HYPERTENSIVE DISORDERS IN PREGNANCY ASSOCIATE PROFESSOR IOLANDA BLIDARU MD, PhD.

HYPERTENSIVE HYPERTENSIVE DISORDERS IN DISORDERS IN PREGNANCYPREGNANCY

ASSOCIATE PROFESSORASSOCIATE PROFESSOR

IOLANDA BLIDARUIOLANDA BLIDARU

MD, PhDMD, PhD..

IntroductionIntroduction

1.1. Hypertensive disorders of Hypertensive disorders of pregnancy are leading causes of pregnancy are leading causes of maternal mortality.maternal mortality.

2.2. Worldwide: 50,000 women die Worldwide: 50,000 women die each year.each year.

DefinitionsDefinitions

Hypertension in pregnancyHypertension in pregnancy – BP of 140/90 or more BP of 140/90 or more == abnormal. abnormal.

– If there is a rise of 30 mmHg or more in the If there is a rise of 30 mmHg or more in the systolic blood pressure or 15 mmHg or systolic blood pressure or 15 mmHg or more in the diastolic blood pressure more in the diastolic blood pressure iin 2 n 2 occasions 6 hours apart.occasions 6 hours apart.

– Mean arterial BPMean arterial BP > 105 mmHg .> 105 mmHg .

Systolic + 2 Diastolic Systolic + 2 Diastolic Mean arterial BP = -----------------------------Mean arterial BP = -----------------------------

33

ClassificationClassification

Gestational hypertension (PIH).Gestational hypertension (PIH).

Preeclampsia (mild, severe).Preeclampsia (mild, severe).

Eclampsia.Eclampsia.

Superimposed preeclampsia Superimposed preeclampsia upon chronic hypertension.upon chronic hypertension.

Chronic hypertension with Chronic hypertension with pregnancy.pregnancy.

DefinitionsDefinitionsGestational hypertension:Gestational hypertension: – Hypertension for first time after 20 w, Hypertension for first time after 20 w,

without Proteinuria. BP returns to normal without Proteinuria. BP returns to normal before 12 weeks postpartumbefore 12 weeks postpartum (formerly PIH) (formerly PIH). .

Chronic hypertension with pregnancyChronic hypertension with pregnancy: : – Hypertension antedates pregnancy and Hypertension antedates pregnancy and is is

detected before 20 w, & lasts more than 12 detected before 20 w, & lasts more than 12 weeks postpartum.weeks postpartum.

DefinitionsDefinitions– Preeclampsia:Preeclampsia:

The development of hypertension and The development of hypertension and Proteinuria after 20 w Proteinuria after 20 w ((earlierearlier in in vesicular mole or twinsvesicular mole or twins))..

– Eclampsia (in Greek= Flash of light):Eclampsia (in Greek= Flash of light): The occurrence of tonic-clonic The occurrence of tonic-clonic convulsions convulsions (without any neurological (without any neurological disease)disease) in a woman with pre-eclampsia. in a woman with pre-eclampsia.


Superimposed pre-eclampsia: ¤ It is the new development of

Proteinuria after 20 weeks gestation in a patient with chronic hypertension.


ProteinuriaProteinuria:: ≥ ≥ 300mg/24 hours urine.300mg/24 hours urine. ≥ ≥ +1 dipstick.+1 dipstick.

Heavy Proteinuria :Heavy Proteinuria := ≥ 2g/24 hours= ≥ 2g/24 hours≥ ≥ +2 in dipstick.+2 in dipstick.

PreeclampsiPreeclampsiaa

Epidemiology of Epidemiology of preeclampsiapreeclampsia

IncidenceIncidence Is a disease of humans only.Is a disease of humans only.Is the most common medical disorder Is the most common medical disorder complicating pregnancy →complicating pregnancy → 5-15%5-15%Is the most common hypertensive disorder in Is the most common hypertensive disorder in pregnancy.pregnancy.More common in primigravidas and elderly More common in primigravidas and elderly multipara.multipara.More common in winter.More common in winter.More in black race. More in black race.

EpidemiologyEpidemiology

Risk factorsRisk factorsChronic hypertension.Chronic hypertension.Chronic nephritis.Chronic nephritis.Past history.Past history.Family history.Family history.Obesity.Obesity.Multiple pregnancy.Multiple pregnancy.

