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194]

Original Article

Towards Zero Mortality in Sickle Cell Pregnancy: A Prospective

Study Comparing Haemoglobin SS and AA Women in Lagos,
Nigeria
Ochuwa Adiketu Babah1,2, Monsurat Bolanle Aderolu2,3, Ayodeji A. Oluwole1,2, Bosede B. Afolabi1,2
1
Department of Obstetrics and Gynaecology, Faculty of Clinical Sciences, College of Medicine, University of Lagos, 2Department of Obstetrics and Gynaecology,
Lagos University Teaching Hospital, Idi‑Araba, 3Department of Obstetrics and Gynaecology, Alimosho General Hospital, Igando, Lagos, Nigeria

Abstract
Introduction: Sickle cell disease in pregnancy carries increased risk of maternal and perinatal morbidity and mortality. Past studies on
pregnancy complications in sickle cell disease women were limited by relatively small sample sizes, and use of retrospective and hospital
discharge data. Study Design: This prospective case-control study compared booked pregnant Haemoglobin (Hb) SS women with AA
controls from two tertiary centres in Lagos, in order to precisely identify their complication and mortality rates and identify associated factors.
Eligible pregnant HbSS and HbAA women were recruited from antenatal clinics at booking and follow-up visits. Information was collected
on a proforma and data was analyzed using IBM SPSS version 20. Results: We found higher complication rate in HbSS group, commonest
complications being vaso-occlusive crisis (RR 1.47, 95% CI 1.22 – 1.78), pregnancy induced hypertension (RR 1.31, 95% CI 1.08 – 1.57),
urinary tract infection (RR 1.32, 95% CI 1.12 – 1.57), and intrauterine growth restriction (RR 1.2, 95% CI 1.05 – 1.34). HbSS group had
higher systolic and mean arterial blood pressure values in early puerperium compared to HbAA group (p = 0.014 and 0.024 respectively).
No maternal death recorded in both group. Incidence of low birth weight <2.5Kg was 38% in HbSS and 4% in HbAA subjects, p = 0.001.
However, overall maternal and perinatal outcomes were comparable in both groups (p = 1.000). Conclusion: Although sickle cell disease
poses higher obstetric risk in pregnancy, maternal and perinatal outcome can be as good as in the non-sickle cell pregnant women if adequate
and prompt individualized care is given to this group of women.

Keywords: Complications, haemoglobin AA, haemoglobin SS, maternal outcome, perinatal outcome, sickle cell disease pregnancy

Introduction the pattern of pregnancy complications to which SCD women

Sickle cell disease (SCD) is the most common inherited disease
worldwide, with 75% of cases in Sub‑Saharan Africa.[1] In
Nigeria, about 24% of the population carry the sickle cell trait
and approximately 150,000 children are born annually with
sickle cell anaemia, with a prevalence of 2% of newborns
affected by sickle cell anaemia.[2]
The World Health Organisation at the 59th  World Health
Assembly in 2006 estimated that half of SCD patients in
Sub‑Saharan Africa will die before adulthood.[1,2] However,
with improvement in the health‑care system in recent years
and increased childhood survival, more women with SCD
are seen growing into adulthood and presenting for antenatal
care. Considering the burden sickle cell anaemia poses in
pregnancy,[3] there is a need to have a clearer understanding of
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are predisposed.
There are discrepancies in the findings of earlier studies on
pregnancy complications in SCD. Several studies reported
complications such as anaemia, gestational hypertension,
pre‑eclampsia, severe crises, post‑partum haemorrhage,
pulmonary diseases, maternal infection, preterm delivery,
increased incidence of low birth weight and foetal distress
in labour as being prevalent, with an increased perinatal
mortality.[4‑7] Afolabi et al. in an earlier study in Lagos, Nigeria
Address for correspondence: Dr. Ochuwa Adiketu Babah,
P.M.B 12003, Lagos University Teaching Hospital, Surulere, Lagos, Nigeria.
E‑mail: ochuwab@yahoo.co.uk
This is an open access journal, and articles are distributed under the terms of the Creative
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tweak, and build upon the work non‑commercially, as long as appropriate credit is given and
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For reprints contact: reprints@medknow.com

