Chapter 31 – Premature Rupture of the Membranes

Brian M. Mercer, MD Rupture of the fetal membranes is an integral part of the normal parturition process at term and is inevitable in the process of preterm birth. Spontaneous rupture of the membranes (SROM) at term and preterm can occur any time before or after the onset of contractions. SROM before the onset of contractions is referred to as premature rupture of the membranes (PROM). Membrane rupture at term usually occurs as a result of a physiologic process of progressive membrane weakening. Preterm PROM generally results from pathologic weakening of the fetal membranes, which has several causes. Although delivery after PROM may be required by the presence of advanced labor, intrauterine infection, vaginal bleeding due to placental abruption, or non-reassuring fetal status, the physician often needs to make the decision whether to actively pursue delivery or conservatively manage the pregnancy. Management of PROM hinges on knowledge of gestational age, the neonatal risks related to immediate delivery, and an understanding of the anticipated clinical course and relative risks of intrauterine infection, abruptio placentae, and fetal distress or death from umbilical cord accident or intrauterine infection with conservative management.

Physiology and Pathophysiology of Membrane Rupture
The fetal membranes consist of the amnion, which lines the amniotic cavity, and the thicker chorion, which adheres to the maternal decidua. Initially, the amnion and chorion are separate layers. The amnionic sac is visible on first trimester ultrasound scans until it fuses with the chorion by the end of the 14th week of gestation. Subsequently, the amnion and chorion are connected by a collagen-rich connective tissue layer, with the amnion represented by a single cuboidal epithelial amnion layer and subjacent compact and spongy connective tissue layers, and a thicker chorion consisting of reticular and trophoblastic layers. Together, the amnion and chorion form a stronger unit than either layer individually. Physiologic membrane remodeling occurs with advancing gestational age, reflecting changes in collagen content and type, changes in intercellular matrix, and progressive cellular apoptosis. These changes lead to structural weakening of the membranes, which is more evident in the region of the internal cervical os.[1–8] Membrane weakening can be stimulated by exposure to local matrix metalloproteinases (e.g., MMP-1, MMP-2, MMP-9), decreased levels of membrane tissue inhibitors of matrix metalloproteinases (e.g., TIMP-1, TIMP-3), and increased poly[ADP-ribose]polymerase (PARP) cleavage.[6,9] Term or preterm uterine contractions can also lead to membrane rupture resulting from increased bursting pressure due to increased intra-amniotic pressure and from “strain hardening” with repeated uterine contractions. If the fetal membranes do not rupture before labor, the work to cause membrane rupture at the internal cervical os decreases with advancing cervical dilatation because of the lack of anchoring to the supportive decidua and enhanced ability to stretch with contractions.[1] Preterm membrane rupture can arise through a number of pathways that ultimately result in accelerated membrane weakening. Bacterial collagenases and proteases can directly cause fetal membrane tissue weakening.[10] An increase in local host cytokines or an imbalance in the interaction between MMPs and TIMPs in response to microbial colonization can have similar effects.[11] There is specific evidence linking urogenital tract infection and colonization with preterm PROM. Amniotic fluid cultures after PROM are frequently positive (25% to 35%),[12–19] and histologic evaluation in the setting of preterm birth frequently has demonstrated acute inflammation and bacterial contamination along the choriodecidual interface.[20] Although these findings may reflect ascending infection after PROM, it is likely that ascending colonization and infection are directly involved in the pathogenesis of preterm PROM in many cases. Genital tract pathogens that have been associated with PROM include Neisseria gonorrhoeae, Chlamydia trachomatis, Trichomonas vaginalis, and group B β-hemolytic streptococcus.[20–26] Although group B streptococcus (GBS) bacteriuria has been associated with preterm PROM and low-birth-weight infants[27] and an association between cervical colonization and preterm PROM is possible,[28] it does not appear that vaginal GBS carriage is associated with preterm PROM.[29,30] Although there is a well-established association between bacterial vaginosis and preterm birth, including that related to preterm PROM,[31,32] it remains unclear whether bacterial vaginosis merely identifies women with a predisposition to abnormal genital tract colonization and inflammation, facilitates ascent of other bacteria to the upper genital tract, or is directly pathogenic and causative of membrane rupture. Physical effects related to preterm contractions and prolapsing membranes with premature cervical dilatation can predispose the fetal membranes to rupture, as can the increased intrauterine pressure seen with polyhydramnios.[4,33] It is likely that certain connective tissue disorders (e.g., Ehlers-Danlos syndrome) can result in intrinsic weakening of the membranes. Clinical associations with preterm PROM include low socioeconomic status, lean maternal body mass (<19.8 kg/m2), nutritional deficiencies (e.g., copper, ascorbic acid), and prior cervical conization. During pregnancy, maternal cigarette smoking, cervical cerclage, second- and third-trimester bleeding, pulmonary disease, prior episodes of preterm labor or contractions, and uterine overdistention with polyhydramnios or multiple gestations have been linked to preterm PROM.[4,33–45] Although one or more risk factors may lead to membrane rupture, the ultimate clinical cause of PROM is often not evident at delivery. In some cases, factors leading to membrane rupture are subacute or chronic in nature. Women with a prior preterm birth have

increased risk for preterm birth due to PROM in subsequent pregnancies, especially if the prior preterm delivery resulted from PROM.[46] Asymptomatic women with a short cervical length (<25 mm) remote from delivery are also at increased risk for subsequent preterm birth due to preterm labor or PROM. Some women may have polymorphisms for inflammatory proteins that alter their inflammatory response and increase the risk for preterm birth.[47,48]

Copyright © 2010 Elsevier Inc. All rights reserved. Read our Terms and Conditions of Use and our Privacy Policy. For problems or suggestions concerning this service, please contact:

g. A history of preterm birth after PROM confers a 3. The optimal way to prevent complications from preterm PROM is to prevent its occurrence. Prevention of preterm PROM would be particularly appealing because labor and intrauterine infection or other complications necessitating delivery often ensue soon after membrane rupture occurs.[51. P = . it is unknown whether correction of these factors can avert this complication. Ancillary tests such as fetal fibronectin screening or transvaginal cervical sonography should be incorporated into routine practice only after effective interventions to prevent PROM have been identified for those with an abnormal test result.50] (see Chapter 29). Broad-based preventive strategies such as progesterone supplementation can be considered for those at risk due to less specific risk factors such as a history of spontaneous preterm birth[49. and the combination of a prior preterm birth due to PROM. work during pregnancy. clinical efforts continue to be focused on evaluation and treatment of women who present with symptoms of preterm PROM.. 95% confidence interval [CI]. and bacterial vaginosis are associated with preterm birth due to PROM.5%.3%). Although one study suggested that vitamin C supplementation had value in preventing preterm PROM (7. pulmonary disease in pregnancy).6% versus 24.1%. When assessed at 22 to 24 weeks' gestation. For problems or suggestions concerning this service. Copyright © 2010 Elsevier Inc. All rights reserved. Although most other risk factors are fixed in that they cannot be removed or remedied in a particular woman.8 kg/m2). urinary tract and sexually transmitted infections. and most preterm births due to preterm labor or PROM occur in women considered to be at low risk for these events.82). 1. nulliparas with a short cervix and a positive cervicovaginal fibronectin screening result at 22 to 24 weeks had a one-in-six chance (16.7%) of delivering a preterm infant because of PROM. low maternal body mass index (<19. and a positive fetal fibronectin screening result increased the risk of delivery at less than 35 weeks because of preterm PROM by 10.Prediction and Prevention Because PROM at term usually is part of the normal parturition process. studies in which vitamin C was given alone or with other supplements to women without prior preterm birth as a risk factor indicate a trend toward increased preterm birth with such treatments (relative risk [RR] = 1. medical complications (e. poor nutrition. please contact: online.3-fold increased risk for recurrent preterm birth due to the same cause (13. Perhaps the strongest risk factor for preterm PROM is a history of prematurity or PROM. P < .com . a short cervical length. P < . Because prior obstetric outcome has such a strong influence on subsequent pregnancy outcomes.5-fold higher risk of subsequent delivery before 28 weeks (1.02). we are able to predict only a small fraction of women destined to deliver preterm. and severe polyhydramnios.01). the focus of efforts has been on the prediction and prevention of preterm birth caused by PROM.[46] Identification of a cervical length shorter than 25 mm on transvaginal ultrasound also confers an increased risk of subsequent PROM in nulliparas and multiparas. In this study. Potentially modifiable risk factors for preterm PROM include cigarette smoking.38.01) and a 13. Because most cases of preterm PROM cannot be predicted or prevented. knowledge of risk can help to counsel women about suspicious symptoms and the importance of timely evaluation if preterm PROM occurs. it is useful to evaluate nulliparas separately from those with prior deliveries. Other than treatment of infections. Read our Terms and Conditions of Use and our Privacy Policy.5% versus 4.[46] Unfortunately. despite knowledge of a broad range of potential risk factors for preterm birth.52] Vitamin C supplementation to prevent preterm birth due to PROM thus cannot be recommended until there is solid evidence of acute pulmonary diseases.04 to 1.[53] Those with an early preterm birth have the highest risk for a recurrence.9-fold (25% versus 2.8% versus 0.

60% to 70% deliver within 1 week. 93% of women will deliver within 1 week.Clinical Course PROM affects approximately 8% of pregnancies at term. All rights reserved. delivery within 1 week is the most common outcome after preterm PROM at any gestational age.[54] Preterm PROM is also associated with brief latency from membrane rupture to delivery.[58] Copyright © 2010 Elsevier Inc. leakage stopped in most cases with conservative management. Read our Terms and Conditions of Use and our Privacy Policy.[ .[44. please contact: online. but 1 in 5 will have a latency of 4 or more weeks if they are managed conservatively. although a normal fluid volume sometimes took time to re-accumulate (in a range of 8 to 51 days).57.[35] Although the likelihood of spontaneous resealing of the membranes after preterm PROM is low (3% to 13%).56] With PROM near the limit of viability. with 86% to 94% resealing spontaneously.58] In a study of women with PROM after second-trimester amniocentesis. and 50% to 60% of those who are managed conservatively will deliver within 1 week. and 95% of these women will deliver within 28 hours of membrane rupture. When PROM occurs before 34 weeks' On average. For problems or suggestions concerning this service. the prognosis for those with PROM occurring after amniocentesis is much better. latency increases with decreasing gestational age at membrane rupture.

