Hypertension disorders in

pregnancy
 Examination questions
• 77. Classification of Hypertension in
Pregnancy. Gestosis. Etiology. Management.
• 78. Severe preeclampsia. Clinical signs.
Diagnosis. Treatment.
• 79. Eclampsia. Clinical signs. Probable
complications. Differential diagnosis.
Management. Termination of pregnancy.
• 80. Emergency treatment and termination of
pregnancy in severe preeclampsia or
eclampsia cases.
 Hypertension in Pregnancy
• the most common medical complications
of pregnancy = 5-10% of all pregnancies
• 16% of maternal mortality in developed
countries = a major cause of maternal and
perinatal morbidity and mortality worldwide
• include
– 30% of hypertensive disorders in pregnancy
are due to chronic hypertension
– 70% are due to gestational hypertension
 Hypertension. Definitions.
• systolic blood pressure (SBP) of 140 mm
Hg or greater
• or a diastolic blood pressure (DBP) of 90
mm Hg or greater
• must be present on at least 2 occasions at least 6 hours
apart but no more than 1 week apart
– an appropriate size of cuff should be used (length 1.5 times
upper arm circumference or a cuff with a bladder that encircles
80% or more of the arm)
– Proper patient position is an upright, after a 10-minute or longer
rest period (patient sitting up or in the left lateral recumbent
position with the patient's arm at the level of the heart)
– The patient should not use tobacco or caffeine for 30 minutes
preceding the measurement
 Classification
1. Gestational hypertension (formerly
pregnancy-induced hypertension that
included transient hypertension)
2. Preeclampsia
3. Eclampsia
4. Chronic hypertension
5. Preeclampsia superimposed
 Classification
• Gestational hypertension = Hypertension developing after
20 weeks gestation or during the first 24 hours postpartum without
proteinuria or other signs of preeclampsia
– Transient hypertension = Hypertension that resolves by 12
weeks postpartum
– Chronic hypertension = Hypertension that does not resolve by
12 weeks postpartum
• Preeclampsia = Hypertension typically developing after 20
weeks gestation with proteinuria
• Eclampsia = the occurrence of seizure activity in woman with
preeclampsia without other identifiable causes
• Chronic hypertension = Hypertension diagnosed prior to
pregnancy, prior to 20 weeks gestation, or after 12 weeks
postpartum
• Preeclampsia superimposed = The development of
preeclampsia or eclampsia in a woman with preexisting or chronic
hypertension
 Gestational hypertension
1. BP = 140/90 mm Hg for first time during pregnancy  
2. No proteinuria  
3. BP returns to normal < 12 weeks' postpartum  

• Incidence 6-17% in healthy nulliparous and 2-4% in

multiparous women
• Final diagnosis made only postpartum  
• 46% of women with gestational hypertension will develop
proteinuria and progress to preeclampsia

• the majority of cases of mild gestational hypertension are

diagnosed at or beyond 37 weeks
– treatment generally is not warranted
– pregnancy outcome similar to term normotensive pregnancies
 Chronic Hypertension
Chronic Hypertension  
1. BP = 140/90 mm Hg before pregnancy or diagnosed
before 20 weeks' gestation not attributable to
gestational trophoblastic disease (molar pregnancy)   
2. or Hypertension first diagnosed after 20 weeks'
gestation and persistent after 12 weeks' postpartum

Superimposed Preeclampsia (on chronic hypertension)   

1. New-onset proteinuria 300 mg/24 hours in
hypertensive women but no proteinuria before 20
weeks' gestation   
2. A sudden increase in proteinuria or blood pressure or
platelet count < 100,000/mm3 in women with
hypertension and proteinuria before 20 weeks' gestation
 Proteinuria in pregnancy
• Abnormal proteinuria in pregnancy = the
excretion of ≥300 mg of protein in 24 hours
– semiquantitative dipstick measurement possible for
emergency
1+ or greater correlates with 30 mg/dL
– a clean sample need to be used, (blood, vaginal
secretions, and bacteria)
• Edema is a common finding in the 50% gravid
– typical form - lower extremity edema
– Pathologic edema is seen in the face, hands, or lungs
or excessive, rapid weight gain of ≥ 5 pounds (1.8kg)
per week
 Preeclampsia 
Minimum criteria     
• BP = 140/90 mm Hg after 20 weeks gestation    
• Proteinuria ≥ 300 mg/24 hours or 1+ dipstick  