How to cite this article: Babah OA, Aderolu MB, Oluwole AA, Afolabi BB.
DOI: Towards zero mortality in sickle cell pregnancy: A  prospective study
10.4103/npmj.npmj_177_18 comparing haemoglobin SS and AA women in Lagos, Nigeria. Nigerian
Postgrad Med J 2019;26:1-7.

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Babah, et al.: Towards zero mortality in sickle cell pregnancy
did not identify preeclampsia as a predominant complication[8]
and Odum et al. in another study in Lagos, Nigeria did not
identify it as a complication in sickle cell pregnancies.[9]
Surprisingly, pre‑eclampsia and urinary tract infection were
observed more in haemoglobin (Hb) AS than HbSS women
in other studies.[7,10] Most of these studies were retrospective,
and it is our belief that this prospective study would help us
clarify some of these discrepancies.
In a meta‑analysis by Oteng‑Ntim et  al., it was observed
that pregnant women with SCD were at higher risk for
complications including pre‑eclampsia compared to the
general population even in developed countries with
advanced care and that women with the most severe form
of SCD were six times more likely to die during or shortly
after pregnancy.[11] Blood pressure has been reported to be
lower in sickle cell individuals, although Obilade et al. did
not find this in their study on pregnant women with SCD.[12]
With a good knowledge of the pattern of blood pressure
and incident complications in pregnant SCD women in our
environment, we will be able to promptly anticipate and
identify complications arising in pregnancy, during delivery
and puerperium. We will also institute measures to reduce
the incidences of near miss, which was found to be as high
as 33% by Resende Cardoso et al.[13]
Reports of maternal and foetal deaths continue to alternate
with descriptions of entirely uneventful pregnancies. Low‑ and
middle‑income countries generally report increased maternal
and perinatal morbidity and mortality in association with
SCD.[14,15] Studies in high‑income countries report more
favourable foetal outcomes without appreciable risk for
increased maternal morbidity.[6,14] Earlier studies done in Lagos,
Nigeria had maternal death rates of 5.3% and 6.6% among
pregnant women with SCD.[8,9]
The objectives of this study were to compare the incidence
of complications, maternal and foetal outcome such as
admissions and mortality and to determine factors affecting the
foetomaternal outcome in pregnant HbSS women compared
to HbAA.
Methodology
Study design
This was a prospective comparative study of HbSS and
HbAA pregnant women conducted between October 2014
and December 2015.
Study setting
The study was conducted at the Department of Obstetrics
and Gynaecology of Lagos University Teaching Hospital, Idi
Araba (LUTH), Lagos, Nigeria, and Lagos State University
Teaching Hospital, Ikeja  (LASUTH), Lagos, Nigeria.
This study had the approval of the Health Research and
