DOI 10.1515/jpm-2013-0078      J. Perinat. Med.
2013; 41(6): 647–649
Opinion paper
Abdul Qader Tahir Ismail* and Soma Lahiri
Management of prelabour rupture of membranes
(PROM) at term
Abstract: Over a 20-month period we identified several
cases of neonatal pneumonia associated with prelabour
rupture of membranes (PROM) at term. PROM complicates
8%–10% of all pregnancies, yet 60% of cases occur at term.
Ascending infection is a contributing factor and the inci-
dence of chorioamnionitis in these patients is relatively
high, especially with prolonged membrane rupture. The
signs and symptoms NICE recommends patients look out
for are not always present as the majority of infections are
subclinical, yet associated maternal and neonatal morbid-
ity of chorioamnionitis is potentially devastating. A survey
of maternity units in the West Midlands reveals significant
variance in management of these cases. Given the lack of
consensus and clear evidence on optimal management of
PROM at term, we believe early detection of developing
infections could be enhanced by using a combination of
investigations (at presentation, 12 and 24 h), as well as cur-
rent advice to self-monitor temperature and vaginal loss.
Keywords: Chorioamnionitis; prelabour rupture of mem-
branes at term.
*Corresponding author: Abdul Qader Tahir Ismail, Department of
Obstetrics and Gynaecology, Walsall Manor Hospital, Moat Road,
Walsall, WS2 9PS, UK, Tel.: +44 1922 721 172,
E-mail: aqt.ismail@bnc.oxon.org
Soma Lahiri: Department of Obstetrics and Gynaecology, Walsall
Manor Hospital, Walsall, UK
Over a 20-month period at Walsall Manor hospital we
received 647 women with prelabour rupture of membranes
(PROM), associated with seven cases of neonatal congeni-
tal pneumonia [of which two had Group B streptococcus
(GBS) positive skin swabs]. PROM ranged from 12 to 45 h
until delivery, either spontaneous, induced, or caesarean
section (for foetal distress). There were no maternal symp-
toms or pyrexia. These cases resulted in the analysis of
whether our management was evidence based.
Current National Institute for Health and Care Excel-
lence (NICE) (UK) guidelines on management of term PROM
recommend 24  h of expectant management followed by
induction [17]. Antibiotics should not be prescribed even
if PROM is prolonged. Women should self-monitor, and
if pyrexial, feeling unwell, or the colour or smell of their
vaginal loss changes/becomes offensive, they should seek
medical attention. A high vaginal swab (HVS) should not
be offered. A telephone survey of the 18 maternity units
in the West Midlands revealed differing practice. Nearly a
third used IV benzyl penicillin to treat women with PROM
of 18–24 h. The other two that routinely used antibiotics
did so at 48 h. Only ten units induced at 24 h, with the rest
varying between offering it at time of ROM to 96 h later. This
reveals a significant discrepancy from NICE guidelines, and
general variance in management of PROM at term.
Therefore, what does the evidence say? PROM compli-
cates 8%–10% of all pregnancies, yet 60% of cases occur
at term [7, 8]; 79%–95% of women will labour spontane-
ously within 12–24 h [6]. Incidence of chorioamnionitis in
these women is 6%–10%, but as high as 40% with pro-
longed rupture ( > 24 h) [19]. Chorioamnionitis is typically
as a result of ascending bacterial infection from the genital
tract, usually in the presence of ruptured membranes, for
which it is considered a contributing factor. The inflam-
matory response results in prostaglandin release, “ripen-
ing” of the cervix, and labour.
Chorioamnionitis can be clinical, or subclinical/
histological, which is defined as tissue infiltration by
neutrophils, macrophages, and lymphocytes, resulting in
clinical signs of inflammation but beginning earlier with
production of chemotactic signals. Therefore absence of
clinical signs does not mean lack of inflammation/infec-
tion. In fact, the majority of cases are subclinical, with
detection of amniotic microbial invasion in 30% of women
with term PROM, lending weight to the theory of a causa-
tive link between the two [19].
