Ausi
NZ J
Obstet Gynaecol 1990. 30: 3: 191
Acute and Subacute Polyhydramnios in Singleton Pregnancies Els Desmedt', Olivia A. Henry', Lionel H. Steinbergz and Norman A. Beischer' Mercy Maternity Hospital and Department of Obstetrics and Gynaecology, University of Melbourne, Victoria Summary: Over a 10-year period when 51,022 singleton infants were delivered, 19 pregnancies (1 in 2,685) were complicated by acute polyhydramnios, 17 (1 in 3,000) by subacute polyhydramnios and 501 (1 in 102) by chronic polyhydramnios. The incidence of major congenital malformations in singleton pregnancies associated with acute polyhydramnios was 63% and the perinatal mortality rate was 74%. When subacute polyhydramnios occurred in singleton pregnancies, the incidence of major congenital malformations was 65%, similar to acute polyhydramnios, but the perinatal mortality rate was only 35%. The comparable figures for chronic polyhydramnios in singleton pregnancies were a major malformation incidence of 14% and perinatal mortality rate of 10%. The type of onset of polyhydramnios, acute, subacute or chronic is therefore the most important indicator of prognosis. In patients with gross polyhydramnios, acute renal failure must be specifically excluded.
1 . Research Fellow. 2. Registrar. 3. Professor.
associated factors identified. The diagnosis of acute polyhydramnios was made when all of the following criteria were fulfilled: 1) onset of excessive amniotic fluid within 1 week of diagnosis. 2) uterus large for dates. 3) pain due to enlarged uterus. 4) respiratory symptoms. Subacute polyhydramnios was diagnosed when symptoms were more gradual in onset and the remaining criteria listed above were satisfied. Chronic polyhydramnios had a gradual onset and, although the amount of excess amniotic fluid varied enormously, the associated symptoms were usually mild. Ultrasonographic findings were used to classify the degree of polyhydramnios as mild, moderate, severe or gross (2). The associated fetal and maternal complications and the fetal outcome in those pregnancies complicated by acute polyhydramnios were analysed. As there can be clinical confusion with subacute polyhydramnios, the case records of patients with this condition were also reviewed to assess whether o r not they constitute a different disease entity. Glucose tolerance testing (GTT) was performed at 30-32 weeks' gestation using a 50 g glucose load. The criterion for diagnosis of gestational diabetes was the combination of a capillary plasma glucose level of > 9 mmol/l at 1 hour and > 7 mmol/l at 2 hours. The criterion for diagnosis of hypoglycaemia was a glucose level of < 4 mmol/l fasting and < 3 mmol/l at 3 hours (3).
Address for correspondence: Professor N.A. Beischer, Mercy Maternity Hospital, Clarendon Street, East Melbourne, Australia, 3002.
There were 537 cases of polyhydramnios in the 51,022 singleton pregnancies, an incidence of 1.03%;
Acute polyhydramnios is a rare complication of pregnancy characterized by a rapid increase in amniotic fluid volume which results in an enlarged tender uterus that causes pain and respiratory symptoms. The diagnosis is usually made in the second trimester and often results in premature labour. The onset in subacute polyhydramnios is more gradual over 1 or 2 weeks; the associated symptoms are less severe and may be difficult to differentiate from other obstetrical conditions such as premature labour or abruption of the placenta. Polyhydramnios is a clinical diagnosis which can be confirmed by ultrasound or at the moment of rupture of the membranes. Weir et al (1) studied acute polyhydramnios in twins and reported very poor perinatal results with a low incidence of major malformations, but very little attention has been paid to the acute condition in singleton pregnancies. PATIENTS AND METHODS
From January 1, 1979, until December 31, 1988, there were 51,022 singleton deliveries at the Mercy Maternity Hospital, Melbourne; those pregnancies complicated by polyhydramnios were identified and the records reviewed to enable a diagnosis of acute, subacute or chronic polyhydramnios to be made and
RESULTS
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19 (3.570) fulfilled the criteria for diagnosis of acute polyhydramnios, 17 (3.2%) for subacute and 501 (93.3%) for chronic polyhydramnios.
