Transcript hypertension in pregnancy

HYPERTENSION IN
PREGNANCY
ESAM ALSABARY
DEFINITION
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Systolic blood pressure greater than
or equal to 140 mmHg,
OR a diastolic BP greater than or
equal to 90 mmHg in two occasions
4/24 apart.
OR one diastolic reading greater than
110 mmHg.
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Incidence: 3-10%
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Incidence of eclampsia: 1/2000
Classification of HT in
pregnancy:
1- Preeclampsia (PE) formerly known
PIH: Raised BP after 20/40, with PTN
urea, which may associate with:
A- HELLP.
B- Neuro complication like: headache, visual
disturbances & hyperreflexia.
C- Sever epigastric pain and or R.
hypochondrial pain.
D- Renal insufficiency.
2- Gestational Hypertension:
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Increase in BP to greater or equal
to 140/90 mmHg after 20/40.
It resolves within 3/12 post partum.
No protein urea.
No neurological symptoms.
No biochemical changes.
May progress to PE if started
< 30/40
3- Chronic HT
( Primary & Secondary ):
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A BP more than or equal to 140/90
mmHg,
Either before the pregnancy or
before 20/40 & does not associate
with any additional feature of PE &
persist longer than 12 weeks post
partum.
4- Superimposed PE on Chronic
Hypertension
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New onset of PTN urea with HT.
Labile BP in spite of antihypertensive
medications.
May be complicated by HELLP.
New onset of headache, epigastric pain & visual
disturbances.
Note: The prognosis is worse than either of
the conditions alone
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Aetiology & Pathogenesis of PE
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Not very clear HOWEVER
? It is a disease of the placenta.
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Immunological Factors may paly a role.
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Genetic Factors. ex Primigravid women with a family history
of preeclampsia (eg, affected mother or sister) have a two
to five fold higher risk of the disease than primigravid
women with no such history
It does not require a foetus ( it occurs with hydatidiform
mole ).
It develops with abdominal pregnancy
( uterus not required ).
Events in the Placenta
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IMPAIRED TROPHOBLAST INVASION
In normal pregnancy: the cytotrophoblast
invades the endothelium and highly
muscular layer of the maternal spiral
arteries transformation from small
muscular arterioles to large capacitance
This allows
increased blood flow (oxygen,
nutrients) to the fetus.
vessels of low resistance 
Placenta: two lesions may occur
1- Deficient placentation.
2- Acute atherosis.
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Both explain the cause of IUGR in a
PE mother.
Immunological Factors
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Exposure to paternal/fetal antigens appears to
protect against PE.
In a report of 1,011 consecutive women
delivered in one unit:
PIH was approximately 12% among
primigravidae, 5% among same-paternity
multigravidae, and 24% among newpaternity multigravidae
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The maternal syndrome of PE:
It is variable in:
Time of onset.
Speed of progression.
& the extent to which it involves different
organs.
The maternal syndrome of PE
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It is a systemic endothelial damage.
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Both functional & structural damage.
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It ↓ the production of prostacyclin (it
is produced by the endothelium  it
is a vasodilator and antiplatelete
aggregant).
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↑ Thromboxane A2: it is a
vasoconstrictor and platelet
aggregator.
In PE the ratio of Thromboxane A2 /
prostacyclin has been found to be
increased.
Risk Factors for Developing PE:
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First pregnancy.
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Multiple pregnancy.
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PIH in previous pregnancy.
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Family history of PE ( mother or sister )
risk increase four folds.
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Chronic HT.
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New partner.
Continue risk factors
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Gestational DM.
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Vascular & connective tissue disease.
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Nephropathy.
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Antiphospholipid syndrome.
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Obesity.
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Age 35y & older or very young age.
Investigations
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Gestation < 20/40  Investigate
for secondary causes of HT like:
Renal a. stenosis, Coarctation of
aorta, Abnormal thyroid
function……etc
FBE, U&Es, TFTs, Renal
imaging……etc
Gestation > 20/40:
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FBE + blood film: picture of
haemolysis.
PLT count: if drop > 30% compare
to previous level  significant
LFTs: increase in ALT & AST.
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S. uric acid: predictive value of
33% if increases 0.12 mmol/lit
above a previously recorded
baseline.
Coagulation profile: increase in
D-dimer, increase in APTT, PT &
decrease fibrinogen.
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Urinary PTN: Albumine/creatinine
ratio of 30mg/mmol is equal to
300mg of PTN in 24h urine
collection.
Fetal wellbeing: U/S & CTG
Complications of PE
A- CNS:
On the mother
1- Eclampsia.
2- Brain haemorrhage.
3- Cerebral oedema.
4- Retinal oedema & detachment.
B- Renal system:
Renal cortical & tubular necrosis.
C- Respiratory:
Laryngeal oedema.
Pulmonary oedema.
D- Liver:
1- Jaundice.
2- Hepatic infarction.
3- HELLP syndrome.
4- Hepatic rupture.
