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Obstetric complications when the fetus has congenital heart disease
volume
110 number 7
August 1, 1971
Americanjournal of Obstetrics and Gynecology
OBSTE.TRICS Obstetric complications when the fetus has congenital heart disease II. Clinical considerations
JEREMY
MACAFEE,
M.D.,
M.R.C.O.G.,
F.R.C.S.
(CLASO.)+
NORMAN
A.
(EDIN.),
DENYS PATH., Victoria,
W.
BEISCHER,
M.D.,
M.G.O.,
F.R.A.C.S.,
F.R.C.O.G.”
FORTUNE,
M.B.,
M.R.C.P.(EDIN.),
F.R.C.S.
M.R.C.
M.C.P.A. AustraEia
In 201 consecutive pregnancies in which the fetus had cardiac abnormalities, the over-all incidence of prenatal complications was less than that in a control series (P < O.OOl), although there was a significant-increase in the percentage of infants who were small for dates (P < O.OiJl). Th ere was no significant difference in the incidence of fetal distress in labor in the 2 groups. Fetal cardiac malformations per se did not result in an increase in the cesarean section rate.
I N ,4 s T u n Y of maternal estriol excretion in 20 pregnancies in which the fetal heart was malformed, the infant was small for dates in 6 of the 9 cases in which low estriol values were rec0rded.l This finding prompted us to establish whether or not the incidences
of intrauterine growth retardation and other prenatal complications are increased when the fetus has congenital heart disease. As far as we are aware, the literature contains no reference to this subject or to the incidence of fetal distress in labor and, hence, the cesarean section rate in such pregnancies. This information is relevant in any discussion about the significance of low maternal estriol excretion when the fetal heart is malformed. Therefore, we have reviewed the
From the Royal Women’s Hospital and Department of Obstetrics and Cynaecology, *Present Hospital, Melbourne,
University
of Melbourne.
address: Mercy Maternity Clarendon Street, East Australia 3002.
891
892
Macafee,
Be&her,
and Fortune
August J. Obstet.
Amer.
1, 1971 Gynec.
Table I. The fetal outcome and birth weights in 201 casesof congenital heart disease Fetal Anomalies of the cnrdiovascular system
Associated extracardiac anomalies
Minor
Nil Nil
Major Major Minor
Major Minor Major
Major
The
weight
of 33 placentas
Above 90th percentile (%)
Placental
weight
Below 10th fierce+
Above 90th percentile (o/o)
Fetal distress (%I
124 41 14 16 6
22.9 23.7 36.4 6.7 50.0
5.6 17.1 21.4 6.2 33.3
50.0 17.1 78.6 43.7 66.7
21.8 29.3 50.0 50.0 83.3
13.7 12.2 7.1 18.7 -
17.5 11.7 23.1 30.8 20.0
6.8 17.6 15.4 15.4 -
201
23.1
9.9
45.3
29.3
12.9
17.8
10.0
Stillbirths (%I
tile (%)
was not recorded.
Method
The diagnosis of congenital heart disease in those infants who died was established at autopsy. The diagnosis in the survivors was made by a specialist cardiologist aided by cardiac catheterization and the findings at corrective operation. Deaths during the first 6 months of life have been included with the neonatal deaths. Multiple pregnancies were excluded. The ‘201 caseswere divided into 5 groups according to the severity of the abnormality in the cardiovascular systemand the presence or absence of anomalies in other systems (Table I). The types of defects in the largest group where no extracardiac anomalies were present are shown in Table II. This series of 201 cases includes the 20 reported previouslyl in which maternal urinary estriol assayswere performed. and
Below 10th percentik (%)
Total No. Of cases
obstetric records of 201 consecutive patients who were delivered of fetuseswith congenital heart diseaseat the Royal Women’s Hospital, Melbourne, during the 13 years from 1958 to 1970. This report presents the findings in these patients.
