First-trimester cord entanglement in monoamniotic twins.
OBJECTIVE: Monoamniotic twinning occurs in only 1% of twin pregnancies, but carries a high perinatal mortality rate. Early and reliable diagnosis is essential if attempts are to be made to reduce the complication rate. We report color Doppler demonstration of cord entanglement in the first trimester, which is diagnostic of monoamnionicity. METHODS: Two patients with twin pregnancies were examined in the first trimester with pulsed and color Doppler insonation of their umbilical arteries. RESULTS: Cord entanglement was suspected and proved by demonstrating differing fetal heart rate patterns in the same direction on umbilical artery Doppler analysis of a common mass of cord vessels. Following appropriate counselling, medical amnioreduction was induced at 20 weeks of gestation to reduce fetal movements and worsening cord entanglement. Delivery was by elective Cesarean section at 32 weeks' gestation and monoamnionicity was confirmed. CONCLUSION: We report a new sign for the demonstration of monoamnionicity in twin pregnancies in the first trimester. This should improve the reliability of early diagnosis, but further studies are required to confirm that, if cord entanglement occurs, it is usually present by the end of the first trimester. (+info)
Molecular mechanisms of neutrophil-endothelial cell adhesion induced by redox imbalance.
Previous studies have implicated a role for intracellular thiols in the activation of nuclear factor-kappaB and transcriptional regulation of endothelial cell adhesion molecules. This study was designed to determine whether changes in endothelial cell glutathione (GSH) or oxidized glutathione (GSSG) can alter neutrophil adhesivity and to define the molecular mechanism that underlies this GSSG/GSH-induced adhesion response. Treatment of human umbilical vein endothelial cell (HUVEC) monolayers for 6 hours with 0.2 mmol/L diamide and 1 mmol/L buthionine sulfoximine (BSO) decreased GSH levels and increased the ratio of GSSG to GSH without cell toxicity. These redox changes are similar to those observed with anoxia/reoxygenation. Diamide plus BSO-induced thiol/disulfide imbalance was associated with a biphasic increase in neutrophil adhesion to HUVECs with peak responses observed at 15 minutes (phase 1) and 240 minutes (phase 2). N-Acetylcysteine treatment attenuated neutrophil adhesion in both phases, which indicated a role for GSH in the adhesion responses. Interestingly, phase 1 adhesion was inversely correlated with GSH levels but not with the GSSG/GSH ratio, whereas phase 2 neutrophil adhesion was positively correlated with GSSG/GSH ratio but not with GSH levels. Intercellular adhesion molecule-1 and P-selectin-specific monoclonal antibodies attenuated the increased neutrophil adhesion during both phases, whereas an anti-E-selectin monoclonal antibody also attenuated the phase 2 response. Pretreatment with actinomycin D and cycloheximide or with competing ds-oligonucleotides that contained nuclear factor-kappaB or activator protein-1 cognate DNA sequences significantly attenuated the phase 2 response, which implicated a role for de novo protein synthesis. Surface expression of intercellular adhesion molecule-1, P-selectin, and E-selectin on HUVECs correlated with the phase 1 and 2 neutrophil adhesion responses. This study demonstrates that changes in endothelial cell GSSG/GSH cause transcription-independent and transcription-dependent surface expression of different endothelial cell adhesion molecules, which leads to a 2-phase neutrophil-endothelial adhesion response. (+info)
Altered connective tissue in children with congenital dislocation of the hip.
The umbilical cord was employed as a source of collagen in 10 children with congenital dislocation of hip. The amount of collagen and its solubility were measured in slices of the cords and in the umbilical veins and compared with the values in normal subjects. Both the amount of collagen and its solubility were decreased in children with congenital dislocation of the hip. (+info)
Characteristics of blood flow in intrauterine growth-restricted fetuses with hypercoiled cord.
OBJECTIVE: To clarify the characteristics of fetoplacental blood flow of growth-restricted fetuses with hypercoiled umbilical cord. SUBJECTS: Eight growth-restricted fetuses with hypercoiled cord. METHODS: Flow velocity waveforms of the umbilical cord artery and vein, fetal abdominal aorta and fetal inferior vena cava were analyzed. RESULTS: The resistance index in the umbilical artery in the hypercoiled cases was lower than that in normal fetuses. Early-diastolic reversed flow was observed in the abdominal aorta in some cases. In all cases, umbilical venous pulsation was observed in the entire cord until delivery. In one case, fetal heart failure occurred, resulting in pre-mature delivery. An atrophic type of single umbilical artery was observed in four cases. CONCLUSION: Fetal blood flow disturbance caused by a hypercoiled umbilical cord may be a cause of growth restriction. (+info)
Prenatal diagnosis of a lean umbilical cord: a simple marker for the fetus at risk of being small for gestational age at birth.