Increased certainty of preeclampsia = severe preeclampsia   

• BP = 160/110 mg Hg  
• Proteinuria 2.0 g/24 hours or ≥ 2+ dipstick    
• Serum creatinine > 1.2 mg/dL unless known to be previously elevated
• Platelets < 100,000/mm3
• Microangiopathic hemolysis (increased lactate dehydrogenase (LDH))
• Elevated ALT or AST 
• Persistent headache or other cerebral or visual disturbance 
• Persistent epigastric pain

Incidence = 2-7% in healthy nulliparous womenwith singletone

pregnancies
14% - in women with twin gestation
18% - in those with previous preeclampsia
 Eclampsia 
• Seizures (fits) that cannot be attributed to
other causes in a woman with preeclampsia
• Eclampsia can occur in the second half of pregnancy, during labour,
or after the birth
• Eclampsia is an important condition because once women have an
eclamptic fit they have a high risk of being seriously ill and dying
• 358,000 women died in 2008 due to complications of pregnancy and
childbirth worldwide
– 99% of these deaths are women in low- and middle-income
countries
– 15% (53,700) of maternal deaths are associated with eclampsia.
Eclampsia is more common in low- and middle-income countries
than in high-income countries
 Etiology

• The etiologic agent responsible for the

development of preeclampsia remains
unknown
 Risk factors
1. Nulliparity
2. Chronic or vascular disease (pregestational diabetes, renal
disease, chronic hypertension, rheumatic disease, connective
tissue disease)
3. Molar pregnancy
4. Fetal hydrops
5. Multifetal gestation
6. Obesity and insulin resistance
7. Prior pregnancy complicated by preeclampsia
8. Antiphospholipid antibody syndrome and thrombophilia
9. Family history of preeclampsia or eclampsia
10.Fetal aneuploidy
11.Maternal infections
12.Maternal susceptibility genes
13.Extremes of maternal age
14.Partner-related factors (limited sperm exposure, donor
insemination [oocyte and embryo donation])
 Pathophysiology
• Cardiovascular
– intense vasoconstriction with segmental spasm that occurs particularly
in arterioles and is thought to be due to increased vascular reactivity =
lead to higher arterial blood pressures (afterload)
– hemoconcentration = lower intravascular volumes and less tolerance for
the blood loss associated with delivery
• Hematologic
– thrombocytopenia (platelet count <100,000/mm3)
– microangiopathic hemolysis, as seen in HELLP syndrome, and can be
diagnosed by schistocytes seen on peripheral smear and increased
lactate dehydrogenase (LDH) levels
• Renal
– decreased renal perfusion and subsequent decreased glomerular
filtration rate (GFR). In normal pregnancy, the GFR is increased up to
50% above prepregancy levels. Because of this, serum creatinine levels
in preeclamptic patients rarely rise above normal pregnancy levels (0.8
mg/dL)
– oliguria (defined as <500ml in 24 hours) may occur due to renal
insufficiency.
– pathognomonic renal lesion = glomerular capillary endotheliosis,
(swelling of the glomerular capillary endothelial and mesangial cells)
 Pathophysiology
• Hepatic
– 20% of maternal mortality in preeclampsia is related to hepatic
complications. The pathologic liver lesions seen on autopsy are
periportal hemorrhages, hepatocellular necrosis, ischemic lesions,
intracellular fatty changes, and fibrin deposition.
• Central Nervous System
– Eclamptic convulsions are major cause of maternal mortality in the Third
World.
– The exact etiology of eclampsia is unknown but is thought to be
attributed to coagulopathy, fibrin deposition, and vasospasm
– The most common finding in the brain is edema, which likely is due to
vascular autoregulation dysfunction. Radiologic studies may show
evidence of cerebral edema and hemorrhagic lesions, particularly in the
posterior hemispheres, which may explain the visual disturbances seen
in preeclampsia. Other CNS abnormalities include headaches and
visual disturbances such as scotomata; blurred vision; and rarely,
temporary blindness
• Fetus and Placenta
– acute atherosis of decidual arteries is the hallmark placental lesion 
poor perfusion
– oligohydramnios; intrauterine growth restriction; placental abruption;
fetal distress; and ultimately, fetal demise
 Severity of Preeclampsia
Abnormality Mild Severe
Diastolic blood pressure < 100 mm Hg ≥110 mm Hg
Proteinuria Trace to 1+ Persistent ≥ 2+
Headache Absent Present
Visual disturbances Absent Present
Upper abdominal pain Absent Present
Oligouria Absent Present
Convulsion Absent Present
Serum creatinine Normal Elevated
Thrombocytopenia Absent Present
Liver enzyme elevation Minimal Marked
Fetal growth restriction Absent Obvious
Lung edema Absent Present
Methods to prevent pre-eclampsia
 Antihypertensive drug therapy for
mild to moderate hypertension
during pregnancy
• There is a halving in the risk of developing severe hypertension
associated with the use of antihypertensive drug(s) (19 trials, 2409
women; RR 0.50; 95% CI 0.41 to 0.61; risk difference (RD) -0.10 (-
0.12 to -0.07); number needed to treat (NNT) 10 (8 to 13))
• but little evidence of a difference in the risk of pre-eclampsia (22
trials, 2702 women; RR 0.97; 95% CI 0.83 to 1.13).
• no clear effect on the risk of the baby dying (26 trials, 3081 women;
RR 0.73; 95% CI 0.50 to 1.08), preterm birth (14 trials, 1992 women;
RR 1.02; 95 % CI 0.89 to 1.16), or small-for-gestational-age babies
(19 trials, 2437 women; RR 1.04; 95 % CI 0.84 to 1.27).
• Beta blockers seem better than methyldopa for reducing the risk of
severe hypertension (10 trials, 539 women, RR 0.75 (95 % CI 0.59
to 0.94); RD -0.08 (-0.14 to 0.02); NNT 12 (6 to 275))
 It remains unclear whether antihypertensive drug therapy for
mild to moderate hypertension during pregnancy is worthwhile
 Diuretics for the prevention
of pre-eclampsia

