Constriction of the umbilical cord as a cause of fetal demise following midtrimester amniocentesis

Two cases of constriction of the umbilical cord resulting in fetal demise following midtrimester amniocentesis are presented. In both cases, real-time ultrasonography prior to amniocentesis revealed a viable fetus. Fetal demise was identified immediately following the procedure in the first case and one month later in the other. A localized constriction at the fetal end of the umbilical cord in both, with torsion of the constricted segment in the second case, was observed. Wharton's jelly was noted to be deficient in this segment of the cord in the first case. The mechanism of fetal demise is discussed. It is suggested that this abnormality should be considered when fetal demise follows midtrimester amniocentesis.     

Vibrio spp., the dominant flora in shrimp hatchery against some fish pathogenic viruses

BACKGROUND: Single fetal demise in a twin pregnancy is a rare event, the common causes being twin-twin transfusion syndrome, chromosomal or congenital anomalies and abnormalities of the umbilical cord and placenta. Umbilical vein thrombosis is a very rare cause of single fetal demise in twins. CASE: Three days after a reassuring biophysical profile, a 40-year-old primigravida with twin pregnancy presented at 38 weeks' gestation in early labor when demise of 1 of the twins was recognized. She underwent a cesarean section for arrest of labor, delivering twin A, a stillborn female weighing 2, 360 g and twin B, a liveborn male weighing 2,200 g. Umbilical vein thrombus was noted in twin A. CONCLUSION: Umbilical vein thrombosis is a rare and sudden cause of fetal demise.     

Thrombolytic therapy with tissue plasminogen activator for prevention of vasospasm in experimental subarachnoid hemorrhage: its efficacy and problems

Parvovirus B19 infection has been associated with fetal anaemia, hydrops, and in some cases demise. Most of the reported cases of fetal hydrops were detected in second-trimester fetuses. We report a series of three cases in which human parvovirus infection was associated with hydropic changes at an earlier gestational age. Spontaneous resolution of hydrops occurred in all fetuses. A greater understanding of the natural history of human parvovirus infection is needed prior to deciding on the mode of therapy (conservative management versus in utero fetal therapy).     

Poststapedectomy otitis media and meningitis

Fetal and neonatal paroxysmal supraventricular tachycardia (PST) requires attention because it may be associated with cardiac pathology and neonatal demise. Continuous monitoring of fetal heart rate and the ability to record clearly interpretable electrocardiograms from fetal scalp electrodes makes discovery and diagnoses of these fetal arrhythmias relatively simple. This report describes the discovery of this arrhythmia during routine DOPPLER ultrasound fetal monitoring and its documentation as PST by fetal scalp electrocardiography. (Fig. 1) The fetal heart rate during PST was 300 BPM, higher than previously reported. In contrast to previous reports, it did not appear post-natally and no pathology was found. Although the significance of transient fetal PST is not known, prudence indicates close observation of the neonate. This case demonstrates the value of fetal monitoring for the discovery, diagnosis and documentation of fetal arrhythmias during labor.     

Pooling of clodronate urinary excretion data: a new pharmacokinetic method to study drugs with highly variable gastrointestinal absorption

OBJECTIVE: Our purpose was to study effects of vibroacoustic stimuli on electrocortical activity and heart rate changes in fetal sheep in utero. STUDY DESIGN: Seven chronically instrumented near-term fetal sheep were repeatedly stimulated by an electronic artificial larynx for 32 seconds during periods of rapid-eye-movement and non-rapid-eye-movement sleep. Responses to vibroacoustic stimulation were obtained by spectral analysis of the electrocorticogram (fast Fourier transform) and by assessment of changes in fetal heart rate and fetal heart rate variability. RESULTS: During non-rapid-eye-movement sleep vibroacoustic stimulation led to electrocorticogram desynchronization that consisted of a marked reduction of delta and theta band power (p < 0.05). A concomitant fetal heart rate decrease and fetal heart rate variability increase were also noted (p < 0.05). During rapid-eye-movement sleep vibroacoustic stimulation induced a significant increase in alpha and beta band power (p < 0.05) and a slight deviation in basal fetal heart rate and fetal heart rate variability (p < 0.05). CONCLUSION: Vibroacoustic stimulation of fetal sheep provokes reproducible changes in fetal electrocortical activity and heart rate patterns. These changes, which are not easily identifiable in gross polygraphic assessments of the fetal behavioral state, are indicative of fetal arousal.     

