By Dr Shanza aurooj
Post Graduate Trainee
Gynea unit III
SPH Quetta
 Gestational Hypertension
 Pre-eclampsia
 Chronic hypertesion
essential
secondary
 Pre-eclampsia superimposed on chronic
hypertension
 Eclampsia
 Gestational hypertension
new hypertension presenting after 20 weeks without
significant proteinuria and features of
preeclampsia,BP levels return to normal within 3
months postpartum
 Pre-eclampsia
is new hypertension presenting after 20 weeks with
significant proteinuria.
 Severe pre-eclampsia
is pre-eclampsia with severe hypertension and/or
with symptoms,and/or biochemical and/or
haematological impairment. after 20 weeks
 Eclampsia is a convulsive condition associated
with pre-eclampsia
 Chronic hypertension is hypertension that is
present before 20 weeks characterized by a BP
of 140/90 mmHg or greater . It can be primary
or secondary in aetiology
 Pre-eclampsia superimposed on chronic
hypertension is hypertension present before 20
weeks with development of symptoms of pre-
eclampsia after 20 weeks
 Significat proteinuria excretion of 300mg/24hr of
urinary proteins in 24hr urine collection or a
concentration of 30mg/dl >1+ on dipstick in atleast
two random urine samples collected 4 to 6 hrs apart
 Grades of hypertension
Mild hypertension
diastolic blood pressure 90–99 mmHg, systolic blood
pressure140–149 mmHg.
Moderate hypertension
diastolic blood pressure 100–109 mmHg, systolic blood
pressure 150–159 mmHg.
Severe hypertension
diastolic blood pressure 110 mmHg or greater, systolic
bloodpressure 160 mmHg or greater
A pregnancy specific syndrome characterized by
variable degrees of placental dysfunction and a
maternal response featuring systemic infammation
 The etiology of preeclampsia is unknown. However,
placental delivery reverses the symptoms of
preeclampsia, suggesting that the placenta has a
controlling role in the condition. Additionally, women
with increased placental tissue for gestational age, such
as hydatiform moles and twin pregnancies, have an
increased incidence of preeclampsia.
 Several theories attempt to explain the
pathophysiology of preeclampsia
 Most popular theory holds that improper placental
development results in placental vascular endothelial
dysfunction and a relative uteroplacental insufficiency.
The vascular endothelial dysfunction results in
increased permeability, hypercoagulability, and diffuse
vasospasm
Changes in normal pregnancy
 In normal pregnancy spiral arteries of the placental bed undergoes
a series of physiological changes
 cytotrophoblasts replace the endothelial cells in the spiarl arteries
resulting in destruction of medial elastic and muscular tissue,these
physiological changes reach the inner third of myometrium and
create a low vascular arterioler system that allows a dramatic
increase in blood supply necessary to serve the growing fetus.The
end result is that 100 to 120 spiral arteries are converted into dilated
inelastic tubes without maternal vasomotor control
Changes in preeclampsia
 In pre-eclampsia about half to 2/3rd of spiral arteries escape this
transformation ,in these arteries the myometrial segment remain
anatomically intact,do not dilate,many vessels are occluded by
fibrinoid material and exhibit adjacent foam cell invasion
(atherosis).Atherosis and thrombosis leads to microinfarcts in
placenta and are responsible for abruption due to decidual
necrosis,separation and hemmorhage.
Cardiovuscular system
Severe pre-eclampsia is characterized by vasoconstriction and a leaky
microcirculation,with extravasation of fluid in E.C.S and relative hypovolemia
leading to hemoconcentration,edema and swelling often facial particularly
peroorbital edema in contrast to physiological pedal edema
Renal system
Primary renal manifestation of endothelial cell activation is inflammatory
swelling of glomeruler endothelial capillaries causing an increase in the renal
vascular resistance with a decrease in the renal blood flow resulting in decreased
GFR and EFRP complicating to ANURIA or OLIGURIA leading to ARF.
The first change in the renal system involvement is tubular dysfunction resulting
in decreased uric acid clearance from the body and hyperuicemia,the next event is
proteinuria due to loss of negative charge from the GBM ,finally there is rise in
levels of urea and creatinine . Proteinuria further leads to hypoalbunemia with
extravasation of fluid in ECS resulting in genearilzed edema and,ascites,pleural
effusion,pulmonary,cerebral and laryngeal edema.
Abnormal hemostasis
Platelet activation a feature of normal pregnancy is exaggerated in
pre-eclampsia as sysytemic endothelial cell activation cause platelet
adherence to site of endothelial damage.Platelets consumption
result in thrombocytopenia while platelet adherence leads to
formation of microthrombi effecting microcirculation leading to
increased intravuscuar coagulation with a rise in fibrin
degradation products and hemolysis of RBC’s in microvessels
leading to HELLP syndrome.
HELLP syndrome
It is Hemolysis,elevated liver enzymes and low platelets caused
by abnormal hemostasis and liver involvement due to excessive
fibrinogen deposition in hepatic sinusoids also obstructing blood
flow leading to hepatic capsular distension and epigastric
pain,nausea,vomiting. It may complicate to subcapsular
hematoma and liver rupture presenting with severe epigastric
pain,shoulder pain,shock, hemoperitoneum,respiratory difficulties
or pleural effusion.
 Nulliparity
 extremes of maternal age
 multifetal gestation
 pre-eclampsia in a previous pregnancy
 family history
 chronic hypertension or renal disease
 chronic infections
 maternal low birth weight
 obesity and insulin resistance
 Pre-gestational DM
 smoking
 maternal genes
 chronic inflammatory conditions like (SLE & RA)
 Anti-phospholipid antibody syndrome
 molar pregnancy
Symptoms of pre-eclampsia
 severe headache
 problems with vision, such as blurring or flashing before the eyes
 severe pain just below the ribs
 vomiting
 sudden swelling of the face, hands or feet.
 Seizures (eclampsia) grand mal in character with tonic clonic phases
Physical signs:
 Asymptomatic hypertension is discovered on routine prenatal
examination.
 Diffuse edema has a high specificity for preeclampsia.
 Neurologic findings such as papilledema and hyperreflexia must be
addressed quickly, as they can herald the onset of eclampsia.
 Petechiae and bruising could suggest coagulopathy.
 Right upper quadrant or mid epigastric tenderness develops as a
result of hepatocellular necrosis.