[67] Copyright © 2010 Elsevier . For problems or suggestions concerning this please contact: online.8%) leading to death (0.66] Maternal sepsis (0.60–62] Conservative management of PROM provides the opportunity for subclinical deciduitis to progress to overt infection and for ascending infection to occur. Endometritis occurs in 2% to 13% of cases.14%) is a uncommon complication of preterm PROM occurring near the limit of viability.62] Chorioamnionitis can complicate 13% to 60% of cases when PROM occurs remote from term. a risk that increases to 24% with membrane rupture lasting longer than 24 hours.Complications after Premature Rupture of the Membranes Maternal Complications Chorioamnionitis complicates 9% of pregnancies with term PROM.[63.65. All rights reserved.[54. Read our Terms and Conditions of Use and our Privacy Policy.[59] The risk of intrauterine infection increases with the duration of membrane rupture and with declining gestational age.[34.55.64] Placental abruption is diagnosed in 4% to 12% of pregnancies complicated by PROM and can occur before or after the onset of membrane rupture.[20.54.55.

and placental abruption. but it may also reflect less aggressive obstetric interventions for fetal compromise before the limit of viability. Copyright © 2010 Elsevier Inc. particularly with fetal malpresentation. umbilical cord compression.8% to 22%. Fetal heart rate patterns consistent with umbilical cord compression due to oligohydramnios are commonly seen after PROM. For problems or suggestions concerning this . please contact: online.69.Fetal Complications The risks to the fetus are primarily those related to intrauterine infection. All rights reserved. Read our Terms and Conditions of Use and our Privacy Policy. Fetal death occurs in 1% to 2% of cases of conservatively managed PROM.70] This particularly high risk of fetal loss may reflect increased susceptibility to umbilical cord compression and hypoxia or intrauterine infection.[68] Umbilical cord prolapse can occur after membrane[36. which is more common with preterm gestations.[56] The reported incidence of fetal death after PROM at 16 to 28 weeks ranges from 3.

[88–91] Pulmonary hypoplasia develops over weeks after membrane rupture occurs. mid-trimester PROM is no longer a relevant clinical entity. Conservative management may result in fetal or neonatal loss before viability.83.001) after controlling for other factors. and cerebral palsy. early gestational age at birth has been associated with neonatal white matter damage (P < . with resultant failure of lung growth.88] Overall. It is most accurately diagnosed pathologically based on radial alveolar counts and lung weights. when the risks of long-term sequelae are highest.[82–87] With PROM occurring during the late pseudoglandular or canalicular stage of pulmonary development. and late-onset bacterial or fungal infection. With current survival rates of about 25% to 85% after delivery at 23 to 26 weeks' gestation. Immediate delivery will result in neonatal death. please contact: online.9%) delivering after PROM at 16 to 26 weeks' gestation. Alternatively.4%) because there has been adequate alveolar development to support extrauterine life by this . and a latency of 28 days.86–88.[74–76] This highlights the need for potential neonatal benefit from delayed delivery if conservative management is to be attempted because this delay offers the opportunity for intrauterine infection to develop.84. including chronic lung disease. and adverse neurologic outcomes. was considered as a separate entity from preterm PROM because neonatal death usually could be anticipated with immediate delivery. before 23 weeks' gestation) is a special circumstance that places the fetus in particular jeopardy.[67] In a review of 201 cases from 11 studies. including pneumothorax. intrauterine infection or inflammation. and the need for high ventilatory pressures because of poor pulmonary compliance. these long-term morbidities are uncommon with delivery after about 32 weeks' gestation. Early PROM before 20 weeks' gestation carries the highest potential for lethal pulmonary hypoplasia (≈50% with PROM before 19 weeks' gestation). restriction deformities can occur in up to 27% of fetuses. pulmonary hypoplasia is suggested by a small chest circumference with severe respiratory distress or persistent pulmonary hypertension and radiographic findings such as small.72.[71. Early preterm birth can lead to long-term complications.[97] Lethal pulmonary hypoplasia is uncommon with PROM after 24 to 26 weeks' gestation (0% to 1. visual or hearing difficulties. compared with 57% for rupture at 24 to 26 weeks' gestation. Respiratory distress syndrome. but there was similar survival after PROM at less than 20 weeks. Fetal lung growth and development can be especially adversely affected when PROM occurs in the early phases of development. mid-trimester PROM.98] However.72] Cerebral palsy and periventricular leukomalacia have been associated with amnionitis.[83. meningitis. sepsis. pulmonary hypoplasia becomes evident in 0% to 26.[71. For problems or suggestions concerning this service. Neonatal sepsis is twofold more common after preterm PROM than after preterm birth due to preterm labor.. and if viability is reached. periventricular leukomalacia. well-aerated lungs with a bell-shaped chest and elevation of the diaphragm. Read our Terms and Conditions of Use and our Privacy Policy. In the past. may lead to failure of the terminal bronchioles and alveoli to develop. which encompasses membrane rupture occurring at about 16 to 26 weeks' gestation. intraventricular hemorrhage.[73] and increased amniotic fluid cytokines and fetal systemic inflammation have been associated with preterm PROM.78–80] Previable PROM occurring before the limit of viability (i. the perinatal survival rate with conservative management of PROM before 23 weeks' gestation was 21%.[77] Despite the described associations between PROM.5% of infants (mean = 5. Neonatal infection can manifest as congenital pneumonia. delivery is likely at an early gestational age. developmental and motor delay. and sepsis are the most common serious acute morbidities.98. and they are common with early preterm birth.[67. it has not been shown that immediate delivery after PROM can prevent these morbidities. the risk of pulmonary hypoplasia is estimated to be 74% to 82%.99] With prolonged oligohydramnios.[83.e.[83. or both. necrotizing enterocolitis. All rights reserved. mental retardation. [92.[83. The neonatal survival rate after PROM occurring before 24 weeks has previously been reported to be approximately 30%. and cerebral palsy. tracheobronchial collapse or loss of intrinsic factors within the tracheobronchial fluid. pneumomediastinum. In general.Neonatal Complications Gestational age at delivery is the primary determinant of the frequency and severity of neonatal complications after PROM. nonlethal pulmonary hypoplasia increases the likelihood of pulmonary[81] These reported outcomes of previable PROM may be optimistic because most studies have been retrospective and have included only patients amenable to conservative management. an amniotic fluid index of 2 cm or less.94–96] With PROM at 15 to 16 weeks.93] In surviving infants.98–101] Copyright © 2010 Elsevier Inc.

Cervical mucus should be avoided during sampling because it can also yield a ferning pattern on microscopy.Diagnosis In more than 90% of cases. the diagnosis of PROM can be confirmed by clinical assessment. and anovaginal Streptococcus agalactiae (i. However.[102–107] The diagnosis of membrane rupture is confirmed by visualization of fluid passing from the cervical canal. including endocervical Neisseria gonorrhoeae and Chlamydia trachomatis.[108. clinical examination. Blood or semen contamination. and other markers may assist in the diagnosis of PROM. passage of the mucous plug.e.0 to 6. but it can be falsely positive if there is heavy blood contamination.1 to 7. and some studies have shown it to introduce vaginal organisms into the cervical canal and to increase the risk of infection. and ferning test results. to assess cervical dilatation and effacement. and to obtain cultures. GBS). If further clarification is needed. and laboratory evaluation. Re-examination after prolonged recumbency or alternate measures can be considered if initial testing is negative. as appropriate. alkaline antiseptics. because a positive test result may reflect decidual disruption rather than membrane rupture in some cases and a negative test result cannot exclude the diagnosis unequivocally. which turns blue at a pH above 6.3. Because optimal clinical care requires an accurate diagnosis. . Digital examination can shorten latency between membrane rupture and delivery. Amniotic fluid usually has a pH of 7.109] Prolonged leakage with minimal residual fluid can lead to false-negative clinical.. including the combination of history. prolactin. Initially. human chorionic gonadotropin (hCG). If the diagnosis is not confirmed on initial inspection. Nitrazine. these tests usually are not more helpful than the initial measures listed previously. whereas normal vaginal secretions have a pH of about 4. attention should be paid to confirming the diagnosis when a suspicious history or ultrasound finding of oligohydramnios is identified. Ferning results from the interaction of amniotic fluid proteins and salts. microscopic inspection can be performed for the presence of arborized crystals (i. The fern test is unaffected by meconium and vaginal pH. Other potentially confounding findings such as urine leakage. 31-1) in an air-dried sample collected from the vaginal side walls or pooled vaginal fluid. increased vaginal discharge with cervical dilatation or membrane prolapse. digital cervical examination should be avoided unless imminent delivery is anticipated because the needed information usually can be obtained with visualization of the cervix..0. and bacterial vaginosis can cause false-positive Nitrazine test results. Assessment of cervicovaginal secretions for fetal fibronectin. ferning) (Fig. A sterile speculum examination should be performed to provide confirmatory evidence of membrane rupture and to inspect for cervicitis and for umbilical cord or fetal prolapse.e. the pH of the vaginal side walls or pooled vaginal fluid can be evaluated using Nitrazine paper. and the presence of semen or vaginal douching should be considered.5.5 to 6. cervical infection.

is suggestive of membrane rupture. This pattern may reflect initial transudation of a small amount of fluid across a weakened membrane or minimal leakage around a firmly applied presenting fetal part. All rights reserved. Ultrasonographically guided amniocentesis with infusion of indigo carmine dye (1 mL of dye in 9 mL of sterile normal saline). Amniocentesis in the setting of oligohydramnios can be difficult. and particular attention should be paid to avoidance of the umbilical cord vessels. can confirm or disprove the diagnosis of membrane rupture. A typical ferning appearance is seen after a swab from the posterior vaginal fornix was smeared on glass slide and the specimen allowed to air dry.FIGURE 31-1 Ferning. The sample was obtained from a patient with premature rupture of the membranes. Women with a suspicious history and initially negative testing should be encouraged to return for reevaluation if symptoms are persistent or recurrent. Orange.) If the diagnosis remains unclear after initial evaluation. please contact: documentation of oligohydramnios by ultrasound. in the absence of fetal urinary tract malformations or significant growth restriction. followed by observation for passage of blue fluid from the vagina onto a perineal pad. University of California at Irvine. Some women with a history suspicious for membrane rupture but a negative speculum examination result and a normal amniotic fluid volume on ultrasound subsequently return with gross membrane . which can have the appearance of a thin. linear fluid space under this circumstance. Copyright © 2010 Elsevier Inc. For problems or suggestions concerning this service. Read our Terms and Conditions of Use and our Privacy Policy. (Image courtesy of Thomas Garite. California.

especially under the circumstance of previable PROM. Fetal well-being is assessed by continuous heart rate monitoring if the . and significant vaginal bleeding. and the patient is evaluated for labor. National Institute of Child Health and Human Development.) Initial Evaluation After the diagnosis of membrane rupture is confirmed. Fetal presentation is assessed. (Adapted from Mercer BM: Preterm premature rupture of the membranes. clinical findings of intrauterine infection. Obstet Gynecol 101:178-193. and ultrasound findings. FIGURE 31-2 Algorithm for management of premature rupture of the membranes (PROM).Management of Premature Rupture of the Membranes Management of PROM is based primarily on the estimated risks for fetal and neonatal complications with immediate delivery weighed against the potential risks and benefits of conservative management to extend the pregnancy after membrane rupture (Fig. as appropriate. 2003. The risks of maternal morbidity should also be considered. Gestational age is established based on the combination of menstrual dates. prostaglandin E2. PGE2. NICHD. The algorithm includes several alternatives for the approach to term and preterm PROM. 31-2). the duration of membrane rupture should be estimated to assist the pediatric caregivers with subsequent management decisions. clinical history.

