312

Tropical and Geographical Medicine

COMPARATIVE STUDIES OF LIVE NEONATES IN MATERNAL SICKLE CELL

HAEMOGLOBINOPATHY IN GHANA
FREDERICK K. ADDAI1, JOHN B. WILSON2 and FRANK JK QUASHIE1
1

Department of Anatomy and 2Department of Obstetrics and Gynaecology, University of Ghana Medical School, Accra, Ghana

Accepted for publication August 3, 1992

Abstract. This study assessed the current status of live neonates born to sickle cell mothers when compared
with those of normal (control) women. Birth weight, placental weight, fetoplacental ratio, and gestational age
for live neonates in singleton births by twenty-nine haemoglobin SS (HbSS), fifty-two haemoglobin SC
(HbSC), and fifty-one (normal) haemoglobin AA (HbAA) mothers were statistically compared.
Neonates of HbSS mothers had a statistically lower than normal mean birth weight and gestational
age, but only a shorter mean gestation significantly distinguished those of the HbSC and HbAA mothers.
Inferentially, neonates delivered by HbSS women were both underweight and preterm, whereas those of HbSC
women were preterm but not underweight, and apparently large for gestational age (LGA). No statistical
differences were found between neonates in terms of placental weights or fetoplacental ratios.
Key words: Neonates; sickle cell; haemoglobinopathy; Ghana

Introduction
A pernicious relationship between sickle cell haemoglobinopathy and pregnancy is established [1, 2, 3].
There is, however, a paucity of information on live neonates delivered by women suffering from sickle
cell disease. Pregnancy coincident with homozygous (HbSS) sickle cell disease is known to be more
hazardous than it is with the doubly heterozygous (HbSC) type [4]. But, comparisons between live
neonates born to the two subsets of patients are lacking, particularly in Ghana. An extensive study has
shown that improvements in the state-of-the-art medical, obstetric, and perinatal care for mothers with
sickle cell haemoglobinopathy in the U.S.A. have resulted in a marked decrease in the risks associated
with their pregnancies and infants [5]. In Accra (Ghana), despite the long existence of a clinical
surveillance programme for sickle cell women throughout pregnancy and after [6], the authors are not
aware of any published studies of babies born by the patients. In the present work, we assessed whether
or not existing clinical management of pregnant mothers with sickle cell haemoglobinopathy in Accra
results in improved perinatal development of their live neonates. Newborn babies of HbSS, HbSC and
HbAA (control) mothers were compared in terms of their birth weight, placental weight, fetoplacental
ratio and gestational age (GA) using the one way analysis of variance (ANOVA) and the two sample ttest [7]. Placental weight and fetoplacental ratio were included in this paper because the placenta has
been suspected by several commentators to hold the key to the enigmatic relationship between sickle cell
disease and pregnancy [3].

Trop. Geogr. Med. 44 (1992) 312-316

Neonates in sickle cell disease, Ghana

313

Subjects and Methods

Data presented in this work were obtained from live births by 132 Ghanaian women. Out of these, 81 were
attendants of a sickle cell clinic run at the Korle-Bu Teaching Hospital in Accra. The sickling genotype was
electrophoretically determined, and when necessary corroborated with clinical and haematological features as well
as family history. Twenty-nine mothers were homozygotes (HbSS) and 52 were double heterozygotes (HbSC) for
sickle cell haemoglobinopathy. The data were collected between June 1988 and October, 1991, the sample sizes
were determined solely by availability of subjects and adequate obstetric histories. In order to preclude
complicating factors, all the women in this study (including controls) had normal vaginal deliveries and singleton
births. Each woman had one pregnancy in this report.
Fifty-one births by women who were negative for the sickling test and had normal haemoglobin genotype
(HbAA) were included in the investigation as controls. This control group comprised mothers who had no history of
hypertension, diabetes, rhesus isoimmunisation, or pre-eclamptic toxaemia. They received routine management at
the antenatal clinic of the hospital and were independently selected. They were included in this work because their
medical and obstetric histories could be confirmed by one of the authors (JBW), and they delivered at the Korle-Bu
Teaching Hospital within the period that data were being collected for the project. Only births resulting in babies
without physical abnormalities of any sort were included as controls.
In both control and sickle cell deliveries, infant birth weights, gestational ages, and maternal (antenatal)
histories were abstracted from the mothers obstetric and ward records. Gestational age was determined from the
first day of the last menstrual period (LMP), and whenever LMP was unclear, early ultrasonography was used to
assess it. Placentae from all but 8 deliveries (by HbSS women) were weighed after washing and excision of their
chorioamniotic membranes and umbilical cords. The 8 missing placentae were mistakenly discarded by labour ward
staff. The weight of each baby per unit weight of its placenta was computed as the fetoplacental ratio. Data
obtained from neonates of the three groups of mothers were statistically compared by the one way analysis of
variance (ANOVA) and two sample t-test.

