Title: Hypertension in Pregnancy
1Hypertension in Pregnancy
- Mojgan Vatani
- Staff Specialist, WCH
2- Definition
- Classification
- Investigation
- Management/Treatment
3Definition
- Normal pregnancy is characterised by a fall in
BP, detectable in the 1st trimester and usually
reaching a nadir in the 2nd trimester. BP rises
towards pre-conception levels towards the end of
the 3rd trimester.
4Hypertension in Pregnancy
- Systolic BP greater than or equal to 140 mmHg
and/or - Diastolic BP greater than or equal to 90 mmHg
- Repeated reading over several hours.
- Important as perinatal mortality and morbidity
rises with diastolic BP above 90 mmHg.
5Recording BP in Pregnancy
- Seated comfortably with her legs resting on a
flat surface. - Left arm
- The standard location is the upper arm, with the
stethoscope at the elbow crease over the brachial
artery - In labour, BP can also be measured in lateral
recumbency (30 degree). Avoid supine posture. - Proper size cuff
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7Cuff size
- Recommendation from American Hearth Association
- Cuff dimension requirements refer to the size of
the compression cavity, NOT the cuff itself. - Cuff width should be equal 40 of the arm
circumference or 1.2 times the diameter of the
arm. - Use the ratio of the arm circumference to the
cuff width, not the cuff length.
8Cuff size
- A larger cuff with an inflatable bladder covering
80 of the arm circumference should be used if
the upper arm circumference is greater than 33
cm.
9BP measurement
- The systolic BP is accepted at the first
Korotkoff sound (K1) heard - The diastolic BP is accepted with the
disapperance of sounds completely (K5). Where K5
is absent, K4 (muffling) should be accepted.
10BP measurement
- Mercury sphygmomanometers remain the gold
standard - Automated BP recorders have been also used.
Require regular calibrating at regular intervals. - 24 hours Ambulatory monitoring is useful in early
pregnancy ( lt20 weeks). To screen for white
coat HT.
11Classification of hypertensive disorders in
pregnancy
- Gestational hypertension
- Chronic hypertension
- Essential
- Secondary
- White coat
- Preeclampsia superimposed on chronic hypertension
- Preeclampsia- eclampsia
12Gestational Hypertension
- Hypertension (HTN) which develops at or after
20/40 in women known to be normotensive at
booking, with no previous history of
hypertension. - Must be present on several readings over several
hours. - Resolves within 12/52 after delivery
- Generally not associated with proteinuria,
although the term PIH is still sometimes
mistakenly used to mean pre-eclampsia. - Approximately 20 of women will have a blood
pressure reading above 140/90 at some stage in
the second half of pregnancy not all of them
will meet the criteria for Gestational HT or
require treatment beyond observation and
monitoring. - In some women with pre-existing hypertension,
the normal fall in blood pressure which occurs in
the first half of pregnancy may put them into the
normotensive range, despite not being on any
treatment.
13Gestational HT continued.
- In normal pregnancy, blood pressure begins to
fall in the first trimester, reaching its lowest
levels around 20/40. - This is due to a decrease in systemic vascular
tone, leading to reductions in both preload and
afterload. - There is a compensatory increase in heart rate
and activation of the volume-restoring
mechanisms, all of which ultimately results in an
increase in cardiac output of approx 40. - This initial drop in peripheral vascular
resistance is probably mediated by oestrogens,
prostaglandins, nitric oxide (and others?). - It appears that prostaglandins reduce the
efficacy of angiotensin II, which would normally
cause vasoconstriction.
14Gestational HT continued
- Both the systolic and diastolic blood pressures
slowly rise through the second half of pregnancy,
to return to pre-pregnant levels around term. - There may be a corresponding reduction in cardiac
output. - At least some of this effect is positional, and
is influenced by the action of the gravid uterus
on venous return to the heart. - A rise of gt 30mmHg systolic or 15mmHg diastolic
may also be abnormal and requires close
monitoring. - A systolic bp gt 170 and / or diastolic gt 110 is
always abnormal in pregnancy the patient should
be admitted for immediate assessment and
management.
15Why worry?
- If blood pressure reaches or exceeds 140/90,
there is an increased risk of morbidity and
mortality to both mother and fetus. - Gest HT increases the risk of pre-eclampsia (PE),
and hence careful monitoring for the development
of this condition is required.