Although narrowing of the biparietal diameter (i. All rights reserved. dolichocephaly) due to oligohydramnios or breech presentation can result in underestimation of gestational age and fetal outpatient management usually is not recommended when PROM occurs after the limit of viability. Prenatal maternal transfer should be undertaken early in the course of management if these resources are not available. it is important to evaluate fetal growth and residual amniotic fluid volume by ultrasound..limit of viability has been reached. please contact: online. For problems or suggestions concerning this service. Read our Terms and Conditions of Use and our Privacy Policy. Copyright © 2010 Elsevier Inc. After preterm PROM. the patient should be cared for in a facility with the ability to provide emergent delivery for placental abruption. and the need for intrapartum prophylaxis should be determined. and the potential of fetal abnormalities that can lead to polyhydramnios should be considered.e.[110] Tables using fetal head circumference rather than biparietal diameter can be consulted as needed. Because of the potential for acute . ultrasound usually is as reliable after PROM as it is with intact membranes. In the absence of available culture results. because conservative management usually is undertaken only if there is a significant risk of neonatal morbidity and mortality with immediate delivery. fetal malpresentation. or fetal distress. a risk factor–based approach should be used for prevention of vertical transmission.[111] If conservative management is planned. GBS carrier status should be ascertained if available from culture results within 6 weeks or there has been a positive urine culture in the current pregnancy. The facility should also have neonatal intensive care facilities and offer acute neonatal resuscitation.

3 hours. available data indicate that women with PROM at term who are not in labor on arrival at the hospital should have labor induced.1%) or neonatal infections (2. decreased rates of chorioamnionitis. given similar efficacy for labor induction. In summary.9% versus 3.0% versus 8.0% versus 2. without increasing the risk of cesarean delivery (13.008). four large studies have since found that induction with oxytocin after term PROM does not increase the risks of maternal or neonatal and the frequencies of chorioamnionitis (4.[54] Neonatal antibiotic therapy was less common with immediate induction (7.2 versus 33.116–118] In the largest study. this choice is somewhat more appealing.5% versus 13. P = . please contact: online. Expectant management of PROM at term was practiced in the 1980s and early 1990s based on studies suggesting that immediate induction after term PROM might increase the risks of infection and cesarean delivery. likely because of a lower concern regarding the potential for neonatal infection with less frequent prolonged rupture of the membranes and less chorioamnionitis. and less frequent neonatal intensive care unit (NICU) admissions with no increase in cesarean delivery rates with prostaglandin administration. usually with an oxytocin infusion.8%).7%.001).[119] Because oxytocin can more easily be discontinued.001) and postpartum febrile morbidity (1. Copyright © 2010 Elsevier Inc.6%. Read our Terms and Conditions of Use and our Privacy Policy. For problems or suggestions concerning this . Meta-analysis of studies comparing prostaglandin induction and conservative management in this setting has found shorter latency.[112–115] However. nor does it make cesarean delivery more likely.7% versus 14.6%. Caregivers should allow an adequate time for the latent phase of labor and minimize digital vaginal examinations until the active phase of labor. to reduce the risk of maternal and neonatal complications. oxytocin induction after term PROM reduced the duration of membrane rupture (17. All rights reserved. P < .Term Premature Rupture of the Membranes There is no substantial fetal benefit to expectant management of pregnancy after membrane rupture at 37 weeks' gestation or later. P < . P < .[54.

increased amnionitis. Amniotic fluid can be collected from the vaginal pool at initial sterile speculum examination or by amniocentesis if vaginal fluid is not available.8%.[130] Based on these findings. This limited benefit was offset by a 2. Specific attention to those enrolled at 32 to 33 weeks' gestation revealed similar trends regarding brief latency. However. P =. Concurrent antibiotic treatment should be given to reduce the risk of intrauterine infection during conservative management (discussed later). but the likelihood of survival is high. and neither group suffered any significant noninfectious neonatal morbidities. consideration should be given to the potential benefits of expeditious delivery unless conservative management to extend latency for 1 or more weeks will be attempted. If antenatal corticosteroids are not to be given to accelerate fetal pulmonary maturity after PROM at 32 to 33 weeks. For problems or suggestions concerning this service.25.06).7% versus 34.7% versus 10. gestational age–dependent neonatal morbidities. controlled trial of conservative management versus immediate induction after PROM at 32 to 36 weeks' gestation. Read our Terms and Conditions of Use and our Privacy Policy.5-fold increased risk of chorioamnionitis (27.[71. With delivery at 32 to 33 weeks' gestation. severe acute morbidities and mortality are uncommon.[121. and reduces umbilical cord pH (7. P = . significantly increases the risk of chorioamnionitis (16% versus documented fetal pulmonary maturity was a requirement for enrollment. Abbott Park.001).9%.122] For these reasons. can occur.Preterm Premature Rupture of the Membranes at 32 to 36 Weeks' Gestation Although infants born at 34 to 36 weeks' gestation (i. women presenting with late preterm PROM at 34 to 36 weeks should be actively delivered.[129] The potential for occult umbilical cord compression during conservative management of PROM is highlighted by the high incidence of recurrent variable decelerations found during intermittent monitoring (19. including respiratory distress syndrome. late preterm birth) have a higher risk of complications than term infants.[122] Alternatively. All rights reserved. P = . P = . IL). suspected neonatal sepsis.003) and increased neonatal antibiotic treatment for suspected infection (78.35 versus . These decisions should take into consideration local population-based risks of infection and neonatal morbidities. conservative management prolonged pregnancy only briefly (36 versus 14 hours. conservative management with antenatal corticosteroid administration for fetal maturation is an appropriate choice.4%) among conservatively managed women. the lecithin-to-sphingomyelin ratio (L/S ratio). P < .[123–128] Modest reductions in the duration of neonatal hospital stay and hyperbilirubinemia with conservative management of PROM at 32 to 33 weeks' gestation have been reported. There are no data regarding optimal management after antenatal corticosteroid treatment is completed. because conservative management increases the risks of chorioamnionitis and prolonged hospitalization and because it is unlikely that conservative management for less than 1 week will result in further significant spontaneous fetal maturation. Each of the TDx/TdXFLx FLM II assay (Abbott Laboratories. P < .3%. In this study.6% versus 28.001) in a randomized. and antibiotic treatment with conservative management. increased neonatal sepsis workups (59.001). delivery should be considered if elective delivery is planned within 7 days after antenatal corticosteroid benefit has been achieved.e. and antenatal corticosteroids for fetal maturation are not typically recommended in this gestational age range. Copyright © 2010 Elsevier Inc. Amniotic fluid studies documenting pulmonary maturity in this gestational age range are useful to identify women who should be offered expeditious delivery. and chronic morbidities are uncommon.. please contact: online. and the phosphatidylglycerol (PG) test can predict pulmonary maturity when performed on vaginal pool specimens.009). the woman with PROM and documented fetal pulmonary maturity at 32 to 33 weeks' gestation is at low risk for complications after immediate delivery and increased risk with conservative management. and it has not been shown to improve neonatal outcomes. If fetal pulmonary testing reveals an immature result or if amniotic fluid cannot be obtained for assessment.120] Conservative management of PROM at 34 to 36 weeks prolongs pregnancy by only days.

generating several meta-analyses. delivery should be pursued and broad-spectrum antibiotics should be initiated because treatment before delivery has been shown to decrease the incidence of neonatal sepsis. A nonreactive result for a nonstress test and a biophysical profile score of 6 or less within 24 hours of delivery have been associated with perinatal infection. a vaginal pool glucose value below 5 mg/dL had a 74.[143] In this promising study. Conservative management includes initial prolonged continuous fetal heart rate and maternal contraction monitoring to assess fetal well-being and identify occult contractions and evidence of umbilical cord compression. a later meta-analysis concluded that antenatal glucocorticoids significantly reduce the risks of respiratory distress syndrome (20% versus 35.[131] Despite this.[136.[15. abruptio placentae. without increasing the risks of maternal (9. fetal heart rate monitoring can identify variable and late decelerations in addition to uterine activity.1%) or neonatal (7.5% versus 15. fetal transverse lie and back up with coexisting advanced cervical dilatation. If initial testing results are reassuring. these results are not likely to be available before the diagnosis is clarified. human immunodeficiency virus infection. Antenatal Corticosteroids Respiratory distress syndrome is the most common acute morbidity after conservatively managed preterm PROM. and long-term sequelae.4%). the counts can be artificially elevated within 5 to 7 days of antenatal corticosteroid administration. intraventricular hemorrhage (7.Preterm Premature Rupture of the Membranes at 23 to 31 Weeks' Gestation Because delivery before 32 weeks' gestation is associated with a high risk for perinatal death. and intrauterine infection.4 °F) with uterine tenderness or with maternal or fetal tachycardia in the absence of another evident source of infection. and it is diagnosed clinically by the presence of maternal fever above 38. particularly remote from term when the fetal heart rate pattern is less likely to be reactive.9%). Because of the high risk of heart rate abnormalities due to umbilical cord compression (32% to 76%). severe neonatal morbidities. In women with conservatively managed PROM remote from term.0% versus 6.[132–134] The latest study of cervical length in women with preterm PROM found that 83% of women delivered within 7 days if the initial cervical length was 1 to 10 mm.2% versus 5. primary herpes simplex virus infection). the patient can be transferred to an inpatient unit or transferred to a facility capable of emergent delivery and acute neonatal resuscitation for modified bed rest. Biophysical profile testing may also be confounded by the presence of oligohydramnios but can be helpful if the nonstress test is equivocal.8% versus 4. amniocentesis may yield helpful results. The presence of leukocytes alone in amniotic fluid after PROM is not well correlated with intrauterine infection. [138–140] Although evaluation of the maternal white blood cell count can be helpful if clinical findings are equivocal. a low initial amniotic fluid volume (amniotic fluid index <5. but only 41 women were evaluated. advanced labor. If the diagnosis of chorioamnionitis is suspected but additional confirmation is needed. currently available studies of initial amniotic fluid volume and cervical length assessment in women with preterm PROM have insufficient power and consistency to guide management. women with PROM between 23 and 31 weeks' gestation usually should be managed expectantly to prolong pregnancy unless there is evidence of intrauterine infection.[132] However.[147] Multivariate analysis of .0 cm or maximum vertical fluid pocket <2. suspected placental abruption. and necrotizing enterocolitis (0.[17] One study suggested that determination of glucose levels from vaginally collected amniotic fluid may be a simple and noninvasive method for identification of intra-amniotic infection. fetal assessment should be performed at least daily for those with initially reassuring test results.137] A nonreactive nonstress test subsequent to an initially reactive result should be considered suspicious.142] A glucose concentration below 16 to 20 mg/dL (sensitivity and specificity of 80% to 90% for a positive culture) and a Gram stain positive for bacteria (sensitivity of 36% to 80% and specificity of 80% to 97% for a positive culture) support the presence of intrauterine infection. Under certain additional circumstances.0 cm) is associated with shorter latency to delivery and increased neonatal morbidity (including respiratory distress syndrome) but not with increased maternal or neonatal infection after PROM.[141] such testing is not available in most clinical laboratories. Although a positive amniotic fluid culture supports clinical suspicion of chorioamnionitis (sensitivity of 65% to 85% and specificity of 85%).0 °C (100. Conservative management requires surveillance for the development of labor..g. compared with 18% for a cervical length more than 30 mm. or a non-reassuring fetal heart rate pattern. the predictive value of a low amniotic fluid volume for adverse outcomes is poor. Chorioamnionitis confers increased risks of perinatal mortality and intraventricular hemorrhage.[144] Antenatal corticosteroid administration after preterm PROM has been extensively studied. delivery may be appropriate despite an early gestational age at membrane rupture (e.2% accuracy rate for identifying women with a positive amniotic fluid culture.135] Continuous monitoring may be appropriate for women with intermittent fetal heart rate decelerations but otherwise reassuring findings. Although the nonstress test and biophysical profile have the ability to confirm fetal well-being in the setting of preterm PROM.141.[63] After the diagnosis of chorioamnionitis is made.6%) infections in women with preterm PROM.6%). A short cervical length on endovaginal ultrasound after preterm PROM has been associated with shorter latency to delivery.[145–147] Although early reviews produced conflicting conclusions about the utility of antenatal corticosteroid treatment after PROM. Although research has found elevated amniotic fluid interleukin levels to be associated with early delivery and perinatal infectious morbidity.[68.

