OBSTETRICS

HYPERTENSIVE DISORDERS OF PREGNANCY

Pre-eclampsia
5% of all pregnancies
10% of 1
st
pregnancy
20-25% with history of chronic hypertensive
vascular disease (CH!"
#apid onset $ rapid turn-over of events
20% of maternal deaths (%riad of hemorrhage&
infection $ hypertension"
Cause of 10% of preterm 'irths
(ncidence
)*tremes of ages
+oung, --fold increase in ris. of developing
gestational hypertension ((mmature cardiovascular
system not ready for the necessary changes in
response to the demands of pregnancy"
/ld (0 -5 years", 1sually with CH! superimposed
Parity, Primigravida $ multigravida
#ace $ ethnicity
2enetic, 3trong family history
)nvironment
#is. 4actors
5ow calcium, -6- 7 869%
Chronic hypertension
:ultifetal gestation, 1-% versus 9% (;igger placenta
with more chorionic villi"
0 -5 years of age
/'esity
;:( < 1=6>, ?6-%
;:( 0 -5, 1-6-%
Classification
2estational hypertension, @ny form of new onset
pregnancy-related hypertension
Pre-eclampsia
)clampsia
Pre-eclampsia superimposed on chronic hypertension
Chronic hypertension
2estational Hypertension
;lood pressure 0 1?0A=0 mmHg for the 1
st
time during
pregnancy
Bo proteinuria
;lood pressure returns to normal < 12 wee.s
postpartum
%ransient hypertension
@ diagnosis of e*clusion
:ay lead to pre-eclampsia& placental insufficiency $
(12#
4urther increase in 'lood pressure late in pregnancy
dangerous
10% eclamptic seiCure develop 'efore overt
proteinuria
Proteinuria, @ sign of worsening hypertensive disease
Closely monitor even without proteinuria
Pre-eclampsia
:inimum criteria
;lood pressure D 1?0A=0 mmHg after 20 wee.s age
of gestation (!ifferentiate from chronic
hypertension"
Proteinuria D -00 mgA 2? hours or D 1E dipstic.
3evere
;lood pressure D 190A110 mmHg
Proteinuria 260 gA 2? hours or D 2E dipstic.
3erum creatinine 0 162 mgAd5 unless previously
elevated
Platelets < 100&000 mm
-
(asoconstriction-
associated"
:icroangiopathic hemolysis, )levated lactate
dehydrogenase (5!H"
Persistent headache& visual distur'ance& epigastric
pain ((ncrease serum transaminase"
/'vious growth restriction
Pulmonary edema, (ncrease permea'ility in
maternal circulation
(ndications of 3everity of Hypertensive !isorders during
Pregnancy
@'normality :ild 3evere
!iastolic ;P < 100 mmHg 110 mmHg
Proteinuria %race to 1E Persistent D 2E
Headache @'sent Present
isual distur'ance @'sent Present
1pper a'dominal pain @'sent Present
/liguria @'sent Present
Convulsions @'sent Present
3erum creatinine Bormal )levated
%hrom'ocytopenia @'sent Present
5iver enCyme :inimal :ar.edly
4etal growth restriction @'sent /'vious
Pulmonary edema @'sent Present
)clampsia
Pre-eclampsia E seiCure (Bot attri'uta'le to any other
condition 'ut pregnancy" or coma
:aternal $ fetal mortality high
Chronic Hypertensive ascular !isease (CH!"
Hypertension that antedates pregnancy
Hypertension that develops 'efore 20
th
wee.
:edical treatment
3uperimposed Pre-eclampsia (Chronic Hypertension or
CH!"
