Retroplacental Hematoma Research Articles

Stillbirth, hypertensive disorders of pregnancy, and placental pathology

IntroductionStillbirth, preeclampsia, and gestational hypertension (PE/GH) have similar clinical risk factors and redundant placental pathology. We aim to discern if stillbirth with PE/GH has a particular phenotype by comparing stillbirths with and without PE/GH. MethodsSecondary analysis of the Stillbirth Collaborative Research Network, a population-based cohort study of all stillbirths and a sample of live births from 2006 to 2008 in five catchment areas. We compared placental pathology between stillbirths and with and without PE/GH, stratified by term or preterm. We also compared placental pathology between stillbirths and live births with PE/GH. Results79/518 stillbirths and 140/1200 live births had PE/GH. Amongst preterm stillbirths, there was higher feto-placental ratio in PE/GH pregnancies (OR 1.24 [1.11, 1.37] per unit increase), and there were more parenchymal infarctions (OR 5.77 [3.18, 10.47]). Among PE/GH pregnancies, stillbirths had increased maternal and fetal vascular lesions, including retroplacental hematoma, parenchymal infarction, fibrin deposition, fetal vascular thrombi, and avascular villi. DiscussionStillbirth pregnancies are overwhelmingly associated with placental lesions. Parenchymal infarctions are more common in PE/GH preterm stillbirths, but there is significant overlap in lesions found in stillbirths and PE/GH.

Placental morphology and fetal implications in pregnancies complicated by pregnancy-induced hypertension

Background: Many disorders of pregnancy, which are associated with a high perinatal morbidity and mortality, are accompanied by gross pathological changes in placenta. Hypertensive disorders of pregnancy are common, and form one of the deadly triads along with hemorrhage and infection that greatly contribute to maternal mortality and morbidity. In addition, they are strongly associated with fetal growth restriction, prematurity, and contributing largely to perinatal mortality and morbidity. A study of placentae was done to find out the morbid and histological changes in placentae of hypertensive mothers and to correlate the findings with the birth weight of new born babies. Materials and Methods: Ninety placentae were studied. The weight of the placenta, placental fetal ratio, retroplacental hematoma, infarction, and histopathological findings were noted. Placental findings were correlated with fetal outcome. Results: The placental weight and fetoplacental weight ratio (5.38:1) was decreased in the hypertensive group. There was an increase in the incidence of infarction (28.8%) and retroplacental hematoma (15.5%) in the hypertensive group. Percentage of cytotrophoblastic proliferation of villi, >30% syncytial knots formation (64.5%), basement membrane thickening of villi (37.8%), and fibrinoid necrosis of villi (46.7%) increased in the placentae from pregnancy-induced hypertension group as compared to the normal group. Conclusions: Hypertensive disorders of pregnancy adversely influence the morphology of placenta. Fetal outcome is poor in the presence of infarction, retroplacental hematoma, basement membrane thickening of villi, and fibrinoid necrosis of villi. The pathological changes observed in the placentae of patients with hypertensive disorders of pregnancy adversely influence the perinatal outcome.

Factors associated with post-cesarean stillbirth in 12 hospitals in Benin: a cross-sectional.

IntroductionIn spite of free caesarean section applied in Benin since 2009, high rates of stillborn babies continue to be recorded. This study aimed to determine the factors associated with post-caesarean stillborn in Benin.MethodsCross-sectional study that covered all women who have delivered by caesarean from December 2013 to February 2014 in twelve hospitals chosen by simple random selection in each of the twelve departments of Benin. Data collected by chart review have been analyzed using the statistical software Epi info 3.5.1. Univariate analysis and multivariable logistic regression were used to identify factors associated with post-caesarean stillbirth at the significance threshold of 5%.ResultsThere were 66 stillborn per 1,000 births of which 58% died before admission to hospital. The risk factors identified were the reference (p = 0.0011), general anesthesia (p = 0.0371), the low birth weight (p = 0.0001), the retro-placental hematoma (p = 0.0083), and the umbilical cord prolapse (p = 0.0229). Acute fetal distress (p = 0.0308) and anesthesia administered by an anesthetist nurse or midwife (p = 0.0337) were protective factors.ConclusionThe majority of cases, in utero death occurred before admission to hospital. Strengthening antenatal refocused consultation, a better access to quality obstetric care and the grant of all obstetric care could reduce stillbirths from caesarean sections in Benin.

