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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Total parenteral nutrition (TPN)-induced liver injury is a common complication in neonates managed with newborn intensive care. In several of these cases, irreversible and even fatal liver damage may develop, with patients dying of liver failure. In spite of multiple studies over several years, the pathogenesis of TPN-induced liver damage remains poorly understood. Clinical data from 24 neonates with clinical history of receiving TPN who died at Yale-New Haven Children's Hospital and had autopsies performed, were collected by medical record review without knowledge of liver pathology findings. Liver histological sections from these patients were evaluated for multiple parameters without knowledge of the clinical course. Continuous data were analyzed by Wilcoxon signed-rank test and Mann-Whitney test, and dichotomous data by Fisher's exact test; P < 0.05 was considered significant. Different histopathological abnormalities with varying degrees of severity were observed. A progression in the severity of histopathological changes in relation to duration of TPN administration (DTPN) was found. While patients with DTPN of < 2 wk had no fibrosis or only mild degrees of fibrosis, patients with more than 6 wk of DTPN developed moderate-to-severe fibrosis. Similar results were observed for cholestasis and bile duct proliferation. We did not find significant differences for birth weight, gestational age, occurrence of necrotizing enterocolitis, sepsis, or enteral feedings between the group with normal-to-mild liver changes ( n = 16), and the group with moderate-to-severe liver changes ( n = 8). On the other hand, DTPN was significantly different between these two groups ( P = 0.008). Also, patients small for gestational age ( P = 0.003) and patients with bronchopulmonary dysplasia ( P = 0.001) were more commonly seen in the group with moderate-to-severe histopathological findings. Intracellular copper was detected in 12.5% of patients with moderate-to-severe liver changes, and was found in 50% of patients with normal-to-mild liver findings ( P = 0.04). Detection of copper from tissue sections also decreased with DTPN, being observed in 57% of patients with < 2 wk DTPN and in none of the patients with > 12 wk DTPN. Our findings confirm the known significant relationship between the duration of TPN and liver injury. While previously described associations with birth weight, gestational age, enteral feedings, necrotizing enterocolitis, and sepsis were not noted, our study suggests that poor intrauterine growth may be a significant clinical risk factor for TPN-induced liver injury. In addition, our findings suggest that copper may have a protective effect against the development of TPN-induced liver damage.
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PMID:Total parenteral nutrition induced liver pathology: an autopsy series of 24 newborn cases. 1554 67

The aim of this study was to assess the effectiveness of active intervention with antenatal maternal corticosteroid and antibiotics therapy in infants delivered between 24 and 28 weeks of gestation after premature rupture of membrane. This retrospective study included pregnant women complicated by preterm delivery at the Dong-A University Hospital from 1998 to 2002. Patients were divided into labor induction group 1 (n=20), observation group 2 (n=19), and medication group 3 (n=20). We evaluated the effects of prolongation of pregnancy and intervention with maternal corticosteroids and antibiotics therapy on perinatal and neonatal outcomes. Each group did not have a significant difference (p<0.05) in neonatal outcomes, such as respiratory distress syndrome, intraventricular hemorrhage, necrotizing enterocolitis, retinopathy of prematurity, pneumonia, bronchopulmonary dysplasia, and sepsis. The mean latency period was 4.7 days and 7.6 days in groups 2 and 3, respectively. Therefore, this study was unable to demonstrate any beneficial effects of corticosteroids in improving neonatal outcomes and prolongation of the latency period with antibiotics.
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PMID:Effect of antenatal corticosteroid and antibiotics in pregnancies complicated by premature rupture of membranes between 24 and 28 weeks of gestation. 1571 10

