Neonatal sepsis

Neonates are susceptible to infection since several elements of the immune system are deficient. At present, the most common pathogens are Group B streptococci and Escherichia coli. Prolonged rupture of membranes with amnionitis is a high-risk setting. Clinical signs suggesting neonatal sepsis include respiratory distress, poor feeding, hypothermia, seizures and hypotonia. After the sepsis work-up is completed, the initial choice of antibiotics is based on the prevailing organisms and antibiotic sensitivities within the community.     

Neonatal bacterial sepsis

Neonatal bacterial infection is a significant cause of morbidity and mortality despite improved survival of premature newborns, better understanding of the pathophysiology of sepsis, advances in supportive care, and more potent antibacterial agents. Early recognition and implementation of appropriate therapy offers the best outcome, and careful assessment of the newborn is essential. Current methods to detect signs of sepsis and to identify the causative microorganism are not 100% sensitive and precise. Continued research on other indicators may yield better diagnostic methods and therapy in the future. Research is necessary to identify the most sensitive markers for diagnosis of sepsis and methods of immune enhancement that are safe and effective.     

Neonatal neutropenia and bacterial sepsis associated with placental transfer of maternal neutrophil-specific autoantibodies

BACKGROUND: Passively acquired neonatal neutropenia is an infrequently reported complication of maternal autoimmune neutropenia (AIN). Two affected siblings are described. The firstborn developed Citrobacter meningitis and was permanently disabled. The second was success-fully managed with pre- and postnatal injections of recombinant human granulocyte colony-stimulating factor (rHuG-CSF). STUDY DESIGN AND METHODS: Neutrophil-specific antibodies were evaluated by flow cytometry (FC), monoclonal antibody immobilization of granulocyte antigens, and granulocyte agglutination assays. RESULTS: A neutrophil-reactive antibody was detected by FC in samples of the mother's serum spanning a 4-year time frame. This antibody reacted with neutrophils from the mother, father, and their first infant and with 18 of 20 target neutrophils tested. In serologic studies, it was shown that the antibody was not specific for the commonly recognized neutrophil-specific alloantigens HNA-1a (NA1), HNA-1b (NA2), HNA-1c (SH), HNA-2a (NB1), or HNA-3a (5b). CONCLUSION: Severe neonatal neutropenia in the two siblings appears to have been caused by placental transfer of a maternal neutrophil-reactive autoantibody of undetermined specificity. Neutrophil counts should be evaluated in infants born to mothers with chronic neutropenia of possible autoimmune origin so that neutropenic infants can be carefully monitored and antibiotics and/or rHuG-CSF administered if indicated.     

Oxidative metabolism in sepsis and sepsis syndrome

The high mortality associated with sepsis syndrome and multiple organ dysfunction syndrome has persisted despite extraordinary research efforts in the laboratory and the intensive care unit. These syndromes produce systemic tissue damage that is likely to result from widespread inflammation and subsequent endothelial injury. This article reviews the oxidative metabolic effects and responses to sepsis syndrome at several levels: the oxygen transport system, the cell, and the mitochondrion. Specifically, aerobic metabolism of carbon substrates and oxygen is altered in sepsis. As a result of systemic inflammation and nonmetabolic oxygen use, oxidative stress may occur both outside and inside the cell. The consequences of these oxidative processes during sepsis may be ongoing cell damage mediated by reactive oxygen and nitrogen oxide species that culminates in multisystem organ failure.     

Evaluation of time to antibiotic administration for suspected late-onset sepsis in the Neonatal Intensive Care Unit: A quality improvement project

Late-onset sepsis is a significant cause of morbidity and mortality, with mortality increasing by 8–9% for each hour delay in antibiotics. The primary objective of this study is to evaluate the time to antibiotic administration for late-onset sepsis after implementation of a newly developed process for performing sepsis evaluations. A retrospective chart review was conducted utilizing electronic medical records to obtain data for select time points within the sepsis evaluation process. There were 42 patients evaluated prior to the quality improvement project (Group 1) and 59 patients evaluated after (Group 2). The average time to antibiotic administration was 2 h and 48 min in Group 1 and 1 h and 7 min in Group 2 (p < 0.0001). Time to antibiotic administration for late-onset sepsis in the Neonatal Intensive Care Unit (NICU) significantly decreased after implementation of a newly developed process, however, several barriers still exist.     

Burn sepsis

Sepsis in the burned individual can arise from multiple causes. However, the unique source is the burn wound itself. It is clear that health is association with maintenance of a bacterial equilibrium in the wound and that infection is a result of an imbalance in favor of the bacteria. The primary host defense mechanism, an intact epithelial barrier, has been lost at the time of burning. A portal of entry has been created, and the bactericidal defenses have been neutralized. All of the host defense mechanisms associated with inflammation are evoked but may be limited by the avascular isolation of much of the wound. In addition to alteration in vascular response associated with the burns, there are adverse changes in the neutrophils themselves. The alterations in nutrition that may follow burn injury further reduce systemic host resistance. Associated diseases, such as diabetes, may present a further hazard. All of the local factors influencing host resistance are adversely affected in the burn wound. There is necrotic tissue, decreased local tissue perfusion, and loss of the mechanical barrier. Quantitative techniques have demonstrated that bacteria are present in the depths of the wound from the time of injury. Infection and burn wound sepsis are clearly represented by the quantitative increase in bacteria to numbers exceeding 10(5) per gram of tissue. In no other instance has the importance of the "amphibiont" organisms been more clearly demonstrated than in the burn wound. Today's nonpathogen has all too often become tomorrow's killer. As therapeutic control becomes effective against the current organism, the ecologic void is filled by another, which, by definition, is resistant to the treatment being employed.     

Intra-abdominal sepsis

Initially, intra-abdominal contamination with endogenous bacteria produces peritonitis and septicemia. If the infection is localized and the patient survives, the late phase is usually abscess formation. Treatment consists of prompt, thorough surgical drainage, with repair of the diseased or traumatized viscera, as well as the use of preoperative, intraoperative and postoperative antibiotics aimed at both aerobic and anaerobic infecting microflora.