E- Coagulation system:
1- DIC
2- HELLP syndrome
F- Placenta:
Abruptio placentae.
Fetal complications
1- IUGR, due to chronic hypoxia.
2- Acute hypoxia due to placental
abruption.
3- Preterm delivery due to severe PE.
TREATMENT
Chronic HT / Gestational HT:
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Methyl dopa.
Labetalol or Nifedipine.
Continue to monitor the patient for
a possibility of superimposed PE.
Aim to deliver at 40/40
Treatment of PE
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Early diagnosis,
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Close medical supervision &
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Timely delivery are the cardinal
requirement for management, &
Delivery is the ultimate cure.
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Once the diagnosis is made 
subsequent management should
depend on the maternal & fetal
wellbeing & the severity of the
disease.
Mild preeclampsia:
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Mother: BP check, urine for PTN,
PLT count & LFTs.
Fetus: US every 2/52 for AFI / AB
ratio & fetal growth,
If IUGR, decrease AFI or ↑ S/D ratio
 US to be done twice a week.
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If the pt is symptomatic ( ex.
Headache, epigastric pain…etc ) 
admit and delivery is to be
considered, especially if GA > 34/40
Mode of delivery: IOL if bishop > 6
Pt is not for bed rest, prolonged
hospitalization.
Antihypertensive drugs to control
Sever preeclampsia
Prompt delivery is recommended if :
Imminent eclampsia.
Multi organ dysfunction.
Fetal distress.
Gestational age > 34/40
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If sever PE happened very early in
the pregnancy  consider
conservative management in a
tertiary centre.
Antihypertensive drugs: to be
considered if diastolic BP is 105110 mmHg or mean BP > 125
mmHg,
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Hydralazine: 5mg iv bolus,
repeated every 15-20 min up to
20mg in total.
If no response or side effects  use
labetolol 20mg iv or Nifedipine
10mg oral.
ANTICONVULSANT DRUG
THERAPY:
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MgSO4 is the drug of choice
ALL PATIENT WITH SEVER PE OR
ECLAMPSIA SHOULD RECEIVE
MgSO4 DURING LABOUR & FOR
24h.
Eclampsia
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The word ECLAMPSIA arises from
Greek “ like a flash of lightening”
Incidence : in UK is 4.9 /10 000
maternities. While in developing
countries it’s much higher.
The fatality rate is 1.8 %.
Seizures : 40 % Postpartum
40 % Antepartum
20 % Intrapartum
Risk Factors
1- Sever PE or imminent eclampsia.
2- Patients in whom PE has been
superimposed on chronic
hypertension.
3- In 10-30% of the patients there are
no risk factors.
Pathogenesis of Seizures
The exact cause is not known .
 Proposed aetiologies:
1) cerebral vasospasm with local
ischemia/infarction.
2) hypertensive encephalopathy with
hyperperfusion, vasogenic
(extracellular) oedema, and
endothelial damage.
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Clinical Features
Maternal:
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Before the fit : disorientation
stage, during which the mother
becomes restless, twitches &
spasmodic respiration.
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Tonic convulsion
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Clonic stage
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coma which may persist for an
hour
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Fetal: bradycardia lasting at least
three to five minutes is a common
finding during and immediately after
an eclamptic seizure, and does not
necessitate emergent caesarean
delivery.
If no improvement in the fetal heart
tracing in spite of active resuscitation
within 10-15 min  C/S
Differential Diagnosis
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Cerebrovascular accident
Hypertensive disease (hypertensive
encephalopathy,
pheochromocytoma).
Space-occupying lesions of the
central nervous system (brain
tumour, abscess).
Metabolic disorders (hypoglycemia,
uraemia, inappropriate Antidiuretic
Hormone secretion resulting in water
intoxication).
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Infection (meningitis, encephalitis).
Thrombotic thrombocytopenic
purpura
Idiopathic epilepsy.
Use of illicit drugs (eg,
Methamphetamine, cocaine)
Management
The aims of the treatment are:
1- Maintain airway patency & prevent
aspiration.
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2- Control the fit.
3-To reduce the blood pressure to prevent
cerebral haemorrhage.
4-To deliver the fetus.
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Initial control of convulsions:
The drug of choice is intravenous
magnesium sulfate.
A Benzodiazepine is another
option.
Phenytoin can also be used, but is
less effective in preventing recurrent
seizures.
Treatment of hypertension:
1- Hydralazine: 5mg iv bolus
2- Labetalol: 20mg iv
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Prevention of subsequent seizures:
Approximately 10 percent of eclamptic
women will have repeated seizures if
managed expectantly. MgSo4 is the drug
of choice for prevention & must be given
for 24/24
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Delivery — Eclampsia is usually
considered an absolute contraindication to
expectant management.
The definitive treatment for eclampsia is
prompt delivery.
Factors to consider in determining the
mode of delivery are gestational age,
Bishop score, whether the patient is in
labor, and fetal condition and position.