Volume 30, Issue 2

Vitamin A (vit A) plays an important role in wound healing and therefore may help in repairing of intestinal mucosal injury. The purpose of this study was to determine if vit A supplementation could promote healing in intestinal mucosal injury as commonly seen in neonatal necrotizing enterocolitis (NEC). Mild intestinal mucosal injury was induced in 10-day-old Sprague-Dawley rats by luminal administration of 1.5% butyric acid (BA) at pH 4.0. Normal saline at the same pH was administered as control. Immediately after administrations of BA or normal saline, animals were randomly assigned to receive high dose vit A (20,000 IU/kg for one dose, i.p.), low dose vit A (5,000 IU/kg for two doses) or vehicle. Animals were followed for 48 hours and then sacrificed for histological examination. Rats with BA-induced intestinal mucosal injury had a reduction in daily weight gain (p < 0.05). Vit A supplementation significantly improved the daily weight gain in the rats with BA-induced intestinal mucosal injury and the effect is dose dependent. At sacrifice, the colon wet weight was significantly heavier and the histological injury scores from both ileum and proximal colon higher in the rats with BA-induced intestinal mucosal injury. All of those parameters were improved with vit A supplementation. We conclude that vit A supplementation ameliorates BA induced-intestinal mucosal injury in newborn rats.

Objective: The purpose of the study was to investigate alimentation of very low birth weight (VLBW) infants and its effect on blood concentration of glucose, urea nitrogen, creatinine and potassium. Methods: The subjects were 100 VLBW infants born between 1993–1999. The gestational age ranged from 23 to 32 weeks and the birth weight from 443 to 1470 g. Intravenous glucose infusions were begun shortly after birth, amino acids on day 3 and lipids on day 4. Blood samples were drawn for determinations of urea nitrogen, creatinine and potassium. Results: Mean caloric intake of glucose rose from 24.7 kcal/kg/day on day 1 to 58.1 kcal/kg/day on day 8 (p < 0.0001) and of amino acids from 1.1 g/kg/day on day 3 to 1.9 g/kg/day on day 8 (p < 0.0001). Potassium administration increased from 1 mq/kg/day on day 2 to 1.9 mq/kg/day on day 8. Urea nitrogen was at a mean level of 21.4 mg/dl on day 4 and declined afterwards (p < 0.0001). Serum potassium levels declined from 5.9 mmol/L on day 2 to 4.1 mmol/L on day 8 (p < 0.0001), while creatinine levels remained stable. Conclusion: Our findings suggest that a catabolic state in VLBW infants begins to be reversed when the caloric intake of 40–50 kcal/kg/day is achieved.

Objective: By determining the early patterns of steroidogenesis in the most common aneuploidies, we have shown that there are differences between aneuploid and euploid pregnancy steroidogenesis patterns. We hypothesize that there are differences in steroidogenesis between specific trisomies, as well. Methods: The records of all patients with a cytogenetic diagnosis of aneuploidy were studied. Serial data on progesterone(P), estradiol(E2) and beta-HCG(bHCG) was collected in the first trimester of aneuploid pregnancies. A matched group of normals at the same gestational ages was used as a control group. The specific trisomies of the above group were catalogued. Results: 31 aneuploid pregnancies were reviewed for progesterone, estradiol and beta-HCG in the first trimester. Data was available for three or more patients with trisomy 16, 18, 21 and 22. Serial measurements between 5 and 10 weeks of pregnancy were obtained for P, E2, and bHCG. Gestational age was determined by LMP and serial sonograms. The progesterone, estradiol and beta-HCG levels were evaluated by calculating the rates of change between 5 and 10 weeks, rather than threshold values. The natural log of the values was used to plot serial data and reduce scatter due to the large natural variation in values between patients. The rates of change of P, E2 and b-HCG in the trisomic pregnancy groups were compared to matched normal pregnancies. The slopes of the curves for the trisomies and euploid pregnancies were calculated and compared. We determined that the rate of change of HCG for each of the trisomies was no different from euploid pregnancies, which is consistent with earlier data. In examining estradiol, trisomy 22 did not have a statistically different pattern of steroidogenesis, where trisomies 16, 18 and 21 were different than euploid (p < 0.05). With progesterone, trisomies 16, 18 and 22 had statistically different rates of change (p < 0.05), however trisomy 21 did not. Conclusions: As we have shown, in pregnancies with aneuploidy, there is a different pattern of steroidogenesis from euploid pregnancies. The difference is detectable in the first trimester by serial measurements of P and E2. In determining steroidogenesis in trisomies 16, 18, 21, and 22, we demonstrate that there is a difference in progesterone and estradiol levels over 5 to 10 weeks among the trisomies that can assist in the diagnosing of abnormal pregnancies in the first trimester. Furthermore, by looking at the rates of change of the individual steroids, the specific aneuploidy may be suspected. A large prospective study may reveal the clinical utility of these observations for early prenatal diagnosis of aneuploidy or probable spontaneous abortion.

