Guideline to hypertensive disorders of pregnancy

1. PRE-ECLAMPSIA AND
ECLAMPSIA: BEST
PRACTICES.
PROF A. O. ADENIJI (MD, FWACS, FMCOG)
MARCH 2021 UPDATE/REVISION COURSE.

2. INTRODUCTION
 Pre‐eclampsia is a multi‐organ syndrome of
pregnancy that manifests after 20 weeks' gestation
with new‐onset hypertension alongside maternal
end‐organ dysfunction and/or fetal growth restriction
(Lowe 2009).
 It is responsible for 50,000 - 60,000 maternal deaths
annually worldwide and complicates 5% of all
pregnancies.
 Currently no effective treatment for pre‐eclampsia
 Delivery is the only cure

3. Definition
 No widely accepted definition of "severe" pre‐eclampsia
 The recent ISSHP (The International Society for the Study
of Hypertension in Pregnancy -2018) statement suggested:
 difficulty in controlling blood pressure and
 deteriorating clinical condition including HELLP syndrome -
Haemolysis, Elevated Liver enzymes and Low Platelets
 impending eclampsia,
 worsening thrombocytopenia (low platelets) or
 worsening fetal growth restriction
 less emphasis regarding increasing proteinuria (Tranquilli
2014).

4. Classification
 Preeclampsia is broadly classified into mild
and severe based on blood pressure and
symptoms/signs
 Mild= Blood pressure 140/90 - 160/100
 Severe= Blood pressure >160/100 +/- signs
and symptoms

5. Pathogenesis
 The exact pathogenesis of pre‐eclampsia is unknown but it
is likely that its evolution is multi‐factorial involving a
complex interplay between the mother, fetus and the
placenta.
 Most salient contemporary theories surrounding the
development of pre‐eclampsia, embrace the fundamental
contribution of the physiological mechanisms that
underlie the establishment of the pregnancy and the
process of placentation (Roberts 2005),
 During which the immature embryo (blastocyst) attaches
onto the uterine lining (endometrial decidua) and begins
the process of embedding into the underlying uterine
vasculature.

6. Pathogenesis contd
 For optimal placentation to occur, the outer (extra villous trophoblast)
layer of the blastocyst is able infiltrate and remodel the maternal spiral
arteries within the uterine walls.
 This invasive process transforms the spiral arteries into large conduits of
low‐resistance vessels that are capable of accommodating adequate
fetal‐placental blood flow during the evolution of pregnancy.
 Should the modification to the spiral arteries be disturbed, placental
development may be impaired;
 a reduction of blood flow ensues ultimately generating a state of uteroplacental
hypoxia, as witnessed with pre‐eclampsia and fetal growth restriction.
 Various hypotheses have been put forward to support interventions that
might delay or reverse this process (Fenton 2014).

7. Aetiology contd
OXIDATIVE STRESS THEORY
 The observation that women with pre‐eclampsia have decreased
plasma and placental concentrations of antioxidants (Hubel 1999) led
to the proposal that placental hypoperfusion may induce a state of
oxidative stress.
 This includes overproduction of highly reactive oxygen molecules or
free radicals, depleting the body’s stores of antioxidants.
 Oxidative stress, coupled with an exaggerated inflammatory response,
may cause the release of maternal factors that result in inappropriate
endothelial cell activation and endothelial cell damage.

8. Aetiology contd
 Endothelial cells line the inside surfaces of blood vessels and their
impairment results in the clinical signs of pre‐eclampsia, such as
hypertension and proteinuria. A woman’s risk of, and response to,
oxidative stress depends on various factors.
 These include the propensity for small low‐density lipoproteins,
hyperhomocysteinaemia, a genetically determined poor resistance to
oxidative stress, and a dietary deficiency of antioxidants (Roberts
2001).

9. Presentation
 The more severe early onset hypertension is associated with fetal growth
restriction.
 Women may present with late-onset hypertension and proteinuria, with
an absence of fetal growth restriction near term.
 This appears to have few long-term consequences for mother or infant.
Conversely, early onset, severe maternal disease is often associated with
fetal intrauterine growth restriction.
 Unrecognized fetal compromise contributes to the rate of fetal demise,
and 1 in 20 stillbirths without congenital abnormality is complicated by
or attributable to pre-eclampsia

10. Presentation contd
 Even in the presence of severe preterm disease, a woman can be
asymptomatic.
 Douglas and Redman reported an absence of hypertension and
proteinuria in 38% of women who presented with an eclamptic fit,
demonstrating that severe maternal adverse events occur even when
the traditional clinical definition of pre-eclampsia is not met.

