PRE-ECLAMPSIA ECLAMPSIA, BEST PRACTICES.pptx

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 - H aemolysis ,  E levated  L iver enzymes and  L ow  P latelets 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/m 2   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 MgSO 4 . 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]

45. 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]

46. 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]

47. 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]

48. 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]

49. 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]

50. 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]

51. 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]

52. 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]

53. Thank you for listening

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