• no clear benefits have been found from the use

of diuretics to prevent pre-eclampsia. Taken
together with the level of adverse effects found,
 the use of diuretics for the prevention of
pre-eclampsia and its complications cannot
be recommended
– Thiazide diuretics were associated with an increased
risk of nausea and vomiting (two trials, 1217 women;
RR 5.81, 95% CI 1.04 to 32.46), and women allocated
diuretics were more likely to stop treatment due to
side effects compared to those allocated placebo (2
trials, 1217 women; RR 1.85, 95% CI 0.81 to 4.22).
 Antioxidants for
preventing pre-eclampsia
• A possible contributing factor to the development of pre-eclampsia may be the
presence of excessive amounts of chemicals called 'free radicals'. Antioxidants, such
as vitamin C, vitamin E, selenium and lycopene, can neutralize free radicals
• There was no significant difference between antioxidant and control groups for the
relative risk of pre-eclampsia (RR 0.73, 95% confidence intervals (CI) 0.51 to 1.06; 9
trials, 5446 women) or any other primary outcome:
– severe pre-eclampsia (RR 1.25, 95% CI 0.89 to 1.76; 2 trials, 2495 women),
– preterm birth (before 37 weeks) (RR 1.10, 95% CI 0.99 to 1.22; 5 trials, 5198
women),
– small-for-gestational-age infants (RR 0.83, 95% CI 0.62 to 1.11; 5 trials, 5271
babies)
– any baby death (RR 1.12, 95% CI 0.81 to 1.53; four trials, 5144 babies)
• Women allocated antioxidants were more likely to self-report abdominal pain late in
pregnancy (RR 1.61, 95% CI 1.11 to 2.34; 1 trial, 1745 women), require
antihypertensive therapy (RR 1.77, 95% CI 1.22 to 2.57; 2 trials, 4272 women) and
require an antenatal hospital admission for hypertension (RR 1.54, 95% CI 1.00 to
2.39; 1 trial, 1877 women). However, for the latter two outcomes, this was not clearly
reflected in an increase in any other hypertensive complications.
  Evidence from this review does not support routine antioxidant
supplementation during pregnancy to reduce the risk of pre-eclampsia and
other serious complications in pregnancy
 Nitric oxide for preventing
pre-eclampsia and its
complications
• There are insufficient data for reliable conclusions about
the effects on pre-eclampsia (four trials, 170 women;
relative risk (RR) 0.83, 95% confidence interval (CI) 0.49
to 1.41) or its complications. One trial (36 women)
compared a nitric oxide donor with nifedipine, and
another (76 women) compared it with antiplatelet agents.
Both were too small for reliable conclusions about
possible differential effects.

