Philippine Society of
Maternal Fetal Medicine (PSMFM), Inc.
A Recognized Affiliate Subspecialty Society of the
Philippine Obstetrical and Gynecological Society (POGS)
BEST PRACTICE RECOMMENDATIONS
ON
PRELABOR RUPTURE OF MEMBRANES
Third Edition
November 2019
Task Force on the Prelabor Rupture of :�1�1 11;�:5 J7',
Best Practice Recommendations on
Prelabor Rupture of Membranes (PROM)
2019
3 rd Edition
TASK FORCE COMMITTEE
Editors in Chief Leah Rivera, MD
Gumersinda C. Javier, MD
Associate Editor: Ma. Cristina Crisologo, MD
Business Manager: Carmela G. Madrigal-Dy, MD
Technical StaffAssistance: Jonnalyn B. Cadion
Members:
Maria Luisa S. Acu, MD Marie Cathleen P. Santiago, MD
Ma. Cristina P. Crisologo, MD Joselito A. Santiago, MD
Carmela G. Madrigal Dy, MD Marjorie I. Santos, MD
Ramon M. Gonzales, MD Emerson D. Tan, MD
Richard Jordias, MD Angelita R. Teotico, MD
Jacinto Blas V. Mantaring III, MD Lucia B. Tiangco, MD
Joseph U. Olivar, MD Ma. Victoria V. Torres, MD
Contributors:
Janice Capoquian, MD Adeline Rose T. Escartin, MD
Cielo F. De Guzman, MD June Joanbelle Gabaldon-Las, MD
Nina Nonette P. Diansuy, MD P aula P. Tolentino-Orlina, MD
Carmela Ann Santos Encabo MD Jacqueline P. Pedroso, MD
PLENARY REVIEWERS
Anna Konsuelo Chua, MD Dazelie Dianne Galagnara, MD
Ma. Cresilda Sabularce, MD Gail A. Bailon, MD
Jan Gay! Rodriguez, MD Ethel Anne Lariego, MD
Carmela S. Encabo, MD Catherine Joie Carelle Roux-Ong, MD
Hannah Mia N. Cacanindin, MD Charisse Guerrero, \1D
Kristine S. Sese, MD
vi
PHILIPPINE SOCIETY OF MATERNAL FETAL MEDICINE, INC.
OFFICERS AND BOARD OF DIRECTORS 2019
Richard C. Jordias, MD
President
Marjorie I. Santos, MD
Vice-President
Maria Estrella Y. Flores, MD
Secretary
Kristine S. Sese, MD
Assistant Secretary
Carmela Madrigal-Dy, MD
Treasurer
Sherri Ann L. Suplido, MD
Assistant Treasurer
Lucia B. Tiangco, MD
PR.O.
Board Members
Catherine Joie Carelle R. Ong, MD
Maria Geraldine Assumption Gavina Torralba, MD
PSMFM REGIONAL COORDINATORS
Region I: Northern Luzon: Christine A. Aguilar, MD
CAR: Cordillera Administrative Region: Andrea Milagros Mapili, MD
Region II: Cagayan Valley: Grace Marie M. Marcos, MD
Region III: Central Luzon: Maellen Joye A. Saldua, MD
Region IV-A: CALABARZON: Julieta A. Villanueva, MD
Region IV-B: MIMAROPA: Marie Scent F. Benedicto, MD
Region V: Bicol: Josephine D. Sanchez
Region VI: Western Visayas: Ma. Ana P. Ausan, MD
Region VII: Central Visayas: Marie Antoniette Joanna P.Mendoza, MD
Region X: Northern Mindanao: Dayres D. Relliquete, MD
Region XI: Southern Mindanao: Dennis John Ortiga, MD
Region XII: Central Mindanao: Alona P. Manangan, MD
Region XIII: Caraga: Kathleen Grace C. Gamotan, MD
ARMM: Autonomous Region in Muslim Mindanao: Potre Mairasna P. Boransing, MD
vii
TABLE OF CONTENTS
CHAPTE R
Grading of the Evidence............................................................. ...... ...
I. . l ...
II. Epidemiology ..................... ....................................................................... 2
Joseph U. Olivar, MD, FPOGS, FPSMFM
June Joanbelle Gabaldon-Las, MD, FPOGS
m. Pathopbysiolog y of PPROM ................................................................... 4
Maria Luisa S. Acu, MD
IV. Diagnostics and Surveillance
IV. l Diagnosis of PROM...................................................................... 16
Marjorie I. Santos, MD
IV.2 Maternal Monitoring ................................................................... 26
Angelita R. Teotico, MD
IV.3 Anterpartum Surveillance........................................................... 36
Ramon M. Gonzales, MD
Paula P. Tolentino-Orlina, MD
V. Management Interventions
V. l Magnesium Sulfate ...................................... ............................;.... 48
Marie Cathleen P. Santiago, MD
.
V.2 Antenatal Corticosteroids......................................................... .. 53
Leah Socorro N. Rivera, MD
Jacqueline Pedroso, MD
.
