Hypertensive Disorders in Pregnancy

By
Francis Kamwendo
@
Nkhota-kota

Adapted from Obstetrics Simplified

by Diaa M. EI-Mowafi
 Classification

1. PRE-EXISTING (CHRONIC) HYPERTENSION

2. PRE-ECLAMPSIA
1. Differential Diagnosis
2. Complications
3. Treatment
4. ECLAMPSIA
Pre-existing (chronic) hypertension:
– Hypertension is present before pregnancy,
detected in early pregnancy (before 20 weeks in
absence of vesicular mole) and postpartum.
– Examples:
• essential hypertension,
• secondary to chronic renal disorders e.g. pyelonephritis
and renal artery stenosis,
• coarctation of the aorta, systemic lupus erythematosus
and pheochromocytoma.
 PRE-EXISTING (CHRONIC) HYPERTENSION

Causes
• Essential hypertension: of unknown aetiology.
• Secondary to chronic renal disorder: e.g.
– Glomerulonephritis.
– Hydronephrosis.
– Pyelonephritis.
– Renal artery stenosis.
• Secondary to cardiovascular disease: e.g.
– Coarctation of the aorta.
– Polyartheritis nodosa.
– Systemic lupus erythematosus.
PRE-EXISTING (CHRONIC) HYPERTENSION

• Causes
• Secondary to endocrine disorders: e.g.
– Primary aldosteronism.
– Phaeochromocytoma.
– Adrenocortical tumours.
– Diabetes mellitus.
Effect of Pregnancy on Chronic Hypertension

• Blood pressure falls by the second trimester in

most of cases, but rises during the third
trimester to a level some what above that in
early pregnancy.
• Deterioration of the underlying disease.
 Effect of Chronic Hypertension on Pregnancy

Maternal: Foetal:
• superimposed pre-
eclampsia/ eclampsia in 15- – Intrauterine growth
20% of cases retardation.
– Intrauterine foetal
death.
 Treatment

• General and medical treatment

• As pre-eclampsia regarding the following:
• Rest
• Antihypertensives
• Observation
Pregnancy-induced hypertension (PIH):
– Transient hypertension:
• Late onset hypertension, without proteinuria or
pathologic oedema
– Pre-eclampsia:
• Hypertension with proteinuria and / or oedema after
20 weeks of pregnancy, but may be earlier in vesicular
mole.
– Eclampsia:
• Pre-eclampsia + convulsions.
Superimposed pre-eclampsia or eclampsia:

– Development of pre-eclampsia or eclampsia in

pre-existing hypertension detected by a further
increase of 30 mmHg or more in systolic blood
pressure or 15 mmHg or more in diastolic blood
pressure.
 PRE-ECLAMPSIA
• Incidence: 5-10%.
• Aetiology:
Although eclampsia had been described
since 200 years, no definite aetiology is
found for PIH and it is still a disease of
theories.
 Predisposing factors
• Primigravidae more than multigravidae.
• Pre-existing hypertension.
• Previous pre-eclampsia.
• Family history of pre-eclampsia.
• Hyperplacentosis i.e. excessive chorionic tissue as in
hydatidiform mole, multiple pregnancy, uncontrolled
diabetes mellitus and foetal haemolytic diseases.
• Obesity.
•
 Theories
• The uteroplacental bed
• Immunological factor
• Genetic factor
• Renin- angiotensin system
• Atrial natriuretic peptide (ANP)
• Prostaglandins
• Neutrophils
 Pathological Changes
• Vasospasm
• Coagulation status
• Sodium and water retention
 Diagnosis

• Signs
• Symptoms
 Signs
• Hypertension:
• Proteinuria (albuminuria):
• Oedema:
 Hypertension

