Hypertension in Pregnancy

Classification
Chronic

hypertension

Gestational

hypertension (only during pregnancy)

Preeclampsia

Superimposed upon chronic

hypertension or Renal Disease

Preeclampsia
Transient

- eclampsia

hypertension (only after pregnancy)

Chronic Hypertension
Defined as hypertension
diagnosed

Before pregnancy

Before the 20th week of gestation

During pregnancy and not resolved

postpartum

Gestational Hypertension
Gestational

Hypertension:
Systolic >140
Diastolic>90
No Proteinurea
25% Develop Pre-eclampsia

Gestational Hypertension
Diagnosis of gestational hypertension:
Detected for first time after midpregnancy
No proteinuria
Only until a more specific diagnosis can be assigned
postpartum
If preeclampsia does not develop and
BP returns to normal by 12 weeks postpartum, diagnosis is
transient hypertension.
BP remains high postpartum, diagnosis is chronic
hypertension.
Proteinurea develops Preeclampsia is diagnosed (25%
incidence)

Hypertension in Pregnancy
Complicates

7-10% of pregnancies
70% Preeclampsia-eclampsia
30% Chronic hypertension
Eclampsia 0.05% incidence
20% of Maternal Deaths
Cause of 10% of Preterm birth
Etiology unknown

Hypertension in Pregnancy
Young

female 3 fold increased risk

Africans 2 fold increased risk
Multifetal pregnancies
Twins
Triplets
Hypertension
Renal

Disease
Collagen Vascular Disease

 Blood

pressure

Measure blood pressure in the sitting position, with the

cuff at the level of the heart. Inferior vena caval
compression by the gravid uterus while the patient is
supine can alter readings substantially, leading to an
underestimation of the blood pressure. Blood pressures
measured in the left lateral position similarly may yield
falsely low values if the blood pressure is measured in
the higher arm and the cuff is not maintained at heart
level.
Allow women to sit quietly for 5-10 minutes before
measuring the blood pressure.

 Record

Korotkoff sounds I (the first sound)

and IV (the muffling of sound) to denote the
systolic blood pressure (SPB) and DPB,
respectively. In about 5% of women, an
exaggerated gap exists between the fourth
(muffling) and fifth (disappearance) Korotkoff
sounds, with the fifth sound approaching zero.
In this setting, record both the fourth and fifth
sounds (eg, 120/80/40 with sound I = 120, sound
IV = 80, sound V = 40).

19 years old lady G1 P0 was seen at the antenatal clinic at 32 weeks

gestation for routine check up. On examination she looked generally
well, blood pressure was 150/95
150/90 pulse 80/m with lower limb oedema
+. Uterus was appropriate for date with a viable fetus. Urine analysis
showed + protein.
Q- what is the diagnosis
Q- what investigations to perform
Q- what treatment to commence

19 years old lady G1 P0 was admitted to the labour word at 32 weeks

gestation complaining of headache. On examination she looked
generally unwell, irritable, epigastric pain, nausea & blood pressure
was 160/110 pulse 90/m with lower limb and abdominal wall oedema
++, reflexes exaggerated. Uterus was small for date with a viable
fetus. Urine analysis showed +++ protein.
Q- what is the diagnosis
Q- what investigations to perform
Q- what treatment to commence

** INCIDENCE: 5-10% 0f all pregnancies . 20% recurrence

This is the third most important cause of maternal mortality
worldwide
** DEFINITION OF HYPEWRTENSION:
D.B.P. > 90 mmHg

or

S.B.P. > 140 mmHg

or

Rise in D.B.P. of at least 15 mmHg (physiological changes) or

Rise in S.B.P. of at least 30 mmHg

** PROTIENUREA:
Proteinurea is defined as urinary excretion
0.3 g protein or greater in a 24-hour
30 mg/dl (+1 or greater on urine dip specimen)

+/-

** OEDEMA: 90% pregnancy. progressive

abandoned

Enlarged placenta e.g.

Pre-existing hypertension, renal
Pre-existing vascular disease
P0 >>>> multip
Family history
New husband

Abnormal trophoblast invasion

first 12 weeks, the decidual segments of the spiral arteries
are invaded increased flow to interrvellous space by 20
weeks trophoblast invades intramyometrial segment of spiral
arteries>>> reduce resistance to blood flow to placenta.(high
volume)
In P-E trophoblast invasion is patchy & spiral arteries retain
their muscular walls. Reason ????

