Hypertensive disorders in pregnancy

Question 1

What are the normal blood pressure changes in pregnancy?

Answer 1

• Blood pressure normally falls to a minimum level in the 2nd trimester- by about 30/15mmHg because of reduced vascular resistance, occurs in both normotensive and chronically hypertensive women, by term, the blood pressure rises again to pre-pregnant levels
• Hypertension due to pre-eclampsia is largely caused by an increase in systemic vascular resistance
• Protein excretion is increased in normal pregnancy, but in the absence of underlying renal disease is less than 0.3g/24hrs

Question 2

What is pregnancy induced hypertension?

Answer 2

when the blood pressure rises above 140/90mmHg after 20 weeks- can be due to pre-eclampsia or transient hypertension
• Gestational hypertension- new hypertension presenting after 20 weeks without proteinuria
Pre-eclampsia

Question 3

What is pre-existing or chronic hypertension?

Answer 3

• This is present when the blood pressure is >140/90mmHg before pregnancy or before 20 weeks gestation or the women is already on hypertensive treatment
• This may be primary hypertension or secondary to renal or other disease, may also be pre-existing proteinuria because of renal disease
• Patients with underlying hypertension are at an increased risk of ‘superimposed’ pre-eclampsia

Question 4

What is pre-eclampsia?

Answer 4

a multisystem syndrome that is usually manifest as new hypertension after 20 weeks with significant proteinuria ((>0.3g/24hrs) and oedema
Cured only by delivery
• Blood vessel endothelial cell damage leads to vasospasm, increased capillary permeability and clotting dysfunction- both the foetus and mother are at risk

Question 5

What are the 2 phenotypes of pre-eclampsia?

Answer 5

o Early-onset- that which causes complications before 34 weeks, typically the foetus is growth restricted
o Late-onset- manifest at any later gestation, not usually associated with growth restriction, although foetal death and damage may occur

Question 6

What is the 1st step of pathophysiology in pre-eclampsia?

Answer 6

Poor placental perfusion
Incomplete trophoblastic invasion of spiral arterioles leads to vasodilation of vessel walls to allow adequate placenta perfusion
This causes oxidative stress- effects can be detected as high- resistance flow in uterine arteries
In late onset PE- growth of an apparently normal placenta reaches its limits- intervillous perfusion may reduce because terminals become over-crowded, causing oxidative stress

Question 7

What is the 2nd step of pathophysiology of pre-eclampsia?

Answer 7

• Both mechanisms cause the oxidative stressed placenta to oversecrete proteins that regulate angiogenic balance
this can be detected as increased sFlt-1 and reduced PIGF levels in the maternal blood
• Widespread endothelial cell damage may follow- causing vasoconstriction, increased vascular permeability and clotting dysfunction, these cause the clinical manifestations of the disease

Question 8

What is the classification of pre-eclampsia?

Answer 8

• Severe pre-eclampsia is pre-eclampsia with severe hypertension and/or with symptoms and/or biochemical and/or haematological impairment
• Hypertension is classified as
o Mild: 140/90 – 149/99mmHg
o Moderate: 150-100 – 159/109mmHg
o Severe: >160/110mmHg
o Mild or moderate- pre-eclampsia without severe hypertension and no symptoms and no biochemical or haematological impairment
o Severe- pre-eclampsia with severe hypertension and/or with symptoms, biochemical or haematological impairment
o Early- <34 weeks
o Late- >34 weeks

Question 9

What is the aetiology of pre-eclampsia?

Answer 9

it is less common in multiparous women unless additional risk factors are present. Recurrence risk is 15% up to 50% if severe before 28 weeks
o Nulliparity
o A previous or family history of pre-eclampsia
o Long interpregnancy interval
o Obesity
o Extremes of maternal age (>40yrs)
o Disorders characterised by microvascular disease (chronic hypertension, chronic renal disease, sickle cell disease, diabetes, autoimmune disease, anti-phospholipid syndrome
o Pregnancies with a large placenta- twins, foetal hydrops or molar pregnancy

Question 10

What are the clinical features of pre-eclampsia?

Answer 10

o	Headache
o	Drowsiness
o	Visual disturbance
o	Nausea/vomiting
o	Epigastric pain- later stage
•	Hypertension is usually the first sign- massive oedema is also found in pre-eclampsia, not postural or of sudden onset

Question 11

What are the maternal complications of pre-eclampsia?

Answer 11

• Early-onset disease is most severe
Eclampsia (grand mal seizure)
• Cerebrovascular haemorrhage- results from a failure of cerebral blood flow autoregulation at MABP
>140mmHg, treatment of hypertension should prevent this
• Liver and coagulation problems: HELLP, DIC, liver failure
Renal failure: identified by careful fluid balance monitoring and creatinine measurement, haemodialysis is required in severe cases
Pulmonary oedema: severe pre-eclampsia is particularly vulnerable to fluid overload. treated with oxygen & furosemide and assisted ventilation may be required- ARDS may develop

Question 12

What is eclampsia?