�tibiotic Therapy in PROM ................................................ .... 62
V.3
armela Madrigal-Dy, MD
V.4 GBS in PPROM Patients 66
.............................................................
Jo_se/ito A. Santiago, MD
Nina Nanette P. Dia
nsuy, MD
viii
V.5 Tocolysis in PPROM .................................................................... 71
Gumersinda C. Javier, MD, Cielo F de Guzman, MD and
Janice C. Capoquian, MD
V.6 Amnioinfusion .............................................................................. 78
Ma. Cristina Pelaez-Crisologo, MD
V.7 Progesterone Use .......................................................................... 82
Joselito A. Santiago, MD
VI. Management According to AOG
VI. I Term Prelabor Rupture of Membranes ..................................... 84
Emerson D. Tan, MD
Carmela Ann Santos Encabo, MD
VI.2 Late Preterm Prelabor Rupture of Membranes........................ 89
Lucia B. Tiangco, MD
VI.3 Periviable Prelabor Rupture of Membranes ............................. 93
Lucia B. Tiangco, MD
VI.4 Previable Preterm Prelabor Rupture of Membranes ............. 100
Lucia B. Tiangco, MD
VII. Intrapartum Management .................................................................. 103
Richard C. Jordias, MD
VIII. Special Situations .................................................................................. 110
Ma. Victoria S. Valmonte-Torres, MD
Adeline Rose T. Escartin, MD
IX. Neonatal Outcomes .............................................................................. 122
Jacinto Blas V Mantaring III, MD
X. PREVENTION OF PPROM ............................................................... 125
Ma. Cristina P Crisologo, MD
ix
CHAPTER 3 PATHOPHYSIOLOGY OF PRETE
PRELABOR RUPTURE OF MEMB
Statements:
I. The etiology of preterm prelabor rupture of membrane (PPROM )
is complex and multifactorial. ln any given patient, one or more
pathophysiologic processes may be evident.
2. A number of clinical risk factors for PPROM have been identified and
they cause PPROM through different pathways.
3. A major etiologic factor contributing to the pathogenesis of PPROM
is infection in the lower reproductive tract, and it triggers a "host
inflammatory response" involving activation of a multifaceted and
multistep pathway. This pathway is characterized by incre ased
production of cytokines and matrix metalloproteinases (MMPs) and
decreased function of the tissue inhibitors of metalloproteinases
(TIMPs), that ultimately leads to weakening and eventual rupture of
the fetal membranes.
4. Evidence suggests that there may be a genetic susceptibility to PPROM
and that genetic and environmental elements are important cofactors in
its development.
5. PPROM has been considered a disease of the fetal membranes.
6. Latest molecular studies reveal that the inflammation-oxidative
stress axis has a major role in causing rupture of the membranes.
Pathologic activation of oxidative stress leads to senescence, membrane
microfractures, sterile inflammation, membrane dysfunction, loss or
reduction in microbial defense capacity culminating in membrane
weakening and PPROM.
Preterm prelabor rupture of membranes (PP ROM) refers to rupture
of the membranes before uterine contractions begin in pregnancies les s
than 37 weeks age of gestation (AOG). It is the single most common fa ctor
2
identified with preterm birth and precedes 40 - 50 % of all preterm births.1-
PPROM complicates up to 3 - 4 percent of pregnancies, wit h 0.5 %
s
occurring in< 27 weeks, I % in 27 to 34 weeks, and I % in 34 to 36 week
and 6 days.3• •
45
4
v di tinctivc a sociation with PPR
n· k factors tho e ' ith a.
Amo ng th e h. . tcd OM, gent• ta1 tract t. nfe o�
. g. a pre io .
u pregna ncy with PPR ct·ton
are the follo win ._ an d cigare tte moking.1
g,
antepartum. bleedin
• Prcviou PPRO M
n on Study conducted by the Na tio
n the Pre Ie n Pre dicti
. 8a ed o lth and Hum an Developm�nt (N I C �D) Maternal-Feta
na 1
In.ututc of C hild Hea
. e Unit . Network, there is a threefold mcrease m the frequenc l
M edicm · . . y of
. vious PPROM compared to thos e
. without (l 3 . 5
PPROM 10 wom en w1111 pre
2.1-5.2). Many other studies have reporta.1
ersus 4.1%,. RR 3 · 3'95¾0CI "�
. .
1 m1lar fin d'mg , wi'th
32¾O as highest reported recurrence rate of PPROM
• Genital tract infection
Genital tract infection i the single most common identifiable risk factor
for PPROM. Epidemiologic studies have_ sho� the foll_o�ing �vidences:
1) Presence of pathologic orgamsms m the amniotic fluid are more
likely in women with ruptured membranes than those with intact
membranes
2) Hi tologic chorioamnionitis is more common in women with
PPROM
3) Genital tract infections, particularly bacterial vaginosis, are more
frequently found in women with PPROM.5
Microorg ani m in the vaginal flora are capable of producing
pho. pholipase , which can cau e the production of prostaglandins which can
then timu late uterine contractions. Some of these bacteria are able invade the
endocervix and fetal membrane triggering the host's genetically detennined
immune re ponse which involves the production of sever inflam atory
al m
mediators that weaken the fetal membranes, even
tually caus ing PPROM.9
• Antepartum bleeding
. �aginal bleeding in the first trime ter is correlated with a m inim al but
St8ti ttcally ignificant inc
rea e in the risk of P PROM.5
!here i an increase ofthree to seven
bleeding occurs in mor times the risk of PPROM is vaginal
e than one lrimc ler..
