Efficacy of vitamin E in protection against methotrexate induced placental injury in albino rats.

Methotrexate (MXT) is a chemotherapeutic drug that has been used in a wide range of clinical practices. Unfortunately, the administration of MXT during pregnancy may induce abortion, fetal deformities, and intrauterine growth retardation. Vitamin E is an antioxidant agent that can ameliorate free radical damage. The current work aimed to shed more light on the possible protective effect of vitamin E against MXT induced placental toxicity and to determine the possible mechanisms; biochemically, histologically, and immunohistochemically. Four groups were used: control pregnant, Vitamin E (VIT E) pregnant, Methotrexate (MXT) pregnant, and Vitamin E Methotrexate (VIT E-MXT) pregnant. The placental tissues were processed for light, immunohistochemical, and electron microscopic study. Other samples were obtained for biochemical study; the placental oxidant/antioxidant status was evaluated. The results showed that MXT caused various placental morphological changes in the form of distorted chorionic projection with an accumulation of hemosiderin granules in the trophoblastic cells. Maternal blood vessels showed a homogenous acidophilic material Edema of the extra-embryonic fetal membranes was noticed. A significant decreased in placental weight as well as increase in the oxidative and inflammatory markers were detected. Increased COX2 and decreased eNOS expressions were observed in the MXT group if compared to the control group. VIT E significantly restored the normal histological and immunohistochemical appearance, placental weight, and oxidant/antioxidant balance. It could be concluded the biochemical, morphological, and morphometric findings suggested that vitamin E coadministration is promising in attenuating the placental toxic effect of methotrexate. In this study, VIT E decreased the inflammatory and oxidative stress effect of methotrexate on the placental tissue by enhancing the level of eNOS.

Four major patterns of placental injury: a stepwise guide for understanding and implementing the 2016 Amsterdam consensus.

The Amsterdam classification system defines four major patterns of placental injury, maternal vascular malperfusion, fetal vascular malperfusion, acute chorioamnionitis, and villitis of unknown etiology, and lists the histologic findings that characterize each. However, there continues to be uncertainty regarding specific definitions, histologic mimics, grading and staging, and what combination of findings is required to diagnose each pattern of injury in a reproducible fashion. The purpose of this review is to clarify some of these issues by suggesting a stepwise approach to more fully realize the potential of this new classification system. In our view, the critical steps for correctly identifying and communicating each pattern of injury are (1) familiarity with the underlying pathophysiology and known clinical associations, (2) incorporation of important gross findings, (3) learning to recognize underlying architectural alterations and defining features at low power, (4) using higher magnification to narrow the differential diagnosis and assess severity (grading) and duration (staging), and (5) adopting a template for generating standardized placental reports that succinctly provide useful information for patient care and research applications.

Cordocentesis-associated fetal loss and risk factors: single-center experience with 6650 cases.

OBJECTIVES: To identify procedural risk factors associated with fetal loss following cordocentesis and to determine the rate of cordocentesis-related fetal loss associated with the current cordocentesis protocol used in our institution. METHODS: This was a retrospective cohort study of pregnancies that underwent midpregnancy cordocentesis in a single center (a tertiary hospital, teaching school), between 1992 and 2018, based on data retrieved from our prospective database. All consecutive cases were validated to retrieve those meeting the eligibility criteria, which included: singleton pregnancy without underlying maternal disease, normal fetus (no structural or chromosomal abnormality or severe disorder), gestational age between 16 and 24 weeks at the time of the procedure and availability of pregnancy outcome. Cases that resulted in termination of pregnancy were excluded. We assessed the effect of prior cordocentesis model training on the fetal-loss rate and procedure-related complications, and evaluated potential risk factors of fetal loss secondary to cordocentesis, including procedure difficulty, placenta penetration, prolonged bleeding, fetal bradycardia, puncture site and early gestational age at procedure. Pregnancy outcomes were compared between the study group and a control group of women, who did not undergo cordocentesis, selected randomly at a 1:1 ratio from our obstetric database. RESULTS: A total of 10 343 procedures were performed during the study period, of which 6650 met the eligibility criteria and were included in the analysis. The fetal-loss rate in the first 60 procedures (early practice) of six operators (n = 360 procedures), who did not have prior model training, was significantly higher than that during the early practice of 18 operators (n = 1080 procedures) with prior model training (6.9% vs 1.6%; P < 0.001); whereas the fetal-loss rate in the next 60 procedures of practice was comparable between the two groups. After excluding the first 360 procedures of the groups without prior model training, the overall fetal-loss rate in pregnancies that underwent cordocentesis was significantly higher than that in the control group (1.6% vs 1.0%; P < 0.001). Considering the fetal-loss rate in the normal controls as background loss, the incremental cordocentesis-associated fetal-loss rate was 0.6%. Penetration of the placenta (odds ratio (OR), 2.65 (95% CI, 1.71-4.10)), prolonged bleeding from the puncture site (OR, 10.85 (95% CI, 5.27-22.36)) and presence of fetal bradycardia (OR, 3.32 (95% CI, 1.83-6.04)) during cordocentesis were independent risk factors associated with fetal loss. CONCLUSIONS: Cordocentesis model training markedly reduces fetal loss during the early learning curve of practice. Thus, cordocentesis practice without prior model training should not be acceptable. Significant procedural risk factors for fetal loss secondary to cordocentesis are placental penetration, prolonged bleeding and fetal bradycardia. Cordocentesis-related fetal loss may be only 0.6%, much lower than the rate reported previously. Copyright © 2020 ISUOG. Published by John Wiley & Sons Ltd.