1). Spontaneous labour occurred in 11 patients (58%), and in 3 (15.7%) labour was induced soon after fetal death or major congenital abnormality
Acute polyhydramnios Tables 1 and 2 show the cIinica1details of the 19 infants and mothers. The age of the mothers ranged from 20-44 years; 7 were primigravidas, and 12 multigravidas. Four patients (Cases 1,3,16 and 18) had chronic polyhydramnios in a previous pregnancy and 1 patient (Case 2) developed chronic polyhydramnios in a subsequent pregnancy, a recurrence rate of 26%. None of these 5 pregnancies with chronic polyhydramnios was associated with perinatal loss. Ail patients were admitted to hospital when they presented with gross uterine distension and associated symptoms. The average fundal height was 7 weeks greater than normal and the estimation made by ultrasound showed the severity of polyhydramnios to be moderate in 3 patients, severe in 7 and gross in 8. (One patient did not have an ultrasound examination). There was only one patient (Case 18) who had amniocentesis performed in an attempt to relieve symptoms and prolong pregnancy. Delivery was postponed for 10 weeks by serial amniocentesis; the patient was delivered of a healthy male infant, birth-weight 2,588 g, by Caesarean section at 34 weeks and no major fetal malformation was present. In these patients with acute polyhydramnios the clinical course was fulminant with an average time of onset at 29.0 weeks and delivery at 31 .O weeks (table
Table 2. Details of the Infants Affected by Acute polyhydrarnnios Sex BirthOutcome Fetal abnormality weight (g) None 1. M 1,094 NND None 2. F 1,ooO NND None 1,528 NND 3. M Idiopathic hydrops fetalis 2,420 NND 4. M None 1,775 Alive 5. M Meningomyelocele, 6. F 1.145 NND diaphragmatic hernia, cleft lip and palate Anencephaly, spina 850 SB 7. F bifida, meningomyelocele diaphragmatic hernia Oesophageal atresia 1,260 Alive 8. M None 1,680 Alive 9. F Anencephaly, spina 10. F 1,400 SB bifida Hydrocephaly, teratoma 11. F 2,352 NND of medulla oblongata 1,512 NND Patent ductus arteriosus 12. M 13. F Spina bifida, men2,310 NND ingomyelocele, hydrocephaly, diaphragmatic hernia None 14. F 3,024 Alive 15. F Hydrops fetalis, single 2,530 NND atrium, microcephaly Anencephaly 16. F 1,010 SB Anencephaly 17. F 1,190 SB 18. M None 2,588 Alive 19. F Anencephaly, spina 1,455 NND bifida SB = stillbirth; NND = neonatal death; M = male; F = female
Table 1. Details of Patients witb Acute Polybydramnios Fundal Ultrasound Labour Delivery Complications height volume Onset Delivery >dates (weeks) , - - _.-, 1. 37 21.6 25.6 5 Gestational diabetes, APH 2 S B 2. 24.0 30 26.0 10 3 S NVD Chorioangiorna of the placenta 3. 27 26.6 28.0 10 4 S F Chorioangioma of the placenta, APH 4. 24 29.4 4 I F 30.0 6 Mild preeclampsia, UTI 5. 24 27.0 30.3 13 4 S cs 6. 44 .. 29.0 30.3 11 4 S NVD 7. 29 30.3 30.6 6 4 S NVD 8. 36 29.4 31.1 10 4 cs Acute renal failure, bilateral hydronephrosis, APH 9. 20 31.0 31.2 3 cs APH 10. 28 31.0 31.4 5 3 S F 11. 22 31.0 31.4 7 4 cs 12. 26 31.4 31.6 6 4 cs Acute renal failure, bilateral hydronephrosis, UTI 13. 22 31.0 32.0 4 4 S F Abruptio placentae 14. 23 32.0 32.6 8 2 S cs Insulin dependent diabetes mellitus 15. 32 28.0 33.1 12 3 S NVD 16. 31 33.3 33.5 5 3 I F 17. 33 30.0 34.0 3 3 I NVD APH, abruptio placentae. 18. 31 24.0 34.1 10 2 cs 19. 28 34.0 34.5 6 3 S F S = spontaneous: I = induced: CS = Caesarean section: F = forcens: NVD = normal vaeinal deliverv: .,, B = breech: APH = antepzkum haemorrhage; UTI = urinary tract infection; Ultrasound volume, ?=moderate, 3 =severe, ’ 4=gross Age Weeks’ gestation
ELSDESMEDT
was diagnosed; the other 5 were electively delivered by Caesarean section. Four patients had an anteparturn haemorrhage of unknown origin, 1 prior to labour (Case 8) and 3 (Cases 1 , 3 and 17) during labour. Haemorrhage and abruption of the placenta followed immediately after rupture of the membranes in Case 13. A sixth patient (Case 9) was found to have a retroplacental clot after delivery. One mother had preexisting insulin dependent diabetes mellitus (IDDM). Only 6 of the remaining 18 patients had a glucose tolerance test performed; in 4 the test was normal, 1 showed gestational diabetes and 1 hypoglycaemia. Five patients had a normal vaginal delivery, 1 an assisted breech delivery, 6 a forceps delivery and 7 were delivered by Caesarean section. In 2 mothers (Cases 8 and 12, table l), delivery by Caesarean section was performed to relieve pressure on the ureters and kidneys which had caused acute renal failure. During and after the Caesarean section, the urine output increased and renal function rapidly returned to normal (4). The other indications for Caesarean section were pain and respiratory distress (Cases 5 and 18), ruptured membranes with a closed cervix (Case 9), hydrocephaly with a tumour of the medulla oblongata (Case 11) and fetal distress (Case 14). The perinatal mortality rate with acute polyhydramnios was 74% (14 infants). The cause of death was fetal malformation in 1 1 infants and prematurity in 3. Twelve of the infants (63%) had major congenital malformations: anencephaly (2), anencephaly and spina bifida (2), anencephaly, meningomyelocele, diaphragmatic hernia (l), meningomyelocele, hydrocephaly and diaphragmatic hernia (l), meningomyelocele, diaphragmatic hernia and