Ethics Committee of Lagos University Teaching Hospital
(Approval number ADM/DCST/HREC/1768) and Health
Service Committee for Lagos State Hospitals to utilise
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Lagos State University Teaching Hospital patients for the
study (Approval number SHMB/728/Vol. VI/).
Study population
The study population comprised pregnant women who booked
and had antenatal care and delivery at the study centres. A total
of 100 pregnant women were studied based on sample size
calculation, of which 50 with HbSS genotype served as cases
and 50 with HbAA genotype served as control.
Selection of patients
Every consenting HbSS woman that met the study criteria
was recruited. Similarly, the next presenting HbAA woman
matched for age, parity and gestational age at booking was
recruited at each antenatal clinic as a control.
Selection based on age was done using age grouping as follows:
16–20, 21–25, 26–30, 31–35, 36–40 and 41–45 years. Parity
was categorised as follows: Para 0, Para 1, Para 2–4 and Para 5
and above. Gestational age at booking was grouped as follows:
12–16, 17–20, 21–24, 25–28, 29–32, 33–36 and 37–42 weeks.
Included in this study were pregnant women between the
age range of 18  years–45  years and pregnant women with
genotype HbSS and HbAA diagnosed in LUTH and LASUTH.
Those excluded were women with diabetes mellitus, renal
failure, heart diseases, chronic essential hypertension, human
immunodeficiency virus‑positive and other medical disorders
and women with multiple gestations.
Sample size determination
Given a prevalence of 45.5% for preterm deliveries in SCD
pregnancy and 17.7% in non‑SCD in a previous study,[16]
the minimum sample size required to give a power of 80%
at a confidence level of 95% was calculated to be 40, using
the formula for calculating sample size when comparing
proportions between two independent groups,[17] n = (Zα/2 + Zβ)2
× (p1[1 − p1] + p2 [1 − p2])/(p1 − p2) 2.
Therefore,
n= (1.96 + 0.84)2 × (0.455 [1 − 0.455] + 0.177 [1 − 0.177])
(0.455 − 0.177)2
n = 39.9, which is approximately 40.
We considered a 20% attrition rate which was 8, thereby
making the minimum sample size required for this study 48 in
each group. We however recruited 50 per group for this study.
Data collection
Structured questionnaires were used to obtain participants’
personal information at booking after counselling and having
obtained written consent. The participants’ phone numbers
were collected, and the investigator’s phone number was
given to the women. The women were informed to call the
investigator anytime they were admitted into the hospital. They
were also called every week to enquire about their health. They
were seen in the labour ward or antenatal ward to get other
information from them, and from their case notes, whenever
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Babah, et al.: Towards zero mortality in sickle cell pregnancy