11. Screening
 Screening for women at risk of pre‐eclampsia is an important part of
antenatal care in order to triage higher‐risk women for more intensive
antenatal surveillance and prophylactic interventions (Meher 2005).
 Most current strategies for risk assessment are based on the general
medical and obstetric history, alongside clinical examination.
 However, there is surprisingly little reliable evidence on the actual
risk associated with individual factors, and how they might interact
(Meher 2005).

12. Screening contd
 Routine screening for pre‐eclampsia is based on measurement of
blood pressure and urinalysis for proteinuria. Overall, 15% to 25% of
women with gestational hypertension progress to pre‐eclampsia
(Saudan 1998).
 Numerous physiological and biochemical screening tests and
algorithms have been developed, however, none so far has proved to
be of good predictive value and few are used in clinical practice
(Akolekar 2011; Oliveira 2014; Poon 2013).
 Increased resistance of the uterine arteries measured through Doppler
ultrasound is a commonly used safe and non‐invasive test to assess for
abnormal blood flow to the placenta, and at present holds some
promises (Papageorghiou 2004).

13. Preventive measures
 The use of antiplatelet agents such as aspirin is associated with a 17%
reduction in the risk of pre‐eclampsia in high‐risk women (Duley
2007);
 Early administration of prophylactic aspirin in high-risk women prior to 16 weeks’
gestation appears to reduce the risk of pre-eclampsia by 17%.
 Furthermore, there is an 8% relative risk reduction of preterm birth
 14% reduction in fetal and neonatal death
 Calcium supplementation (≥ 1g/day) is associated with a significant
reduction in the risk of pre‐eclampsia, particularly for women with
low calcium diets (Hofmeyr 2014).
 Antithrombotic therapies (such as low molecular weight heparin) may
decrease the risk of pre‐eclampsia in women at high risk of placental
dysfunction (Dodd 2013).

14. Preventive measures contd
 Supplementing women with melatonin, a potent antioxidant, may
increase their resistance to oxidative stress and subsequently limit the
systemic and uteroplacental endothelial damage that is observed in
pre‐eclampsia (Hobson 2013).

15. Risk factors
 Strong risk factors
 previous pre-eclampsia or hypertension in pregnancy,
 chronic kidney disease,
 chronic hypertension, diabetes (type 1 or 2), and
 autoimmune disorders e.g. systemic lupus erythematosus or antiphospholipid syndrome.
 Moderate risk factors:
 first pregnancy & teenage pregnancy
 age at >40 years or more,
 a pregnancy interval of greater than 10 years
 body mass index of >35 kg/m2
 family history of pre-eclampsia
 multiple pregnancy .
 The large SCOPE (Screening for Pregnancy Endpoints) cohort study showed that
there was a lower incidence of developing pre-eclampsia with:
 a small-for-gestational-age baby with
 25(OH)D concentrations of more than 75 nmol/L at 15 weeks’ gestation.

16. The vitamin D angle.
 Achkar et al (2015) suggested that women who developed pre-
eclampsia had a significantly lower vitamin D concentration at 14
weeks compared with women in the control group (mean 47.2 versus
52.3 nmol/L, p<0.0001) .
 Levels <30 nmol/L vs 50 nmol/L had a greater risk of developing pre-
eclampsia (aOR = 2.23; 95% CI = 1.29–3.83 — after adjustment for
other variables)
 suggesting that maternal vitamin D deficiency may be an independent
risk factor for the development of pre-eclampsia.

17. Predictors – Glycosylated Fibronetin
 A new test used for the prediction of pre-eclampsia is the
measurement of glycosylated fibronectin (GlyFn) serum levels in the
first trimester
 A longitudinal cohort study by Rasanen et al. (2015) showed levels to
be significantly higher in women with pre-eclampsia ( p<0.01) and to
remain higher throughout pregnancy
 Increased GlyFn levels were significantly associated with increased
blood pressure and small-for-gestational-age neonates.

