Hypertensive Disorders of Pregnancy

1. Hypertensive Disorders of Pregnancy Anita Kazdepka – Ziemińska Klinika Położnictwa, Chorób Kobiecych i Ginekologii Onkologicznej

2. Hypertension The most common and seriousmedical problem in pregnancy. WHY ?

3. Complications Pregnant women with hypertension are more likely to develop: • Multiorgan system dysfunction. • Hepatic failure and acute renal failure. • Cerebral haemorrhage. • Disseminated intravascular coagulation (DIC). • Pulmonary edema. • Placental abruption. Fetal and neonatal complications: • Growth restriction. • Prematurity. • Perinatal death .

4. Incidence • About 10% pregnant women develop hypertension and mild pre-eclampsia • Further 10% of these develop severe pre-eclampsia • Incidence of eclampsia ranges from 1 in 500 to 1 in 30

5. Blood pressure in Normal Pregnancy • Decreases during the first trimester, • Reaching its lowest point at 20 weeks, • Middle trimester - reduction in Systemic Vascular Resistance (SVR) and Arterio-venous (AV) shunting within the uterus and intervillous space – the Blood Pressure (BP) falls below pre-pregnancy or early pregnancy level. This is compensated by relative tachycardia. • 3rd trimester, BP usually rises back to the pre-pregnancy level.

6. Definition • Systolic blood pressure (BP) ≥ 140 mmHg and/or diastolic BP ≥ 90 mmHg • Severe hypertension in pregnancy: systolic BP greater ≥ 160 mmHg and/or diastolic BP ≥ 110 mmHg • Severe hypertension requires urgent assessment and management.

7. Classification • gestational hypertension, • preeclampsia – eclampsia, • chronic hypertension, • chronic hypertension with superimposed preeclampsia.

8. Gestational hypertension • New onset of hypertension arising after 20 weeks gestation • No additional features of preeclampsia • Resolves within 3 months postpartum • The earlier the gestation at presentation and the more severe the hypertension, the higher thelikelihood of developing preeclampsia or an adverse pregnancy outcome.

9. Preeclampsia • A multi-system disorder characterised by hypertension and involvement of one or more other organsystems and/or the fetus. • Raised BP is commonly but not always the first manifestation. • Proteinuria is also common but should not be considered mandatory to make the clinical diagnosis.

10. Preeclampsia • Hypertension + one or more of: significant proteinuria  random urine protein/creatinine ratio greater than or equal to 30 mg/mmol renal involvement  serum or plasma creatinine greater than or equal to 90 micromol/L or  oliguria haematological involvement  thrombocytopenia  haemolysis  DIC liver involvement  raised transaminases  severe epigastric or right upper quadrant pain neurological involvement  severe headache  persistent visual disturbances (photopsia, scotomata, cortical blindness, retinal vasospasm)  hyperreflexia with sustained clonus  convulsions (eclampsia)  stroke pulmonary oedema,intrauterine fetal growth restriction (IUGR),placental abruption

11. Risk factors for preeclampsia • Preeclampsia in a previous pregnancy. • Family history of preeclampsia. • Poor outcome in a prior pregnancy (placental abruption, IUGR, fetal death in utero) • Interdelivery interval greater than 10 years • Nulliparity • Pre-existing medical conditions - chronic hypertension - diabetes (pre-existing or gestational) - renal disease - thrombophilias: antiphospholipid syndrome, protein C and S deficiency,antithrombin III deficiency and Factor V Leiden • Maternal age greater than or equal to 40 years • Body Mass Index (BMI)1 greater than 35 kg/m2 • Multiple pregnancy • Fetal triploidy

14. Eclampsia • Seizures may occur antepartum (38%), intrapartum (18%) or postpartum (44%). • Teenagers are three times more likely to suffer eclampsia than older women.

17. Eclampsia

18. Chronic hypertension Pre-existing hypertension or prior to 20 weeks gestation.

19. Preeclampsia superimposed on chronic hypertension. • Diagnosed where a woman with pre-existing hypertension develops: - systemic features of preeclampsia, - after 20 weeks gestation.

20. Antenatal assessment Goals of antenatal monitoring are to: • control blood pressure, • recognise preeclampsia early, • prevent eclampsia, • optimise birth for both the woman and the fetus.

21. Maternal investigations Tests may be abnormal even when BP elevation is minimal. • Urine dipstick testing for proteinuria - Quantitation by laboratory methods if greater than or equal to “2+” - Spot urine protein:creatinine can be used to detect significant proteinuria (greater than30mg/mmol) - 24 hour urine collection. Full blood count (FBC) Urea, creatinine, electrolytesincluding lactate dehydrogenase (LDH) and urate. Liver function tests (LFT)

22. Preeclampsia investigations If features of preeclampsia are present additional investigations should include: - urinalysis and microscopy on a carefully collected mid-stream urine sample - if there is thrombocytopenia or a falling haemoglobin, investigations for DIC: coagulation studies, blood film, LDH, fibrinogen.