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cleft lip and palate (l), hydrocephaly secondary to a teratoma of the medulla oblongata (l), oesophageal atresia (l), hydrops fetalis (l), hydrops fetalis, single atrium, and microcephaly ( l ) , patent ductus arteriosus (1). Malformations were diagnosed by ultrasound in all of these infants, except the last. Only 2 of the 537 cases of polyhydramnios were associated with a chorioangioma of the placenta; both patients developed acute polyhydramnios, at 24.0 and 26.6 weeks’ gestation respectively, and the babies died from immaturity (table 1 , Cases 2 and 3). Subacute polyhydramnios Tables 3 and 4 show the details of the 17 infants and mothers affected by subacute polyhydramnios. The age of the mothers ranged from 21-39 years; 8 were primigravidas and 9 multigravidas. Two patients (Cases 14/15 and 17) (17.6%) had recurrent polyhydramnios. Cases 14 and 15 are the same mother who developed subacute polyhydramnios twice and in Case 17 the patient had chronic polyhydramnios in a previous pregnancy. All 4 pregnancies of these patients resulted in surviving normal infants. All patients with subacute polyhydramnios had gross uterine distension with an average fundal height of 7 weeks greater than normal and were admitted to hospital. Of the 13 patients who had ultrasonography performed at the time of diagnosis, polyhydramnios was described as moderate in 3, severe in 4 and gross in 6. The average gestation at diagnosis was 28.6 weeks and at delivery 34.1 weeks. In none of these patients was amniocentesis used in an attempt to prolong pregnancy. Eight patients (47%) laboured spontaneously and 6 (35%) had labour induced, the in-
Table 3. Detnils of patients with -SubPeote Polyhydrnmnios ~~
Age
Weeks’ gestation Onset
Delivery
Fundal height >dates (weeks)
~
Ultrasound volume
Labour Delivery
Complications
10 3 I NVD 24 23.5 25.1 25.0 25.6 I 2 S NVD APH,UTI 26 S NVD 9 21 28.0 29.2 29 29.0 29.6 4 3 S F 23 31.0 32.0 9 3 I B cs Severe preeclampsia 30.5 32.1 4 34 22.0 32.2 10 4 S B Preeclampsia 21 I 4 I NVD Gestational diabetes 22 30.0 33.3 cs 25 32.5 33.4 8 4 7 4 S cs APH 26 32.0 34.2 8 4 S cs Generalized oedema, no hypertension 34 24.0 34.6 S cs 36.0 36.4 4 4 27 8 3 I cs Hypertension 39 29.0 37.1 S F 4 22 30.5 39.1 I NVD 6 2 15. 24 26.0 39.6 3 I NVD Gestational diabetes 16. 36 34.0 40.2 10 2 cs 17. 30 24.0 41.0 S = spontaneous; I = induced; CS = Caesarean section; F = forceps; NVD = normal vaginal delivery; B = breech; APH = anteparturn haemorrhage; UTI = urinary tract infection; Ultrasound volume, 2=rnoderate, 3 =severe, 4=grOss
1. 2. 3. 4. 5. 6. I. 8. 9. 10. 11. 12. 13. 14.
-
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dications being stillbirth (2) congenital abnormality (2) and patient discomfort near term (2); the other 3 patients were electively delivered by Caesarean section. Tabk 4. Details of tbe Infants Affected by Snbneute PoIyhydmmnios Sex
Birthweight&) 430
Outcome
Fetal abnormality
Anencephaly, spina bifida Alive Patent ductus arteriosus 2. M 1,095 Alive Oesophageal atresia 1,580 3. M tracheo-oesophageal fistula 4. M 1,054 NND None 5. F 1,090 NND Anencephaly 6. F 1,600 NND Nonimmune hydrops fetalis (alphathalassaemia) 7. M 2,490 SB Idiopathic hydrops fetalis 8. F 1,290 SB Anencephaly, meningomyelocele 9. M 2,114 Alive Duodenal and midgut rotation, small bowel volvulus 10. M 1,775 Alive Bowel obstruction perforation of the small bowel - ascites 11. F 3,076 Alive None 12. F 3,166 Alive Abdominal cyst 13. M 4,995 Alive Bilateral hydronephrosis, vesicoureteric reflux None 3,440 Alive 14. F None 3,035 Alive 15. F None 4,200 Alive 16. F None 3,930 Alive 17. M SB = stillbirth; NND = neonatal death; M = male; F = female 1.
F
SB
Glucose tolerance tests were performed in 13 of the 17 mothers and showed a normal result in 10, gestational diabetes in 2 and hypoglycaemia in one. Antepartum haemorrhage occurred twice prior to labour (Cases 2 and 10) but at delivery there were no signs of placental abruption in either case. Six patients had normal vaginal delivery, 2 assisted breech delivery, 2 forceps delivery and 7 were delivered by Caesarean section. The indications for Caesarean section were contracted pelvis (Cases 9, 11 and 17), obstructed labour (Cases 12 and 13), severe preeclampsia (Case 6), and antepartum haemorrhage (Case 10). The perinatal mortality in the subacute group was 35% (6 infants); 5 died because of a fetal malformation and 1 because of immaturity. Eleven infants (65%) had major congenital malformations; anencephaly (l), anencephaly and spina bifida (l), anencephaly and meningomyelocele (l), oesophageal atresia (l), duodenal and midgut rotation, small bowel volvulus (I), bowel obstruction, perforation of the small bowel and ascites (l), abdominal cyst (l),
bilateral hydronephrosis (I), alpha thalassaemiainduced hydrops fetalis (1) nonimmune idiopathic hydrops fetalis (1) patent ductus arteriosus (1). Malformations were diagnosed by ultrasound in all of these infants except the last.
