Hypertension in pregnancy

1. Hypertensive disorders in
pregnancy

2. Classified into 5categories:
• Hypertension encountered before 20 weeks
of gestation or persists after 6 weeks
postpartum. It can be primary or secondary
in aetiology.
Chronic
hypertension
• Hypertensive condition in which systolic
BP ≥ 140mmHgand / or adiastolic BP ≥
90mmHgin at least 2 occasions, 4 hours
apart, arising de novo after 20 weeks and
resolved within 6 weeks postpartum in a
previously normotensive woman
Pregnancy induced
hypertension
(gestational
hypertension)

3. 3
• New hypertension diagnosed after
20 weeks with significant
proteinuria.
• *Significant proteinuria =24-hour
urine protein of >300mg/day
(0.3g/day)
Pre-eclampsia
• Pre-eclampsia with severe
hypertension and / or with symptoms,
and / or biochemical and / or
haematological derangement.
Severe pre-eclampsia
Eclampsia Pre-eclampsia with convulsion

4. 4
•Degree of hypertension:
– Mild: SBP:140-149 / DBP:90-99
– Moderate: SBP:150-159 / DBP100-109
– Severe: SBP:≥ 160 / ≥110
Etiology
 Indefinite etiology, remainunknown
 Proposed theory:
• Placental origin
• Immunological origin
• Biochemical origin
• Genetics
• Oxidative stress

5. Placental Origin
Normal Placental development :
Thisis why the maternal blood flow to the placenta canbe increases
throughout pregnancy from 50 ml/min in first trimester to 500-750 ml/min at
terms.

6. Abnormal Placental development:
Trophoblast cell
fail to invade
maternal arteries
Spiral arteries
retain their pre-
pregnancy state
Impair perfusion of
fetoplacental unit
Ischaemic necrosis
of acotyledon of
placenta
Placenta release
inflammatory
cytokines like
TNF-α and IL-6.
Dysfunction of
vascular
endothelial cells
Decrease release
of nitric oxide &
other vasodilator
substances
Vasoconstricton
HPT

7. Immunological Origin
• Results from some type of immunereactivity
in the mother caused by the fetus, which
contain the paternalgene.
• This theory is supported by the fact that:
– Thesymptoms of preeclampsia disappears
within a few days after birth of the fetus and its
products.
– Thickening of the kidney glomerularmembranes
(seen in PE,undeterminedcauses)

8. Proposed mechanism
Maternal immune
reaction toward
paternal gene in
fetus.
Deposit &cause
thickening of the
kidney glomerular
membranes
Reduces rate of
glomerular fluid
filtration
Thus, to maintain
normal formation
of urine, arterial
pressure elevated
HPT

9. Biochemical origin
•Imbalance of vasodilators (eg:prostaglandin) andvasoconstrictors
(eg:thromboxane A2)
Genetics
•Genetic factors are thought to play a role in disease susceptibility
•Primigravida women with family history of pre-eclampsia have 2
to 5 folds increased risk of developing the disease compared with
primigravida women with no history of pre-eclampsia
Oxidative stress
•Increase in the levels of placental oxidative stressmay mediate
endothelial cell dysfunction and contribute to the pathophysiology
of pre-eclampsia

10. Biochemical Origin
•Imbalance of vasodilators (prostaglandin) and vasoconstrictors (thromboxaneA2)
Risk factors
Moderate risks
• First pregnancy
• Age40 years or older
• Pregnancyinterval of more than 10years
• BMI of ≥ 35kg/m2 at firstvisit
• Family hx of pre-eclampsia
• Multiple pregnancy
Efficacyof aspirin:
-17%reduction in risk of pre-eclampsia
-8%reduction in relative risk of preterm birth
-14%reduction in fetal/neonataldeath
-10%reduction in SGAbabies
 Advice women with >1 moderate risk factor for pre-eclampsia to take75mg
of aspirin daily from 12 weeks until the birth of the baby (practice: 36 weeks)
• +calcium carbonate 1gBD(promote fetal bone mineralisation & prevention ofgrowth
restriction)
 Aspirin inhibit enzyme cyclo-oxygenase in the platelet and prevent release of thromboxane
A2(vasoconstrictor)

