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CtINICAI P GUIDELINES
on
HYPERTENSIVE COM PTICATIONS OF
PREGNANCY

Second Edition

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Task Force on Clinical Practice Guidelines

ln the Diagnosis and Management of
gl"T-t'-om Hypertensive Complications of pregnancy
 \SE.{\D WAIVER OF
tsILITY

- :'-: rn H1'pertensive Complications

Epidemiology of Hypertensive Complications of pregnancy...................... I

':,:=::i cal and Gynecological Society,
Ramon M. Gonzalez, M.D., Ronaldo R. Santos, M.D.
and Carelle Roux-Ong, MD
-=-:3:s. and its entire membership.
2. The Classification of Hypertensive Complications
-. ::":titioner, the patient, the student, of Pregnancy ................ ....................... 6
,' -::er. any capacity ofthe person or Ernesto S. Uichanco, M.D. and Sherri Ann L. Suplido, M.D.
': - : t. .rr acknorvledge, any, or part, or
: .a:..stic condition or idea/s willfully
: :.,:srbilities ofthe POGS, its officers 3. Predictive Tests for Hypertensive Complications
, - ::rmiftee on the Clinical Practice of Pregnancy ................ ..................... 16
-'r all clinical or other disputes, Ma. Antonia E. Habana, M.D and Ma. Cristina p. Crisologo, M.D.
-:. ies. case discussions/critiquing.
4. Prevention of Preeclampsia ........... ......................25
g-,- - -.:nical case as a distinct and unique
Walfrido W. Sumpaico, M.D. and Milagros T Jocson, M.D.
-- -.:-r an exact location if reference is

5. Gestational Hypertension and Mild Preec1ampsia.....................................2j

: trr serve as a guide, to clarifz, to Pilar Lagman-Dy, M.D. and Carmencita B. Tbngco, M.D.
-:ention or objective of this CPG to
;..lution and treatment for clinical 6. Severe Preeclampsia 32
--.rura-sed to refer to the individual
Mario A. Bernardino, M.D. and Joseph Olivar, M.D.
- the case in question, not this CPG.

:l:nician will find a handy guide that

7. Eclampsia ....................... 55
Raul M. Quillamor M.D. and Diosdado V Mariano, M.D.
't leads to the discovery of clinical
:ntually recovery.
8. Chronic Hypertension ................ ....... 59
,:ees. the Committee on The Clinical Virgilio B. Castro, M.D. and Ann Marie C. Trinidad. M"D.
- 33nt to make each one of us a perfect
9. Complications of Pregnancy lnduced Hypertension
(HELLP, Abruptio Placenta) ............. 6l
Ma. Luisa S. Acu, M.D. and Sol M. pangan, M.D

vll
EPIDEMIOLOGY OF HYPERTENSION IN PREGNANCY
Ramon M. Gonzalez MD, Ronaldo Santos MD and, Carelle Roux-Ong MD

Preeclampsia is a life threatening complication of pregnancy characterized by

hypertension and proteinuria that contribute greatly to maternal morbidity and
mortality. This is primarily due to an abnormal implantation of trophoblasts in the
placenta as well as poor placental perfusion. It occurs in about 3o/o of all pregnancies.
This disease has long been recognized but the exact etiology of preeclampsia is
still obscure despite many attempts to identify possible causes. The etiology
therefore, is more likely to be multifactorial. Clues regarding the etiology may be
derived from the various risk factors that have been identified.

Primiparity

The only well accepted risk factor for preeclampsia is primiparity. Pregnancy-
induced hypertensive disorders, especially preeclampsia have been documented to
occur primarily in the first pregnancy. The concept, therefore, of primiparity is the
epidemiological cornerstone of this disease.r In a population based study in Norway
covering all births since 1967 (about 1.5 million women), the risk of preeclampsia
in first pregnancy was 3%o. It decreased to 1.7%o in the second pregnancy.a

Immunologic Factors

There is circumstantial evidence to support the theory that preeclampsia is

immune mediated. Normal pregnancy is well known to be an immunological
stimulation towards the tolerance pathway and not an immunological depression
of the mother. In the past, the theory was that this immunological tolerance could
be due to blocking antibodies, hiding the father's antigens. More recently, it is
thought that this tolerance involves cytokines through the tolerance network called
T helper 2 (Th2) reaction. Preeclampsia caused by the failure of the trophoblast
invasion can be considered as a kind of rejection reaction by the mother towards
the trophoblast antigens through a failure of the tolerance system allowing the
invasion. This may arise in situations in which effective immunization by a previous
pregnancy is lacking, as in first pregnancies. The immunizationconcept is supported
by observations that preeclampsia develops less often in multiparas who had a
prior term pregnancy.l

Previous Pregnancy Complicated by Preeclampsia / Eclampsia / HELLP

Women who had previous pregnancies complicated by preeclampsia have an

increased risk for recurrence in subsequent pregnancies. Moreoveq severely
preeclamptic women in an initial pregnancy have a recurrence rate of as high as Pregnancy Related Conditions
50%., In a study by Campbell and coworkers, the rate of recurrence of
preeclampsia was 7 .5Yo and 65% when the previous pregnancy was complicated Conditions with arr increased rr--:
by severe preeclampsia. Van Rijn and co-workers showed that there was a25o/o multifetal gestation are at increased :- .
chance of recurrence in women with a history of early onset preeclampsia gestations compared lvith those ii irL
resulting in delivery before 34 weeks of gestation. Those with pre-existing hypertension and preeclanipsia are h..rl
chronic hypertension had higher rates of preeclampsia, aboutT5oh. Sibai and respectively. Although rnLrltiple _eestari, :
Sullivan in separate studies revealed a recurrence rate of preeclarnpsia with the risk for recurrence in subsequenr l:
previous pregnancies with HELLP syndrome to be I 9oh and 43oh respectively. workers examined a total of 550.1 I 8 u -
ln a study by Sibai involving 366 eclamptic women, the rate of recurrence of out tliat for women with a prer i..Lr.
eclampsia in subsequent pregnancies was 2o/o and the risk for developing preeclampsia, tlre recurrence rate * as . -
preecl ampsia was 22oh.5 rvas only 6.\Yo.s

Family History of Preeclampsia Primipaternity

The predisposition to hereditary hypertension undoubtedly is linked to Recently, it has been suggested rr:::
preeclampsia and the tendency for preeclampsia-eclampsia is inherited. Women the relevant risk factor. Irnrlunt ge:::
with preeclampsia were 2.3 times more likely to have a sister who had phenomenon. The role of the father ha.
preeclampsia. Those with gestational hypertension on the other hand, were primipaternity model which cari be in:;:
1.6 times more likely to have a sister with gestational hypertension. If two This rnay be interpreted as an irr.rini.:.
sisters have the same father but different mothers the risk of preeclampsia is through corrtact between the sperrn ::.:
1.8 (95% CI I .01-2.9).4 The pathophysiologic role for genetic and behavioral sexual paftner will expose the rnother :-
factors that cluster families is consistent with the likelihood of preeclampsia among not be tolerant. Thus, chauginu tl.. '
sisters of women with previous preeclamptic pregnancies.r0 preeclampsia may increase her risk ti :r'
prirnipara. This disease therefore. ma.' :
Body Mass Index primigravity. Moreover. if auornan b-:
a preeclamptic pregnancy in a dift-eren: "'.
The relationship between maternal weight and the risk of preeclampsia is is 1.8 (95% Cl 1.2-2.6).4 Paternal c:.
progressive. It increases from 4.3o/o for women with a body mass index (BMI) less substar-rtially to a wotnan's risk of pree :
than I 9.8 kg/m2 to 13 3% in those with a BMI greater than 3 5 kil In a population risk for preeclampsia has also bee::
^r.
based cohort study in N4issouri between 1989-1997 obese and overweight women insemination by an unknotlu dont r
had higher risks of recurrent preeclampsia 19.3% and 14.2o/o respectively compared
with women with normal BMI which was 11.2oh.8 Sexual Co-habitation

Underlying Medical Conditions Robillard, et. al. sLrggested that ::,

and that the longer the duration of ...-:-.
Underlying medical conditions with vascular and connective tissue disorders the lower the risk of preeclampsi; I
or renal implications are at risk for developing preeclampsia. In a study by Stamilio, preeclampsia with the tirning of ci:.-.
the odds ratio was 6.9 (95% Cl Ll-42.3). Among 462 women with pregestational habitation. Within the first four m..nlr..
diabetes, Sibai and co-workers demonstrated a20Yo occurrence of preeclampsia.T months.r Regardless of parity. the ,::::
More so, the frequency of preeclampsia rose with increasing severity of diabetes. inversely related to the incidence --: :
period of sexual co-habitation rr iIh ::.; :
h'-. -:re a recurrence rate of as high
l(r :rre tS, th€ rate of recufrence of
b : --r ious pregnancy was complicated
Fs -\ers showed that there was aZ5o/o
I - :.-rr_\ of early onset preeclampsia
oi -:station. Those with pre-existing
f ;-.=:lampsia, aboutT5%o. Sibai and
lrr- -:rence rate of preeclampsia with
h -: ir-r be 19o/o and 43Yo respectively.
l;lti : .,omen, the rate of recurrence of
tli, l:o ond the risk for developing
pr--::rsion undoubtedly is linked to
h:, .-eclampsia is inherited. r*/omen
Iq relr to have a sister who had
l:.--nsion on the other hand, were
Fn' .=srational hypertension. If two
I - ers the risk of preeclampsia is
h,. - :..Ie for genetic and behavioral
I -. kelilrood of preeclampsia among
F r"= 'nancies.ro
f a probrem of primipater'ity rather
::
'id the risk of preeclampsia is
:;r a body mass index (BMI) less
{-:::-r than 35 kdmr.ln a population
- risk for preeclampsia has arso teen observed
- - obese and overweight women
l'-d ll.2yorespectivelycompared
,' ,:td connective tissue disorders
::, 3nlpSia. In a study by Stamilio,
l6l u,omen with pregestational
= habitation. within the first four months tie
:
i - : rrccurrence ofpreeclampsia.T
,b - :creasing severity of diabetes.
as Pregnancy Related Conditions
conditions with a' in.creased trophobrast
multifetal gestation are at increased risk
rnass rike hydrops fetaris ard
gestations compared rvith those with
for preecrarnp;;;. i,-, worren with r*i'
singretons, the i;;;i"n"" of gestationar
hyperterrsion and preecrarnpsia are
both significantry increased, 13o/o
respectively' AlthoLrgh rnultiple gestations and 5_60/o
are considered at risk for preeclanrpsia,
the risk for recurrence i1 s1lleauent
pregnancies is not crear. Trogstad
workers examined a totar of 550,2 rg and co-
women between 1967 ard r99g. They
out tlrat for women with a previous sirrgreton found
pr"gnun-" cornpricated with
preeclampsia' the recurrence rate
was I4.loz whereas tli" ,"",ir.",rce rate
rvas only 6.8oA.s for twins
Primipaternity
Recently, it has been suggested that prirnipaternity
the relevant risk factor. Immunog.n.ii.
ratrrer than primiparity is
factors ,r,. primipaternity
phenomenon' The role of the father "*prri,-,
lls long been hypothesized to be central in the
prirnipaternity moder which can.be interpreted
by a' irnmu'ogenetic hypothesis.
This rnay be i'terpreted as an immunoiogical
through contact between the sperm and the
habituation to pater'al arrtigens
femare g"nitui t.u.t. Havirrg a lrew
sexual parlner will expose the mother to
new paternal antigens to wjr jch she
not be tolerant. Thus, changing the fat'er, fo,
a wo,ni,-, *;1';',;;;;'"; 'rav
preeclampsia may increase her risk to the
same level that she would have had as
prirnipara. This disease therefore, may be a
primigravity. Moreover. if a woman becornes than
pregnant by a man rvrro has fathered
a preeclamptic pregnancy in a different
wornan, heirisk oideveroping preecrampsia
is 1.8 (95% cI r.2-2.6).a paternar genes in the
fetus ,rrf ,i,.r"rore contribute
substantially to a woman's risk of preecrampsia.
In supporrtf this theory, a higher
i'women rvho had artificial
inseminatiorr by an unknown donor.
Sexual Co-habitation
Robillard, et. ar. s,ggested that preecrampsia
is a,,disease of ,ew coupres,,
and that the longer the duration of co-habitation
(without barrier contraceptives),
the lower the risk of preecrampsia. There
is a rinear decrease of the risk of
preeclampsia with the-tirning of conception
witrri. the first yeu,. or sexuar co_
risk is 40%o.o,rpur.J b 3_5o/oover r2
months'r Regardless,of parity, the length of
inversely related to the incidence of
sexual co-haoitation was noted to be
iregnan"y induced hypertension. A ronger
period of sexual co-habitation with the
fatf,er beiore .on."p,io,r i.duces the risk
of
 preeclampsia. One explanation is that the mother adapts to the imprinted
antigens
from the father. 4. Dildy G, Belfort M, Smulian j
2007:31(3):135-t4t .
5. Agudelo AC, Villar J, Lindh:
Maternal Infection
systematic review and mera-ar
6. Sibai B, Caritis S, Hauth .1. e:. e
Systematic review and meta-analysis of observational studies were done
to among women with pregesra:::
examine the relationship between maternal infection and preeclampsia. 369.
The risk
of preeclampsia was increased in patients with urinary tract infection (oR L57, 7. Mostello D, Kallogjeri D. Tur::
95% L45-1.10) and periodontal disease (oR L76, 95% g 1.43-2.1g). conclusion
cl gestational age at deliven oi ri,
val between births. ln i ,r5r,,
was that urinary tract infection and periodontal diseases increased the risk
of 8. Mostello D, Tegan C, Roman L.
deve lopin g preeclampsia.6
who is at risk? Am J Obsret ,-:..,
9. Darcy C, Epplein M. Johnsc: (
Gestational Age at Delivery in the First pregnancy preeclampsia. Am J Obstet C.,:
10. Eskanazi B, Harley K. Comme:
sia. Int J Obstet Cynecol 2,-t,-.,::
The risk of recurrent preeclampsia is inversely related to the gestational age at
the first delivery: 38.6% for <28 weeks gestation, 29.1% between 29-32 weeks,
ll. Cunningham F, Crant \F. er.
Hill;2005. "
21 .9% for 33-36 weeks and 12.90/o for >37 weeks age of gestation.8 A previous
preterm delivery and small for gestationar age newborn increases the risk of
preeclampsia in subsequent pregnancies.e

Socioeconomic Status

Women from different socioeconomic status share the similar risk ofdeveloping
preeclampsia. This disease is the only major perinatal risk factor which is noi
reported to be evidently associated with poor social status.

Smoking

Altliough smoking during pregnancy causes a variety of adverse pregnancy

outcomes, itoni-c-allv.
;. j .?,i r:7. smoking has consistently been associated with a reduced risk
. r-- -- ,. -
o^ f h y p e rt e n s i o ;,1ii ii fo$p.Wf1*
y.
j:lr..t -"'r;i
-
rl '-
rJ
References

l.

2. factors for preeclampsia.

J. al. Fetal and matemal contributuions to risk of

B MJ 1998;3 I 6:1343-1347 .
rther adapts to the imprinted antigens
4.
5.
6.
f,:bservational studies were done to
ir=ction and preeclampsia. The risk
7. Mostello D, Kallogjeri D, Tungsiripat R, Leet T. Recurrence of preeclamsia: Effects
r,':: urinary tract infection (OR 1.57,
n. -6. 95%Cl 1.43-2.18).Conclusion
Dildy G, Belfort M, Smulian J. preeclampsia recurrence and preventio n. sem perinar
2007:31 (3):135-141 .
Agudelo AC, villar J, Lindheimer M. Matemal infection and risk of preeclampsia:
systematic review and meta-analysis. Am J obstet Gynecol 200g:l9gei:7-22.
sibai B, caritis S, Hauth J, et. al. Risks of preeclampsia and adverse neonatal outcome
among women with pregestational diabetes mellitus. Am J obstet Gynecol
2000:364_
369.
of
gestational age at delivery ofthe first pregnancy, body mass index, paternity,
val between births. Am J Obstet Gynecol 200g: 55.e1_55.e7.
and inter-

lc::al diseases increased the risk of
ltgnancy
cr.<lr related to the gestational
s;eks age of gestation.s A previous
a:: newborn increases the risk of
8. Mostello D, Tegan c, Roman L, Holcomb w, Leet T. preeclampsia in the parous woman:
who is at risk? Am J Obstet Gynecol2002;187(2):425-429.
9. Darcy c, Epplein M, Johnson c, et. al. A sister's risk: family history as a predictor
of
preeclampsia. A m J Ob s te t Gy ne c o I 200 5 :l 93 (3):965 -97 2.
10. Eskanazi B, Harley K. commentary: revisiting the primipaternity
theory of preecramp-
sia. Int J Obstet Gynecol 2001;30:1323 -1324.
age at H. cunningham F, Grant NF, et. al.I4tilliams obstetrics 22il ed. New york Ny:McGraw-
Hill;2005.

lrrii ):rare the similar risk of developing

ir :erinatal risk factor which is not
r:, .-.al status.

Ec: 3 rariety of adverse pregnancy

h :,.::r associated with a reduced risk

: rf,$lsA;*oPEsfY
t.
..
Lg: :-..,.'pibemiological standard of preec-
h:
3:
'.' J Obstet Gynecol Reprod Bio
Tir$w
n
I: r : sis of risk factors for preeclampsia.
'.

kr .-.: maternal contributuions to risk of

I : :.'- r -: I6:1343-1347.
 CLASSIFICATION OF HYPERTENSIVE Definition of Terms

COMPLICATIONS OF PREGNANCY l. Hypertension

Ernesto S. Uichanco, MD and SherriAnn L. Suplido, MD
The National Hi_eh Bi,
Working Group defines hr pe
blood pressure (Bp) of lri-i r-

Modern day obstetrics is still wanting of a classification of hypertensive or higher on more than I ic
disorders of pregnancy that is simple, encompassing and meaningful in the clinical Gynecology (ACOGt. Let..- .

situation. The various classificatiorr systems each have their own defects and an incremenfsl inglss5s 1rf
-lr
deficiencies. The confusions brought about by these nllmerous classification be used as a diagnostic crite
methods may be one of the reasons why it is difficult to come up with researches 140190 mmHg. These crireri-
on the topic with significant results and conclusiorrs. that these women are unl:i..
because similar increases a:_
Local rnedical centers are using a cornbination of the various definitions and this is the case, the \\orkir:.
classification svstenr of h1'pertensive disorders in pregnancy. Some terrns are used these patients.
irrterchanseably. adding to the confusion when trying to give a diaguosis and in The diagnosis of hr per:e:
labeling a patient. The committee is presenting tlris classification system for BP measurement and is bas;:
uniformity and standardization in practice. taken using the same arm: ,.\'-..
II-2, Grade B). KorotkotTr::=
Recommendations of the Consensus Meeting Level I, Grade A).

The committee recomrnends the following classification of hypertensive 2. Proteinuria

cornplications of pregnancy, based on a revierv of three comrnonly,-used
classificatiott system used presently in the Philippines and several recommendations Proteinuria is defined ;.
frorn different societies and guidelines abroad. protein in a 24_hour urirre .:, _
mg/dl) or greater, but shoLrl;
Clossi/icotion of Hypertensive Disorders in Pregnuncy evaluation or and a 24_hour c: :
be defined as greater than lr, ::
A. Gestational Hypertension / Non-Proteinuric Hypertension of Pregnancy / urine sample2 (NGC, Let.el I j ,

Transient Hypefterrsiotr
3. Edema
B. Preeclarnpsia
l. Mild This is defined as sriellir:
2. Severe overnight rest, arrd is rro I,.rrr_:

C. Eclarnpsia 3. Pregnancy Induced Hr.pertens

D. ChronicHypertension This is defined as hr pener,. ,

and regresses postpartu ln. H ..,. ;
E. Chronic Hypertension with Superirnposed Preeclarnpsia should be abarrdoned. as i:. :: =
Level III, Grade D).
iHYPERTENSIVE
F PREGNANCY
r -:-:'- Arn L Suplido MD
:ssit-rcation of hypertensive
"nd nreaningful in the clinical
hrr e their or.vn defects and
-3:e numerous classification
t to come up with researches
L pregnancies. Although
F -:inancl,.
--irhe various definitions and
h -g Some tenns are used
, these patients.
lr . to sive a diagnosis and in
l]r :::is classificatiorr system for
h,.
i* - , :ssification of hypertensive
t : .i of three commonly-used
|c :i tnd several recommendations
:
Fr
rliutt'_l'
- : i{r perlension of Pregnancy'
:'eeclampsia
Definition of Terms
1. Hypertension
The Nationar High Blood pressure Education program
(NHBpEp)
working Group defines hypertension in pregnant
women as having a systoric
blood pressure (Bp). of r 40 mmHg or high-r
or a diastoric Bp of 90 mmHg
or higher on more than l occasion' (Aierican
coilege of obstetrics and
Gynecology (ACoq, Levet IIl. rn the past, it
has beei recommended that
an incrementar increase of.30 mmHg systoric
Bp or l5 mmHg diastoric Bp
be used as a diagnostic criteria, regardless if
absolute values were below
140/90 mmHg. These criteria ur" no longer used
because evidence reveals
that these women are unrikery to suffei adverse p"rinutur
outcomes and
because simirar increases are seen in uncompricated
this is the case, the working Group recommends ..close
observation,, of
The diagnosis of hypertension shourd be based
on office or in_hospitar
BP measurement and is based on the average
of at least two measurements,
taken using the same arm2 (Nationar Guideiine
Crearinghouse (NGC), Level
II-2, Grctde B). Korotkoff phase v is used to designatJdiastoric
Bpz (NGC,
Level I, Grade A).
2. Proteinuria
Proteinuria is defi.ned as the presence of 0.3 g
or 300 mg or more of
protein in a24-hour urine specimen, which
usuaily".orr"rut.. with a +r (30
mg/dl) or greater, but should be confirmed with
a random urine dipstick
evaluation or and a24-hour or timed coilectionr (ACoG
Lever IIl.It may arso
be defined as greater than 30 mg/mmor urinary
creatinine in a spot (random)
/ urine sample2 (NGC, Level II, Grade A_B).
J. Edema
This is defined as sweiling of the hands and the
face or reg edema after an
overnight rest, and is no ro'ger a criterion for
trre diagnosis of preecrampsia.
3. Pregnancylnducetl Hypertension
This is defined as hypertension that deverops
as a consequence ofpregnancy
and regresses postparturn. However, the tenn
pregnancy indLrced hypertension
should be abandoned, as its meaning in crinicar
p.u"ii"" is uncrear , (NGC,
Level III, Grade D).
: HYPERTENSIVE Definition of Terms

)F PREGNANCY t. Hypertension
r: SherriAnn L. Suplido, MD
The Nationar High Blood pressure Education program (NHBpEp)
working Group defines hypertension in pregnant women as having
a systoric
blood pressure (Bp) of r40 mmHg or higher or a diastoric
Bp of 90 mmHg
or higher on more than l occasionr (Aierican coilege
E : a classification of hypertensive of obstetri", or"d
Gynecology (ACoG), Lever IIl. rn the past, it has beJn recommended
ry'ssing and meaningful in the clinical an incremental increase of 30 mmHg systolic Bp or l5
that
r:. :ach have tlreir own defects and mmHg diastolic Bp
be used as a diagnostic criteria, regardress if absorute values
r:: :r these numerous classification were berow
-iicult to come up with researches 140/90 mmHg. These criteria are no longer used because
s ; evidence reveals
that these women are unrikery to suffei adverse perinatar outcomes
f,. - >t0ns. and
because similar increases are seen in uncompricated pregnancies.
Although
this is the case, the working Group recommends .,close observation,,
I'i-:: :n of the various definitions and of
these patients.
P, " pregnancy. Some tenns are used The diagnosis of hypertension should be based on office
rF: :i-\ing to give a diagnosis and in BP measurement and is based on the average of at least
or in_hospital
E-: ' j this classificatiott systern for two measurements,
taken using the same arm2 (National Guideline clearinghouse
(NGC), Level
II-2, Grade B). Korotkoff phase v is used to designate diastoric Bp, (NGC,
Level I, Grade A).
iin g

2. Proteinuria
,- ;lassification of hypertensive
0ti1r"

a -. . ien of three cotnmonly-used

'res and several recommendations Proteinuria is defined as the presence of 0.3 g or 300 mg
rii : r or more of
protein in a24-hour urine specimen, wrricrr usuailyiorrelates
n* with a +r (30
mgldl) or greateq but should be confinned with a random
urine dipstick
evaluation or and a24-hour or timed collectionr (ACoG
t F'.-'gnuncy Levet IIl. rt may also
be defined as greater than 30 mg/mmor urinary
creatinine in a spot (random)
urine sample, (NGC, Level II, Gracte A_B).
ot- .:ic H1'peftension of Pregrtattcy /
3. Bdema

This is defined as sweiling of the hands and the face

or leg edema after an
overnight rest, and is no ronger a criterion for the diagnosis
oipreeclampsia.

