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Medical Problems in Pregnancy

Medical Problems in Pregnancy. Dr Suzy Matts FRCOG Consultant Obstetrics and Gynaecology George Eliot Hospital. Introduction. Most women in pregnancy are healthy However, those with medical disorders require expert care Care may be by the obstetrician, +/- GP and/or medical specialist

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Medical Problems in Pregnancy

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  1. Medical Problems in Pregnancy Dr Suzy Matts FRCOG Consultant Obstetrics and Gynaecology George Eliot Hospital

  2. Introduction Most women in pregnancy are healthy However, those with medical disorders require expert care Care may be by the obstetrician, +/- GP and/or medical specialist May be through normal or specialised ANC Most complex disorders may need multidisciplinary antenatal care in a tertiary centre

  3. Medical Disorders What disorders can you think of that can affect pregnancy?

  4. Medical Disorders Asthma Cystic fibrosis Hypertension/PIH/PET Arrthymias Valvular disease Cardiomyopathy Cyanotic heart disease VSD/ASD Pulmonary hypertension Epilepsy Multiple sclerosis Intracranial hypertension Benign cranial tumours eg pit adenomas Obstetric Cholestasis Acute Fatty Liver of Pregnancy IBS Crohns/Ulceative colitis Thrombophilias VTE Antiphospholipid syndrome SLE Rheumatoid arthritis Sickle cell disease/thalassaemias Anaemia Diabetes Hypo/hyperthyroidism Adrenal disease Cancer

  5. Background • Medical disorders can impact on pregnancy in two ways • Disorders caused by the pregnancy eg • PET/PIH • VTE • Disorders pre-existing by exacerbated by the effects of the pregnancy eg • Heart disease • Asthma • Immune disorders • Epilepsy

  6. These conditions make major contributions to maternal deaths

  7. Exercise-15 minutes • Prepregnancy actions/changes/ issues • Antenatal issues • Effects on mum • Effects on baby • Screening • Medication issues • Contraindications • Delivery issues • Postnatal issues • Neonatal issues GROUPS: ASTHMA EPILEPSY DIABETES ESSENTIAL HYPERTENSION THROMBOPHILIA eg PROTEIN C DEFICIENCY and APLS

  8. DIABETES • Important issue in pregnancy • Major impacts on maternal and fetal health • Requires multidisciplinary care in combined clinic • Pre-existing Type 1 • Pre-existing Type 2 (increasing) • Gestational Diabetes (increasing)

  9. Diabetes Mellitus and Pregnancy-1 • Diabetes mellitus affects all systems in the body-actual or effective insulin deficiency • 3-4 per 1000 pregnancies • Before insulin in 1921, 40% women died during pregnancy (usually DKA) • Remainder died within 2 years of delivery • Fetal loss rate >50%

  10. Diabetes Mellitus and Pregnancy-2 • Introduction of insulin improved outcome • Maternal mortality fell to 2-3% • Now deaths very rare • Fetal loss rates remained high • Initially concentrated on reducing stillbirth but PNMR high • 1970s-effect on fetus of abnormal glucose levels • Optimisation of maternal control and fetal surveillance should lead to PNMR close to non-diabetic • Recent studies show PNMR still double non-diabetic • Fetal anomaly rates 4x those of non-diabetic

  11. Effects of diabetes on pregnancy Miscarriage Fetal malformations Cardiac Neural tube Caudal regressions syndrome (200x↑) IUGR Macrosomia Unexplained IUD PET Effects of pregnancy on diabetes Poorer control Deterioration of renal function Deterioration of opthalmic disease Gestational DM

  12. Effects of Diabetes - fetus

  13. Fetal effects • Macrosomia • Increased risks of birth injury/ shoulder dystocia*** • Major cause of obstetric litigation • LSCS recommended in DM where macrosomia and EFW >4000g • Polyhdramnios • Fetalmalpresentations and possible increased risk preterm labour • Hyperinsulinaemia • Severe hypoglycaemia (risk of CP) • Polycythaemia • Thrombotic effects • Jaundice • Hypocalcaemia • HOCM

