See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/283778720 Physiology of Labor Article · February 2015 DOI: 10.1007/978-3-319-13890-9_1 CITATIONS READS 0 1,516 3 authors, including: Helena Strevens Jim G Thornton Lund University University of Nottingham 51 PUBLICATIONS 756 CITATIONS 371 PUBLICATIONS 6,696 CITATIONS SEE PROFILE Some of the authors of this publication are also working on these related projects: PITCHES trial View project Inflammation and biomarkers in gestational diabetes View project All content following this page was uploaded by Jim G Thornton on 13 April 2016. The user has requested enhancement of the downloaded file. SEE PROFILE Ann. N.Y. Acad. Sci. ISSN 0077-8923 A N N A L S O F T H E N E W Y O R K A C A D E M Y O F SC I E N C E S Issue: Women’s Health and Disease Management of premature prelabor rupture of the membranes Helena Strevens,1 Kirsten Allen,2 and Jim G. Thornton2 1 Department Obstetrics and Gynecology, University Hospital, Lund, Sweden. 2 Department of Obstetrics and Gynaecology, Nottingham City Hospital NHS Trust, Nottingham, UK Address for correspondence: Jim G. Thornton, M.D., F.R.C.O.G., Department of Obstetrics and Gynaecology, University of Nottingham, Nottingham City Hospital NHS Trust, Hucknall Road, Nottingham, UK. [email protected] Premature prelabor rupture of the fetal membranes affects about 3% of pregnancies. The cause is usually infection, especially at earlier gestations. The prognosis and the risks of delivery are both much worse at earlier gestations. Before viable pregnancy, termination may be offered. Once the fetus is viable, steroids to mature the fetal lungs and antibiotics to reduce infection are the mainstays of treatment. Delivery is recommended in the presence of signs of clear-cut infection at early gestational ages. At later ones, balancing the risks of infection from conservative treatment against the risk of prematurity from delivery is difficult. Published trials to date have not given clear guidance, but a number are ongoing. Keywords: prematurity; infection; rupture of membranes Introduction The etiology, complications, and management of premature prelabor rupture of the fetal membranes all vary with the gestational age at which the rupture occurs. At previable gestational ages, the prognosis, with or without treatment, is relatively poor, with a high risk of delivery before fetal survival is possible and a high risk of pulmonary hypoplasia and other deformities even if the pregnancy continues. At later gestational ages, management consists of antibiotics, steroids to advance lung maturity, and induction if the risks of intrauterine infection are higher than the risks of prematurity. Although the risk of delivery falls with advancing gestational age, the risk of chorioamnionitis goes in the opposite direction, so calculating this balance of risks is not straightforward. We begin with a description of the etiology, epidemiology, and diagnosis. Various treatments that have been considered are then discussed, namely amnioinfusion, techniques to close amniotic leakage, cervical cerclage, tocolysis, antibiotics, maternal steroids, and timed delivery. Finally, summary evidence relating to management of premature rupture of membranes (ROMs) will be presented for four gestational age bands, namely for less than 16 weeks, for 16–24 weeks, for 24–36 weeks, and for more than 36 weeks. These are relatively arbitrarily chosen gestational age bands, and it should be recognized that both prognosis and management at the borders may vary. Etiology and natural history Local infection in the fetal membranes underlying the cervix is believed to be an important mechanism of membrane rupture. In some cases, primary infection causes membrane weakening and local prostaglandin release. In other cases, uterine distension, cervical weakness, or cone biopsy1 are the primary cause of cervical shortening, and bacteria pass through the cervix as a secondary mechanism. There is fairly strong evidence that infection plays a larger role at lower gestational ages.2 Despite occasional suggestions that collagen abnormalities similar to the various types of Ehlers Danlos might be associated with premature ROM3,4 no definite associations with any specific genetic collagen weaknesses has been confirmed. Without