18. Predictors 2
 Studies have shown that levels of cell-free fetal DNA (cffDNA) are
raised in women with pre-eclampsia.
 The hypothesis for increased levels of cffDNA is of abnormal
placentation, hypoxia reperfusion injury, and release of apoptotic
fragments containing cffDNA into maternal circulation .
 A systematic review showed that whilst cffDNA may have a role in
disease prediction in pre-eclampsia, its use is probably limited to the
early second trimester because its detection rate is too low at later
gestations (Contro et al, 2017)

19. Blood pressure control
 The NICE recommends keeping systolic blood pressure below 150
mmHg and diastolic blood pressure below 80–100 mmHg and using
labetalol as first-line treatment for hypertension over this threshold.
 The results of the Control of Hypertension In Pregnancy Study (CHIPS)
reported in 2016 demonstrated that:
 those with “tight” control achieved a lower blood pressure (by 5 mmHg) and there
was no increase in adverse perinatal outcome (adjusted OR 0.98, 95% CI 0.74–1.3)
and birth weight less than the tenth percentile (1.3, 0.93–1.8).
 However, there were reduced rates of severe maternal hypertension ( p<0.001)
with tighter control. it may be concluded that in these women who are at high risk
of the complications of severe hypertension, seizures, and intracerebral
hemorrhage, there may be benefit in tighter control of blood pressure

20. Antihypertensives
 Severe hypertension is treated with short-acting parenteral
antihypertensive agents, most frequently intravenous hydralazine or
labetalol.
 This is because of the speed of onset of action but means that they
require more intensive monitoring and can affect the fetus if large shifts
in blood pressure occur.
 A systematic review showed that, in most women, nifedipine achieved
treatment success similar to that of hydralazine (84% with nifedipine;
relative risk 1.07, 95% CI 0.98–1.17) or labetalol (100% with nifedipine;
relative risk 1.02, 95% CI 0.95–1.09).
 <2% of women who received nifedipine experienced hypotension.
 There were no differences in adverse maternal or fetal outcomes.
 Thus, the authors suggest that oral nifedipine is a suitable treatment for
severe hypertension in pregnancy and post-partum.

21.  A meta-analysis by Shekhar et al. (2016) confirmed these
findings, providing further evidence that oral Nifedipine is
a reasonable antihypertensive for the treatment of severe
pregnancy hypertension of any classification.

22. Delivery consideration in preeclampsia
 Clinical convention offers women with pre-eclampsia delivery at 37
weeks’ gestation as per NICE guidance and the guideline from the
American College of Obstetricians and Gynecologists.
 Prior to 34 weeks’ gestation, management is expectant with elective
delivery not considered due to worse neonatal adverse outcomes
(respiratory distress syndrome risk ratio 2.3, 95% CI 1.39–3.81 and
necrotizing enterocolitis risk ratio 5.54, 95% CI 1.04–29.56) .
 Between 34 and 37 weeks’ gestation, the optimum time to deliver to
prevent morbidity for the mother and baby remains unknown.

23. Complications of preeclampsia.
 A diagnosis of pre-eclampsia may result in a range of complications
with significant long-term implications for the mother.
 The diagnosis may have future implications for the management of
the health of the mother, as a history of pre-eclampsia is an
independent risk factor for cardiac events and stroke.
 Women from the Impact of Hypertension and Preeclampsia
Intervention Trial At Near term (HYPITAT) trial, which investigated
the optimum time for delivery in women with gestational
hypertension or pre-eclampsia, received a cardiovascular follow-up 2–
5 years post-delivery. (Lancet 2015)
 The results showed that almost half of the early onset pre-eclampsia
women subsequently developed hypertension
 As opposed to 39% and 25% of women in the pregnancy-induced
hypertension and late-onset pre-eclampsia groups, respectively.

24. Eclampsia
 Eclampsia is defined as the occurrence of one or more convulsions in
a pre-eclamptic woman in the absence of any other neurological or
metabolic causes.
 It is an obstetric emergency affecting approximately 5/10,000
pregnancies, with a maternal mortality rate of 1.8% and a fetal
mortality rate of up to 30%.
 The majority of seizures occur in the post-natal period (44%), but
they can also occur in the antepartum (38%) or intrapartum (18%)
settings.