and reduced infant morbidities. In a clinical trial with adequate power to evaluate antibiotic therapy during conservative management of women with preterm PROM before 32 weeks' gestation.9% versus 7. [148] Three studies in which prophylactic antibiotics were given concurrent to antenatal corticosteroids found treatment to reduce respiratory distress syndrome (18. chronic lung disease (bronchopulmonary dysplasia: 20. including death. P = .05). Oral amoxicillin-clavulanic acid treatment was associated with increased necrotizing enterocolitis (RR = 4. The antibiotic study group had less neonatal GBS sepsis (0% versus 1. and severe necrotizing enterocolitis. Benefit persisted for 3 weeks after randomization despite discontinuation of antibiotics at 7 days. patent ductus arteriosus (11.57).009) and pneumonia (2.88) was also reduced.[56.56 to 1. 0.9% versus 6.5% among controls). but oral erythromycin therapy was not (RR = 1.66 to 1. less overall maternal infection and chorioamnionitis.3%.14.05 or less for each.2%) without an increase in neonatal sepsis (9.161] In summary. The benefits and risks of a single rescue course remote from initial corticosteroid administration remain to be determined.0%).71) and within 7 days (RR = 0.3% versus 8.3% versus 48.98 to 10.60.7%). delivery within 48 hours (RR = 0.5%. and there was a trend toward less sepsis. and they were analyzed separately. 95% CI.01).05).[149–151] The National Institutes of Health Consensus Development Panel recommended a single course of antenatal corticosteroids for women with PROM before 30 to 32 weeks' gestation in the absence of intra-amniotic infection. P < . Antibiotic treatment increased the likelihood of continued pregnancy after 7 days of treatment by twofold. respiratory distress syndrome.2%). the study authors recommended erythromycin as a better choice. P < ..5% versus 13.[144] An alternative conclusion from the latest meta-analysis is that penicillins other than .[154] Respiratory distress syndrome was less common in another retrospective review of repeated courses of antenatal corticosteroids (34. CI. Antibiotic therapy also significantly reduced individual gestational age–dependent morbidities. a single course of antenatal corticosteroids should be considered when PROM occurs before 32 weeks' gestation and for women with documented pulmonary immaturity at 32 to 33 weeks' gestation. there was no reduction in respiratory distress syndrome.3% versus 2% for a single course or 1.04) were reduced for those who were not GBS carriers. the National Institutes of Child Health and Human Development Maternal Fetal Medicine Units (NICHD-MFMU) Research Network assigned women with PROM to initial aggressive intravenous therapy for 48 hours (2 g of ampicillin IV every 6 hours and 250 mg of erythromycin IV every 6 hours) followed by oral therapy for 5 days (250 mg of amoxicillin PO every 8 hours and 333 mg of enteric-coated erythromycin base PO every 8 hours) to provide limited-duration. severe intraventricular hemorrhage.156.03).5% versus 48.[144. given 12 hours apart) is considered appropriate.157] In the latest one.03) perinatal mortality (1.8%).6%.[153] In another retrospective analysis of repeated antenatal corticosteroids. but intraventricular hemorrhage and amnionitis were less common. including respiratory distress syndrome (40. broad-spectrum antibiotic (ampicillin-amoxicillin plus erythromycin) therapy for women with preterm PROM before 32 weeks' gestation prolongs pregnancy sufficiently to reduce neonatal gestational age–dependent morbidities and reduce the frequencies of maternal and neonatal infections.[160.[157] The need for surfactant administration (RR = 0.6%. P = . P = . In a retrospective study that controlled for gestational age and other factors.68). antibiotic treatment after preterm PROM significantly reduced chorioamnionitis (relative risk [RR] = 0.2%).82) compared with placebo therapy.4% versus 15. Repeated weekly antenatal corticosteroids are not recommended after preterm PROM. Because of the increased risk of neonatal necrotizing enterocolitis with amoxicillin-clavulanate.7% versus 20.159] GBS screening was performed.72) in this analysis. including neonatal infection (RR = 0. P = .[157] The study that dominated this meta-analysis included women with PROM up to 36 weeks' gestation and included a population at low risk for necrotizing enterocolitis overall (i. early sepsis.e. with no increase in perinatal infections.[158] The meta-analysis found treatment with “all penicillins” (excluding amoxicillin-clavulanic acid) versus placebo to be associated with fewer births within 48 hours and 7 days of PROM. given 24 hours apart) or dexamethasone (four doses of 6 mg IM. P = . fewer positive neonatal blood cultures. and composite morbidities (29. even though benefits were limited to reduction in delivery at 48 hours.9% versus 45.[152] Data regarding repeated weekly courses of antenatal corticosteroids after preterm PROM are conflicting.05).prospective observational trials suggested a benefit of antenatal corticosteroid use regardless of membrane rupture. two or more courses of antenatal corticosteroids were associated with increased early neonatal sepsis (15.00.5%. 1. and major cerebral abnormalities on ultrasound before discharge (RR = 0.3% versus 5.4% versus 43. Betamethasone (two doses of 12 mg IM. P = . but the studies lacked size and power to demonstrate equivalent effectiveness.83) and oxygen therapy (RR = 0. and it was the only one of 10 studies that found a significant increase in necrotizing enterocolitis with antibiotic therapy. 0. and a reduced need for oxygen therapy. Babies born to women treated with ampicillin plus erythromycin had a reduced incidence of one or more major infant morbidities (53% versus 44% rate of composite morbidity. Two other studies have attempted to determine whether antibiotic therapy of shorter duration could provide similar benefit.001). CI.80). fewer positive neonatal blood cultures. and fewer major intracranial cerebral ultrasound abnormalities. and stage 3 or 4 necrotizing enterocolitis (2. broad-spectrum antimicrobial coverage before delivery. More than two dozen randomized clinical trials have been summarized in several metaanalyses. Chorioamnionitis was reduced with the study's antibiotics (23% versus 32. less neonatal infection. Antibiotics did not influence the risk of necrotizing enterocolitis (RR = 1. 0. with P values of 0. and neonatal sepsis (8.[155] Based on current evidence that antenatal corticosteroids are effective for induction of fetal pulmonary maturity without increasing the risk of infection and that most women will remain pregnant for the 24 to 48 hours needed to achieve corticosteroid benefit after PROM.0%. GBS carriers were treated with ampicillin for 1 week and again in labor. Adjunctive Antibiotics Antibiotic therapy is given during conservative management of preterm PROM to treat or prevent ascending decidual infection to prolong pregnancy and to reduce gestational age–dependent morbidity while limiting the risk of neonatal infection.6%.97).5% for no courses.80). P < .

Therapeutic tocolysis administered only after contractions occur has not been shown to be effective in prolonging latency. the risks and benefits of this approach have not been determined. but hematogenous transmission can occur to the fetus in utero in some cases. and antiviral therapy was inconsistent in this series.5 days. After latencies ranging from 1 to 35 days.177] and infection can result in mortality rates of 50% to 60% and serious sequelae in up to 50% of survivors. Women with a diagnosis of chorioamnionitis should receive broad-spectrum intrapartum antibiotic therapy. and it remains plausible that prophylactic tocolysis could delay delivery long enough to allow antibiotic suppression of subclinical decidual infection and for corticosteroid effects on the fetus. Cesarean delivery was performed for women with active lesions at the time of delivery.[173–175] No study has found cerclage retention after PROM to reduce the frequency or severity of infant morbidities after preterm PROM.amoxicillinclavulanic acid are an acceptable treatment for preterm PROM and that the benefits of erythromycin are limited to brief pregnancy prolongation.[162–167] After preterm PROM. Tocolysis Evidence from prospective studies of tocolysis after PROM is similar to that from studies of tocolysis for preterm labor with intact membranes. tocolytic therapy should not be considered an expected practice after preterm PROM. none of the 26 infants developed neonatal herpes infection (CI. a case series of women with conservatively managed PROM before 32 weeks' gestation coincident to active recurrent herpes simplex virus lesions suggests that conservative management may be considered.[43.169. but the biologic mechanism for this association is unclear. Based on these data.179] Based on two case series including a total of 35 women with an active maternal genital herpesvirus infection. and fewer positive neonatal blood cultures.[174] Because cerclage retention after PROM has not been shown to improve perinatal outcomes and there are potential risks related to leaving the cerclage in situ.[167] A report from the Collaborative Study on Antenatal Steroids suggested tocolytic use after PROM was associated with subsequent neonatal respiratory distress syndrome. Pending further study in this area.[180–182] However. Shortages in intravenous and oral antibiotics have led to the need for alternative antibiotic choices. 0% to 10.[168] Overall. In a retrospective comparison of aggressive tocolysis with limited treatment for contractions only during the first 48 hours.170] Because no prospective studies have been performed regarding management of preterm PROM with a cerclage in situ. but it may be appropriate in pregnancies at high risk for neonatal complications with early preterm birth. and each has demonstrated statistically insignificant trends toward increased maternal infectious morbidity with only brief pregnancy prolongation. the available prospective studies have not found tocolytic treatment after PROM to increase or prevent neonatal morbidities after PROM. provided the cerclage is removed on admission after PROM. Maternal Herpes Simplex Virus Infection Neonatal herpes simplex infection most commonly results from direct maternal-fetal transmission at delivery.[178. aggressive therapy was not associated with longer latency (3. P = . regardless of prior antibiotic treatments. Neonatal infection rates after primary and secondary maternal infections occur in 34% to 80% and 1% to 5% of cases. erythromycin. The risk of adverse perinatal outcomes does not appear to be different when PROM occurs with a cerclage or without one. Tocolytic therapy has not been studied when antenatal corticosteroids and antibiotics were administered concurrently.[111] Known GBS carriers and those who deliver before carrier status can be determined should receive intrapartum prophylaxis to prevent vertical transmission. While deferred removal might enhance pregnancy prolongation for corticosteroid administration. One study found increased infant mortality and mortality due to sepsis with cerclage retention after PROM. conservative management of PROM complicated by recurrent maternal herpes simplex virus infection may be .[176. prophylactic tocolysis with β-agonists before the onset of contractions can prolong pregnancy briefly.[171–172] Several small studies comparing pregnancies of preterm PROM in which the cerclage was retained or removed have yielded consistent patterns. removal is recommended when PROM occurs.[173] One study that compared different practices at two institutions found longer latencies with cerclage retention. particularly if the indication for initial cerclage placement was not strong. Oral ampicillin.8 versus 4. Cervical Cerclage Preterm PROM complicates about one fourth of pregnancies with a cervical cerclage and one half of pregnancies requiring an emergent cerclage.4%).[183] Antenatal corticosteroids and antibiotics were not administered. less need for oxygen therapy. it has been generally accepted that increasing latency after membrane rupture of more than 4 to 6 hours increases risk of neonatal infection and that cesarean delivery should be performed expeditiously to prevent fetal infection in this setting. recommendations reflect the data available from retrospective cohorts. respectively.16). and azithromycin are likely appropriate alternatives if needed. Up to a 7-day course of parenteral and oral therapy using ampicillin-amoxicillin and erythromycin is recommended for women undergoing conservative management of preterm PROM remote from term. but this finding could reflect population or practice differences at these institutions rather than the effect of cerclage retention. Adjunctive antibiotic administration to prolong latency must be distinguished from intrapartum prophylaxis to prevent vertical transmission of GBS from mother to baby.[157] This is not inconsistent with the NICHD-MFMU approach.