treatment, miscarriage or premature labor typically ensues within a few weeks of the rupture occurring. Depending on the gestational age, doi: 10.1111/j.1749-6632.2010.05654.x c 2010 New York Academy of Sciences. Ann. N.Y. Acad. Sci. 1205 (2010) 123–129 123 Strevens et al . Premature membrane rupture the baby may die or face all the complications of prematurity. Infection in the amniotic sac also becomes increasingly likely with time from rupture, as a result of spread up the genital tract. Such infection adds to the fetal complications, in particular increasing the risk of cerebral palsy.5 Placental abruption is also more common in association with premature ROMs, although this may partly be an artifact of misdiagnosis of cases of abruption—if retained blood separates into organized clot and plasma, and the latter leaks through the cervix it may be misdiagnosed as amniotic fluid. Even in the absence of infection the harmful fetal effects of premature ROM include postural deformities and pulmonary hypoplasia as a direct result of lack of amniotic fluid. Resealed rupture of membranes Despite all the above complications, the fetal prognosis, even in the second trimester is not absolutely hopeless, since occasionally the hole in the membranes reseals, amniotic fluid reforms and the pregnancy proceeds normally to term.6,7 have concluded that this drug reduces the risk of premature delivery. However, none of the studies reported the effect on premature membrane rupture separately. Reports of apparent benefits of progesterone on preterm birth are still treated with caution by many experts, because the methodologically highest quality studies showed no benefit and the long-term safety of such hormonal treatment remains unproven.20 This is why many large trials are ongoing. Prophylactic antibiotics given early in pregnancy, either routinely21 or selectively to treat ureaplasma ureolyticum,22 or asymptomatic bacteriuria,23 do not in general prevent preterm birth. Antibiotics to treat bacterial vaginosis in pregnancy may possibly reduce preterm birth when started before 20 weeks’ gestation, but there is no evidence that they reduce preterm rupture of membranes.24 One large and methodologically good-quality trial as judged by the Cochrane reviewers25 has suggested that a screening programe for vaginal infection reduces preterm birth, but preterm membrane rupture was not reported.26 Epidemiology and prevention Diagnosis Premature ROMs occurs in about 3% of pregnancies.8 It is more common in women who have had a previous preterm birth, either with or without ruptured membranes9,10 and can be predicted in ongoing pregnancies with cervical length assessment and fetal fibronectin measurement in cervical fluid.11 Many other factors such as low socioeconomic status, cigarette smoking, previous cervical cone biopsy,1 amniocentesis, and multiple pregnancy are associated with an increased risk of premature labor, and probably also with premature ROMs. Unfortunately, apart from prophylactic cerclage in women at high risk of premature birth, there is no evidence that any other preventive treatment is effective. Prophylactic cerclage in women at high risk of preterm labor shows a nonsignificant trend toward reducing the risk of premature ROMs, relative risk (RR) 0.31 [95% confidence interval (CI) 0.08–1.28].12 This reduction is plausible since prophylactic cerclage also reduces the overall chance of premature birth. Many randomized trials and almost as many systematic reviews13–19 have measured the effect of progesterone on the risk of preterm birth, and some Tests of membrane rupture The diagnosis of membrane rupture is not straightforward. Patients may mistake a leakage of urine, a profuse vaginal discharge, or a leakage of separated serum from a retro-placental clot for amniotic fluid. Conversely, they may fail to report a slow leakage of amniotic fluid that they misdiagnose as a vaginal discharge or as urine. A sterile speculum examination in which fluid containing vernix or meconium is seen coming through the cervix is diagnostic. If fluid is seen pooling in the posterior fornix, a simple test for a neutral pH (“amnistix” or nitrazine yellow that changes to blue/purple) is suggestive that it is amniotic, since normal urine and vaginal discharge have an acid