A flat decelerative fetal heart rate tracing with normal fetal heart rate variability

We report two cases for which computer interpretation of nonstress test indicated a flat decelerative trace in spite of normal fetal heart rate variability. Fetal behavioral state in the first case and signal loss in the second case were possibly responsible for this computerized interpretation of the tracings in the absence of fetal distress.     

Cardiotocogram compared to Doppler investigation of the fetal circulation in the premature growth-retarded fetus: longitudinal observations

It was our objective to compare computerized fetal heart rate analysis with blood flow velocity waveform analysis of the arterial and venous fetal circulation in intrauterine growth retardation. We report five illustrative cases with longitudinal observations of fetal Doppler findings and fetal heart rate between 23 and 32 weeks of gestation. Blood flow waveforms were recorded from the umbilical artery, middle cerebral artery, descending aorta, ductus venosus and inferior vena cava. Fetal heart rate was analyzed by a computer system according to the Dawes-Redman criteria. The time sequence of deterioration is described individually for each fetus. An abrupt increase in pulsatility of ductus venosus waveforms with loss of forward flow velocity during atrial contraction preceded abnormally low short-term variation of fetal heart rate. With advanced gestational age and concomitant maternal disease, we observed severe alterations of flow velocity waveforms within 12 h of normal Doppler measurements, which is in contrast to findings in the second trimester, in which severely abnormal venous waveforms were observed over a period of several weeks before intrauterine death occurred. In a fetus with terminally low short-term variation, normal venous waveforms indicated fetal well-being despite an abnormal cardiotocogram (CTG). We challenge the current concept that the CTG is the best available parameter to determine the optimal time for elective delivery of premature growth-retarded fetuses. Deterioration in ductus venosus blood flow seems to precede an abnormal CTG and thus heralds the need for delivery.     

5-Hydroxytryptamine1D-like receptors mediate contraction of partially depolarized rabbit renal arteries

OBJECTIVE: Our purpose was to correlate measures of Doppler-detected fetal movements with standard fetal heart rate parameters and perinatal outcomes. STUDY DESIGN: This prospective, multiinstitutional trial used the Hewlett-Packard M1350A monitor to record simultaneous fetal heart rate baseline, variability, accelerations, decelerations, and number of fetal movements, and duration and percent of total time. These data were compared at 10- and 30-minute intervals during nonstress tests and were correlated with fetal heart rate baseline parameters and maternally perceived fetal movements and with outcomes of infants delivered within 7 days of the last test. RESULTS: At six centers 1704 actocardiograms from 884 third-trimester patients were analyzed. Doppler-detected fetal movement counts, durations, and percent of total time correlated weakly with all baseline fetal heart rate parameters (all values < 0.20). All fetal movement parameters increased significantly in successive 10-minute blocks and in periods of increased or normal fetal heart rate variability compared with those with fetal heart rate variability. The sensitivity, specificity, and predictive values of the percent of total movement time were comparable to those of standard nonstress test parameters. The risk of poor perinatal outcomes after nonreactive nonstress tests was lower in cases with fetal movements than in those without. CONCLUSIONS: Doppler actocardiography may help to discriminate fetal states during antepartum testing. It may prevent inappropriate diagnosis of fetal compromise when the nonstress test is nonreactive or nonreassuring.     

Effects of intravenous meperidine and meperidine with promethazine on uterine activity and fetal heart rate during labor

A prospective study of the effects of the i.v. injection of 75 mg meperidine, alone or combined with 25 mg promethazine, was conducted by continuous and direct monitoring of the fetus and of intrauterine pressure. The study was carried out in 16 primiparas and 24 multiparas in active spontaneous labor with cervical dilatation of 3 to 4 cm. Administration of meperidine and of meperidine with promethazine was associated with an increase in uterine activity of 31 to 45% (Montevideo units), respectively. The most marked effects were on the amplitude of the uterine contractions. There was no significant change in uterine tone. A tetanic response was recorded in two patients who vomited after the administration of meperidine with promethazine and was followed by slowing of the fetal heart rate. In no other cases were there significant changes in fetal heart rate. Except for the latter two patients, no adverse effect of meperidine or of meperidine with promethazine on the fetal heart rate was noted. The condition of the newborns at birth was excellent in all but three cases, in two of which maternal amniotic infection and high fever were present.     