 There is insufficient evidence to draw reliable

conclusions about whether nitric oxide donors and
precursors prevent pre-eclampsia or its
complications
 Antiplatelet agents for
preventing pre-eclampsia and
its complications
• There is a 17% reduction in the risk of pre-eclampsia associated with the
use of antiplatelet agents ((46 trials, 32,891 women, RR 0.83, 95% CI 0.77
to 0.89), number needed to treat (NNT) 72 (52, 119)). Although there is no
statistical difference in RR based on maternal risk, there is a significant
increase in the absolute risk reduction of pre-eclampsia for high risk (risk
difference (RD) -5.2% (-7.5, -2.9), NNT 19 (13, 34)) compared with
moderate risk women (RD -0.84 (-1.37, -0.3), NNT 119 (73, 333)).
• Antiplatelets were associated with an 8% reduction of preterm birth (29
trials, 31,151 women, RR 0.92, 95% CI 0.88 to 0.97); NNT 72 (52, 119)),
• a 14% reduction in fetal or neonatal deaths (40 trials, 33,098 women, RR
0.86, 95% CI 0.76 to 0.98); NNT 243 (131, 1,666)
• 10% reduction in small-for-gestational age babies (36 trials, 23,638 women,
RR 0.90, 95% CI0.83 to 0.98). There were no statistically significant
differences between treatment and control groups for any other outcomes.
 Antiplatelet agents, largely low-dose aspirin, have moderate benefits
when used for prevention of pre-eclampsia and its consequences.
Further information is required to assess which women are most likely
to benefit, when treatment is best started, and at what dose
 Calcium supplementation during
pregnancy for preventing
hypertensive disorders
• The average risk of high blood pressure was reduced with Ca supplementation rather
than placebo (12 trials, 15,470 women: RR 0.65, 95% CI 0.53 to 0.81).
• also a reduction in the average risk of pre-eclampsia associated with Ca
supplementation (13 trials, 15,730 women: RR 0.45, 95% CI 0.31 to 0.65). The effect
was greatest for high-risk women (5 trials, 587 women: RR 0.22, 95% CI 0.12 to
0.42), and those with low baseline calcium intake (8 trials, 10,678 women: RR 0.36,
95% CI 0.20 to 0.65).
• The average risk of preterm birth was reduced in the calcium group overall (11 trials,
15,275 women: RR 0.76, 95% CI 0.60 to 0.97) and amongst women at high risk of
developing pre-eclampsia recruited to four small trials (568 women: RR 0.45, 95% CI
0.24 to 0.83).
• There was no overall effect on the risk of stillbirth or death before discharge from
hospital (11 trials 15,665 babies; RR 0.90, 95% CI 0.74 to 1.09). The composite
outcome maternal death or serious morbidity was reduced (4 trials, 9732 women; RR
0.80, 95% CI 0.65 to 0.97). Most of the women in these trials were low risk and had a
low Ca diet. Maternal deaths were reported in only one trial. One death occurred in
the Ca group and six in the placebo group, a difference which was not statistically
significant (RR 0.17, 95% CI 0.02 to 1.39).
 Ca supplementation appears to approximately halve the risk of pre-eclampsia,
to reduce the risk of preterm birth and to reduce the rare occurrence of the
composite outcome 'death or serious morbidity'
 Rest during pregnancy for
preventing pre-eclampsia
• There was a statistically significant reduction in the relative risk
of pre-eclampsia with 4-6 h rest per day (1 trial, 32 women; RR
0.05, 95% CI 0.00 to 0.83), but not of gestational hypertension
(RR 0.25, 95% CI 0.03 to 2.00), compared to normal activity.
• Rest of 30 minutes per day plus nutritional supplementation was
associated with a reduction in the risk of pre-eclampsia (1 trial,
74 women; RR 0.13, 95% CI 0.03 to 0.51) and also of gestational
hypertension (RR 0.15, 95% CI 0.04 to 0.63). The effect on
caesarean section was unclear (RR 0.82, 95% CI 0.48 to 1.41)
  There is no information about outcomes such as perinatal
mortality and morbidity, maternal morbidity, women's views,
adverse effects, and costs. Current evidence is insufficient
to support recommending rest or reduced activity to women
for preventing pre-eclampsia and its complications
 Antithrombotic therapy for improving
maternal or infant health outcomes in
women considered at risk of placental
dysfunction
• 5 studies, involving 484 women. 4 studies compared heparin
(alone or in combination with dipyridamole) with no treatment;
and 1 compared trapidil (triazolopyrimidine).
• While there were no statistically significant differences
identified for the primary outcomes following heparin
treatment, it was associated with a reduction in the risk of pre-
eclampsia, eclampsia, and infant birthweight less than the
10th centile for gestational age.
 The review identified no significant differences for the
primary outcomes perinatal mortality, preterm birth less
than 34 weeks' gestation, and childhood
neurodevelopmental handicap, although the number of
studies and participants was small. Further research is
required.
 Progesterone for
preventing pre-eclampsia
• There was insufficient evidence to demonstrate any clear
differences between the two groups on the risk of pre-
eclampsia (1 trial, 128 women; RR 0.21, 95% CI 0.03-1.77),
• death of the baby (2 trials, 296 women; RR 0.72, 95% CI 0.21
to 2.51),
• preterm birth (1 trial, 168 women; RR 1.10, 95% CI 0.33-
• 3.66),
• small-for-gestational-age babies (one trial, 168 women; RR
0.83, 95% CI 0.19 to 3.57) or major congenital defects (one
trial, 168 women; RR 1.65, 95% CI 0.28 to 9.62)
 There is insufficient evidence for reliable conclusions
about the effects of progesterone for preventing pre-
eclampsia and its complications. Therefore, progesterone
should not be used for this purpose in clinical practice at
present
 Another ways to diminish the
risk of pre-eclampsia