Maternal sequelae of chorioamnionitis include
increased risk of caesarean section, wound infection,
bacteraemia, and postpartum haemorrhage [13, 15,
20]. For the baby, prolonged rupture of membranes is a
major risk factor for early onset neonatal sepsis, which,
if untreated, has mortality as high as 50% [3]. Rates of
neonatal infections in PROM is 2%–3%, which is ten times
higher than in normal deliveries but this figure doubles
Unauthenticated
Download Date | 12/29/17 10:41 PM
648      Ismail and Lahiri, Management of PROM at term
in cases of chorioamnionitis [9]. Other neonatal complica-
tions include depressed APGAR scores, IVH, and neonatal
encephalopathy [2, 12, 22].
There is strong evidence linking PROM with chorioam-
nionitis and subsequent neonatal morbidity. A Cochrane
review of trials including patients with PROM but other­
wise uncomplicated pregnancies compared planned to
expectant management and found that women in the
former group had a significantly shorter delay from PROM
to delivery, corresponding to a reduced risk of developing
chorioamnionitis [6]. Secondary analysis showed associa-
tion between longer time periods from membrane rupture
to delivery and a higher incidence of neonatal infection.
Secondary analysis of data from the International Multi-
centre Term Prelabour Rupture of Membranes Study found
duration of active labour to be the strongest independent
predictor of clinical chorioamnionitis [21].
Therefore, patients with PROM at term are at increased
risk of chorioamnionitis. Even with induction at 24 h,
delays occur as a result of obstetric emergencies, patients
refusing induction, and others with prolonged labour. Fur-
thermore, the true burden of disease is hidden due to rela-
tively higher rates of subclinical chorioamnionitis, which
would not be picked up by self-monitoring. The UK does
not have a GBS screening program. Up to a third of women
have vaginal colonisation, which is an independent pre-
dictor for chorioamnionitis [21], and their babies are at a
25 fold higher risk of early onset GBS sepsis [4]. By the time
women deliver, PROM may have exceeded the 18 h stated
References
[1] Aina-Mumuney AJ, Althaus JE, Henderson JL, Blakemore MC,
Johnson EA, Graham EM. Intrapartum electronic fetal monitoring
and the identification of systemic fetal inflammation. J Reprod
Med. 2007;52:762–8.
[2] Alexander JM, McIntire DM, Leveno KJ. Chorioamnionitis and the
prognosis for term infants. Obstet Gynecol. 1999;94:274–8.
[3] Anderson-Berry A, Bellig L, Ohning B. Neonatal sepsis. http://
emedicine.medscape.com/article/978352-overview#a0199.
Accessed September, 2011.
[4] Boyer KM, Gotoff SP. Strategies for chemoprophylaxis of GBS
early-onset infections. Antibiot Chemother. 1985;35:267–80.
[5] Buhimschi CS, Abdel-Razeq S, Cackovic M, Pettker CM,
Dulay AT, Bahtiyar MO, et al. Fetal heart rate monitoring patterns
in women with amniotic fluid proteomic profiles indicative of
inflammation. Am J Perinatol. 2008;25:359–72.
[6] Dare MR, Middleton P, Crowther CA, Flenady VJ, Varatharaju B.
Planned early birth versus expectant management (waiting) for
prelabour rupture of membranes at term (37 weeks or more).
Cochrane Database Syst Rev. 2006;(1):Art. No. CD005302.
DOI: 10.1002/14651858.CD005302.pub2.
in the Royal College of Obstetricians and Gynaecologists
(RCOG) guideline as a risk factor for early onset neonatal
GBS sepsis (2.0–8.7 fold increased risk) [17].
Given the above, what is the “right” answer? Some
units have a policy of routine IV antibiotics once PROM is
prolonged, however, as ROM is in itself an indication for
the presence of infection, is it wise to wait until rupture is
prolonged before intervening? Given the lack of consensus
and clear evidence on optimal management, we believe
early detection of developing infections could be enhanced
by using a combination of investigations along with current
advice to self-monitor temperature and vaginal loss [11, 16].
