Hypertension in pregnancy: maternal and fetal outcomes according to
laboratory and clinical features
Mark A Brown and Megan L Buddle
MJA 1996; 165: 360-365
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Objectives: To determine the predictive value of
clinical and laboratory parameters for maternal and fetal
complications in pregnant women with hypertension.|
Design: Prospective data collection.
Setting: Two primary referral hospitals in the
southern suburbs of Sydney between March 1987 and July 1994.
Subjects: 1183 pregnant women with hypertension
managed conjointly by a physician and obstetrician.
Intervention: Uniform management protocol, plus
antihypertensive medications if systolic blood pressure was
persistently ≥ 160 mmHg and/or diastolic blood pressure ≥ 90
Main outcome measures: Maternal and fetal
complications, as defined by the Australasian Society for the Study
of Hypertension in Pregnancy Consensus Statement.
Results: Of 825 women with pre-eclampsia (502 mild;
323 severe), univariate analysis showed that hyperuricaemia,
proteinuria and severe hypertension were significantly associated
with a higher rate of maternal and fetal complications. In
multivariate analyses without confounders, only primiparity, low
serum albumin levels and absence of diabetes were significantly
associated with severe pre-eclampsia. Severe pre-eclampsia, high
haemoglobin levels and low platelet count were associated with
higher rates of small-for-gestational-age babies, but only low
serum albumin levels were associated with increased perinatal
mortality rates. Low birthweight was associated with severe
hypertension and severe pre-eclampsia.
Conclusions: Simple clinical and laboratory
parameters are useful predictors for maternal and fetal outcomes in
pregnancies complicated by hypertension.
Hypertensive disorders in pregnancy are common and their incidence
appears to be increasing.1 These disorders comprise
hypertension de novo in pregnancy (variably called
pre-eclampsia, gestational or transient hypertension), and
chronic forms of hypertension (essential and secondary
hypertension), and have multiple modes of clinical presentations.
With the current emphasis on outpatient management of pregnant women
with non-proteinuric hypertension,2 clinicians require readily
available clinical and laboratory parameters as indicators of the
likely outcome of pregnancies complicated by hypertension. Such
information is often difficult to obtain because of the selective
nature of cases and complications reported by high-risk
tertiary-care obstetric units, and is confounded by the varying
treatments given to pregnant women before referral.3,4
Our study examined prospectively the maternal and fetal outcomes in
women with hypertension in pregnancy, and the associated clinical
and laboratory features. In particular, we sought to determine
whether complications were greater if the woman had hyperuricaemia,
severe hypertension and/or proteinuria, was nulliparous, or
presented with hypertension early in the pregnancy. We also sought to
determine which clinical and laboratory features were associated
with severe pre-eclampsia.
The study group consisted of all pregnant women with hypertension who
were referred by their obstetrician to one physician (M A B) at primary
referral hospitals (St George or Hurstville community hospitals) in
Sydney between March 1987 and July 1994.
Indications for referral were:
- Hypertension failing to
settle after overnight rest in hospital, or repeated measurement in a
- The presence of proteinuria or other abnormal urinalysis, abnormal
biochemistry (serum electrolytes and creatinine levels, liver
function tests) or thrombocytopenia;
- Recurrent admissions for hypertension; or
- A suspected secondary cause for hypertension.
The definitions, classifications and complications of
hypertension in pregnancy used in our study were those of the
Australasian Society for the Study of Hypertension in Pregnancy
(ASSHP) (Boxes 1 and 2).5
The maternal biochemical and haematological data used in our
analysis were those recorded immediately before delivery.
Complications were those having occurred by the time of discharge
from hospital or by the postpartum check-up (after three months).
Each patient's management was overseen by one physician (M A B) in
conjunction with the patient's obstetrician. A standardised
management protocol was followed by all staff during the course of
this study (Box 3).
All data were stored in a database program (iBANK) and analysed using
Minitab statistical package6 and BMDP statistical
For initial bivariate analyses, the frequency of adverse events
within groups was tested by χ2 analysis and, where
significant, by 2 x 2 contingency tables. Biochemical and
haematological indices and birthweights were compared using
Student's t tests, and significance assessed using Hochberg's
method for interpreting multiple comparisons.
