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Oligohydramnios - Assessment of Amniotic Fluid Volume

Severe oligohydramnios in a fetus with renal agenesis at 14 weeks gestation
Oligohydroamnios due to premature preterm rupture of the membranes

Findings:

A sonogram at 14 weeks reveals severe oligohydramnios due to renal agenesis. Transverse scan in the late second trimester reveals severe oligohydramnios. This was a case of premature preterm rupture of the membranes.

Discussion:

Amniotic fluid serves a number of important functions in the normal development of the fetus: it protects the fetus against physical trauma, it allows growth of the fetus free from restriction or distortion by adjacent structures, it provides for a thermally stable environment and allows fetal lung development to proceed normally. A number of anatomic sites are important in the regulation of amniotic fluid. The volume of amniotic fluid at any time represents a balance between those structures producing or allowing passage of fluid into the amniotic cavity: chorion frondosum and membranes, skin, urinary tract and respiratory tract; and those involved in the removal of amniotic fluid: gastrointestinal tract, respiratory tract and the amniotic-chorionic interface at the uterine wall. In early pregnancy, the chorio-amnion acts almost as a molecular sieve allowing for the free passage of water and solutes, electrolytes, creatinine and urea. Little embryonic contribution to the amniotic fluid takes place at this time as evidenced by the presence of "chorio-amniotic fluid" both prior to or in the absence of a living embryo. In the mid to late first trimester, diffusion through the fetal skin occurs and continues until fetal keratinization at 24-26 weeks gestation.

From:Wallenburg HCS. The amniotic fluid: I Water and electrolyte homeostasis. J Perinat. Med 5:193-205, 1977

Weisman et al calculated the volume of amniotic fluid in the first trimester. They found that the quantity of amniotic fluid increased from approximately 1 ml at 7 weeks to 25 ml at 10 weeks and 60 ml at 12 weeks. An interesting point made by these authors is that if an early amniocentesis is performed, removing 1 ml per gestational week, at 9 weeks 72% of the amniotic fluid volume will be removed while at 17-18 weeks less than 10% of the total volume is removed.

In the second and third trimesters fetal urination plays an important role in the production of amniotic fluid. The excretion of hypotonic urine by the fetal kidneys has been reported as early as 12 weeks. At 18 weeks gestation, fetal urine production has been estimated to be between 7 and 17 ml day and increases steadily throughout pregnancy. At term it is approximately 800 ml/ day, which approximates the total amniotic fluid volume at this stage. The presence of normal amniotic fluid volume in the 2nd and 3rd trimesters implies that at least one functioning kidney must be present. A reduction in fetal renal arterial blood flow or an increase in renal tubular reabsorption from anti-diuretic hormone (both a result of fetal hypoxemia) will result in a diminution of amniotic fluid volume. In addition to the fetal kidneys, the lungs also contribute to the total amniotic fluid volume. While the exact amount of fluid secreted by the respiratory tract is not known, it is presumed to be in the range of 300-400 ml per day.

The removal of amniotic fluid throughout pregnancy is largely a result of fetal swallowing. Approximately half the daily urine produced is removed by fetal swallowing. Fetal swallowing has been estimated to be as low as 200 ml per day to as high as 1500 ml per day. While at approximately 20 weeks the percentage of amniotic fluid volume swallowed is small, approximately 5%, at term the fetus may swallow as much as 50% of the total amniotic fluid volume. In a model of amniotic fluid volume dynamics by Mann et al they found that relatively low rates of swallowing in proportion to urine and lung fluid production account for the gradual increase in amniotic fluid volume in the first and second trimesters. They also found that increased swallowed amniotic fluid volume contributes to the reduction in amniotic fluid volume near term and possibly to the development of oligohydramnios in post-term patients. It is unlikely that fetal urination and swallowing can explain the total variation in amniotic fluid volume. Trans- and intramembranous flow between the amniotic space and mother and fetus are also likely to play a role in the fluctuations of AFV. Kilpatrick et al and others have noted often dramatic changes in the AFV after maternal hydration.

