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Polyhydramnios

Polyhydramnios due to unilateral UPJ obstruction (arrow)
Jejunal Atresia with markedly dilated loops of bowel and polyhydramnios

Findings:

In both cases polyhydramnios is seen. In the first case (on the left) unilateral UPJ obstruction is seen. In the case on the right, the etiology is bowel obstruction from jejunal atresisa.

Discussion:

Polyhydramnios is an excess accumulation of amniotic fluid at some time during pregnancy. It has a reported incidence which varies from 0.2% to 3.3%. The incidence obviously depends upon how this abnormality is defined. (This will be described below) The author prefers the use of the term polyhydramnios rather than "hydramnios" which may often be used to describe the same condition. Pathologically and clinically it is defined as an excess of amniotic fluid which is greater in amount than 1500 to 2000 cc. Although reasonably accurate assessment of excess amniotic fluid can be made with dye-dilution studies, for many years the diagnosis was made and confirmed at the time of delivery; a less than ideal way to accurately estimate volume. In the past ten years ultrasound has played a pivotal role in correctly making this diagnosis in the patient who presents "large for dates".

The methodology used in arriving at this diagnosis varies tremendously and is controversial. Most clinicians agree that ultrasound is the appropriate tool to estimate amniotic fluid volume. Many sonologists utilize a subjective estimate of amniotic fluid [defining polyhydramnios when a fetus in the mid to late 2nd or 3rd trimester appears to float in the amniotic fluid, displaced away from the anterior uterine wall or placenta], others measure the single deepest amniotic fluid volume pocket [defining polyhydramnios when the deepest pocket is greater than 8 cm] and still others use the amniotic fluid index ( a summation of the deepest pocket in 4, cord and extremity-free, quadrants on the maternal abdomen) [here, polyhydramnios exists when the amniotic fluid index is greater than 24 cm]. It is unlikely that any cases of true polyhydramnios will escape detection when the amniotic fluid volume is analyzed subjectively by even a moderately experienced examiner. The greater problem is that too many false positive cases are likely to occur when only subjective criterion are employed. Many cases of normal pregnancies in the early 2nd trimester may appear to have too much amniotic fluid. Care must be taken to avoid diagnosing polyhydramnios under this circumstance. Likewise, many cases of mild polyhydramnios will be in pregnancies with normal fetuses and normal pregnancy outcomes. It is for this reason that that the author prefers to use the subjective assessment as a first line of screeening and apply objective measurements such as the amniotic fluid index in those cases where the amniotic fluid seems excessive.

Technique of Measuring the Amniotic Fluid Index (AFI) From: Dildy FA, Lira N, Moise Jr KJ, Riddle GD, Deter RD. Amniotic fluid volume assessment:comparison of ultrasonographic estimtes versus direct measurements with a dye-dilution technique in human pregnancy.Am J Obstet Gynecol 167:986-94, 1992
Measurement of the Largest Vertical Pocket > 8cm.

An interesting study by Carlson et al. attempted to compare the utility of subjective estimation of the severity of polyhydramnios (mild, moderate and severe) vs the amniotic fluid index value of > 24 cm and assessment of the single deepest amniotic fluid pocket. Using the description of severe polyhydramnios they found only 11 of 24 anomalies versus 22 of 24 anomalies using an amniotic fluid index of >24 cm. In their study, using an amniotic fluid index of >24 cm not only predicted 49 of 50 cases of true polyhydramnios confirmed at delivery, but this measurement also included 92% of all anomalies and 100% of all trisomies and fetal and neonatal deaths. They had 7 patients in whom the amniotic fluid index was < 24 cm but in which one pocket of fluid was > 8 cm. None of these fetuses or neonates had fetal anomalies, aneuploidy, perinatal death, NICU admission or a diagnosis of polyhydramnios at delivery.

The etiology of polyhydramnios can be due to a variety of maternal and neonatal disorders. Perhaps the most notable maternal disorder associated with polyhydramnios is diabetes mellitus. Most series quote diabetes as a common cause of increased amniotic fluid. These cases, under further examination, are almost always in patients with poor diabetic control. Erythroblastosis fetalis and assoicated hydrops may result in polyhydramnios. For that matter, any fetal condition resulting in hydrops will often manifest polyhydramnios. Multiple births, usually monochorionic may also be associated with polyhydramnios.

Fetal stuctural and chromosomal abnormalities are responsible for a significant number of cases in which polyhydramnios is seen. Central nervous system abnormalities were once the most common cause for polyhydramnios due to fetal structural abnormalities. This is no longer true and perhaps in part due to recognition of severe CNS abnormalities in the second trimester with termination prior to the development of polyhydramnios. Gastrointestinal tract abnormalites are now perhaps the most common structural cause with atresia or obstruction ie duodenal atresia or esophageal atresia the likely explanation. Other fetal structural defects include cardiovascular, urinary tract abnormalites and skeletal abnormalities. Two urinary tract abnormalities; congenital mesoblastic nephroma and unilateral ureteropelvic junction (UPJ) obstruction may be associated with polyhydramnios. Although somewhat paradoxical, the polyhydramnios associated with UPJ obstruction may be due to impairment of the concentrating ability of the kidney resulting in high urine output. The association of lethal skeletal abnormalities with polyhydramnios is also interesting. While no good explanation for this association has come forth there is no question that this association exists.