,o."
Placental abru t'on
. · P i account fo 0- 5% of PP
Produced in abruption-re1ated v . r 1 1 ROM · The throlll b'tn
agmal bleeding bind to dec idual proteases•
- 6
. e contraction s who require transfer
Women with PPROM with regul uterin
.
to a tertiary hosp1taI or antenatal cort1co � stero1·ds may be con sidered. for a short
. . lytic agents in women w ith PPROM
course of tocolysis . The benefit o� g1v1�g toc
_ �io nitis when con sidering antenatal
may outweigh. the risk of developing c n
.
. ;
er to a 1ac1 ty� l �
1 ''" th appropriate neo natal intensive
steroids adm1m · or n-ansf
strat1on
. . .
"l
. n ne eds to be carefully thought of m the
care equipment..HO\\,ever' .this. dec1s1o .
.
i fe ctio which at t im es m ay only
setting of_ a possi_ble pr�-� xistm!:tra teri e n n n
;n ofchorioam nionitis, delayin g delive
present with utenne act1V1ty. In se g ry
. by tocolys1s _ admi·rn·stration could lead to adverse
from an I�tiected envir· o.nment.
effects smce an association h as been found between intrauteri n e i n fection,
. . .
. ts
pro taglandm and cytoleine release and delivery. In this situatio n , toco 1ys1s n ot
recommended. 7
oue,.,tio n No. 2: How long should tocolytic a gents be used in PPROM to
prolong pregnancy?
Recommendation: Tocolytic agents should be given for 48 hours to allow for
completion of corticosteroids.
Quality of Evidence: +
Strength of Recommendation: Weak
Summary of Evidence:
In 2014, a Cochrane database analysis of tocolytics in PPROM was done
which included 8 studies and 408 women. Seven ofstudies compared tocolysis
versus no tocolysis. Tocolysis was found to be associated with longer latency
and
fewer births within 48 hours and seven days compared to no tocolysis.
Tocolysis
was also associated with an Apgar less than seven at five minute
s and higher
incidence of neonates requiring ventilation. Tocolysis also i
ncreased incide nce of
chorioa.mnionitis. However, antibiotics and corticostero
ids (which are both part
of standard care) were not consistently administe
red in the studies.8
In a retrospective study done by Phupong
and Khulmala in 2015, 23 l women
with PPROM between 28 and 34 weeks
were either given tocolysis or not, in the
form of terbutaline based on the disc
retion ofthe attending physician. It tried to
determine the factors associated with
prolonged latency periods in preterm pre abor
rupture ?f membrane (PPROM) l
. Among the factors, it noted
resulted 1_n a latenc� period of tha t toc olytics
e" 2 days with adjusted ORs
6.02� �hich established the sho of2.74 (98%CI 1.25·
rt-term benefit of48 hours
providmg enough time for with use oftocolysis,
corticosteroid administra
tion and fetal Jung maturity.'
72
V.6 Amnioinfusion
la. Cristina Peiaa-Cri.sologo. MD. FPOGS, FPSMFJ,
Definition of Terms:
Amnioinfusion: refers to the instillation of fluid into the amniotic cavity, via
either the transabdominal or transcervical route. 1
Oligohydramnios in preterm fetuses is a poor prognosticating factor
for pnhnonary bypopl.asia Restoring amniotic fluid to adequate levels may
theoretically lead to better perinatal outcomes, by means of amnioinfusion (AI).
For preterm pregnancies where prolongation of the gestation is endeavored,
the ultrasound-guided transabdominal approach has been favored The clinical
questions in 1his chapter will consider oligohydramnios only as a result ofpretenn
rupture of membranes, whether preterm or term.
There is no evidence to support the use of"prophylactic" amnioinfusion as
a routine procedure after the diagnosis of PROM if there is normohydramnios.
Question No. 1: Can amnioinfusion be used in PPROM patients with
oligo'h dramnios to impro e maternal and infant outcomes in pregnancies
24-33 weeks gest.ationa1 age?
Recommendation: Among women with preterm prelabor rupture ofmembranes
beyond 26 w.eeks amnioinfusion may be performed with caution.
Quality of Evidence: +
Strength of Recommendation: Weak
Sammaf')' .of Evidence:
ln PPROM patients with documented oligohydramnios, earlier studie s2 have
shown potential benefit for amnioinfusion when, after Al, there is documented
increase in amniotic fluid levels such that by sonologic assessment, a single vertical
pocket i.s greater than 2cm; these pregnancies reported better perinatal outc?rne!
and lower pulmonary bypoplasia rates, compared to those who had pers1sten
oJigobydramnios.
78