Chronic polyhydrarnnios The time of onset of chronic polyhydramnios (mean 31.6 weeks) was 3 weeks later than that of acute and subacute polyhydramnios, and the maturity at delivery (mean 37.6 weeks) was 4 to 8 weeks greater. The incidence of Caesarean section was similar to that for acute and subacute polyhydramnios but the incidence of diabetes was higher and the incidence of major congenital malformations and the perinatal mortality rate were much lower (14% and 10% respectively). Table 5. Comparison of Results According to Type of Polyhydramnios in Singleton Pregnancies, 1979-1988, Mercy Maternity Hospital Polyhydramnios
Hospital populaAcute Subacute Chronic tion singleton pregnancies (n=19) (n=17) (n=501) (n=51,022) Gestation at: onset (weeks) delivery (weeks)
-
29.0 31.0
28.6 34.1
31.6 37.6
7
7
3
Labour spontaneous induced elective Caesarean section
58% 16%
47% 35%
29%
66.3% 24.6%
26%
18%
29%
9.1%
Delivery vaginally forceps breech Caesarean section
26% 32%
41% 21%
37%
35% 12% 12% 41%
37%
@.8% 22.1% 2.2% 14.9%
Diabetes*
10.5%
11.7%
19.3%
2.9%
Major congenital malformations
63%
65%
14%
4.3%
Perinatal mortality rate 74% 35% 10% * = diabetes; gestational and preexisting
1.9%
Fundal height > dates (weeks)
5%
42%
1%
Table 5 summarizes the details of all cases of acute, subacute and chronic polyhydramnios in singleton pregnancies. Statistics from the total hospital population for the years 1979-1988 are included for comparison. DISCUSSION
There were many similarities between acute and subacute polyhydramnios when it occurred in singleton pregnancies. Patients presented with gross
ELS DESMEDT
polyhydramnios with an average fundal height of 7 weeks greater than normal and the onset was at approximately 29.0 weeks. The groups differed in the speed of accumulation of excessive amniotic fluid and the perinatal mortality rate in the acute group (74%) was double that of the subacute (35%) although the incidence of major malformations was similar in both (63% and 65% respectively) (table 5). In all cases of acute polyhydramnios in singleton pregnancies reported in the literature since 1980, an associated major abnormality of the fetus or a chorioangioma of the placenta is described (5-10). The incidence of major fetal malformation in patients with chronic polyhydramnios at the Mercy Maternity Hospital was 14% and the perinatal mortality rate was lo%, 5 times greater than that of the hospital overall (table 5); it is therefore important that all patients with polyhydramnios have an ultrasound examination performed. Conversely, the presence of excessive amniotic fluid should alert the ultrasonographer to the high possibility of fetal or placental abnormality so that detailed structural examination can be undertaken and amniocentesis or fetal blood sampling for chromosomal analysis be performed when appropriate. Acute polyhydramnios in twins is associated with a very high perinatal mortality rate (virtually 100%) and a low malformation rate (1). The present series revealed a very different picture with acute polyhydramnios in singleton pregnancies where the major malformation rate was very high (63%) and approximately 1 in 4 infants (26V0) survived (table 5). Maternal morbidity associated with acute polyhydramnios was common; apart from pain and respiratory distress inherent in the definition, 6 patients had an antepartum haemorrhage and 2 developed acute renal failure secondary to pressure of the uterus on the ureters. It is important but not always easy to differentiate acute polyhydramnios from placental abruption which is also characterized by a large tender uterus and sudden onset of symp-
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toms. Ultrasonography may be required to distinguish between the 2. Acute polyhydramnios is a rare pregnancy complication (0.04%) with a slightly better outcome in singleton pregnancies. Because of the high perinatal loss, associated maternal morbidity, especially increased risk of acute renal failure, and a high Caesarean section rate (37%) it requires the full attention of both obstetric and paediatric staff.
Acknowledgements We wish to thank our colleagues for access to the clinical records of patients under their care, Dr Christine Acton and her staff for provision of the ultrasound reports, and Miss Mary Sheedy, Medical Records Administrator, for assistance with data collection. This study was funded by the Mercy Maternity Hospital Research Foundation. References 1. Weir PE, Ratten GJ, Beischer NA. Acute polyhydramnios - a complication of monozygous twin pregnancy. Brit J Obstet Gynaecol 1979; 86: 849-853. 2. Zamah NM, Gillieson MS, Walters JH, Hall PF. Sonographic detection of polyhydramnios: A five-year experience. Am J Obstet Gynecol 1982; 143: 523-527. 3. Oats JN, Beischer NA. Gestational Diabetes. Aust NZ J Obstet Gynaecol 1986; 26: 2-10. 4. Carey MP, Ihle BV, Woodward CS, Desmedt E. Ureteric obstruction in the gravid uterus. Aust NZ J. Obstet Gynaecol 1986; 29: 308-313. 5 . Broecker BH, Redwine FO, & Petres RE. Reversal of acute polyhydramnios after fetal renal decompression. Urology 1988 31: 6062. 6. Conaghan CJ, Mac Lean AB, Duff GB, Bashford DH, Hunter LA. Midtrimester acute polyhydramnios and fetal sacrococcygeal teratoma. Obstet Gynecol 1984; 10: 41-44. 7. Ott WJ. Acute polyhydramnios and a fetal ovarian cyst. J Reprod Med 1985; 3 0 887-889. 8. Stevens MJ, Dumon J, Jacquemyn Y et al. Antenatal ultrasonographic diagnosis of trismony 18. Eur J Obstet Gynecol Reprod Biol 1987; 26: 353-358. 9. Van de Bor M, Vermey RA, Van Pel R. Acute polyhydramnios associated with fetal hepatoblastoma. Eur J Obstet Gynecol Reprod Biol 1985; 2 0 65-69. 10. Wong PC, Arulkumaran S, Ratnam SS, Pang M. Acute polyhydramnios and cord presentation - complication of chorioangioma of the placenta - a case report. Int J Gynaecol Obstet 1986; 24: 61-64.
