ANTENATAL OBSTETRICS
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.
● Offer birth to women with refractory severe chronic hypertension, after a course of corticosteroids (if required) has been completed.
Neonatal complications
Neonatal complications are also more commonly reported for women with chronic hypertension than for normotensive women, including higher rates of perinatal mortality, fetal growth restriction and admission to neonatal special care.1
POSTPARTUM MANAGEMENT
Peak postpartum blood pressure usually occurs at 3–5 days.
It is recommended that women with chronic hypertension should have blood pressure measured at the following times postpartum, and treatment titrated to keep blood pressure lower than 140/90 mmHg:5
● Daily for the first 2 days postpartum;
● At least once between day 3 and day 5 postpartum;
● As clinically indicated if antihypertensive treatment is changed after delivery.
Women with previously diagnosed chronic hypertension can be discharged when their blood pressure is stable and
<140/90 mmHg or <150/100 mmHg with treatment.20 Medications that are safe for breastfeeding are listed in Table 8.3. Usually women can continue taking their antenatal antihypertensive agent. Enalapril is a good alternative for women with proteinuria associated with renal disease. It is the only ACEI/ARB that has been investigated for excretion into breast milk and is found in only small amounts.21
Hypertension may also be diagnosed postpartum, if blood pressure remains persistently elevated after 6 weeks.
Community care should be alerted to the presence of unre-solved hypertension and instructed to monitor and investigate appropriately.
All women with chronic hypertension should be offered a medical review at the postnatal review (6–8 weeks after delivery) for future pre-pregnancy counselling.5 Assessment of future cardiovascular risk should also be made includ-ing serum lipids, family history and smokinclud-ing history. Each 2-mmHg rise in systolic blood pressure is associated with a 7% increased risk of mortality from ischaemic heart disease and a 10% increased risk of mortality from stroke.8 Women should be advised that statin and fibrate treatment should be stopped before or at conception.22
It is recommended that oestrogen-containing contraceptives be avoided in women with hypertension, due to their potential to exacerbate sodium retention23 and hypertension.24
Table 8.3 Drugs safety in breastfeeding (adapted from Bramham et al.20)
Drug Dose Comments
NICE recommendation and widely used in UK Alpha and/or beta blockers
Labetalol 100–600 mg 2–3 times daily Only small quantities detected in breast milk
Atenolol 25–100 mg once daily Second-line use for women who require once-daily
formulation Calcium channel antagonists
Nifedipine SR 10–20 mg twice daily Amount in breast milk too small to be harmful;
manufacturer suggests avoid but widely used without reports of neonatal side effects
Amlodipine 5–10 mg once daily Second-line use for women who require once-daily
formulation. Amount in breast milk too small to be harmful. Manufacturer suggests avoid but used in clinical practice without report of harm
Nifedipine MR 30–60 mg once daily
Angiotensin-converting enzyme inhibitor (ACEI)
Enalapril 5–20 mg twice daily Can be used in breastfeeding when previously on ACEI;
other first-choice agents cannot be used or cardiac/
renal protection needed. Excreted into breast milk in low concentrations but amount probably too small to be harmful
(continued)
66 Chronic hypertension
ANTENATAL OBSTETRICS
CONCLUSION
Women with chronic hypertension in pregnancy have increased maternal and neonatal morbidity, and require pre-pregnancy counselling and heightened antenatal surveil-lance. Hypertension identified for the first time in pregnancy should be investigated for secondary causes and evidence of end-organ damage. All women should be offered low-dose aspirin, and lifestyle modifications advised to reduce risk of complications.
Key References
1. Bateman BT, Bansil P, Hernandez-Diaz S, Mhyre JM, Callaghan WM, Kuklina EV. Prevalence, trends, and out-comes of chronic hypertension: a nationwide sample of delivery admissions. Am J Obstet Gynecol. 2012;206:134.
e131–8.
2. Mathews TJ, Hamilton BE. Delayed child-bearing: more women are having their first child later in life. National Center for Health Statistics Data Brief. Bethesda, MA:
CDC, 2009:21.
3. Kelly T, Yang W, Chen CS, Reynolds K, He J. Global bur-den of obesity in 2005 and projections to 2030. Int J Obesity 2008;32:1431–7.
4. Livingston JC, Sibai BM. Chronic hypertension in preg-nancy. Obstet Gynecol Clin North Am 2001;28:447–63.
5. National Institute for Clinical Excellence. Hypertension in Pregnancy: The management of hypertensive disorders during pregnancy Clinical Guideline 107. London: NICE, 2010 wwwniceorguk/CG107.2010.
6. Cnossen JS, Vollebregt KC, de Vrieze N, et al. Accuracy of mean arterial pressure and blood pressure measure-ments in predicting pre-eclampsia: systematic review and meta-analysis. BMJ 2008;336:1117–20.
7. Coresh J, Selvin E, Stevens LA et al. Prevalence of chronic kidney disease in the United States. JAMA.
2007;298:2038–2047.
