You are on page 1of 6

Pregnancy Hypertension 11 (2018) 12–17

Contents lists available at ScienceDirect

Pregnancy Hypertension
journal homepage: www.elsevier.com/locate/preghy

Indications for delivery in pre-eclampsia T


a,⁎ c b c c c a,b
N. Varnier , M.A. Brown , M. Reynolds , F. Pettit , G. Davis , G. Mangos , A. Henry
a
Department of Women’s and Children’s Health, St George Hospital, Kogarah, NSW, Australia
b
School of Women’s and Children’s Health, UNSW Medicine, Sydney, Australia
c
Department of Renal Medicine, St George Hospital, Kogarah, NSW, Australia

A B S T R A C T

Objective: Examine the frequency with which the most accepted indicators for delivery in pre-eclampsia are used
in a population with predominantly late-onset (birth > 32 weeks) pre-eclampsia (PE).
Methods: Retrospective cohort study using the St George Public Hospital (SGH) Hypertension in Pregnancy
database. Demographic, pregnancy, and outcome details were extracted and verified by comparison with data
collection sheets.
Results: From 2001 to 2013, 908 women (970 babies) with PE were included, of which a subgroup of 303
women (33%) had clearly delineated delivery triggers available. This subgroup of women had similar demo-
graphic and outcome characteristics to the total PE population.
In this group, the most common maternal trigger for delivery apart from gestational age 37+ weeks was
difficult to control/severe hypertension (114 cases, 38%) and the most common fetal trigger intrauterine growth
restriction (IUGR: 14 cases, 4%). 78 (35%) of term women had no specific delivery trigger other than gestation.
A primary maternal trigger and/or associated complication was slightly more common in those delivering <
37 weeks vs 37+ weeks (52 vs 38%, p = .03), while a fetal or combined maternal/fetal complication was over
four times more common in preterm women (25 vs 6%, p < .001).
Conclusion: In our population of predominantly late-onset PE, maternal triggers for delivery (predominantly
severe hypertension) far outweigh fetal triggers (predominantly IUGR). Fetal and mixed indicators for delivery
were relatively more common in women delivering preterm, possibly reflecting the severity of placental dys-
function in this subgroup.

1. Background indicators for delivery in hypertensive pregnancies [5,6]. As noted in


the SOMANZ and ISSHP guidelines [6,7], triggers for delivery in the
Management of the hypertensive expectant mother has evolved with case of pre-eclampsia include gestational age 37 weeks or more
concurrent understanding of the pathophysiology of disease and out- (reaching “term”), deteriorating maternal condition (manifest as any of
comes. Hypertensive disorders complicate 6–8% of all pregnancies, uncontrollable blood pressure, severe persistent maternal symptoms
with 3–4% complicated specifically by pre-eclampsia [1,2]. Although despite blood pressure control, or laboratory evidence of deteriorating
there are multiple temporizing management strategies for pre- maternal end-organ function) and deteriorating fetal condition. Mul-
eclampsia and gestational hypertensive disorders, definitive manage- tiple triggers may be present.
ment is delivery of the placenta (and therefore of the fetus) [3]. Fol- Whilst some studies cite ‘severe disease’ as an indication for delivery
lowing delivery, most symptoms of pre-eclampsia resolve within days to [6,8] we are not aware of studies describing the relative frequency with
weeks, and blood pressure has been shown to return to normal gen- which each specific delivery trigger (or combination of triggers) occurs.
erally within a maximum of three months. However, as preterm or early Additionally, many studies focus on severe early-onset pre-eclampsia
term delivery increases risk of morbidity for mother and baby [4], where delivery occurs prior to 34 weeks due to the high rate of maternal
difficulties arise in deciding what particular set of circumstances should and fetal complications in early-onset cases [6,9,10]. However, the
lead to delivery rather than expectant management of hypertensive predominant burden of hypertensive disorders of pregnancy still occurs
disorders of pregnancy. in the far more numerous late onset cases. A recent meta-analysis
Progression of pre-eclampsia, failure to control maternal blood suggested that the early-onset preeclampsia rate was 0.38 per 100 de-
pressure, or failure of fetal growth are common recommended liveries compared to 2.72 per 100 deliveries for late-onset preeclampsia