NZ J
Obstet Gynaecol 1990. 30: 3: 191
Acute and Subacute Polyhydramnios in Singleton Pregnancies Els Desmedt', Olivia A. Henry', Lionel H. Steinbergz and Norman A. Beischer' Mercy Maternity Hospital and Department of Obstetrics and Gynaecology, University of Melbourne, Victoria Summary: Over a 10-year period when 51,022 singleton infants were delivered, 19 pregnancies (1 in 2,685) were complicated by acute polyhydramnios, 17 (1 in 3,000) by subacute polyhydramnios and 501 (1 in 102) by chronic polyhydramnios. The incidence of major congenital malformations in singleton pregnancies associated with acute polyhydramnios was 63% and the perinatal mortality rate was 74%. When subacute polyhydramnios occurred in singleton pregnancies, the incidence of major congenital malformations was 65%, similar to acute polyhydramnios, but the perinatal mortality rate was only 35%. The comparable figures for chronic polyhydramnios in singleton pregnancies were a major malformation incidence of 14% and perinatal mortality rate of 10%. The type of onset of polyhydramnios, acute, subacute or chronic is therefore the most important indicator of prognosis. In patients with gross polyhydramnios, acute renal failure must be specifically excluded.
1 . Research Fellow. 2. Registrar. 3. Professor.
associated factors identified. The diagnosis of acute polyhydramnios was made when all of the following criteria were fulfilled: 1) onset of excessive amniotic fluid within 1 week of diagnosis. 2) uterus large for dates. 3) pain due to enlarged uterus. 4) respiratory symptoms. Subacute polyhydramnios was diagnosed when symptoms were more gradual in onset and the remaining criteria listed above were satisfied. Chronic polyhydramnios had a gradual onset and, although the amount of excess amniotic fluid varied enormously, the associated symptoms were usually mild. Ultrasonographic findings were used to classify the degree of polyhydramnios as mild, moderate, severe or gross (2). The associated fetal and maternal complications and the fetal outcome in those pregnancies complicated by acute polyhydramnios were analysed. As there can be clinical confusion with subacute polyhydramnios, the case records of patients with this condition were also reviewed to assess whether o r not they constitute a different disease entity. Glucose tolerance testing (GTT) was performed at 30-32 weeks' gestation using a 50 g glucose load. The criterion for diagnosis of gestational diabetes was the combination of a capillary plasma glucose level of > 9 mmol/l at 1 hour and > 7 mmol/l at 2 hours. The criterion for diagnosis of hypoglycaemia was a glucose level of < 4 mmol/l fasting and < 3 mmol/l at 3 hours (3).
Address for correspondence: Professor N.A. Beischer, Mercy Maternity Hospital, Clarendon Street, East Melbourne, Australia, 3002.
There were 537 cases of polyhydramnios in the 51,022 singleton pregnancies, an incidence of 1.03%;
Acute polyhydramnios is a rare complication of pregnancy characterized by a rapid increase in amniotic fluid volume which results in an enlarged tender uterus that causes pain and respiratory symptoms. The diagnosis is usually made in the second trimester and often results in premature labour. The onset in subacute polyhydramnios is more gradual over 1 or 2 weeks; the associated symptoms are less severe and may be difficult to differentiate from other obstetrical conditions such as premature labour or abruption of the placenta. Polyhydramnios is a clinical diagnosis which can be confirmed by ultrasound or at the moment of rupture of the membranes. Weir et al (1) studied acute polyhydramnios in twins and reported very poor perinatal results with a low incidence of major malformations, but very little attention has been paid to the acute condition in singleton pregnancies. PATIENTS AND METHODS
From January 1, 1979, until December 31, 1988, there were 51,022 singleton deliveries at the Mercy Maternity Hospital, Melbourne; those pregnancies complicated by polyhydramnios were identified and the records reviewed to enable a diagnosis of acute, subacute or chronic polyhydramnios to be made and
RESULTS
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19 (3.570) fulfilled the criteria for diagnosis of acute polyhydramnios, 17 (3.2%) for subacute and 501 (93.3%) for chronic polyhydramnios.