Answer 12

grand mal seizure resulting from cerebrovascular vasospasm
mortality can result from hypoxia and concomitant complications of severe disease
treatment is magnesium sulphate and intensive surveillance for other complications

Question 13

What is HELLP syndrome?

Answer 13

H: haemolysis (dark urine, raised lactic dehydrogenase (LDH), anaemia)
EL: elevated liver enzymes (epigastric pain, liver failure, abnormal clotting)
LP: low platelets (normally self-limiting)
treatment is supportive and includes magnesium sulphate prophylaxis against eclampsia

Question 14

What are the foetal complications of pre-eclampsia?

Answer 14

• Perinatal mortality and morbidity of the foetus are increased
Early onset PE: growth restriction, preterm labour required
At term- pre-eclampsia affects foetal growth less, but is still associated with increased morbidity and mortality, at all gestations there is an increased risk of placental abruption

Question 15

What are the investigations for pre-eclampsia?

Answer 15

• If bedstick urinalysis is +ve, the protein is quantified- 24hr urine or protein:creatinine ratio is used
• Blood tests are taken to show elevation of uric acid- the Hb is often high, a rapid fall in platelets due to aggregation on damaged endothelium indicates impending HELLP
• A rise in LFTs (ALT) suggests impending liver damage or HELLP- LDH levels rise with liver disease and haemolysis
• Renal function is often mildly impaired, a rapidly rising creatinine suggests severe complications and renal failure
• To monitor foetal complications an USS helps estimate foetal weight at early gestations and is used to assess foetal growth- umbilical artery Doppler and CTG are required to evaluate foetal well-being

Question 16

What is the screening and prevention for pre-eclampsia?

Answer 16

• Early prediction- uterine artery Doppler at 20 weeks, the sensitivity for PE at any stage in pregnancy is about 40% for a 5% screen-positive rate, for early-onset PE the figures are much better
ate prediction, the ratio of sFlt-1 to PIGF in maternal blood later in pregnancy, particularly in women with mild hypertension- useful in determining who will actually develop pre-eclampsia
• Prevention: low-dose aspirin (75mg) before 16 weeks (evening) reduces the risk of pre-eclampsia and is now NICE recommended, high-dose vitamin D with Ca2+ supplementation might also be effective

Question 17

When are patients with pre-eclampsia admitted?

Answer 17

• Necessary with severe hypertension and presence of proteinuria, if hypertension absent, but proteinuria
≥30 or >0.3g/hr they should be admitted
• Assessment using sFlt-1:PIGF assay may determine which women are most at risk and should be admitted

Question 18

Which medications are used in pre-eclampsia?

Answer 18

• Anti-hypertensives: given if BP reaches 150/100mmHg- Labetalol maintenance is recommended, oral nifedipine is used for initial control, with IV labetalol as 2nd line with severe hypertension. aim for BP is 140/90mmHg
• Magnesium sulphate: used in both treatment and prevention, IV loading dose followed by IV infusion- increased cerebral perfusion so treats underlying pathology of eclampsia- is required then delivery is indicated. Toxicity is severe resulting in respiratory depression, hypotension, loss of patellar reflex
• Steroids: used to promote foetal pulmonary maturity if the gestation is <34 weeks

Question 19

How is the delivery managed in pre-eclampsia?

Answer 19

• Women with pre-eclampsia should be delivered by 36 weeks (after 34 can be induced with prostaglandin)
• Clinical deterioration or maternal complications or reduced SVT on CTG will prompt delivery
• As a general rule- 1 or more foetal/maternal complications are likely to occur within 2 weeks of the onset of proteinuria
• Women with gestational hypertension should be delivered by 40 weeks as usual
• C-section is usual delivery- epidural will help reduce blood pressure
• Anti-hypertensives should be used in labour
• Maternal pushing should be avoided in 2nd stage is BP is 160/110mmHg
• Oxytocin instead of ergometrine should be used in 3rd stage and the latter can increase BP

Question 20

What is the post-natal care for pre-eclampsia?

Answer 20

• Highest BP is usually reached 4-5 days after birth- postnatal treatment is with a beta-blocker, with nifedipine and ACE-i 2nd line
• Treatment may be needed for several weeks

Question 21

What are the causes of pre-existing hypertension in pregnancy?

Answer 21

•	Diagnosed when BP is already treated or exceeds 140/90mmHg before 20 weeks 
o	Obesity
o	Diabetes
o	Renal disease- ADPKD, renal artery stenosis or chronic pyelonephritis
o	Phaechromocytoma
o	Cushing’s syndrome
o	Cardiac disease
o	Coarctation of the aorta

Question 22

What is the management for pre-existing hypertension in pregnancy?

Answer 22

o ACE-i- teratogenic and affect foetal urine production
o Labetalol- normally used
o Nifedipine- 2nd line
• Medication may not be needed in the 2nd trimester because of the physiological fall in BP
• The pregnancy is treated as ‘high-risk’- low dose aspirin is advised, screening using uterine artery Doppler and additional antenatal visits are usual
• Delivery is usually undertaken at 38-40 weeks- although the benefits of this are debated