24. Fetal assessment • Cardiotocograph (CTG) • Ultrasound scan (USS) assessment of: - fetal growth - amniotic fluid volume (AFV) - umbilical artery flow (Doppler)

26. Fetal investigations Fetal investigation Description if preeclampsia -Fetal movement count - Decreased -Non-stress test - Non-reassuring FHR -Biophysical profile - Lower score -Deepest amniotic fluid - Lower pocket -USS assessment of fetal - IUGR growth -Umbilical artery flow - Increased resistance, absent Doppler or reversed end diastolic flow

27. Pathophysiology • Normal pregnancy : cytotrophoblasts invade the uterine spiral arterioles, converting them from small-caliber vessels to large-caliber capacitance vessels capable of carrying larger amount of blood flow through the placenta.

28. Pathophysiology • TWO – STAGE MODEL FOR PREECLAMPSIA Stage 1: reduced placental perfusion Abnormal implantation Stage 2 : maternal syndrome -hypertension - proteinuria -endothelial dysfunction

31. Pathophysiology • Impair/ inadequate trophoblast invasion to the spiral arteries. • Spiral arteries retain their charecteristic (narrow, tortuous, high resistance) • Reduce blood supply to placenta • Result in placental hypoperfusion • As a compensation High BP in maternal

32. Pathophysiology • Vasoconstriction and end-organ damage: - Neurologic: headache, blurred vision, hyperreflexia, clonus, and seizures. Cerebral edema and intracerebral hemorrhage can be seen. - Renal: proteinuria (>300 mg/day), azotemia (decreased renal blood flow and average GFR by 30-40%), acute kidney injury (acute tubular necrosis), increased urate reabsorption (leads to hyperuricemia) - Hematologic: microangiopathic hemolytic anemia, thrombocytopenia, DIC (Disseminated Intravascular Coagulation) - Hepatic: HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) - Cardiovascular: hypertension, decreased cardiac output - Gastrointestinal: elevated liver enzymes, epigastric/right upper quadrant pain, subcapsular hemorrhage, liver rupture - Other: pulmonary edema, peripheral edema

34. PE MANAGEMENT Definitive treatment: DELIVERY! • Based on the ff: • AOG • Severity of PE • Maternal / Fetal condition

35. PES: MANAGEMENT Deliver regardless of gestational age : if proteinuria ( ≥5 grams) is the only criteria for severe disease Corticosteroids should be given if the fetus is less than 34 weeks gestation and birth can be deferred

36. MILD PE: MANAGEMENT Deliver at ≥37 weeks of gestation Labor induction encouraged

37. Acute Management of PES Labetalol first-line therapy (rapid onset of action, good safety profile) 20 mg IV over 2 minutes followed at 10-minute intervals by doses of 20 to 80 mg – up to a maximum total cumulative dose of 300 mg – E.g. Give 20 mg, then 40 mg, then 80 mg, then 80 mg, then 80 mg

38. Acute Management of PES Hydralazine 5 mg IV over 1 to 2 minutes if BP goal is not achieved within 20 minutes, give a 5 to 10 mg bolus depending upon the initial response » The maximum bolus dose is 20 mg » If a total dose of 30 mg does not achieve optimal blood pressure control, another agent should be used. » The fall in blood pressure begins within 10 to 30 minutes and lasts from 2 to 4 hours.

39. Target BP 130 to 150 mm Hg systolic and 80 to 100 mm Hg diastolic OR reduce MAP by no more than 25% over 2hrs • Cerebral or myocardial ischemia or infarction can be induced by aggressive antihypertensive therapy if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation

40. Seizure Prophylaxis MgS04 given to mild / severe PE » Loading dose: 4-6 g, slow IV push, over 15-20 mins » Continuous infusion: 1-2 g/hr OR 5g IM into each buttock (total 10 g) followed by 5 g IM, alternate buttocks ever 4h continued for 24 hours postpartum

41. Prevention of Recurrence Prepregnancy • Weight loss to ideal BMI • Control of glucose in diabetes • Control of BP in CHTN (diet, exercise) • Low dose aspirin in select patients (from 12 wks) •Not recommended: Vitamins C & E • Dietary salt restriction • Anti-HTN therapy to prevent preeclampsia

42. GOALS • Development of effective strategies for the prevention and/or treatment of preeclampsia • Prolong the pregnancy and improve maternal and neonatal health

43. Key Points • • • • • • • Identify Risk Factors Prediction Diagnosis (Classify) Ambulatory or In Patient Management Tertiary Care Postpartum care Prevention

44. Recommendations • Low-dose aspirin (75–100 mg/d )(I-A) and calcium supplementation (ofat least 1 g/d) are recommended.Starting pre-pregnancy or from diagnosis of pregnancy but before 16 weeks’ gestation until delivery. • Heparin (LMWH).