As discussed, infection is a major concern with membrane rupture. While some cases remain subclinical, if chorioamnionitis is diagnosed, prompt eforts to efect delivery, preferably vaginally, are initiated. Because maternal leukocytosis alone is not a consistent inding, ever is the ony reliable indicator or the diagnosis of chorioamnionitis. Institutional practices and protocols vary in deining the temperature threshold. T raditionally, a temperature �38°C (100.4°F) accompanying ruptured membranes has implied infection. At Parkland Hospital, we still adhere to this criterion.
In 2015, a workshop sponsored by the NICHD was convened and suggested renaming this condition "intraamnionic infection and inflammation" (Higgins, 2016). The merits and clinical utility of this novel "triple I" terminology have been questioned (Barth, 2016). Nonetheless, the American College of Obstetricians and Gynecologists (20 17b) recently revised both the definitions and temperature thresholds for intraamnionic infection. Using these new deinitions, the diagnosis of suspected intraamniotic infection is made when the maternal temperature is �39.0°C or when the maternal temperature is 38.0 to 38.9°C and one additional clinical risk factor is present. Suggested factors include low parity, multiple digital examinations, use of internal uterine and fetal monitors, meconiumstained amnionic fluid, and the presence of certain genital tract pathogens. Examples are group B streptococcus and sexually transmitted agents. Isolated maternal fever is deined as any maternal temperature between 38.0°C and 38.9°C with no additional risk factors present, and with or without persistent temperature elevation.
With chorioamnionitis, fetal and neonatal morbidity are substantively increased. lexander and colleagues (1998) studied 1367 very-Iow-birthweight neonates delivered at Parkland Hospital. Approximately 7 percent were born to women with overt chorioamnionitis, and their outcomes were compared with similar newborns without clinical infection. Those in the infected group had higher incidences of sepsis, RDS, earlyonset seizures, intraventricular hemorrhage, and periventricular leukomalacia. The investigators concluded that these very-Iowbirthweight newborns were vulnerable to neurological injury attributable to chorioamnionitis. Yoon and colleagues (2000) found that intraamnionic infection in preterm neonates was related to increased rates of cerebral palsy. Petrova and associates (2001) studied more than 11 million singleton live births in the United States from 1995 to 1997. During labor, 1.6 percent of all women had fever, and this was a strong predictor of infection-related death in both term and preterm neonates.
The proposed microbial pathogenesis for spontaneous preterm labor or ruptured membranes has prompted investigators to give various antimicrobials to forestall delivery. Mercer and associates (1995) reviewed 13 randomized trials performed before 35 weeks. heir metaanalysis indicated that only three of 10 outcomes werepossiby beneited: (1) fewer women developed chorioamnionitis, (2) fewer newborns developed sepsis, and (3) pregnancy was more often prolonged 7 days in women given antimicrobials. Rates of neonatal survival, necrotizing enterocolitis, RDS, or intracranial hemorrhage, however, were unafected.