A sepse é caracterizada por um desequilíbrio entre a resposta pró- e anti-inflamatória às infecções. Um dos principais componentes da resposta do hospedeiro no choque séptico são as interações recíprocas entre o sistema imune e o sistema nervoso central, desta forma o objetivo deste estudo foi investigar o desenvolvimento de alterações neurológicas e sua associação com alterações imunológicas em fases iniciais e tardias após a sepse por ligação e perfuração cecal (CLP). Dividimos em três experimentos: agudo, crônico e efeito da ACh na evolução tardia da sepse. No experimento agudo utilizamos camundongos Balb/c, induzimos sepse por CLP em diferentes gravidades (leve, moderado e grave), 6 horas após o CLP foi realizado teste comportamental SHIRPA e logo após os animais foram sacrificados. No experimento crônico os camundongos Balb/c foram submetidos ao CLP leve, o SHIRPA foi realizado 6 horas e 15 dias após o CLP e os animais foram sacrificados 15 dias após o CLP. No experimento dos efeitos da ACh utilizamos camundongos Balb/c que receberam a droga donepezila (5 mg/kg/dia, oralmente) sete dias antes do CLP leve até o dia do sacrifício e os camundongos homozigotos mutantes VAChT KD também submetidos ao CLP leve. O teste comportamental SHIRPA foi realizado 6 horas após o CLP e os animais sacríficos 15 dias após o CLP. O plasma, o baço e o hipocampo foram removidos em todos os experimentos. Os níveis do S100? foram medidos no plasma. Os baços foram pesados, e por citometria de fluxo foi caracterizado os linfócitos (linfócitos T citotóxicos, linfócitos T auxiliares, linfócitos B, células T reguladoras e células Th17) e morte celular (Apoptose inicial, necrose e apoptose tardia). Os níveis de citocinas no baço, hipocampo e plasma foram determinados por ELISA. Nossos resultados mostram que no experimento agudo, 6 horas após o CLP a encefalopatia é diferente dependendo da gravidade da sepse, e o perfil de linfócitos no baço não é alterado por nenhuma gravidade da sepse. No entanto, a ativação de células do baço foi indicada no nosso estudo por variações na quantidade de citocinas no baço. No experimento crônico observamos que 15 dias após o CLP os animais apresentam encefalopatia séptica, e esta está correlacionada com a diferenciação e morte celular de linfócitos do baço, o que leva a um alto perfil imunossupressor. No experimento da ACh mostramos que a estimulação da transmissão colinérgica, utilizando donepezila, diminui a inflamação, por aumentar linfócitos, morte linfocitária e diminuir citocinas pró-inflamatória. E, ao contrário, a diminuição da transmissão colinérgica, experimento VAChT KD, observouse uma diminuição de linfócitos, sem morte celular e aumento da inflamação. Desta forma, concluímos que a alteração neurológica nos animais com sepse está associada com as alterações imunológicas tardias e que a ACh tem um importante papel no perfil imunológico 15 dias após o CLP / Sepsis is characterized by an imbalance between pro- and anti-inflammatory responses to infection. One of the main components of the host response in septic shock are the reciprocal interactions between the immune system and the central nervous system, so the aim of this study was to investigate the development of neurological disorders and their association with immunological changes in early and late stages after sepsis by cecal ligation and puncture (CLP). We divided in three experiments: acute, chronic and chronic ACh. In acute experiment we use Balb/c mice, induce sepsis by CLP in different severities (mild, moderate and severe), 6 hours after CLP was conducted behavioral test SHIRPA and after the animals were sacrificed. In the chronic experiment Balb/c mice were subjected to CLP mild, the SHIRPA was performed 6 hours and 15 days after CLP, and animals were sacrificed 15 days after CLP. In chronic ACh experiment use Balb/c mice that received the drug Donepezil (5 mg/kg/day, orally) seven days before the CLP mild until the day of sacrifice and use too mice homozygous mutants KD VAChT also submitted to CLP mild. The SHIRPA behavioral test was performed 6 hours after CLP and the animals were sacrificed 15 days after CLP. The plasma, spleen and hippocampus were removed in all experiments. The levels of S100? were measured in plasma. The spleens were weighed, and flow cytometry was characterized lymphocytes (cytotoxic T lymphocytes, helper T lymphocytes, B lymphocytes, regulatory T cells and Th17 cells) and cell death (apoptosis initial, necrosis and DNA fragmentation). Cytokine levels in the spleen, hippocampus and plasma were determined by ELISA. Our results show that in the acute experiment, 6 hours after CLP encephalopathy is different depending on the severity of sepsis, since the profile of the spleen lymphocytes is not changed by any severity of