Complications
Maternal complications
 Abruption placenta
 DIC/HELLP syndrome
 Acute Renal Failure
 Eclampsia
 Liver failure & Hemmorhage
 Stroke
 Death
 Long term cardiovascular morbidity
Neonatal complications
 Preterm delivery
 IUGR
 Hypoxic neurological injury
 Perinatal death
 Low birth weight with long term morbidity
DIFFERENTIALS
 Disseminated Intravascular Coagulation
 Fatty Liver
 Cholecystitis
 Perforated peptic ulcer
 Systemic Lupus Erythematosus
 Thrombotic Thrombocytopenic Purpura
BASELINE
•CBC
•BLOOD GROUP
•HEPATITUS B & C
Urine analysis of a clean catch specimen
Proteinuria 2+ or higher is significant and warrants further
evaluation to rule out preeclampsia.
A 24-hour urine collection with more than 300 mg of protein
RFT’s
• UREA > 40 mmol/l or >11 mg/dl
• Creatinine>1 mg/dl
• Serum uric acid levels >6.3 mg/dl
LFT’s
• AST or ALT >50 IU/L
• Biluribin >25 IU/L
Clotting profile
• PT/APTT
• Fibrin degradation products
Ultrasound
 Confirmation of normal fetal development is important
and standard prenatal care in all pregnancies.Points to
study in US are
 Fetal biometry(AC,HC,BPD,FL)
 AOL & estimated fetal weight
 Placental localization
Doppler velocimetry
 Screening test in first trimester to detect changes in
spiral arteries and is considered abnormal if there is an
early diastolic notch or high RI
Management can be discussed under following headings
 Prevention
 Antihypertensive treatment
 Anticonvulsant treatment
 Steroids for lung maturation
 Fluid balance
 Mode and timing of birth
 Fetal monitoring in high risk patient
 Intrapartum care
 Postnatal monitoring,treatment and investigations
 Breast feeding
 Advice and follow up care
Primary prevention
 Pre pregnancy weight control in high risk patients
 Vitamin B and folate supplementations
 Cessation of smoking
 Control of Hypertension in women having chronic hypertension
 Control of sugar levels in women having Diabetes pre-pregnancy
Secondary prevention
 Calcium supplementations:it reduces parathyroid and renin release
thereby reducing intracellular calcium and smooth muscle
contractility,the ideal patient is the one who is obese with raised BP at
booking visit
 Antiplatelet agents:low dose aspirin is recommended in high risk
patients as it inhibits thromboaxane synthesis thus altering the balance in
favor of PGI usually before 23 weeks and therefore helps in proper
placentation in a dose of 75mg OD starting from 12 weeks until birth
 For other agents like Mg and Zinc supplements,fish oil,salt restriction,
antioxidants like vitamin C,E there is insufficient data to recommend
their use in primary prevention
Degree of
hypertension
Mild hypertension
(140/90 to 149/
99 mmHg)
Moderate hypertension
(150/100 to 159/
109 mmHg
Severe hypertension
(160/110 mmHg or
higher)
Admit to hospital NO YES YES
Treat NO With oral labetalol† as
first-line treatment to
keep:
diastolic blood
pressure between
80–100 mmHg
systolic blood
pressure less than
150 mmHg
With oral labetalol† as
first-line treatment to
keep:
diastolic blood
pressure between
80–100 mmHg
systolic blood
pressure less than
150 mmHg
Measure
blood
pressure
At least four times a
day
At least four times a day More than four times a
day, depending on
clinical circumstances
Test for
proteinuria
Do not repeat
quantification of
proteinuria
Do not repeat
quantification of
proteinuria
Do not repeat
quantification of
proteinuria
Blood tests Monitor using the
following tests twice a
week: kidney function,
electrolytes, full blood
count, transaminases,
bilirubin
Monitor using the
following tests three
times a week: kidney
function, electrolytes, full
blood count,
transaminases, bilirubin
Monitor using the
following tests three
times a week: kidney
function, electrolytes, full
blood count,
transaminases, bilirubin
 Only offer women with pre-eclampsia
antihypertensive treatment other than labetalol
after considering side-effect profiles for the
woman, fetus and newborn baby.
 Alternatives include methyldopa† and
nifedipine†
Adult Dose 5-10 mg IV;
repeat 20min to maximum of 60
mg
Contraindications
Documented
hypersensitivity, dissecting
aortic aneurysm, mitral valve
rheumatic heart disease
Interactions:MAO inhibitors
and beta-blockers may
increase hydralazine toxicity;
pharmacological effects of
hydralazine may be
decreased by indomethacin
Adverse effects headache,
flushing, overshoot
hypotension, peripheral
edema, implicated in
myocardial infarction;
Pregnancy C (safety not
established)
Hydralazine (Apresoline) -- First-line therapy against preeclamptic
hypertension in past decades. Decreases systemic resistance through direct
vasodilation of arterioles resulting in reflex tachycardia..
Labetalol (Normodyne) -- Second-line therapy
that produces vasodilatation and decrease in systemic
vascular resistance. Has alpha-1 and beta antagonist
effects and beta-2 agonist effects. Has more rapid onset
than hydralazine and less overshoot hypotension.
Adult Dose 50-100 mg
IV; repeat 30min to a maximum of
300 mg
Preganacy C (safety not
established)
Contraindications
Documented
hypersensitivity,
cardiogenic shock,
pulmonary edema,
bradycardia, heart block,
uncompensated CHF,
reactive airway disease
Precautions Caution in
impaired hepatic function;
discontinue therapy if there are
signs of liver dysfunction; in
elderly patients, a lower
response rate and higher
incident of toxicity may be
observed; intensified
bronchospasms, heart block,
CHF
Nifedipine
 Potent direct vasodilators,rapid onset of action,safe and effective
 Adverse effects severe headache,hypotension and flushing
Nitroprusside (Nitropress) -- Used when hydralazine and labetalol are
ineffective. Reduces peripheral resistance by acting directly on
arteriolar and venous smooth muscle.
 Pregnancy C - Safety for use during pregnancy has not been
established.
 adverse effects of nitroprusside include tinnitus, blurred vision,
altered mental status, hypotension, and methemoglobinemia
Diazoxide powerful direct vasodilator
 mini-bolus dose of 15mg of diazoxide is as effective as hydralazine
with less side effects
When to use?
 If a woman in a critical care setting who has severe
hypertension or severe pre-eclampsia has or
previously had an eclamptic fit, give intravenous
magnesium sulphate*.
