Hypertension in Pregnancy

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Hypertension in Pregnancy

• Mojgan Vatani
• Staff Specialist, WCH

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• Definition
• Classification
• Investigation
• Management/Treatment

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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.

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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.

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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

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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.

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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.

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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.

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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.

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Classification of hypertensive disorders in
pregnancy

• Gestational hypertension
• Chronic hypertension
• Essential
• Secondary
• White coat
• Preeclampsia superimposed on chronic hypertension
• Preeclampsia- eclampsia

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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.

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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.

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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.

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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.

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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.

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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

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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)
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HYPITAT trial

• IOL is associated with improved maternal outcome
  and should be advised.

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Essential Chronic HT

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

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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.

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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.

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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.

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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

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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.

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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.

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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.

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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).

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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.

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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.

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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.

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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.

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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

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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.

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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.

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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

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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.

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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

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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

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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

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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

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• 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

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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

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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.

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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.

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• Checked BP multiple times over the next few days.
• Started on Methyl-Dopa 250 mg TDS
• Bloods all normal. PCR normal.

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• 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

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• 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

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• 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!

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• 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!

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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

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• 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.

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• 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

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• Decided for elective LSCS at 36 weeks.
• Baby 4260g
• Postop BP and bloods stable.
• Good recovery.