A number of investigators have calculated the volume of amniotic fluid throughout gestation. Brace et al found that the volume of amniotic fluid progressively rises from 8 weeks gestation reaching its statistical maximum (variance analysis) at 22 weeks gestation and remaining at this level (630-817 ml) through 39 weeks. These authors calculated the mean changes in AFV calculated on a weekly basis (based upon a polynomial regression equation). At 8 weeks the volume was increasing at 10 ml / week, at 13 weeks the AFV increased to 25 ml / week and reached a maximum of 60 ml / week at 21 weeks gestation. The weekly volume increment then decreased and reached zero at 33 weeks gestation at which point the mean volume reached its peak. After term the amniotic fluid volume declines at a rate of approximately 8% per week. During the first half of pregnancy amniotic fluid volume is closely correlated with fetal weight. The ratio of amniotic fluid to fetal volume increases until about 30 weeks gestation and then appears to decline. The late 3rd gestation fetus urinates and drinks a volume of amniotic fluid equal to 20-30% of its body weight per day, whereas an adult, for comparison, urinates and drinks approximately 2-3% of its body weight per day.

Ultrasound and Amniotic Fluid Estimation

The recognition of the importance of amniotic fluid in fetal development made it imperative to develop methods of assessing the amniotic fluid volume throughout pregnancy. While ultrasound has many advantages, not the least of which is it's noninvasive nature it also has inherent problems. The biggest difficulty relates to the tomographic nature of this modality. Sonographic scans across the gravid uterus are two dimensional "slices" of the intrauterine contents. A decision about the amount of amniotic fluid volume requires that the examiner sum the individual pockets of amniotic fluid at the time of scanning or interpretation of the recorded films. While most experienced sonologists are capable of making a subjective decision about the amount of fluid, the lack of objectivity is troublesome to some.

Assessment of Oligohydramnios

Oligohydramnios may be due to a variety of conditions: renal abnormalities: including renal agenesis, bilateral obstruction, bilateral renal dysplasia; intrauterine growth retardation, preterm premature rupture of the membranes, and post-term pregnancy. Regardless of the cause most investigators have noted increased perinatal morbidity and occasionally fetal or neonatal death in the presence of oligohydramnios.

Sonographic assessment of oligohydramnios has been largely based in the past on the subjective judgment of the sonologist. While experienced sonologists and sonographers are quite capable of making such judgments, it is impossible to disseminate "criteria" for use by less experienced examiners.. Furthermore, there is no mechanism to be certain that even the most experienced examiners employ the same visual cues when attempting to diagnose too little fluid. An excellent step was made in the visual evaluation by Manning et al when these authors described a simple measurement to judge oligohydramnios. This measurement has come to be known as the "one centimeter rule". Though devised to assess pregnancies where growth retardation was suspected, it was also utilized in the evaluation of post-term patients. The "one centimeter rule" originally described in the early 1980's was modified a number of times by others, to increase as well as decrease the maximum allowable amniotic fluid pocket to define oligohydramnios: including measurements of 2 cm, 3 cm and 0.5 cm. Unfortunately, this "rule" and others have been subsequently proven too stringent a criterion to employ.

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 Amniotic Fluid Pocket as part of AFI determination

In 1987 Phelan et al and subsequently Rutherford et al and Moore et al developed a sonographic assessment of the amniotic fluid volume which has come to be known as the amniotic fluid index (AFI). This measurement is based upon the division of the gravid uterus into 4 quadrants with measurement of the deepest amniotic fluid pocket in each quadrant that is free of fetal parts or umbilical cord. These 4 measurements are added together and the sum referred to as the amniotic fluid index (AFI). While a number of investigators have designed tables relating gestational age to AFI, values greater than 5 cm and less than 18-20 cm are felt by most examiners to be normal.

