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⢠Hypertensive disease in pregnancy is a major
cause of maternal and fetal morbidity and
mortality.
⢠Pregnancy-related hypertension is divided into
3 categories:-
ďą Pregnancy-induced hypertension:
⢠Hypertension that develops as a consequence
of pregnancy, and regresses postpartum
1) Hypertension without proteinuria or
pathological edemaâtransient hypertension
2) Normotensive, pregnant patients who have
sustained hypertension, proteinuria, and
edema after the 20th week of gestation, with
preeclampsia (Mild, Severe).
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3) Eclampsia (= Preeclampsia along with
convulsions or fits)
ďą chronic hypertension begins prior to
pregnancy.
⢠A BP greater than 140 mm Hg/90 mm Hg
occurs prior to the 20th week of gestation, is
not associated with significant proteinuria or
end-organ damage, and continues well after
delivery.
ďą Pregnancy-aggravated hypertension:
⢠Underlying hypertension worsened by
pregnancy
⢠The category consists of patients with chronic
hypertension with superimposed
preeclampsia/Eclampsia.
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Causes
⢠Despite extensive research, no definitive
cause has been identified.
⢠Theories about causes!!:
ď Immunological causes ďinadequate/poor
invasion of trophoblasts to spiral arteries
ď Genetic causes
ď Dietary deficiencies ď FA deficiency
ď âHormonalâ or Endothelial dysfunction in
which there is imbalance production of
vasodilator & vasoconstrictor substances by
the endothelia (Toxaemia, Endothelins,
Endothelium-derived relaxing factor, Nitric
oxide, Prostaglandines)
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Risk factors:
⢠Nulliparity
⢠Multiple pregnancy
⢠Underlying chronic hypertension of any type
⢠Age; young < 20 yrs and older > 35 years
(have 4 times)
⢠Chronic disease of the kidneys with
impairment of renal function
⢠Ethnicity
⢠Socioeconomic status
⢠Poor prenatal care
⢠Strong family history of
preeclampsia/eclampsia
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⢠Obstetric conditions associated with an
abundance of chorionic villi (eg, twin
gestations, molar pregnancies, triploidy,
nonimmune hydrops fetalis)
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Pathophysiology
⢠The cause of preeclampsia/eclampsia remains
unknown
⢠Many investigators have proposed genetic,
immunologic, endocrinologic, nutritional, and
even infectious agents as the cause for
preeclampsia/eclampsia
⢠Presumably, the placenta and fetal
membranes play a role in the development of
preeclampsia because of the prompt
resolution of the disease following delivery
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⢠Uteroplacental ischemia is postulated to
predispose to the production and release
of biochemical mediators that enter the
maternal circulation, causing widespread
endothelial dysfunction and generalized
arteriolar constriction and vasospasm
⢠Females with pregnancy-induced
hypertension have been noted to have an
increased responsiveness to a variety of
endogenous substances (prostaglandins,
thromboxane) that can cause vasospasm
and platelet aggregation.
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Early in pregnancy
⢠Note: site of action: placenta!
⢠Impairment of âplacentationâ â spiral
arteries retain their ability to contract â
local vasospasm â local hypoxia â local
intravascular imbalance between
vasoconstrictory and vasodilatatory
Prostaglandines
⢠Generalized intravascular effects of
angiotensin II â Failure in drop of blood
pressure during second trimester of
pregnancy and increased pressor
response, damage of the vessel walls
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Any time between week 20 and 40 of
pregnancy
⢠Note: systemic disease!
⢠Generalized vasospasm â> hypertension
⢠Generalized leakage of intravascular fluid and
molecules (i.e. proteins) to the extravascular
tissue â> proteinuria and generalized edema
⢠Decrease in the volume of intrvascular fluid â>
impairment of renal function â oliguria
⢠Imbalance of intravascular Prostaglandines and
clotting factorsâ> disseminated intravascular
coagulation (DIC)
⢠Spasms of spiral arteries â> fetal growth
retardation
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Clinical features of preeclampsia/eclampsia
Major symptoms: Hypertension, Proteinuria,
Generalized Edema âpreeclampsia
⢠Preeclampsia + convulsions/fitsâeclampsia
Other features:
⢠Headache
⢠RUQ abdominal pain
⢠Decreased urine output
⢠Shortness of breath or dyspnea on exertion
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⢠Hand and facial edema
⢠Visual disturbances
⢠Confusion and apprehension
⢠Nausea and vomiting
Physical: Findings
⢠Sustained systolic BP increases by 30 mm Hg,
and diastolic BP increases by 15 mm Hg, or
absolute BP higher than 140 mm Hg/90 mm Hg.
