Hypertension in Pregnancy

Tony Nicoll

Consultant Obstetrician

Ninewells Hospital

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Outline

• Objectives• Physiology• Classification• Pre-eclampsia• Pathogenesis • Management• Eclampsia• Conclusions

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Objectives

• Understand the processes involved in antenatal care, surveillance in pregnancy, and the roles of the professionals involved (Outcomes 1-11)

• Demonstrate a knowledge of the common problems encountered in obstetric practice (Outcomes 3,4,5,8)

Hypertension in Pregnancy• Hypertension affects 10-15% of all pregnancies

• Mild pre-eclampsia affects 10% of primigravid women

• Severe pre-eclampsia affects 1% of primigravid women

• Eclampsia affects 1/2000 pregnancies

• Death from eclampsia = 2%

• Pre-eclampsia is the commonest cause of iatrogenic

prematurity

• Up to 25% of antenatal admissions are due to hypertension

Blood Pressure in Pregnancy

• Blood pressure (BP) proportional to systemic vascular resistance and cardiac output

• Pregnancy Vasodilatation• BP falls in early pregnancy• Nadir reached at 22-24 weeks• Steady rise until Term• BP falls after delivery but subsequently rises and

peaks at day 3-4 P/N

Hypertension

• ≥140/90 mmHg on 2 occasions

• DBP >110 mmHg

• ACOG - >30/15 mmHg compared to booking BP

Hypertension in Pregnancy

• Pre-existing hypertension

• Pregnancy Induced Hypertension (PIH)

• Pre-eclampsia

Pre-existing Hypertension

• Diagnosis prior to pregnancy• Likely if hypertension in early pregnancy

(PET / PIH diseases of second half of pregnancy)• May be retrospective diagnosis if BP has not

returned to normal within 3 months of delivery• Consider secondary causes - renal / cardiac,

Cushing’s, Conn’s, Phaeochromocytoma• Risks include PET (X2), IUGR and abruption

PIH

• Second half of pregnancy

• Resolves within 6/52 of delivery

• No proteinuria or other features of pre-eclampsia

• Better outcomes than pre-eclampsia

• 15% progression to pre-eclampsia - depends on

gestation

• Rate of recurrence is high

Pre-eclampsia

Pre-eclampsia

• Hypertension

• Proteinuria (≥0.3g/l or ≥0.3g/24h)

• Oedema

• Absence does not exclude the diagnosis

Pre-eclampsia• A pregnancy-specific multi-system disorder with

unpredictable, variable and widespread

manifestations

• May be asymptomatic at time of first presentation

• Diffuse vascular endothelial dysfunction widespread

circulatory disturbance

• Renal / Hepatic / Cardiovascular / Haematology /

CNS / Placenta

Pathogenesis

• Genetic predisposition

• Stage 1 - abnormal placental perfusion

• Stage 2 - maternal syndrome

Pathogenesis• Abnormal placentation and trophoblast invasion failure

of normal vascular remodelling • Spiral arteries fail to adapt to become high capacitance, low

resistance vessels• Placental ischaemia widespread endothelial damage

and dysfunction• Mechanism unclear (??oxidative stress / PGI2 : TXA2

imbalance / NO)• Endothelial Activation

Capillary Permeability Expression of CAM Prothrombotic Factors Platelet aggregration• Vasoconstriction

Normal Placentation

Pre-eclampsia

Non- Pregnant

A Multi-system Disorder

• CNS

• Renal

• Hepatic

• Haematological

• Pulmonary

• Cardiovascular

• Placental

CNS Disease

• Eclampsia

• Hypertensive encephalopathy

• Intracranial haemorrhage

• Cerebral Oedema

• Cortical Blindness

• Cranial Nerve Palsy

Renal disease

GFR• Proteinuria serum uric acid (also placental ischaemia) creatinine / potassium / urea• Oliguria /anuria• Acute renal failure

