When there is too much amniotic fluid, this is called polyhydramnios. According to the American Pregnancy Association, it occurs in 1 percent of all pregnancies. Too much fluid can also be produced during multiple pregnancies, when the mother is carrying more than one fetus.
Maternal symptoms can include abdominal pain and difficulty breathing due to the enlargement of the uterus. Testing for maternal diabetes may be recommended, and frequent ultrasounds will be obtained to monitor the levels of amniotic fluid in the uterus.
In more severe cases, fluid may need to be reduced with either amniocentesis or a medication called indomethacin. This reduces the amount of urine the baby produces. Sometimes, fluid leaks before the waters break. According to the American Pregnancy Association, only 1 in 10 women will experience a dramatic flow of fluid as the waters break. For most, it will start as a trickle, or leak. Sometimes, what looks like fluid leaking is actually urine, because the uterus is pressing on the bladder.
If the fluid has no color and no smell, it will be amniotic fluid, and you should contact a healthcare provider as labor will normally begin soon. If the fluid is green, brownish-green, or foul-smelling, this may indicate the presence of meconium or an infection. Medical advice should be sought. If leaking or rupture happens before 37 weeks , this is known as premature rupture of membranes PROM.
Depending on how early this happens, it can have serious consequences for the mother and the unborn child. It affects around 2 in pregnancies.
This is known as premature rupture preterm, but it is also possible to have premature rupture at term. That is when 37 weeks or more of pregnancy are complete, but labor does not start spontaneously within 6 hours of the membrane rupturing.
It is important to seek medical help as soon as possible and to avoid having sex or introducing anything into the vagina, as this could lead to an infection. Anyone who is concerned about leaking or levels of amniotic fluid during pregnancy should discuss this with their healthcare provider.
Amniocentesis is a test that detects chromosomal abnormalities in the fetus. A sample of amniotic fluid is taken from the amniotic sac. The test may…. A developing child survives for around 9 months without coming into contact with the outside world.
How do babies breathe in the womb? This MNT…. Esophageal atresia, duodenal or jejunal atresia, annular pancreas, midgut volvulus, diaphragmatic hernia, omphalocele, gastroschisis. Down syndrome, trisomy 13 and 18, Pena-Shokeir syndrome, multiple congenital anomalies, myotonia dystrophica. Obstet Gynecol Surv , 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.
Pedersen, however, found no association between amniotic fluid glucose concentration and volume. 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. The extracellular fluid could possibly be transferred across the placenta and membranes into the amniotic cavity. Alternatively, the interstitial fluid in the placenta could perhaps interfere with water transfer between the fetal and maternal compartments, resulting in fetal volume overload, polyuria, and ultimately polyhydramnios.
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. 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, either through volume overload, increased renal blood flow, and polyuria, 27 or through a hydropic placenta.
Placental chorioangiomas and sacrococcygeal teratomas are other abnormalities in which large arteriovenous shunts may lead to high-output cardiac failure and ultimately 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.
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. The maternal signs and symptoms of polyhydramnios are usually caused by the overdistended uterus and its compressing effect on intrathoracic and intra-abdominal organs. Elevation of the diaphragm can result in dyspnea and occasionally respiratory distress. The diagnosis of polyhydramnios had formerly been a clinical one, retrospectively based on the presence of more than 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.
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 cm was arbitrarily defined as excessive amniotic fluid volume. 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.
Malpresentations are also encountered more frequently, as a result of both the abundance of amniotic fluid in which the fetus may maneuver and the earlier gestational age at the time of delivery. 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. These pregnancies progressed uneventfully after resolution of the polyhydramnios, with no adverse sequelae observed.
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. 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.
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.
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 to ml. Periodic evaluation of maternal electrolytes and serum protein may need to be assessed if frequent amniocenteses are required 18 although no studies have demonstrated the efficacy of such surveillance.