Results
weight
Neonatal and infant deaths (b/o)
comment
Incidence. During the period reviewed, the incidence of fetal heart abnormality diagnosed in our hospital was 1 in 459 births, there having been 92,355 patients delivered during these 13 years. The over-all incidence of congenital heart diseaseis now calculated to be approximately 8 per 1,000 live births,2 so it would appear that only 25 per cent of
Table II. Types of major anomalies of the cardiovascular system in 124 fetuses without extracardiac anomalies Type of anomaly Complete transposition of the great vessels Hypoplasia of the Ieft ventricle including mitral and aortic atresia and endocardial fibroelastosis Significant ventricular septal defect Aortic stenosis Fallot’s tetrad Pulmonary atresia Tricuspid atresia Atrioventricularis communis Patent ductus arteriosus Coarctation of aorta Anomalous drainage of the pulmonary veins Pulmonary stenosis Truncus arteriosus Double aortic arch Large atria1 septal defect Miscellaneous
Total Figures
1
No. of cases 19
18 (1) 17 (2) 9 7 (21 7 6 4 (2) 4 2 2 1 1 1 24 124
in parentheses
denote
number
of stillbirths.
casesare recognized in obstetric institutions. The high death rate in the present series (Table I) indicates that obstetric statistics are concerned mainly with very severe fetal heart defects and those in which the malformation is an incidental finding at autopsy. Prenatal complications (Table III). In the group of 165 casesin which the fetus had an isolated cardiac defect, the incidence of “normal” pregnancy (60 per cent) was high in comparison with that in the control series3(P < O.OOl), and, therefore, it seems reasonable to conclude that congenital heart
Volume
110
Number
7
Obstetric
complications
with fetal heart disease
893
Table III. Obstetric complications in 201 singleton pregnancies resdting in infants with cardiac malformations Cardiouascular Without cxtfacardiac defect (165) Prenatal
comfilication
Prolonged pregnancy Hypertension Pre-eclampsia Antepartum hemorrhage Anemia (Hemoglobin < 10 Gm./lOO ml.) Urinary tract infection and renal disease Diabetes mellitus Polyhydramnios Rhesus immunization Rubella Normal pregnancy (none of the above) *In
the
control
seri~s,~
patien:s
known
in the
No.
%
20 18 17 15 9 a 7 4 4
12.1 10.9 10.3 9.1 5.5 4.8 4.2 2.4 2.4 0.6 60.0
9: first
trimester
to have
diabetes
malformation Control series (597)” ...-of No. [ 10
With extracardiac defects (36) No.
(
%
1 1 5 2 2 1 2 10 3 4 12 mellitus
2.8 2.8 13.9 5.5 5.5 2.8 5.5 27.8 8.3 11.1 33.3 and
rhesus
a7 72 65 12 88 25 6 1
I46 12.1 IO.9 ?.O 14.7 ‘I.2 I .o 0.2
23;
immunization
38.5
were
-.-._l_ excluded.
Table IV. Maternal age and parity in pregnancies in which the fetus had cardiac abnormalities and in the controI series -Maternal age and parity 19 20 30 40
years to 29 to 39 years
and below years years and above
Cardiac
series
Control
series
._I
No.
%
No.
%
27 107 60 7
13.4 53.2 29.8 3.5
97 354 133 13
16.2 59.3 22.3 2.2
78 100 23
38.8 49.7 11.4
256 316 25
42.8 52.9 4.2
201
99.9
597
99.9
Parity Primipara Para 1 to 4 Para 5 and above Totals
diseaseof the fetus is not characterized by an increase in maternal prenatal complications. We have no explanation for this unexpected finding, particularly as the distribution of maternal age and parity was similar in the two groups (Table IV). In comparison with that in the control series, there was a high incidence of antepartum hemorrhage (P = 0.001)) and perinatal deaths occurred in 10 of these 15 cases. The cardiac anomalies were an incidental finding at autopsy in these infants. The incidence of polyhydramnios was only 2.4 per cent in these casesin which congenital heart diseasewas the sole abnormality, which does not support Greenhill’s” statement that cardiac malformations such as aortic stenosis are a cause of polyhydramnios. However, as
expected, when there was also an extracardisc defect, the incidence of polyhydramnios was very high (27.8 per cent, P < 0.001). Paradoxically, in the 41 casesin which the infants had minor cardiac malformations, there was a high incidence of obstetric complications which explained the high stillbirth rate (17.1 per cent) in this group (Table I). Fetal distress (Table I). In the 201 pregnancies, the incidence of fetal distressduring labor (a fetal heart rate above 160 or below 120 per minute, the presence of meconium, or both) was 23.1 per cent, which was not significantly different from the figure of 27.6 per cent recorded in the control series.3 Therefore, a fetal cardiac anomaly is not likely to result in an increased useof cesarean section becauseof fetal distressin labor.
