This technique may be useful in the prenatal diagnosis of conotruncal anomalies and in the assessment of the spatial relationships of abnormal vascular connections in the upper mediastinum. P01.34Maternal lipopolysaccharide depresses fetal cardiovascular function in mouse S. Rounioja, J. Räsänen, H. Autio-Harmainen, M. Ojaniemi, V. Glumoff, K. Mäkikallio, M. Hallman University of Oulu, FinlandBackground: Intra-amniotic lipopolysaccharide (LPS) causes a fetal inflammatory response and cardiac dysfunction in mice. We hypothesized that the placenta serves as a barrier against bacterial toxins delaying the onset of a fetal inflammatory response and cardiac failure. Methods: At 14-15 days of gestation DBA strain mice were randomized to receive LPS (∼ 70 µg) or vehicle intraperitoneally. Doppler ultrasonography of fetal cardiovascular hemodynamics was performed before and six hours after LPS. The expression and production of cytokines and other inflammatory mediators were determined using ribonuclease protection assay and cytometric bead array. Histopathology and immunostaining of toll-like receptor (TLR) in placenta were carried out. Results: Six hours after LPS injection, there was no evidence of stasis in maternal lung or liver, although tumor necrosis factoralpha (TNF-á) and interleukin (IL)-6 were increased in serum (p < 0.05). In contrast, placenta showed severe dilatation and stasis most distinctly in maternal vessels. The expression of TNF-á, IL-1á and IL-6 (p < 0.05) increased in placenta, whereas no inflammatory activation was evident in fetal tissues, and amniotic fluid revealed no increase in cytokines. The expression of TLR2 (p < 0.05) was increased in labyrinthine macrophages, which could serve as target for LPS. The fetal cardiac outflow mean velocity, was lowered (p < 0.005) in the LPS group. The pulsatility indices (PI) of the umbilical artery and the descending aorta and the PI for veins from the ductus venosus were higher after LPS. In the LPS group 65% of the fetuses had atrioventricular valve regurgitation, compared to only 4% in the vehicle group. Conclusions: Maternally administered LPS acutely induced cytokine expressions in placental tissue with histologic lesions. Inflammatory response was not evident in the fetal compartment. However, placental congestion increased the cardiac afterload, leading to fetal cardiovascular dysfunction.

No abstract

Considerada la estadística de los últimos once años del instituto, es posible extraer algunos datos sobre la mortalidad de los hijos de las mujeres afectadas por toxemias gravídicas, que tienen importancia para el estudio del pronóstico, y del tratamiento que se haya de seguir en tales casos desde el punto de vista pediátrico, lo que combinado con el criterio puramente obstétrico, que considera primordialmente a la madre, puede llevar a conclusión favorable para ambos.

No abstract

Poster abstracts anomalies may be associated. We present a case of ectopia cordis and toracoabdominal wall defect diagnosed in the first trimester scan. 32 year old women, with a history of a spontaneous abortion at 8 weeks with no complications. No personnel or family history of birth defects. In her first ultrasound, at 12 th weeks, we encountered a life fetus with several anomalies. The thorax was small and the heart was located anteriorly to the thoracic cavity. This malformation was associated with the absence of skull and a wall defect with extrusion of abdominal organs. Due to the poor diagnosis associated with this malformation, the patient decided to terminate pregnancy. The fetus was sent to anatomopathology that concluded the presence of polimarformations: 1. Absence of skull, 2. Toracoabdominal wall defect with ectopia cordis and omphalocele, 3. Presence of an amniotic band with isquemic lesion of one foot, 4. severe escoliosis. These were associated with amniotic band syndrome. The anomalies observed in the present case may be due to rupture of the amnion, chromosomal abnormalities or maternal disease. The anomalies found in the ultrasound did not exclude the diagnosis of Pentalogy of Cantrell. The diagnosis of amniotic band sequence was made due to the anatomopathological findings.