⢠Severe preeclampsia (sustained systolic BP
>160 mm Hg or diastolic BP >110 mm Hg with
end-organ damage)
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Variability of symptoms:
⢠Degree of hypertension
⢠Degree of proteinuria
⢠Risk of DIC secondary to intravascular
hypovolaemia
⢠Risk of eclampsia
⢠Edema
⢠Involvement of the liver (= HELLP
Syndrome)
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Dynamics of the disease:
⢠Onset of symptoms early or late in
pregnancy
⢠Progress of disease rapid or slow
⢠General condition severely impaired or
fair
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Lab Studies
No single laboratory test or set of laboratory
determinations is useful in predicting maternal or
neonatal outcome in women with eclampsia
Laboratory studies that should be ordered include
the following:
⢠Complete blood cell count-Anemia due to the
microangiopathic hemolytic anemia
⢠Platelet count-Thrombocytopenia due to HELLP
syndrome
⢠Twenty-fourâhour urine for protein/creatinine-elevated
due to decreased intravascular volume and GFR.
⢠Electrolytes
⢠Liver function tests (ie, lactate dehydrogenase [LDH],
aspartate aminotransferase [AST])
⢠Uric acid
⢠Serum glucose
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⢠The most common hematologic abnormality in
obstetric disorders is thrombocytopenia,
occurring in 17% of patients with eclampsia.
⢠DIC appears to be uncommon in patients with
eclampsia.
Imaging Studies
⢠CT scan of the head in patients (1) who have
been involved in a trauma, (2) who are
refractory to magnesium sulfate therapy, and
(3) who have atypical presentations (such as
seizures >24 h after delivery).
⢠MRI
1. Angiography-The principle finding observed
with eclampsia on angiography is widespread
arterial vasoconstriction of the intracranial
vessels.
⢠Transabdominal sonogram
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Treatment of Preeclampsia
⢠To monitor the condition of the patient and
the fetus is perhaps more important than the
âtreatmentâ.
ďśMild PE:
⢠No drug treatment necessary
⢠Can even stay at home,
⢠Make then sure that progress of disease is
discovered by outpatient monitoring
⢠Maternal and fetal monitoring (viability, growth,
maturity)
⢠Delivery should be aimed vaginally at GA 38wks
unless other factors necessitates C/S
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ďśSevere PE:
⢠Immediate hospital admission
⢠Bed rest
⢠Antihypertensives (hydralazine)
⢠Sedatives and /or magnesium sulfate
⢠Careful monitoring of the maternal and
fetusďlung maturity enhancement
(betamethasone GA < 34wks 12 mg bd/24hrs b4
delivery OR Dexamethasone 6mg bd)
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Treatment of Eclampsia
⢠AâBâC
⢠Control convulsions (anticonvulsants,
sedatives, magnesium sulfate)
⢠Control blood pressure (hydralazine)
⢠Deliver after control of convulsions and
blood pressure
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ďąControl of convulsion:
⢠MgSO4 4g in 20ml NS as bolus i/v statâ10-
20min; then 4g in 1L RL/NS as maintenance
⢠If seizure occurs in first 20 min after loading
dose, the convulsion usually is short, and no
additional treatment is indicated. If seizure
occurs >20 min after the loading dose, an
additional 2g i/v in 10ml NS bolus (2-5min) in
each attack of the convulsion is indicated.
⢠Diazepam, if necessary
ďąHypertension control:
⢠Hydrallazine (40mg in 500ml 5%D 8hrly till dBP
90-100 mm Hg)âOnset of action 15 min; peak effect 30-60
min; duration of action 4-6 h .
