Hypertension in

pregnancy

Dr Simmer Gill

Sydney Adventist Hospital

Definition and Criteria

Systolic BP > or equal to 140 mmhg

Diastolic > or equal to 90 mm hg

Rise in BP >30/15 from booking BP- not a criteria but may

hold significance in presence of uric acid or a proteinuria

or foetal growth problems

SBP >/= 160 or DBP >/=110 requires treatment

BP >170/110 has adverse pregnancy outcomes

Recording of BP in Pregnancy

Seated comfortably, In labour- lateral recumbency

Mercury Sphygmometer ideal

BP to be recorded on 2 separate occasions 6 hours or more

apart

Home BP reading acceptable

24 hr ABPM (Ambulatory BP monitoring) -only to identify

white coat HTN

Classifications

Gestational HTN

Preeclampsia and eclampsia

Chronic HTN- essential, secondary, white coat.

Preeclampsia superimposed on chronic HTN

HELLP syndrome

Pathophysiology

CVS effects – increased BP and cardiac output

Haematologic effects- third spacing of fluid due to increased BP,

decreased oncotic pressure and increased vascular permeability

Renal effects- atherosclerotic like changes in Renal vessels –

decreased GFR and proteinuria. Uric acid filtration is also decreased

Neurological effects- Hyperreflexia sustained clonus and grand mal

seizures

Pulmonary oedema- decreased colloid oncotic pressure and increased

vascular permeability

Haemostatic Changes- increased platelet activation with increased

endothelial fibronectin and decreased antithrombin III and alpha 2

antiplasmin – endothelial damage

Pathophysiology –cont’d

Uterine Vascular changes

Trophoblastic mediated vascular changes – effects the musculature of

spiral arterioles causing low resistance and high flow system.

Inadequate maternal vascular response to the above - endothelial

damage within the vessels

Haemostatic Changes- increased platelet activation with increased

endothelial fibronectin and decreased antithrombin III and alpha 2

antiplasmin – endothelial damage

Changes in Prostanoids- PGI -2 and TXA -2- promotes vasoconstriction

Vasoconstriction and endothelial damage lead to vasospasm causing -

Foetal effects of IUGR, Oligohydramnios and low birth weight

Investigations

Specific history to look for clinical symptoms of PET in a woman with

new onset HTN after 20 weeks is very valuable

U A with a dipstick to look for proteinuria

Urine protein creatinine ratio and culture if > +1 protein on urine

dipstick

PET bloods- FBC, EUC, LFTs, retest in 3 days if normal in new onset

If low platelets or Hb- do Coagulation profile, LDH and fibrinogen to

exclude haemolysis

Foetal Growth, AFI and Umbilical artery dopplers

Severe early onset PET- exclude SLE, APLS, underlying renal disease

Pheochromocytoma although rare is potentially fatal- 24 hr urinary

catecholamines

Placental growth factor like tyro kinase 1- significance not known

Gestational HTN

New onset BP usually after 20 weeks

5-10% of Pregnancies beyond 1st trimester

15-25% women initially diagnosed with Gestational HTN may develop Preeclampsia

Earlier onset of Gestational HTN are more likely to progress to Preeclampsia

No maternal or foetal features of PET

BP returns to normal within 3 months postpartum

Earlier onset and more severe essential HTN will have higher risk of progress to PET and adverse pregnancy outcome