16Gestational HT Management.
- 1. Exclude PE Ix for mother and fetus.
- 2. Monitor to identify early development.
- Mild to moderate HTN may not need to be treated
140-150/90-100 can be managed with observation
treatment will not prevent the development of PE. - Bp 170/110 is indicative of PE (in the absence of
other underlying cause), and must be treated as
an emergency, with admission and urgent blood
pressure lowering. - Even in this instance, treatment is aimed at
preventing the maternal complications of acute
hypertension, and will not prevent progression of
PE.
17Management
- HYPITAT trial
- IOL vs. expectant management for Gest HT or mild
PE after 37 weeks - Multicentre, open-label RCT
- 756 women
- 377 patients in IOL group and 379 in expectant
management - In IOL group 117(31) developed poor maternal
outcome compared with 166(44) allocated to
expectant management
18HYPITAT trial
IOL(n377) Expectant(n379) RR (95CI,pvalue)
SVD 273(72) 253(67) 1.09(0.99-1.19,0.091)
Instrumental delivery 50(13) 54(14) 0.93(0.65-1.33,0.64)
CS 54(14) 72(19) 0.75(0.55-1.04,0.085)
No cases of maternal or neonatal death or
eclampsia. No difference between the LSCS in the
groups. Most LSCS were done for FTP both 1st and
2nd stage and Fetal distress. More use of
antihypertensive drugs (oral or IV) in expectant
group. ICU care of 6(2) of IOL and 14(4) of
expectant group. Severe HT recorded more in
expectant group (Systolic 15 vs. 23) (Diastolic
16 vs. 27). HELLP syndrome recorded more in
expectant group(1 vs. 3)
19HYPITAT trial
- IOL is associated with improved maternal outcome
and should be advised.
20Essential Chronic HT
- HT confirmed before pregnancy or before 20
completed weeks gestation without a known cause.
21Chronic Hypertension
- Hypertension which is present either prior to
conception or 20/40. - HTN which persists 12/52 after delivery.
- May be primary or secondary if secondary, the
underlying disease process may have implications
for the pregnancy (esp renal disease). - High risk to fetus uteroplacental
insufficiency, IUGR (8-16) placental abruption
(0.7-1.5) and pre-term delivery (12-34). - 20 risk of developing superimposed PE.
22Chronic Hypertension
- Primary / essential / idiopathic HTN accounts for
the majority of chronic HTN in adults the causes
are unknown. - Secondary hypertension arises from an
identifiable cause, and may have a specific
treatment or even cure. Secondary HTN accounts
for less than 10 of HTN cases seen. - Abnormality in one or more of the systems that
regulate arterial pressure (vascular, renal,
hormonal and central and peripheral adrenergic
systems) underlies secondary (and presumably
primary) HTN.
23Secondary HT
- Important causes in pregnancy
- Chronic kidney disease e.g. reflux nephropathy,
adult polycystic kidney disease - Renal artery stenosis
- Systemic disease with renal involvement e.g. DM,
SLE - Endocrine disorders e.g. phaechromocytoma,
Cushings syndrome and primary hyperaldosteronism - Coarctation of the aorta.
24Causes of Secondary HTN
- Renal disease, both acute and chronic, carries
higher risk of complications to both mother and
fetus. - Drugs eg OCP, venlafaxine, NSAIDs,
corticosteroids, cyclosporin. - Primary hyperaldosteronism
- Renal artery stenosis both atherosclerotic and
due to fibromuscular dysplasia - Cushings syndrome
- Hypothyroidism
- Hyperthyroidism
- Hyperparathyroidism
- Phaeochromocytoma rare, but dangerous to both
if occurs. - Obstructive sleep apnoea
- Coarctation of the aorta
25Factors implicated in Primary HTN
- Genetics HTN about 50 more likely in people
with one or both parents hypertensive. Most
likely multiple genes involved, with variations
in sodium and chloride channels in renal tubules
or calcium channels in smooth muscles being
suggested. - Ethnic background Aboriginals, Torres St
Islanders, Pacific Islanders Maori more likely. - Sodium intake HTN seen mainly in societies where
Na intake gt 100meq/day (2.3g), seldom seen where
it is lt 50meq/day (1.2g). - Alcohol excess
- Caffeine excess - ? In women only.
- Obesity
- Metabolic syndrome (Syndrome X).
