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Amnioinfusion in Preterm PROM: Effects on Amnion and Cord Histology

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Amnioinfusion in Preterm PROM: Effects on Amnion and Cord Histology Journal of Perinatology (2008) 28, 97–101 r 2008 Nature Publishing Group All rights reserved. 0743-8346/08 $30 www.nature.com/jp ORIGINAL ARTICLE Amnioinfusion in preterm PROM: effects on amnion and cord histology A Locatelli1, M Andreani1, A Ghidini1, M Verderio1, A Pizzardi1, P Vergani1 and CM Salafia2 1Department of Obstetrics and Gynecology, University of Milano-Bicocca, Monza, Italy and 2Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA and lower incidence of pulmonary hypoplasia compared with Objective: To investigate the effects of transabdominal amnioinfusion expectant management.1–6 A recent randomized study7 confirmed (TA) on the histology of amnion (A) and umbilical cord (UC). a significant prolongation of pregnancy in cases managed with Study Design: From a cohort of 56 singleton pregnancies with amnioinfusion. premature rupture of membranes (PROM) at p24.6 weeks, we excluded However, the infusion of normal saline into the amniotic fluid those who did not develop severe oligohydramnios (n ¼ 12). Of the 44 is not fully a physiologic replacement of amniotic fluid, with its patients, 29 consented to TA and 15 declined the procedure. TA was wealth of growth factors and nutritive components. It is thus performed with normal saline solution. conceivable that exposure of the membranes to normal saline could have some deleterious effects on the integrity or histologic Result: Women who consented to TA underwent a median of three features of the amnion and umbilical epithelia. Because the effects procedures had a gestational age at PROM of 18.7 weeks and at delivery of of amnioinfusion on placental histology have not been addressed 26.1 weeks, with a latency of 50 days. Compared with subjects who so far, we have investigated whether amnioinfusion in women with declined the procedure, TA had a beneficial effect on clinical variables, second trimester PROM and severe oligohydramnios has an effect mediated primarily by a longer latency. TA was not associated with on the histopathologic integrity of the epithelial surfaces of the identifiable effects on the histologic features of A or UC. amniochorionic membranes and umbilical cord and the Conclusion: A and UC histology is not significantly affected by exposure underlying connective tissue. Since acute inflammation and to saline solution even for prolonged periods of time. uteroplacental ischemia, two factors implicated in the causation of Journal of Perinatology (2008) 28, 97–101; doi:10.1038/sj.jp.7211876; PROM, may also affect the integrity of the epithelial surfaces, in published online 29 November 2007 the analysis we have taken into account the presence and severity of these two processes at histology. Keywords: amnioinfusion; placental histology; preterm premature rupture of membranes Methods Introduction We have accessed a database of consecutive singleton pregnancies When premature rupture of membranes (PROM) occurs in the with preterm PROM at <25.0 weeks lasting >4 days admitted at early second trimester and is associated with severe our institution between January 1998 and December 2004. oligohydramnios, standard approaches have traditionally included Diagnosis of rupture of the membranes was made by observation of termination of pregnancy or expectant management. However, persistent vaginal pooling on sterile speculum examination and alternative strategies have been explored for treatment and repair of serial ultrasonographic observations. Gestational age (GA) was membrane rupture, such as use of serial amnioinfusions, established by menstrual history and confirmed by intracervical tissue sealants, gelatin sponge embolization and ultrasonographic examination before 20 weeks. amniopatch.1–3 Amnioinfusion is the only approach that has been Included in the present study were those with (1) evaluated by independent investigators in nonrandomized series oligohydramnios, defined as deepest pocket of amniotic fluid and it has been shown to lead to higher perinatal survival rates p2 cm and persisting for 4 days or longer, (2) no major fetal anomalies and (3) placental slides available for histopathological Correspondence: Dr A Locatelli, Clinica Ostetrica e Ginecologica, University of Milano- examination. Bicocca, San Gerardo Hospital, Monza (MI), Italy. All patients were given hospital bed rest during the first week E-mail: [email protected] Received 17 April 2007; revised 13 September 2007; accepted 9 October 2007; published online and received an initial 7-day course of antibiotic prophylaxis 29 November 2007 (sulbactam–ampicillin 3 g every 8 h or amoxicillin–clavulanic Amnioinfusion in preterm PROM A Locatelli et al 98 acid 2 g every 8 h i.v.). Digital