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most of the system changes were based on minor critical incidents which were often detected only after a longer period of time. This shows the value of our "low-threshold" critical incident monitoring. Repeated checks along the drug delivery process (prescription, preparation, administration) are an important means to reduce adverse drug events.

We investigated an outbreak of Serratia marcescens in the neonatal intensive care unit (NICU) of the University Hospital of Zurich. S. marcescens infection was detected in 4 children transferred from the NICU to the University Children's Hospital (Zurich). All isolates showed identical banding patterns by pulsed-field gel electrophoresis (PFGE). In a prevalence survey, 11 of 20 neonates were found to be colonized. S. marcescens was isolated from bottles of liquid theophylline. Despite replacement of these bottles, S. marcescens colonization was detected in additional patients. Prospective collection of stool and gastric aspirate specimens revealed that colonization occurred in some babies within 24 hours after delivery. These isolates showed a different genotype. Cultures of milk from used milk bottles yielded S. marcescens. These isolates showed a third genotype. The method of reprocessing bottles was changed to thermal disinfection. In follow-up prevalence studies, 0 of 29 neonates were found to be colonized by S. marcescens. In summary, 3 consecutive outbreaks caused by 3 genetically unrelated clones of S. marcescens could be documented. Contaminated milk could be identified as the source of at least the third outbreak.

Increased loss of antithrombin is present in children with chylothorax, potentially predisposing these children to an increased risk of thrombosis. Repeated antithrombin substitution should be considered in critically ill children with chylothorax.

An immunocompetent 9-year-old boy with disseminated cat scratch disease involving spleen, cervical and abdominal lymph nodes, skull, and one clavicle is reported. Antibodies to Rochalimaea quintana and R. henselae were detected, at increasing, then decreasing concentration. DNA extracted from the biopsied skull lesion was amplified by polymerase chain reaction and hybridized with species-specific oligonucleotides proving the presence of R. henselae in affected tissue. Our findings suggest that R. henselae plays a pathogenic role in cat-scratch disease.

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Aims: To evaluate the prevalence of congenital prothrombotic disorders in children with peripheral venous and arterial thromboses. Methods: Deficiencies in antithrombin (AT), proteins C (PC) and S (PS), and increased lipoprotein (a), and the presence of factor V (FV) G1691A, prothrombin G20210A and methylenetetrahydrofolate reductase (MTHFR) mutations were investigated. Results: Forty-eight patients (mean age, 3.4 years) were investigated. Of these patients, 23 had venous thrombosis, 22 had arterial thrombosis, and 3 had both. No patients had AT, PC or PS deficiency. FV G1691A mutation was present in 2 (7.6%) and 3 (12%) patients with venous and arterial thromboses, respectively. The prothrombin G20210A mutation was present in 1 (4%) patient with arterial thrombosis. Homozygous MTHFR C677T mutation was detected in 4 (18%) and 2 (9%) patients with venous and arterial thromboses, respectively. Increased lipoprotein (a) was present in 2 (10%) and 1 (4.5%) patients with venous and arterial thromboses, respectively. Regarding acquired risk factors, 79% of all thrombotic events were related to catheter usage. An underlying disease was present in 96% of the patients. Conclusions: Compared to acquired risk factors, congenital prothrombotic disorders are rarely present in children with peripheral venous and arterial thromboses. These results do not support general screening of children with venous and arterial thromboses for congenital prothrombotic disorders.

Early detection of pathophysiological factors associated with permanent brain damage is a major issue in neonatal medicine. The aim of our study was to evaluate the significance of the CO₂ reactivity of cerebral blood flow (CBF) in neonates with perinatal risk factors. Fourteen ventilated neonates with perinatal risk factors (pathological cardiotocogramm, low cord pH, postpartal encephalopathy) were enrolled into this prospective study. The study was performed 18–123 h after birth. CBF was measured using the nonivasive intravenous ¹³³Xe method. Two measurements were taken with a minimal PaCO₂-difference of 5 mm Hg. From the two CBF values the CO₂ reactivity was calculated. Outcome was evaluated 1 year after birth. The CBF values at a lower PaCO₂ ranged from 6.6 to 115.2 ml/100 g brain issue/min (median = 18.2) and at a higher PaCO₂ level from 7.1 to 125.7 ml/100 g brain tissue/min (median = 18.75). The calculated CO₂ reactivity ranged from –9.6 to 6.6% (median 1.1%) change in CBF/mm Hg change in PaCO₂. CO₂ reactivity correlated with lowest pH (r² = 0.35, p = 0.02). Two infants died, one of neonatal sepsis, the other of heart failure. Neurological outcome at the age of 1 year was normal in 11 patients, 1 had severe cerebral palsy. From the 12 surviving patients the patient with severe neurological deficit showed the highest CBF values (125.7 ml/100 g/min). Impaired chemical coupling of cerebral blood flow is compatible with intact neurological outcome in neonates with perinatal risk factors. CO₂ reactivity in these newborns correlates with the lowest pH and may reflect the severity of perinatal asphyxia.