Novel pathological findings of placenta with fetal heart failure associated with congenital heart disease

Novel pathological findings of placenta with fetal heart failure associated with congenital heart disease

P93. Early-onset eclampsia with intrauterine fetal death after placental abruption at 22 weeks gestation: A case report and literature review

Background Eclampsia is one of the complications of preeclampsia, and associated with increased risks of maternal and prenatal mortality and morbidity. The incidence of eclampsia varies worldwide, and ranges from 4/10,000 (0.04%) deliveries to 7.4/10,000 (0.07%) deliveries in Japan. The time of eclamptic episode can be antepartum, intrapartum, or postpartum. However, report of eclampsia occurs at Case report A 37-year-old primiparous Japanese woman who had no history of hypertension suddenly developed convulsion attack in local clinic at 22 weeks and 2 days gestation was transported to our tertiary center. On admission, she was recovered from convulsions, and blood pressure was 136/88 mmHg with proteinuria and oliguria. After the decision of course observe, she had a magnetic resonance imaging (MRI) of the brain which showed features consistent with posterior reversible encephalopathy syndrome (PRES). While being managed with magnesium sulface and antenatal corticosteroid therapy, she developed placental abruption(confirmed with retroplacental hematoma with transabdominal ultrasound) and intrauterine fetal death at 22 weeks and 4 days gestation. After the patient and her husband’s choice of vaginal delivery, uterine cervical dilation was performed. However, she presented an increase of blood pressure up to 170/90 mmHg, immediate cesarean section with general anesthesia was performed. On postpartum, she was given intensive care with nicardipine and magnesium sulface infusions, and she made improvement significantly. Eight days later, her brain showed an improvement of PRES in follow-up MRI. She was discharged from hospital on 8days post-operation without recurrence of eclampsia. Discussion This case highlights the occurrence of eclampsia and rapidly progressed placental abruption at very early gestation as 22 weeks gestation. Mattar F. and Sibai B.M. showed case series of eclampsia including early onset cases in the last century [1] , but confirmation with MRI of the brain were not performed. It must be noted that some cases reported formally as eclampsia include cerebral hemorrhage in pregnancy, since cerebrovascular disorders occurs more frequently than we expected [2] . Clinicians should care both eclampsia and brain stroke to all pregnant course.

Abnormal placental findings in the case of a pregnant woman with biliary tract hydatid disease

We report the case of a 33 weeks pregnant woman who was admitted in our hospital for recent jaundice. The controversial results of medical investigations and the patient’s clinical outcome indicated the necessity for immediate caesarian-section along with exploratory laparotomy. The surgeons extracted gelatinous membranes from the main biliary duct. At the Department of Pathology from University Emergency Hospital from Bucharest, we received the placental components, were we noted the presence of one true umbilical cord knot and meconium impregnation, a non-slatted gallbladder of 18 cm long and the numerous, heterogeneous membranes. On histopathological examination we found uteroplacental hypoxia-related features in the placenta together with retroplacental hematoma, umbilical cord edema, and inflammatory content of the gallbladder and hydatid cyst fragments on the common bile duct samples. The premature new-born survived and both the mother and the infant were discharged in good health condition after 2 weeks.

Complications and maternal mortality from severe pre-eclampsia during the first 48 hours in an intensive care unit in Morocco

