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Hypertensive Disorders in Pregnancy

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Title: Hypertensive Disorders in Pregnancy


1
Hypertensive Disorders in Pregnancy
  • Azza Alyamani
  • Prof. of Obstetrics Gynecology

2
  • Classification
  • Women who are pregnant and hypertensive
  • must be divided into
  • chronic hypertension.
  • pregnancy induced hypertension (PIH)
  • or gestational hypertension.
  • those with PIH further subdivided
  • proteinuric PIH
    (preeclampsia)minority
  • non-proteinuric PIH majority

3
  • Therefore
  • women with hypertension in pregnancy are
    classified as having
  • 1. preeclampsia (proteinuric hypertension).
  • 2. non proteinuric hypertension.
  • 3. chronic hypertension
  • primary (essential)
    hypertension. 95.
  • secondary hypertension.5.
  • ..renal dis.
  • ..adrenal dis.
  • ..hyperthyroidism.
  • The aetiology and management of the three
    conditions are different .

4
  • Incidence
  • Worldwide , maternal mortality from
    hypertensive
  • disease accounts for
  • 100.000 deaths
    per year.
  • preeclampsia occurs in 5 .
  • non proteinuric PIH 15.
  • it accounts to 15 20 of maternal
    mortality in
  • the developed cuonteris.

5
  • Definition
  • pregnancy induced hypertension (PIH) is
  • Hypertension that occurs after 20 weeks
    gestation and unrelated to other pathology.
  • protienuria is the excretion of 300mg or more
    of protein in 24 hours urine.
  • hypertension and protienuria define
    preeclampsia.

6
  • Preeclampsia
  • is a multisystem disorder involving the
    placenta , liver , kidneys , blood , neurological
    and
  • cardiovascular systems.
  • both maternal and fetal morbidity /
    mortality are more likely to occur with early
    onset disease as
  • placental abruption ,acute renal failure
    ,cerebral Hge ,DIC and IUGR ,prematurity as
    delivery is
  • the only cure.
  • therefore , ANC is directed towards
    identifying women with hypertension and
    protienuria.

7
  • severity ranges from
  • a mild disorder (transient hypertension
    in the later part of the pregnancy) to
  • a life-threatening disorder with seizure
    HELLP syndrome, fetal hypoxia, and
    growth retardation.
  • more severe disease 0.5 per 1000
    deliveries

8
  • Chronic Hypertension
  • is the presence of persistent hypertension of
    whatever cause , before 20 weeks gestation
  • or
  • persistent hypertension beyond 6 weeks
  • postpartum.
  • sustained bl. p of 140/90 mmHg or gt on two
    occasions 6 hours apart is considered
  • hypertensive.

9
  • Aetiology
  • Pregnancy induced hypertension (PIH)
  • Preeclampsia
  • is unknown , believed to be involved
  • immune maladaptation.
  • placental ischemia.
  • oxidative stress.
  • genetic predisposition.

10

Genetic Predisposition
Faulty interplay bet. invading trophoblast and
decidua
Decreased bl. supply to feto-placental unit
Release of circulating factors
Endothelial cell alteration
IUGR
Hypertension
Proteinuria
11
  • Management
  • Screening for preeclampsia
  • Risk Factors
  • 1. ve family history in the first degree
    relative
  • increase the risk of PET 4 8 fold.
  • 2. primiparety
  • 3. medical disorders as
  • history of PET.
  • chronic hypertension.
  • diabetes.
  • obesity.
  • antiphospholipid syndrome.
  • molar pregnancy.
  • multiple pregnancy.
  • hydrops fetalis.

12
  • Screening and assessment for chronic
  • hypertension
  • Women who is found to be hypertensive before
    pregnancy can be advised about
  • 1. weight loss.
  • 2. restrict salt and alcohol intake.
  • 3. change her antihypertensive agents ,
    diuretics ,
  • angiotensin-converting enzyme (ACE)
    inhibitors
  • and ß blockers to other alternatives.