- Low birth weight - ? Problems with renal
development in utero and in early infancy.
26End-organ damage in HTN 1
- Acute rises in blood pressure can be associated
with end-organ damage - Malignant hypertension retinal changes
papilloedema, haemorrhages and exudates.
Malignant nephrosclerosis, resulting in acute
renal failure, haematuria and proteinuria. - Hypertensive encephalopathy cerebral oedema
(sudden hyperperfusion due to loss of
autoregulation). Presents as progressive
headache, NV, irritability, confusion, seizures
and coma. - Flash pulmonary oedema in patients with RAS.
- Intracranial haemorrhage either intracerebral
or subarachnoid. - Lacunar infarcts.
27End-organ damage in HTN 2
- Chronic HTN causes debilitating conditions the
risk is greater if other cardiovascular risk
factors are also present. - Cerebrovascular disease HTN is the main risk
factor, and treating blood pressure will
significantly reduce the risk of stroke (both
ischaemic and haemorrhagic). - Coronary artery disease heart attacks (MI),
angina etc. - Heart failure systolic and diastolic, with LVH,
which predisposes to arrhythmia. - Peripheral vascular disease limb ischaemia,
poor healing etc. - Retinal disease visual loss
- Renal disease small scarred kidneys due to
nephrosclerosis. HTN also accelerates damage due
to any other cause.
28Ix of Chronic HTN
- CBE, EUC, LFT, TFTs, Urate and BSL.
- 24hr urine collections for protein and
catecholamines. If unable, should have urinary
proteincreatinine. - Spun urine for casts and sediment.
- Fetal scans for growth including dopplers where
relevant. - Other tests frequently done in specialist HTN
clinics. - Monitoring bloods and urine for development of
PE at approximately 4/52 intervals more
frequently if indicated. - require regular growth scans.
- Low threshold for admission (or review in DAU) if
bp gt 160/100 or develops signs and symptoms of PE
(even with normal blood pressure readings).
29Management - Lifestyle
- Reduction in salt intake
- Reduction in alcohol intake
- Weight loss / maintenance within healthy range
- Regular physical activity (30mins at least 5x/wk)
- Smoking cessation
- Dietary modification
- Bed rest (while traditional) has not been shown
to be useful. Reduction in employment hours may
be.
30Treatment Gestational HT and Chr HTN
- Methyldopa is the drug of first choice in a
non-urgent situation starts at 250mg daily -gt
3g/day. - Major SEs drowsiness / fatigue, oedema,
depression / anxiety, headache, fever. Rarely
causes SLE-type syndrome, haemolytic anaemia,
jaundice and cytopaenias. Hypotension in the
neonate may occur. - Nifedipine, a calcium channel blocker has also
been used with good effect and good outcome.
Side effects include ankle swelling, facial
flushing and constipation. Starts at 30mg daily
(SR) -gt 120mg daily. - Labetalol, a non-selective beta blocker can also
be used. Starts at 100mg bd up to 2400mg daily.
There is a possibility that atenolol, a selective
beta blocker, contributes to low weight babies
placentas it is generally not used. - Methyldopa, labetalol and nifedipine are safe for
use if breast feeding. - Diuretics, ACE-Is, AIIRAs contraindicated in
pregnancy / lactation enalapril has been used
safely in lactating women.
31Treatment continued
- In mild hypertension (BP lt 150 / 100),
conservative management is recommended. - Meta-analysis has suggested that treating mild
HTN does reduce the risk of severe HTN in women
by 30 50, and may avoid the need for
additional antihypertensives. - It provides no benefit in terms of preventing PE,
pre-term delivery, SGA babies, abruption or
perinatal mortality. - There appears to be a link between treatment of
mild HTN and fetal growth restriction a 10mmHg
fall in MAP was associated with an average
reduction of 176g in birth weight.
32Pre-eclampsia / Eclampsia
- PE is sometimes still referred to as toxaemia a
term that covers HTN or proteinuria in pregnancy
from any cause. - The exact cause or causes are unknown PE is a
disease of the placenta (a viable fetus may not
be present), and appears to be based in
inadequate maternal or uteroplacental
circulation. - This leads to placental hypoxia, oxidative stress
and infarction, which in turn leads to damage of
the endothelium and release of multiple
inflammatory and pro-coagulant factors. - This endothelial dysfunction becomes widespread
within the maternal vasculature, and leads to the
varied presentation of PE.