PET- preeclamptic toxaemia

Multisystemic disorder unique to human pregnancy

Includes HTN plus one or more organs and/or foetus

Renal- proteinuria, raised creatinine, urates & oliguria

Haematological-Thrombocytopenia, thrombolysis and DIC

Liver- raised transaminases, epigastric pain or RUQ pain

Neurological- convulsions hyperreflexia and sustained

clonus, headache, visual disturbance and stroke

Pulmonary oedema- decreased oncotic pressure and

increased vascular permeability

Foetal growth restriction oligohydramnios and abnormal

dopplers

Risk Factors for Preeclampsia

Nulliparity

Multiple pregnancy

Previous H/O preeclampsia

Family H/O preeclampsia

Obesity

AMA

Pre-existing HTN

APLS

Pre-existing Diabetes

Underlying Renal disease or autoimmune disease

Interpregnancy interval > 10 years

Eclampsia

Addition of convulsions in a woman with Preeclampsia

Occurs in 0.5- 4% of the deliveries

Most cases occur around the 24 hours of labour

3% cases may be diagnosed between 2-10 days of

postpartum

25% have seizures before labour 50% during labour and

other 25 % after delivery

Chronic HTN

Usually before the 20 weeks of gestation

Usually lasts more than the 6 weeks postpartum period

Can be essential or secondary to chronic disease

BP >140/90

Chronic Diseases causing HTN in pregnancy are

-chronic renal disease or renal artery thrombosis

- Coarctation of the aorta

-Systemic diseases involving kidneys like SLE, DM

-Endocrine disorders-pheochromocytoma, Cushing and

hyperaldosteronism

PET superimposed on Chronic HTN

Pre-existing HTN is a strong risk factor for PET

25 % women with Chronic HTN may develop PET

Women with Chronic hypertension develops features of

PET after 20 weeks is indicator

SGA is common with Chronic hypertension but

oligohydramnios and abnormal umbilical artery dopplers

are required to diagnose PET

HELLP syndrome

HTN patients with Haemolysis (H), elevated liver

enzymes( EL) and low platelets(LP)

4-12 % pt with severe Preeclampsia and eclampsia may

develop HELLP syndrome

First symptoms are always missed- nausea, emesis, and

non specific viral like syndrome

Cardiovascular stabilisation and correction of

coagulopathy sometimes even before delivery is mainstay

of treatment

Management of HTN in pregnancy

Delivery is definitive management for preeclampsia

Timing of delivery depends on severity of the disease and gestational age of the foetus.

BP >/= 160/ 100 needs treatment with AHTN drugs

Mild HTN- between 140-160/90-100- treatment is optional

Regular follow up in day assessment units play a vital role in diagnosing PET in pre-existing essential and chronic HTN Patients

Ace inhibitors and angiotensin receptor blockers are C/I in pregnancy

Drug Dose Action Contraindicati

ons

Practise Points

Methyl dopa

Clonidine

250-750mg

tds

75-300µg td

Central Depression Slow onset of action over 24 hours,

dry mouth, sedation, depression,

blurred vision

Withdrawal effects: rebound

hypertension

Labetalol

Oxprenolol

100-400mg

q8h

20-160 mg

q8h

Blocker with mild alpha vasodilator

effect

Blocker with intrinsic

sympathomimetic activity

Asthma,

chronic airways

limitation

Bradycardia, bronchospasm,

headache, nausea, scalp tingling

(labetalol only) which usually

resolves within 24 hours

Nifedipine 20mg -60 mg

slow release

bd

Ca channel antagonist Aortic stenosis Severe headache in first 24 hours

Flushing, tachycardia, peripheral

oedema, constipation

Prazosin 0.5-5 mg q8h blocker Orthostatic hypotension especially

after first dose

Hydralazine 25-50 mg q8h Vasodilator Flushing, headache, nausea, lupus-

like syndrome

Anti-HTN for mild/ moderate HTN

Foetal monitoring

Accurate dating of pregnancy

SFH is a poor screening tool for SGA

U/S by experienced operator is ideal

UAD – only foetal surveillance modality to reduce Foetal intervention but has limited value after 36 weeks

Systematic review has shown no benefits of BPP or CTG or their combination

No foetal testing can predict placental abruption or cord accidents

Foetal surveillance through DAU associated with good perinatal outcome for women with stable well controlled HTN

Foetal Surveillance

Hypertension Modality Frequency

Chronic hypertension Early dating ultrasound

U/S for foetal growth/AFV/Doppler

First trimester

3rd trimester: repeat as indicated

Gestational hypertension U/S for foetal growth/AFV/Doppler At time of diagnosis and 3-4 weekly

Preeclampsia U/S for foetal growth/AFV/Doppler

Cardiotocography

At time of diagnosis and 2-3 weekly

Twice weekly or more frequently if

indicated

Preeclampsia with FGR Cardiotocography

U/S for foetal /AFV/Doppler

U/S for foetal growth

Twice weekly or more frequently if

indicated

On admission and weekly or more

frequently if abnormalities in Doppler

flow or amniotic fluid volume are

detected.

