Abstract

The physiologic cascade that results in PROM is cyclic and probably can be entered at many points--through the production of collagenases, peroxidases, phospholipases, or prostaglandins. It can be initiated or exacerbated by bacteria. In addition, PROM is the result of direct bacterial insults or host-mediated autodestruction in response to bacterial presence or challenge. It may be affected by physical properties and stresses that are mechanical. This review of the mechanical factors that support normal chorioamnion membranes may provide an understanding of where the support can be eroded, thus leading to PROM. With this basic overview of the pathophysiology contributing to PROM, the clinician can justify clinical decisions better, depending on the patient's presentation and gestational age. The judicious use of various tocolytic agents, antimicrobial agents, and/or corticosteroids singly or in combination is predicated on the effect each of these iatrogenically administered agents will have on the mother and fetus. As more investigations are done, we will gain greater insight into the mechanical factors involved in causing PROM.

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