11. 11
 High risks
• Hypertensive disease during previous pregnancy
• Chronic kidney disease
• Autoimmune disease such asSLEor APS
• Type 1 or Type 2DM
• Chronic hypertension
Advice women at high risk of pre-eclampsia to take
75mg of aspirin daily from 12 weeks until 36 weeks of
pregnancy
• +calcium carbonate 1gBD

12. 12
Signs & symptoms ofpre-eclampsia
• Severe headache
• Problems with vision,such
asblurring or flashing
before the eyes
• Epigastric pain
• Vomiting
• Sudden swelling of theface,
hands or feet (oedema)
• Hyperreflexia
• Papilloedema
• clonus

13. Multi-systemic effect of pre-eclampsia
Maternal complications
• CVA
• Eclampsia
• Thrombosis
• Pulmonary oedema
• Pulmonary embolism
• PPH
• Heart failure
• Liver failure
• Renal failure
• DIVC
• HELLPsyndrome
• Retinal damage
• Maternal death
• Increased risk of LSCS
Fetal complications
• SGA/IUGR
• Preterm labour
• Placenta abruptio
• Oligohydramnios
• IUD
• Respiratory distress
syndrome
• Intraventricular
haemorrhage

14. Cardiovascular system
Normal pregnancy:
• Marked peripheral vasodilatation →fall in total
peripheral resistance despite increase plasma volume&
cardiac rate.
Pre-eclampsia :
• Marked peripheral vasoconstriction due to imbalanceof
vasoactive substances →HPT
• HPT+loss of endothelial cell integrity due to local
disturbances in control of vessel toneproduced by
endothelium of vessel wall→ greater vascular
permeability & generalizedoedema.

15. Renalsystem
• Thickened glomerular tufts that containprotein
deposit in the basement membrane →
Glomeruloendotheliosis
• Associated with impaired glomerular filtration &
selective loss of intermediate weight proteins(eg :
albumin & transferrin)
Proteinuria: >300mg per volume in 24 hourcollection
Raisedplasma urate levels: >0.35mmol/litres
Reduction in plasma oncotic pressure
Exacerbate development of oedema

16. Haematological system
Damageof
endothelium
Adherence of
platelet to
damaged area
Reduce
platelet
count-risk of
bleeding
Increase fibrin
deposition-risk
of thrombosis
Increase
production of
fibrin
Afalling platelet count and changesin clotting factors may proceed to disseminate
intravascular coagulation with micro-angiopathic hemolysis secondary to small vessel
blockage, revealed by anaemia and the presence of fragmented red cells in peripheral
blood.

17. Hepatic System
• Vasoconstriction in the hepatic bed leads to
periportal fibrin deposition, haemorrhageand
hepatocellular necrosis.
o Leadsto elevated liver enzymes may occur as
part of the HELLPsyndrome (haemolyticanaemia,
elevated liver enzymes, and low plateletcount

18. Neurological system
• In Pre-eclampsia:
– Cerebral oedema & haemorrhagic lesions especiallyin
posterior hemisphere
– Thus, headache & visual disturbances occurs (eg:
scotomata, blurred vision.
• In Eclampsia:
– 1 or more convulsions, not contributable to other cerebral
conditions in apatient withpre-eclampsia
– Cerebral vasoconstriction leads to focal ischemia&
abnormal electrical activity, thus, triggersseizures.
• 38%occur antenatally
• 18%occur intrapartum
• 44%post partum (esp 1st 24-48H)

19. Fetal & Placenta
• Poor perfusionplacental insufficiency,thus
resulting in :
– Oligohydramnios
– IUGR
– PlacentaAbruptio
– IUD
– Preterm labour

20. Investigations
• Todetect any evidence of PE,complications of PE&
obtain baseline results for future comparison
(monitoring)
• FBC
• Coagulation profile
• LFT
• RP
• UFEME/24H urine protein
• PBF
• GSH/GXM
• Uric acid
• Ultrasound assessmentfor fetal growth, AFI,umbilicalartery
doppler