13
  • Diagnosis
  • Screening tests
  • to predict PET and superimposed preeclampsia
  • on chronic hypertension.
  • (1) US
  • it is quick ,non-invasive and inexpensive .
  • Uterine artery Doppler
  • analysis of its waveform is an early
    predictor of
  • poor placental perfusion and development of
    PET ,
  • there is resistance circulation with notch.
  • Its predictive value is greater at 24 weeks
    or more.

14
Uterine art. Doppler in PET
  • diastolic
    notch

15
  • (2) Biochemical tests
  • in preeclampsia
  • HB , and Hematocrit concentrations.
  • CBC with platelets count.
  • serum uric acid .
  • endothelial activation markers are
    increased.
  • urinary excretion of Ca and
    microalbuminuria

16
  • in severe chronic hypertension
  • urine analysis.
  • 24h urine for protein , creatinine
    clearance,
  • catecholamine metabolites and free
    cortisol.
  • bl. Urea and electrolytes as Na k.
  • Lupus anticoagulant and
    anticardiolipin in APS.
  • serum lipids.
  • in addition
  • (3) fundoscopy.
  • (4) ECG ECHO.
  • (5) X ray chest.

17
Symptoms Signs

18
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19
  • Criteria of severe preeclampsia
  • blood pressure gt 160 mmHg systolic
    or
  • gt 110 mm Hg diastolic
  • Proteinuria gt 3 g in 24 hours
  • Persistent and severe cerebral or
    visual disturbances (headache,
    blurred vision)
  • Persistent and severe epigastric pain
    or right upper quadrant pain.
  • Pulmonary edema or cyanosis.
  • Oliguria ( lt 500 ml urine / 24 hour).
  • Eclampsia ( grand mal seizures).
  • HELLP syndrome.

20
  • Maternal and fetal assessment
  • the GA at which woman present with
    hypertension
  • is an important factor in establishing risk .
  • Late onset hypertension after 37weeks rarely
    result in serious maternal or fetal
    complications.
  • Superimposed pre eclampsia on chronic
    hypertension is diagnosed by identifying
    proteinuria, raised uric acid levels or failing
    platelets count .
  • chronic hypertension is associated with
    preeclampsia
  • in 20 and abruptio placenta in 2.

21
  • Uterine artery Doppler velocity waveforms
  • is used to assess risk .
  • bl.pressure and urine analysis are checked
  • every 2 weeks.
  • sudden and profound rise should alert the
  • clinician to the possibility of
    PET.
  • high uric acid and low platelet count
  • may pre date proteinuria by some
  • weeks.

22
  • Management
  • Pre eclamptic Toxaemia
  • A) PET remote from term
  • Early onset PET is associated with
  • a. placental insufficiency
  • resulting in IUGR and fetal death. Therefore
  • Fetal Wellbeing must be carefully
    considered.
  • 1. monitoring of fetal movements.
  • 2. serial symphesis -fundal height .
  • 3. serial US to confirm fetal
    growth ,AF
  • volume and Umbilical A. Doppler
  • waveform .

23
  • b. involvement of other organ systems
  • resulting in increased maternal morbidity
  • and mortality.
  • 1.serial platelets count
  • as platelets are consumed due to
    endothelial
  • activation.
    Thrompocytopenia
  • lt100.000/ml. delivery should be
    considered.
  • 2.increased HB and haematocrit values
    indicate
  • hypovolaemia.
  • 3.clotting abnormalities indicate DIC.
  • .

24
  • 4.raised uric acid
  • a measure of fine renal tubular
    function is used
  • to assess severity of the disease.
  • raised urea and creatinine
  • indicate late renal involvement .
  • 5.severe proteinuria
  • gt 3g /24 hours urine resulting in
    fall of
  • circulating albumin and increasing
    the risk of
  • pulmonary edema.

25
  • 5.HELLP syndrome
  • it is severe variant of PET,
    Haemolysis ,
  • Elevated Liver enzymes and Low
    Platelets .
  • PET can cause subcapsular hematoma,
    liver
  • rupture and hepatic infarction which
    result in
  • raised liver transaminases as AST
    indicating
  • hepatocellular damage and
  • liver involvement
  • and the need to consider delivery.