Epidemiology – RiskEpidemiology – Risk factorfactorss

Polyhydramnios.Polyhydramnios.

Vesicular mole.Vesicular mole.

Diabetes mellitus. Diabetes mellitus.

Nulliparity.Nulliparity.

TeenageTeenage / over 35 years / over 35 years pregnancy. pregnancy.

Afro-American ethnicityAfro-American ethnicity..

StressStress..

Etiology= Etiology= theoriestheories

1. 1. Abnormal trophoblastic Abnormal trophoblastic invasioninvasion

Incomplete invasion → atherosisIncomplete invasion → atherosis

The development of uteroplacental vessels

1-st wave → before 12 w. → invasion + modification of spiral arteries up to the border between decidua and myometrium.

2-nd wave → 12 - 16 w. → invasion of the intramyometrial segments of spiral arteries.

Remodeling of spiral arteries into dilated, low-resistance uteroplacental vessels.

Significance - pathogenesis of preeclampsia, IUGR.

Triggers for PETriggers for PE

Genetic ModulatorsGenetic Modulators

Pre-existing Vascular PathologyPre-existing Vascular Pathology

Central players

Cytokines

Ros


2. Immunological Factor2. Immunological Factorss abnormal trophoblast invasionabnormal trophoblast invasion

primigravidasprimigravidas

Multipara with 1st pregnancy Multipara with 1st pregnancy from a new husband. from a new husband.

Abundant trophoblastAbundant trophoblast (vesicular (vesicular mole and multiple pregnancymole and multiple pregnancy))..

EtiologyEtiology = = theoriestheories3. Vasculopathy and 3. Vasculopathy and

inflammatory changes inflammatory changes Endothelin Endothelin 11 ((potent vasoconstrictorpotent vasoconstrictor).).

Nitric Oxide Nitric Oxide ((vasodilatorvasodilator).).

Vascular Endothelial Growth Factor (VEGF).Vascular Endothelial Growth Factor (VEGF).

PE - an PE - an inflammatory disease = activated inflammatory disease = activated leukocytes in the maternal circulationleukocytes in the maternal circulation. .


4. Nutritional factors4. Nutritional factors• Dietary deficienciesDietary deficiencies• Zn, Ca, MgZn, Ca, Mg• obesityobesity


5. Genetic Predisposition5. Genetic Predisposition

Genetic factors including inherited

predisposing genes

PATHOGENESISPATHOGENESIS

I. Arteriolar vasospasm I. Arteriolar vasospasm

II. Endothelial cell activationII. Endothelial cell activationIncreased pressor responses (AII)Increased pressor responses (AII)

Prostaglandins (decreased prostacyclin / Prostaglandins (decreased prostacyclin /

thromboxane A2 ratio)thromboxane A2 ratio)

Nitric oxideNitric oxide

Endothelins (endothelin-1)Endothelins (endothelin-1)

Angiogenic factors (VEGF, PIGF)Angiogenic factors (VEGF, PIGF)

PathologyPathologyPEPE is the clinical is the clinical ice-ice-

berg tipberg tip manifestation manifestation of the disturbances in of the disturbances in the the maternal maternal homeostasis, involving homeostasis, involving many systems and many systems and organs.organs.

Pathophysiological Pathophysiological ChangesChanges

Cardiovascular systemCardiovascular system (hemodynamic (hemodynamic changes, blood volume, platelets, changes, blood volume, platelets, coagulation, hemolysis)coagulation, hemolysis)

KidneyKidney (proteinuria, anatomical changes) (proteinuria, anatomical changes)LiverLiverBrainBrain (cerebral blood flow, blindness, (cerebral blood flow, blindness,

cerebral edema)cerebral edema)Uteroplacental perfusionUteroplacental perfusion

Multisystem Features Of Multisystem Features Of PreeclampsiaPreeclampsia

Hypertension Proteinuria

Eclampsia HELLP syndrome

Intra-uterine growth restriction

Multi-organ disease

Cerebral vessels

Fetus

Liver

Systemic blood vessels Kidneys

DiagnosisDiagnosis

11 ) )PredictionPrediction

22))CCllinical inical ppresentationresentation & & SeveritySeverity

33))EclampsiaEclampsia

DiagnosisDiagnosisI. Prediction:I. Prediction:

High risk factors.High risk factors.Rapid weight gain during the Rapid weight gain during the 2nd half of pregnancy (due to 2nd half of pregnancy (due to occult edema). occult edema). Any increase above 3/4 kg/week in late Any increase above 3/4 kg/week in late pregnancy is abnormal.pregnancy is abnormal.