Objective: The hypothesis is that a risk score derived from the risk index (RI) is correlated with perinatal outcomes. Study design: The RI is a weighted numerical score based on gestational risk factors applied to 782 gravidas antepartum. Management was independent of the score. Birth weight, Apgar scores, and cesarean birth were correlated with risk score. Results: The break point score in this non-Gaussian cohort was 6. Using 6, 80. 2% were low and 19.8% high risk. Birth weight < 2500 gm was inversely correlated (p < .001) and occurred in 13% of the high risk ( 3 6) and 4.9% of the low risk (< 6) group, relative risk (RR) 2.7. C-section correlated (p < .001), and occurred in 51% of the high and 23% of the low risk group, RR 2.4. risk score inversely correlated with 5 minute Apgar (RR 4.7 p < .002) but not the 1 minute Apgar score. Conclusion: The RI identified gravidas at risk for low birth weight, low 5 minute Apgar score, and cesarean birth.

There is increasing evidence from studies on animals and humans that surfactant administration may have a great impact on cerebral perfusion. These effects may result from direct pulmonary or hemodynamic changes (or a combination of both), but may also be due to rapid alterations of blood gases. Type of surfactant and mode of administration seem to play an important role. Results from the pertinent literature are summarised with a special emphasis on how to avoid potentially harmful side effects of surfactant therapy in preterm infants.

A prospective multicenter study was designed to assess the frequency, etiology, and mortality of nosocomial neonatal sepsis diagnosed between 1996 and 1997 in the neonatology services of 27 acute-care hospitals in Spain (“Grupo de Hospitales Castrillo”). Nosocomial sepsis is defined in the literature using chronological criteria (> 3–7 days of life at the onset of symptoms); accordingly, there is the possibility of including late-onset maternally acquired sepsis or of excluding early-onset nosocomial sepsis (< 3–7 days of life). For these reasons, in this study, cases of nosocomial sepsis that developed at ≤3–7 days after birth (early onset) were also recorded and maternally acquired sepsis diagnosed beyond 3–7 days of life were excluded. Using these criteria in a total of 30,993 admissions to the neonatal units of the participating hospitals, the nosocomial sepsis rate was 2.1% with an incidence density of 0.89 per 1000 patient days. Sepsis rate was significantly more frequent among very low birth weight (VLBW) infants (15.6%) than among those weighing ≥1500 g (1. 16%) ( P < 0.001). Fifty-eight percent of all isolates were Gram-positive organisms, mainly Staphylococcus epidermidis (42 %). Gram-negative organisms were isolated in 29.5%of cases ( Escherichia coli and Klebsiella spp. were the most commonly isolated pathogens) and fungal infections in 12 %, with absolute predominance of Candida spp. The overall mortality rate was 11.8% and the following subgroups had significantly higher ( P < 0.001) mortality rates: sepsis caused by Gram-negative organisms (19% vs. 5.1% in Gram-positive pathogens) and sepsis caused by Pseudomonas aeruginosa (33.3% vs. 9.4% for the total number of sepsis caused by the remaining causative pathogens). Sepsis caused by S. epidermidis showed a significantly lower mortality rate (5.5%) compared with overall sepsis for the remaining etiologies (14.2%) ( P < 0.001). In VLBW infants, the mortality rate was significantly higher than in infants weighing > 1500 g (17.3% vs. 6.5 %, P <0.001).

Aim: To examine the effect of overexpression of human intracellular copper-zinc superoxide dismutase (CuZnSOD1) gene on fetal mice brain exposed to in-utero ischemic reperfusion injury. Design: Transient in-utero ischemia (7 min) was induced in pregnant transgenic mice overexpressing human CuZnSOD1 and wild-type mice by occluding the blood supply to the uterine artery on day 17 of pregnancy, followed by 24 hours of reperfusion. The level of lipid peroxidation in fetal mice brains was compared between the transgenic and non-transgenic (control) fetal mice. Motor and coordination skills of transgenic and control adult mice (six to eight months old) which were exposed to ischemic reperfusion injury in-utero were compared by the rope grip test and visible platform task. Results: We first measured CuZnSOD1 activity in the brains of the transgenic fetal mice and confirmed that the enzyme activity is 4.2-fold higher than control. We also established that ischemia reperfusion on day 17 of pregnancy led to increased level of TBARS (Thiobarbituric acid reactive substance) in brains of wild-type fetal mice when compared to sham operated mice (72.5 ± 3.4 vs. 49.4 ± 1.5 nmol/mg. p < 0.001). The increase was markedly accentuated in the CuZnSOD1 transgenic mice, and significantly higher compared to control mice exposed to ischemia-reperfusion (85.6 ± 4.0 vs. 69.5 ± 2.3 nmol/mg, p < 0.001). Moreover, we found that the transgenic mice that were subjected to in-utero ischemia reperfusion exhibited a significantly higher rate of failures in the rope grip test and poorer performance in the visible platform task, when compared to non-transgenic mice exposed to identical insult. Conclusions: Oxygen free radicals play an important role in the pathogenesis of perinatal hypoxia. Overexpression of the enzyme CuZnSOD1 in transgenic mice exposes their brains to increased damage during ischemic-reperfusion insult.