The maternal-outcome variable was severity of pre-eclampsia.
Logistic regression analysis was used to analyse the following
variables as predictors of severe pre-eclampsia: parity; gestation
at presentation; age; plasma uric acid level; serum albumin,
haemoglobin and haematocrit levels; and diabetes. Proteinuria,
platelet count and serum creatinine levels were not analysed because
abnormalities of these form part of the diagnosis of severe
Fetal-outcome variables were birthweight,
small-for-gestational-age (SGA) and perinatal mortality (PNM).
Each of the following variables was analysed as a predictor of poor
fetal outcome: maternal complications, age, parity, diabetes,
gestation at presentation and laboratory data. Multiple regression
analysis was used for birthweight and logistic regression analysis
for SGA and PNM.
For regressions, backward elimination was used until all remaining
predictors were statistically significant (P < 0.05).
From March 1987 to July 1994, 1183 pregnant women with hypertension
fulfilled the criteria for referral to a physician (M A B) and were
entered into the study, representing 6.7% of all confinements at the
two hospitals. During this period, 2121 women were documented in
hospital records as having hypertension in pregnancy, representing
12% of all confinements.
There were 825 women (70%) with pre-eclampsia (mild, 502; severe,
323), 82 (7%) with superimposed pre-eclampsia, 223 (19%) with
essential hypertension, and 53 (4%) with secondary hypertension
(predominantly renal disease).
Oral antihypertensive medications were given to 563 women (48%),
additional parenteral antihypertensives were required by 281
(24%), and 339 (29%) received no antihypertensive medications.
Thirteen women (1%) received "prophylactic" low-dose aspirin.
Five women (0.4%) required dialysis during or after pregnancy and
four women (0.3%) had convulsions. Seventy-three women (6%) had
pre-existing or gestational diabetes mellitus.
Of the 1242 babies born to the women in the study, there were 15
perinatal deaths (12 per 1000 hypertensive pregnancies). There was
one maternal death (0.08%) in a 29-year-old woman who
presented at 29 weeks' gestation with severe pre-eclampsia and who
delivered immediately and died unexpectedly the next day. Despite
autopsy, the cause of death was not established.
Predictors of outcomes in women with pre-eclampsia|
Hyperuricaemia was significantly associated with higher
rates of all maternal complications and SGA babies and babies with
lower average birthweights than normal plasma uric acid levels (Box 4).
Severe hypertension was significantly associated with higher
maternal complication rates and earlier gestation at delivery than
mild hypertension (Box 4). This group of women had babies of a lower
average birthweight, a higher proportion of SGA babies and a higher
perinatal mortality rate.
Proteinuria was significantly associated with similar maternal and
fetal complication rates as severe hypertension, and the proportion
of SGA babies was similar to non-proteinuric hypertension (Box 4).
Parity did not affect maternal complication rates, except for a
higher prevalence of severe hypertension and liver disease in
nulliparae (Box 5).
Early gestation at presentation with hypertension (at or before 32
weeks' gestation) was significantly associated with a higher
prevalence of proteinuria than later presentation (Box 5).
Severe pre-eclampsia was associated with low serum albumin
(odds ratio [OR], 0.93; 95% confidence interval [CI], 0.90-0.97;
P = 0.0001), primiparity (OR, 0.51; 95% CI, 0.33-0.79;
P = 0.002) and the absence of diabetes (OR, 0.21; 95% CI,
0.05-0.93; P = 0.04).
SGA was associated with severe pre-eclampsia (OR, 2.5; 95% CI,
1.6-3.9; P = 0.0001), high maternal haemoglobin levels (OR,
3.7; 95% CI, 1.1-12.8; P = 0.04) and low platelet counts (OR,
1.4; 95% CI, 1.1-1.8; P = 0.02).
Birthweight was positively associated with gestation at
presentation (regression coefficient [β], 41; standard error [SE],
5; P < 0.0001) and serum albumin levels (β, 28; SE, 5;
P < 0.0001) and inversely associated with severe
hypertension (β, 2193; SE, 69; P < 0.005) and severe
pre-eclampsia (β, 2311; SE, 60; P < 0.0001).