Tests for PredictionTests for PredictionRoll over test is positiveRoll over test is positive (rise of diastolic blood (rise of diastolic blood pressure 20 mmHg or more after turning from left pressure 20 mmHg or more after turning from left lateral to dorsal position).lateral to dorsal position).

Increased pressor response to AII.Increased pressor response to AII.

Uric acid: is elevated (> 5.9mg/dL).Uric acid: is elevated (> 5.9mg/dL).

Hypercalciuria.Hypercalciuria.

Doppler velocimetry to detect Uteroplacental hypo Doppler velocimetry to detect Uteroplacental hypo perfusion.perfusion.

Tests for PredictionTests for Prediction

Coagulation activation Coagulation activation (increased PAI-1/PAI-2 ratio; (increased PAI-1/PAI-2 ratio; PAI = plasminogen activator inhibitors).PAI = plasminogen activator inhibitors).

Oxidative stress.Oxidative stress.

Cytokines.Cytokines.

Placental peptides (HCG, CRH, VEGF, PIGF, inhibin A, Placental peptides (HCG, CRH, VEGF, PIGF, inhibin A, activin A).activin A).

Fetal DNA in the maternal serum.Fetal DNA in the maternal serum.

Diagnosis of PEDiagnosis of PE

Hypertension Hypertension + + ProteinuriaProteinuria ==

Two facets of a complex Two facets of a complex pathophysiological processpathophysiological process

A): SignsA): Signs : :::

it is a disease of signsit is a disease of signs:

2 cardinal signs2 cardinal signs

HypertensionHypertension – usually precedes Proteinuria, usually precedes Proteinuria,

ProteinuriaProteinuria

+ + // - Edema - Edema

- / + - / +EdemaEdema

occult or manifest:occult or manifest:The lower extremities.The lower extremities.Abdominal wall, vulva or may Abdominal wall, vulva or may be generalized.be generalized.

usually after hypertension.usually after hypertension.

B) Symptoms (non B) Symptoms (non specificspecific))

Headache.Headache.

Blurring of vision.Blurring of vision.

Nausea and vomiting.Nausea and vomiting.

Epigastric pain (distension of the liver Epigastric pain (distension of the liver capsule)capsule)

Oliguria or anuriaOliguria or anuria

Severity of Pre-Severity of Pre-eclampsiaeclampsia

The severity of pre-eclampsia The severity of pre-eclampsia ((assessed assessed byby tthe frequency and intensity of the he frequency and intensity of the signs signs andand symptoms symptoms))

1.1.Mild PEMild PE

2.2.Severe PESevere PEThe more The more the severity of PEthe severity of PE, the more likely , the more likely

is the need is the need to terminate pregnancy.to terminate pregnancy.

Differential Dg., mild & Differential Dg., mild & severe PEsevere PE

AbnormalityMildSevereSevereDiastolic blood pressure< 100 mg Hg110 mm Hg or higher110 mm Hg or higher

ProteinuriaTrace to 1g/24hPersistent 2g or more/24hPersistent 2g or more/24h

HeadacheAbsentPresentPresent

Visual disturbancesAbsentPresentPresent

Upper abdominal painAbsentPresentPresent

OliguriaAbsentPresentPresent

ConvulsionAbsentPresent (eclampsia)Present (eclampsia)

Serum creatinineNormalElevatedElevated

ThrombocytopeniaAbsentPresentPresent

Liver enzyme elevationMinimalMarkedMarked

Fetal growth restrictionAbsentObviousObvious

Pulmonary edemaAbsentPresentPresent

DEFINITION OF DEFINITION OF ECLAMPSIAECLAMPSIA::

Eclampsia is the occurrence of seizures (generalized tonic-clonic convulsions

that cannot be attributed to other causes) in a woman with preeclampsia .

