HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC...

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HYPERTENSIVE DISORDERS HYPERTENSIVE DISORDERS IN PREGNANCY IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC & ADOLESCENT GYNECOLOGIST

Transcript of HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC...

Page 1: HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC & ADOLESCENT GYNECOLOGIST.

HYPERTENSIVE DISORDERS HYPERTENSIVE DISORDERS IN PREGNANCYIN PREGNANCY

DR. SALWA NEYAZI

ASSISSTANT PROF KSU/ CONSULTANT OBGYN

PEDIATRIC & ADOLESCENT GYNECOLOGIST

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TYPES OF HYPERTENSIVE DISEASE IN TYPES OF HYPERTENSIVE DISEASE IN PREGNANCYPREGNANCY

1-Gestational hypertension 1-Gestational hypertension

2-PET2-PET

3-Eclampsia3-Eclampsia

4-Chronic hypertension4-Chronic hypertension

5-PET superimposed on chronic hypertension5-PET superimposed on chronic hypertension

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11--Gestational hypertensionGestational hypertension

BP ≥ 140/90 mm Hg for the first time during pregnancyBP ≥ 140/90 mm Hg for the first time during pregnancy

No proteinuriaNo proteinuria

BP returns to N < 12 Wk postpartumBP returns to N < 12 Wk postpartum

Final Dx made only postpartumFinal Dx made only postpartum

May have other signs of PET eg. Headache, epigastric May have other signs of PET eg. Headache, epigastric discomfort or thrombocytopeniadiscomfort or thrombocytopenia

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PETPET

Minimum criteriaMinimum criteria

BP ≥ 140/90 mm Hg after 20 Wk gestationBP ≥ 140/90 mm Hg after 20 Wk gestation

Proteinuria ≥ 300 mg/24 hrs or ≥ 1Proteinuria ≥ 300 mg/24 hrs or ≥ 1+ + dipstickdipstick

Increased certainty of PETIncreased certainty of PET

BP ≥ 160/110 mm HgBP ≥ 160/110 mm Hg

Proteinuria ≥ 2 gm/24 hrs or ≥ 2Proteinuria ≥ 2 gm/24 hrs or ≥ 2+ + dipstickdipstick

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

Platelets < 100 000/mm³Platelets < 100 000/mm³

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Increased certainty of PETIncreased certainty of PET

Microangiopathic hemolysis (increased LDH)Microangiopathic hemolysis (increased LDH)

Elevated ALT or ASTElevated ALT or AST

Persistant headache or other cerebral/ visual Persistant headache or other cerebral/ visual disturbancedisturbance

Persistant epigastric painPersistant epigastric pain

ECLAMPSIAECLAMPSIA

Seizures that can not be attributed to other causes in Seizures that can not be attributed to other causes in a woman with PET. 1% of Pt with PET develop ECa woman with PET. 1% of Pt with PET develop EC

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CHRONIC HYPERTENSIONCHRONIC HYPERTENSION

BP ≥BP ≥ 140/90 mm Hg before pregnancy or Dx before 20 140/90 mm Hg before pregnancy or Dx before 20 Wk gestationWk gestation

HPT first Dx after 20 Wk gestation & persistant after 12 HPT first Dx after 20 Wk gestation & persistant after 12 Wk postpartumWk postpartum

PET SUPERIMPOSED ON CHRONIC HYPERTENSIONPET SUPERIMPOSED ON CHRONIC HYPERTENSION

New onset proteinuria ≥ 300 mg/24 hrs in hypertensive New onset proteinuria ≥ 300 mg/24 hrs in hypertensive women but no proteinuria before 20 Wk gestationwomen but no proteinuria before 20 Wk gestation

A sudden increase in proteinuria or BP or A sudden increase in proteinuria or BP or

Plt count < 100 000/ mm³in women with HPT & Plt count < 100 000/ mm³in women with HPT & proteinuria before 20 Wk gestationproteinuria before 20 Wk gestation

