Preterm Premature (Prelabor) Rupture of Membranes

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Official reprint from UpToDate www.uptodate.com ©2016 UpToDate

Author 

Patrick Duff, MD

Section Editor 

Charles J Lockwood, MD, MHCM

Deputy Editor 

Vanessa A Barss, MD, FACOG

Preterm premature (prelabor) rupture of membranes

 All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Dec 2015. | This topic last updated: Jan 04, 2016.

INTRODUCTION — Premature rupture of membranes (PROM) refers to membrane rupture before the onset of 

uterine contractions (also known as prelabor rupture of membranes); preterm PROM (PPROM) refers to PROM

before 37 weeks of gestation.

The management of PPROM is among the most controversial issues in perinatal medicine. Points of contention

include:

Risk factors, diagnosis, and management of PPROM at 23 to 37 weeks of gestation will be discussed here. Issues

specifically relating to management of PROM prior to 23 weeks of gestation and at term are discussed separately.

(See "Midtrimester preterm premature rupture of membranes" and "Management of premature rupture of the fetal

membranes at term".)

INCIDENCE — Preterm premature rupture of membranes (PPROM) occurs in 3 percent of pregnancies and is

responsible for, or associated with, approximately one-third of preterm births [1].

PATHOGENESIS — The pathogenesis of spontaneous membrane rupture is not completely understood. The

strength and integrity of fetal membranes derive from extracellular membrane proteins, including collagens,

fibronectin, and laminin. Matrix metalloproteases (MMPs) decrease membrane strength by increasing collagen

degradation [2]. Tissue inhibitors of MMPs (TIMMPs) bind to MMPs and shut down proteolysis, thereby helping to

maintain membrane integrity [2,3]. A variety of pathologic events can disrupt this homeostasis and initiate a

cascade of biochemical changes that culminate in PROM. Although the pathway varies depending on the initiating

event, it is likely that all pathways lead to a final common pathway ending in membrane rupture. (See

"Pathogenesis of spontaneous preterm birth".)

CLINICAL FINDINGS

Risk factors — Mater nal physiologic, genetic, and environmental factors likely predispose to development of 

preterm premature rupture of membranes (PPROM) in many cases. These risk factors are similar to those for 

preterm labor (table 1), but most patients have no identifiable risk factors. (See "Risk factors for preterm labor and

delivery".)

 A history of PPROM in a previous pregnancy, genital tract infection, antepartum bleeding, and cigarette smoking

have a particularly strong association with PPROM [4].

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0/7ths

Expectant management versus intervention●

Use of tocolytics●

Duration of administration of antibiotic prophylaxis●

Timing of administration of antenatal corticosteroids●

Methods of testing for maternal/fetal infection●

Timing of delivery●

Previous PPROM — Studies have consistently reported that a history of PPROM is a strong risk factor for 

recurrence. As an example, the Preterm Prediction Study, a large prospective study conducted by the

National Institute of Child Health and Human Development (NICHD) Maternal-Fetal Medicine Units (MFMU)

●

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1/11/2016 Preterm premature (prelabor) rupture of membranes

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In addition, several genetic polymorphisms of genes related to infection, inflammation, and collagen degradation

have been identified as potential risk factors for PPROM.

Patient presentation — The classic clinical presentation of PPROM is a sudden "gush" of clear or pale yellow

fluid from the vagina. However, many women describe intermittent or constant leaking of small amounts of fluid or 

 just a sensation of wetness within the vagina or on the perineum.

Findings on physical examination — Direct observation of amniotic fluid coming out of the cervical canal or 

pooling in the vaginal fornix is pathognomonic of PPROM. If amniotic fluid is not immediately visible, the woman can

be asked to push on her fundus, Valsalva, or cough to provoke leakage of amniotic fluid from the cervical os.

For patients who are not in active labor, examination of the cervix and vagina is performed using a sterile speculum.

Digital examination should be avoided because it may decrease the latency period (ie, time from rupture of 

membranes to delivery) and increase the risk of intrauterine infection [12-14]. The cervix may appear dilated and/or  effaced and, rarely, prolapse of a fetal part or the umbilical cord may be detected.

Findings on ultrasonography — Fifty to 70 percent of women with PPROM have low amniotic fluid volume on

initial sonography [15].

Clinical course — The majority of pregnancies with PPROM deliver within one week of membrane rupture. In a

randomized trial of PPROM at 24 to 32 weeks, the median time to delivery of 239 group B streptococcal (GBS)

negative patients managed expectantly with prophylactic antibiotics was 6.1 days; 27 percent delivered within 48

hours, 56 percent delivered within 7 days, 76 percent delivered within 14 days, and 86 percent delivered within 21

days [16]. However, the duration of the latency period inversely correlates with gestational age at membrane rupture

Network, observed that women with a history of PPROM had a 13.5 percent rate of PPROM in a subsequent

pregnancy compared to 4.1 percent in women with no such history (RR 3.3, 95% CI 2.1-5.2) [5]. Others have

reported recurrence rates at high as 32 percent [6]. Women with a history of PPROM are at risk for recurrent

PPROM or preterm birth without PPROM [7,8].

Genital tract infection — Genital tract infection is the single most common identifiable risk factor for 

PPROM. Three lines of epidemiologic evidence strongly support this association: (1) women with PPROM are

significantly more likely than women with intact membranes to have pathogenic microorganisms in the

amniotic fluid, (2) women with PPROM have a significantly higher rate of histologic chorioamnionitis than

those who deliver preterm without PPROM, and (3) the frequency of PPROM is significantly higher in women

with certain lower genital tract infections (particularly b