These would involve a speculum examination at presenta-
tion to verify ROM, high vaginal swab (although not helpful
in the acute setting, results could guide antibiotic therapy
if subsequent neonatal infection develops), blood infection
markers (C-reactive protein and differential white blood cell
counts) [14, 18], observations (heart rate, temperature) [10],
and cardiotocography (CTG) [1, 5]. Relevant investigations
can be repeated at 12 and 24 h when the woman presents
for induction, if she has not yet spontaneously laboured. If
introduction of such guidelines could be shown to reduce
incidence of neonatal infections secondary to chorioam-
nionitis as a result of early detection and appropriate man-
agement, an update to NICE guidelines may ensure a more
uniform management of women with term PROM.
Received April 9, 2013. Accepted May 27, 2013. Previously published
online July 4, 2013.
[7] Duff P. Management of premature rupture of membranes in
term patients. Clin Obstet Gynecol. 1991;34:723–9.
[8] Duff P. Premature rupture of the membranes in term patients.
Semin Perinatol. 1996;20:401–8.
[9] Gerdes JS. Clinicopathologic approach to the diagnosis of
neonatal sepsis. Clin Perinatol. 1991;18:361–81.
[10] Gibbs RS, Duff P. Progress in pathogenesis and management
of clinical intraamniotic infection. Am J Obstet Gynecol.
1991;164:1317–26.
[11] Gilstrap LC 3rd, Cox SM. Acute chorioamnionitis. Obstet
Gynecol Clin North Am. 1989;16:373–9.
[12] Hagberg H, Wennerholm UB, Savman K. Sequelae of chorioam-
nionitis. Curr Opin Infect Dis. 2002;15:301–6.
[13] Hauth JC, Gilstrap LC 3rd, Hankins GD, Connor KD. Term
maternal and neonatal complications of acute chorioam-
nionitis. Obstet Gynecol. 1985;66:59–62.
[14] Lee SY, Park KH, Jeong EH, Oh KJ, Ryu A, Park KU. Relationship
between maternal serum C-reactive protein, funisitis and
early-onset neonatal sepsis. J Korean Med Sci. 2012;27:
674–80.
Unauthenticated
Download Date | 12/29/17 10:41 PM

[15] Mark SP, Croughan-Minihane MS, Kilpatrick SJ. Chorio-
amnionitis and uterine function. Obstet Gynecol.
2000;95:909–12.
[16] Newton ER. Chorioamnionitis and intraamniotic infection. Clin
Obstet Gynecol. 1993;36:795–808.
[17] NICE. Intrapartum care. Secondary intrapartum care 2009.
http://www.nice.org.uk/nicemedia/live/11837/36275/36275.
pdf. Accessed September, 2011.
[18] Popowski T, Goffinet F, Maillard F, Schmitz T, Leroy S,
Kayem G. Maternal markers for detecting early-onset
neonatal infection and chorioamnionitis in cases of premature
rupture of membranes at or after 34 weeks of gestation: a
two-center prospective study. BMC Pregnancy Childbirth.
2011;11:26.
[19] Romero R, Ghidini A, Bahado-Singh R. Premature rupture of the
membranes. Philadelphia: JB Lippincott; 1992.
Ismail and Lahiri, Management of PROM at term      649
[20] Rouse DJ, Landon M, Leveno KJ, Leindecker S, Varner MW,
Caritis SN, et al. The Maternal-Fetal Medicine Units cesarean
registry: chorioamnionitis at term and its duration-relationship
to outcomes. Am J Obstet Gynecol. 2004;191:211–6.
[21] Seaward PG, Hannah ME, Myhr TL, Farine D, Ohlsson A,
Wang EE, et al. International Multicentre Term Prelabor
Rupture of Membranes Study: evaluation of predictors of
clinical chorioamnionitis and postpartum fever in patients with
prelabor rupture of membranes at term. Am J Obstet Gynecol.
1997;177:1024–9.
[22] Willoughby RE Jr, Nelson KB. Chorioamnionitis and brain injury.
Clin Perinatol. 2002;29:603–21.
The authors stated that there are no conflicts of interest regarding
the publication of this article.
Unauthenticated
Download Date | 12/29/17 10:41 PM