Corresponding author.
E-mail address: n.varnier@yahoo.com (N. Varnier).

https://doi.org/10.1016/j.preghy.2017.11.004
Received 17 January 2017; Received in revised form 3 September 2017; Accepted 20 November 2017
Available online 08 December 2017
2210-7789/ © 2017 International Society for the Study of Hypertension in Pregnancy. Published by Elsevier B.V. All rights reserved.
N. Varnier et al. Pregnancy Hypertension 11 (2018) 12–17

[11]. Similar findings were noted in the SCOPE study which found an Table 1
early onset PE rate (i.e. < 34-weeks’ gestation) of 0.5% [12]. SOMANZ triggers for delivery (7).
We therefore examined the frequency with which the most com-
Maternal Fetal
monly recognised triggers for delivery are considered responsible in the
setting of pre-eclampsia ≥32 weeks’ gestation (gestation limited by Gestational age > 37/40 Placental abruption
study hospital special care nursery capacity). We also aimed to examine Uncontrollable blood pressure Severe growth
restriction
the associations of demographic, pregnancy and outcome factors, in-
Deteriorating platelet count Non-reassuring fetal
cluding time from presentation to delivery, with each delivery indica- Intravascular haemolysis status
tion, in order to potentially guide future patient counselling and man- Deteriorating liver function
agement. Deterioration renal function
Persistent neurological symptoms
Persistent epigastric pain, nausea or vomiting
2. Methods
with abnormal LFTs
Pulmonary oedema
We conducted a retrospective cohort study at St George Hospital, a
metropolitan Sydney teaching hospital with approximately
2700 births/annum. The primary data source accessed was the complications with underlying maternal and pregnancy characteristics,
Hypertension in Pregnancy (HIP) database, used since 1987 to docu- the following data was also analysed: maternal age and parity; obstetric
ment the management of any hypertensive pregnancy at the hospital. history, medical history including chronic hypertension, pre-existing
The data is collected in a standardised data collection sheet by mid- renal disease, pre-existing diabetes; pregnancy history (singleton or
wifery staff at the time of confinement and subsequently transposed multiple pregnancy, gestational diabetes); gestation at first presentation
into an electronic database. The study was limited to a 12-year period of hypertension; presentation to delivery interval; gestational age at
from which the most comprehensive data was available (January 1, delivery, birth weight, mode of birth. To ensure accurate information
2002 to December 31, 2013) for St George Public Hospital patients. about delivery triggers, original HIP data from January 2010 to
The definition of hypertension in pregnancy has been the subject of December 2013 was cross-checked against patient medical records.
recent review [13]. For the purposes of this study, the parameters
outlined by the SOMANZ/ISSHP guidelines [14] which guide treatment 2.1. Data analysis
protocols at the study hospital, were used. Thus, patients with hy-
pertension in pregnancy were those with a systolic blood pressure Data were analysed using SPSS (IBM SPSS Statistics for Windows,
≥140 mmHg or diastolic ≥90 mmHg. A sustained finding of hy- Version 22.0). Chi-square test or Fisher exact tests were used as ap-
pertension in pregnancy was routinely treated with oral anti- propriate to test for significant differences between categorical vari-
hypertensive agents as per local protocol. Severe hypertension in this ables. Student’s t-test and ANOVA were used as appropriate to compare
Unit at the time of the study was defined as a systolic blood pressure continuous variables. All tests were two-tailed, with statistical sig-
≥170 mmHg or diastolic blood pressure ≥110 mmHg (treated urgently nificance defined as a probability value of < .05. Subgroup analysis was
with standard release nifedipine). This unit maintained a consistent performed for women who were term (37 or more completed weeks at
treatment policy throughout the data collection period and continues to time of delivery) vs preterm, and for singleton vs twin pregnancy.
maintain the same treatment policy. ‘Tight’ control is favoured [15],
aiming for blood pressure readings below systolic blood pressure 2.2. Ethics approval
≥140 mmHg or diastolic ≥90 mmHg. Patients are routinely com-
menced on oxprenolol 40 mg three times per day (TDS); methyldopa at The study was approved as low/negligible risk research by the
a starting dose of 250 mg TDS if beta-blockers are contraindicated. South Eastern Sydney Local Health District Human Research and Ethics
These medications are titrated to maximum recommended doses Committee (HREC 13/152, LNR/13/POWH/384).
through close assessment in a day stay unit and admission if required.
Additional agents are added as required. The use of more than two 3. Results
agents and sustained suboptimal control of blood pressure constitutes
‘difficult to control BP’. 3557 deliveries of pregnancies affected by hypertension were re-
Pre-eclampsia (PE) was diagnosed as hypertension at > 20 weeks’ corded in the database for the study period. After exclusion of women
gestation with evidence of effect on one or more other body systems with gestational or essential hypertension only, those delivering at the
[16,17] including cardiovascular, renal, hepatic/coagulation systems, private hospital (with no access to records for verification of delivery
neurological symptoms and the fetus and placenta. The HIP database triggers), and women < 32 weeks’ gestation transferred out, 908
also records whether PE is de novo or superimposed on essential hy- women had a final diagnosis of PE. Of these, 304 (287 singleton
pertension. pregnancies and 17 twins; n = 287 de novo PE, 17 superimposed PE)
The primary inclusion criterion was final diagnosis of de novo or had delivery trigger data and 604 outcome data only. Baseline demo-
superimposed PE. Only pregnancies delivered at gestation greater than graphic and pregnancy data is shown in Table 2. As shown in Table 2,
32 completed weeks were eligible as delivery prior to this gestation is demographic data and outcomes were similar between our background
not undertaken at the study hospital, and triggers for delivery may have PE population and the study (delivery trigger) population, suggesting
differed at the hospital to which the mother had been transferred. the subgroup with trigger data is representative of our total PE popu-
Primary data sought were the recorded trigger or triggers for delivery as lation. Average maternal age was 30.7 ± 6.1 years, mean gestation
suggested by SOMANZ [6] and shown in Table 1. For the term group, (GA) at time of diagnosis 36.3 ± 2.6 weeks, and at delivery
where GA of 37+ weeks was in itself sufficient to trigger delivery, any 37.7 ± 1.9 weeks (74% GA 37+ weeks at delivery). There were no
additional maternal or fetal complications from Table 1 were recorded. significant differences between term and preterm groups regarding
Note was also made where PE was diagnosed but was not the primary preeclampsia type (de novo vs superimposed), however women with PE
indicator for delivery; in these cases, another obstetric indicator for delivering preterm were significantly older, more likely to have a twin
delivery was present (e.g. cholestasis or premature rupture of mem- pregnancy, and more likely to be multiparous (Table 2).
branes) with subsequent intrapartum or postpartum diagnosis of pre- The most common maternal trigger for delivery or associated term
eclampsia. complication was difficult to control/severe hypertension (114 cases,
To examine the association of preterm delivery triggers and term 38%) and the most common fetal trigger was intrauterine growth