they were on admission. Information obtained included the

Table 1: Sociodemographic characteristics of study
number of antenatal visits, packed cell volume, any previous
population
crises and treatment for urinary tract infection, chest infection
and anaemia. While in labour, their blood pressures were Sociodemographic variable HbAA HbSS Total
measured using a digital blood pressure monitor (Microlife Age group (years)
3BTO‑A blood pressure monitor). Blood pressure was recorded 16‑20 1 (2) 1 (2) 2 (2)
in the first and second stages of labour, immediate post‑partum 21‑25 7 (14) 7 (14) 14 (7)
and 6‑h post‑partum. The SpO2 was also monitored whenever 26‑30 21 (42) 21 (42) 42 (21)
they were on admission and in labour. The blood loss at 31‑35 16 (32) 16 (32) 32 (16)
delivery was estimated by visual assessment. They were also 36‑40 4 (8) 4 (8) 8 (4)
41‑45 1 (2) 1 (2) 2 (2)
seen while in the post‑natal ward to update their information.
χ2=0.000, P=1.000
The primary outcome measures were maternal indices such as Marital Status
incidence of hypertensive disorders in pregnancy, incidence Married 48 (96) 46 (92) 94 (94)
of urinary tract infections, caesarean section rates, incidence Single 2 (4) 4 (8) 6 (6)
of post‑partum haemorrhage, pseudotoxaemia, incidence of Fisher’s exact test=0.678, P=0.339
retained placenta, wound status and incidence of puerperal Socioeconomic status
complications such as breast engorgement and perinatal indices I 17 (34) 14 (28) 31 (31)
such as birth weight, APGAR score, incidence of stillbirth II 10 (20) 17 (34) 27 (27)
and neonatal unit admission rate. We defined pseudotoxaemia III 15 (30) 15 (30) 30 (30)
in this study as a combination of albuminuria and systolic IV 8 (8) 4 (8) 12 (12)
V 0 (0) 0 (0) 0 (0)
hypertension occurring during a bone pain crisis.[18] We also
χ2=3.438, P=0.329
defined foetal outcome as delivery of a live baby or stillbirth
Parity
in this study.
0 15 (30) 15 (30) 30 (30)
The secondary outcome measures were average blood pressure 1 23 (46) 23 (46) 46 (46)
in mmHg, during labour and in the puerperium, frequency of 2‑4 12 (24) 12 (24) 24 (24)
admission, gestational age at delivery, duration of labour and χ2=4.800, P=0.308
blood loss at delivery. Gestational age at booking (weeks)
<16 5 (10) 5 (10) 10 (10)
Data management 17‑20 19 (38) 19 (38) 38 (38)
All data collected were subjected to statistical analysis using 21‑24 7 (14) 7 (14) 14 (14)
SPSS version 20 (IBM corp., USA). The Chi‑square test was 25‑28 8 (16) 8 (16) 16 (16)
used in comparing categorical variables where applicable and 29‑32 9 (18) 9 (18) 18 (18)
Fischer’s Exact test was used where an expected value is <5. 33‑36 2 (4) 2 (4) 4 (4)
General Linear Model Univariate Analysis of Variance to assess χ2=0.000, P=1.000
factors that can influence maternal outcome such as maternal Figures are presented as frequency (percentages). Grade I is the highest
social class, while Grade V is the lowest social class. HB: Haemoglobin
age, parity, gestational age at booking, blood pressures in
during labour and puerperium, duration of labour and estimated
blood loss at delivery. It was also used to assess factors women compared to HbAA pregnant women (92% and 38%,
affecting foetal outcome. The Pearson’s Product‑Moment respectively, P = 0.001, relative risk [RR] =7.750, confidence
Correlation Coefficient was used in assessing correlation interval  [CI] 2.9535–20.3361). Table 2 summarises the
between maternal weight and foetal birth weight after testing incidence and pattern of complications in each group.
for normality of the population distribution. P <  0.05 was Admissions were significantly more frequent in the HbSS
considered to be statistically significant. Socioeconomic status pregnant women (P = 0.001). The incidence of preterm delivery
was determined using the occupation of subject and that of
was significantly more in the HbSS compared to HbAA group
her husband, using the National Readership Survey grades.[19]
(P = 0.022). The caesarean section rate was higher in HbSS
than HbAA group (80% versus 34%), most being conducted as
Results emergencies. For those who had normal delivery, it was found
The mean age ± standard error of mean of the participants that the duration of second stage of labour was significantly
was 29.84  ±  0.431  years. They were all booked women. longer in the HbSS compared to the HbAA parturient with
Majority (38%) booked after 16 weeks but before 20 weeks a mean difference of 38.33  minutes, P = 0.003. Table 3
gestational age, with only 10% booking before 16  weeks, summarises these findings. Of the 50 HbSS women studied,
while 4% of the women booked late in pregnancy after 13 (26%) had blood transfusion while 2 of the 50 HbAA (4%)
32‑week gestational age. Table  1 shows details of the studied had blood transfusion (P = 0.002, RR = 1.2973, CI
participants’ demographic characteristics. Complications 1.0904–1.5435). There was no maternal death recorded in
occurred significantly more frequently in HbSS pregnant either group in this study.

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Babah, et al.: Towards zero mortality in sickle cell pregnancy

Table 2: Incidence of complications in haemoglobin AA and haemoglobin SS parturient