21. 21
Management
• Assessmentand evaluation of patient
• Control of blood pressure (aimBP<150/100)
• Fetal assessment
• Prevention of eclampsia - useof MgSO4
• Plan for delivery – timing andmode
• Useof IM dexamethasone (24-34 weeks) –for
lung maturity

22. 22
Pre-pregnancy care
• Women considered tobe at high risk of pre-
eclampsia should be referred for pre-
pregnancy counselling (to be seenat PPC)to
identify modifiable riskfactors.
– Lifestyle modification (eg: cessation of smoking
and diet adjustment)
– Revisemedications to optimize medical conditions
and cessation of potentially teratogenic agents(eg:
warfarin-> warfarin embryopathy & ACE-I->renal
dysgenesis, lung hypoplasia)
– Drugs of choice: methyldopa, labetalol,nifedipine

23. 23
Antihypertensive drugs
• Methyldopa (oral)
– MOA:
- altered to α-methylnorepinephrine, stimulates
inhibitory α-2 adrenergic receptors inhypothalamus
- Reducessympathetic tone, total peripheralresistance
& bloodpressure.
- No direct effect on cardiacfunction.
– SE: depression, drowsiness, headache, liver
disorder, postural hypotension
– CI: acute hepatic disease,history ofdepression
– Starting dose: 250mgTDS
– Maximum dose: 1gTDS

24. 24
Antihypertensive drugs
• Nifedipine (oral)
– MOA:
- Calcium channel blocker.
- Inhibits the passageof calcium through the gated channels of
smooth and cardiac muscle (vasodilation and musclerelaxation)
- Causesdilation of coronary & systemic arteries,decrease
peripheral resistance, systemic BP&afterload.
– SE: severe headache (mimic worsening disease), flushing,
dizziness, palpitations, ankle oedema
– CI: Acute MI
– Starting dose: 10mgTDS
– Maximum dose: 20mgTDS

25. 25
Antihypertensive drugs
• Labetalol (oral orIV)
– MOA:
- Exhibits selective α-1 antagonist and nonselectiveβ-2
antagonist effects.
- Causesadecrease in systemic arterial blood pressure&
systemic vascular resistance without asubstantial
reduction in resting heart rate, cardiac output, or
stroke volume
– SE: tremor, headache, scalptingling
– CI: AVheart block, heart failure, bronchialasthma
– Starting dose: 100mgTDS
– Maximum dose: 400mgTDS

26. 26
Antihypertensive drugs
• Hydralazine (IV)
– MOA:
- decreases BPby exerting direct relaxant effect on
vascular smooth muscle
– SE: reflex tachycardia, Naand H2Oretention,
vertigo, myocardial stimulation, SLElikesyndrome
– CI: tachycardia

27. 27
Monitoring of mother andfoetus
Maternal monitoring Fetal monitoring
•Vital signs
•Full blood count
•Serumrenal profile
•Serumliver profile
•Urinalysis
•Sign and symptom of worsening disease
process – nausea and vomiting, persistent
severe headache, blurred vision
•Fundal height
•Fetal kick chart
•Fetal heart (cardiotocography)
•Doppler of umbilical artery
•Ultrasound (fetal size,amniotic fluid)-4
weekly or more frequent asindicated

28. Timing of delivery
• PIHnot on treatment – 40weeks
• PIHon treatment – 38 weeks
• SeverePIH– 37 weeks
• Pre-eclampsia – 34-37 weeks
• Eclampsia – immediate delivery oncestable

29. 29
Indications for MgSO4 asprophylaxis
Severe pre-eclampsia
Severe PIH(SBP>160mmHg, DBP>110mmHg)
Hypertensive crisis
Imminent premature delivery (<32 weeks) forfetal
neuroprotection
Indications for MgSO4 astreatment
Eclampsia
If the patient is symptomatic of impending eclampsia
• 58%reduced risk of eclampsia
• Maternal mortality lower among women allocated with MgSO4
*MOA remains unclear. Possiblemechanisms:
-acts asvasodilator, protecting blood brain barrier to decrease
cerebral oedema and relieve vasoconstriction.