894
Macafee,
Beischer, and Fortune
E E 2000
1000
28
30
32
34 GESTATION
36
38
40
42
44
IN WEEKS
Fig. 1. Birth weight and duration of pregnancy in 201 cases of congenital heart disease. A = stillbirth; + = neonatal death; 0 = infant survived. The tenth and ninetieth percentiles for birth weight according to gestational age for this community are shown.5 The incidence of cesarean section was 8.0 per cent or almost double the hospital figure of 4.7 per cent. However, fetal distress was the indication for only 2 of the 16 cesarean sections performed in this series, the remainder being indicated by previous uterine scars (7), diabetes mellitus (2), placenta previa ( 2)) abruptio placentae ( 1) , hypertension (l), and obstructed labor (1). It would appear, therefore, that the higher cesarean section rate was not due to the cardiac anomalies per se. Fetal results (Table I). The over-all stillbirth rate was 9.9 per cent, and most of these deaths were accounted for by prenata1 complications (Table III), severe neural tube deformities (2 cases), and nonimmunologic hydrops fetalis (2 cases). There were, however, 6 cases where no obvious obstetric cause was evident to account for the stillbirth, and in these the defects were atrioventricularis communis (2)) ventricular septal defect (2, 1 of which was large), mitral and aortic atresia (I), and Fallot’s tetrad ( 1). These defects are certainly not characterized by intrauterine death, yet they can-
not be dismissed as being unrelated. The high neonatal and infant death rate is easily understood, considering the severity of the defects (Table II), but it is noteworthy that the birth weight distribution of these deaths showed a wide scatter, suggesting that the severity of the cardiac defect was not directly related to the degree of intrauterine growth retardation (Fig. 1) .
Birth weight and incidence of prematurity (Table I). There were 59 infants (29.3 per cent) in this series with birth weights below the tenth percentile for the period of gestation5 (Fig. 1, P < 0.001). This supports previous reports that congenital heart disease is associated with a high incidence of intrauterine growth retardation.+* When there was an associated extracardiac defect, more than 50 per cent of infants were small for dates. The fallibility of the clinician in the diagnosis of growth retardation before the birth of an infant was evident in this as in other series”; in only 14 of the 201 patients was a clinical diagnosis of fetal growth retardation made before the infant was born. The incidence of delivery before 37 weeks’
Obstetric
complications
with
fetal
heart
disease
895
+ .
1000-
+
. +
+
_ m
+
800-
.
+
+
+
% 9g
++
*
.
+
+
* + +*+ + . + +++“+*+. +‘I + ” +.+ I... +-*r;‘~~~ . ..+ ++ + .+ . *ti+* . . ++ +
.C
+
600-
A 4 z : cc 400-b i:
.+ +. ++
. .
-t* .+
+.
* *
+ +*r .
l
+
+
+.
+
.
.
.
200’
. .
28
30
36
34
32
GESTATION
Fig. 2.
