For the majority of women with PROM at term, amniorrhexis most likely occurs as a result of proteolytic enzyme-mediated weakening of the fetal membranes in the region of the cervix or lower uterine segment.[7,8] Histologic examination of the fetal membranes in women with PROM at term demonstrates localized thinning of the chorioamnion and regional decreases in the collagen content compared with specimens from term parturients who had intact membranes at labor onset.[8] Proteolytic enzymes involved in weakening of the fetal membranes may originate from bacteria present in the lower genital tract, maternal inflammatory cells, or seminal secretions. One of the key proteolytic enzymes implicated in prelabor amniorrhexis is phospholipase A2, an enzyme produced by microbial organisms, principally anaerobic bacteria. This enzyme catalyzes the breakdown of phospholipids to arachidonic acid. Arachidonic acid is then converted into prostaglandins by cyclooxygenase and into leukotrienes by lipooxygenase. The presence of these eiconasoids can lead to uterine contractions with increased intrauterine pressure, localized weakening of the fetal membranes, and decreased lubrication between the chorion and amnion--a cascade of events ultimately resulting in rupture of the fetal membranes.