Bew onset proteinuria D -00 mgA 2? hours (Bo
proteinuria 'efore 20 wee.s age of gestation"
3udden increase in
Proteinuria
;lood pressure
Platelet count < 100&000
Hypertension E proteinuria < 20 wee.s age of
gestation
/nly treatment is termination of pregnancy if
eclampsia is present
History
2estational age
Hypertension prior to 20 wee.s almost always due
to chronic hypertension
Page 1 of 9 CH#@;(
Bew onset or worsening hypertension after 20
wee.s, )valuation for manifestations of pre-
eclampsia (;ecause management is different"
!iagnosis of severe hypertension or pre-eclampsia
in 1
st
or early 2
nd
trimester, #ule out gestational
tropho'lastic disease (3till la'eled as pre-eclampsia
even if 'efore 20 wee.s"
:aternal ris. factor for pre-eclampsia
1
st
pregnancy
Bew partnerA paternity, @dapted to genetic
component of prior 'a'ies& 'ut can produce new
anti'odies to new pregnancy
@ge < 1> years or 0 -5 years
History of pre-eclampsia
4amily history of pre-eclampsia in a 1
st
degree
relative
:edical ris. factor
Chronic hypertension
3econdary causes of chronic hypertension
Hypercortisolism
Hyperaldosteronism
Pheochromocytoma
#enal artery stenosis
Pre-e*isting dia'etes mellitus (%ype 1 or 2"
especially with microvascular disease
#enal disease
3ystemic lupus erythematosus
/'esity
%hrom'ophilia
PlacentalA fetal ris. factor
:ultiple gestation
Hydrops fetalis
2estational tropho'lastic disease
%riploidy
:ortalityA :or'idity
Hypertension
/ne of the leading cause of mortality
!iastolic 'lood pressure 0 110 mmHg associated
with increase ris. for placental a'ruption $
intrauterine growth restriction ((12#"
3uperimposed pre-eclampsia, Causes most of the
mor'idity due to chronicity of hypertension
:aternal complications in severe cases
)clamptic seiCure
(ntracere'ral hemorrhage
Pulmonary edema
:yocardial dysfunction
@cute renal failure
!isseminated intravascular coagulation
4etal complications
@'ruptio placenta
(ntrauterine growth restriction
Pre-term delivery, ;ecause termination of
pregnancy is the only treatment
(ntrauterine fetal death
Points to #emem'er
Hypertension is diagnosis whenF
Ghen the resting 'lood pressure is 1?0A=0 mmHg or
higher
Horot.off phase is used to define diastolic
pressure
;lood pressure is ta.en in a sitting position with the
cuff at the level of the heart
!iastolic 'lood pressure 0 =5 mmHg, - fold increase
in fetal death rate
Gorsening ;P especially accompanied 'y proteinuria,
/minous
3evere or early pre-eclampsia ( 2nd or early -rd ",
prevalence of throm'ophilias
Gorsening proteinuria preterm delivery
)pigastric pain 7 wA serum hepatic transaminase
levels, 3ign to terminate pregnancy
%hrom'ocytopenia, Platelet activation $ aggregation,
3ign of worsening
Hypertensive !isorders due to Pregnancy increase in
womenF
)*posed to chorionic villi for the 1
st
time
)*posed to super-a'undance of chorionic villi
)*isting vascular disease
2enetically predisposed
Pre-eclampsia 3yndrome
ascular endothelial damage $ vasospasm
%ransudation of plasma
(schemic $ throm'otic seIuela
Potential Causes of Hypertension in Pregnancy
@'normal tropho'lastic invasion
(mmunological intolerance
:aternal maladaptation
!ietary deficiencies
2enetic influences
Bormal %ropho'lastic (nvasion
#emodeling of uterine spiral arteries Proliferation
of e*travillous tropho'last (nfiltration of the spiral
arteries into the deciduas $ myometrium
%ropho'last replace endothelium 5umen with
'igger diameter
@'normal %ropho'lastic (nvasion
(ncomplete tropho'lastic invasion
!ecidual vessels& not myometrial vessels (Ghich are
the vessels responsi'le for the normal 'lood supply"
lined with endovascular tropho'last
%he more defective tropho'last invasion the greater
the severity of hypertensive disorder
!ecrease uteroplacental perfusion