The seizures are grand mal and may appear antepartum, intrapartum, or

postpartum (48 hours postpartum up to 10 days postpartum) .

ECLAMPSIAECLAMPSIA

☼ Almost without exception, preeclampsia precedes the onset of eclamptic convulsions .

☼ The incidence: about 1 in 3250 up to1 in 2000 deliveries.

DIAGNOSIS OF DIAGNOSIS OF ECLAMPSIAECLAMPSIA

Eclamptic seizure stages (4 stages):Eclamptic seizure stages (4 stages):–Premonitory stage (1/2 minute): Premonitory stage (1/2 minute):

Eye rolled up.Eye rolled up.

Twitches of the face and hands. Twitches of the face and hands. –Tonic stage (1/2 minute): Tonic stage (1/2 minute):

Generalized tonic spasm with Generalized tonic spasm with opisthotonus.opisthotonus.

Cyanosis.Cyanosis.

Tongue may be bitten between the Tongue may be bitten between the clenched teeth. clenched teeth.

DIAGNOSIS OF DIAGNOSIS OF ECLAMPSIAECLAMPSIA::

Clonic stage (1-2 minutes): Clonic stage (1-2 minutes): Convulsions.Convulsions.

Tongue may be bitten.Tongue may be bitten.

Face is congested and cyanosed.Face is congested and cyanosed.

Conjunctival congestion.Conjunctival congestion.

Blood stained froth from the mouth.Blood stained froth from the mouth.

Stertorous breathing,Stertorous breathing,

Temperature may rise.Temperature may rise.

Involuntary passage of urine or stool.Involuntary passage of urine or stool.

Gradually convulsions stop.Gradually convulsions stop.

DIAGNOSIS OF DIAGNOSIS OF ECLAMPSIAECLAMPSIA::

ComaComa – Variable duration due to respiratory and Variable duration due to respiratory and

metabolic acidosis.metabolic acidosis.– Deep coma Deep coma →→ cerebral hemorrhage. cerebral hemorrhage. – Labor starts shortly after the seizure.Labor starts shortly after the seizure.– Sometimes labor does not start and Sometimes labor does not start and

convulsions recur again the so called convulsions recur again the so called ‘‘intercurrent eclampsiaintercurrent eclampsia’’ and carries a and carries a bad prognosis.bad prognosis.

CLASSIFICATIONS OF CLASSIFICATIONS OF ECLAMPSIAECLAMPSIA

– Intercurrent EclampsiaIntercurrent Eclampsia: : eclamptic seizures recur in the eclamptic seizures recur in the same pregnancy.same pregnancy.

– Recurrent EclampsiaRecurrent Eclampsia: : eclampsia recurs in subsequent eclampsia recurs in subsequent pregnancy.pregnancy.


– Ante partum (65%)Ante partum (65%) with the best with the best prognosis.prognosis.

– Intrapartum (20%).Intrapartum (20%).

–Postpartum (15%)Postpartum (15%) with the worst with the worst prognosis as it indicates extensive prognosis as it indicates extensive pathology and multisystem pathology and multisystem damage.damage.


1)Mild1)MildComa > 6 hours.Coma > 6 hours.

2) Severe (Eden's criteria):2) Severe (Eden's criteria):Temperature > 39Temperature > 39 ˚̊CC (pneumonia or pontine (pneumonia or pontine hemorrhage)hemorrhage)

Systolic Bp > 200 Systolic Bp > 200 (cerebral hemorrhage risk)(cerebral hemorrhage risk)

Pulse > 120/min Pulse > 120/min (acute heart failure).(acute heart failure).

Anuria or Oliguria Anuria or Oliguria (renal failure).(renal failure).

Respiratory rate > 40/min Respiratory rate > 40/min (pneumonia)(pneumonia)

More than 10 fits More than 10 fits ((status eclampticusstatus eclampticus).).

PATHOLOGY OF ECLAMPSIAOF ECLAMPSIA

► Pathological deterioration of function in several organs and systems, as a consequence of vasospasm and ischemia.

► Maternal and fetal consequences often occur simultaneously.

► The major cause of fetal compromise occurs as a consequence of reduced uteroplacental

perfusion .


