Relevant bibliographies by topics / Human abdominal sepsis][Sepsis

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Human abdominal sepsis][Sepsis'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Human abdominal sepsis][Sepsis"

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Carlson, G. L., M. Saeed, R. A. Little, and M. H. Irving. "Serum leptin concentrations and their relation to metabolic abnormalities in human sepsis." American Journal of Physiology-Endocrinology and Metabolism 276, no. 4 (April 1, 1999): E658—E662. http://dx.doi.org/10.1152/ajpendo.1999.276.4.e658.

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Circulating leptin concentrations are raised in animal models of inflammation and sepsis. The purpose of this study was to determine the effect of sepsis on serum leptin concentration in humans and to examine the relationship between leptin and the metabolic consequences of sepsis. Resting energy expenditure, insulin sensitivity, and fasting serum leptin, plasma insulin, and cortisol concentrations were measured in 20 subjects with intra-abdominal sepsis and 20 healthy control subjects, before and during a 2-h period of euglycemic hyperinsulinemia. Fasting serum leptin concentrations were similar in septic and control subjects. In simple regression analysis, serum leptin concentrations correlated significantly with percent body fat in both septic patients ( r = 0.64, P < 0.005) and healthy subjects ( r = 0.75, P < 0.0001). Multiple regression analyses additionally indicated that percent body fat, fasting plasma insulin, and plasma cortisol, but not sepsis, were significant and independent determinants of serum leptin concentration. No relationship between leptin and resting energy expenditure or insulin sensitivity was identifiable. A major metabolic role for leptin in human sepsis therefore appears unlikely.
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Pieracci, F. M., and P. S. Barie. "Management of Severe Sepsis of Abdominal Origin." Scandinavian Journal of Surgery 96, no. 3 (September 2007): 184–96. http://dx.doi.org/10.1177/145749690709600302.

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Severe sepsis is a life-threatening condition that may occur as a sequela of intra-abdominal infections (IAIs) of all types. Diagnosis of IAIs is predicated upon the combination of physical examination and imaging techniques. Diffuse peritonitis usually requires urgent surgical intervention. In the absence of diffuse peritonitis, abdominal computed tomography remains the most useful test for the diagnosis of IAIs, and is essential to both guide therapeutic interventions and evaluate suspected treatment failure in the critically ill patient. Parameters most consistently associated with poor outcomes in patients with IAIs include increased illness severity, failed source control, inadequate empiric antimicrobial therapy, and healthcare-acquired, as opposed to community-acquired infection. Whereas community-acquired IAI is characterized predominantly by enteric gram-negative bacilli and anaerobes that are susceptible to narrow-spectrum agents, healthcare-acquired IAI (e.g., anastomotic dehiscence, postoperative organ-space surgical site infection) frequently involves at least one multi-drug resistant pathogen, necessitating broad-spectrum therapy guided by both culture results and local antibiograms. The cornerstone of effective treatment for abdominal sepsis is early and adequate source control, which is supplemented by antibiotic therapy, restoration of a functional gastrointestinal tract (if possible), and support of organ dysfunction. Furthermore, mitigation of deranged immune and coagulation responses via therapy with recombinant human activated protein C may improve survival significantly in severe cases complicated by septic shock and multiple organ dysfunction syndrome.
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Siegler, Benedikt Hermann, Marc Altvater, Jan Niklas Thon, Christopher Neuhaus, Christoph Arens, Florian Uhle, Christoph Lichtenstern, Markus Alexander Weigand, and Sebastian Weiterer. "Postoperative abdominal sepsis induces selective and persistent changes in CTCF binding within the MHC-II region of human monocytes." PLOS ONE 16, no. 5 (May 3, 2021): e0250818. http://dx.doi.org/10.1371/journal.pone.0250818.