Amniotic Fluid Index Values in Normal Pregnancy (Moore & Cayle)

AFI (mm) Percentile Values

Week

2.5th

5th

50th

95th

97.5th

Number

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

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 162:1168-73, 1990

In fact the "one centimeter rule" has now been replaced by the "5 cm rule". While most studies have found that the AFI more closely relates to the amniotic fluid volume based upon dye-dilution studies and in many cases is more accurate than measuring a single pocket it also has its deficiencies. Interobserver errors, particularly at AFI values < 10 have been reported to be as high as 10 - 20%. Likewise while positive predictive accuracies are quite high for the group with AFI ? 5 cm, the sensitivities for the detection of oligohydramnios are poor; between 18% and 40%. In one study comparing the AFI to dye-dilution methods Dildy et al found that the AFI overestimated the actual volume by as much as 88.7% at lower volumes and underestimated the actual volume by as much as 53.9% at higher volumes. In Moore and Cayle's original work patients with AFI < 5 cm represented the group below the 1st percentile, patients between 5.1 and 8.0 cm were representative of the group between the 1st and 5th percentiles. They suggested that oligohydramnios be defined as the group in which the AFI was below the 5th percentile. While this increases the sensitivity, one study by Baron et al correlating the likelihood of abnormal fetal heart rate tracing and need for cesarean section for fetal distress found no difference in the group in which the AFI was between 5.1 and 8.0 and the group in which the AFI was between 8.0 cm and 20 cm. Several groups have tried to refine the results of the AFI to gain additional information. In one study, Myles et al looked at the distribution of fluid between upper quadrants and the lower quadrants. In two groups with the same AFI, those with greater fluid in the upper quadrants had a greater incidence of meconium staining, 1 minute Apgar scores < 7, variable decelerations, late decelerations, cesarean delivery for fetal distress and arterial pH < 7.2 than did those where the fluid in the lower quadrants was greater. In another study, Sadovsky evaluated additional cord containing amniotic fluid pockets in women where the AFI was <5 cm. In the subgroup where the cord-containing pocket was greater than 5 cm, there was no evidence of an increase in poor outcome, normally seen in women with oligohydramnios. A recent report by Magann et al found that utilizing multiple assessments eg AFI + deepest pocket did not add to the accuracy. In their report the accuracy of ultrasound estimates of abnormal AFV were relatively low.

Accuracy of AFV Assessment - Multiple Evaluations (Magann et al):

Correct AFV Estimates

Subjective Assess.

Larg. Vert. Pocket

AFI
2-Diam. Pocket

Oligohydramnios

41%
12%
12%
53%

Normal

80%
92%
95%
85%

Polyhydramnios

48%
15%
18%
44%

Pred.Value of Nl. Ultrasound Result

69%
61%
63%
69%

Magann EF, Chauhan SP, Whitworth NS, Saltzman AK, Morrison JC. Dept of OB/GYN, University of Mississippi, Jackson MS. Society of Perinatal Obstetricians-Jan 1997, Anaheim, Am J Obstet Gynecol 176:S130:440

Pitfalls in AFV Estimation

Normally it is quite easy to reach a conclusion on the total amniotic fluid volume whether one uses subjective or objective methods of assessment. Three potential piftalls exist which one should be aware of: 1) An umbilical cord-filled amniotic fluid pocket should not be used in assessment of AFV. Color Doppler flow imaging will often assist one in identifying the umbilical cord. 2) Fat tends to scatter the ultrasound beam and as such may introduce artifactual echoes into the amniotic fluid. Obese patients may seem to have significantly reduced fluid due to these artifactual echoes. Utililizing a lower frequency transducer may often assist one in correctly assessing AFV in these patients. 3) In the 3rd trimester "free-floating particles" perhaps due to vernix may make the true amniotic space less conspicuous.