• Blood pressure of 140/90 mmHg or more or

an increase of 30 mmHg in systolic and/or 15
mmHg in diastolic blood pressure over the
pre- or early pregnancy level.
 How to measure the blood pressure in
pregnancy 1
• The patient should rest for at least 30 min. after arriving to
the clinic.
• Remove any tight clothing from the right arm.
• The patient lies comfortably on the left side that her back
makes an angle of about 30o with the bed. The right arm
is supported to be with the sphygmomanometer at the
same level with the patient’s sternum i.e. her heart. Each
cm above or below the level of the heart induces a
difference of 0.7mmHg in blood pressure reading. She
should lie undisturbed in this position for 2-3 min. before
blood pressure is measured.
 How to measure the blood pressure in
pregnancy 2
• The cuff should be applied to the right upper arm with
the connecting tubes pointing downwards, the centre
of the rubber bag in the cuff is directly over the
brachial artery leaving ante-cubital fossa free.
• Apply cuff firmly but not tightly around the arm.
• Feel the brachial artery and apply the stethoscope
directly over it without undue pressure.
• Pump up cuff rapidly to 20-30 mmHg above the point
at which the pulse sound disappears, and take blood
pressure reading without delay.
 How to measure the blood pressure in
pregnancy 3
• Let air out slowly so that mercury falls steadily by 2-3 mm/sec.
• Blood pressure measurement phases (Korotkoff):
– Korotkoff I¾ Appearance of the sound¾ systolic reading.
– Korotkoff II¾ Accentuation of the sound.
– Korotkoff III ¾ Sound becomes harsh.
– Korotkoff IV¾ Sound becomes muffled¾ diastolic reading.
– Korotkoff V¾ Disappearance of the sound.
• Korotkoff I and IV is the reading for systolic and diastolic blood
pressure respectively. If you wait the disappearance of the sound
to take the diastolic reading (as in non-pregnant state) you may
reach down to zero because of the hyperdynamic circulation
during pregnancy.
 How to measure the blood pressure in
pregnancy 4
• Use the right arm for measuring because it is
more convenient to the physician, but if the
reading is 10 mmHg or more higher in the left
arm use it in the future readings.
• The blood pressure should be measured in
two occasions at least 6 hours apart.
 Proteinuria (albuminuria)
• It is urinary protein greater than 0.3gm/L in 24
hours collection or greater than 1gm/L in two
random samples obtained at least 6 hours
apart.
• It indicates glomerular damage and almost
always occurs after hypertension.
• Proteinuria is usually in the range of 1-3 gm
daily, of which 50-60% is albumin but in severe
cases it may exceed 15gm.
 Oedema
• It is weight gain of more than 1 kg in any one
week or 2.25 kg in any one month.
• Clinical oedema is present in about two-thirds
of patients with PIH. However, two-thirds of
pregnant women with clinical oedema do not
develop hypertension.
 Symptoms
These are usually manifestations of severe pre-eclampsia.
• Headache: usually frontal but may be occipital. It is due
to cerebral oedema and hypertension.
• Visual disturbances: blurring of vision, flashes of light or
blindness.
• Epigastric or right upper quadrant pain: due to
enlargement and subcapsular hemorrhage of the liver.
• Nausea and vomiting: due to congestion of gastric
mucosa and/ or cerebral oedema.
• Oliguria or anuria: due to kidney pathology.
 Investigations
• Complete urine examination: for proteinuria, pus cells, RBCs, casts,
specific gravity, culture and sensitivity.
• Kidney function tests: serum uric acid > 6 mg % is abnormal during
pregnancy. It is more specific for pre-eclampsia than creatinine.
• Coagulation status: Platelet count, fibrinogen and FDP as DIC may
develop.
• Eye fundus examination.
• Tests for foetal well being: as
– ultrasound,
– daily foetal movement count,
– non-stress test,
– oxytocin challenge test (if needed).
 N.B.
• Imminent eclampsia: It is a state in which the patient
is about to develop eclampsia. Usually there are:
– blood pressure much higher than 160 /110 mmHg,
– heavy proteinuria (+++or ++++),
– hyperreflexia,
– severe continuous headache,
– blurring of vision,
– epigastric pain.
• Fulminating pre-eclampsia: a rapidly deteriorating
pre-eclampsia to be imminent eclampsia
 Pre-eclampsia Pre-existing
(chronic)
Hypertension
Parity usually usually
primigravida multigravida.
Past History of pre-eclampsia of hypertension in
may be present between
pregnancies.
Hypertension after the 20th week before pregnancy,
of pregnancy during the first 20
(except in vesicular weeks and persists
mole) and after 6 weeks
disappears within 6 postpartum.
weeks postpartum
Proteinuria If present, it If present, it
develops after develops before
hypertension hypertension due
to underlying renal
disease.
 Pre-eclampsia Pre-existing (chronic)
Hypertension
Hyperreflexia may be present. absent.

Fundus Examination Normal or retinal vessels Sclerotic changes.

spasm, oedema, exudate
and papilloedema (oedema
of the optic disc).
Serum Uric Acid Its increase is not Its increase is propotionate
proportionate to serum to serum creatinine
creatinine
 Differential Diagnosis
• Other causes of hypertension
• Other Causes of proteinuria
• Other causes of oedema
 Other Causes of proteinuria

• Contamination of urine by vaginal discharge this is excluded

by examination of a midstream sample after cleansing the
introitus with sterile water or saline or by using a catheter.
• Urinary infection: excluded by microscopic examination and
culture of urine.
• Congestive heart failure and severe anaemia due to hypoxia
of the kidney.
• Orthostatic proteinuria: Proteinuria is detected at the end of
the day while it is absent in the morning. This is due to
pressure of the lumbar spines on the left renal vein during
standing
 Other causes of oedema
• General causes: cardiac, hepatic, renal or
nutritional oedema.
• Local causes: as inflammatory or deep vein
thrombosis (usually unilateral).
• Pressure of the gravid uterus on the pelvic
veins may produce ankle oedema.
 Complications