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INCIDENCE & RISK FACTORSINCIDENCE & RISK FACTORS

PET occurs in 6-8% of all live birthPET occurs in 6-8% of all live birth

RISK FACTORSRISK FACTORS

Extremes of reproductive age Extremes of reproductive age 15 < & >35 Y15 < & >35 Y

NulliparityNulliparity

Black raceBlack race

Hx of PET in a 1Hx of PET in a 1stst degree degree female relativefemale relative

Hx of PET in prior pregnancyHx of PET in prior pregnancy

DMDM

Chronic renal diseaseChronic renal disease

Ch HPTCh HPT

Multiple pregnancy Multiple pregnancy twins 13 twins 13 vs 6%vs 6%

Hydatidiform moleHydatidiform mole

Nonimmune hydrops fetalisNonimmune hydrops fetalis

Obesity Obesity 4.3% 4.3% BMI < 19.8 BMI < 19.8 kg/m²kg/m²

13.3% 13.3% BMI ≥ 35 BMI ≥ 35 kg/m²kg/m²

Smoking Smoking ↓ risk of HPT ↓ risk of HPT

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PATHOGENESISPATHOGENESIS

Endothelial cell injury Endothelial cell injury ↓ ↓ prostacyclin & ↑ thromboxaneA2↓ ↓ prostacyclin & ↑ thromboxaneA2

Rejection phenomenon (inadequate matenal Ab response)Rejection phenomenon (inadequate matenal Ab response)

Compromised placental perfusionCompromised placental perfusion

Altered vascular reactivity Altered vascular reactivity ↑sensitivity to vaspressin EPN, ↑sensitivity to vaspressin EPN, NEPN & angiotensinNEPN & angiotensin

↓ ↓ GFR with retention of salt & waterGFR with retention of salt & water

↓ ↓ intravascular volumeintravascular volume

↑ ↑ CNS irritabilityCNS irritability

DICDIC

Uterine muscle stretch & ischemiaUterine muscle stretch & ischemia

Dietary factors Dietary factors

Genetic factorsGenetic factors

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PATHOGENESISPATHOGENESIS

Summary of current hypothesis:Summary of current hypothesis:

Immunological disturbance Immunological disturbance abnormal placental abnormal placental

implantation implantation ↓ placental perfusion ↓ placental perfusion production of production of

substances that activate or injure endothelial cells of thesubstances that activate or injure endothelial cells of the

blood vessels blood vessels multiple organ system involvement multiple organ system involvement

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PATHOPHYSIOLOGYPATHOPHYSIOLOGY

MULTIPLE ORGAN SYSTEM MULTIPLE ORGAN SYSTEM INVOLVMENTINVOLVMENT

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11 - -CNSCNS

Similar to hypertensive encephalopathySimilar to hypertensive encephalopathy

Petechial HgPetechial Hg

Gross hemorrhages due to ruptured arteriesGross hemorrhages due to ruptured arteries

Thrombosis of the arteriolesThrombosis of the arterioles

MicroinfarctsMicroinfarcts

Fibrinoid necrosis in the walls of blood vesselsFibrinoid necrosis in the walls of blood vessels

Cerebral edema Cerebral edema confusion, blurred vision / coma confusion, blurred vision / coma

Brain stem herniation is a serious complication of cerebral Brain stem herniation is a serious complication of cerebral edema edema death death

MECHANISM MECHANISM cerebral hyperperfusion ,vasospasm cerebral hyperperfusion ,vasospasm &forced dilation&forced dilation

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11 - -CNSCNS

CT ScanCT Scan ½ of the pt ½ of the pt focal hypodensities in the focal hypodensities in the white matter / post half of the cerebral hemisphere & white matter / post half of the cerebral hemisphere & occasionally in the grey matter occasionally in the grey matter may represent may represent petechial Hgpetechial Hg

Severe cases Severe cases IV Hg or subarachnoid HgIV Hg or subarachnoid Hg

MRIMRI Abnormalities in the cortical & subcortical white Abnormalities in the cortical & subcortical white matter of the occipital & parietal areasmatter of the occipital & parietal areas

EEGEEG nonspecific changesnonspecific changes

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22--PULMONARY SYSTEMPULMONARY SYSTEM

