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PREGNANCY HPN
DR. Te-Santos
Classifcation of Hypertensive Disorders
in Prenancy
Gestational HPN/transient/ non-
proteinuric HPN in pregnancy
Preeclampsia = mild
= severe
Ecclampsia
Chronic HPN
Chronic HPN with superimposed
preeclampsia
e!nition o" terms
HPN # systolic $P o" 1%& mmHg or higher
'r a diastolic $P o" (& mmHg or
higher on more than one occasion
Proteinuria # presence o" )&&mg or &*) g or
more o" protein in a +% hr urine specimen
o 'r a ,1 or more in the urine dipstic-
e.uivalent to )& mg/d/
Edema # swelling o" hands and "ace or legs
a"ter an overnight rest
Gestational HPN # elevated $P without
proteinuria a"ter +& wee-s o" gestation* $P
returns to normal 1+wee-s postpartum
Preeclampsia # multiorgan disease process
characteri0ed 1y the presence o" HPN and
proteinuria a"ter +&w-s o" gestation in a
woman with a previously normal $P
2ild preeclampsia # i" patient does not
mani"est any signs and symptoms o"
severe preeclampsia
3evere preeclampsia # mani"est any o" the
4
o $P516&mmHg systolic or 511&mmHg
diastolic ta-en at least 6 hours apart on
+ occasions while patient is on 1ed rest
o Proteinuria 5 7g/ +% hrs or 5,) in +
random urine samples collected at
least % hrs apart
o Elevated serum creatinine
o Pulmonary edema
o 'liguria 8 7&&m// +%hrs
o 2icroangiopathic hemolysis
o 9hrom1ocytopenia
o Hepatocellular dys"unction elevated
3GP9 3G'9
o /ugr/ oligohydramnios
o 3ymptoms suggesting end organ
involvement
Headache/ visual dist / right upper
. pain
Ecclampsia # HPN in pregnancy with
proteinuria and convulsions*
Chronic HPN # HPN present 1e"ore
pregnancy or 1e"ore +&
th
wee- o"
pregnancy and persists longer than
1+w-s post delivery
Chronic HPN w superimposed
preeclampsia
o Char* $y elevated $P that
antecedes pregnancy or persists
postpartum w ss: o" preeclampsia*
'ther criteria;
o 1* New onset proteinuria in a
woman w HPN 1e"ore +& w-s
gestation
o +* 3udden increase in proteinuria i"
already present in early gestation
o )* 3udden increase in HPN
o %* evt o" HE//P3
P<EEC/=2P3>=
?idespread vascular endothelial
dys"unction and vasospasm w multiorgan
systemic clinical "eatures such as HPN@
proteinuria@ cere1ral and hepatic
dys"unction
HPN in preeclampsia is secondary to
placental hypoper"usion thus lowering
systemic $P and use o" antihypertensive
medications has never 1een demonstrated
to cure or reverse the primary pathogenic
process o" this condition
2aternal immunologic intolerance to
paternally derived placental and "etal
antigens
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Genetic 1asis "or the disorder has 1een
implicated as studies have shown that 1&-
%&B o" daughters and 11-)CB o" sisters o"
women with preeclampsia also developed
the disease
P=9H'GENE3>3 >N 9HE ED9 'E
P<EEC/=2P3>=
Placental implantation with a1normal
tropho1lastic invasion and vascular
remodeling causing placental
hypoper"usion and leading to the release o"
systemic vasoactive compounds that
causes e:aggerated inFammatory
response@ vasoconstriction@ endothelial
damage@ capillary lea-@ and
hypercoagula1ility and platelet dys"unction*
Gestational HPN occurs in 6B o"
pregnancies
Preeclampsia occurs in 7-GB o"
pregnancies
Chronic HPN complicates )B o"
pregnancies
3uperimposed preeclampsia complicates
+&-+7B o" pregnant women with chronic
HPN
<>3H E=C9'<3 E'< P<EEC/=2P3>=
2aternal o1stetrics "actors;
o Nulliparity@ h: o" preeclampsia@ multiple
gestation@ gestational hpn@ molar
pregnancy
2aternal co-mor1id conditions
o Chronic HPN@ pregestational vascular/
endothelial/ renal dis/ pregestational
dia1etes
2aternal genetic "actors
o =ntiphospholipid anti1ody syndrome@
"actor D leiden mutation@ !rst degree
relative w preeclamptic pregnancy
2aternal li"estyle "actors
o '1esity@ smo-ing
'ther "actors
o ="rican-american race@ ageI%& yrs
Paternal o1stetrics "actors
o Paternity 1y male who "athered a
previous preeclamptic pregnancy in
another woman@ paternity 1y male 1orn
"rom a preeclamptic pregnancy
P<E>C9>DE 9E393 E'< P<EEC/=2P3>=
1* 3C<EEN>NG 9E393
2=P # mean arterial pressure = $P ,1/)
the pulse pressure Jsystolic $P # diastolic
$PK
2=P value in the +
nd
tri I (& mmHg
2=P value in the )
rd
tri I 1&7 mmHg
<oll over test # 1etween +G to )+ wee-s o"
pregnancy* /e"t lat recum1ent position then
roll over to the supine position* $P readings
were ta-en immediately and a"ter 7 mins@
an increase o" at least +& mmHg in the $P
is positive roll over test and assoc with a )
"old increase o" developing preeclampsia
/=$ 9E393
oppler velocimetry # diminished 1lood
Fow
>ncreased systo / dia ratio J stuart inde:K
=1sence or reversed end diastolic 1lood
Fow J=<EK
$ilateral notching o" uterine arteries at 1+-
1% wee-s
E>$<'NEC9>N # a glycoprotein derived "r
liver and endothelial cells and released into
plasma
= mar-er o" vascular disruption and
endothelial cell activation* >ncrease in
preeclampsia 1ut not in chronic HPN
Hematocrit # increased levels/
hemoconcentration in preeclampsia
Proteinuria # amts greater than )&&mg/ +%
hr urine denote poor prognosis
Lric acid # elevated connotes increased
perinatal mortality and severity o"
preeclampsias
9>2>NG 'E E/>DE<A E'< GE39=9>'N=/
HPN / 2>/ P<EEC/=23>=
3hould 1e delivered at
o 5%& wee-s ='G
o 5 )C wee-s ='G
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?ith a "avora1le cervi: / 1ishop
score I7 "etal weight 8 1& Btile
N39 non reactive
= )% wee-s and a1ove with the
presence o" la1or
<$'?