30. Management of Pre-Eclampsia
– Anti-hypertensive medication:
• Aim BP<150/100
• 1st line: labetalol(oral/IV)
• 2nd line: nifedipine,methyldopa
– PEprofiles: FBC,RP
,LFT
,Coagulation profiles, uric acid
– Fetal monitoring: Growth scan,AFI,umbilicalartery
doppler
– CTG
– IM dexamethasone ifconsidering delivery (24-34 weeks)
– For IV MgSO4asprophylaxis or symptomatic of impending
eclampsia

31. Indication for EarlyDelivery
- Timing of delivery:
• Determine by severalfactors:
Severe refractory hypertension= BPremains
uncontrolled despite maximal medicaltherapy
Deteriorating maternal or fetalconditions
Availability of neonatalcare
Completion of corticosteroid
• After 37weeks: recommend delivery within24-
48hours

32. 32
Management of Eclampsia
• Anti-convulsant – MgSO4
– Loading dose:
• IV =4g(8mls) +12mls NSgiven over 15minutes
• Recurrent convulsion =further dose 2g(4mls) +8mls NS
given over 15minutes
• IM =10g with 5g(10mls) given ateach buttock
– Maintenance dose:
• 24.7g +500mls NSto run at 21mls/hour =1g/hour
• Maintenance dose to continue up till 24hours post-
delivery or 24 hours from the last convulsion
(whichever occurslater)

33. 33
Management of Eclampsia
o Sideeffects of MgSO4:neuromuscular blockade,
loss of tendon reflex, respiratory & cardiac
depression
• Sign of toxicity : respiratory rate depression, prolong QRS
complex, cardiac arrest
• Aim urine output at least (30mls/hour) – to prevent
retention of magnesium in thecirculation
* Urine output is not a sign of toxicity
• Antihypertensive drugs: hydralazine,labetalol
• Plan for delivery once patientstable

34. 34
MgSO4 level(mmol/L) Effects
0.8 to 1.0 Normal plasma level
1.7 to 3.5 Therapeutic range
2.5 to 5.0 ECGchanges (P-Qinterval prolonged,
widen QRScomplex)
4.0 to 5.0 Reduction in deep tendon reflex
>5.0 Lossof deep tendon reflexes
>7.5 Sino-atrial and atrioventricular blockade,
respiratory paralysis and CNSdepression
>12 Cardiac arrest
Antidote for MgSO4 toxicity:
- 1gm Calcium gluconate (10ml of 10% solution) given IV slow bolus over 3minutes

35. HELLPSyndrome
•Variant of severe pre-eclampsia/eclampsiawith
biochemical evidenceof
– Haemolysis (H)
– Elevated Liver enzymes (EL)
– Low platelets (LP)
•Occursat various gestational ages-ranging from mid-
2nd trimester of pregnancy until several days
postpartum(20%)
• A/w increase maternal and perinatalcomplication
- Mortality rate: maternal-24%, perinatal-30-40%

36. 36
Management of HELLPsyndrome
• Early recognition- investigations and evaluation of
patient
• Control HPT
• Assessfetal condition
• Plan for delivery – timing andmode
• Platelet transfusion if <50,000/uL orsymptomatic
• Prevention of seizure- use of MgSO4

37. 37
Post-partum care
• All patients should have their their blood
pressure monitored during home visits orin
primary health carecentres.
• Ensurecompliance if patient isdischarged
with medication.
• Patients should be counselled about
contraception, spacing and risk of developing
similar problems in subsequentpregnancies
• Longterm follow-up is advised for
development of chronichypertension

38. References
• NICEclinical guideline107
• Labour ward manual SGH
• Clinical Protocols in O&Gfor Malaysians
Hospitals
• Obstetrics by Tenteachers
• Journal of cerebral circulation:Magnesium
sulphate treatment for the prevention of
elampsia
• European journal of obstetric &gynaecology
and reproductive biology

39. THANKYOUFORYOURATTENTION
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