HYPERTENSIVE DISORDERS

IN PREGNANCY (HDP)
 SCOPE OF THE PROBLEM
Commonest medical problem encountered in
pregnancy, complicating 10-15% of all
pregnancies.
Includes all conditions of hypertension which
present in pregnancy
Leading cause of maternal mortality and
morbidity.
Antenatal care is largely geared towards the
detection of hypertension and pre-eclampsia.
NICE Guideline August 2010 (Reducing risk)

NHS Evidence update on HDP May 2012

 RISK FACTORS
General
- Age <20 years and >40 years
- Obesity BMI 35kg/m2

Genetic factors
- Mother had pre-eclampsia, 20-25% risk of developing pre-eclampsia
- Sister with a history of pre-eclampsia, risk can be as high as 35-40%

Obstetric factors
- Primiparity first time exposure to chorionic villi
- First pregnancy with a new partner
- Multiple pregnancy
- Previous pre-eclampsia
- Hydrops with large placenta
- Long birth interval ( >5 years)
- Hydatidiform mole

Medical factors
+ pre-existing vascular disease
- Pre-existing hypertension
- Renal diseases
- Diabetes
- Antiphospholipid antibodies
- Connective tissue disease
- Inherited thrombophilia
 RISK FACTORS (NICE)

High risk ( Aspirin 75/150mg from 12 weeks until

birth of child):

- Previous HDP
- Chronic kidney disease
- Autoimmune diseases
- Type I/II Diabetes Mellitus
- Chronic hypertension
 RISK FACTORS (NICE)

Moderate risk (more than 1 of the following)

- 1st pregnancy
- Age > 40
- Pregnancy interval of >10 years
- BMI of 35kg/m2 at 1st visit
- Family history of PE
- Multiple pregnancy
 PHYSIOLOGICAL CHANGES IN
BLOOD PRESSURE DURING
PREGNANCY

Systolicand diastolic blood pressure

decreases 10-15 mmHg during the first two
trimesters.
Increases 10 mmHg during the last
trimester
Returning to baseline towards term.

Chronic hypertension can therefore be

masked during the first half of a pregnancy.
THEORIES OF PATHOGENESIS
o Genetic predisposition (maternal, paternal,
thrombophilias)
o Abnormal placental implantation (defects in
trophoblasts and spiral arterioles)
Angiogenic factors (increased sFlt-1,
decreased placental growth factor levels)
Cardiovascular maladaptation and
vasoconstriction
Immunologic intolerance between
fetoplacental and maternal tissue
Platelet activation

Vascular endothelial damage or dysfunction

 PATHOGENESIS
Involves a genetic predisposition
Multiple system disorders originating in the
placenta.
Trophoblastic invasion is abnormal, placenta
doesnt undergo normal vascular remodeling
and causes uteroplacenta ischemia.
Results in endothelial cell activation that
leads to increased capillary permeability,
increased prothrombotic factors, platelet
thrombosis and increased vascular tone.
Also results in an increased in thromboxane
A2 synthesis that contributes to platelet
activation and vasoconstriction.
 HYPERTENSIVE DISORDER IN
PREGNANCY

Blood pressure of 140/90mmHg taken

after a period of rest on 2 occasions in a
previously normotensive woman.

or

Riseof systolic blood pressure of 30mmHg

and / or a rise in diastolic blood pressure of
15mmHg compared to pre-pregnancy
levels.
 HYPERTENSIVE DISORDER IN
PREGNANCY

HDP may be divided into

1. Chronic Hypertension /
Pre-existing hypertension.
2. Gestational Hypertension
3. Pre-eclampsia
4. Eclampsia
5. Chronic Hypertension with superimposed
Pre-Eclampsia
PRE-EXISTING HYPERTENSION

Essential or Primary Hypertension

- Idiopathic

Secondary Hypertension
- A definite cause of hypertension can be
identified.

- At increased risk of superimposed pre-

eclampsia, small for gestational age infants and
placenta abruption
 SECONDARY HYPERTENSION

Hypertension in any young person should

not be attributed to essential
hypertension before secondary causes
have been excluded.
 CAUSES OF SECONDARY
HYPERTENSION

Congenital / Hereditary
- Coarctation of aorta
- Congenital renal artery stenosis

Endocrine Disease
- Phaeochromocytoma
- Conns syndrome
- Cushings syndrome
CAUSES OF SECONDARY
HYPERTENSION
Renal Disease
-Chronic Glomerulonephritis
-Lupus Nephritis
-Adult polycystic kidney disease

Vasculitis
- Systemic lupus erythematosus
- Systemic sclerosis
 GESTATIONAL
HYPERTENSION
Hypertension after the 20th week of pregnancy
in a previously normotensive woman.

It may be associated with proteinuria.

Tends to recur in subsequent pregnancies.