3. Pregnancy Induced Hypertension

This is defined as hypertension that deverops as a consequence

ofpregnancy
and regresses postpartum. Howeveq the tenn pregnancy
induced hypertensiolr
should be abandoned, as its meaning in crinical pru"ii"" is uncrear : (h,GC.
Level III, Grade D).
 Gestational Hypertension
along with convulsions or th
with preeclampsia.3
The NHBPEP working Group has recommended that the term ,,gestational
hypertension" replace the term "pregnancy induced hypertension,, to describe
cases in which elevated BP without proteinuria develops in a woman after 20
9. ChronicHypertension
weeks of gestation and BP levels return to normal l2 weeks postpartumr (AC7G
Level III). Chronic hypertension is .
pregnancy or persists postpan
5. Preeclampsia on High Blood pressure in pr,
week of pregnancy or hr pen,
Preeclampsia is a multiorgan disease process characterized by the presence III).The diagnosis is also mace
of lrypertension and proteinuria occurring after 20 weeks of gestation in a before conception. It is class;l
woman with a previously normal Bp.
> 180/l l0 mmHg, and is als..
l2 weeks post delivery.r
Severe preeclampsia
10. Chronic Hypertension rr.irh
Preeclampsia is characterized as severe if the patient manifests any of the
following3 (ACOG Level III: This is characterized br eie
postpartum with associated s j.
' BP > 160 mmHg systolic or >1 10 mmHg diastolic taken at least 6 hours
apaft on 2 occasions while the patient is on bed rest criteria include "new-onset p:.
20 weeks gestation, sudden ir
' Proteinuria>S gl24 hrs or >+3 in 2 random urine samples collected at
least 4 hours apart gestation, a sudden increase ::
I
. Elevated serum creatinine syndromer. The acronrm HEL
. Pulmonary edema characterized by hernolr sis. el
. Oliguria < 500 ml/24 hrs
. Microangiopathichemolysis 11. Unclassified Hypertension
. Thrombocytopenia
' Hepatocel lular dysfunction (elevated alan ine transarninotransferase or Hypertension when es:e
aspartase am inotransferase) classification is put to ensure
. Intrauterine growth restriction or oligohydramnios not confused by the inclusi..n
. Symptorns suggestingend-organ involvement: to be placed in a defin ite cater
Headache to a more definitive catesor\.
Visual disturbances the recent guidelines and lilsr
Epigastric or right upper quadrant abdominal pain Unspecified Hypertens iorr.
Should any other classit'l;
1 Mild preeclampsia that the system of classit'lc:
presented for clarifi cation.
Preeclampsia is characterized as mild if the patient does not manifest any The measurement of B p '.r
of the signs and symptoms of severe preeclampsia.
the Multi-sectoral Task F;:
Hypertension convened br ri.
8. Eclampsia (Table 2.1), the NHBpEp \\
Pregnancy, the ACOG the R,-,.
Eclampsia is defined as hypertension in pregnancy with proteinuria
(RCOG) and the NGC.

on',mended that the term "gestational
1 :nduced hypertension" to describe
in.rria develops in a woman after 20
n'mal l2 weeks postpartumr (ACOG
lrrrC€SS characterized by the presence
ns after 20 weeks of gestation in a
re rf the patient rnanifests any of the
mnHg diastolic taken at least 6 hours
n:ent is on bed rest
r I random urine samples collected at
a:.J alan ine transaminotransferase or
r c iigohydramnios
I l:\ rrlYement:
rJ::nt abdominal pain
d if the patient does not manifest any
e'.,:rnpSia.
;iln in pregnancy with proteinuria
along with convulsions or the occurrence of grand mal seizures in a patient
with preeclampsia.3
9. ChronicHypertension
Chronic hypertension is clraracterized by elevation of BP that antecedes
pregnancy or persists postpartum. It is defined by the NHBpEp working Group
on High Blood Pressure in Pregnancy as hypertension present before the 20th
week of pregnancy or hypertension present before pregnancyr (ACoG Levet
III). The diagnosis is also made in a woman taking anti-hypertensive medications
before conception. It is classified as mild (Bp > r40190 mmHg) or severe (Bp
> 180/110 mmHg, and is also present if the hypertension persists longer than
l2 weeks post delivery.3
10. Chronic Hypertension with Superimposed Preeclampsia
This is characterized by elevation ofBP that antecedes pregnancy or persists
postpartum with associated signs and symptoms of preeclampsia. Diagnostic
criteria include "new-onset proteinuria" in a woman witlr hypertension before
20 weeks gestation, sudden increase in proteinuria if already present irr early
gestation, a sudden increase in hypertension, or the development of HELLP
syndrome3. The acronym HELLP describes a variant of severe preeclampsia
characterized by hemolysis, elevated liver enzymes, and low platelet count.
11. Unclassified Hypertension
Hypertension when essential clinical infbrmation is lacking (This
classification is put to ensure that "pregnancy induced" and "chronic" are
not confused by the inclusion ofequivocal cases and to enable all patients
to be placed in a definite category. Postpartum, patients may be reclassified
to a more definitive category.) This is now no longer encountered in any of
the recent guidelines and literature except for ICD-9 2l0l which included
Unspecified Hypertension.
Should any other classification system is to be used, it is recommended
that the system of classification be mentioned and proper definitions
presented for clarification.
The measurement of BP will follow the recommendations preserrted by
the Multi-sectoral rask Force on the Detection and Management of
Hypertension convened by the Philippine Society of Hypertension, 1997
(Table 2.1), the NHBPEP working Group on High Brood pressure in
Pregnancy, the ACoG, the Royal college of obstetricians and Gynecologists
(RCOG) and the NGC.
Tahle 2.1. Method of Indirect Measurement of Blood Pressure Basis for the Recommendations

l. A mercury manometer is ideal for accurate measurement. Aneroid, digital or other The above recommendations ri er.
automated devices provide reasonable alternatives2 NGC, Level II, Grade A), pro- used in the Philippines. A rer ieu
vided that they satisfy technical requirements for accuracy, and are calibrated and hypertensive disorders in pregnanc-r
tested on a regular basis. Automated methods, however, need to be used with cau- appeared to take their origins from
tion, as they may give inaccurate BP readingsT (RCOG Level II-2, Grade B).The fol Iorving sources, namely:
manometer cuff should cover at least 213 of the length of the patient's arm, or the
lenglh 1.5 times upper arm circumference while the bladder should cover at least
80% of the arm circumference.
A. William's Textbook of Obstel
B. International Statistical Cla=
2. The patient should be seated (or supine) or in the left lateral recumbent position Problems by the World Heal:-
with anns bared, supported, and at heart level7 (RCOG Level II-1, Grade A)2. C. XIIth World Congress of Gr r
They should have rested for at least 5 to l0 minutes, and should not have smoked D. ACOG Practice Bullerin \..
or ingested caffeine within 30 minutes before measurement.3 The edge of the cuff eclampsia and Eclampsia anci
should be placed I inch above the elbow crease, with the bladder directly over Hypertension in Pregrrancr
brachial artery. E. RCOG Evidence-based Cii
Management of Severe preec ..
J. The bladder should be inflated to 30 mrnHg above the point of radial pulse extinc- F. NHBPEP Reporl on Hr penen,
tion as deterrnined by a preliminary palpatory determination. lt should then be
G. NGC Guideline on Diasn - s
deflated at a rate of 2 rnmHg/beat, with the stethoscope bell placed directly over
Hypertensive Disorders oi p:-;,
the brachial artery.
H. lnternational Statistical C lr..
4. Systolic pressure should be recorded at the appearance ofthe I't clear tapping Problerns (ICD- I 0)
sound (Korokoff phase l). Diastolic pressure should be recorded at the disappear-
ance of these sounds (Korotkoffphase V): (NGC, Level I, Grade l), unless these A summary and comparison of :r.
are still present near 0 mrnHg in which case, softening of the sounds should be presented in Tables 2.2 and 2.3.
used as diastolic pressure (Korotkoffphase IV).

5. For every visit, the mean of readings, taken at least 2 minutes apart, should be 1. Clussification of Hypertensit,e D
regarded as the patient's BP. If the first 2 regarded differ by 5 mmHg or more, a 3'd lltil I iam's Tbxt bo o k of O b s t e t r i c s
reading shor-rld included in the average.

This is perhaps the mosr popu.:

If BP is being taken for first time, the procedure should be repeated with the
tl-re
Philippines, our country most srrrrn J
other arm. Subsequent determination should then be perforrned on the arm with a
higlrer pressLlre reading. States.
In the past editions of \\ illiar:r'.
7. lf BP is consistently lrigher in one ann, the arm with the higher values should be hypertension" was utilized. Tlre l::c
used for all BP rneasr-rrements.2 (I{GC, Levbl III, Grade B) adapts the current scherne of the \\,,-
The diagnosis of chronic lrr pe :
Arnbr-rlatory BP monitoring (by 24-hour or horne measurement) may be useful to . l Hypertension ( l-10 90 nr::::
detect isofated ofllce (white coat) hyperlension.2 (NGC, Level II, Grade B)
2. Hypertension detected be:--:
9. Patients should be instrr.rcted on proper BP measurement technique if they are to 3.
perfornr home BP monitoring.2 (NGC, Level III, Grade B)
Persistent hypertensirrrr l::.

t0
L-,: P:essure
rn.i: trement. Aneroid, digital or other
te: .3s: (NGC, Level II, Grade A), pro-
ns .,': accuracy, and are calibrated and
fo" .-...rrever, need to be used with cau-
€.' ^?COG Level II-2, Grade B).The
r:--= iength
of the patient's arm, or the
r: .: the bladder should cover at least
''- ::te left lateral recumbent position
et: rRCOG Level II-1, Grade A)2.
i: .: .rtes. and should not have smoked
:s :-- 3asurerlent.r The edge of the cuff
tr:::e. rvith the bladder directly over
a:or e the point of radial pulse extinc-
or determination. It should then be
siethoscope bell placed directly over
r 3ppearance of the 1.t clear tapping
: should be recorded at the disappear-
'"O(, Level I, Grade l),
unless these
e. softening of the sounds should be
Vr
! 3i least 2 minutes apart, should be
irJed differ by 5 mmHg or more, a 3'd
o!-3dure should be repeated with the
r:en be perfonned on the arm with a
Lrnr ri ith the higher values should be
Grode B)
"ll.
onre rreasurement) may be useful to
rn.: r-\GC, Level II, Grade B)
reasurement technique if they are to
ill Grade B)
Basis for the Recommendations
The above recommendations
were based on a discussion on the classifications
used in the Philippines. A review of the crassifications
and definitions of
hypertensive disorders in pregnancy used in rocar
hospitars aJ medicar centers
appeared to take their origins from definitions
fol lowing sources, namely:
and classifi.u,ion. used in the
A. William's Textbook of Obstetric s,22nd Edition
B. Internationar Statistical classification of Disease and Rerated Hearth
Problems by the World Health Organization
C. XIIth world congress of Gynecorogy &
obstetrics in Rio De Janeiro
D. ACOG Practice Bulletin No. 33 on Diagnosis
and Management of pre-
eclampsia and Eclampsia and ACOG practice
Builetin No. 29 on chronic
Hypeftension in Pregnancy
E. RcoG Evidence-based crinicar Guiderine Number r
0A o' The
Management of Severe preeclampsia/ Eclampsia
F. NHBPEP Report on Hyperterrsion in pregnancy 2000
G. NGC Guiderine on Diagnosis, E,varuation and Management
of the
Hypertensive Di sorders of
pregnancy
H' International Statistical Classification of Diseases
and Related Health
Problems (tCD-t0)
A summary and comparison of the above classifications and definitions
are
presented in Tables 2.2 and 2.3.
A. classi/ication of Hypertensive Disorders compricoting pregnancy
lltil I ia m's Tbxt from
bo o k of O bstet r ic s
This is perlraps the most popular definition and classification
used in the
Philippines, our country most stro'gry influenced by teachings
frorn the United
States.
In the past editions of wiiliam's obstetrics, the term ,.pregnancy
induced
hypertension" was utilized. The latest edition, which
is the 22nd edition, also
adapts the current scheme of the worki.g Group
of the NHBpEp in 2000.
The diagnosis of chronic hypertension is suggested
by the foilowing:
1. Hyperte'sio, (r40r90 mmHg or greater) antecedent to pregnancy
2. Hypertension detected before 20 weeks, or
3. Persistent hypertension long after delivery
l1
 Additional factors that support the diagnosis are multiparity, hypertension The unclassified hy penen,
cases when essential clinical
complicating a previous pregnancy and a strong family history of hypertension'
often. This is important ro ens
are not confused by the inclu,
Diagnosis of pregnancy-aggravated hypertensiorl or superirnposed
be placed in a definite careg.-
preeclaipsia is givln when a pre-existing chronic hyperterrsion worsen and is
encountered in any ofthe rec
usually accompanied by proteinuria or pathologic edema'
ln this proposal, compli,
example, severe hypertensi..r
separately. Suggested criter j:
Internationol Ststistical CtassiJicution of Disease ond Related Health
Problems by the Worlcl Health Organization (ICD-10)
A. Diastolic BP of ll(,, r:
B. Diastolic Bp of I 1Lr r
In this comprehensive classification of diseases' there is a section on occasions 4 or mr.re I
.,Oedema, proteinuria and hyperlensive disorders iu pregnancy, childbirth and
the puerpeiium". This classification may be easily compared to the ACOG
classification and the NHBPEP Working Group presented above and D. ACOG Prsctice Bulletin .\o.
corresponding classes may be matched. without a corresponding category eclampsia, Eclampsio tnd .i
though is the class gestational edema and proteinuria without hypertension Hypertension in Pregnsnc). ot
(lcD 10 code 012.2). Perhaps this may be indicative ott broader outlook at the Pressure in Pregnancl.
possible complications of pregnancy with regards to this topic - possibly
initially starting as to involve other organ systems even prior to the clinical The NHBPEP \\'orkinr C
manifestation of overt elevation in BP. Another difference irr the classification recently issued a report ider:: .-.
is ICD l0 code 013, where gestational hypertension without significant namely: chronic hr periens --

proteinuria, or gestational hypertension not otherwise specified are also known eclampsia, a serious. s\:ie: :
Obstetrics
as mild preeclampsia. According to the 22nd edition of Williams other findings: chronic hr le::=
and the Working Group, to make the diagnosis of gestational hypertertsion, gestational hypertension. .: - .

there should be no protlinuria. The ICD l0 also included the term

"Moderate scheme and the criteria l.: ::
Preeclampsia" (lCD 10 code 014). schemes and the current i- - --
This is the classification system used mainly by the group of the FetalAs preeclampsia eliminatie.n :: -
"
A Patient but the term EPH Gestosis (Ederna, Proteinuria, Hypertension) is the group recommends usr:i
used to correspond to the terrn "preeclampsia"' edema as a criteriorr. beca...: .-
women and absolute requ ::::
24 hours for the diagnosis f -,
XIIth Worltt Congress of Gynecology & Obstetrics in women with nonprotei:--,
pathophysiologic perturb,:i..- - .
This is a classification based solely on the physical signs of hyperlension before delivery. The {COC .
and proteinuria - with the intention of defining clinical categories without Working Group, as repLrrreJ .-
necessarily implying a particular etiology or pathology. Edema is not included For a more detarled t're:..: .

because it was noted not to have prognostic significance' see Table 2.2.
In this classification, gestational hypertension, proteinuria and proteinuric
hypertension are further subdivided into anteparturn, intrapartum or postpartum
types because of possible differences in clinical, pathologic and prognostic
significance.

12
rsnosis are multiparity, hypertension
;trong family history of hypertension.
ed hypertension or superirnposed
r chronic hypertension worsen and is
rthologic edema.
n of Disease ond Reloted Hesltlt
nion (ICD-I0)
l ,-'l diseases, there is a section on
i**.rders in pregnancy, childbirth and
i he easily compared to the ACOG
kine Group presented above and
\\ itlrout a corresponding category
xj croteinuria witlrout hypertension
: indicative ou broader outlook at the
hir regards to this topic - possibly
n s\ stems even prior to the clinical
r::.er difference in the classification
I :.' pertension without significant
il -:leru ise specified are also known
Il .l edition of Williams Obstetrics
g: :sis of gestational hypertension,
![ . .o included the term "Moderate
lr,irlr by the group of the FetalAs
de^-:. Proteinuria, Hypertension) is
F5:
Oh:tetrics
I :- . phl sical signs of hypeftension
t' :ns clinical categories without
c,r :'thology. Edema is not included
lic .
=nificance.
t'[tr- i:!-\n. proteinuria and proteinuric
t: :ruln. intrapartum or postpartum
s - ;al. pathologic and prognostic
The uncrassified hypertension and/or proteinuria
in pregnancy is used for
cases when essentiar crinicar information
is racking
often' This is important to ensure that .,chroni",, - *nLr-, happens quite
or;g..tutionur,, categories
are not confused by the incrusion ofequivocar
cases and enabre patients to
be placed in a definite category. This crassification
however, is no ronger
encountered in any of the recent guiderines
and ratest riterature.
In this proposar, comprications are to be crassified
separatery. For
example, severe hypertension and severe
proteinuria should be defined
separately. Suggested criteria for "severe"
hypertension are as follows:
A. Diastolic mmHg or more on any one occasion, or
B' Diastoric llBp "1120
of lr0 mmHg or more on two or more consecutive
occasions 4 or more hours apart
D' AC,G Practice Builetin No. 33 on Diagnosis and Monagement
eclampsia, Ecrampsio onct AC0G prac"tice
of pre-
nureti-io'.' 29 on crtronic
Hypertension in pregnancy and NHBpEp wtorking
Group on High Btooct
Pressure in pregnoncy
The NHBpEp Working Group on High Blood pressure
in pregnancy
recently issued a report identifying four hypertensive
disorders
namely: chronic hypertension that p."dut., pr"gnun.y, of pregnancy
preecrampsia-
eclampsia, a serious, systemic syndrome or
etevat"ea Bp, proteinuria and
other find ings; chron ic hypertension witrr rrp"ri
rpo*J prJ". run.'psia; and
gestational hypertension, or nonproteinuric
t yp.rt"nrion irp..gnuncy. This
scheme and the criteria for each category
differ from fo.me, diagnostic
schemes and tlre current schemes of otrrer groups.
Important features of the
preeclampsia elimination of a change in
Bp as a diagnostic wrrerein
the group recommends using cut-off of r40190;," "rite.ion
edema as a criterion, because this finding
Hg, eriminationof
is so common in"hearthy pregnant
women and absorute requirement of proteinuria
of more than 300 mg per
24 hours for the diagnosis. The gestaiionar
hypertension category is used
in women with nonproteinuric hypertension'of
pregnanry in which the
pathophysiologic perturba_tions ofth. pr.".lampsia
,inoron-'" do not occur
lefore delivery. The ACoG adapt the present scheme of the NHBpEp
working Group, as reported in ttre acoc practice
Builetin No. 29 and 33.
For a more detaired breakdown of the three
crassification systems, prease
see Table 2.2.
l3
Table2.2z Classification of Hypertensive Disorders in Pregnancy
wHo (tcD-r0)
Gestational hypertension
w/o sig. proteinuria
References
Xllth World Congress Williams Obstetrics 22nd
Ed/NH BPEP Workins G rouP/ACOG t. Report of the National _ :-
The ternl "pregllancy induced High Blood Pressure ir: ?-._-
hlpertension" is r.rorv replaced by
gestational hypertension I
2. Diagnosis. evaluarion,.. l,
National Cuideline Cl::: - _:
I
5 Types olHypertensive Disease in I
3. American College of oL.:.1- _
Pregnancy:
Bulletins-Obstetrics. \ C,_, ._
Gestational hypertension (rv/o A. Cestational Hypertension/
proteinuria) Transierrt Hypertens ion management of preeclarr::. . .

4. Sibai BM. Diagnosis. Ct-rir- .r

B. Pre-eclarnsia
hemolysis, elevated Iir er r:r. -
pt I ):981-991 .
Same Mild
Gestational hypertension Severe 5. Barton JR, Sibai B\1. D .;:
with sig. Proteinuria zytnes. and low platelets :.. -:-
6. Magann EF. Martin J\ .rr. 1...;
Clin Obstet G),necsl lc,qn:l:
Eclampsia Eclanrpsia C. Eclanrpsia
7. Royal College of Oh:rerr;-,:-r
Pre-existing hypertension Chronic hypertelNion w/o D. Chronio H)?ertension eclampsia,z Eclanrpsia: Er .::-,
proteinuria
8. American College of Ob::;:: ,
Pre-existing h) pertenslolr Chronic hypertension w/ E. Preeclanrpsia superimposed on Bulletins-Obstetrics. .\ CCta :
w/ superimposed superimposed preeclantpsia Chronic Hypertension
sion in Pregnanc). /)Asr.r .. ,.
preeclampsia
[Jsed intercharrgeably rvith gestational
9. Cunningham, et.al. \\ iljrar.
Unspecifi ed hypertension Unspecifi ed lrypertension _

rv/o proteinuria hlpertensiorr

Gestational proteinuria
Gestational ederna & (r.r'lo h1'pertens ion)
proteinuria w/o
Chronic renal disea;e
hypertension (rv/ or rv/o l.rlpertension)
Unclassified proteitruria
(wo hYDertension)

Table 2.3: Definitions

\\'illia
ms Obstetrics \\'HO (lcD - l0) \l lth World Congress
22nd Ed/NHBPEP
\\'orking Group/ACOG

BP >140/90 ntnt Hg BP -140/90 Diastolic BI'} I l0 rnmHg

Incremcntal incrcase in 'f30mnrHg systolic or Diastolic BP 90 nrnrlJg
Hypertension BP is no longer included I l5 mmHg diastolic (4 hours apart)
Korotkotl-phase V is used (6 hours apart) (Korotkollphase lV)
to define diastolic BP (KorotkofTphase lV)

> 300 rng per 24 lrours
30 nrg/dl (+l) dipstick in
Proteinuria randorr urine sanrples
Abandoned as diagnostic
Edenra criterion
0.3 g/l- in 24 hr collection 300 rng in 24 hours
0.1 g/L or 2+ in 2 r'andont I g/t, or 2+ in 2 randont
6 ltours apart ,1hours apart
0.3 g/L or l+ on reagent
(SG >1.030 & pH < 8)
Sri,elling olhands & l-ace
Weight gain ol5 lbs
(2.27 kd in a *eek

t4
:: ?::snancv References
\\ illiams Obstetrics 22nd
Ed/\HBPEP Workins C roup/ACOG t. Report of the National High Blood pressure Education program
The term "pregnancy ir]duced working Group on
High Blood Pressure in pregnancy. .,trn J Obstel CynecolZOdO;
hrpertension" is norv replaced by lS:1t;:St_-SZZ.
gestational hypertension 2. Diagnosis, evaluation and management of the hypertensive
disorders of pregnancy.
National Guideline crearinghouse. t'ttp,z***.gria.tin..nouluuouizln.ru.iun.urp*.
.{ Trpes olHlpenensive Disease in 3. American college of obstetricians and Gynecologists.
Pregnancy:
ACoG committee on practice
Bulletins-obstetrics. ACoG practice Bulletin N]o. 33, January
i: .\. Gestaticlnal Flypertension/ 2002. Diagnosis and
management of preecrampsia and ecrarnp sia. obstet
Transient Hypertension Gynecor )ooz;osltlrtse-taz .
Sibai BM. Diagnosis, controversies, andmanagement of
the syndrome o f
hemolysis, elevated liver enzymes, and low ptaGtet
Pre-eclamsia count. obster Gynecor 2004;103(5
pt l):981 -991 .
Mild
Severe 5. Barton JR, Sibai BM. Diagnosis and management of hemorysis,
erevated river en-
zymes, and low platelets syndrome. Clin perinatol 2004:31 (aj:g07_g33.
6. Magann EF, Martin JN Jr. Twelve steps to optimal management
of HELLp syndrome.
Cl in Obstet Gynecol 1999;42(3):532-550.
Eclampsia
7. Royal college of obstetricians and Gynaecologists. The Management
D. Chronic Hlpertension of severe pre_
eclampsia,/ Eclampsia: Evidence-based clinicalbuideline Numier l0 A, 2006, March.
8. American college of obstetricians and Gynecologists. ACoG
E Preeclaurpsia superirnposed on
committee on practice
Bulletins-obstetrics. ACoG practice Bulletin No. zs, July 2001.
Chronic Hypertension Chronic Hyperten_
sion in Pregnancy. Obstet Gynecol 2001;9g: 177_1g5.
I- sed interchangeably r.vith gestational
9. Cunningham, et.al, Williams Obstetrics. 22 ed.2005.
h\pertension

l( D_ l0) \'llth World Congress

Diastolic BI') I l0 nrmHg

il i .,- llf Diastolic BP 90 ntmHg
-.:. (4 hours apart)
q.- (Korotkofl phase IV)
q-.::r I\')
r -- -.'llection 300 nrg in 24 hours
- I rrndonr I g/1. or 2+ in 2 randonr
4 hours apart
0.3 g/L or l+ on rcagent
(SG >1.030 & pl{ < 8)
::--. & lace
.- : .:s
r . ,' .'lk

15
 PREDICTIVE TESTS FOR HYPERTENSIVE preeclampsia, the search t-or r
development or assist in the dere;
COMPLICATIONS OF PREGNANCY is still of utmost importance. The
Ma. Antonia E. Habana, MD and Ma. Cristina P. Crisologo, MD impact not only on the medical r:
such as referral to a tertian cenrer
prevalent medical condition. The;
or prediction of hypertensir e cc:r
Hypertensive complications of Pregnancy are more likely to develop in a
woman who - The following are suggesrei :
( I ) is exposed to abnormal chronic villi for the first time
(2) is exposed to super abundance of chorionic villi, or with twins or l. Case Finding as part of Gene:.
hydatidiform mole Opportunities for case ir
(3) has preexisting vascular disease, or service providers are encouri.
(4) is genetically predisposed to hypertension developing during pregnancy patient visit and consultarion ,

if the patient complains tbr u:

and Siston
The tendency to develop preeclampsia is said to be heritable. cooper for potential risk factors. :.-
(1971) examined the possi'bility that susceptibilify to preeclampsia is dependent showed that these Seerr] ttr Si
upon u single recessive gene. chesley and cooper (1986) reanalyzeti chesley's onset preeclampsia, uhich n:
extensive data and .on"lud.d that the single gene hypothesis fits well, but hypertensive statesT. (Let'ei t'i
multifactorial inheritance cannot be excluded. Risk factors for hypertensive
complications of pregnancy are found in Table 3'1'ri 2. Screening Maneuvers

Table 3.1. Risk Factors for Hypertension in Pregnancy a. Mean Arterial Pressure
Factor Risk Ratio The mean arterial pres
Diabetes mellitus 2:l l13 tl'te pulse pressure [\f
2-3:1 MAP value in the secon:
Hypertension in previous pregnancy
Nulliparity 3:l 6l-71% and specificin c:
Change ofpaftner for second or
(MAP -3) >'t05 mmHe i.
3:1 eclampsia.r8 The louer cr
subsequent PregnancY
3:1 the mid+rimester drop in Bi
Age > 40 years
Twin gestation 4:l proliferation at this time i
Family history of pregnancy induced
Therefore, the absence ..i.
hypertension (PIH) 5:1 < 90 mmHg may' predic:
Chronic hypertension l0:1 vasodilatation and shoul; :
Chronic renal disease 20 1 authors suggest that tlie \1
Anti-phosphol ipid sYndrome l0: I hypertension or essenri-i.
Angiotensinogen gene suggest the sensitir irr c: ::
Homozygous 20:1 be of little value in predi;l::

4:l at MAP and BP measurer-..

