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Pleural effusions and pulmonary hypoplasia
Pleural effusions and pulmonary hypoplasia Ramon A. Castillo, M.D., Lawrence D. Devoe, M.D. Greer Falls, M.D., Gerald B. Holzman, M.D., Hamid A. Hadi, M.D., and Hossam E. Fadel, M.D. Augusta, Georgia Nine cases of fetuses with pleural effusions are presented in which the diagnosis was made by ultrasound before the thirtieth week of gestation. A ratio of lung span to hemithorax diameter was calculated and ranged from 0.44 to 0.77 (mean 0.60). At autopsy, pulmonary hypoplasia was confirmed in all cases by criteria based on the ratio of lung weight to total body weight. Because pleural effusions occurring in the midtrimester can be detected and may lead to pulmonary hypoplasia, consideration should be given to definitive in utero therapy when no other major fetal abnormality is detected. (AM J OssTET GvNECOL 1987; 157:1252-5.)
Key words: Effusions, pulmonary hypoplasia, ultrasound Increased use of real-time ultrasonography has resulted in early prenatal recognition of m
From the Departments of Obstetrics and Gynecology and Pathology, Medical College of Georgia. Received for publication December 11, 1986; revised june 11, 1987; acceptedjuly 15, 1987. Reprint requests: Ramon A. Castillo, M.D., Department of Obstetrics and Gynecology, Maternal-Fetal Medicine Section, Medical College of Georgia, Augusta, GA 30912.
1252
vey was performed and quantification of each pleural effusion was done. This measurement, described previously: consists of a ratio between the lung span and the fetal hemithorax determined in transverse or lon. gitudinal views. Also as part of the prenatal evaluation the following tests were performed: amniocentesis for fetal karyotype, delta optical density at 450 nm, and viral cultures. Analysis of maternal blood included a Kleihauer-Betke test, complete hemogram, blood type and antibody screen, glucose screen, and hemoglobin electrophoresis. Results Four pregnancies were electively terminated and one patient underwent induction of labor after intrauterine fetal death had been documented. In the other four cases, the fetuses were delivered alive after the spon. taneous onset of labor. Autopsy was performed in each case and the results of each examination are presented in Table I. In three cases no anatomic abnormalities were found and there were no fluid accumulations in other serous cavities (Cases 1, 5, and 6). In Cases 2 and 8, no significant structural abnormalities were present, but a karyotypic disorder was found. In the remainder at least one other major anomaly was present although a direct association between these abnormalities and pulmonary hypoplasia could not be established. All fetuses were found to have pulmonary hypoplasia as defined by the criteria of Reale and Esterly. 7 This definition consists of a ratio of total lung weight to total body weight that falls more than 2 SD below the normal value of 0.022 ± 0.002 and is constant throughout gestation. Comment The development of the fetal lung encompasses different stages that have characteristic anatomic findings:
Pleural effusions
Volume 157 Number 5
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Table I. Summary of cases Gestational age at delivery (wk) and outcome
Age (yr)
Gravidity
Parity
Gestational age at diagnosis (wk)
22
2
1-0-0-1
26
32 SVD
46
0.003
2
26
6
4-0-1-3
26
40 SVD
44.5
0.005
3
21
3
1-0-1-1
22
23 E.Ab.
62
0.009
4
18
24
24
64
0.002
5
29
30
38 SVD
0.009
6
24
26
27.5 SVD
50 61.3 77.9 51.5
7
25
3
2-0-0-2
25
28.5 IVD
60
0.0027
8
32
3
1-0-1-1
18
19 E.Ab.
63.6
0.0023
9
23
2
1-0-0-1
18
19 E.Ab.
61.2
0.009
Case No.