Condition is expected to return to normal after

pueperium but some may remain hypertensive
after pueperium.
 PRE-ECLAMPSIA (PE)
Pregnancy specific
Multi-systems disorder

Manifestations can be unpredictable,

variable and widespread.
Classic signs: Hypertension, proteinuria
and edema.
BUT absent of classic signs doesnt
exclude the diagnosis.
 PRE-ECLAMPSIA (PE)
Common symptoms:
- headache
- epigastric / right upper quadrant
pain
- nausea / vomiting
- rapidly progressive edema
- visual disturbance
 PRE-ECLAMPSIA (PE)
Clinical examination
- vital signs, includes BP, PR, temperature
and SpO2
- urine dipstick, body weight
- non-dependant edema
- heart and lungs
- abdomen : uterus larger than date
tenderness
lie & presentation
fetal heart
- reflexes : hyper-reflexia
clonus
- eye : fundoscopy
 PRE-ECLAMPSIA (PE)
Investigations:
- Full blood count
(thrombocytopenia, increased hematocrit and
hemoglobin levels)
- Renal function test
(raised urea, creatinine and uric acid levels)
-Liver function test
(raised transaminases, LDH and bilirubin)
- Coagulation profile
(prolonged clotting time)
- 24 hour urinary protein excretion(>0.3g/24hrs) or
urine protein to creatinine ratio(30mg/mmol)
- Uterine artery Doppler
( bilateral notches and increased resistance index at 24
weeks predict PE)
 PRE-ECLAMPSIA (PE)

Fetalsurveillance
- Cardiotocography (CTG)
- Ultrasound and umbilical artery
doppler
- Corticosteroid for fetal lung maturity
 PRE-ECLAMPSIA (PE)
Admit patient to a high dependency area and
inform specialist or consultant to be involved in
patient care.
Monitor maternal BP, pulse rate and fetal heart
rate every 15 minutes until mother is stabilized.
Set up IV access and IV solution for resuscitative
therapy.
Close monitoring of fluid balance with urine output
( >30ml/hour).
If DBP is >110mmHg, start IV antihypertensive
(Hydralazine or Labetolol)
To start or continue with oral antihypertensive and
consider increasing the dosage.
Role of IV MgSO4
Dexamethasone or Betamethasone for preterm
fetus and timing of delivery
 PRE-ECLAMPSIA (PE)
Several possible crises may develop:

Eclampsia
HELLP syndrome
Pulmonary edema
Cerebral hemorrhage
Cortical blindness
Placenta abruption
Disseminated intravascular coagulation
Renal failure
Hepatic rupture
 ECLAMPSIA
A tonic clonic (grand-mal) convulsion occurring in
association with features of pre-eclampsia, occurs
in 1 in 2000 pregnancies.

More than 1/3 of women experience first

convulsion before development of hypertension
and proteinuria.

Convulsion may occur antepartum (38%),

intrapartum (18%) or postpartum (44%).
 ECLAMPSIA
Goals of treatment: Mothers always come
first!

1 To treat convulsion and prevent

recurrence.

2. To control the blood pressure.

3. To stabilize the mother.

4. To deliver the fetus

 ECLAMPSIA
Obstetric emergency
Red alert system should be initiated (introduced
by MOH in 1992)
- O&G specialist and registrar
- Anesthetics specialist and registrar
- Sister on call
- Blood bank technician
Lateral recovery position
Resuscitation ABC
IV MgSO4 loading dose of 4g over 10-15 minutes,
followed by a maintenance infusion of 1g/hour for
24 hours.
 DRUG THERAPY
Methyldopa:
- centrally acting antihypertensive, stimulate central
inhibitory-adrenergic receptors
- used for many years without serious adverse effects on
the fetus or children up to age of 7 years.
- sedation, postural hypotension, depression, hemolytic
anemia.

Calcium antagonist or - adrenergic blockers :

- facial flushing, headache and edema.

-Blockers
- fewer maternal side effects than methyldopa
- should not be given to women with history of asthma
- concern regarding fetal growth inhibition
- Labetolol, and -adrenergic blocker. 1st line.
 OTHER ANTI-
HYPERTENSIVE
Diuretics
- generally avoided as can cause further depletion of
intravascular volume.
- reserved for heart failure and pulmonary edema.
- unknown teratogenicity

Angiotensin-converting enzyme inhibitors (enalapril,

captopril)
- should not be used as they may cause
oligohydramnios, renal failure and hypotension in fetus
- safe in post-partum for women who breast feed

Angiotensin II receptor blockers (losartan)

- Lack data in pregnancy but similar to ACE inhibitor
therefore should be avoided.
 POSTPARTUM
MANAGEMENT
Although delivery is a cure for pre-eclampsia,
the manifestations may take weeks to resolve.

Intensive monitoring following delivery with

attention to BP control, fluid balance,
hematology and biochemistry.

Anti-hypertensive

Breast feeding

Contraception
RECURRENCE/PRE-PREGNANCY
COUNSELING
Women who have pre-eclampsia in their 1st
pregnancy have about 10% risk of developing
pre-eclampsia in their 2nd pregnancy

Risk
is increased if there is any underlying
medical risk factors.

Recurrence risk is also higher in women who

has early onset pre-eclampsia necessitating
delivery; before 28 weeks is associated with a
40% chance of recurrence.
 PROPHYLAXIS
Low dose Aspirin
- Inhibits platelet cyclo-oxygenase therefore thromboxane A2 synthesis
- Safe in pregnancy
- Large randomized trails suggesting that aspirin may be effective in reducing risk of
early onset pre-eclampsia
- Evidence shown that it reduces incidence of pre-eclampsia in women with acquired
thrombophilia.
- Should be started pre-conception or before 12 weeks gestation

Calcium
- Meta-analyses have supported a lower risk with calcium supplement of1.5g-2g per day,
largest trial to date found no beneficial effect.

Antioxidant
- Free radical scavengers
- Vitamin C 1g /day and vitamin E 400IU.day from 18-22 weeks gestation in high risk
group was associated with a 50% reduction in the incidence of pre-eclampsia.

Folic acid
- Hyperhomocysteinaemia has been associated with early onset pre-eclampsia
- Folate supplement reduces homocysteine level
- Not harmful in pregnancy
QUESTIONS ????