Hypertensive disorders in Hypertensive disorders in PregnancyPregnancy

Presenter

Dr Peter N Ebeigbe , FMCOG,FWACS

DEPT OF OBGYN,DELSU,ABRAKA

FORMATFORMAT

Introduction Classification Definitions

BP

Proteinuria Assessing

proteinuria Etiology/Pathophs

Risk factorsManagementProphylaxisConclusion

IntroductionIntroduction

A major cause of maternal and perinatal morbidity and mortality in developing countries-12% of maternal mortalities worldwide

Most common medical complication of pregnancy worldwide

WHO estimates 15% of pregnant women would have some form of hypertensive disorder in pregnancy, labour and puerperium.

In Nigeria…..In Nigeria…..Incidences as high as 21.6-26.2% of

all deliveries in hospital based studies.(Salako et al 2002,Onah 1996)

National survey showed that Eclampsia contributed 13.0% of all obstetric complications of pregnancy and 16.7% of deaths in public sector referral facilities.(Fmoh 2003)

Pre-eclampsia complicates 5-6% of all deliveries

……..Nigerian statistics continued..Nigerian statistics continuedPre-eclampsia contributed 77.9% 0f

hypertensive disorders of pregnancy in UBTH (Onyiruka and Okolo 2004)

Eclampsia complicates 1 in 76 to 1 in 335 deliveries with case fatality rates of 9.3-42.2% with higher rates in rural areas and Northern Nigeria

Comparatively eclampsia complicates I in 2041 deliveries in the UK and 1 in 3704 deliveries in Nova Scotia ,Canada.

ClassificationClassificationVaried in literatureMost widely used are those by Davey

and MacGillivray 1988…. Based on the occurrence of hypertension and proteinuria

And the classification by Hughes 1972 recommended by the working group of the National High Blood Pressure Education program(1990) of the USA

Classification…Davey and Classification…Davey and MacGillivray 1988.MacGillivray 1988. A.Gestational hypertension and/or proteinuria 1.Gestational hypertension (without proteinuria) 2.Gestational proteinuria 3.Gestational proteinuric

hypertension(preeclampsia B.Chronic hypertension and chronic renal

disease 1.chronic hypertension (without proteinuria) Weaknesses

…….contd.contd 2.chronic renal disease(proteinuria with or

without hypertension)

3.chronic hypertension with superimposed preeclampsia(proteinuria developing in pregnancy in known chronic hypertension)

C.Unclassified hypertension and /or proteinuria.

1 unclassied hypertension

2 ,, proteinuria

3 ,, proteinuric hypertension.

……..contd..contd

D .Eclampsia

The occurrence of generalised convulsions during pregnancy,labour,or within 7 days of delivery and not caused by epilepsy or other convulsive disorders.

Classification…..Hughes 1972Classification…..Hughes 1972

Pregnancy induced hypertension 1.Hypertension without proteinuria or

pathological edema 2.Pre-eclampsia-with proteinuria and /or

pathological edema a. mild b. severe 3 Eclampsia-proteinuria and /or pathological

edema with convulsions.

…………contdcontd

Coincidental hypertension:chronic underlying hypertension that antecedes pregnancy or persists postpartum

Pregnancy –aggravated hypertension:underlying hypertension worsened by pregnancy

1. Superimposed preeclampsia 2.superimposed eclampsia

contdcontd

Transient hypertension:Hypertension which develops after the midtrimester of pregnancy and is characterised by mild elevations of blood pressure that do not compromise the pregnancy.This form of hypertension regresses after delivery but may return in subsequent gestations.

DEFINITIONS…..B.PDEFINITIONS…..B.P

one measurement of Diastolic Blood Pressure of 110mmHg or more or two consecutive measurements of Diastolic Blood Pressure of > 90mmHg 4 hours or more apart.

Some authorities recommend blood pressure greater than 140mmHg systolic or 90mmHg diastolic

or a rise of 30mmHg or 15mmHg above the normal pre-pregnancy values after the 20th week of pregnancy.

Taking Blood pressureTaking Blood pressure

Diagnosis utilizing only a change from baseline has limited sensitivity( 21-52% and 7-23% for the DBP And SBP respectively

Take BP with patient sitting or lying on her side with a 30 degrees tilt.The upper arm at the same level as the heart after 10 minutes of rest

Korotkoff IV or V?Korotkoff IV or V?

Correct size of upper arm cuff should be used.the bladder of the cuff should encompass 80% of the upper arm.

Work by Wichman et al 1984 claimed that frequently muffling of sounds heard down to zero and that gap btw IV and V was so great as to render V inaccurate……based on this ALL BODIES recommended use of K4

Subsequent work showed these assertions were wrong

………………..IV OR V?..IV OR V?

