At term, rupture of fetal membranes occurs as a normal part of labor due to a combination of cellular apoptosis and increased collagenase activity. Shearing forces accompanying uterine contractions aid this process. The etiology of PPROM is multifactorial, involving mechanical, infectious and inflammatory processes. Mechanical forces encountered in preterm labor, cervical incompetence or polyhydramnios can all induce the production of prostaglandins. This increases uterine irritability, decreases synthesis of fetal membrane collagen and increases collagenase activity. The subsequent exposure of the membranes to vaginal flora increases the likelihood of attack by bacterial proteases, endotoxins and enzymes such as phospholipase. The role of infection in the causation of PPROM is supported by the identification of pathologic micro-organisms in human vaginal flora soon after membrane rupture. An association between colonization of the genital tract by group B streptococci (GBS), Ureaplasma urealyticum, Chlamydia trachomatis, and Neisseria gonorrhoeae has been established. Although earlier smaller studies showed an association between bacterial vaginosis (BV) and PPROM, prospective studies have found that BV is not a risk factor for PPROM at less than 35 weeks. In general, intrauterine infection may predispose women to PPROM through the secretion of bacterial proteases that induce the degradation of collagen and the extracellular matrix. Additionally, the host inflammatory response to bacterial infection mediated by cytokines and prostaglandins produced by neutrophils and macrophages may predispose the patient to PPROM. In the majority of cases, however, the exact etiology of PPROM is not known. The risk of recurrence of preterm birth from PPROM in a future pregnancy approaches 14%.

The population at risk for PPROM is similar to the population at risk for preterm birth. Risk factors associated with PPROM include a history of preterm birth or PPROM in a previous pregnancy, preterm labor in the current pregnancy, cervical insufficiency, cervical conization, cerclage, maternal smoking, low socio-economic status, low maternal Body Mass Index, second-trimester vaginal bleeding, and amniocentesis. Additionally, a substantial portion of PPROM cases are related to urinary tract infections and sexually transmitted infections (STI). Patients with a history of PPROM or spontaneous preterm birth should therefore be screened for the presence of genitourinary infections and STI in early pregnancy and treated accordingly. Of note, evaluation for asymptomatic BV and its treatment have not proven effective in preventing PPROM.

The first step in the management of PPROM is confirmation of the diagnosis. In most cases, the history and physical examinations will provide ample evidence for a diagnosis of PPROM, with patient history having an accuracy of 90%. If the clinical history is equivocal, a sterile speculum examination is undertaken. Visualization of amniotic fluid passing from the cervix or the presence of pooling in the posterior fornix of the vagina is diagnostic. Amniotic fluid is more alkaline (pH > 6) than vaginal secretions and will stain pH-sensitive indicators such as nitrazine paper blue. False-positive results on nitrazine testing may be seen with blood or semen contamination, antiseptic solutions or bacterial vaginosis. Microscopic evaluation of amniotic fluid allowed to dry on a clean slide will reveal the characteristic pattern of ferning. This is due to the interaction of amniotic fluid, proteins and salts. A false-positive but atypical ferning pattern may be seen when contamination with cervical mucus is present. On the other hand, false-negative ferning or nitrazine testing can occur with prolonged leakage.

If the diagnosis of PPROM is strongly suspected but cannot be confirmed by the tests above, an ultrasound examination showing diminished amniotic fluid volume (AFI) is supportive of the diagnosis. If the diagnosis remains in doubt, dilute indigo carmine may be injected into the uterine cavity and its egress detected on a vaginal tampon or perineal pad.

At the time of the initial speculum examination, the cervix should be inspected for evidence of cervicitis or umbilical cord prolapse. Cervical effacement and dilation can be evaluated visually (correlation coefficient with digital examination = 0.74) in order to reduce infectious morbidity, as digital examinations have been associated in multiple studies with a significantly shortened latency.

After PPROM, the latency period from membrane rupture to delivery decreases inversely with advancing gestational age. For example, at 20–26 weeks’ gestation, the mean latency period is close to 12 days; at 32–34 weeks’ gestation, it is only 4 days. The natural history of PPROM therefore allows significant prolongation of pregnancy in some cases of PPROM. A central tenet of care of the patient with PPROM is that pregnancy prolongation should be considered only when significant fetal benefit could be expected, in the absence of significant fetal and maternal risk.