Hypertension In Pregnancy

Hypertensive disorders in Pregnancy Presenter

Dr Peter N Ebeigbe , FMCOG,FWACS DEPT OF OBGYN,DELSU,ABRAKA

FORMAT  Introduction  Classification  Definitions

BP Proteinuria  Assessing proteinuria  Etiology/Pathophs

 Risk

factors  Management  Prophylaxis  Conclusion

Introduction 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…..  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  Pre-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.

Classification  Varied

in literature  Most 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 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)

….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 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 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.

……contd  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

contd  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.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 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?  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?  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?  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… Davey and MacGillivray 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 

Assessing 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 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 methods  Sulphosalicylic

acid,Trichloroacetic acid,Alkaline benzothonium chloride.  Short comings similar to dipstick strips

Quantitative methods 24 hour urine protein  Gold standard  Commonest error –diff in collection of accurately timed specimen or incompleteness of collection  Not easy in out patient settings  Up to 36 hour waiting period for results and to take decision

Quantitative methods contd 2-hour urinary protein estimation  Good correlation with 24 hr urine protein results  Somanthan found sensitivity of 80% compared to 50% for dipstick  Good for outpatient setting,time saving

Quantitative 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 …..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…..  Immunologic

mechanisms  Genetic predisposition  Dietary deficiencies  Vasoactive compounds  Endothelial dysfunction

Multiple modular approach… evidence  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

contd  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

Pathogenesis  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 FACTORS Genetic  Women whose mothers had preeclampsia have a 20-25% risk  In women with a sister with a history of preeclampsia risk may be as high as 35-40%

Obstetric 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 factors  Pre-existing

hypertension  Renal disease  Diabetes(pre-existing or gestational)  Antiphospholipid syndrome  Connective tissue diseases  Inherited thrombophylia…assotd with early onset PIH

MANAGEMENT  Screening

for pre-eclampsia  Treatment of hypertension  Fetal surveillance  Decision regarding delivery Mild cases,with no evidence of preeclampsia may be managed on outpatient basis

Monitoring 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 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 delivery  Only

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 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 hypertension    



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 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 Hospital, 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  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 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  Assist

second stage  Avoid use of Ergometrine  Comment on Early onset PIH

Prophylaxis  Low

dose aspirin Collaborative 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.

prophylaxis  Calcium

…evidence inconclusive  Antioxidants..vit c inconclusive  Folic acid too

Recurrence  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.

Conclusion  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……. Thank you for

Listening