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Background Postoperative abdominal infections belong to the most common triggers of sepsis and septic shock in intensive care units worldwide. While monocytes play a central role in mediating the initial host response to infections, sepsis-induced immune dysregulation is characterized by a defective antigen presentation to T-cells via loss of Major Histocompatibility Complex Class II DR (HLA-DR) surface expression. Here, we hypothesized a sepsis-induced differential occupancy of the CCCTC-Binding Factor (CTCF), an architectural protein and superordinate regulator of transcription, inside the Major Histocompatibility Complex Class II (MHC-II) region in patients with postoperative sepsis, contributing to an altered monocytic transcriptional response during critical illness. Results Compared to a matched surgical control cohort, postoperative sepsis was associated with selective and enduring increase in CTCF binding within the MHC-II. In detail, increased CTCF binding was detected at four sites adjacent to classical HLA class II genes coding for proteins expressed on monocyte surface. Gene expression analysis revealed a sepsis-associated decreased transcription of (i) the classical HLA genes HLA-DRA, HLA-DRB1, HLA-DPA1 and HLA-DPB1 and (ii) the gene of the MHC-II master regulator, CIITA (Class II Major Histocompatibility Complex Transactivator). Increased CTCF binding persisted in all sepsis patients, while transcriptional recovery CIITA was exclusively found in long-term survivors. Conclusion Our experiments demonstrate differential and persisting alterations of CTCF occupancy within the MHC-II, accompanied by selective changes in the expression of spatially related HLA class II genes, indicating an important role of CTCF in modulating the transcriptional response of immunocompromised human monocytes during critical illness.
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Koca, Uğur, Çimen Gülben Olguner, Bekir Uğur Ergür, Emel Altekin, Aydın Taşdöğen, Seden Duru, Pelin Girgin, et al. "The Effects of Dexmedetomidine on Secondary Acute Lung and Kidney Injuries in the Rat Model of Intra-Abdominal Sepsis." Scientific World Journal 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/292687.

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In the present study, the effects of dexmedetomidine on secondary lung and kidney injuries were studied in the rat model of intra-abdominal sepsis by immunohistological and biochemical examinations. We measured serum creatinine, kidney tissue malondialdehide and plasma neutrophil gelatinase-associated lipocalin levels. In order to evaluate tissue injury we determined kidney tissue mononuclear cell infiltration score, alveolar macrophage count, histological kidney and lung injury scores and kidney and lung tissue immunoreactivity scores. We demonstrated that dexmedetomidine attenuates sepsis-induced lung and kidney injuries and apoptosis in the rat model of sepsis. There is still need for comparative studies in order to determine the effects of dexmedetomidine on organ functions in early human sepsis.
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Luo, Lingtao, Su Zhang, Yongzhi Wang, Milladur Rahman, Ingvar Syk, Enming Zhang, and Henrik Thorlacius. "Proinflammatory role of neutrophil extracellular traps in abdominal sepsis." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 7 (October 1, 2014): L586—L596. http://dx.doi.org/10.1152/ajplung.00365.2013.

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Excessive neutrophil activation is a major component in septic lung injury. Neutrophil-derived DNA may form extracellular traps in response to bacterial invasions. The aim of the present study was to investigate the potential role of neutrophil extracellular traps (NETs) in septic lung injury. Male C57BL/6 mice were treated with recombinant human (rh)DNAse (5 mg/kg) after cecal ligation and puncture (CLP). Extracellular DNA was stained by Sytox green, and NET formation was quantified by confocal microscopy and cell-free DNA in plasma, peritoneal cavity, and lung. Blood, peritoneal fluid, and lung tissue were harvested for analysis of neutrophil infiltration, NET levels, tissue injury, as well as CXC chemokine and cytokine formation. We observed that CLP caused increased formation of NETs in plasma, peritoneal cavity, and lung. Administration of rhDNAse not only eliminated NET formation in plasma, peritoneal cavity, and bronchoalveolar space but also reduced lung edema and tissue damage 24 h after CLP induction. Moreover, treatment with rhDNAse decreased CLP-induced formation of CXC chemokines, IL-6, and high-mobility group box 1 (HMGB1) in plasma, as well as CXC chemokines and IL-6 in the lung. In vitro, we found that neutrophil-derived NETs had the capacity to stimulate secretion of CXCL2, TNF-α, and HMGB1 from alveolar macrophages. Taken together, our findings show that NETs regulate pulmonary infiltration of neutrophils and tissue injury via formation of proinflammatory compounds in abdominal sepsis. Thus we conclude that NETs exert a proinflammatory role in septic lung injury.
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Zantl, Niko, Annette Uebe, Brigitte Neumann, Hermann Wagner, Jörg-Rüdiger Siewert, Bernhard Holzmann, Claus-Dieter Heidecke, and Klaus Pfeffer. "Essential Role of Gamma Interferon in Survival of Colon Ascendens Stent Peritonitis, a Novel Murine Model of Abdominal Sepsis." Infection and Immunity 66, no. 5 (May 1, 1998): 2300–2309. http://dx.doi.org/10.1128/iai.66.5.2300-2309.1998.

