Gomez Ricardo, Romero Roberto, Nien Jyh Kae, Medina Luis, Carstens Mario, Kim Yeon Mee, Espinoza Jimmy, Chaiworapongsa Tinnakorn, Gonzalez Rogelio, Iams Jay D, Rojas Iván
Center for Perinatal Diagnosis and Research CEDIP, Hospital Dr. Sótero del Río, P. Universidad Católica de Chile, Puente Alto, Chile.
J Matern Fetal Neonatal Med. 2007 Feb;20(2):167-73. doi: 10.1080/14767050601135485.
Antibiotic administration has become part of the standard of care for patients with preterm premature rupture of membranes (PROM). Yet, the natural history of intrauterine infection/inflammation during antibiotic therapy remains largely unknown. This study was conducted to determine if antibiotic administration to the mother eradicates intra-amniotic infection and/or reduces the frequency of intra-amniotic inflammation, a risk factor for impending preterm labor/delivery and adverse neonatal outcome.
A subset of patients with preterm PROM admitted to our institution underwent amniocenteses before and after antibiotic administration in order to guide clinical management. Amniotic fluid analysis consisted of a Gram stain, culture for aerobic and anaerobic bacteria as well as genital mycoplasmas, and amniotic fluid white blood cell (WBC) count. Microbial invasion of the amniotic cavity (MIAC) was defined as a positive amniotic fluid culture. Intra-amniotic inflammation was defined as an amniotic fluid WBC count >or=100/mm(3). Patients were given antibiotics and steroids after the 24(th) week of gestation. Antibiotic treatment consisted of ampicillin and erythromycin for 7 days for patients without evidence of intra-amniotic inflammation or MIAC, and ceftriaxone, clindamycin and erythromycin for 10-14 days for those with intra-amniotic inflammation or MIAC.
Forty-six patients with preterm PROM whose first amniocentesis was performed between 18 and 32 weeks (median 27.4 weeks) were included in the study. The overall prevalence of intra-amniotic inflammation in the first amniocentesis was 39% (18/46). Seven had a positive amniotic fluid culture for microorganisms. At the time of the second amniocentesis, six of the seven patients with a positive amniotic fluid culture had microorganisms. Of 18 patients with intra-amniotic inflammation at admission, only three showed no evidence of inflammation after antibiotic treatment. Among patients with no evidence of intra-amniotic inflammation at admission, 32% (9/28) developed inflammation despite therapy. Five of these nine patients had positive amniotic fluid cultures.
(1) Antibiotic administration (ceftriaxone, clindamycin, and erythromycin) rarely eradicates intra-amniotic infection in patients with preterm PROM; (2) intra-amniotic inflammation developed in one-third of patients who did not have inflammation at admission, despite antibiotic administration; (3) a sub-group of patients with documented inflammation of the amniotic cavity demonstrated a decrease in the intensity of the inflammatory process after antibiotic administration.
抗生素给药已成为胎膜早破早产患者标准治疗的一部分。然而,抗生素治疗期间宫内感染/炎症的自然病程仍很大程度上未知。本研究旨在确定对母亲使用抗生素是否能根除羊膜腔内感染和/或降低羊膜腔内炎症的发生率,羊膜腔内炎症是即将发生早产/分娩及不良新生儿结局的一个危险因素。
我院收治的一部分胎膜早破早产患者在使用抗生素前后接受了羊膜腔穿刺术,以指导临床管理。羊水分析包括革兰氏染色、需氧菌和厌氧菌以及生殖道支原体培养,以及羊水白细胞(WBC)计数。羊膜腔微生物入侵(MIAC)定义为羊水培养阳性。羊膜腔内炎症定义为羊水白细胞计数≥100/mm³。患者在妊娠24周后给予抗生素和类固醇。对于无羊膜腔内炎症或MIAC证据的患者,抗生素治疗为氨苄西林和红霉素连用7天;对于有羊膜腔内炎症或MIAC的患者,头孢曲松、克林霉素和红霉素连用10 - 14天。
本研究纳入了46例胎膜早破早产患者,其首次羊膜腔穿刺在18至32周(中位时间27.4周)进行。首次羊膜腔穿刺时羊膜腔内炎症的总体发生率为39%(18/46)。7例羊水微生物培养阳性。在第二次羊膜腔穿刺时,7例羊水培养阳性患者中有6例仍有微生物。入院时有羊膜腔内炎症的18例患者中,抗生素治疗后只有3例无炎症迹象。入院时无羊膜腔内炎症证据的患者中,32%(9/28)尽管接受了治疗仍发生了炎症。这9例患者中有5例羊水培养阳性。
(1)抗生素给药(头孢曲松、克林霉素和红霉素)很少能根除胎膜早破早产患者的羊膜腔内感染;(2)三分之一入院时无炎症的患者尽管使用了抗生素仍发生了羊膜腔内炎症;(3)一部分有记录的羊膜腔炎症患者在抗生素给药后炎症过程强度有所降低。