pH. However false positives and false negatives can occur with this test. Various other immunoassays for proteins specific to amniotic fluid have been developed. These include alpha-feto protein, and placental alpha microglobulin-1 (PASMG-1) AmniSure,27 but their test accuracy remains uncertain. An ultrasound assessment of the amniotic fluid volume provides supportive evidence but again is not diagnostic. Absent or reduced fluid may result from fetal renal problems or severe growth restriction, and the fluid 124 c 2010 New York Academy of Sciences. Ann. N.Y. Acad. Sci. 1205 (2010) 123–129 Strevens et al . volume may be near-normal if the leakage is only partial. Tests of fetal lung maturity Amniocentesis and measurement of the level of surfactant by the lecithin:sphyngomyelin (L:S) ratio has been recommended to test fetal lung maturity and guide the timing of delivery. However, it is rarely used for this indication in modern practice, partly because trials of timed delivery have not reported results stratified into those with or without positive fetal lung maturity tests. Tests of infection High vaginal and endo-cervical swabs for culture and sensitivity to antibiotics should be taken at the same time as a speculum examination is performed to make the diagnosis. However, these are often not revealing because the vagina is rarely a sterile location even in the absence of clinical infection. In the United States, transabdominal amniocentesis is occasionally performed to diagnose amnionitis.28 The amniotic fluid is normally sterile so the presence of microorganisms is likely to be a sign of clinically important infection and an indication for delivery. Such a policy is rarely followed in Europe where obstetricians are fearful that the very act of needling the amniotic sack may introduce or spread infection, or directly provoke preterm labor, and it is argued that in the presence of infection delivery tends to occur fairly soon anyway. Management Clinical chorioamnionitis Some years ago, the suggestion gained currency that, if delivery was imminent, antibiotics should be deferred until after cord clamping, even in the presence of clinical chorioamnionitis, on the grounds that fetal swabs would allow bacterial sensitivity to be measured more accurately. However, the only trial of this policy, which compared predelivery administration of antibiotics with delaying administration until after delivery, in the presence of clinical chorioamnionitis29 showed such overwhelming fetal benefit from predelivery administration that it was suspended. Antibiotic trials in premature ROMs subsequent to the Gibbs trial have confined themselves to patients without clear evidence of chorioamnionitis and have shown less clear-cut benefits. Nevertheless, the lesson of the Gibbs trial should not be forgotten. Premature membrane rupture In the presence of signs of chorioamnionitis, antibiotic administration should not be deferred even if delivery is imminent. In the absence of signs of infection, the largest and best designed trial (ORACLE 1),30 which was performed on patients with preterm labor with ruptured membranes, failed to demonstrate any substantive fetal benefit from antibiotics overall. However, in those who were given erythromycin there was a reduction in preterm labor and respiratory distress. Even in this group, the trend toward reduced perinatal mortality did not reach conventional levels of significance. Choice of antibiotics The results of the ORACLE trial clearly indicate that erythromycin is preferable to coamoxiclav as the antibiotic of choice with premature ROMs and no clear signs of infection. Co-amoxiclav was associated with an increased fetal risk of necrotising enterocolitis. Steroids to provoke fetal lung maturity There is overwhelming randomized trial evidence that for deliveries predicted to deliver before 34 weeks, the administration of corticosteroids to the mother reduces both the risk of neonatal respiratory distress syndrome and perinatal mortality.31 Early concerns that steroids might be less effective, or even harmful in the presence of ruptured membranes have also been shown to be unfounded. Among women with premature ROMs at first dose, the latest systematic review shows a reduction in risk of fetal or neonatal death of RR 0.62 [95% CI 