Lung-thoracic ratio (%)
Lung weightbody weight ratio*
0.0012
Prenatal findings
Postnatal findings
Body edema Pleural effusions Ascites 46,XY Body edema Pleural effusions Ascites 47,XY + 21 Body edema Pleural effusions Ascites 46,XY
Severe hydrops Hypoplastic lungs
Body edema Pleural effusions Neck cystic mass 46,XY Pleural effusions 46,XY Body edema Pleural effusions 46,XX Fetal cell preparation 4% Body edema Pleural effusions Bilateral clubfoot Tachycardia 46,XY Body edema Pleural effusions Ascites 45,XO Body edema Neck cystic mass Pleural effusions 46,XY
Severe hydrops Hypoplastic lungs Severe hydrops Dysmorphic fascies Hypoplastic lungs Liver hyperplasia with focal areas of necrosis Severe hydrops Cystic hygroma Hypoplastic lungs Hypoplastic lungs Hypoplastic lungs Hypoplastic lungs Bilateral clubfoot Pena Shokeir type I
Severe hydrops Hypoplastic lungs Severe hydrops Hypoplastic lungs Cystic hygromas
SDV = Spontaneous vaginal delivery. E.Ab. = Elective abortion. IVD = Induced vaginal delivery. *Expected = 0.022 ± 0.002.
(1) the glandular stage between the fifth and the seventeenth weeks, (2) the canalicular stage between the thirteenth and the twenty-fifth weeks, (3) the alveolar phase that occurs from the twenty-fourth week to approximately the eighth decade oflife. 8 The intrauterine environment must provide a number of factors for these stages to proceed uneventfully; adequate anmiotic fluid volume; presence of fetal breathing activity, intact muscular activity, and adequate intrathoracic and extrathoracic volumes that are capable of allowing the ~ung to expand. When one or more of these factors are not present or are significantly altered, the result is a spectrum of disorders ranging from minimal lung disease to severe pulmonary hypoplasia. 3 • 4 · 8
In the present series, each fetus had bilateral pleural effusions that were quantified by the lung-thoracic ratio. In our institution any accumulation of fluid that can be quantified with this measurement is copsidered to be "significant." In Case 5 this measurement was repeated at 32 and 36 weeks' gestation with an objective decrease in the amount of the effusions (Fig. l, A to C). Despite the reduction in pleural fluid in this fetus, the histopathologic findings were consistent with lung hypoplasia (Fig. 1, D). Therefore regardless of the cause the fluid accumulations appear to function as spaceoccupying lesions and restrict the development of the fetal lung, a sequence of events that was recognized by Potter in 1952 in fetuses with diaphragmatic hernias."
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Castillo et al.
November 1987 Am J Obstet Gynecol
Fig. 1. Lung-thoracic ratios obtained at (A) 30 weeks', (B) 32 weeks', and (C) 36 weeks' gestation. Despite a reduction in the amount of pleural fluid the lungs were hypoplastic (D) with a ratio of lung weight to total body weight (LIT ratio) of 0.009.
However, it is clear that the sole presence of these effusions at birth is not enough to establish severe lung damage since adequate pulmonay function in some of these babies has been reported." It seems that the gestational age at which these effusions develop may play a critical role in the development of severe and irreversible damage to the fetal lung. Studies of morphologic lung development as well as a case report of persistent hypoplasia of the lung after repair of congenital diaphragmatic hernia suggest that such lesions appearing in the alveolar phase of lung development may not produce irreversible damage. Once the process is corrected, the development of alveoli may proceed although these may be significantly decreased in number. 8 · 10 These same studies and our histopathologic analysis of the nine hypoplastic lungs show that there are some changes in the bronchial tree and in the arterioles of hypoplastic lungs that indicate that the onset of this process occurred before the twenty-fourth to twenty-sixth week of gestation. These changes are reduced bronchial airway generation and increased muscularity of pulmonary blood vessels.
