Belly Tales

The Diary of a New Midwife

Premature Rupture of Membranes at Term

Filed under: Academia, Complications, Education, Hospitals, Journal Articles, Labor and Birth, Research — The Midwife at 12:00 pm on Saturday, March 3, 2007

I’ve been meaning to post this post for ages, but was never able to finish it during the school year last year. All of this comes from the research project that I worked on last year for 2 semesters as part of my research class, and even though I had to radically alter the goal and purpose of my research proposal in the end, along the way I had the opportunity to do some of the research I was really interested in doing in the first place, and it definitely needs to be shared. This is rather a long post, and it gets somewhat technical in places, but bear with me; a lot of the information here can help you fend off an unnecessary induction or cesarean, so it’s well worth reading. And with that, here we go:

Premature rupture of membranes (or prelabor rupture of membranes, aka PROM) occurs when a woman’s water breaks before she actually goes into active labor. It can happen to women at any point in their pregnancy, and when it happens to women who are still preterm, the danger to herself and her baby is much higher, as are the risks of infection (and many studies have demonstrated that in fact, preterm PROM, aka PPROM, is often caused by infection in the first place). However, the majority of PROM occurs in women who are at term gestation (37+ weeks)—90% of all cases, in fact (Zamzami, 2005), and it’s pretty common, too: PROM at term occurs in 8% of all births. (Hannah et. al., 1996)

In our hospitals today, there is sort of an unspoken rule—let’s call it the 24-Hour Rule. It goes something like this: if you haven’t delivered your baby within 24 hours of breaking your water, something is going to have to be done. In many cases, this something is induction, and in many cases, waiting a full 24 hours before inducing is something that never happens. Providers are often way too impatient and antsy for that, and will generally talk a woman into induction long before the 24 hours has passed. Many providers have the policy of immediately inducing a woman with PROM, either by using prostaglandin gels like cervadil followed by IV oxytocin (pitocin), or by just starting on the pit right away. The rationale for this type of management (often called active management) stems from research that was done in the 1960s (Shubeck, 1966; Rusell & Anderson, 1962) which found that the longer a woman was ruptured, the greater the chance of infection, chorioamnionitis (an acute infection of the chorion, which is part of the placenta), and maternal and/or fetal sepsis.

These early studies advocated immediate induction, and were the beginning of active management. The idea that the length of PROM is responsible for maternal infection is something which has sort of been hard-wired into modern obstetrical practice right now, and in my own experience, I have seen the 24-Hour Rule in effect many a time. Providers often use it to justify the need for an induction or augmentation, i.e. “we need to get your labor moving along, because you’ve been ruptured now for 8 hours…12 hours…18 hours…and you’re still not in active labor”, and as studies have shown, inductions and augmentations, especially for PROM, often lead to cesarean (Mozurkewich & Wolf, 1997; Grant et. al., 1992; Tan & Hannah, 2001). I have seen this deadline held over women’s heads before, and in my most humble opinion, it does absolutely NOTHING to help a woman relax, labor effectively, and have a vaginal delivery. (What’s that old Bradley joke about telling a man he better orgasm soon or else his penis will have to be cut apart to get to the sperm? No pressure, now!)

The thing is…the research from the ’60s, which forms the basis of the 24-Hour Rule, has more holes in it than swiss cheese. For one thing, these studies were retrospective, instead of prospective, which means that they relied on going back and looking at records after the births had already occurred, and never tried to control for any of the gazillion variables that might have affected these birth outcomes other than PROM. Similarly, these early studies were non-randomized, meaning that there might have been selection bias at play which could have muddied the findings. Additionally, both term and preterm pregnancies were mixed together when examining the effects of PROM, which seriously confounds results since preterm infants are much more susceptible to infection, and as I mentioned above, preterm PROM often occurs because of infection in the first place (McGregor & French, 1997). These studies had very imprecise definitions for infection, and the management protocols used were neither uniform or clearly discussed. And of course, NICUs and antibiotic therapy have improved so much in the past 40 years that many of the babies that died of infection in these early studies probably wouldn’t have died if they had been born today. So, as you can see, the studies from the 1960s had a lot of problems, and the fact that modern obstetrical practices are still based in part on the findings in these studies is an even BIGGER problem.

What have more recent studies shown? Well, many studies have shown that strict adherence to active management is often unnecessary, and in some cases, does more harm than good (seems to be a repeating theme when you start to look at obstetrical research—funny, that. And here is where it gets very technical. I’m putting the rest of this behind a cut, for those of you who are interested.)