Mitigating placental injuries through up-regulating DAF in experimental APS mice: new mechanism of progesterone.

Anti-phospholipid syndrome (APS) is characterized by recurrent pathological pregnancy, arterial or venous thrombosis in the presence of anti-phospholipid antibody (aPL). Complement activation is recognized as an intermediate link leading to placental thrombosis and placental inflammation in APS model mice. Decay accelerating factor (DAF, CD55), MAC-inhibitory protein (MAC-IP, CD59) and membrane co-factor protein (MCP, CD46) are important complement inhibitory proteins (CIPs) highly expressed in normal placenta to curb excessive complement activation and its mediated injuries. Anti-ß2 glycoprotein I (anti-ß2GPI) antibody is an important aPL. We found that placental DAF and CD46 decreased in ß2GPI passively immunized APS model mice, accompanied by C3 deposition, neutrophil infiltration and increased proinflammatory cytokine levels detected in its placenta. Progesterone supplement can up-regulate DAF but not CD46 expression, curb C3 activation and decrease proinflammatory cytokines levels to reduce fetal loss frequency. Progesterone receptor antagonist (mifepristone) or knock-down DAF with specific siRNA, above the protective effects of progesterone, were significantly weakened. Another sex hormone, oestrogen, has no significant effect on placental DAF and C3 contents and fetal loss frequency in the APS mice model. This may be an important mechanism by which progesterone induces maternal-fetal immune tolerance. At the same time, it may provide evidence for the use of progesterone in APS abortion patients.

Placental malperfusion in response to intrauterine inflammation and its connection to fetal sequelae.

Exposure to intrauterine inflammation (IUI) is associated with short- and long-term adverse perinatal outcomes. However, little data exist on utilizing placenta to prognosticate fetal injury in this scenario. Our study aimed to utilize imaging modalities to evaluate mechanisms contributing to placental injury following IUI exposure and correlated it to concomitant fetal brain injury. CD1 pregnant dams underwent laparotomies and received intrauterine injections of either lipopolysaccharide (LPS; a model of IUI) or phosphate-buffered saline (PBS). In utero ultrasound Doppler velocimetry of uterine and umbilical arteries and magnetic resonance imaging (MRI) of placental volumes with confirmatory immunohistochemical (vimentin) and histochemistry (fibrin) analyses were performed. ELISA for thrombosis markers, fibrinogen and fibrin was performed to analyze thrombi in placenta. Fetal brain immunohistochemistry was performed to detect microglial activation (ionized calcium-binding adaptor molecule 1, Iba1). On ultrasound, LPS group demonstrated elevated resistance indices, pulsatility indices and a greater occurrence of absent end-diastolic flow in the umbilical and uterine arteries. In the fetus, there was an increased cardiac Tei indices in the LPS group. MRI revealed decreased volume of placenta in the LPS group associated with placental thinning and placental endothelial damage on immunohistochemistry. Decreased fibrinogen content and more thrombi staining in placenta exposed to maternal LPS indicated the hypercoagulability. Furthermore, the expression of Iba1was significantly associated with placental thickness (r = -0.7890, Pearson correlation coefficient). Our data indicate that IUI can trigger events leading to maternal placental malperfusion and fetal vessel resistance, as well as predispose the developing fetus to cardiac dysfunction and brain damage. Furthermore, our data suggest that prenatal ultrasound can be a real-time clinical tool for assessing fetal risk for adverse neurologic outcomes following the potential IUI exposure.