Heterzygous
MAP of 90 mm Hg or rii!-:3
CI2.0-5.0) and a negarir;
Regardless of tlre lack of existing prophylactic and therapeutic means to address women deemed to be ar i-r..

t6
R HYPERTENSIVE
F PREGNANCY
I is still of utmost importance. The availability of such *urk..f
r Cristina P. Crisologo, MD
c) are more likely to develop in a
t r the first time
c:orionic villi, or with twins or
xi..n developing during pregnancy
rj: r.-, be heritable. Cooper and Siston
ibrl:n to preeclampsia is dependent
.o; :er (1986) reanalyzed Chesley's
gie uene hypothesis fits well, but
!e': Risk factors for hypertensive
-
e,:.
r', . .J therapeutic means to address
preeclampsia, the search for non-invasive markers that
could predict the
development or assist in the detection of this life-threatening pregnancy
disorder
iould have decisive
impact not only on the medical management of pregnant women
and their child,
such as referral to a tertiary center, but also on the health costs
associated with this
prevalent medical condition. There are many proposed strategies
on the detection
or prediction of hypertensive complication of pregnancy.
The following are suggested predictive tests for preecrampsia:
1. Case Finding as part of General physical Examination
opportunities for case finding are common in generar practice. Hearth
service providers are eucouraged to measure the blood pressure (Bp) at
each
patient visit and consultation (either on outpatient or on ernergency
basis) even
if the patient complains for unrerated symptoms. Reviewing maternal history
for potential risk factors, coupled with uterine artery Doppler urr"rr,n.ni
showed that these seem to serect two different populationi - early and late_
onset preeclampsia, which might suggest a different pathogenesis for
these
hypertensive statesi. (Level II, Grarte A)
2. Screening Maneuvers
a. Mean Arterial pressure
The mean arterial pressure (MAp) is defined as diastolic Bp (DBp) +
113 the pulse pressure [MAp = DBp + t/3 (systolic Bp (SBp)_DBp)].
A
MAP value in the second trimester (MAp -2) > g0 mmHg (sensitivity of
6l-71% and specificity of 62-74%o) or a MAP value in the third trimester
(MAP -3) >105 rnmHg has resurted in an increased incidence of pre-
eclampsia.r8 The lower critical cut off in the second trimester represents
the rnid-trimester drop in BP which strengthens the beliefthat throphoblastic
proliferation at this time has resulted in dilatation of the spiral arterioles.
Therefore, the absence of a rnid-trirnester drop in Bp despite MAp _2
values
< 90 mmHg may predict future PIH based on the abience
of arteriolar
vasodilatation and should alert the physician for closer follow-up. Several
authors suggest that the MAp -2 varue may be more predictive for
chronic
hypertension or essential or transient hypertension.re.20 Recent reports
suggest the sensitivity of this test may be much lower (22-35yo)
and. may
be of little value in predicting preeclampsi a.2tln asystematic
review looking
at MAP and BP measurements in predicting preeclampsia, second
trimester
MAP of90 mm Hgor more showed a positive rikelihood ratio of3.5 (95y0
cl 2.0-5.0) and a negative rikelihood ratio of 0.46 (95% ClO. r6-0.75). In
women deemed to be at high risk, a diastolic Bp of 75 mm Hg
or more at
t7
 13 to 20 weeks' gestation best predicted preeclampsia: positive likelihood f. Hyperbaric Inder r HB
ratio 2.8 (g5%Cl1.8-3.6), negative likelihood ratio 0.39 (95% CI 0.18- The FIBI \\ils ..1 ,..
0.71). Thus, when BP is measured in the first or second trimester of
tolerance limit fbr si .:.
its predictire eI'tr..,,
pregnancy the MAP is a better predictor for preeclampsia than systolic
BR diastolic BP, or an increase of BP.e (Level I, Grade B)
ambulatory Bp rrr, : :
methods, sensitir irr i -- .,.
(Level II-2)
b. Supine Pressure Test or Roll Over Test
Originally described by Gant, et. al. in 1974, women were seen between 3. Laboratory Tests
28-32 weeks of pregnancy when their diastolic BP in the superior arm Wlren evalrratirrs nt... :,-
were first stabilized in the left lateral recumbent positiorr. The women and predictive r,alues _<l:. .. :
were then rolled over to the supine position and BP readings were taken acceptability arrd qualir., -
immediately and after 5 minutes. An increase of at least 20 mmHg irr the
diastolic pressure constituted a positive roll over test. A positive roll over a. Doppler Velrrcirr.ii:.
test is associated with a 3-fold increase of developing preeclampsia,
similar Dirninislrecl hl, : '
to the results of the angiotensin sensitivity test. Gant, et. al' (1973) and diastolic ratio ( Sru:n , .-:,
Oney and Kaulhausenlf qSZ) infused angiotensin II and demonstrated diastolic(AREDTbl.._
increased pressor response in primigravidas, with 20 rnmHg as the
positive 14 weeks is a usc.firl :
response. However, the positive predictive value of this test in predicting disorders irr hi!.lt-::... :-.
preeclampsia is only 33Yo- (Level I, Grade B) predicting hr perren.... . :
pregnancy fi'orn Q. :- :-.
values irrcreaseJ I'r.:r _
c. Combination of the MAP-2 and Roll Over Test
negative predictir e r., ,"=
Performed singly, the MAP -2 test or the roll over test predicted a600/o
velocimetn' ol tlte i;:.:r .
risk hypertension or preeclampsia later in pregnancy but rvhen a MAP -2 effective test tr) prej ;:
uulr" >90 mmHg and a positive roll over test are combined, the predictiorl
.

both rrterine allcric. ::: ..

rate increas ed to J 8o/o.22 (Grade B)
before 34 ueek: rr i:i. .,
contrast. \\'omelt u ithi,.:
d. 48-hour BP Monitoring I% having delir en bc: :.
ln the first trimester, the test accurately diagrrosed 93% of the 60 rvomen in twin pre_errancies. i: r.
wlio later developed PIH or preeclarnpsia. This rose to 99%by the third
r

results defined br rrr ii. :

trimester. The test does not require monthly monitoring during pregnancy vs. 18.2%o for preeci.r::::
which was done duringthe study to validate the test. It additionally exatnines tlornogranls. Ulet.i lte J::, :.
lower BP in women and fluctuations between activity and the rest during lorv serrsitir it1 irr 1.pg.r;,- ...
different trimesters. This allows diagnosis before BP becomes elevated'23 values of trterirre D.,r:..- -
(Grade C) those reported in Lrrr:c....::
cornplications ()ccLlr :r l

e. 24 hours Arnbulatory BP and Heart Rate wavelorms. Tlris srrt:=...

The sensitivity in predicting preeclampsia for MAP of > 85 mmHg at causingpreeclanrpsi. ], . -
20 weeks was 65oh,with a positive predictive value for a test combining tlrat is unrelated [o r]r!,r---:
MAP > 85 mmHg and a heart rate > 90 bpm were 53Vo at'rd 45% respectively.
The efficiency of the test is increased by combining the awake ambulatory
b. Fibronectin
This glycoprotejn r. j_
heart rate and BP measurement together.23 (Gracle C)
cells, and its release i:r: :

l8
d preeclarnpsia: positive likelihood
rkelihood ratio 0.39 (95% CI 0.18-
in the first or second trimester of
:tor for preeclarnpsia than systolic
' ,Level I, Grade B)
t
in I91 4, women were seen between
r drastolic BP in tlie superior arm
I recumbent position. The women
sition and BP readings were taken
increase of at least.20 mmHg in the
e roll over test. A positive roll over
oi developing preeclampsia, similar
tir in test. Gant, et. al. (1973) and
J angiotensin II and demonstrated
r idas. with 20 rnmHg as the positive
irir e value of this test in predicting
ru.le B)
)r er Test
r.r the roll over test predicted a600/o
:r in pregnancy but when a MAP -2
,ei- test are combined, the prediction
telr diagnosed93oh ofthe 60 wornen
p.ia. This rose to 99% by the third
rn:lr lr monitorirrg durirrg pregnarlcy
date the test. It additionally exarnines
ler\\een activity and the rest during
rt sis before BP becomes elevated.23
;lampsia for MAP of > 85 mmHg at
redictive value for a test combining
)pm \\'ere 53oh and 45o% respectively.
:-r cornbining the arvake arnbulatory
er.:] (Grade C)
f. Hyperbaric Index (HBI)
The HBI was carculated as a tirne-specified
Bp excess over a pre_set
tolerance rimit for systoric Bp. diastoric rjpand
MAp. Irr a stLrcry cornparing
its predictive efficacy ,uvith standard sphygrnon.,ono',-,",.y
and 4g-rrour
ambulatory BP morritoring, the preaiciivLlalu"
,uu, iorv tbr all three
nrethods' sensitivity between 54 ancl 77%o,
(Level II-2)
specifrcity betrveen 4l and 7gyo.14
3. Laboratory Tests
when evaruating ne.w screening stra.tegies, not
onry sensitivity, specificity
and predictive values should be taken int-o account,
bLrt atso costs, patient,s
acceptability arrd quality control.
a. Doppler Velocimetry
Diminished brood flow rnay be reflectecr as a'
i'creasecr systoric/
diastolic ratio (Stuart Index) or the more orninous
absence or reversed end
diastolic (ARED) blood flow.raBilateral notching
of ,,t"ri,r" arteries at l2-
l4 weeks is a u.sefur toor in predicting the deveiof,rr.,rt orrrypertensive
disorders in high-risk pregnancies. ThJsensiti"iryiit,irurerar
notcrring in
predicting hyperte'sive disorders of pregnancy
decreased rvith advancTng
pregnancy from 9l to35o/o,arrd the,p..ifi.irya'd
the positive predictiv;
I values increased frorn 41 to 94%o o,id fro,n i
to 7}yo', rcspectiverl,. T.he
negative predictive varues ra'ged fronr 86 to 97o/o.a (Lever
velocimetry of the uterine and uteroplacental arteri
II-rl Eopprer
es atZA rveeks is an
effective test to predict prH. persistence of trre earry
d{astoric notch in
botlr Lrterine afteriesstrongry correrates^witrr severe
nrir r..luiri,rg derivery
before 34 weeks with a sensitivity of gr%o on.r
contrast, women without a notch corrstitute a
,p".it.ity of g7o/o. rr.r
very iow risk groLrp r.r,,ith <
lohhavingderivery before 34 weeks.25 wrren ,seito
prJL, rrvpefte'siorr
in twin pregnancies,.the sensitivity of abrornrar uterine
aftery Dopprer
defi'ed by twin ,.,orogru,ri vs. singretor., non.,og.un-.,s r.vas
results
36.402
vs. for preecrampsia. Despite usi,ig speciaily?onstructed
18.2%o
twin
nomogralns' Lrterine altery Doppler stLrdies in
t*I1 gestatiolts had arr overall
low sersitivity in predicting adverse obstetric
oLrtcJme. Negative predictive
values of uterine Dopprer studies in twin gestations
or. tori",. conrparecr to
those repofted in unselected singleton pre-{nancies,
i.e. r'aterrral and fetal
cornplicatior.ls.occur more frequentiy Jespit"
,ror,.,.',or .-rterine artery
waveforms. This suggests that tirere is an additionar
pathomecrra'ism,
causing preeclampsia and consequent growth
restrictio' in trvin gestations.
tlrat is unrelated to uteroplacentil insufilciency.ro (Levet
II_2)
b. Fibronectin
..
Th is glycoproteirl. is derived principally
frorn the liver and epdothelial
cells' and its rerease into prasrna is a nrarker of.ydscurar
disrLrption and
l9
a
o Hypocalciuria and the
endothelial cell activation. lncreased levels have been found to predict b' ,

preeclampsia but not in chronic hypertension. In a study among 125 eclampsia lrom clrron i.
pregnant women, the elevated maternal plasma fibronectin level over 40
mg/dL is capable of predicting preeclampsia in the third trimester with a h. Glucose Intolerance
sensitivity of 73oh and a specificity of 92o/o. These results suggest that Irrsulin resistarrcc i,
serial plasma fibronectin measurements before 24 weeks of gestation may hypertension, but th
be helpful in the early detection of preeclampsia in normotensive gravid lrypertension ari si n " de
women who are destined to become clinically preeclarnptic.t2 (Level II'2) case-control studr. ri ,--:
had sign ificanr lr lr ir:;
c. Hematocrit test and a significantl'.
Preeclampsia represents a state of hemoconcentration and incrbased tests (> or : 7.8 n:r:r '
hematocrit levels. A fall in repeat hematocrit values may denote clinical Relative glucose irrr.. l.
irnprovement.26 developed rlorlprrric -
hypertensiolr cls.. l:, -
Proteinuria baseline systolic:i::
Arnounts greater than 300 mgl24 hr urine sample or dipsticks values normotensive at base -
of +1 or more have been said to denote poor prognosis, however, a for these and other p --:;
systematic review concluded that even increasing levels of proteinuria are test remained a sic:t .-:
not predictive of poor maternal nor fetal outcomes.13 Deemed more and, specifical lr. rr' r.rl
important than the proteinuria values is the urinary protein/creatinine ratio
in its ability to predict hyperlensive complications during pregnancy. For i. Inhibin A and circL:l:: ''
protein/creatinine ratio 130-150 mg/g, sensitivity ranged from 90-990/o, weeks age of gesta:: -
and specificity ranged from33-65Yo; for protein/creatinine ratio 300 mg/ preeclarnpsia at les. ::': '
g, serisitivity ranged frorn 8l -98oh and specificity ranged from 52-99o/o; with onset of preec I:r ^'
ior protein/creatinine ratio 600-700 mg/g, sensitivity ranged from 85-87%,
.

the correspon d irr s se::.

and specificity ranged from 96-970%. Random protein/creatinine ratio low. these rnarker: rl:- -:
determinations are helpful primarily when they are below 130- I 50 mg/g,
in women \\ itlr ..'
in that 300 mg or more proteinuria is unlikely below this threshold. hypertension. i
Midrange protein/creatinine ratio (300 mgig) has poor sensitivity and
specificity, requiring a full 24-hour urine for accurate results'r4
4. In the recent years. other b j -'
.
predictors for preeclanrps:,
d. Serum uric acid
Uric acid values correlate with the developmerrt of preeclampsia, its sufficiently sensitir e arr: ::
severity and increased perinatal mortality'26 predictive value. Ser era I :: -
combination, that rnieht i.: :-
e. Hemoglobinuria, elevated alanine transaminotransfrase (ALT) and from srnall case studies rr:: '
thrombocytopenia comprise the diagnosis of the HELLP syndrome. for worldwide large scal.- ::
specificity of these pr,.rr:i.
Matemal serum alpha fetoprotein (MSAFP) levels > 2 multiples of median subtypes of preeclarnpsia b:::
(MOM) were associated with a higher incidence of preeclampsia compared tests.2 The follor.lins tah,e s
tc controls. This elevation also correlated with a higher likelihood of markers for preeclarnpsia. -.
developing adverse perinatal outcomes such asfrowth restriction,freterm
delivery and,intrauterine fetal demise.r5

20
 Rrpone,C Alrcred levels Because of the abundance of tests evaluating the predictive
r':mtriletions ercalso value of differe't
parameters in predicting preeclampsia, a systematic
i: n prcdktion correlated review of these reviews were
rith: conducted. where murtipre studies were avairable, onry
a body mass index of >
34, alpha-fetoprotein, fibronectin (cellular and total), and
uterine artery Doppler
(bilateral notching) rreasurements reached specificity
above 90oh. orly Doppler
(anylu n i lateral notchi ng, res istance i ndex, and
corn binatiol s) r,easurements were
II-GR over 60oh sensitive. Fufther research should focus on
HELLP tests which offer muclr higher
levels of sensitivity than tests currently available. High
SG.A sensitivity is a more useful
SGA attribute in early detection of preeclampsia tharr spec-ificity
b"cause consideration
ILGR trl benefits, harms and costs indicates a much greater pr"f.r"n""
for minimizing
Preterm talse negatives than false positives, althouglr the ideal would
be to avoid both.il
:
del iverl

References

IUGR l. Brown MA, Mackenzie C, Dunsrnuir W, Roberls L, Ikin K, Matthews

J, Mangos G,
Polvhydramn Davis G' Can we predict recurrence of pre-eclarnpsia or gestational
hypertension? BJOG
ios 2007;lt 4(8):984-93.
Trisomy 2l 2. Grill S, RusterholzC,zanerti-Ddlrenbach R, Tercanli S, Holzgreve
Preterm Iabor o. Potential markers I Hahn S, Lapaire
of preeclampsia * a review. Reprod Biol Endocrin ol 2009;7:70.
J. Caritis S, Sibai B, Hauth J, Lindheimer M, VanDorsten p, KrebanoffM,
Thom E, Landon
Trisomy 2l M, Paul R, Miodovnik M, Meis p, Thurnau G, Dorrbrowski M,
McNeilis D, Roberls J.
Trisomy l8 Predictors of pre-eclanrpsia in women at high risk. National Institute
of Child Health
SGA and-Human Development Network of Maternal-Fetal Medicine
Units. AJoG
IUGR 1998;179:4,946-51 .

birthiveieht 4. Vainio M, Kujansuu E, Koivisto AM, Miienpiiii J. Biraterar notching

of uterine arteries
Type-2 at l2-14 weeks of gestation for prediction of hypertensive disorders
of pregnancy.
diabetes Acta obstetr et gynecol Scan 2005;g4:ll, 1062-7.
nrell itus 5. Sibai BM, Koch MA, Freire S, pinto e Sirva JL, Rudge MV,
Marrins-costa S, Bartz J,
Gestational de Barros Santos c, Cecatti JC, costa R, Ramos JG,
Spinnato JA. Serurn inhibin A and
diabetes angiogenic factor levels in. pregnancies with previous preeclampsia
and/or chronic
mellitus hypertension: are they usefur markers for prediction of
subsequent preecramfsiaz n;oc
Obesity 2008;199:3,268.e 1-9.
IUCR 6_ odegird RA, Vatten LJ, Nirsen ST, Sarvesen KA, Austguren R. Risk factors and clini-
Vascular cal manifestations of pre-eclampsia. BJOG 2000 Nov;iOZ1 I
I ): l4l0_6.
isorders 7. Llurba E, carreras E, Gratac6s E, Juan M, Astor J, Vives
d A, Herrnosiila E, carero I,
Mill6n P' Garcia-Vardecasas B, cabero L. Maternar history and
uterine a,tery ooppte,
4. : , L trime.t/er, 2. lrime.ster) or the in the assessment of risk for development of early- and late-onset
preeclampsia and
n.,. :.tl peripherul bloocl. intrauterinegrowth restrictio'. obstetGynecollnt200g:2756r3.
Epub 2009May27.
in: 8. Vollebregt KC, cisorf J, Guelen r, Boer K, van Montfrans
il- .i,tgl PIG F; trtlacerttol grott, th c, woFH. Limited accu-
racy of the hyperbaric index, ambulatory blood pressure
: ,ttrtl nretalloprotease 12,. pTX3. and sphygmomanometry mea_
,t .1 . I(/GR. lntrottterine grovth lyrelents in predicting gestationar hypertension anu pre"crlmpsia J Hypertens
2010;28(t):t27 -34.
i.t sis eleyaled liver en:1,n79s,. 1e11,
9. Cnossen JS, Vollebregt KC, de Vrieze N, ter Riet
G Mol BW, Franx A, Khan KS, van
der Post JA' Accuracy of nrean arteriar pressure and brood pi.rrrr.
measurements in
predicting pre-eclampsia: systematic review and rneta-analysis.
BMJ
2000;336(7 653):t I t 7 -20.

23
 l0' Geipel A, Berg c, Germer U, Katalinic A, Krapp M, Smrcek J, Gembruch U. Doppler
assessment of the uterine circulation in the second trimester in twin pregnancies: pre-
PREVENTI(
diction of pre-eclampsia, fetal growth restriction and birth weight discordance. Ultra- Milagros J. Tia-Jccs
sound Obstet Gynecol 2002;20(6):541 -5.
ll. cnossen JS, ter Riet G Mol Bw, van der post JA, Leeflang Mlvl, N,leads CA. Hyde c,
Khan KS. Are tests for predicting pre-eclampsia good enough to make screening vi-
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Strategies to effectir e..,
2009;88(7):75 8-65.
l2' investigatiorrs for decade. i-
Aydin I Varol FG, Sayin NC. Third trimester maternal plasma total fibronectin levels
in pregnancy-induced hypertension: results of a tertiary center. clin Appl rhromb Systernatic Reviews re\ eal-J j
Hemost. 2006;12( I ):33-9. aimed at preventing preec
=
13. Thangaratinam S, coomarasamy A, o'Mahony F, Sharp S, Zamora J, Khan KS, Ismail significantly reduce the risk . I
KM. Estimation of proteinuria as a predictor of complications of pre-eclampsia: a ./uSe of antiplatelet agellts.
systematic review. BMC Med. 2009;24:7-10.
14. Papanna R, Mann LK, Kouides RW, Glantz JC. Protein/creatinine ratio in preeclamp-
sia: a systematic review. Obstet Gynecol. 2008;l l\(l):135-44.
The meta-anal\ si> b,r r:
I 5. Toal M, Chaddha V, Windrim R, Kingdom J. Ultrasound detection of placental insuf- controlled trials (RCTs, t i -- .

ficiency in women with elevated second trimester serum alpha-fetoprotein or human given calciurn supplernc,.t,.., -
chorionic gonadotropin. J Obstet Gynaecol Can. 2008;30(3): l9g-206. of gestation (AOG) Lrnril ::
16. Solomon cG, craves SW, Greene MF and Seely EW. Glucose intolerance as a predic- hypertension (RR 0.70. sj: : :
tor of hypertension in pregnancy. Hypertension. 1 99 4 ;23 :7 I 7 -7 2l 0.33-0.69) wlren cornparer : :-
17. ACOG Technical Bulletin, Jan 1996
the risk of preterm birrh r RR
I 8. Page and Christianson, lgT6
19. Chesley and Sibai, 1974
death prior to discharge , RR
20. Chesley and Sibai, 1988
2l . Chesley and Sibai, 1987 The meta-anall sis b-i D,_.:..
22. Sumpaico and Santillan, 1982 preeclarnpsia and its cornp I i ca: : --
23. Kyle and Clark, 1993 agents lvith either placebr- .:
24. Vollebregt,20l0 reduction (by l7%) in rhe r:..
25. Pangan,1997
agents (RR 0.83, 95%CI [r ---,.
26. Sumpaico,1995
27. Lim and Cardenas, 1996 placental abruptiorr betu eer: :r.
Women included in the stu,ire,
preeclarnpsia. lrrten ention: \ rr
60 mg to 150 mg/dar ) and .iir,.
with ASA except in one Srudr ,. ,
of ASA rrp to 75 upp..:- ,
'r,g

Recommendations

l. Calciurn strpplementari..:.r :
risk flor derelopirre Frcr_ -
before 32 weeks AOC .:
develop ing hypertens irrn :.!
I, Grude A)

24

t -'i^. Leeflang MM, Meads CA, Hyde C,
F,5:: good enoughto make screening vi-
pe::isal. Acta Obstet Gynecol Scand
n:aiernal plasma total fibronectin levels
;; : tertiary center. CIin Appl Thromb
I i. Sharp S, Zamora J, Khan KS, Ismail
r ,: complications of pre-eclampsia: a
C P:otein/creatinine ratio in preeclamp-
8., l):135-44.
1r
L :::sound detection ofplacental insuf-
s:ii serum alpha-fetoprotein or human
rr i-r08;30(3):I98-206.
ri;. !
"\.
Glucose intolerance as a predic-
n '. ;91:23:7
17 -721
PREVENTION OF PREECLAMPSIA
Milagros J. Tia-Jocson, MD and Walfrido W. Sumpaico, MD
Strategies to effectively prevent preeclampsia have been the subject of
investigations for decades. In fact, the latest issue of the Cochrane Database
of
Systematic Reviews revealed a number of meta-analyses on various interventions
aimed at preventing preeclarnpsia. However, the only strategies found to
significantly reduce the risk of this cornplication areredlcium supplementation and
/uSe of antiplatelet agents.
The meta-analysis by Hofmeyr, et. ar.,r which included l2 randornized
controlled trials (RCTs) of good quality, showed tlrat pregnant rvornen who were
given calciunr supplemerrtation at dose of 1.5 to 2 gper day before 32 weeks age
of gestation (AOG) until delivery, had significantly recluced incidence of
hypertension (RR 0.70,95yo cl0.57-0.86) and preeclarnpsia (RR 0.4g, 95% ct
0.33-0.69) when compared to those taking placebo. There was no overall effect on
the risk of preterm bifth (RR 0.81,950 CI 0.64-l.03) nor on stillbirth or neonatal
death prior to discharge (RR 0.89, 95% U 0.73- L09)r.
The meta-analysis by Duley, et. al. on use of antiplatelet agents for preventing
preeclarnpsia and its complications,2 which included 59 RCTs cornparing antiplatelei
agents rvith either placebo
or no antiplatelet agerrt, also showed a sigriificant
reduction (by l7%) in the risk of preeclampsia among those given uniiplut"l"t
agents (RR 0.83, 95% C!0.77-0.89). There was no overall difference in the risk
of
placental abruption between the comparison groups (RR L l0,gsohcl0.g9-1.37).
Women inclLrded in the studies were either at moderate to high risk in developing
preeclarnpsia. lnterventions varied as to the doses of aspirin (ASA), (ranging frorn
60 mg to I 50 mg/day) and dipyridamore (200 mg to 400 rnglday in combination
with ASA except in one study), although conclusion of the author, ,uu, that
doses
of ASA up to 75 mg appear to be safer.2
Recommendations
l. calciLrrn sLrpplementation to pregnant worren (both low risk a'd those
at
risk for developing preecrampsia), given at a dose of 1.5 to 2 g per day
before 32 weeks AoG untir derivery, appears to decrease the risk of
developing hypertension by around a third and preecrarnpsia by harf. (Lever
I, Grade A)
25
2. Use of antiplatelet agents, eitherASA or dipyridamole, has also been shown to
reduce tlre risk of preeclampsia by lTYo among moderate to high risk women.
GESTATIONAL H'
This intervention has rrot been shown to increase the risk of placentalabruption. PRE
(Level I, Grade 41 Pilar Lagman-Dy l.t -

3. There are insr-rfficient evidence to support the use of anti-oxidants (vitamin C,

vitamin E, lycopene, red palm oil, selenium)3, nitric oxidea, rest during Gestational Hypertension
pregnancys, exercise6, diureticsT, reduced salt intakes, marine oil or other
prostaglarrdin precursore and garlicr0 in the prevention of preeclampsia. (Level Definitiorr: Blood pressure (Bp r c
I-II, Grade A-B). after 20 weeks gestational aoe ;. -

Mild Preeclampsia
References
Definition:
l. Hofineyr GJ, Atallah AN, Duley L. Calcium supplementation during pregnancy for L BP of J40 rnmHg slsr,rii- -:
preventing hypertensive disorders and related problems. Cochrane Database Syst Rev
upri-r{ht sittirrg BP afier a l,_r--
2006, Issue 3.
2. Duley I, Henderson-Smart DJ, Meher S, King JF. Antiplatelet agents for preventing in a wonran with prer iousl,. :
pre-eclampsia and its complications. Cochrone Datobase fysl Rev 2007, lssue 2. 2. Proteinuria. defined as ur:r::-
3. Rumbold A, Duley I, Crowther CA, Haslam RR. Antioxidants for preventing pre- hour urirre specimerr.
eclampsia. Cochrane Database,Sys/ Rer 2008, Issue l.
4. Meher S, Duley I. Nitric oxide for preventing pre-eclampsia and its complications. Approximatell 3 5oro (11' ,,\ .':'i
Cochrane Dalabase Sysl Rer' 2007, Issue 2. <34 weeks develop preeclanrpsr:. :
5. Meher S, Duley l. Rest during pregnancy for preventing pre-eclampsia and its compli-
and perinatal cornplicatioDs { l6: : ,:
cations in women with normal blood pressure. Cochrane Database Syst Rel 2006,
maternal and fetal surveillance. l.
Issue 2.
6. Meher S, Duley L. Exercise or other physical activity for preventing pre-eclampsia and establislred.
its cornplications. Cochrane Database Syst Revietrs 2006, Issue 2.
7. Churchill D, Beevers GCG, Meher S, Rhodes C. Diuretics for preventing pre-eclamp- The following should be pan .-
sia. Cochrone Database Sy.st Ret,2007, lssue I . Mild Preeclampsia:
8. Duley L, Henderson-Smart D. Reduced salt intake cornpared to normal dietary salt, or
high intake, in pregnancy. Cochrone Dalabose,Sysl Rel 1999, Issue 3. l. Home Health Care
9. Makrides M, Duley, Olsen S. Marine oil, and other prostaglandin precursor, supple-
mentation for pregnancy uncornplicated by pre-eclampsia or intrauterine growth re-
striction. Cochrane Dalabase Sysl Rer' 2006, lssue 3. As long as the criteria ic,i
l0. Meher S, Duley L. Garlic for preventing pre-eclampsia and its complications. Cochrane recornnrended lor wornen s irn
Databose S);st Rer, 2006, Issue 3. This rnay continue as lonr ri :
restrictiorr is not suspected. Se
the day is essential. Horne B
evaluation visits by a r isitin" n
wolneu should be instructed ;:
honte rrarragement, ther ars .r
and they are allorved to be up e:l,
about recording fetal kick cc;::
(Grade B)

26
_q:nteria can be managed at home:
nJation
I gestational hypertension/preeclampsia at an earlier age tend to have an earlier
< l- on dipstick
tersion/rnild preeclarrpsia during
rperience rather than the result of
on. lrospital admission for bed rest
nension to severe preeclampsia and
Sr-uptio placenta, with irnprovement
gtj in l97l by a British team who
r :r patients with nonproteinuric
nr. .\s a result of this policy, they
en ..rrl1, patients with proteinuric
rI s:udr. they reported on I 35 patients
a:Ctrmized trial. They showed tlrat
,e :,.. advantage over 'ambulation as
a, lisease.e Hospitalization was not
il _:r"o*th or reduction in the neonatal
he :Jea of outpatient management of
3.
h using outpatient management of
ir;reasing pressure to curb rnedical
t rr:s endorsed by American College
p::r ided the patient lrad a thorough
n:cnded for a select group ofpatients
ar ittempt to reduce hospitalization,
s. sereral programs were introduced
at home. All such programs involved
rt depends rnostly on maternal status
BP. and gestational age) at time of
I preeclarnpsia with proteinuria are
associated with a lower gestational age at delivery, shorter pregnancy
prolongation, and an increased requirement for antepuriurn hospitaliz;ion
as
compared with pregnancies with gestational hypertension.8 women who develop
gestational age at delivery, a worsening of the disease status, and worse fetal
outcome when compared with those who develop the disease at term.16
2. Timing of Delivery
The delivery of patients with gestational hypertension/mild
preeclampsia will depend on fetal gestational age and feial testing as well
as maternal BP, amount of proteinuria, and maternal symptoms. patients
having any of the following should be hospitalized and considered for
delivery: (Grade A)
Gestational age > 40 weeks
Gestational age > 37 weeks if there is:
Bishop score >5
Fetal weight <1Oth percentile
Non-reactive non-stress test (NST)
Gestational age34 weeks and above with the presence of:
Labor
Rupture of membranes
Vaginal bleeding
Abnormal biophysical profile
Criteria for severe preeclampsia
Expectant management should be considered for women remote from
term who have mild preeclampsia. (Grade C)
Monitoring of Fetal Well-Being
The patient should be evaluated by a physician for maternal and fetal
well-being at least once weekly. This weekly check-up should include the
following:
a. BP at each visit (Grade A)
b. Platelet count and Iiver enzymes at regurar intervals (Grade B)
c. NST at regular intervals (Grade B)
d. Fetal growth every 2 to 3 weeks (Grade B)
In contrast, patients with gestational age < 3 7 weeks who do not satisfy
the criteria for home management should be immediately hospitalized.
Subsequently management should depend on results of maiernal and fetal
conditions. (Grade A)
29
 Frangieh AY, Sibai B\1. Ou:p,
4. Medications 7.
preeclampsia. Contemporar.'
8. Crowther CA, Bouu mees:e: :
Magnesium sulfate and other anti-convulsants are not recommended and prevent disease proeressi:: .
should be withheld in cases of gestational hypertension/mild preeclampsia. non-proteinuric hvpertens: : -
(Grade B) 9. Matthews DD. Aganral \. S- -
Patients with mild preeclampsia and gestational hypertension will be given urea levels in pregnant *,::,
anti-hypertension medications only if there is an increase in BP readings from 1 980;87: I 095.
baseline.rT Please refer to the recommendations for medications in the section 10. Barton JR, Stanzino C.;. S :,
tional hypertension :: :-:
rern :
on severe preeclampsia.
11. Matthews DD. Patel lR. S:-:-
Low dose aspirin and high dose calcium are not recommended for the Gynecol l97l:78:610.
prevention of the progression to severe preeclampsia. (Grade B) 12. Feeney JE. Hlpenensi::
I 984;288:1 046.
t3. Tuffnell DJ, Lilford R-I. 3-::,,
Summary hypertension in preen:r::. . -
14. American College of Obs:e:-'
Management of women with gestational hypertension/mild preeclampsia must sion in pregnanc). \\'ashin_r::

always coirsider maternal safety first and then the delivery of a newborn who will
15. Dawson AJ, Middlemiss C. C
care scheme: The effect ..i: h:
not iequire intensive and prolonged neonatal care. Outpatient management of 16. Hamlin RHJ. The prer ent --:
patients with gestational hypertension/mild preeclampsia has been documented to 17. Sibai BM, Barton JR. {i; S =
L" *or. cost-effective than similar in-patient therapy. Therefore, outpatient bed rest versus bed resr r.:::
managenlent.must provide evaluation of maternal and fetal status similar to that of Am J Obstet Gy,necol l9ql. :
in-patient management.