⢠Ca2+ channel blockers
⢠Methyldopa
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o Note:
⢠Calcium gluconate 1 g IV may be
administered slowly for evidence of
magnesium toxicity
⢠Uterine hypoperfusion may result if blood
pressure is lowered too quickly
⢠Uterine vasculature always is maximally
vasodilated, and a decrease in maternal
blood pressure tends to decrease
uteroplacental perfusion.
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Further Inpatient Care:
⢠Blood pressure, neurologic status, and
urine output should be monitored closely
Further Outpatient Care
ďˇ Patients with eclampsia should be
followed up postpartum to evaluate for
evidence of essential hypertension,
residual deficits from the eclamptic
seizure, and patient education.
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Systemic derangements in
eclampsia include the following:
Cardiovascular
â Generalized vasospasm
â Increased peripheral vascular resistance
â Increased left ventricular stroke work index
â Decreased central venous pressure
â Decreased pulmonary wedge pressure
Hematologic
â Decreased plasma volume
â Increased blood viscosity
â Hemoconcentration
â Coagulopathy
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⢠HELLP is the medical term for one of the
most serious complications of pre-
eclampsia, in which there is a combined
liver and blood clotting disorder.
⢠H stands for Haemolysis (rupture of the
red blood cells, microangiopathy);
⢠EL stands for Elevated Liver enzymes in
the blood (reflecting liver
damage/necrosis);
⢠LP stands for Low blood levels of
Platelets; vital for normal clotting (due to
DIC).
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⢠HELLP is as dangerous as eclampsia
(convulsions) and probably more common,
although it is less easy to diagnose.
⢠HELLP syndrome may be preceded by clear
signs of pre-eclampsia - most typically high
blood pressure, protein in the urine and swelling
of hands, feet or face
⢠But, like eclampsia, it can also arise out of the
blue without any of the classic warning signs
⢠The typical presenting symptom is 'epigastric
pain', sometimes accompanied by vomiting and
headaches.
⢠This pain is sometimes confused with the
discomfort of heartburn, a very common problem
during pregnancy
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⢠But, the pain of HELLP syndrome is not burning,
does not spread upwards towards the throat and
is not relieved by antacid.
⢠The pain is often very severe and is associated
with tenderness over the liver
When does it occur?
⢠As with eclampsia, HELLP syndrome is most
likely to occur immediately after delivery -
sometimes developing with devastating speed.
However, it can arise at any stage during the
second half of pregnancy - and some rare cases
have been recorded even earlier.
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What are the risks?
HELLP syndrome may be associated with one or
more of the following problems:
⢠severely disturbed blood clotting function,
leading to heavy, uncontrollable bleeding,
particularly after surgery;
⢠severe liver damage, which can lead to failure or
even rupture of this vital organ;
⢠severe kidney problems, including kidney failure;
⢠breathing difficulties, which may be severe
enough for the mother to need artificial
ventilation.
⢠stroke (cerebral haemorrhage) with or without
eclampsia (convulsions).
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How is it treated
⢠All treatment is aimed at supporting the
mother's systems which have failed (liver,
kidney, lungs, clotting) until such time as they
have recovered enough to cope on their own.
⢠Once the syndrome is diagnosed the baby
should be delivered as soon as the
mother's condition is stable, regardless of
the maturity of the baby, since delivery is the
only cure for this life-threatening
condition.
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How is the baby affected?
⢠HELLP is a maternal problem which has
no specific effects on the unborn baby
⢠However, as with all cases of severe pre-
eclampsia, the baby may suffer growth
retardation and even distress as a result of
the underlying causeâ a shortage of
maternal blood flow to the placenta. But in
most cases of HELLP delivery is for the
mother's benefit, sometimes with tragic
results for babies who are too premature
to survive outside the womb.
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What happens in the next pregnancy
⢠About 1 sufferer in every 20 will suffer a
recurrence of HELLP in her next pregnancy
⢠However, there is no way of predicting who is
most likely to suffer a recurrence
⢠For optimum safety, any woman who has
suffered HELLP in one pregnancy should be
considered 'at risk' in the next pregnancy and
monitored carefully throughout.
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⢠No specific means of prevention, although
treatment with low-dose aspirin may be
recommended in cases where the
syndrome developed relatively early in
pregnancy - i.e. before 32 weeks.