Rosiglitazone blocks first trimester in-vitro placental injury caused by NF-κB-mediated inflammation.

Increased inflammation and abnormal placentation are common features of a wide spectrum of pregnancy-related disorders such as intra uterine growth restriction, preeclampsia and preterm birth. The inflammatory response of the human placenta has been mostly investigated in relation to cytokine release, but the direct molecular consequences on trophoblast differentiation have not been investigated. This study measured the general effects of LPS on both extravillous and villous trophoblast physiology, and the involvement of the transcription factors PPARγ and NF-κB, specifically using 1st trimester explants and HTR-8/ SVneo cell line models. While both proteins are known for their roles in inflammatory pathways, PPARγ has been identified as an important molecule in trophoblast differentiation, suggesting its potential role in mediating a crosstalk between inflammation and trophoblast differentiation. Here, LPS (1 µg/ml) exposure of first trimester placental villous explants resulted in secretion of inflammatory cytokines, induction of apoptosis and reduction in trophoblast cell proliferation. Additionally, LPS significantly reduced expression of the trophoblast differentiation proteins GCM1 and ß-hCG, and increased invasion of the extravillous trophoblast. Activation of PPARγ by Rosiglitazone (10 µM) reversed the LPS-mediated effects on inflammatory cytokine release, trophoblast apoptosis and proliferation compared to controls. Lastly, markers of trophoblast differentiation and invasion reverted to control levels upon activation of PPARγ and concomitant inhibition of NF-κB (either by Rosiglitazone or NF-κB specific inhibitor), revealing a new role for NF-κB in trophoblast invasion. This study reveals a novel PPARγ - NF-κB axis that coordinates inflammatory and differentiation pathways in the human placenta. The ability to reverse trophoblast-associated inflammation with Rosiglitazone offers promise that the PPARγ - NF-κB pathway could one day provide a therapeutic target for placental dysfunction associated with both inflammation and abnormal trophoblast differentiation.

Placental Histology After Minor Trauma in Pregnancy: A Pilot Study.

OBJECTIVE: Trauma in pregnancy may cause placental abruption. Consequences of moderate placental injury on neurodevelopment are unknown. The aim was to evaluate placental histology after maternal trauma. METHODS: A prospective study was conducted at 2 tertiary medical centers in the Netherlands. Placentas from women exposed to maternal trauma ≥ 20 weeks' gestational age were histologically examined. Neurological follow-up of the infants was performed at 1 year of age by means of Alberta Infant Motor Scale. Histological findings were compared to placentas from pregnancies without trauma. PRINCIPAL RESULTS: Thirteen placentas were investigated in the trauma group. The control group consisted of 15 placentas. Placental pathology was seen more often in the trauma cases (11 of the 13) than in the controls (6 of the 15), P = .024. Neurological follow-up was normal. CONCLUSIONS: In this small population, majority of the placentas showed pathology after minor trauma in pregnancy without consequences for neurodevelopment at 1 year.

Hydrogen sulfide alleviates placental injury induced by maternal cigarette smoke exposure during pregnancy in rats.

Maternal cigarette smoke exposure (CS) during pregnancy is a well recognized causative factor for placental injury. Hydrogen sulfide (H2S), a gaseous signal molecule, has been shown to exert a protective effect against tissue injury in many organs. This study aimed to investigate whether H2S could alleviate CS-induced placental injury in rats. Pregnant SD rats were randomly divided into 4 groups: NaCl, CS, CS + NaHS (a donor of H2S) and NaHS. On gestational day 21, placental and fetal weights were measured. Placental H2S content was assessed by methylene blue method. Placental histological changes were examined by light microscopy and transmission electron microscopy. The results showed that administration of NaHS significantly attenuated CS-induced decrease in placental and fetal weights. Moreover, NaHS injection markedly alleviated CS-induced reduction in placental H2S content. Meanwhile, NaHS treatment obviously improved CS-induced morphological changes of placental junctional and labyrinthine zones. More notably, NaHS administration in CS rats was also found to ameliorate placental ultrastructural alterations, as indicated by decrease in the thickness of placental barrier, prevention of apical microvilli loss, alleviation of endoplasmic reticulum swelling and reduction in the number of vacuoles in trophoblast cells. Taken together, these findings demonstrate that administration of NaHS can alleviate CS-induced placental injuries in rats, suggesting that H2S may have therapeutic potential for treatment of placental injury caused by CS.