Pseudo-AF pocket filled with Umbilical Cord

Color Doppler flow imaging shows umbilical cord filling pocket

Echogenic fluid in term pregnancy. Umbilical Cord=arrows

 

Fat scattering the ultrasound beam, creating the appearance of oligohydramnios

Intrauterine Growth Retardation

The earliest sonographic evaluations of the potentially growth-retarded patient recognized the important role of amniotic fluid. The first use of sonographic evaluation of decreased amniotic fluid was in the diagnosis of the growth retarded fetus. Manning et al and others recognized the high incidence of oligohydramnios in these patients. Initially the finding of the single largest amniotic fluid pocket to be no greater than one-centimeter was found to be predictive of IUGR. Unfortunately, this criterion was too stringent and was not sensitive enough to allow it alone to detect these patients. Subsequently, other methods such as the amniotic fluid index have replaced the largest pocket evaluation. In theory, the hypoxemia resulting from poor placental perfusion results in a redistribution of cardiac output so that the brain is protected with increased blood flow relative to the abdomen and kidneys. The decreased renal perfusion and increased anti-diuretic hormone release from hypoxemia result in decreased urine output and oligohydramnios. In addition, decreased fluid in the amniotic space can result in pressure against the umbilical cord and further complicate the already decreased perfusion to the fetus. Assessment of the amniotic fluid volume is now an important part of antenatal evaluation along with the non-stress test in the fetus with suspected growth retardation.

Post-Term Patients

Post-term patients have increased morbidity with an increased risk of meconium aspiration, fetal postmaturity syndrome and fetal death. Amniotic fluid begins to decline near term and may do so precipitously in the post-term patient. While the relationship between decreased amniotic fluid and perinatal morbidity is not known for certain, several theories have been proposed to explain this relationship. Perhaps the most popular theory is that placental insufficiency in these patients results in a redistribution of cardiac blood flow such that renal perfusion is decreased resulting in oligohydramnios, while cerebral blood flow is increased. Recent work by Bar-Hava et al have shown that this mechanism is unlikely to play a major role in the post-term patient and that increased reabsorption in the fetal kidneys may be more important. An additional explanation is the decreased weight which may be seen in the post-term patient. There appears to be a relationship between fetal weight and amniotic fluid production.

Pulmonary Hypoplasia

Patients with prolonged oligohydramnios from any cause: renal, premature preterm rupture of the membranes, etc have an increased risk of developing pulmonary hypoplasia, which is invariably fatal. It has long been known that amniotic fluid is an important factor in the normal development of the fetal lungs. What has been less clear is how oligohydramnios interferes with this normal developmental process. There are normally four stages of fetal lung development: 1) embryonic, from conception to the 5th week 2) pseudoglandular, from the 5th to the 17th week, 3) canalicular, from the 16th week to the 24th week, and 4) terminal sac or alveolar period, from the 24th week to term and beyond. By the 16th week of gestation, all of the branches of the tracheobronchial tree up to the terminal bronchioles are established. Oligohydramnios resulting in pulmonary hypoplasia characterized by inadequate development of pulmonary acini and restricted vascularization normally occurs during the canalicular stage of development. Several theories have been postulated in the past to explain pulmonary hypoplasia developing in patients with severe oligohydramnios; these include: 1) abnormal fetal breathing, 2) increased pressure on the fetal thorax and 3) abnormal pulmonary fluid egress. Abnormalities of fetal breathing are unlikely to be the cause as normal fetal breathing movements occur in animals as well as in humans with oligohydramnios-related pulmonary hypoplasia. Compression of the fetal thorax is also unlikely to be the cause as amniotic sac pressure in patients with oligohydramnios is low. It has been postulated that fetal lung fluid acts as an internal stent for the developing surrounding lung. Normally the upper airways produce resistance to the egress of fluid out of the trachea. In the presence of oligohydramnios and low amniotic pressure, it is theorized that the pressure gradient results in the loss of this lung fluid. In addition, interesting work by Harding et al in sheep has shown that the rise in pulmonary airway pressure relative to amniotic sac pressure may also be a result of increased spinal flexion and resulting increased abdominal and thoracic pressure in the fetus with oligohydramnios. In a recent study by Kilbride et al. patients were evaluated who had premature rupture of the membranes < 29 weeks gestation. While most patients did not change their amniotic fluid status over time, as many as 20% of patients did. While the prognosis was dismal and likelihood of pulmonary hypoplasia in the group where the amniotic fluid pockets were < 1 cm was great, there was no association between patients with moderate oligohydramnios (1-2 cm pockets) and pulmonary hypoplasia. Thus it would be inappropriate to group all patients with an AFI < 5 cm together in an attempt to prognosticate the development of pulmonary hypoplasia.

