Hypertensive disorders in

Pregnancy
Presenter
Dr Peter N Ebeigbe ,
FMCOG,FWACS
DEPT OF
OBGYN,DELSU,ABRAKA
FORMAT
 Introduction  Riskfactors
 Classification  Management
 Definitions
 Prophylaxis
BP
 Conclusion
Proteinuria
 Assessing
proteinuria
 Etiology/Pathophs
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
 Transienthypertension: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 pre-

eclampsia 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
 Inabilityto 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
 Assistsecond 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