Intrauterine fetal death caused by seatbelt injury.

OBJECTIVE: Severe motor vehicle accidents involving pregnant women can result in fetal and neonatal death. We describe a case in which fetal death occurred due to relatively mild seatbelt injuries and present the characteristic magnetic resonance imaging (MRI) findings of the placenta. CASE REPORT: A 26-year-old primigravid woman at 20 weeks gestation was involved in an automobile accident. Although she suffered only a seatbelt injury, fetal death subsequently occurred. Contrast-enhanced MRI showed the region compressed by the seatbelt as a low-intensity band without enhancement, and serum alpha-fetoprotein and hemoglobin F levels were elevated. CONCLUSION: Careful monitoring, including blood and abdominal examinations, should be performed when pregnant women suffer seatbelt injuries.

Potentially Avoidable Peripartum Hysterectomies in Denmark: A Population Based Clinical Audit.

OBJECTIVE: To audit the clinical management preceding peripartum hysterectomy and evaluate if peripartum hysterectomies are potentially avoidable and by which means. MATERIAL AND METHODS: We developed a structured audit form based on explicit criteria for the minimal mandatory management of the specific types of pregnancy and delivery complications leading to peripartum hysterectomy. We evaluated medical records of the 50 Danish women with peripartum hysterectomy identified in the Nordic Obstetric Surveillance Study 2009-2012 and made short narratives of all cases. RESULTS: The most frequent indication for hysterectomy was hemorrhage. The two main initial causes were abnormally invasive placenta (26%) and lacerations (26%). Primary atony was third and occurred in 20%. Before hysterectomy another 26% had secondary atony following complications such as lacerations, retained placental tissue or coagulation defects. Of the 50 cases, 24% were assessed to be avoidable and 30% potentially avoidable. Hysterectomy following primary and secondary atony was assessed to be avoidable in 4/10 and 4/13 cases, respectively. Early sufficient suturing of lacerations and uterine ruptures, as well as a more widespread use of intrauterine balloons alone or in combination with uterine compression sutures (the sandwich model), could presumably have prevented about one fourth of the peripartum hysterectomies. CONCLUSION: More than 50% of peripartum hysterectomies seem to be avoidable by simple measures. In order to minimize the number of unnecessary peripartum hysterectomies, obstetricians and anesthesiologists should investigate individual cases by structured clinical audit, and disseminate and discuss the results for educational purposes. An international collaboration is warranted to strengthen our recommendations and reveal if they are generally applicable.

Incidence of fetal bradycardia and effect of placental injury on fetal heart rate during second-trimester genetic amniocentesis.

A prospective study was conducted for comparing the incidence of fetal bradycardia and level of fetal heart rate change following a second-trimester genetic amniocentesis with and without placental injury. A total of 257 and 495 participants in injured and non-injured groups were analysed. The incidence of fetal bradycardia following amniocentesis was not statistically different between the two groups (1.17%, [95% CI 0.24, 3.37] and 0.20%, [95% CI 0.005, 1.12]) in injured and non-injured placenta groups, respectively; p = 0.118). The mean change in baseline fetal heart rate before and after amniocentesis was also not significantly different between the two groups (p = 0.844). No fetal death or pregnancy loss occurred within 4 weeks after the procedure. All 4 bradycardia participants were normal and healthy and had an appropriate weight for their gestational age. We conclude that placental injury during a second-trimester genetic amniocentesis due to advanced maternal age poses only a low risk of fetal bradycardia, and there is no evidence of differences between subjects with injured and non-injured placenta in the changes in fetal heart rate.

An Autopsy Case of a Pregnant Woman With Severe Placental and Fetal Damage From Domestic Violence.