• acute tubular necrosis• renal cortical necrosis

Liver Disease

• Epigastric/ RUQ pain• Abnormal liver enzymes• Hepatic capsule rupture

• HELLP SyndromeHaemolysis, Elevated Liver Enzymes, Low Platelets

• high morbidity/ mortality

Haematological Disease

Plasma Volume• Haemo-concentration• Thrombocytopenia• Haemolysis• Disseminated Intravascular Coagulation

Cardiac / Pulmonary Disease

• Pulmonary oedema ARDS• iatrogenic• disorder related

• Pulmonary Embolus

• High mortality

Placental Disease

• Intrauterine growth restriction (IUGR)

• Placental Abruption

• Intrauterine Death

Symptoms

• Headache • Visual disturbance• Epigastric / RUQ pain• Nausea / vomiting• Rapidly progressive oedema

• Considerable variation in timing, progression and order of symptoms

Signs

• Hypertension• Proteinuria• Oedema• Abdominal tenderness• Disorientation• SGA• IUD• Hyper-reflexia / involuntary movements / clonus

Investigations• Urea & Electrolytes

• Serum Urate

• Liver Function Tests

• Full Blood Count

• Coagulation Screen

• CTG

• Ultrasound - biometry, AFI, Doppler

Management• Assess risk at booking

• Hypertension < 20 weeks - look for secondary

cause

• Antenatal screening - BP, urine, MUAD

• Treat hypertension

• Maternal & fetal surveillance

• Timing of Delivery

• PIH can be managed as O/P in Day Care Unit

Risk Factors

• Maternal Age (>40 years 2X)• Maternal BMI (>30 2X) • Family History (20-25% if mother affected, up to

40% if sister)• Parity (first pregnancy 2-3X)• Multiple pregnancy (Twins 2X)• Previous PET (7X)• Molar Pregnancy / Triploidy

• Multiparous women develop more severe disease

Medical Risk Factors

• Pre-existing renal disease

• Pre-existing hypertension

• Diabetes Mellitus

• Connective Tissue Disease

• Thrombophilias (congenital / acquired)

Predicting Pre-eclampsia

Normal MUAD

Notch

Maternal Uterine Artery Doppler

20 - 24 weeks

Antenatal Screening• When to refer to AN DCU?

BP 140/90

(++) proteinuria

oedema

symptoms - esp persistent headache

• For every 1000 “Low-risk” patients:

100 hypertensive

60 normal - 20 will return

20 DCU follow up - 10 admitted

20 admitted

When to admit?1. BP >170/110 OR >140/90 with (++) proteinuria

2. Significant symptoms - headache / visual disturbance / abdominal pain

3. Abnormal biochemistry

4. Significant proteinuria - >300mg / 24h

5. Need for antihypertensive therapy

6. Signs of fetal compromise

Inpatient Assessment

• Blood Pressure - 4 hourly

• Urinalysis - daily

• Input / output fluid balance chart

• 24 hour urine collection - if proteinuria on urinalysis

• Bloods - FBC, U&Es, Urate, LFTs. Minimum X2 per week

Fetal Surveillance

• Fetal Movements

• CTG - daily

• Ultrasound

Biometry

Amniotic Fluid Index

Umbilical Artery Doppler

Normal

AEDF

REDF

Treatment of Hypertension

• Treat regardless of aetiology

• With MAP ≥150 mmHg there is significant risk of cerebral

haemorrhage

• Most treat if BP ≥150/100 mmHg

• BP ≥ 170/110 mmHg requires immediate Rx

• Aim for 140-150/90-100 mmHg

• Control of blood pressure does not reduce the risk of

developing pre-eclampsia

Treatment of HypertensionMode of Action

Starting Dose

Maximum Dose

Contra-

indicationsBreast

Feeding

Methyl Dopa

Centrally acting agonist

250mg bd 1 gram tds Depression Yes

Labetolol +

antagonist100mg bd 600mg qid Asthma Yes

Nifedipine SR

Ca channel antagonist

10mg bd 40mg bd Yes

Hydralazine Vasodilator 25mg tds 75mg qid Yes

(Avoid Diuretics / ACE Inhibitors)

When to Deliver?