OBJECTIVE: The purpose of this study was to investigate whether the prenatal diagnosis of a 'lean' umbilical cord in otherwise normal fetuses identifies fetuses at risk of being small for gestational age (SGA) at birth and of having distress in labor. The umbilical cord was defined as lean when its cross-sectional area on ultrasound examination was below the 10th centile for gestational age. METHOD: Pregnant women undergoing routine sonographic examination were included in the study. Inclusion criteria were gestational age greater than 20 weeks, intact membranes, and singleton gestation. The sonographic cross-sectional area of the umbilical cord was measured in a plane adjacent to the insertion into the fetal abdomen. Umbilical artery Doppler waveforms were recorded during fetal apnea and fetal anthropometric parameters were measured. RESULTS: During the study period, 860 patients met the inclusion criteria, of whom 3.6% delivered a SGA infant. The proportion of SGA infants was higher among fetuses who had a lean umbilical cord on ultrasound examination than among those with a normal umbilical cord (11.5% vs. 2.6%, p < 0.05). Fetuses with a lean cord had a risk 4.4-fold higher of being SGA at birth than those with a normal umbilical cord. After 25 weeks of gestation, this risk was 12.4 times higher when the umbilical cord was lean than when it was of normal size. The proportion of fetuses with meconium-stained amniotic fluid at delivery was higher among fetuses with a lean cord than among those with a normal umbilical cord (14.6% vs. 3.1%, p < 0.001). The proportion of infants who had a 5-min Apgar score < 7 was higher among those who had a lean cord than among those with normal umbilical cord (5.2% vs. 1.3%, p < 0.05). Considering only patients admitted in labor with intact membranes and who delivered an appropriate-for-gestational-age infant, the proportion of fetuses who had oligohydramnios at the time of delivery was higher among those who had a lean cord than among those with a normal umbilical cord (17.6% versus 1.3%, p < 0.01). CONCLUSION: We conclude that fetuses with a lean umbilical cord have an increased risk of being small for gestational age at birth and of having signs of distress at the time of delivery. (+info)
Early prenatal diagnosis of cord entanglement in monoamniotic multiple pregnancies.
OBJECTIVES: Cord entanglement is a severe complication in monoamniotic multiple pregnancies. Three cases were reviewed to determine how early ultrasound diagnosis might improve counselling and management. METHODS: In two monoamniotic twin and one dichorionic diamniotic triplet pregnancies, cord entanglement was detected between 10 and 18 gestational weeks by color Doppler and pulsed Doppler velocimetry. Pregnancies were followed up on a weekly basis with special observation of fetal behavior and use of color Doppler velocimetry. RESULTS: In Case 1, a monoamniotic twin pregnancy with cord entanglement close to the umbilical insertions was diagnosed at 10 weeks. Longitudinal follow-up showed intrauterine death of both twins at 15 weeks. In Case 2, entanglement of the umbilical cords of two monoamniotic triplets within a dichorionic diamniotic triplet pregnancy was diagnosed at 10 weeks. The pregnancy continued uneventfully until 35 weeks when cord entanglement was confirmed at Cesarean section. All triplets have since developed normally. In Case 3, monoamniotic twins were diagnosed at 18 weeks. Color Doppler detected side-by-side insertion of the umbilical cords and Doppler velocimetry suggested an entanglement at the chorionic plate. The pregnancy was complicated by polyhydramnios. Cesarean section at 36 weeks confirmed cord entanglement at the chorionic plate. Postnatal computer angiography and morphological examination of the placenta showed the presence of superficial artery-to-artery and vein-to-vein anastomoses and of deep arteriovenous shunts. The development of the twins was uneventful. CONCLUSIONS: Diagnosis of cord entanglement is feasible early in gestation. Future protocols are proposed to document the gestational age at detection, the location, and the Doppler flow patterns and to facilitate the assessment of short- and long-term development. (+info)
Abnormal ductus venosus blood flow: a clue to umbilical cord complication.
We report a case of umbilical cord complication causing, fetal hypoxemia and acidemia. At 30 weeks of gestation, the patient was referred because of slightly increased amniotic fluid volume and a non-reactive cardiotocogram. Biometry was appropriate for gestational age. Umbilical artery and fetal aortic Doppler findings were normal, whereas diastolic blood flow velocities in the middle cerebral artery were increased and the ductus venosus showed severely abnormal flow velocity waveforms with reversal of flow during atrial contraction. Since other reasons for fetal hypoxemia could be excluded, careful examination of the umbilical cord was performed. Traction of the hypercoiled umbilical cord due to its course around the fetal neck and shoulders was suspected. Cesarean section confirmed the sonographic findings and fetal blood gases revealed fetal acidemia. This case indicates that investigation of fetal venous blood flow may also help to identify fetal jeopardy due to reasons other than increased placental vascular resistance. (+info)
The cardiovascular and cerebrovascular responses of the immature fetal sheep to acute umbilical cord occlusion.
1. In premature fetal sheep (89-93 days gestation) we examined the fetal response to asphyxia induced by 30 min of complete umbilical cord occlusion. Fetuses were also studied during the first 3 days after asphyxia. We measured heart rate, blood pressure, carotid and femoral blood flows, vascular resistance, electroencephalographic activity and cerebral changes in haemoglobin concentration by near infrared spectroscopy (NIRS). 2. Fetuses tolerated 30 min of asphyxia and the cardiovascular response was characterized by three phases: initial redistribution of blood flow away from the periphery to maintain vital organ function, partial failure of this redistribution and near terminal cardiovascular collapse, with profound hypotension and cerebral and peripheral hypoperfusion. 3. Post-asphyxia carotid blood flow and NIRS data demonstrated that between 3-5 h there was a significant secondary reduction in cerebral blood flow, blood volume and oxygenation despite normal perfusion pressure and heart rate. There was also a secondary fall in femoral blood flow which persisted throughout recovery. 4. These data demonstrate that the immature fetus can survive a prolonged period of asphyxia, but paradoxically the capacity to survive exposes the fetus to profound hypotension and hypoperfusion. A secondary period of significant cerebral hypoperfusion and reduced oxygen delivery also occurred post-asphyxia. These cardiovascular and cerebrovascular responses may contribute to the patterns of cerebral injury seen in the human preterm fetus. (+info)