RESUMEN
Clinical chorioamnionitis, the most common infection-related diagnosis in labor and delivery units, is an antecedent of puerperal infection and neonatal sepsis. The condition is suspected when intrapartum fever is associated with two other maternal and fetal signs of local or systemic inflammation (eg, maternal tachycardia, uterine tenderness, maternal leukocytosis, malodorous vaginal discharge or amniotic fluid, and fetal tachycardia). Clinical chorioamnionitis is a syndrome caused by intraamniotic infection, sterile intraamniotic inflammation (inflammation without bacteria), or systemic maternal inflammation induced by epidural analgesia. In cases of uncertainty, a definitive diagnosis can be made by analyzing amniotic fluid with methods to detect bacteria (Gram stain, culture, or microbial nucleic acid) and inflammation (white blood cell count, glucose concentration, interleukin-6, interleukin-8, matrix metalloproteinase-8). The most common microorganisms are Ureaplasma species, and polymicrobial infections occur in 70% of cases. The fetal attack rate is low, and the rate of positive neonatal blood cultures ranges between 0.2% and 4%. Intrapartum antibiotic administration is the standard treatment to reduce neonatal sepsis. Treatment with ampicillin and gentamicin have been recommended by professional societies, although other antibiotic regimens, eg, cephalosporins, have been used. Given the importance of Ureaplasma species as a cause of intraamniotic infection, consideration needs to be given to the administration of antimicrobial agents effective against these microorganisms such as azithromycin or clarithromycin. We have used the combination of ceftriaxone, clarithromycin, and metronidazole, which has been shown to eradicate intraamniotic infection with microbiologic studies. Routine testing of neonates born to affected mothers for genital mycoplasmas could improve the detection of neonatal sepsis. Clinical chorioamnionitis is associated with decreased uterine activity, failure to progress in labor, and postpartum hemorrhage; however, clinical chorioamnionitis by itself is not an indication for cesarean delivery. Oxytocin is often administered for labor augmentation, and it is prudent to have uterotonic agents at hand to manage postpartum hemorrhage. Infants born to mothers with clinical chorioamnionitis near term are at risk for early-onset neonatal sepsis and for long-term disability such as cerebral palsy. A frontier is the noninvasive assessment of amniotic fluid to diagnose intraamniotic inflammation with a transcervical amniotic fluid collector and a rapid bedside test for IL-8 for patients with ruptured membranes. This approach promises to improve diagnostic accuracy and to provide a basis for antimicrobial administration.
Asunto(s)
Corioamnionitis , Sepsis Neonatal , Hemorragia Posparto , Femenino , Recién Nacido , Embarazo , Humanos , Corioamnionitis/diagnóstico , Corioamnionitis/tratamiento farmacológico , Corioamnionitis/etiología , Claritromicina/uso terapéutico , Hemorragia Posparto/tratamiento farmacológico , Sepsis Neonatal/diagnóstico , Sepsis Neonatal/tratamiento farmacológico , Antibacterianos/uso terapéutico , Líquido Amniótico/microbiología , Inflamación/metabolismo , TaquicardiaRESUMEN
OBJECTIVE: To compare clinical features and inflammatory effects for mothers and newborns between cases with or without funisitis among histlogical chorioamnionitis (HCA) at term. METHODS: We recruited 42 patients who were diagnosed with HCA at term. The women were classified into group HCA1/2 (HCA without funisitis, n = 22) and group HCA3 (HCA with funisitis, n = 20). Medical records and cardiotocograms were retrospectively reviewed to analyze predelivery maternal signs, abnormal FHR patterns, and neonatal outcomes. Differences between the two groups were evaluated using the Mann-Whitney U-test. RESULTS: The maternal CRP and WBC level of group HCA3 was observed to be significantly greater than that of group HCA1/2. Moreover, neonatal CRP levels at days 0, 1 and 2 of group HCA3 were significantly greater than of group HCA1/2. The ratios of abnormal FHR patterns of the two groups for recurrent late deceleration and prolonged deceleration were 26% and 43%, respectively, which was not statistically significant between the two groups. CONCLUSION: We showed that HCA at term, particularly for funisitis, elevates the levels of maternal and neonatal CRP. Neonatal inflammatory signs, including elevated CRP levels, should be considered when managing cases of abnormal elevated CRP levels during labor at term.