Cystic hygroma colli in triplo-X syndrome.
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Biomedical subjects
Publications and source records attributed to A Van Assche.
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We report an unusual pregnancy with a complete hydatiform mole coexisting with a normal fetus and placenta. This report stresses the importance of a correct diagnosis and the dilemmas the clinician is faced with when managing such a case. Malignant trophoblastic disease occurs in 55% of complete hydatiform mole and fetus. Two-thirds require combination chemotherapy.
Postdural puncture headache (PDPH) is the most common complication of accidental or deliberate dural puncture. It also occurs after epidural or spinal analgesia for labor and delivery. Treatment may be conservative with analgesics and/or caffeine. Definitive treatment can be accomplished with an epidural blood patch (EBP). We present a case of postpartum convulsions which were temporally related to a caffeine infusion and an EBP.
The analgesic efficacy and incidence of maternal, fetal and neonatal side-effects of combined spinal epidural (CSE) and epidural (EPI) analgesia, using a mixture of bupivacaine 0.125%, epinephrine (1.25 micrograms.ml-1) and sufentanil (0.75 microgram.ml-1) for the relief of labor pain, were randomly and prospectively compared in 110 parturients. A 29 gauge Whitacre tip spinal needle was used to perforate the dura in CSE patients. Compared to EPI, CSE resulted in rapid (326 +/- 22 vs 766 +/- 79 sec, p < 0.05), excellent analgesia, using less bupivacaine (23.5 +/- 2.3 vs 33.9 +/- 2.9 mg, p < 0.05) and sufentanil (12.5 +/- 1.0 vs 16.5 +/- .7 micrograms, p < 0.05). A tendency to improved patient satisfaction in the CSE group was observed. The incidence of maternal or neonatal side effects was similar in both groups. No PDPH was observed. We conclude that CSE analgesia results in excellent pain relief during labor with immediate gratification as compared to epidural analgesia.
The use of epinephrine as a test dose for epidural analgesia in obstetrics remains controversial. Isoproterenol as a test dose may be efficacious in the parturient. However, the effects of isoproterenol on the uterine blood flow (UBF) and umbilical blood flow (UMB) in the parturient are unknown. In a randomized, double-blind study, the hemodynamic variables in 60 nonlaboring women at term were studied 5 min before and for 10 min after an intravenous injection of either 5 micrograms isoproterenol or 5 micrograms saline. The UBF was assessed in 35 women and the UMB in 25 women using a color Doppler technique. The results of 50 women were used for further analysis. Maternal heart rate (MHR) was measured continuously, and maternal mean arterial pressure was measured every minute. MHR did not change after saline but increased significantly after injection of isoproterenol. UBF also increased significantly after isoproterenol during the same time interval. UMB did not change. Other hemodynamic variables did not change. We conclude that isoproterenol, 5 micrograms, may be a suitable test dose for epidural analgesia in obstetrics.
A primipara with an uncomplicated pregnancy was induced for labor. As uterine contractions commenced, an antepartum bleeding occurred, followed by fetal distress. An anemic fetus was delivered by cesarean section. The placenta was annular in shape with velamentous blood vessels, one of which was ruptured and sealed off by a fresh thrombus. A zonary or ring-shaped placenta is extremely rare: to our knowledge, this is the first case to be published.
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A review of clinical and pathological data on 10,000 consecutive deliveries revealed that the incidence of unexpected and intractable asphyxia at birth despite adequate resuscitation was 0.24%. Lung hypoplasia appeared to be the underlying non-viable condition in 22 out of 24 infants. Attention is drawn to congenital neuromuscular disorders which were found to be the cause of lung hypoplasia in at least 4 out of 22 infants. Some helpful hints for diagnosis are given which may contribute to the final decision making.
