Evaluation and Work-Up of Mid-gestation Oligohydramnios:

When the diagnosis of oligohydramnios is made in the second trimester, it is vitally important to obtain a complete history and physical from the patient, as well as a targeted ultrasound. The patient should be questioned for any history consistent with rupture of the membranes, leakage of bloody fluid, or wetness of her underwear. If there is a question of the possible rupture of the membranes, a sterile speculum examination should be performed in an attempt to obtain fluid that can be examined for evidence of rupture. Specific tests include examining for microscopic ferning, checking for a neutral pH on nitrazine paper, and looking for pooling in the posterior vagina. When ferning is present, the sodium chloride concentration is high enough for crystallization or ferning to occur. The sodium chloride concentration of the AF is sufficient to cause ferning, whereas vaginal secretions usually do not fern. Determining the pH of the vaginal fluid can identify the neutral pH of AF as different from the acidic pH of normal vaginal secretions. Next, a targeted ultrasound should be performed to examine for the amount of AF present, the presence of normal anatomy including fetal kidneys and bladder, and finally, for appropriate interval growth. If the fetus is normally grown with kidneys and bladder visualized, more often than not, the fetal membranes have been prematurely ruptured. If kidneys and bladder cannot be seen, then the diagnosis is most likely renal agenesis. The difference between the prognoses of these two entities is dramatic. Renal agenesis is uniformly fatal, whereas PROM can have a reasonable prognosis if it occurs after fetal viability and if infection is not present.

Third-Trimester Oligohydramnios:

Although severe oligohydramnios has an increased PMR later in the third trimester, it is still not as high as earlier in pregnancy. It is reported a 50-fold increase in PMR when the LVP of AF was less than 1 cm. This data has led many clinicians to induce or deliver women with oligohydramnios, even when there were no other indications for delivery (6, 7). This study was problematic in that approximately 40% of the patients also had IUGR or hypertensive disorders, or both. This could easily explain the increase in mortality. Other studies have reported similar increases in perinatal mortality associated with oligohydramnios, but most have not corrected for other underlying medical conditions. When oligohydramnios is diagnosed in the prolonged pregnancy, there is an increased risk of meconium staining of the AF, meconium aspiration syndrome, fetal distress in labor, and increased cesarean delivery rates. For these reasons, induction of labor is indicated with oligohydramnios in the prolonged pregnancy. An important question currently under investigation is whether or not a patient with isolated oligohydramnios will have a worse pregnancy outcome if decreased AFV is the only finding. Because induction is indicated for oligohydramnios in the post-date period, many clinicians believe that induction is indicated for oligohydramnios at or close to term.

Management of Oligohydramnios:

Because of the increase in perinatal morbidity and mortality associated with oligohydramnios in the prolonged pregnancy, most authors recommend delivery in these cases. As discussed earlier, however, the patient who presents with isolated oligohydramnios in the third trimester may be a candidate for continued observation. Several investigators have attempted to treat oligohydramnios with the oral administration of water in the hope of "hydrating" the fetus through the mother. Animal studies have demonstrated that there is a close relationship between the hydration or dehydration of the mother and the fetus (5). Attempts to dehydrate the mother have resulted in dehydration of the fetus and in some cases vice versa. In human pregnancies, it is found that the maternal intravascular volume was low in cases of idiopathic oligohydramnios, and that by increasing the intravascular volume, the oligohydramnios resolved. In the initial randomized study of the use of oral hydration as a treatment for women with a low AFI, women were put into two groups: the treatment group was told to drink 2 liters of water within 4 hours of a repeat AFI, and a control group that did not drink the 2 liters of water. The treatment group had a significantly greater increase in AFI on repeat testing (6.3 cm) than the control group (5.1 cm). They concluded that the oral administration of water could increase the AFI in women with oligohydramnios. A follow-up study by the same group observed that women with normal AFV could increase or decrease their AFI depending upon the amount of water the mothers drank (8). Several researchers have reported success in improving AFV in women with oligohydramnios by the injection of a crystalloid solution into the amniotic compartment during an amniocentesis. The injection of fluid also allows for a more complete ultrasound examination of the fetus, which previously was not available owing to the lack of AF. Most of these studies, however, have been case reports, and because no large prospective studies have been performed, the routine use of amniocentesis for cases of marked oligohydramnios in mid-gestation cannot be justified by the literature.