 Consider giving intravenous magnesium sulphate*
to women with severe preeclampsia who are in a
critical care setting if birth is planned within 24 hours
 If considering magnesium sulphate* treatment, use the
following as features of severe pre-eclampsia:
 severe hypertension and proteinuria or
 mild or moderate hypertension and proteinuria with one or
more of the following:
1. symptoms of severe headache
2. problems with vision, such as blurring or flashing before the
eyes
3. severe pain just below the ribs or vomiting
4. papilloedema
5. signs of clonus (≥3 beats)
6. liver tenderness
7. HELLP syndrome
8. platelet count falling to below 100 x 109 per litre
9. abnormal liver enzymes (ALT or AST rising to above 70
iu/litre).
 Use the Collaborative Eclampsia Trial[2]
regimen for administration of magnesium
sulphate*:
 loading dose of 4 g should be given
intravenously over 5 minutes, followed by an
infusion of 1 g/hour maintained for 24 hours
 recurrent seizures should be treated with a
further dose of 2–4 g given over 5 minutes.
 Do not use diazepam, phenytoin as an
alternative to magnesium sulphate* in women
with eclampsia.
(NICE GUIDELINE)
Continous intravenous infusion
 Give 4-6 gm of loading dose in 100 ml of IV fluid administered
over 15-20 min
 Begin 2 gm/h in 50 ml of IV maintainance infusion
 Measure serum magnesium level at 4-6 hrs and adjust between 4-7
meq/l
 Magnesium sulfate is discontinued 24 hrs after delivery
 Give loading dose of 4 g of magnesium sulfate as a 20% solution
intravenously at a rate of 1g/min
 Follow with 10g of magnesium sulfate ,one half(5 g) injected deeply in the
upper outer quadrant of both buttocks using a 3-inch long 20 guage
needle
 If convulsions persist after 15 minutes give 2 gm more IV as a
20%solution as 1g/min.,for a large women 4 gm can be given slowly and
safely
 Every 4 hrs thereafter give 5 gm of Mg sulphate in alternate buttocks after
assuring
1. the patellar reflex is present
2. Respirations are not depressed
3. Urine output during the previous 4 hrs exceed 400ml
Discontinue 24 hrs after delivery
(William obstetrics)
Magnesium Sulfate –
First-line therapy for seizure prophylaxis.
Antagonizes calcium channels of smooth muscle.
Adult Dose 4-6 g IV over 20 min, with maintenance of 1-2 g/h
Contraindications Hypermagnesemia, heart block, severe
hepatitis renal disease, Addison disease, myocardial damage
Overdose calcium gluconate, 10-20 mL IV of 10%; serum
magnesium level should be checked one hour after initiation of
therapy with goal of therapeutic level of 4-7 mEq/L
Phenytoin (Dilantin) -- The major site of action is the motor cortex where it
acts by preventing the spread of seizure activity.
Indicated for eclampsia.
Adult Dose 20 mg/kg IV infused at a rate of 12.5 mg/min, not to exceed
1500 mg/24h
Contraindications Documented hypersensitivity, sinoatrial block, sinus
bradycardia, Adam-Stokes syndrome
Pregnancy D - Unsafe in pregnancy
Diazepam (Valium) -- For treatment of seizures resistant to magnesium
sulfate. Depresses all levels of CNS (eg, limbic and reticular formation),
possibly by increasing activity of GABA.
Indicated for status epilepticus in eclamptic patients.
Adult Dose 5-10 mg IV, repeat to total of 30 mg
Contraindications Documented hypersensitivity; narrow angle glaucoma
Fetal respiratory depression, fetal heart beat variability, maternal respiratory
depression, delivery of fetus imminent
Pregnancy D - Unsafe in pregnancy
Precautions Monitor respiratory status during administrati on
Corticosteroids for fetal lung maturation
• If birth is considered likely within 7 days in women with pre-
eclampsia:
give two doses of betamethasone* 12 mg intramuscularly 12
hours apart in women between 24 and 34 weeks
 consider giving two doses of betamethasone* 12 mg
intramuscularly12 hours apart in women between 35 and 36
weeks.
Corticosteroids to manage HELLP syndrome
Do not use dexamethasone or betamethasone for the treatment of
HELLP syndrome.
 Do not use volume expansion in women with
severe pre-eclampsia unless hydralazine is
the antenatal antihypertensive.
 In women with severe pre-eclampsia, limit
maintenance fluids to 80 ml/hour unless there
are other ongoing fluid losses (for example,
haemorrhage).
 Manage pregnancy in women with pre-eclampsia conservatively
(that is, do not plan same-day delivery of the baby) until 34 weeks.
 Consultant obstetrician should document in the woman's notes the
maternal (biochemical, haematological and clinical) and fetal
thresholds for elective birth before 34 weeks in women with pre-
eclampsia.
 Consultant obstetrician should write a plan for antenatal fetal
monitoring during birth.
Before 34 weeks
 Offer birth to women with pre-eclampsia before 34 weeks, after
discussion with neonatal and anaesthetic teams and a course of
corticosteroids has been given if:
 severe hypertension develops refractory to treatment
 maternal or fetal indications develop as specified in the consultant
plan
After 34 weeks
 Recommend birth for women who have pre-eclampsia
with severe hypertension after 34 weeks when their
blood pressure has been controlled and a course of
corticosteroids has been completed (if appropriate).
Between 34+0 to 36+6 weeks
 Offer birth to women who have pre-eclampsia with mild
or moderate hypertension at 34+0 to 36+6 weeks
depending on maternal and fetal condition,risk factors
and availability of neonatal intensive care.
At 37+0 weeks
 Recommend birth within 24–48 hours for women who
have pre-eclampsia with mild or moderate
hypertension after 37+0 weeks (nice guideline)
 Carry out cardiotocography at diagnosis of severe
gestational hypertension or pre-eclampsia.
 If conservative management of severe gestational
hypertension or pre-eclampsiais planned, carry out
all the following tests at diagnosis:
• ultrasound for fetal growth and amniotic fluid
volume assessment
• umbilical artery doppler velocimetry.
 If the results of all fetal monitoring are normal in
women with severe gestational hypertension or pre-
eclampsia, do not routinely repeat cardiotocography
more than weekly.
 In women with severe gestational hypertension or
pre-eclampsia, repeat cardiotocography if if any of
the following occur:
 the woman reports a change in fetal movement
 vaginal bleeding
 abdominal pain
 deterioration in maternal condition.