Kappy et. al. (1979) challenged the 24-Hour Rule, asserting that active management unnecessarily increased the cesarean section (CS) rate, and that expectant management of PROM could reduce the rising CS rate while at the same time keep infection to a minimum. Using a prospective, nonrandomized, observational design, the rates of infection were studied in 110 women with preterm PROM and 78 women with term PROM. In both groups, patients were managed expectantly until they either delivered or signs and symptoms of infection appeared, at which point the patients were induced. No digital examinations were performed on patients until they were in active labor, and no tocolytic agents or prophylactic antibiotics were given unless a patient showed signs and symptoms of infection, at which point the patient was induced. Kappy et. al. found that only 13% of all term women had clinical signs of infection at delivery, and only 3% had chorioamnionitis. There were no maternal deaths, and no neonatal deaths attributed to sepsis. Unlike earlier studies, Kappy et. al. separated preterm and term births, used standardized and clearly defined indicators of PROM (sterile speculum exam to detect vaginal pooling, followed by positive nitrazine tests and microscopic ferning to confirm rupture) and standardized and precise definitions of infection (clinical signs confirmed by positive blood, sputum, spinal or placental cultures). The weaknesses of this study included its nonrandomized design, the fact that no effort was made to control for infectious risk factors such as GBS, and only infants showing clinical signs of infection were cultured. Nevertheless, Kappy et. al. were able to conclude that “the conservative approach in the term pregnancy with PROM…seems to decrease the incidence of cesarean sections without an appropriate increase in the infectious morbidity”.

Duff et. al. (Duff, Huff & Gibbs, 1984) supported these results with a randomized control trial that demonstrated that “expectant management resulted in a lower frequency of both cesarean delivery and intrapartum infection than…the practice of immediately inducing labor”. In this study, 134 women with PROM were assigned either to an oxytocin induction group or to an expectant management group where they were observed as inpatients until the onset of labor. The researchers found a statistically significant increase in the number of cesarean deliveries and intra-amniotic infections in the induction group versus the expectant group—20% versus 7%, p<0.05, for cesarean deliveries, and 17% versus 4%, p <0.05, for intra-amniotic infections. This study used a non-blinded, randomized, prospective design (in other words, one of the strongest study designs you can use, and the “gold standard” for research), standardized definitions for maternal and neonatal infection, and uniform and clearly defined indications for cesarean section. Women participating in the study were from a homogenous population of carefully screened low-risk women at term without complicating risk factors such as diabetes, postdates pregnancy, meconium-stained fluid, hypertensive disorders, intraamniotic infection or malpresentation. However, again no mention was made of GBS status, potential bias could have occurred in the use of two distinct management teams, not all neonates were screened for sepsis, and the use of antibiotics during management was not specified.

A study conducted by Grant et. al. (1992) also found that expectant management significantly lowered the cesarean rate while at the same time posing no additional infectious risk to women or infants. In this study, 444 term primigravidas with PROM were blindly randomized to either an immediate induction group or induction the following morning (9-33 hours later, depending on when the woman arrived on the unit). It was found that there were fewer cesareans in the group that was allowed to wait 9-33 hours before induction (11.1% versus 17.4%, p = 0.06) with no significant increase in the rates of neonatal or maternal infection. It’s also interesting to note that women in the immediate induction group were more likely to ask for epidural anesthesia (70.3% versus 57.3%, p < 0.005), which supports the idea that induction leads to increased demand for epidurals, and that epidurals lead to increased cesarean rates.

The largest study to date, the TERM PROM study (Hannah et. al., 1996), examined 5041 women from 72 centers throughout Canada, Israel, Australia and the UK with PROM at term who were randomized to one of four groups: immediate induction with oxytocin (induction-oxytocin); immediate induction with vaginal prostaglandin gel first, followed by oxytocin if active labor had not started (induction-prostaglandin gel); expectant management for up to 4 days unless signs of infection or fetal distress were noted, followed by oxytocin induction if labor had not started after four days (expectant-oxytocin); and expectant management for up to 4 days, followed by induction with prostaglandin gel (expectant-prostaglandin). The study protocol was standardized and well-defined, and the randomization process was blinded (i.e. a very rigorous study design). Vaginal exams were discouraged; however, approximately one third of the women, equally divided among all four groups, received vaginal exams during the initial cervical assessment. Approximately 78% of the women in both expectant management groups went into labor spontaneously within 4 days of PROM and did not require induction. The researchers found no differences in the rate of neonatal infections or cesareans, but an increase in maternal infectious morbidity was noted in the women of the expectant management groups, with 8.6% of the expectant groups developing clinical chorioamnionitis versus 4% in the immediate induction groups.