examination was avoided until of connective tissue. In the umbilical cord, we analyzed epithelial active labor. After the initial 7-day hospital stay, the patient was or Wharton’s jelly necrosis, PMN number, distance and integrity in discharged home on bed rest if GA was <25 weeks; vaginal cultures the cord vessels and in the Wharton’s jelly. For the purpose of the were obtained every 2 weeks, and positive results for potentially analysis, epithelial integrity was graded in a semiquantitative scale pathogenic bacteria were treated. After 25 weeks’ gestation, women from 1 to 4 based on the distribution of the nuclei, which normally were admitted to the hospital until delivery and they received at are distributed at regular intervals reflecting the size of each least one course of corticosteroid therapy (betamethasone 12 mg epithelial cell. Scattered nuclear dropout with retained cytoplasm i.m. daily  two doses). In the presence of preterm labor, (considered a sign of cell death with loss of nuclear staining but tocolytic treatment (i.v. ritodrine) was administrated in the absence undissolved cytoplasm) was graded 1. Grade 4 was complete loss of of clinical signs of chorioamnionitis or abruptio placentae. Fetal all epithelium on the amnion basement membrane, or a naked heart rate was monitored daily, and biophysical profile was basement membrane without viable cells (with nuclei and performed twice a week. Amniotic fluid volume was assessed cytoplasm), or dead ‘ghost’ cells (no nuclear staining but preserved sonographically weekly on the outpatients, and every other day cytoplasm/cell shape). from admission until delivery. Chorionic and basal plate were evaluated in particular for Consenting women with persistent (>4 days) oligohydramnios evidence of acute inflammation or uteroplacental ischemia, the (maximum cord-free pocket of amniotic fluid <2 cm) were offered two principal pathologic processes that have been implicated in the serial amnioinfusions. Under sonographic guidance a 20-gauge needle causation of PROM and that may affect histologic features of was inserted transabdominally into the amniotic cavity. Transplacental amnion and umbilical cord. Histologic evidence of acute passage was avoided whenever possible. We targeted either a small inflammation was established by the number of neutrophils, their pocket of residual fluid or loops of cord between the fetal limbs, using integrity and the extent of tissue invasion in amnion, color flow mapping to avoid puncturing the umbilical cord. The choriodecidua and chorionic plate. Evidence of placental damage correct positioning of the needle was checked either by aspiration of a related to uteroplacental vascular pathology included abnormalities little amount of amniotic fluid or by ultrasonographic visualization of of uteroplacental vessels, fibrinoid necrosis and atherosis, a free dispersion of normal saline solution within the amniotic cavity. abruption, villous infarcts, terminal villous fibrosis, increased The volume infused of normal saline solution was aimed at restoring a syncytiotrophoblast knotting, cytotrophoblast (‘X-cell’) proliferation normal amount of amniotic fluid; we noted that infusion of 10 ml per and villous hypovascularity. For the purpose of the analysis, the week of GA was usually sufficient for this purpose. In no case did the two pathologic processes (acute inflammation and uteroplacental procedure last longer than 15 min. If oligohydramnios recurred and ischemia) were evaluated in a stochastic way (as present or absent) persisted for >4 days, the procedure was repeated. Amnioinfusion was as well as in a semiquantitative way, by averaging the scores of deemed successful if the mean deepest pocket of fluid during the acute inflammatory and uteroplacental ischemia lesions. latency period was >2 cm. Delivery was expedited in the presence of clinical Statistical analysis chorioamnionitis; fetal tachycardia with diminished variability, Histologic and clinical characteristics of women who underwent recurrent late or severe variable decelerations, or a biophysical amnioinfusion were compared with those of women with similar profile score <6; abruptio placentae; or GA >34 weeks. severity of oligohydramnios who did not undergo the procedure, Placental pathology sampling and examination were performed using one-way ANOVA and Fisher’s exact test; a P<0.05 was following a standard protocol. For each case, at least two samples considered significant. Linear regression analysis was used to assess of the following were obtained: extra-placental membranes near the independent effect of amnioinfusion on epithelial integrity of the point of rupture and near the placenta; chorionic plate amnion and umbilical cord after controlling for acute including the whole wall, distant from the marginal edge; decidua inflammation and uteroplacental
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