• Altered dietary salt for preventing pre-eclampsia, and its complications

– Low salt intake in pregnancy is unlikely to prevent pre-eclampsia
• Plasma volume expansion for treatment of pre-eclampsia
– Not enough evidence to show the effects of plasma volume expansion for women
with pre-eclampsia
• Marine oil, and other prostaglandin precursor, supplementation
– Not enough evidence to say if fish oil supplementation in pregnancy helps reduce
the risk of pre-eclampsia and small-for-date babies
• Vitamin E and C supplementation in pregnancy
– Not enough evidence to determine if giving women vitamin E during pregnancy
helps prevent preeclampsia, their babies dying, being born small or too soon.
Preterm birth may have been increased with vitamin C supplementation
• Pyridoxine (vitamin B6) supplementation in pregnancy
– No evidence that routine supplementation with vitamin B6 during pregnancy is of
any benefit and it may cause harm if too much is taken (numbness, difficulty in
walking, less birthweight)
• Magnesium supplementation in pregnancy
– There is not enough high quality evidence to show that dietary magnesium
supplementation during pregnancy is beneficia
 Maternal and Fetal Complications in
Severe Preeclampsia
• Maternal • Fetal
– Abruptio placentae (1-4%) – Preterm delivery (15-67%)
– Disseminated – Fetal growth restriction
(10-25%)
coagulopathy/HELLP
syndrome (10-20%) – Hypoxia/neurologic injury
(<1%)
– Pulmonary edema/aspiration – Perinatal death (1-2%)
(2-5%)
– Long-term cardiovascular
– Acute renal failure (1-5%) morbidity associated with
– Eclampsia (<1%) low birth weight (fetal origin
– Liver failure or hemorrhage of adult disease)
(<1%)
– Stroke (rare)
– Death (rare)
– Long-term cardiovascular
morbidity
 Management of mild gestational
hypertension or preeclampsia
Mild gestational
hypertension or preeclampsia

Maternal and ≥34-37 weeks

fetal evaluation Bishop score ≥6
Labor/rupture of membranes
Abnormal fetal testing
Intrauterine growth restriction

YES
NO

Management
Maternal and fetal assesment Delivery
 Management
Maternal and fetal assesment
• Goals?
• Methods?
How should the woman be monitored?

• BP
– In unstabile woman - each 15’ until - then every 30’
– in stable and asymptomatic woman – every 4 hours
• at least daily (the results are normal)
– full blood count
– liver function
– renal function tests
• Clotting studies are not required if the platelet count
is over 100 x 106/l.
• Fluid balance with charting of input and output
– in the acute situation - hourly
How should the fetus be assessed?
• Cardiotocography
– continuous CTG – in women in labour with
severe pre-eclampsia
• Ultrasound (if conservative management is
planned)
– measurement of fetal size
– umbilical artery Doppler (The value of Doppler
in other fetal vessels has yet to be clarified)
– liquor volume
 Antihypertensive treatment
• in women with a SBP>160 mmHg or a DBP>110
mmHg
– In women with other markers of potentially severe disease,
can be considered at lower degrees
• LABETALOL (should be avoided in women with known asthma),
given orally or i/v, NIFEDIPINE given orally (not
sublingually) or HYDRALAZINE i/v can be used for the
acute management of severe hypertension,
METHYLDOPA

• Atenolol (FGR), angiotensin converting enzyme

(ACE) inhibitors, angiotensin receptor-blocking
drugs (ARB) and diuretics (reserved for pulmonary oedema)
should be avoided.
 Management of severe pre-eclampsia
Severe pre-eclampsia <34 weeks

1 Admit to labor/delivery area Maternal and fetal evaluation 24 hours

IV Magnesium sulfate Corticosteroids for lung maturity
Antihypertensives if BP, if SP≥160mmHg, DP ≥110mmHg, mean BP>125mmHg

2 Eclampsia Suspected abruptio placentae

Pulmonary edema Dissemenated coagulopathy Delivery before
Acute renal falure <23weeks gestation
Nonreassuring fetal status completion of steroids