 In women with severe gestational hypertension or pre-eclampsia, do
not routinely repeat ultrasound for fetal growth and amniotic fluid
volume assessment or umbilical artery doppler velocimetry more
than every 2 weeks.
 If the results of any fetal monitoring in women with severe gestational
hypertension or pre-eclampsia are abnormal, tell a consultant
obstetrician
 For women with severe gestational hypertension or pre-eclampsia,
write a careplan that includes all of the following:
o the timing and nature of future fetal monitoring
o fetal indications for birth and if and when corticosteroids should be
given
o when discussion with neonatal paediatricians and obstetric
anaesthetists should take place and what decisions should be made
 Blood pressure
During labour, measure blood pressure:
• hourly in women with mild or moderate hypertension
• continually in women with severe hypertension.
• Continue use of antenatal antihypertensive treatment during labour.
 Haematological and biochemical monitoring
Determine the need for haematological and biochemical tests during labour in
women with mild or moderate hypertension using the same criteria as in the
antenatal period even if regional analgesia is being considered.
 Care during epidural analgesia
Do not preload women who have severe pre-eclampsia with intravenous fluids
before establishing low-dose epidural analgesia and combined spinal epidural
analgesia.
 Do not routinely limit the duration of the
second stage of labour: in women with stable
mild or moderate hypertension or if blood
pressure is controlled within target ranges in
women with severe hypertension.
 Recommend operative birth in the second stage
of labour for women with severe hypertension
whose hypertension has not responded to
initial treatment.
Blood pressure
In women with pre-eclampsia who did not take antihypertensive treatment and have
given birth, measure blood pressure:
 at least four times a day while the woman is an inpatient
 at least once between day 3 and day 5 after birth
 on alternate days until normal if blood pressure was abnormal on days 3–5.
In women with pre-eclampsia who did not take antihypertensive treatment and have
given birth, start antihypertensive treatment if blood pressure is 150/100 mmHg or
higher.
Ask women with pre-eclampsia who have given birth about severe headache and
epigastric pain each time blood pressure is measured.
In women with pre-eclampsia who took
antihypertensive treatment and have given
birth, measure blood pressure:
o at least four times a day while the woman is an inpatient
o every 1–2 days for up to 2 weeks after transfer to
community care until the woman is off treatment and has no
hypertension.
For women with pre-eclampsia who have taken
antihypertensive treatment and have given
birth:
 continue antenatal antihypertensive treatment
 consider reducing antihypertensive treatment if their blood
pressure falls below 140/90 mmHg
 reduce antihypertensive treatment if their blood pressure falls
below 130/80 mmHg.
 If a woman has taken methyldopa† to treat pre-eclampsia, stop
within 2 days of birth.
 Offer women with pre-eclampsia who have given birth transfer
to community care if all of the following criteria have been met:
1. there are no symptoms of pre-eclampsia
2. blood pressure, with or without treatment, is 149/99 mmHg or
lower
3. blood test results are stable or improving.
 Write a care plan for women with pre-eclampsia who have given
birth and are being transferred to community care that includes
all of the following:
• who will provide follow-up care, including medical review if
needed
• frequency of blood pressure monitoring
• thresholds for reducing or stopping treatment
• indications for referral to primary care for blood pressure review
• self-monitoring for symptoms.
 Offer women who have pre-eclampsia and are
still on antihypertensive treatment 2 weeks
after transfer to community care a medical
review.
 Offer all women who have had pre-eclampsia a
medical review at the postnatal review (6–8
weeks after the birth).
 Offer women who have had pre-eclampsia and
who still need antihypertensive treatment at
the postnatal review (6–8 weeks after the birth)
a specialist assessment of their hypertension.
Haematological and
biochemical monitoring
 In women who have pre-eclampsia with mild
or moderate hypertension, measure platelet
count, transaminases and serum creatinine 48–
72 hours after birth
 do not repeat platelet count, transaminases or
serum creatinine measurements if results are
normal at 48–72 hours.
 If biochemical and haematological indices are
improving but stay within the abnormal range
repeat measurements as clinically indicated
and at the postnatal review (6–8 weeks after the
birth).
 If biochemical and haematological indices are
not improving , repeat platelet count,
transaminases and serum creatinine
measurements as clinically indicated.
 carry out a urinary reagent-strip test at the
postnatal review (6–8 weeks after the birth).
 Offer women who had pre-eclampsia and still
have proteinuria (1+ or more) at the postnatal
review (6–8 weeks after the birth) a further
review at 3 months after the birth to assess
kidney function and consider offering them a
referral specialist kidney assessment.
 In women who still need antihypertensive treatment in the postnatal period,avoid
diuretic treatment for hypertension if the woman is breastfeeding or expressing
milk.
 Tell women who still need antihypertensive treatment in the postnatal period that
the following antihypertensive drugs have no known adverse effects on babies
receiving breast milk:
 labetalol
 nifedipine
 enalapril
 captopril
 atenolol
 metoprolol
 Tell women who still need antihypertensive treatment in the postnatal period that
there is insufficient evidence on the safety in babies receiving breast milk of the
following antihypertensive drugs:
• ARBs
• amlodipine
• ACE inhibitors other than enalapril† and captopril†.
 Assess the clinical wellbeing of the baby, especially adequacy of feeding, at least
daily for the first 2 days after the birth.
Long-term risk of cardiovascular disease
increased later in life
Long-term risk of end-stage kidney disease
Tell women with a history of pre-eclampsia who
have no proteinuria and no hypertension at the
postnatal review (6–8 weeks after the birth) that
although the relative risk of end-stage kidney
disease is increased the absolute risk is low and no
further follow-up is necessary
Thrombophilia and the risk of pre-eclampsia
Do not routinely perform screening for thrombophilia
in women who have had pre-eclampsia.
Risk of recurrence of hypertensive
disorders of pregnancy
 Tell women who had gestational hypertension that their
risk of developing:
• gestational hypertension in a future pregnancy ranges from about
16 to 47%
• pre-eclampsia in a future pregnancy ranges from 2 to 14%
 Tell women who had pre-eclampsia that their
• risk of gestational hypertension in a future pregnancy ranges
from about 13 to 53%
• pre-eclampsia in a future pregnancy is up to about (16%)
• pre-eclampsia in a future pregnancy is about (25%) pregnancies if
their preeclampsia was complicated by severe pre-eclampsia,
HELLP syndrome or eclampsia and led to birth before 34 weeks,
and about (55%) pregnancies if it led to birth before 28 weeks.
