GESTATIONAL HTN

BP reading 140/90
mmHg for the first
time after 20 weeks
of pregnancy
No proteinuria
BP returns to
normal within 12
weeks postpartum
(if the BP elevation
persists, the woman
is diagnosed as
having chronic
hypertension)
Final dx is only
made postpartum
May even be
associated with an
increased birth
weight

HYPERTENSIVE DISORDERS IN
PREGNANCY-INDUCED HTN
PRE-ECLAMPSIA
ECLAMPSIA
Mild pre-eclampsia
CNS
BP 140/90 mmHg after
involvement
20 weeks gestation
with the
Proteinuria 1+ by urine occurrence of
dipstick or a total protein
convulsions that
level 300 mg/24 hours
cannot be
- Pre-eclampsia can develop attributed to
before the 20 week of
other causes
gestation in hydatidiform
mole and in the presence of
lupus anticoagulant
Severe pre-eclampsia
BP 160 mmHg systolic
or 110 mmHg diastolic
Proteinuria 2+ by urine
dipstick or a total protein
level of 2 gm/24 hours

PREGNANCY
PREGNANCY-AGGRAVATED
HTN
Development of PE or
eclampsia in pre-existing
hypertension detected by a
further increase of
> 30 mmHg in SBP or >15
mmHg in DBP
or
New onset proteinuria of
>300 mg/24 hours in
hypertensive women but
with no proteinuria before
20 weeks gestation
or
A sudden increase in
proteinuria or a drop in
platelet count to
<100,000/mm3 with HTN
and proteinuria before
20wk gestation

PREDISPOSING FACTORS
Age: PG<20, all women > 35
Parity: PG have double incidence
Lower socio-economic status
Genetic predisposition: Recessive trait
Obstetric complications: multiple and molar pregnancy, fetal hemolytic diseases (hydrops fetalis),
polyhydramnios
Existing medical conditions: chr BP, ren D, DM, SLE, antiphospholipid AS.
Previous PE. The recurrence rate for PE with the same male partner is ~ 20%, and usually
becomes apparent at later gestation than in the first pregnancy
Obesity: 4.3% for a women with a body mass index <19.8 kg/m2 to 13.3% for those > 35 kg/m2

CHRONIC HTN WITH

PREGNANCY
Hypertension is
present before
pregnancy or
detected before 20
weeks Or
Hypertension first
diagnosed after 20
weeks gestation and
persisted after 12
weeks postpartum

FACTORS THAT PET

Prolonged exposure
to paternal Ag
Smoking, but if PE
occurs then perinatal
mortality triples
Placenta previa

PRE-ECLAMPSIA
CAUSE (UNKNOWN)

THEORIES
(I) Defective trophoblastic
invasion of the spiral arteries
(II) Immunologic factor
(III) Increased pressor
responses
(IV) Prostaglandins imbalance
(V) Genetic predisposition
(VI) Inflammatory factors
Ischemia could be due to:
- Underlying vascular changes (HTN/
Failure of physio chgs of spiral
arteries)
- Increased myometrial resistance of
the myometrial vessels, which could
be related to a heightened
myometrial tension produced by the
large fetus in a primiparous women,
by twins, or by polyhydramnios
The poorly perfused trophoblast
release factor X which enters
maternal circulation and causes
endothelial dysfunction Imbalance
between different classes of locally

PATHOPHYSIOLOGY
VASOSPASM
Excess
Decreased
production/
production/sensiti
sensitivity to
vity to
vasoconstrictors vasodilators
Angiotensin II
Prostacyclin
Serotonin
Nitric oxide
Endothelin
INTRAVASCULAR COAGULATION
Platelet activation
Thrombocytopenia
Reduced production of anti-thrombin
III
PLASMA VOLUME CONTRACTION
Redistribution of fluid from the intravascular to interstitial fluid spaces so
that total ECF volume remains
unaltered

ORGAN HYPOPERFUSION
Kidney: GFR, proteinuria,
hyperuricaemia, oliguria
Liver: SGOT, SGPT,
epigastric pain
Brain: visual scotomata due
to occipital lobe ischemia,
headache, convulsions
(eclampsia)
Placenta: IUGR, placental

Stimulation of the maternal immune system by the early

conceptus Produce blocking Ab to antigenic sites on the
placenta, thus preventing the rejection of the fetus and placenta.
Hypoimmune response results in damage of the placenta and
subsequent PE.
PE less common in previously stimulated immunity conditions as:
Previous pregnancy, Consanguineous marriages, Increased

PRE-ECLAMPSIA
DIAGNOSIS
INDICATIONS OF SEVERITY OF
INDICATIONS TO TERMINATE PREGNANCY
PRE-ECLAMPSIA
IN PRE-ECLAMPSIA
HISTORY
INVESTIGATION
Presence of symptoms
MATERNAL FACTORS
FETAL FACTORS
Persistent
headache
or
Personal hx
Completed 37 weeks
Obvious IUGR
CBC: PCV and
other cerebral or visual
Past hx
Abnormal liver/ renal

thrombocytopenia
disturbances
Menstrual hx
functions
Oligohydramnios
SGOT, SGPT:
- Persistent epigastric pain
Obstetric hx
Severe preeclampsia/
, IUFD
Elevated liver enzymes
Complaints and
eclampsia regardless of
Presence of
Creatinine clearance, Diastolic BP 110 mmHg