sepsis. However, the spleen cell activation was shown in this study by variations in the quantity of cytokines in the spleen. In the chronic experiment we observed that 15 days after CLP animals have septic encephalopathy, and this correlates with cell differentiation and the death of spleen lymphocytes, which leads to a high immunosuppressive profile. Since in the chronic ACh experiment have shown that stimulation of cholinergic transmission, using donepezil, reduces inflammation by increasing lymphocytes, lymphocyte death and decreasing proinflammatory cytokine. And, conversely, the reduction in cholinergic transmission, KD VAChT experiment, we observed a decrease of lymphocytes, and increase cell death without inflammation. Thus, we conclude that the neurological deficits in animals with sepsis is associated with immunological late changes and ACh plays an important role in the immune profile 15 days after CLP

La réponse immuno-inflammatoire au cours du choc septique associe une importante réponse inflammatoire initiale responsable de l'état de choc et le développement secondaire d'altérations du système immunitaire. Les polynucléaires neutrophiles (PNN) jouent un rôle central dans la réponse immunitaire. Des données récentes de la littérature décrivent également un rôle immunosuppresseur jusqu'alors méconnu pour ces cellules. Nous avons exploré leur possible implication dans la physiopathologie du choc septique.Le but de ce travail était l'exploration des altérations phénotypiques, fonctionnelles et transcriptomiques des PNN lors de la phase immunosuppressive du choc septique. Nos résultats montrent une diminution de la capacité de migration des PNN ainsi qu'une diminution de la production de composés bactéricides (myéloperoxydase, lactoferrine) alors que la réponse aux cytokines et la phagocytose n'apparaissent pas altérées. Le contenu en myéloperoxydase et la présence de PNN immatures CD10dimCD16dim étaient indépendamment associés à une mortalité plus élevée. De manière intéressante, CD177 était le gène le plus différentiellement exprimé entre les patients et les volontaires sains. CD177 et CD10 étaient inversement corrélés. Ainsi, la diminution du chimiotactisme, la perte de myéloperoxydase, la présence de cellules immatures et leurs liens avec la mortalité pourraient contribuer au contexte d'immunosuppression présent chez les patients septiques. Au final, les pistes d'exploration futures convergent vers la population de PNN immatures et le rôle spécifique du CD177 dans les états septiques sévères / Severe septic syndromes deeply impair innate and adaptive immunity and are responsible for sepsis-induced immunosuppression. While neutrophils represent the first line of defense against infection, little is known about their phenotype and functions few days after sepsis, when the immunosuppressive phase is maximal (i.e., between day 3 and 8). The objective of this study was thus to perform a global evaluation of neutrophil alterations in immunosuppressed septic patients based on phenotypic, functional and transcriptomic studies. Our results highlight a markedly altered neutrophil chemotaxis (functional and chemokine receptor expressions), oxidative burst, lactoferrin content and an increased number of circulating immature granulocytes (i.e., CD10dimCD16dim). In contrast, phagocytosis and activation capacities were conserved. It is interesting to note that a diminished myeloperoxidase expression appeared as the best predictor to identify a group of septic shock patients at high risk of death. Similarly, patients with lower proportions of CD10dimCD16dim granulocytes had a significant better survival compared with patients presenting a higher percentage. CD177 mRNA, coding for an activation molecule in chemotaxis but also known to be overexpressed in immature cells, had the highest fold change modulation between patients and controls. Considering the potential dual roles of CD177 neutrophil (i.e., maturation / chemotaxis), its participation in septic shock pathophysiology deserves further investigation. To conclude, circulating neutrophils present with phenotypic, functional and morphological alterations few days after sepsis onset. These dysfunctions may participate in the deleterious role of sepsis-induced immunosuppression. The present results open new perspectives in the mechanisms favoring nosocomial infections after septic shock. They deserve to be further investigated in a larger clinical study and in animal models recapitulating these alterations

