Effect of Bifidobacterium lactis on the incidence of nosocomial infections in very-low-birth-weight infants: a randomized controlled trial.

BACKGROUND: Nosocomial infections endanger preterm infants. OBJECTIVE: The aim of the present controlled randomized trial was to investigate whether Bifidobacterium lactis reduces the incidence of nosocomial infections in infants with very low birth weight (VLBW; <1,500 g) <30 weeks of gestation. PATIENTS AND METHODS: In a randomized controlled trial, 183 VLBW infants <30 weeks of gestation were stratified according to gestational age (23-26 and 27-29 weeks) and early antibiotic therapy (days 1-3, yes or no) and randomly assigned to have their milk feedings supplemented with B. lactis (6 x 2.0 x 10(9) CFU/kg/day, 12 billion CFU/kg/day) or placebo for the first 6 weeks of life. Primary outcome was the 'incidence density' of nosocomial infections defined as periods of elevated C-reactive protein (>10 mg/l) from day 7 after initiation of milk feedings until the 42nd day of life (number of nosocomial infections/total number of patient days). The main secondary outcome was necrotizing enterocolitis (NEC; >or=stage 2). RESULTS: There were 93 infants in the B. lactis group and 90 in the placebo group. There was no significant difference between the two groups with regard to the incidence density of nosocomial infections (0.021 vs. 0.016; p = 0.9, chi(2) test). There were 2 cases of NEC in the B. lactis group and 4 in the placebo group. None of the blood cultures grew B. lactis. CONCLUSION: In the present setting, B. lactis at a dosage of 6 x 2.0 x 10(9) CFU/kg/day (12 billion CFU/kg/day) did not reduce the incidence density of nosocomial infections in VLBW infants. No adverse effect of B. lactis was observed.

Neonatal and neurodevelopmental outcome in infants born before 30 weeks of gestation with absent or reversed end-diastolic flow velocities in the umbilical artery.

UNLABELLED: The objective of our study was to examine the outcome of infants born at a gestational age < 30 weeks with absent or reversed end-diastolic flow velocity (AREDFV) in the umbilical artery in comparison with gestational age-matched eutrophic controls. A group of 40 infants who had AREDFV were matched for gestational age and date of birth with 40 appropriate for gestational age infants. Perinatal outcome variables were retrospectively reviewed. In 16 out of the 40 matched pairs, a standardized neurological examination was done and, depending on age, the Kaufman Assessment Battery for Children or the Bayley Scales of Infant Development were applied at a corrected age of 13 to 100 months to assess neurodevelopmental outcome. The results were compared using Fisher's Exact Test or Mann Whitney U Tests as appropriate. In the AREDFV group, 26/40 (65%) survived until discharge compared to 39/40 (97.5%) in the control group (P < 0.001). AREDFV was associated with a higher rate of chronic lung disease, retinopathy of prematurity > or = grade III and impaired intestinal motility. More AREDFV infants suffered from permanent neurological sequelae compared with control infants: 44% versus 25% were mentally retarded (P = 0.033), and 38% versus 19% showed severe motor impairment (P = 0.073). CONCLUSION: Absent or reversed end-diastolic flow velocity is not only associated with a higher mortality and morbidity during the neonatal period, but the surviving infants of this high risk group have an increased risk for mental retardation and severe motor impairment as compared with appropriate for gestational age preterm infants of the same gestational age.

Delivery room management of extremely low birth weight infants: spontaneous breathing or intubation?

OBJECTIVE: To study the effect of two different delivery room (DR) policies on the rate of endotracheal intubation and mechanical ventilation (EI/MV) and short term morbidity in extremely low birth weight infants (ELBWI; <1000 g, >/=24 weeks). METHODS: Retrospective cohort study of 123 inborn ELBWIs born in 1994 and in 1996. DR policies have changed. Until 1994, ELBWIs were intubated immediately after delivery when presenting the slightest signs of respiratory distress or asphyxia after initial resuscitation using a face mask and a handbag. During 1995, the guidelines for respiratory support were changed. In 1996, continuous (15 to 20 seconds), pressure controlled (20 to 25 cm H2O) inflation of the lungs using a nasal pharyngeal tube, followed by continuous positive airway pressure (CPAP; 4 to 6 cm H2O) was applied to all ELBWIs immediately after delivery to establish a functional residual capacity and perhaps to avoid EI/MV. In addition to the changes in respiratory support, the prevention of conductive and evaporative heat loss was improved in 1996. For analysis of morbidity and mortality, infants were matched for gestational age and birth weight. RESULTS: The rate of EI/MV in the DR decreased from 84% in 1994 to 40% in 1996. In 1996, 25% of the ELBWIs were never intubated (7% in 1994), but 35% of the ELBWIs needed secondary EI/MV, primarily because of respiratory distress syndrome (RDS). Initial ventilator settings, ventilator days, mortality, and morbidity were not different between ELBWIs with EI/MV in the DR and infants with secondary EI/MV attributable to RDS in the intensive care unit. ELBWIs with no EI/MV that was caused by RDS had a lower morbidity (ie, bronchopulmonary dysplasia, intraventricular hemorrhage >grade 2 and/or periventricular leukomalacia), mortality, and fewer hospital days (mean: 79 vs 105 days). The incidence of gastrointestinal adverse effects like feeding intolerance or necrotizing enterocolitis was not increased in 1996. PaCO2 was significantly higher at admission to the neonatal unit in ELBWIs with CPAP in 1996 (54 +/- 15 mm Hg, 7.2 +/- 2.0 kPa) compared with infants with EI/MV in 1994 (38 +/- 11 mm Hg, 5.1 +/- 1. 5 kPa. A total of 26% of spontaneously breathing infants had hypercapnia (PaCO2 >/=60 mm Hg [8.0 kPa]), compared with 7% of infants with EI/MV in 1994. Within the first few hours of life, PaCO2 decreased to 46 (32 to 57) mm Hg (6.1 [4.3 to 7.6] kPa) in never intubated ELBWIs (n = 17), but increased to 70 (57 to 81) mm Hg (9.3 [7.6 to 10.8] kPa) in ELBWIs (n = 14) with RDS and secondary EI/MV (age 5.5 [1 to 44] hours). CONCLUSIONS: In our setting, the individualized intubation strategy in the DR restricted EI/MV to those ELBWIs who ultimately needed it, without increasing morbidity or mortality in infants with secondary EI/MV attributable to RDS. We speculate that an individualized intubation strategy of the ELBWI is superior to immediate intubation of all ELBWIs with slight signs of respiratory distress after birth.