Proteinuria
of
2+
or
more
by
hx of present
the gestational age
congenital fetal
serum creatinine, uric
urine dipstick or a total protein
pregnancy
In selected cases of
malformations
acid, total protein in
level of 2 gm/liter in a 24-hour severe PET, where the
incompatible
urine, and blood urea:
urine sampling
expertise and
with life
impaired
PHYSICAL EXAM

Abnormal
lab
findings
equipment
are
available,

Coagulation
profile:
Hypertension
Obvious fetal growth
expectant management
PT, PTT, clot. and
Edema
restriction
may be undertaken for
bleed. time in DIC.
Obstetric exam
Neurological effects:
fetal indications
Fibrinogen and FDP to
Scotomata, hyperreflexia
diagnose DIC
Eclamptic convulsions
Fetal Surveillance
MANAGEMENT
CONVULSION
ANTIHYPERTENSIV TIMING OF DELIVERY FLUIDS
END-ORGAN COMPLICATIONS
PROPHYLAXIS
ES
Magnesium sulphate
Hydralazine
Once the dx of
Carefu Consumption coagulopathy: Administer
(MgSO4)
Nifedipine
severe preeclampsia l.
platelets/FFP only if clinical bleeding.
Blocks neuromuscular
Labetalol
has been
Colloid Intracranial hemorrhage:Severe
conduction through
Sodium
established,
s.
headache in the post partum with pre~ or
blocking the release of
nitroprusside
termination of
eclampsia. CT scan
acetylcholine at NMJ.
pregnancy becomes
Rx: Combined obstetric and neuro in 3
Toxicity: Neurotoxicity
mandatory after
hosp
(Loss of patellar reflex) ,
patient stabilization
Sub capsular hematoma:Severe
Resp depression (RR
Mode of delivery
epigastric pain+hepatomegaly. US.
<12/min), Cardiac toxicity
depends upon
Rx:Correct coagulopathy. If liver rupture,
(cardiac arrest)
whether: The woman
transfusion + liver surgery.
Antidote: Calcium
is in labor, The
HELLP syndrome: Abnormal vascular

gluconate

progress of labor,
The cervix is fit for
induction.

tone, vasospasm and coagulation defects.

Rx:Delivery regardless GA. Steroids.
Platelets only if <20k/ml. Csection in
platelets >50k/ml.

CLINICAL FEATURES
Premonitory phase
Tonic phase
Clonic phase
Coma

ECLAMPSIA
MANAGEMENT
EMERGENCY TREATMENT
MONITORING DURING HOSPITAL STAY
1. Clear airway passages
Close observation:
2. Apply an oxygen mask
Every 30 minutes assess pulse, BP and respiratory rate
3. Protect the patient from harm during
Maintain a fluid balance chart monitoring fluid intake
seizures
and urinary output
4. Control convulsions with MgSO4
Limit IV fluid administration unless excessive blood loss
5. Control high BP to avoid fatal
If convulsions occur despite MgSO4 therapy:
complications
CT scan should be performed
6. Deliver fetus
If severe respiratory insufficiency occurs:
7. Avoid diuretics and hyperosmotic
ICU admission and ventilation
agents
Measuring blood gases and blood pH levels
8. Close observation

HISTORY
Past history:
Hypertension treated before pregnancy
with various antihypertensive medication
Renal problems
Obstetric history:
Hypertension during previous pregnancies
Previous superimposed pre-eclampsia
Previous IUFD, IUGR and abortions
Family history of hypertension

CHRONIC HYPERTENSION
DIAGNOSIS
EXAM
Hypertension: Presenting before
20 weeks gestation
Cardiac enlargement: May be
present
Edema: Occurs when preeclampsia or heart failure occurs
as a complication of hypertension

INVESTIGATIONS
Urine analysis: Proteinuria indicates
occurrence of superimposed preeclampsia
Renal function: Serum creatinine, uric
acid and BUN
Fundus examination: Changes
indicating chronic hypertension

MANAGEMENT
ANTIHYPERTENSIVE THERAPY
- Antihypertensive therapy recommended when SBP > 160-170 and DBP > 105-110, as such treatment decreases the
maternal cerebral and cardiovascular complications.
- In acute control of severe HTN, the objective of therapy is a gradual reduction of blood pressure to a level of about 140150 / 90-100 mmHg
BP should be assessed every 15 minutes initially, once the blood pressure is stabilized the interval can be lengthened to 30
minutes
- Lowering the blood pressure rapidly over minutes abrupt and profound in BP cardiac output to the uterus with
possible fetal hypoxia. Continuous fetal heart rate monitoring should be performed during initial therapy to detect such
effect and allow early remedial action
HYDRALAZINE (Vasodilator), NIFEDIPINE (Ca Channel Blocker), LABETOLOL (Beta-blocker) - most commonly used.
Labetalol should be avoided in asthma. Atenolol, ACE inhibitor, ARB and diuretics should be avoided
Diuretics are not recommended
Angiotensin converting enzyme inhibitors are contraindicated with pregnancy

Termination if:
Fetal maturity reached
Fetal distress and severe IUGR
Additional complications occur (severe preeclampsia, abruptio placentae)