Pulmonary edemaPulmonary edema

May occur with sever PET OR ECMay occur with sever PET OR EC

Usually postpartumUsually postpartum

May be due to excessive fluid administration with May be due to excessive fluid administration with crystalloids crystalloids + + ↓ plasma colloid pressure due to ↓ plasma colloid pressure due to proteinuriaproteinuria

↑ ↑ in Pt with ch HPT & hypertensive cardiac diseasein Pt with ch HPT & hypertensive cardiac disease

Aspiration of gastric content with ECAspiration of gastric content with EC

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3-CVS3-CVS

Plasma volume is reduced, the cause is unknownPlasma volume is reduced, the cause is unknown theories:theories:

1-Generalized vasoconstriction with ↑ vascular 1-Generalized vasoconstriction with ↑ vascular permeability permeability Advocate the use of vasodilators Advocate the use of vasodilators

2-1ry hypovolemia 2-1ry hypovolemia hypoperfusion of the uterus hypoperfusion of the uterus release of pressor substances release of pressor substances HPT HPT

Advocate the use of volume expanders & avoidance Advocate the use of volume expanders & avoidance of diureticsof diuretics

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33--CVSCVS

High systemic vascular resistance & hyperdynamic High systemic vascular resistance & hyperdynamic ventricular functionventricular function avoid aggressive fluid avoid aggressive fluid adminstrationadminstration

Loss of the normal refractoriness to angiotensin IILoss of the normal refractoriness to angiotensin II

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44--BLOODBLOOD

HemoconcentrationHemoconcentrationThrombocytopenia < 150 000 Thrombocytopenia < 150 000 15-20% of PT 15-20% of PTFibrinogen ↑Fibrinogen ↑Thrombin time ↑ in 1/3 of the Ptwith ECThrombin time ↑ in 1/3 of the Ptwith ECFDP ↑ FDP ↑ 20% of the Pt 20% of the PtDIC DIC 5% 5%Microangiopathic hemolytic anemia Microangiopathic hemolytic anemia 5%5%HEELP HEELP hemolytic anemia, ↑↑ liver enzymes, low Plthemolytic anemia, ↑↑ liver enzymes, low Plt

-LDH > 600 U/L-LDH > 600 U/L -T bilirubin >1.2 mg/dl-T bilirubin >1.2 mg/dl -AST > 70U/L-AST > 70U/L -Plt < 100 000/mm³-Plt < 100 000/mm³Found in 10% of the Pt with severe PETFound in 10% of the Pt with severe PET

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5-KIDNEY5-KIDNEY

Characteristic lesion Characteristic lesion glomeruloendotheliosis glomeruloendotheliosis swelling swelling of the gromelular capillary endothelium of the gromelular capillary endothelium ↓↓GFR ↓↓GFR↓↓ ↓↓ creatinine clearance/ ↑↑plasma creatinine creatinine clearance/ ↑↑plasma creatinine ↑↑ ↑↑ uric aciduric acidProteinuriaProteinuriaRenal tubular necrosis &renal failureRenal tubular necrosis &renal failure

6-Eyes6-Eyes

Visual disturbances Visual disturbances due to retinal artery vasospasm due to retinal artery vasospasmRetinal detachment Retinal detachment Cortical blindness Cortical blindness occipital lobe ischemia infarction or occipital lobe ischemia infarction or edema lasting hrs –up to 8 daysedema lasting hrs –up to 8 days

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77--LiverLiver

Minimal involvement with fibrin depositionMinimal involvement with fibrin deposition

Periportal hemorrhagic necrosis Periportal hemorrhagic necrosis ↑↑ serum liver ↑↑ serum liver enzymesenzymes

Bleeding from these lesions Bleeding from these lesions Subcapsular hematoma Subcapsular hematoma hepatic rupture hepatic rupture

Hepatic infarctionHepatic infarction

HEELP SYNDROMEHEELP SYNDROME

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88--Endocrine & metabolic changesEndocrine & metabolic changes