 Inter-pregnancy interval and recurrence of
hypertensive disorders of pregnancy
Tell women who have had pre-eclampsia that there is no
additional risk of recurrence with inter-pregnancy interval
up to 10 years
 Body mass index and recurrence of
hypertensive disorders of pregnancy
Advise women who have had pre-eclampsia to achieve and
keep a BMI within the healthy range before their next
pregnancy (18.5–24.9 kg/m2)
Pre eclampsia & eclampsia

Pre eclampsia & eclampsia

  • 1.
    By Dr Shanzaaurooj Post Graduate Trainee Gynea unit III SPH Quetta
  • 2.
     Gestational Hypertension Pre-eclampsia  Chronic hypertesion essential secondary  Pre-eclampsia superimposed on chronic hypertension  Eclampsia
  • 3.
     Gestational hypertension newhypertension presenting after 20 weeks without significant proteinuria and features of preeclampsia,BP levels return to normal within 3 months postpartum  Pre-eclampsia is new hypertension presenting after 20 weeks with significant proteinuria.  Severe pre-eclampsia is pre-eclampsia with severe hypertension and/or with symptoms,and/or biochemical and/or haematological impairment. after 20 weeks
  • 4.
     Eclampsia isa convulsive condition associated with pre-eclampsia  Chronic hypertension is hypertension that is present before 20 weeks characterized by a BP of 140/90 mmHg or greater . It can be primary or secondary in aetiology  Pre-eclampsia superimposed on chronic hypertension is hypertension present before 20 weeks with development of symptoms of pre- eclampsia after 20 weeks
  • 5.
     Significat proteinuriaexcretion of 300mg/24hr of urinary proteins in 24hr urine collection or a concentration of 30mg/dl >1+ on dipstick in atleast two random urine samples collected 4 to 6 hrs apart  Grades of hypertension Mild hypertension diastolic blood pressure 90–99 mmHg, systolic blood pressure140–149 mmHg. Moderate hypertension diastolic blood pressure 100–109 mmHg, systolic blood pressure 150–159 mmHg. Severe hypertension diastolic blood pressure 110 mmHg or greater, systolic bloodpressure 160 mmHg or greater
  • 6.
    A pregnancy specificsyndrome characterized by variable degrees of placental dysfunction and a maternal response featuring systemic infammation
  • 7.
     The etiologyof preeclampsia is unknown. However, placental delivery reverses the symptoms of preeclampsia, suggesting that the placenta has a controlling role in the condition. Additionally, women with increased placental tissue for gestational age, such as hydatiform moles and twin pregnancies, have an increased incidence of preeclampsia.  Several theories attempt to explain the pathophysiology of preeclampsia  Most popular theory holds that improper placental development results in placental vascular endothelial dysfunction and a relative uteroplacental insufficiency. The vascular endothelial dysfunction results in increased permeability, hypercoagulability, and diffuse vasospasm
  • 8.
    Changes in normalpregnancy  In normal pregnancy spiral arteries of the placental bed undergoes a series of physiological changes  cytotrophoblasts replace the endothelial cells in the spiarl arteries resulting in destruction of medial elastic and muscular tissue,these physiological changes reach the inner third of myometrium and create a low vascular arterioler system that allows a dramatic increase in blood supply necessary to serve the growing fetus.The end result is that 100 to 120 spiral arteries are converted into dilated inelastic tubes without maternal vasomotor control Changes in preeclampsia  In pre-eclampsia about half to 2/3rd of spiral arteries escape this transformation ,in these arteries the myometrial segment remain anatomically intact,do not dilate,many vessels are occluded by fibrinoid material and exhibit adjacent foam cell invasion (atherosis).Atherosis and thrombosis leads to microinfarcts in placenta and are responsible for abruption due to decidual necrosis,separation and hemmorhage.
  • 12.
    Cardiovuscular system Severe pre-eclampsiais characterized by vasoconstriction and a leaky microcirculation,with extravasation of fluid in E.C.S and relative hypovolemia leading to hemoconcentration,edema and swelling often facial particularly peroorbital edema in contrast to physiological pedal edema Renal system Primary renal manifestation of endothelial cell activation is inflammatory swelling of glomeruler endothelial capillaries causing an increase in the renal vascular resistance with a decrease in the renal blood flow resulting in decreased GFR and EFRP complicating to ANURIA or OLIGURIA leading to ARF. The first change in the renal system involvement is tubular dysfunction resulting in decreased uric acid clearance from the body and hyperuicemia,the next event is proteinuria due to loss of negative charge from the GBM ,finally there is rise in levels of urea and creatinine . Proteinuria further leads to hypoalbunemia with extravasation of fluid in ECS resulting in genearilzed edema and,ascites,pleural effusion,pulmonary,cerebral and laryngeal edema.
  • 13.
    Abnormal hemostasis Platelet activationa feature of normal pregnancy is exaggerated in pre-eclampsia as sysytemic endothelial cell activation cause platelet adherence to site of endothelial damage.Platelets consumption result in thrombocytopenia while platelet adherence leads to formation of microthrombi effecting microcirculation leading to increased intravuscuar coagulation with a rise in fibrin degradation products and hemolysis of RBC’s in microvessels leading to HELLP syndrome. HELLP syndrome It is Hemolysis,elevated liver enzymes and low platelets caused by abnormal hemostasis and liver involvement due to excessive fibrinogen deposition in hepatic sinusoids also obstructing blood flow leading to hepatic capsular distension and epigastric pain,nausea,vomiting. It may complicate to subcapsular hematoma and liver rupture presenting with severe epigastric pain,shoulder pain,shock, hemoperitoneum,respiratory difficulties or pleural effusion.
  • 14.
     Nulliparity  extremesof maternal age  multifetal gestation  pre-eclampsia in a previous pregnancy  family history  chronic hypertension or renal disease  chronic infections  maternal low birth weight  obesity and insulin resistance  Pre-gestational DM  smoking  maternal genes  chronic inflammatory conditions like (SLE & RA)  Anti-phospholipid antibody syndrome  molar pregnancy
  • 15.
    Symptoms of pre-eclampsia severe headache  problems with vision, such as blurring or flashing before the eyes  severe pain just below the ribs  vomiting  sudden swelling of the face, hands or feet.  Seizures (eclampsia) grand mal in character with tonic clonic phases Physical signs:  Asymptomatic hypertension is discovered on routine prenatal examination.  Diffuse edema has a high specificity for preeclampsia.  Neurologic findings such as papilledema and hyperreflexia must be addressed quickly, as they can herald the onset of eclampsia.  Petechiae and bruising could suggest coagulopathy.  Right upper quadrant or mid epigastric tenderness develops as a result of hepatocellular necrosis.