We present an autopsy case of a pregnant woman who was a victim of domestic violence. The deceased showed injuries mainly to her head and abdomen. Postmortem examination revealed 1400 mL of abdominal hemorrhage, ablation of the perimetrium, placental avulsion, and intracranial hematoma. The cause of death was diagnosed as hemorrhagic shock. The uterus contained a fetus of 7 months' gestational age. Fetal autopsy revealed laceration of the lungs, laceration and avulsion of the liver, and 15 mL of hemoperitoneum. Both placental and fetal injuries suggested repeated severe attacks to the abdomen, such as those expected to result from kicking or hitting.

Effect of placenta penetration during cordocentesis at mid-pregnancy on fetal outcomes.

OBJECTIVES: To compare the rates of fetal loss, low birth weight, and preterm birth between pregnancies undergoing cordocentesis at mid-pregnancy with placenta penetration and those without it. METHODS: Consecutive cases of cordocenteses were prospectively recorded. The inclusion criteria for analysis were: (1) singleton pregnancies, (2) no fetal abnormalities, (3) gestational age of 18-22 weeks, and (4) procedures performed by experienced operators. The primary outcome was fetal loss rate, and the secondary outcomes were rates of failed procedures, low birth weight, and preterm birth. RESULTS: Of 6147 cordocenteses recorded, 2829 met the inclusion criteria with complete data for analysis. Of these, 654 procedures were further excluded because the puncture site was at cord insertion. The remaining 2175 cases, consisting of 615 procedures with placenta penetration and 1560 cases with no penetration, were analyzed. Cordocenteses with placenta penetration had a significantly higher rate of fetal loss (3.6% vs 1.3%, p = 0.01) as well as of low birth weight and preterm birth. CONCLUSION: Cordocentesis with placenta penetration carries a higher risk for fetal loss, preterm birth, and low birth weight. This information may be helpful in prenatal diagnosis counseling, and it may encourage performers to avoid placenta penetration, if possible.

Comparison between 20G and 22G needle for second trimester amniocentesis in terms of technical aspects and short-term complications.

OBJECTIVE: To compare short-term complications of amniocentesis using 20G versus 22G needle. METHODS: A total of 200 women referred for mid-trimester amniocentesis were randomized to a 20G (Group I, n = 100) or 22G amniocentesis needle (Group II, n = 100). The primary outcome was intrauterine bleeding at needle insertion. The operator reported technical aspects and patient's reactions immediately after the procedure. Women's perception of discomfort 30 min after the procedure and complications after 2 weeks were recorded. RESULTS: Intrauterine bleeding at needle insertion was similar between groups (4/100 vs 8/100). When only transplacental taps were analyzed, bleeding was significantly lower in Group I (4/20 vs 8/14, p = 0.035). Fluid retrieval was faster in Group I (9.6 vs 26.8 sec, p < 0.001). In all, 65% of women in Group I versus 30% in Group II reported discomfort during the procedure, although discomfort 30 min after the procedure and complications within 2 weeks after the procedure were similar in the two groups. CONCLUSION: Amniocentesis with 20G needle is associated with lower risk of intrauterine bleeding in case of transplacental needle insertion and allows for faster fluid retrieval, as compared with 22G needle. Nevertheless, 20G needle is associated with more immediate discomfort during the procedure.

Finite element modeling of human placental tissue.

Motor vehicle crashes account for a large portion of placental abruption and fetal losses. To better understand the material properties of the human placenta, a Finite Element (FE) model of human placenta tissue was created and verified using data from uniaxial tension tests. Sixty-four tensile tests at three different strain rates of 7% strain/s, 70% strain/s, and 700% strain/s from six whole human placentas were used for model development. Nominal stresses were calculated by dividing forces at the grips by the original cross-sectional area. Nominal strains were calculated by dividing cross-head displacement by the original gauge length. A detailed methodology for interpreting experimental data for application to material model development is presented. A model of the tension coupon was created in LS-DYNA and stretched in the same manner as the uniaxial tension tests. The behavior of the material was optimized to the uniaxial tension test using a multi-island genetic algorithm. The results demonstrate good correlation between experiments and the model, with an average difference of 2% between the optimized FE and experimental first principal stress at the termination state. The material parameters found in this study can be utilized in FE models of placental tissues for behavior under dynamic loading.