CARDIOVASCULAR CHANGES

► increased cardiac afterload caused by hypertension ,

► cardiac preload, affected by pathologically diminished hypervolemia of pregnancy or iatrogenically increased by intravenous crystalloid or oncotic solutions

► endothelial activation with extravasation into the extracellular space, especially the lung.

PATHOLOGYPATHOLOGY OF OF ECLAMPSIAECLAMPSIA

BLOOD VOLUME

► hemoconcentration → hallmark of eclampsia .

► the woman with eclampsia → unduly sensitive to vigorous fluid therapy )an attempt to expand the contracted blood volume to normal pregnancy levels). She is sensitive as well to even normal blood loss at delivery.

PATHOLOGY OF ECLAMPSIAOF ECLAMPSIAHEMATOLOGICAL CHANGES. COAGULATION

► the level of plasma clotting factors → decreased;

► erythrocytes may be traumatized → display bizarre shapes and undergo rapid hemolysis

► intravascular coagulation

► maternal thrombocytopenia can be induced acutely; the lower the platelet count, the greater are maternal and fetal morbidity and

mortality.


KIDNEY

►proteinuria

►renal perfusion and glomerular filtration reduced

►plasma uric acid concentration is typically elevated

►glomerular capillary endotheliosis = glomerular capillary endothelial swelling + subendothelial deposits of protein material )electron microscopy)

►renal tubular lesions → acute renal failure from tubular necrosis )oliguria / anuria and azotemia);

rarely, renal cortical necrosis develops.


LIVER

► elevation of serum aspartate aminotransferase levels

►periportal hemorrhagic necrosis → bleeding from these lesions may cause hepatic rupture, or a subcapsular hematoma.

PATHOLOGY OF ECLAMPSIAOF ECLAMPSIABRAIN

►central nervous system → convulsions of eclampsia

► visual symptoms, blindness, retinal artery vasospasm, retinal detachment

► symptomatic cerebral edema: lethargy, confusion, and blurred vision to obnubilation and coma .

►nonspecific electroencephalographic abnormalities .

The principal postmortem cerebral lesions are edema, hyperemia, focal anemia, thrombosis, and hemorrhage.

InvestigationsInvestigations

A. LaboratoryA. Laboratory– UrineUrine:: 24 hour urine, Proteinuria. 24 hour urine, Proteinuria.– Kidney functionsKidney functions: serum creatinine, urea, : serum creatinine, urea,

creatinine clearance and uric acid. creatinine clearance and uric acid. – Liver functionsLiver functions: bilirubin, enzymes )SGPT : bilirubin, enzymes )SGPT

and SGOT).and SGOT).– BloodBlood:: CBC, HCt, Hemolysis indices, Platelet CBC, HCt, Hemolysis indices, Platelet

count.count.– Coagulation ProfileCoagulation Profile: Bleeding + clotting time: Bleeding + clotting time

InvestigationsInvestigations

B.B. InstrumentalInstrumentalEye Fundus ExaminationEye Fundus Examination..

C. Imaging techniques:C. Imaging techniques:CTCT scan for the brain. scan for the brain.

UltrasonograghyUltrasonograghy..

EE. . DopplerDoppler Velocimetry.Velocimetry.

VI. Differential DiagnosisVI. Differential Diagnosis

A. A. Hypertension With PregnancyHypertension With Pregnancy..

B. Proteinuria With PregnancyB. Proteinuria With Pregnancy. .

C. C. Edema With PregnancyEdema With Pregnancy::

VI. Differential DiagnosisVI. Differential Diagnosis

D. Convulsions With D. Convulsions With PregnancyPregnancy::

EpilepsyEpilepsy

Uremic convulsionsUremic convulsions

Meningitis / EncephalitisMeningitis / Encephalitis

TetanusTetanus

Strychnine poisoning Strychnine poisoning

Brain tumorsBrain tumors

E. Coma With E. Coma With PregnancyPregnancy::

HypoglycemicHypoglycemic

Hyperglycemic Hyperglycemic coma.coma.

Uremic coma.Uremic coma.

Hepatic coma.Hepatic coma.

Alcoholic coma.Alcoholic coma.

Cerebral comaCerebral coma..