Ureaplasma urealyticum and Mycoplasma hominis colonized 20-40% of newborns and are more frequent in premature. They are responsible for localized infections such as pleural effusion, pneumopathy, adenopathy, abscess or systemic sepsis. An important hyperleukocytosis is often associated with pulmonary infections. Their responsibility, as pathogen agents, is questionable in some non bacterial meningitis. There is large controversy for their role as cofactor, in chronic lung disease (bronchopulmonary dysplasia) and periventricular leukomalacia, because of a too low number of newborns in prospective trials. Genital mycoplamas are resistant to beta lactamines. Macrolides have a good sensitivity, particularly josamycine, but Mycoplasma hominis is resistant to erythromycin. For systemic sepsis, fluoroquinolones such as ciprofloxacine have less deleterious effects than IV erythromycin.
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PMID:[Ureaplasma urealyticum and Mycoplasma hominis infections in newborns: personal data and review of the literature]. 1589 30

The purpose of this study was to identify the risk factors for bronchopulmonary dysplasia (BPD) in a population of very low birth weight (BW) newborns treated with mechanical ventilation in the first week of life who survived the 28 days. The effects of antenatal steroids, sepsis, patent ductus arteriosus (PDA), fluid management and ventilator support strategies were investigated. This was a prospective study of a cohort of 86 newborns with BW below 1500 g who were born alive between the period of September 2000 to November 2002, treated at the University Hospital of Medical School Campinas, Brazil. The BPD was defined as the oxygen dependence in the 28 days, with consistent radiology findings. A logistic regression analysis was realized to identify the risk factors associated to BPD. Among the very low BW newborns, 45 developed BPD. The univariate analysis showed that besides BW and gestational age (GA), other factors such as FiO(2) > or = 0.60 (RR : 2.03; 95% CI: 1.4-2.94), PIP > or = 21 cm H(2)O (RR : 1.73; 95% CI: 1.12-2.65), surfactant therapy (RR : 1.68; 95% CI: 1.14-2.48), fluid volume on day 7 >131 ml/kg/day (RR : 1.81; 95% CI: 1.18-2.78), presence of PDA (RR : 1.95; 95% CI: 1.36-2.8) and pneumothorax (RR : 1.71; 95% CI: 1.18-2.45) were associated to an increase in the risk of BPD. When the variables were analysed concomitantly, using the multivariate logistic regression model, the most important risk factors for the development of BPD were GA < or = 30 weeks (RR : 2.76; 95% CI: 1.23-6.19), PIP > or = 21 cm H(2)O (RR : 1.92; 95% CI: 1.04-3.54), fluid volume on day 7 >131 ml/kg/day (RR : 2.09; 95% CI: 1.14-3.85) and presence of PDA (RR : 1.94; 95% CI : 1.03-3.65). The risk for BPD due to the association of these four factors was 96.4%. Finally, it was observed that the most important risk factors for BPD were prematurity, PDA and elevated levels of PIP as well as fluid volume.
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PMID:Risk factors for bronchopulmonary dysplasia in very low birth weight newborns treated with mechanical ventilation in the first week of life. 1592 45

A male infant born vaginally after a gestation period of 25 4/7 weeks with a birth weight of 875 g underwent surgical correction for oesophageal atresia with a distal tracheo-oesophageal fistula. Postoperative complications included seam leakage, mediastinitis with sepsis, transient elevated diaphragm, recurrent fistula and seam stenosis. Persistent ductus arteriosus was closed surgically. The further course of disease was characterised by periventricular haemorrhage, recurrent infections, bronchopulmonary dysplasia and retinopathy. Anaemia caused by the premature birth and frequent blood sampling necessitated multiple transfusions of filtered, Cytomegalovirus(CMV)-free erythrocyte concentrate. At the age of 3 months, the patient developed cholestatic jaundice that was attributed to a CMV infection contracted through breast milk. The patient recovered spontaneously. At the age of 2 years, the patient had mildly impaired psychomotor development. Reactivation of CMV during lactation is common in CMV-seropositive women. This carries a high risk of transmission of the virus through breast milk, especially for extremely premature neonates. In these infants, an early acquired postnatal CMV infection may lead to serious disorders.
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PMID:[Primary cytomegalovirus infection in the postnatal period]. 1668 92