References

l. ACOC practice Bulletin No. 33. American College of Obstetricians and Cynecolo-
gists. Diagnosis and management of preeclampsia and eclampsia. Obstet Gynecol
lOOZ:gg,tSg-t67 (Level 1ll1 <http://www.acoe.com/publications/educational-bulletins/
Pb033.htm>
2. neport of the National High Blood Pressure Education Program Working Group on
High Blood Pressure in Pregnancy. Am J Obstet Gynecol 2000;183:S I -S22. (Level Ill)
http://www.ncbi.nlm.nih.gov/entre/query. fcgi?cmd:Retrieve&db:PubMed&list-uids
: | 09203 46 &dopeAbstract
3. Cabbe SG Neibyl JR, Simpson JL (Eds). Obstetrics: Normal and Problem Pregnan-
cies. 4,r, Ed. Hypertension, Chapter 28. Churchill Livingstone, New York, 2002- 945-
1004, (Level III)
4. Cunningham GF, et. al. (Eds) Williams Obstetrics,2lu Edition. Hypertensive Disor-
ders in Pregnancy, Section 7. McCraw-Hill, 2001 .24:567-618. (Level III)
5. Chobanian AV, et. al. The seventh report of the joint national committee on prevention,
detection. evaluation, and treatment of high blood pressure. JAMA 2003;289:2560-
2571 . (Level III) http://jama.ama-assn.orglcgilcontentlfulll2S9l1912560
6. Hofnreyr GJ, Atallah AN, Duley L. Calcium supplementation during pregnancy for
pr.ueniing hypertensive disorders and related problems. Cochraine Library Syst Revs.
irttp://www. ih s.gov/generalweb/webapps/sitelink/ s ite. as p? link=http:.ll
www.cochranelibrary.com/enter/

30

n'- ilsants are not recommended and
ra :) pertension/mild preeclampsia.
;t=:'lional hypertension will be given
E€ ) an increase in BP readings from
h - is for medications in the section
t ,: are not recommended for the
!e:.rmpsia. (Grade B)
!r.::n sion/mi ld preeclampsia must
l:-= :elirery of a newborn who will
lr -::;. Outpatient management of
;=: '-ps'a has been documented to
k: .rerapl'. Therefore, outpatient
n- .:.d fetal status similar to that of
lf, ';e of Obstetricians and Gynecolo-
iur* " . : and eclampsia. Obstet Gynecol
l- - :rblicationsieducational-bulletins/
:::-::rion Program Working Group on
3 .. :;ol 2000;183:Sl -S22. (Level III)
h' -- :=Retrieve&db:PubMed&list_uids
b;.-' :': \ormal and Problem pregnan-
rT - ingstone, New York, 2002.945-
u
E- -, ll" Edition. Hypertensive Disor-
13- -::-<67-618. (Level III)
b -: ::rional committee on prevention,
I r ': ::essure. JAMA 2003;289:2560-
i : -'=rr fulll289l1912560
! : -:: 3rentation during pregnancy for
irn - .:s. Cochraine Library Syst Revs.
[E'= :nk' site.asp?link=hftp:ll
7 - Frangieh AY Sibai BM. Outpatient management of gestational hypertension and mild
preeclampsia. Contemporary OB-Gyn 1996:67.
8. Crowther CA, BouwmeesterAM, Ashurst HM. Does admission to hospital for bed rest
prevent disease progression or improve fetal outcome in pregnancy complicated by
non-proteinuric hypertension? Br J Obstet Gynecot 1992;99:13.
9. Matthews DD, Agarwal V, Shuttleworth TP. The effect of rest and ambulation on plasma
urea levels in pregnant women with proteinuric hypertensi on. Br J Obstet Gynecol
1 980;87: I 095.
10. Barton JR, Stanzino GJ, Sibai BM. Monitored outpatient management of mild gesta-
tional hypertension remote from term. Am J obstet Gynecol 1994:170:765.
I l.
Matthews DD, Patel IR, Sengupta SM. outpatient management of toxemia. Br J obstet
Gynecol l97l;78:610.
12. Feeney JE. Hypertension in pregnancy managed by community midwives. BMJ
1984;288:1046.
13. Tuffnell DJ, Lilford RJ, Buchan PC, et. al. Randomized controlled trial of day care for
hypertension in pregnancy. Lance t I 992;339 :224.
14. American College of Obstetricians and Cynecologists. Technical Bulletin: Hyperten-
sion in pregnancy. Washington DC, 219,Ianuary 1996.
15. Dawson AJ, Middlemiss c, coles EC. A randomized study of a domiciliary antenatal
care scheme: The effect on hospital admissions. Br J obstet Gynecol I 9g9;96: I 3 19.
16. Hamlin RHJ. The prevention of eclampsia-preeclampsia. Lancet l9g2;l:64.
t7. Sibai BM, Barton JR, Aki S. A randomized prospective comparison of nifedipine and
bed rest versus bed rest alone in the management of preeclampsia remote from term.
Am J Obstet Cynecol 1992;167,879.
31
r
SEVERE PREECLAMPSIA IAELE 1

Marlo A. Bernardino, M.D. and Joseph U. Olivar, M.D. crffila lbr lhe drgnorh of smr trrch

SInptoms of cenfal nenDUs Sr&eJr:

-'y".l:T.dv'1rlg]91..... .... .

The objectives in the management of severe preeclarnpsia include the following: S]rndoms of lluer c€p6ule

L To reduce its severity or prevent progression ofthe disease process ..

Sl0ns
....111Pil|9i.9t tytlu.
rJ

2. To prevent convulsions Elood presrurc crlterla

3. To control severe hypertension :cr30.l i
4. To deliver the mother of a fetus at the optirnum time and with the Sai.:l=:
least trauma :rr*i f
5. To detect and appropriately treat end-organ damage
6. To completely restore tlre health of the mother .{:-e c:r:

:,-; -...
':r:1t'
Background !t -€!a :
rl:;T(:r'r
!€ :c -E:r
Incidence
0ll0urla and/or renal laJlure
As the most common medical disorder of pregnancy, hypertension is
lta€-:r f
reported to complicate 5-60/o of all pregnancies worldwide,r witlr 5-l 0 ohbeing a?',fi;ri
:.:i'{;!'i
severe.2 It is the 2nd most comrnon cause of maternal death irr the United States.rJ
Se"f :-:-c
Locally, the incidence of severe preeclampsia is 2-5o/o and is the 2nd most
common cause of maternal death.a It is also associated with a high perinatal Uoagulopafy ;'ffT= l
mortality and morbidity rate, which is primarily due to iatrogenic prernaturity.5 3x ti::;r
The development of preeclampsia cannot be accurately predicted nor effectively
;il,nii"iicn'd #iiiJ
fe di4mci ol rnm prwhmprl u
ioii riii
llpir:w ::,tqr
iiffi 6i iri,
dcfird D
oiiir;; ;: *-; :
prevented. Delivery of the fetus and placenta remains the olly definitive Nwia &ptwtmngtnwoltmrymlnpn nt,oc Lx c t
treatment.6 For all these reasons, the timing of delivery is critical to optimize Adapted from Norwitz. Expe::_:,
maternal and perinatal outcome. term. Am J Obstet Gvnecol ),', .

C loss iJicat io n of Pre e c lamps io

Management
Preeclampsia is classified as mild and severe. Milel preeclampsia refers to
disease that meets the criteria for the diagnosis of preeclampsia but is not severe
The main objective in rhe man
disease. A diagnosis of severe preeclampsia requires evidence of new-onset
the safety of the mother and rh: :
proteinuric hypertension occurring at> 20 weeks age of gestation with > I of a
includes stabilization of rhe ncii.
series of complications (see Table l). It is emphasized that only I of the listed
and assessment of fetal uell-bein.
criteria in Table I is required for the diagnosis of severe preeclampsia. The
established, traditional manaserne:
distinction between mild and severe preeclarnpsia is important because it
delivery. Because these pregnar.
dictates management,5 and one must not be complacent with inild preeclampsia6
morbidity and mortalit), and u:ri
because apparently mild disease may progress rapidry t4 swere disease.6
agreement that such patients shr.u I :

32
CLAMPSIA TASlt 1
Crlbrlr lhr fiH ftgnoiF 0f ssBrs prugolampslr
Joseph U. Olivar, M.D

_ry"*r.dysfr$rll..
synpt0m6 ot ltver c€psute -srbl;;il;ffiilil;lpilirbrt;;h1ilp;;"q"dif;rd/.;iid#i;prtr"---
re preeclarnpsia include the following:
dltbntlon il rupture
t progression ofthe disease process

Gcaal0n6 at re8t al least 6 iour6 apatl

generallzed Eehures and/or uneo(plalned preedemsla and
coma ln the rettln0 0l ln lhe absence
s at the optirnum time and with the ot other neurologlc condltlofls

Pulmonary edema or Exce$llE lluld arcumulatlon In he lung6

at end-organ damage
CerebrwaEcular accldefit Acub 106€ 0f braln functon (a6 evldenced by fmal neurol0glc ElgnE, altered menlaj shl!6, and/or
h oithe mother (drokd comal becauEe ot a dl8furbrce In lhe vafDulatuB hal supplleG blood b the bnaln
cortlcal bllndne66 Parllal 0r tolal lois of vt6t0n rn a normii:iipirariis ediiliilcadffitd;madio iii;
'riilat
reglon ol he occlpllal cortcx
Es'tlmabd fetal wel0hl <5h percentlle torgeslatlonal qqe or <1oth percenflle furge8tailonal roe
udth evldence oflelal comprcmlse (0llgohydramnlo8, abnormal umblllcal artery Owpler
wlcclme'tryl

er .rf pregnancy, hypertension is

:ies norldwide,r with 5-10 % being
a::rnal death irr the United States.r.3
rp.ia is 2-5%o and is the 2"d rnost
(. rssociated rvith a high perinatal
to iatrogenic prematurity.5
r-r: -r dLre
a; ; u rate ly pred icted nor
effectively
;enta rernains the only definitive
r ; i delivery is critical to optimize Adapted from Norwitz. Expectant management of severe preeclampsia remote from
term. Am J Obstet Gvnecol 2008 .

n'ere. ,1,[ild preeclampsia refers to
is ..f preeclampsia but is not severe
ia requires evidence of new-onset
'e;ks ase of gestation with > I of a
mphasized that only I of the listed
mis of severe preeclampsia. The
:[:ntpsia is important because it
rn: p lacent with rni ld preeclampsia6
s. rapidly rO servere disease.6
Managemenl
The main objective in the management of severe preeclampsia must always be
the safety of the mother and the fetus.5 The initial management of preeclampsia
includes stabilization of the mother's condition, confirmation of gestational age
and assessment of fetalwell-being. Once the diagnosis of severe preeclampsia is
established, traditional management has focused on maternal safety with expedited
delivery. Because these pregnancies are associated with high rates of maternal
morbidity and mortality and with potential risks for the fetus, there is general
agreement that such patients should be delivered if the disease develops > 34 weeks

JJ
of gestation.ls Although delivery is always appropriate for the mother, it may not Recently, the results .- : s;
be optimal for the premature fetus (< 34 weeks).e Complications of prematurity described expectantman3ge:-:
include respiratory distress syndrome, intraventricular hemorrhage, necrotizing have suggested that su.-h i-"
enterocolitis, sepsis and even death. In the past, it was believed that infants born increasing matemal morbl: :.
prematurely to severely preeclamptic women had lower rates of neonatal morbidity In 2005, Sibai pub,:s-::
and mortality than infants of similar gestational age born to non-preeclamptic preeclampsia<34ueeks
women. In contrast, several recent case-control studies have demonstrated that
premature infants born after severe preeclampsia have neonatal complications and
Admit to labor and delivery su :e
mortality similar to those of other premature infants of similar gestational age and
have higher rates of admission to neonatal intensive care unit (NICU).r0 In addition, r Maternaljetal era -:::- ':-
case-control studies have revealed that fetuses of preeclamptic women do not exhibit r Magnesium sulfaie J:- l: -:
. Antihypertenswes ' s -r:: :
accelerated I ung or neurological maturation. i 0 _.

diastolic BP > 1i3 ---=- :'

There are 3 circumstances in which expectant management of severe pressure (MAP) >' 25 - - -':
preeclampsia remote from term (< 34 weeks) is clearly acceptable. The first is
severe preeclampsia by proteinuria.s Neither the amount of protein spilled in the
urine nor the rate of increase correlates with maternal or perinatal outcome.rr'r2 As Any of the following present?
such, proteinuria > 5 grams per 24 hours is not, in itself, an indication for delivery.s
The second is severe preeclampsia on the basis of intrauterine groMh restriction
o Eclampsia
. Pulmonary eden'a
(IUGR) alone with good fetal testing. Although not candidates for immediate r Acute renalfailure
delivery such patients should be treated as in-patients5 with at least daily fetal . Disseminated intra ' as r-.:- :
well-being studies. Third, there is precedent in the literature to support the expectant
. Suspected abruP:: a '-ae":.
o Non-reassuring ie:a s'::-:
management of women with severe preeclampsia blood pressure (BP) criterion. . Labor or rupture c' -.--a''-'
This approach, although potentially dangerous for the motheq has been substantiated gestation
in a number of clinical trials.T'8 There are only 2 published randomized trials on
the expectant management of severe preeclampsia. In 1990, Odendaal, et. al. studied
38 patients with severe preeclampsiaat2S-34 weeks of gestation. Twenty patients
HELLP syndrome iF€-: '. -r
underwent aggressive treatment (steroid therapy followed by delivery in 48 hours), enzymes, ano Lo*. F a::t':
and l8 patients were treated expectantly (steroid therapy followed by delivery Persistent sympto,l. s
only for maternal and fetal indications). In the conservative group, the authors I

reported no increase in maternal complications but with statistically significant No+ I

prolongation ofpregnancy (mean, 7.1 days), a reduction in neonates that required

ventilation (11% vs 35Yo), and a reduction in total neonatal complications (33 vs I

l5yo).7 Sibai, et. al. studied 95 patients with severe preeclampsia at28-32 weeks
of gestation: 46 patients underwent aggressive treatment and 49 were assigned to
FGC_] 23-32 weeks

expectant management. In women who were treated conservatively, there was no

increase in maternal complications, but there was a statistically significant
I t Steroids
prolongation of pregnancy (mean 15.4 vs 2.6 days),less time in NICU (20.2vs l-r---,'i;;l o Antihype
36.6 days), and a reduce incidence of respiratory distress syndrome (22.4o/o vs I pr"gn"n.y I
a Daily eva
tEtd -- -
50.5%).8These 2 trialsT'8 demonstrated improved perinatal benefit with reasonable Delivery i

maternal safety when expectant management was conducted in a select group of

Delivery i
patients with severe preeclampsiaat23-34 weeks of gestation,'3

34
lFn ::iate for the mother, it may not
d.. Ct'rmplications of prematurity
x::- ;ular hemorrhage, necrotizing
tfr. : \\as believed that infants born
bc ',r er rates of neonatal morbidity
ir= .rge born to non-preeclamptic
f: s:udies have demonstrated that
En - 'r e neonatal complications and
ir:-:s of similar gestational age and
-
t$i rare unit (NICU).r0 In addition,
, .
t':-=eclamptic women do not exhibit
!il:.Jtant management of severe
| :"' :1early, acceptable. The
first is
&c ':rtrunt of protein spilled in the
r=-:al or perinatal outcome.rl,r2 As
;ir :.elf. an indication fordelivery.5
fti ntrauterine groMh restriction
lr:.- not candidates for immediate
i-:,:rents5 with at least daily fetal
lE :erature to support the expectant
p: . blood pressure (BP) criterion.
hr :.- e mother, has been substantiated
! i published randomized trials on
rfu- In 1990, Odendaal, et. al. studied
lfrrrS of gestation. Twenty patients
I : :. I.ru ed by delivery in 48 hours),
r: J therapy followed by delivery
le :lnservative group, the authors
rs :ut ri'ith statistically significant
F; -Jtion in neonates that required
E,i= neonatal complications (33 vs
n =:e preeclampsia at 28-32 weeks
r r:rtment and 49 were assigned to
te::ed conservatively, there was no
lrc $s5 a statistically significant
d:1s). less time in NICU (20.2 vs
lc1 distress syndrome (22.4o/o vs
C oerinatal benefit with reasonable
ras conducted in a select group of
*-i of gestation.'3
Recently, the results of several retrospective and observational studies that
described expectant management of severe preeclampsiaat24-34 weeks of gestation
have suggested that such management improves perinatal outcome without
increasing maternal morbidity.t+-zt
In 2005, Sibai published an algorithm in the expectant management of
preeclampsi a < 34 weeks.
Admit to labor and delivery suite
Maternal-fetal evaluation for 24 hours
. Magnesium sulfate for 24 hours
o Antihypertensives if systolic BP >160 mmHg,
diastolic BP > 110 mmHg, or mean arterial
pressure (MAP) >125 mmHg
Any of the following present?
o Eclampsia
o Pulmonary edema
o Acute renal failure
Yes
r Disseminated intravascular coagulation ----+
. Suspected abruptio placenta
. Non-reassuring fetal status
. Labor or rupture of membranes >34 weeks'
gestation
Steroids
No
I I
t.x;4 --l---I TrJJ, *""k" frg-34-*k"l
I I
. Steroids . Steroids
l-T--rin.rt"l r Antihypertensives if needed o Delivery after 48
I pr"gntn.y I . Daily evaluation of maternal- hours
fetal condition
. Delivery if: with indications
(see Table 2)
. Delivery at 32-34 weeks
35
Table 2. Indications for Delivery During Expectant Management '4eterioration in fetal status unir
expectantly should be obserr eJ
fetal reasons.
lndlcations lur delivery
Variable lndicalion Maternal Co mp licat io n s
Maternal Persistent severe headache or visual changes; eclampsia
Shoilness of brealh 0r chest tightness wilh rales and/or pulse oximetry of The main aim of the erpe :
{g4ib 0n roorn air or pulmonary edema from term is lrolonging gestal:,r:
Epigaslric/right upper quadrant pain wilh AST or ALT >2 times the upper deterioration in maternal cond r:
limils ol normal may occur. Thus, any protocc, : --

Uncontrolled severe hypertension. despite maximum doses ol for maternal complications.i DL:
antihypertensive agenls in reported studies include: HEI
0liguria (.:500 mU24 hr) or a serum creatinine leuel of ;-1.5 mg/dL 8.5o ), eclampsia and acute :e:.
Expectant management r' - i:
Persistent plalelet counl. <100.000 /mm3
maternal oxygenatiort. Pr,-'. .l:
$uspected abruptto placentae. progressive labor. and/or rupture ol
membranes
dysfunction (HELLP sr ri:. *
particularly provide er alual: -:
Felal Severe FGB {estimated fetal weigltt, <slh percentile ior gestational age)
the risks of placental abrui: ----
Penistent severe oligohydramnios (amniotic lluid index, {5 cm}

Repetilive late or variable {etal heafl rate decelerations Severe Preeclampsin < l-f x.'i/
Persistent biophysical proiile, -4 (evaluations 6 h0urs apan)
Only few literatures are :!-:
Umbilical artery Doppler imaging with reverse diaslolic blood flow
during expectqnt treattttent . :- :
Felal death gestation. Severe preeclantps .
;i i ;h,i'; n.il;i;#, ;si ;;ili t#i *i*" associated with higlt pertn:::
treatment in the forrn of inr::,
Adapledfrotn Sibai and Barton, 200778
Note: Hypertension is uncontrolled tvhen the BP remains in Ihe settere range despite maximum
mortality rate.ra'26 If the tei-..
doses of antihypertensite ogents. According tct mosl reports, Ihe maximum dose of hydralazine expected and these * ill recL:.:;
is 20 mg tV: Nifedipine 50 mg PO and Nicardipine drip l0 mg/hour the other hand, atternptS tt- l:--
expose the mother to se\ ei. -
Pe ri n ata I Co mp I ic at io ns perinatal death rate ransed fr--::
without handicap.r*:-:: The': '
Though the main aim of expectant management is to improve perinatal outcome had eclampsia and HELLP .'.-
by prolonging gestation and reducing neonatal morbidities (acute and long term)r3 weeks age of gestation.:- F,.;::
due to prernaturity, expectant treatment has potential cornplications. Bombrys and colleagLre s:
During expectant management of patients with severe preeclampsia at24-34 management of ser ere pree;1::
weeks of gestation, the rate of perinatal death ranged from 0 to 16.6 o%.7'8 Abruptio weeks, maternal complicati--: .
placerrtaisalsoareportedcomplicationanditrangedfrom4.lYoto22.9o/o.8'22 ln Thus, the authors reconune: J-J
addition, delivery for non-reassuring fetal status ranged from26-75%o.18'20 In all at23 weeks, the perinatal sl:n -.
the reported studies, intensive fetal monitoring for early detection of fetal is yet unknown. For \\ Lrltterr r':. '

comprornise is recommerrded. The most common irrdication for delivery was approached 600h. and it ar e:-.-,

36
ItXr:-:-3llt
Gterioration in fetal status underscoring the need that these pregnancies managed
expectantly should be observed in centers that are capable ofrapid intervention for
fetal reasons.

Maternal Comp lic atio ns

pulse oximelry of The main aim of the expectant management of severe preeclampsia remote
from term is y'rolonging gestation without jeopardizing maternal safety. Progressive
or ALT :'2 times the upper deterioration in maternal condition during the clinical course of severe preeclampsia
may occur. Thus, any protocol for management of severe preeclampsia has potential
"rJ mum doses oJ for matemal complications.5 During expectant management, maternal complications
in reported studies include: HELLP syndrome (4.1-27 .lo%), pulmonary edema (0-
8.5oA), eclampsia and acute renal failure (<lo%;.t''u''o
Expectant management must provide heightened surveillance to ensure adequate
maternal oxygenation, provide prompt intervention for symptoms of lrepatic
and/or rupture of
dysfunction (HELLP syndrome or subcapsular hematoma of the liver), and
particularly provide evaluation of the fetal status and maternal presentation given
the risks of placentalabruption.5
rndex, {5 cm}

Severe Preeclampsia < 25 weeks

!'" :;:J se|ere range despite maximum
ry, :he ntarimum dose of hydralazine
i'f,- .t? hour.
E-: ] to improve perinatal outcome
nr , -:idities (acute and long term)r3
E-: rl complications.
r:-:i from 0 to 16.6 o%.7,8 Abruptio
r:-:3d from 4.lYo to 22.9%o.8'22 In
D,i :insed from26-75o/o.18'20 In all
r -: for early detection of fetal
n: --n indication for delivery was
Only few literatures are published regarding maternal and perinatal outcomes
during expectqnt treatment of patients with severe preeclampsia at <25 weeks of
gestation. Severe preeclampsia that develops in the rnid-trimester of pregnancy is
associated with high perinatal mortality and morbidity rates.ra-r6'23 Aggressive
treatment in the form of immediate delivery will usually result in high neonatal
mortality 1s1s.t4.26 If the fetus survives, significant neonatal complications are
expected and these will require prolonged hospitalization in the NICU.4,23-25'28 On
the other hand, attempts to prolong pregnancy may result in fetal death and may
expose the mother to severe morbidity.ra.t6,24,25,2'7 Overall, in these studies, the
perinatal death rate ranged frorn T loh to l00Yo, with few newborn infant surviving
without handicap.ra,2?'28 There was one reported maternal death in a patient who
had eclampsia and HELLP syndrome who underwent expectant treatment at 23
weeks age of gestation.2T Furlhermore. maternal morbidities were very high.5
Bombrys and colleagues2e found small studies that focused on expectant
management of severe preeclampsia before 28 weeks. In pregnancies before 23
weeks, maternal complications were common and there were no infant survivors.
Thus, the authors recommended pregnancy termination for these women. For those
at 23 weeks, tlre perinatal survival rate was I 8%, but long tenn perinatal morbidity
is yet unknown. For women with pregnancies at 24 to 26weeks, perinatal survival
approached 60Yo, and it averaged 90Yo for those at 26 weeks.