A patient with a history of habitual abortion, deep venous thrombosis, thrombocytopenia, high titer IgG anticardiolipin antibodies and a clearly positive lupus anticoagulant, was treated during her seventh pregnancy with high-dose intravenous immunoglobulins (IVIg) from the third month onwards. Every month, a daily infusion of 400 mg immunoglobulins per kg body weight was given during five consecutive days. The patient's pregnancy ended preterm with a live birth, delivered by caesarian section because of a placental abruption. The 1070 g (P20-P25) weighing girl was in good health, apart from a bradycardia, due to dysfunction of the atrioventricular conduction. Each treatment with IVIg resulted in a slight reduction of both anticardiolipin antibodies and lupus anticoagulant levels and in an increase in platelet count. During the six-month observation period, a gradual decline in antiphospholipid antibodies and an increase in platelet count was found. The potential role of anti-idiotypic antibodies, present in the IVIg used for treatment, was studied. In vitro, IVIg were able to reduce the binding of the patient's anticardiolipin antibodies to cardiolipin coated microtiter plates. The presence of anti-idiotypic antibodies in IVIg was further documented by affinity chromatography and by realtime biospecific interaction analysis (BIA) on a BIA-core instrument. Affinity purified anticardiolipin antibodies were retarded on a column of insolubilized IVIg and a weak interaction was found between IVIg and affinity purified antiphospholipid antibodies, coupled to the BIA-core biosensor. In addition, the same technology revealed increased levels of anti-antiphospholipid antibodies in the patient's plasma following IVIg therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
Blood pressure, proteinuria, and plasma fibronectin and plasminogen activator inhibitor-1 levels were measured in 120 apparently healthy normotensive primigravid women during the first, second, and third trimesters of pregnancy and 2 days post partum. Thirty-two women developed hypertension (diastolic blood pressure greater than or equal to 90 mm Hg) that in 17 women was associated with proteinuria (greater than 0.3 gm/day). Fibronectin levels were 83% +/- 22% of normal (mean +/- SD) during the first trimester and 75% +/- 20% at term in the healthy women but increased from 94% +/- 36% to 187% +/- 36% in the women who developed gestational hypertension (with or without proteinuria) (p less than 0.0001). Plasminogen activator inhibitor-1 levels increased from 26 +/- 19 ng/ml to 110 +/- 86 ng/ml in healthy women and from 32 +/- 35 ng/ml to 290 +/- 90 ng/ml in hypertensive women (p less than 0.001). Increased levels of fibronectin at 25 to 36 weeks of pregnancy (greater than or equal to mean + 2 SD of the healthy women, or greater than 140%) were found in 31 of the 32 women with gestational hypertension with or without proteinuria and in 5 of the 88 healthy women (sensitivity 96%, specificity 94%). Fibronectin levels increased 3.6 +/- 1.9 weeks earlier than the onset of hypertension and/or proteinuria. Increased levels of plasminogen activator inhibitor-1 at 25 to 32 weeks (greater than or equal to 280 ng/ml) were found in 16 of the 32 women who developed gestational hypertension with or without proteinuria and in 4 of the 88 healthy women (sensitivity 50%, specificity 95%). We conclude that increased fibronectin levels are the best predictor of gestational hypertension with or without proteinuria and that its level in plasma increases several weeks before the development of hypertension.
The effect of maternal hyperalimentation on intrauterine growth retardation was studied by performing unilateral uterine vessel ligation on day 17 in Wistar rats. Test animals were given food supplements by gavage for three days postoperatively whereas control animals received saline. The caloric intake and weight gain of the test dams was significantly greater than that of the controls from days 17 to 20 but not over the longer period, day 14 to 23. The survival and growth of fetuses in the unoperated horn were similar in test and control rats. Fetal survival in the ligated horn was doubled by maternal food supplementation but the growth and development of the survivors were not improved.
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We describe two infants dying neonatally of respiratory failure despite all attempts at resuscitation. The most striking finding at autopsy was eventration and reduced muscle content of the diaphragm. Microscopic examination of the skeletal muscles, in combination with retrospective evaluation of the family history, disclosed severe X-linked centronuclear myopathy in the first patient and congenital myotonic dystrophy in the second. These disorders are probably more frequent than reported before. Their identification is important, not only for genetic counseling of the involved families but also for providing the neonatologist a sufficient explanation for the failure of resuscitation.
In three patients with neonatal Bartter syndrome associated with polyhydramnios, analysis of the amniotic fluid showed normal sodium, normal-to-low potassium, but high chloride concentrations. This finding clearly suggests a renal chloride reabsorption defect as the primary cause of the neonatal form of Bartter syndrome. It is suggested that whenever polyhydramnios occurs, the electrolyte composition of the amniotic fluid should first be analysed in order to establish the diagnosis of Bartter syndrome.
A case of Monocephalus diprosopus, associated with craniorachischisis and duplication of most of the foregut derivates is presented. The major part of the cardiovascular system remained single but the heart exhibited severe defects, including a complete persistent atrioventricular canal, transposition of the great arteries and atresia of the pulmonary valve. This report further supports the hypothesis that certain-types of incomplete twinning and neural tube defects may be caused by a single teratogenic mechanism.
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Evidence exists of an association between the presence of a "lupus" anticoagulant in plasma, recurrent fetal loss, and repeated thromboembolic accidents, also in the absence of systemic lupus erythematosus. Presented is an example of this association, with morphologic and biologic studies to elucidate its pathogenesis. In the case reported, the placenta showed massive infarction. In the spiral arteries of the basal plate of the placenta, lesions of intimal thickening, fibrinoid necrosis, acute atherosis, and intraluminal thrombosis were observed. The plasma of the patient contained a lupus anticoagulant and inhibited the formation of prostacyclin by rat aortic rings. Vascular production of prostacyclin is a major natural defense mechanism against thrombosis. Lack of generation of prostacyclin may account for the decidual vasculopathy and consequent placental infarction and for the generalized thrombotic tendency of some patients with lupus anticoagulant.
In a 31-year-old woman with a history of recurrent arterial thrombosis, both of whose pregnancies had resulted in intrauterine death at 23 and 24 weeks, a "lupus" anticoagulant was identified. The patient's IgG fraction, containing the lupus anticoagulant, reduced the release of prostacyclin (PGI2) from rat aorta rings or pregnant human myometrium. This inhibitory effect was abolished in the presence of arachidonic acid. The production of 6-keto-PGF1 alpha by cultured bovine endothelial cells was also decreased in the presence of the patient's IgG fraction. The plasma level of 6-keto-PGF1 alpha was reduced. An antibody in this patient may interfere with the production or release of PGI2 by the vessel wall, possibly by interfering with the availability of arachidonic acid. This mechanism could play a role in this patient's arterial disease and obstetric problems.