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ABSTRACT Despite considerable progress, peritonitis and sepsis remain life-threatening conditions. To improve the understanding of the pathophysiology encountered in sepsis, a new standardized and highly reproducible murine model of abdominal sepsis termed colon ascendens stent peritonitis (CASP) was developed. In CASP, a stent is inserted into the ascending colon, which generates a septic focus. CASP employing a stent of 14-gauge diameter (14G stent) results in a mortality of 100% within 18 to 48 h after surgery. By inserting stents of small diameters, mortality can be exactly controlled. Thus, CASP surgery with insertion of a 22G or 18G stent (22G or 18G CASP surgery) results in 38 or 68% mortality, respectively. 14G CASP surgery leads to a rapid invasion of bacteria into the peritoneum and the blood. As a consequence, endotoxemia occurs, inflammatory cells are recruited, and a systemic inflammatory response syndrome develops. Interestingly, the most pronounced upregulation of inflammatory cytokines (gamma interferon [IFN-γ], tumor necrosis factor alpha [TNF-α] and interleukin-12) is observed in spleen and lungs. CASP surgery followed by stent removal at specific time intervals revealed that all animals survived if intervention was performed after 3 h, whereas removal of the septic focus after 9 h did not prevent death, suggesting induction of autonomous mechanisms of a lethal inflammatory response syndrome. 18G CASP surgery in IFN-γ receptor-deficient (IFNγR−/−) mice revealed an essential role of IFN-γ in survival of sepsis, whereas TNF receptor p55-deficient (TNFRp55−/−) mice did not show altered survival rates. In summary, this study describes a novel animal model that closely mimics human sepsis and appears to be highly suitable for the study of the pathophysiology of abdominal sepsis. Importantly, this model demonstrates a protective role of IFN-γ in survival of bacterial sepsis.
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Leinhardt, D. J., J. Arnold, K. A. Shipley, M. M. Mughal, R. A. Little, and M. H. Irving. "Plasma NE concentrations do not accurately reflect sympathetic nervous system activity in human sepsis." American Journal of Physiology-Endocrinology and Metabolism 265, no. 2 (August 1, 1993): E284—E288. http://dx.doi.org/10.1152/ajpendo.1993.265.2.e284.

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Plasma norepinephrine concentrations ([NE]) when raised in patients with sepsis are thought to indicate increased activity of the sympathetic nervous system (SNS). However, increased SNS activity may occur without a concomitant rise in plasma [NE]. Measurement of NE kinetics (clearance and spillover) is a more accurate and direct assessment of SNS activity. In the present study plasma [NE] and NE kinetics were measured in six patients with intra-abdominal sepsis (septic) using tritiated NE infused to achieve a plateau plasma concentration. The measurements were repeated in the same patients after they had recovered (nonseptic). NE clearance and spillover were both significantly higher (P < 0.05) in the septic compared with the nonseptic state. However, there was no statistically significant difference in plasma [NE] between the two conditions. Plasma [NE] indicates no alteration in SNS activity during the septic state, whereas NE kinetics indicate increased activity of the SNS during sepsis. The results suggest that plasma [NE] is a poor indicator of SNS activity during septic illness.
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Worth, P. J., S. F. Monaghan, R. K. Thakkar, M. L. Tran, A. Ayala, W. G. Cioffi, and D. S. Heffernan. "Compartmentalized Lymphocyte Response To Abdominal Versus Non-abdominal Sources Of Sepsis In Humans." Journal of Surgical Research 165, no. 2 (February 2011): 238. http://dx.doi.org/10.1016/j.jss.2010.11.505.

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Lehmann, Christian, Maral Aali, Juan Zhou, and Bruce Holbein. "Comparison of Treatment Effects of Different Iron Chelators in Experimental Models of Sepsis." Life 11, no. 1 (January 14, 2021): 57. http://dx.doi.org/10.3390/life11010057.

