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.

OBJECTIVE. The neonatal abstinence scoring system proposed by Finnegan is used widely in neonatal units to initiate and to guide therapy in babies of opiate dependent mothers. The purpose of this study was to assess the variability of the scores in newborns and infants not exposed to opiates during the first three days of life and during 3 consecutive days in week 5 or 6. PATIENTS AND METHODS. Healthy neonates born after 34 completed weeks of gestation whose parents denied opiate consumption and gave informed consent were included in this observational study. Infants with signs or symptoms of disease or with feeding problems were excluded. A modified scoring system was used every 8 hours during 72 hours by trained nurses. 102 neonates were observed for the first 3 days of life and 26 neonates in week 5 to 6. A meconium sample and a urine sample at week 5 to 6 were stored from all infants to be analysed for drugs when the baby scored high. Given a non-Gaussian distribution the scores were represented as percentiles.RESULTS. During the first three days of life median scores remained stable at 2, but the variability increased, with the 95 th percentile rising from 5.5 on day 1 to 7 on day 2.At week 5 to 6 median values were higher during day time (50th percentile = 5, 95th percentile = 8) than night time (50th percentile = 2, 95th percentile = 6, p=0.02).CONCLUSION. Scores increase from day 1 -3 to week 5 -6 and show day-nightcycles with 5 to 6 weeks. Values above 8 can be considered pathological. This data may help to raise suspicion of narcotic withdrawal and to guide therapy.

Background: Most clinical trials of sepsis treatment modalities fail at their primary objective of establishing superiority over placebo when added to background standard of care. While there is no definitive explanation for the high failure rate, it might be stated that our attempts to insert a new therapeutic agent into standard of care encounters severe problems with definition of exactly what stage is ongoing, and what are the criteria for progression or resolution from that time point onwards. Clearly there is need for a means of defining steps in the septic process that would apply to individuals, and to better define the course of sepsis in each patient after they are enrolled in a trial. Methods: For core model development, 30 septic patients were studied for time-related progression in relation to biomarkers, employing a Load Model in a neural net algorithm in MatLab. Causative bacterial infections were linked to primary infection sites. In order to minimize overparameterization, the model was allowed to estimate outputs using the best three input parameters. Bacterial load was tracked from origin using clinical and microbiologic data to provide an estimate at the start of sepsis. The bacterial load as well as clinical and laboratory parameters were model inputs with the output parameter being organ failures and/ or mortality. Results: At onset of sepsis, human bacterial load estimates ranged from between 10 8 and 10 11 CFU, which is consistent with inocula in animal models of sepsis. Sepsis proceeds to organ failures and mortality in a series of steps that are initially linked to bacterial load and inflammatory response, followed by coagulopathy, ischemia, oxygen deprivation in organs and tissues, and culminating in organ failures. The later stages of sepsis are all driven by metabolic parameters, and there seems to be little benefit to blocking inflammation at later stages. Substrate and oxygen deficiencies must be addressed first. Conclusion: Neural net progression models based on biomarkers and physiological markers are able to describe the evolution of sepsis to septic shock, organ failures, and provide some evidence that mortality may be a consequence of the stages of sepsis. Overall, these models appear useful to the task of sorting out organ failure endpoints and mechanisms in individual patients with sepsis progression across sepsis to septic shock. P2Extracellular matrix turnover, angiogenesis and endothelial function in acute lung injury: relationship to pulmonary dysfunction and outcome S Sayed * , N Idriss, H Sayyed Faculty of Medicine, Assuit University, Assuit, Egypt E-mail: 1@bmc.com Critical Care 2012, 16(Suppl 3):P2 Background: Acute lung injury (ALI) is a syndrome with a diagnostic criteria based on hypoxemia and a classical radiological appearance, with acute respiratory distress syndrome at the severe end of the disease. Facts recommended the occurrence of rupture of the basement membranes and interstitial matrix remodeling during ALI. Matrix metalloproteinases (MMPs) participate in...

Background: Most clinical trials of sepsis treatment modalities fail at their primary objective of establishing superiority over placebo when added to background standard of care. While there is no definitive explanation for the high failure rate, it might be stated that our attempts to insert a new therapeutic agent into standard of care encounters severe problems with definition of exactly what stage is ongoing, and what are the criteria for progression or resolution from that time point onwards. Clearly there is need for a means of defining steps in the septic process that would apply to individuals, and to better define the course of sepsis in each patient after they are enrolled in a trial. Methods: For core model development, 30 septic patients were studied for time-related progression in relation to biomarkers, employing a Load Model in a neural net algorithm in MatLab. Causative bacterial infections were linked to primary infection sites. In order to minimize overparameterization, the model was allowed to estimate outputs using the best three input parameters. Bacterial load was tracked from origin using clinical and microbiologic data to provide an estimate at the start of sepsis. The bacterial load as well as clinical and laboratory parameters were model inputs with the output parameter being organ failures and/ or mortality. Results: At onset of sepsis, human bacterial load estimates ranged from between 10 8 and 10 11 CFU, which is consistent with inocula in animal models of sepsis. Sepsis proceeds to organ failures and mortality in a series of steps that are initially linked to bacterial load and inflammatory response, followed by coagulopathy, ischemia, oxygen deprivation in organs and tissues, and culminating in organ failures. The later stages of sepsis are all driven by metabolic parameters, and there seems to be little benefit to blocking inflammation at later stages. Substrate and oxygen deficiencies must be addressed first. Conclusion: Neural net progression models based on biomarkers and physiological markers are able to describe the evolution of sepsis to septic shock, organ failures, and provide some evidence that mortality may be a consequence of the stages of sepsis. Overall, these models appear useful to the task of sorting out organ failure endpoints and mechanisms in individual patients with sepsis progression across sepsis to septic shock. P2 Extracellular matrix turnover, angiogenesis and endothelial function in acute lung injury: relationship to pulmonary dysfunction and outcome