Unlike earlier studies, a similar number of babies in all four groups were sampled and cultured for neonatal sepsis, regardless of what management group their mothers had been assigned to. Overall, this study presented a very strong case for arguing that immediate induction does not increase the cesarean rate, and that expectant management may increase maternal infection rates. Nevertheless, it still had a few weaknesses. For one thing, multiparas were pooled with nulliparas, and there was no standardization of Bishop’s score (cervical ripeness); 6-15% of the women had ripe cervices, versus 29-54% which were considered unripe, and in 33-65% of the women, the cervical status was unknown. Additionally, the researchers stated that “digital vaginal examinations were avoided,” but the expectant management groups had considerably more digital vaginal exams than the immediate induction groups. This is very important to note, given that digital vaginal exam after PROM has been found to be an independent risk factor for maternal and fetal infection.(Shutte et. al., 1983; Lenihan, 1984)

Even more recent studies (Zanzami, 2005) have found that in the absence of other obstetric and maternal or fetal risk factors, PROM at term is not an additional risk factor on its own. “Expectant management of PROM at term enhances a patient’s chance of normal delivery without an incrase in fatal and/or maternal morbidity.”

Now, this is not to say that other studies haven’t found the contrary to be the case. For example, Wagner et. al. (1989) found an increase in infection rates in babies born to women with PROM who had been managed expectantly versus actively, although this study also found that the number of vaginal exams performed increased the infection rate (which other studies have confirmed). Rydhstrom & Ingemarsson (1991) found no difference in the cesarean rates in a randomized trial between active management and expectatant management, and Akyol et. al. (1999) actually found that the cesarean rate was lower in the immediate induction group of their study when compared to the expectant management group who were randomized to induction after 24 hours had passed. However, it’s important to note that this increase in cesarean rate was in a group of women who had already failed to go into spontaneous labor within 24 hours. The majority of women will go into labor within 24 hours, so inducing those who didn’t might imply other variables at work which would make induction particularly unsuccessful.

My thoughts on the subject? If your water breaks and your labor doesn’t start right away, that’s fine: 8-12% of all women experience this problem, and it happens most often at term. If the fluid is clear and you can feel the baby moving, call your provider by all means and discuss your options with her, but try to stay home for as long as possible! Go for a walk, bake some cookies, scrub out the bathtub, do some yoga, try to get those contractions to kick in (just don’t have sex, now that your membranes are ruptured). Most women will go into labor on their own within 24 hours, and so long as NO digital vaginal exams are performed (i.e. using fingers; a sterile speculum exam is somewhat better, but still isn’t 100% risk-free), the risks of infection are low. If your provider urges an induction, ask for more time; studies have shown that inductions for PROM often don’t work that well, and women who are induced have a higher risk for developing an infection or having a cesarean (Zanzami, 2005; Hannah et. al., 1996), in part because once the induction process begins, vaginal exams and other interventions which increase the rate of infection, like internal monitoring, are often done.

Talk with your provider about giving your body AT LEAST 12 (and preferably 24) hours to get going on its own, and chances are very good that it will. If, after 24 hours you’re still not in active labor, don’t panic; about 15-20% will not do so within 24 hours (Kappy et. al. 1979). In a clinical trial that measured a 12-hour expectant management regimen versus a 72-hour regimen, the rates of infection, chorioamnionitis and neonatal morbidity were the same in both groups. (Shalev et. al, 1995) In other words, you can probably wait up until 72 hours, so long as no signs and symptoms of infection occur (although your risk of infection does marginally increase the longer you’re ruptured, especially after 24 hours). Also, keep in mind that one of the side effects of an epidural is fever! One of the warning signs of infection is a rising temperature, but if you’ve just had an epidural, it could be from the epidural, and not really an infection at all—especially if your provider has kept his/her fingers out of your vagina! (Goetzl, et. al. 2001)

(Having just issued all of this advice, though, please go read my Quick Disclaimer before you go forth holding my word as gospel. I’m not a midwife! I’m a student, and I have NO idea what your personal situation might be. Each labor and birth is unique, full of a million and one variables, and needs to be handled individually by a health care provider you trust.)

