The incidence of fetal asphyxia in six hundred high-risk monitored pregnancies J.
A.
S. R.
LOW,
M.D.
PANCHAM,
D.
WORTHINGTON,
R.
W.
Kingston,
M.D. M.D.
BOSTON, Ontario,
M.D. Canada
Six hundred high-risk monitored obstetric patients were reviewed for evidence of fetal asphyxia at delivery. The over-all incidence was 20 per cent, i.e., 8 times the incidence in a normal obstetric population. Highly significant indicators of risk for asphyxia were severe toxemia (79 per cent), prematurity with further medical or obstetric complications (36 per cent), and clinical fetal distress, particularly meconium staining with fetal heart rate abnormality (33 per cent). All obstetric, medical, or gestational complications in this review were associated with a normal obstetric population.
an increased
risk
for fetal
Methods Six hundred monitored high-risk pregnancies were analyzed for evidence of fetal asphyxia at delivery.
and of Paediatrics,
Presented at the Thirtieth Annual Meeting of the Society of Obstetricians and Gynaecologists of Canada, Murray Bay, Quebec, Canada, June 20-23, 1974. Reprint requests: Dr. J. A. Low, Department Obstetrics and Gynaecology, Queen’s University, Kingston, Ontario, Canada.
when
compared
to that
in
The definition of fetal asphyxia was an umbilical cord artery buffer base of less than 36.1 mEq. per 1iter.l Uterine contractions were measured by means of an intra-amniotic catheter. Instantaneous fetal rate was obtained from a scalp electrode. Serial acid base assessments (pH, Pcoz, buffer base PoZ) were performed on fetal capillary blood during labor as indicated and on the umbilical cord artery and vein at delivery. The indications for monitoring were the standard obstetric criteria of risk. Some patients had more than one problem; therefore, the number of indications exceeds the number of patients. There were two main categories of indications for monitoring. The first group included those patients in whom a high-risk factor was present, i.e., a maternal obstetric, medical, or fetal complication; these fetuses presumably had an increased potential for morbidity and death. The second group included patients who displayed abnormal uterine activity, had a failed induction of labor, or were trials of labor for previous cesarean section or cephalopelvic disproportion. Abnormal uterine activity included patients with failure to progress in the absence of fetopelvic disproportion or abnormal response to oxytocin stimulation. Failed induction included those patients with spontaneous or artificially ruptured membranes and
THE co N c E PT of the high-risk pregnancy has received extensive endorsement in the recent literature. The clinical implication of risk is an increase in perinatal morbidity and death. Morbidity is difficult to define and has in the past been based on low Apgar scores, early neonatal behavior or longterm central nervous system dysfunction. The increased awareness of this intrapartum risk has led to the widespread use of fetal monitoring units. The purpose of this review of a high-risk monitored obstetric population is to determine the risk of fetal asphyxia at delivery as identified by metabolic acidosis and expressed as an umbilical cord artery buffer base.
From the Department of Obstetrics Gynaecology and the Department Queen’s University.
usphyxia
of
456
Volume Number
121 4
in whom labor was not established in 24 hours despite at least one course of clinical oxytocin stimulation. The fetuses in these patients were presumably normal but at risk because of these abnormal labor and delivery factors. Results The incidence of fetal asphyxia at delivery in 600 high-risk monitored pregnancies was 20 per cent (Table I). Of the 834 indications for monitoring, 22.5 per cent were associated with fetal asphyxia. Six hundred and seventy-four antepartum or intrapartum indices of risk were associated with a 24 per cent incidence of fetal asphyxia; of the 160 in the abnormal labor group, 18 per cent had asphyxia (Table II) . The incidence of fetal asphyxia in patients with high-risk factors is outlined in Table III. Clinical fetal distress was present on 198 occasions, 53 (27 per cent) of which were associated with asphyxia. Table IV shows the incidence of fetal asphyxia, increasing from 10 per cent with clinical fetal heart rate abnormality to 28 per cent with meconium staining of the amniotic fluid and 33 per cent when both criteria were present. The incidence of fetal asphyxia in 64 premature ( < 37 weeks) infants was 31 per cent. Table V shows that there was a higher incidence of fetal asphyxia with prematurity when associated with a further complication, such as toxemia or antepartum hemorrhage, than with prematurity alone. In 98 postterm pregnancies (> 42 weeks), the incidence of fetal asphyxia was 18 per cent. The incidence of asphyxia was no greater in the 27 patients who were 43 weeks’ gestation or greater when compared to the 71 who were 42 completed weeks of gestational age. Table VI shows that the presence of meconium in the amniotic fluid was associated with 27 per cent fetal asphyxia as compared to 12 per cent with clear fluid. The gestational abnormality group was too small to permit detailed analysis (Table III). Of 38 cases of suspected intrauterine growth retardation, the diagnosis was confirmed in 20 cases, of which 7 infants had asphyxia (< tenth percentile on the weight-gestational scale of Gruenwald). Of the remaining 18 without intrauterine growth retardation, only 3 had fetal asphyxia. There were 14 breech presentations, of which 7 infants developed asphyxia. Each breech infant had one or more additional complications so that the development of asphyxia was associated with a combination of
Fetal
asphyxia
Table I. Incidence obstetric
in monitored
pregnancies
of fetal asphyxia
in a high-risk
population Fetal
Patients Indications
for
monitoring
No.