Complications HbAA (n=50) HbSS (n=50) P Risk ratio 95% CI
Non‑sickle cell‑related complications
Abruptio placentae 0 (0.0) 1 (2.0) 1.000 1.0204 0.9808‑1.0616
Upper respiratory tract infection 1 (2.0) 5 (10.0) 0.204 1.0889 0.9848‑1.2040
Pregnancy‑induced hypertension 3 (6.0) 14 (28.0) 0.003* 1.3056* 1.0834‑1.5732*
Vaginal candidiasis 1 (2.0) 3 (6.0) 0.617 1.0426 0.9620‑1.1299
Asymptomatic bacteriuria 0 (0.0) 1 (2.0) 1.000 1.0204 0.9808‑1.0616
Eclampsia 1 (2.0) 3 (6.0) 0.617 1.0426 0.9620‑1.1299
Cardiomyopathy 0 (0.0) 1 (2.0) 1.000 1.0204 0.9808‑1.0616
Intrauterine growth restriction 0 (0.0) 8 (16.0) 0.006* 1.1905* 1.0548‑1.3436*
Malaria 3 (6.0) 9 (18.0) 0.065 1.1463 0.9891‑1.3286
Pneumonia 0 (0.0) 1 (2.0) 1.000 1.0204 0.9808‑1.0616
Post‑partum haemorrhage 3 (6.0) 5 (10.0) 0.715 1.0444 0.9301‑1.1728
Pre‑eclampsia 1 (2.0) 4 (8.0) 0.362 1.0652 0.9727‑1.1665
HELLP syndrome 0 (0.0) 1 (2.0) 1.000 1.0204 0.9808‑1.0616
Preterm contractions 1 (2.0) 1 (2.0) 1.000 1.000 0.9455‑1.0576
Preterm delivery 5 (10.0) 14 (28.0) 0.022* 1.2500* 1.0275‑1.5207*
Wound dehiscence 0 (0.0) 3 (6.0) 0.242 1.0638 0.9919‑1.1410
Retained placenta 1 (2.0) 4 (8.0) 0.362 1.0652 0.9727‑1.1665
Foetal hypospadia 1 (2.0) 0 (0.0) 1.000 1.0204 0.9808‑1.0616
IUFD 1 (2.0) 1 (2.0) 1.000 1.000 0.9455‑1.0576
Urinary tract infection 1 (2.0) 13 (26.0) 0.001* 1.3243* 1.1184‑1.5682*
Preterm rupture of membrane 0 (0.0) 1 (2.0) 1.000 1.0204 0.9808‑1.0616
Breast engorgement 3 (6.0) 1 (2.0) 0.617 0.9592 0.8850‑1.0395
Gluteal abscess 0 (0.0) 1 (2.0) 1.000 1.0204 0.9808‑1.0616
Sickle cell‑related complications
Pseudotoxaemia 0 (0.0) 3 (6.0) 0.242 1.0638 0.9919‑1.1410
Vaso‑occlusive crisis 0 (0.0) 16 (32.0) 0.000* 1.4706* 1.2159‑1.7786*
Acute kidney injury 0 (0.0) 2 (4.0) 0.495 1.0417 0.9844‑1.1023
Sequestration crisis 0 (0.0) 1 (2.0) 1.000 1.0204 0.9808‑1.0616
Severe anaemia 0 (0.0) 1 (2.0) 1.000 1.0204 0.9808‑1.0616
Haemolytic crisis 0 (0.0) 1 (2.0) 1.000 1.0204 0.9808‑1.0616
Acute chest syndrome 0 (0.0) 3 (6.0) 0.242 1.0638 0.9919‑1.1410
Osteomyelitis 0 (0.0) 1 (2.0) 1.000 1.0204 0.9808‑1.0616
Figures in paracentesis are presented as frequency percentage of individual group. χ2 used in calculating P values and Fischer’s Exact test used where a value
is <5. *Are values that are statistically significant. IUFD: Intrauterine foetal death, CI: Confidence interval, HELLP: Haemolysis, elevated liver enzymes,
low platelets, HB: Haemoglobin