HELLP-syndrome
Severe FGR or oligohydroamnios
Reversed bloodflow in UA Steroids
Persistent symptoms
Trombocitopenia
48h delay of labor is possible
Gestational age 33-34 weeks
Labor or membrane rupture

<23 weeks 6 days or >24weeks 0 days

Daily evaluation of mothers
3 Counseling
and fetal condition
4 Termination of pregnancy Delivery at 33-34 weeks
 How should seizures be prevented?
• MgSO4 should be considered for women with pre-eclampsia for
whom there is concern about the risk of eclampsia = usually in
the context of severe pre-eclampsia once a delivery decision
has been made and in the immediate postpartum period

• Women allocated MgSO4 had a 58% lower risk of an eclamptic

seizure, (95% CI 40–71%)

• If MgSO4 is given, it should be continued for 24 hours following

delivery or 24 hours after the last seizure, which ever is the later,
unless there is a clinical reason to continue
– 44% of eclampsia reported to occur postnatally

• Patient observation:
– urine output
– maternal reflexes
– respiratory rate
– oxygen saturation
 If seizure had occur
1. The principles of management should follow
the basic principles of airway, breathing and
circulation
a. to place the woman in the left lateral position
b. assess the airway, breathing and administer oxygen
c. check pulse and blood pressure
2. MgSO4 therapy
1. loading dose of 4 g by infusion pump over 5–10’
2. further infusion of 1 g/hour maintained for 24 h after
the last seizure
3. for recurrent seizures - further bolus of 2 g MgSO4
or an increase in the infusion rate to 1.5- 2.0 g/hour
 Magnesium sulphate
compared with diazepam
• Magnesium sulphate was associated with a reduction in
maternal death (seven trials;1396 women; risk ratio (RR)
0.59, 95% confidence interval (CI) 0.38 to 0.92) and
recurrence of seizures (seven trials;1390 women; RR
0.43, 95% CI 0.33 to 0.55) compared to diazepam
• There were no clear differences in other measures of
maternal morbidity.
• There was no clear difference in perinatal mortality (four
trials; 788 infants; RR 1.04, 95% CI 0.81 to 1.34) or
neonatal mortality (four trials; 759 infants; RR 1.18, 95%
CI 0.75 to 1.84)
 Magnesium sulphate for women with eclampsia
reduces the risk ratio of maternal death and of
recurrence of seizures, compared with diazepam
 Magnesium sulphate
compared with phenytoin
• Magnesium sulphate was associated with a substantial reduction in
the recurrence of seizures, when compared to phenytoin (6 trials,
972 women; RR 0.34, 95% CI 0.24 to 0.49)
• There were reductions in the risk of pneumonia (one trial, RR 0.44,
95% CI 0.24 to 0.79), ventilation (one trial, RR 0.68, 95% CI 0.50 to
0.91) and admission to an intensive care unit (one trial, RR 0.67,
95% CI 0.50 to 0.89) associated with the use of magnesium
sulphate rather than phenytoin.
• For the baby, magnesium sulphate was associated with fewer
admissions to a special care baby unit (SCBU) (one trial, 518
babies; RR 0.73, 95% CI 0.58 to 0.91) and fewer babies who died or
were in SCBU for more than seven days (one trial, 643 babies; RR
0.77, 95% CI 0.63 to 0.95)
• There was no clear difference in perinatal deaths (two trials, 665
babies; (RR 0.85, 95% CI 0.67 to 1.09).
  Magnesium sulphate is the drug of choice for women with
eclampsia. The use of phenytoin should be abandoned
 Magnesium sulphate versus
lytic cocktail for eclampsia
• lytic cocktail = usually chlorpromazine, promethazine and pethidine
• Magnesium sulphate was associated with fewer maternal deaths
(RR 0.14, 95% CI 0.03 to 0.59; 3 trials, 397 women) and was better
at preventing further seizures (RR 0.06, 95% CI 0.03 to 0.12; 3
trials, 397 women) than lytic cocktail.
• Magnesium sulphate was also associated with less respiratory
depression (RR 0.12, 95% CI 0.02 to 0.91; 2 trials, 198 women),
less coma (RR 0.04, 95% CI 0.00 to 0.74; 1 trial, 108 women), and
less pneumonia (RR 0.20, 95% CI 0.06-0.67; 2 trials, 307 women)
• There was no clear difference in the RR for any death of the baby
(RR 0.35, 95% CI 0.05 to 2.38, random effects; 2 trials, 177 babies)
 Magnesium sulphate, rather than lytic cocktail, for women with
eclampsia reduces the RR of maternal death, of further
seizures and of serious maternal morbidity (respiratory
depression, coma, pneumonia). Magnesium sulphate is the
anticonvulsant of choice for women with eclampsia; the use of
lytic cocktail should be abandoned
 Complex treatment
• Antihypertensive treatment
• Fluid balance management
– In usual circumstances, total fluids should be limited to 80
ml/hour or 1 ml/kg/hour
• Pregnancy termination
– If the gestation is greater than 34 weeks, delivery after
stabilisation is recommended
– If less than 34 weeks and the pregnancy can be prolonged in
excess of 24 hours - steroids reduce fetal respiratory mortality
– Prolonging the pregnancy at very early gestations may improve
the outcome for the premature infant but can only be considered
if the mother remains stable (mean of 7-15 days with no increase in
maternal complications)
– Vaginal delivery is generally preferable after 34 weeks with a
cephalic presentation (vaginal prostaglandins for induction)
– for gestation <32 weeks, caesarean section is more likely
 How should the woman be
managed following delivery?
• Clinicians should be aware of the risk of late
seizures and ensure that women have a careful
review before discharge from hospital
– 44% of eclampsia occurs postpartum
– eclampsia has been reported up to 4 weeks
postnatally
– most women will need inpatient care at least 4 days
following delivery
– before discharge careful review to ensure improving
clinical signs is needed
• Anti-hypertensive medication should be continued
after delivery as dictated by the BP
– It may be necessary to maintain treatment for up to 3
months
 Follow-up and final diagnosis
• 6 weeks postnatal by the general practitioner
– BP
– proteinuria
• If hypertension or proteinuria persists then
further investigation is recommended
– may have renal disease
• 13% of women with pre-eclampsia will have
underlying chronic or essential hypertension that
was not suspected antenatally
 Clinical examination question 2
Patient a 26-year-old woman was admitted to pathological pregnancy
department been primigravida at 34 weeks’ gestation. In her history
chronic tonsillitis, scarlet fever were presented. Also prior to
pregnancy she had had periodical headaches, face edema,
according to this problem she had never been examined. At present
she is not complaining. At clinical examination – widespread edema
of extremities, abdominal wall, face; BP 150/100 and 160/110
mmHg, fundus high 30cm, abdominal circumference 90 cm; uterus
in normal tone, painless. Fetus lie is longitudinal, above the pelvic
inlet is palpated softened and of irregular shape large part of fetus
body. Fetal heart rate is at umbilicus level, 144 beats per min, clear.

