Transcript HYPERTENSIVE DISORDER IN PREGNANCY.ppt

AHMED ABDULWAHAB
ASSISTANT PROFESSOR
AND CONSULUTANT OB/GY
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Objectives .
Definition of preeclampsia .
Etiology .
Effect of hypertensive disorder in pregnancy .
The theory of development of preeclampsia .
Pathological changes associated with
preeclampsia .
Definition of Eclampsia .
Management of preeclampsia and Eclampsia
Role of antihypertensive .
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the hypertensive disorder are major
contributor to maternal and perinatal
morbidity and mortality.
CLASSIFICATION AND DIFINTION.
Blood pressure reading depends on maternal
position and gestational age, it is lower in left
lateral position and higher in sitting position,
arterial B/P normally decline in 1st ,and 2nd
trimester and rise to pre pregnant level in the
3rd trimester.
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Cont.
The diagnosis of hypertension is made when
the systolic B/P is equal or greater than
140mmHg or diastolic of greater or equal
90mmHg.
Preeclampsia/ eclampsia.
Chronic hypertension, If the hypertension is
known prior to pregnancy or develops prior
to 20 weeks gestation and persist 12 weeks
postpartum.
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Cont,
Mostly essential hypertension but small
percentage will have secondary hypertension
due to renal ,vascular, or endocrinological
causes.
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3-Chronic hypertension with superimposed
preeclampsia.
It is diagnosed when the patient is known to
have hypertension and the process is
aggravated by pregnancy and usually carries
a worse prognosis , it is suspected by new
develop of proteinuria or sudden significant
increases in B/P or proteinuria after the 20
weeks of pregnancy.
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4- gestational hypertension.
When hypertension appears for the first time
after 20 weeks of pregnancy or within 48 to
72 hours after delivery without proteinuria
and disappears by 12 weeks postpartum.
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PREECLAMSIA.
It is a syndrome unique to pregnant human,
characterized by the new onset of
hypertension and or proteinuria and or
edema in the second half of gestation.
It may arise earlier after 14 weeks and then
we should suspect hdatidiform mole or
multiple pregnancy.
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Etiology.
It is the disease of theories.
Genetics , immunologic, nutritional
,endocrinologic, and infection all have been
proposed as a causes.
Because the condition disappears after
delivery, most attention has directed on the
placenta, membranes and the fetus,
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Uteroplacental ischemia may be central to the
development of the disease, and the ischemia
may result in production and release of
toxins that enter the circulation and causes
wide spread endothelial dysfunction that
causes imbalance in vasoconstrictors
prostaglandin thromboxane A2 and
vasodilator prostacyclin E2 production.
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PATHOPHYSIOLOGY.
The underlying pathophysiologic abnormality
is generalized vasospasm .
Renal blood flow and GFR in preeclampsia are
significantly lower than in normal pregnancy
this vasoconstriction causes to damage to the
glomerular membranes and increase the
permeability to proteins that leads to
proteinurria
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PATHOLOGY.
1- lack of decidualization of the myometrial
segment of the spiral arteries .
In normal pregnancy the second wave
trophoblast invade the muscular and elastic
layer of the spiral artery by fibrinoid and
fibrous tissue that becoming unresponsive to
vasoconstrictors substances, this is limited in
preeclamppsia
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The typical renal lesion in preeclampsia is
glomerular capillary endotheliosis .
Hemorrhage and necrosis will occur in many
organs secondary to arteriolar
vasoconstriction such as liver, brain, and
retina.
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Clinical and laboratory manifestation.
Most can be explained on the basis of the
endothelial dysfunction and vasospasm.
Weight gain and edema.
It occurs early and reflect an expansion of the
extra vascular fluid compartment, and
haematocrit may also increased reflecting
hypovolumia and hemo concentration .
Elevation of blood pressure.
Particularly the diastolic B/P, which may
occur days or weeks after the onset of
pathological fluid retention.
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Protienuria .
May occur days or weeks after the onset of
hypertension, or manifest during labor or
even postpartum.
Renal function test.
Increase in serum uric acid is the earliest
change, decrease in creatinine clearance with
increase in blood urea and creatinine
condition may progress to frank oligouria and
renal failure.
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Coagulation system.
Thrombocytopenia is the most common
abnormality , DIC may occur and represent
severe preeclampsia .
Liver function.
Focal hemorrhage and infraction leading to
upper quadrant and epigastric pain and
elevated liver enzymes and increase level of
bilirubin in significant haemolysis .
Hepatic rupture is rare .
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Placental function.
Vasospasm will lead to infraction and
decrease uteroplacental perfusion that will
cause intrauterine growth restriction IUGR,
oligohydramnios , fetal heart abnormalities
and retroplacental hemorrhage or abruption.
Central nervous system.
Visual disturbance, blurred vision , increase
reflexes irritability or hypereflexia.
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Evaluation and management.
Delivery is the only definitive cure for
preeclampsia BUT the question is which is
more good for the mother and the baby? So
delivery is indicated when the presence of the
fetus inside the uterus is attended by certain
risks that outweigh pre maturity
complications, or the maternal condition is
not responding to appropriate management
regardless of fetal maturity.
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Initial maternal assessment will involve .
Any past history of hypertension or renal
disease prior to pregnancy or previous
pregnancy.
Symptoms of sever preeclampsia like
headache, visual changes, nausia and
vomiting, abdominal or epigasteric pain .
Examination .
B/P , weight gain, edema, fundal height, and
reflexes.
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Investigation .
Urine for protein, CBC, liver function test,
urea and electrolyte ,uric acid .
Fetal assessment.
Fetal growth chart by ultrasound biophysical
profile Doppler study and fetal kick chart non
stress test.
If the mother disease is mild and no evidence
of fetal compromise management consist of
bed rest and observation.
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The patient should be delivered by the time
she reached 38 weeks or she started to
develop signs and symptoms of worsening
the disease, or there is evidence of fetal
compromise .
In mild cases patient can be managed as
outpatient .
Criteria of severe preeclampsia .
Severe hypertension systolic more than
160mmHg and diastolic equal or more than
110mmHg..
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Heavy proteinuria 5 gm in 24 hour urine
collection .
Oliguria less than 500ml per 24 hour .
Cerebral or visual disturbance.
Pulmonary edema and cyanosis .
Epigasteric or right upper quadrant pain .
HELLP syndrome .characterized by.
Haemolysis, Elevated liver enzyme, Low
platelet .
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ECLAMPSIA.
Is the presence tonic- clonic seizures that
usually complicate severe PET .
25% occur ante nataly before labor 50%
during labor and 25% occur post nataly after
delivery.
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Management of eclampsia .
It is a true obstetric emergency .
Stabilize and deliver.
Room is dark with minimum noise.
Clear airway and give oxygen mask .
Insert IV line for blood test and drug and fluid
administration .
Foley catheter for input and output charting .
The best and safest drug for controlling
convulsion is magnesium sulfate
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After stabilization delivery Is considered
either by induction of labor or by caesarian
section .
Prophylaxis against convulsion with
magnesium sulfate continued after delivery
for 24 hours after the last convulsion.
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Antihypertensive therapy.
Should be initiated when diastolic B/P is more
than 105mmHg to prevent CNS hemorrhage .
Hydralazine and labetalol are used to control
severe hypertension .
Nifedipine is an other option .
Alpha methyldopa is save to be use in chronic
hypertension .
Angiotensin converting enzyme inhibitor
should not be used.