HYPERTENSIVE DISORDERS IN PREGNANCY

By: Dr Biruktawit .H

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 0UTLINE
• Introduction
• Incidence
• Classification
• Risk Factors
• Etiopathogenesis
• Investigation
• Management

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 Introduction
• Pregnancy related hypertension is defined as a
systolic blood pressure >140 mm Hg or
diastolic blood pressure >90 mm Hg in two
occasions at least 6 hours apart, but not more
than 7 days; or a single BLOOD PRESSURE
recording of 160/110 mm Hg in a woman
who was normotensive prior to 20 weeks of
gestation.

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 Incidence
• Hypertensive disorders complicate 5 to 10
percent of all pregnancies.
• They are one member of the deadly triad of
obstetrics along with hemorrhage and
infection.

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 Classification

• The basic classification was retained, as it

describes four types of hypertensive disease:
1. Gestational hypertension
2. Preeclampsia and eclampsia syndrome
3. Chronic hypertension of any etiology
4. Preeclampsia superimposed on chronic
hypertension

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 Gestational Hypertension
• BP 140/90mmHg or more for the first time in
pregnancy, onset after 20weeks of gestation.
• No proteinuria
• BP returns to normal <12weeks postpartum
 

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 Chronic hypertension
• Hypertension with onset before pregnancy or
before 20th week gestation   
• Use of antihypertensive medications before
pregnancy   
• Persistence of hypertension beyond 12 weeks
postpartum

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 Preeclampsia
• Hypertension
–1. Blood pressure ≥ 140/90mmHg
• Measured on two consecutive occasions 6 hrs or more apart, but not more than7 days.
OR
–2. Single blood pressure measurement ≥ 160/110mmHg in women who was
normotensive prior to 20weeks of gestation.
Proteinuria
–Qualitative
• 2+ protein on reagent strip or
• +1 on dipstick if sp.gravity <1.03
–Quantitative
• 24 hrs urine protein ≥ 300mg
• Two random urine protein concentration of 100mg/dl collected 4hrs or more apart
[Edema (especially non-dependent)]
–No longer considered a required component

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• pregnancy-specific syndrome that can affect virtually
every organ system.
• proteinuria is an objective marker and reflects the
system-wide endothelial leak, which characterizes
the preeclampsia syndrome

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 Severity signs of Preeclampsia

• Any one of the following:

– Blood pressure sustained above 160/110
– Headache/visual disturbances
– Epigastric pain/RUQ pain
– HELLP syndrome
Deranged LFT
Thrombocytopenia
Hemolysis
– Pulmonary edema
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 Eclampsia
• Seizure activity in preeclamptic women that is
unrelated to other central nervous system
disorders (epilepsy, meningitis, mass lesion,
intracranial hemorrhage), with or without
resultant coma.
• The majority of eclampsia occurs intra partum
(50%) with the remainder equally occuring in
the ante partum and post partum periods.

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 4. Superimposed preeclampsia
• If new-onset or worsening baseline hypertension is
accompanied by new-onset proteinuria or other
one of the severity sign then superimposed
preeclampsia is diagnosed.
• It also tends to be more severe and often is
accompanied by fetal-growth restriction

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 Risk Factors
• Nulliparity
• Previous pregnancy with preeclampsia
• Family history of preeclampsia
• Chronic hypertension
• Diabetes mellitus
• primipaternity
• Obesity
• Rh-issoimmunization
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 Risk Factors
• Renal disease
• Connective tissue diseases
• Multiple gestation
• Hydatidiform mole
• Certain fetal anomalies (triploidy)
• Age <18yr OR >35yr
• Black race
• Low socioeconomic status
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• The etiology of preeclampsia is not known;but
suggestive theory
1. Placental implantation with abnormal trophoblastic
invasion of uterine vessels
2. Immunological maladaptive tolerance between
maternal, paternal (placental), and fetal tissues
3. Maternal maladaptation to cardiovascular or
inflammatory changes of normal pregnancy
4. Genetic factors including inherited predisposing genes
and epigenetic influences.
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• The etiology of preeclampsia is not known;
however, a growing body of evidence suggests
that maternal vascular endothelial injury plays
a central role in the disorder.
• Some reports suggest that endothelial damage
in preeclampsia results in decreased
endothelial production of prostaglandin I2
(prostacyclin), a potent vasodilator and
inhibitor of platelet aggregation.
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 Pathophysiology

Brain
• Pathologic findings in preeclampsia-induced
cerebral injury include fibrinoid necrosis,
thrombosis, microinfarcts, and petechial
hemorrhages, primarily in the cerebral cortex.
• Cerebral edema may be observed.
• Subarachnoid or intraventricular hemorrhage
may occur in severe cases.
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 Lungs

• noncardiogenic pulmonary edema.

• In eclampsia, pulmonary injury may result
from aspiration of gastric contents, leading to
pneumonia, pneumonitis, or adult
respiratory distress syndrome.

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 Liver

• In severe cases involving hepatocellular necrosis

and DIC, intrahepatic hematomas may progress
to liver rupture.
• Right upper quadrant pain or epigastric pain
are classic symptoms attributed to stretching of
Glisson's capsule.
• Elevation of serum transaminases is a hallmark
of HELLP (hemolysis, elevated liver enzymes,
and low platelets) syndrome.
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 Kidneys

• The classic renal lesion of preeclampsia,

"glomeruloendotheliosis," is characterized by
swelling and enlargement of glomerular
capillary endothelial cells, leading to
narrowing of the capillary lumen.