  • 16.
    Complications Maternal complications  Abruptionplacenta  DIC/HELLP syndrome  Acute Renal Failure  Eclampsia  Liver failure & Hemmorhage  Stroke  Death  Long term cardiovascular morbidity Neonatal complications  Preterm delivery  IUGR  Hypoxic neurological injury  Perinatal death  Low birth weight with long term morbidity
  • 17.
    DIFFERENTIALS  Disseminated IntravascularCoagulation  Fatty Liver  Cholecystitis  Perforated peptic ulcer  Systemic Lupus Erythematosus  Thrombotic Thrombocytopenic Purpura
  • 18.
    BASELINE •CBC •BLOOD GROUP •HEPATITUS B& C Urine analysis of a clean catch specimen Proteinuria 2+ or higher is significant and warrants further evaluation to rule out preeclampsia. A 24-hour urine collection with more than 300 mg of protein RFT’s • UREA > 40 mmol/l or >11 mg/dl • Creatinine>1 mg/dl • Serum uric acid levels >6.3 mg/dl LFT’s • AST or ALT >50 IU/L • Biluribin >25 IU/L Clotting profile • PT/APTT • Fibrin degradation products
  • 19.
    Ultrasound  Confirmation ofnormal fetal development is important and standard prenatal care in all pregnancies.Points to study in US are  Fetal biometry(AC,HC,BPD,FL)  AOL & estimated fetal weight  Placental localization Doppler velocimetry  Screening test in first trimester to detect changes in spiral arteries and is considered abnormal if there is an early diastolic notch or high RI
  • 20.
    Management can bediscussed under following headings  Prevention  Antihypertensive treatment  Anticonvulsant treatment  Steroids for lung maturation  Fluid balance  Mode and timing of birth  Fetal monitoring in high risk patient  Intrapartum care  Postnatal monitoring,treatment and investigations  Breast feeding  Advice and follow up care
  • 21.
    Primary prevention  Prepregnancy weight control in high risk patients  Vitamin B and folate supplementations  Cessation of smoking  Control of Hypertension in women having chronic hypertension  Control of sugar levels in women having Diabetes pre-pregnancy Secondary prevention  Calcium supplementations:it reduces parathyroid and renin release thereby reducing intracellular calcium and smooth muscle contractility,the ideal patient is the one who is obese with raised BP at booking visit  Antiplatelet agents:low dose aspirin is recommended in high risk patients as it inhibits thromboaxane synthesis thus altering the balance in favor of PGI usually before 23 weeks and therefore helps in proper placentation in a dose of 75mg OD starting from 12 weeks until birth  For other agents like Mg and Zinc supplements,fish oil,salt restriction, antioxidants like vitamin C,E there is insufficient data to recommend their use in primary prevention
  • 22.
    Degree of hypertension Mild hypertension (140/90to 149/ 99 mmHg) Moderate hypertension (150/100 to 159/ 109 mmHg Severe hypertension (160/110 mmHg or higher) Admit to hospital NO YES YES Treat NO With oral labetalol† as first-line treatment to keep: diastolic blood pressure between 80–100 mmHg systolic blood pressure less than 150 mmHg With oral labetalol† as first-line treatment to keep: diastolic blood pressure between 80–100 mmHg systolic blood pressure less than 150 mmHg Measure blood pressure At least four times a day At least four times a day More than four times a day, depending on clinical circumstances Test for proteinuria Do not repeat quantification of proteinuria Do not repeat quantification of proteinuria Do not repeat quantification of proteinuria Blood tests Monitor using the following tests twice a week: kidney function, electrolytes, full blood count, transaminases, bilirubin Monitor using the following tests three times a week: kidney function, electrolytes, full blood count, transaminases, bilirubin Monitor using the following tests three times a week: kidney function, electrolytes, full blood count, transaminases, bilirubin
  • 23.
     Only offerwomen with pre-eclampsia antihypertensive treatment other than labetalol after considering side-effect profiles for the woman, fetus and newborn baby.  Alternatives include methyldopa† and nifedipine†
  • 24.
    Adult Dose 5-10mg IV; repeat 20min to maximum of 60 mg Contraindications Documented hypersensitivity, dissecting aortic aneurysm, mitral valve rheumatic heart disease Interactions:MAO inhibitors and beta-blockers may increase hydralazine toxicity; pharmacological effects of hydralazine may be decreased by indomethacin Adverse effects headache, flushing, overshoot hypotension, peripheral edema, implicated in myocardial infarction; Pregnancy C (safety not established) Hydralazine (Apresoline) -- First-line therapy against preeclamptic hypertension in past decades. Decreases systemic resistance through direct vasodilation of arterioles resulting in reflex tachycardia..
  • 25.
    Labetalol (Normodyne) --Second-line therapy that produces vasodilatation and decrease in systemic vascular resistance. Has alpha-1 and beta antagonist effects and beta-2 agonist effects. Has more rapid onset than hydralazine and less overshoot hypotension. Adult Dose 50-100 mg IV; repeat 30min to a maximum of 300 mg Preganacy C (safety not established) Contraindications Documented hypersensitivity, cardiogenic shock, pulmonary edema, bradycardia, heart block, uncompensated CHF, reactive airway disease Precautions Caution in impaired hepatic function; discontinue therapy if there are signs of liver dysfunction; in elderly patients, a lower response rate and higher incident of toxicity may be observed; intensified bronchospasms, heart block, CHF
  • 27.
    Nifedipine  Potent directvasodilators,rapid onset of action,safe and effective  Adverse effects severe headache,hypotension and flushing Nitroprusside (Nitropress) -- Used when hydralazine and labetalol are ineffective. Reduces peripheral resistance by acting directly on arteriolar and venous smooth muscle.  Pregnancy C - Safety for use during pregnancy has not been established.  adverse effects of nitroprusside include tinnitus, blurred vision, altered mental status, hypotension, and methemoglobinemia Diazoxide powerful direct vasodilator  mini-bolus dose of 15mg of diazoxide is as effective as hydralazine with less side effects
  • 28.
    When to use? If a woman in a critical care setting who has severe hypertension or severe pre-eclampsia has or previously had an eclamptic fit, give intravenous magnesium sulphate*.  Consider giving intravenous magnesium sulphate* to women with severe preeclampsia who are in a critical care setting if birth is planned within 24 hours
  • 29.