J/
Preeclampsia with HELLP B2. How should the BP be
When taking the BP. tt
The clinical course of women with HELLp syndrome is characterized by angle. The cuff should
progressive and sudden deterioration in the maternal condition.2e Because this at the level ofthe hearr
syndrome is associated with increased rates of maternal morbidity and mortality, the diagnosis. Korotk,,
some authors consider its presence an indication for immediate delivery, except diastolic BP. (Leyt,' ,' -
for the benefit of steroid for fetal lung maturity in gestation at24-34 weeks.5
There are 3 studies30r2 published regarding expectant management in patients Automated methods :l
with HELLP syndrome at < 34 weeks of gestation. Their results suggest that
expectant treatment is possible in a select group of women with alleged HELLP The BP should be ch
syndrome at<34 weeks of gestation. However, despite pregnancy prolongation in stabilized and then e
some of these cases, the overall perinatal outcome was not improved, compared assessment. The BP :h
with cases of similar gestational age who were delivered within 48 hours after midnight and rrrorn ing
steroid therapy. Since the sample size in these studies is inadequate, such approach and the w'onlan is stah
is currently experimental.5
Wltert takirr: t ': :-
and the crrff .lr-.. -: -
Clinical Considerations and Recommendations hearr. l\1 rrlt ip l< :;,, -. :
of natural ran..ri ". ir
A. What are the clinical features of severe preeclampsia? diastolic BP.:-
A diagnosis of severe preeclampsia requires evidence of new onset AutorttaleJ lr:;: - -
proteinuric hypertension along with > I of a series of complications systolic BP." It ir.:. :::
(summarized in Table l). (Level III, Grade C) should be ureJ l, ' j-- -
units no longel h.rr - .
Although the classification of severity of preeclampsia is primarily based with another r ali.i.l<: :
on the level of BP and tlre degree of proteinuria, other organs may be potentially
Initial assessnr-:'
involved and clinicians should be vigilant when assessing the maternal risk.sa rnore freqrrerrt llrr'l.. -

It is emphasized that only I of the listed clinical features in addition to B3. How should proteinuri
hypertension (> 140190 mmHg) and proteinuria (> 300 ngl24 hours) is required
The usual screening trr
for the diagnosis of severe disease.5 Ultimately as many clinical criteria are
measurement can he. t;
subjective, women should be managed according to a careful clinical assessment
(-) dipstick mar not h
rather than relying overly on precise criteria.ra
hour urine protein ccrll
Grade C)
B. Assessment of the Woman
Bl. what is the initial management in a woman rvith severe preeclampsia?
While it has rt b; -,
In a woman with severe preeclampsia, immediate admission preferably
from urine dipstick :;s:
in a high risk unit is mandatory, eevel I, Grarte A) : lglL arrd -l = -:g L :
possible nith the ir..-
Hospitalization is considered in women with severe preeclampsia.6 proteinuria m ar il ,. -: , ,
|ospitalization is irrdicated in cases in which the woman is unreliable, cases.c ltt r ieri r'r .' -
{ 2 systolic BP >150 mmHg or diastolic Bp>,f00 mmHg,fieavy proteinuria collection is rea t r:r :r' -
or fersistent maternal symptoms.35,16
clirrical rrrgeni\ d ,:. -.

38

ELLP syndrome is characterized by
r maternal condition.2e Because this
r,-'f maternal morbidity and mortality,
:ation for immediate delivery, except
rin in gestation at 24-34 weeks.5
inu expectant management in patients
restation. Their results suggest that
rt-rup of women with alleged HELLP
er. despite pregnancy prolongation in
utcome was not improved, compared
*ere delivered within 48 hours after
e studies is inadequate, such approach
rtions
re preeclampsia?
r requires evidence of new onset
r > 1 of a series of complications
ir.de C)
iq of preeclampsia is primarily based
ir:.lria. otherorgans may be potentially
nt rr hen assessing the maternal risk.3a
sted clinical features in addition to
:inuria (> 300 mgl24 hours) is required
tiirately as rnany clirrical criteria are
cording to a careful clinical assessment
leria.r'
a \l oman with severe preeclampsia?
sia. im mediate admission preferably
. ,Level I, Grade A)
I \\olnen with severe preeclampsia.6
:s in rvhich the woman is unreliable,
lic BP >'{00 mmHg,fieavy proteinuria
82. How should the BP be taken?
When taking the BB the woman should be rested sitting at 45-degree
angle. The cuff should be of the appropriate size and should be placed
at the level of the heart. Multiple readings should be used to confirm
the diagnosis. Korotkoff phase V is the appropriate measurement of
diastolic BP. (Level I, Grade A)
Automated methods should be used with caution. (Level II-2, Grade B)
The BP should be checked every 15 minutes until the woman is
stabilized and then every J0 minutes in the initial phase of the
assessment. The BP should be checked every 4 hours except between
midnight and morning if a conservative management plan is in place
and the woman is stable and asymptomatic. (Level III, Grude C)
When taking the BP the woman shoLrld be appropriately positioned
and the cuff should be of an appropriate size placed at the level of the
heart. Multiple readings are required to accurately assess the BP because
of natural variations. Korotkoff phase V is the appropriate method for
diastolic BP.r7
Automated metlrods can systernatically underestimate parlicularly the
systolic BP.38 It has been suggested that mercttry sphygnrornanometers
should be used to establish baseline BP as a reference.ro However, many
units no longer have tnercury splrygmornatrotleters and a baseline check
with another validated device wor-rld be an alterrtative.
Initial assessment of the woman with severe preeclalnpsia requires
more frequeirt morritoring of the BP untilthe rvotnan is stabilized.rl
83. How should proteinuria be measured?
The usual screening test is vfsual dipstick assessment. A (+)l dipstick
measurement can be taken as evidence of proteinuria but a negative
(-) dipstick may not be accurate. Ideally, a nlore accurate test q4
hour urine protein collection) is required to confirm this. (Level III,
Grade C)
While it has to be acknorvledged that there is poor predictive value
from urine dipstick testing,aoapproximate equivalence is +l : 0.3 glL,+2
: lglL arrd +3 :3glL. False negative as well as f-alse positive results are
possible with the use of dipstick assesslnetttaO because the degree of
proteinuria may fluctuate widely over the 24 hour period, even in severe
cases.6 In view of this, laboratory testing usually by a l.+ hour urine
collection is recomrnended to conf-irm significant proteinuria uttless the
clinical urgency dictates irnmediate delivery.''
39
 84. What other laboratory exams should be requested? preeclampsia reduces tl'
The following laboratory exams should be requested in cases of severe MgSOo had a 580% lo*.
preeclampsia: complete blood count (CBC) with platelet count, The relative risk redu,
peripheral blood smear, liver enzymes aspartase aminotransfrase preeclampsia. More *.-
(AST), alanine transaminotransfrase (AA), creatinine, uric acid, severe (109) to prer,
lactate dehydrogenase (LDH) and total bilirubin. (Level III, Grade C) preeclampsia (63). \\ ht
output, maternal ret-le
A falling platelet count is associated with worsening disease and is important.3a
itself a risk to the mother.as A platelet count persistently less than 100 x MgSOo can be si\<
106/L should be a consideration for delivery. On the other hand, it is not intermittent intramusc r-
until the count is less than 100 x l06lLthat there may be an associated
coagulation abnormality.a6 Clotting studies are not required if the platelet C2. How should seizure b,
count is over 100 x 106/L. The principles of mat
A diagnosis of HELLP syndrome needs confirmation of hemolysis, airway, breathing. ant
either by LDH levels (> 600U/L), blood film to look for fragmented red
cells or total bilirubin >1.2 mgldL; elevated liver enzymes (AST or ALT MgSO, is the theraPr
>70UlL) and low platelet (< 100 x 106/L).5 If only I or 2 of the 3 criteria of 4 g should be girr
are met, the diagnosis iq partial HELLP syndrome.6 infusion of I gi hour t
In preeclarnpsia, there can be a rise in uric acid that correlates with (Level I, Gracle .i
poorer outcome for both mother and the fetus.aT This rise confirms the
diagnosis of preeclampsia but the levels should not be used for clinical
Table S tntravenous and Itre
decision-making. Renal function is generally maintained in preeclampsia
Preschmpsb and Ecbtrg*
until the late stage unless HELLP syndrome develops.a8 If creatinine is
found to be elevated early in the disease process, underlying renal disease Intravenous Intusim
should be suspected. In severe disease, serum creatinine can be seen to
rise and is associated with a worsening outcome a8 but renal failure is not 2. Beqin 2 g/hr in 100 mL o;
uncommon in preeclampsia and when it does occur, it is usually associated 3. Measure serum magne3 '-
with hemorrhage, HELLP syndrome or sepsis.3a m/dL).

4. Flaqnesium sulfate s c s.:-:'

C. Anti-Seizure Prophylaxis Intermittent Intra mustu la r In jed€'5

C1. How should seizure be prevented?

Magnesium sulfate (MgSOo) is the drug of choice for the prevention
of convulsions. This drug should be considered for women with 2. Follow Promptly wrih :C E :' i:'r -:;-:
preeclampsia for whom there is concern about the risk of eclampsia. quadrant of both buttccks l"c;-:- : 3- -:-
discomfort.) if conv, s o1: Pe': =: ::€' -:
This is usually in the context of moderate to severe preeclampsia (at to exceed 1 g/min. lf tne w:-:- : :';. -
least 150-160/100-110 mmHg), once a delivery decision is made and in
3. Every 4 hr thereaiter ! r: 5 : 3' : )::
the immediate postpartum period. In women with mild diseaseo the quadrant of alternate :-::c:i:. :-: :- r :'
decision is less clear and will depend on individual case assessment. a. the patellar reflex s l"'::':
(Level I, Grade A)
b. respirations are nci Jet':::::
c. urine outDut the P'ev a-! i " :::-=:::
The MagPie Trial (Magnesium sulfate for Prevention of Preeclampsia)
has demonstrated that administration of MgSO. to women with Magnesium sulfate is drscs'r: - -:: :i '- :

40
id be requested?
rold be requested in cases ofsevere
ront (CBC) with platelet count,
tr mes aspartase aminotransfrase
nese (ALT), creatinine, uric acid,
btal bifirubin. (Level III, Grade C)
ia:;: n ith worsening disease and is
tr rrunt persistently less than 100 x
&. i en. On the other hand, it is not
f- :hat there may be an associated
G-: :s are not required if the platelet
r : =:ds confirmation of hemolysis,
k.,.: ;llm to look for fragmented red
de , ,:ed liver enzymes (AST or ALT
l{'' - r j Ifonly I or2 ofthe 3 criteria
I-I s'" ndrome.6
r:: n uric acid that correlates with
d :-: fetus.aT This rise confirms the
*- = siiould not be used for clinical
pr ;:,..i11 rnaintained in preeclampsia
F-::rme develops.a8 If creatinine is
&i< rlt)c€SS, underlying renal disease
G:. serum creatinine can be seen to
h_: :tcome a8 but renal failure is not
l -: l r'es occur, it is usually associated
'\":=f'515.
tdrug of choice for the prevention
5 be considered for women with
:cern about the risk of eclampsia.
rderate to severe preeclampsia (at
r e delivery decision is made and in
, In rromen with mild disease, the
ld on individual case assessment.
d:'ie lor Prevention of Preeclampsia)
a:r-.n of MgSOo to women with
preeclampsia reduces the risk of an eclamptic seizure.a2 Women allocated
MgSO, had a 58o/a lower risk of an eclamptic seizure (95% Cl 40-71%).
The relative risk reduction was similar regardless of the severity of
preeclampsia. More women need to be treated when preeclampsia is not
severe (109) to prevent one seizure when compared with severe
preeclampsia (63). When MgSOo is given, regular assessment of the urine
output, maternal reflexes, respiratory rate and oxygen saturation is
important.3a
MgSOo can be given in 2 ways: continuous intravenous infusion and
intermittent intramuscular injections (see Table 3)'
C2. How should seizure be controlled?
The principles of management should follow the basic principles of
airway, breathing, and circulation. (Level III, Grade C)
MgSOois the therapy of choice to control seizures. A loading dose
of 4 g should be given over 5-10 minutes, followed by a further
infusion of 1 g/hour maintained for 24 hours after the last seizure.
(Level I, Grade A1
lable 3 Intravensus and lfitran$fc$hr tlagnesium S$ffate Dosage Schedules for
sdr€re PreccbmFsb and refimPsia
contin uous Intrdvenous Inf usion
l, 6ive 4-to 6-g loading dose of magnesium sulfate diluted in 100 mL of IVfluid admrnistered over 15-20 min.
2. Begin 2 g/hr in 100 mL of IV maintenance infusion.
3. Measure serum magnesium level at 4-6 hr and adjust infusion to matntain levels between 4-7 nEqlL
(4'8-8.4
midL).
. lvlagnesium sulfate is discontinued 24 hr after delivery.
Intermittent Intramuscular Injections
f. C* q g of magnesium sulfate (lvlgS04. 7H2O USP) as a 20% solution intravenously at a rate not to exceed 1
g/min.
2. Follow pr0mptly with 10 g of 500/! magnesium sulfate solution, one-half (5 q) injected deeply in the upper
outer
quadrant of both buttocks through a 3-inch-long, 20-gauge needle. (Addition of 1.0 mL of 2%lidocaine minimizes
discomfort.) Ifconvulsions persist after 15 min, give up to 2 g more intravenously as a 20% solution at a rate not
to exceed 1 g/min. If the woman is large, up to 4 g may be given slowly'
3. Every 4 hrthereafter grve 5 g of a 50% solution of magnesium sulfate in]ected deeply in the upper outet
quadrant of alternate buttocks, but only after ensuring that:
a. the patellar reflex is Present
b. respirations are not dePressed
c. urine output the previous 4 hr exceeded 100 mL
l'4agnesium sulfate is discontinued 24 hr after delivery.
41
I Recurrent seizures should be treated with either a further bolus of 2 g D. How should fluid balance tt
MgSOo, or an increase in the infusion rate to 1.5 g or 2 g/hour. (Level I, Fluid restriction is advisab
Grade A) intrapartum and PostPa rt u t

should be limited to 80 ml I
Do not leave the woman alone but call for help. Ensure that it is safe to
approach the woman and do effort to prevent materrral injury during the Close fluid balance * ith cha
convulsion. Place the wollan in left lateral recumbent position and administer is advisable in the acutt irtl
oxygen. Assess the airway and breathing and check the pulse and BP. The use period. , l-erel Ill
of the pulse oximeter is helpful.a3 Once stabilized, plans should be made to
deliveithe woman but there is no particular hurry and a delay of several hours Pulmonar;- edr--tn: ir : : :"'
to make sure the correct care is in hand is acceptable, assuming that there is no been associalgj s ith ir.:n::--
acute fetal concern such as fetal bradycardia.ra the benef-it ol flLrid e\13'r:
MgSOo is the therapy of choice and diazepam and phenytoin should no with goocl ntaterltal - .::
longerle used as first-line drugs.aa The intravenous route has few side effects' specific urine ottttrtl: r' ---:
Magnesiuni toxicity is unlikely with the recommended regimens and the levels restriction sh,'LIIJ 'lc '. -: - .:
do not neecl to be routinely measured. MgSOo is rnostly excreted irr the urine' is comtnott u itll se" ;-': I -::.
Urine output should be closely observed and if it becomes reduced below 20 balance is lnLrre i i::- - .- . .- -

rnlihour, tire rnagnesium inf'usion should be halted.34 Because magnesium is

cleared almost exclusively by renal excretion, plasma magnesium concentration E. How should the fetus hc e:
is excessive if glomerular filtration is decreased substantively. The initial A baseline cardiotocogreP
stanclard dose o1 MgSO, can be safely administered without knowledge of information about fetal r.
renal function. Renal function is thereafter estimated by measuring plasma predictive information. -
creatinine, and whenever it is L3 mg/dl or higher, only half ofthe rnaintenance
MgSOrdose is given.6 Magnesium toxicity can also be assessed by clinical Women in labor rr ith st
asiess,nent of the maternal deep tendon reflexes (DTRs) and respiratory rate' electronic fetal monitoring
If there is loss of the DTRs and the respiratory rate falls below l2 cpm, the
MgSO. infusion should be halted. Calciurn gluconate i g (10 ml) over 10 If conservative managentt
minutes can be given if there is concern of MgSO, toxicity'34 fetus rvith ultrasound mcas
In the collaborative eclarnpsia trial,aa a further bolus of 2 g MgSO, was screcning (BPS) and amniu
administered for recurrent seizures. An alternative is to increase the infusion weekly, umbilical arten l
rate to 1.5 g or 2 g/hoLrr. Ifthere are repeated seizures, then alternative agents (NST) should be underte
such as diazeparn or thiopentolle may be used, but only as a single dose, since delivery to be oPtimized.
prolonged usc of cliazeparl is associated r.vith an increase in maternal death.aa
if convirlsions persist, intubation is likely to be necessary to protect the airway CTG is the maittstar --:
and ntaintain oxygenation. T'ransfer to intensive care facilities r.vith interrnittent fetal rvell-being at that ti:::;
positive pressure r.,entilation is appropriate in tltese circumstances.3a labor. then continuous EF\1
Patients with severe preeclampsia rvho are expectantly rnarraged should
receive N{gS0o for24 hours. If BP is controlled adequately and fetaltesting is The rnain Patholtrgr al-::
reassuring, MgS0r is discontinued. MgS0. is cleared by the kidneys 4 hours insufficiency leadirte tl II
after the last dose. After this tinle, the risk of convulsion is again present. time of the initial presc:.:':
MgS0o should be given ortce the BP rises again and remaius in the severe to assess fetal grt''ir lil \ i: -
range, orrvhen delivery is planned. This should be cotttinued upto 24 hours best method of asses=n',::.
postpafium. Reduced amniotic iltrr; i -

42
Ir rrh either a further bolus of 2 g
I rrre to 1.5 g or 2 g/hour. (Level I,
Er : help. Ensure that it is safe to
,
F-, <nt maternal injury during the
. Ctose fluid balance with charting of input and output is essential. A catheter
t:r -:-, Jrnbent position and administer
g a- : : heck
the pulse and BP. The use
r i:.-.lized, plans should be made to
da: -.rn and a delay of several hours
l"r- -.i:iable, assuming that there is no
r: ,-
I: ,.r:pam and phenytoin should no
hri-: :irouS route has few side effects.
R* -'nended regirnens and the levels
E. is rlostly excreted in the urine.
_ is comrnort with severe preeclarnpsia. If there is associated hemorrhage, fluid
l: - r it becontes reduced below 20
d : - ,:lted.ja Because magnesium is
[ ' .tsrna magnesium concentration
&, :..:ed substantively. The initial
a: :ristered without knowledge of
f,-- :stimated by measuring plasma
r - -:rer. only half ofthe maintenance
E . -rn also be assessed by clinical
!r -: ..es (DTRs) and respiratory rate.
tr
-, -I rate falls below l2 cpm, the
c:--. Jluconate I g (10 ml) over l0
r-'.1 *SO., toxicity.3l
* , ,.rther bolus of 2 g MgSO., was
L:- irti\e is to increase the infusion
a:: , :eizul'es, then alternative agents
L: : . Lrut only as a single dose, since
li . .rn increase in maternal death.aa
r I . '-: lte c€Ssary to protect the airway
E-: : care facilities with interrnittent
!!; :iresecircumstances.sa
ri ,-:'i expectantly rnanaged should
r --: adequately and fetal testing is
r-- . cieared by the kidneys 4 hours
: ." . 1'convulsion is again present.
i€: :Jrin and rernaius in the severe
;, ' ,:ld be continued up to 24 hours
How should fluid balance be managed?
Fluid restriction is advisable to reduce the risk of fluid overload in the
intrapartum and postpartum periods. In usual circumstances, total fluids
shoulrl be limited to 80 mt/hour or I ml/kg/hour. (Level III, Grade C)
is advisable in the acute situation, especially in the immediate postpartum
period. (Level III, Grade C)
Pulmonary ederna is a significant cause of maternal death.3S This has often
been associated with inappropriate fluid marlagemerlt. There is no evidence of
the benefit of fluid expansionae and a fluid restriction regimen is associated
with good nraternal outcolre.4i There is no evideuce that maintetrance of a
specific urine output is important to prevent renal failure, which is rare.3a Fluid
restriction shoLrld be rnaintained until there is postpartutn diuresis, as oliguria
balance is more difficult and fluid restriction is inappropriate.ro
E. How should the fetus be assessed?
A baseline cardiotocography (cTG) should be undertaken. This gives
information about fetal wetl-being at that time but does not give any
predictive information. (Level II-2, Gracle B)
Women in labor with severe preeclampsia should have continuous
electronic fetal monitoring (EFM). (Level II-2, Grade B)
If conservative management is planned, then further assessment of the
fetus rvith ultrasound measurements of fetal size every 2 weeks, biophysical
screening (BPS) and amniotic fluid index (AFI) measurement at least twice
weekly, umbilical artery Doppler once a week and daily nonstress test
(NST) should be undertaken. Serial assessment will allow timing of
delivery to be optimized. (Level I, Grade A)
CTC is the mainstay of fetal monitoring. It gives information concerning
fetal well-being at that time bLrt has little predictive value. [f tlie woman is in
labor. then continuous EFM is appropriate.5o
The main pathology affecting the fetus, apart from prematurity is placental
insufficiertcy leading to IUGR. Ultrasound assessment of fetal size, at the
time of the initial presentation with hypertension, is a valuable measurement
to assess fetal growth. Measurement of the abdominal circurnference is the
best method of assessment since IUGR in this case is usually asymmetrical.
Reduced amniotic fluid volume is also associated with placental insufficiency
43
 and fetal growth restriction. Serialestimations of amniotic fluid
volume can hypertension and then. if
detect fetal compromise. Randomized trials have shown that investigation that hydralazine ma1 be ie
with umbilical artery Doppler using absent or reversed-end diastolic flow, enough to preclude its uri
fetal
improves neonatal out"o,r,"t'and serial investigations of this and other The National High t
vessels can be used to follow pregnancies under treatment and optimize Working Group Report *--i
delivery.5r the journal of American
urgent control of ser ere h
F. How should we control the BP?
>
Fl. Anti-hypertensive treatment should be started in woman with BP
160/110 mmHg. In woman with other markers of potentially
severe
Drugs for Urgent Control of Ser ere
diseaseo treatment can be considered at lower degrees of hypertension.
Drug (FDA Risk*) Dose and Rou::
(Level III, Grade C) i\.
Labetalol ( C ) l0 to 20 mg
20 to l0 nrir:::;,
Thereisconsensusthatseverehypertensioninpregnancy,definedas for infusion: I :.
> I 60/ I l0 mmHg requires treatment because these women are at increased
-hemorrhage,
risk of intracereiral and that treatment decreases the risk of
maternal death.5] There is also a consensus that, if the BP
is below 160/
ll0nrrnHg,thereisnoimmediateneedforanti-hypertensivetherapy.An
exceptionmaybeiftherearemarkersofpotentiallymoreseveredisease, Hydralazine ( C ) 5 mg I\ ..: I\1.
test results. Since, 20 to {0 n-:,:,
such as treauy proteinuria or disordered hematological repeat er er-. i
in this situation, alarming rise in BP may be anticipated, anti-hypertensive to 10.0 mg 1'.:: l:
treatment at lower BP levels may be justified'38 l! 6y -lQ 65 1\1

Nifedipine ( C ) Tablets rec.':: -

F2. What BP is the aim of anti-hypertensive therapy? mg PO. re:\..=::
Theaimofanti-hypertensivetherapyistokeepsystolicBPbetween
140 and 155 mmH! and diastolic BP between 90 and 105
mmHg. (Level lV Nicardipine D5\\ 90 r:.1 -
soluset
III, Grade C)
Concentr:t:-: =
Start drip :: .

lntreatingSeverehypertension,itisimportanttoavoidhypotension, I mg hrr
because the d-egree to which placental blood flow is autoregulated is not Titrate !-\ jl.
established, and aggressive lowering may cause fetal distress' mg hrt.
Itlarinu:-- :. s
Consideration should be given to initiating agents for treatment of
acute
may be \:]
severe hypertension at iower doses, because these patients :-:-.:-: :'-
intravascularly volume depleted and .may be at increased risk for
hypotension.53 Nole: Since Laber.:.
control of set'ere h ;.
F3. Labetalol given orally or intravenously intravenous hydralazine'
or be considered, and tlit: :: -.

oralnifedipinecanbeusedfortheacutemanagementofsevere The maximum dose oJ ar-;. ':..'. -:

adverse effects include tacit - ':'':
hypertension. (Level I, Grade A)
Patients tvith resistant J?r'c/. '
delivered.
The preferred therapeutic agents are labetalol, nifedipine or hydralazine.
Labetalol has the advantage that it can be given initially by mouth in severe