25. Risk factors
Same as for preeclampsia

26. Clinical features
 The hallmark feature of eclampsia is a new onset tonic-clonic type
seizure, in the presence of pre-eclampsia (new onset hypertension
and proteinuria after 20 weeks’ gestation).
 The seizures typically last around 60 to 75 seconds, followed by a
variable lasting post-ictal phase. Maternal convulsions may
cause fetal distress and bradycardia.
 Seizures are not preceded by aura.
 Other signs and symptoms essentially as in severe preeclampsia.
 Early presentation improves prognosis.

27. Symptoms /signs of imminent eclampsia
 Headache (usually frontal).
 Hyper-reflexia.
 Nausea and vomiting.
 Generalised edema.
 Right upper quadrant pain +/- jaundice.
 Visual disturbances e.g. flashing lights, blurred or double vision.
 Change in mental stage.

28. Investigations
 FBC: ↓ Hb, ↓ platelets.
 E & U: ↑ urea, ↑ creatinine, ↑ urate,
 Hourly urine output and urinalysis.
 LFTs: ↑ ALT, ↑ AST, ↑ bilirubin.
 Clotting studies: Usually deranged
 Blood glucose: to rule out hypoglycemia
 Abdominal ultrasound may be performed to estimate the gestational age
and to rule out placental abruption which can complicate eclampsia.
 Continuous CTG monitoring is likely to indicate evidence of fetal
distress and bradycardia.
 It may be necessary to rule out other causes of seizures if there is any
doubt regarding the diagnosis of eclampsia using E.E.G, cranial CT/ MRI.

29. Treatment
 Mobilize relevant personnel to assist with management
 A, B, C,D, E of resuscitation, pass oropharyngeal airway (Airway,
Breathing, Circulation, Disability & Exposure)
 Auscultate to rule out aspiration.
 May need I.C.U care, nurse in left lateral position.
 Abort seizure with MgSO4 and continue for 24hrs after last seizure
 The patient should be assessed for signs of hypermagnesaemia (hyper-
reflexia, respiratory depression), and the fetus monitored via continuous
CTG. Urine output should be monitored.
 Effect delivery by most expeditious route after stabilizing the patient
 Monitor patient closely for complications and manage accordingly

30. Magnesium sulphate regimen
 Prophylaxis in Severe PE
 Pritchard Regimen
 Zuspan Regimen
Note: Magnesium sulphate should be continued for 24 h after delivery/ last seizure, whichever is later.

31. Antihypertensive therapy
 The two most commonly used intravenous anti-hypertensives
are labetalol and hydralazine. A target mean arterial pressure (MAP) of
<120mmHg is used.
 A rapid decrease in maternal blood pressure can cause fetal heart rate
abnormalities. Therefore, continuous CTG monitoring is used during and for
30 minutes after giving IV anti-hypertensives.
 Oral anti-hypertensives should be given once patient is fully conscious

32. Delivery
 Definitive treatment of eclampsia is delivery of the fetus.
 However, the mother must be stable before delivery – with any
seizures controlled, severe hypertension treated and hypoxia
corrected. This is the case regardless of any fetal compromise.
 Caesarean section is the ideal mode of delivery. However,
intrapartum seizures in established labour may be managed by
vaginal delivery.
 After delivery, the patient will require HDU care until she is
stable – well controlled blood pressure, adequate urine output,
and discontinuation of MgSO4. This usually takes a minimum of
24 hours.
 Fluid balance monitoring is important to prevent pulmonary
edema and detect acute kidney injury.

33.  Indicators of complications of eclampsia should also be
monitored – such as platelets, transaminases and
creatinine levels.