:aternal !isease is characteriCed 'yF
asospasm
@ctivation of coagulation system
Pertur'ation in hormonal $ autocoid systems related
to volume $ 'lood pressure control
/*idative stress $ inflammatory-li.e response
Pathologic changes that are ischemic in nature
Pathophysiology
:aternal vascular disease& faulty placentation
(2enetic& immunologic or inflammatory factors"&
Page 2 of 9 CH#@;(
e*cessive tropho'last #educed uteroplacental
perfusion )ndothelial activation
asospasm Hypertension& seiCures& oliguria&
a'ruption& liver ischemia asoactive agents,
Prostaglandins& nitric o*ide& endothelins further
reduce uteroplacental perfusion
Capillary lea. )dema& hemoconcentration&
proteinuria
@ctivation of coagulation %hrom'ocytopenia
Bo*ious agents, Cyto.ines& lipid pero*idases
#educed uteroplacental perfusion
asculopathy $ (nflammatory Changes
!ecidua contains cells when activated release no*ious
agents as mediators to provo.e endothelial inJury
@ disease due to e*treme state of activated
leu.ocytes& cyto.ines $ interleu.ins contri'ute to
o*idative stress 5ipid-laden macrophages
(atherosis" @ctivation of microvascular coagulation
( platelet" permea'ility
Highly to*ic radicals
(nJure endothelial cells
:odify nitric acid production
(nterfere prostaglandin 'alance
(mmunological 4actors
#is. of pre-eclampsia is enhanced where formation of
'loc.ing anti'odies to placental antigenic sites might
'e impaired
!ecreased proportion of helper % cells, Helper %
lymphocytes secrete cyto.ines that promote
implantation
%hose wA anticardiolipin anti'odies& placental
a'normalities $ pre-eclampsia develop more
commonly
Butritional 4actors
!ietary deficiencies
Kinc& calcium $ magnesium
!iet high in fruits $ vegeta'les, @nti-o*idant
activity
/'esity
)ndothelial activation
3ystemic inflammatory response associated with
atherosclerosis
C-reactive protein& an inflammatory mar.er&
increased in o'esity
Pathogenesis
;asic pathology, asospasm
ascular constriction resistance $ hypertension
)ndothelial damage interstitial lea.age
;lood constituents& platelets $ fi'rinogen deposited
endothelially
!isruption of endothelial Junction proteins
Gidespread )ndothelial !ysfunction
:anifest as dysfunction of multiple organ system
Central nervous system
Hepatic
Pulmonary
#enal
Hematological
)ndothelial damage leads to pathologic capillary lea.
#apid weight gain& edema
Bormal weight gain
!uring 1
st
trimester,
Gomen hardly gain weight
!uring the 2
nd
$ -
rd
trimester, Craving $ appetite increase, 2ain ?
poundsA 1 month (12 pounds in 2
nd
trimester&
12 pounds in -
rd
trimester"
Pathological edema, Patient
wa.es up in the morning $ cannot wal. 'ecause
foot is edematous already (!ependent edema on
normal pregnancy is seen after a day of
prolonged wal.ing& not immediately on wa.ing
up"
Pulmonary edema
Hemoconcentration
!iseased Placenta, uteroplacental 'lood flow
Bon-reassuring fetal heart rate pattern
5ow scores on ;P3
/ligohydramnios
(12#
Hypertension in Pre-eclampsia is due to vasospasm
with arterial constriction $ relatively intravascular
volume
Hyperresponsive to vasoactive peptides angiotensin ((
$ epinephrine
)ndothelial Cell @ctivation
)ndothelial prostacyclin (P2(2" production is in pre-
eclampsia& throm'o*ane @2 secretion 'y platelets &
prostacyclin, throm'o*ane ratio is sensitivity
to angiotensin (( vasoconstriction 3ynthesis $
release of vasoconstrictors $ platelet-aggregating
agents Bitric o*ide& result& not the cause
Pathophysiology
Cardiovascular
cardiac after load caused 'y hypertension
cardiac preload due to ( cystalloid or oncotic
solutions
)ndothelial activation wA e*travasation into
e*tracellular space& especially lungs
Hemoconcentration, Hallmar. of pre-eclampsia
2eneraliCed vasoconstriction
)ndothelial dysfunction with vascular permea'ility