Candidal infections are one of the common causes of late-onset sepsis (LOS) among very low birthweight (VLBW) infants, and are associated with substantial morbidity and mortality. The aim of this study was to evaluate the perinatal and neonatal risk factors for fungal LOS compared with bacterial LOS in VLBW infants. This was a population-based observational study of VLBW infants in 28 neonatal intensive care units across Israel, with information on 11,830 infants born between 1995 and 2002 from the Israeli National VLBW infant database. The study population comprised 3054 infants with one or more episodes of LOS. Univariate analysis and logistic regression models were used to compare perinatal and neonatal risk factors between infants with fungal sepsis only (N=179) and those with bacterial sepsis only (N=2630). The mean birthweight and gestational age of infants with candidal LOS were significantly lower (940 g; 27.1 weeks) than those in the bacterial LOS group (1027 g; 28.3 weeks) (P<0.001). Logistic regression analysis showed that candidal sepsis, in contrast to bacterial sepsis, was independently associated with decreasing gestational age and bronchopulmonary dysplasia (BPD). In addition, BPD only [odds ratio (OR) 1.84; 95% confidence intervals (CI) 1.03-3.23] and BPD with postnatal steroid therapy (OR 2.66; 95% CI 1.59-4.46) were independently associated with an increased risk for candidal sepsis.
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PMID:Candidal versus bacterial late-onset sepsis in very low birthweight infants in Israel: a national survey. 1727 63

Although antenatal steroids reduce risk factors for bronchopulmonary dysplasia (BPD) in preterm infants, their effect on BPD is conflicting. We hypothesised that the lack of protective effect found in some studies could derive from over-adjustment during analysis, caused by controlling for factors intermediate in the causal pathway between treatment and outcome. We prospectively studied a cohort of infants 23-32 weeks gestation <1500 g, admitted to 10 tertiary-level neonatal units in Lombardy (Italy) in 1999-2002; 1118 neonates out of 1314 survived to 36 weeks; 15.9% developed BPD (oxygen requirement at 36 weeks); 82% were treated with steroids. In univariable analysis, steroids were not significantly protective against BPD; some intermediate factors (mechanical ventilation, greater severity of illness as measured by Clinical Risk Index for Babies score, patent ductus arteriosus) were significantly positively associated with (i.e. were risk factors for) BPD (OR = 11.0, 1.55, 4.42, respectively, all P < 0.001), and negatively associated with (i.e. prevented by) steroids (OR = 0.58, 0.92, and 0.58, respectively, all P < 0.01). In multiple logistic regression models using propensity scores, without the above-mentioned intermediate risk factors, steroid-treated infants had a lower risk of BPD (OR 0.59 [95% CI 0.36, 0.97], P = 0.036); male sex (OR = 2.08), late-onset sepsis (OR = 4.26), and birthweight (OR = 0.63 for 100 g increase) were also associated with BPD, all P < 0.001. When intermediate risk factors for BPD were also added to the model, the effect of steroids disappeared; ventilation (OR = 3.03), increased illness severity (OR = 1.11), and patent ductus arteriosus (OR = 1.90) were significant risk factors. This study suggests that including variables that are potential mediators in the causal chain can obscure the ability to detect a protective effect of treatment. We observed such a phenomenon in our analyses of the relationship between antenatal steroids and BPD, suggesting that steroid effect is partly mediated through a reduction in the classical risk factors.
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PMID:Antenatal steroids and risk of bronchopulmonary dysplasia: a lack of effect or a case of over-adjustment? 1756 92