600 834
119 188
of fetal asphyxia for monitoring
indication
Indication
for
High-risk Abnormal
monitoring
1
No.
Total
20 22.5
per
I-
674 160
pregnancies labor group
asphyxia
7%
Total
Table II. Incidence
159 29
24 18
834
Table III. Incidence patients
with
of fetal asphyxia indices
high-risk
in obstetric
1 Fetal High-risk
indices
1 No.
Clinical fetal distress Abnormal maturity Prematurity Postmaturity Gestational abnormality Suspect intrauterine growth retardation Breech Twins Rh isoimmunization Maternal medical abnormality Diabetes Hypertension Obstetric complications Toxemia Antepartum hemorrhage Other Total
Table IV. Incidence clinical
457
asphyxia
IA;o.
198
53
27
64 98
20 17
31 18
38 14 12 21
10 7 3 2
26 50 14 10
32 30
6 7
19 23
100 46 14 674
25 10 1
25 22 7
of fetal asphyxia
in
fetal distress 1 “eta: Clinical
fetal
Clinical fetal heart abnormality Meconium staining fluid Meconium staining
distress
asphz
No.
rate 30
3
10
113
32
28
55
18
33
of amniotic plus
heart rate abnormality
fetal
458
Low et al.
Table V. Incidence of the premature
February Am. .I. Obstet.
of fetal asphyxia group
in 64 patients
Fetal
Prematurity Prematurity
I NO.
I No.
14 50
2 18
alone with complications
Table VII. Incidence 100 cases of toxemia
asphyxia 1
NO.
14 36
Mild toxemia Severe toxemia Totai
Table VIII. of fetal asphyxia pregnancies
98 postterm
No.
No.
Clear Meconium
57 41
7 11
patients
in
asphyxia
No.
71 19 100
Incidence abnormal
with
I
1
%
10 15
asphyxia I
Abnormal
of fetal asphyxia labor
labor
Failed induction Abnormal uterine activity Cephalopelvic disproportion Trial of labor-previous cesarean section Total
% 12 17
98
--
14 79
in
Fetal
Fetal
Amniotic fluid
in
Fetal
%
64
Table VI. Incidence
of fetal asphyxia
15. 1975 Cynrcol.
asphyxia
No.
No.
3P a7 30
8 15 4
% 25 17 13
11 160
?
18
I
factors and not the abnormal presentation alone. There were 62 diabetic or hypertensive complications of pregnancy in the study. In 32 diabetic patients, the incidence of fetal asphyxia was 19 per cent. In 18 Class A pregnant diabetic patients, 3 had asphyxia; in 14 cases of Classes B, C, D diabetes combined, 3 had asphyxia. In 30 pregnancies complicated by hypertension (blood pressure 140/90) without toxemia, 7 infants (23 per cent) had fetal asphyxia. The incidence of fetal asphyxia in 100 patients with toxemia was 25 per cent. Table VII shows a marked increase in fetal asphyxia from 14 per cent in mild toxemia to 79 per cent in severe toxemia (blood pressure 160, systolic; 110 or greater, diastolic, proteinuria, 5 Gm. per 24 hours or more). In the 15 cases of severe toxemia with asphyxia, the fetus was further complicated in 9 cases by intrauterine growth retardation and in 6 by prematurity. Antepartum hemorrhage was a primary or associated complication in 46 cases, 10 (22 per cent) of which had fetal asphyxia. In 14 cases where definite pathology was identified (abruptio placentae, major infarcts, circumvallate placenta, vasa previa), 6 had fetal asphyxia. In the remaining 32 cases where no pathologic explanation of bleeding was established, only 4 had asphyxia. The abnormal labor group is outlined in Table VIII. There were 32 cases of failed induction of
labor was present in 23 cases; 6 of these had asphyxia at delivery. There were 9 patients who had labor induced without any major complications; 2 developed asphyxia. In 87 cases of abnormal uterine activity, there were 15 ( 17 per cent) who had fetal asphyxia. In 30 patients who had trials of labor for fetopelvic disproportion, 4 (13 per cent) had asphyxia.