Although there was no significant difference in average blood
pressure values during the first and second stage of labour, the
HbSS group had significantly higher mean systolic BP and
mean arterial blood pressure (MAP) values at 6‑h post‑partum
compared to the HbAA group (P = 0.014 and 0.024, respectively).
The details of these findings are summarised in Table 4.
HbSS women are more likely to have lighter babies than the
HbAA women, mean ± standard deviation of birth weight of
2.56 ± 0.62 kg and 3.23 ± 0.52 kg, respectively, P = 0.001.
The incidence of low birth weight below 2.5 kg was 38% in
HbSS and 4% in HbAA participants (P = 0.001). We further
assessed the correlation between maternal weight and foetal
birth weight in both groups combined, and we found a weak
positive but statistically significant correlation between the two
parameters, r = 0.333, P = 0.001. There was also a moderate
positive correlation between gestational age at delivery and
foetal birth weight, r = 0.653, P = 0.001. After adjusting for
maternal weight and gestational age at delivery, the difference
in foetal weight between the two groups was found to be
statistically significant (P = 0.003).
The HbSS has a higher incidence of birth asphyxia defined
by APGAR score <7 in this study. At 1 min, the proportion of
HbSS and HbAA with APGAR score <7 was 25/49 (51.0%)
versus 5/49 (10.2%), respectively, P = 0.001, while at 5 min,
the incidence reduced to 5/49  (10.2%) versus 0/49  (0.0%),
respectively, P = 0.001. The HbAA group had median APGAR
scores of 8 at 1 min and 9 at 5 min, while the HbSS group
had median APGAR scores of 6 at 1  min and 8 at 5  min.
Neonatal unit admission rate was significantly higher for the
HbSS babies compared to the HBAA group, 21/50  (42%)
versus 2 (4%), respectively, P = 0.001. Perinatal death was
comparable in both groups, live births were 49  (98%) and
stillbirths 1 (2%) in each group, P = 1.000, odds ratio = 1.000,
95% CI = 0.061–16.444.

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Babah, et al.: Towards zero mortality in sickle cell pregnancy

Table 3: Maternal outcome in haemoglobin AA and haemoglobin SS parturient

Parameter HbAA (n=50) HbSS (n=50) Total
Median maternal admission, frequency 0 1 0
Mean gestational age at, delivery±SD (weeks) 38.10±0.476 36.80±0.931 37.45±2.129
χ2, P 10.186, 0.002
Mode of delivery (%)
ElC/S 9 (60.0) 6 (40.0) 15 (100.0)
EmC/S 8 (19.0) 34 (81.0) 42 (100.0)
Forceps 1 (100.0) 0 (0.0) 1 (100.0)
SVD 32 (76.2) 10 (23.8) 42 (100.0)
Total 50 (50.0) 50 (50.0) 100 (100.0)
Mean duration of labour (min)
1st stage 402.82 458.10 P=0.415
2nd stage 12.97 51.30 P=0.003
3rd stage 13.36 10.90 P=0.664
Total duration 423.94 485.30 P=0.412
Figures are presented as frequency percentage of individual group, P<0.05 is considered to be statistically significant. SD: Standard deviation, SVD:
Spontaneous vaginal delivery, ElC/S: Elective caesarean section, EmC/S: Emergency caesarean section, HB: Haemoglobin