0.46–0.82]. Bedrest Many authors advocate bed rest, especially when membrane rupture occurs before viability on the grounds that this encourages the hole in the membranes to reseal. Such resealing does occasionally occur,6,7 and in such cases the amniotic fluid reaccumulates and pregnancy proceeds normally to term. However, there is no evidence that bed rest encourages this process and it carries the inevitable risk of increasing thromboembolic risks for the mother. Tocolysis Most trials of tocolysis for suspected preterm labor have excluded pregnancies with premature ROMs. Although the drugs do generally prolong the pregnancy, they have, even with such exclusion, failed to demonstrate any reduction in substantive fetal c 2010 New York Academy of Sciences. Ann. N.Y. Acad. Sci. 1205 (2010) 123–129 125 Strevens et al . Premature membrane rupture Figure 1. Neonatal mortality in Sweden, 2001–2002. adverse outcomes. Some authorities (e.g., NICE) have therefore concluded that tocolysis has no place in premature ROMs. However, the lack of evidence of effectiveness with either intact or ruptured membranes may be a result of lack of power, or an artifact of the fact that most trials excluded pregnancies at the highest risk. It is implausible that effective tocolysis never improves fetal outcomes at the limits of viability. There is evidence that this is the case. For example, figures for neonatal death in Sweden between 2001 and 2002 (Fig. 1, courtesy of Professor I. Ingemarssson, Lund, Sweden) where tocolysis is widely used whether the membranes are ruptured or not, and where gestational age is routinely recorded to the nearest day based on early scan, show a notably sharp decrease in mortality between weeks 24 and 25. One plausible explanation is the effective use of tocolytics after 24 weeks. Drugs to reseal the membranes There have been various attempts over the years to reseal holes in the membranes with endoscopically administered mixtures of fibrin glue and platelets.32,33 Results have been somewhat better after iatrogenic membrane rupture than when the membranes rupture spontaneously, presumably because infection is less likely to be a causative factor in the former cases. However there have been no randomized trials, and the practice has not yet entered regular clinical use. 126 Cervical cerclage There is no place for the insertion of a cervical suture of any type after membrane rupture has occurred. The risk of introducing infection is too great. If a suture has been inserted previously, it should usually be removed because of the risks of providing a focus for infection. Management by gestational age Less than 16 weeks’ gestation At these very early gestational ages the diagnosis may be difficult. A typical history of ruptured membranes may not be clear-cut, so a detailed ultrasound assessment should be performed. If this reveals severely reduced or absent amniotic fluid, renal agenesis or urinary outflow obstruction should be excluded. Once these abnormalities have been excluded, rupture of the membranes remains the most likely diagnosis. The prognosis at this early gestational age is very poor, with at least half of such patients delivering within 1 week and 85% by 4 weeks. There is a very high risk of pulmonary hypoplasia in the small fraction of babies who reach viability and survival to hospital discharge is rare. Most authorities would offer termination of pregnancy in this situation. If there is any sign of chorioamnionitis in the mother, pyrexia, abnormal vaginal discharge, raised white blood cell count, or other acute phase reactant (e.g., ESR, CRP, etc.), antibiotics should be given to reduce the risk of serious maternal septic c 2010 New York Academy of Sciences. Ann. N.Y. Acad. Sci. 1205 (2010) 123–129 Strevens et al . complications. In the presence of infection, delivery usually ensues rapidly, but if it does not, termination is recommended. 