Increased activation of the transcription factor NFkappaB in the neutrophils has been associated with the pathogenesis of sepsis, acute lung injury (ALI), bronchopulmonary dysplasia (BPD), and other neutrophil-mediated inflammatory disorders. Despite recent progress in analyzing early NFkappaB activation in human neutrophils, activation of NFkappaB in persistently stimulated neutrophils has not been previously studied. Because it is the persistent NFkappaB activation that is thought to be involved in the host response to sepsis and the pathogenesis of ALI and BPD, we hypothesized that continuously stimulated human neutrophils may exhibit a late phase of NFkappaB activity. The goal of this study was to analyze the NFkappaB activation and expression of IkappaB and NFkappaB proteins during neutrophil stimulation with inflammatory signals for prolonged times. We demonstrate that neutrophil stimulation with lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNFalpha) induces, in addition to the early activation at 30-60 min, a previously unrecognized late phase of NFkappaB activation. In LPS-stimulated neutrophils, this NFkappaB activity typically had a biphasic character, whereas TNFalpha-stimulated neutrophils exhibited a continuous NFkappaB activity peaking around 9 h after stimulation. In contrast to the early NFkappaB activation that inversely correlates to the nuclear levels of IkappaBalpha, however, in continuously stimulated neutrophils, NFkappaB is persistently activated despite considerable levels of IkappaBalpha present in the nucleus. Our data suggest that NFkappaB is persistently activated in human neutrophils during neutrophil-mediated inflammatory disorders, and this persistent NFkappaB activity may represent one of the underlying mechanisms for the continuous production of proinflammatory mediators.
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PMID:NFkappaB is persistently activated in continuously stimulated human neutrophils. 1759 47

An 8-mo-old infant born at 24-wk of gestation died unexpectedly 12 h after his ninth uneventful general anesthetic. Preoperatively, he required low-flow nasal oxygen due to bronchopulmonary dysplasia, chronic diuretic therapy, and IV alimentation. As planned preoperatively, the infant remained tracheally intubated after his elective surgery and went to the Neonatal Intensive Care Unit in stable condition. However, over the next 6 h, he developed fever. The diagnosis of postoperative sepsis was considered. One hour before his death his temperature reached 43 degrees C. Autopsy documented Duchenne's muscular dystrophy and renal tubules containing myoglobin.
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PMID:Postoperative hyperthermia, rhabdomyolysis, critical temperature, and death in a former premature infant after his ninth general anesthetic. 1834 16

This study evaluated early neurobehavioral outcomes in ventilated preterm infants randomized to receive morphine analgesia or placebo in the Neurological Outcomes and Pre-emptive Analgesia in Neonates (NEOPAIN) trial. Eight hundred and ninety-eight infants between 23 and 32 weeks of gestation were randomized to receive preemptive morphine analgesia (morphine) or placebo. Infants also received additional analgesia (AA) with open-label morphine. The Neurobehavioral Assessment of the Preterm Infant (NAPI) was used to evaluate 572 of 793 survivors (72.1%) at 36 weeks of postconceptual age. The Neonatal Medical Index (NMI) was used to evaluate the severity of medical complications. Regression analyses were used to determine the effect of covariates. Infants were equally distributed in morphine and placebo groups with similar neonatal and demographic characteristics. Infants assessed with the NAPI were more likely to have sepsis ( P = 0.03), bronchopulmonary dysplasia ( P = 0.02), and longer length of stay ( P = 0.008). Infants randomized to the morphine group had higher NMI scores (odds ratio [OR]; 95% confidence interval [CI]: 1.75; 1.23 to 2.50; P = 0.002). Use of AA was associated with higher NMI scores (OR; 95% CI: 4.5; 2.9 to 5.9; P < 0.001). Of the NAPI subscales, the (mean +/- standard deviation [SD]) popliteal angle cluster scores were significantly higher in the morphine group compared with placebo (51.2 +/- 33.2 versus 45.0 +/- 33.5; P = 0.03). AA use was associated with lower (mean +/- SD) MOTOR scores in the morphine group (48.2 +/- 16.1 versus 52.7 +/- 19.1; P = 0.03) and with lower POPLITEAL ANGLE cluster scores in both the morphine group (41.5 +/- 34.0 versus 59.5 +/- 30.1; P < 0.0001) and the placebo group (40.8 +/- 36.8 versus 49.4 +/- 28.0; P = 0.004). No differences were noted in the other NAPI subscales cluster scores in either subgroup. We conclude that morphine analgesia may result in subtle neurobehavioral differences in premature infants.
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PMID:Neurobehavior of preterm infants at 36 weeks postconception as a function of morphine analgesia. 1790 73


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