Therefore it is suggested that if there are significant fluid accumulations in the pleural space before the alveolar phase and if this fluid accumulation persists throughout the remainder of pregnancy, the fetal lung could be irreversibly damaged. Since 1982 at least five fetuses have been treated in utero by decompression of the thorax by means of either repeated pleural taps or placement of a pleural amniotic shunt.'· 11 • 15 While the fetal outcomes are not always good, our experience suggests that untreated significant pleural effusions detected by the second trimester of pregnancy can lead to significant lung hypoplasia and perinatal death. In summary, when pleural effusions are detected by ultrasound, a detailed anatomic survey of the fetus should be performed and accompanied by a complete antenatal workup as recommended for fetuses with nonimmune hydrops. If no major anomalies or significant karyotypic abnormalities are documented and the effusions are detected before the third trimester, prenatal therapy should be considered. Finally, aggressive neonatal support is mandatory at the time of delivery
Volume 157 Number 5
since there is no absolute way of determining before, birth which babies will have a pulmonary function incompatible with life. REFERENCES I. Defoort P, Thiery M, Antenatal diagnosis of congenital chylothorax by gray scale sonography, J Clin Ultrasound I978;6:4 7-8. 2, Bovicelli L, Rizzo N, Orsini LF, Calderoni P, Ultrasonic real-time diagnosis of fetal hydrothorax and lung hypoplasia, JCU I981';9:253-4. 3. Page DP, Stocker JT Anomalies associated with pulmonary hypoplasia, Am Rev Respir Dis I982;I25:2I6-2l. 4. Castillo RA, Devoe LD, Hadi HA, MartinS, Geist D. Nonimmune hydrops fetalis: clinical experience and factors related to a poor outcome. AM J 0BSTET GYNECOL I986;I55:8I2-6, 5. Weiner C, Varner M, Pringle K, Hein H, Williamson R, Smith WL Antenatal diagnosis and palliative treatment of nonimmune hydrops fetalis secondary to pulmonary extralobar sequestration. Obstet Gynecoli986;68:275-80, 6, Nimrod C, Davies D, Iwanicki S, Harder J, Persaud D, Nicholson S. Ultrasound prediction of pulmonary hypoplasia, Obstet Gynecol I986;68:495-7, 7. Reale FR, Esterly JR. Pulmonary hypoplasia: a morphometric study of the lungs of infants with diaphragmatic hernia, anencephaly, and renal malformations. Pediatrics I973;5I:9I-6,
Pleural effusions
8. Tomashefski JF Jr, Vawter GF, Ried LM. Pathological observations on infants who do not survive the respiratory distress syndrome. In: Nelson GH, ed. Pulmonary development: transition from intrauterine to extrauterine life. New York: Marcel Dekker, I985:387-429, 9. Lange IR, Manning FA. Antenatal diagnosis of congenital pleural effusions. AM J 0BSTET GYNECOL I98I;I40: 839-40. 10. Hislop A, Reid L Persistent hypoplasia of the lung after repair of congenital diaphragmatic hernia. Thorax I976; 3I :450-5, II. Petres RE, Redwine FO, Cruikshank DP. Congenital bilateral chylothorax: antepartum diagnosis and successful intrauterine surgical management. JAMA I982;248: I360-l. I2. Schmidt W, Harms E, Wolf D. Successful prenatal treatment of non-immune hydrops fetalis due to congenital chylothorax: case report. Br J Obstet Gynaecol I985; 92:685-7. 13. Benacerraf BR, Frigoletto FD Jr. In utero treatment of a fetus with diaphragmatic hernia complicated by hydrops. AMJ 0BSTET GYNECOL 1986;155:8I7-8. 14. Seeds JW, Bowes WA Jr. Results of treatment of severe fetal hydrothorax with bilateral pleuroamniotic catheters. Obstet Gynecol 1986;68:577-80: 15, Benacerraf BR, Frigoletto FD Jr, Wilson M. Successful midtrimester thoracentesis with analysis of the lymphocyte population in the pleural effusion. AM J OBSTET GYNECOL I986; 155:398-9.
Antenatal diagnosis and management of monoamniotic twins John F. Rodis, M.D., Anthony M. Vintzileos, M.D., Winston A. Campbell, M.D., Jeffrey L. Deaton, M.D., Fred Fumia, M.D., and David J. Nochimson, M.D. Farmington, Connecticut Double survival of monoamniotic twins is rare. Three consecutive cases in which double survival occurred are presented. Accurate antenatal diagnosis, intensive fetal surveillance, and operative delivery should improve neonatal outcome. (AM J OssTET GvNECOL 1987;157:1255-7.)
Key words: Monoamniotic twins, antenatal diagnosis
The incidence of monozygotic twins is approximately one in 250 pregnancies, with little racial or geographic differences worldwide, as opposed to dizygotic twins. Only l% to 2% of monozygotic twins are monoamniotic. The perinatal mortality rate of monoamniotic twins has been reported to be as high as 50%.'·" We present three consecutive cases of monoamniotic twins From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, The University of Connecticut Health Center. Received for publication December 18, 1986; accepted june 18,
1987,
Reprint requests: John F. Rodis, M.D., Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, The University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06032.
with double survival in all and discuss the antenatal diagnosis and management.