↓↓ ↓↓ plasma renin, angiotensin II & aldosterone to the plasma renin, angiotensin II & aldosterone to the normal prepregnancy valuesnormal prepregnancy values

Vasopressin levels are NVasopressin levels are N

Atrial natriuretic peptide ↑↑ Atrial natriuretic peptide ↑↑

Volume expansion in PET Volume expansion in PET ↑ ANP ↑ ANP ↑ COP &↓ ↑ COP &↓ periephal vascular resistanceperiephal vascular resistance

Expansion of the extracellular fluid volume (edema) Expansion of the extracellular fluid volume (edema) Proteinuria Proteinuria ↓↓ plasma oncotic pressure ↓↓ plasma oncotic pressure displacement of intravascular fluid to interstitiumdisplacement of intravascular fluid to interstitium

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99--Uteroplacental perfusionUteroplacental perfusion

Vasospasm Vasospasm compromised placental perfusion compromised placental perfusion ↑↑ ↑↑ perinatal morbidity & mortalityperinatal morbidity & mortality

Doppler velocimetry (systolic /diastolic velocity ratio of Doppler velocimetry (systolic /diastolic velocity ratio of umbilical& uterine arteries )umbilical& uterine arteries )20% N20% N

15% N Umbilical / Abnormal uterine15% N Umbilical / Abnormal uterine

40% Both Abnormal40% Both Abnormal

Histological changes in placental bedHistological changes in placental bed

Defective trophoblastic invasion of spiral arteries / decidual Defective trophoblastic invasion of spiral arteries / decidual vessels but not myometrial vessels are invaded by vessels but not myometrial vessels are invaded by trophoblasttrophoblast

Charecteristic lipid rich lesions in the uteroplacental arteriesCharecteristic lipid rich lesions in the uteroplacental arteries

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PREVENTIONPREVENTION

Calcium supplementation??Calcium supplementation??

Fish oil Fish oil ineffectiveineffective

Low dose aspirin Low dose aspirin selective supression of throboxane selective supression of throboxane synthesis by the plt & sparing endothelial prostacyclin synthesis by the plt & sparing endothelial prostacyclin production production Not effective in preventing PETNot effective in preventing PET

Antioxidants Antioxidants Vit C & E supplementation Vit C & E supplementation significant significant reduction in PETreduction in PET

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SYMPTOMS & SIGNSSYMPTOMS & SIGNS

↑ ↑ BPBP

ProteinuriaProteinuria

Edema of the face & hands ( but it has been dropped of Edema of the face & hands ( but it has been dropped of the definition due to poor predictive value)the definition due to poor predictive value)

Headache Headache

Visual disturbance Visual disturbance

Epigastric painEpigastric pain

Exaggerated reflexesExaggerated reflexes

Page 23: HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC & ADOLESCENT GYNECOLOGIST.

Fetal & maternal risksFetal & maternal risks

Fetal Fetal

IUGRIUGR

Oligohydramnios Oligohydramnios

Placental infarctsPlacental infarcts

Placental abruptionPlacental abruption

PrematurityPrematurity

Uteroplacental Uteroplacental insufficiencyinsufficiency

Perinatal death Perinatal death

MaternalMaternal

CNS CNS seizures & strokeseizures & stroke

DICDIC

↑↑ ↑↑ CSCS

Renal failureRenal failure

Hepatic failure or ruptureHepatic failure or rupture

DeathDeath

Page 24: HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC & ADOLESCENT GYNECOLOGIST.

CLASSIFICATION OF PETCLASSIFICATION OF PET

SEVERE PETSEVERE PET

Systolic BP >160 mmHg or diastolic >110 mmHg on two Systolic BP >160 mmHg or diastolic >110 mmHg on two occasions at least 6 hrs apartoccasions at least 6 hrs apart

Proteinuria ≥ 5 g/24 hrs Proteinuria ≥ 5 g/24 hrs

Oliguria < 500 cc /24 hrsOliguria < 500 cc /24 hrs

Cerebral or visual symptomsCerebral or visual symptoms

Epigastric or Rt upper quadrant painEpigastric or Rt upper quadrant pain

Pulmonary edema or cyanosisPulmonary edema or cyanosis

Low PLtLow PLt

↑↑ ↑↑ liver enzymesliver enzymes

IUGRIUGR

MILD PET MILD PET any PET that is not considered severe any PET that is not considered severe

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MANEGEMENT OF PET & MANEGEMENT OF PET & ECEC

Page 26: HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC & ADOLESCENT GYNECOLOGIST.