Placental weights in 168 cases of congenital death; l = infant survived. The tenth and ninetieth to gestational age for this community are shown.*0
gestation was 27.9 per cent (56 of 201) which was double that of the over-all hospital population; the figure fell to 20 per cent when cases with extracardiac defects were excluded. Placental weight (Table I). The placental weights according to the period of gestation demonstrated a fairly wide distribution (Fig. 21. There was a higher than expected proportion of cases above the ninetieth percen tilelo in some groups, and this was accounted for by 4 cases of hydrops fetalis. In this series, a small-for-dates infant was a more common
38
40
42
IN WEEKS
heart disease. A = stillbirth; + = neonatal percentiles for placental weight according
finding (29.3 per cent) than was a small placenta ( 17.8 per cent). This study has shown that when the fetal heart is malformed there is no increase in the rates of prenatal complications or fetal distress in labor. Therefore, fetal cardiac defects are not more likely to result in an increased use of cesarean section. We wish to thank the medical staff of the hospital for their co-operation in this study and Mr. J. S&ramp for preparation of the illustrations. Dr. A. W. Venables was the cardiologist responsible for the care of the infants in this series.
REFERENCES
1. Macafee, J., Beischer, N. A., Fortune, D. W., and Brown, J. B.: AMER. J. OBSTET. GYNEC. 110: 653, 1971. L’. Carlgren, L. E.: Proc. Ass. Europ. Paediat. Cardiol. 5: 2, 1969. :1. Beischer, N. A., Bhargava, V. L., Brown, J. B., and Smith, M. A.: J. Obstet. Gynaec. Brit. Comm. 75: 1021, 1968. -4. Grecnhill, J. P.: Obstetrics, Philadelphia, 1966, W. B. Saunders Company, p. 827. i. Kitchen, W. H.: Australian Paediat. J. 4: 29, 1968.
6. 7.
8. 9.
10.
Campbell, M.: Brit. Med. J. 2: 895, 1965. Butler. N. R.. and Alberman. E. D.: Perinatal Proble’ms, Edinburgh, 1969, ‘E. & S. I,ivingstone, Ltd., p. 305. Howie, R. N., and Phillips, L. 1.: New Zeal. Med. J. 71: 65, 1970. MacLeod, S. C., Brown, J. B., Beischer, N. A., and Smith, M. A.: Amt. New Zeal. J. Obstet. Gynaec. 7: 25, 1967. Kitchen, W. H.: .i\ustralian Paediat. J. 4:
105, 1968.
110 number 7
August 1, 1971
Americanjournal of Obstetrics and Gynecology
OBSTE.TRICS Obstetric complications when the fetus has congenital heart disease II. Clinical considerations
JEREMY
MACAFEE,
M.D.,
M.R.C.O.G.,
F.R.C.S.
(CLASO.)+
NORMAN
A.
(EDIN.),
DENYS PATH., Victoria,
W.
BEISCHER,
M.D.,
M.G.O.,
F.R.A.C.S.,
F.R.C.O.G.”
FORTUNE,
M.B.,
M.R.C.P.(EDIN.),
F.R.C.S.
M.R.C.
M.C.P.A. AustraEia
In 201 consecutive pregnancies in which the fetus had cardiac abnormalities, the over-all incidence of prenatal complications was less than that in a control series (P < O.OOl), although there was a significant-increase in the percentage of infants who were small for dates (P < O.OiJl). Th ere was no significant difference in the incidence of fetal distress in labor in the 2 groups. Fetal cardiac malformations per se did not result in an increase in the cesarean section rate.
I N ,4 s T u n Y of maternal estriol excretion in 20 pregnancies in which the fetal heart was malformed, the infant was small for dates in 6 of the 9 cases in which low estriol values were rec0rded.l This finding prompted us to establish whether or not the incidences
of intrauterine growth retardation and other prenatal complications are increased when the fetus has congenital heart disease. As far as we are aware, the literature contains no reference to this subject or to the incidence of fetal distress in labor and, hence, the cesarean section rate in such pregnancies. This information is relevant in any discussion about the significance of low maternal estriol excretion when the fetal heart is malformed. Therefore, we have reviewed the
From the Royal Women’s Hospital and Department of Obstetrics and Cynaecology, *Present Hospital, Melbourne,
University
of Melbourne.
address: Mercy Maternity Clarendon Street, East Australia 3002.
891
892
Macafee,
Be&her,
and Fortune
August J. Obstet.
Amer.