Causality and control: key to the experiment

Maternal betamethasone administration causes a transient but considerable reduction in fetal body and breathing movements and in fetal heart rate variation. The aim of the present prospective study was to investigate whether there is evidence of circulatory changes in fetal, placental or uterine arteries, consistent with hypoxemia. Eighteen women at risk for preterm delivery received betamethasone to enhance fetal lung maturation. Doppler studies were performed before treatment, and 24 and 72 h after the second dose of betamethasone. Blood flow velocity waveforms were obtained from both uterine arteries, umbilical arteries, fetal descending aorta, fetal renal artery, and fetal cerebral arteries. No significant changes occurred in the pulsatility index of any of these blood vessels, suggesting that the transient reduction in fetal heart rate variation and fetal body and breathing movements following maternal betamethasone administration is not mediated through fetal hypoxemia.     

Simultaneous determination of nerisopam, a novel anxiolytic agent showing polymorphic metabolism, and its N-acetyl metabolite from human plasma by a validated high performance liquid chromatographic method

OBJECTIVE: Our goal was to determine the effect of chronic and acute umbilical-placental embolization on placental hemodynamic and fetal heart rate patterns in relation to fetal oxygenation in the near-term ovine fetus. STUDY DESIGN: Daily fetal placental embolization was performed during 10 days in 9 sheep fetuses until fetal arterial oxygen content decreased by approximately 30%. Nine control fetuses received saline solution. Mean and pulsatile umbilical blood flow, perfusion pressure, placental vascular resistance, fundamental impedance, pressure pulsatility index, and umbilical artery resistance index corrected to a fetal heart rate of 160 beats/min were measured. On day 10 both groups were acutely embolized until fetal arterial pH decreased to approximately 7.00. Fetal heart rate was measured with the Sonicaid System 8000 (Oxford Sonicaid, Oxford, United Kingdom). RESULTS: Chronic fetal placental embolization was associated with a progressive reduction in umbilical blood flow (p < 0.00001) and fetal arterial oxygen content (p < 0.001) whereas fetal heart rate patterns remained unaltered. A chronic increase in umbilical artery resistance index corrected to a fetal heart rate of 160 beats/min could be entirely explained only if the changes in umbilical artery pressure pulsatility index and the fundamental impedance were taken into account, in addition to the changes observed in placental vascular resistance. During acute embolization leading to a 50% reduction in umbilical blood flow (p < 0.0002) and a three times increase in placental vascular resistance (p < 0.0001), the most consistent change in fetal heart rate patterns related to progressive metabolic acidosis was an 84% decrease in absolute acceleration frequency (p < 0.0001) whereas short-term fetal heart rate variability remained unaltered. CONCLUSION: Changes in umbilical artery resistance index induced by chronic umbilical-placental embolization resulting in fetal hypoxemia occurred before any changes in fetal heart rate patterns were detectable. A decrease in the absolute acceleration frequency was the only component of fetal heart rate patterns related to progressive metabolic acidosis in the near-term ovine fetus.     

Effect of dexamethasone and betamethasone on fetal heart rate variability in preterm labour: a randomised study

OBJECTIVE: To compare the effects of betamethasone and dexamethasone on fetal heart rate in appropriately grown fetuses. METHODS: Eighty-two pregnant women (97 fetuses) with preterm labour were randomly allocated to receive betamethasone (n=42) or dexamethasone (n=40) for fetal lung maturation in a nonblinded fashion. Computerised cardiotocogram (CTG) parameters were compared before, during and after treatment. RESULTS: A decrease in fetal heart rate variability was found with betamethasone but no significant changes were found with dexamethasone. Fetal heart rate variability returned to pre-treatment values within a week after cessation of treatment with betamethasone. Neonatal outcome was similar in the two groups. CONCLUSIONS: These findings might prove useful in the management of compromised fetuses with decreased fetal heart rate variability in which the CTG should be used together with other parameters to assess fetal wellbeing during corticosteroid treatment. Dexamethasone may be preferable as the drug of choice since it was associated with significantly less alteration in fetal heart rate variability compared with betamethasone.     