13
N. Varnier et al. Pregnancy Hypertension 11 (2018) 12–17

Table 2
Demographic and pregnancy characteristics.

Excluded PE population Study population P values no trigger vs Term delivery Preterm delivery P values term vs
(n = 604 women, 649 (n = 304 women, 321 study population (n = 225) (n = 79) preterm delivery
babies) babies)
N (%) N (%) N (%) N (%)

Parity
- Primiparous 384 (64) 213 (70) .052 166 (74) 47 (60) .02
- Multiparous 220 (36) 91 (30) 59 (26) 32 (41)

Plurality
- Singleton 559 (93) 287 (94) .30 222 (99) 65 (82) .001
- Twin 45 (7) 17 (6) 3 (1) 14 (18)

PE subtype
- De-novo 564 (93) 287 (94) .55 214 (95) 73 (92) .46
- Superimposed 40 (7) 17 (6) 11 (5) 6 (8)

Mean ± SD Mean ± SD Mean ± SD Mean ± SD


Maternal age, years 30.3 ± 5.6 30.7 ± 6.1 .39 30.2 ± 6.0 32.0 ± 6.1 .02
Birthweight, singletons (kg) 3.05 ± 0.74 3.07 ± 0.66 .79 3.26 ± 0.55 2.50 ± 0.54 < .001
GA at diagnosis (weeks) 36.2 ± 2.7 36.3 ± 2.6 .65 37.7 ± 1.9 34.1 ± 1.8 < .001
GA at delivery (weeks) 37.5 ± 2.1 37.7 ± 1.9 .32 38.6 ± 1.3 35.1 ± 1.0 < .001
GA 37 + weeks at delivery, 427 (71) 225 (74) .29 – – –
n (%)

PE = preeclampsia; SD = standard deviation; GA = gestational age.