The role of Gilbert's syndrome (GS) in neonatal hyperbilirubinemia, characterized by bilirubin levels higher than 223 μMol/L during the first seven days of life, has been investigated, evaluating the frequency of GS genotype (A(TA) 7 TAA polymorphism in the promoter of the gene encoding UGT1). The frequency of GS was significantly higher in the hyperbilirubinemic group, even though neither the peak of bilirubin, nor the day on which the highest value was found, differed according to genotype. The normalization of bilirubin levels was slower in neonates with GS. These results confirm the idea that GS is one of the factors contributing to neonatal hyperbilirubinemia, but that other factors play a role in determining neonatal jaundice. The slower decrease of bilirubin levels in A(TA) 7 TAA homozygous neonates confirms that GS is an important factor in determining a prolonged neonatal jaundice.

Aims: To evaluate the sonographic appearance of suspected fetal cardiac rhabdomyomas and their evolution until delivery and in the postnatal period. Methods: The study group consisted of 6 patients at 23–37 weeks of gestation referred to our Ultrasonic Unit, between March 1992 and December 1998, for suspected fetal cardiac rhabdomyomas. Results: The cardiac tumors were single in three cases and multiple in the other cases. The size ranged from 11 to 47 mm. In two cases the tumors arose from the right ventricle, in one case from the interventricular septum and in three cases from the left ventricle. Five infants are alive and in satisfactory hemodynamic compensation, but three of them developed tuberous sclerosis. In two infants a regression in the maximum diameter of the tumor masses has been observed. One child underwent surgical treatment at the age of six months and the baby died after surgery. Conclusions: Two-dimensional and Doppler echocardiography are useful non invasive methods to diagnose fetal cardiac rhabdomyomas and to monitor their influence on the fetal cardiac function. However they do not allow us to recognize which fetuses presenting with features compatible with rhabdomyomas will develop tuberous sclerosis.

Objective: In cohorts of infants with proven neonatal alloimmune thrombocytopenia (NAIT) an unusual high rate of preterm infants has been reported, raising the question of whetherNAIT contributes to the high rate of intracranial hemorrhage in preterm infants. Methods: We genotyped the HPA-1-allele in a large cohort of term (n = 205) and very low birth weight infants (VLBW-infants, n = 299) with polymerase-chain-reaction and restriction enzyme digestion. Results: HPA-1a/b is the only fetal HPA-1-genotype in which alloimmunization and NAIT could occur. Genotype distribution did not differ between term and VLBW-infants (p = 0.26). Furthermore, neither HPA-1a/b genotype nor platelet count at birth were of significant prognostic value in predicting subsequent intracranial haemorrhage or death inVLBW-infants (p = 0.93 and p = 0.19 respectively). Conclusion: Our data did not support the hypothesis that routine screening of preterm infants or their mothers for HPA-1-genotype is of additional value in the care of these infants.

Aims: The authors compare their experience of 17 cases of sacrococcygeal teratoma (SCT) with the literature in an attempt to clarify the natural history of this tumor and to identify factors related to its prognosis and management. Methods: The obstetrical, neonatal and surgical data were analyzed for 17 cases of SCT observed between July 1985 and December 1998. Results: Three fetuses died in utero or shortly after birth. In the remaining 14, the tumors were removed. Twelve of the infants are currently tumor-free, with good sphincter control and lower-limb function. The remaining two died: one had a malignant tumor, and the other had a recurrence of an embryonal carcinoma. Recurrent tumors (mature histotypes) were also removed from two of the 12 patients who survived. Conclusions: Benign SCTs generally have favorable prognosis. Negative prognostic factors for SCT include solid tumors, those detected early in pregnancy, malignant histotypes, polyhydramnios, placentomegaly, and fetal hydrops.

We report a case of Dubin-Johnson Syndrome in a neonate presenting with severe direct hyperbilirubinemia, which failed to respond to phenobarbital treatment. Ursodeoxycholic Acid added to therapy was well tolerated, and resulted in declining bilirubin concentration. We suggest ursodeoxycholic acid in treatment for Dubin- Johnson Syndrome with severe direct hyperbilirubinemia presenting in the neonatal age.

Perforation of the urinary bladder is a rare complication with a considerable degree of morbidity and mortality in modern neonatal intensive care units. We report a case of urinary bladder perforation, which probably was triggered by prolonged urinary retention secondary to morphine infusion, using credé maneuver on an already. over-distended bladder, and inserting an umbilical catheter as urethral catheterization in an extremely low birth weight infant.