Case reports Case 1. A 22-year-old primigravida was transferred to the University of Connecticut Health Genter at 33'¥7 weeks' gestation because of preterm labor in a known twin gestation. Previous sonograms at 16, 20, and 24 weeks, as well as on adminssion, failed to reveal a dividing amniotic membrane. One placenta was seen, and amniotic fluid volume appeared normal around both female fetuses. No fetal anomalies were noted. At cesarean section both female fetuses occupied one amniotic sac. Twin B had a nuchal cord. The umbilical cords were intertwined and knotted and the placenta was monochorionic and monoamniotic (Fig. 1). Both
1255
Key words: Effusions, pulmonary hypoplasia, ultrasound Increased use of real-time ultrasonography has resulted in early prenatal recognition of m
From the Departments of Obstetrics and Gynecology and Pathology, Medical College of Georgia. Received for publication December 11, 1986; revised june 11, 1987; acceptedjuly 15, 1987. Reprint requests: Ramon A. Castillo, M.D., Department of Obstetrics and Gynecology, Maternal-Fetal Medicine Section, Medical College of Georgia, Augusta, GA 30912.
1252
vey was performed and quantification of each pleural effusion was done. This measurement, described previously: consists of a ratio between the lung span and the fetal hemithorax determined in transverse or lon. gitudinal views. Also as part of the prenatal evaluation the following tests were performed: amniocentesis for fetal karyotype, delta optical density at 450 nm, and viral cultures. Analysis of maternal blood included a Kleihauer-Betke test, complete hemogram, blood type and antibody screen, glucose screen, and hemoglobin electrophoresis. Results Four pregnancies were electively terminated and one patient underwent induction of labor after intrauterine fetal death had been documented. In the other four cases, the fetuses were delivered alive after the spon. taneous onset of labor. Autopsy was performed in each case and the results of each examination are presented in Table I. In three cases no anatomic abnormalities were found and there were no fluid accumulations in other serous cavities (Cases 1, 5, and 6). In Cases 2 and 8, no significant structural abnormalities were present, but a karyotypic disorder was found. In the remainder at least one other major anomaly was present although a direct association between these abnormalities and pulmonary hypoplasia could not be established. All fetuses were found to have pulmonary hypoplasia as defined by the criteria of Reale and Esterly. 7 This definition consists of a ratio of total lung weight to total body weight that falls more than 2 SD below the normal value of 0.022 ± 0.002 and is constant throughout gestation. Comment The development of the fetal lung encompasses different stages that have characteristic anatomic findings:
Pleural effusions
Volume 157 Number 5
1253
Table I. Summary of cases Gestational age at delivery (wk) and outcome
Age (yr)
Gravidity
Parity
Gestational age at diagnosis (wk)
22
2
1-0-0-1
26
32 SVD
46
0.003
2
26
6
4-0-1-3
26
40 SVD
44.5
0.005
3
21
3
1-0-1-1
22
23 E.Ab.
62
0.009
4
18
24
24
64
0.002
5
29
30
38 SVD
0.009
6
24
26
27.5 SVD
50 61.3 77.9 51.5
7
25
3
2-0-0-2
25
28.5 IVD
60
0.0027
8
32
3
1-0-1-1
18
19 E.Ab.
63.6
0.0023
9
23
2
1-0-0-1
18
19 E.Ab.
61.2
0.009
Case No.
Lung-thoracic ratio (%)
Lung weightbody weight ratio*
0.0012
Prenatal findings
Postnatal findings
Body edema Pleural effusions Ascites 46,XY Body edema Pleural effusions Ascites 47,XY + 21 Body edema Pleural effusions Ascites 46,XY
Severe hydrops Hypoplastic lungs
Body edema Pleural effusions Neck cystic mass 46,XY Pleural effusions 46,XY Body edema Pleural effusions 46,XX Fetal cell preparation 4% Body edema Pleural effusions Bilateral clubfoot Tachycardia 46,XY Body edema Pleural effusions Ascites 45,XO Body edema Neck cystic mass Pleural effusions 46,XY
Severe hydrops Hypoplastic lungs Severe hydrops Dysmorphic fascies Hypoplastic lungs Liver hyperplasia with focal areas of necrosis Severe hydrops Cystic hygroma Hypoplastic lungs Hypoplastic lungs Hypoplastic lungs Hypoplastic lungs Bilateral clubfoot Pena Shokeir type I
Severe hydrops Hypoplastic lungs Severe hydrops Hypoplastic lungs Cystic hygromas
SDV = Spontaneous vaginal delivery. E.Ab. = Elective abortion. IVD = Induced vaginal delivery. *Expected = 0.022 ± 0.002.