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Growing evidence indicates that dysregulated iron metabolism with altered and excess iron availability in some body compartments plays a significant role in the course of infection and sepsis in humans. Given that all bacterial pathogens require iron for growth, that iron withdrawal is a normal component of innate host defenses and that bacterial pathogens have acquired increasing levels of antibiotic resistance, targeting infection and sepsis through use of appropriate iron chelators has potential to provide new therapeutics. We have directly compared the effects of three Food and Drug Administration (FDA)-approved chelators (deferoxamine—DFO; deferiprone—DFP; and deferasirox—DFX), as were developed for treating hematological iron overload conditions, to DIBI, a novel purpose-designed, anti-infective and anti-inflammatory water-soluble hydroxypyridinone containing iron-selective copolymers. Two murine sepsis models, endotoxemia and polymicrobial abdominal sepsis, were utilized to help differentiate anti-inflammatory versus anti-infective activities of the chelators. Leukocyte adhesion, as measured by intravital microscopy, was observed in both models, with DIBI providing the most effective reduction and DFX the poorest. Inflammation in the abdominal sepsis model, assessed by cytokine measurements, indicated exacerbation by DFX and DFO for plasma Interleukin (IL)-6 and reductions to near-control levels for DIBI and DFP. Peritoneal infection burden was reduced 10-fold by DIBI while DFX and DFP provided no reductions. Overall, the results, together with those from other studies, revealed serious limitations for each of the three hematological chelators, i.e., as potentially repurposed for treating infection/sepsis. In contrast, DIBI provided therapeutic benefits, consistent with various in vitro and in vivo results from other studies, supporting the potential for its use in treating sepsis.
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O'Connell, Rachel L., Glenn K. Wakam, Ali Siddiqui, Aaron M. Williams, Nathan Graham, Michael T. Kemp, Kiril Chtraklin, et al. "Development of a large animal model of lethal polytrauma and intra-abdominal sepsis with bacteremia." Trauma Surgery & Acute Care Open 6, no. 1 (January 2021): e000636. http://dx.doi.org/10.1136/tsaco-2020-000636.

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BackgroundTrauma and sepsis are individually two of the leading causes of death worldwide. When combined, the mortality is greater than 50%. Thus, it is imperative to have a reproducible and reliable animal model to study the effects of polytrauma and sepsis and test novel treatment options. Porcine models are more translatable to humans than rodent models due to the similarities in anatomy and physiological response. We embarked on a study to develop a reproducible model of lethal polytrauma and intra-abdominal sepsis, which was lethal, though potentially salvageable with treatment.MethodsOur laboratory has a well-established porcine model that was used as the foundation. Animals were subjected to a rectus crush injury, long bone fracture, liver and spleen laceration, traumatic brain injury and hemorrhage that was used as a foundation. We tested various colon injuries to create intra-abdominal sepsis. All animals underwent injuries followed by a period of shock, then subsequent resuscitation.ResultsAll animals had blood culture-proven sepsis. Attempts at long-term survival of animals after injury were ceased because of poor appetite and energy. We shifted to an 8-hour endpoint. The polytrauma injury pattern remained constant and the colon injury pattern changed with the intention of creating a model that was ultimately lethal but potentially salvageable with a therapeutic drug. An uncontrolled cecal injury (n=4) group resulted in very early deaths. A controlled cecal injury (CCI; n=4) group had prolonged time prior to mortality with one surviving to the endpoint. The sigmoid injury (n=5) produced a similar survival curve to CCI but no animals surviving to the endpoint.ConclusionWe have described a porcine model of polytrauma and sepsis that is reproducible and may be used to investigate novel treatments for trauma and sepsis.Level of evidenceNot applicable. Animal study.
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Dissertations / Theses on the topic "Human abdominal sepsis][Sepsis"

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Vasconcelos, P. R. L. de. "Hepatic metabolism during sepsis." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233530.

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Lattuada, Marco. "Effect of Ventilatory Support on Abdominal Fluid Balance in a Sepsis Model." Doctoral thesis, Uppsala universitet, Klinisk fysiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-207218.