A sepse é caracterizada por um desequilíbrio entre a resposta pró- e anti-inflamatória às infecções. Um dos principais componentes da resposta do hospedeiro no choque séptico são as interações recíprocas entre o sistema imune e o sistema nervoso central, desta forma o objetivo deste estudo foi investigar o desenvolvimento de alterações neurológicas e sua associação com alterações imunológicas em fases iniciais e tardias após a sepse por ligação e perfuração cecal (CLP). Dividimos em três experimentos: agudo, crônico e efeito da ACh na evolução tardia da sepse. No experimento agudo utilizamos camundongos Balb/c, induzimos sepse por CLP em diferentes gravidades (leve, moderado e grave), 6 horas após o CLP foi realizado teste comportamental SHIRPA e logo após os animais foram sacrificados. No experimento crônico os camundongos Balb/c foram submetidos ao CLP leve, o SHIRPA foi realizado 6 horas e 15 dias após o CLP e os animais foram sacrificados 15 dias após o CLP. No experimento dos efeitos da ACh utilizamos camundongos Balb/c que receberam a droga donepezila (5 mg/kg/dia, oralmente) sete dias antes do CLP leve até o dia do sacrifício e os camundongos homozigotos mutantes VAChT KD também submetidos ao CLP leve. O teste comportamental SHIRPA foi realizado 6 horas após o CLP e os animais sacríficos 15 dias após o CLP. O plasma, o baço e o hipocampo foram removidos em todos os experimentos. Os níveis do S100? foram medidos no plasma. Os baços foram pesados, e por citometria de fluxo foi caracterizado os linfócitos (linfócitos T citotóxicos, linfócitos T auxiliares, linfócitos B, células T reguladoras e células Th17) e morte celular (Apoptose inicial, necrose e apoptose tardia). Os níveis de citocinas no baço, hipocampo e plasma foram determinados por ELISA. Nossos resultados mostram que no experimento agudo, 6 horas após o CLP a encefalopatia é diferente dependendo da gravidade da sepse, e o perfil de linfócitos no baço não é alterado por nenhuma gravidade da sepse. No entanto, a ativação de células do baço foi indicada no nosso estudo por variações na quantidade de citocinas no baço. No experimento crônico observamos que 15 dias após o CLP os animais apresentam encefalopatia séptica, e esta está correlacionada com a diferenciação e morte celular de linfócitos do baço, o que leva a um alto perfil imunossupressor. No experimento da ACh mostramos que a estimulação da transmissão colinérgica, utilizando donepezila, diminui a inflamação, por aumentar linfócitos, morte linfocitária e diminuir citocinas pró-inflamatória. E, ao contrário, a diminuição da transmissão colinérgica, experimento VAChT KD, observouse uma diminuição de linfócitos, sem morte celular e aumento da inflamação. Desta forma, concluímos que a alteração neurológica nos animais com sepse está associada com as alterações imunológicas tardias e que a ACh tem um importante papel no perfil imunológico 15 dias após o CLP / Sepsis is characterized by an imbalance between pro- and anti-inflammatory responses to infection. One of the main components of the host response in septic shock are the reciprocal interactions between the immune system and the central nervous system, so the aim of this study was to investigate the development of neurological disorders and their association with immunological changes in early and late stages after sepsis by cecal ligation and puncture (CLP). We divided in three experiments: acute, chronic and chronic ACh. In acute experiment we use Balb/c mice, induce sepsis by CLP in different severities (mild, moderate and severe), 6 hours after CLP was conducted behavioral test SHIRPA and after the animals were sacrificed. In the chronic experiment Balb/c mice were subjected to CLP mild, the SHIRPA was performed 6 hours and 15 days after CLP, and animals were sacrificed 15 days after CLP. In chronic ACh experiment use Balb/c mice that received the drug Donepezil (5 mg/kg/day, orally) seven days before the CLP mild until the day of sacrifice and use too mice homozygous mutants KD VAChT also submitted to CLP mild. The SHIRPA behavioral test was performed 6 hours after CLP and the animals were sacrificed 15 days after CLP. The plasma, spleen and hippocampus were removed in all experiments. The levels of S100? were measured in plasma. The spleens were weighed, and flow cytometry was characterized lymphocytes (cytotoxic T lymphocytes, helper T lymphocytes, B lymphocytes, regulatory T cells and Th17 cells) and cell death (apoptosis initial, necrosis and DNA fragmentation). Cytokine levels in the spleen, hippocampus and plasma were determined by ELISA. Our results show that in the acute experiment, 6 hours after CLP encephalopathy is different depending on the severity of sepsis, since the profile of the spleen lymphocytes is not changed by any severity of sepsis. However, the spleen cell activation was shown in this study by variations in the quantity of cytokines in the spleen. In the chronic experiment we observed that 15 days after CLP animals have septic encephalopathy, and this correlates with cell differentiation and the death of spleen lymphocytes, which leads to a high immunosuppressive profile. Since in the chronic ACh experiment have shown that stimulation of cholinergic transmission, using donepezil, reduces inflammation by increasing lymphocytes, lymphocyte death and decreasing proinflammatory cytokine. And, conversely, the reduction in cholinergic transmission, KD VAChT experiment, we observed a decrease of lymphocytes, and increase cell death without inflammation. Thus, we conclude that the neurological deficits in animals with sepsis is associated with immunological late changes and ACh plays an important role in the immune profile 15 days after CLP