(ntravascular compartment spaces contracted $ filled
3ensitive to vigorous fluid therapy administration
3ensitive even to normal 'lood loss
;lood $ Coagulation
%hrom'ocytopenia
100&000A5, /vert throm'ocytopenia, 3evere
disease
%he platelet count& the maternal $ fetal
mor'idity $ mortality
H)55P 3yndrome
4ragmentation hemolysis
serum lactate dehydrogenase levels
)ndothelial disruption wA platelet adherence $
fi'rin deposition
Hidneys
Page - of 9 CH#@;(
renal perfusion $ glomerular filtration
plasma uric acid concentration
2* plasma creatinine 7 2-- mgAd5
/liguria
Proteinuria
5ate to develop
Luantitative not accurate
2?-hour measurement
5iver
)levated serum hepatic transaminases
HELLP syndrome
Hepatic rupture
3u'capsular hematoma
3welling of 2lissonMs capsule
;rain
cere'ral perfusion& due to loss of autoregulation
leading to cere'ral edema
Causing headache& visual symptoms to o'tundation
leading to seiCure $ coma
Prediction
#oll-/ver %est
2>--2 wee.s
#esponse induced after lying laterally assume
supine position
!iastolic difference 0 20 mm Hg --% PP
1ric acid due to renal urate e*cretion
4i'ronectin, !ue to endothelial cell activation
Coagulation @ctivation, throm'ocytopenia $ platelet
dysfunction
/*idative 3tress - lipid pero*idasesN activity of
antio*idants
Presence of fetal !B@
1terine artery !oppler elocimetry
3ymptoms of Pre-eclampsia
)dema, #apidly nondependent may 'e a signal to
developing pre-eclampsia
#apid weight gain, @ result of edema due to capillary
lea. $ renal Ba $ fluid retention
isual distur'ances, scintillations $ scotomata due to
cere'ral vasospasm (temporary"
Headache of new onset& descri'es as frontal&
thro''ing or similar to migraine (Bo classic headache"
(Prodromal signs of impending eclampsia"
)pigastric pain, due to hepatic swelling $
inflammation& with stretching of liver capsuleN may
'e of sudden onset& it may 'e constant
Physical 4indings in Pre-eclampsia
;lood pressure
3itting positionN cuff level of the heart
3;P 0 190 mm H'& !;P 0 110 mm H; severe,
Consider delivery
Proteinuria
#etinal vasospasm or retinal edema
#ight upper Iuadrant a'dominal tenderness
;ris. or hyperactive rele*es are common& 'ut clonus
is a sign of neuromuscular irrita'ility
!ifferential !iagnosis
!ocumentation of ;P 'efore conception or 'efore 20
wee.s @A2, CH!
;P presenting at midpregnancy ( 20 -2> wee.s", may
'e early pre-eclampsiaN gestational or unrecogniCed
CH!
%hrom'ocytopenic Purpura
Hemolytic 1remic 3yndrome
@cute 4atty 5iver of Pregnancy
5a'oratory %ests
High-#is. Patients 'ut with normal ;P
Hg'& Hct (hemoconcentration is a hallmar. of pre-
eclampsia"
3erum uric acid
(f urine protein (E1"& 2?-hr urine collection
(;ecause proteinuria is la'ile"
@ccurate dating $ assessment of fetal growth
:enstrual history
@ppearance of Iuic.ening
Correlation with fundic height
1
st
>-12 wee.s, @ccurate for
dating
;aseline 13 at 25-2> wee.s
Patients presenting with HPB < 20 wee.s
3ame as a'ove
)arly 'aseline 13 for dating $ 'iometry
Patients with HPB after midpregnancy
2?-hr urine for protein determination
Hg'& Hct $ platelet count
3erum creatinine& uric acid $ transaminase level
3erum al'umin& 5!H& 'lood smear $ coagulation
profile
OOChronic hypertensive has less predisposition for
eclampsia& since the patient is used to that level of 'lood
pressureOO
:anagement
/'Jectives in the management,
%ermination of pregnancy wA least possi'le trauma
to mother $ fetus
;irth of an infant who su'seIuently thrives
Complete restoration of health to the mother
)arly Prenatal !etection
Gith overt hypertension 7 evaluate severity of
new-onset hypertension
Githout hypertension
>1->= mmHg diastolic (2
nd
trimester is associated with physiologic lowering
of 'lood pressure 'ecause of placenta formation"
0 2 l'sAwee.s