34. Post partum care-inpatient
 Regular symptom review – e.g headaches, epigastric pain.
 Daily urinalysis until urine is protein free
 72 hrs post-partum – FBC, LFTs, creatinine.
 Pre-conceptional counselling – advice regarding minimizing
risk factors and prophylaxis for future pregnancies.
 Discharge home when target BP is achieved and patient is
asymptomatic

35. Post partum care-outpatient
Consider CT Head – if persistent neurological
deficit.
Measure BP – blood pressure is checked
4hrly post-partum - Adjust antihypertensive
medication as necessary.
Follow-up at 6 weeks – check BP
, proteinuria
and creatinine. Repeat FBC, LFTs,
electrolytes, urea and creatinine if not
previously returned to normal

36. Eclampsia complications
Maternal Complications Fetal Complications
HELLP syndrome (3 %)
Disseminated Intravascular
Coagulopathy (DIC) (3 %)
Acute Kidney Injury (4 %)
Adult respiratory distress
syndrome (3 %)
Cerebrovascular haemorrhage
(< 2 %)
Permanent CNS damage.
Death (1.8 %)
Intrauterine growth restriction
(IUGR).Prematurity.
Infant respiratory distress
syndrome.
Intrauterine fetal death.
Placental abruption.

37. Documentation
 Document all events in the management clearly and in chronological
order.

38. NICE GUIDELINES – NATIONAL INSTITUTE FOR CARE AND EXCELLENCE
(2019)
1.1 Reducing the risk of hypertensive disorders in pregnancy
Antiplatelet agents
 1.1.2 Advise pregnant women at high risk of pre-eclampsia to take 75–150 mg of aspirin daily from 12 weeks until the birth of
the baby. Women at high risk are those with any of the following:
 chronic kidney disease
 autoimmune disease such as systemic lupus erythematosus or antiphospholipid syndrome
 type 1 or type 2 diabetes
 chronic hypertension. [2010, amended 2019]
 1.1.3 Advise pregnant women with more than 1 moderate risk factor for pre-eclampsia to take 75–150 mg of aspirin daily from
12 weeks until the birth of the baby. Factors indicating moderate risk are:
 first pregnancy
 age 40 years or older
 pregnancy interval of more than 10 years
 body mass index (BMI) of 35 kg/m2 or more at first visit
 family history of pre-eclampsia
 multi-fetal pregnancy. [2010, amended 2019]

39. Other pharmaceutical agents
 1.1.4 Do not use the following to prevent hypertensive disorders during pregnancy:
 nitric oxide donors
 progesterone
 diuretics
 low molecular weight heparin. [2010]
 Nutritional supplements
 1.1.5 Do not recommend the following supplements solely with the aim of preventing hypertensive
disorders during pregnancy:
 magnesium
 folic acid
 antioxidants (vitamins C and E)
 fish oils or algal oils
 garlic. [2010]
Diet
 1.1.6 Do not recommend salt restriction during pregnancy solely to prevent gestational hypertension
or pre-eclampsia. [2010]

40. 1.2 Assessment of proteinuria in hypertensive disorders of
pregnancy
 1.2.1 Interpret proteinuria measurements for pregnant women in the context of a full clinical
review of symptoms, signs and other investigations for pre-eclampsia. [2019]
 1.2.2 Use an automated reagent-strip reading device for dipstick screening for proteinuria in
pregnant women in secondary care settings. [2019]
 1.2.3 If dipstick screening is positive (1+ or more), use albumin:creatinine ratio or
protein:creatinine ratio to quantify proteinuria in pregnant women. [2019]
 1.2.4 Do not use first morning urine void to quantify proteinuria in pregnant women. [2019]
 1.2.5 Do not routinely use 24-hour urine collection to quantify proteinuria in pregnant
women. [2019]
 1.2.6 If using protein:creatinine ratio to quantify proteinuria in pregnant women:
 use 30 mg/mmol as a threshold for significant proteinuria
 if the result is 30 mg/mmol or above and there is still uncertainty about the diagnosis of pre-
eclampsia, consider re-testing on a new sample, alongside clinical review. [2019]
 1.2.7 If using albumin:creatinine ratio as an alternative to protein:creatinine ratio to
diagnose pre-eclampsia in pregnant women with hypertension:
 use 8 mg/mmol as a diagnostic threshold
 if the result is 8 mg/mmol or above and there is still uncertainty about the diagnosis of pre-
eclampsia, consider re-testing on a new sample, alongside clinical review. [2019]