significant relationship with foetal outcome in both groups

Table 4: Blood pressure pattern in labour and early
combined (P = 0.001) and in HbAA only (P = 0.001).
puerperium in haemoglobin AA and haemoglobin SS
women
Average blood pressure (mmHg) HbSS HbAA P
Discussion
Systolic first stage of labour 124.8±15.7 126.9±18.1 0.558 In comparison with earlier studies, we found a higher
Diastolic first stage of labour 72.8±12.2 77.9±14.3 0.079 complication rate in the HbSS pregnant women compared to
MAP first stage of labour 90.3±12.4 93.5±15.0 0.272 their HbAA counterparts, reiterating the fact that pregnancy in
Systolic second stage of labour 126.4±13.2 125.6±11.4 0.757 HbSS women is high risk. The most common complications
Diastolic second stage of labour 76.3±11.1 78.6±8.9 0.279 in HbSS pregnant women as observed in this study were
MAP second stage of labour 91.5±15.6 94.3±9.0 0.313 vaso‑occlusive (bone pain) crises (32%), pregnancy‑induced
Systolic 6 h post‑partum 128.3±17.7 120.6±12.8 0.014 hypertension  (28%), malaria  (18%), intrauterine growth
Diastolic 6 h post‑partum 78.5±12.0 75.1±10.0 0.129 restriction  (16%) and urinary tract infection  (13%). The
MAP 6 h post‑partum 95.1±13.1 88.8±14.0 0.024 incidence of bone pain crisis in this study is slightly higher than
Figures are presented as mean±SD values. MAP: Mean arterial blood was reported in an earlier study by Afolabi et al. in this centre
pressure, SD: Standard deviation, HB: Haemoglobin
in 1996–2000 (25.3%)[8] but much lower than the incidence
reported by Resende Cardoso et  al.  (77.8%).[13] The lower
Factors that can influence maternal outcome such as maternal prevalence reported in our centre previously might be because
age, parity, gestational age at booking, blood pressures in during it was a retrospective study, which unlike prospective studies
labour and puerperium, duration of labour and estimated blood
may not give room for adequate data collection or maybe as
loss at delivery were assessed, and it was found that when a
a result of environmental differences.
combined assessment of both groups was done, only MAP
at 6‑h post‑delivery (P = 0.039) and estimated blood loss at We also found higher incidences of pregnancy‑induced
delivery (P = 0.022) significantly influence maternal outcome. hypertension, preterm delivery, intrauterine growth restriction
This association remained similar in the HbAA group only with and urinary tract infection in the HbSS pregnant women
MAP at 6‑h post‑delivery (P = 0.034) and estimated blood loss compared to their HbAA counterparts. This observation is
at delivery (P = 0.017) being statistically significant. Statistical similar to findings in other studies.[8,9,20,21] The three HbSS
significant was however lost in HbSS group (P = 0.105 for MAP patients who had acute chest syndrome were admitted into
at 6‑h post‑delivery and P = 0.076 for estimated blood loss). the intensive care unit, managed by partial exchange blood
transfusion, oxygen supplementation, good hydration,
There was no statistically significant relationship between
antibiotic coverage and aggressive pulmonary therapy.[9]
maternal age and foetal outcome (P = 0.725) or between parity and
foetal outcome (P = 0.084), but there was a statistically significant The proportion of women with gestational hypertension and
relationship between gestational age at delivery and foetal pre‑eclampsia was higher in the HbSS group than the HbAA
outcome when both groups were assessed together (P = 0.001) group in this study. It has been established that women with
and when each group was assessed alone  (HbSS group, SCD have lower ratio of prostacyclin/thromboxane, and this
P = 0.021 and HbAA group, P = 0.001). Only average diastolic may indicate an increased tendency to vasoconstriction[12] and
blood pressure in the first stage of labour showed statistically may explain why HbSS women are more prone to developing