2 weekly

Inpatient Management of Severe PET

Acute BP lowering antihypertensives- Labetalol 20mg IV, rpt 10

min(Max-80mg)

Nifedipine 10-20 mg oral rpt 45 mins to max of 40 mg

Hydralazine5-10 mg IV bolus max 30 mg. Hydralazine can be given

as infusion for maintenance

Thromboprophylaxis- Mechanical / chemical if 2 or more risk

factors

Fluid Management- worsen peripheral and cause pulmonary

oedema, small bolus can be considered before hydralazine therapy

or regional anaesthesia before delivery

Multi disciplinary team management with Haematologist, renal

physician, anaesthetist and paediatrician is vital in management

of PET patients

Inpatient Management- cont’d

Management of haematology and hepatology derangements- monitor biochemistry daily or twice a day

Platelets transfusion in severe thrombocytopenia as there is anaesthetic concerns for levels lower than 80 and risk of PPH for levels less than 50

FFP may be required to manage Coagulopathy

Consider Mg so4 for decreasing seizure activity risk – 4 gm loading dose and 1-2 gm /hr as maintenance

Eclampsia – Resuscitation- Airway, Breathing, Circulation, Drugs

IV diazepam or clonazepam while Mg so4 is prepared

Mgso4 to continue for 24 hr after the last seizure.

Management of Preeclampsia

WHEN TO DELIVER ????????

If previable- consult tertiary centre as TOP may be required or very extreme preterm delivery

Between 24 -32 weeks- consult tertiary centre

Consider antenatal corticosteroids and Mgso4

Aim to prolong pregnancy where possible

Between 32- 37 weeks-consult Paediatric team

Consider AN steroids esp. if <34 weeks or if considering caesarean delivery

Deliver in a centre with appropriate paediatric care

More than 37 weeks – Plan Delivery on the best day in the best way

Indications for delivery

Maternal Foetal

Gestational age >37 weeks Placental abruption

Inability to control HTN Severe IUGR

Worsening Biochemistry Non reassuring Foetal status

Intravascular haemolysis

Persistent Neurological symptoms

Persistent epigastric pain nausea and

abnormal LFTS

Pulmonary oedema

Hypitat and Hypitat II

HYPITAT- Lancet –Aug 2009- IOL is associated with improved

maternal outcome and should be advised for women with mild

hypertensive disease more than 37 weeks of gestation

HYPITAT II- Lancet – Mar 2015- Women with non severe

hypertensive disorders at 34-37 weeks of gestation immediate

delivery might reduce the already small risk of adverse

maternal outcomes. However it significantly increases the risk

of neonatal RDS, therefore routine immediate delivery does not

seem to be justified and expectant monitoring can be

considered till clinical situation deteriorates.

Anaesthetic considerations

Whenever possible an anaesthetist should be informed of women with Preeclampsia much before labour or before operative delivery.

Appropriate anaesthetic management is vital in reducing both foetal and maternal morbidity.

Relevant issues include- anaesthetic risk assessment, fluid management, BP control, eclampsia prophylaxis and planning of analgesia and anaesthesia

EDB is a useful adjunct to antihypertensives to control BP and improve both renal and uteroplacental blood flow

Regional blocks are preferred for C/S but GA may be required due to foetal compromise or maternal reasons like thrombocytopenia, haemodynamic instability, Pulmonary oedema or altered consciousness post eclampsia

Postpartum care

Consider HDU care for very severely affected patients, especially if

on MGSO4 therapy

Biochemistry may worsen on first day or 2 before getting better

NSAIDS are C/I as may adversely affect HTN, renal functions and

platelets

BP may take days, weeks or up to 3 months to normalise

Resolution is still reassured in preeclampsia if there is no underlying

pathology

Psychological and family support should be offered postpartum

Preconception prophylaxis of PET

Low dose Aspirin- prevents platelet aggregation and causes

vasodilatation, also has anti-inflammatory affect

Calcium supplements reduces risk of pre eclampsia particularly

in high risk women who has low dietary intake of calcium

There is a potential role of Heparins to prevent preeclampsia

secondary to hypertension in thrombophilic women

Antioxidant therapy with vit C and E shows no benefit but Folic

acid supplements may play a role by improving systemic and

placental endothelial function

Long term consequences

Women with preeclampsia may develop these later in life

Chronic HTN, CV disease, IHD, Peripheral vascular disease, DVT

End stage renal disease, type 2 DM, elevated TSH and all cancers

Women with preeclampsia may note some cognitive and visual

impairment

Systematic review of 18 studies show that offspring of preeclamptic

pregnancies are at higher risk of obesity, CVD and both systolic and

diastolic HTN

THANK YOU