41.  1.3 Management of chronic hypertension in pregnancy
Pre-pregnancy advice
 1.3.1 Offer women with chronic hypertension referral to a specialist in hypertensive disorders of pregnancy to discuss the risks and
benefits of treatment. [2010, amended 2019]
 1.3.2 Advise women who take angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers[2 ] (ARBs):
 that there is an increased risk of congenital abnormalities if these drugs are taken during pregnancy
 to discuss alternative antihypertensive treatment with the healthcare professional responsible for managing their hypertension,
if they are planning pregnancy
 to discuss alternative treatment with the healthcare professional responsible for managing their condition, if ACE inhibitors or
ARBs are being taken for other conditions such as renal disease. [2010, amended 2019]
 1.3.3 Stop antihypertensive treatment in women taking ACE inhibitors or ARBs if they become pregnant (preferably within 2 working
days of notification of pregnancy) and offer alternatives. [2010]
 1.3.4 Advise women who take thiazide or thiazide-like diuretics:
 that there may be an increased risk of congenital abnormalities and neonatal complications if these drugs are taken during
pregnancy
 to discuss alternative antihypertensive treatment with the healthcare professional responsible for managing their hypertension,
if they are planning pregnancy. [2010, amended 2019]
 1.3.5 Advise women who take antihypertensive treatments other than ACE inhibitors, ARBs, thiazide or thiazide-like diuretics that
the limited evidence available has not shown an increased risk of congenital malformation with such treatments. [2010, amended
2019]

42.  Treatment of chronic hypertension
 1.3.6 Offer pregnant women with chronic hypertension advice on:
 weight management
 exercise
 healthy eating
 lowering the amount of salt in their diet. Provide this advice in line with the NICE guideline on hypertension in adults: diagnosis
and treatment. [2019]
 1.3.7 Continue with existing antihypertensive treatment if safe in pregnancy, or switch to an alternative
treatment, unless:
 sustained systolic blood pressure is less than 110 mmHg or
 sustained diastolic blood pressure is less than 70 mmHg or
 the woman has symptomatic hypotension. [2019]
 1.3.8 Offer antihypertensive treatment to pregnant women who have chronic hypertension and who are not already on treatment if
they have:
 sustained systolic blood pressure of 140 mmHg or higher or
 sustained diastolic blood pressure of 90 mmHg or higher. [2019]
 1.3.9 When using medicines to treat hypertension in pregnancy, aim for a target blood pressure of 135/85 mmHg. [2019]
 1.3.10 Consider labetalol to treat chronic hypertension in pregnant women. Consider nifedipine for women in whom labetalol is not
suitable, or methyldopa if both labetalol and nifedipine are not suitable. Base the choice on any pre-existing treatment, side-effect
profiles, risks (including fetal effects) and the woman's preference. [2019]
 1.3.11 Offer pregnant women with chronic hypertension aspirin 75–150 mg once daily from 12 weeks. [2019]
 1.3.12 Offer placental growth factor (PlGF)-based testing to help rule out pre-eclampsia between 20 weeks and up to 35 weeks of
pregnancy, if women with chronic hypertension are suspected of developing pre-eclampsia. (See the NICE diagnostics guidance on PlGF-
based testing to help diagnose suspected pre-eclampsia). [2019]

43. Antenatal appointments
 1.3.13 In women with chronic hypertension, schedule additional antenatal appointments based on
the individual needs of the woman and her baby. This may include:
 weekly appointments if hypertension is poorly controlled
 appointments every 2 to 4 weeks if hypertension is well-controlled. [2010, amended 2019]
Timing of birth
 1.3.14 Do not offer planned early birth before 37 weeks to women with chronic hypertension whose blood
pressure is lower than 160/110 mmHg, with or without antihypertensive treatment, unless there are other
medical indications. [2010, amended 2019]
 1.3.15 For women with chronic hypertension whose blood pressure is lower than 160/110 mmHg after 37
weeks, with or without antihypertensive treatment, timing of birth and maternal and fetal indications for
birth should be agreed between the woman and the senior obstetrician. [2010]
 1.3.16 If planned early birth is necessary, offer a course of antenatal corticosteroids and magnesium
sulfate if indicated [2010, amended 2019]