Bold values designate statistically significant values.

restriction (IUGR: 14 cases, 4%) (Table 3). Seventy-eight (35%) term population was severe or difficult to control blood pressure, and the
women had no specific complication other than their PE diagnosis and most common fetal indicator was suspected intrauterine growth re-
were thus delivered on the basis of their gestation alone, while 27 striction. Severe hypertension was also the most common associated
women (11%) only developed pre-eclampsia intrapartum or post- feature of term PE, occurring in approximately one-third of cases, while
partum. A primary maternal trigger/associated complication was one-third had no associated concerning maternal or fetal features and
slightly more common in those delivering < 37 weeks vs 37+ weeks were delivered on the basis of term gestation alone. On comparison of
(52 vs 38%, p = .02), while a fetal or combined maternal/fetal com- the term and preterm PE populations, the presence of both a maternal
plication was over four times more common in preterm women (25 vs and fetal indication for delivery was much more common in preterm PE
6%, p < .001). Overall, maternal and fetal indications for delivery (25% vs 6%).
were more common in women delivered pre-term (Table 3).
Pregnancy outcomes are shown in Table 4. Over half of pregnancies 4.1.1. Preterm vs term women
were induced (n = 172; 57%); 23% of women laboured spontaneously Although there were a significantly higher proportion of preterm
and 20% (n = 70) had an elective caesarean section (‘elective cae- patients with maternal triggers than term patients (Table 3), maternal
sarean’: constitutes a pre-labour caesarean section, planned at a time complications (predominantly severe hypertension) were still present in
acceptable to both the woman and the team) [18,19]. There was a over one-third of term women. Additionally, rates of serious compli-
significantly greater proportion of elective Caesarean and fewer at- cations such as liver/haematological dysfunction and eclampsia did not
tempted inductions of labour in the preterm group. Mean birth weight differ between groups, consistent with our group’s previous research
was 3.07 ± 0.66 kg. As expected, birthweight was significantly lower showing adverse maternal outcomes across the gestational age spec-
in the preterm group, although the proportion of singleton babies of trum [4]. Conversely, presence of a primary fetal indication for delivery
birthweight < 10th centile for gestation [20] did not differ significantly (predominantly IUGR or suspected fetal distress from ultrasound/car-
(18% in term group, 25% in preterm group). In the preterm group when diotocograph findings), or mixed maternal/fetal final indication for
the delivery trigger was either fetal or mixed fetal/maternal, 19/20 delivery, was over four times more common in the preterm group. This
women (95%) had a Caesarean, of which 11/19 (58%) were emergent/ may reflect differing preeclampsia phenotypes, with a greater degree of
urgent. overt placental pathology in the preterm group [21]. Moreover, it may
Regarding demographic subgroups, there were no significant dif- reflect a higher clinical threshold for proceeding with preterm delivery
ferences in delivery triggers/associated complications between women and therefore, more advanced disease by the time delivery is triggered.
having their first and subsequent deliveries, (Table 5) however parous Clinically, this was reflected in a very high rate of caesarean section
women were more likely to deliver preterm. Women with twin preg- (half of which were emergency cases after an attempt at induction) in
nancies were, unsurprisingly, more likely to deliver preterm (82% vs the 20 preterm women who had both a maternal and fetal indication for
23%). They were also more likely than singleton pregnancies to have a delivery. Although the numbers in this subgroup are small, it does
mixed maternal/fetal indication for delivery (24% vs 4%, p = .006) and suggest that these patients should not be quoted (normal pregnancy)
less likely to have no specified trigger or a non-PE diagnosis as the population statistics regarding Caesarean rates/induction outcomes,
indication for delivery (p < .001). and that after discussion elective Caesarean is reasonable to offer if that
is the maternal preference.
4. Discussion Also noted in the preterm delivery group was that a higher pro-
portion were parous rather than nulliparous. This may be a chance
4.1. Main findings statistical finding due to multiple comparisons. It may also represent
close surveillance of a known higher-risk group in our cohort, and
In this cohort of preeclamptic women ≥32 weeks’ gestation man- prompt diagnosis and management of late preterm preeclampsia when
aged at a single unit with consistent diagnosis and management pro- it arose, as over half the parous women in this study had a prior history
tocols, the most common maternal indicator for delivery in the preterm of a hypertensive disorder of pregnancy.