16–24 weeks’ gestation At these slightly more advanced gestational ages, the prognosis is still poor, but not hopeless.34 Reported case series survival rates may be as high as 46%.35–37 However, such figures should be interpreted with caution since survival is much better at the upper end of this gestational age range and it is unclear from some reports whether ascertainment was complete and whether poor prognosis cases in which labor was induced were included. Amniotic fluid infusion has been advocated as a possible treatment with the idea that by replacing the missing fluid it might reduce the risk of pulmonary hypoplasia.38,39 It may well do this, but it tends to leak away fairly rapidly after infusion so it often has to be repeated, and the transabdominal needling might introduce infection or stimulate preterm labor. This is why amnioinfusion has not yet entered clinical practice outside randomized controlled clinical trials.40,41 An ongoing pilot trial of amnioinfusion for ruptured membranes at 16–24 weeks (http://www.controlledtrials.com/ISRCTN81932589) will soon indicate the feasibility of such a trial. 24–30 weeks’ gestation In the absence of clear-cut signs of infection all authorities would manage such pregnancies conservatively, since the risks of delivery clearly outweigh the risks of observation in utero. Nevertheless, there is a significant risk of chorioamnionitis with observation and most authorities would advocate the prophylactic administration of broad-spectrum antibiotics, such as erythromycin. Steroids should be given to reduce the risk of respiratory distress syndrome. Although bed rest is frequently advocated, it is not evidence based and carries risks of increasing maternal morbidity. Similarly, the evidence for tocolysis at these early gestational ages is very weak. It should be restricted to use in randomized controlled trials, or those few pregnancies at the limit of viability where the risks of delivery are judged to clearly outweigh the risks of infection. 30–34 weeks’ gestation There has been one systematic review of induction of labor at this gestational age band.42 It suggested Premature membrane rupture that a policy of induction reduced chorioamnionitis. However, it should be interpreted with caution. Two of the four trials included in the meta-analysis restricted themselves to patients in whom a test of lung maturity had been performed before entry and none of the trials administered antibiotics or steroids before entry. Finally, although there was an apparent benefit in terms of reduced chorioamnionitis, there was no effect on perinatal death, neonatal sepsis, respiratory distress syndrome (RDS), intraventricular hemorrhage (IVH), necrotising enterocolitis (NEC), or neonatal length of stay. The best policy is probably to treat such patients conservatively, with antibiotic cover until labor, signs of fetal compromise, or signs of chorioamnionitis ensue. If a cervical suture is in place at the time membrane rupture occurs, the choice of removal or not is difficult. Nonrandomized studies comparing a policy of suture removal with retention have given conflicting results.43,44 However, since infection is relatively common at this gestational age, most authors recommend that cervical sutures should be removed when membrane rupture is confirmed, the only exception being when the suture is known to have been buried, such as the Shirodkar or transabdominal suture. 34–36 weeks’ gestation At this relatively advanced gestation, many authorities recommend induction on the grounds that there is little to gain from a slight increase in maturity, and the risks of infection from delay, which might increase cerebral palsy, outweigh this. Such calculations might be right but there are no data from randomized controlled trials to support them. Fortunately, this deficit will soon be remedied by the Australian PPROMT (Pre-term Pre-labour Rupture of the Membranes close to Term ISRCTN 44485060) trial. In this trial, participants with ruptured membranes between 34 ± 0 days and 36 ± 6 days are allocated either to have labor induced immediately or to be observed until another clinical indication for induction develops. The primary outcome is neonatal sepsis and the sample size is 1,812 women. In the meantime both policies of induction or observation are acceptable. Conflicts of interest The authors declare no conflicts of interest. c 2010 New York Academy of Sciences. Ann. N.Y. Acad. Sci. 1205 (2010) 123–129 127 Strevens et al . Premature membrane rupture References 1. Crane, J.M.G. et al. 2006. Transvaginal ultrasonography in the prediction of preterm birth after treatment for cervical intraepithelial neoplasia. Obstet. Gynecol. 