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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Newborns present a certain degree of immunological immaturity, which makes them highly susceptible to infection. As interleukin-2 (IL-2) is a cytokine that increases the immune response, we performed this study with the object of determining whether there are differences in the serum levels of IL-2 in healthy newborns and those affected by neonatal sepsis in order to establish if there is an increase in the production of IL-2 in systemic neonatal infection. We studied three groups of newborns: group 1-20 healthy full-term newborns; group 2-19 healthy preterm newborns; and group 3-11 infected newborns. The study was performed before the seventh day of life. IL-2 levels were determined by radioimmunoassay (RIA). Covariant analysis showed no significant differences in IL-2 values between the healthy groups (1 + 2) and the infected group (3) (p = 0.7814).
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PMID:Assessment of interleukin-2 (IL-2) in sera of healthy and infected newborns. 773 17

The aim of this study was to determine the reasons for admission, charges made, and causes of death in a tertiary referral neonatal unit in India. Records of the Christian Medical College Hospital, Vellore, Tamil Nadu, India, were reviewed for the period 1 January-31 December 1992. The principal cause of death was ascertained with reference to predetermined diagnostic criteria. There were 5592 livebirths, 138 stillbirths and 1809 admissions to the nurseries (1603 inborn, 206 outborn). Suspected sepsis accounted for 24 per cent of admissions, 14 per cent required preterm care, 13 per cent phototherapy and 8 per cent were full term low birth weight babies admitted for observation. There were 87 early neonatal deaths, 4 per cent (49) of inborn admissions and 18 per cent (38) of outborn admissions. A further 11 babies were discharged to receive terminal care at home and nine were discharged, critically ill, against medical advice. Causes of death were respiratory problems of prematurity (49 per cent), lethal congenital malformations (22 per cent), complications of asphyxia (20 per cent) and sepsis (5 per cent). The median duration of nursery care was 2 days (range 1-21) and the median charge made Rs 714 (range 122-5036). Although the pattern of admissions and deaths still reflects the substantial problems of suspected sepsis, asphyxia, and congenital malformations, problems of immaturity may be on the increase. We caution against hospital-based statistics that fail to take account of babies who are discharged alive in the knowledge that death is imminent. Considered strategies for the provision or selective provision, of neonatal care in India, are called for.
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PMID:Reasons for admission, causes of death and costs of admission to a tertiary referral neonatal unit in India. 777 5

Infection remains a major cause of death and complication in pediatric surgery today. Impaired host resistance from such circumstances as immaturity, cancer chemotherapy, or AIDS predisposes to opportunistic infection by fungi, viruses, mycobacteria, and even protozoa. This review considers recent advances in five areas: 1) sepsis, 2) soft-tissue and wound infections, 3) chest infections, 4) abdominal infections, and 5) miscellaneous (including nosocomial) infections. Of particular importance are the new concepts of sepsis. The new terminology distinguishes stages in the septic process and a complex interaction of inflammatory mediators. The systemic inflammatory response syndrome may progress independently of the original infection to multiorgan dysfunction syndrome, and death. The reports cited herein are, for the most part, retrospective observational studies. There is a great need for prospective, randomized trials to answer questions about the optimal management of, and prevention of, pediatric surgical infections.
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PMID:Surgical infections in children. 806 46

The functional immaturity of PMNs is one of the major causes of overwhelming sepsis in newborns. In this study, we observed functions and surface markers of PMNs to investigate what causes the functional immaturity of PMNs in newborns. As results, the percentage of EA rosette forming PMNs (58.5 +/- 15.5%) and the chemotactic movement (0.14 +/- 0.09 mm) of cord blood PMNs were significantly lower than those of adult peripheral blood PMNs (70.8 +/- 9.9%, 0.60 +/- 0.34 mm). Cord blood PMNs showed decreased glass adherence and ADCC activity. The expression of Fc gamma RII or Fc gamma RIII was a little lower than those of adult peripheral blood PMNs, but the expression of Fc gamma RI (43.1 +/- 26.8%) was significantly higher than that of adult peripheral blood PMNs (3.2 +/- 1.8%). There was a significant difference in LFA-1 expression between EA rosette forming PMNs (92.9 +/- 9.1%) and EA rosette non-forming PMNs (25.6 +/- 22.6%). From these results, it is assumed that neonatal PMNs may consist of heterogeneous populations. And the relatively high percentage of EA rosette non-forming PMNs which express a low level of LFA-1 may be responsible for the functional immaturity of cord blood PMNs.
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PMID:Possible roles of LFA-1 and Fc gamma receptors on the functional immaturities of cord blood polymorphonuclear leukocytes. 837 91

