Germain S, Nelson-Piercy C. Liver and gastrointestinal disease. Maternal Medicine Module. RCOG Strat-OG 2nd edn. London: RCOG, 2007.
RCOG. Obstetric Cholestasis. Green-top Guideline No.
43 London: RCOG, 2011. Available from: files/
GT43ObstetricCholestasis2006.pdf.
van der Woude CJ, Kolacek S, Dotan I, et al.; European Crohn’s Colitis Organisation (ECCO). European evi-denced-based consensus on reproduction in inflamma-tory bowel disease. J Crohns Colitis 2010:493–510.
Key References
1. Girling JC, Dow E, Smith JH. Liver function tests in pre-eclampsia: importance of comparison with a reference range derived for normal pregnancy. Br J Obstet Gynaecol 1997;104:246–50.
2. Jarvis S, Nelson-Piercy C. Nausea and vomiting in preg-nancy BMJ 2011;342:d3606
3. Mazzotta P, Magee LA. A risk–benefit assessment of pharmacological and non-pharmacological treat-ments for nausea and vomiting of pregnancy. Drugs 2000;59:781–800.
KEY POINTS
Obstetric cholestasis
● Liver function tests should be requested in any pregnant woman with pruritus without obvious rash.
● Liver function tests should be repeated serially if the itching involves the palms and soles.
● Other causes of pruritus and abnormal liver function tests, including viral hepatitis and gallstones causing extrahepatic obstruction, should be excluded.
● Severe cholestasis is associated with a significantly increased risk of preterm delivery and stillbirth.
● Fetal risks increase with increasing bile acid levels.
● UDCA improves symptoms and liver function tests
Acute fatty liver of pregnancy 127
ANTENATAL OBSTETRICS
4. Kametas N, Nelson-Piercy C. Hyperemesis gravidarum, gastrointestinal and liver disease in pregnancy. Obstetrics Gynaecol Reprod Med 2008;18:69–75.
5. Nelson-Piercy C, Fayers P, de Swiet M. Randomised, placebo-controlled trial of corticosteroids for hypereme-sis gravidarum. Br J Obstet Gynaecol 2001;108:1–7.
6. Moran P, Taylor R. Management of hyperemesis grav-idarum: the importance of weight loss as a criterion for steroid therapy. QJM 2002; 95:153–8.
7. Vermeire S, Carbonnel F, Coulie PG et al. Management of inflammatory bowel disease in pregnancy. J Crohns Colitis 2012;6:811–23.
8. Alstead EA, Nelson-Piercy C. Inflammatory bowel dis-ease in pregnancy. Gut 2002;52:159–61.
9. Vinet E, Pineau C, Gordon C et al. Biologic therapy and pregnancy outcome in women with rheumatic diseases.
Arthritis Rheum 2009;61:587–92.
10. Hyrich KL, Verstappen SM. Biologic therapies and pregnancy: the story so far. Rheumatology (Oxford).
2014;53:1377-85.
11. Locatelli A, Roncaglia N, Arreghini A et al. Hepatitis C virus infection is associated with a higher inci-dence of cholestasis of pregnancy. Br J Obstet Gynaecol 1999;106:498–500.
12. Kenyon AP, Nelson-Piercy C, Girling J et al. Obstetric cholestasis, outcome with active management: a series of 70 cases. Br J Obstet Gynaecol 2002;109:282–8.
13. Kenyon AP, Nelson-Piercy C, Girling J et al. Pruritus may precede abnormal liver function tests in pregnant women with obstetric cholestasis: a longitudinal analysis. Br J Obstet Gynaecol 2001;108:1190–2.
14. Glantz A, Marschall HU, Mattson LA. Intrahe patic cholesta-sis of pregnancy: relationship between bile acid levels and fetal complication rates. Hepatology 2004;40:467–74.
15. Geenes V, Chappell LC, Seed PT, Steer PJ, Knight M, Williamson C. Association of severe intrahepatic cholestasis of pregnancy with adverse pregnancy outcomes: A prospective population-based case-control study. Hepatology 2014;59:1482-91.
16. Chappell LC, Gurung V, Seed PT, Chambers J, Williamson C, Thornton JG; PITCH Study Consortium.
Ursodeoxycholic acid versus placebo, and early term delivery versus expectant management, in women with intrahepatic cholestasis of pregnancy: semifactorial ran-domised clinical trial. BMJ 2012;344:e3799.
17. Knight M, Nelson-Piercy C, Kurinczuk JJ et al. A prospec-tive national study of acute fatty liver of pregnancy in the UK. Gut 2008;57:951–6.
INTRODUCTION: PULMONARY DISEASE IN PREGNANCY
The physiological changes occurring within the respiratory sys-tem are summarised in Tables 16.1 and 16.2. Symptomatically, pregnant women may complain of new-onset rhinitis, which
may result from oestrogen-induced oedema, hyperaemia and hypersecretion of the upper airways. Although mostly harm-less, this contributes to the greater difficulties encountered during intubation of pregnant women. Much more common is the complaint of shortness of breath or ‘air hunger’. This dyspnoea is experienced by approximately half of all preg-nant women by 20 weeks’ gestation and by three-quarters by 30 weeks. It rarely occurs at rest and does not significantly impair normal activities. The postulated mechanism is high
Chapter 16 Respiratory conditions
Louise Kenny
MRCOG standards
Taken from Core Curriculum Module 9: Maternal Medicine, http://www.rcog.org.uk/files/rcog-corp/
uploaded-files/ED-CORE-9.pdf
Theoretical skills
• Understand the epidemiology, aetiology,
pathophysiology, clinical characteristics and prog-nostic features of pulmonary diseases in pregnancy.
• Understand the impact that pregnancy may have on pre-existing pulmonary disease and the influence the illness may have on pregnancy.
• Specific mention is made of asthma, infection, embolism and aspiration syndrome. However, vembolism and aspiration syndrome are dealt with elsewhere within this text. Pre-existing common pulmonary disease and infection are discussed here in detail.
Practical skills
• Diagnose, investigate and manage pulmonary disease in pregnancy with specific reference to asthma, infection, embolism and aspiration syndrome.
• Manage a pregnancy complicated by pre-existing pulmonary disease.
• Request and interpret pulmonary investigations with reference to pregnancy.
Table 16.1 Normal arterial blood gas values and the effect of pregnancy
Pre-pregnancy By term PaO2 11–13 kPa
(83–98 mmHg)
13 kPa (98 mmHg)
PaCO2 4.8–6.0 kPa (36–45 mmHg)
3.7–4.2 kPa (28–32 mmHg)
HCO3- 24–30 mmol/L 18–21 mmol/L
pH 7.35–7.45 7.4–7.45
Table 16.2 The effect of pregnancy on lung function
Lung function Change by term Actual volume change Total lung capacity 4% decrease 200–400 mL
Functional residual 10–20% decrease 300–500 mL capacity Expiratory reserve 15–20% decrease 100–300 mL volume Tidal volume 30–50% increase 200 mL
Minute (or expired volume in 1 min) ventilation
30–50% increase 3 L/min
Residual volume 20–25% decrease 200–300 mL Respiratory rate No change
Vital capacity No change
Peak flow No change
Metabolic rate 15% increase Oxygen
consumption (VO2)
20–33% increase