44
imations of amniotic fluid volume can
I trials have shown that investigation
rbsent or reversed-end diastolic flow
,l investigations of this and other fetal
lncies under treatment and optimize
ruld be started in woman with BP >
other markers of potentially severe
red at lower degrees of hypertension.
hlpertension in pregnancy, defined as
rt because these women are at increased
rnd that treatment decreases the risk of
ransenslrs that, if the BP is below 160/
need for anti-hypertensive therapy. Arr
;.ers of potentially more severe disease,
lered hematological test results. Since,
P mar be anticipated, anti-hypertensive
x -iustified.r8
rtensive theraPY?
erapv is to keep systolic BP between
BP befrveen 90 and 105 mmHg. (Level
n. it is important to avoid hypotension,
:nral blood flow is autoregulated is not
cr. ering may caLtse fetal distress.
initiating agents for treatment of acute
oses. because these patients may be
d and.rnay be at increased risk for
enously intravenous hydralazine' or
lr the acute management of severe
c :re labetalol, nifedipine or hydralazine.
can be given initially by mouth in severe
hypertension and then, ifneeded, intravenously. A review has suggested
that hydralazinemay be less preferable, although the evidence is not strong
enough to preclude its use.5a
The National High Blood Pressure Education Program (NHBPEP)
Working Group Report on High Blood Pressure in Pregnancy published in
the journal of American Heart Association the recommended drugs for
urgent control ofsevere hypertension in pregnancy.
Drugs for Urgent Control of Severe Hypertension in Pregnancy
(C ) l0 to 20 mg IV, then 20 to 80 mg every Because of a lower incidence of
-Labetalol 20 to 30 minutes, maximum of 300 mg; maternal hypotension and other
for infusion: I to 2 mg/min adverse effects, its
use now
supplants that of
hydralazine;
avoid in women with asthma or
congestive heart failure. Not
available locally.
Hydralazine ( C ) 5 mg IV or IM, then 5 to l0 mg every A drug of choice according to
20 to 40 minutes; once BP controlled NHBEP; long experience of safety
repeat every 3 hours; for infusion: 0.5 and efficacy
to I 0.0 mg/hr; lf no success with 20 mg
IV or 30 mg lM, consider another drug
Nifedipine ( C ) Tablets recommended only: l0 to 30 Should be used with caution if
mg PO, repeat in 45 minutes if needed concomitantly used with MgSOa
lV Nicardipine D5W 90 mL + Nicardipine l0 mg in Should be used with caution if
soluset concomitantly used with MgSOI
Concentration - 0.1 mg/ mL
Start drip at l0 ugtts/min (equivalent to
I mg/hr)
Titrate every hour (increments of I
mg/hr).
Maximum dose l0 mg/hr
Note: TheIV infusion site must be
changedeveryl2hours
Note: Since Labetalol is not locally available, hydralazine is thefirsl line drug in the urgent
control ofsevere hypertension in pregnancy. Ifno success fi,ith 20 mg IV, another drug should
be considered, and this is usually a calcium channel blocker (oral nifedipine or IV nicardipine).
The maximum dose of oral nifedipine is 50 mg PO and l)mg/hourfor IV nicardipine. Maternal
adverse effects include tachycardia, palpitation, peripheral edema, headache andfacialflushing.
Patients with resistant severe hypertension after maximum doses of these drugs should be
delivered.
45
t*.,. mav assist in the prolongation
l'"
Ft- -= \\omen with BP between 150-
L t.'.:-rnal treatment is associated with
llc- ,:i and a reduction in the need for
F .u :: treatment, a prolongation of
l :, : :sible as long as there is no other
F. . nost commonly used therapies.
;fo -: rerm follow-up of the delivered
;.- :t.'\rt on High Blood pressure
r : \merican Heart Association the
!€- rf _sestational hypertension and
r::- .,.hich they are familiar. A recent
---
d ': rhere is insufficient data to favor
r::) have concluded that agents other
blc:.;.rl or nifedipine) are preferable
lti ,ir erse effects.5a
[,zr rns (ACE) inhibitors, angiotensin
J d iu retics should be avoided during
F-jse in fetalgrowth restriction. ACE
or::: indicated because of unacceptable
c:: relatively contraindicated for
d ',: pulmonary edema.3a
suld be given orally not sublingually
if concomitanily used with MgSOo.
ne:al11,are now not recommended for
rp:egnant patients because of reports
n hr pertensive patients with coronary
n. etlicacy and safety of long_acting
iti ser ere hypertension in pregnancy.i
um antagonists for Bp control in
rnr use of MgSOo to prevent seizures;
drug interactions between nifedipine and MgSO4 were reported to cause
neuromuscular blockade, myocardial depression, or circulatory collapse
in some cases.60 In a recent evaluation,6r these medications are commonly
use together without increased risk.
Table 4. Drugs for Gestational or Chronic Hypertension in
Pregnancy.
0.5 to 3,0 qid in 2 divi4Bd doses 0rug 0f chol4e accDr'1lng to NH6EP: salsly aner
lirst trinie$ler well d0cument8,l, includinq 7 years
f0llDw'uF Df oltsfllnq
200 t0 1200 n]g,rd hr 2 tr) 3 dlvlded dDses May be a.ss,rcialed wlth fetal gr0wlh rBstrictl0n
in 30 t0 120 mg,rd 0t a slow-release preFarfllion I'day inhlbit l.1bor ond have sfner{i$tlc ac{lon wlth
nrflgneslum sultate in BP lowFrlng; llttle
e,(perience with ,rther cilclum 4ntry bl{lckers
50 t0 301"1 m0,rd ln 2 t0 .1 dlvided dosFs Few contrDlled lrials long Brperience $1th lrl#
adlirse events do(:unrentPd: usnlul ln
con]binntion with syrnpatholytic agentr may cause
ne,natal ttuonrb'rcytoFenla
0eFe06 0n spPclllc aoent decrirse 0teroplaDBnlal blaDd 11Dtu: may
hlay
imparr fetal resp0nse l0 hypoxlc stres$: risk ol
gr0rlth rBstrlctiDn when st,lrled ln llrsl 0r se.c0nd
trlnrester (alenDlol): mry be a$soclated with
neonalal hyloqly,:6nrla ilt hiqher do$es
1?.5 to 25.0 nrq/d Malority Dl c0ntrr)lled sludies ln nDrmolensiye
fre{nnnl wr})Fn nllrFr lltan h'/lurleniltr
oatienls: can cause vDlunre c0ntractiDn and
electrDl!1e dis0rdefs: nrrl be uselul ln
co'rlhinalion viith mplhyld0pa and ya"sodllalDr t0
mitrqdl8 conpinsatory llrid retenti0n
Contraindlcated AGE-ls flnd 0ngiotEnsln Leads tr te.tal |rss in animalsi hurnan use
tlpe 1 r€ffptor anlagoni.rls (gl+ ossdclalEd with cardiar defects, fel{pathy,
Dll girhldranrnios, !Jr0*1h restrlct16n. renal
agenesis and n€r)natal anurlc tenal lallure,
whlch may be latal
F7. How is postpartum hypertension managed?
Anti-hypertensive drugs should be given if the BP exceed 150 mmHg
systolic or 100 mmHg diastolic during the postpartum. (Level III, Grade
c)
Agents commonly used in the antepartum period may be used or
continued postpartum. (Level III, Grade C)
Diuretics can be used during the postpartum period. (Level I, Grade
A)
Itis prudent to avoid nonsteroidal anti-inflammatories in postpartum
women who are hypertensive. (Level III, Grade C)
47
 Postpartum, no guidelines currently exist with regard to anti- lL Delivery
hypertensive medications but Tan and de Swiet62 have suggested that anti- I{1. When is the $'oman r
hypertensive drugs should be given if the BP exceeds 150 mmHg systolic Pregnancies >3{ nr
or 100 mmHg diastolic in the first 4 days of the puerperium. preeclampsia is be
Choice of antihypertensive agent in the postpartum period is often stabilization. Lr,,..' .'
r

influenced by breast feeding,63 but in general, the agents commonly used

in the antepartum period may be continued postpartum. If the fetusis less tha
The medication may be discontinued when the BP normalizes. Home deferred, corticoste rc
BP monitoring by the patient is helpful in this regard.53 the benefits of conse
In select cases of women with severe preeclampsia, there seems to be (Level I, Grade .J

some benefit to a brief course of furosemide diuresis in the days

postpartum.s lf the gestarir.i ::.
A few case reports have suggested that nonsteroidal anti-inflammatories preeclampsia. del :r =:,
may contribute to BP elevation postpartum,65 and the effects on BP in non- gestational ase app:,rr
pregnant individuals are well documented. Thus, in postpartum patients outcomes are er;:..e-:
who are already hypertensive, these drugs should be used cautiously or gestations. and the p::<
should perhaps be avoided. less compelling.

Use of Corticosteroids Prolonging the p::,

G1. Is corticosteroid therapy indicated for fetal lung maturity? outcome for the pren.
Between 24-34 weeks, corticosteroids should be given to enhance fetal mother remains stable '
Iung maturity. The recommended regimens are the following: in neonatal complica::
Betamethasone 12 mg IM every 24 hours for 2 doses of severe earlr-cnse:
Dexamethasone 6 mg IM every 12 hours for 4 doses (Level I, Grade A) complications. Ser er:r
in different settinrts u.
In pregnancies less than34 weeks and the pregnancy can be prolonged
, in excess of 24 hours, steroids help to reduce fetal respiratory H2. What is the mode of r

mortality.66"67 There is probable benefit from steroid therapy even if The mode of delir en
delivery is less than24 hours after administration.6s-6e presentation of the fer
likelihood of success r

G2. Does steroid therapy have a role in the treatment of HELLP syndrome? cervix. (Grade C,
The use of dexamethasone or other steroids for therapy specific for
HELLP syndrome is not recommended and this approach should be In allsituations. a;
considered experimental. (Level I, Grade A) delivery is generallr ;
cesarean section is mi:
Two trialsTo-Trcompared treatment with dexamethasone vs. placebo in After 34 u'eeks u ith c:
women with HELLP syndrome. Both studies revealed outcomes that were considered.5 r' The r.t'sI,
not significantly different between 2 groups. One study?2 suggests that the mother. \/a,einal p:---
corticosteroids use lead to a more rapid resolution of the biochemical and Anti-hypertensir e rre:::
hematological abnormalities but there is no evidence that they reduce and labor.sl
morbidity.

48
rE::ently exist with regard to anti-
E Je Srviet62 have suggested that anti-
r r::he BP exceeds 150 mmHg systolic
4 J:1 s of the puerperium.
rn: in the postpartum period is often
:i-. 3eneral, the agents commonly used
oE:inued postpartum.
G::ed rvhen the BP normalizes. Home
[:-'i in this regard.s3
sE',3re preeclampsia, there seems to be
c; furosemide diuresis in the days
H :hat nonsteroidal anti-inflammatories
q::1um.65 and the effects on BP in non-
r--::ted. Thus, in postpartum patients
s€ ir-ugs should be used cautiously or
:d for fetal lung maturity?
roids should be given to enhance fetal
rd regimens are the following:
rcr.r 2{ hours for 2 doses
y 12 hoursfor4 doses (Level I, Grade A)
ei-s and the pregnancy can be prolonged
ls :elp to reduce fetal respiratorY
I
':enefit from steroid therapy even
r aJ:n ini stration.68-6e
i the treatment of HELLPsyndrome?
]ler steroids for therapy specific for
rended and this approach should be
I i Grade A)
rcnt * ith dexamethasone vs. placebo in
oth studies revealed outcomes that were
n i groups. One studyT2 suggests that
rapid resolution of the biochemicaland
there is no evidence that they reduce
H. Delivery
Hl. When is the woman with severe preeclampsia delivered?
Pregnancies >34 weeks of gestation complicated by severe
preeclampsia is best managed by delivery after maternal
stabilization. (Level I, Grade A)
Ifthe fetus is less than 34 weeks of gestation and delivery can be
deferred, corticosteroids should be given, although after24 hours,
the benefits of conservative management should be reassessed.
(Level I, Grade A)
If the gestation is greater than 34 weeks and complicated by severe
preeclampsia, delivery after stabilization is recommended.3a As the
gestational age approaches 34 weeks, short and long term neonatal
outcomes are excellent, fetal survival is already similar to that of term
gestations, and the potential benefits of expectant management becomes
less compelling.
Prolonging the pregnancy at very early gestation may improve the
outcome for the premature infant but can only be considered if the
mother remains stable.68'6eTwo small RCTs?3'7a have reported a reduction
in neonatal complications with an expectant approach to management
of severe early-onset preeclampsia with no increase in maternal
cqmplications. Several case series have also reported similar outcomes
in different settings with gestations as early as 24 weeks T'8'68'6e
H2. What is the mode of delivery?
if The mode of delivery should be determined after considering the
presentation of the fetus and the fetal condition, together with the
likelihood of success of induction of labor after assessment of the
cervix. (Grade C)
In all situations, a carefully planned delivery is appropriate. Vaginal
delivery is generally preferable but if gestation is below 32 weeks,
cesarean section is more likely as the success of induction is reduced.
After 34 weeks with cephalic presentation, vaginal delivery should be
considered.5'34The obstetrician should discuss the mode of delivery with
the mother. Vaginal prostaglandins will increase the chance of success.
Anti-hypertensive treatment should be continued throughout assessment
and labor.3a
49
 How shoultl the woman be managed following delivery?
ensure that
I1. Clinicians should be aware oftn" risk of late seizures and (Level
-1.

women have a careful review before discharge from the hospital.

III, Grade C)
delivery as
Anti-hypertensive medication should be continued after
6.
12.
maintain treatment for up
dictatJ by the Bp. lt may be necessary to
7.
to 3 months. &evel III, Grade C)

at 6 weeks may
13. Women with persisting hypertension and proteinuria
haverenaldiseaseanost'o"tobeconsideretlforfurtherinvestigation.
(Level III, Grade C)

who develop
Severe preeclampsia can occur postpartum' Women
postnatally (headaches' visual
lryperlension o. ry,tpioms of preeclampsia
pain) should be assessed'75
disturbances, ltaLlsea u,.rd uo,.,-riti,.tg or epigastric
th-e optimum
As eclarnpsia has been reported up to 4 weeks postnatally'
of eclampsia
le'gth of inpatie't postnatal stay is unclear but the incidence
postpartum day'?lThe decision
u,.ti."u"r. preeclampsia falls after the 4th
aboutdischargefromhospitalneedstoconsidertheriskoflateseizures,
MostwomenwithSeverepreeclampsiaoreclampsiawillnee-d-inpatient
assessment of the woman
care for 4 days or more following delivery. careful
disacharge'r'
to ensure iniproving clirrical signs is needed before
Arrti-lrypertensivetherapyshouldbecontinuedafterdelivery'
at around 24 hours
AlthoLrgh, initially, BP may fail, it usually rises agairr
be made in a
postpariunr. A reclLrction in anti-hypertensive therapy should
womall cannot go home on
,t.f*ir. fashion' There is llo reason why the
treatment, to be weaned off therapy as an outpatient.
After preeclampsia,
BPcarrtaketrpto3moltthstoreturtrtonormal.Durirrgtlristirrre,BP
slrouldnotbeallowedtoexceedl60/l00nrmHg.Thereisinsufficient
evidencetorecomnlendanyparlicrrlardrug,lrowever,itisgoodpractice
because of its adverse
to avoid the use of rnethydopain the postnatal period
metoprolol are also
effect profile, particularly depression' Atenolol and
four-rd to be cotrcentrated in the breastmilk'r4'5i

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[-- ^:e. Errr J Obstet Gynecol Reprod Biol
a-'. i. Koopman C, Bots ML, Bruinse
,t ::rlonged prednisolone administration to
c,r :3nn. [-ur J Obstet Cynecol Reprod Biol
n3,,l.rgists. The rnanagement of Severe
iu :;.;ne No l0 (A). London: RCOG Press;
rii - letal \'tedicine. Evidence Based Guide-
g:-.:rt ol Severe Preeclampsia. January
m:,:3nlent of hypertensive pregnancies by
95::l:777-81.
'1 .I The Sixth Report of the Confidential
B; \ rgdom. London: RCOG Press; 2004.
r ''-.ides accurate measurement of blood
[ . :-: --.
i: -::re detection of proteinuria in hyperten-
wr'- . ) B.IOG 2005: I 12: 412-17.
c :.,'OG Press; 2003.
rt-:: uith preeclampsia, and their babies,
g = lrial:A randomized placebo-controlled
43. Trufnell DJ, et. al. Outcome of severe preeclampsia/ eclampsia in Yorkshire 1999/
2003. BJOG 2005;l I 2:875-80.
44. Which anticonvulsant for women with preeclampsia? Evidence from the Collabora-
tive Eclampsia Trial. Lancet 1995;345(8963): 1455-63.
45. Redman CW, et. al. Early platelet consumption in preeclampsia. Br Med J
I 978;(6 I 1t):467 -9.
46. Sharma SK, et. al. Assessment of changes in coagulation in parturient with preeclamp-
of gestation:
sia using thromboelastography. Anesthesiology 1999;90:385-90.
47. Martin JN, et. al. Early risk assessment of severe preeclampsia: admission battery of
symptoms and laboratory tests to predict likelihood of subsequent significant maternal
morbidify. Am,l Obstet Gynecol 1999;180:1407-14.
48. Martin JN, et. al. The spectrum of severe preeclampsia: comparative analysis of HELLP
(hemolysis, elevated liver enzymes and low platelet count) syndrome classification.
Am J Obstet Gynecol 1999;180:1373-84.
49. Duley L, et. al. Plasma volume expansion for treatment of women with preeclampsia.
Cochrane Database Syst Ret, 2000(2):CD001805.
50. RCOG. The Use of Electronic Fetal Monitoring. Evidence Based Clinical Guideline
No.8. London: RCOG Press;2001.
51. Calan HL, et. al. lntrauterine Growth Restriction (IUGR): biometric and doppler as-
sessment. Prenat Diagn 2002;22:331-7.
52. Alfirevic Z, et. al. Doppler ultrasonography in high risk pregnancies: systematic re-
view with meta-analysis. Am J Obstet Gynecol 19951,172:1379-87.
53. Report of the National High Blood Pressure Education Program Working Group on
High Blood Pressure in Pregnancy. An J Obstet Gynecol 2000;183:S1-S22.
54 Magee LA, et. al. Hydralazine for treatment of severe hypertension in pregnancy: meta-
analysis. B MJ 2003;327 :955 -60.
HW.
55. Magee LA, et. al. Fortnightly Review: management of hypertensioninpregnancy. BMJ
1999:,318:1322-6.
56. El-Qarmalawi AM, et. al. Labetalol vs. methyldopa in the treatment of pregnancy in-
duced hypertension. Int J Gynaecol Obstet 1995;;49 125-30.
57. Duley L, et. al. Drugs for treatment of very high blood pressure during pregnancy.
Cochrane Database Sysl Rer:2006; 3:CD001449.
58. Furberg CD, et. al. Nifedipine. Dose-related increase in mortality in patients with coro-
nary heart disease. Circulation 1995;92:1326-1331.
59. Brown MA, et. al. Efficacy and safefy of nifedipine tablets for the acute treatment of
27
severe hypertension in pregnancy. Am J Ob.gtet Gynecol 2002:187:1046-1050.
60. Ben-Ami M, et. al. The combination of magnesium sulfate and nifedipine: a cause of
neuromauscular blockade. Br J Obstet Gynaecol 19941'10l:262-263.
61 Magee LA, et. al. Therapy with both magnesium sulfate and nifedipine does not in-
crease the risk of serious magnesium related maternal side effects in women with preec-
lanrpsia. Am J Obstet Gynecol 2005:193:l 53-163.
62. Tan LK, de Swiet M. The management of postpartum hypertension. BJOG
2002.109:733-736.
63. Beardmore KS, et, al. Excretion of anti-hypertensive medication into human breastmilk:
a systematic review. Hypertens Pregnancy 2002;21:85-95.
64 Ascarelli MH, et. al. Postpartum preeclampsia management with Furosemide: A ran-
dornized clinical trial. Obstet Gynecol 2005;105:29-33.
65. Makris A, et. al. Postpartum hypertension and non-steriodal analgesia. Am J Obstet
Gyne co I 200 4:l 90 :57 7 -57 8.
53
66. Crowley P. Prophylactic corticosteroids for preterm birth. Cochrane Database Syst E(
Rev 2000 (2): CD000065. Raul M. Qu, a-
67. Leveno KJ, Cunningham FC, Lindheimer MD, Roberts JM, Cunningham FG (eds):
Chesley's Hypertensive Disorder of Pregnancy 3'd ed. New York, ln Press, 2009, p.395.
68. Magan EF, et. al. Neonatal salvage by weeks'gestation in pregnancies complicated by
HELLP syndrome. J Soc Gynecol Investig 19(X;l:206-9.
69. Bramovici D, et. al. Neonatal outcome in severe preeclampsia at24-36 weeks gesta- The aims in the treatment of ecll
tion: Does the HELLP Syndrome matter? Am J Obstet Gynecol 1999;180:221-5' o control of seizure
70. Fonseca JE, et. al. Dexamethasone treatment does not improve the outcome of women . correction of h1 poria a:r
with HELLp syndrome. A Double blind placebo-controlled, randomized clinical trial. . colttrol of blood pressu:i
Am J Obstet Gynecol 193:1591,2005.
71. KatzL, et. al. Postpartum dexamethasone for women with. HELLP Syndrome' A double
. delivery after colltrcl .i
blind, placebo- controlled, randomized clinical trial. ,4m J Obstel Gynecol 198.283. el'
2008. The protocol of actire nlallaSe:: ,

72. Clenny TL, VieraAJ. corticosteroid for HELLP syndrome. BMJ2004;329;270-2.

73. N4urphy DJ, Stirrat GM. Mortality and morbidity associated with early onset preec- A. Hospitalization - required ft
ampsi a. Hyp ert e ns P re g n a n cy 2000 ;l 9 :221 -3 1'
I

Z+. Had'dad B, Deis S. Coffinet F, Paniel BJ, Cabral D, Sabai BM. Maternal and perinatal
outcome during expectant managenlent of 239 severe preeclampsia women between B. Control of seizures and Pn
24-33 weeks gestation. Am J Obstet Gynecol 2004;190-1590-7'
75. Atterburry JL, et. al. clinical presentation of women readrnitted with postpartum se- Magnesium sLrltate r \i:'
vere preeclampsia or eclamp sia. J Obstet Gynecol Neonatal Nurs 1998;27:134-41 . the preventiorr of ecl;.ilrr: .
76. Lubarsky SL, Sibai BM. Late postpartum eclampsia revisited ' obstet seizures. Tlre EclarrrP.i.l L
G y ne co I 1 99 4;83 :502-5. superiority of \lgSO- c" =:
77. Sibai BM. Expectant management of preeclampsia. oBG Management 2005;3:18-36. convulsions. Signiticart.. :,
78. Sibai BM, Bartom JR. E,xpectant management of severe preeclampsia remote from patients given \lgSO il-,:; '
term: patient selection treatment, and delivery lndications' Ant J Obstet Gynecol
2007l'514:E I -E9.
significalrt reductl(rll itt ;:,:
the three grouPS.
The reconlttla"63.i \1:i
eclampsia har e been Pr: , -

severe preeclernp:i;.1' \=-i

1. Loadingdoses.': -
"
g to each bulli;" .

delir e11.
2. Loading dose .'l j
=
hour. lncorptrrat-i I .

I 000 ml D5 \\ t'i' \ ,
(2 g/hr). r ia infus:i;'
hr after 2J hcur.

The follou ing pre:...:

succeeding doses:
I . Urine output trt Jl .;
hours

54
 ior preterm birth. Cochrane Database Syst
ECLAMPSIA
:r \lD, Roberts JM, Cunningham FG (eds): Raul M. Quillamor, MD and Diosdado V. Mariano, MD
NewYork, [n Press,2009,p.395.
ren!-)'3'd ed.
e'xs'gestation in pregnancies complicated by
'r 1994;l:206-9.
n s3\ere preeclampsia at24-36 weeks gesta- The aims in the treatment of eclampsia are:
| ),n J Obstet Gynecol 1999:'180'221-5. o control of seizure
teir does not improve the outcome of women
rl acebo-controlled, randomized cl inical trial.
. correction of hypoxia and acidosis
. control of blood pressure (BP)
:l: * omen with. HELLP Syndrome. A double . delivery after control of seizure
.1:.:cal trial. Am J Obstet Cynecol 198.283. el,
The protocol of active management of eclampsia consists ofi
H : -LP syndrome. BMJ 2004;329;27 0-2.
r,rrbidity associated with early onset preec-
Hospitalization - required forall patients with eclampsia. (Level I, Grade A)
t: -l 1.
C::ral D, Sabai BM. Maternal and perinatal
.-: l,l9 severe preeclampsia women between Control of seizures and prevention of recurrence
e; 1004;190-1590-7.
',r-. :: *onren readmitted with postpartum se- Magnesium sulfate (MgSOo) is currently considered the drug of choice in
-:.,;rcol ,\-eonatal Nurs 1998;27:134-41.
i the prevention of eclarnptic seizures as well as tl.le reduction of recurrent
's::.rriun1 eclampsia revisited. Obstet seizures. The Eclampsia Collaborative Trial Group in 1995 has establislred the
slrperiority of MgSOo over diazepam and phenytoin in the treatment of
e;,.rpsia. O BG ltlanage ment 2005 ;3 :18-36.
convulsions. Significantly fewer recurrences of seizures were noted among
:i-:elit of severe preeclampsia remote from
;. .,cry Indications. Am J Obstet Gynecol patients given MgSOo than those given diazepam or phenytoin, although no
significant reduction in maternal and perinatal mortalities was noted among
the three groups.
The recommended Mgsoo dosage schedules for severe preeclampsia and
eclampsia have been previously mentiolled in the chapter on lllanagement of
severe preeclampsia (Section Six) but they are restated here for ellphasis:

1. Loadingdoses of4 g IV slowlyover5-10 minutesand l0 gdeep IM (5

g to each buttock), then 5 g lM every 4 hours until 24 hours after
delivery.
2. Loading dose of 4 g IV followed immediately by IV infusion of 2 g per
hour. Incorporate20 g MgSOo(four l0-ml ampules of 500/o MgSO,,) to
1000 rnl D5W orNonnosol-M, and infuse IV at a rate of 100 ml/hour
(2 glhr), via infusion pump or soluset.e One may reduce the drip to I g/
hr after 24 hours.

The following precautions must be observed prior to administration of

succeeding doses:
l. Urine output of at least 30 rnl for the past hour or 100 ml for the past 4
hours

55
 Give hydralazine bY lV bcl
2. Presence of Patellar reflex until the desired BP is attained
3. Respiratory rate of not less than I 2/minute recommended because of the ins
for
4. IV Calcium gluconate ( l0 ml of lToh solution) available at bedside a. Clonidine IM 75-l,i(,1 :'
MgSOo overdose b. Nifedipine 5 or l0 ms
5.Serummagnesiumlevelsmaybetakenatcertainirrtervalstomonitor minutes. The subl i n si: :
(Level III, Grade Q' Maintenance of plasma
fo, magneiium toxicity'4-'7 because of the acute :-.
t-t'tugn"iirn1 levels at rneqlL almost always prevents eclamptic
levels of 8-10 studies on fetal efie':
convulsions.2 Patellar reflexes disappear with plasma
c. Labetalol call be 'Jlr.'-
rneqil]. This sign warns of impending magnesium toxicity
since
at 12 meqlL' followed by respiratory desired BP is It.'t :::'
respiratory deprlssion develops
every l0 ttrittLrtc' : -.
and cardiac ParalYsis and arrest'
treated.-' Tlti: .::.---
6.Ifapatienti,tou"transferredtoanotlrerhospital,thefullloading congesti\ e lter:: :' -- -
dosemusthavebeengivenandthepatientshouldbeaccompaniedby
aresporrsiblehealthp-ersonnel,withprovisionsforcontrolofseizures
(Level II-2' Grade B)
and other complications, if they occur'
D. Deliverv after control t, f
IfMgSo4isnotavailable,otheranti-seizureoptionsthatmaybeusedare:
It is generalll accePtec :*,
Diazepam
constitutes a significarl'. :::-J
pregnancy should be ternl::1.:
Aloadingdoseofl0mglVover2minutes,repeatedifconvulsionsrecurred, It is recommended tr'tLi..-
saline for 24
followed by an intravenois infusion of 40 rng in 500 ml normal as the patient becomes CtrlrS-.
consciousness, with the
hours. The rate of infusion is titrated based on the levelof fetal maturity in the PrBS€r^i:
aimofovercomingrestlessnessandkeepingthepatient.se{1!edbutarousable. B)
During the next 24-hours, an infusiotr of 20 mg diazepam
in 500 ml normal saline It has been obserred th:t:
phenytoin in the management of can be induced e\ en \\ ith an " -.
is given and slowly reduced. It may be used with
coirvulsions in the absence of MgSO o'(Level II-2' Grade
B) can be performed if labor Pr-- .