1, 1971 Gynec.
Table I. The fetal outcome and birth weights in 201 casesof congenital heart disease Fetal Anomalies of the cnrdiovascular system
Associated extracardiac anomalies
Minor
Nil Nil
Major Major Minor
Major Minor Major
Major
The
weight
of 33 placentas
Above 90th percentile (%)
Placental
weight
Below 10th fierce+
Above 90th percentile (o/o)
Fetal distress (%I
124 41 14 16 6
22.9 23.7 36.4 6.7 50.0
5.6 17.1 21.4 6.2 33.3
50.0 17.1 78.6 43.7 66.7
21.8 29.3 50.0 50.0 83.3
13.7 12.2 7.1 18.7 -
17.5 11.7 23.1 30.8 20.0
6.8 17.6 15.4 15.4 -
201
23.1
9.9
45.3
29.3
12.9
17.8
10.0
Stillbirths (%I
tile (%)
was not recorded.
Method
The diagnosis of congenital heart disease in those infants who died was established at autopsy. The diagnosis in the survivors was made by a specialist cardiologist aided by cardiac catheterization and the findings at corrective operation. Deaths during the first 6 months of life have been included with the neonatal deaths. Multiple pregnancies were excluded. The ‘201 caseswere divided into 5 groups according to the severity of the abnormality in the cardiovascular systemand the presence or absence of anomalies in other systems (Table I). The types of defects in the largest group where no extracardiac anomalies were present are shown in Table II. This series of 201 cases includes the 20 reported previouslyl in which maternal urinary estriol assayswere performed. and
Below 10th percentik (%)
Total No. Of cases
obstetric records of 201 consecutive patients who were delivered of fetuseswith congenital heart diseaseat the Royal Women’s Hospital, Melbourne, during the 13 years from 1958 to 1970. This report presents the findings in these patients.
Results
weight
Neonatal and infant deaths (b/o)
comment
Incidence. During the period reviewed, the incidence of fetal heart abnormality diagnosed in our hospital was 1 in 459 births, there having been 92,355 patients delivered during these 13 years. The over-all incidence of congenital heart diseaseis now calculated to be approximately 8 per 1,000 live births,2 so it would appear that only 25 per cent of
Table II. Types of major anomalies of the cardiovascular system in 124 fetuses without extracardiac anomalies Type of anomaly Complete transposition of the great vessels Hypoplasia of the Ieft ventricle including mitral and aortic atresia and endocardial fibroelastosis Significant ventricular septal defect Aortic stenosis Fallot’s tetrad Pulmonary atresia Tricuspid atresia Atrioventricularis communis Patent ductus arteriosus Coarctation of aorta Anomalous drainage of the pulmonary veins Pulmonary stenosis Truncus arteriosus Double aortic arch Large atria1 septal defect Miscellaneous
Total Figures
1
No. of cases 19
18 (1) 17 (2) 9 7 (21 7 6 4 (2) 4 2 2 1 1 1 24 124
in parentheses
denote
number
of stillbirths.
casesare recognized in obstetric institutions. The high death rate in the present series (Table I) indicates that obstetric statistics are concerned mainly with very severe fetal heart defects and those in which the malformation is an incidental finding at autopsy. Prenatal complications (Table III). In the group of 165 casesin which the fetus had an isolated cardiac defect, the incidence of “normal” pregnancy (60 per cent) was high in comparison with that in the control series3(P < O.OOl), and, therefore, it seems reasonable to conclude that congenital heart
Volume
110
Number
7
Obstetric
complications
with fetal heart disease
893
Table III. Obstetric complications in 201 singleton pregnancies resdting in infants with cardiac malformations Cardiouascular Without cxtfacardiac defect (165) Prenatal
comfilication
Prolonged pregnancy Hypertension Pre-eclampsia Antepartum hemorrhage Anemia (Hemoglobin < 10 Gm./lOO ml.) Urinary tract infection and renal disease Diabetes mellitus Polyhydramnios Rhesus immunization Rubella Normal pregnancy (none of the above) *In
the
control
seri~s,~
patien:s
known
in the
No.