Severe pre-eclampsia is a serious pathology of pregnancy because it is associated with a high risk of progression to fatal complications such as eclampsia, HELLP syndrome, retroplacental hematoma, and acute kidney injury, particularly in low-income countries [1]. The first 48 hours after patients have been admitted with severe pre-eclampsia to an intensive care unit (ICU) are crucial, and the quality of management during this period profoundly affects maternal prognosis. The aim of the present study was to determine the clinical and biological characteristics during the first 48 hours after women with severe preeclampsia were admitted to an ICU in Morocco. A retrospective study covering the seven-year period from January 1, 2007, to January 1, 2014, was conducted at the multipurpose ICU at the Regional Hospital of Oujda, eastern Morocco. Ethics Committee approval and informed consent were not needed because of the nature of the study. Inclusion criteria were patients with severe pre-eclampsia at 20weeks or more of pregnancy who had been admitted to the ICU during pregnancy or in the postpartum period (less than seven days after delivery). Severe pre-eclampsia was defined as severe arterial hypertension (systolic ≥160 mm Hg and/or diastolic ≥110 mm Hg), proteinuria (≥2 g/L or≥2+), and/or signs of visceral involvement. Exclusion criteria were pre-existing comorbidities (arterial hypertension, diabetes, nephropathy, and cardiomyopathy). Acute kidney injury was defined using the RIFLE classification (Risk, Injury, Failure, Loss of kidney function, End-stage kidney disease. A total of 138 patients met the criteria and were included in the study. The clinical and biological characteristics at the time of enrollment and the obstetric complications observed during the first 48 hours in the ICU are reported in Table 1. Eclampsia was the main complication of severe pre-eclampsia in the present study. Concerning the frequency of obstetric complications of pre-eclampsia reported in other studies, rates of eclampsia, HELLP syndrome, retroplacental hematoma, and acute kidney injury were reported, respectively, as 43.5%, 27.1%, 24.8%, and 58.7% by Bouazziz et al. [2] and 31.2%, 42.8%, 8.5%, and 19% by Lelong et al. [3]. In Lataifeh et al. [4], maternal mortality related to pre-eclampsia was 17.6% compared with 6.5% in the present study. Hypertensive disorders are themain reason for admission to the ICU in a large number of low-resource countries, which raises the question: what are the risk factors for pre-eclampsia in this population? Prospective studies with more rigorous criteria and methodology are needed.

Acute Kidney Injury in Pregnancy: A Single-Center Study in Tunisia

Acute kidney injury is a rare but serious complication of pregnancy. It is still common in developing countries. The causes can be varied. It is imperative to distinguish these conditions to make appropriate therapeutic decisions which can be lifesaving for the mother and fetus. This study examined the incidence and etiology of acute kidney injury in pregnancy, the morbidity, fetomaternal mortality, and renal prognosis among pregnant patients developing acute kidney injury. This is a retrospective observational study involving cases of acute kidney injury during pregnancy and hospitalized in our department from 1995 to 2015. The study involved 10 patients. The average age of patients was 31.6 years. Personal history of preeclampsia was found in 2 patients. The average term of pregnancy in which appeared the acute kidney injury was 33 weeks. All patients had preeclampsia. Five of them had a retro-placental hematoma, 2 had eclampsia and another post-partum hemorrhage. Five patients underwent renal biopsy for a persistent acute kidney injury with an average delay of 26 days. The histological results were: partial cortical necrosis in one case, thrombotic microangiopathy in two cases, acute tubular necrosis in one case, and membranoproliferative glomerulonephritis in one case. Six of our patients had an antihypertensive treatment. Seven patients have required renal replacement therapy. The ultimate evolution was good in 9 patients with recovery of diuresis and total recovery of renal function. Only one patient had kept with advanced renal failure requiring hemodialysis. She has been transplanted after 2 years with normal graft function. The pregnancy care and quality of access to care remain fundamental to prevent complications of pregnancy, including acute kidney injury.

Placental hypoxic overlap lesions: a clinicoplacental correlation.

This retrospective analysis is aimed to study clinical and placental associations of placental acute, chronic, and acute-on-chronic (overlap) hypoxic lesions. Frequencies of 32 clinical (maternal and fetal) and 47 placental (gross and microscopic) phenotypes were compared by the Yates χ(2) with the Holm-Bonferroni correction among consecutive placentas from 2831 ≥ 16-week gestations: 778 placentas with chronic hypoxic lesion(s) (diffuse patterns of hypoxic placental injury, chorangiosis, excessive extravillous trophoblasts, microscopic chorionic pseudocysts, clusters of decidual multinucleate trophoblasts), 481 placentas with acute hypoxic lesion(s) (infarction, intravillous hemorrhage, deep meconium penetration, membrane laminar necrosis), 585 placentas with hypoxic overlap lesion(s) (coexisting at least one lesion from each of the above groups), and 987 placentas without placental hypoxic lesions, adjusted for gestational age. The control group was dominated by premature rupture of membranes, inflammatory pattern of placental injury, and poor prenatal care. The fetal and placental hypoxic patterns were associated not only with increased frequency of clinical hypoxia-associated conditions, but also abnormal umbilical cord coiling, intervillous thrombi, retroplacental hematomas, and placental features of fetal thrombotic vasculopathy, particularly in association with hypoxic overlap lesions. Placental hypoxic overlap lesions are associated with clinical complications of pregnancy and predispose to thrombotic lesions, some most likely stasis-induced.