Para descrever a incidência, fatores de risco e evolução clínica da sepse neonatal hospitalar por Klebsiella spp. foi realizado um estudo retrospectivo e prospectivo de 45 neonatos com sepse e Klebsiella spp. na hemocultura. A taxa geral de sepse hospitalar por Klebsiella spp foi de 3,7%, identificando K. pneumoniae (91%), K. oxytoca (9%), e 55,6% de cepas multirresistentes. Os principais fatores de risco foram uso prévio de antibióticos, prematuridade, baixo peso e catéter central. Houve complicações em 28,9% dos casos, com mortalidade de 11%. A sepse por Klebsiella spp. foi freqüente nas unidades neonatais, com taxa elevada de complicações e mortalidade, principalmente na infecção por cepas multirresistentes / In order to describe the incidence, risk factors and clinical evolution of hospital-origin sepsis by Klebsiella spp. in neonatal units, a retrospective and prospective study of 45 neonates with sepsis and Klebsiella spp. at the hemoculture was carried out.The overall hospital sepsis rate by Klebsiella spp. was 3.7%, with the identification of K. pneumoniae (91%), K. oxytoca (9%) and 55.6% of multi-resistant strains. The main risk factors were previous antibiotic use, prematurity, low weight and central catheter.There were complications in 28.9% of the cases, with a mortality rate of 11%.The sepsis by Klebsiella spp. was frequent at the neonatal units, with a high rate of complications and mortality, especially in multi-resistant strain infections

Sepsis is associated with high mortality and morbidity. Immediate recognition and treatment is crucial to prevent complications that can be highly detrimental and cause a significant impact on the U.S. healthcare economy. Numerous studies have been conducted to improve patient outcomes and lower healthcare costs from sepsis and septic shock. Many of these studies were focused on exploring healthcare providers' knowledge and compliance to the Surviving Sepsis Campaign (SSC) guidelines. This study aimed to explore and identify barriers to the implementation of the sepsis bundles and strategies to enhance healthcare providers' adherence to these bundles. A systematic review of articles was conducted using the ACE Star Model of Knowledge Transformation. Studies such as randomized controlled trials (RTC's), systematic reviews, retrospective studies, and prospective observational studies conducted in Intensive Care Units (ICUs) within the past 10 years were utilized, guided by the American Association of Critical Care Nurses' (AACN's) grading system. Sources of evidence were obtained from PubMed, CINAHL, and GoogleScholar. The results of this study are aimed at helping support the evidence-based clinical practice among providers caring for patients with sepsis and septic shock in an ICU setting using evidence-based guidelines. The results of this study provide an opportunity for healthcare systems to relieve financial burdens from sepsis and thus contribute to pos

La septicémie et les troubles associés demeurent une cause majeure de mortalité dans les unités de soins intensifs. Des récents travaux ont mis en lumière un lien inattendu entre les mitochondries et les fonctions des cellules immunitaires. Des modifications des fonctions mitochondriales ont pu être observées dans les cellules sanguines périphériques lors de septicémies. Dans le cadre de ce travail de thèse, nous avons cherché à évaluer si la mitophagie pouvait avoir un impact sur les fonctions des phagocytes dans le contexte d’une infection bactérienne. La mitophagie est une autophagie dédiée aux mitochondries qui régit l'élimination des mitochondries dysfonctionnelles. Nous avons démontré ici in vivo et in vitro que les macrophages exposés aux bactéries à Gram négatif ou à leurs composants de la paroi cellulaire (Lipopolysaccharides, LPS) présentent une inhibition marquée de la mitophagie qui constitue un mécanisme de protection contre la septicémie. L'activation des macrophages avec une combinaison LPS/IFNγ entraîne une inhibition précoce de la mitophagie dépendante de PINK1 selon une voie dépendante de STAT1-Caspase 11. Cette inhibition de la mitophagie contribue à