Progress in pathogenesis and management of clinical intraamniotic infection.

In the past decade, gratifying progress has been achieved in our understanding of clinical intraamniotic infection. With a usual incidence of 1% to 4%, clinical intraamniotic infection mainly develops as an ascending process after prolonged rupture of the membranes and labor, but other cases may be hematogenous in origin whereas still others complicate intrauterine procedures. The most common organisms isolated in amniotic fluid of cases of intraamniotic infections are anaerobes, genital mycoplasmas, group B streptococci, and Escherichia coli. The latter two are found most commonly in maternal or neonatal bacteremia complicating intraamniotic infection. Although the diagnosis remains largely a clinical one, laboratory tests have been suggested to confirm the diagnosis in women with symptoms. These include amniotic fluid Gram stain, gas-liquid chromatography, and leukocyte esterase measurement. Maternal treatment consists of antibiotic therapy and delivery. Studies to date have used a penicillin plus an aminoglycoside, with some authors advocating the addition of clindamycin after cesarean delivery. Other broad-spectrum regimens may be equally effective. Complications of clinical intraamniotic infections include an increase in cesarean section rate and in maternal and neonatal bacteremia. Poor neonatal outcomes in intraamniotic infection are more likely in the following cases: (1) when E. coli or group B streptococci are present in the amniotic fluid; (2) when the infant has a low birth weight; (3) when maternal antibiotic therapy is delayed until after delivery.