Normal pregnancy: marked peripheral vasodilatation. 4 fold increase

in prostacyclin (PGI2) normal thromboxane and increased nitric oxide by
vascular endothelium
Pre-eclampsia: no change/reduction in prostacyclin and N.O.
synthesis. Vasospasm and endothelial cell dysfunction>>> platelet
activation and micro aggregate formation
It is a multi organ affecting disease/ syndrome
*hemorrhage and necrosis in many organs,, arteriolar constriction
*kidneys: glomerioloendotheliosis
*acute atherosis of spiral arteries, platelets microaggregates&thrombosis

Pathophysiologic Abnormalities in Preeclampsia

Generalizedvasospasm
Activationofcoagulationsystem
Abnormalhemostasis
Alteredthromboxane-prostacyclinratio
Endothelialcellinjury
Abnormalhemodynamics
Reduceduteroplacentalbloodflow

Pathophysiology
Heart:

Generally unaffected; cardiac

decompensation in the presence of preexisting
heart disease.

Kidney:

Renal lesions (glomerular

endotheliosis); GFR and renal blood flow
decrease; hyperuricemia; proteinuria may appear
late in clinical course; hypocalciuria; alterations
in calcium regulatory hormones; impaired
sodium excretion; suppression of renin
angiotensin system.

Pathophysiology
Coagulation System:

Thrombocytopenia;
low antithrombin III; higher fibronectin.

Liver:

HELLP syndrome (hemolysis, elevated ALT

and AST, and low platelet count).

CNS:

Eclampsia is the convulsive phase of

preeclampsia. Symptoms may include headache
and visual disturbances, including blurred vision,
scotomata, and, rarely, cortical blindness.

Symptoms of Preeclampsia

Visual

disturbances typical of preeclampsia are

scintillations and scotomata. These disturbances are
presumed to be due to cerebral vasospasm.
Headache is of new onset and may be described as
frontal, throbbing, or similar to a migraine
headache. However, no classic headache of
preeclampsia exists.
Epigastric pain is due to hepatic swelling and
inflammation, with stretch of the liver capsule. Pain
may be of sudden onset, it may be constant, and it
may be moderate-to-severe in intensity.

Symptoms of preeclampsia
While

mild lower extremity edema is common in

normal pregnancy, rapidly increasing or
nondependent edema may be a signal of
developing preeclampsia. However, this signal
theory remains controversial and recently has been
removed from most criteria for the diagnosis of
preeclampsia.
Rapid weight gain is a result of edema due to
capillary leak as well as renal sodium and fluid
retention.

Physical Findings in
Preeclampsia
Blood

Pressure
Proteinurea
Retinal vasospasm or Retinal edema
Right upper quadrant (RUQ) abdominal
tenderness stems from liver swelling and
capsular stretch

Physical findings in
Preeclampsia
Brisk, or hyperactive, reflexes are common

during pregnancy, but clonus is a sign of

neuromuscular irritability that raises concern.
Among pregnant women, 30% have some
lower extremity edema as part of their normal
pregnancy. However, a sudden change in
dependent edema, edema in nondependent areas
such as the face and hands, or rapid weight gain
suggests a pathologic process and warrants
further evaluation

Why screening
Accuracy. Uterine artery doppler at 24 weeks, notching on both
uterine arteries identifies 80% who will develop PET,,, 5% false
positive

** Maternal

** Fetal

Methods Used to Prevent Hypertensive Disorders of Pregnancy

Properprenatalcare
Low-saltdiet
Diuretics
Antihypertensivedrugs
Nutritionalsupplementation
Magnesium(365mg/d)
Zinc(20mg/d)
Calcium(1500200mg/d)
Fishoil
AntithromboticagentsLow-doseaspirin(50150mg/d)
Dipyridamole(225300mg/d)
Subcutaneousheparin(15,000IU/d)

Low doses of aspirin do help prevent

pre-eclampsia, but there is little
information about whether they are of
benefit for treatment of established preeclampsia cochrane 22 April 2003
Pre-eclampsiaisaconditioninpregnancyinvolvinghighblood
pressureandproteinintheurine.Itcanleadtoserious
complicationsanddeath.Aspre-eclampsiaaffectsbloodclotting,
antiplatelets(drugslikeaspirinwhichcanpreventbloodclots)are
usedforpre-eclampsia.Thereviewoftrialsfoundthatlowdoses
ofaspirinloweredtheriskofpre-eclampsiaalittle(15%lowering
intherisk),withasimilarloweringintheriskofthebabydying
(14%)andaverysmallloweringintheriskofthebabybeing
borntooearly(8%).Doseslessthan75mgappeartobesafe.
Higherdosesmaybebetter,butastherisksofadverseeffects
mayalsoincrease,moreresearchisneeded.