33Complications of PE
- CNS eclamptic convulsions, cerebral
haemorrhage, cerebral oedema, cortical blindness,
retinal oedema, retinal detachment - Renal renal cortical necrosis, renal tubular
necrosis, nephrotic syndrome - Respiratory laryngeal oedema, pulmonary oedema
- Liver jaundice, hepatic infarction, hepatic
rupture, HELLP syndrome - Coagulation system DIC, microangiopathic
haemolysis, HELLP - Placenta infarction and bleeding, abruption
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35Increased risk of PE
- Primigravida, primipaternity, increasing maternal
age - Previous PE, family Hx of PE
- Obesity, Metabolic syndrome, PCOS
- Diabetes, HTN, chronic renal disease,
antiphospholipid syndrome and other
thrombophilias, migraine, asthma - Stressful job
- Advanced gestational age
- Multiple pregnancy, hydatidiform mole, Trisomies.
36Diagnosis of PE
- New-onset of proteinuria and HTN after 20/40.
- Proteinuria on dipstick has high false positive
rate need to confirm on 24hr collection or
urinary PCR. - Symptoms include headache, visual disturbances,
nausea and vomiting, upper abdominal pain,
excessive weight gain and generalised oedema
(gt0.5kg/wk), acute dyspnoea. There may be no
symptoms. - Signs include IUGR, reduced urine output,
pulmonary oedema, peripheral oedema, confusion,
hyperreflexia and clonus. - PE can be diagnosed in the absence of
hypertension or proteinuria.
37Investigations in PE
- CBE Thrombocytopaenia, microangiopathic
haemolysis, reduced plasma volume (high
haematocrit) - Urate, creatinine, urinary PCR renal impairment
- LDH, AST, ALT liver dysfunction (HELLP)
- US for fetal growth, doppler studies, amniotic
fluid index. CTG. - Ix to exclude other causes may be appropriate
38Treatment
- In preeclamptic women with a gestational age gt 30
weeks, significant organ dysfunction indicates
the need to deliver the baby - Before 30 week's gestation aim to prolong the
pregnancy - Steroids should be given once diagnosis of PE is
established if lt 34/40 - Progressive organ dysfunction (eg worsening LFTs
despite treatment) is an indication for delivery - Close monitoring for variables such as blood
pressure, urine output etc. - Invasive monitoring may be required eg arterial
lines, CVCs.
39Treatment
- Admission
- For severe HTN (gt170/110) acute blood pressure
lowering required. - Nifedipine tablets - 20 mg every 30 minutes - not
gt 80 mg in first 2 hours. Watch for hypotension.
- Intravenous labetalol 20mg increments up to
300mg or infusion at 1 -2 mg/min. Effective in 5
10 mins, lasts 3 6 hours. - Intravenous hydralazine bolus or infusion
- Reducing systolic BP initially by only 20-30 mm
Hg and diastolic by 10-15 mm Hg should protect
the mother from cerebral haemorrhage without
jeopardising the fetus - Oral nifedipine is frequently first choice, IV
treatment is generally reserved for true
hypertensive crisis
40Treatment continued
- Continuous electronic fetal monitoring during
acute treatment - The risk of sudden hypotension with vasodilators
such as nifedipine can be minimised by the use of
concomitant plasma expansion - Appropriate fluid replacement also required for
management of kidney and liver involvement - After initial stabilization, the following drugs
could be used for maintenance treatment - Nifedipine - maximum daily maintenance dose 160
mg - Labetalol - maximum daily maintenance dose 3,000
mg - Methyldopa - maximum daily maintenance dose 3,000
mg
41Treatment
- Neurological
- Terminate ongoing convulsions with intravenous
magnesium sulphate 4 - 6 g (MgSO4) Treat blood
pressure - Prophylaxis of further convulsions with magnesium
sulphate, initially intravenous 4 g loading dose
followed by 1-3 g / hr for 24 hrs after birth - The decision to start prophylactic treatment
should be based on a thorough assessment of the
individual's risk to develop eclamptic seizures.
