Hypertensive Disorders in Pregnancy-Kabera Rene

8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene

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National University of Rwanda

Family and Community Medicine

Hypertensive Disorders in Pregnancy

KABERA Ren,MD

PGY IV Resident

Family and Community MedicineNational University of Rwanda


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Introduction

Hypertensive disorders complicating pregnancy are common

and form one of the deadly triad, along with hemorrhageand infection, that contribute greatly to maternal morbidity

and mortality.


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Classification

Gestational hypertension

Preeclampsia.

Eclampsia.

Preeclampsia superimposed on chronic hypertension.

Chronic hypertension.


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BP 140/90 mm Hg for first time during pregnancy

No proteinuria

BP returns to normal < 12 weeks' postpartum

Final diagnosis made only postpartum

May have other signs or symptoms of preeclampsia, forexample, epigastric discomfort or thrombocytopenia

Gestational hypertension has replaced the term pregnancy-

induced hypertension to describe women who develop

hypertension without proteinuria after 20 weeks of gestation.


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Gestational hypertension is a provisional diagnosis that

includes women eventually diagnosed with preeclampsia orchronic hypertension, as well as women retrospectively

diagnosed with transient hypertension of pregnancy.

Fifty percent of women diagnosed with gestational

hypertension between 24 and 35 weeks develop

preeclampsia


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Preeclampsia Minimum criteria

BP 140/90 mm Hg after 20 weeks' gestation

Proteinuria 300 mg/24 hours or 1+ dipstick

Increased certainty of preeclampsia

BP 160/110 mg Hg

Proteinuria 2.0 g/24 hours or 2+ dipstick

Serum creatinine > 1.2 mg/dL unless known to be previously elevated

Platelets < 100,000/mm3

Microangiopathic hemolysis (increased LDH)

Elevated ALT or AST

Persistent headache or other cerebral or visual disturbance

Persistent epigastric pain


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Preeclampsia

Described as a pregnancy-specific syndrome of reduced organ

perfusion secondary to vasospasm and endothelial activation. Proteinuria is an important sign of preeclampsia

Significant proteinuria is defined by 24-hour urinary protein

exceeding 300 mg per 24 hours, or persistent 30 mg/dL (1+dipstick) in random urine samples.

Renal biopsy specimens: glomerular lesion.

The minimum criteria for the diagnosis of preeclampsia are

hypertension plus minimal proteinuria.

The more severe the hypertension or proteinuria, the more

certain is the diagnosis of preeclampsia


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Preeclampsia

Epigastric or right upper quadrant pain is thought to result from

hepatocellular necrosis, ischemia, and edema that stretchesthe Glisson capsule.

This characteristic pain is frequently accompanied by

elevated serum hepatic transaminase levels and usually is a

sign to terminate the pregnancy.

The pain presages hepatic infarction and hemorrhage or

catastrophic rupture of a subcapsular hematoma. Fortunately,

hepatic rupture is rare.


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Preeclampsia

Thrombocytopenia is characteristic of worsening preeclampsia

Thrombocytopenia is due platelet activation and aggregationas well as microangiopathic hemolysis induced by severe

vasospasm.

Evidence of gross hemolysis such as hemoglobinemia,hemoglobinuria, or hyperbilirubinemia is indicative of severe

disease.

Other factors indicative of severe hypertension include

cardiac dysfunction with pulmonary edema as well as obviousfetal growth restriction.


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Preeclampsia

Exact mechanism not known

Immunologic

Genetic

Placental ischemia

Endothelial cell dysfunction Vasospasm

Hyper-responsive response to vasoactive hormones (e.g.

angiotensin II & epinephrine)


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Preeclampsia

Abnormality Mild Severe

1. Diastolic blood pressure < 100 mg Hg 110 mm Hg or higher

2. Proteinuria Trace to 1+ Persistent 2+ or more

3. Headache Absent Present

4. Visual disturbances Absent Present

5. Upper abdominal pain Absent Present6. Oliguria Absent Present

7. Convulsion Absent Present

8. (eclampsia)

9. Serum creatinine Normal Elevated

10. Thrombocytopenia Absent Present

11. Liver enzyme elevation Minimal Marked

12. Fetal growth restriction Absent Obvious

13. Pulmonary edema Absent Present


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Eclampsia

Seizures that cannot be attributed to other causes in a woman

with preeclampsia The seizures are generalized and may appear before,

during, or after labor.