Oligohydramnios is defined as a decrease in the volume of amniotic fluid, relative to the gestational age. The incidence in an unselected population without membrane rupture ranges from 0. Acute onset is most commonly the result of membrane rupture, whereas chronic oligohydramnios may reflect a structural abnormality of the fetal urinary tract or a pathophysiologic response to chronic or intermittent fetal hypoxemia.
Risk factors for oligohydramnios are shown in Table 2. Fetal growth restriction Postterm pregnancy Repetitive cord compression. Fetal anomalies Renal agenesis Renal anomalies e. Non-steroidal anti-inflammatory medications Twin-to-twin transfusion Premature rupture of membranes. Spontaneous premature rupture of membranes PROM is the most common cause of acute oligohydramnios. Chronic oligohydramnios may be the product of major fetal anomalies or prenatal hypoxia.
These anomalies are associated with decreased amniotic fluid formation. Chronic or intermittent fetal hypoxia may also result in reduced amniotic fluid volume. Chronic low-grade fetal hypoxia may be a consequence of long-standing uteroplacental insufficiency or maternal hypoxia, whereas prenatal cord compression may lead to either prolonged or repetitive episodes of acute hypoxia of varying intensity and duration.
Corroborative evidence for this pathophysiologic process leading to oligohydramnios exists in both animal and human models. A redistribution of fetal cardiac output has been noted in pregnant ewes made hypoxic. Under ordinary circumstances, this decreased renal perfusion would ultimately result in reduction of fetal urine production and oligohydramnios.
Support for redistribution of cardiac output away from the fetal kidneys as the operative mechanism is also provided by several human observations. Wladimiroff and Campbell measured hourly human fetal urine production rate HFUPR by measuring bladder volume on two occasions 1 hour apart.
A normal curve of HFUPR versus gestational age in 92 normal pregnancies from 30 to 41 weeks was established. Additionally, all nine subjects that delivered infants whose weights were less than the fifth percentile had HFUPRs below the normal range. However attractive the theory of redistribution of flow is, there may be additional operative mechanisms.
In an animal model subjected to hypoxemia, glomerular filtration was maintained despite decreased renal blood flow. A final, hypothesized cause of unexplained oligohydramnios is amniotic rupture with an intact chorion. Corroborative evidence for this process exists in amniotic band syndrome, in which it is theorized that the fetus is partially extruded into the extra-amniotic space.
To date, no experimental confirmation of this pathway for oligohydramnios has been provided. Regardless of the precise mechanism, the presence of oligohydramnios in the absence of structural anomalies or membrane rupture suggests an altered normal physiological process.
Its presence also increases the risk for prenatal cord compression. Unfortunately, it is not known what prognostic significance one should attribute to the observation, particularly in a pre-term fetus.
Absence of amniotic fluid at the time of artificial rupture of the membranes is also strongly suggestive of oligohydramnios and, in the absence of a sonographic diagnosis, may be the first indication of its presence.
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. Data presented in these studies are listed in Table 3 and summarized below. Vertical 2 cm. 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.
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. Similarly, Goldstein and Filly also demonstrated good correlation between subjective and objective evaluations of amniotic fluid volume. In , the concept of the "1 cm rule" was introduced in a selected high-risk patient population.
Volume was arbitrarily classified as decreased if the largest fluid pocket measured less than 1 cm in broadest dimension. However, subsequent studies were less optimistic, showing both a lower prevalence and sensitivity of' oligohydramnios as a predictor of IUGR.
The 1 cm rule was re-evaluated in 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. While in the womb, the baby floats in the amniotic fluid.
The amount of amniotic fluid is greatest at about 34 weeks gestation into the pregnancy, when it averages mL. About mL of amniotic fluid surrounds the baby at full term 40 weeks gestation.
The amniotic fluid constantly moves circulates as the baby swallows and "inhales" the fluid, and then releases it. Too much amniotic fluid is called polyhydramnios. This condition can occur with multiple pregnancies twins or triplets , congenital anomalies problems that exist when the baby is born , or gestational diabetes. Too little amniotic fluid is known as oligohydramnios.
This condition may occur with late pregnancies, ruptured membranes, placental dysfunction , or fetal abnormalities.
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