References:

Akyol, D., Mungan, T., Unsal, A. & Yuksel, K. (1999) Prelabour Rupture of the Mmebranes at Term—No advantage of Delaying Induction for 24 Hours. Australia and NZ Journal of Obstetrics & Gynecology, 39(3): 291-295.

Duff, P., Huff, R.W. & Gibbs, R. (1984) Management of Premature rupture of Membranes and Unfovarable Cervix in Term Pregnancy. Obstetrics & Gynecology 63(5): 697-702.

Duncan, S.L.B & Beckley, S. (1992) Prelabour rupture of the membranes—why hurry? British Journal of Obstetrics and Gynaecology, 99: 543-545.

Ezra, Y., Michaelson-Cohen, R., Abramov, Y. & Rojansky, N. (2004) Prelabor rupture of the membranes at term: when to induce labor? European Journal of Obstetrics & Gynecology and Reproductive Biology, 115:23-27.

Grant, J.M., Serle, E., Mahmood, T., Sarmandal, P., & Conway, D.I. (1992). Management of prelabour rupture of membranes in term primigravidae: a report of a randomized prospective trial. British Journal of Obstetrics & Gynaecology, 99(7): 557-562.

Goetzl, L., Cohen, A., Frigoletto, F., Ringer, S.A., Lang, J., & Lieberman, E. (2001). Maternal Epidural Use and Neonatal Sepsis Evaluation in Afebrile Mothers. Pediatrics, 108(5): 1099-1102.

Hannah, M.E., Ohlsson, A., Farine, D., Hewson, S.A., Hodnett, E.D., Myhr, T.L. et. al. (1996). Induction of Labor Compared with Expectant Management for Prelabor Rupture of the Membranes at Term (TERM PROM study). New England Journal of Medicine, 334(16), 1005-1010.

Kappy A.K. et. al. (1979) Premature Rupture of Membranes: A conservative approach. American Journal of Obstetrics & Gynecology 134(6): 655-661.

Lenihan, J.P. (1984) Relationship of Antepartum Pelvic Examinations to Premature Rupture of the Membranes. Obstetrics & Gynecology, 83(1): 33-37.

Marshall, V.A. (1993) Management of premature rupture of membranes at or near term. Journal of Nurse-Midiwfery, 38(3): 140-145.

McGregor, JA, French, JI. (1997) Evidence-based prevention of preterm birth and rupture of membranes: infection and inflammation. Journal of the Society of Obstetricians and Gynaecologists of Canada, 13: 835-852.

Mozurkewich, E.L. & Wolf, F.M. (1997) Premature rupture of membranes at term: a meta-analysis of three management schemes. Obstetrics & Gynecology, 89(6):1035-1043.

Rhdhstrom, H & Ingemarsson, I. (1991) No Benefit from consevative management in nulliparous women with premature rupture of membranes (PROM) at term. Acta Obstetrica Gynecologica Scandinavia, 70: 543-547.

Russell, K., & Anderson, G. (1962) The aggressive management of ruptured membranes. American Journal of Obstetrics and Gynecology, 83(7): 930-937.

Shalev, E., Peleg, D., Eliyahu, S. & Nahum, Z. (1995). Comparison of 12- and 72- hour Expectant Management of Premature Rupture of Membranes in Term Pregnancies. Obstetrics & Gynecology, 85(5): 766-768.

Shetty, A., Burt, R. Rice, P & Templeton, A. (2005) Women’s perceptions, expectations and satisfaction with induced labour—A quastionnaire-based study. European Journal of Obstetrics & Gynecology and Reproductive Health.

Shubeck, F., Benson, RC., Clark Jr, WW., Berendes, H., Weiss, W., & Deutschberger, R. (1966). Fetal hazard after rupture of membranes. A report from the Collaborative Project. Obstetrics & Gynecology, 28(1), 22-31.

Shutte, M.F., Treffers, P.E., Kloostermoan, G.J. & Soepatmis, S. (1983) Management of premature rupture of membranes: The risk of vaginal examination to the infant. American Journal of Obstetrics & Gynecology, 146(4): 395-400.

Tan, BP & Hannah, M.E. (2001) Oxytocin for prelabour rupture of membranes at or near term (Cochrane Review). In: The Cochrane Library, No. 2., Oxford: Update Software, 2001.