For problems or suggestions concerning this service. All rights Read our Terms and Conditions of Use and our Privacy Policy.. please contact: online.g.appropriate if membrane rupture occurs remote from term and the potential for mortality or serious sequelae with delivery is considered to be high. Copyright © 2010 Elsevier Inc. acyclovir) during conservative management can reduce viral shedding and the frequency of . Antiviral therapy (e.

severe oligohydramnios after PROM before 20 weeks is the strongest predictor of subsequent lethal pulmonary hypoplasia.g. Serial fetal biometric evaluation (e. Discharged patients are typically readmitted to hospital after the limit of viability has been reached to allow early intervention for infection. including a realistic appraisal of potential fetal and neonatal outcomes according to the available information for gestational age–appropriate outcomes. and the physician's experience with these techniques. please contact: online. Copyright © 2010 Elsevier Inc. and deep venous thrombosis can also occur with prolonged bed rest.e. suspicious vaginal discharge. labor. and there are inadequate data to recommend that any of these approaches be incorporated into routine clinical practice.184] In addition to the maternal risks of conservative management previously delineated. the available facilities. or the degree of neonatal pulmonary hypoplasia at the time of initial presentation with PROM.g. previable PROM in a pregnancy complicated by persistent second-trimester bleeding. These methods are described in a review. the ultimate gestational age at delivery. After an initial ultrasound assessment. For women who decide that the risks of conservative management exceed the potential[191] The maternal risks and fetal benefits of these interventions have not been adequately evaluated. cryoprecipitate. repeated evaluation can be performed every 1 to 2 weeks to determine whether there is re-accumulation of amniotic fluid and to evaluate lung growth. Prediction of specific neonatal outcomes after previable PROM is extremely difficult because it is not possible to predict extended latency. Membrane rupture after amniocentesis is associated with cessation of leakage and subsequent successful pregnancy outcomes in most cases. prior cesarean delivery) and preference. Administration of antenatal corticosteroids for fetal maturation at this time is appropriate. Read our Terms and Conditions of Use and our Privacy Policy.72. Data to guide the management for women who choose conservative management of previable PROM are lacking. abdominal pains. Women who are discharged should be advised to abstain from intercourse and limit physical activity. lung length.[88. misoprostol).96. or by dilatation and evacuation. There is no consensus about the advantages of inpatient versus outpatient management. bone demineralization.Previable Premature Rupture of the Membranes before 23 Weeks' Gestation Although the cause is often not apparent. delivery can usually be accomplished with vaginal prostaglandin E2. with a high-dose oxytocin infusion.[71. which carries a poor prognosis... For problems or suggestions concerning this service. and there are significant financial and social implications of prolonged hospitalization. The patient with previable PROM and no other indication for immediate delivery should be counseled regarding the risks and benefits of expectant management. oral or vaginal prostaglandin E1 (i. . clinical antecedents can be helpful in determining the likely outcomes in some cases of previable PROM. the patient may choose to reconsider her decision regarding ongoing expectant management.. Treatments to seal the membrane defect or restore normal amniotic fluid volume include transabdominal amnioinfusion and membrane sealing with fibrin. severe oligohydramnios. or any vaginal bleeding. Persistent.185–190] If pulmonary hypoplasia becomes evident before the limit of viability or there is persistent. or gel-foam plugs. muscle wasting. They should return immediately in case of fever. chest circumference). evident amnionitis. gestational age. and non-reassuring fetal heart rate patterns. platelet. or an elevated level of maternal serum α-fetoprotein more likely reflects an abnormality of placentation. Initial inpatient evaluation may include strict bed and pelvic rest to enhance the opportunity for resealing and for early identification of infection and placental abruption. ratios to adjust for overall fetal size (thoracic to abdominal circumference. Hospitalization for the duration of amniotic fluid leakage may be appropriate in some circumstances. All rights reserved. thoracic circumference to femur length) and Doppler studies of fetal pulmonary artery and ductus arteriosus waveform modulation with fetal breathing movements can demonstrate whether fetal pulmonary growth has occurred over time. Alternatively. The optimal approach depends on the patient's characteristics (e. placental abruption. These results have a high predictive value for neonatal mortality due to pulmonary hypoplasia.

All rights reserved. Attention to early diagnosis and management of complications that occur after PROM can lead to good perinatal outcomes in many cases. please contact: . there is the potential for significant perinatal morbidity and mortality. Conservative management of PROM remote from term can reduce infectious and gestational age–dependent morbidities.Summary When term or preterm PROM occurs. infants delivered after early preterm or previable PROM are at high risk for perinatal complications. Expeditious delivery of the patient with term and late preterm PROM can reduce the risk of perinatal infections without increasing the likelihood of operative delivery. which can be reduced by considered and timely obstetric interventions. Read our Terms and Conditions of Use and our Privacy Policy. many of which cannot be avoided with current technologies and management algorithms. For problems or suggestions concerning this Regardless of management approach. Copyright © 2010 Elsevier Inc.

Taylor DJ. 182:409-416. Campos GA. et al: Amnion type IV collagen composition and metabolism: Implications for membrane breakdown. Bottoms SF: Conservative vs. 14(2):895-900. McLaren J. 166:794-802. Lei H. N Engl J Med 1998. Taylor DJ. Liggins GC: Collagen content of human amniotic membranes: Effect of gestation length and premature rupture. Am J Obstet Gynecol 2003. Hum Reprod 1999. Moretti ML. 19. 167:1092-1095. 11. Aust N Z J Obstet Gynaecol 1991. Romero R. et al: A program of cell death and extracellular matrix degradation is activated in the amnion before the onset of labor. Skinner SJM. 1:322-324. Taylor DJ. 179:1248-1253. Fetal Diagn Ther 1995. randomized trial of 220 patients. Obstet Gynecol 1979. Cotton DB. Prevost RR. Am J Obstet Gynecol 1998. Obstet Gynecol 1981. Athayde N. Bell SC: Structural characteristic of term human fetal membranes: A novel zone of extreme morphological alteration within the rupture site. Am J Perinatol 1984. 5. et al: Term human fetal membranes have a weak zone overlying the lower uterine pole and cervix before the onset of labor. 17. . Bell SC: Increased incidence of apoptosis in non-labor affected cytotrophoblast cells in term fetal membranes overlying the cervix. aggressive management of preterm rupture of membranes. Davies ET. Preterm Birth Causes. Ellwood D: Amniocentesis in the management of preterm premature rupture of the membranes. Moore RM. Garite TJ. Stetzer B. 14. Sibai BM: Erythromycin therapy in preterm premature rupture of the membranes: A prospective. Broekhuizen FF. 2. Kalluri R. 10:290-296. Obstet Gynecol 1985. McLaren J. Kitzmiller J: Preterm premature rupture of the membranes. 159:661-666. Prevention and Management. leukocyte esterase activity.References 1. Meyer WJ: Comparison of gram stain. 15. Oyarzun E. Gonik B. 189:1481-1488. 13. Am J Obstet Gynecol 1992. Romero R. 3. ed. Bell SC: Increased concentration of pro-matrix metalloproteinase 9 in term fetal membranes overlying the cervix before labor: Implications for membrane remodeling and rupture. Strauss JF: Premature rupture of the fetal membranes. Carroll SG. 12. Malak TM. In: Fuchs F. Reprod 1999. Furth EE. A randomized trial of amniocentesis. 18. 16. et al: Intraamniotic infection and the onset of labor in preterm premature rupture of the membranes. Braly P: The use of amniocentesis in patients with premature rupture of membranes. J Clin Invest 1997. Hamilton PR: Amniocentesis for Gram stain and culture in preterm premature rupture of the membranes. Quintero R. El Khwad M. 338:663-670. Dudley J. Am J Obstet Gynecol 2000. BJOG 1994. 7. Biol. 66:316-321. Papaioannou S. Parry S. Bell SC: Mapping of zones of altered morphology and choriodeciduaic connective tissue cellular phenotype in human fetal membranes (amnion and deciduas) overlying the lower uterine pole and cervix before labor at term. Gauthier DW. 10. Linzey EM. Malcolm G. 57:487-489. 72:720-726. Furth EE. Edwin SS. McParland PC. Gilman M. Freeman RK. Nicolaides KH: Maternal assessment in the prediction of intrauterine infection in preterm prelabor amniorrhexis. 101:375-386. Biol Reprod 2005. Stubblefield PG. Mercer BM. Am J Obstet Gynecol 1992. 1984:298. Am J Obstet Gynecol 1988. and amniotic fluid glucose concentration in predicting amniotic fluid culture results in preterm premature rupture of membranes. 98:1971-1978. 8. 54:226-230. et al: A role for matrix metalloproteinase-9 in spontaneous rupture of the fetal membranes. Kalluri R. 31:331-336. 6. Lei H. 60:176-182. 4. 9. New York: Macmillan.