Placental pathologies on fetal MRI are associated with high impairment rates: a prospective long-term outcome study

Objective: Placental anomalies visualized at midgestation by MRI are shown to be related to pregnancy outcome. We performed a prospective cohort study to investigate the influence of placental pathologies diagnosed with fetal MRI on long-term neurodevelopmental outcome.Methods: In our hospital-based, cross-sectional study, all fetal MRI examinations of pregnancies with vascular placental pathology (i.e. infarction with/without hemorrhage, subchorionic thrombi/hemorrhages, intervillous thrombi/hemorrhages or retroplacental hematoma) between 2003 and 2007 were included. The extent of the pathology was expressed as the percentage of abnormality related to the whole placental volume. Pathohistological reports were correlated to MRI findings. Infants were prospectively investigated using Bayley developmental scales at the age of 2–3.5 years. Impairment was categorized as a Bayley scale two SDs below normal (<85 points).Results: There were 31 singletons and 25 offspring of multiple pregnancies included in the analyses. Impairment rates were 32.2% in singletons and 32.0% in multiple births. No correlation between neuro/motordevelopmental outcome at 2–3.5 years and the type, extent or gestational week at the time of diagnoses of placental vascular pathologies was found.Conclusion: The long-term outcome of children with vascular placental pathologies on fetal MRI was associated with a high impairment rate after 2–3.5 years, both on motor- and neurodevelopmental Bayley scales. Neurological impairment did not correlate with the extent of placental involvement, intrauterine growth restriction, gestational age at birth or multiple state.

English

OBJECTIVE: Study of placental morphological changes in intrauterine growth restricted babies. MATERIAL & METHODS: The Study was carried out at Mahatma Gandhi Medical College & Hospital, Jaipur, from January 2011 to January 2012. The placentae were collected from 50 cases of mothers of normal for date babies &50 cases of mothers of IUGR babies. Placental changes studied in both the groups, grossly and histopathologically. RESULTS: The placentae were collected from fifty mothers of normal for date babies & fifty mothers of growth restricted babies. It was observed that mean placental & fetal weights were 385 + 15gm in IUGR as compared to control group 500 + 15 gm Total gross & microscopic pathology in each group were 46% & 94% respectively in IUGR group as compared to 8% each in control groups. Mean fetal weight was low in IUGR group in relation to socioeconomic status, smoking & various disease factors. CONCLUSION: Gross morphology and histopathology of placentae were studied. Gross changes were developmental anomalies, placenta extrachorialis 2% & placenta bipartite 2%. Mean placental diameter in IUGR group was found to be less 15.58 cms as compared to 18.48cms in control group. Tesselation and subchorionic fibrosis was present in 70% & 76% in IUGR group which was found to be less as compared to 90% & 94%in control group1.Calcification, infarction and retroplacental haematoma were present in 54%, 56% & 26% in IUGR which was found more in comparison to 24% &12%in control group. It was concluded

Study of Placental Insufficiencies in IUGR Babies in Term Pregnancies

&lt;p&gt;&lt;strong&gt;Introduction:&lt;/strong&gt; In intrauterine growth restricted babies, at term, the placenta might hold the key to the etiology. This present study is aimed at comparison of data of gross and pathological study of placentae from normal weight (control) and IUGR groups and attempted to establish a relationship between placenta pathology and intrauterine growth retardation in term pregnancy.&lt;/p&gt;&lt;p&gt;&lt;strong&gt; Aims and Objectives:&lt;/strong&gt; 1. To study placental factors associated with IUGR. 2. To study prevalence of placental factors in details. Material and Methods: A study of 100 patients, with more 37 and less 42 weeks of gestation wasconducted for 2yrs in a tertiary care hospital. A thorough general examination&amp;amp;amp;Systemic examination which included per abdominal examination including uterine height, abdominal girth, symphysio fundal height, estimated fetal weight, abdominal grips, fetal heart auscultation, and per vaginal examination. Routine and specific investigations will be sent for clinical correlation. Placenta obtained after delivery was send for macroscopic and microscopic examination to pathologist. The reports obtained will be used to study placental causes in IUGR and placenta in detail.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Result:&lt;/strong&gt; Average placental weight of term pregnancy is 400 gms and placental coefficient is 0.18. decidual surface area is 254 cm2 and its thickness is 2.72cm. Retroplacental haemorrhage is closely associated with PIH. Microscopic infarction is found with high frequency (p&amp;lt;0.005). Placenta of IUGR fetus, gross pathological changes like severe infarction with or without retroplacental haematoma can obviously be noted but they are not found to be statistically significant. Placental coefficient is increased in cases of anemia. Syncytial knot formation in excess and thickening of basement membrane is well correlated.&lt;/p&gt;