• The only cure for pre-eclampsia is delivery

• Mother must be stablised before delivery

• Consider expectant management if pre-term

• Most women delivered within 2 weeks of

diagnosis

Indications for Delivery

• Term gestation

• Inability to control BP

• Rapidly deteriorating biochemistry / haematology

• Eclampsia

• Other Crisis

• Fetal Compromise - REDF, abnormal CTG

Crises in Pre-eclampsia

• Eclampsia• HELLP syndrome• Pulmonary Oedema• Placental Abruption• Cerebral Haemorrhage• Cortical Blindness• DIC• Acute Renal Failure• Hepatic Rupture

Steroids• Promote fetal lung surfactant production• ↓ neonatal respiratory distress syndrome (RDS)

by up to 50% if administered 24-48h before delivery

• Administer up to 36 weeks• Only significant effects up to 34 weeks. Proven

benefit up to 1 week• Betamethasone preferred to Dexamethasone

• 1 course = 12mg Betamethasone IM X2 injections 24 hours apart

Eclampsia

Eclampsia

• Tonic-clonic (grand mal) seizure occuring with features of pre-eclampsia

• >1/3 will have seizure before onset of hypertension / proteinuria

• Ante-partum (38%) / Intra-partum (16%) / post-partum (44%)

• More common in teenagers• Associated with ischaemia / vasospasm

Management of Severe PET / Eclampsia

• Control BP

• Stop / Prevent Seizures

• Fluid Balance

• Delivery

Antihypertensives

• IV Labetolol

• IV Hydralazine

• Beware hypotension – fetoplacental unit

Seizure Treatment / ProphylaxisMAGNESIUM SULPHATE

Loading dose: 4g IV over 5 minutes

Maintenance dose: IV infusion 1g/h

If further seizures administer 2g Mg SO4

If persistent seizures consider diazepam 10mg IV

Fluid Balance

• Main cause of death = pulmonary oedema(Capillary leak / fluid overload / cardiac failure)

• Oliguria in 30%. Does not require intervention

• Any doubts about renal function urine osmolality

• Fluid challenges are potentially dangerous

• Safer to run a patient “dry” - 80 ml/h

Labour and Delivery

• Aim for vaginal delivery if possible• Control BP• Epidural anaesthesia• Continuous electronic fetal monitoring• Avoid ergometrine• Caution with iv fluids

Postpartum Management

• Breast feeding• Contraception• BP management• Counselling• Future risk

– Depends on other medical factors– Gestation dependent (28/40 - 40%, 32/40 - 30%)

• Long term CVD risk

Low Dose Aspirin

• Aspirin - inhibits cyclo-oxygenase prevents TXA2 synthesis

• 75mg Aspirin 15% reduction in PET (NNT=90)• May be more beneficial in preventing severe early onset

pre-eclampsia (MRC CLASP Trial)• Safe• Used for high risk women - Renal, DM, APS, Multiple

risk factors, previous PET• Commence before 12 weeks

NICE Aug 2010

Calcium, Antioxidants & Folic Acid

• Calcium supplementation (>1gram / day) may reduce risk of hypertension (30%), PET (52%) and maternal death (20%). Did not affect pre-term birth or stillbirth (Hofmeyr et al Cochrane Database 2006)

• Antioxidants not effective (Poston et al. VIP Study, Lancet 2006)

• Mid trimester folic acid also appears to be effective in preventing pre-eclampsia (73% reduction) (Wen et al AJOG 2008)

Conclusions• Hypertension in pregnancy is common

• Pre-eclampsia is a multi-system disorder with unpredictable and variable manifestations

• Pathogenesis involves abnormal placentation and widespread endothelial dysfunction

• Supportive management requires maternal and fetal surveillance

• No cure other than delivery

• Maternal risks balanced against risks of prematurity