  14. Perinatal mortality by plasma glucose levels

  15. Pregnancy is diabetogenic • Fetus has little capacity for gluconeogenesis • enzymes are deactivated by low oxygen tensions • Glucose obtained from maternal blood • therefore dependent on maternal nutritional status • Maternal endocrine controls designed to keep blood glucose levels within tight limits • Insulin secretion prevents hyperglycaemia by increasing glucose utilisation for glycogen and fat synthesis and storage • Gut absorption and gluconeogenesis prevent hypoglycaemia

  16. Pregnancy is diabetogenic • Progesterone increases maternal appetite and stimulates deposition of glucose in fat stores • Also increases renal gluconeogenesis • Increased protein catabolism • Human placental lactogen (hPL, hPS) acts like growth hormone (GH) • Placental variant of GH • Polypeptide hormone • Produced from end of 1st trimester onwards • Mobilises fatty acids for maternal metabolism

  17. Pregnancy is diabetogenic • Relative insulin insensitivity in later pregnancy • Effects of hPL- exaggerated rate and amount of insulin release due to relative insulin insensitivity (requirements may increase by ~30%) • Reduced insulin sensitivity also due to effects of increased levels of cortisol, oestrogen and progesterone • Prolonged hyperglycaemia after eating • Reduced uptake of glucose by maternal tissues more by placental uptake • Facilitated diffusion only saturated at maternal levels of 20 mmol/l

  18. Gestational diabetes • Development of severe glucose intolerance in pregnancy-may require insulin treatment • ADA recommends all women should have 50g OGTT 24-28 weeks • UK-women with specific risk factors screened – 75g OGTT • Limit to <32 weeks due to slower gastric emptying and unpalatability in late pregnancy • Alternatives: HbA1C, blood glucose series

  19. Risk factors for GDM • Family history • One first degree relative • Two second degree relatives • Poor obstetric history • Esp. death of previous macrosomic baby • Significant glycosuria • Polyhydramnios • Macrosomic infant in this pregnancy • Polycystic ovary syndrome • Wt >100kg or BMI >30 • South Asian, Middle Eastern or African origin

  20. Oral glucose tolerance test-interpretation (WHO) **=diagnostic of GDM

  21. Diabetes and Pregnancy-Key Points • Pregnancy is diabetogenic, worsening pre-existing diabetes and precipitating gestational DM • Increasing obesity increases incidence gestational and Type 2 DM • Poorer control worsens fetal and maternal outcomes • Hyperglycaemia is associated with acute fetal demise: hypoglycaemia is associated with cerebral palsy

  22. Diabetes Antenatal Combined Clinic • One stop clinic for women with diabetes in pregnancy-all consultant units • See all professionals on one visit-may or may not be in same room, depending on size of clinic! • Obstetrician • Diabetes physician • Diabetes nurse • Diabetes specialist midwife • Sonographers • Dietician • (psychologist)

  23. Management • Pre-pregnancy • Optimise control-aim for BM 4-7 • HbA1C 6.0% or less • High dose folic acid 5mg/day • Stop smoking, weight reduction of BMI raised • Early Pregnancy • Early booking at 6 weeks • Combined clinic every 1-2 weeks • Early dating/viability scan

  24. Management • Screening • Combined test at 12 weeks (sl lower sensitivity in DM) • Detailed USS including extended cardiac views • Diabetic control • May need diet, oral HG or insulin • Aim for BM 4-7 • Keep HbA1C <6.0% • Retinal screening every trimester • Dietetic support

  25. Management • Pregnancy Care • Regular antenatal care • Serial growth scans 28. 32. 36 weeks • Monitoring for PET • Fetal wellbeing monitoring from 34 weeks • Elective delivery IOL or LSCS • 38-39 weeks in pre-existing DM • 38 wks in GDM on insulin, may be 41 weeks if GDM on diet with normal BMs and fetal growth

