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

2. The most common and serious medical problem in pregnancy.
Hypertension
The most common and serious medical 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 the likelihood of developing preeclampsia or an adverse pregnancy outcome.

9. Preeclampsia
A multi-system disorder characterised by hypertension and involvement of one
or more other organ systems 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. Pre-existing hypertension or prior to 20 weeks gestation.
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 than 30mg/mmol)
- 24 hour urine collection.
Full blood count (FBC)
Urea, creatinine, electrolytes including 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 investigation Description if preeclampsia
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 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 (of at least 1 g/d) are recommended. Starting pre-pregnancy or from diagnosis of pregnancy but before 16 weeks’ gestation until delivery.
Heparin (LMWH).