PubMed · 2563514
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
1989-02-18. Chorioamnionitis: cause or effect?. https://pubmed.ncbi.nlm.nih.gov/2563514/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
OBJECTIVE: Meconium in amniotic fluid has been associated with an increased prevalence of chorioamnionitis. In an effort to delineate the mechanism of this association, we determined the effect of meconium on the neutrophil's capacity for phagocytosis and microbial killing by oxidative burst in vitro. STUDY DESIGN: Sterile meconium samples were obtained from four fetuses at the time of breech delivery and were then pooled and lyophilized. Neutrophils were purified from whole blood of each of 13 pregnant nonlaboring patients. Phagocytosis and the oxidative burst of neutrophils in the presence and absence of meconium were assessed by single-cell analysis with flow cytometry. Phagocytosis was measured as the mean fluorescence intensity produced after 30 minutes of incubation with fluorescein-labeled Escherichia coli. Oxidative burst was measured as the mean fluorescence intensity resulting from the oxidation of internalized reduced dichlorodihydrofluorescein after 15 minutes of stimulation with phorbol myristate acetate. Oxidative burst was expressed as the neutrophil oxidative index and the net fluorescence intensity. Neutrophil oxidative index was equivalent to the quotient of the mean fluorescence intensity for phorbol myristate acetate-stimulated and unstimulated cells. Net fluorescence intensity was equivalent to the absolute difference between stimulated and unstimulated cells. RESULTS: Exposure of neutrophils to light and very light meconium each resulted in significantly lower mean neutrophil oxidative index compared with unexposed controls (3.2 +/- 4.9 and 4.2 +/- 5.9 vs 16.2 +/- 7.5, p = 0.00002 and p = 0.0007, respectively) and significantly lower mean net fluorescence intensity than that of control cells (112 +/- 220 and 188 +/- 294 vs 613 +/- 328, p = 0.0001 and p = 0.005, respectively). Phagocytosis was significantly impaired in the presence of moderate meconium compared with control cells (2239 +/- 393 vs 4645 +/- 2071, p = 0.0001). Light meconium did not significantly affect phagocytosis. CONCLUSION: Meconium has significant effects on neutrophil function in vitro. Both light and very light meconium inhibit the oxidative burst. Moderate meconium inhibits phagocytosis.
A randomised prospective clinical trial was conducted over a 7-year period (1987-1993) in the Department of Obstetrics and Gynaecology, University of Patras. The purpose of this study was to compare two management protocols of Preterm Premature Rupture of Membranes (PPROM). Two-hundred forty-one women entered the study and were assigned randomly to one of two groups. Group A consisted of 105 subjects who were managed expectantly (tocolysis used for 48 h only, if necessary, to permit full course of steroid therapy), while Group B consisted of 136 subjects, in whom aggressive tocolysis was utilised. The differences in the latency period (time from rupture of membranes to the onset of labour) were not statistically significant between the two groups. On the contrary, statistically significant differences in the incidence of chorioamnionitis and postpartum endomyometritis were found between the two groups (higher in Group B). Twelve subjects in Group A (12/105, 11.4%) and 40 in Group B (40/136, 29.4%) had chorioamnionitis. The relative risk (RR) was 2.47 (95% C.I. 1.42-4.66, P < 0.001). Endomyometritis was diagnosed in 20 subjects in Group A (20/105, 19%) and in 45 in Group B (45/136, 33.3%). The RR was 1.74 (95% C.I. 1.10-2.75, P < 0.05). These data suggest that long term prophylactic tocolytic therapy in patients with PPROM, while without demonstrated benefit, may result in an increased risk of maternal infectious morbidity, and raise the cost of treatment.
The article presents a survey of preterm rupture of the amniotic membranes at term (more than 1 hour prior to uterine contractions) and preterm (< 37 weeks). The diagnosis of rupture can be suspected from the history alone in 90% of the cases, and confirmed by inspection. In doubtful cases the pH in fluid from the posterior fornix of the vagina is determined and microscopy is performed. Amniotic fluid is alkaline. Microscopy of a dried specimen shows "ferning" when amniotic fluid is present (crystallization test). Staining with Nil blue will reveal orange foetal cells in fresh specimens, usually only late in pregnancy (after the 38 week). The crystallization test is useful, however, in all three trimesters. The cause of membrane rupture and of chorioamnionitis may be infection. Chorioamnionitis is a serious clinical condition, but can be subclinical and may occur with intact membranes. It can lead to preterm delivery. It is important that chorioamnionitis be diagnosed (maternal fever, tachycardia, uterine contractions, abdominal pain, foul smelling vaginal discharge and elevated C-reactive protein). The condition is treated with antibiotics and labour must be induced.