ManegementManegement

OBJECTIVES OBJECTIVES

Terminaton of pregnancy with the least possible trauma Terminaton of pregnancy with the least possible trauma to the mother & fetusto the mother & fetus

Birth of an infant who subsequently thrivesBirth of an infant who subsequently thrives

Complete restoration of health to the motherComplete restoration of health to the mother

1- Hospitalization1- Hospitalization

Women with new onset BP ≥ 140/90Women with new onset BP ≥ 140/90

Worsening BP Worsening BP

Development of proteinuria in addition to existing BP Development of proteinuria in addition to existing BP

Page 27: HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC & ADOLESCENT GYNECOLOGIST.

INITIAL HOSPITAL MANAGEMENTINITIAL HOSPITAL MANAGEMENT

Observe for headache , visual disturbance, epigastric Observe for headache , visual disturbance, epigastric pain & rapid wt gainpain & rapid wt gain

Wt dailyWt daily

Analysis for proteinuria every 2 days / dailyAnalysis for proteinuria every 2 days / daily

BP in sitting position every 4 hrs except during sleepBP in sitting position every 4 hrs except during sleep

Blood investigations Blood investigations Hct, Plt, S creatinine, liver Hct, Plt, S creatinine, liver enzymesenzymes

Frequent evaluation of fetal size & AF Frequent evaluation of fetal size & AF

Reduced physical activity but not absolute bed restReduced physical activity but not absolute bed rest

N diet & fluid intakeN diet & fluid intake

Page 28: HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC & ADOLESCENT GYNECOLOGIST.

FURTHER MANAGEMENTFURTHER MANAGEMENT

Depends on:Depends on:Severity of PET Severity of PET Duration of gestationDuration of gestationCondition of the CxCondition of the CxComplete resolution of the signs & symptoms does not Complete resolution of the signs & symptoms does not occur till after deliveryoccur till after delivery

Lines of managementLines of managementTermination of pregnancyTermination of pregnancyAntihypertensive therapyAntihypertensive therapyAnticonvulsant therapyAnticonvulsant therapyHome health care Home health care if BP improved within few days Pt if BP improved within few days Pt can be managed as outpatient can be managed as outpatient Home BP & urine Home BP & urine protein monitoring . Instruction to come to hospital if she protein monitoring . Instruction to come to hospital if she has waning symptoms . Rest at home has waning symptoms . Rest at home

Page 29: HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC & ADOLESCENT GYNECOLOGIST.

Termination of pregnancyTermination of pregnancy

IndicationsIndicationsTerm pregnancy with mild or severe PETTerm pregnancy with mild or severe PETSevere PET regardless of the gestational ageSevere PET regardless of the gestational age

Warning signs Warning signs headache , visual disturbance, epigastric headache , visual disturbance, epigastric pain, oliguriapain, oliguriaEclampsia Eclampsia Pt must be stabilized & delivered immediatelyPt must be stabilized & delivered immediately

Preterm with mild PET Preterm with mild PET Assess fetal wellbeing by NST, Assess fetal wellbeing by NST, BPP, DopplerBPP, Doppler

Methods of terminationMethods of terminationIOL with prostaglandines to ripen the Cx followed by IV IOL with prostaglandines to ripen the Cx followed by IV oxytocinoxytocinElective CS Elective CS Severe PET with unfavorable Cx Severe PET with unfavorable Cx

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Antihypertensive therapyAntihypertensive therapy

Mild PETMild PET

There is no benefit of antihypertensive therapy There is no benefit of antihypertensive therapy

Reduction in the maternal BP with labetalol or nifedipine Reduction in the maternal BP with labetalol or nifedipine IUGRIUGR