Oligohydramnios in Labor:

When AF is removed from the amniotic compartment, variable decelerations in the fetal heart rate may develop. These decelerations resolve when the AF is replaced, suggesting that cord compression may be the cause of the decelerations. Multiple investigators have studied amnioinfusion as a technique by which to treat variable decelerations in labor. Although most report a decrease in the frequency of variable decelerations, few have demonstrated any decrease in perinatal morbidity or mortality, or the cesarean delivery rate. Amnioinfusion has been studied as a possible therapy in the case of thick meconium. In several prospective studies, it has been shown to improve neonatal outcomes, including meconium visualized below the newborn vocal cords, and meconium aspiration syndrome. A recent, multicenter, randomized trial of 1,998 women in labor at 36 weeks' gestation or later with thick meconium did not find that amnioinfusion reduced the risk of moderate or severe meconium aspiration syndrome or perinatal death (8). The authors concluded that amnioinfusion should not be recommended to prevent meconium aspiration syndrome.

Polyhydramnios

With the increasing use of real-time ultrasound, the diagnosis of polyhydramnios has been on the rise. Previously, the diagnosis of polyhydramnios was made when the uterus was large for gestational age or the fetus could not be easily palpated by Leopold's maneuvers. The diagnosis was often not made until the time of delivery, when large gushes of AF preceded or followed the delivery of the newborn. Polyhydramnios has an impact on perinatal morbidity and mortality based largely on the amount of fluid present, and when in gestation it presents. The earlier in gestation it occurs and the greater the amount of fluid, the higher the morbidity and mortality. The incidence of polyhydramnios has been reported to be about 1% in large population-based studies. The most common cause for severe polyhydramnios in mid-gestation is congenital malformations, with or without aneuploidy, and monozygotic twins.

Fetal and Maternal Causes of Polyhydramnios:

Fetal conditions: congenital anomalies; gastrointestinal obstruction; CNS abnormalities; cystic hygromas; non-immune hydrops; sacrococcygeal teratoma; aneuploidy; twin-to-twin transfusion syndrome; and muscular dystrophy syndromes

Maternal conditions: idiopathic; and poorly controlled diabetes mellitus (CNS: central nervous system)

Evaluation and Work Up:

The pregnant woman who presents with a rapidly enlarging uterus in mid-pregnancy, or who presents in preterm labor, will most likely have a fetus with a congenital malformation or aneuploidy, or both. Severe polyhydramnios in the second trimester has a significant PMR, which is most commonly due to prematurity or aneuploidy. The more common congenital malformations associated with severe polyhydramnios include the host of defects associated with gastrointestinal obstruction. Esophageal atresia with or without tracheoesophageal fistula can present with early-onset severe polyhydramnios owing to the blockage of fetal swallowing. With certain malformations, AFV may still be normal because a tracheoesophageal fistula, for example, provides for the movement of fluid into the stomach, and thus, polyhydramnios may not develop. Other gastrointestinal obstructions such as duodenal atresia may result in polyhydramnios. Whenever a structural defect is seen in a fetus, consideration should be given to performing a karyotype owing to the dramatic increase in aneuploidy seen with one or more structural defects. Knowing the karyotype of the fetus with a defect may allow for further treatment options, or possible pregnancy termination. The fetus with polyhydramnios and trisomy 18 would be a candidate for pregnancy termination at any point in the pregnancy owing to the lethal nature of trisomy 18. Another common cause of acute, severe, polyhydramnios in the second trimester is the condition associated with the twin-to-twin transfusion syndrome (TTS). This may be found in single placenta, monozygotic twin pregnancies. With identical twins who share a single placenta, 90% of the fetuses will have vascular connections between the arteries and veins on the surface of the placenta. The most common connection is the artery-to-artery connection, followed by the vein-to-vein connection. The least common connection is the artery of one twin connecting to the vein of the other.