14
N. Varnier et al. Pregnancy Hypertension 11 (2018) 12–17

Table 3 previously reported (6–10%) [21,22]. This could be related to the


Maternal and fetal indicators for delivery. length of pregnancy in a higher risk population who are not routinely
induced at 37 weeks unless PE has been diagnosed. It may also reflect in
Term Preterm P value
delivery, n delivery, n part increased local ascertainment of intrapartum and early postpartum
(%) (%) cases (vs antenatal diagnosis), as timing of diagnosis can be differ-
Total Total entiated both through the HIP database and our centre’s obstetric da-
n = 225 n = 79 tabase.
Any Maternal 84 (37.3) 41 (51.9) .02
Trigger/ 4.2. Comparative literature
association×
Maternal triggers Difficult to control/ 78 (34.7) 36 (45.6) .06 Whilst a number of guidelines are available regarding the general
Severe Hypertension*
indicators for delivery in pre-eclampsia, a review of available literature
Liver or haematological 5 (2.2) 5 (6.3) .13
dysfunction failed to yield any comparative studies reviewing the actual frequency
Eclampsia 1 (0.4) 0 (0) 1.0 of each indicator for delivery (search carried out using OVID MedLine
Gestational Diabetes 14 (6.2) 2 (2.5) .21 and PubMed, included search terms: “pre-eclampsia”, “delivery”, “in-
Other† 11 (4.9) 10 (12.7) .02
dication”, “trigger”, “induction”).
No specific trigger (PE 59 (26.2) 15 (19) .20
but spontaneous Although ‘severe disease’ is often cited as a key indicator for de-
labour) livery in pre-eclampsia this is not always defined in a standard manner,
GH/EH†† 9 (4) 0 (0) .12 though the ISSHP has sought to address this recently [1,6,23]. More-
Preeclampsia alone††† 43 (19.1) 11 (13.9) .30 over, the literature is commonly focused on the early-onset population
Postdates 5 (2.2) N/A
[9] and fails to consider the clinical reality of a late-onset pre-
Any Fetal Trigger 20 (8.9) 22 (27.8) < .001
Fetal triggers Intrauterine 6 (2.7) 8 (10.1) .01 eclampsia, mostly occurring above 34-weeks’ gestation. This study as-
GrowthRestriction sesses the frequency of each indicator as delineated in the local SO-
(IUGR) MANZ guidelines, which are similar to the recent ISSHP guidelines
Abnormal CTG/Fetal 6 (2.7) 7 (8.9) .05
[13].
distress (incl. abnormal
doppler)
PROM/PPROM 2 (0.9) 1 (1.3) 1.0 4.3. Strengths and limitations
Other*** 6 (2.7) 6 (7.6) .09
Final Indication for Delivery The main strengths of this study are a) As far as we are aware, ex-
Primary maternal indication 85 (37.8) 41 (51.9) .03
amination of the relative frequency of triggers for delivery across a late
Primary fetal indication 10 (4.4) 7 (8.9) .14
Mixed maternal/fetal indication 3 (1.3) 13 (16.5) < .001 preterm/term preeclamptic population has not been performed, and b)
Non-PE primary indication 24 (10.7) 7 (8.9) 0.65 the study was carried out in a single centre whose management pro-
Spontaneous pre-term delivery – 9 (11.4) tocols are consistent, managed by one team and a single agreed man-
No specified delivery trigger 78 (34.7) –
agement protocol, thus minimising the effect of individual preferences
Intra- or post-partum diagnosis, IOL for non- 25 (11.1) 2 (2.5) .02
BP reason
or bias upon timing of delivery. The major limitations of the study are
its retrospective nature and its modest sample size, with indications for
GH: gestational hypertension; EH: essential hypertension; PROM: premature rupture of delivery data limited to the proportion of cases with original datasheets
membranes; PPROM: preterm, premature rupture of membranes, IOL: induction of la- available (as indications for delivery have only been added to our
bour, CTG: cardiotocograph. electronic database more recently). However, analysis has been carried
Bold values designate statistically significant values.
×
out on the data available and comparison with the subgroup of verified
For term group, preeclampsia alone sufficient to trigger delivery: Table 3 shows
whether additional maternal or fetal indicators were also present.
data has confirmed accuracy of recording.
* Blood pressure requiring treatment with two or more agents. Retrospective studies carry their own inherent limitations, including