Results
The medical records of the sickle cell patients showed that none of them had any other serious ailments
apart from occasional crises during the course of pregnancy.
Summarized results of neonatal factors assessed in this investigation are presented in table 1. In
table 2 the one way analysis of variance (ANOVA) comparing babies of HbSS, HbSC, and HbAA
mothers shows that their mean birth weights and gestational ages were significantly different, whereas
their mean placental weights and fetoplacental ratios were not. Two sample t-test comparisons
summarized in table 3 indicates that the mean birth weight and mean gestational age for neonates born to
HbSS women were statistically lower than corresponding values for babies of both HbSC and HbAA
mothers. Table 3 also shows that there was no significant difference between the mean birth weight for
infants of HbSC and HbAA women, but the mean gestational age for the former was statistically lower
than that for the latter neonates.

Discussion
In accord with the WHO definition of a premature baby as one born before the thirty-seventh completed
week of gestation [8]; there is agreement between our results and earlier ones that babies born to HbSS
mothers are on the average premature and underweight [1, 2]. Besides, our results on neonates of HbSS
women support the finding that low birth weight often coincides with prematurity [9]. Based on mean
neonatal birth weight and length of gestation, our results suggest that the existing management practice
for sickle cell patients in Ghana has not altered the finding that pregnancy in HbSC is more benign that in
HbSS [4].
.

F.K. Addai et al.

314

Table 1. Synopsis of Neonatal factors assessed from singleton births by women with either HbSS or HbSC form of sickle cell
disease, and control mothers. Weights are in kg
Variable/Statistic

HbSS

Number of Neonates
Mean birth weight
Range
S.D. (S.E.M.)
95% C.I.*

HbSC

29
2.59
1.20-3.70
0.64 (0.12)
(2.41, 2.77)

HbAA (control)

52
3.10
1.90-4.30
0.48 (0.07)
(2.96, 3.24)

51
3.10
2.20-4.25
0.42 (0.06)
(2.96, 3.24)

Mean placental weight

Range
S.D. (S.E.M.)
95% C.I.*

0.44 (n = 21)
0.30-0.62
0.10 (0.02)
(0.40, 0.48)

0.48
0.29-0.67
0.08 (0.01)
(0.45, 0.51)

0.47
0.29-0.77
0.10 (0.01)
(0.44, 0.50)

Mean F/P** ratio

Range
S.D. (S.E.M.)
95% C.I.*

6.23 (n = 21)
3.00-9.35
1.58 (0.34)
(5.68, 6.78)

6.60
3.96-10.18
1.22 (0.17)
(6.25, 6.95)

6.81
5.00-10.00
1.19 (0.17)
(6.50, 7.17)

Mean GA*** (Wks.)

Range
S.D. (S.E.M.)
95% C.I.*

35.24
30-39
2.36 (0.44)
(34.63, 35.85)

36.44
32-40
1.33 (0.18)

37.25
35.41
1.48 (0.21)

(35.98, 36.90)

(36.79, 37.71)

*
**
***

C.I. Confidence Interval for the mean.

F/P
=
Fetolacental (ratio).
GA
=
Gestational age.

Table 2. Summary of a one way analysis of variance (ANOVA) of neonatal variables obtained from singleton
births by mothers with either HbSS or HbSC type of sickle cell haemoglobinopathy, and HbAA (normal) mothers
Variable

F-statistic (d.f.)