Lopez et al showed in a large sample that muffling of sounds were rarely audible till zero <0.5%

Mean difference btw both phases was around 6mmHg

Phase 5 showed better association with other outcome variables …proteinuria,IUGR ,hyperuricemia

……..IV OR IV?..IV OR IV?

Brown et al comparing direct intrarterial to mercury sphygmomanometry in 28 women found that phase IV overestimated direct DBP by 9(2,12) and phase V by 4(2,7)

Proteinuria… Proteinuria… Davey and Davey and MacGillivrayMacGillivray significant proteinua as one 24hour urine

collection with total protein excretion of 300mg and more; or two random clean catch or catheter urine specimens with 2+(1g albumin/L) or more on a reagent strip or 1+(0.3g albumin/L) if the specific gravity is less than 1030 and pH less than 8.

A few authors suggest that since 0.3g/L of albumin is the upper limit of urinary albumin excretion in pregnancy, levels of albumin of 0.5g/L may be more accurate in definition of significant proteinuria in pregnancy.

Assessing proteinuriaAssessing proteinuria

Qualitative methods

Test strips

Dipstick

High false negative rates 40-53.7%

False negative rate 28%.

Sensitivity 73.5%specificity 44.2%

(Ebeigbe et al 2004)

Dipstick testsDipstick tests Meyer et al …trace or –ve had negative

predictive value of only 34% 3+ or 4+ positively predictive of severe

pre-eclampsia in only 36%.Automated devices increase true positive

urinalysis from 48% to 74%False + rxn…concentrated urine,highly

alkaline urine(ph>8),contamination with vaginal discharge,antiseptic,UTIs

False –ve rxn….very dilute urine,bence jones proteins ,mucoproteins

Turbidimetric methodsTurbidimetric methods

Sulphosalicylic acid,Trichloroacetic acid,Alkaline benzothonium chloride.

Short comings similar to dipstick strips

Quantitative methodsQuantitative methods

24 hour urine proteinGold standardCommonest error –diff in collection

of accurately timed specimen or incompleteness of collection

Not easy in out patient settingsUp to 36 hour waiting period for

results and to take decision

Quantitative methods contdQuantitative methods contd

2-hour urinary protein estimationGood correlation with 24 hr urine

protein resultsSomanthan found sensitivity of 80%

compared to 50% for dipstickGood for outpatient setting,time

saving

Quantitative methodsQuantitative methods

Random urine protein-creatinine ratio Sensitivity 91-93% Specificity 88.5-90% Less than a third false positive rate of

dipsticks and less than a fourth its false negative rates

Widely used in Australia and New Zealand

Etiology …..theoriesEtiology …..theories

Any satisfactory theory should account for hypertension more commonly developing in women

Exposed to chorionic villi for the first time Exposed to superabundance of chorionic

villi as in twins or hydatidiform mole Has preexisting vascular disease Is genetically predisposed to hypertension

in pregnancy

Theories…..Theories…..

Immunologic mechanismsGenetic predispositionDietary deficienciesVasoactive compoundsEndothelial dysfunction

Multiple modular approach…Multiple modular approach…evidenceevidence Poor placentation

Deficient trophoblast invasion

Failure of adaptation of maternal vessels

Increased incidence of placental insufficiency

Hyperplacentosis

Increased incidence in twin,diabetic molar pregnancies and rhesus incompatibility

contdcontd

Fetal/placental response Activation of circulating neutrophils Abnormal lymphocyte function Increased lipid peroxide production Maternal response Decreased cellular protection from free radical activity Generalized membrane instability Diminished vascular endothelial function Increased vascular resistance /vasoconstriction hypertension,renal impairment,convulsion,platelet

consumption etc

PathogenesisPathogenesis

Lack of vascular adaptation to pregnancy Spiral arteries fail to adapt to become high

capacitance,low resistance vessels Precise mechanism by which ischaemic

placenta leads to widespread endothelial cell damage not known

Endothelial cell activation leads to capillary permeability,increased endothelial expression of cell adhesion molecules and prothrombotic factors,platelet thrombosis and increased vascular tone.