Antibiotics are the leading cause of drug-induced kidney disease, and among them the aminoglycosides (AMG) are the main nephrotoxic agents, bringing about kidney damage via a direct dose-dependent mechanism. The combination of an aminoglycoside and a penicillin derivative is still the most commonly recommended and used first-line treatment modality in the empirical therapy of neonatal sepsis, despite the low therapeutic index of AMG. The immaturity of neonatal kidney function, particularly in preterm neonates, makes newborn infants particularly susceptible to AMG-induced kidney damage. Numerous factors intervene in bringing about AMG-induced kidney damage, such as factors related to the antibiotic itself (intrinsic toxicity, administration route, type of monitoring of blood concentrations), those related to the subject treated (neonatal age, constitutional sensitivity), and others related to associated pathology (neonatal anoxia, renal hypoperfusion, respiratory distress/mechanical ventilation, hyperbilirubinaemia/phototherapy, electrolyte disorders, and even the acute sepsis calling for antibiotic therapy), as well as pharmacological factors (concomitant therapies such as diuretics, indomethacin and other antibiotics, particularly glycopeptides and cephalosporins).
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PMID:[Aminoglycosides, risk factors and neonatal kidney]. 905 89

This paper reports the creation of India's national neonatal-perinatal database. The database has a continuous reporting format, uniform in its definitions, and is checked and compiled at a nodal center, which is a necessity for planning and monitoring health care. Data were compiled from intramural births of 16 centers, which included neonatal morbidity and mortality data for the year 1995. Furthermore, the database comprised data on 38,592 births, 37,082 of which were live-born and 1510 stillborn. Statistics show that the incidence of low birth weight (LBW) was 32.8% and that of preterms 12.3%, while two-thirds of the LBW infants were term babies. Among institutional births, the incidence of birth asphyxia would approximate 5%, while septicemia was observed in 3.9% of intramural live births. Birth asphyxia, septicemia, and causes related to immaturity account for almost three-fourths of the neonatal deaths, a majority of which could be prevented.
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PMID:Neonatal morbidity and mortality: report of the National Neonatal-Perinatal Database. 956 38

The immaturity of neonatal phagocytic immunity contributes to increased mortality during neonatal sepsis. Neonates have both quantitative and qualitative neutrophil defects with decreased bone marrow neutrophil storage pool (NSP) reserves, an inability to increase neutrophil production, and defective neutrophil functional activity. Neonates respond to overwhelming sepsis with depletion of the NSP and the development of peripheral neutropenia. The myelopoietic cytokines granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) have been documented to induce neutrophilia in neonatal animals and human infants, increase the NSP, and upregulate neutrophils for improved functional activity. Preclinical studies in neonatal rats demonstrate increased survival with prophylactic G-CSF during experimental group B streptococcal sepsis. In pilot phase I/II human trials, G-CSF and GM-CSF were demonstrated to be both safe and well tolerated and to induce significant increases in absolute neutrophil count and NSP. Prophylactic GM-CSF in the very low birth weight neonate may reduce the incidence of nosocomial infections. Phase III trials are needed to further delineate the clinical usefulness of these myelopoietic cytokines in neonates with a high predisposition to sepsis.
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PMID:Potential use of granulocyte colon-stimulating factor and granulocyte-macrophage colony-stimulating factor in neonates. 966 63

In Japan, chronic lung disease (CLD) is defined as an oxygen requirement greater than that obtainable in room air at 28 days of age, with symptoms of persistent respirator distress and a hazy or emphysematous and fibrous appearance upon chest x-ray. A total of 4964 infants weighing less than 1500 g at birth and born in 1990 were admitted to and cared for at level II and III neonatal care centers in Japan. A total of 4293 infants (86.3%) survived at 28 days after birth. Analyses of infants who developed CLD through their preceding illnesses and chest x-ray findings resulted in the classification of CLD into six types. Types I and II are defined as CLD following the acute stage respiratory distress syndrome (RDS). Type I is the typical case of bronchopulmonary dysplasia (BPD) as described previously, whereas Type II shows atypical radiological findings, namely only diffuse haziness without typical emphysema and fibrosis. Type III has a history of intrauterine inflammation. Chest x-ray shows the typical bubbling and cystic appearance described in the original report of Wilson-Mikity syndrome or neonatal pulmonary emphysema in the very low birth weight infant. Type III also has atypical radiological findings in cases with intrauterine infection. Type IV does not have a history of either intrauterine inflammation or RDS but shows typical emphysematous and fibrous appearance upon chest x-ray. Type V includes those with atypical chest x-ray appearance similar to Type II but without history of RDS and intrauterine inflammation. CLD is a heterogeneous condition which shows different spectra. However, the cardinal event is common to all types--the excessive inflammatory response caused by various insults to the immature airways and alveoli, such as oxygen, barotrauma, infection and so on. The excessive inflammatory response leads to lung tissue damage and the abnormal healing process due to immaturity, (such as vitamin A deficiency and insufficient oxygen radical scavenging system) and results in dysplasia and metaplasia of the respiratory system. The treatment of respiratory distress due to CLD also acts as an insult to the lungs and thus forms a vicious cycle. The different spectra of the disease are most possibly attributed to the difference in the timing and the kind of insults to the lungs. In Type I and II CLD, the insults are given in the first hours of life when the infants with surfactant deficiency receive high concentrations of oxygen for stabilization before the surfactant replacement. In Type III and III' CLD the insults are most likely given before birth. Excessive and sustained inflammatory response in the lungs with different onset times may result in the development of Type IV and V CLD. The strategy for the prevention of CLD should be different according to the origins and causes. The prevention of Type I and II CLD, or CLD following RDS, should be accomplished by successful prophylactic surfactant replacement therapy. Another procedure may be the application of high frequency oscillatory ventilation (HFOV) in the acute stage of RDS or at the time of stabilization right after birth. Types III and III' CLD present the most difficult challenge for prevention strategy because the disease process already started before birth. At the moment there are no effective measures for prevention. The strategy for the prevention of Type IV and V CLD may reside in the early detection and treatment of patent ductus arteriosus, sepsis and airway infection including pneumonia.
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PMID:Chronic lung disease of the very low birth weight infant--is it preventable? 967 27