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In patients affected by acute respiratory failure or acute respiratory distress syndrome (ARDS) the leading cause of death is failure of different vital organs other than the lungs, so called multiple organ dysfunction syndrome (MODS). The abdominal organs have a crucial role in the pathogenesis of this syndrome. There is a lack of knowledge regarding the mechanisms by which mechanical ventilation can affect the abdominal compartment. One hypothesis is that mechanical ventilation can interfere with abdominal fluid balance causing edema and inflammation. We addressed the question whether different levels of ventilatory support (mechanical ventilation with different levels of positive end-expiratory pressure, PEEP, and spontaneous breathing with or without PEEP) can influence abdominal edema and inflammation in both healthy and endotoxin-exposed animals. The effect on lymphatic drainage from the abdomen exerted by different degrees of ventilatory support was evaluated (paper I). We demonstrated that endotoxin increases abdominal lymph production, that PEEP and mechanical ventilation increase lymph production but also impede lymphatic drainage; spontaneous breathing improves lymphatic drainage from the abdomen. By adapting a non-invasive nuclear medicine imaging technique and validating it (paper II), we have been able to evaluate extravascular fluid accumulation (edema formation) in the abdomen over time (paper III) demonstrating that edema increases during endotoxemia, mimicking a sepsis-like condition, and that spontaneous breathing, compared to mechanical ventilation, reduces extravascular fluid. Pro-inflammatory cytokines TNF-α and IL-6 in intestinal biopsies are reduced during spontaneous breathing compared to mechanical ventilation. Abdominal edema results in increased intra-abdominal pressure (IAP): in paper IV we analyzed the effect of increased intra-abdominal pressure on the respiratory system. Pulmonary shunt fraction increased with high IAP both in healthy and LPS animals, resulting in decreased level of oxygenation. These changes are only partially reversible by reducing IAP. In conclusion, mechanical ventilation is a life-saving tool but the possible side effect at the extra-pulmonary level should be considered, and the introduction of some degree of spontaneous breathing when clinically possible is a suggested choice.
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Bleszynski, Michael Sean. "Impact of open abdomen and Vacuum Assisted Closure Device in surgical abdominal sepsis." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/61001.

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Introduction: Surgical abdominal sepsis has traditionally been managed with by a single staged procedure, otherwise known as primary abdominal closure (PAC). An on demand laparotomy may be performed for post-operative clinical deterioration. Open abdomen and a planned re-laparotomy with vacuum assisted closure (VAC) is an alternate method to single staged procedure. Inflammatory cytokines can potentially help stratify severity of sepsis and guide surgical management. The objective of the study was to identify if inflammatory cytokines could differentiate between PAC and VAC. Secondary objectives were to see if cytokines could predict mortality and characterize longitudinal cytokine profiles during open abdomen management. Severity of disease between surgical groups was compared using the Acute Physiology and Chronic Health Assessment (APACHE)-IV predictive mortality rate (PMR) calculator. Methods: Prospective case series between December 2011 to June 2013. Patients were included if they met criteria of severe abdominal sepsis/septic shock requiring urgent source control laparotomy (SCL). Blood and peritoneal samples were obtained pre- and post-operatively at primary SCL in patients who underwent PAC and VAC management. Peritoneal fluid (PF) samples were obtained once the peritoneum was entered. Blood and peritoneal samples were obtained for re-look laparotomies in the VAC group. Samples were centrifuged within 1 hour and stored at -70 degrees Celsius. Samples were analyzed with a Human Cytokine 30-plex Panel and concentrations were reported as pg/ml. Results: 12 patients were included (4 PAC and 8 VAC). PF cytokine concentrations of IL 6, IL-17, IL-5 and HGF were significantly higher in VAC compared to PAC. Peritoneal fluid at primary SCL did not differentiate between survivors and non-survivors. Pre-operative serum RANTES was significantly elevated in survivors compared to non-survivors. Pre operative serum VEGF, IL-1b, FGF-b, IL-5, IL-4, IL-7 and post-operative serum VEGF, IL-7 differentiated between VAC survivors and non-survivors at second SCL. Conclusion: VAC management was utilized in patients with elevated peritoneal cytokines compared to single staged procedures. Increased peritoneal inflammatory cytokine concentrations in VAC represent a more severe degree of local sepsis. Pro and anti-inflammatory cytokines are both elevated in the early and late phases of surgical abdominal sepsis.
Medicine, Faculty of
Surgery, Department of
Graduate
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Perry, Sara Elizabeth. "The phenotypic characterization of the monocyte in human sepsis." Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268902.

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Sartelli, M., F. M. Abu-Zidan, L. Ansaloni, M. Bala, M. A. Beltran, W. L. Biffl, F. Catena, et al. "The role of the open abdomen procedure in managing severe abdominal sepsis: WSES position paper." BioMed Central, 2015. http://hdl.handle.net/10150/610338.