Study of Placental Insufficiencies in IUGR Babies in Term Pregnancies

Introduction: In intrauterine growth restricted babies, at term, the placenta might hold the key to the etiology. This present study is aimed at comparison of data of gross and pathological study of placentae from normal weight (control) and IUGR groups and attempted to establish a relationship between placenta pathology and intrauterine growth retardation in term pregnancy. Aims and Objectives: 1. To study placental factors associated with IUGR. 2. To study prevalence of placental factors in details. Material and Methods: A study of 100 patients, with more 37 and less 42 weeks of gestation wasconducted for 2yrs in a tertiary care hospital. A thorough general examinationaSystemic examination which included per abdominal examination including uterine height, abdominal girth, symphysio fundal height, estimated fetal weight, abdominal grips, fetal heart auscultation, and per vaginal examination. Routine and specific investigations will be sent for clinical correlation. Placenta obtained after delivery was send for macroscopic and microscopic examination to pathologist. The reports obtained will be used to study placental causes in IUGR and placenta in detail. Result: Average placental weight of term pregnancy is 400 gms and placental coefficient is 0.18. decidual surface area is 254 cm2 and its thickness is 2.72cm. Retroplacental haemorrhage is closely associated with PIH. Microscopic infarction is found with high frequency (p<0.005). Placenta of IUGR fetus, gross pathological changes like severe infarction with or without retroplacental haematoma can obviously be noted but they are not found to be statistically significant. Placental coefficient is increased in cases of anemia. Syncytial knot formation in excess and thickening of basement membrane is well correlated.

Follow-up Study of Lympho-Histiocytic Villitis and Incidental Retroplacental Hematoma

Placentas are usually submitted for pathologic examination based on obstetrical indications. We hypothesized that the placenta may have diagnostic value to the infant independent of obstetrical events. We specifically tested whether lymphohistiocytic villitis (noninfectious) would predict autoimmune or alloimmune disease based on transfer of activated maternal T-cells to the fetus and whether clinically silent placental separations (retroplacental hematomas, RPH) would predict neurologic injury in the infant. All placentas from consecutive deliveries had a routine pathologic examination of the placenta. The infants with placentas demonstrating inflammation of >1% of villi or RPH >2 cm and matched controls had their hospital charts reviewed and parental interviews by telephone at 5 to 7 years of age. The children of consented patients were also searched for in the office visits of the University of Louisville Pediatric Neurology and Rheumatology divisions. One thousand six hundred eighty-four patients consented to the follow-up study. We found no cases of autoimmune disease among 17 children with villitis >1%. Of 16 infants with RPH, 1 had cerebral palsy but with other placental findings, 1 had lethal hydranenecephaly, and the remainder had no adverse outcome. Of 15 children seen by a pediatric neurologist, none had the same placental lesion. The specific lesions of lymphohistiocytic villitis or asymptomatic RPH do not predict significant pediatric disease by 7 years of age. At least for these 2 lesions, the placenta does not have diagnostic value to the infant.

Relation of placental diagnosis in stillbirth to fetal maceration and gestational age at delivery

To study the relation of retention of dead fetus resulting in its maceration and gestational age at delivery to placental diagnosis. Some 75 clinicoplacental phenotypes have been retrospectively analyzed in 520 consecutive stillbirths, 329 macerated and 191 nonmacerated, and at three gestational age interval cohorts (330 second trimester, 102 preterm third trimester, and 88 term). Chi-square and clustering methods (Ward dendrograms and multidimensional scaling) were used for statistical analysis. Maternal diabetes mellitus, induction of labor, fetal growth restriction, various umbilical cord abnormalities, and placental clusters of sclerotic/hemosiderotic chorionic villi were more common in macerated stillbirths, while clinicoplacental signs and symptoms of ascending infection and placental abruption, i.e., retroplacental hematoma, premature rupture of membranes, and acute chorioamnionitis in nonmacerated stillbirths. Placental abnormalities were less common in the second trimester, other than the acute chorioamnionitis. Patterns of chronic hypoxic placental injury were common in preterm third trimester, while signs of in-utero hypoxia (abnormal cardiotocography, meconium, and histological erythroblastosis of fetal blood) in term pregnancy. In addition to classical statistics, the clustering analyses added new information to placental investigation of cause of stillbirth. Macerated third trimester stillbirths have multifactorial etiology more likely than the second trimester stillbirths and the likely stasis-induced fetal thrombotic vasculopathy secondary to occult umbilical cord compromise should be sought in placental investigation in such cases. Nonmacerated stillbirths are associated with ascending infection and placental abruption.