Recording fetal heart rate as a behavioral measure.

Employed the fetal EKG with 4 electrodes placed on the maternal abdomen 1 just above the symphysis pubis, and the other across the abdomen at the level of the fundus uteri. The relationship between maternal and fetal heart rates were explored by also recording the maternal EKG. Difficulties in measuring fetal heart rate are discussed and possible solutions presented. It is concluded that fetal heart rate is a difficult but possible measure for exploration of fetal behavior. (17 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Dexamethasone and fetal heart rate variation

OBJECTIVE: To determine the effect of maternal administration of dexamethasone on fetal heart rate and its variation. DESIGN: Retrospective analysis of computerised data derived from cases studied over three years. SETTING: High risk pregnancy unit, John Radcliffe Hospital, Oxford. SUBJECTS: Twenty-eight pregnant women, at 27 to 32 weeks of gestation, to whom dexamethasone was given to accelerate pulmonary maturation in the expectation of preterm delivery. METHODS: Dexamethasone (two doses of 12 mg intramuscularly, 12 h apart) was given on 51 occasions at weekly intervals (one to four occasions per patient). Complete data were available for cardiotocograph analysis from computerised measurement of fetal heart rate variables for two days before and four days after dexamethasone and, in 19 women, measurements of umbilical arterial flow velocity waveforms before and after dexamethasone. RESULTS: In 10 pregnancies without fetal distress there was a highly significant (P < 0.01) transient rise in short term fetal heart rate variation after dexamethasone administration, from means (SE) 6.4 (0.28) to 9.8 (0.4) ms. In 18 pregnancies with subsequent delivery for fetal distress (abnormal fetal heart rate pattern) and high umbilical arterial resistance index [mean 0.93 (0.06 SE)], the rise in short term fetal heart rate variation was less (P < 0.01), from mean (SE) 5.4 (0.26) to 6.1 (0.48) ms. In a further case of discordant twin pregnancy, the larger twin continued to respond to dexamethasone administrations with a rise in fetal heart rate variation for five weeks; the smaller twin, with maintained tachycardia and reduced umbilical arterial end-diastolic flow velocity, failed to respond after the first two weeks. CONCLUSION: The results show that maternal dexamethasone administration normally causes a rise in fetal heart rate variation for up to a day. This rise is reduced in pre-eclampsia or intrauterine growth retardation, associated with a reduction in umbilical flow, perhaps because of a consequential lower concentration of steroid in the fetus. The results contrast with those for betamethasone which has been reported to reduce fetal heart rate variation.     

Amnioinfusion-induced malpresentation

Amnioinfusion is a valuable and common intrapartum procedure for the relief of cord compression and to dilute thick meconium. Like most procedures, it is not without risk and we report a case of malpresentation following amnioinfusion. Intrapartum fetal demise occurred after malpresentation during amnioinfusion resulting in a change of fetal presentation from vertex to unrecognized shoulder presentation. Further study is needed regarding changes in volume of amniotic fluid and saline as well as intrauterine manipulation and the effect on fetal presentation. Careful attention must be paid to infused volumes during amnioinfusion.     

Prostaglandin E2 induction of labor for fetal demise

Intrauterine fetal demise is a source of anxiety to both patient and physician. Heretofore, the standard treatment was either careful observation until the patient went into labor or attempt at induction of labor with oxytocin. Unfortunately, oxytocin stimulation has not proven to be uniformly successful for this problem. Prostaglandin E2 suppositories have been shown to be effective in inducing uterine evacuation after intrauterine fetal demise. In the opinion of the authors, this approach will in the future replace the sometimes dangerous and emotionally laden convention of watchful delayed therapy.     