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The open abdomen (OA) procedure is a significant surgical advance, as part of damage control techniques in severe abdominal trauma. Its application can be adapted to the advantage of patients with severe abdominal sepsis, however its precise role in these patients is still not clear. In severe abdominal sepsis the OA may allow early identification and draining of any residual infection, control any persistent source of infection, and remove more effectively infected or cytokine-loaded peritoneal fluid, preventing abdominal compartment syndrome and deferring definitive intervention and anastomosis until the patient is appropriately resuscitated and hemodynamically stable and thus better able to heal. However, the OA may require multiple returns to the operating room and may be associated with significant complications, including enteroatmospheric fistulas, loss of abdominal wall domain and large hernias. Surgeons should be aware of the pathophysiology of severe intra-abdominal sepsis and always keep in mind the option of using open abdomen to be able to use it in the right patient at the right time.
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Januszkiewicz, Anna. "In vivo protein synthesis determinations in human immune cells /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-219-5/.

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Cajander, Sara. "Dynamics of Human Leukocyte Antigen-D Related expression in bacteremic sepsis." Doctoral thesis, Örebro universitet, Institutionen för medicinska vetenskaper, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-56125.

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Monocytic human leukocyte antigen-D related (mHLA-DR) expression determined by flow cytometry has been suggested as a biomarker of sepsisinduced immunosuppression. In order to facilitate use of HLA-DR in clinical practice, a quantitative real-time PCR technique measuring HLA-DR at the transcription level was developed and evalutated. Levels of HLA-DR mRNA correlated to mHLADR expression and were robustly measured, with high reproducibility, during the course of infection. Dynamics of mHLA-DR expression was studied during the first weeks of bloodstream infection (BSI) and was found to be dependent on the bacterial etiology of BSI. Moreover, mHLA-DR was shown to be inversely related to markers of inflammation. In patients with unfavourable outcome, sustained high C-reactive protein level and high neutrophil count were demonstrated along with low mHLA-DR expression and low lymphocyte count. This supports the theory of sustained inflammation in sepsis-induced immunosuppression. The association between mHLA-DR and bacterial etiology may be linked to the clinical trajectory via differences in ability to cause intractable infection. Staphylococcus aureus was the dominating etiology among cases with unfavourable outcome. With focus on patients with S. aureus BSI, those with complicated S. aureus BSI were found to have lower HLA-DR mRNA expression during the first week than those with uncomplicated S. aureus BSI. If these results can be confirmed in a larger cohort, HLA-DR measurement could possibly become an additional tool for early identification of patients who require further investigation to clear infectious foci and achieve source control. In conclusion, PCR-based measurement of HLA-DR is a promising method for measurements of the immune state in BSI, but needs further evaluation in the intensive care unit setting to define the predictive and prognostic value for deleterious immunosuppression. The etiology of infection should be taken into consideration in future studies of translational immunology in sepsis.
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González, Lisorge Ada. "Estudio sobre la sepsis grave de origen abdominal. Utilidad de la procalcitonina y otros marcadores pronósiticos." Doctoral thesis, Universidad de Murcia, 2013. http://hdl.handle.net/10803/128673.