1. What is the most likely diagnosis?

2. What information from the patient’s history need to be checked?
3. Make the plane of patient’s investigation
4. Outline the management of this woman
5. Give the prognosis for mother and fetus
 Clinical examination question 3
Mrs. М. is a 28-year-old woman. Now she is pregnant for 3rd time and
at 31-32 weeks’ gestation. She reported about one ectopic and one
preterm pregnancy at 31 week, when she had emergency C-section
because of severe pre-eclampsia. Her daughter with a birthweight of
1200g died on the 5 day after birth.
At presentation she has BP 170/100 mmHg. Urine dipstick shows no
proteinuria. Fetus is in breech presentation, it’s heart rate is 150
beats/min. During last week she was treated for pre-eclampsia in
pathological pregnancy department. Under the monitoring her BP
was from130/90 to 150/100 mmHg. Proteinuria less or above 1 g/l.
Abnormal fetal testing on cardiotocography.

1. Make the working diagnosis and proove it

2. What information from the patient’s history need to be checked?
3. Make the plane of patient’s investigation
4. Outline the management of this woman
5. If the termination of pregnancy is needed, what method will be
appropriate?
6. Give the prognosis for mother and fetus
 Clinical examination question 4
A 22-year-old patient is admitted from home complaining of headache.
She is in her first pregnancy of 39-40 weeks. Clinical examination
reveals atypical edema, BP 170/110 and 180/ 115 mmHg. Fetus
head is engaged, labor activity is absent. Fetal heart rate is 140
beats/min. During vaginal examination she has a seizure.

1. Make the working diagnosis and proove it.

2. What clinical conditions (diagnosis) need to be assumed when
pregnant have convulsions?
3. What emergency care need to be provided?
4. Make the plane of patient’s investigation
5. Outline the management of this woman
6. If the termination of pregnancy is needed, what method will be
appropriate?
7. Give the prognosis for mother and fetus
 Clinical examination question 5
A 17-year-old pregnant patient is admitted from home with the history
of a painfull contractions, headache, visual disturbances, nausea
and one-time vomiting. BP is 160/120 and 170/110 mmHg. Edema
is seen in lower extremities. Uterine contractions’ frequency is 4 per
10 min, of a proper force, above 50” of their duration. Fetus head is
in the pelvic inlet plane by it’s large segment. FHR 124 beats/min.
Vaginal examination, performed under the i/v anesthesia, revealed
cervical enlargement of 7-8 cm, fetal membranes intact, fetus head
in the pelvic inlet plane in ROA position. Promontorium is
unreachable, exostoses are absent.