Recent study reported that a fourth of eclamptic seizuresdeveloped beyond 48 hours postpartum


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Superimposed Preeclampsia

New-onset proteinuria 300 mg/24 hours in hypertensive women

but no proteinuria before 20 weeks' gestation A sudden increase in proteinuria or blood pressure or platelet

count < 100,000/mm3 in women with hypertension and proteinuriabefore 20 weeks' gestation

All chronic hypertensive disorders, regardless of their cause,predispose to development of superimposed preeclampsia andeclampsia.

The diagnosis of chronic underlying hypertension is made when:

Hypertension (140/90 mm Hg or greater) is documentedantecedent to pregnancy.

Hypertension (140/90 mm Hg or greater) is detected before 20weeks, unless there is gestational trophoblastic disease.


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Chronic Hypertension

BP 140/90 mm Hg before pregnancy or diagnosed before

20 weeks' gestation not attributable to gestationaltrophoblastic disease

Hypertension first diagnosed after 20 weeks' gestation andpersistent after 12 weeks' postpartum.


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Etiology

Chorionic villi for the first time.

Superabundance of chorionic villi, as with twins or hydatidiformmole.

Preexisting vascular disease.

Genetically predisposed to hypertension developing duringpregnancy.

Abnormal trophoblastic invasion of uterine vessels. Immunological intolerance between maternal and fetoplacental

tissues.

Maternal maladaptation to cardiovascular or inflammatory

changes of normal pregnancy. Dietary deficiencies.

Genetic influences.


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Diagnosis

Hypertension is diagnosed when the resting blood pressure is

140/90 mm Hg or greater. Edema has been abandoned as a diagnostic criterion

because it occurs in too many normal pregnant women to be

discriminant.


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Pathophysiology


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Pathophysiology Prostacyclinis produced by endothelial cells and

thromboxane A2 by platelets from their common precursor

arachidonic acid via the cyclooxygenase pathway.

Thromboxane A2 promotes platelet aggregation and

vasoconstriction, whereas prostacyclininhibits platelet

aggregation and promotes vasodilation. The balance between platelet thromboxane A2 and

prostacyclinfosters localized platelet aggregation and

consequent clot formation while preventing excessive

extension of the clot and maintaining blood flow around it.

The thromboxane A2-prostacyclin balance can be shifted

toward prostacyclin by administration of low doses of aspirin.


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Pathophysiology Aspirin produces irreversible inhibition of cyclooxygenase by

acetylating serine residue in its active site.

Obviously, this reduces production of both thromboxane A2 andprostacyclin.

Endothelial cells produce new cyclooxygenase in a matter of hourswhereas platelets cannot manufacture the enzyme, and the level

rises only as new platelets enter the circulation. This is a slow process because platelets have a half-life of about 4

days.

Administration of small amounts of aspirin for prolonged periodsreduces clot formation and has been shown to be of value in

preventing myocardial infarctions, unstable angina, transientischemic attacks, and stroke.


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PathophysiologyBrain

There are two distinct but related types of cerebralpathology.

The first is gross hemorrhage due to ruptured arteries caused

by severe hypertension

The second type of cerebral lesion is variably demonstrated

with preeclampsia but probably is universal with eclampsia.

These are more widespread, focal, and seldom fatal.

The principal postmortem lesions are edema, hyperemia,

ischemias, thrombosis, and hemorrhage


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Pathophysiology

Cardiac/Pulmonary Increased CO & SVR

CVP normal or slightly increased

Plasma volume reduced

Pulmonary edema Decrease oncotic/collid pressure

Capillary/endothelial damage leak

Vasoconstriction

increase PWP and CVP

Occurs 3 % of preeclamptic patients


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Pathophysiology

Liver Usually mild

Severe PIH or preeclampsia complicated by HELLP

periportal hemorrhages

ischemic lesion

generalized swelling

hepatic swelling epigastric pain


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Pathophysiology

Kidney Adversely affected proteinuria

GFR and CrCl decrease

BUN increase, may correlate w/ severity

RBF compromised

ARF w/ oliguria PIH, esp. w/ abruption, DIC, HELLP


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Pathophysiology

Uterus

Activity increased

Hyperactive/hypersensitive to oxytocin

Preterm labor frequent

Uterine/placental blood flow decreased by 50-70%

Abruption incidence increased


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Management

Basic management objectives for any pregnancy complicated

by preeclampsia are: Termination of pregnancy with the least possible trauma to

mother and fetus.