labor,
delivery.
of
which
An
8
(25
obstetric
per
cent)
indication
Comment Standard obstetric criteria of risk have been based on the clinical observation of the association between antepartum and intrapartum complications and subsequent outcome of the fetus. This review is an attempt to assess these factors on the basis of biochemical evidence of asphyxia at delivery. Because there are no widely accepted laboratory criteria of fetal asphyxia, the definition used in this review was the identification of metabolic acidosis based on an umbilical cord artery buffer base of less than 36.1 mEq. per liter. This figure represents 2 standard deviations below the mean in a previously reported normal obstetric popu1ation.l Every complication of pregnancy examined in this review was associated with an increased risk of fetal asphyxia at delivery. The over-all incidence of asphyxia in this high-risk group was 8 times greater than in the normal obstetric population. Clinical
had
asphyxia
at
with
for
induction
of
Meconium
criteria
a high
of
fetal
incidence
staining
of the
distress
of
were
asphyxia
amniotic
fluid
associated
at
delivery.
showed
an
Volume Number
121 4
elevenfold increase in asphyxia when compared to the incidence in the normal population with clear fluid. The low incidence of asphyxia when only clinical fetal heart rate abnormalities were present re-emphasizes the difficulty of interpretation or fetal heart rate patterns by auscultation as an indicator of asphyxia. There was an increased incidence of fetal asphyxia in premature infants. However, this was probably principally a reflection of other obstetric, medical, and gestational complications. Postterm pregnancies had a sevenfold increase in asphyxia when compared to the incidence in the normal term pregnancies. The increased incidence of fetal asphyxia with meconium staining of the amniotic fluid points to the value of this observation as an additional indicator of risk in this group. There is evidence in the literature to suggest an increased perinatal mortality rate after 43 weeks’ gestation”; however, in this review, there was no further increase in the incidence of asphyxia past 43 weeks’ gestation. The difficulty in the diagnosis of intrauterine growth retardation is emphasized by about a 50 per cent predictive accuracy. However, when the diagnosis is correct, there is a marked increase in
Fetal
asphyxia
in monitored
pregnancies
459
the incidence of asphyxia as previously reported and again evidenced in this review.’ Severe toxemia was associated with the highest incidence of fetal asphyxia in this review. Associated factors were intrauterine growth retardation and prematurity. The incidence of fetal asphyxia was higher in cases of antepartum hemorrhage associated with definite pathology when compared to those cases without an identified cause. The significance of maternal medical disorders is shown by the increased risk of fetal asphyxia in obstetric patients whose pregnancies were complicated by diabetes or hypertension. The high risk of the Class A diabetic pregnancy is demonstrated by the presence of asphyxia in 3 fetuses. Abnormal labor was associated with a sevenfold increase in asphyxia. In the failed induction group, the increased incidence of fetal asphyxia might, in part, be related to associated complications. This review has defined and analyzed fetal asphyxia on the basis of an umbilical cord artery buffer base of less than 36.1 mEq. per liter. Every complication studied was associated with an increased incidence of asphyxia. Therefore, highrisk indices have been reasonable predictors of intrapartum asphyxia in this review.
REFERENCES
1.
2.
Low, J. A., Pancham, S. R., Worthington, D., and Boston, R. W.: AM. J. OBSTET. GYNECOL. 120: 862, 1974. Butler, N. R., and Bonham, D. G.: The First Report
of the British Perinatal Mortality Survey, Edinburgh, 1963, E. & S. Livingston, Ltd., Section F, p. 118. 3. Low, J. A., Boston, R. W., and Pancham, S. R.: AM. J. OBSTET. GYNECOL. 113: 351 1972.