1. Make the diagnosis and proove it.

2. What emergency care need to be provided?
3. Make the plane of patient’s investigation, what results are most
likely?
4. Outline the management of this woman
5. Outline the follow-up of this patient
6. Give the prognosis for mother and fetus
 Clinical examination question 6
Multiparous 32-years-old patient being admitted from home is
complaining of need to push, headache, visual disturbances,
epigastric pain, nausea. BP =190/120 and 170/110 mmHg. Patients’
face and cruses are edematic. Uterine contractions are frequent,
strong, patient is pushing. Fetus head is inside the pelvic cavity,
FHR 100 beats per min. Vaginal examination, performed under the
i/v anesthesia, revealed full cervical enlargement, fetal membranes
ruptured, fetus head in the pelvic outlet plane. Sagital suture in
anterior-posterior diameter, small fontanelle under symphysis pubis.

1. What is the patient’s diagnosis? Proove it.

2. What emergency care need to be provided?
3. Make the plane of patient’s investigation, what results are most
likely?
4. Outline the management of this woman
5. Outline the follow-up of this patient
6. Give the prognosis for mother and fetus
 Clinical examination question 7
A 19-year-old patient in her first pregnancy at 37-38 weeks’ gestation
presents to delivery suite. She has no past medical history of note.
Her pelvic sizes: 26-29-32-21cm. Abdominal circumference –
100cm, fundus high – 36cm. Uterine contractions are 40-45”, strong,
regular, frequency 4 per 10min. Fetus lie longitudinal, it’s head
inside the pelvic cavity. FHR 128 bpm, above pubis. BP 130/ 100 -
140/110 mmHg. Patients’ face and cruses are edematic. During
pushing she has seizure.

1. What is the patient’s diagnosis? Proove it.

2. What emergency care need to be provided?
3. What complications may appear in time and after the seizure?
4. Outline the management of this woman
5. Outline the follow-up of this patient
6. Give the prognosis for mother and fetus
 Clinical examination question 8
A 32-year-old woman in her first pregnancy at 32 weeks’ gestation is
examining by an obstetrician in outpatient clinic. She reports about
chronic hypertension in her history, BP during pregnancy 130/80 –
135/90 mmHg. At present she is complaining of decrease in fetal
physical activity. BP 150/100 and 160/110 mmHg. Patient’s face
and cruses are edematic. Her weight gain1,5kg per 2 weeks. Urine
dipstic shows 3+ proteinuria.

1. What is the patient’s diagnosis? Proove it.

2. What methods may be applied to evaluate fetal physical activity?
3. Give the prognosis for mother and fetus
4. Outline the management of this woman
5. Make the plane of patient’s investigation, what results are most
likely?
 Clinical examination question 9
A 20-year-old primigravida presents in clinic at 36-37 weeks gestation.
She was referred by community midwife. She is not complaining by
herself. Cruses edema is significant. BP 150/90 and 140/ 90 mmHg.
Urine dipstic shows 3+ proteinuria. Uterus is of a normal tone, but
contracts on palpation. Fetus head is engaged, FHR 132 bpm.
Patient’s pelvic sizes: 25-28-29-20 cm.

1. What is the most likely diagnosis? Proove it.

2. What information in patient’s history need to be checked?
3. Make the plane of patient’s investigation.
4. Outline the management of this woman
5. Outline the plane of vaginal delivery
6. Give the prognosis for mother and fetus
Clinical examination question 10
23-year-old primigravida is presented in clinic. Now she is at 36 weeks’
gestation. She reports about preexisting chronic pyelonephritis.
According to individual chart of pregnant - she was booked at 8
weeks gestation, but last 6 weeks she had pathological weight gain,
cruses edema, hypertension. At present patient is not complaining
by herself. BP is 160/100 and 150/100 mmHg. Significant edema is
seen in the face, hands, cruses, abdominal wall. An ultrasound scan
revealed fetus sizes corresponding 33 weeks’ gestation. Proteinuria
2g/l.

1. What is the patient’s diagnosis? Proove it.

2. Make the plane of patient’s investigation. What results do you
suspect?
3. Give the prognosis for mother and fetus
4. Outline the management of this woman
5. Discuss the possible methods of the pregnancy termination