All women with severe hypertension should receive
MgS04 during the initial stabilization
42Treatment
- If PE is non-threatening and stable, or lt 30/40
aim to prolong pregnancy. - PE bloods done at least 2x/wk, alternate daily or
daily. - Fetal monitoring
- Ultrasound and umbilical artery Doppler
velocimetry - Ultrasound estimation of fetal growth rate every
2 weeks - Doppler studies
- Estimation of amniotic fluid volume
- Cardiotocography (CTG)
- Daily CTG
- In the preterm fetus a non-reactive CTG tracing
indicates the need for more detailed biophysical
monitoring - In the mature fetus a non-reactive CTG tracing
may be an indication for delivery
43- In preeclampsia close to term, the fetus will
usually tolerate labour and vaginal birth - Intrapartum continuous electronic fetal
monitoring is recommended - When delivery is indicated pre-term because of
severe preeclampsia, particularly when the
indication for birth is fetal, delivery by
caesarean section will usually be in the best
interests of both baby and mother - Anaesthetic review before labour / birth
44Postpartum
- All of the features of preeclampsia will
eventually resolve - New maternal complications may occur up to a week
after birth - Women who require delivery for maternal
indications usually need monitoring in a high
dependency area and laboratory tests may need
repeating 4-6 hourly - Careful monitoring of fluid balance
- Oliguria should alert concern for developing post
partum renal failure - In the woman who is showing clinical improvement,
blood tests are not routinely indicated post
partum - Antihypertensive drugs are usually continued but
can be weaned as the blood pressure continues to
settle
45And finally..
- Recurrence is likely in up to half of women with
preeclampsia or gestational hypertension,
especially if this occurred early in pregnancy.
Recurrent gestational hypertension may herald
future essential hypertension - Investigations for an underlying thrombophilic
state, renal disease or auto-immune disease are
not routinely indicated but should be undertaken
in women with recurrent or early onset severe
preeclampsia or if there is evidence of
significant placental vasculopathy - Future pregnancies should be managed in
conjunction with a high risk pregnancy service. - Aspirin may be of benefit in preventing
recurrence.
46Case 1
- 28 yo, G2P1
- First pregnancy IOL at 38 weeks for gestational
HT. Forceps delivery of 2.9 kg baby girl. BP
settled quickly postpartum. No medication
required. - 1st visit at 10 weeks at the hospital and BP is
170/110.
47- Checked BP multiple times over the next few days.
- Started on Methyl-Dopa 250 mg TDS
- Bloods all normal. PCR normal.
48- 1st Trimester maternal serum screening low risk.
- Again seen at hospital at 15 weeks BP 140/80
- Morphology normal
- Seen at 21 weeks and BP 180/120
49- Admitted for 3 days.
- Methyldopa increased to 500 mg TDS
- BP settled to 140/80
- Bloods all normal. PCR normal
- BP in ANC at 23 weeks 170/110.
- Bloods again normal. PCR 15.
- Methyldopa increased to 500 mg QID
50- Review at 25 weeks.
- BP 220/120
- Mild headache. No other symptoms.
- Nifedipne 20 mg and repeated again. BP 150/100
- Bloods Plts 130, crea 80, urate 0.40, LFT
normal. PCR 2000!
51- Admitted to HDU
- Ultrasound EFW 530 gm ( lt5), AEDF, abnormal MCA
doppler and DV abnormal but not reversed. AFI 8
cm. - What to do now!
52Case 2
- 27 yo
- G3P0, x2 early m/c
- Type I DM diagnosed age 12. On Lantus and
Novorapid. - HbA1C 5.6 at booking
- Multiple Sclerosis diagnosed 18 months prior to
pregnancy - Has been on Interferon treatment for 14 months
53- Folate prepregnancy
- GP shared care ( country patient)
- Poorly controlled diabetes during pregnancy!
- Admitted at 326 days with headache, feeling
unwell and proteinuria. T/F to WCH. - BP 130-140/90-95
- Plts normal, Crea 76, Urate 0.42, LDH 340, PCR
98.
54- u/s fetal macrosomia EFW 1.95 Kg ( around 98),
Liquor 25 cm and dopplers normal. Breech. - BP settled. Stable.
- D/C. Stay in Adelaide
- PE monitoring as outpatient.
- PE remained stable.
- Diabetes poorly controlled. U/S at 354 weeks
baby 4 Kg! AFI 30 cm. Umbilical artery doppler
raised. - BSLs high
55- Decided for elective LSCS at 36 weeks.
- Baby 4260g
- Postop BP and bloods stable.
- Good recovery.