Two Cases of Twin-twin Transfusion Syndrome

 

 

In this case, at first glance it appears that both fetuses reside within the same polyhydramniotic sac. There should be no reason, however for the slightly smaller more anterior twin to be fixed in its position unless it was within its own sac. The donor twin within the polyhydramniotic sac has evidence of fetal ascites.
In this case the severely growth retarded twin (arrow) in an oliogohydramniotic sac is adherent to the anterior uterine wall.

 

As was mentioned above, twin pregnancy particularly monochorionic, can be associated with marked polyhydramnios. The twin-twin transfusion syndrome is clearly the most common explanation for polyhydramnios among twins. The marked polyhydramnios in one sac may often lead to the mistaken diagnosis of monoamniotic twins. Therapeutic serial amniocenteses have often proven quite beneficial in alleviating the excessive fluid and often correcting the abnormality.

When no structural abnormalities are detected, polyhydramnios is said to be idiopathic. Prior to reaching this conclusion two other entities should be considered: growth disturbances and chromosomal abnormalities. Studies comparing patients with normal amniotic fluid volume and those with polyhydramnios have found a significantly higher incidence of fetuses with birth weights greater than 4000 g or > 90th percentile weight for gestational age in the polyhydramniotic group. Polyhydramnios is clearly associated with chromosomal abnormalities often trisomies 21, 18 and 13. Studies have reported incidences of 1.7% to 3.2% of fetuses with polyhydramnios with chromosomal abnormalities. While structural abnormalities are often seen in patients with polyhydramnios and chromosomal abnormalities, they may be absent even after careful examination. Some centers recommend amniocentesis in the group of patients with severe polyhydramnios and no metabolic or sonographic explanation.

Aside from association with fetal and maternal abnormalities, polyhydramnios itself may result in perinatal morbidity. The reported prevalence of preterm births in patients with polyhydramnios is between 11.1% and 29.4%. The prevalence of prematurity was highest among those with malformations (39%) followed by those with diabetes mellitus (22.2%) in a study by Many et al. In addition, abdominal pain and premature uterine contractions may lead to premature rupture of the membranes and preterm delivery. Rupture of the membranes with sudden decompression of the uterus may lead to abruptio placentae.

In patients with severe polyhydramnios and difficulties with pain and breathing therapeutic amniocenteses are often performed. The problem is that fluid often tends to reaccumulate quite rapidly. In the past decade treatment of excessive amniotic fluid has been accomplished with the use of maternally ingested prostaglandin synthetase inhibitors such as indomethacin. Indomethacin freely passes the placental barrier and can be detected in fetal blood within 15 minutes after administration. Its main mechanism of action is in the reduction of fetal urine output. Two potential ill-effects of this treatment may be over-treatment with resultant oligohydramnios and premature closure of the ductus arteriosus. These may often reverse with cessation of treatment.

References:

Barnhard Y, Bar-Hava I, Divon MY. Is polyhydramnios in an ultrasonographically normal fetus an indication for genetic evaluation? Am J Obstet Gynecol 173:1523-1527, 1995

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. [Letter}. Am J Obstet Gynecol 612:1344-5, 1990

Landy HL, Isada NB, Larsen JW Jr.. Genetic implications of idiopathic polyhydramnios. Am J Obstet Gynecol 157:114-7,1987

Many A, Hill LM, Lazebnik N. The association between polyhydamnios and preterm delivery. Obstet Gynecol 86:389-391, 1995

Damato N, Filly RA, Goldstein RB, Callen PW et al. Frequency of fetal anomalies in sonographically detected polyhydramnios. J Ultrasound Med 12:11-15, 1993

Stoll CG, Alembik Y, Dott B. Study of 156 cases of polyhydramnios and congenital malformations in a series of 118,265 consecutive births. Am J Obstet Gynecol 165:586-590, 1991

Benacerraf BR. Sonographic evaluation of a pregnancy with a size greater than its dates. Syllabus: A special course in ultrasound. 82nd Scientific Assembly and Annual Meeting of the Radiological Society of North America. Dec., 1996, 273-279

Benson CB, Coughlin BF, Doubilet PM. Amniotic fluid volume in large-for-gestational-age fetuses of nondiabetic mothers. J Ultrasound Med 10:149-151, 1991

Sohaey R, Nyberg DA, Sickler GK, Williams MA. Idiopathic polyhydramnios: association with fetal macrosomia. Radiology 190:393-396, 1994

Smith CV, Plambeck RD, Rayburn WF, Albaugh KJ. Relation of mild idiopathic polyhydramnios to perinatal outcome. Obstet Gynecol 79:387-389, 1992

Brady K, Polzin WJ, Kopelman JN, Read JA. Risk of chromosomal abnormalities in patients with idiopathic polyhydramnios. Obstet Gynecol 79:234-238, 1992

Carlson D, Platt LD, Medearis AL, Horenstein J. Quantifiable polyhydramnios: diagnosis and management. Obstet Gynecol 75:989, 1990

Mamopoulos M, Assimakipoulos E, Reece EA, Andreou A, Zheng X-Z, Mantalenakis S. Maternal indomethacin therapy in the treatment of polyhydramnios. Am J Obstet Gynecol 162:1225-1229, 1990

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Peter W. Callen, M.D.
Professor of Radiology, Obstetrics, Gynecology and Reproductive Science
University of California Medical Center, San Francisco, California

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