Daginal 1leed
=1normal $P3
3evere preeclampsia
<emote "r term # e:pectant m:
=ntepartum testing # at the time o"
d: and +: wee- until delivery
N39
$PP
Eetal growth monitoring every +
wee-s to watch "or restriction
oppler velocimetry # to assess
"etal status i" >LG< is present
EMPEC9=N9 2=N=GE2EN9 'E
3EDE<E P<EEC/=2P3>=
$e"ore )%w-s ='G
2other appears sta1le and "etal
condition is reassuring
E:pectant m: may 1e considered
1ut only in a tertiary center
2ust 1e evaluated in a delivery until
"or +%hrs 1e"ore a decision "or
e:pectant m: can 1e made
No severe growth restriction / "etal
distress
maternal urine output is ade.uate
normal la1 results
HPN is controlled
Eetal monitoring
o N39 daily@ $P3 /+: wee-
o Eetal growth determination at +
wee- intervals@ um1ilical artery
oppler 1/wee-
3EDE<E P<EEC/=2P3>=
="ter +%w-s ='G # vaginal delivery is the
route o" delivery* C3 is "or o1stetric
indication*
Nonreassuring "etal status@ rupture
mem1ranes@ in la1or@ maternal distress #
should 1e delivered regardless o" age
)+ wee-s ='G and received steroid #
should 1e delivered
C<>9E<>= E'< E/>DE<A
Nonreassuring "etal heart status
Lncontrolled $P
'ligohydramnios =E> less than 7cm
3evere >LG<
'liguria 8 7&&ml/ +%h
3eriNum creatinine level at least 1*7 mg /dl
Pulmonary edema
Chest pain
Persistent and severe headache
< upper .uad tenderness
HE//P syndrome
+%hr urine collection "or protein
<ecord Fuid inta-e and urine output
/E9@ C$C@ uric acid@ /H@ renal ": test +:
/wee-
3teroids 1e"ore )% wee-s
Patients should 1e instructed to resort any
headache@ visual changes@ epigastric pain@
decreased "etal movt
3E>OL<E3 9M =N P<'PHA/=M>3 ? 2=G
3L/E=9E
2g sul"ate # prevention o" primary and
reduction o" recurrent eclamptic
sei0ures
>2 route # %g >D loading dose over 7-1&
mins* 9hen 7g at each 1uttoc-* 9hen 7g
>2 every %hrs until +% hrs a"ter delivery
>D route # %g >D loading dose 4Pd 1y the
>D in"usion o" 1g/hr maintained "or +%hrs
a"ter the last sei0ure*
>ndicated "or all patients w severe
preeclampsia
CH<'N>C HPN
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Goal o" treatment is to maintain $P at a
level that minimi0es maternal
cardiovascular ris-
<ecommendations;
1* /ow dose aspirin 67 to G7mg P' at
1edtime daily "r 1+ wee-s until 1irth
+* =nti-HPNsive therapy
2ethyldopa +7& # 7&&mg P' $>-Q>
Jma: +g/dayK
/a1etalol 1&&-%&&mh 9> J1+((
mg/dayK
Ne!dipine P= ta1 1&-+&mg P'
$>9> Jma: 1G&mgK
M/ slow release +&-6& mg P' '
HE//P 3AN<'2E
Hemolysis/ elevated liver en0ymes
/ow platelet ct
Lsually develops suddenly in )
rd
trimester or immediate postpartum
<apid progression* 'nset occurs
antepartum in C&B and postpartum in
)&B
3evere epigastric pain / right upper .
pain #most important symptom
Hepatic imaging w a1dominal ut0* C9
scan @ mri
Lsually resolves within a wee-
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