Perinatal mortality was associated only with low serum
albumin levels (OR, 0.88; 95% CI, 0.82-0.95; P < 0.0003),
but there were too few perinatal deaths to support a useful formal
Outcomes in women with all forms of hypertension in pregnancy|
Box 6 shows the maternal and fetal outcomes in women with the different
forms of hypertension in pregnancy.
Maternal and fetal outcomes were better for women with essential
hypertension than for the other groups. Twenty-seven per cent (or 10%
if proteinuria was included in the diagnosis) of women with essential
hypertension developed superimposed pre-eclampsia.
Women with superimposed pre-eclampsia delivered their babies
earlier, had babies with lower average birthweights, significantly
more SGA babies and significantly higher rates of all maternal
complications than women with essential hypertension alone.
Women with secondary (predominantly renal) hypertension had
similar maternal and fetal outcomes to women with superimposed
pre-eclampsia (data available from author).
In our prospective study, there was uniform management of all women
with hypertensive disorders in pregnancy. As the database excluded
very mild cases of hypertension in pregnancy, an inherent bias
exists, but our study provides a general estimate of fetal and
maternal outcomes for women with hypertension managed in primary
During the study period, 12% of all confinements were complicated by
hypertension, which is either similar to or higher than previous
Hjertberg et al. noted a 5% incidence of
hypertension in pregnancy, of whom 83% had hypertension
de novo in pregnancy.12 In our study, 70%
of women had pre-eclampsia (hypertension de novo in
pregnancy), 19% had essential hypertension alone, 7% had
superimposed pre-eclampsia, and 4% had a renal or other secondary
cause. These results are similar to those from a smaller study in a
tertiary referral unit.13
When analysed separately, hyperuricaemia, proteinuria and severe
hypertension were associated with higher rates of all maternal and
fetal complications, while parity was associated with severe
hypertension and liver disease. Presentation before 32 weeks'
gestation impacted negatively on fetal outcome. We have reported
previously on the adverse impact of proteinuria on maternal and fetal
Hyperuricaemia is an established marker of severe pre-eclampsia,
correlating histologically with the severity of renal
lesions,15 and clinically with
adverse fetal outcomes.16 We found that
hyperuricaemia, when considered alone, was associated with higher
maternal complication rates and fetal growth retardation, but, with
multivariate analysis, was not a significant predictor of adverse
maternal or fetal outcomes. Hyperuricaemia remains a useful marker
of pre-eclampsia, but women with normal serum uric acid levels and
pre-eclampsia may still develop complications.
Severe hypertension was confirmed by multivariate analysis to be
associated with low birthweight babies, and, in univariate
analysis, with a higher incidence of all fetal complications and a
higher incidence of SGA babies. Therefore, the more severe the
hypertension, the more the likelihood of fetal as well as maternal
Pre-eclampsia has long been considered a disorder of
primigravidae.17 However, it is clear that
pre-eclampsia does occur in second or subsequent pregnancies
(particularly following a change of partner); in our study,
approximately two-fifths of the women with pre-eclampsia were
parous women. Parous women had a lower incidence of severe
hypertension and liver disease when compared with nulliparae, but
there were no other differences in outcomes between these groups.
Therefore, equal risk to the fetus should be assumed in both groups of
women once hypertension has developed in the second half of
The gestation at presentation in pre-eclampsia influences fetal
outcome because of the likelihood of early delivery, but we are
unaware of any prospective studies that relate gestation at
presentation to maternal complication rates. Apart from
proteinuria, maternal complication rates for women presenting
before 33 weeks' gestation in our study were similar to those who
presented later. Two retrospective studies have reported a higher
incidence of maternal complications in women with pre-eclampsia of
early onset.18,19 Our patients
presenting early with pre-eclampsia had milder disease than that
reported by Sibai et al.20 As expected, the earlier
the gestation with pre-eclampsia the lower the birthweight (because
gestation did not proceed as far as those presenting later), but the
likelihood of having an SGA baby was not increased.
Although maternal diabetes was associated with a lower risk of severe
pre-eclampsia, only 6% of our study population had diabetes.
Therefore, it should not be assumed that diabetes protects pregnant
women against severe pre-eclampsia.