expliquer la reprogrammation métabolique observée dans les macrophages classiquement activés (macrophages M1) et conduit à une augmentation de la production de ROS mitochondriaux (mROS). En tant que molécules de signalisation, les mROS conduisent à l'activation des macrophages de manière dépendante de HIF-1α et NF-κB. En outre, ces molécules contribuent à la clairance bactérienne dans les phagocytes activés. Il est intéressant de noter que nous avons démontré in vitro et in vivo que la modulation pharmacologique de la mitophagie permet d'imiter ou de réprimer les effets du LPS sur la polarisation des macrophages, la libération des cytokines et l'activité bactéricide. Pour conclure, ce travail démontre que l'inhibition de la mitophagie est une caractéristique de l'activation LPS-dépendante des macrophages et un mécanisme de protection contre les bactéries à Gram négatif. Cette étude souligne également une relation inconnue entre la signalisation IFNγ, les caspases inflammatoires et la mitophagie. Enfin, nos travaux mettent en lumière l'impact des modulateurs pharmacologiques de la mitophagie sur la fonction des macrophages et ouvrent de nouvelles opportunités pour le développement de nouvelles stratégies thérapeutiques pour stimuler la défense de l'hôte. / Sepsis and related organ dysfunctions remain a leading cause of mortality in intensive care units. Increasing evidences have shed light on an unexpected link between mitochondria and immune cell functions. Alterations in mitochondrial functions have been reported in peripheral blood cells in sepsis. We hypothesize here that mitophagy might impact on phagocyte functions in the context of bacterial infection. Mitophagy is a mitochondria-dedicated autophagy that governs the elimination of dysfunctional mitochondria. We demonstrated here in vivo and in vitro that macrophages exposed to Gram-negative bacteria or their cell wall component LPS display a marked inhibition of mitophagy that constitutes a protective mechanism against sepsis. LPS/IFNγ-driven macrophage activation results in early inhibition of PINK1-dependent mitophagy through a STAT1-Caspase 4/11 pathway. This inhibition of mitophagy contributes to explain the metabolic reprogramming observed in classically activated macrophages and leads to a rise in mitochondrial ROS (mROS) production. As signaling molecules, mROS lead to macrophages activation in a HIF-1α- and NF-κB-dependent manner. Furthermore, these molecules contribute to bacterial clearance in activated phagocytes. Interestingly, we demonstrated in vitro and in vivo that pharmacological modulation of mitophagy allows either mimicking or repressing the effects of LPS on macrophages polarization, cytokine release and bactericidal activity. To conclude, this work demonstrates that inhibition of mitophagy is a feature of LPS-dependent macrophage activation and a protective mechanism against Gram-negative bacteria. This study also highlights an unknown relationship between IFNγ-signaling, inflammatory caspases and mitophagy. Finally, our work point out the impact of pharmacological modulators of mitophagy on macrophage function and open new opportunities for the development of novel strategies to boost host defense

Background: Inhaled carbon monoxide (CO) appears to have beneficial effects on endotoxemia-induced impairment of hypoxic pulmonary vasoconstriction (HPV). This study aims to specify correct timing of CO application, it’s biochemical mechanisms and effects on inflammatory reactions. Methods: Mice (C57BL/6; n = 86) received lipopolysaccharide (LPS, 30 mg/kg) intraperitoneally and subsequently breathed 50 ppm CO continuously during defined intervals of 3, 6, 12 or 18 h. Two control groups received saline intraperitoneally and additionally either air or CO, and one control group received LPS but breathed air only. In an isolated lung perfusion model vasoconstrictor response to hypoxia (FiO2 = 0.01) was quantified by measurements of pulmonary artery pressure. Pulmonary capillary pressure was estimated by double occlusion technique. Further, inflammatory plasma cytokines and lung tissue mRNA of nitric-oxide-synthase-2 (NOS-2) and heme oxygenase-1 (HO-1) were measured. Results: HPV was impaired after LPS-challenge (p < 0.01). CO exposure restored HPV-responsiveness if administered continuously for full 18 h, for the first 6 h and if given in the interval between the 3rd and 6th hour after LPS-challenge (p < 0.05). Preserved HPV was attributable to recovered arterial resistance and associated with significant reduction in NOS-2 mRNA when compared to controls (p < 0.05). We found no effects on inflammatory plasma cytokines. Conclusion: Low-dose CO prevented LPS-induced impairment of HPV in a time-dependent manner, associated with a decreased NOS-2 expression.