Premature Rupture of Membranes

Premature rupture of the membranes (PROM) is rupture of the amniotic sac that occurs prior to the onset of uterine contractions. This is reported to occur in approximately 10% of pregnancies at term and between 0.7% and 2.0% of pregnancies before 37 weeks. While PROM occurring at term is usually managed by induction of labor, preterm PROM is often treated conservatively. While most patients at term will begin labor soon after membrane rupture, the earlier in gestation that membrane rupture occurs the more likely the latency period will be long. Patients who rupture early in pregnancy have the added risk of pulmonary hypoplasia. Pulmonary hypoplasia has been reported in patients with PROM particularly when the rupture occurs prior to 26 weeks and when the duration of the rupture is at least two weeks and often > 5 weeks. As was mentioned above, a critical amount of amniotic fluid is necessary for normal lung development to occur. Lack of fluid, as might occur with PROM, results in a lack of the normal internal stenting force in the developing fetal lungs. The likelihood of pulmonary hypoplasia developing is dependent upon as much on the time of membrane rupture as the amount of residual fluid and the length of time of oligohydramnios.

Patients with preterm PROM have an increased risk of chorioamnionitis (between 25% and 46%), fetal morbidity and death (between 37% and 78%). The likelihood of these complications is dependent upon the timing of membrane rupture and the amount of residual amniotic fluid and length of time of persistent oligohydramnios. One series by Hadi et al reported an overall survival rate of 55%. When delivery occurred before 25 weeks of gestation 6.7% survived. For the cases delivered between 26 and 34 weeks of gestation, the survival rate was 89.4%. While the prognosis is often poor, the earlier the time of membrane rupture, it is not universally grave for all patients. Several series have reported "resealing" of the leak with reaccumulation of fluid and normal outcomes. While these are uncommon events, they must be considered at the time of counseling.

Aside from the issues of pulmonary hypoplasia, patients with PROM have a higher incidence of cesarean section for fetal distress than do patients with oligohydramnios from other causes. in the studies of Sarno et al, the cesarean section rate for fetal distress was 19% for PROM compared to less than 1% for other causes of oligohydramnios.

Even when the evidence is overwhelming that PROM is the likely explanation for decreased fluid, the fetal urinary bladder should be idenitified to exclude renal agenesis as the primary etiology.

Intrapartum Oligohydramnios in High-Risk Patients

In the past 5 years there have been a number of studies in which oligohydramnios (defined by an AFI less than or equal to 5 cm) in laboring patients was associated with a poor peripartum outcome. As such, there are centers in which the results of the AFI are used to triage patients. Recently however, there have been reports disputing the utility of a low AFI . In a recent paper by Chauhan et al. the authors found the sensitivity and positive predictive values of an amniotic fluid index less than the 5th percentile for gestational age to predict a pH < 7.00 were 0.8% and 22%, respectively and for an amniotic fluid index less than or equal to 5.0 cm, 0.5% and 11% respectively. In this study, "receiver-operator characteristic curves indicated that an AFI between 0 and 20 cannot predict accurately which patients will have cesarean sections for distress or be delivered of a newborn with a low Apgar score at 5 minutes or a pH < 7.10". The patients in this study were high-risk patients with either medical or obstetric complications.