26
  • Delivery
  • should be considered once fetal lung maturity
    is likely ( at 32 weeks gestation) ,especially if
    either
  • multi-organ involvement or fetal compromise is
  • proved.
  • Corticosteroids are given to enhance fetal
    lung maturity. Steroid therapy may enhance
    recovery from HEELP syndrome.
  • Delivery before term is usually by CS .such
    patients are risk of thromboembolism and should
    be given prophylactic SC heparin and stockings.

27
  • Indications of termination of pregnancy
  • in PET
  • 1. uncontrollable hypertension.
  • 2. deteriorating liver or renal
    function.
  • 3. progressive fall in platelets.
  • 4. neurological complications as
    cerebral Hge.
  • 5. deteriorating fetal condition as
    non-reactive
  • CTG.

28
  • B) PET near term
  • Lat onset preeclampsia rarely results in
  • serious morbidity to mother or fetus .
  • Drug therapy should be considered
  • a) antihypertensive
  • the aim is to lower the bl.
    pressure and
  • lower the risk of maternal
    cerebrovacular
  • accident without uterine
    bl. flow and
  • compromising the fetus.

29
  • 1. Labetolol
  • a ß blockers .
  • can be given IV and orally.
  • safe during pregnancy.
  • 2. Methyldopa
  • centrally acting agent.
  • very safe during pregnancy.
  • only given orally .
  • takes 24 h for its effect.
  • 3. Nifedipine
  • is Ca channel blocker .
  • with rapid onset of action.
  • cause severe headache.

30
  • NB
  • Diuretics ,Angiotensin-converting enzyme
    (ACE)
  • inhibitors and ß-blockers are
    contraindicated .
  • b) Low dose aspirin
  • results in significant reduction in
    preeclampsia
  • associated fetal death and preterm
    delivery.
  • c) for prophylaxis
  • Ca , fish oil , antioxidants , vit. C
    , vit. E

31
  • Management of severe fulminating preeclampsia
    and impending eclampsia
  • 1. IV antihypertensive
  • Hydralazine / labetolol
  • IV infusion titration rapidly against
    changes in
  • the blood pressure .
  • 2. Anticonvulsant therapy
  • Magnesium Sulfate
  • it is the anticonvulsant of choice
    as ttt. of
  • eclampsia and also as prophylaxis
    which
  • reduce the risk of fits to half.
  • Diazepam and phenytoin can be
    used but
  • less effective .

32
  • mode of action
  • anticonvulsant.
  • muscle relaxant.
  • vasodilator.
  • reduce the intracerebral
    ischaemia.
  • dose
  • 2 g IV as a loading dose
    then
  • 1-2 g / h as maintenance
    infusion.
  • toxicity is detected by
  • absence of the patellar
    reflexes.
  • respiratory arrest .
  • may be cardiac arrest.
  • antidote is
  • 10 ml of 10 Ca gluconate.

33
  • 3. Fluid management
  • a Folly's catheter should be inserted
    and fluid
  • balance recorded.
  • oliguria without a rising serum
    urea or
  • creatinine is a manifestation of
    severe PET
  • and not renal failure.
  • however , if creatinine or
    potassium rises ,
  • haemodialysis is necessary.
  • diuretics should only be given if
    there are
  • signs of pulmonary edema.

34
  • Postpartum Care
  • in severe PET and eclampsia, a severe
    type of
  • of eclamptic fits occur postpartum ,
    intensive
  • monitoring is required for 48 h. after
    delivery.
  • bl. Pressure is frequently at its
    highest levels
  • 3 -4 days after delivery . Therefore ,
  • antihypertensive therapy is need to be
  • continued after discharge home.

35
  • a postnatal care visit 6 -8 w. is
    mandatory for
  • measuring bl.p , urine analysis ,
    RFT, LFT and
  • predisposing factors as thrompophilia
    or APS
  • should be excluded.
  • in women with severe chronic
    hypertension
  • must be carefully monitored for at
    least 48h
  • after delivery as they are at
    increased risk of
  • renal failure , pulmonary edema and
  • hypertensive encephalopathy.

36
  • Thank you
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