  26. Management • Neonatal • Paediatric alert • Neonatal surveillance at delivery-may be with mother • Monitor BMs to ensure no neonatal hypoglycaemia • Postnatal • Pre-Existing: Return to prepregnancy insulin / oral HG agent regime • GDM: stop treatment and monitor BMs for 48 hours to ensure return to normal and no persistence of IGT

  27. Thyroid and Pregnancy • hCG has thyrotrophic function • May suppress TSH during first trimester • Thyrotoxicosis may be a feature of hydatidiform pregnancy where levels of hCG are extremely elevated • Thyroid function remains essentially normal in pregnancy • Marked increase in thyroid binding globulin (? Effect of oestrogen?) • Increase in bound thyroxin (T4) t3 (more active)and rT3 (inactive) • Free T4 and T3 are unaltered or slightly reduced • NOTE: increased BMR, tachycardia, elevated body temperature and increased CO are normal in pregnancy but may mimic the effects of hyperthyoidism

  28. Thyroid and Pregnancy • Hypothyroid: • Check TFT (TSH) at booking and every trimester • Likely to need increase in thyroxine dose during pregnancy • If anti-thyroid antibodies, inform paeds who will need to check fetal TFT at birth

  29. Thyroid and Pregnancy • Hyperthyroid • May worsen due to HCG • Risks-hyperemesis, miscarriage • Can use carbimazole but not PTU (or radio-I2) to treat • Regular TFTs and multidisciplinary care • If well controlled, no other impact on pregnancy care (fetal growth, delivery etc) • Inform Paeds to check fetal thyroid function, especially if pt has thyroid Abs

  30. Pre-Eclampsia

  31. Definition • Hypertension and proteinuria with onset ≥20 weeks • Oedema from classical definition dropped as not discriminating clinically • Diastolic ≥90mmHg on 2 occasions 4-6 hours apart OR ≥110mmHg on one occasion • Proteinuria >300mg/24 hours • Symptoms • Differentiation from PIH/renal disease George Eliot Hospital, Nuneaton

  32. Hypertensive disorders George Eliot Hospital, Nuneaton

  33. Incidence • 2-3% pregnancies • 5-7% primips • 1.8% PET will develop eclampsia (from Collaborative Eclampsia Trial = 49/ 100000) • Rates eclampsia 26.8/100 000 maternities (UKOSS reporting system 2003-5) • Worldwide 1.5-8 million develop PET with 150 000 deaths • Deaths 2003-5: 0.85/100000 maternities • 18 deaths • 10 cerebral haemorrhage, 2 cerebral infartion • 6 were eclamptic, 8 had HELLP syndrome George Eliot Hospital, Nuneaton

  34. Importance • Maternal morbidity • Blindness • Neurological • renal • Fetal death • Abruption, hypoxia, IUGR • Fetal morbidity • Prematurity (PET is cause of >40% iatrogenic preterm dels) with risks respiratory and neurodevelopmental complications (inc.learning difficulty/IQ in up to 60%) George Eliot Hospital, Nuneaton

  35. Primiparous First pregnancy with new partner Family history (1 in 3 risk if mother had PET) Twins/multiples Pregestational Diabetes Essential hypertension Renal disease SLE Antiphospholipid syndrome Thrombophilias Age >40 Obesity Risk Factors:-Pre-Eclampsia George Eliot Hospital, Nuneaton

  36. Pathophysiology • “The disease of theories” • Pregnancy specific syndrome • Placenta has a central role to play • Reduced placental perfusion • Inadequate vascular remodelling at ~16 wks • Genetic component in some women tho’ not in others • No candidate genes or consistent results George Eliot Hospital, Nuneaton