Birth of an infant who subsequently thrives.

Complete restoration of health to the mother.


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Antepartum Hospital Management

Hospitalization is considered at least initially for women with

new-onset hypertension, especially if there is persistent orworsening hypertension or development of proteinuria.

A systematic evaluation is instituted to include the following:

Detailed examination followed by daily scrutiny for clinical

findings such as headache, visual disturbances, epigastric

pain, and rapid weight gain.

Weight on admittance and every day thereafter.


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Management Analysis for proteinuria on admittance and at least every 2

days thereafter. Blood pressure readings in the sitting position with an

appropriate-size cuff every 4 hours, except between midnight

and morning.

Measurements of plasma or serum creatinine, hematocrit,

platelets, and serum liver enzymes, the frequency to be

determined by the severity of hypertension.

Frequent evaluation of fetal size and amnionic fluid volumeeither clinically or with sonography.


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Management of chronic hypertension

Methyldopa (Aldomet),labetalol, and nifedipine (Procardia)

are oral agents commonly used to treat chronic hypertensionin pregnancy.

The beta blocker atenolol (Tenormin) has been associated with

IUGR,

Women in active labor with uncontrolled severe chronic

hypertension require treatment with intravenous labetalol or

hydralazine.


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Management of Severe Preeclampsia

Magnesium sulfate: Loading dose of 4 to 6 g diluted in 100

mL of normal saline, given IV over 15 to 20 minutes, followedby a continuous infusion of 2 g per hour

Assess serum magnesium level if urine output is < 30 mL perhour or there is a loss of deep tendon reflexes, decreased

respiratory rate, or altered mental status Therapeutic range for serum magnesium is 4 to 7 mg per dL

Corticosteroids (if between 24 and 34 weeks of gestationand not previously administered)

Betamethasone (Celestone), 12 mg IM initially, then repeat in24 hours or Dexamethasone, 6 mg IM initially, then repeatevery 12 hours for three additional doses


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Management of Severe Preeclampsia For systolic blood pressure > 160 mm Hg or diastolic >

110 mm Hg, one of the following should be given toachieve a systolic measurement of 140 to 155 mm Hgand/or a diastolic measurement of 90 to 105 mm Hg:

Hydralazine, 5 to 10 mg IV every 15 to 30 minutes(maximal dose: 30 mg)

Labetalol, 20 mg IV initially; if the initial dose is noteffective, double the dose to 40 mg and then 80 mg at 10-minute intervals until target blood pressure is reached or atotal of 220 mg has been administered; the maximal dose

of IV labetalol is 220 mg in a 24-hour period Calcium gluconate, 1 g IV; keep at bedside in case of

respiratory depression from magnesium sulfate use


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Management Eclampsia Protecting the airway and minimizing the risk of aspiration by

placing the woman on her left side, suctioning her mouth, and

administering oxygen. intubations should be immediately available.

Close observation, soft padding, and use of side rails on the

bed may help prevent trauma from falls or violent seizureactivity.

After the convulsion has ended and the patient is stabilized,

plans should be made for prompt delivery.

In rural or remote areas, physicians need to consider the risk

of transfer versus the benefits of tertiary maternal and

neonatal care.


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Management of eclampsia Magnesium sulfate is the drug of choice because it is more

effective in preventing recurrent seizures than phenytoin(Dilantin) or diazepam (Valium).

If a patient has already received a prophylactic loading

dose of magnesium sulfate and is receiving a continuous

infusion, an additional 2 g should be given intravenously.

Otherwise, a 6-g loading dose is given intravenously over 15

to 20 minutes, followed by maintenance infusion of 2 g per

hour. A total of 8 g of magnesium sulfate should not be exceeded

over a short period of time


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References American Academy of Family Physician : www.aafp.org

Williams obstetrics Review of Medical Physiology


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End

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