The consistent relationship between low serum albumin levels and
adverse maternal and fetal outcomes was independent of proteinuria
and implies that hepatic albumin synthesis is altered in severe
pre-eclampsia. The association between high maternal haemoglobin
levels and SGA babies presumably reflects a reduced plasma volume and
haemoconcentration, which is associated with poor fetal
In conclusion, for women with pre-eclampsia, the traditional
clinical markers of proteinuria, parity and severe hypertension
remain useful clinical indices of maternal risk, while severe
pre-eclampsia, severe hypertension, elevated haemoglobin and low
serum albumin levels portend increased fetal risk.
We wish to thank the obstetricians of St George and Hurstville
community hospitals, Professor J A Whitworth, Ms Jodie Wilkinson and
Dr M Jones (Intstat Australia Pty Ltd).
- Crawford JS. Epidemic pre-eclampsia. Lancet 1987; 1:
Tuffnell DJ, Lilford RJ, Buchan PC, et al. Randomised controlled
trial of day care for hypertension in pregnancy. Lancet 1992;
Horvath JS, Korda A, Child A, et al. Hypertension in pregnancy. A
study of 142 women presenting before 32 weeks' gestation. Med J
Aust 1985; 143: 19-21.
Clarke M, Mason ES, Macvicar J, Clayton DG. Evaluating perinatal
mortality rates: effects of referral and case mix. BMJ 1993;
Australasian Society for the Study of Hypertension in Pregnancy.
Consensus Statement on Management of Hypertension in Pregnancy:
Executive Summary. Med J Aust 1993; 158: 700-702.
Minitab [computer program], version 9.1. Pennsylvania State
College: Minitab Inc, 1993.
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hypertension in pregnancy on fetal and neonatal condition. Int J
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Andrews WW, Cox SM, Sherman ML, Leveno KJ. Maternal and perinatal
effects of hypertension at term. J Reprod Med 1992; 37: 73-76.
Safflas AF, Oldson DR, Franks AL, et al. Epidemiology of
pre-eclampsia and eclampsia in the United States, 1979-1986. Am J
Obstet Gynecol 1990; 163: 460-465.
Pietrantoni M, O'Brien WF. The current impact of the hypertensive
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Hjertberg R, Bellrage P, Hanson U. Conservative treatment of mild
and moderate hypertension in pregnancy. Acta Obstet Gynecol
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Hypertens Pregnancy 1983; B2: 21-28.
Brown MA, Buddle ML. The importance of non proteinuric
hypertension in pregnancy. Hypertens Pregnancy 1995; 14:
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clinical and pathologic study based on renal biopsies. Medicine
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Redman CWG, Beilin LJ, Bonnar J, Wilkinson PH. Plasma urate
measurements in predicting fetal death in hypertensive pregnancy.
Lancet 1976; 2: 1370-1373.
Chesley LC. Diagnosis of pre-eclampsia. Obstet Gynecol
1985; 65: 423-425.
Sibai BM, Taslimi M, Abdella TN, et al. Maternal and perinatal
outcome of conservative management of severe pre-eclampsia in
midtrimester. Am J Obstet Gynecol 1985; 152: 32-37.
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complicated by severe pre-eclampsia of early onset. S Afr Med J
1987; 72: 608-610.
Sibai BM, Mercer BM, Schiff E, Friedman SA. Aggressive versus
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(Received 9 Oct 1995, accepted 13 May 1996)
Departments of Medicine, Renal Medicine and Obstetrics, St George
and Hurstville community hospitals, University of NSW.
Mark A Brown, MB BS, FRACP, MD, Associate Professor of
Megan L Buddle, SRN, Hypertension Unit Registered
No reprints will be available.
Correspondence: Associate Professor
M A Brown, Department of Renal Medicine, St George Hospital, Kogarah,
1: ASSHP classifications and definitions of hypertension in pregnancy|
Hypertension: A sitting systolic blood pressure (BP) ≥ 140 mmHg and/or diastolic BP (phase IV Korotkoff sound) ≥ 90 mmHg, or a rise in systolic BP of ≥ 25 mmHg and/or diastolic BP ≥ 15 mmHg from first-trimester BP (two readings taken six hours apart).