Wagner, M.V., Chin, V.P., Peters, C.J., Drexler, B., & Newman, L.A. (1989) A Comparison of Early and Delayed Induction of Labor with Spontaneous Rupture of Membranes at Term. Obstetrics & Gynecology, 74(1):93-97.

Zamzami, Y. (2005) Prelabor Rupture of membranes at term in low-risk women: induce or wait? Achives of Gynecology and Obstetrics, Oct. 6: 1-5 [e-pub. ahead of print.]

6 Comments »

Comment by emjaybee

March 8, 2007 @ 10:30 pm

Really impressive, thank you for posting this. If only my midwives had read it, perhaps they wouldn’t have pushed me into the induction/pit/epidural/c-section spiral.

Tell me…is there a lot of debate that inducing with pit doesn’t increase use of epidurals? My own experience and that of many women is that pit contractions are so much harder and faster that an epidural is necessary. I had had very gentle contractions, but about 2 hours after pit started, they suddenly sped up so fast I couldn’t brace against them or do anything to manage them (separate rant), though I suppose my anecdote =! data. I held out for 5 hours w/out epidural, but the pain was incredibly intense and unrelenting in a way that seemed different than what I was expecting.

Comment by The Student

March 9, 2007 @ 3:04 pm

I don’t think there’s much debate about the fact that using pitocin often leads to an epidural. Pitocin IS a lot stronger than natural labor, and the biggest difference is that during natural labor, the body has the ability to create beta endorphins and enkephalins which boost a woman’s natural pain tolerance. This happens slowly, though, as slow, natural labor is unfolding, so that by the time a woman is in true, active labor, her pain threshold is actually a lot higher than it would be otherwise; she has natural pain killers at work helping her (even though it’s still quite painful!). With pitocin, the contractions ramp up so quickly that I don’t think the body’s natural pain defenses have time to kick in, which is why pit becomes so painful so quickly, and in many ways, I do think that an epidural is the more humane option to use when a woman is receiving pitocin titration. I often tell women on pitocin, especially those who were committed to natural childbirth and feel like they’re failing on some level by requesting an epidural, to keep in mind that there is *nothing* natural about pitocin. Once that pitocin starts, you have to start to look at the labor differently than you did before, and this requires being able to roll with the punches, and use pain medication if you need it. Pitocin HURTS. It’s really difficult to get through without pain medicine, and I don’t think women need to feel like they’re letting themselves down by asking for pain relief. 5 hours on pitocin without pain relief is quite an accomplishment!

Comment by mcsarahb

April 26, 2007 @ 11:51 am

Thank you so much for this. I am a midwifery student doing a similar project and would love to use your reference list if you don’t mind. This topic is pretty controversial at my university hospital, especially because there is a large homebirth community that often transfers care to our faculty practice after days of rupture. The potential implications are complicated, and thus, my interest and choice of topic for my IP paper.

Comment by The Student

April 27, 2007 @ 8:24 pm

Wow, neat! Of course use the references! They are only a small portion of all the references I ended up needing for my project, but they’re a great starting place. Could I read your paper when you’re done? This topic still interests me a great deal, and I’m always interested to see what other people are writing about and thinking about regarding this.

Comment by mcsarahb

May 1, 2007 @ 11:36 pm

Of course. I will send it to you in June. Thanks!

Comment by arcem

May 2, 2007 @ 3:30 pm

Even though there is a clear relationship between the use of pitocin and the use of epidurals, there is still some controversy whether pitocin contraction pain is stronger, therefore leads to epidurals. It would be very difficult to conduct a study that measures pain levels in natural labor v.s. pain levels in pitocin induced/augmented labors without taking into consideration length of labor, position of the baby, and other confounding factors. Therefore studies have not been able to determine this. Pitocin is many times used in labors that are longer, not progressing, complicated by infection, malposition, etc, which confounds results. Researchers in these studies concluded that it was the more difficult labors that ended in more epidurals, rather than the pitocin itself.

In my experience as a student nurse midwife though, pitocin labors are very difficult to cope with for a woman. The rate of contractions can be very intense. A natural labor can have contractions that are more spaced out and there is a sense of control that is missing in pitocin labors. It almost seems as if once a woman is hooked on to pitocin, she has lost ownership of her labor. Maybe that also leads to more epidural use. These are issues that are very hard to study though, but leave it to midwives/SNMs to bring them to the table for discussion…:).

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