RISK FACTORSRISK FACTORS

GeneticWomen whose mothers had

preeclampsia have a 20-25% riskIn women with a sister with a history

of preeclampsia risk may be as high as 35-40%

Obstetric risk factorsObstetric risk factors

Primiparity Multiple gestation Pregnancy for a new consort Previous preeclampsia Hydrops with a large placenta Hydatidiform mole Triploidy (particular association with early

onset PIH)

Medical risk factorsMedical risk factors

Pre-existing hypertensionRenal diseaseDiabetes(pre-existing or gestational)Antiphospholipid syndromeConnective tissue diseasesInherited thrombophylia…assotd

with early onset PIH

MANAGEMENTMANAGEMENT

Screening for pre-eclampsiaTreatment of hypertensionFetal surveillanceDecision regarding delivery

Mild cases,with no evidence of pre-eclampsia may be managed on outpatient basis

Monitoring for pre-eclampsiaMonitoring for pre-eclampsia

Serum urea,creatinine ,uric acid ,CBC,Liver function

Regular urinalysis and if + or more>more specific estimation of proteinuria

Uterine artery Doppler blood flow estimation at 20-24 weeks.presence of a prediastolic “notch”.A persistent high resistance waveform is predictive of subsequent pre-eclampsia.high negative predictive value…..useful in high risk women

Fetal surveillanceFetal surveillance

Risk of IUGR high in pre-existing hypertension and pre-eclampsia….USS to assess growth,liquor volume and umbilical artery blood flow

Women with early onset PIH or likely to require delivery before 34 weeks should receive dexamethasone or betamethasone for lung maturation

Decision regarding timing of Decision regarding timing of deliverydeliveryOnly cure for pre-eclampsia is

delivery This should be done after adequate

control of blood pressure, coagulopathy ,eclamptic seizures and haemodynamic stability

Expectant management should be in well equipped centres only

Indications for deliveryIndications for delivery

Inability to control blood pressure Eclampsia Rapidly worsening maternal

BCH/Haematology e.g platelets<100 x109 /L

Fetal distress/severe IUGR/Reversed umbilical artery diastolic flow

Symptoms and signs of imminent eclampsia

Treatment of acute severe Treatment of acute severe hypertensionhypertension Standard protocol in every unit .when do you

transfer to ICU? Manage in unit with adequate nurses and doctors

per patient BP control most important drug intervention Choice of antihypertensive….hydralazine (I.v

bolus),labetalol (continous I.v infusion) or Nifedipine (orally)

Sublingual nifedipine causes too rapid a fall in BP and uteroplacental perfusion and should be avoided.

Management of EclampsiaManagement of Eclampsia D.O.C for both primary and secondary

prophylaxis is Magnesium sulphate .Believed to act as a cerebral vasodilator Eclampsia should be treated with I.V

Magnesium sulphate followed by an infusion for 24-48 hours after delivery or after the last seizure to prevent further seizures

Give loading dose of 4g(diluted to 40mls) over 5-10 minutes followed by maintainance dose of 1g /hour

Recurrent seizures further bolus of 2g

Pritchard regimen…Parkland Pritchard regimen…Parkland Hospital, 1955Hospital, 1955

Give 4g of MgSO4 as 20% solution intravenously at a rate not to exceed 1g/min

Follow promptly with 10g of 50%MgSO4 solution,one half (5g) injected deeply in both buttocks thru a 3-inch-long 20 gauge needle(addition of 1.0ml of 2 % lidocaine minimizes discomfort)

If convulsions persist after 15 minutes give up to 2g more I.v as a 20% solution at a rate not to exceed 1g/min.4g if woman large

…….contd.contd

Every 4 hours give 5g of 50%solution deep IM after assuring that

patellar reflex is present

Respiration not depressed(>12/min)

urinary output in previous 4 hours exceeded 100mls.

Discontinue MgSO4 24 hours after delivery

MNGT OF DELIVERYMNGT OF DELIVERY

Regional analgesia/anaesthesia advantageous in pre-eclampsia for labour or C-section

Reduced pre and after load,provides adequate analgesia

Avoids BP fluctuations associated with G.A and intubation

Not safe with thrombocytopenia

…….delivery.delivery

Assist second stageAvoid use of ErgometrineComment on Early onset PIH

ProphylaxisProphylaxis

Low dose aspirinCollaborative low-dose Aspirin Study in

Pregnancy (CLASP) Trial.evidence aspirin may be effective in reducing risk of early –onset Preeclampsia.

Reasonable to give 75mg/day in high risk patients…hypertension and renal disease,hypertension and diabetes,recurrent or severe preeclampsia in previous pregnancies.

prophylaxisprophylaxis

Calcium …evidence inconclusiveAntioxidants..vit c inconclusiveFolic acid too

RecurrenceRecurrence

Women with preeclampsia in their first pregnancy have a 10% risk of it occurring in second pregnancy.

Risk increased if they have underlying medical disorder.

ConclusionConclusion

Hypertension disorders in pregnancy remain a major cause of MMM and PRMM

With etiology poorly understood and no efficient predictive tools ,reduction in MMM hinges on early detection and prompt and efficient management.

THANKS…….THANKS…….

Thank you for

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