Neonatal hypocalcaemia associated with rotavirus diarrhoea.

UNLABELLED: We observed an association between rotavirus diarrhoea and hypocalcaemia in several patients and therefore started a prospective evaluation with measurement of calcium levels in all patients with rotavirus infection during a period of 8 months. We report on 54 infants with rotavirus gastro-enteritis. Serum concentrations of sodium, potassium, and total and ionized calcium were measured on admission. If hypocalcaemia was detected, total and ionized calcium were measured every day until recovery. Calcium was supplemented as calcium gluconate which was added to milk. Out of 54 newborns with rotavirus gastro-enteritis, 20 developed hypocalcaemia. All these newborns had severe diarrhoea. Seven infants were admitted because of convulsions, but EEG and ultrasonographic examination of the brain revealed no abnormalities. Once the infants' clinical condition and the consistency and frequency of the stool had improved, calcium concentrations increased and remained within the reference range without supplementation. CONCLUSION: Rotavirus gastro-enteritis seems to be a cause of neonatal hypocalcaemia.

[Olivo-ponto-cerebral hypoplasia--case report of a neurodegenerative disease manifesting at birth with a fatal outcome]. / Olivo-ponto-cerebellare Hypoplasie--Fallbericht einer neurodegenerativen Erkrankung mit Manifestation bei Geburt und fatalem Verlauf.

We report on a boy with pontocerebellar hypoplasia Type II according to the classification of Barth. The clinical signs were noted at birth and consisted of muscular hypertonus, central hypopnoe requiring artificial ventilation, chorea, hyperthermia above 40 degrees C and myoclonic seizures resistant to all therapeutic modalities. At birth, the boy was noted to have macrocephaly, but was microcephalic by 3 months of age. He failed to develop any mental or motor facilities. After cessation of all therapy the child died at the age of 3 1/2 months. Postmortem examination of the brain revealed loss of neurons and gliosis affecting the olivo-ponto-cerebellar system, signs characteristic of PCH.

[Emergency therapy of neonatal hyperammonemia with high dosage glucose]. / Notfalltherapie neonataler Hyperammonämien mit hochdosierter Glukose.

In severe neonatal hyperammonemia, therapy must be started immediately to prevent irreversible CNS damage. Endogenous ammonia production can be quickly reduced if an anabolic condition is induced by means of high-dose glucose infusion. We applied this treatment to four newborn infants with hyperammonemia, this being a symptom of an inborn error of metabolism. The dangerous metabolic dysfunction was brought under control without dialysis within 24-48 hours in all four patients.

[Severe combined immune defect. Presentation of exfoliative dermatitis with eosinophilia and lymphadenopathy]. / Schwerer kombinierter Immundefekt. Auftreten von Exfoliativer Dermatitis mit Eosinophilie und Lymphadenopathie.

BACKGROUND: We report on 9 infants with severe combined immunodeficiency (SCID), who additionally showed signs of Omenn syndrome with an exfoliative dermatopathy, alopecia, enlarged lymph nodes, a hepatomegalia and a striking blood eosinophilia. The immunological evaluation revealed the characteristic abnormalities of SCID with cellular and humoral immunodeficiency. All patients however had the unusual finding of mature T cells in the peripheral blood. By HLA typing these cells were noted to be of maternal origin in 5 patients. In the other 4 patients the T cells were of host origin. We asked for additional differences between both patient groups. METHOD: Both patient groups were analyzed and compared with regard to case histories, clinical, laboratory and histopathological parameters. RESULTS: No clinical or laboratory differences could be detected. The histomorphologic analysis of patients with or without maternal T cells was identical. The skin biopsies showed dense cell infiltrations of lymphocytes, histiocytes and eosinophils, in the enlarged lymph nodes the latter two cell types predominated. Therefore the only difference between the 2 patient groups was the presence or absence of maternal T cells. CONCLUSION: Since the Omenn syndrome is found in association with maternal as well as patient derived T cells, we postulate that the peculiar symptoms of this syndrome are the result of a T cell induced inflammatory reaction, similar but not identical to a graft versus host reaction, occurring on the basis of an inborn SCID.

[Pathogenesis and histomorphology of the so-called Omenn syndrome]. / Pathogenese und Histomorphologie des sogenannten Omenn-Syndroms.

1. The Omen-syndrome is not a disease on its own, but a complication of congenital SCID. 2. In contrast to patients with classical SCID, patients with Omenn-syndrome possess mature T-cells, which are either of maternal or of host origin. 3. These T-cells are involved in the pathogenesis of the characteristic tissue changes, in particular of skin and lymph nodes (Langerhans-histiocytosis with eosinophilia). 4. The detection of immunodeficiency in Omenn-syndrome is difficult since the lymph nodes are enlarged in contrast to patients with classical SCID. The histomorphological analysis of lymph nodes in Omenn-syndrome is considerably complicated by secondary changes closely resembling dermatopathic lymphadenopathia.