1). Spontaneous labour occurred in 11 patients (58%), and in 3 (15.7%) labour was induced soon after fetal death or major congenital abnormality
Acute polyhydramnios Tables 1 and 2 show the cIinica1details of the 19 infants and mothers. The age of the mothers ranged from 20-44 years; 7 were primigravidas, and 12 multigravidas. Four patients (Cases 1,3,16 and 18) had chronic polyhydramnios in a previous pregnancy and 1 patient (Case 2) developed chronic polyhydramnios in a subsequent pregnancy, a recurrence rate of 26%. None of these 5 pregnancies with chronic polyhydramnios was associated with perinatal loss. Ail patients were admitted to hospital when they presented with gross uterine distension and associated symptoms. The average fundal height was 7 weeks greater than normal and the estimation made by ultrasound showed the severity of polyhydramnios to be moderate in 3 patients, severe in 7 and gross in 8. (One patient did not have an ultrasound examination). There was only one patient (Case 18) who had amniocentesis performed in an attempt to relieve symptoms and prolong pregnancy. Delivery was postponed for 10 weeks by serial amniocentesis; the patient was delivered of a healthy male infant, birth-weight 2,588 g, by Caesarean section at 34 weeks and no major fetal malformation was present. In these patients with acute polyhydramnios the clinical course was fulminant with an average time of onset at 29.0 weeks and delivery at 31 .O weeks (table
Table 2. Details of the Infants Affected by Acute polyhydrarnnios Sex BirthOutcome Fetal abnormality weight (g) None 1. M 1,094 NND None 2. F 1,ooO NND None 1,528 NND 3. M Idiopathic hydrops fetalis 2,420 NND 4. M None 1,775 Alive 5. M Meningomyelocele, 6. F 1.145 NND diaphragmatic hernia, cleft lip and palate Anencephaly, spina 850 SB 7. F bifida, meningomyelocele diaphragmatic hernia Oesophageal atresia 1,260 Alive 8. M None 1,680 Alive 9. F Anencephaly, spina 10. F 1,400 SB bifida Hydrocephaly, teratoma 11. F 2,352 NND of medulla oblongata 1,512 NND Patent ductus arteriosus 12. M 13. F Spina bifida, men2,310 NND ingomyelocele, hydrocephaly, diaphragmatic hernia None 14. F 3,024 Alive 15. F Hydrops fetalis, single 2,530 NND atrium, microcephaly Anencephaly 16. F 1,010 SB Anencephaly 17. F 1,190 SB 18. M None 2,588 Alive 19. F Anencephaly, spina 1,455 NND bifida SB = stillbirth; NND = neonatal death; M = male; F = female
Table 1. Details of Patients witb Acute Polybydramnios Fundal Ultrasound Labour Delivery Complications height volume Onset Delivery >dates (weeks) , - - _.-, 1. 37 21.6 25.6 5 Gestational diabetes, APH 2 S B 2. 24.0 30 26.0 10 3 S NVD Chorioangiorna of the placenta 3. 27 26.6 28.0 10 4 S F Chorioangioma of the placenta, APH 4. 24 29.4 4 I F 30.0 6 Mild preeclampsia, UTI 5. 24 27.0 30.3 13 4 S cs 6. 44 .. 29.0 30.3 11 4 S NVD 7. 29 30.3 30.6 6 4 S NVD 8. 36 29.4 31.1 10 4 cs Acute renal failure, bilateral hydronephrosis, APH 9. 20 31.0 31.2 3 cs APH 10. 28 31.0 31.4 5 3 S F 11. 22 31.0 31.4 7 4 cs 12. 26 31.4 31.6 6 4 cs Acute renal failure, bilateral hydronephrosis, UTI 13. 22 31.0 32.0 4 4 S F Abruptio placentae 14. 23 32.0 32.6 8 2 S cs Insulin dependent diabetes mellitus 15. 32 28.0 33.1 12 3 S NVD 16. 31 33.3 33.5 5 3 I F 17. 33 30.0 34.0 3 3 I NVD APH, abruptio placentae. 18. 31 24.0 34.1 10 2 cs 19. 28 34.0 34.5 6 3 S F S = spontaneous: I = induced: CS = Caesarean section: F = forcens: NVD = normal vaeinal deliverv: .,, B = breech: APH = antepzkum haemorrhage; UTI = urinary tract infection; Ultrasound volume, ?=moderate, 3 =severe, ’ 4=gross Age Weeks’ gestation
ELSDESMEDT
was diagnosed; the other 5 were electively delivered by Caesarean section. Four patients had an anteparturn haemorrhage of unknown origin, 1 prior to labour (Case 8) and 3 (Cases 1 , 3 and 17) during labour. Haemorrhage and abruption of the placenta followed immediately after rupture of the membranes in Case 13. A sixth patient (Case 9) was found to have a retroplacental clot after delivery. One mother had preexisting insulin dependent diabetes mellitus (IDDM). Only 6 of the remaining 18 patients had a glucose tolerance test performed; in 4 the test was normal, 1 showed gestational diabetes and 1 hypoglycaemia. Five patients had a normal vaginal delivery, 1 an assisted breech delivery, 6 a forceps delivery and 7 were delivered by Caesarean section. In 2 mothers (Cases 8 and 12, table l), delivery by Caesarean section was performed to relieve pressure on the ureters and kidneys which had caused acute renal failure. During and after the Caesarean section, the urine output increased and renal function rapidly returned to normal (4). The other indications for Caesarean section were pain and respiratory distress (Cases 5 and 18), ruptured membranes with a closed cervix (Case 9), hydrocephaly with a tumour of the medulla oblongata (Case 11) and fetal distress (Case 14). The perinatal mortality rate with acute polyhydramnios was 74% (14 infants). The cause of death was fetal malformation in 1 1 infants and prematurity in 3. Twelve of the infants (63%) had major congenital malformations: anencephaly (2), anencephaly and spina bifida (2), anencephaly, meningomyelocele, diaphragmatic hernia (l), meningomyelocele, hydrocephaly and diaphragmatic hernia (l), meningomyelocele, diaphragmatic hernia and