@ntepartum :anagement
!etailed e*amination6 5oo. for worsening signs
!aily weight
!etermination of proteinuriaN repeat every 2 days
;P reading every ? hours in sitting position
Plasma or serum creatinine& Hct& platelets $ liver
enCymes
#egular evaluation of fetal siCe $ @mniotic fluid
volume
4urther :anagement depends on,
3everity of pre-eclampsia
!uration of gestation
Page ? of 9 CH#@;(
Condition of the cervi*
:ild Pre-eclampsia
Ghen fetus is preterm& tendency is to temporiCe6
5onger stay in utero will ris. of neonatal death or
serious mor'idity, Pustified only in :ild Pre-eclampsia
:aternal surveillance
4etal surveillance
@nti-hypertensives
Gatch-out for any worsening
:ild Pre-eclampsia
D -8 wee.s
3ta'le condition& unfavora'le cervi*, !eliver at ?0
completed wee.s
4avora'le cervi*& fetal Jeopardy& visual
distur'ances& persistent headaches, :agnesium
sulfate delivery
< -8 wee.s
@m'ulatory management& home 'lood pressure
monitoring& maternal $ fetal evaluation 2*A wee.,
hospitaliCe if condition change
Persistent hypertension& persistent proteinuria&
a'normal la'oratory test& a'normal fetal growth&
unrelia'le patient, Heep in hospital
3urveillance of 4etal Gell-'eing
@ccurate @A2
;P3
B3%
!oppler 4low velocimetry
5A3 ratio for lung maturity
3evere Pre-eclampsia with Preterm 4etus, )*pectant
management
@nti-convulsants
@nti-hypertensive
3teroid administration < -2 wee.s
Bo improvement, termination of pregnancy
(ndication for !elivery in Pre-eclampsia
:aternal (ndications,
%erm fetus
Platelet count < 100&000 cellsAmm-
Progressive deterioration of liver $ renal functions
3uspected a'ruptio placenta
Persistent headacheN visual distur'ances
)pigastric pain& or vomiting
4etal (ndications,
3evere (12#
Bon-reassuring fetal heart rate pattern
/ligohydramnios
(mminent 3igns of Convulsions
Headache
isual distur'ances
)pigastric pain
/liguria, /minous sign
3evere Pre-eclampsia Q %ermination of Pregnancy
Prime /'Jectives for %ermination
%o forestall convulsions
%o prevent intracranial hemorrhage $ damage to
vital organs
%o deliver healthy infant
%ermination
Gith good ;ishop score, (nduce for vaginal delivery
Poor score, Cesarean section
@ntihypertensive !rug %herapy
%o prolong pregnancy or modify perinatal outcomes
%reatment-induced decreases in maternal ;P may
adversely affect fetal growth (!o not 'ring down to
normal 'lood pressure"
@C) ( angiotensin-converting enCymes" 'e avoided
during 2nd $ -rd trimester
/ligohydramnios
(12#
#!3
Beonatal hypotension
Beonatal death
HydralaCine& Ca-channel 'loc.ers& la'etalol
@nticonvulsant therapy
@dministered to prevent seiCures in severe Pre-
eclampsia
:agnesium sulfate
?-9 g ( loadN followed 'y 2-- gAhour to maintain
levels > mgAd5
Precautions,
5evels >-12 mgAd5 7 loss of
refle*es& diplopia& flushing or slurring of speech
5evels 012 mgAd5 - muscular
paralysis& ventilatory failureN circulatory collapse
Calcium 2luconate, 10-20 m5 ( in 10% solution
Prevention
!ietary manipulation
3alt-restriction is ineffective
Ca-supplementation incidence
fish oil
5ow-dose @spirin, 3elective throm'o*ane suppression
with resultant dominance of endothelial
prostacyclin
@ntio*idants
itamin )
itamin C
)clampsia
Pre-eclampsia complicated 'y generaliCed tonic-
clonic convulsions
4atal, coma wAo convulsions
/nce it has ensued& ris. to mother $ fetus
Prognosis is always serious
:aJor complications
@'ruptio
Beurological deficits
@spiration pneumonia
Pulmonary edema
Cardiopulmonary arrest
@cute renal failure
:aternal death
:anagement
Page 5 of 9 CH#@;(
Control of convulsions - :g3/? (Gait for -0
minutes to 1 hour so magnesium levels will 'e at its
pea. during delivery"
( anti-hypertensives
!elivery
)clampsia may still occur during the post partum
period
!1H@G))
H@PP+ ;(#%H!@+ ;))))
Page 9 of 9 CH#@;(