THE HELLP SYNDROME

hemolysis (H) +

elevated liver enzymes (EL) +

low platelets (LP)

almost 20% of women with severe preeclampsia or eclampsia

Major complications

abruptio placentae )10 %), neurological deficits )7 %), aspiration pneumonia )7 %), pulmonary edema )5 %), cardiopulmonary arrest )4 %), acute hepato-renal failure )4 %), maternal death )1 %).

PreventionPreventionPreventionPrevention

Low dose aspirin: 75 mg/day.Low dose aspirin: 75 mg/day.Decrease TxADecrease TxA22 (from Platelets). (from Platelets).

Calcium supplementationCalcium supplementation::↑↑ production of prostacyclin (PGIproduction of prostacyclin (PGI22) )

from endothelial cells.from endothelial cells.

Antioxidants – vitamine C, EAntioxidants – vitamine C, E

Dietary manipulationsDietary manipulations – salt – salt restriction, fish oilrestriction, fish oil

The most effective preventive The most effective preventive measures for measures for occurance of occurance of

pre-eclampsia pre-eclampsia IS IS PREVENTION OF PREVENTION OF

PREGNANCYPREGNANCY “contraception”“contraception”

PreventionPreventionPreventionPrevention

Treatment of Treatment of preeclampsiapreeclampsia

Expectant Treatment.Expectant Treatment.

Control of Hypertension.Control of Hypertension.

Prevention of convulsions.Prevention of convulsions.

Termination of pregnancy.Termination of pregnancy.

1) Expectant Treatment1) Expectant Treatment

RestRest: Complete Physical and mental rest.: Complete Physical and mental rest.

Diet:Diet: Increase protein and carbohydrate Increase protein and carbohydrate

with low Na diet )!?).with low Na diet )!?).

Sedation:Sedation: Phenobarbital & Diazepam. Phenobarbital & Diazepam.

Observation Observation )maternal & fetal).)maternal & fetal).

1) Expectant Treatment 1) Expectant Treatment (Observation)(Observation)

Maternal:Maternal:– Blood pressure.Blood pressure.– Pulse and Respiratory rate.Pulse and Respiratory rate.– Urine output.Urine output.– Proteinuria.Proteinuria.– Any new symptoms.Any new symptoms.– Investigations (Investigations (creatinine, creatinine clearance, creatinine, creatinine clearance,

blood picture, coagulation profile,….)blood picture, coagulation profile,….)

Fetal:Fetal: fetal well-beingfetal well-being

2) Control of 2) Control of HypertensionHypertension

2) Control of 2) Control of HypertensionHypertension

A) Parenteral drugs:A) Parenteral drugs:

–1) Hydralazine1) Hydralazine:: a peripheral VD. a peripheral VD.

The best Antihypertensive drug used during The best Antihypertensive drug used during Pre-eclampsia and Eclampsia.Pre-eclampsia and Eclampsia.

– 2) Labetalol (Trandate2) Labetalol (Trandate)): : α + non selective β-α + non selective β-adrenergic blocker resulting in VD.adrenergic blocker resulting in VD.

– 3) Diazoxide (Hyperstat3) Diazoxide (Hyperstat)):: in in severe severe dangerous resistant hypertension as a last dangerous resistant hypertension as a last resort. resort.

2)Control of 2)Control of HypertensionHypertension

B )Oral drugsB )Oral drugs1) α-methyl DOPA (aldomet):1) α-methyl DOPA (aldomet): α-adrenergic agonist α-adrenergic agonist →→

depletion of catecholamine stores. depletion of catecholamine stores. DoseDose: 500mg 3-4 times/day : 500mg 3-4 times/day orally.orally.

2) Monohydralazine (Aprisoline):2) Monohydralazine (Aprisoline): weak weak antihypertensive (given alone) + β- blockersantihypertensive (given alone) + β- blockers

– 3) β- adrenergic blockers3) β- adrenergic blockers: : Atenolol (tenormin), Atenolol (tenormin), Labetalol (Trandate).Labetalol (Trandate).

– 4) Prazocin (minipres4) Prazocin (minipres):): postsynaptic α-adrenergic postsynaptic α-adrenergic receptor blocker receptor blocker →→ VD and reflex tachycardia. VD and reflex tachycardia.

– 5) Calcium Channel Blocker5) Calcium Channel Blocker: : NifedipineNifedipine (Adalat or Epilat) .(Adalat or Epilat) .