Necrotizing enterocolitis (NEC) causes approximately 4000 deaths/y and significant morbidity among U.S.-born preterm infants alone. Various combinations of inadequate tissue oxygenation, bacterial overgrowth, and enteral feeding with immaturity may cause the initial damage to intestinal mucosa that culminates in necrosis. Presently, there is not a way to predict the onset of the disease or to prevent its occurrence. As part of risk-benefit assessment, we compared disease in hospitalized preterm infants fed a commercial (control) preterm formula or an experimental formula with egg phospholipids for a randomized, double-masked, clinical study of diet and infant neurodevelopment. Infants fed the experimental formula developed significantly less stage II and III NEC compared with infants fed the control formula (2.9 versus 17.6%, p < 0.05), but had similar rates of bronchopulmonary dysplasia (23.4 versus 23.5%), septicemia (26 versus 31%), and retinopathy of prematurity (38 versus 40%). Compared with the control formula, the experimental formula provided 7-fold more esterified choline, arachidonic acid (AA, 0.4% of total fatty acids), and docosahexaenoic acid (0.13%). Phospholipids are constituents of mucosal membranes and intestinal surfactant, and their components, AA and choline, are substrates for intestinal vasodilatory and cytoprotective eicosanoids (AA) and the vasodilatory neurotransmitter, acetylcholine (choline), respectively. One or more of these components of egg phospholipids may have enhanced one or more immature intestinal functions to lower the incidence of NEC in this study. Regardless of the potential mechanism, a larger randomized trial designed to test the effect of this egg phospholipid-containing formula on NEC seems warranted.
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PMID:Lower incidence of necrotizing enterocolitis in infants fed a preterm formula with egg phospholipids. 977 36

We investigated colonization with Ureaplasma urealyticum (Uu) in infants <30 weeks gestation and assessed the relationship to other risk factors influencing respiratory morbidity, plus the effect of treatment with erythromycin. Ventilated preterm infants [n = 155; median GA 26 (23-29) weeks] were cultured for Uu in endotracheal aspirate and nasopharynx. Colonized infants were randomly assigned to treatment with erythromycin 40 mg/kg/d, intravenously or orally. The rate of colonization was 29/155 (19%) and the Uu-colonized infants had lower mean gestational ages than the culture-negative infants (25 vs 26 weeks). For the colonized infants PROM (48% vs 12%), chorioamnionitis in the mother (46% vs 17%) and vaginal delivery (71% vs 29%) were more common. More colonized infants needed supplemental oxygen at 36 weeks' postconceptual age (p < 0.05). Erythromycin treatment was effective in reducing colonization with negative control cultures in 12/14 (86%) of treated infants. No significant differences were found between the colonized treated infants (n = 14) and those not treated (n = 14) in time with supplemental oxygen. Oxygen requirement at 36 weeks was related to lower gestational age, late appearance of PDA, late onset sepsis and signs of chorioamnionitis in the mother. We conclude that the Uu colonization is related to increasing immaturity, the presence of prolonged rupture of membranes, signs of chorioamnionitis and vaginal delivery. Treatment with erythromycin reduced colonization but did not significantly alter length of time with supplemental oxygen.
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PMID:Ureaplasma urealyticum, erythromycin and respiratory morbidity in high-risk preterm neonates. 982 77


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