Third-Trimester Polyhydramnios:

When polyhydramnios occurs in the third trimester of pregnancy, it is usually mild and not associated with a structural defect. Despite the fact that a diagnosis can be determined for the majority of early-onset cases, for the vast majority of cases in the third trimester, a diagnosis cannot be found. Thus, these cases are given the diagnosis of idiopathic. Despite this, however, the other causes of polyhydramnios must be ruled out before the idiopathic label can be applied. In many cases, polyhydramnios may be transient. If polyhydramnios is persistent, the fetus should be examined closely for congenital malformations and aneuploidy, and monitored to prevent an intrauterine fetal death. In addition, the mother should be watched closely for other medical complications of pregnancy (9).

Management of Polyhydramnios:

Treatment options for patients with polyhydramnios are usually tailored to the underlying cause of the polyhydramnios. With mild idiopathic polyhydramnios, in which the work-up is negative, and follow-up ultrasound demonstrates persistent polyhydramnios, the only possible intervention might be antepartum testing with fetal kick counts, or non-stress tests. When poorly controlled diabetes mellitus is the cause of the polyhydramnios, proper glycemic control may be beneficial as a treatment option (10). With the current aggressive management of diabetes in pregnancy, it is rare to see severe polyhydramnios associated with diabetes. Usually, if the diabetes is not well controlled, then the mother will undergo antepartum testing to assess fetal well-being. Polyhydramnios associated with a fetal structural abnormality such as an obstruction to swallowing, usually requires invasive testing by amniocentesis to rule out aneuploidy (11). Often, the degree of polyhydramnios in these cases is severe and the resulting over-distention of the uterus causes preterm labor long before the due date.

Polyhydramnios associated with a fetal structural abnormality such as an obstruction to swallowing, usually requires invasive testing by amniocentesis to rule out aneuploidy. Often, the degree of polyhydramnios in these cases is severe and the resulting over-distention of the uterus causes preterm labor long before the due date. In these cases, one medical treatment option involves the administration of a prostaglandin inhibitor such as indomethacin, which works by decreasing fetal urine production (12). Prostaglandin inhibitors have been shown to decrease fetal urine output significantly. This effect occurs within 5 hours of starting the medication and decreases AFV within 24 hours. Although indomethacin has been shown to be relatively safe when given over a short period of time, such as 72 hours, prolonged usage may be associated with risks to the fetus. Prolonged use has been shown to cause premature closure, or narrowing, of the ductus venosus within the fetal heart and renal abnormalities in the newborn period. Complications related to indomethacin use worsen with advancing gestational age, and such treatment beyond 31 to 32 weeks of gestation should be avoided. Because of the adverse effects on the fetus associated with the long-term use of indomethacin, it probably has limited use in pregnancy for the treatment of severe polyhydramnios. For those pregnancies complicated by the TTS or for the fetus with obstructed swallowing, repetitive amnioreductions may be required to reduce the AFV until the fetus reaches viability. Severe cases of TTS, if left untreated, can have a PMR approaching 100%. Repetitive amnioreductions, in which an amniocentesis is performed and AF is withdrawn until the AFI is normal, can reduce the PMR from 100% to about 50%. Further options for the treatment of the TTS include the ablation of the connecting blood vessels by laser photocoagulation via fetoscopy. A recent large prospective trial found that the laser ablation of the connecting blood vessels resulted in better outcomes for the twin pregnancy as compared with amnioreduction alone (13). A major problem with laser ablation is that only certain centers perform the procedure, and most insurance companies will not pay for the procedure. This is not the case with amnioreductions, which can be performed anywhere and, therefore, are usually covered by insurance. Although laser ablation treatment may "cure" the cause of the TTS, amnioreduction only treats the symptoms (14). As a result, the amnioreduction method of treatment may require repeated procedures every 1 to 2 weeks for the remainder of the pregnancy.