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cleft lip and palate (l), hydrocephaly secondary to a teratoma of the medulla oblongata (l), oesophageal atresia (l), hydrops fetalis (l), hydrops fetalis, single atrium, and microcephaly ( l ) , patent ductus arteriosus (1). Malformations were diagnosed by ultrasound in all of these infants, except the last. Only 2 of the 537 cases of polyhydramnios were associated with a chorioangioma of the placenta; both patients developed acute polyhydramnios, at 24.0 and 26.6 weeks’ gestation respectively, and the babies died from immaturity (table 1 , Cases 2 and 3). Subacute polyhydramnios Tables 3 and 4 show the details of the 17 infants and mothers affected by subacute polyhydramnios. The age of the mothers ranged from 21-39 years; 8 were primigravidas and 9 multigravidas. Two patients (Cases 14/15 and 17) (17.6%) had recurrent polyhydramnios. Cases 14 and 15 are the same mother who developed subacute polyhydramnios twice and in Case 17 the patient had chronic polyhydramnios in a previous pregnancy. All 4 pregnancies of these patients resulted in surviving normal infants. All patients with subacute polyhydramnios had gross uterine distension with an average fundal height of 7 weeks greater than normal and were admitted to hospital. Of the 13 patients who had ultrasonography performed at the time of diagnosis, polyhydramnios was described as moderate in 3, severe in 4 and gross in 6. The average gestation at diagnosis was 28.6 weeks and at delivery 34.1 weeks. In none of these patients was amniocentesis used in an attempt to prolong pregnancy. Eight patients (47%) laboured spontaneously and 6 (35%) had labour induced, the in-
Table 3. Detnils of patients with -SubPeote Polyhydrnmnios ~~
Age
Weeks’ gestation Onset
Delivery
Fundal height >dates (weeks)
~
Ultrasound volume
Labour Delivery
Complications
10 3 I NVD 24 23.5 25.1 25.0 25.6 I 2 S NVD APH,UTI 26 S NVD 9 21 28.0 29.2 29 29.0 29.6 4 3 S F 23 31.0 32.0 9 3 I B cs Severe preeclampsia 30.5 32.1 4 34 22.0 32.2 10 4 S B Preeclampsia 21 I 4 I NVD Gestational diabetes 22 30.0 33.3 cs 25 32.5 33.4 8 4 7 4 S cs APH 26 32.0 34.2 8 4 S cs Generalized oedema, no hypertension 34 24.0 34.6 S cs 36.0 36.4 4 4 27 8 3 I cs Hypertension 39 29.0 37.1 S F 4 22 30.5 39.1 I NVD 6 2 15. 24 26.0 39.6 3 I NVD Gestational diabetes 16. 36 34.0 40.2 10 2 cs 17. 30 24.0 41.0 S = spontaneous; I = induced; CS = Caesarean section; F = forceps; NVD = normal vaginal delivery; B = breech; APH = anteparturn haemorrhage; UTI = urinary tract infection; Ultrasound volume, 2=rnoderate, 3 =severe, 4=grOss
1. 2. 3. 4. 5. 6. I. 8. 9. 10. 11. 12. 13. 14.
-
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dications being stillbirth (2) congenital abnormality (2) and patient discomfort near term (2); the other 3 patients were electively delivered by Caesarean section. Tabk 4. Details of tbe Infants Affected by Snbneute PoIyhydmmnios Sex
Birthweight&) 430
Outcome
Fetal abnormality
Anencephaly, spina bifida Alive Patent ductus arteriosus 2. M 1,095 Alive Oesophageal atresia 1,580 3. M tracheo-oesophageal fistula 4. M 1,054 NND None 5. F 1,090 NND Anencephaly 6. F 1,600 NND Nonimmune hydrops fetalis (alphathalassaemia) 7. M 2,490 SB Idiopathic hydrops fetalis 8. F 1,290 SB Anencephaly, meningomyelocele 9. M 2,114 Alive Duodenal and midgut rotation, small bowel volvulus 10. M 1,775 Alive Bowel obstruction perforation of the small bowel - ascites 11. F 3,076 Alive None 12. F 3,166 Alive Abdominal cyst 13. M 4,995 Alive Bilateral hydronephrosis, vesicoureteric reflux None 3,440 Alive 14. F None 3,035 Alive 15. F None 4,200 Alive 16. F None 3,930 Alive 17. M SB = stillbirth; NND = neonatal death; M = male; F = female 1.
F
SB
Glucose tolerance tests were performed in 13 of the 17 mothers and showed a normal result in 10, gestational diabetes in 2 and hypoglycaemia in one. Antepartum haemorrhage occurred twice prior to labour (Cases 2 and 10) but at delivery there were no signs of placental abruption in either case. Six patients had normal vaginal delivery, 2 assisted breech delivery, 2 forceps delivery and 7 were delivered by Caesarean section. The indications for Caesarean section were contracted pelvis (Cases 9, 11 and 17), obstructed labour (Cases 12 and 13), severe preeclampsia (Case 6), and antepartum haemorrhage (Case 10). The perinatal mortality in the subacute group was 35% (6 infants); 5 died because of a fetal malformation and 1 because of immaturity. Eleven infants (65%) had major congenital malformations; anencephaly (l), anencephaly and spina bifida (l), anencephaly and meningomyelocele (l), oesophageal atresia (l), duodenal and midgut rotation, small bowel volvulus (I), bowel obstruction, perforation of the small bowel and ascites (l), abdominal cyst (l),
bilateral hydronephrosis (I), alpha thalassaemiainduced hydrops fetalis (1) nonimmune idiopathic hydrops fetalis (1) patent ductus arteriosus (1). Malformations were diagnosed by ultrasound in all of these infants except the last.