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Babah, et al.: Towards zero mortality in sickle cell pregnancy
hypertensive disorders in pregnancy compared to non‑SCD
women.
The difference in the incidence of gestational hypertension in
the two groups studied was statistically significant. However,
there was a loss of statistical significance in the incidence
of pre‑eclampsia when both groups were compared. This
might be because this study was not specifically power
for pre‑eclampsia. Granger et  al. in an earlier study found
a reduction in uteroplacental circulation to be a vital
initiating event in the development of pregnancy‑induced
hypertension, and it was thought that placental ischaemia
may play a role.[22] In subsequent studies, it was established
that placental ischaemia is not a causal factor in pre‑eclampsia
but a consequence of the disease.[23,24] This may further
explain why there was a statistically significant difference
in the incidence of gestational hypertension in HbSS women
compared to HbAA group but not so with pre‑eclampsia, as
SCD is association with recurrent plugging of blood vessels
by sickled cells which causes ischaemia and can result in a
reduction in uteroplacental circulation, thus increasing the risk
of gestational hypertension.
HbSS women had a higher incidence of preterm delivery
probably because of a higher complication rate in them,
which led to early delivery. The incidence of preterm birth
among HbSS and HbAA group in this study was 28% and
10%, respectively. A recent meta‑analysis found that preterm
delivery was more than twofold increased risk in women with
HbSS compared to women without SCD.[11]
Unlike several studies that have reported an increased
incidence of spontaneous miscarriages and ectopic pregnancy
in HbSS pregnant women, this study did not record any of these
complications, probably because the women were recruited
late to detect these complications.[7,19,25] None of the women
recruited was lost to follow‑up probably because adequate
counselling was given at the time of recruitment and most of
the women were also educated.
This study did not report any maternal death, unlike previous
studies.[6‑9,21] Majority of the HbSS women were recruited
from LUTH, and about 80% of them were managed by
one of the authors. The other institution that the remaining
women were recruited from is also a tertiary institution. The
fact that the women had no additional comorbidities may
also have contributed to the favourable prognosis. However,
the women with SCD studied in the past suffered mortalities
from complications developed during pregnancy and not from
co‑morbidities.[8,9]
There was also no increased risk of IUFD in both groups which
is similar to the findings in some previous studies[26,27] probably
due to improved foetal monitoring and prompt intervention.
Low birth weight is one of the most consistent findings in
neonates born to mothers with SCD.[7,28,29] Almost half of
the neonates in this study were of low birth weight which
reflected in the number of neonatal unit admission. We found
6 Nigerian Postgraduate Medical Journal  ¦  Volume 26  ¦  Issue 1  ¦  January-March 2019
an increased risk of Apgar score below 7 at 1 min, but there
was no difference at 5 min. This is likely to be a reflection of
the neonatal care offered to these groups of patients as they
were managed in tertiary institution. There was no neonatal
death reported in both groups studied.
Contrary to earlier reports that blood pressure tends to be lower
in HbSS individuals,[30] this study found a slight increase in
blood pressure in labour in HBSS compared to HbAA women,
with a significant fall in the MAP in early puerperium in HbSS
women. The reason for this is unknown. However, bearing in
mind the fact that systolic blood pressure is commonly affected
by emotional issues, anxiety and stress, we presume that the
increase in blood pressure in labour in HbSS parturient may be
attributable to the higher level of anxiety and stress that labour
and delivery pose on this group of women. It is thus advisable
to shorten second stage of labour in this group of parturient.
Despite the increased complication rates reported among
HbSS pregnant women compared to their HbAA counterpart
as reported in this study, the overall maternal and perinatal
outcomes were comparable in both groups probably because
of the individualised care and close monitoring.
This study is however limited by the possibility that some
patients may have chronic undiagnosed medical conditions
such as early‑stage renal disease and Class I heart disease
which may be asymptomatic at recruitment. Second, some of
the outcome measures such as estimated blood loss at delivery
are subjective and liable to observer error as assessment was
done by visual inspection. However, this study is strengthened
by the prospective recruitment of 50 pregnant women with
SCD and controls that were carefully matched.
Conclusion
Complications found in this study were comparable to some
earlier studies. In addition, prolonged second stage and
increased MAP and systolic BP in the puerperium were new
findings. However, although SCD poses higher obstetric risk in
pregnancy, the maternal and perinatal outcomes can be as good
as in the non‑SCD pregnant women if adequate and prompt
healthcare is given to this group of women, especially where
adequate workforce exists to offer them individualised care.
This will also promote awareness of the disease among affected
women and encourage them to present early for booking,
assessment and appropriate management of symptoms.
Financial support and sponsorship
The cost of the research was borne solely by the authors.
Conflicts of interest
There are no conflicts of interest.
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