Phenytoin Cesarean sectioll i: I-<:;: ' r

I. vaginal deli\ er\ : -

although the $ose
There is no consensus about an ideal phenytoin regimen, 2. there is failure.'::
may be varied accordi'g to the patienf's weight. Since
phenytoin is only 3. there is letal c.-::'.:
recommended for the prev"ention of seizures, l0 mg diazeparn
IV should be given
dose of 1 g slow IV
to control the seizures. Th"reuft"r, an initial phenytoin loading Anticonvulsant theraPr ::
(over 20 min) is given with continuous cardiac monitoring, and followed by
(Level II-2, Grade
delivery. ln colnatose fr:.::
hours.
succeeding doses o1 1 00 mg every 6 hours for the next 24 Computed TomograPhl tCT,
B)

C. Anti-hyPertensive theraPY

Patients with severe hypertension should be starled on IV

therapy' The drugs
and nifedipine (Level
that may be used arehydraiazrne (drug of choice); clonidine
II-2, Grode B); and labetalolT . (Level I, Grade A)

I - ltinute
f . ' : solution) available at bedside for
be :'renat certain intervals to monitor
L; irttde C). Maintenance of plasma
fL , most always prevents eclamptic
,C ::Jpear with plasma levels of 8-10
n:..lJing magnesium toxicity since
u =: I rneq/L, followed by respiratory
L every 10 minutes but not to exceed a total of 220 mg per episode
il: .rnorher hospital, the full loading
ILL; :atient should be accompanied by
* :: provisions for control of seizures
r --:rur. (Level II-2, Grade B)
Jz'.:e options that may be used are:
r.l:::. repeated if convulsions recurred,
[i ::rg in 500 ml normal saline for 24
on the level of consciousness, with the
n. :he patient sedated but arousable.
n".: diazeparn in 500 ml normal saline
'..:ih phenytoin in the management of
e.' il-), Grade B)
rl-.enrtoin regimen, although the dose
'5 ueight. Since phenytoin is only
;. . tl rng diazepam IV should be given
phenr toin loading dose of I g slow IV
ardiac monitoring, and followed by
rr ihe next 24 hours. (Level II-2, Grade
ic be starled on IV therapy. The drugs
j.e): clonidine and nifedipine (Level
rr.
tii,lI
Give hydralazine by lv boluses of 5 or l0 mg at20to 30 minute intervals
until the desired BP is attained. Administering hydralazine via an lV drip is not
recommended because of the instability of the preparation. (Level II-1, Grade B)
a. Clonidine IM 75-150 mcg is the next recommended drug.
b. Nifedipine 5 or l0 mg can be given orally and takes effect within I 5-50
minutes. The sublingual route is not recommended for pregnant patients
because ofthe acute fluctuations in BP levels and the absence ofgood
studies on fetal effects of calcium antagonists. (Level II-2, Grade C1
c. Labetalol can be given with an initial dose of 20 mg IV bolus. If the
desired BP is not attained within l0 minutes, give 40 mg, then 80 mg
treated.T'8 This drug should be avoided in women with asthma or
congestive heart fai lure.
D. Delivery after control of seizures
It is generally accepted that continuation of pregnancy in eclamptic patients
constitutes a significant threat to maternal and fetal well being such that
pregnancy should be terminated.
It is recommended to induce labor or to perform a cesarean section as soon
as the patient becomes consciolrs and oriented, since ternporization to gain
fetal maturity in the presence of eclampsia is always risky. (Level II-3, Grade
B)
It has been observed that the uterus is sensitive to oxytocin so that labor
can be induced even with an o'unfavorable" cervix and assisted vaginal delivery
can be performed if labor progresses.
Cesarean section is reserved ifi
I . vaginal delivery does not appear easy and imminent
2. there is failure of progress after induction, or
3. there is fetal compromise
Anticonvulsant therapy should be continued for at least 24 hours after
delivery. In comatose patients, a neurologic evaluation ,uvith possibly a
Computed Tomography (CT) scan should be performed.
57
r- CHRONIC
References
Virgilio B. Castro 1'rli
and Prac-
l. Creasy RK, Resnik R. Creasy & Resnik's Maternal-Fetal Medicine Principles
tice, Sixth Edition. 2009, Saunders Elsevier.
2. Cunningham FG Leveno K, et. al. Williarns Obstetrics 23"1 Edition 20 10, The McCraw-
Hill Companies, Inc.
J. Duley L, Henderson-Smart D. Magnesium sulfate versus diazepam for eclampsia' Definition
hrane Data bct se'S1sl Rer' (4):CD000 I 27' 2003'
C oc
pregnancy in-
4. Greer I, Walker J, et. al. Second line therapy with nifedipine in severe Chronic hypertension. Ceil:.c
duced hypertension. C/lr Exp Hypertens B8:277.1989' predating pregnanc) or de\ elcp::
RCOG Guideline Number 10, March 2006: The Management of Severe Preeclampsia/ that persists l2 weeks pt-rSIF3r:-:
Eclampsia.
of Eclampsia. Obstetr C)'necol maternal, fetal and neonatal ffror1:
Sibai gNa. Diagnosis, Prevention, and Managenlent
2005;105:402-10.
pregnancy occur in \\ Lrnler '.\':
ACOG 2002. hypertension, and in uomen
7. "ri--
8. National High Blood Pressure Education Prograrri 2000 half of pregnancy.
9. Anderson 1986. Anti-hypertensire agent: i
hypertension, to prolons pre::
maximizing the gestational alc -

medications that rnav liar e air e:.,

at a level that minimizcs n:::;-
Prevention of preeclampsia i: J<:
that either specific BP targets r:
modify the risk of superimpc..
hypertension. The challenge :s
medications and u'hat ler el oi BP
is less complex, because onl\ a s:l
been adequately evaluated in pre::

Recommendations

L Low dose aspirin (65-85 n:

birth should be considereJ ::
superimposed preeclantps : :
pregnancy, chronic renal dis:,
erythematosis or antiphcspir --

hypertension). (Gr ad e .1
Some women ?t€ nrtrr€ r'c:
of at least 75 mg'dar ttt3-r ::
thromboxatte. Horre\er. I J-
synthesis.

2. Angiotensin conr ertirtg e:z'. :

blockers (ARBs) or€ c.'rti: -

58
 CHRONIC HYPERTENSION
' Virgilio B. Castro, MD and Ann Marie C. Trinidad, MD
.,1-Fetal Medicine Principles and Prac-

'::rics 23'd Edition 2010, The McCraw-

..1re versus diazepam for eclampsia. Definition

i.
:h nifedipine in severe pregnancy in-
- -. I 989.
Chronic hypertension, defined as blood pressure (BP) 140/90 mmHg either
predating pregnancy or developing before 20 weeks gestation and hypertension
, '.lanagernent of Severe Preeclampsia/
that persists 12 weeks postpartum. This complication may result in significant
-: rint of E,clarnpsia. Obstetr Gynecol maternal, fetal and neonatal mortality and morbidity. Hypertensive disorders during
pregnanay occur in women with pre-existing primary or secondary chronic
hypertension, and in women who develop new-onset hypertension in the second
,'r 1000 half of pregnancy.
Anti-hypertensive agents are mainly used to prevent and treat severe
hypertension, to prolong pregnancy for as long as safely possible, thereby
maximizing the gestational age of the infant and to minimize fetal exposure to
medications that may have adverse effects. The goalof treatment is to maintain BP
at a level that minimizes maternal cardiovascular and cerebrovascular risk.
Prevention of preeclampsia is desirable; however, current evidence has not shown
that either specific BP targets in pregnancy or specific anti-hypertensive agents
modify the risk of superimposed preeclampsia in women with pre-existing
hypertension. The challenge is in deciding when to use anti-hypertensive
medications and what level of BP to target. The choice of anti-hypertensive agents
is less complex, because only a small proporlion of currently available drugs have
been adequately evaluated in pregnant women, and many others are contraindicated.

Recommendations

l. Low dose aspirin (65-85 rng PO) at bedtime everyday from 12 weeks until
birrh should be considered in women with historical risk factors to decrease
superimposed preeclampsia (e.g. hypertensive disease during a previous
pregnancy, chronic renal disease, autoimmune disease such as systemic lupus
erythematosis or antiphospholipid syndrome, type I or type 2 diabetes, chronic
hypertension). (Grade A)
Some women are more resistant than others to the effects of aspirin, a dose
of at least 75 mglday may be necessary to inhibit both platelet and placental
thromboxane. However, a dose of 100 rng/day may affect fetal prostacyclin
synthesis.

2. Angiotensin converting enzyme (ACE inhibitors) and angiotensin II receptor

blockers (ARBs) are contraindicated during pregnancy. (Level II-2, Grade A)

59
3. The beta blocker atenolol may be associated with groMh restriction and is not
COMPLICATIONS C
recommended for use in pregnancy. (Grade B)
HYPERTENSION (HEl
4. Anti-hypertensivetherapyshouldbereinstitutedifBPexceeds 150-l60systolic Ma. Luisa S. Ac-
or 100-1 l0 diastolic. Initial anti-hypertensive therapy include the following:
a. Methyldopa 250-500 mg PO BID-QID (max2 dday) HELL
b. Labetalol 100-400 mg PO BID-TID (max 1200 mglday)
c. Nifedipine PA (intermediate release) tablets ( l0-20 mg PO BID-TID, Definition
max 180 mg/day) or XL (slow release) preparation (20-60 mg PO
OD, max 120 mg/day) . The acronym HELLP \\as cie:
subset of severe PreeclamPsi:
Methyldopa and labetalol are the first line antihypertensive therapies. (Level I, anemia, ,moderate to se\ ere
Grade A) erythrocltes on PeriPheral si::e:
with right upper quadratrt ePii':,
EL : elevated liver €rZ\ Ill€S. ;i
Obstetric Management . Two classification s\ stcnls :.i
significant matertral ntc-rrb i,j i:'.
-

l. Baseline ultrasound at 18-20 weeks and repeat scan at 28-32weeks to monitor outcomes.
fetal growth and to check amniotic fluid volume. . The Tennessee Classit-rcatic:l: :
2. If with growth restriction or superimposed preeclampsia, antenatal fetal following criteria oI€ lllit: '
surveillance should include umbilical artery Doppler velocimetry. (Grade A) platelets 100,000'1rnl or lcss
3. For women with pre-existing hypertension laboratory exams at initial visit aminotransfase (AST) l0 IL L
include complete blood count (CBC), serum creatinine, serum potassium and abnormal peripheral snl ea:
urinalysis. (Grade B) dehydrogenase (LDH) 600 lL ,

4. If with suspicion of preeclampsia, creatinine clearance and24 hour urine protein When some but not all these
are encouraged. (Grade A)
"incomplete" HELLP is use:
5. Vaginal delivery should be considered unless a cesarean section is required for
. The MississippiTriple Class S'
the usual obstetric indication. (Grade B) their platelet cottnts: class r :
50,000/rnl, evidence of heP:rli;
6. If vaginal delivery is planned and the cervix is unfavorable, then cervical
transfrase (ALT) > 70 IL L,. "
ripening should be used to increase the chance a successful vaginal delivery.
600 IU/L); class 2 requires s:r:'i
(Grade A)
( >50,000 to < 100.0[ttt ;-'
7. Women with long standing hypertension should be evaluated for end-organ
thrombocytopenia (platel ::.
disease including cardiomegaly, renal insufficiency and retinopathy. (Grade
dysfunction (AST artd or \Lf
c)
600 ru/L).

Pathophysiology

. The pathophysiologl oi HE--

that placenta-derived prrrl-:: :
damage hepatic cells. sugg:.::-
liver-targetted acute inilr: : .

process.5

60
r ::.d rvith growth restriction and is not
G.-:-le B)
tk .::ruted if BP exceeds I 50- 160 systolic
n=: 'ir e therapy include the following:
) B:f-QID (max 2 e/day)
lD-IID (max 1200 mg/day)
re ;rse) tablets (10-20 mg PO BID-TID,
or" :elease) preparation (20-60 mg PO
:li:c antihypertensive therapies. (Level I,
rc :-peat scan at 28-32 weeks to monitor
U,: \ rrlume.
in-.:..sed preeclampsia, antenatal fetal
I a::en Doppler velocimetry. (Grade A)
Er-,s.on laboratory exams at initial visit
. s<rum creatinine, serum potassium and
ri;..re clearance and 24hour urine protein
l:'.ess a cesarean section is required
t!
he :ervix is unfavorable, then cervical
h< :hance a successful vaginal delivery.
sr,-n should be evaluated for end-organ
ri rnsufficiency and retinopathy. (Grade
COMPLICATIONS OF PREGNANCY INDUCED
HYPERTENSION (HELLR ABRU PTIO PLACENTA)
Ma. Luisa S. Acu, MD and Sol M. Pangan, MD
HELLP SYNDROME
Definition
. The acronym HELLP was created by Louis Weinstein in 1982 to describe a
subset of severe preeclampsia/eclarnpsia witlrrnricroangiopathic hemolytic
anemia,'moderate to severe thrombocytopenia, disrupted or destroyed
erythrocytes on peripheral smear, and abnormal liver function tests presenting
with right upper quadrant/epigastric pain, nausea and vorniting (H : hemolysis,
EL = elevated liver enzymes, and LP: low platelets).|
. Two classification systems have been created to stratify patients' risks for
significant maternal rnorbidity, to guide therapeutic intervention and assess
outcomes.
. The Tennessee Classification2 defines "con-lplete" HELLP syndrome if all the
following criteria are met: (l) moderate to severe thrombocytopenia witlr
platelets I 00,000/rnl or less; (2) hepatic dysfunction with aspartase
aminotransfase (AST) l0lUlL or greater; (3) evidence of hemolysis with an
abnormal peripheral smear in addition to either total serum lactate
dehydrogenase (LDH) 600 IU/L or greater, or bilirubin 1.2 mgldL or greater.
When some but not all these parameters are present, the term "partial" or
"incomplete" HELLP is used.
for
. The Mississippi Triple Class Systernr divides patients into 3 classes based on
their platelet counts: class I requires severe thrombocytopenia (platelets <
50,000/ml, evidence of hepatic dysfunction (AST and/or alanine transamino-
transfrase (ALT) > 70lUlL), and evidence of liemolysis (total serum LDH >
600 lU/L), class 2 requires similar criteria except thrombocytopenia is moderate
( >50,000 to < 100,000/rnl ); and class 3 includes patients with mild
thrombocytopenia (platelets >100,000 but < 150,000/rnl), mild hepatic
dysfunction (AST and/or ALT > 40lUlL), and hernolysis (total serum LDH >
600 ru/L).
Pathophysiology
. The pathophysiology of HELLP remains unclear. Strand, et.al.a postulated
that placenta-derived proteins are shed into the maternal circulation which
damage hepatic cells, suggestingthat HELLP syndrome is a placenta-instigated,
liver-targetted acute inflammatory condition and disordered immunologic
process.5
61
Ctinical Presentation magnesium sulfate (\1gS
maternal condition. and t'l
. Usually develops suddenly in the third trimester or immediate postpartum. There is no general agreen,
Progression is usually rapid with 35-50
o%
decrease in platelets per day and HELLP syndrome betcre -:-
rise in AST and ALT until 24-48 hours postpartum when levels begin to stable except for m i ld ltr ITr .'.:
recover.6-8 fetal condition.2e rs (Grtit (.

. Onset of disease occurs antepartum in 70o/o, and postpartum in 30o/o of Aggressive high dose cr:'.:
cases.15 Hypertension and proteinuria may be mild and may not directly maternal and neonatal ou:;:
correlate with laboratory parameters. Patients are usually seen complaining mgevery l2 hours. or int::r:
of malaise (90%), epigastric or right upper quadrant pain (90o/o), or nausea until delivery, and addrtri:
or vomiting (50%), and some with non-specific viral-like symptoms.'3 reported improvement i: l:
. The most important symptom is severe epigastric/right upper quadrant pain, (BP). shorler hospital =:"r .

found in 100% of Weinstein's original series of 29 advanced cases, often Most of these studies are r:
heralds rapidly progressive disease.
r'3'e in inclusion criteria. ch.':.
. A patient with severe preeclampsia who suddenly develops severe writhing reported.2e The .{ randJi:'rrt
epigastric/upper abdominal pain, may have hepatic hematoma or rupture, improved laboraton ralu<.
and constitutes an obstetric emergency. Rupture of a subcapsular liver given dexarnetltasone. n.- :
hematoma is one of the most dreaded, life-threatening complication of the need for transfusion. pu.:
HELLP syndrome. If suspected, hepatic irnaging with transabdominal complications \vere 5/1pri n.:
ultrasound, computed tomography (cT), or magnetic resonance imaging there is insufficient er idence
(MRI), can be performed'ra syndrome decreases ttta.irr :
. Significant maternal morbidity occllrs with worsening thrombocytopenia' The results of trro recent :
very high LDH, AST and/or uric acid levels.3'rr double-bl ind, placebo-cr'ntr
. HELLP usually resolves within a week postpartum'5'6'2s to date, on the use of high j
. Sixty percent of maternal mortalities occur with class 1 disease and the in patients with HELLP srr.
most common cause is cerebral hemorrhage/stroke. Other causes of death for all HELLP s35s3. flgr,r.
are cardiac arrest, disseminated intravascular coagulopathy (DIC), acute disease, of the Fonseca c:s
respiratory distress syndrome (ARDS), renal failure, sepsis, hepatic rupture HELLB there rvas a shrlnei
and hypoxic encephaloPathY.ro of hospitalization irr those rr
Replacement of clotting ta:
Management and platelet transfusitrn l-.,-:
needed. (Level IIL Gr.t.i. i
. Liver function tests and platelet counts should be done in all preeclamptic Epidural or spirral 3nc:'.: ;
women, especially with suspected HELLP. (Level II, Grade B) preeclarnpsia. Aggres'lr e :
. Best rnanaged in a center with intensive care facilities for hepatologic, count to 75,000/rnmr. the :
hematologic and obstetric emergencies. (Gratle B) anesthesia (from 0o o t.' l-:
. There is a consensus of opinion that prompt delivery is indicated if the labor. and possible r asin,l
syndrome develops beyorrd 34 weeks gestation, or earlier if there is Most of the patients coul: :

multiorgan dysfunction, DIC, liver infarction or hemorrhage, renal failure, platelet couttt is grc3t3: :-
suspected abruptio placenta, or nonreassuring fetal status. In these damage.25

situations, treatment consists of prophylaxis against convulsions with

62

ird trimester or immediate postpartum.
-jr,)%o decrease in platelets per day and
ours postpartum when levels begin to
n in 70Yo, and postpartum in 30o/o of
rria may be mild and may not directly
. Patients are usually seen complaining
I upper quadrant pain (90%), or nausea
nt n-specific viral-like symptoms.ll
:re epigastric/right upper quadrant pain,
nal series of 29 advanced cases, often
* ho suddenly develops severe writhing
rar have hepatic hematoma or rupture,
enc). Rupture of a subcapsular liver
:d. life-threatening complication of the
hepatic irnaging with transabdominal
rCT). or magnetic resonance imaging
urs u ith worsening thrombocytopenia,
id lel els.3'rr
eek postparlutn.5'6'2s
ies occur with class 1 disease and the
nr-rrhage/stroke. Other causes of death
tnr ascular coagulopathy (DIC), acute
rS r. renal failure, sepsis, hepatic rupture
unts should be done in all preeclamptic
HELLP. (Level II, Grade B)
rensir e care facilities for hepatologic,
cie:. (Gracle B)
rat prompt delivery is indicated if the
eeks gestation, or earlier if there is
int-arction or hemorrhage, renal failure,
ntrnr€&SSUring fetal status. In these
prophylaxis against convulsions with
l 63
magnesium sulfate (MgSOo,, control of hypertension, stabilization of
maternal condition, and then delivery.r6 (Level III, Grade B)
There is no general agreement, however, on the management of women with
HELLP syndrome before 34 weeks gestation when the maternal condition is
stable except for mild to moderate abnormalities in blood tests with a reassuring
fetal condition.2e'r6 (Grade C)
Aggressive high dose corticosteroid therapy has been advocated to improve
maternal and neonatal outcome in HELLP. Intravenous dexamethasone 1 0- 1 2
mg every l2 hours, or intramuscular betamethasone 10-12 mg every 12 hours,
until delivery, and additional 3 more doses after delivery, were given with
reported improvement in laboratory values, improvement in blood pressure
(BP), shorter hospital stay and an increased use of regional anesthesia.r6-23'2i
Most of these studies are retrospective and have critical design flaws, mainly
in inclusion criteria, choice of historical controls and/or clinical outcome
repofted.2e The 4 randomized trials were not placebo controlled. Although
improved laboratory values and urine output were obtained in the patients
given dexamethasone, no differences in serious maternal rnorbidity such as
need for transfusion, pulmonary edema, renal failure, or serous hepatic
complications were shown.2e Hence a Cochrane review (2004) concluded that
there is insufficient evidence to deterrnine whether corticosteroid use in HELLP
syndrome decreases major maternal and perinatal morbidity.24
The results of two recent studies, Fonseca25 and Katz26, both randomized,
double-blind, placebo-controlled clinical trials, with the largest sarnple sizes
to date, on the use of high dose dexamethasone to improve maternal outcome
in patients with HELLP syndrome, do not support routine use of this regimen
for all HELLP cases. Howeveq a subgroup analysis according to severity of
disease, of the Fonseca cases, showed that among the patients with class I
HELLP, there was a shorter average platelet count recovery and less duration
of hospitalization in those who received dexamethasone (4.6 versus 10.4 days).
Replacement of clotting factors witlr frozen plasma and factor concentrates,
and platelet transfusion for counts below 50,000/mmr should be given as
needed. (Level III, Grade B)
Epidural or spinal anesthesia is the preferred anesthesia for patients with
preeclampsia. Aggressive liigh dose corticosteroids can increase the platelet
count to 75,000/mm3 , the threshold deerned adequate to undertake regional
anesthesia (from 0% to 42Yo), and to enable cervical ripening, induction of
labor, and possible vaginal delivery.27,28 (Level II, Grade B)
Most of the patients could be discharged after 4-8 days hospitalization, if the
platelet count is greater than 100,000/mm3 and no evidence of end-organ
damage.25
 18. Magann EF, Bass D. Chu'i.t:ij
References tum corticosteroids: disea-'c .
-1 : I 1:
Obstet Gynecol 1991:I
l. Weinstein L.Syndrome of hemolysis, elevated liver enzymes, and low platelet count: 19. Magann EF, Penl KC -lr. \
a severe consequence of hypertension in pregnancy. Am J Obstet Gynecol 1982;142:159- Postpartum corticostero i ds : a;
67. Gynecol 1994;17 1: I I 5-t-8.
2. Sibai BM, Taslimi MM, el-Nazer A, Amon E, Mabie BC, Ryan GM. platernal- 20. van Runnard Heimel PH. .tu:
perinatal outcome associated with the syndrome of hemolysis, elevated liver enzymes, HW. A randomized Placebr ;"
and low platelets in severe preeclampsia-eclampsia. Am J Obstet Gynecol 1986;155:501- to patients with HELLP s1 r:Jr-
9. tions. Am J Obstet Gtnec,:' 1
3. Martin JN Jr, Rinehart K, Magann EF, Terrone DA, Blake PG. The
May WL, 21. lslerCM, Banilleaur PS. \:3:
spectrum of severe preeclampsia: comparative analysis by HELLP sybdrome classifi- ized trial comparing the eftl::
cation. Am J Obstet Gynecol 1999;180:1373-84. ment of antePartum HELLP s1
4. StrandS, StrandD, SeufertR, MannA, LotzJ, BlessingM, et.al. Placenta-derived 22. Vigil-DeGracia B Carcia-C::
CD95 ligand causes liver damage in HELLP syndrome. Gastroenterology HELLP syndrome. Inr -i C',':-
2004;126:849-58. 23. YalcinOT, SenerT, Ha:s H-
5. Martin JN Jr, Magann EF, Isler CM. HELLP sybdrome: the scope of disease and in patients with HELLP s1 ::-
treatment. ln: Belfort MA, Thornton S, Saade GR, editors. Hypertension in preg- 24. MatchabaP, Moodlel -1. C--::.
nancy. Chap 7. Oxford: Marcel Dekker;2003.p.141-88. Review) ln: The Cochrene -
6. Martin JN Jr, Blake PG, Perry KG, McCaul JF, Hess LW, Martin RW. The natural ware.
history of HELLP syndrome: pattems of disease progression and regression. Am J 25. Fonseca JE, Nlendez F. C::.
O bstet Gynec o I 19911'164 1500- I 3. prove the outcome of rrcr::::
7. Katz VL, Thorp JM, Rozas L, Bowes WA Jr. The natural history of thrombocytope- trolled, randomized clini;: ::
nia associated with preeclampsia. Am J Obstet Gynecol 1990;163:1142'3. 26. KatzL, de Amorin \{\lR. :.,
8. Makkonen N, Harju M, Kirkinen P. Postpartum recovery after severe preeclampsia for women with hemolls:s. :
and HELLP sybdrome. J Perinat Med 1996;24:641-9. drome: a double-blind. Pl"-'
9. Faridi A, Rath W. Differential HELLP syndrome diagnosis. Z Gerburstschilfe Gynecol 2008:198:l8l e: -lS
I 996;200:88-95.
27. O'brienJM, Shumate S.\. S:
10. IslerCM, RinehartBK, TerroneDA, MartinRW, MagannEF, MartinJNJr' Mater- ofcorticosteroid theraPl in :
nal mortality associated with HELLP syndrome. Am J Obstet Gynecol 1998;181:924- and low Platelet count' s)::
Obstet Gynecol 2001: I86.l:
8.
71. CatanzariteVA, SteinbergSM, MosleyCA, LaudersCF, CousinsLM, SneiderJM. 28. Rose CH, ThigPen BD. ts;
Severe preeclampsia with fulminant and extreme elevationof aspartate aminotrans-
implications of antePartum ;'c:
ferase and lactate dehydrogenase levels: high risk for maternal death. Am J Perinatol
2004;104:l0l l-4,
1995:'12:310-3.
29. Sibai BM, Barton JR. Der::
12. Martin JN Jr, Rose CH, Briery CM. Understanding and managing HELLP syndrome:
hemolysis, elevated lir er enr
the integral role of aggressive glucocorticoids for mother and child. Am J Obstet Gynecol
2005;193: I 587-90.
2006;195:914-34.
13. Sibai BM. The HELLP syndrome (hemolysis, elevated liver enzymes, and low plate-
lets): much ado about nothing? Am J Obstet Gynecol 1990;162:311-6.
14. WickeC, PereiraPL, NeeserE, Fleschl, RodegerdtsEA, BeckerHD. Subcapsular
liver hematoma in HELLP syndrome: evaluation of diagnostic and therapeutic options
- A unicenter study. Am J Obstet Gynecol 2004;190:106-112.
15. SibaiBM, RamadanMK, Ustal, SalamaM, MercerBM, FriedmanSA. Maternal
morbidity and mortality in 442 pregnancies with hemolysis, elevated liver enzymes,
and low platelets (HELLP syndrome). Am J Obstet Gynecol 1993;169:1000-6.
16. Sibai BM. Diagnosis, controversies, and management of the syndrome of hemolysis,
elevated liver enzymes and low platelet aounl. Obstet Gynecol 2004;103:981-91.
17. Martin JN Jr, Magann EF. High-dose dexamethasone:a promising therapeutic option
for HELLP. Contemp Ob Gyn 1999;44:55-65.