%
20 18 17 15 9 a 7 4 4
12.1 10.9 10.3 9.1 5.5 4.8 4.2 2.4 2.4 0.6 60.0
9: first
trimester
to have
diabetes
malformation Control series (597)” ...-of No. [ 10
With extracardiac defects (36) No.
(
%
1 1 5 2 2 1 2 10 3 4 12 mellitus
2.8 2.8 13.9 5.5 5.5 2.8 5.5 27.8 8.3 11.1 33.3 and
rhesus
a7 72 65 12 88 25 6 1
I46 12.1 IO.9 ?.O 14.7 ‘I.2 I .o 0.2
23;
immunization
38.5
were
-.-._l_ excluded.
Table IV. Maternal age and parity in pregnancies in which the fetus had cardiac abnormalities and in the controI series -Maternal age and parity 19 20 30 40
years to 29 to 39 years
and below years years and above
Cardiac
series
Control
series
._I
No.
%
No.
%
27 107 60 7
13.4 53.2 29.8 3.5
97 354 133 13
16.2 59.3 22.3 2.2
78 100 23
38.8 49.7 11.4
256 316 25
42.8 52.9 4.2
201
99.9
597
99.9
Parity Primipara Para 1 to 4 Para 5 and above Totals
diseaseof the fetus is not characterized by an increase in maternal prenatal complications. We have no explanation for this unexpected finding, particularly as the distribution of maternal age and parity was similar in the two groups (Table IV). In comparison with that in the control series, there was a high incidence of antepartum hemorrhage (P = 0.001)) and perinatal deaths occurred in 10 of these 15 cases. The cardiac anomalies were an incidental finding at autopsy in these infants. The incidence of polyhydramnios was only 2.4 per cent in these casesin which congenital heart diseasewas the sole abnormality, which does not support Greenhill’s” statement that cardiac malformations such as aortic stenosis are a cause of polyhydramnios. However, as
expected, when there was also an extracardisc defect, the incidence of polyhydramnios was very high (27.8 per cent, P < 0.001). Paradoxically, in the 41 casesin which the infants had minor cardiac malformations, there was a high incidence of obstetric complications which explained the high stillbirth rate (17.1 per cent) in this group (Table I). Fetal distress (Table I). In the 201 pregnancies, the incidence of fetal distressduring labor (a fetal heart rate above 160 or below 120 per minute, the presence of meconium, or both) was 23.1 per cent, which was not significantly different from the figure of 27.6 per cent recorded in the control series.3 Therefore, a fetal cardiac anomaly is not likely to result in an increased useof cesarean section becauseof fetal distressin labor.
894
Macafee,
Beischer, and Fortune
E E 2000
1000
28
30
32
34 GESTATION
36
38
40
42
44
IN WEEKS
Fig. 1. Birth weight and duration of pregnancy in 201 cases of congenital heart disease. A = stillbirth; + = neonatal death; 0 = infant survived. The tenth and ninetieth percentiles for birth weight according to gestational age for this community are shown.5 The incidence of cesarean section was 8.0 per cent or almost double the hospital figure of 4.7 per cent. However, fetal distress was the indication for only 2 of the 16 cesarean sections performed in this series, the remainder being indicated by previous uterine scars (7), diabetes mellitus (2), placenta previa ( 2)) abruptio placentae ( 1) , hypertension (l), and obstructed labor (1). It would appear, therefore, that the higher cesarean section rate was not due to the cardiac anomalies per se. Fetal results (Table I). The over-all stillbirth rate was 9.9 per cent, and most of these deaths were accounted for by prenata1 complications (Table III), severe neural tube deformities (2 cases), and nonimmunologic hydrops fetalis (2 cases). There were, however, 6 cases where no obvious obstetric cause was evident to account for the stillbirth, and in these the defects were atrioventricularis communis (2)) ventricular septal defect (2, 1 of which was large), mitral and aortic atresia (I), and Fallot’s tetrad ( 1). These defects are certainly not characterized by intrauterine death, yet they can-
not be dismissed as being unrelated. The high neonatal and infant death rate is easily understood, considering the severity of the defects (Table II), but it is noteworthy that the birth weight distribution of these deaths showed a wide scatter, suggesting that the severity of the cardiac defect was not directly related to the degree of intrauterine growth retardation (Fig. 1) .