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 COMPLICATIONS
FETAL:
• IUGR.
• Oligohydramnios.
• Placental abruption.
• prematurity.
• NRFHRP due to utero-placental insufficiency.
• Increased perinatal morbidity & mortality.

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MATERNAL:
• seizures
• DIC
• Pulmonary edema
• Acute kidney injury
• Hepatic failure or rupture
• Maternal mortality

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 Investigations

– Base line
• Blood group
• CBC
• U/A
• RFT, LFT,
• Obstetric U/S

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 MANAGEMENT
• The decision to proceed with immediate
delivery versus expectant management is
based upon several factors, including
disease severity
fetal maturity
maternal and fetal condition
cervical status

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 Gestational Hypertension
Manage on outpatient basis (especially if at
<36wks)
• Follow BLOOD PRESSURE, U/A & fetal
condition weekly
• Counsel the woman & her family about
danger signals indicating sever preeclampsia
or eclampsia.

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 Management of Pre-eclampsia with severity feature

1 General measures - supporting the specific

treatments
2 Prevent convulsion with magnesium sulfate
3 Control hypertension
4 Delivery as soon as possible

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1) General Measures
• Admit the patient urgently
• Manage in left lateral position (relieves
pressure on inferior vena cava)
• Prepare equipment for convulsion
management, at bedside (mouthpiece, airway,
suction equipment, mask & bag, oxygen)

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• Never leave the patient alone (if convulsion
occurs, aspiration may cause death)
• Observe vital signs, FHB & reflexes hourly
• Anti pain - for RUQ pain, headache etc

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3) Anticonvulsant therapy (seizure prophylaxis)
• Seizure prophylaxis should be instituted
• In all pre-eclamptics during labor &
continued for 12-24 hrs after delivery
• In all severe pre-eclamptics during
admission & continued during period of
evaluation & observation.
• Magnesium sulfate is the drug of choice
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Diazepam
• May be used as alternative, if mgs04 is not available,
although there is a greater risk for neonatal respiratory
depression because diazepam passes the placenta freely.

• NB It is difficult to predict who will seize.

• It is not directly related to degree of hypertension or
level of proteinuria (Blood pressure is not a reliable
predictor of the risk of seizures, some may seize with
blood pressure of 140/90)
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4) Anti -hypertensive therapy
• Anti - hypertensive drugs should be used if the
DBLOOD PRESSURE remains at ≥ 110 mmhg
• The goal is to keep the diastolic blood
pressure 90-100 mm hg in labor.
• Hydralazine, Nifedipine, Methayl dopa

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 ECLAMPSIA

1. General measures
2. Control of convulsions (to stop ongoing convulsion &
prevent repeated convulsion)
3. Correction of hypoxia & acidosis -by clearing airway &
giving O2by mask at 6L/min
4. Blood pressure control & stabilization of the condition
of the mother & fetus
5. Fluid balance & diuresis
6. Delivery & intra partum/post partum care
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i) Anticonvulsant Therapy
• Administer anticonvulsant drugs to stop the
ongoing convulsion & prevent repeated
attacks
• Be aggressive & avoid under treatment, to be
successful
• Magnesium sulphate is the drug of choice in
eclampsia

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 Magnesium sulfate schedules for severe pre-
eclampsia and eclampsia

Loading dose
• Magnesium sulfate 20% solution, 4 g IV over 5 minutes.
• Follow promptly with 10 g of 50% magnesium sulfate solution, 5 g in each
buttock as deep IM injection with 1 mL of 2% lignocaine in the same syringe.
• If convulsions recur after 15 minutes, give 2 g magnesium sulfate
(50%solution) IV over 5 minutes.
Maintenance dose
• 5 g magnesium sulfate (50% solution) + 1 mL lignocaine 2% IM every 4 hours
into alternate buttocks.
• Continue treatment with magnesium sulfate for 24 hours after delivery or
the last convulsion, whichever occurs last.

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Withhold or delay drug if:
• Respiratory rate falls below 16 per minute.
• Patellar reflexes are absent.
• Urinary output falls below 30 mLper hour over
preceding 4 hours.
Keep antidote ready :
• Give calcium gluconate 1 g (10 mL of 10%solution)
IV slowly until respiration begins to antagonize the
effects of magnesium sulfate.
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• Delivery remains the only definitive treatment
for PIH
• Timely delivery minimizes maternal &
neonatal morbidity & mortality

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Indications for delivery
1.Pregnancy at > 37wks GA.
2. Gestation >34 wks GA, with severe pre-
eclampsia
3. Severe pre-eclampsia remote from term «28
or 30 wks GA)

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Route of delivery
• Vaginal delivery is preferable to cesarean
section for women with PE (even if with sever
disease).

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Cesarean delivery is indicated
• If the cervix is unfavorable (firm, thick, closed) esp.
in seriously ill
patients
• With poor progress of labor
• If patient has not entered active labor within 8hrs
of induction of labor
• If there is evidence of fetal distress, or there
obstetric indications
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Atypical Eclampsia:
• Is occurrence of convulsions before 20th week
of gestation OR 48hrs after delivery.
• Management is similar to ecclampsia!!!

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Thank you

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