Other primary maternal indication for delivery than preeclampsia (e.g. cholestasis) – lack of data fields that may be relevant to interpretation of outcome,
with subsequent intrapartum or postpartum development of preeclampsia. such as BMI which was not until recently included in this study hos-
††
Delivered for GH/EH but then developed preeclampsia intrapartum or postpartum. pital’s databases. Despite cross-checking for triggers data against both
†††
Preeclampsia is the only indicator for delivery (e.g. routine delivery at 37 weeks or
our datasheets and patient files/electronic records, there remains scope
following diagnosis beyond term).
*** Includes: Small for gestational age, Malposition, Oligohydramnios, Antepartum
for error in interpretation of clinician decision-making which could
Haemorrhage, Decreased fetal movement. only be overcome with a prospective study design.

In the term group, the majority of patients had at least one asso- 4.4. Future research
ciated abnormality/complication of their pre-eclampsia, with only 19%
having no other concurrent abnormality. The most common compli- Subgroup numbers in the preterm (32–37 weeks) triggers group
cation was severe hypertension (35%), with only a small minority of remain small, and further studies from other Units are needed to see
term cases having a diagnosed fetal complication or major maternal whether these data are applicable nationally or internationally.
complication such as eclampsia. This is consistent with findings from
the HYPITAT study [1] wherein continued expectant management at 5. Conclusion
term leads to higher likelihood of severe hypertension, and that unless
new evidence arises to suggest risks of early term delivery in PE out- This study quantifies the frequency of triggers/indications for de-
weigh benefits, PE alone at 37+ weeks is sufficient trigger for delivery. livery in pre-eclampsia ≥32 weeks’ gestation. It confirms that severe/
In this group, we also found a significant minority where PE was not difficult to control maternal blood pressure is the most common in-
part of decision making regarding delivery: 11% of women laboured dicator for delivery across gestations, with fetal triggers/complications
spontaneously and were then noted to have PE either intra-partum or occurring in a minority of cases, although substantially higher in the
postpartum, while 11% underwent induction for a non-PE reason and preterm group. A mixed maternal/fetal indication, which was sig-
were subsequently diagnosed with PE. The rate of diagnosis of intra- nificantly more common in preterm gestation, supports an increased
partum or postpartum PE in this group was noted to be higher than placental severity of pre-term disease with consequent increased po-
tential for intervention or poor fetal outcome.

15
N. Varnier et al. Pregnancy Hypertension 11 (2018) 12–17

Table 4
Pregnancy outcome data.

Overall group, n (%) Term delivery, n (%) Preterm delivery, n (%) P-value (term vs preterm)
Total n = 304 women, 321 babies Total n = 225 women 228 Total n = 79 women 93 babies##
babies#
Mean ± SD Mean ± SD Mean ± SD

Birth weight (singletons only), kg 3.07 ± 0.66 3.26 ± 0.55 2.50 ± 0.54 < .001
Gestation at delivery, weeks 37.7 ± 1.9 38.6 ± 1.3 35.1 ± 1.0

N (%) N (%) N (%)


Birthweight < 10th centilea (singletons) 56 (19.5) 40 (18.0) 16 (24.6) .24
Spontaneous labour* 70 (23.0) 58 (25.8) 12 (15.2) .054
No established labour 62 (20.4) 31 (13.8) 31 (39.2) < .001
Induction 172 (56.6) 136 (60.4) 36 (45.6) .02
MOD: Vaginal delivery 115 (37.8) 89 (39.6) 26 (32.9) .30
Assisted vaginal delivery 72 (23.7) 59 (26.2) 13 (16.5) .08
Caesarean section** 117 (38.5) 77 (34.1) 40 (50.6) .01
- Emergency/urgent caesarean 82 (27.0) 56 (24.8) 26 (32.9) .17
- Elective caesarean 35 (11.5) 21 (9.3) 14 (17.7) .04

SD = standard deviation; MOD = Mode of delivery.