et al: Infection in the pathogenesis of preterm labor. 32. Klebanoff MA. Mazor M. Tucker JM. 159:397-404. Schwarz RH. McGregor JA. Halim A. Am J Obstet Gynecol 1981. Edwards WB: Infectious complications of cervical cerclage. 77:343-347. Obstet Gynecol 1998. Obstet Gynecol 1984. . Nugent RP. 33. Am J Obstet Gynecol 2004. James LS: Premature rupture of membranes. et al: Group B streptococcus and premature rupture of membranes and preterm delivery. Gibbs RS: A rabbit model for ascending infection in pregnancy: Intervention with indomethacin and delayed ampicillin-sulbactam therapy. Meis PJ. McDuffie Jr RS. 60:93-98. Kanayama N. Ernest JM. 41. preterm delivery. J Infect Dis 1994. 173:157-167. Eschenbach DA. Gosselink CA. Mazor M. Tuomala RE. Obstet Gynecol 1982. Ekwo EE. and group B streptococcal colonization of mothers. Nugent RP. Am J Obstet Gynecol 1996. 30. 31. Am J Obstet Gynecol 1995. 64:615-620. Chao S. Am J Obstet Gynecol 1996. Matorras R. Obstet Gynecol 1991. 22:495-503. Gosselink CA. Hebel JR. Regan JA. Hillier SL. Am J Obstet Gynecol 1990. Lancet 1980. VIP Study Group. 27. 22. 141:1065-1070. 28. Obstet Gynecol 1982. 333:1737-1742. Neisseria gonorrhoeae. 141:184-186. 34. J Reprod Med 1989. 23. 1:192-194. et al: Prevention of premature birth by screening and treatment for common genital tract infections: Results of a prospective controlled evaluation. et al: Risk factors for prematurity and premature rupture of membranes: A prospective study of the vaginal flora in pregnancy. Knight RD: The effect of labor on the rheologic response of chorioamniotic membranes. Omeñaca F. 174:843-849. Goldenberg RL. Wu YK. Woolson R.20. 38. 39. Garcia Perea A. 25. Grunebaum AN. et al: The association of Chlamydia trachomatis. 21. Romero R. Ekwo EE. and group B streptococci with preterm rupture of the membranes and pregnancy outcome. 37. Semin Perinatol 1988. The Vaginal Infections and Prematurity Study Group. 24. N Engl J Med 1995. 169:708-712. Am J Obstet Gynecol 1988. Int J Epidemiol 1993. 42. 170:724-728. Regan JA. 156:1165-1168. Garite T: Premature rupture of the membranes before fetal viability. Jolley PT. Romero R. 12:262-279. Am J Obstet Gynecol 1984. Naeye R: Factors that predispose to premature rupture of the fetal membranes. 174:1354-1360. Heddleston L. Naeye RL. et al: Etiologies of preterm birth in an indigent population: Is prevention a logical expectation?. 27:14-18. Kuivaniemi H. 34:797-801. Moawad A: Risks for premature rupture of amniotic membranes. Harger JH. Parker R. Davis RO. French JI. 163:130-137. Romero R. 35. 26. Oyarzun E. the inflammatory response and the risk of preterm birth: A role for genetic epidemiology in the prevention of preterm birth. Am J Obstet Gynecol 1987. 29. et al: Risk factors for preterm premature rupture of fetal membranes: A multicenter case-control study. et al: Stretching of fetal membranes increases the concentration of interleukin-8 and collagenase activity. Lavery JP. 190:1509-1519. Alger LS. Charles D. et al: Colonization with group B streptococci in pregnancy and adverse outcome. Kubota T: Relationship between maternal group B streptococcal colonization and pregnancy outcome. Chaiworapongsa T. Gynecol Obstet Invest 1989. Miller CE. Maradny EE. Moore ML: Causes of low birth-weight births in public and private patients. Hsing AW. McDonald HM. 150:965-972. Peters EC: Causes and consequences of premature rupture of the fetal membranes. Tromp G: Bacterial vaginosis. 80:166-172. Obstet Gynecol 1982. Minkoff H. 40. Taylor J. 92:926-930. Moawad A: Unfavorable outcome in penultimate pregnancy and premature rupture of membranes in successive pregnancy. 60:87-92. O'Loughlin JA. Am J Obstet Gynecol 1981. 43. Lovchik JC. et al: Association between bacterial vaginosis and preterm delivery of a low-birth-weight infant. 36. et al: Changes in vaginal flora during pregnancy and association with preterm birth. et al: Is there an association between colonization with group B Streptococcus and prematurity?. Am J Obstet Gynecol 1993.

46. Am J Perinatol 1990. Mercer BM. 179:126-134. Klebanoff M. Meis PJ. 51. Am J Clin Nutr 2005. Christian JS: Management of term patients with premature rupture of membranes and an unfavorable cervix. Obstet Gynecol 1982. et al: Conservative management of second trimester post-amniocentesis fluid leakage. 7:374-379. Am J Obstet Gynecol 2003. 81:859-863. 70:183-186. 319:972-978. Millar LK. Mills AA. Main DM. Feldman DM. Harbert Jr GM: Use of β-methasone in management of preterm gestation with premature rupture of membranes. Farine D. Gabbe SG: Risk factors for preterm premature rupture of the fetal membranes. Goldenberg RL. Morton DG: Premature rupture of the fetal membranes: A review. Van Deerlin PG. Obstet Gynecol 1985. Yamamoto SY. N Engl J Med 1996. da Fonseca EB. et al: for the National Institutes of Child Health and Human Development Maternal Fetal Medicine Units (NICHD-MFMU) Network: The preterm prediction study: Effect of gestational age and cause of preterm birth on subsequent obstetric outcome. Moawad AH. 55. Schwartz . 66:168-175. Am J Obstet Gynecol 1999.”. Roberts AK. Simpson GF. 181:1216-1221. Krohn M. et al: Outcome of pregnancies complicated by ruptured membranes after genetic amniocentesis. Am J Obstet Gynecol 2000. 60. 56. 62. Moorhead J: Cases with ruptured membranes that “reseal. Freeman RK: Chorioamnionitis in the preterm gestation. Meis PJ. Gunn GC. National Institutes of Child Health and Human Development Maternal Fetal Medicine Units (NICHD-MFMU) Network . 50. Am J Obstet Gynecol 2000. Martius J. Am J Obstet Gynecol 1998. Obstet Gynecol 1989. Am J Perinatol 1992. Hillier SL. National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network . 59. Hadley CB. Monzon-Bordonaba F. Ripoll C. 348:2379-2385. 74:93-97. Morales WJ: The effect of chorioamnionitis on the developmental outcome of preterm infants at one year. et al: A comparison of early and delayed induction of labor with spontaneous rupture of membranes at term. Bittar RE. . Goldenberg RL. 183:738-745. Chin VP. 180:1297-1302. 74:745-747. 48. 346:1271-1279. Johnson JWC. et al: A relaxin mediated pathway to preterm premature rupture of the fetal membranes that is independent of infection. Mercer B. 163:1024-1032. Gold RB. Am J Obstet Gynecol 1970. et al: Prevention of recurrent preterm delivery by 17 alpha-hydroxyprogesterone caproate. 188:419-424. Arheart K: Antimicrobial therapy in expectant management of preterm premature rupture of the membranes. Wagner MV. Am J Obstet Gynecol 1999. Rumbold A. 183:937-939. Cochrane Database Syst Rev 2005. Guise JM. Mishell DR. 57. et al: Association of polymorphism within the promoter of the tumor necrosis factor alpha gene with increased risk of preterm premature rupture of the fetal membranes.CD004072 53. Goyer GL. Borgida AF. Lancet 1995. N Engl J Med 2003. 54. 63. et al: A case-control study of chorioamnionic infection and histologic chorioamnionitis in prematurity. Am J Obstet Gynecol 1990. Egerman RS. 9:56-60. Thom E. Carvalho MH. Mercer BM. Casanueva E. Crowther CA: Vitamin C supplementation in pregnancy. 64. 59:539-545. 106:469-482. Peters CJ.44. et al: Induction of labor compared with expectant management for prelabor rupture of membranes at term. Obstet Gynecol 1987. 334:1005-1010. Zugaib M: Prophylactic administration of progesterone by vaginal suppository to reduce the incidence of spontaneous preterm birth in women at increased risk: A randomized placebo-controlled double-blind study. 47. 52. Ohlsson A. Duff P. Tolentino M. N Engl J Med 1988. et al: The preterm prediction study: Prediction of preterm premature rupture of the membranes using clinical findings and ancillary testing. 45. Obstet Gynecol 1989. Garite TJ. Boesche MH. 58. et al: Vitamin C supplementation to prevent premature rupture of the chorioamniotic membranes: A randomized trial. Hannah ME. 49. 61.

et al: Interleukin-6 concentrations in umbilical cord plasma are elevated in neonates with white matter lesions associated with periventricular leukomalacia. 41:389-394. Romero R. 84. Hannah ME. Jun JK. Obstet Gynecol 1984. Pediatrics 2001. neonatal brain white matter lesions. Rib DM. 81. 75. Semin Perinatol 1996. Nochimson DJ. Freeman RK: Fetal heart rate patterns and fetal distress in patients with preterm premature rupture of membranes. 80. Obstet Gynecol 1989. 177:19-26. 76. Puterman ML. Farquharson D: Neonatal outcome after prolonged preterm rupture of the membranes. Bauer CR. 193:947-951. Am J Obstet Gynecol 1996. Dewan H. Obstet Gynecol 1989. Paul RH. et al: Risk factors for pulmonary hypoplasia in second-trimester premature rupture of membranes. 78. 71. 73:921-926. Yoon BH. 74:347-350. 86. Piecuch R. 174:1433-1440. Kilpatrick SJ. 159:390-396. Am J Perinatol 1993. 82. et al: Amniotic fluid inflammatory cytokines (interleukin-6. Wu YW. JAMA 2000. Hibbard JU. 155:471-479. Obstet Gynecol 1997. van der Mooren K. Schucker JL. 85. J Reprod Med 1993. 83. 73. 101:178-193. Survival and cost. Paterlini G. Woods JR: Maternal and neonatal outcome associated with prolonged premature rupture of membranes below 26 weeks' gestation. Mercer BM: Midtrimester premature rupture of the membranes. Oh W. Am J Obstet Gynecol 1997. Mercer BM: Perinatal intervention and neonatal outcomes near the limit of viability. 74. VanMarter LJ. Am J Obstet Gynecol 2005. Sibai B: Maternal and perinatal outcome of expectant management of premature rupture of the membranes in midtrimester. 284:1417-1424. and tumor necrosis factor-α). . Am J Obstet Gynecol 1994. 77. Ghidini A. Wladimiroff JW: Ductus arteriosus flow velocity modulation by fetal breathing movements as a measure of fetal lung development. Colford Jr JM: Chorioamnionitis as a risk factor for cerebral palsy: A meta-analysis. Hibbard MC.65. Beydoun SN. 162:46-52. 156:1235-1238. van Eyck J. NICHD Neonatal Research Network. 68. Garite TJ. Bengtson JM. Yoon BH. et al: High expression of tumor necrosis factor-alpha and interleukin-6 in periventricular leukomalacia. Am J Obstet Gynecol 1986. Milligan JE: Does prolonged preterm premature rupture of the membranes predispose to abruptio placentae?. 10:369-373. Ghidini A. Ismail M. Barss VA. 170:1359-1364. Am J Obstet Gynecol 1987. 79. 38:945-951. Am J Obstet Gynecol 1988. Bottoms SF. 177:406-411. Romero R. Aust N Z J Obstet Gynaecol 2001. 90:803-808. Vergani P. Locatelli A. Ehrenberg HM. Weinbaum PJ: Preterm premature rupture of the membranes: A risk factor for the development of abruptio placentae. Collin MF. et al: Obstetric determinants of neonatal survival: Influence of willingness to perform cesarean delivery on survival of extremely low-birth-weight infants. Yang SH. 69. et al: Very low birth weight outcomes of the National Institute of Child Health and Human Development Neonatal Research Network. Mercer BM: Preterm premature rupture of the membranes. Gonen R. 191:1398-1402. Sherer DM. Ling EW. Moberg LJ. Yoon BH. Am J Obstet Gynecol 2004. et al: Gestational age at preterm premature rupture of membranes: A risk factor for neonatal white matter damage. Obstet Gynecol 2003. Morris JM: A systematic review of pregnancy outcome following preterm premature rupture of membranes at a previable gestational age. Louis JM. Kim CJ. Schlueter MA. 87. Locatelli A. Yasin SY: Premature rupture of the membranes before 28 weeks: Conservative management. 163:558-566. 176:960-966. Am J Obstet Gynecol 1997. 67. 64:60-64. et al: Outcome of infants born at 24-26 weeks' gestation. Am J Obstet Gynecol 1990. 70. Moretti M. 20:389-400. January 1995 through December 1996. Rotschild A. interleukin 1b. Am J Obstet Gynecol 1997. Lemons JA. Arendt E: Pregnancy outcome after expectant management of premature rupture of the membranes in the second trimester. Vintzileos AM. I. 107:E1-E8. Campbell WA. Am J Obstet Gynecol 1990. Iams JD. 72. et al: Pregnancy outcome after premature rupture of the membranes at or before 26 weeks' gestation. and cerebral palsy. 66. Romero R.