Mit der Entdeckung des Selens als essentielles Spurenelement und der Glutathionperoxidase als Selenoenzym sowie der Tatsache, daû Selenmangel relativ weit verbreitet ist, wurde erstmals ein Zusammenhang zu einigen schweren Erkrankungen hergestellt (Keshan-Krankheit, Kaschin-Beck-Syndrom). Interessant ist dabei, daû sich trotz dieser und anderer bekannter Selenmangelerkrankungen eine Therapie in der Humanmedizin nur langsam zu etablieren beginnt, waÈ hrend die Selensupplementation in der VeterinaÈ rmedizin bereits Standard ist. Die Autoren beschaÈ ftigen sich seit 1990 mit der Rolle des Spurenelements Selen bei septischen Krankheitsbildern in der Intensivmedizin, beim ReperfusionsphaÈnomen nach gefaÈûchirurgischen Eingriffen und in der Onkologie. Sie konnten zeigen, daû die adjuvante Therapie der akuten Pankreatitis und der Sepsis mit Natriumselenit einen positiven Effekt auf das Outcome der Patienten zu haben scheint (eine multizentrische, doppelblinde, randomisierte Sepsisstudie zur Validierung dieser Ergebnisse ist in Vorbereitung). Neue Erkenntnisse zur Beeinflussung von Transkriptionsfaktoren durch Selen bei systemischem Inflammationssyndrom und Sepsis erlauben eine wissenschaftlich fundierte Interpretation der klinischen Ergebnisse. Weitere molekularbiologische Untersuchungen werden das Spurenelement Selen zu einem der interessantesten Forschungsprojekte der naÈ chsten 10 Jahre in Intensivmedizin und Onkologie machen. / Since selenium was discovered as an essential trace element being widely distributed, and since glutathione peroxidase is known as a selenoenzyme, associations with several severe diseases were established (Keshan disease, Kaschin-Beck syndrome). Despite these known selenium deficiency diseases a related human therapy is still not established so far. In veterinary medicine, however, substitution of selenium is already a standard therapy. Our laboratory investigates the role of selenium since 1990. This includes investigations about the effects of selenium in acute inflammatory diseases in intensive care, in the reperfusion phenomenon following vascular surgery, and in oncology. In acute pancreatitis and sepsis, adjuvant therapy using sodium selenite seems to have positive effects on the overall outcome of patients (a multicenter, double-blind, randomized trial on sepsis is being prepared). New findings concerning the influence of selenium on transcription factors in inflammatory processes will permit a scientifically sound interpretation of clinical results. With further investigations in molecular biology the trace element selenium will become, in the next decade, one of the most interesting topics in intensive care and oncology. / Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.