Treatment of Treatment of PreeclampsiaPreeclampsia

3) Prevention of convulsions3) Prevention of convulsions

4) Termination of pregnancy4) Termination of pregnancy

Treatment of EclampsiaTreatment of EclampsiaPPrinciplesrinciples

1. Control of convulsions (i.v. MgSO4 loading dose, followed by continuous MgSO4).

2. Antihypertensive medication - intermittent administration.

3. Avoidance of diuretics (unless obvious pulmonary edema), of hyperosmotic agents, limitation of intravenous fluid administration (unless excessive fluid loss).

4. Delivery of the fetus to achieve a “cure”.

Treatment of EclampsiaTreatment of Eclampsia1) General and first aid measures:1) General and first aid measures:

– Isolation in a single, quiIsolation in a single, quieet, semi-dark room, an efficient t, semi-dark room, an efficient nurse.nurse.

– Equipments )Equipments )Oxygen source, Suction apparatus, bed Oxygen source, Suction apparatus, bed with movable head and legs with limb ties).with movable head and legs with limb ties).

– The patient in The patient in Trendlenburg Trendlenburg positionposition )to avoid )to avoid aspiration of secretions).aspiration of secretions).

– Insert a catheter, Insert a catheter, nothing by mouth, fluid chart.nothing by mouth, fluid chart.– Full laboratory investigation.Full laboratory investigation.

Treatment of EclampsiaTreatment of Eclampsia

2) Observation2) Observation::– Pulse, temperature, BP and respiratory rate.Pulse, temperature, BP and respiratory rate.

– Level of consciousness.Level of consciousness.

– Duration of coma.Duration of coma.

– Fetal heart sounds.Fetal heart sounds.

– Urine output and albuminuria.Urine output and albuminuria.

– Number of convulsions. Number of convulsions.


3) Sedation:3) Sedation:

Morphine Morphine 10-20mg IM 10-20mg IM

DiazepamDiazepam

– for maintaining by 10mg IV or IM/8 hours. for maintaining by 10mg IV or IM/8 hours.

Lytic cocktailLytic cocktail

– 25mg25mg chlorpromazine + chlorpromazine + 50mg50mg phenergan + phenergan +

100mg 100mg pethidine.pethidine.

Treatment of EclampsiaTreatment of Eclampsia 4) Control of 4) Control of Convulsions:Convulsions:

A) Magnesium Sulfate (MgSO4):A) Magnesium Sulfate (MgSO4):It is the drug of choice.It is the drug of choice.

Mechanisms: Mechanisms: CNS depression, mild VD, mild CNS depression, mild VD, mild diuresis, inhibits platelet aggregation, diuresis, inhibits platelet aggregation, ↑ ↑ PGIPGI22

synthesis.synthesis.

IV regimenIV regimen:: initially 4-6 g (20%) in 100ml initially 4-6 g (20%) in 100ml solution (given over 15-20 minutes), solution (given over 15-20 minutes), then, 2 then, 2 g/hour by IV drip. g/hour by IV drip.

IM regimen:IM regimen: 10 g of 50% solution deeply IM (5 g 10 g of 50% solution deeply IM (5 g in each buttock), in each buttock), maintain with 5 g/6 hours of 50% maintain with 5 g/6 hours of 50% solution.solution.

Side effectsSide effects of MgSO4of MgSO4 (small safety (small safety margin)margin)

– lost patellar reflexlost patellar reflex– myometrial inhibition myometrial inhibition → → uterine inertiauterine inertia– respiratory depressionrespiratory depression– cardiac depressioncardiac depression– curara-like action.curara-like action.– Synergistic effect with Ca++ channel blockers.Synergistic effect with Ca++ channel blockers.– Neonatal hypermagnesemia.Neonatal hypermagnesemia.– Decreased beat to beat variability in FHR.Decreased beat to beat variability in FHR.

AntidoteAntidote : : 10ml of 1010ml of 10%% calcium calcium gluconate gluconate

4) Control of Convulsions:4) Control of Convulsions:Phyenitoin (Epanutin)Phyenitoin (Epanutin)

Diazepam (Valium)Diazepam (Valium) – Initially 20-40mg IV slowly over 5 minutes. Initially 20-40mg IV slowly over 5 minutes. – then 10-20mg/6hours. then 10-20mg/6hours.