Bold values designate statistically significant values.
a
For gestational age as per Australian birthweight centiles (23).
* Australian averages: Spontaneous labour: 54.2%, No labour: 19.4%, Induction: 26.3%; NSW: 54.1, 18.6%, 27.3% (18).
** Australian average 32% (18).
#
222 singleton, 3 twin pregnancies.
##
65 singleton, 14 twin pregnancies.

Table 5
Maternal and fetal indicators for delivery by parity.

Nulliparous, n (%) Multiparous, n (%) P value


Total n = 213 Total n = 91

Any maternal trigger/association 87 (41) 38 (42) .88


Maternal triggers Difficult to control/Severe Hypertension* 78 (37) 36 (40) .63
Liver or haematological dysfunction 9 (4) 2 (2) .52
Eclampsia 1 (0.5) 0 (0) 1.0
Gestational diabetes 13 (6) 3 (3) .32
Other† 12 (6) 11 (12) .06
No specific trigger (PE but spontaneous labour) 56 (26) 18 (20) .68
GH/EH†† 7 (3) 2 (2) .73
Preeclampsia alone††† 35 (16) 19 (21) .35
Postdates 6 (3) 0 (0) .18
Any fetal trigger 29 (14) 13 (14) .88
Fetal triggers Intrauterine Growth Restriction (IUGR) 10 (5) 4 (4) .91
Abnormal CTG/Fetal distress (incl. abnormal Doppler) 9 (4) 5 (5) .63
PROM/PPROM 3 (1) 0 (0) 1.0
Other*** 8 (4) 4 (4) .76
Final Indication for Delivery
Primary maternal indication 85 (40) 40 (44) .55
Primary fetal indication 13 (6) 4 (4) .54
Mixed maternal/fetal indication 8 (4) 8 (9) .08
Non-PE primary indication 24 (11) 7 (8) .33
Spontaneous pre-term delivery 6 (3) 3 (3) 1.0
No specified delivery trigger 57 (27) 22 (24) .73
Intra- or post-partum diagnosis, IOL for non-BP reason 20 (9) 7 (8) .62

GH: gestational hypertension; EH: essential hypertension; PROM: premature rupture of membranes; PPROM: preterm, premature rupture of membranes, IOL: induction of labour, CTG:
cardiotocograph.
* Blood pressure requiring treatment with two or more agents.

Other primary maternal indication for delivery than preeclampsia (e.g. cholestasis) – with subsequent intrapartum or postpartum development of preeclampsia.
††
Delivered for GH/EH but then developed preeclampsia intrapartum or postpartum.
†††
Preeclampsia is the only indicator for delivery (e.g. routine delivery at 37 weeks or following diagnosis beyond term).
*** Includes: Small for gestational age, Malposition, Oligohydramnios, Antepartum Haemorrhage, Decreased fetal movement.

Acknowledgement online version, at http://dx.doi.org/10.1016/j.preghy.2017.11.004.

The authors would like to extend their thanks to Ms Jennifer Beddoe References
who is responsible for maintenance of the database which is herein
referenced. [1] C.M. Koopmans, D. Bijlenga, H. Groen, S.M. Vijgen, J.G. Aarnoudse, D.J. Bekedam,
et al., Induction of labour versus expectant monitoring for gestational hypertension
or mild pre-eclampsia after 36 weeks' gestation (HYPITAT): a multicentre, open-
Appendix A. Supplementary data label randomised controlled trial, Lancet 374 (9694) (2009) 979–988 PubMed
PMID: 19656558.
[2] M.A. Brown, Pre-eclampsia: a lifelong disorder, Med. J. Aust. 179 (4) (2003)
Supplementary data associated with this article can be found, in the