Admissions en réanimation des femmes en cours de grossesse ou en post-partum : circonstances et pronostic. Une série rétrospective de 96 cas

PurposeVery few studies had been published about admission of obstetric patients in French intensive care units (ICU). Patients and methodsFiles of women who had been admitted during pregnancy or the postpartum period to ICU of an academic hospital between January 1st 1997 and 31st December 2006 were analyzed. Diagnosis at admission, severity, main treatments and outcome were studied during two successive periods of 5 years. ResultsThere were 96 admissions (0.95% of all admissions to ICU). They included 34 complications due to arterial hypertension (35%), among them 10 cases of pre-eclampsia, eight of eclampsia, seven of Hemolysis-Liver Enzymes-Low Platelet (HELLP) syndrome and two of retroplacental hematoma ; 26 postpartum haemorrhages (27%); and 36 miscellaneous diagnosis including two sepsis, four acute pulmonary oedema, four cardiomyopathy, three pulmonary embolism, and three acute liver steatosis. Mean Simplified Acute Physiologic Score (SAPS II) was 18.5±11.2 and mean Sequential Organ Failure Assessment (SOFA) 2.1±2.3. The main treatments were mechanical ventilation (50% of all cases) and transfusion (32%). The average ICU stay was 5.7±5.4 days. Two maternal deaths were observed (aortic dissection and peripartum cardiomyopathy). The number of patients admitted for postpartum haemorrhage increased from five to 21 over the two successive periods of the study. ConclusionThe number of women admitted to ICU during pregnancy or the postpartum period is low. Admissions for hemorrhage have increased. Regular monitoring of maternal morbidity and mortality gives relevant clues for assessing the quality of obstetrical care.

Treatment of Von Willebrand Disease Women Undergoing Childbirth with a Von Willebrand Factor Product with a Low Content of Factor VIII: Results From 4 Multicenter Studies

AbstractAbstract 3375 Introduction:Von Willebrand disease (VWD) is relative to an abnormality, either quantitative or qualitative, of von Willebrand factor (VWF). Among patients with severe VWD, pregnant women are at increased risk of bleeding especially for the peripartum period both for vaginal delivery and Caesarean section. In patients with type 3 VWD and in patients with a functional defect, the treatment with VWF is required for the prevention of bleeding during the delivery. Predisposition towards an increased risk of thrombosis in pregnant women is well establish and this predisposition to thrombosis results from the hypercoagulable state of pregnancy with increased factor VIII and VWF levels. As endogenous factor VIII production in patients with VWD is intact, the treatment with a VWF concentrate with a low factor VIII content provides hemostatic levels of factor VIII, by stabilization of endogenous factor VIII, while providing efficient primary hemostasis. We report the efficacy and safety of Wilfactin, a triple-secured VWF concentrate almost devoid of factor VIII, for the preventive treatment of bleeding during the delivery period. Methods:Data from 4 prospective multicenter studies including one fully monitored post-marketing study were pooled. As recommended in the protocols, if needed, the unscheduled childbirth was managed by VWF with the coadministration of factor VIII at the first infusion. When time permitted, two infusions of Wilfactin were administered: one at 12–24 hours and one 30 minutes-1 hour prior to childbirth. The investigators were asked to evaluate the efficacy on a 4-point scale (Excellent, Good, Moderate, None) at the end of treatment. Results:Across all studies, 22 VWD women delivered 24 children. Wilfactin was used to prevent bleeding in 9 vaginal deliveries in 9 women (3 type 1, 5 type 2 and 1 type) and 15 Cesarean deliveries in 13 women (3 type 1, 9 type 2 and 3 type 3). There were no notable differences in the evaluation of efficacy between vaginal and Caesarean deliveries. The efficacy was rated as ‘good/excellent' in 20 of 21 (95%) evaluated deliveries and ‘moderate' in one cesarean due to a moderate, but controlled bleeding. Blood transfusion was required for a retroplacental hematoma in one Cesarean section but the efficacy of the product was rated as excellent by the investigator. Over the total course of therapy for childbirth, the median dose per infusion was higher for vaginal delivery (42 IU/kg) than for Cesarean section (27 IU/kg). Women received more infusions for Cesarean section than for vaginal delivery (15 vs 8) and more treatment days (10 vs 6, respectively) but, the total dose per type of treatment was quite similar (374 vs 272 IU/kg). A priming dose of factor VIII at the first infusion of Wilfactin was given to ensure rapid coagulation before starting 5 Cesarean sections and 4 vaginal deliveries. For 4 other Cesarean sections, the hemostatic level of factor VIII was achieved by an initial infusion of Wilfactin 12 to 24 hours before the procedure. No special measures to increase factor VIII were required for the other 11 deliveries. The overall tolerability was very good; neither VWF inhibitor nor thrombotic complications were reported. An additional data is to note that 2 patients were treated with long-term prophylaxis regimen during pregnancy because of placental hematoma. Conclusion:Good hemostatic efficacy, absence of thrombotic or other severe complications shown in the clinical trials with Wilfactin are encouraging for its use in the management of pregnant VWD women for vaginal delivery or Cesarean section. Disclosures:No relevant conflicts of interest to declare.