Calcium supplements may prevent high blood

pressure and help prevent preterm labour
cochrane 22 April 2003
Main results:
Eleven studies were included, all of good quality. There was a modest
reduction in high blood pressure with calcium supplementation . The effect
was greatest for women at high risk of hypertension (relative risk 0.45, 95%
confidence interval 0.31 to 0.66) and those with low baseline dietary calcium
(relative risk 0.49, 95% confidence interval 0.38 to 0.62).
Reviewers' conclusions:
Calcium supplementation appears to be beneficial for women at
high risk of gestational hypertension and in communities with low
dietary calcium intake. Optimum dosage requires further
investigation.

SERIOUS

COMPLICATIONS: -

HELLP SYNDROME

ABRUPTIO PLACENTAE

PULMONARY OEDEMA

ACUTE RENAL FAILURE

CEREBRAL HAEMORRHAGE

VISUAL DISTURBANCES & BLINDNESS

HEPATIC RUPTURE

ELECTROLYTIC IMBALANCE

POSTPARTUM COLLAPSE

HYPERTENSION DURING PREGNANCY

OBJECTIVES OF MANAGEMENT
CURE

/ PREVENT PROGRESSION -

CLOSE MONITORING

REDUCE

BLOOD PRESSURE -TATRGET- 140/90

PROMOTE

FOETAL MATURITY

PROLONG

PREGNANCY (34 - 36 WEEKS)

TO ACHIEVE FOETAL MATURITY TERMINATION

DELIVERY- BEST DAY, BEST WAY & BEST PLACE

PREVENT /

MANAGE COMPLICATIONS

HYPERTENSION DURING PREGNANCY

MATERNAL

MONITORING

LOOK

FOR APPEARANCE OF OMINOUS

FEATURES

DAILY- RECORD

B.P 4 TIMES, MONITOR

URINE OUTPUT & TEST FOR PROTEINURIA
QUALI. / QUANT
ALT.DAY- BODY WEIGHT
EVERY 4TH DAY- URIC ACID, PLATELET
COUNT, L.F.T. (LDH)
WEEKLY- CREATININE

HYPERTENSION DURING PREGNANCY

FOETAL

MONITORING

DAILY -

CLINICAL FOETAL MONITORING FHS, FUNDAL Ht. ABDOMINAL GIRTH,

LIQUOR, FOETAL MOVEMENT COUNT, C.T.G

USG

- ON ADMISSION & THEN 3 WEEKLY

FOR FOETAL BIOPHYSICAL PARAMETERS,
PLACENTA AND LIQUOR VOLUME

DOPLLER

USG FOR PLACENTAL BLOOD

FLOW VELOCITY EVERY 4TH DAY

L/S

RATIO FOR MATURITY

MANAGEMENTOFPRE-ECLAMPSIA
theprinciplesare:
*earlyrecognitionofthesymptomlesssyndrome
*awarenessofseriousnatureoftheconditioninitssevereform
withoutover-reactingtomilddisease
*agreedguidelinesforadmissiontohospital,investigation,anduse
ofantihypertensiveandanticonvulsanttherapy
*well-timeddeliverytopre-emptseriousmaternalorfetal
complicationspostnatalfollow-upandcounsellingforfuture
pregnancies.

ClinicalobservationandinvestigationExamination(overand
aboveroutine):
palpationofthefemoralpulses(toexcludecoarctationof
aorta)lookforhyperreflexiaandankleclonus
checkopticfundiforsilverwiring,arterio-venousnipping,
exudatesandhaemorrhage.

Laboratoryinvestigation
Proteinuria-.Ifpresentalsocheckurine microscopyand cultureto
excludeurinaryinfection.
*Serumuratelevelsincreaseearlyinpre-eclampsia.Levels
>350pmol/Lareabnormalinpregnancybutgraduallyincreasing
levelsaremoresignificant.

Serumureaand creatinine. Risinglevelsaresignificantbutnot

suchsensitiveindicatorsofpre-eclampsiaasuricacid.Theupper
limitsofnormalinpregnancyare5mmol/Lforserumureaand100
pmol/Lforcreatinine,buttrendsareevenmoreimportantthan
specificlevels.
PlateletcountgraduallyfallsifdisseminatedIntravascular
coagulationisoccurring.