8. NICE. Clinical Management of Primary Hypertension in Adults. Clinical Guideline 127. London: NICE, 2011 www.nice.org.uk/CG127. 2011.
9. Smith MC, Moran P, Ward MK, Davison JM. Assessment of glomerular filtration rate during pregnancy using the MDRD formula. BJOG 2008;115:109–12.
10. Cooper WO, Hernandez-Diaz S, Arbogast PG et al. Major congenital malformations after first-trimester exposure to ACE inhibitors. N Engl J Med 2006;354:2443–51.
11. Bullo M, Tschumi S, Bucher BS, Bianchetti MG, Simonetti GD. Pregnancy outcome following expo-sure to angiotensin-converting enzyme inhibitors or angiotensin receptor antagonists: a systematic review.
Hypertension 2012;60:444–50.
12. Li DK, Yang C, Andrade S, Tavares V, Ferber JR. Maternal exposure to angiotensin converting enzyme inhibitors in the first trimester and risk of malformations in offspring:
a retrospective cohort study. BMJ 2011;343:5931.
13. Butters L, Kennedy S, Rubin PC. Atenolol in essen-tial hypertension during pregnancy. BMJ 1990;301:587–9.
14. El Guindy AA, Nabhan AF. A randomized trial of tight vs.
less tight control of mild essential and gestational hyper-tension in pregnancy. J Perinat Med 2008;36:413–18.
15. Magee LA, von Dadelszen P, Chan S et al. The Control of Hypertension In Pregnancy Study pilot trial. BJOG.
2007;114:770. e713–20.
16. von Dadelszen P, Ornstein MP, Bull SB, Logan AG, Koren G, Magee LA. Fall in mean arterial pressure and fetal growth restriction in pregnancy hypertension: a meta-analysis. Lancet 2000;355:87–92.
17. Chappell LC, Enye S, Seed P, Briley AL, Poston L, Shennan AH. Adverse perinatal outcomes and risk fac-tors for preeclampsia in women with chronic hyperten-sion: a prospective study. Hypertension 2008;51:1002–9.
18. Duley L, Henderson-Smart DJ, Meher S, King JF.
Antiplatelet agents for preventing pre-eclampsia and its complications. Cochrane Database Syst Rev 2007;2:CD004659.
19. Brown MA, Lindheimer MD, de Swiet M, Van Assche A, Moutquin JM. The classification and diagnosis of the hypertensive disorders of pregnancy: statement from the International Society for the Study of Hypertension in Pregnancy (ISSHP). Hypertens Pregnancy 2001;20:IX–XIV.
Drug Dose Comments
NICE recommendation and widely used in UK Contraindicated
Other ACEIs and ARBs Not recommended Minimal data on use during lactation. Manufacturers suggest avoid
Diuretics Not recommended Excessive thirst in breastfeeding women; large doses
may suppress lactation Table 8.3 Drugs safety in breastfeeding (adapted from Bramham et al.20) (continued)
Conclusion 67
ANTENATAL OBSTETRICS
20. Bramham K, Nelson-Piercy C, Brown MJ, Chappell LC.
Postpartum management of hypertension. BMJ 2013;346:894.
21. Redman CW, Kelly JG, Cooper WD. The excretion of enalapril and enalaprilat in human breast milk. Eur J Clin Pharmacol 1990;38:99.
22. Pechère-Bertschi A, Maillard M, Stalder H, Bischof P, Fathi M, Brunner HR, Burnier M. Renal hemodynamic and tubular responses to salt in women using oral con-traceptives. Kidney Int 2003;64:1374–80.
23. Williamson PM, Buddle ML, Brown MA, Whitworth JA.
Ambulatory blood pressure monitoring (ABPM) in the normal menstrual cycle and in women using oral contraceptives: Comparison with conventional blood pressure measurement. Am J Hypertens 1996;
9:953–8.
24. Briggs GG, Freeman RK, Yaffe SJ (eds). Drugs in Pregnancy and Lactation: A reference guide to fetal and neonatal risk, 9th edn. 2011, Philadelphia, PA: Lippincott Williams &
Wilkins.
INTRODUCTION
Diabetes mellitus (DM) is a collection of metabolic disorders with hyperglycaemia as the common feature and is predomi-nantly classified outside pregnancy into two major subtypes, type 1 and type 2. Type 1 is typically due to a deficiency of insu-lin and tends to present in a younger age group, whereas type 2 is considered to be a disease of insulin resistance presenting in an older age group. Persistent hyperglycaemia in both disorders causes organ damage affecting the eyes, kidneys, nerves and cardiovascular system. Pre-existing diabetes (type 1 or type 2) is associated with a higher risk of a poor obstetric outcome. In 1990, the St Vincent Declaration set a series of targets to improve the outcome of pregnant women with diabetes, with the aim that the risks should approximate those of the non-diabetic populations. Unfortunately, the 2007 CEMACH (Confidential Enquiry into Maternal and
Child Health) report on diabetes in pregnancy found that current care falls well short of this target.1