1273 Gestational Hypertension and Neonatal Outcome - Moroccan Data

The objective:Evaluation of fetal and neonatal immediate impact of pregnancy hypertensive disease, and a comparison between the severity of gestational hypertensive disease and neonatal outcome.Materials and MethodsThis work was based...

PP169. Management of fetal and maternal prognosis during severe toxemia

Severe gravidic toxemia gives heavy maternal and fetal morbidity and mortality. The purpose of our data is to identify bad maternal and fetal factors during severe toxemia and the outcome of pregnancy. It is a retrospective and comparative study about 200 cases of severe toxemia reported during 8 years 2004-2011 among 25,000 deliveries (control group). Toxemia is considered severe when blood pressure⩾160/100mHg, proteinuria ⩾2g/l, bad neurosensorial signs, hemostasis disorders, kidney and liver failure, some fetal tests: delay intra-uterine growth acute fetal suffering, fetal death. Frequency of severe toxemia 8‰, primiparous 58% vs. 35% control, gestational diabetes 12% vs. 10% control, oedema 87% vs. 45% control. Maternal morbidity is dominated by hemostasis disorders: low platelet count<80,000 23% vs. 8%, hypofibrinogenemia <4g/l 13% vs. 2%, HELLP syndrome eight cases vs. 0. We raised eight cases of eclampsia crises, 22 cases of retroplacental hematoma vs. 10 control. Blood transfusion 15% vs. 10% control, inhibitors of VII factor administered in two cases vs. 0. We do not deplore any maternal mortality. Fetal prognosis is very compromised ,the delay intra uterine growth 44% vs. 18% control, prematurity 66% vs. 15% control, perinatal mortality 60‰ vs 12‰ control More toxemia appears early during pregnancy more maternal and especially fetal prognosis is compromised. New drugs, predictive tests and preventives measurements improve maternal outcome better than fetals' one.

A 32 weeks twin pregnancy in a non-communicating rudimentary horn: Case report

Introduction: Pregnancy in a rudimentary horn represents a serious implication of this rare uterine anomaly. In 90% of cases, rupture of the horn occurred in the second trimester. In this report, we present a rare case of intact twin pregnancy in a non-communicating rudimentary horn that reached 32 weeks of gestation. Case presentation: A 25 years old Caucasian woman pregnant for 32 weeks presented with shock, acute lower abdominal pain and considerable vaginal bleeding. The patient was shocked and the uterus was tender and tense. Trans-abdominal ultrasound scan revealed a twin intrauterine pregnancy with no cardiac activity in both fetuses, fetal biometry was equivalent to 32 weeks and there was a huge retroplacental hematoma. Urgent laparotomy was performed and a huge intact right sided rudimentary horn was identified. Vertical incision was done with extraction of the dead twins, and the horn was excised. Conclusion: Despite being rare, rudimentary horn pregnancy should be suspected regardless of the gestational age. Placental abruption should also be considered as an unusual presentation of this condition.