  37. Pathophysiology of PET George Eliot Hospital, Nuneaton

  38. 2 stage process • Inadequate implantation • Poor remodelling • Cytokines produced + growth factors • placental apoptosis/necrosis • Shedding of microparticles into circulation • Markers seen preceding PET • Inflammation and endotheial activation STAGE 1:Reduced placental perfusion STAGE 2: Maternal syndrome (multisystem disorder) George Eliot Hospital, Nuneaton

  39. Prevention of PET: Aspirin • Several small trials suggested reduction in rates PET with low dose aspirin therapy • Large multicentre trial (CLASP) in 9364 women did not demonstrate benefit for wholescale prophylaxis for low risk women • Trend towards reduction in likelihood to preterm delivery • No significant increased risk of haemorrhages • No statistically significant effect on stillbirths/ neonatal deaths • Non significant (12%) reduction in incidence PET Lancet 1994; 343: 619-629 George Eliot Hospital, Nuneaton

  40. CLASP • Trial suggested only benefits in women at high risk of severe early onset IUGR ? How to identify • Benefits thus suggested in women with previous severe early onset PET and IUGR • ?relationships to APLS (not investigated in original trial) George Eliot Hospital, Nuneaton

  41. Prevention: Aspirin • More recent study showed aspirin treatment produced at RR of 0.9 (95% CI 0.84-0.97) for PET • Moderate but consistent reductions in PET, preterm delivery and serious outcomes Lancet 2007 George Eliot Hospital, Nuneaton

  42. Prevention: Calcium • Calcium levels lower in women with PET compared to ‘normal’ pregnancy • Australian Randomised Study in 456 singleton nullips from <24/40 showed reduction in risk PET with 1.8g calcium/day compared to placebo • RR 0.44 95% CI 0.21-0.90 Aus NZ J Obstet Gynaecol 1999; 39: 12-18. George Eliot Hospital, Nuneaton

  43. Prevention: Calcium • Calcium for Eclampsia Prevention Study (CPEP) Am J Obstet Gynecol 1997; 177: 1003-10 • 4589 US women in multicentre trial • All nullips • Analysis of risk factors for development of subsequent PET did not show any benefit from Ca++ supplementation George Eliot Hospital, Nuneaton

  44. Prevention: Calcium • Cochrane Review Cochrane Database 2000 (3), OUS. • 9 studies, all good quality • Ca++ dose > 1g/day • Modest reduction in risk PET for all women (RR 0.72, 95% CI 0.6-0.86) • Greatest effect where highest risk- RR 0.22, 0.11-0.43 and low dietary intake (0.32, 0.21-0.49) • No effect on preterm delivery • Smaller effects seen for hypertension • Ca++ appears of benefit for women at high risk of developing PET • Also women from communities with low dietary intake • Optimum dosage requires further evaluation George Eliot Hospital, Nuneaton

  45. Prevention: Antioxidants • Vitamin C 1000mg and Vit E 400 IU/day • 58% reduction in PET in treated group Chappell et al, Lancet 1999 354: 810-5 • A number of trials ongoing globally • All using above dosages • 3 reported so far-NO difference in rates treatment vs placebo. George Eliot Hospital, Nuneaton

  46. Diagnosis: Pre-Eclampsia • Classic triad • Hypertension 140/90 • Proteinuria >300mg in 24 hours (RCOG) • Oedema (least reliable) • BP rise should be from booking >30/15 • Proteinuria and raised BP x 2 occasions 6 hrs apart (or once if DBP ≥110 and heavy proteinuria >2+ (=1g/24h)) George Eliot Hospital, Nuneaton

  47. Mild PET • Classically asymptomatic • BP 140/90 (ish) • Maybe trace-+ proteinuria • Often incidental finding at CMW clinic attendance George Eliot Hospital, Nuneaton

  48. What questions should you ask?

  49. What questions should you ask? • Headache (classically severe) • Effects hypertension • Visual disturbances (‘flashing lights’) • Sign of cerebral vasospasm/impending eclampsia • Epigastric pain • Hepatic congestion/liver capsule stretching • Is baby moving normally? • Fetal wellbeing

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