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Hypertension in Pregnancy

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Title: Hypertension in Pregnancy


1
Hypertension in Pregnancy
  • Mojgan Vatani
  • Staff Specialist, WCH

2
  • Definition
  • Classification
  • Investigation
  • Management/Treatment

3
Definition
  • 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.

4
Hypertension 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.

5
Recording 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

6
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7
Cuff 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.

8
Cuff 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.

9
BP 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.

10
BP 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.

11
Classification of hypertensive disorders in
pregnancy
  • Gestational hypertension
  • Chronic hypertension
  • Essential
  • Secondary
  • White coat
  • Preeclampsia superimposed on chronic hypertension
  • Preeclampsia- eclampsia

12
Gestational 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.

13
Gestational 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.

14
Gestational 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.

15
Why 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.

16
Gestational 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.

17
Management
  • 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

18
HYPITAT 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)
19
HYPITAT trial
  • IOL is associated with improved maternal outcome
    and should be advised.

20
Essential Chronic HT
  • HT confirmed before pregnancy or before 20
    completed weeks gestation without a known cause.

21
Chronic 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.

22
Chronic 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.

23
Secondary 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.

24
Causes 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

25
Factors 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.

26
End-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.

27
End-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.

28
Ix 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).

29
Management - 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.

30
Treatment 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.

31
Treatment 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.

32
Pre-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.

33
Complications 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

34
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35
Increased 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.

36
Diagnosis 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.

37
Investigations 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

38
Treatment
  • 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.

39
Treatment
  • 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

40
Treatment 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

41
Treatment
  • 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

42
Treatment
  • 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

44
Postpartum
  • 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

45
And 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.

46
Case 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!

52
Case 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.
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