Proteinuria: ≥ 300 mg/day (24-hour urine collection) or persistently (over two or more days) ≥ 2+ protein (1 g/L) on urinalysis (dipstick testing). As urinalysis was performed daily, non-proteinuric hypertension that progressed to proteinuric hypertension was always detected.
Hyperuricaemia: Plasma uric acid level > 0.35 mmol/L.
Pre-eclampsia: The development of hypertension after 20 weeks' gestation in a woman with no known history of hypertension or renal disease and whose blood pressure (BP) was normal in the first half of the pregnancy and returned to normal after delivery:
(i) mild pre-eclampsia: hypertension only;
(ii) severe pre-eclampsia: hypertension and evidence of maternal organ dysfunction (see Maternal complications, Box 2).
Essential hypertension: Hypertension in the first half of pregnancy (often occurring before pregnancy) without a demonstrable secondary cause, or the appearance of hypertension in the second half of pregnancy in a woman whose BP failed to return to normal within three months after delivery.
Superimposed pre-eclampsia: The development of proteinuria and/or hyperuricaemia in the second half of pregnancy in a woman with essential hypertension.
Secondary hypertension: To exclude a secondary cause of hypertension, all women had serum potassium levels measured and had urinalysis, microscopy and a clinical examination; urinary catecholamines and renal ultrasound were performed in selected cases. Within this group, superimposed pre-eclampsia was not diagnosed as a separate entity as it was too difficult to ascertain whether changes (e.g., increasing proteinuria) reflected superimposed
pre-eclampsia or progression of the underlying (usually renal) disease.
ASSHP = Australasian Society for the Study of Hypertension in Pregnancy.5
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2: ASSHP complications of hypertension in pregnancy|
|(i)||Severe hypertension: Blood pressure (BP) ≥ 170 mmHg systolic and/or ≥ 110 mmHg diastolic;|
|(ii)||Proteinuria (Box 1);|
|(iii)||Haematological abnormalities: haemolysis (haemoglobin < 110g/L, with reticulocytosis, fragments) or thrombocytopenia (< 150 x 109/L platelets);|
|(iv)||Renal impairment: serum creatinine level ≥ 0.10 mmol/L;|
|(v)||Liver disease: elevated serum aspartate aminotransferase level > 40 IU/L, with or without severe epigastric pain;|
|(vi)||Neurological disturbances: visual scotoma; severe headaches with hyperreflexia; hyperreflexia with sustained clonus (> 3 beats).|
|(i)||Small-for-gestational-age (SGA): birthweight below the 10th centile for gestation, corrected for sex;|
|(ii)||Perinatal mortality (PNM): stillbirths and neonatal deaths per 1000 hypertensive pregnancies.|
|ASSHP = Australasian Society for the Study of Hypertension in Pregnancy.5|
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3: Management protocol during pregnancy|
- Blood pressure (BP) measurements six times per day;
- Fetal cardiotocograph recordings on alternate days (or more often if clinically indicated);
- Daily urinalysis;
- Biochemistry and haematological testing at least twice weekly;
- Bedrest if there is evidence of intrauterine fetal growth retardation, or maternal neurological features or severe hypertension.
- Oral antihypertensive therapy (single agent or combinations) of oxprenolol, hydralazine, methyldopa, prazosin or nifedipine was instituted if the systolic BP was persistently > 160 mmHg or diastolic BP persistently > 90 mmHg after overnight bedrest in hospital.
- Parenteral antihypertensive therapy (sublingual nifedipine or intravenous hydralazine) was given for severe hypertension (Box 2).
- Convulsion prophylaxis (intravenous phenytoin followed by oral phenytoin) was used for women with neurological disturbances (Box 2).
Indications for delivery.
Delivery (by induction) was scheduled after 38 weeks' gestation if the BP remained stable and the cervix was favourable.
Indications for delivery before 38 weeks' gestation were:5
- Fetal compromise: premorbid (cardiotocographic) tracing of fetal heart rate or failure of fetal growth (assessed by doppler ultrasound).
- Inability to control maternal BP;
- Persistent neurological disturbances (see Box 2);
- Progressively rising liver enzyme or serum creatinine levels, or worsening thrombocytopenia.