107: 37–44. 2. Bendon, R.W., O. Faye-Petersen, Z. Pavlova, et al. 1999. Fetal membrane histology in preterm premature rupture of membranes: comparison to controls, and between antibiotic and placebo treatment. Pediatr. Dev. Pathol. 2: 552–558. 3. Thornton, J.G., J. Hill & H.A. Bird. 1988. Complications of pregnancy and benign familial joint hyperlaxity. Ann. Rheumat. Dis. 47: 228–231. 4. Hermanns-Lê, T., G. Piérard & G. Quatresoozx. 2005. Ehlers-Danlos-like dermal abnormalities in women with recurrent preterm premature rupture of fetal membranes. Am. J. Dermatopathol. 27: 407–410. 5. Wu, Y.W. & J.M. Colford Jr. 2000. Chorioamnionitis as a risk factor for cerebral palsy: a meta-analysis. JAMA 284: 1417–1424. 6. Carlan, S.J., W.F. O’Brien, M.T. Parsons, et al. 1993. Preterm premature rupture of membranes: a randomised study of home vs hospital management. Obstet. Gynaecol. 81: 61–64. 7. Johnson, J.W.C., R.S. Egerman & J. Moorhead. 1990. Cases with ruptured membranes that ‘reseal’. Am. J. Obstet. Gynaecol. 163: 1024–1032. 8. Mercer, B.M. 2003. Preterm premature rupture of the membranes. Obstet. Gynecol. 101: 178–193. 9. Goldenberg, R.L., J.D. Iams, B.M. Mercer, et al. 1998. The preterm prediction study: the value of new vs. standard risk factors in predicting early and all spontaneous preterm births. Am. J. Public Health. 88: 233–238. 10. Mercer, B.M., R.L. Goldenber, et al. 1999. The preterm prediction study: effect of gestational age and cause of preterm birth on subsequent obstetric outcome. Am. J. Obstet. Gynecol. 181: 1216–1221. 11. Honest, H., C.A. Forbes, K.H. Durée, et al. 2009. Screening to prevent spontaneous preterm birth: systematic reviews of accuracy and effectiveness literature with economic modelling. Health Technol. Assess. 13: 1–627. 12. Drakeley, A.J., D. Roberts & Z. Alfirevic. 2003. Cervical stitch (cerclage) for preventing pregnancy loss in women. Cochrane Database Syst. Rev. doi: 10.1002/14651858.CD003253, Art. No.: CD003253. 13. Dodd, J.M., V. Flenady, R. Cincotta & C.A. Crowther. 2006. Prenatal administration of progesterone for preventing preterm birth in women considered to be at risk of preterm birth. Cochrane Database Syst. Rev. doi: 10.1002/14651858. CD004947.pub2, Art. No.: CD004947. 14. Rode, L., J. Langhoff-Roos, C. Andersson, et al. 2009. Systematic review of progesterone for the prevention of preterm birth in singleton pregnancies Acta Obstet. Gynecol. Scand. 88: 1180–1189. 15. Sanchez-Ramos, L., A.M. Kaunitz & I. Delke. 2005. Progestational agents to prevent preterm birth: a meta-analysis of randomized controlled trials. Obstet. Gynecol. 105: 273– 279. 16. Dodd, J.M., V.J. Flenady, R. Cincotta & C.A. Crowther. 2008. Progesterone for the prevention of preterm birth: a systematic review. Obstet. Gynecol. 112: 127–134. 128 17. Dodd, J.M., C.A. Crowther, R. Cincotta, et al. 2005. Progesterone supplementation for preventing preterm birth: a systematic review and meta-analysis. Acta. Obstet. Gynecol. Scand. 84: 526–533. 18. Mackenzie, R., M. Walker, A. Armson, et al. 2006. Progesterone for the prevention of preterm birth among women at increased risk: a systematic review and meta-analysis of randomized controlled trials. Am. J. Obstet. Gynecol. 194: 1234–1242. 19. Coomarasamy, A., S. Thangaratinam, H. Gee & K.S. Khan 2006. Progesterone for the prevention of preterm birth: a critical evaluation of evidence. Eur. J. Obstet. Gynecol. Reprod. Biol. 129: 111–118. 20. Thornton, J.G. 2007. Progesterone and preterm labor—still no definite answers. N. Engl. J. Med. 357: 499–501. 21. Thinkhamrop, J., G.J. Hofmeyr, O. Adetoro & P. Lumbiganon. 2002. Prophylactic antibiotic administration in pregnancy to prevent infectious morbidity and mortality. Cochrane Database Syst. Rev. doi: 10.1002/14651858. CD002250, Art. No.: CD002250. 22. Raynes-Greenow, C.H., C.L. Roberts, J.C. Bell, et al. 2004. Antibiotics for ureaplasma in the vagina in pregnancy. Cochrane Database Syst. Rev. doi: 10.1002/14651858. CD003767.pub2, Art. No.: CD003767. 23. Smaill, F.M. & J.C. Vazquez. 2007. Antibiotics for asymptomatic bacteriuria in pregnancy. Cochrane Database Syst. Rev. doi: 10.1002/14651858.CD000490.pub2, Art. No.: CD000490. 24. McDonald, H.M., P. Brocklehurst & A. Gordon. 