ACI ACI contraindicated contraindicated IUGR, boney malformations, limb IUGR, boney malformations, limb contracture, PDA, pulmonary hypoplasia, RDS, contracture, PDA, pulmonary hypoplasia, RDS, hypotension &death hypotension &death

Severe PET Severe PET

Antihypertensive therapy is used to control BP untill the Pt Antihypertensive therapy is used to control BP untill the Pt delivers or in preterm for 48 hrs to allow time for delivers or in preterm for 48 hrs to allow time for glucocorticoid administration for fetal lung maturity then glucocorticoid administration for fetal lung maturity then deliverydelivery

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Antihypertensive therapy for severe PET & ECAntihypertensive therapy for severe PET & EC

Hydralazine Hydralazine

IV infusion or IV 5-10 mg bolus at 15-20 min interval IV infusion or IV 5-10 mg bolus at 15-20 min interval

when diastolic BP ≥100-110 mm Hg or systolic BP ≥ when diastolic BP ≥100-110 mm Hg or systolic BP ≥ 160 mmHg160 mmHg

Nifedipine 10 mg po repeated in 30 min Nifedipine 10 mg po repeated in 30 min

Labetalol 10 mg IV / 20 mg after 10 min/ 40mg after Labetalol 10 mg IV / 20 mg after 10 min/ 40mg after 10min/80 mg (not to exceed 220 mg)10min/80 mg (not to exceed 220 mg)

Nitroprusside Nitroprusside used only in PT not responding to other used only in PT not responding to other drugsdrugs

Diuretics not recommended because intravascular Diuretics not recommended because intravascular volume depletion already exists in PET volume depletion already exists in PET

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Fluid therapyFluid therapy

Hyperosmotic agents not recommended because Hyperosmotic agents not recommended because intravascular influx of fluid intravascular influx of fluid subsequent escape of subsequent escape of fluid to vital organs fluid to vital organs pulmonary edema & cerebral pulmonary edema & cerebral edemaedema

LR 60-120 ml/hr Excessive fluid administration LR 60-120 ml/hr Excessive fluid administration pulmonary edema & cerebral edemapulmonary edema & cerebral edema

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PREVENTION /CONTROL OF CONVULSIONSPREVENTION /CONTROL OF CONVULSIONSMagnesium sulfate IV infusion Magnesium sulfate IV infusion 4 gm loading dose in 100 4 gm loading dose in 100 ml of IV fluid over 20 min ml of IV fluid over 20 min 2 gm /hr maintenance 2 gm /hr maintenance

Measure serum MG level at 4-6hrs maintain at 4-7 mEq /LMeasure serum MG level at 4-6hrs maintain at 4-7 mEq /L

D/C 24 hrs after deliveryD/C 24 hrs after delivery25% of seiz occur post partum25% of seiz occur post partum

Avoid toxicity by :Avoid toxicity by :

-monitoring patellar reflexes-monitoring patellar reflexes

-respiratory rate-respiratory rate

-urine output-urine output

Antidote Antidote calcium gluconate 1gm IVcalcium gluconate 1gm IV

MgS ↓ myometrial contractilityMgS ↓ myometrial contractility

Compared to phenytoin or diazepam Compared to phenytoin or diazepam 50% ↓ in maternal 50% ↓ in maternal mortality ,67% ↓ in convulsionsmortality ,67% ↓ in convulsions

Infants were less likely to be admitted to NICU/ intubationInfants were less likely to be admitted to NICU/ intubation

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PrognosisPrognosis

Maternal death rare Maternal death rare due to cerebral Hg, aspiration due to cerebral Hg, aspiration pneumonia, hypoxic encephalopathy, thromboembolism, pneumonia, hypoxic encephalopathy, thromboembolism, hepatic rupture, renal failure, ansthesiahepatic rupture, renal failure, ansthesia

Recurrence Recurrence 25-33% primipara 25-33% primipara

70% multipara70% multipara

PG, PET before 30 wk PG, PET before 30 wk 40% 40%

HEELP HEELP 5%5%

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CHRONIC HYPERTENSION CHRONIC HYPERTENSION in pregnancyin pregnancy