Other Conditions Leading to Oligohydramnios

There have been reports of oligohydramnios complicating chorionic villus sampling procedures. In a recent series by Cheng et al 2.7% of chormosomally normal pregnancies developed oligohydramnios versus 0% in the control amniocentesis group. They theorized that chorionic villus sampling may cause a placental or endometrial injury that may result in perigestational hemorrhage. This may result in altered fetoplacental perfusion. In their series none of the patients developing oligohydramnios survived.

Prostaglandin inhibitors such as indomethacin can cause a dramatic reduction in the volume of amniotic fluid, probably as a result of decreased fetal urine production. The fetal kidneys are sensitive to indomethacin as early as 21 weeks gestation and may respond to the drug's affects as early as 5 hours after administration. This "side-effect" of the medication is used at times in patients with polyhydramnios to decrease the amniotic fluid through maternal ingestion.

 

References:

Wallenburg HCS. The amniotic fluid: I Water and electrolyte homeostasis. J Perinat. Med 5:193-205, 1977

Chamberlain MB, Manning FA, Morrsion L et al. Ultrasound evaluation of amniotic fluid II. The relationship of increased amniotic fluid volume to perinatal outcome. Am J Obstet Gynecol 150:250, 1984

Moore TR, Longo J, Leopold G et al. The reliability and predictive value ao an amniotic fluid scoring system in severe second trimester oligohydramnios. Obstet Gynecol 73:739, 1989

Moore TR. Oligohydramnios. Contemporary OB/Gyn 15-26, 1996

Bar-Hava I, Divon MY, sardo M, Barnhard Y. Is oligohydramnios in postterm pregnancy associated with redistribution of fetal blood flow? Am J Obstet Gynecol 173:519-522, 1995

Baron C, Morgan MA, Garite TJ. The impact of amniotic fluid volume assessed intrapartum on perinatal outcome. Am J Obstet Gynecol 173:167-174, 1995

Moore TR, Cayle JE. The amniotic fluid index in normal human pregnancy. Am J Obstet Gynecol 162:1168-73, 1990

Marks AD, Divon MY. Longitudinal study of the amniotic fluid index in post-dates pregnancy. Obstet Gynecol 79:229-233, 1992

Manning FA, Hill LM, Platt LD. Qualitative amniotic fluid volume determination by ultrasound: antepartum detection of intrauterine growth retardation. Am J Obstet Gynecol 139:254-258, 1981

Chamberlain PF, Manning FA, Morrison I, Harmon CR, Lange IR. Ultrasound evaluation of amniotic fluid volume. I The relationship of marginal and decreased amniotic fluid volumes to perinatal outcome. Am J Obstet Gynecol 150:245-249, 1984

Fisk NM, Parkes MJ, Moore PJ, Hanson MA, Wigglesworth J, Rodeck CH. Mimicking low amniotic pressure by chronic pharyngeal drainage does not impair lung development. Am J Obstet Gynecol 166:991-996, 1992

Spong CY, McKindsey F, Ross MG. Amniotic fluid index predicts the relief of variable decelerations after amnioinfusion bolus Am J Obstet Gynecol 175:1066-70, 1996

Crowley P. Non-quantitative estimation of amniotic fluid volume in suspected prolonged pregnancy. J Perinat Med j8:249-51,1980

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 32:54-2, 1987

Dieckmann WJ, Davis ME. The volumetric determination of amniotic fluid with Congo red. Am J Obstet Gynecol 25: 623-7,1933

Charles D, Jacoby HE. Preliminary data on the use of sodium aminohippurate to determine amniotic fluid volumes. Am J Obstet Gynecol 95:266-9, 1966