Significance level

Birth weight
Placental weight
F/P ratio
GA*

13.16 (2, 129)

2.00 (2, 121)
1.73 (2, 121)
14.34 (2, 129)

P < 0.01
P > 0.05
P > 0.05
P < 0.01

*GA

Gestational age

An intriguing finding of ours is that neonates born by HbSC mothers were on the average
delivered significantly earlier (in fact, premature by definition), but had a mean birth weight that was
similar to that of infants delivered by control/HbAA women. This result is comparable to that of
Powars et al. [5] who found that the gestation of HbSC mothers in the U.S.A. did not change within
the decade between 19721982, even though their infant birth weights significantly increased to well
within the normal range for the black population as a whole. We interpret our results to mean that
babies born by HbSC mothers are large for gestational age (LGA). This is because in normal
pregnancy birth weight increases with length of gestation up to the 42nd week [9], and evidence for
further intra-uterine growth is lacking only after 41 weeks [10]. The neonates of HbSC women
however, attained birth weights equivalent to those for normal babies a week or two earlier

Neonates in sickle cell disease, Ghana

315

.
Table 3. Summarized results showing comparisons between neonates of HbSS (group 1), HbSC (group 2), and
HbAA (group 3) mothers using the two sample t-test

Variable/statistic

1 : 2#

1 : 3#

Birth weight

t = 4.25

t = 4.25

t = 0.0

Level of significance (d.f. = 129)

95% C.I.*

P < 0.01
(0.28, 0.74)

P < 0.01
(0.28, 0.74)

P > 0.05
(-0.20, 0.20)

Gestational age

t = 3.08

t = 5.15

t = 2.45

Level of significance (d.f. = 129)

95% C.I.*

P < 0.01
(0.43, 1.97)

P < 0.01
(1.24, 2.78)

P < 0.02
(0.16, 1.46)

*C.I
#1:2

=
=

2 : 3#

Confidence Interval for the difference between the means in the group compared.
Comparison between groups 1 and 2; and applies respectively to 1 : 3 and 2 : 3.

To explain how this may occur for infants of HbSC women and not for those of HbSS, it is
informative that sickling in the latter is a continuing process whilst it is intermittent I the former
[11]. We propose that LGA neonates of HbSC mothers reflect the better health that they obtain
under improved clinical management. As to why these babies of HbSC mothers are born
prematurely, we suggest that it is linked to their attaining an equivalent normal birth weight at an
earlier date. Thus, combined with their averagely normal (term) placental weights the babies
congest the uterus and trigger early parturition. This hypothesis is supported by the work of
Mckeown and Record [12] who provided evidence that in multiple pregnancy crowding
(distension) in the uterus may account for early onset of labour. On the other hand, both the low
birth weight and preterm delivery of neonates born to HbSS mothers may be attributed to the
continuous sickling they suffer.
The fact that the mean gestational age for babies born to control women is just over 37 weeks
is difficult to explain in the absence of birth weight and gestation date covering several years
[13] for Ghanaian neonates. We can only speculate that lower gestational age and birth weight
in Ghanaian babies may be related with a subjective observation (ours) that Ghanaian women
tend to have shorter heights and smaller pelves. More research is required to elucidate this issue,
a fact which underscores the importance of the present report.
In conclusion, babies born to HbSC mothers are LGA apparently due to improved
management of their pregnancy and haemoglobinopathy; whereas neonates of HbSS mothers do
not show similar perinatal development with the same clinical care, presumably because the
health benefits obtained by the mothers are reduced by the continuous sickling they suffer.
We gratefully acknowledge the assistance of the labour ward staff, Korle-Bu Teaching Hospital, Accra, in the
clinical coordination of the project; and Mr. D.B. Addo in the preparation of the manuscript.
This project has been supported by the University of Ghana Medical School through a research grant.
Correspondence to: F.K. Addai, PhD, Department of Anatomy, University of Ghana Medical School, P. O. Box
4236, Korle-Bu, Accra, Ghana.

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F.K. Addai et al.

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