44. xxxxxxxxxxxx
 1.5 Management of pre-eclampsia
 Assessing pre-eclampsia
 1.5.1 Assessment of women with pre-eclampsia should be performed by a healthcare professional trained in
the management of hypertensive disorders of pregnancy. [2010, amended 2019]
 1.5.2 Carry out a full clinical assessment at each antenatal appointment for women with pre-eclampsia, and
offer admission to hospital for surveillance and any interventions needed if there are concerns for the
wellbeing of the woman or baby. Concerns could include any of the following:
 sustained systolic blood pressure of 160 mmHg or higher
 any maternal biochemical or haematological investigations that cause concern, for example, a new and
persistent:
 rise in creatinine (90 micromol/litre or more, 1 mg/100 ml or more) or
 rise in alanine transaminase (over 70 IU/litre, or twice upper limit of normal range) or
 fall in platelet count (under 150,000/microlitre)
 signs of impending eclampsia
 signs of impending pulmonary oedema
 other signs of severe pre-eclampsia
 suspected fetal compromise
 any other clinical signs that cause concern. [2019]

47.  Timing of birth
 1.5.7 Record maternal and fetal thresholds for planned early birth before 37 weeks in women with pre-
eclampsia. Thresholds for considering planned early birth could include (but are not limited to) any of the
following known features of severe pre-eclampsia:
 inability to control maternal blood pressure despite using 3 or more classes of antihypertensives in appropriate doses
 maternal pulse oximetry less than 90%
 progressive deterioration in liver function, renal function, haemolysis, or platelet count
 ongoing neurological features, such as severe intractable headache, repeated visual scotomata, or eclampsia
 placental abruption
 reversed end-diastolic flow in the umbilical artery doppler velocimetry, a non-reassuring cardiotocograph, or stillbirth.
Other features not listed above may also be considered in the decision to plan early birth. [2019]
 1.5.8 Involve a senior obstetrician in any decisions on timing of birth for women with pre-eclampsia.
[2010, amended 2019]
 1.5.9 Discuss with the anaesthetic team if birth is planned in a woman with pre-eclampsia. [2010,
amended 2019]
 1.5.10 Discuss with the neonatal team if birth is planned in a woman with pre-eclampsia, and neonatal
complications are anticipated. [2010, amended 2019]
 1.5.11 Offer intravenous magnesium sulfate and a course of antenatal corticosteroids if indicated, if early
birth is planned for women with preterm pre-eclampsia, in line with the NICE guideline on preterm labour
and birth. [2010, amended 2019]
 1.5.12 Decide on timing of birth in women with pre-eclampsia as recommended in table 3. [2019]

49. Postnatal investigation, monitoring and treatment (including after discharge from critical
care)
 Blood pressure
 1.5.13 In women with pre-eclampsia who did not take antihypertensive treatment and have given birth, measure
blood pressure:
 at least 4 times a day while the woman is an inpatient
 at least once between day 3 and day 5 after birth
 on alternate days until normal, if blood pressure was abnormal on days 3–5. [2010]
 1.5.14 In women with pre-eclampsia who did not take antihypertensive treatment and have given birth, start
antihypertensive treatment if blood pressure is 150/100 mmHg or higher. [2010]
 1.5.15 Ask women with pre-eclampsia who have given birth about severe headache and epigastric pain each time
blood pressure is measured. [2010]
 1.5.16 In women with pre-eclampsia who took antihypertensive treatment and have given birth, measure blood
pressure:
 at least 4 times a day while the woman is an inpatient
 every 1–2 days for up to 2 weeks after transfer to community care until the woman is off treatment and has no
hypertension. [2010]
 1.5.17 For women with pre-eclampsia who have taken antihypertensive treatment and have given birth:
 continue antihypertensive treatment (see section 1.9 for choice of antihypertensive during the postnatal period)
 consider reducing antihypertensive treatment if their blood pressure falls below 140/90 mmHg
 reduce antihypertensive treatment if their blood pressure falls below 130/80 mmHg. [2010, amended 2019]