J Pediatr Surg 1983. Ultrasound Obstet Gynecol 2000. 104. Bottoms SF. 86:18-25. diagnosis. Am J Obstet Gynecol 1983. et al: Experimental pulmonary hypoplasia due to Oligohydramnios and its reversal by relieving thoracic compression. Obstet Gynecol 1995. Harding R. Hooper SB. Kloosterman GJ. Gabbe SG: The microbiologic effect of digital cervical examination. et al: Effects of digital vaginal examinations on latency period in preterm premature rupture of membranes. Aust N Z J Obstet Gynaecol 1992. 110. Blott M. Rizzo G. Glick PL. 106. Imseis HM. Machin G. Am J Obstet Gynecol 1985. 75:338-340. Hadi HA. Capponi A. 19:658-663. 98. Sokol RJ: Clinical interpretation of ultrasound measurements in preterm pregnancies with premature rupture of the membranes. Dowd J. Gonik B. 146:395-400. meconium. 69:358-362. 101. Ludwiczak MH. 96. Hobbins JC: Amniotic fluid arborization: Effect of blood. Blott M. Miodovnik M. Towers CV. Strickland D: Premature rupture of the membranes between 20 and 25 weeks' gestation: Role of amniotic fluid volume in perinatal outcome.88. Moessinger AC. 148:540-543. Arch Dis Child 1979. Askenazi SS. 180:578-580. Graham A. and pH alterations. Perlman M: Pulmonary hypoplasia: Lung weight and radial alveolar count as criteria of diagnosis. Nicolaides KH: Preterm prelabor amniorrhexis: Outcome of live births. et al: The impact of digital cervical examination on expectantly managed preterm rupture of membranes. Adzick NS. 95. Harrison MR. 107. 108. Amon E. Collins MH. . Am J Obstet Gynecol 1990. 92. Obstet Gynecol 1992. 64:248-250. Major CA. Chervenak FA. 170:1139-1144. 89. Winn HN. 105. et al: Oligohydramnios-induced lung hypoplasia: The influence of timing and duration in gestation. Lewis DF. et al: Neonatal pulmonary hypoplasia and perinatal mortality in patients with midtrimester rupture of amniotic membranes: A critical analysis. and antenatal prediction. Obstet Gynecol 1987. Munson LA. J Pediatr Surg 1984. 63:1146-1151. 182:1638-1644. Pediatr Res 1986. 183:1003-1007. Chen M. 94. et al: Blood flow velocity waveforms from fetal peripheral pulmonary arteries in pregnancies with preterm premature rupture of the membranes: Relationship with pulmonary hypoplasia. Alexander JM. 153:562-563. Moya FR. Brown CL. 102. Reece EA. 91. Harrison ML. et al: Experimental pulmonary hypoplasia and oligohydramnios: Relative contributions of lung fluid and fetal breathing movements. Arch Dis Child 1988. 93. Welch RA. 163:1904-1913. Koos BJ. 20:951-954. Obstet Gynecol 1990. Am J Obstet Gynecol 1984. Carroll SG. Blanco JD. 90. Treffers PE. Obstet Gynecol 1984. Lauria MR. Zador IE. Lombardi SJ. Varela-Gittings F. 15:98-103. Am J Obstet Gynecol 2000. Hodson CA. Boehm FH: Ferning of amniotic fluid contaminated with blood. Blanc WA. Glick PL. Obstet Gynecol 1995. Rosemond RL. 100. Am J Obstet Gynecol 1994. Schutte MF. Desai R: Use of DNA estimation for growth assessment in normal and hypoplastic fetal lungs. Romero R: Pulmonary hypoplasia: Pathogenesis. 18:347-353. Arch Dis Child 1981. Dickson KA: A mechanism leading to reduced lung expansion and lung hypoplasia in fetal sheep during Oligohydramnios. Soepatmi S: Management of premature rupture of membranes: The risk of vaginal examination to the infant. Permezel M: Pregnancy outcome following preterm premature rupture of the membranes at less than 26 weeks' gestation. Valenzuela GJ: Is there a need for digital examination in patients with spontaneous rupture of the membranes?. 109. Am J Obstet Gynecol 2000. 56:601-605. 86:466-475. Greenough A: Neonatal outcome after prolonged rupture of the membranes starting in the second trimester. 97. Am J Obstet Gynecol 1999. Wigglesworth JS. Nakayama DK. Nimrod C. Mercer BM. Trout WC. 80:630-634. Obstet Gynecol 1993. 99. 54:614-618. Angelini E. et al: The effect of very prolonged membrane rupture on fetal development. Hirsch CE: Cervical dilation: Accuracy of visual and digital examinations. 32:120-124. 81:215-216. 103.

South Med J 1986. 82:775-782. Am J Obstet Gynecol 1983. Poseiro JJ. Clark RH. Major CA. 114. Obstet Gynecol 2000. Am J Obstet Gynecol 1993. 170:1835-1836. Repke JT. 75:54-56. 180:349-352. Am J Obstet Gynecol 2006. Boe N. Am J Obstet Gynecol 1987. Mercer BM. Mercer BM. 122. Mercer BM. 112. Huff RW. 133. Obstet Gynecol 2002. 194:438-445. American College of Obstetricians and Gynecologists (ACOG) : Prevention of early-onset group B streptococcal disease in newborns. Semin Perinatol 2006. 128. et al: The NICHD-MFMU antibiotic treatment of preterm PROM study: Impact of initial amniotic fluid volume on pregnancy outcome. et al: Premature rupture of membranes at 34 to 37 weeks' gestation: Aggressive vs. Ross KC: Amniotic fluid indices of fetal pulmonary maturity with preterm premature rupture of response to 131. 127. 113. 124. J Reprod Med 1982. 169:573-576. Golde SH: Use of obstetric perineal pads in collection of amniotic fluid in patients with rupture of the membranes. Torday J. Edwards RK. Acker D. Gibbs RS: Management of premature rupture of membranes and unfavorable cervix in term pregnancy. Committee opinion no. Serle E.and 72-hour expectant management of premature rupture of membranes in term pregnancies. Miller GL: Management of premature rupture of the membranes. Ultrasound Obstet Gynecol 1998. Ultrasound Obstet Gynecol 2004. Ladfors L. December 2002. Lewis DF. Am J Obstet Gynecol 1994. 119. Ross EL. 123. 117. Jonas HS. Mattsson LA. Capponi A. Morales WJ. Fuchs I. et al: Comparison of phospholipids in vaginal and amniocentesis specimens of patients with premature rupture of membranes. 146:710-712. Shalev E. 96:102-105. BJOG 1996. Lazar AJ: Expectant management of rupture of membranes at term. Escobar GJ. 63:697-702. Crocker L. Duff P. 27:283-286. Peleg D. Eriksson M. Tan BP. 178:126-130. Schwarcz R: Phosphatidylglycerol determination in the amniotic fluid from a PAD placed over the vulva a method for diagnosis of fetal lung maturity in cases of premature ruptured membranes. Obstet Gynecol 1978. 156:454-457. 52:17-21. Haney EI. Obstet Gynecol 1984. 121. Duff P. 116. 129. Estol PC.CD000178 120. 130. Whybrew D. Fayez JA. Sibai B: Induction vs. expectant management in PROM with mature amniotic fluid at 32-36 weeks: A randomized trial. 100:1405-1412. Shaver DC. Rizzo G. 79:955-958. conservative management. 11:23-29. et al: Use of Amniostat-FLM in detecting the presence of phosphatidyl glycerol in vaginal pool samples in preterm premature rupture of membranes. Henrich W. Cravello C. Van der Walt D. Mahmood T. Obstet Gynecol 1995. 115. Hasan AA. Grant JM. 24:550-553. et al: The value of transvaginal ultrasonographic examination of the uterine cervix in predicting preterm delivery in patients with preterm premature rupture of membranes. Thurnau GR. 20:65-71. 279. Silver RK: Timing of labor induction after premature rupture of membranes between 32 and 36 weeks' gestation. et al: Management of prelabour rupture of the membranes in term primigravidae: Report of a randomized prospective trial. Eliyahu S. BJOG 1992. S Afr Med J 1989. 132. Tsoi E. Hannah ME: Prostaglandins for prelabour rupture of membranes at or near term. Allbert JR. .111. Naef 3rd RW. Towers CV. Greene JD: Short-term outcomes of infants born at 35 and 36 weeks' gestation: We need to ask more questions. J Perinat Med 1992. Am J Obstet Gynecol 1998. Phillippe M. Rabello YA. 30:28-33. Venter PF: Management of term pregnancy with premature rupture of the membranes and unfavourable cervix. Spinnato JA. 118. 103:755-762. 126. 125. Fall O: A randomised trial of two expectant managements of prelabour rupture of the membranes at 34 to 42 weeks. Nahum Z: Comparison of 12. et al: The effects of vaginal contamination on two pulmonary phospholipid assays. 85:1-3. 99:557-562. Am J Obstet Gynecol 1999. Berck DJ: Preterm premature rupture of membranes: A continuing dilemma. Angelini E. Am J Obstet Gynecol 1993. Cochrane Database Syst Rev 2000. Neerhof MG. et al: Sonographic measurement of cervical length in preterm prelabor amniorrhexis.