64

!rE=J liver enzymes, and low platelet count:
Fc- :.r q'. Am J Obstet Gynec ol 1982;1 42'.159'
,*r,. E. Mabie BC, Ryan GM. Matemal-
lF: re of hemolysis, elevated liver enzymes,
Es-:sia- Am J Obstet Gynecol 1986;155:501-
, f1 'aann EF, Terrone DA, Blake PG. The
Fn: .. analysis by HELLP sybdrome classifi-
u-:-_.-3-1.
L'-":'zJ. BlessingM, et. al. Placenta-derived
rir :.!LLP syndrome. Gastroenterology
li:-,P sybdrome: the scope of disease and
L S',de GR, editors. Hypertension in preg-
9J,,. -: p.l4l-88.
l{:- JF. Hess LW, Martin RW. The natural
lqn : :ease progression and regression. Am J
;t:. .: The natural history of thrombocyope-
tr'- :et G),necol 1990;1 63:1142-3.
::
hs;::rtum recovery after severe preeclampsia
rl i:: .l_l:641_9.
L-Ll srndrome diagnosis. Z Gerburstschilfe
iltr':.r
RW, Magann EF, Martin JN Jr. Mater-
;c::ne. Am J Obstet Gynecol 1998;181:924-
I ii:.. Lauders CF, Cousins LM, Sneider JM.
E 3\!reme elevationof aspartate aminotrans-
r :,:gh risk for maternal death. Am J Perinatol
de:standing and managing HELLP syndrome:
sc,:. iormotherand child. AmJ Obstet Gynecol
x.,. sis. elevated liver enzymes, and low plate-
)r : : : r G y'ne c ol 1990:1 62:3 I 1 -6.
1.. S.odegerdtsEA, BeckerHD. Subcapsular
ra-uation of diagnostic and therapeutic options
r--. 1004; I 90 :106-1 12.
r:a \1, Mercer BM, Friedman SA. Maternal
nc:es rvith hemolysis, elevated liver enzymes,
,trt J Obstet Gynecol 1993;169:1000-6.
nd nanagement of the syndrome of hemolysis,
t ;..unt. Obstet Gynecol 2004;103:981-91.
rderamethasone:a promising therapeutic option
r: i 5 -65.
t
18. Magann EF, Bass D, Chouhan SP, Sullivan DL, Martin RW Martin JN Jr. Antepar-
tum corticosteroids: disease stabilization in patients with HELLP syndrome. Am J
Obstet Gynec ol 1994;17 I :11 48-53.
19. Magann EF, Perry KG Jr, Meydrech EF, Harris RL, Chouhan SR Martin JN Jr.
Postpartum corticosteroids: accelerated recovery fom HELLP syndrome. Am J Obstet
Gynec ol 1994;17 I :11 5 4-8.
20. van Runnard Heimel PH, Juisjes AJM, Franx A, Koopman C, Bots ML, Bruinse
HW. A randomized placebo controlled trial of prolonged prednisolone administration
to patients with HELLP syndrome remote from term: maternal and neonatal complica'
lions. Am J Obstet Gynecol2004;l9l:S41.
21. Isler CM, Barrilleaux PS, Magann EF, Bass JD, Martin JN Jr. A prospective random-
ized trial comparing the efficacy of dexamethasone and betamethasone for the treat-
ment of antepartum HELLP syndrome. Am J Obstet Gynecol 2001;184:1332'7.
22. Vigil-DeGracia P, Carcia-Caceres E. Dexamethasone in the postpartum treatment of
HELLP syndrome. Int J Gynaecol Obstet 1997;59:217'21.
23. Yalcin OT, Sener ! Hass H, Ozalp S, OkurA. Effects of postpartum corticosteroids
in patients with HELLP syndrome. Int J Gynaecol Obstet 1997;61:l4l-8.
24. Matchaba R Moodley J. Corticosteroids for HELLP syndrome in pregrancy. (Cochrane
Review) In: The Cochrane Library, Issue 4, 2004:CD002076 Oxford: Updates Soft-
ware.
25. Fonseca JE, Mendez F, Catano C, Arias F. Dexamethasone treatment does not im-
prove the outcome of women with HELLP syndrome: a double blind, placebo-con-
trolled, randomized clinical trial. Am J Obstet Gynecol2005;193:1591-8'
26. KatzL, deAmorin MMR, Figueroa JN, Pinto eSilva JL. Postpartum dexamethasone
for women with hemolysis, elevated liver enzymes, and low platelets (HELLP) syn-
drome: a double-blind, placebo-controlled, randomized clinical trial. Am J Obstet
Gynecol 2008;l 98:283.e 1-283.e8.
27. O'brien JM, Shumate SA, Satchwell SL, Milligan DA, Barton JR. Maternal benefit
of corticosteroid therapy in patients with HELLP (hemolysis, levated liver enrymes,
and low platelet count) syndrome: impact on the rate of regional anesthesia. Am J
O b s te t Gy ne c o I 2002;1 86:457 -9.
28. Rose CH, Thigpen BD, Bofill JA, Cushman J, May WL, Martin JN Jr. Obstet
implications of antepartum corticosteroid therapy for HELLP syndrome. Obstet Gynecol
2004;104:l0l l-4.
29. Sibai BM, Barton JR. Dexamethasone to improve maternal outcome in women with
hemolysis, elevated liver enzymes, and low platelets syndrome. Am J Obstet Gynecol
2005; I 93:1 587-90.
65
 ABRUPTIO PLACENTA Hypertensive diseases ir p

placenta. However. the ser er:t'.

Definition the incidence of abruption

Abruptio placenta is defined as premature separation of a normally implanted Table 1. Evidence and Streng:r ,:'
placenta. Approximately 0.5-1% of all pregnancies are complicated by abruptio Placenta Based on Published Sl-: :,
placenta. Abruption may be "revealed," in which case blood tracks between the Itisk liactors
membranes and the decidua, and escapes through the cervix into the vagina. The Chronic h1'pcrtension

less common "concealed" abruption occurs when blood accumulates behind the Mild and Scrc'rc I't'cee lrtttl"
placenta, with no obvious external bleeding. Total abruption involves the entire Chronic hypct'tcnsion u ith P:.'.
relalive risk; Oll. -,
placenta, in which case it typically leads to fetal death, while in partial abruption, RR, {rc,1.1\ ..
stutlies. lleprinte d.fi'ortt L .'. :

only a portion of the placenta is detached from the uterirre wall. G.l'n c. ( I ),q-l' t J r h.t t, r -
) t L t t t

There are no randomized controlled studies that have specifically 1.i14tin1 1111 ll illi,ttttt a li - :

studied abruptio placenta. Majority of the studies published in English are

observational (i.e. cohort, case-control, or case series). Most large sttrdies
Clinical Presentation
with abruptio placenta have examined the risk factors for this condition.
Studies dealing on management strategies for abruptio placenta are usually
The clinical presettt.rti. -
limited by srnall sample size. The levels of available evidence for the
asymptomatic cases to tll. s-
diagnosis and management of abruptio placenta are mostly II-l,lI-2, and
morbidity. The classicalll d:s:
III. There are rto trials to assess any intervention for prevention of abruptio
bleeding and abdorninal p;::r
placenta or its comPlications.
bleeding occurs itt tlte sec.'n: :
It is also possible to har e :
Clinical Importance
these signs. The amount ol r a.
abruption. The set'erit1 oi sr ::'
Abruptio placenta has a wide spectrum of clinical significance, varying
whether it is revealed or ;.'r,
from cases with rninor bleeding and little or Ilo consequences, to massive
correlation between the ertei-.:
abruption leadiug to fetal death and severe maternal morbidity.
with stillbirtlt occurrinc, itt rrti.:
The maternal effect of abruptio placenta depends primarily on its severity,
separation.
whereas its effect on tlre fetus is determined both by its severity and the
Typically. there is trterit.;
gestatiopal age at which it occurs. Maternal complications include antepartum
amplitude uterine contracl i.-:..
and postparturn hernorrhage, disserninated intravascular coagulation (DIC) and
on palpation. Backache ntar i.
acute renal failure, need for blood transfusions, hysterectotny, and less
location is posterior. There r':
commonly, maternal death. Fetal complications include a high perinatal
mortality, preterm delivery, fetal hypoxia and/or exsanguination, and growth than 50% of the placenta h:s
restriction. abruptio placenta ma) occur '.
This high perinatal mortality is largely due to preterm delivery, because evidence of abruptio placent" :

approximately one half of the excess perinatal deaths are associated with early asymptomatic patients. F i rral 11.

deiivery. Abrr-rptio placenta may be irnplicated in up to l0% of preterm births. labor.

Althougft abruptio placenta is an important cause of spontaneous preterm A variety of fetal heart r::,
birth, it is also often an indication for iatrogenic preterm delivery. Premature abruptio placenta. Tltere n.:. :
separation of the placenta before delivery may deprive the fetus of oxygen variability, bradycardia. trr 3 : l
and nutrition, leadilg to long-term haldicap among survivors. in cases ofconcealed abrupt.-:

66
PLACBNTA
rture separation of a normally implanted
resnancies are complicated by abruptio
in *hich case blood tracks between the
through tlre cervix into the vagina. The
lrs l'hen blood accurnulates behind the
ing. Total abruption involves the entire
:o t'etaldeath, while in partial abruption,
ed from the uterirre wall.
,lied studies that have specifically
ithe studies published in English are
ll. or case series). Most Iarge studies
d rhe risk factors for this condition.
gies for abruptio placenta are usually
er els of available evidence for the
ic placenta are mostly II-1, II-2, and
terr ention for prevention of abruptio
t:;in of clirrical significance, varying
ii::.e or no consequences, to massive
e::- lnatenlal rnorbidity.
r::a depends primarily on its severity,
ei-:ined both by its severity and the
r-,. cornpl ications include antepartum
R; rtravascular coagulation (DIC) and
r" .iusions, hysterectomy, and less
n: :;ations include a high perinatal
ri" :rd/or exsanguination, and growth
g: -. due to preterm delivery, because
n- ':.rl deaths are associated with early
l--,::d in up to l0% of preterrn births.
!F' -:,ilrt cause of spontaneous preterm
i:- - -enic preterm delivery. Premature
FR:_. lav deprive the fetus of oxygen
!r: :ap among survivors.
I 67
Hypertensive diseases in pregnancy are strongly associated with abruptio
placenta. However, the severity of hypertension does not necessarily correlate with
the incidence of abruption.
Tabte l. Evidence and Strength of Association Linking Major Risk Factors with Abruptio
Placenta Based on Published Studies
[{isk f]actols Stlength ol'ljviclcnce lll{ ot OI{
Chronic hypcrlcnsion ++ 1.8 ,, 5.1
Mild and Scvcrc Procclampsia +1 0 .1 -.1.5
Chronic h1'pcrtcnsion rvith Precclarnpsia l+l 7.lt
'fhese e.stinrctlc.s ure llrc ranges o./'llR or Ol?.[otnd in itttlelrcntlent
RR, relative risk; Ol?, odd,s rcttio.
studies. Reprinted.front I'eo L.,lnanth(.'L', I'inlzileos,lIl. l)lucentol uhrrqtlion. ln: Sc'iurro.J, editor.
Ovnecology'and r.>bstetrics. tr'ol 2. tlcrgerstov'n (l'lD1 Lippincott, Il'illiams & lL"ilkins: 2003. iC) 2003
Lippincott ll'i I liams & ll'ilkins.
Clinical Presentation
The clinical presentatiorr of abruptio placenta varies widely from totally
asymptomatic cases to those where there is fetal death rvith severe maternal
morbidity. The classically described symptoms of abrLrptio placenta are vaginal
bleeding and abdominal pain. Abruptio placenta must be considered wltenever
bleeding occurs in the second halfofpregnancy.
It is also possible to have severe abruptio placenta without or just of one of
these signs. The amount of vaginal bleeding correlates poorly with the degree of
abruption. The severity of symptoms depends on the location of the abruption,
whether it is revealed or concealed, and the degree of abruption. There is a
correlation between the extent of placental separation and the risk of stillbinh,
with stillbirth occurring in most cases in which there is greater than 50% placental
separation.
Typically, there is uterine hypertonus with associated high-frequency. low-
amplitude uterine contractions. The uterus is frequently tender and may feel hard
on palpation. Backache may be tlre only symptom, especially when the placental
location is posterior. There rnay be acute fetal distress, and in cases rvhere more
than 50o/o of the placenta has separated, fetal demise. Rarely fetal death due to
abruptio placenta may occur with no other symptoms or signs. In some cases,
evidence of abruptio placenta may be found on ultrasonographic examination of
asymptomatic patients. Finally, abruptio placenta may present as idiopathic preterm
labor.
A variety of fetal heaft rate patterns have been described in association with
abruptio placenta. There may be recurrent late or variable decelerations, reduced
variability, bradycardia, or a sinusoidalfetal heart rate pattern. More infrequently,
in cases of concealed abruption associated with fetal death, the first clinical sign
le :;sult of DIC. In addition, there may
ca.._' proceeds fairly rapidly in cases of
I a:..rciated with acute tubular necrosis
r:: and renal failure.
rue primarily on clinical presentation.
r.rc: of the placenta has separated and
presentation is the presence of painful
gir red vaginal bleeding after the 20th
r t rn€fl with abruptio placenta are the
r.n - reassuri n g testing (60%),'ut'erine-
uterine contractions >5 / l0 minutes
l0: : of abruptio placenta present with
presenting sign is fetal death. Severity
ickll the woman is seen following
ocd of extensive separation causing
rintaining a high index of suspicion
; ol shock is warranted.
o "afl I pregnant patient with vaginal
;ation of the placenta. Before a pelvic
ultrasonographic examination should
ng out other causes of third trimester
ram seems to show an abruPtion, the
ruptio placenta is extremely high.
)es not rule out an abruptio placenta.
I findings are confusing, magnetic
er define the location of the placenta
ognosis in abruptio placenta. Nyberg
rf 69 cases of abruptio placenta, found
he ultrasonographically estimated
location, with the worst prognosis
; all causes of abdominal pain and
append icitis, urinary tract infections,
'ian pathology, and muscular pain.
usefulness in the diagnosis of abruptio
sed to rule out abruptio placenta, nor
does a positive test necessarily confirm it. However, a)(Teihauer-Betke test
allows quantification of feto-maternal transfusion to guide dosing of Rh-immune
globulin in Rh-negative women.
Classification
Class I -mildest type,48Yo
l. No vaginal bleeding to mild bleeding
2. Slightly tender uterus
3. Normal maternal blood pressure (Bp) and heart rate (HR)
4. No coagulopathy
5. No fetal distress
Class 2 - moderate, 27o/o
l. No vaginal bleeding to mild bleeding
2. Moderate to severe uterine tenderness with possible tetanic contractions
3. Maternal tachycardia with orthostatic changes in Bp and HR
4. Fetal distress
5. Low fibrinogen levels present
Class 3 -severe,24o/o
l. No vaginal bleeding to heavy bleeding
2. Yery painful tetanic uterus
3. Maternal shock
4. Coagulopathy
5. Fetal death
Management
The goals in the management of abruptio placenta are to assess, controland
restore the amount of blood lost and to deliver a viable infant to prevent coagulation
disorders. History, physical examination, laboratory and ultrasonographic studies
guide management.
Admission is required if abruptio placenta is considered. The following should
be performed once it is diagnosed:
L Obtain intravenous access using 2 large-bore lV lines.
2. Institute crystalloid resuscitation.
3. Begin external fetal monitoring for both fetal heart rate and contractions.
4. Type and cross-match blood.
5. Foley catheter should be placed and the hourly urine output should be
monitored closely.
 6' Begin blood transfusion if patient is hemodynamically unstable
after The mode of deliverl, is dep,
fluid resuscitation. and the fetus:
7. Correct coagulopatlry. l In most cases, for mild :
8. Administer Rh immune globulin if patient is Rh_negative. fetal compromise-r asina

The management of abruptio pracenta depends on the presentation,

2. Moderate abruption 1lad
the delivery typicalll. br ceso
gestatio'al age, and the degree of maternal and fetal compromise.
presentation is widely variable, it is important
Because the 3. Severe abruption (grade _l
to individ ualize management on is indicated if patient is s
a case-by-case basis. More aggressive management,
desirable in cases of severe In cases ofsevere abruption r
I
abruption, may not be appropriate in mildei of abruption. long as the mother is stable. i:
"ur", is at or near
Prornpt delivery is indicated if the pregnancy
term. The main traindications, to allon the parie:
question is whether vaginal delivery can be achieved without
fetal or maternal is contracting vigorouslr. and ..::.
death or severe morbidity. In cases in which there is evidence
of fetal Amniotomy is frequenrl-r s,-
comprornise and delivery is not imminent, cesarean delivery
should be proven to decrease bleedjn: :
performed promptly, because total placental detachment
could occur without thromboplastin into the matei"
warning.
rupture of the membr-ancs n-ti-r r:
whe' both maternal and fetal status are reassuring, conservative sac may facilitate cerr ical dilar:::
management, with the goar of vaginar derivery, is reasonabre.
Labor, if Oxytocin is given in standa:l
established, should be allowed to progress, otlrerwise induction
of labor should no previous uterine surgen anj ::
be considered. Both mother and fetus should be monitored
closely during labor. noted. There is no evidence rha: .
Should the fetal heart rate tracing becorne non-reassuring,
witir brady-cardia, entry of thromboplastin into rhe i,:
loss of variability, or persistent Iate decererations, promptlesarean
derivery is There is a significanr risk of ;:,
indicated. Sirnilarly, slrould maternal compromisr o."ur,
the fetus should be access should be established and bi
delivered promptly.
aggressively. Meticulous amenriri
However, if <34 weeks, expectant managemert for mird (grade
l ) abruption clinicians frequently underestintar.
may allow tirne for glucocorticoid administration. Maternal
oifetal compromise It is prudent to involve an ane
necessitates delivery. A decision to delivery interval
of <l:20 minutes is labor does not progress rapidll.
associated with a substantial reduction in neonatal morbidity
and mortality in disproportion, fetal malpresentat io r
cases of fetal bradycardia. when there is partial abruptio
placenta and the delivery may be necessar\ to arri:
maternal arrd fetal status are reassuring, the patient may
be managed Bleeding from surgical rncisr:
conservatively. Preterm birth is the leading cause of perinatal
death in women control, and it is important ttr Sr3i.
with abruptio placenta, and to optimize perinatar ort.o*.r, it
is desirable, if derangement during surqen. _{tre: :
pos.sible, to prolong gestation. However, it cannot
be overemphasized that these with particular attention paid r,. r :::
patients require extremely close monitoring, because
there is a signifibant risk In addition, the uterus should be ..b*
of fetal death. In cases where the gestational age is between
24 and34 weeks, and is not increasing in size. anc
steroids should be administered to promote fetaliung
maturation. patients should uterus may be hypotonic. and occa-
be delivered in a center with adequate neonatal facilities
and the parents should should be drawn for complete bl..i j
be counseled by a neonatologist regarding potential
treatments and outcomes intervals untilthe patient is stable t
for the neonate. Prolonged hospitarization and monitoring
rnay be necessary. It associated with severe preec Iarr,i.
may be possible to discharge these patients to outpatient
management if the may be normotensive due to hr o_-.,
fetal status is reassuring once they have remained stable
for severar davs. suspicion for severe preeclarnpsi: .

from an obvious cause such as lr3.j

70
l: : hemodynamically unstable after
if ::rtient is Rh-negative.
m:' Jepends on the presentation, the
ce- :,rd fetal compromise. Because the
tr:.1;rt to individualize management on
m::er.nent, desirable in cases of severe
Jd:: cases of abruption.
re-:rancy is at or near term. The main
be :chieved without fetalor maternal
n ,ihich there is evidence of fetal
i:.:irt. cesarean delivery should be
mi:l detachment could occur without
la:r-is ere reassuring, conservative
rl Jelivery, is reasonable. Labor, if
is- rtherwise induction of labor should
,u lJ be monitored closely during labor.
rn3 non-reassuring, with bradycardia,
l!e :atior.rs, prompt cesarean delivery is
:r:.promise occur, the fetus should be
rna{ernent for mild (grade I ) abruption
str.rtion. Maternal or fetal compromise
:1.',err interval of <l: 20 minutes is
;'i neonatal morbidity and mortality in
:) partial abruptio placenta and the
r.:tg. the patient may be managed
in_::ause of perinatal death in women
perinatal outcomes, it is desirable, if
it ;annot be overemphasized that these
'ins. because there is a signifibant risk
lrral age is between 24 and 34 weeks,
e tetal lung maturation. Patients should
rlrl3tal facilities and the parents should
n: potential treatments and outcomes
rn endrnonitoring rnay be necessary. It
ents to outpatient management if the
rernained stable for several days.
The mode of delivery is dependent primarily on the condition of the mother
and the fetus:
l. In most cases, for mild abruption (grade I), no evidence of maternal or
fetal compromise-vaginal delivery is indicated.
2. Moderate abruption (grade 2) evidence of fetal non-reassuring testing-rapid
delivery typically by cesarean is indicated.
3. Severe abruption (grade 3), fetal demise, often with DIC - vaginal delivery
is indicated if patient is stable.
In cases of severe abruption with fetal death, regardless of gestational age, as
long as the mother is stable, it is reasonable, in the absence of other con-
traindications, to allow the patient to have a vaginal delivery. Typically, the uterus
is contracting vigorously, and labor rapidly progresses.
Amniotomy is frequently sufficient to speed up delivery. Amniotomy is not
proven to decrease bleeding from spiral arteries and reduce the entry of
thromboplastin into the maternal circulation. If the fetus is reasonably mature,
rupture of the membranes may hasten delivery. If the fetus is immature, the intact
sac may facilitate cervical dilatation.
Oxytocin is given in standard doses to effect vaginal delivery if there has been
no previous uterine surgery and there are no rhythmic superimposed contractions
noted. There is no evidence that oxytocin might predispose to DIC by enhancing
entry of thromboplastin into the maternal circulation.
There is a significant risk of coagulopathy and hypovolemic shock. Intravenous
access should be established and blood and coagulation factors should be replaced
aggressively. Meticulous attention should be paid the amount of blood loss;
clinicians frequently underestimate this.
It is prudent to involve an anesthesiologist in the patient's care early. when
labor does not progress rapidly, and in cases in which there is feto-pelvic
disproportion, fetal malpresentation, or a prior classical cesarean delivery cesarean
delivery may be necessary to avoid worsening of the coagulopathy.
Bleeding from surgical incisions in the presence of DIC may be difficult to
control, and it is important to stabilize the patient and to correct any coagulation
derangement during surgery. After delivery the patient should be monitored closely,
with particular attention paid to vital signs, amount of blood loss, and urine output.
In addition, the uterus should be observed closely to ensure that it remains contracted
and is not increasing in size, and blood loss should be monitored closely. The
uterus may be hypotonic, and occasionally hysterectomy may be necessary. Blood
should be drawn for complete blood count (CBC) and coagulation studies at regular
intervals until the patient is stable. Finally, s,6me cases of abruptio placenta may be
associated with severe preeclampsia, which may be masked because the patient
may be normotensive due to hypovolemia. Thus, there should be a high index of
suspicion for severe preeclampsia in patients with abruptio placenta not resulting
from an obvious cause such as trauma or cocaine use. In such cases, the patients
7l
may benefit from close volume status monitoring, early recognition of hypovolemia,
and adequate blood replacement
The extensive extravasation of blood into the uterine musculature, a condition __v
t_
known as Couvelaire's uterus, seldom interferes with myometrial contractions to t-'"'"'"
I -Al rC a a

cause atony. It is not an indication for hysterectomy.

_[_
Tocolysis [-n""ttut,*
I f"tul statrs
It is generally taught that tocolytics, especially sympathomimetics such as
I
i

terbutaline, are contraindicated in the presence of vaginal bleeding, because side

effects such as tachycardia could mask the clinical signs of blood loss. However, a
few retrospective cohort and case-control studies have evaluated the use of t
a-.----- --
tocolytics fincluding syrnpathomimetics) in the presence of bleeding in the second
half of pregnancy, including patients with suspected stable abruptio placenta before
35 weeks gestation. Based on these repofts tocolytics may be used in caution in
stable women remote from term. A
Most cases of abruptio placenta cannot be predicted or prevented. Howevel
in some cases, maternal and infant outcomes can be optimized through attention to
the risks and benefits of conservative management, ongoing evaluation of fetal
and maternal well-being, and through expeditious delivery where appropriate.
Algorithm for the management of abruptio placenta in term or near term (A)
Fet!s airvc
and preierm births (B). In all cases, CBC and coagulation indices should be checked; less :har. 2:
blood or blood volume should be replaced; coagulopathy should be corrected; and lveeks
intake, output, and renal function should be monitored.a

References

l. Obstetric evidence based guidelines by Vincenzo Berghella, 2007|'p 193-200.

2. Cunningham L, et. al. Williams Obstetrics, 23'd edition, 20 l0; p 761-769' I Stabie
3. Neilson JP. Interventions for treating placental abruption. Cochrane Database Syst
Rev 2009. I
I

4. Oyelese ! Ananth CV. Placental abruption. Obstet Gynecol 2006;108:1005-1016.(

l

5. Birnischke K, Kaufmann P. Pathology of the human placenta. 4th ed. New York (NY):
Springer; 2000. Mane;:
6. SalleiON Jr, Nagey DA, Pupkin MJ, Crenshaw MC Jr. Tocolysis in the management w; r>gr Yd. !:

of third trimester bleeding. J Perinatol 1990;10:125-8.

7. Towers cv Pircon RA, Heppard M. ls tocolysis safe in the management of third-
trimester bleeding? Am J Obstet Gynecol 1999;180:1572-8.
8. Ananth CV Berkowitz GS, Savitz DA, Lapinski RH. Placental abruption and adverse
perinatal outcomes. JAMA 1999;282: 1646-51.
9. i.,lyberg DA, Cyr DR, Mack LA, Wilson DA, Shuman WP' Sonographic spectrum of
placental abruption. AJR Am J Roentgenol 1987;148:l6l-4.
10. blantz C, Purnell L. Clinical utility of sonography in the diagnosis and treatment of
placental abruption. J U I t r a s ou n d lr4 e d 2002;21 :837 40.

72
toring, early recognition of hypovolemia,

into the uterine musculature, a condition

:erferes with myometrial contractions to
sterectomy.

. especially sympathomimetics such as

)senceofvaginal bleeding, because side
: clinical signs of blood loss. However, a lFa lure lc trogress
stable rncther
trol studies have evaluated the use of
in the presence of bleeding in the second
Lu'
;uspected stable abruptio placenta before
rrts tocolytics may be used in caution in
A
not be predicted or prevented. However, rl
il

1es can be optimized through attention to l

,anagement, ongoing evaluation of fetal I

I
xditious delivery where appropriate.
ruptio placenta in term or near term (A)
Fetus alive Fetus alive
nd coagulation indices should be checked;
less than 24
J: coagulopathy should be corrected; and weeks
be monitored.a

r Vincenzo Berghella, 2007 p 193-200.

trics. 23'd edition, 2010; p 761-769. Reassurrrig felal
placental abruption. Cochrane Database Syst stalus
Slaole mother
prion. Obstet Gynecol 2006;l 08:l 005-1016.(
oithe human placenta. 4th ed. New York (NY):
Manage
Crenshaw MC Jr. Tocolysis in the management conservatlvely
i I s90;1 0: I 25-8.
ls tocolysis safe in the management of third-
;r/ 1999;I80:1572*8.
,. Lapinski RH. Placental abruption and adverse Give steroids
Tocolytics as indrcated
l6-16 5l .
Closely monitor fetus and mother
DA, Shuman WP. Sonographic spectrum of Monthly growth ultrasonograms
".n
:e nc, l 1987 i| 48: l 6 l -4.
'f sonography in the diagnosis and treatment of
;1002:21 :83740.

IJ
 APPENDIX
LEVELS OF EVIDENCE AND GRADES OF RECOMMENDATION

LEVEL DEFINITIOhI

Evidence obtained from at least one properly randomized controlled

trial
Evidence obtained from well-designed controlled trials without
I
I il-1
randomization
l
Evidence obtained from well-designed cohort or case-control
l II-2 analytic studies, preferably from more than one center or research
group.

Evidence obtained from multiple time series with or without the

II-3 intervention.

Opinions of respected authorities, based on clinical experience

ru descriptive studies and case reports or reports of expert committees

GRADE DEFINITION

There is good evidence to support the recommendation of the

A practice in the management of hypertensive complications of
pregnancy.

There is fair evidence to suppofi the recommendation of the practice

B
in the management of hypertensive complications of pregnancy.
There is insufficient evidence to recommend for or against the
C
inclusion of the practice in the management of hypertensive
compl ications of pregnancy.

There is fair evidence to support the recommendation that the

D practice be excluded in the management of hypertensive
compl ications of pregnancy.

There is good evidence to support the recommendation that the

E practice be excluded in the management of hypertensive
complications of pregnancy.

A good practice point (GPP) is a recommendation for best practice

GPP
based on the experience ofthe Task Force

74