2007. Antibiotics for treating bacterial vaginosis in pregnancy. Cochrane Database Syst. Rev. doi: 10.1002/14651858. CD000262.pub3, Art. No.: CD000262. 25. Sangkomkamhang, U.S., P. Lumbiganon, W. Prasertcharoensook & M. Laopaiboon. 2008. Antenatal lower genital tract infection screening and treatment programs for preventing preterm delivery. Cochrane Database Syst. Rev. doi: 10.1002/14651858.CD006178.pub2, Art. No.: CD006178. 26. Kiss, H., L. Petricevic & P. Husslein. 2004. Prospective randomised controlled trial of an infection screening programme to reduce the rate of preterm delivery. BMJ 329: 371–374. 27. Cousins, L.M., D.P. Smok, S.M. Lovett, et al. 2005. AmniSure placental alpha microglobulin-1 rapid immunoassay versus standard diagnostic methods for detection of rupture of membranes. Am. J. Perinatol. 22: 317–320. 28. Romero, R., R. Quintero, E. Oryazun, et al. 1988. Intraamniotic infection and the onset of labour in preterm premature rupture of membranes. Am. J. Obstet. Gynecol. 159: 661– 666. 29. Gibbs, R.S., N.J. Dinsmoor, E.R. Newton & R.S. Ramamurthy. 1988. A randomized trial of intrapartum versus immediate postpartum treatment of women with intraamniotic infection. Obstet. Gynecol. 72: 823–827. 30. Kenyon, S., D.J. Taylor, W. Tarnow-Mordi, on behalf of the ORACLE Collaborative Group. 2001. Broad-spectrum antibiotics for preterm, prelabour rupture of fetal membranes: the ORACLE I randomised trial. Lancet 357: 979– 988. c 2010 New York Academy of Sciences. Ann. N.Y. Acad. Sci. 1205 (2010) 123–129 Strevens et al . 31. Roberts, D. & S.R. Dalziel. 2006. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst. Rev. doi: 10.1002/14651858.CD004454.pub2, Art. No.: CD004454. 32. Young, B.K., A.P. MacKenzie, A.S. Roman, et al. 2004. Endoscopic closure of fetal membrane defects: comparing iatrogenic versus spontaneous rupture cases. J. Matern Fetal. Neonatal. Med. 16: 235–240, doi: 10.1080/jmf.16.4.235.240. 33. Devlieger, R., L.K. Millar, G. Bryant-Greenwood, et al. 2006. Fetal membrane healing after spontaneous and iatrogenic membrane rupture: a review of current evidence. Am. J. Obstet. Gynecol. 195: 1512–1520. 34. Kilbride, H.W., J. Yeast & D.W. Thibeault. 1996. Defining limits of survival: lethal pulmonary hypoplasia after midtrimester premature rupture of membranes. Am. J. Obstet. Gynecol. 175: 675–681. 35. Morales, W.J. & T. Talley. 1993. Premature rupture of membranes at <25 weeks: a management dilemma. Am. J. Obstet. Gynecol. 168: 503–507. 36. Winn, H.N., M. Chen, E. Amon, T.L. Leet, et al. 2000. Neonatal pulmonary hypoplasia and perinatal mortality in patients with midtrimester rupture of amniotic membranes—a critical analysis. Am. J. Obstet. Gynecol. 182: 1638–1644. 37. Manuck, T.A., A.G. Eller, M.S. Esplin, et al. 2009. Outcomes of expectantly managed preterm premature rupture of membranes occurring before 24 weeks of gestation. Obstet. Gynecol. 114: 29–37. Premature membrane rupture 38. Locatelli, A., P. Vergani, G. Di Pirro, et al. 2000. Role of amnioinfusion in the management of premature rupture of membranes at <26 weeks gestation. Am. J. Obstet. Gynecol. 183: 878–882. 39. Tranquilli, A.L., S.R. Giannubilo, V. Bezzeccheri, et al. 2005. Transabdominal amnioinfusion in preterm premature rupture of membranes: a randomised controlled trial. BJOG 112: 759–763. 40. Gramellini, D., S. Fieni, C. Kaihura, et al. 2003. Antepartum amnioinfusion: a review. J. Matern. Fetal. Neonatal. Med. 14: 291–296. 41. NICE. 2006. Interventional procedures overview of therapeutic amnioinfusion for oligohydramnios during pregnancy (excluding labour). Available at: www.nice.org. uk/IP338overview. Accessed May 25, 2010. 42. Hartling, L., R. Chari, C. Friesen, et al. 2006. A systematic review of intentional delivery in women with preterm prelabor rupture of membranes. J. Matern. Fetal. Neonatal. Med. 19: 177–187, doi: 10.1080/14767050500451470. 43. Ludmir, J., T. Bader, L. Chen, et al. 1994. Poor perinatal outcome associated with retained cerclage in patients with premature rupture of membranes. Obstet. Gynecol. 84: 823– 826. 44. Jenkins, T.M., V. Berghella, P.A. Shlossman, et al. 2000. Timing of cerclage removal after preterm premature rupture of membranes: maternal and neonatal outcomes. Am. J. Obstet. Gynecol. 183: 847–852. c 2010 New York Academy of Sciences. Ann. N.Y. Acad. Sci. 1205 (2010) 123–129 View publication stats 129