Laboratoryinvestigation
Liverfunction-this shouldbecheckedoncepersistentproteinuria
ispresent,orifplateletcountissignificantlyreduced.Itcanbe
detectedbyelevationofliverenzymes(notalkalinephosphatase,
whichisnormallyraisedbecauseitisproducedbytheplacenta).

Coagulationstudies shouldbecarriedoutifplateletcountis
reduced,andinseveredisease.

Testsoffetalgrowthandwell-being
Eachofthesetestsshouldberepeatedasoftenasisclinically
necessary.

** definite treatment is delivery (ending the pregnancy).

But,
Mother vs. Fetus

** Mild pre-eclampsia:
diastolic /90-95 & proteinurea trace-1+

** Moderate pre-eclampsia

** Severe pre-eclampsia
** Does the treatment improve the condition? Then why. Adv/disadv

Managementofmild(non-proteinuric)pre-eclampsia
Theprinciplesare:
*uncomplicatedhypertensionissuitableforcarefulsupervision
athomebytheprimaryhealthcareteam

*anti hypertensive therapy is not indicated

* admission to hospital is indicated when:
+-SBP is 160 and/or DBP 100 mmHg or greater -proteinuria is detected in
a clean (i.e. mid-stream) urine sample in the absence of a urinary
infection
}-the patient is symptomatic with e.g. visual disturbances, unusual
headache, epigastric pain, or vomiting (URGENT!) there is clinical
evidence of intrauterine growth retardation +tests of fetal welfare have
deteriorated -4-a previous bad obstetric history suggests that closer
surveillance would be worthwhile.

MANAGEMENT OF SEVERE HYPERTENSION

The maternal risks of cerebrovascular accident and of left ventricular or renal
failure begin to increase significantly when hypertension is severe.
The choice has then to be made between delivery and antihypertensive
therapy.
Among the factors to be considered are:
~gestational age-it is seldom justified to commence long-term oral therapy
from 34 weeks
the severity of other signs and symptoms availability of intensive neonatal
care facilities. >K Treatment neither influences the progression of underlying
preeclampsia nor significantly improves fetal outcome. It helps to protect the
mother and enables many pregnancies to continue that otherwise would be
ended because of maternal risk.

CONTROL OF ACUTE SEVERE HYPERTENSION

There is no consensus on the optimum acute treatment.
The important objective is to reduce the blood pressure to safe levels (but not
too low!).
Parenteral hydralazine is used most commonly but oral nifedipine should be
considered .
LONGER-TERM CONTROL OF SEVERE HYPERTENSION
Thecombineda-and(B-blockingagentlabetalol is commonly
used.
Thepotentvasodilatorandcalciumchannelblockernifedipine is a
usefulsecond-linetreatment.Itsmajordrawbackissevere
headache.
Angiotensin-converting enzyme (ACE) inhibitors havedeleteriousfetal
effectsandtheiruseisnotrecommended.Ifawomanwith
chronichypertensionbecomespregnantonanACEinhibitor,

LONGER-TERM CONTROL OF SEVERE HYPERTENSION

There is still insufficient trial evidence to determine whether the benefits outwe
any disadvantages.
If it is to be used, the suggested indications are: ,-DBP >_100 mmHg
-pregnancy <_34 weeks
*fetal and maternal state otherwise good.
Methyldopa remains the drug of first choice.
Thecombineda-and(B-blockingagentlabetalol is commonlyused.

Thepotentvasodilatorandcalciumchannelblockernifedipine is ausef
second-linetreatment.Itsmajordrawbackissevereheadache.

Angiotensin-converting enzyme (ACE) inhibitors havedeleteriousfetaleffec

andtheiruseisnotrecommended.Ifawomanwithchronic
hypertensionbecomespregnantonanACEinhibitor,changetoanoth
anti-hypertensioeagentisadvised.

TTimingofdelivery

Themostcommongroundsfordeliveryare:
progressivefetalcompromise(i.e.whenthebabyissafer
delivered)
uunacceptablerisktomaternalhealth,e.g.uncontrollableBP,
impendingrenalfailureorheartfailure,HELLPsyndrome,DIC,
eclampsia(seebelow).
.

The mode of delivery (caesarean section versus vaginal) depends

on:
-the seriousness of the situation
-the gestational age
-the degree of fetal/maternal compromise.
Epidural analgesia is the method of choice for labour (as long as a
coagulation defect has been excluded).
Appropriate facilities for the care of the newborn available