Chronic polyhydrarnnios The time of onset of chronic polyhydramnios (mean 31.6 weeks) was 3 weeks later than that of acute and subacute polyhydramnios, and the maturity at delivery (mean 37.6 weeks) was 4 to 8 weeks greater. The incidence of Caesarean section was similar to that for acute and subacute polyhydramnios but the incidence of diabetes was higher and the incidence of major congenital malformations and the perinatal mortality rate were much lower (14% and 10% respectively). Table 5. Comparison of Results According to Type of Polyhydramnios in Singleton Pregnancies, 1979-1988, Mercy Maternity Hospital Polyhydramnios
Hospital populaAcute Subacute Chronic tion singleton pregnancies (n=19) (n=17) (n=501) (n=51,022) Gestation at: onset (weeks) delivery (weeks)
-
29.0 31.0
28.6 34.1
31.6 37.6
7
7
3
Labour spontaneous induced elective Caesarean section
58% 16%
47% 35%
29%
66.3% 24.6%
26%
18%
29%
9.1%
Delivery vaginally forceps breech Caesarean section
26% 32%
41% 21%
37%
35% 12% 12% 41%
37%
@.8% 22.1% 2.2% 14.9%
Diabetes*
10.5%
11.7%
19.3%
2.9%
Major congenital malformations
63%
65%
14%
4.3%
Perinatal mortality rate 74% 35% 10% * = diabetes; gestational and preexisting
1.9%
Fundal height > dates (weeks)
5%
42%
1%
Table 5 summarizes the details of all cases of acute, subacute and chronic polyhydramnios in singleton pregnancies. Statistics from the total hospital population for the years 1979-1988 are included for comparison. DISCUSSION
There were many similarities between acute and subacute polyhydramnios when it occurred in singleton pregnancies. Patients presented with gross
ELS DESMEDT
polyhydramnios with an average fundal height of 7 weeks greater than normal and the onset was at approximately 29.0 weeks. The groups differed in the speed of accumulation of excessive amniotic fluid and the perinatal mortality rate in the acute group (74%) was double that of the subacute (35%) although the incidence of major malformations was similar in both (63% and 65% respectively) (table 5). In all cases of acute polyhydramnios in singleton pregnancies reported in the literature since 1980, an associated major abnormality of the fetus or a chorioangioma of the placenta is described (5-10). The incidence of major fetal malformation in patients with chronic polyhydramnios at the Mercy Maternity Hospital was 14% and the perinatal mortality rate was lo%, 5 times greater than that of the hospital overall (table 5); it is therefore important that all patients with polyhydramnios have an ultrasound examination performed. Conversely, the presence of excessive amniotic fluid should alert the ultrasonographer to the high possibility of fetal or placental abnormality so that detailed structural examination can be undertaken and amniocentesis or fetal blood sampling for chromosomal analysis be performed when appropriate. Acute polyhydramnios in twins is associated with a very high perinatal mortality rate (virtually 100%) and a low malformation rate (1). The present series revealed a very different picture with acute polyhydramnios in singleton pregnancies where the major malformation rate was very high (63%) and approximately 1 in 4 infants (26V0) survived (table 5). Maternal morbidity associated with acute polyhydramnios was common; apart from pain and respiratory distress inherent in the definition, 6 patients had an antepartum haemorrhage and 2 developed acute renal failure secondary to pressure of the uterus on the ureters. It is important but not always easy to differentiate acute polyhydramnios from placental abruption which is also characterized by a large tender uterus and sudden onset of symp-
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toms. Ultrasonography may be required to distinguish between the 2. Acute polyhydramnios is a rare pregnancy complication (0.04%) with a slightly better outcome in singleton pregnancies. Because of the high perinatal loss, associated maternal morbidity, especially increased risk of acute renal failure, and a high Caesarean section rate (37%) it requires the full attention of both obstetric and paediatric staff.
Acknowledgements We wish to thank our colleagues for access to the clinical records of patients under their care, Dr Christine Acton and her staff for provision of the ultrasound reports, and Miss Mary Sheedy, Medical Records Administrator, for assistance with data collection. This study was funded by the Mercy Maternity Hospital Research Foundation. References 1. Weir PE, Ratten GJ, Beischer NA. Acute polyhydramnios - a complication of monozygous twin pregnancy. Brit J Obstet Gynaecol 1979; 86: 849-853. 2. Zamah NM, Gillieson MS, Walters JH, Hall PF. Sonographic detection of polyhydramnios: A five-year experience. Am J Obstet Gynecol 1982; 143: 523-527. 3. Oats JN, Beischer NA. Gestational Diabetes. Aust NZ J Obstet Gynaecol 1986; 26: 2-10. 4. Carey MP, Ihle BV, Woodward CS, Desmedt E. Ureteric obstruction in the gravid uterus. Aust NZ J. Obstet Gynaecol 1986; 29: 308-313. 5 . Broecker BH, Redwine FO, & Petres RE. Reversal of acute polyhydramnios after fetal renal decompression. Urology 1988 31: 6062. 6. Conaghan CJ, Mac Lean AB, Duff GB, Bashford DH, Hunter LA. Midtrimester acute polyhydramnios and fetal sacrococcygeal teratoma. Obstet Gynecol 1984; 10: 41-44. 7. Ott WJ. Acute polyhydramnios and a fetal ovarian cyst. J Reprod Med 1985; 3 0 887-889. 8. Stevens MJ, Dumon J, Jacquemyn Y et al. Antenatal ultrasonographic diagnosis of trismony 18. Eur J Obstet Gynecol Reprod Biol 1987; 26: 353-358. 9. Van de Bor M, Vermey RA, Van Pel R. Acute polyhydramnios associated with fetal hepatoblastoma. Eur J Obstet Gynecol Reprod Biol 1985; 2 0 65-69. 10. Wong PC, Arulkumaran S, Ratnam SS, Pang M. Acute polyhydramnios and cord presentation - complication of chorioangioma of the placenta - a case report. Int J Gynaecol Obstet 1986; 24: 61-64.