5) Control of hypertension5) Control of hypertension

6)Other drugs:6)Other drugs:– Prophylactic digitalisProphylactic digitalis to guard against HFto guard against HF– AntibioticAntibiotic for infection.for infection.– IV glucoseIV glucose - a liver support, - a liver support, ↑↑ urine output and urine output and

improves hemoconcentration.improves hemoconcentration.


5) Control of hypertension5) Control of hypertension

6)Other drugs:6)Other drugs:

– Prophylactic digitalisProphylactic digitalis to guard against HF to guard against HF

– Antibiotic Antibiotic for infection.for infection.

– IV glucoseIV glucose - a liver support, - a liver support, ↑↑ urine output and urine output and

improves hemoconcentration.improves hemoconcentration.

7)Termination of 7)Termination of PregnancyPregnancy

MethodsMethods: :

– CS - CS - Indications:Indications:Eclampsia.Eclampsia.

Retinal hemorrhage.Retinal hemorrhage.

Deteriorated cardiac, renal or liver Deteriorated cardiac, renal or liver functions.functions.

Severe PE not controlled after 24 hours.Severe PE not controlled after 24 hours.

Mild PE reaching 38 weeks, not Mild PE reaching 38 weeks, not controlledcontrolled..

Deterioration of the fetal conditions.Deterioration of the fetal conditions.

Other obstetric indications.Other obstetric indications.

8) Intrapartum 8) Intrapartum management:management:

vaginal delivery is safer and better than CS vaginal delivery is safer and better than CS (???)(???)..

Artificial rupture of membranes and Artificial rupture of membranes and oxyoxytocin driptocin drip..Epidural anesthesia is the best for both CS and Epidural anesthesia is the best for both CS and vaginal delivery )if vaginal delivery )if disseminated intravascular disseminated intravascular coagulationcoagulation is excluded). is excluded).

Avoid straining in the second stage.Avoid straining in the second stage.

Shorten the 2nd stage by forceps or ventouse.Shorten the 2nd stage by forceps or ventouse.

No ergometrine Intrapartum.No ergometrine Intrapartum.

Prognosis:Prognosis:

BP usually normalize after placental BP usually normalize after placental delivery.delivery.Hypertension may persist.Hypertension may persist.Postpartum eclampsia - the worst Postpartum eclampsia - the worst prognosis.prognosis.Maternal mortalityMaternal mortality - 2% in severe - 2% in severe preeclampsia and 10% in eclampsia.preeclampsia and 10% in eclampsia.Perinatal mortalityPerinatal mortality rate = 5% in mild rate = 5% in mild cases, 25% in severe cases and 30% in cases, 25% in severe cases and 30% in eclampsia.eclampsia.

CHRONIC HYPERTENSION AND PREGNANCY

► increased perinatal mortality and morbidity

► increased risk for the superimposed PE and abruptio placentae → 10 to 15%.

DiagnosisCHRONIC HYPERTENSION

AND PREGNANCY

history hypertension - before

week 20 of pregnancy general physical

examination repeated blood pressure

determinations eye examination renal function

assessment blood urea nitrogen cardiac evaluation.

periodic sonographic measurement of fetal diameters

nonstress test / contraction stress / biophysical score


Prenatal care

Interruption of pregnancy the systolic blood pressure is > 180 - 200mm Hg or the diastolic pressure is 110mm Hg or more degenerative changes in the retinal arterioles previous cerebral hemorrhage or PE during previous pregnancies renal function is reduced

Antenatal visitsHospitalization


Medical treatment

Methyldopa

Clonidine

Prazosin

Propranolol

Atenolol

Labetalol

Calcium channel blockers

alone or in combination

Hydralazine

The angiotensin-converting enzyme inhibitors (Captopril, Enalapril, Lisinopril) are

not recommended in pregnancy.


Obstetrical treatmenttermination of the pregnancy → CS if superimposed PE that cannot be controlled with medical treatment.

induction of labor as soon as fetal maturity is present )if the blood pressure remains stable or falls slightly and if PE does not develop).

HYPERTENSIVE DISORDERS IN PREGNANCY ASSOCIATE PROFESSOR IOLANDA BLIDARU MD, PhD.

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