(1) the glandular stage between the fifth and the seventeenth weeks, (2) the canalicular stage between the thirteenth and the twenty-fifth weeks, (3) the alveolar phase that occurs from the twenty-fourth week to approximately the eighth decade oflife. 8 The intrauterine environment must provide a number of factors for these stages to proceed uneventfully; adequate anmiotic fluid volume; presence of fetal breathing activity, intact muscular activity, and adequate intrathoracic and extrathoracic volumes that are capable of allowing the ~ung to expand. When one or more of these factors are not present or are significantly altered, the result is a spectrum of disorders ranging from minimal lung disease to severe pulmonary hypoplasia. 3 • 4 · 8
In the present series, each fetus had bilateral pleural effusions that were quantified by the lung-thoracic ratio. In our institution any accumulation of fluid that can be quantified with this measurement is copsidered to be "significant." In Case 5 this measurement was repeated at 32 and 36 weeks' gestation with an objective decrease in the amount of the effusions (Fig. l, A to C). Despite the reduction in pleural fluid in this fetus, the histopathologic findings were consistent with lung hypoplasia (Fig. 1, D). Therefore regardless of the cause the fluid accumulations appear to function as spaceoccupying lesions and restrict the development of the fetal lung, a sequence of events that was recognized by Potter in 1952 in fetuses with diaphragmatic hernias."
1254
Castillo et al.
November 1987 Am J Obstet Gynecol
Fig. 1. Lung-thoracic ratios obtained at (A) 30 weeks', (B) 32 weeks', and (C) 36 weeks' gestation. Despite a reduction in the amount of pleural fluid the lungs were hypoplastic (D) with a ratio of lung weight to total body weight (LIT ratio) of 0.009.
However, it is clear that the sole presence of these effusions at birth is not enough to establish severe lung damage since adequate pulmonay function in some of these babies has been reported." It seems that the gestational age at which these effusions develop may play a critical role in the development of severe and irreversible damage to the fetal lung. Studies of morphologic lung development as well as a case report of persistent hypoplasia of the lung after repair of congenital diaphragmatic hernia suggest that such lesions appearing in the alveolar phase of lung development may not produce irreversible damage. Once the process is corrected, the development of alveoli may proceed although these may be significantly decreased in number. 8 · 10 These same studies and our histopathologic analysis of the nine hypoplastic lungs show that there are some changes in the bronchial tree and in the arterioles of hypoplastic lungs that indicate that the onset of this process occurred before the twenty-fourth to twenty-sixth week of gestation. These changes are reduced bronchial airway generation and increased muscularity of pulmonary blood vessels.
Therefore it is suggested that if there are significant fluid accumulations in the pleural space before the alveolar phase and if this fluid accumulation persists throughout the remainder of pregnancy, the fetal lung could be irreversibly damaged. Since 1982 at least five fetuses have been treated in utero by decompression of the thorax by means of either repeated pleural taps or placement of a pleural amniotic shunt.'· 11 • 15 While the fetal outcomes are not always good, our experience suggests that untreated significant pleural effusions detected by the second trimester of pregnancy can lead to significant lung hypoplasia and perinatal death. In summary, when pleural effusions are detected by ultrasound, a detailed anatomic survey of the fetus should be performed and accompanied by a complete antenatal workup as recommended for fetuses with nonimmune hydrops. If no major anomalies or significant karyotypic abnormalities are documented and the effusions are detected before the third trimester, prenatal therapy should be considered. Finally, aggressive neonatal support is mandatory at the time of delivery
Volume 157 Number 5