Horsager R, Nathan L, Leveno KJ. Correlation of measured amniotic fluid volume and sonographic predictions of oligohydramnios. Obstet Gynecol 83:955-8, 1994

Sepulveda W, Flack NJ, Fisk NM. Direct volume measurement at midtrimester amnioinfusion in relation to ultrasonographic indexes of amniotic fluid volume. Am J Obstet Gynecol 170:1160-1163, 1994

Harding R, Hooper SB, Dickson KA. A mechanism leading to reduced lung expansion and lung hypoplasia in fetal sheep during oligohydramnios. Am J Obstet Gynecol 163:1904-13, 1990

King JC, Mitzner W, Butterfield AB, Queenan JT. Effect of induced oligohydramnios on fetal lung development. Am J Obstet Gynecol 154:823-830, 1986

Philipson EH, Sokol RJ, Williams T. Oligohydramnios: clincial associations and predictive value for intrauterine growth retardation. Am J Obstet Gynecol 146:271, 1983

Cheng EY, Luthy DA, Hickik DE, Hollenbach KA, Resta RG, Mahony BS, Luthardt FW. Transcervical chorionic villus sampling and midtrimester oligohydramnios. Am J Obstet Gynecol 165:1063-8, 1991

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Magann EF, Morton ML, Nolan TE, Martin Jr JN et al. Comparative efficacy of two sonographic measurements for the detection of aberrations in the amniotic fluid volume and the effect of amniotic fluid volume on pregnancy outcome. Obstet Gynecol 83:959-62, 1994

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Chauhan SP, Washburne JF, Magann EF, Perry Jr KG et al. A randomized study to assess the efficacy of the amniotic fluid index as a fetal admission test. Obstet Gynecol 86:9-13, 1995

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Croom CS, Banias BB, Ramos-Santos E, Devoe LD et al. Do semiquantitative amniotic fluid indexes reflect actual volume? Am J Obstet Gynecol 167:995-999, 1992

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

Sadovsky Y, Christensen MW, Scheerer L, Crombleholme WR. Cord-containing amniotic fluid pocket: a useful measurement in the management of oligohydramnios. Obstet Gynecol 80:775-777, 1992

Myles TD, Strassner HT. Four-Quadrant assessment of amniotic fluid volume: distribution's role in predicting fetal outcome. Obstet Gynecol 80:769-74, 1992

Hashimoto B, Filly RA, Belden C, Callen PW, Laros RK. Objective method of diagnosing oligohydramnios in postterm pregnancies. J Ultrasound Med 6:81-84, 1987

Hadi JA, Hodson CA, Strickland D. Premature rupture of the membranes between 20 and 25 weeks gestation:role of amniotic fluid volume in perinatal outcome. Am J Obstet Gynecol 170:1139-44, 1994

Johnson JWC, Egerman RS, Moorhead J. Cases with ruptured membranes that "reseal". Am J Obstet Gynecol 163:1024-32, 1990

Bengtson JM, VanMarter LJ, Barss VA, Greene MF et al. Pregnancy outcomes after premature rupture of the membranes at or before 26 weeks gestation. Obstet Gynecol 73:921, 1989

Magann EF, Chauhan SP, Whitworth NS, Saltzman AK, Morrison JC. Dept of OB/GYN, University of Mississippi, Jackson MS. Society of Perinatal Obstetricians-Jan 1997, Anaheim, Am J Obstet Gynecol 176:S130:440

Sarno AP, Ahn MO, Phelan IP. Intrapartum amniotic fluid volume at term: association of ruptured membranes, oligohydramnios and increased fetal risk. J Reproducive Med 35:719-23, 1990

Chauhan SP, Hendrix NW, Morrison JC, Magann EF, Devoe LD. Intrapartum oligohydrmanios does not predict adverse peripartum outcome among high-risk parturients. Am J Obstet Gynecol 176:1130-8, 1997

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