Summary:

Amniotic fluid is seldom considered important until polyhydramnios or oligohydramnios occurs, either of which may significantly impact perinatal survival. Amniotic fluid is dynamic, with large volume flows into and out of the amniotic compartment each day. Clinical estimates of actual amniotic fluid volume through ultrasound measurements of the AFI or LVP are not very accurate at predicting true volume. Oligohydramnios, when associated with IUGR or prolonged gestations, is associated with significant increases in perinatal morbidity and mortality. Preterm or term isolated oligohydramnios, with an otherwise normal fetus, is not associated with an increase in perinatal morbidity or mortality. Early-onset or severe polyhydramnios is associated with a significant increase in aneuploidy, congenital malformations, preterm delivery, and perinatal mortality. The cause of mild polyhydramnios, especially in the latter part of the third trimester, is usually idiopathic, or related to diabetes mellitus, and has little positive or negative impact on perinatal survival. Amniotic fluid volume as estimated by the amniotic fluid index, can be increased or decreased by the amount of water ingested orally. Indomethacin, which decreases fetal renal and possibly pulmonary fluid production, can decrease AFV over time when taken orally. Absorption of amniotic fluid directly from the amniotic compartment into the blood vessels on the fetal surface of the placenta can explain the large differences between fetal swallowing and urine production.

References:

  1. Magann EF, Doherty DA, Field K, et al. Biophysical profile with amniotic fluid volume assessments. Obstet Gynecol 2004;104:5-12
  2. Magann EF, Doherty DA, Chauhan SP, et al. Dye-determined amniotic fluid volume and intrapartum/neonatal outcome. J Perinatol 2004;24:423-427
  3. Magann EF, Doherty DA, Chauhan SP, et al. How well do the amniotic fluid index and single deepest pocket indices (below the 3rd and 5th and above the 95th and 97th percentiles) predict oligohydramnios and hydramnios? Am J Obstet Gynecol 2004;190:164-167
  4. Magann EF, Doherty DA, Chauhan SP, et al. Is there a relationship to dye determined or ultrasound estimated amniotic fluid volume adjusted percentiles and fetal weight adjusted percentiles? Am J Obstet Gynecol 2004;190:1610-1615
  5. Faber JJ, Anderson DF. Absorption of amniotic fluid by amniochorion in sheep. Am J Physiol 2002;282:H850
  6. Casey BM, McIntire DD, Bloom SL, et al. Pregnancy outcomes after antepartum diagnosis of oligohydramnios at or beyond 34 weeks' gestation. Am J Obstet Gynecol 2000;182:909-911
  7. Rainford M, Adair R, Scialli AR, et al. Amniotic fluid index in the uncomplicated term pregnancy: Prediction of outcome. J Repro Med 2001;46:589-594
  8. Gilbert WM. Amniotic fluid disorders. In Obstetrics: Normal and Problem Pregnancies; 5th edition. Eds: Gabbe SG, Niebyl JR, Simpson JL. Publisher: Churchill Livingstone Elsevier; 2007
  9. Bartha JL, Martinez-Del-Fresno P, Comino-Delgado R. Early diagnosis of gestational diabetes mellitus and prevention of diabetes-related complications. Eur J Obstet Gynecol Reprod Biol 2003;109:41-49.
  10. Thomas A, Kaur S, Somville T. Abnormal glucose screening test followed by normal glucose tolerance test and pregnancy outcome. Saudi Med J 2002;23:814-816
  11. Pauer HU, Viereck V, Krauss V, et al. Incidence of fetal malformations in pregnancies complicated by oligo- and polyhydramnios. Arch Gynecol Obstet 2003;268: 52-59
  12. Pierce J, Gaudier FL, Sanchez-Ramos L. Intrapartum amnioinfusion for meconium-stained fluid: Meta-analysis of prospective trials. Obstet Gynecol 2000;95:1051-1061
  13. Fraser WD, Hofmeyr J, Lede R, et al. Amnioinfusion for the prevention of the meconium aspiration syndrome. N Engl J Med 2005;353:909-912
  14. ACOG Practice Bulletin. Ultrasonography in pregnancy. Number 101, February 2009

Published: 10 August 2009

Women's Health & Education Center
Hospital Campus Medical Building
300 Stafford Street #265
Springfield, MA 01104
United States of America
Tel: 413-733-1177
www.womenshealthsection.com