50. Fetal monitoring in pre-eclampsia or severe gestational hypertension
 1.6.5 Carry out cardiotocography at diagnosis of pre-eclampsia or severe gestational hypertension.
[2010]
 1.6.6 If conservative management of pre-eclampsia or severe gestational hypertension is planned,
carry out all the following tests at diagnosis:
 ultrasound for fetal growth and amniotic fluid volume assessment
 umbilical artery doppler velocimetry. [2010]
 1.6.7 If the results of all fetal monitoring are normal in women with pre-eclampsia or severe
gestational hypertension, do not routinely repeat cardiotocography unless clinically indicated.
[2010, amended 2019]
 1.6.8 In women with pre-eclampsia or severe gestational hypertension, repeat cardiotocography if
any of the following occur:
 the woman reports a change in fetal movement
 vaginal bleeding
 abdominal pain
 deterioration in maternal condition. [2010]
 1.6.9 In women with pre-eclampsia or severe gestational hypertension, repeat ultrasound for fetal
growth and amniotic fluid volume assessment or umbilical
 artery doppler velocimetry every 2 weeks, with subsequent surveillance and monitoring determined by the
findings of these scans. [2010, amended 2019]

51. Intrapartum care
 1.7.1 Give advice and treatment to women with hypertensive disorders of
pregnancy in line with the NICE guideline on intrapartum care, unless there are
recommendations in this guideline on the same topic. Offer care in accordance
with the NICE guideline on intrapartum care for women with hypertension
whether treated or untreated, and not just on the basis of blood pressure in
labour. [2010, amended 2019]
 1.7.2 Give women with chronic hypertension advice and care in line with the
NICE guideline on intrapartum care for women with existing medical conditions
or obstetric complications and their babies. [2019]
Blood pressure
 1.7.3 During labour, measure blood pressure:
 hourly, in women with hypertension
 every 15–30 minutes until blood pressure is less than 160/110 mmHg in women with
severe hypertension. [2010, amended 2019]
 1.7.4 Continue use of antenatal antihypertensive treatment during labour.
[2010]

52. Management of second stage of labour
 1.7.7 Do not routinely limit the duration of the second stage of labour in women
with controlled hypertension. [2010, amended 2019]
 1.7.8 Consider operative or assisted birth in the second stage of labour for women
with severe hypertension whose hypertension has not responded to initial
treatment. [2010, amended 2019]

53. Anticonvulsants
 1.8 Medical management of severe hypertension, severe pre-eclampsia or eclampsia in a critical care
setting
 1.8.1 If a woman in a critical care setting who has severe hypertension or severe pre-eclampsia has or previously
had an eclamptic fit, give intravenous magnesium sulfate. [2010]
 1.8.2 Consider giving intravenous magnesium sulfate to women with severe pre-eclampsia who are in a critical care
setting if birth is planned within 24 hours. [2010]
 1.8.3 Consider the need for magnesium sulfate treatment, if 1 or more of the following features of severe pre-
eclampsia is present:
 ongoing or recurring severe headaches
 visual scotomata
 nausea or vomiting
 epigastric pain
 oliguria and severe hypertension
 progressive deterioration in laboratory blood tests (such as rising creatinine or liver transaminases, or falling platelet
count). [2010, amended 2019]
 1.8.4 Use the Collaborative Eclampsia Trial regimen for administration of magnesium sulfate:
 A loading dose of 4 g should be given intravenously over 5 to 15 minutes, followed by an infusion of 1 g/hour maintained
for 24 hours. If the woman has had an eclamptic fit, the infusion should be continued for 24 hours after the last fit.
 Recurrent fits should be treated with a further dose of 2–4 g given intravenously over 5 to 15 minutes. [2010, amended
2019]
 1.8.5 Do not use diazepam, phenytoin or other anticonvulsants as an alternative to magnesium sulfate in women
with eclampsia. [2010, amended 2019]

54. Antihypertensives
 1.8.6 Treat women with severe hypertension who are in critical care during
pregnancy or after birth immediately with 1 of the following:
 labetalol (oral or intravenous)
 oral nifedipine
 intravenous hydralazine. [2010, amended 2019]
 1.8.7 In women with severe hypertension who are in critical care, monitor their
response to treatment:
 to ensure that their blood pressure falls
 to identify adverse effects for both the woman and the baby
 to modify treatment according to response. [2010]
 1.8.8 Consider using up to 500 ml crystalloid fluid before or at the same time as the
first dose of intravenous hydralazine in the antenatal period. [2010]

55. Corticosteroids for fetal lung maturation
 1.8.9 If early birth is considered likely within 7 days in women with pre-eclampsia,
offer a course of antenatal corticosteroids in line with the NICE guideline on
preterm labour and birth. [2010, amended 2019]

56. Thank you for listening

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