Maternal: Foetal:

– Convulsions and coma (eclampsia). – Intrauterine growth

– Cerebral haemorrhage. retardation (IUGR).
– Renal failure.
– Intrauterine foetal death.
– Heart failure.
– Liver failure. – Prematurity and its
– Disseminated intravascular complications.
coagulation.
– Abruptio placentae.
– Residual chronic hypertension in
about 1/3 of cases.
– Recurrent pre-eclampsia in next
pregnancies.
 Treatment
• Prophylactic
• Curative
 Prophylactic
• Proper antenatal care:
– To detect the high risk patients who may develop PIH through the
screening tests.
– Early detection of cases who have already developed PIH and examine
them more frequently.
• Low dose aspirin:
– It inhibits thromboxane production from the platelets and the AII
binding sites on platelets.
– A low dose (60 mg daily) selectively inhibits thromboxane due to higher
concentration of such a low dose in the portal circulation than systemic
affecting the platelets when they pass through the portal circulation.
The Prostacyclin production from the systemic vessels will not be
affected.
 Curative
• Delivery of the foetus and placenta is the only
real treatment of pre-eclampsia. As the
conditions are not always suitable for this, the
treatment aims to prevent or minimize the
maternal and foetal complications (see before)
till reasonable maturation of the foetus.
 General measures:
Observation:

Maternal: Foetal:

• blood pressure twice daily. • daily foetal movement

• urine volume and count,
proteinuria daily, • serial sonography,
• oedema daily, • non-stress and stress test if
• body weight twice weekly, needed.
• fundus oculi once weekly,
• blood picture including
platelet count, liver and
renal functions particularly
serum uric acid on
admission.
 Medical treatment
• Antihypertensives:
– decrease the maternal cerebral and cardiovascular complications but do not affect the foetal outcome.
– Alpha-methyl-dopa (Aldomet):
• It reduces the central sympathetic drive.
• Dose: 250-500 mg every 6-8 hours up to a maximum dose of 4 gm/day. Its effect appears after 48 hours.
• A loading single dose of 2 gm may act within 1-2 hours.
• Side effects: headache, athenia and nightmares.
– Hydralazine (Apresoline):
• It is a vasodilator, increases renal and uteroplacental blood flow.
• Dose: 20 mg slowly IV initially followed by 5mg every 20 min. until diastolic blood pressure is 100-110 mmHg. This
regimen is used for severe and acute hypertension. Oral hydralazine can be used in the chronic situation as a second
line treatment in a dose of 25-75 mg/ 6 hours.
• Side effects: tachycardia, headache, flushing, nausea and vomiting.
– Calcium channel blockers (Nifedipine):
• It is a vasodilator acting by blocking the Ca influx into smooth muscle cells.
• It can be given sublingually (acts within 10 minutes) or orally (acts within 30 minutes) in a dose of 10-20 mg 2-3 times
daily.
• The higher the starting blood pressure the greater is the hypotensive effect.
• Side effects: headache and flushing.
 Obstetric measures
• Timing of delivery
• Method of delivery
• Intrapartum care
• Postpartum care
 Timing of delivery: Severe pre-eclampsia is usually treated conservatively till the end of the 36th week to ensure reasonable
maturation of the foetus. Indications of termination before 36th week include:

Foetal: deteriorating placental function as Maternal: deteriorating maternal

judged by: condition as judged by:

– intrauterine growth – blood pressure is sustained

retardation, or exceeds 180/110 mmHg,
– oligohydramnios, – urine proteinuria > 5
– reduced foetal gm/24 hours,
movements, – oliguria,
– abnormal foetal heart – evidence of DIC, or
patterns, or – imminent or already
– failing biochemical results. developed eclampsia.
 Method of delivery:

– Vaginal delivery may be commenced in vertex

presentation by:
• amniotomy + oxytocin if the cervix is favourable.
• prostaglandin vaginal tablet (PGE2) if the cervix is not
favourable.
– Caesarean section is indicated in:
• Foetal distress.
• Late deceleration occurs with oxytocin challenge test.
• Failure of induction of labour.
• Other indications as contracted pelvis, and malpresentations.
 Intrapartum care:

– Close monitoring of the foetus is indicated.

– Proper analgesia to the mother.
– Anti-Hypertensives may be given if needed.
– 2nd stage of labour may be shortened by forceps.
 Postpartum care:

– Methergin (Ergometrine) is better avoided as it

may increase the blood pressure.
– Continue observation of the mother for 48 hours.
– Anti- hypertensive drugs are continued in a
decreasing dose for 48 hours.
Thank you