Hallazgos placentarios en casos de parálisis cerebral / Placental findings in cases of cerebral palsy

Objetivos: hay evidencias de que un elevado número de casos de parálisis cerebral (PC) se originan antes de nacer. Existe interés en determinar las causas que provocan esta grave complicación. Han sido descritas varias lesiones placentarias en estos pacientes. El objetivo es individualizar lesiones placentarias asociadas a PC en nuestro medio y poder contribuir a la determinación de factores de riesgo.Material y método: se estudiaron 39 placentas de pacientes con PC que nacieron en el Centro Hospitalario Pereira Rossell (CHPR). Se compararon los hallazgos con un grupo control de 75 placentas, correspondientes a embarazos de similar edad gestacional que no desarrollaron PC. Se evaluó la duración de la gestación, peso al nacer, peso placentario y alteraciones macroscópicas e histológicas de la placenta. Resultados: fue relevante, desde el punto de vista estadístico, el hallazgo de: a) placentas grandes en niños prematuros; b) meconio evolucionado; c) corioamnionitis con respuesta fetal histológica en niños prematuros; d) hematomas retroplacentarios parciales en niños prematuros con corioamnionitis, con o sin respuesta fetal histológica; e) vasculopatía trombótica fetal en gestaciones de término. Conclusiones: el estudio de la placenta aporta elementos valiosos en los pacientes con PC. Su resultado debería ser integrado a las historias clínicas pediátricas y ser considerado cuando se evalúa a los pacientes con PC y encefalopatía neonatal.

Background: there is strong evidence that a great number of cases of cerebral palsy (CP) are originated before birth. There is an interest in determining the causes of this dreadful complication. Many placental lesions have been described in these patients. The purpose of this research is to determine the placental lesions found in our cases of CP and to contribute to the investigation of risk factors. Material and method: the placentas from 39 patients with CP that were born at the Hospital Pereira Rossell in Montevideo were analyzed. The findings were compared to a control group of 75 placentas from patients of a similar gestational age without CP. The authors studied the gestational age, weight at birth, placenta weight and abnormal macroscopic and histological findings. Results: it was relevant from a statistical point of view the findings of: a) large placenta in premature babies; b) prolonged meconium; c) chorioamnionitis with fetal response in premature babies; d) partial retroplacental hematoma in premature babies with chorioamnionitis; e) fetal thrombotic vasculopathy in full term gestations. Conclusions: placental examination provides valuable evidence in lesions originated before birth in many cases of CP. The results should be included in the clinical history of the pediatric patients. They should be taken into consideration when evaluating patients with CP or with neonatal encephalopathy.

O espessamento da membrana basal do epitélio amniótico e as síndromes hipertensivas durante a gestação / The amniotic epithelium basal membrane thickening and hypertensive syndromes during pregnancy

Existem estudos sugerindo a associação entre o espessamento da membrana basal do epitélio amniótico (MBEA) e as intercorrências maternas e fetais. Objetivos: Neste estudo avaliamos a espessura da MBEA em pacientes com hipertensão durante a gestação. Métodos: Utilizamos 66 placentas, 46 de pacientes hipertensas e 20 controles. Após os exames macroscópico e microscópico, foi realizada a análise morfométrica. Resultados: A espessura da MBEA foi maior nas pacientes com síndromes hipertensivas durante a gestação, comparadas às do grupo controle (p=0,04): nas placentas com inflamação associada à hipertensão e nas placentas com alteração morfológica placentária (AMP) compatível com hipertensão e hipóxia perinatal. Conclusões: O espessamento da membrana basal do epitélio amniótico mostrou associação com às síndromes hipertensivas durante a gestação e deve ser mais um parâmetro a ser utilizado para avaliação das lesões placentárias relacionadas as síndromes hipertensivas durante a gestação.

Introduction: Some studies in the literature suggest the relationship between the amniotic epithelium basal membrane (AEBM) thickening and fetal outcome problems. Objective: To evaluate the thickness of the AEBM in patients with hypertension syndromes during gestation. Method: 66 placentas, 46 from hypertensive patients and 20 from normal controls were studied. After the gross and microscopic exams, the morphometric analysis of AEBM was performed. Results: Compared with the control group, the AEBM was thicker in the patients with hypertensive syndromes during gestation (p=0,04) as well as in placentas with inflammation associated with hypertension and in placentas with pathological alteration compatible with hypertension and perinatal hypoxia. Conclusion: The thickening of AEBM showed association with hypertensive syndromes during gestation and should be an additional parameter for the evaluation of placenta lesions related to hypertensive syndromes during gestation.