since there is no absolute way of determining before, birth which babies will have a pulmonary function incompatible with life. REFERENCES I. Defoort P, Thiery M, Antenatal diagnosis of congenital chylothorax by gray scale sonography, J Clin Ultrasound I978;6:4 7-8. 2, Bovicelli L, Rizzo N, Orsini LF, Calderoni P, Ultrasonic real-time diagnosis of fetal hydrothorax and lung hypoplasia, JCU I981';9:253-4. 3. Page DP, Stocker JT Anomalies associated with pulmonary hypoplasia, Am Rev Respir Dis I982;I25:2I6-2l. 4. Castillo RA, Devoe LD, Hadi HA, MartinS, Geist D. Nonimmune hydrops fetalis: clinical experience and factors related to a poor outcome. AM J 0BSTET GYNECOL I986;I55:8I2-6, 5. Weiner C, Varner M, Pringle K, Hein H, Williamson R, Smith WL Antenatal diagnosis and palliative treatment of nonimmune hydrops fetalis secondary to pulmonary extralobar sequestration. Obstet Gynecoli986;68:275-80, 6, Nimrod C, Davies D, Iwanicki S, Harder J, Persaud D, Nicholson S. Ultrasound prediction of pulmonary hypoplasia, Obstet Gynecol I986;68:495-7, 7. Reale FR, Esterly JR. Pulmonary hypoplasia: a morphometric study of the lungs of infants with diaphragmatic hernia, anencephaly, and renal malformations. Pediatrics I973;5I:9I-6,
Pleural effusions
8. Tomashefski JF Jr, Vawter GF, Ried LM. Pathological observations on infants who do not survive the respiratory distress syndrome. In: Nelson GH, ed. Pulmonary development: transition from intrauterine to extrauterine life. New York: Marcel Dekker, I985:387-429, 9. Lange IR, Manning FA. Antenatal diagnosis of congenital pleural effusions. AM J 0BSTET GYNECOL I98I;I40: 839-40. 10. Hislop A, Reid L Persistent hypoplasia of the lung after repair of congenital diaphragmatic hernia. Thorax I976; 3I :450-5, II. Petres RE, Redwine FO, Cruikshank DP. Congenital bilateral chylothorax: antepartum diagnosis and successful intrauterine surgical management. JAMA I982;248: I360-l. I2. Schmidt W, Harms E, Wolf D. Successful prenatal treatment of non-immune hydrops fetalis due to congenital chylothorax: case report. Br J Obstet Gynaecol I985; 92:685-7. 13. Benacerraf BR, Frigoletto FD Jr. In utero treatment of a fetus with diaphragmatic hernia complicated by hydrops. AMJ 0BSTET GYNECOL 1986;155:8I7-8. 14. Seeds JW, Bowes WA Jr. Results of treatment of severe fetal hydrothorax with bilateral pleuroamniotic catheters. Obstet Gynecol 1986;68:577-80: 15, Benacerraf BR, Frigoletto FD Jr, Wilson M. Successful midtrimester thoracentesis with analysis of the lymphocyte population in the pleural effusion. AM J OBSTET GYNECOL I986; 155:398-9.
Antenatal diagnosis and management of monoamniotic twins John F. Rodis, M.D., Anthony M. Vintzileos, M.D., Winston A. Campbell, M.D., Jeffrey L. Deaton, M.D., Fred Fumia, M.D., and David J. Nochimson, M.D. Farmington, Connecticut Double survival of monoamniotic twins is rare. Three consecutive cases in which double survival occurred are presented. Accurate antenatal diagnosis, intensive fetal surveillance, and operative delivery should improve neonatal outcome. (AM J OssTET GvNECOL 1987;157:1255-7.)
Key words: Monoamniotic twins, antenatal diagnosis
The incidence of monozygotic twins is approximately one in 250 pregnancies, with little racial or geographic differences worldwide, as opposed to dizygotic twins. Only l% to 2% of monozygotic twins are monoamniotic. The perinatal mortality rate of monoamniotic twins has been reported to be as high as 50%.'·" We present three consecutive cases of monoamniotic twins From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, The University of Connecticut Health Center. Received for publication December 18, 1986; accepted june 18,
1987,
Reprint requests: John F. Rodis, M.D., Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, The University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06032.
with double survival in all and discuss the antenatal diagnosis and management.
Case reports Case 1. A 22-year-old primigravida was transferred to the University of Connecticut Health Genter at 33'¥7 weeks' gestation because of preterm labor in a known twin gestation. Previous sonograms at 16, 20, and 24 weeks, as well as on adminssion, failed to reveal a dividing amniotic membrane. One placenta was seen, and amniotic fluid volume appeared normal around both female fetuses. No fetal anomalies were noted. At cesarean section both female fetuses occupied one amniotic sac. Twin B had a nuchal cord. The umbilical cords were intertwined and knotted and the placenta was monochorionic and monoamniotic (Fig. 1). Both
1255