     If consideringmagnesium sulphate* treatment, use the following as features of severe pre-eclampsia:  severe hypertension and proteinuria or  mild or moderate hypertension and proteinuria with one or more of the following: 1. symptoms of severe headache 2. problems with vision, such as blurring or flashing before the eyes 3. severe pain just below the ribs or vomiting 4. papilloedema 5. signs of clonus (≥3 beats) 6. liver tenderness 7. HELLP syndrome 8. platelet count falling to below 100 x 109 per litre 9. abnormal liver enzymes (ALT or AST rising to above 70 iu/litre).
  • 30.
     Use theCollaborative Eclampsia Trial[2] regimen for administration of magnesium sulphate*:  loading dose of 4 g should be given intravenously over 5 minutes, followed by an infusion of 1 g/hour maintained for 24 hours  recurrent seizures should be treated with a further dose of 2–4 g given over 5 minutes.  Do not use diazepam, phenytoin as an alternative to magnesium sulphate* in women with eclampsia. (NICE GUIDELINE)
  • 31.
    Continous intravenous infusion Give 4-6 gm of loading dose in 100 ml of IV fluid administered over 15-20 min  Begin 2 gm/h in 50 ml of IV maintainance infusion  Measure serum magnesium level at 4-6 hrs and adjust between 4-7 meq/l  Magnesium sulfate is discontinued 24 hrs after delivery
  • 32.
     Give loadingdose of 4 g of magnesium sulfate as a 20% solution intravenously at a rate of 1g/min  Follow with 10g of magnesium sulfate ,one half(5 g) injected deeply in the upper outer quadrant of both buttocks using a 3-inch long 20 guage needle  If convulsions persist after 15 minutes give 2 gm more IV as a 20%solution as 1g/min.,for a large women 4 gm can be given slowly and safely  Every 4 hrs thereafter give 5 gm of Mg sulphate in alternate buttocks after assuring 1. the patellar reflex is present 2. Respirations are not depressed 3. Urine output during the previous 4 hrs exceed 400ml Discontinue 24 hrs after delivery (William obstetrics)
  • 33.
    Magnesium Sulfate – First-linetherapy for seizure prophylaxis. Antagonizes calcium channels of smooth muscle. Adult Dose 4-6 g IV over 20 min, with maintenance of 1-2 g/h Contraindications Hypermagnesemia, heart block, severe hepatitis renal disease, Addison disease, myocardial damage Overdose calcium gluconate, 10-20 mL IV of 10%; serum magnesium level should be checked one hour after initiation of therapy with goal of therapeutic level of 4-7 mEq/L
  • 34.
    Phenytoin (Dilantin) --The major site of action is the motor cortex where it acts by preventing the spread of seizure activity. Indicated for eclampsia. Adult Dose 20 mg/kg IV infused at a rate of 12.5 mg/min, not to exceed 1500 mg/24h Contraindications Documented hypersensitivity, sinoatrial block, sinus bradycardia, Adam-Stokes syndrome Pregnancy D - Unsafe in pregnancy Diazepam (Valium) -- For treatment of seizures resistant to magnesium sulfate. Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Indicated for status epilepticus in eclamptic patients. Adult Dose 5-10 mg IV, repeat to total of 30 mg Contraindications Documented hypersensitivity; narrow angle glaucoma Fetal respiratory depression, fetal heart beat variability, maternal respiratory depression, delivery of fetus imminent Pregnancy D - Unsafe in pregnancy Precautions Monitor respiratory status during administrati on
  • 35.
    Corticosteroids for fetallung maturation • If birth is considered likely within 7 days in women with pre- eclampsia: give two doses of betamethasone* 12 mg intramuscularly 12 hours apart in women between 24 and 34 weeks  consider giving two doses of betamethasone* 12 mg intramuscularly12 hours apart in women between 35 and 36 weeks. Corticosteroids to manage HELLP syndrome Do not use dexamethasone or betamethasone for the treatment of HELLP syndrome.
  • 36.
     Do notuse volume expansion in women with severe pre-eclampsia unless hydralazine is the antenatal antihypertensive.  In women with severe pre-eclampsia, limit maintenance fluids to 80 ml/hour unless there are other ongoing fluid losses (for example, haemorrhage).
  • 37.
     Manage pregnancyin women with pre-eclampsia conservatively (that is, do not plan same-day delivery of the baby) until 34 weeks.  Consultant obstetrician should document in the woman's notes the maternal (biochemical, haematological and clinical) and fetal thresholds for elective birth before 34 weeks in women with pre- eclampsia.  Consultant obstetrician should write a plan for antenatal fetal monitoring during birth. Before 34 weeks  Offer birth to women with pre-eclampsia before 34 weeks, after discussion with neonatal and anaesthetic teams and a course of corticosteroids has been given if:  severe hypertension develops refractory to treatment  maternal or fetal indications develop as specified in the consultant plan
  • 38.
    After 34 weeks Recommend birth for women who have pre-eclampsia with severe hypertension after 34 weeks when their blood pressure has been controlled and a course of corticosteroids has been completed (if appropriate). Between 34+0 to 36+6 weeks  Offer birth to women who have pre-eclampsia with mild or moderate hypertension at 34+0 to 36+6 weeks depending on maternal and fetal condition,risk factors and availability of neonatal intensive care. At 37+0 weeks  Recommend birth within 24–48 hours for women who have pre-eclampsia with mild or moderate hypertension after 37+0 weeks (nice guideline)
  • 39.
     Carry outcardiotocography at diagnosis of severe gestational hypertension or pre-eclampsia.  If conservative management of severe gestational hypertension or pre-eclampsiais planned, carry out all the following tests at diagnosis: • ultrasound for fetal growth and amniotic fluid volume assessment • umbilical artery doppler velocimetry.  If the results of all fetal monitoring are normal in women with severe gestational hypertension or pre- eclampsia, do not routinely repeat cardiotocography more than weekly.  In women with severe gestational hypertension or pre-eclampsia, repeat cardiotocography if if any of the following occur:  the woman reports a change in fetal movement  vaginal bleeding  abdominal pain  deterioration in maternal condition.
  • 40.