Semin Perinatol 1996. Vintzileos AM. Weiss JD. et al: Preterm premature ruptured membranes: A randomized trial of steroids after treatment with antibiotics. 173:269-274. Am J Obstet Gynecol 2000. S Afr Med J 1999. Dexiprom Study Group. Harding JE. et al: A comparative study of the diagnostic performance of amniotic fluid glucose. Weinbaum PJ: The use of the nonstress test in patients with premature rupture of the membranes. 139. Am J Obstet Gynecol 1986. 142. 138. 143. et al: Effect of single vs. 98:144-150. Minior VK: Repeated courses of steroids in preterm membrane rupture do not increase the risk of histologic chorioamnionitis. Clin Perinatol 1997. Edwards MS. Am J Obstet Gynecol 1989. Abbasi S. et al: Antenatal corticosteroid administration and neonatal outcome in very low birth weight infants: The NICHD Neonatal Research Network. Carlan SJ. Phelan JP. Farhouh LJ. immediate postpartum treatment of intraamniotic infection. 147. interleukin-6. Nochimson DJ. Romero R. Knight DB. Davis J. Richmond LB. multiple courses of antenatal corticosteroids on maternal and neonatal outcome. 151. Leveno KJ. Am J Obstet Gynecol 1993. et al: for the NICHD-MFMU Network: Antibiotic therapy for reduction of infant morbidity after preterm premature rupture of the membranes: A randomized controlled trial. Smith CV. Ramamurthy RS: A randomized trial of intrapartum vs. Sperling RS.134. et al: A low vaginal “pool” amniotic fluid glucose measurement is a predictive but not a sensitive marker for infection in women with preterm premature rupture of membranes. Lewis DF. Am J Obstet Gynecol 1999. Liggins GC: Do antenatal corticosteroids help in the setting of preterm rupture of membranes?. Gibbs RS: Intra-amniotic infection and premature rupture of the membranes. immediate postpartum treatment of women with intra-amniotic infection. Lovett SM. 137. Hanley ML. Obstet Gynecol 2001. 24:43-57. National Institutes of Health Consensus Development Panel : Antenatal corticosteroids revisited: Repeat courses. Am J Obstet Gynecol 1995. et al: The use of dexamethasone in women with preterm premature rupture of membranes'a multicentre. Dinsmoor MJ. 32:1-4. Am J Obstet Gynecol 1995. 160:890-906. Yoon BH. white blood cell count. Campbell WA. 150. et al: A prospective. J Reprod Med 1987. 184:131-139. 145. 135. 136. Miodovnik M. 20:418-425. 1972 to 1994. 173:322-335. Thurnau G. and Gram stain in the detection of microbial invasion in patients with preterm premature rupture of membranes. 72:823-828. 140. August 17–18. Obstet Gynecol 1988. Obstet Gynecol 1997. 14:309-313. Younes N. O'Brien WF: Randomized trial of endovaginal ultrasound in preterm premature rupture of membranes. Vintzileos AM: Biophysical testing in premature rupture of the membranes. Platt LD: Clinical utility of the nonstress test in the conservative management of women with preterm spontaneous premature rupture of the membranes. double-blind. Am J Obstet Gynecol 2006. Buhimschi CS. Vermillion ST. 169:839-851. Ghidini A. Ohlsson A: Treatments of preterm premature rupture of the membranes: A meta-analysis. Salafia CM. Hamar BG. 154. 89:458-461. et al: Intrapartum treatment of acute chorioamnionitis: Impact on neonatal sepsis. National Institutes of Health Consensus Development Conference Statement. Cox SM. Sfakianaki AK. Pattinson RC. Gibbs RS: A comparison of intrapartum vs. 89:865-870. 148. Am J Obstet Gynecol 1997. Gibbs RS. Gilstrap 3rd LC. Belady PH. Mazor M. Soper DE. Pang J. Am J Perinatol 1997. 155. 182:1243-1249. 141. Hirsch D. Makin JD. 278:989-995. 194:309-316. Am J Obstet Gynecol 1988. Verter J. 155:149-153. 2000. 153. Chasedunn-Roark J: Neonatal sepsis after betamethasone administration to patients with preterm premature rupture of membranes. controlled clinical trial of ampicillin-sulbactam for preterm premature rupture of membranes in women receiving antenatal corticosteroid therapy. Funk M. 159:579-583. randomised trial. Diogo MJ. 146. Obstet Gynecol 1987. 181:320-327. Crowley PA: Antenatal corticosteroid therapy: A meta-analysis of the randomized trials. Am J Obstet Gynecol 2001. 70:861-865. JAMA 1997. . placebo-controlled. Obstet Gynecol 1996. 152. Brody K. Mercer B. Ramamurthy RS. Wright LL. 176:1030-1038. Greenspoon J. 88:801-805. Newton ER. 144. 149. double blind randomized.

66:621-623. 189:799-802. 177. Obstet Gynecol 1985. 173. Am J Obstet Gynecol 1988. Taylor DJ. et al: Effect of Ritodrine on labor after premature rupture of the membranes. Miles AM. Cook CR. 148:263-268. 164. 187:1147-1152. Katz Z.CD001058 158. Am J Obstet Gynecol 1984. Vontver LA. 159:216-222. Am J Obstet Gynecol 1988. Garite TR: The role of cervical cerclage in the management of preterm premature rupture of the membranes. Robichaux AG. et al: for the National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network: What we have learned regarding antibiotic therapy for the reduction of infant morbidity. Leideman T. Neilson J: Antibiotics for preterm rupture of membranes. Cochrane Database Syst Rev 2003. 178. Combs CA. Int J Gynaecol Obstet 1989. Egarter C. Perinatal Care 1978. Das AF. Chuang T: Neonatal herpes: Incidence. Am J Obstet Gynecol 1987. Obstet Gynecol 1994. McElrath TF. Semin Perinatol 2003. Am J Prev Med 1988. Obstet Gynecol 1990. et al: Poor perinatal outcome associated with retained cerclage in patients with premature rupture of membranes. 165:555-558. Warsof SL: Oral Ritodrine and preterm premature rupture of membranes. 162. 165. 317:1246-1251. 160. Klugman M: The therapeutic efficacy and cost-effectiveness of aggressive tocolysis for premature labor associated with premature rupture of the membranes. Am J Obstet Gynecol 2000. Ingemarsson I. . Weiner CP. 313:1327-1330. Clothier B. Part II. prelabor rupture of fetal membranes: The ORACLE I Randomized trial. 27:217-230. Shlossman PA. expectant management. et al: Antibiotic treatment in premature rupture of membranes and neonatal morbidity: A meta-analysis. 166. 157:388-393. Cook VD. 172. J Matern Fetal Med 1998. 170. 167. McCune M. Stagno S. et al: Antibiotic therapy in preterm premature rupture of membranes: Are seven days necessary? A preliminary. Mercer BM. 190:1723-1731. tocolytic therapy. Norwitz ER. et al: Effects on infants of a first episode of genital herpes during pregnancy. Molgilner BM: The outcome of pregnancies complicated by preterm rupture of the membranes with and without cerclage. Am J Obstet Gynecol 1413. randomized clinical trial. 55:187-190. 159. Obstet Gynecol 1980. Lancet 2001. Am J Obstet Gynecol 1991. Am J Obstet Gynecol 2002. Brown ZA. Benedetti J. Visintine AM. 157. Blickstein I. Leitich H. Kenyon S. 158:106-110. Am J Obstet Gynecol 2004. Harger JH: Comparison of success and morbidity in cervical cerclage procedures.156. 169. Tarnow-Mordi WOracle Collaborative Group: Broad spectrum antibiotics for preterm. Lancet M. Bader T. 171. 174:589-597. Treadwell MC. 188:1413-1416. N Engl J Med 1987. 4:47-53. How HY. 2:32-41. 357:979-988. Garite TJ. Chen L. Whitley RJ: Herpesvirus infections of pregnancy. Keegan KA. Fishman A: Aggressive tocolysis does not prolong pregnancy or reduce neonatal morbidity after preterm premature rupture of the membranes. Lewis DF. Bottoms SF: Prognostic factors and complication rates for cervical cerclage: A review of 482 cases. Jenkins TM. Kenyon SL. Goldenberg RL. Segel SY. Renk K. N Engl J Med 1985. Zachman RD. expectant management in patients with premature rupture of membranes at 25 to 30 weeks of gestation. Am J Obstet Gynecol 1996. 168. Bronsteen RA. Freeman RK. Nahmias AJ. 163. 179. 174. et al: Timing of cerclage removal after preterm premature rupture of membranes: Maternal and neonatal outcomes. 176. Nageotte MP: A randomized trial of Ritodrine tocolysis vs. Curet LB. Josey WE: Genital herpes.discussion 1416-1417 161. Levy DL. 7:8-12. Lieberman ES. and respiratory distress syndrome. Adair CD. Boulvain M. Clark R. Am J Obstet Gynecol 2003. 56:543-548. Ludmir J. Rao AV. Christensen KK. Karas H. Herpes simplex virus and varicella zoster infections. et al: Association between ruptured membranes. Heffner LJ: Perinatal outcome after preterm premature rupture of membranes with in situ cervical cerclage. Yeast JD. et al: Preterm premature rupture of membranes: Aggressive tocolysis vs. 175. et al: Duration of antibiotic therapy after preterm premature rupture of fetal membranes. 183:847-852. 84:823-826. 28:237-242. Berghella V. prevention and consequences.

Mercer B. 175:477-483. and Doppler velocity correlates. Blott M. September 2002. 190. 161:606-612. et al: Fetal membrane healing after spontaneous and iatrogenic membrane rupture: A review of current evidence. Nahmias AJ. Tibboel D. For problems or suggestions concerning this service. American College of Obstetricians and Gynecologists (ACOG) : Perinatal care at the threshold of viability. Am J Obstet Gynecol 1989. Robben SG. please contact: online. Amstey MS. JAMA 1993.180. 110:825-837. 189. 183. 184. Laudy JA. Major CA. 163:558-566. 37:515-520. Am J Obstet Gynecol 2006. abdominal circumference ratios for the prediction of pulmonary hypoplasia in premature rupture of the membranes remote from term. Josey WE. Am J Obstet Gynecol 1992. Wladimiroff JW: Ductus arteriosus flow velocity modulation by fetal breathing movements as a measure of fetal lung development. Int J Gynaecol Obstet 2002. 188. Millar LK. no. 181. Devlieger R. van Eyck J. Amstey MS: Management of pregnancy complicated by genital herpes virus . et al: Prenatal prediction of pulmonary hypoplasia: Clinical. Yoshimura S. All rights reserved. Bryant-Greenwood Lezotte DC: Role of cesarean delivery in preventing neonatal herpes virus infection. 185. et al: Ultrasonographic prediction of lethal pulmonary hypoplasia: Comparison of eight different ultrasonographic parameters. 270:94-95. Riddick E. Rodis JF. et al: Perinatal risk associated with maternal genital herpes simplex virus infection. Early Hum Dev 1990. 79:181-188. Dudley D: Serial thoracic vs. 163:838-844. 21:143-151. Naib ZM. 166:658-663. Read our Terms and Conditions of Use and our Privacy Policy. Masuzaki H. Campbell S: The ultrasonographic assessment of the fetal thorax and fetal breathing movements in the prediction of pulmonary hypoplasia. 182. Greenough A. Campbell WA. 187. 191. Gotoh H. Am J Obstet Gynecol 1996. Am J Obstet Gynecol 1971. D'Alton M. biometric. 109:250-258. et al: Comparison of six different ultrasonographic methods for predicting lethal fetal pulmonary hypoplasia. 186. 195:1512-1520. Pediatrics 2002. 38. Am J Obstet Gynecol 1990. Obstet Gynecol 1971. Gibbs RS. Am J Obstet Gynecol 1990. Nicolaides KH. Copyright © 2010 Elsevier Inc. Kitzmiller JL: Perinatal survival with expectant management of midtrimester rupture of membranes. ACOG practice bulletin. van der Mooren K. Vintzileos AM.

Master your semester with Scribd & The New York Times

Special offer for students: Only $4.99/month.

Master your semester with Scribd & The New York Times

Cancel anytime.