Birth weight and incidence of prematurity (Table I). There were 59 infants (29.3 per cent) in this series with birth weights below the tenth percentile for the period of gestation5 (Fig. 1, P < 0.001). This supports previous reports that congenital heart disease is associated with a high incidence of intrauterine growth retardation.+* When there was an associated extracardiac defect, more than 50 per cent of infants were small for dates. The fallibility of the clinician in the diagnosis of growth retardation before the birth of an infant was evident in this as in other series”; in only 14 of the 201 patients was a clinical diagnosis of fetal growth retardation made before the infant was born. The incidence of delivery before 37 weeks’
Obstetric
complications
with
fetal
heart
disease
895
+ .
1000-
+
. +
+
_ m
+
800-
.
+
+
+
% 9g
++
*
.
+
+
* + +*+ + . + +++“+*+. +‘I + ” +.+ I... +-*r;‘~~~ . ..+ ++ + .+ . *ti+* . . ++ +
.C
+
600-
A 4 z : cc 400-b i:
.+ +. ++
. .
-t* .+
+.
* *
+ +*r .
l
+
+
+.
+
.
.
.
200’
. .
28
30
36
34
32
GESTATION
Fig. 2.
Placental weights in 168 cases of congenital death; l = infant survived. The tenth and ninetieth to gestational age for this community are shown.*0
gestation was 27.9 per cent (56 of 201) which was double that of the over-all hospital population; the figure fell to 20 per cent when cases with extracardiac defects were excluded. Placental weight (Table I). The placental weights according to the period of gestation demonstrated a fairly wide distribution (Fig. 21. There was a higher than expected proportion of cases above the ninetieth percen tilelo in some groups, and this was accounted for by 4 cases of hydrops fetalis. In this series, a small-for-dates infant was a more common
38
40
42
IN WEEKS
heart disease. A = stillbirth; + = neonatal percentiles for placental weight according
finding (29.3 per cent) than was a small placenta ( 17.8 per cent). This study has shown that when the fetal heart is malformed there is no increase in the rates of prenatal complications or fetal distress in labor. Therefore, fetal cardiac defects are not more likely to result in an increased use of cesarean section. We wish to thank the medical staff of the hospital for their co-operation in this study and Mr. J. S&ramp for preparation of the illustrations. Dr. A. W. Venables was the cardiologist responsible for the care of the infants in this series.
REFERENCES
1. Macafee, J., Beischer, N. A., Fortune, D. W., and Brown, J. B.: AMER. J. OBSTET. GYNEC. 110: 653, 1971. L’. Carlgren, L. E.: Proc. Ass. Europ. Paediat. Cardiol. 5: 2, 1969. :1. Beischer, N. A., Bhargava, V. L., Brown, J. B., and Smith, M. A.: J. Obstet. Gynaec. Brit. Comm. 75: 1021, 1968. -4. Grecnhill, J. P.: Obstetrics, Philadelphia, 1966, W. B. Saunders Company, p. 827. i. Kitchen, W. H.: Australian Paediat. J. 4: 29, 1968.
6. 7.
8. 9.
10.
Campbell, M.: Brit. Med. J. 2: 895, 1965. Butler. N. R.. and Alberman. E. D.: Perinatal Proble’ms, Edinburgh, 1969, ‘E. & S. I,ivingstone, Ltd., p. 305. Howie, R. N., and Phillips, L. 1.: New Zeal. Med. J. 71: 65, 1970. MacLeod, S. C., Brown, J. B., Beischer, N. A., and Smith, M. A.: Amt. New Zeal. J. Obstet. Gynaec. 7: 25, 1967. Kitchen, W. H.: .i\ustralian Paediat. J. 4:
105, 1968.