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CHRONIC HYPERTENSIONCHRONIC HYPERTENSIONIncidence of ch HPT 0.5-4%Incidence of ch HPT 0.5-4%

80% essential HPT80% essential HPT

20% due to renal disease20% due to renal disease

Symptoms & signsSymptoms & signs

↑↑risk in risk in Age > 30, obese, multipara, DM, renal disease, Age > 30, obese, multipara, DM, renal disease, black race, family Hx black race, family Hx

Difficult to deffirentiate HPT with superimposed PET from Difficult to deffirentiate HPT with superimposed PET from HPT with renal disease HPT with renal disease both have proteinuriaboth have proteinuria

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INVESTIGATIONSINVESTIGATIONS

Chest x ray Chest x ray cardiomegaly cardiomegaly

ECG ECG Lt vent hypertrophy Lt vent hypertrophy

↑ ↑ serum creatinine, ↓ creatinine clearance & proteinuria serum creatinine, ↓ creatinine clearance & proteinuria 5-10% 5-10%

MATERNAL COMPLICATIONSMATERNAL COMPLICATIONS

Superimposed PET in 1/3 of PtSuperimposed PET in 1/3 of Pt

↑ ↑ risk of abruptio placentae 0.4-10% risk of abruptio placentae 0.4-10% DIC, acute DIC, acute tubular & cortical necrosistubular & cortical necrosis

If renal function is well creatinine < 1.5 mg/dl If renal function is well creatinine < 1.5 mg/dl pregnancy does not change the coarse of renal pregnancy does not change the coarse of renal diseasedisease

If renal function is affected prior to pregnancy If renal function is affected prior to pregnancy deterioration of renal function occur more rapid in deterioration of renal function occur more rapid in pregnancy pregnancy

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FETAL COMPLICATIONSFETAL COMPLICATIONS

Prematurity 25-30%Prematurity 25-30%

IUGR 10-15%IUGR 10-15%

Stillbirth & fetal distress due to abruptio placentae or ch Stillbirth & fetal distress due to abruptio placentae or ch intrauterine asphyxia intrauterine asphyxia

Page 39: HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC & ADOLESCENT GYNECOLOGIST.

TREATMENTTREATMENT

No benefit of treating mild CH HPT ( 140-179/90-109)No benefit of treating mild CH HPT ( 140-179/90-109)

in pregnancy in pregnancy should be monitered for worsening HPT or should be monitered for worsening HPT or superimposed PET superimposed PET

Pt with severe CH HPT should have their BP controlled Pt with severe CH HPT should have their BP controlled before pregnancy & continue Rx in pregnancybefore pregnancy & continue Rx in pregnancy

αα Methyle Dopa Methyle Dopa

Calcium channel blockersCalcium channel blockers

B blockers can be used but B blockers can be used but IUGR IUGR

Labetalol Labetalol

Page 40: HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI ASSISSTANT PROF KSU/ CONSULTANT OBGYN PEDIATRIC & ADOLESCENT GYNECOLOGIST.

Obstetric managementObstetric management

Serial U/S for fetal growth. BPP, NSTSerial U/S for fetal growth. BPP, NST34wk34wk

Follow up every 2 wks till 30 then weeklyFollow up every 2 wks till 30 then weekly

Warn the mother about symptoms of superimposed PETWarn the mother about symptoms of superimposed PET

Investigations Investigations Renal function test,uric a , calcium ,LFT, Renal function test,uric a , calcium ,LFT, 24hrs urine for creatinine clearance & protein, CBC, 24hrs urine for creatinine clearance & protein, CBC, Urinalysis, ECG.GTTUrinalysis, ECG.GTT

Early U/S for dating of pregEarly U/S for dating of preg

Not allowed to continue past 40wksNot allowed to continue past 40wks

IOL at40 wksIOL at40 wks

Regular diet no salt restrictionRegular diet no salt restriction

IOL IOL for superimposed PET,IUGR, fetal distress, worsening for superimposed PET,IUGR, fetal distress, worsening renal functionrenal function