16
N. Varnier et al. Pregnancy Hypertension 11 (2018) 12–17

182–183 PubMed PMID: 12914506. (SCOPE) Cohort Study, Hypertension 64 (2014) 644–652.
[3] B. Jim, S. Sharma, T. Kebede, A. Acharya, Hypertension in pregnancy: a compre- [13] A.L. Tranquilli, G. Dekker, L. Magee, J. Roberts, B.M. Sibai, W. Steyn, et al., The
hensive update, Cardiol. Rev. 18 (4) (2010). classification, diagnosis and management of the hypertensive disorders of preg-
[4] F. Pettit, G. Mangos, G. Davis, A. Henry, M.A. Brown, Pre-eclampsia causes adverse nancy: a revised statement from the ISSHP, Pregnancy Hypertens. 4 (2014) 97–104.
maternal outcomes across the gestational spectrum, Pregnancy Hypertens. 5 (2015) [14] Lowe SA, et al., Guidelines for the management of hypertensive disorders of
198–204. pregnancy 2008, SOMANZ Guidelines, 2008.
[5] L.A. Magee, M. Helewa, J.M. Moutquin, P. von Dadelszen, Hypertension Guideline [15] L.A. Magee, et al., Less-tight versus tight control of hypertension in pregnancy, N.
Committee, Strategic Training Initiative in Research in the Reproductive Health Engl. J. Med. 372 (2015) 407–417.
Sciences Scholars, Diagnosis, evaluation, and management of the hypertensive [16] K. van der Tuuk, C.M. Koopmans, H. Groen, B.W. Mol, M.G. van PampusHYPITAT
disorders of pregnancy, J. Obstet. Gynaecol. Can. 30 (3 Suppl.) (2008) S1–S48 Study Group, Impact of the HYPITAT trial on doctors' behaviour and prevalence of
PubMed PMID: 18817592. eclampsia in the Netherlands, BJOG 118 (13) (2011) 1658–1660 PubMed PMID:
[6] S.A. Lowe, L. Bowler, K. Lust, L.P. McMahon, M.R. Morton, R.A. North, M. Paech, J. 21985398.
M. Said, The SOMANZ guideline for the management of hypertensive disorders of [17] Pregnancy NHBPEPWGoHBPi, Report of the National High Blood Pressure
pregnancy 2014, http://www.somanz.org. Education Program Working Group on high blood pressure in pregnancy, Am. J.
[7] M.A. Brown, M.D. Lindheimer, M. de Swiet, A. Van Assche, J.M. Moutquin, The Obstet. Gynecol. 183 (1) (2000) S1–S22 PubMed PMID: 10920346.
classification and diagnosis of the hypertensive disorders of pregnancy: statement [18] RANZCOG Women's Health Committee, Timing of Elective Caesarean Section at
from the International Society for the Study of Hypertension in Pregnancy (ISSHP), Term (C-Obs 23), 2014.
Hypertens. Pregnancy 20 (1) (2001) IX–XIV PubMed PMID: 12044323. [19] RANZCOG Women's Health Committee, Categorisation of Urgency for Caesarean
[8] Practice CoO, Emergency therapy for acute-onset, severe hypertension with pre- Section (C-Obs 14), 2015.
eclampsia or eclampsia, in: Gynaecologists ACoOa (Ed.), Committee Opinion No. [20] L.Z.Z. Hilder, M. Parker, S. Jahan, G.M. Chambers, Australia's Mothers and Babies
514, Obstet Gynaecol, 2011, pp. 1465–1468. 2012, AIHW, Canberra, 2014.
[9] D. Churchill, et al., Interventionist versus expectant care for severe pre-eclampsia [21] B. Huppertz, Placental origins of preeclampsia: challenging the current hypothesis,
between 24 and 34 weeks’ gestation, Cochrane Database Syst. Rev. (2013). Hypertension 51 (4) (2008) 970–975.
[10] B. Sibai, G. Dekker, M. Kupferminc, Pre-eclampsia, Lancet 365 (2005) 785–799. [22] T. Dobbins, et al., Australian national birthweight percentiles by sex and gestational
[11] S. Lisonkova, K.S. Joseph, Incidence of preeclampsia: risk factors and outcomes age, 1998–2007, Med. J. Aust. 197 (2012) 291–294.
associated with early- veresus late-onset disease, Am. J. Obstet. Gynaecol. 209 [23] A. Tanquilli, The definition of severe and early-onset preeclampsia. Statements from
(2013) 544. the International Socety for the Study of Hypertension in Pregnancy, Pregnancy
[12] Kenny Lea, Early pregnancy predition of preeclampsia in nulliparous women, Hypertens. 3 (2013) 44–47.
combining clinical risk and biomarkers: the Screening for Pregnancy Endpoints

17

You might also like