Women whose pregnancies could not be prolonged beyond 30 weeks' (and occasionally 32 weeks') gestation were sometimes transferred before delivery to a tertiary referral unit with neonatal intensive care facilities. Outcomes of this group were included in our analysis.
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|For box 4 click here|
5: Maternal and fetal outcomes in women with pre-eclampsia (mild and severe) according to parity and gestation at presentation (see text for definitions). Data are percentages or means (standard deviation). |
|Gestation at presentation|
|Nulliparae|| Parous||P|| ≤ 32 wks||> 32 wks|| P|
|Age (years)||27 (5)||30 (5)|| < 0.0001*||29 (5)||28 (5)||0.30|
|Gestation at presentation (weeks)||36 (4)||35 (6)||0.009||27 (7)||37 (2)||< 0.0001*|
|Gestation at delivery (weeks)||38 (3)||38 (2)|| 0.89||35 (4)||38 (2)||< 0.0001*|
|Plasma creatinine (mmol/L)||.07 (.04)||.07 (.02)||.18||.08 (.08)||0.07 (.02)|| 0.51|
|Plasma uric acid (mmol/L)||.40 (.20)||.37 (.04)|| .01||.38 (.09)||0.39 (0.17)||0.66|
|Plasma albumin (g/L)||33 (5)||34 (5)|| .34||31 (8)||34 (4)||0.002*|
|Haemoglobin (g/L)||119 (23)||122 (16)|| .03||117 (37)||121 (15)||0.20|
|Haematocrit (%)||35.1 (5.5)||35.9 (5.6)|| .10||33.7 (8.7)||35.7 (4.7)||0.02|
|Platelets (x 109/L)||223 (82)||232 (82)|| .11||206 (95)||230 (79)||0.009*|
|PNM (per 1000)||17||3||0.06||54||4||< 0.0001*|
|Birthweight (g)||2984 (701)||2985 (694)|| 0.98||2312 (960)||3105 (561)||< 0.0001*|
* Statistically significant . SGA = small-for-gestational-age. PNM = perinatal mortality.
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6: Maternal and fetal outcomes in women with different forms of hypertension in pregnancy (ASSHP classifications). Data are percentages or means (standard deviation).|
|Pre-eclampsia||Essential hypertension|| Superimposed pre-eclampsia||P*|
|Age (years)||28 (5)||30 (5||30 (5)||> 0.0001†|
|Gestation at presentation (weeks)||35 (5)||26 (10)||28 (10)|| < 0.0001†||0.17|
|Gestation at delivery (weeks)||38 (3)||38 (2)||36 (1)||0.0007†||< 0.0001†|
|Hyperuricaemia (%)||58||16||83||< 0.0001†||0.0001†|
|Severe hypertension||21%||13%||38%||0.0005†||< 0.0001†|
|Renal insufficiency||7%||0||9%||0.62||< 0.0001†|
|Liver disease||10%||1%||11%||0.79||< 0.0001†|
|Plasma creatinine (mmol/L)||0.07 (0.04)||0.06 (0.02)||0.07 (0.02)||0.78||< 0.0001†|
|Plasma uric acid (mmol/L)||0.39 (0.16)||0.32 (0.25)||0.46 (0.35)||0.09||0.002†|
|Plasma albumin (g/L)||33 (5)||35 (6)||33 (5)||0.81||0.04|
|Haemoglobin (g/L)||120 (20)||119 (14)|| 117 (17)||0.14||0.52|
|Haematocrit (%)||35.4 (5.5)||35.1 (4.0)|| 34.7 (5.4)||0.29||0.64|
|Platelets (x 109/L)||226 (82)||256 (68)|| 235 (78)||0.36||0.03|
|SGA (%)||19||9||28||0.20||< 0.0001†|
|PNM (per 1000)||12||9||12||0.93||0.80|
|Birthweight (g)||2984 (701)||3260 (652)|| 2795 (935)||0.08||0.0001†|
|* Significance of difference between outcomes for women with pre-eclampsia and superimposed pre-eclampsia (and for women with essential hypertension and superimposed pre-eclampsia). †Statistically significant. SGA = small-for-gestational-age. PNM = perinatal mortality. ASSHP = Australasian Society for the Study of Hypertension in Pregnancy.5
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