Blunt trauma in pregnancy.

Trauma is the most common cause of nonobstetric death among pregnant women in the United States. Motor vehicle crashes, domestic violence, and falls are the most common causes of blunt trauma during pregnancy. All pregnant patients with traumatic injury should be assessed formally in a medical setting because placental abruption can have dire fetal consequences and can present with few or no symptoms. Evaluation and treatment are the same as for nonpregnant patients, except that the uterus should be shifted off the great vessels. After initial stabilization, management includes electronic fetal monitoring, ultrasonography, and laboratory studies. Electronic fetal monitoring currently is the most accurate measure of fetal status after trauma, although the optimal duration of monitoring has not been established. Prevention of trauma through proper seat belt use during pregnancy and recognition of domestic violence during prenatal care is important.

Diagnostic mid trimester amniocentesis: how safe?

OBJECTIVE: Genetic mid-trimester amniocentesis is a common invasive procedure. The origin of the commonly quoted 0.5% rate of procedure-related pregnancy loss after amniocentesis is obscure and is in conflict with the only randomized prospective study that reported a procedure-related rate of loss of 1.0%. This review was performed to establish an estimate of procedure-related pregnancy loss after mid-trimester amniocentesis. The impact of placental puncture on the rate of loss and the risk of direct needle injury to the fetus were also examined. STUDY DESIGN: The National Library of Medicine database was used to identify English language reports of >1000 amniocenteses with sufficient detail and follow up data to allow the calculation of the rate of spontaneous pregnancy loss after amniocentesis but before 28 completed weeks. These reports were divided into 2 groups to assess the impact of the ultrasound technique. Group I described only preamniocentesis ultrasound evaluation; group II described primarily concurrent ultrasound needle guidance. Pregnancy loss between the 2 groups was compared. The impact of placental puncture and reported direct fetal trauma were examined. The significance of differences was tested using chi-square analysis, with significance at a probability value of < or =.05. RESULTS: Twenty-nine reports that totaled 68,119 amniocenteses were examined. In a comparison of all studies in group I with all studies in group II, there was a lower rate of loss after amniocenteses with the use of concurrent guidance (1.4%) compared with the use of preamniocentesis ultrasound evaluation (2.1%) that was significant ( P <.001). Among only the 5 controlled studies that used preamniocentesis ultrasound evaluation, the difference in rate of loss between amniocentesis patients and control subjects was 0.6% ( P =.0042; 95% CI, 0.19, 1.03), which was identical to the difference in the rate of loss of 0.6% between amniocentesis patients and control subjects from the 5 controlled studies that used concurrent ultrasound needle guidance ( P <.0001; 95% CI, 0.31, 0.90). Multiple case reports and small series of presumed fetal needle trauma were reviewed, but most of these attributed causation to the amniocentesis needle based only on circumstantial association. Two cases with direct evidence of fetal needle trauma are discussed. Finally, the rate of loss after placental puncture from among 9 reports that provided this detail was 1.4% and not different from the overall rate of loss that was noted in group II. CONCLUSION: This examination of experience with 68,119 amniocenteses from both controlled and uncontrolled studies provides a substantive basis for several conclusions: (1) Contemporary amniocentesis with concurrent ultrasound guidance in controlled studies appears to be associated with a procedure-related rate of excess pregnancy loss of 0.6% (95% CI, 0.31, 0.90). To determine the total rate of loss, this must be added to the reported natural rate of loss without amniocentesis among control patients of 1.08%. (2) The use of concurrent ultrasound guidance appears to reduce the number of punctures and the incidence of bloody fluid. Concurrent ultrasound guidance was associated with a reduced rate of loss when all studies were compared, but not among controlled studies. (3) Direct fetal needle trauma is rare, and rarely proved, but may occur more frequently than is reported because of a failure to diagnose and a failure of the consistent production of sequelae. (4) This experience does not substantiate an increased rate of pregnancy loss if placental puncture is required.