Bakgrund: Ungefär hälften av alla vuxna som vårdas på sjukhus erhåller en perifer venkateter (PVK) för intravenöst behandling. Det finns risk för lindriga eller allvarliga komplikationer. Den vanligaste komplikationen är tromboflebit och den allvarligast är infektion. I Sverige är det sjuksköterskan som ansvarar för insättning, skötsel, borttagande och dokumentation av PVK. Omvårdnaden vid handhavande av PVK är eftersatt och sjuksköterskan bör förvissa sig om att deras kunskaper är uppdaterad och evidensbaserad för att minska risken för komplikationer. Syfte: Studiens syfte var att beskriva faktorer av betydelse som kan förebygga PVK relaterade komplikationer med fokus på tromboflebit och infektion. Metod: En litteraturstudie som är baserad på 15 artiklar, 2009-2014. Resultat: Faktorer av betydelse för att förebygga tromboflebit och infektion i samband med PVK är inläggningsteknik, anatomisk placering, PVK storlek, slutna- eller öppna system och hur länge en PVK är in situ. Utbildning av personalen och feedback förbättrade handhavandet av PVK och följsamheten till riktlinjer. Slutsats: Flera faktorer påverkar om patienten utvecklar tromboflebit eller infektion i samband med PVK. Flera går att förebygga genom att följsamheten till riktlinjer förbättras och utförda omvårdnadsåtgärder dokumenteras. / Background:About half of all adults who are being cared for in hospital receivea peripheral venous catheter (PVC) for intravenous treatment. There is a risk of mild or serious complications. The most common complication is thrombophlebitis and the most serious is infection. In Sweden it isthe nurse who is responsible for the insertion, management, removal and documentation of PVC. Nursing care in PVCis neglected and the nurse should ensure that their knowledge is up-to-date and evidence-based in order to reduce the risk of complications.Aim:The aim of the studywas to describe factors that can prevent PVCrelated complications with focus on thrombophlebitis and infection.Method:Aliterature review based on 15articles, 2009-2014. Results:Factors of importance to prevent thrombophlebitis and infection associated with the PVCis insertion technique, anatomic location, PVCsize, closed or open system and how long PVCis in situ. Staff training and feedback improved management of PVCand adherence to guidelines. Conclusion:Several factors affect if the patient developsfrom thrombophlebitis or infection associated with PVC. Many are preventable by adherence to the guidelines be improved and performed nursing interventions should be documented.

Bakgrund: Sepsis är vanligt förekommande och ett av de allvarligaste sjukdomstillstånden med hög mortalitet. Tillståndet medför stort lidande för den drabbade patienten. Tidig identifiering och snabb behandling är avgörande för patientens överlevnad och fortsatta hälsa. Sjuksköterskan ansvarar för omvårdnaden av patienter med sepsis och har därmed en viktig roll vid identifiering och behandling av sjukdomstillståndet. Syfte: Syftet var att beskriva faktorer som kan påverka sjuksköterskans identifiering av sepsis.   Metod: En litteraturöversikt valdes som metod till denna uppsats. Datainsamling skedde via databaserna Cinahl Complete och PubMed och resulterade i tio kvantitativa och en kvalitativ artikel som svarade på syftet. Utvalda artiklarhar kvalitetsgranskats och sedan analyserats utifrån de fyra analysstegen som finns beskrivna i Friberg. Resultat: Fyra kategorier framkom: sjuksköterskans kunskap, bedömningsinstrument, implementering av protokoll och riktlinjer samt arbetsmiljö.   Sammanfattning: Som ett resultat av analysen framkom flera faktorer som kan påverka sjuksköterskans identifiering av sepsis. Bristande kunskap och avsaknad av utbildning, hög arbetsbelastning, vårdprotokoll, riktlinjer och screeningverktyg var faktorer som kan påverka sjuksköterskornas identifiering av sepsis. Det behövs mer utbildning för att kliniskt verksamma sjuksköterskors kunskap om sepsis ska öka. / Background: Sepsis is common and one of the most serious diseases with a high mortality. The condition causes great suffering to the affected patient. Early identification and treatment are crucial for the patient's survival and continued health. The nurse is responsible for the care of patients with sepsis and play an important role in identifying and treating the condition.  Aim: The aim was to describe factors that may affect the nurse's identification ofsepsis. Method: A literature review was chosen as the method of this essay. Data collection wasperformed using the databases Cinahl Complete and PubMed and resulted in ten quantitative and one qualitative article that answered the purpose. Selectedarticles have been quality reviewed and then analyzed using the four analysing steps described in Friberg.  Results: Four categories emerged: the nurse's knowledge, assessment instruments, implementation of protocols and guidelines and work environment. Summary: As a result of the analysis, several factors emerged that may affect the nurse´s identification of sepsis. Lack of knowledge and lack of education, highworkload, care protocols, guidelines and screening tools were some of the factors that emerged in the results of the literature review. More education is needed to increase clinically active nurses' knowledge of sepsis.