Interaction of dexamethasone and Salmonella enteritidis immune lymphokines on Salmonella enteritidis organ invasion and in vitro polymorphonuclear leukocyte function

OBJECTIVE: To evaluate the effects of gemeprost on utero-placental and luteal circulation and on the embryo/fetus in normal first trimester pregnancies. STUDY DESIGN: Sixty-seven women with a normal first trimester pregnancy requesting termination of pregnancy for psychosocial reasons were randomly allocated to pre-operative treatment with vaginal suppositories containing placebo or gemeprost. The women underwent transvaginal color and spectral Doppler ultrasound examination before the application of the suppository, 4 h after the application of the suppository but before the abortion, and on the seventh post-operative day. Blood flow velocities in the uterine and subchorionic arteries, the intrachorionic area and arteries in the wall of the corpus luteum and the embryonic/fetal heart rate were measured. RESULTS: The median value for pulsatility index (PI) in the dominant uterine artery was 2.4 before treatment with gemeprost and 8.5 4 h after treatment (P = 0.0006); the corresponding values for time-averaged maximum velocity (TAMXV) being 27 cm/s and 10 cm/s (P = 0.0006). Four (14%) of 28 embryos/fetuses in the gemeprost group were dead 4 h after treatment with gemeprost and the median heart rate of those still alive was significantly lower than before treatment (130 vs. 163 bpm; P = 0.003). In the placebo group, the results for the uterine arteries and the embryonic/fetal heart rate did not differ significantly between the first and second ultrasound examinations. The median values for PI and TAMXV in the arteries of the corpus luteum wall at the first ultrasound examination were 0.71 and 18 cm/s, respectively, in the placebo group and 0.71 and 20 cm/s, respectively, in the gemeprost group. These values remained almost unchanged at the second and third ultrasound examinations in both groups. CONCLUSION: Gemeprost has profound effects on utero-placental circulation in the first trimester and can induce embryonic/fetal bradycardia and sometimes embryonic/fetal demise. It has no unequivocal effect on luteal circulation.     

Acute thoracic inlet obstruction in achalasia of the oesophagus

Eleven women with fetal distress as manifested by a decrease of fetal movements up to cessation underwent amniocentesis for amniotic fluid evaluation under continuous FHR monitoring. All the fetuses showed abnormal heart rate response, manifested by absence of FHR acceleration or early or late deceleration. The pathologic response, or lack of response of fetal heart rate during amniocentesis is suggested as an additional test to evaluate the severity of fetal distress.     

Gait patterns in children with hemiplegic spastic cerebral palsy

Our objective was to study uterine and umbilical artery flow resistance during the oxytocin challenge test (OCT). The study population was 21 women with suspected placental insufficiency; one woman was excluded because of a positive OCT with reactive fetal heart rate pattern. We carried out simultaneous electronic fetal heart rate monitoring and Doppler velocimetry of uterine and umbilical artery flow during the OCT. The uterine artery flow resistance increased significantly during contractions in both OCT-positive (n = 5) and OCT-negative (n = 15) cases compared with basal values, but the increase was significantly higher in positive cases. The umbilical artery flow resistance increased significantly during contractions in OCT-positive cases, but was almost unchanged in negative cases. During uterine inactivity, there were no differences between the groups for any vessel. This study showed that fetal heart rate decelerations during the OCT are associated with rapid and exaggerated increases of vascular resistance in both uterine and umbilical arteries. The causal relationship is unknown, but the findings indicate pathophysiological mechanisms revealed only during uterine contractions.     

Prevalence of fetal heart rate decelerations in self-referred low-risk patients in the third trimester

We tested the hypotheses that fetal heart rate decelerations are present during the third trimester in most low risk pregnant women, the prevalence of decelerations is a function of the length of time fetal heart rate monitoring occurs and their presence is not associated with an adverse prognosis. We performed a retrospective chart review of 114 self-referred low-risk pregnant patients who presented to the labor and delivery triage area of a tertiary care hospital at 26-41 weeks gestation. None required admission to the hospital. The control group consisted of patients who delivered immediately before and after the delivery of the study patient. Normal long-term variability and fetal baseline heart rate were found in all electronic fetal monitoring tracings. Accelerations were present in 91% and decelerations in 65% of patients. There was no correlation between length of time of monitoring and the incidence of decelerations. At delivery, there were no differences in birthweight, gestational age, 5-min Apgar scores or cord pH between the control and study patients. Variable decelerations were a common finding in the third trimester of low-risk pregnant patients who self referred to labor and delivery triage. They were not prognostic of an adverse perinatal outcome.