     In womenwith severe gestational hypertension or pre-eclampsia, do not routinely repeat ultrasound for fetal growth and amniotic fluid volume assessment or umbilical artery doppler velocimetry more than every 2 weeks.  If the results of any fetal monitoring in women with severe gestational hypertension or pre-eclampsia are abnormal, tell a consultant obstetrician  For women with severe gestational hypertension or pre-eclampsia, write a careplan that includes all of the following: o the timing and nature of future fetal monitoring o fetal indications for birth and if and when corticosteroids should be given o when discussion with neonatal paediatricians and obstetric anaesthetists should take place and what decisions should be made
  • 41.
     Blood pressure Duringlabour, measure blood pressure: • hourly in women with mild or moderate hypertension • continually in women with severe hypertension. • Continue use of antenatal antihypertensive treatment during labour.  Haematological and biochemical monitoring Determine the need for haematological and biochemical tests during labour in women with mild or moderate hypertension using the same criteria as in the antenatal period even if regional analgesia is being considered.  Care during epidural analgesia Do not preload women who have severe pre-eclampsia with intravenous fluids before establishing low-dose epidural analgesia and combined spinal epidural analgesia.
  • 42.
     Do notroutinely limit the duration of the second stage of labour: in women with stable mild or moderate hypertension or if blood pressure is controlled within target ranges in women with severe hypertension.  Recommend operative birth in the second stage of labour for women with severe hypertension whose hypertension has not responded to initial treatment.
  • 43.
    Blood pressure In womenwith pre-eclampsia who did not take antihypertensive treatment and have given birth, measure blood pressure:  at least four times a day while the woman is an inpatient  at least once between day 3 and day 5 after birth  on alternate days until normal if blood pressure was abnormal on days 3–5. In women with pre-eclampsia who did not take antihypertensive treatment and have given birth, start antihypertensive treatment if blood pressure is 150/100 mmHg or higher. Ask women with pre-eclampsia who have given birth about severe headache and epigastric pain each time blood pressure is measured.
  • 44.
    In women withpre-eclampsia who took antihypertensive treatment and have given birth, measure blood pressure: o at least four times a day while the woman is an inpatient o every 1–2 days for up to 2 weeks after transfer to community care until the woman is off treatment and has no hypertension. For women with pre-eclampsia who have taken antihypertensive treatment and have given birth:  continue antenatal antihypertensive treatment  consider reducing antihypertensive treatment if their blood pressure falls below 140/90 mmHg
  • 45.
     reduce antihypertensivetreatment if their blood pressure falls below 130/80 mmHg.  If a woman has taken methyldopa† to treat pre-eclampsia, stop within 2 days of birth.  Offer women with pre-eclampsia who have given birth transfer to community care if all of the following criteria have been met: 1. there are no symptoms of pre-eclampsia 2. blood pressure, with or without treatment, is 149/99 mmHg or lower 3. blood test results are stable or improving.  Write a care plan for women with pre-eclampsia who have given birth and are being transferred to community care that includes all of the following: • who will provide follow-up care, including medical review if needed • frequency of blood pressure monitoring • thresholds for reducing or stopping treatment • indications for referral to primary care for blood pressure review • self-monitoring for symptoms.
  • 46.
     Offer womenwho have pre-eclampsia and are still on antihypertensive treatment 2 weeks after transfer to community care a medical review.  Offer all women who have had pre-eclampsia a medical review at the postnatal review (6–8 weeks after the birth).  Offer women who have had pre-eclampsia and who still need antihypertensive treatment at the postnatal review (6–8 weeks after the birth) a specialist assessment of their hypertension.
  • 47.
    Haematological and biochemical monitoring In women who have pre-eclampsia with mild or moderate hypertension, measure platelet count, transaminases and serum creatinine 48– 72 hours after birth  do not repeat platelet count, transaminases or serum creatinine measurements if results are normal at 48–72 hours.  If biochemical and haematological indices are improving but stay within the abnormal range repeat measurements as clinically indicated and at the postnatal review (6–8 weeks after the birth).
  • 48.
     If biochemicaland haematological indices are not improving , repeat platelet count, transaminases and serum creatinine measurements as clinically indicated.  carry out a urinary reagent-strip test at the postnatal review (6–8 weeks after the birth).  Offer women who had pre-eclampsia and still have proteinuria (1+ or more) at the postnatal review (6–8 weeks after the birth) a further review at 3 months after the birth to assess kidney function and consider offering them a referral specialist kidney assessment.
  • 49.
     In womenwho still need antihypertensive treatment in the postnatal period,avoid diuretic treatment for hypertension if the woman is breastfeeding or expressing milk.  Tell women who still need antihypertensive treatment in the postnatal period that the following antihypertensive drugs have no known adverse effects on babies receiving breast milk:  labetalol  nifedipine  enalapril  captopril  atenolol  metoprolol  Tell women who still need antihypertensive treatment in the postnatal period that there is insufficient evidence on the safety in babies receiving breast milk of the following antihypertensive drugs: • ARBs • amlodipine • ACE inhibitors other than enalapril† and captopril†.  Assess the clinical wellbeing of the baby, especially adequacy of feeding, at least daily for the first 2 days after the birth.
  • 50.
    Long-term risk ofcardiovascular disease increased later in life Long-term risk of end-stage kidney disease Tell women with a history of pre-eclampsia who have no proteinuria and no hypertension at the postnatal review (6–8 weeks after the birth) that although the relative risk of end-stage kidney disease is increased the absolute risk is low and no further follow-up is necessary Thrombophilia and the risk of pre-eclampsia Do not routinely perform screening for thrombophilia in women who have had pre-eclampsia.
  • 51.
    Risk of recurrenceof hypertensive disorders of pregnancy  Tell women who had gestational hypertension that their risk of developing: • gestational hypertension in a future pregnancy ranges from about 16 to 47% • pre-eclampsia in a future pregnancy ranges from 2 to 14%  Tell women who had pre-eclampsia that their • risk of gestational hypertension in a future pregnancy ranges from about 13 to 53% • pre-eclampsia in a future pregnancy is up to about (16%) • pre-eclampsia in a future pregnancy is about (25%) pregnancies if their preeclampsia was complicated by severe pre-eclampsia, HELLP syndrome or eclampsia and led to birth before 34 weeks, and about (55%) pregnancies if it led to birth before 28 weeks.
  • 52.
     Inter-pregnancy intervaland recurrence of hypertensive disorders of pregnancy Tell women who have had pre-eclampsia that there is no additional risk of recurrence with inter-pregnancy interval up to 10 years  Body mass index and recurrence of hypertensive disorders of pregnancy Advise women who have had pre-eclampsia to achieve and keep a BMI within the healthy range before their next pregnancy (18.5–24.9 kg/m2)