Closure of the ductus venosus in premature infants: findings on real-time gray-scale, color-flow Doppler, and duplex Doppler sonography.

OBJECTIVE: Our objective was to use gray-scale, color-flow, and duplex Doppler sonography to study the anatomy, flow pattern, and time of closure of the ductus venosus in healthy premature infants. SUBJECTS AND METHODS: We prospectively examined the ductus venosus in 130 premature infants whom we divided into two groups: Group I comprised 27 neonates of gestational age 28-32 weeks, and group II comprised 103 neonates of gestational age 33-36 weeks. Neonates who had undergone umbilical vessel manipulation were excluded from the study. All examinations included gray-scale, color-flow, and duplex Doppler sonography. Patency, length, color flow, and Doppler characteristics of the ductus venosus were recorded. Neonates were examined 1-2 days after birth, 6-7 days after birth, and subsequently every 3-4 days until ductus closure was observed. The time of closure of the ductus for the two groups was compared using the chi-square test. RESULTS: The ductus venosus was patent during the initial examination in 128 of the 130 neonates. Doppler waveform was venous with little variation in velocity. Ductus length slightly exceeded 1 cm in both groups. We found a statistically significant difference in the percentage of infants having a patent ductus venosus after the initial examination: At 1 week after birth, ductus patency was shown in 85% of the infants in group I and in 56% of the infants in group II; at 2 weeks, the respective percentages were 42% and 14%; and at 3 weeks, 27% and 0%. CONCLUSION: The ductus venosus is patent 1-2 days after birth in virtually all premature infants. From 6 days after birth and onward, a significantly greater percentage of smaller premature infants (i.e., 28-32 weeks' gestational age) have a patent ductus venosus than do larger premature infants (i.e., 33-36 weeks' gestational age).

Leukemoid reaction induced by prenatal administration of betamethasone.

A case of leukemoid reaction in a premature baby whose mother was antenatally treated by betamethasone is reported. The neonatal and maternal factors which might lead to leukocytosis or leukemoid reaction were excluded. The presented case is the last in a series of eight previously reported cases of leukemoid reaction, in which the common denominator was the antenatal administration of betamethasone.

The use of an audiotaped analysis in a continuous case seminar.

The use of an audiotaped analysis in a continuous case seminar is evaluated. We compare this case seminar to the traditional one in which an analyst presents process notes, and find that the use of the tape lends itself readily to teaching microanalysis, principles of technique, and observation of affect. Listening to anonymous taped sessions allowed for the possibility of a freer climate for discussion, as none of the seminar participants had a personal relationship with the taped analyst. The disadvantages posed by the absence of the analyst during the seminar also are addressed.

Total leukocyte and neutrophil count changes associated with antenatal betamethasone administration in premature infants.

The white blood cell counts of 84 premature infants were included in a retrospective study of 45 infants treated antenatally with betamethasone and 39 non-treated infants. A significant increase in neutrophil and immature neutrophil forms was found in the treated group when the drug was administered to the mother close to delivery. This effect lasted for three days. Afterwards, although the counts were not significantly high compared to the control group, their physiological decrease was delayed. This study indicates that the known stimulating effect of steroids on total leukocyte and neutrophil counts in adult humans and fetal lambs, also occurs in premature infants. This fact supports recent reports which propose the antenatal maternal administration of betamethasone as a cause of leukemoid reaction or leukocytosis after birth.

Evidence that 3 alpha-hydroxy-5 alpha-pregnan-20-one is the metabolite responsible for anesthesia induced by 5 alpha-pregnanedione in the mouse.

Mice were anesthetized with [3H]5 alpha-pregnanedione (5 alpha). Brain levels for 5 alpha and its metabolites were quantitated and compared at time points following injection and at two behavioral endpoints that are characteristic of the anesthetized state. The results support the hypothesis that 3 alpha-hydroxy-5 alpha-pregnan-20-one (3 alpha), a metabolite of 5 alpha, mediates this anesthetic response, and they weigh against the hypothesis that 5 alpha itself is solely responsible for activity. Anesthesia occurred at 3-8 min following injection. During this period, levels of 3 alpha derived from 5 alpha were comparable to those seen when 3 alpha was administered alone. It is estimated that 5 alpha, if active at all, is at least 3-5 times less potent than 3 alpha.

In vivo studies identify 5 alpha-pregnan-3 alpha-ol-20-one as an active anesthetic agent.

Mice were anesthetized with 5 alpha-[3H]pregnan-3 alpha-ol-20-one. Brain levels for 5 alpha-pregnan-3 alpha-ol-20-one and its five major metabolites (5 alpha-pregnanedione, k0, k1, k2, k3) were compared at behavioral endpoints that are characteristic of the anesthetized state. The results support the hypothesis that 5 alpha-pregnan-3 alpha-ol-20-one mediates the anesthetic response, and they weigh against the hypothesis that any of its metabolites is solely responsible for the onset or the maintenance of the anesthetized state. For an administered dose of 3 mg/kg, brain levels (means +/- SEM) for 5 alpha-pregnan-3 alpha-ol-20-one at the time of the loss of the righting response (n = 10) and at the time of the return of the righting response (n = 6) were 7.24 +/- 0.61 pmol/mg of brain tissue and 3.63 +/- 0.26 pmol/mg of brain tissue, respectively. No metabolite level was lower at the return of the righting response than at the loss of the righting response. 5 alpha-Pregnan-3 alpha-ol-20-one brain levels increased consistently with the percentage of anesthetized mice. This was not the case for any of the metabolites. Fifty percent of the mice were anesthetized when the 5 alpha-pregnan-3 alpha-ol-20-one level was 4.5 pmol/mg of brain tissue.

Meconium peritonitis: a benign course in a premature infant.

A case of a premature infant with meconium peritonitis and intraperitoneal calcifications is described. The course of illness was mild and recovery complete. No evidence of congenital intestinal obstruction or cystic fibrosis was found.

Familial combined sinus node and atrioventricular conduction dysfunctions.

Eighteen members of a family were investigated for cardiac conduction abnormalities following the discovery of a second-degree atrioventricular block in a fetus at 35 weeks of gestation. The conduction disturbance was diagnosed by ultrasonography. Seven of the family members were diagnosed as suffering from sinus node dysfunction and/or various degrees of atrioventricular block. Three of them were children aged 9 months to 6 years and all were asymptomatic. The symptomatic family members were two adults. One of them had a pacemaker inserted for a complete atrioventricular block and Adam-Stokes attacks while the other had had several fainting attacks. The clinical, electrocardiographic and ultrasonographic findings of the family members are presented. Previous reports in literature have documented the dominant transmission of familial sinus node dysfunctions or of familial cardiac conduction disturbances. The coexistence of both dysfunctions in the same family has not been emphasized in previous reports. A review of these previously reported families, as well as our patients, suggests the need of investigation and follow-up of the families in which one member of any age is diagnosed as suffering from an "idiopathic" disturbance of the cardiac conduction system.

Soft tissue calcification: a complication of vitamin E injection.

Two cases of gross soft tissue calcification following intramuscular administration of vitamin E in two premature babies are described. The drug was administered for prevention of retinopathy of prematurity. The relation between this complication and both the dosage used and the duration of the treatment is discussed. In spite of the extent of the calcifications, a benign course was observed. Other reports about this complication are reviewed.