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INTRODUCCIÓN: La sepsis es una de las principales causas de morbimortalidad en las unidades de cuidados intensivos (UCIs). La sepsis grave de origen abdominal es uno de los cuadros más frecuentes en las UCIs Posquirúrgicas. Su mortalidad es elevada y oscila entre 40% y el 70% según las series. Sin embargo, es un cuadro que suele tener poco protagonismo en la literatura científica. Los biomarcadores son elementos fundamentales para el diagnóstico, seguimiento y pronóstico de la sepsis. Uno de los biomarcadores más estudiados en las últimas décadas ha sido la procalcitonina. Muchos autores consideran que su cinética se relaciona con la evolución, el pronóstico o con un tratamiento correcto de diversas patologías. Las escalas de gravedad, como el Acute Physiology And Chronic Health Evaluation II (APACHE II) y la escala Sequential Organ Failure Assessment (SOFA) tienen utilidad pronóstica en pacientes críticos. El APACHE II no es específico para pacientes sépticos, pero identifica pacientes con gravedad aumentada. La escala SOFA es un sistema específico de valoración de la gravedad del paciente séptico. Se diseñó para evaluar la afectación orgánica secundaria a la sepsis, aunque posteriormente, también se ha empleado con fines pronósticos. El objetivo principal de esta Tesis Doctoral es identificar los factores que influyen en la evolución (Éxitus o supervivencia) de los pacientes con sepsis grave de origen abdominal. Analizamos la utilidad de la procalcitonina como marcador de supervivencia y evaluamos si las escalas de gravedad, APACHE II y SOFA, permiten predecir la mortalidad de estos pacientes. MATERIAL Y MÉTODO: Se incluyeron en el estudio todos los pacientes con diagnóstico de sepsis grave de origen abdominal ingresados en una Unidad de Cuidados Críticos Posquirúrgicos entre los años 2007 y 2008. Se recogieron datos demográficos, los valores de la procalcitonina en los días primero, tercero y séptimo de ingreso y se calcularon las puntuaciones de las escalas APACHE II y SOFA al ingreso y de la escala SOFA en los días tercero y séptimo. RESULTADOS: Estudiamos 69 pacientes. La mortalidad de nuestra serie fue del 23,19% (IC95%: 13,19;33,19%). La edad media de estos pacientes fue 64,94 años (IC95%: 61;69 años). La mayoría de los pacientes (57,97%) presentó sepsis de origen comunitario (p<0,05). La patología previa más frecuente fue la hipertensión arterial (49,27%; IC95%: 37,27;61,27%), seguida de la diabetes mellitus (24,63%; IC95%: 14,43;34,83%) El foco de infección más frecuente fue el intestino grueso (40,57%; IC95%: 28,57;52,57%). La puntuación APACHE II media al ingreso fue de 16,43 puntos (IC95%: 14,95;17,91puntos) y fue superior entre los Éxitus (p<0,00001). La puntuación SOFA media al ingreso fue de 6,46 puntos (IC95%: 5,71;7,2puntos). En el estudio de regresión logística binario, los dos factores que más influyeron en la mortalidad de estos pacientes fueron la edad y el ascenso de las puntuaciones de la escala SOFA entre los días primero y séptimo. La procalcitonina presentó una dinámica diferente entre Éxitus, cuyos valores se mantuvieron elevados y Supervivientes, en los que los valores disminuyeron con el tiempo (p<0,05). El valor de procalcitonina que mejor identificó pronóstico fue el del día séptimo (AUC-ROC 0,768), niveles mayores o iguales a 3,5ng/mL detectaron mortalidad con una sensibilidad del 55% y una especificidad del 73%. CONCLUSIONES: En nuestra serie de pacientes con sepsis grave posquirúrgica de origen abdominal, el valor de procalcitonina en el séptimo día de observación se relaciona con el pronóstico. El ascenso en la puntuación de la escala SOFA entre los días primero y séptimo, junto con la edad, fueron los elementos que mejor identificaron el pronóstico de los pacientes con sepsis grave de origen abdominal.
Sepsis represents a major cause of morbidity and mortality in Intensive Care Units (ICU). Severe sepsis of intraabdominal origin is a frequent pathology in Surgical ICU. It presents a high mortality rate, 40% in some series, but even 70% has been reported. Nevertheless, it has little prominence in scientific literature. Biomarkers are main elements in the battery of diagnostic, monitoring and prognostic tests. Procalcitonin has been one of the most studied markers in lasts decades. Many authors consider its dynamics well related with evolution, outcome or a correct treatment of different pathologies. Severity scales, such as Acute Physiology and Chronic Health Evaluation II (APACHE II) and Sequential Organ Failure Assessment score (SOFA) are some of the prognostic tools used in critical patients. APACHE II is not specific for septic patients, but has utility identifying patients with augmented severity. SOFA score is a specific system for severity assessment in septic patients. It identifies and allows the monitoring of organ failure secondary to sepsis. Initially it was design for the evaluation of organ dysfunction during the ICU stay of these patients, though its prognostic value has also been proved. The purpose of this Doctoral Thesis is to study which elements characterize patients with severe sepsis of intraabdominal origin, and try to identify which factors can influence the outcome of these patients. We assess the utility of procalcitonin and severity scores, APACHE II and SOFA, as outcome predictors in patients with severe sepsis of intraabdominal origin. PATIENTS AND METHOD: We included all patients admitted in a Surgical Intensive Care Unit with the diagnosis of severe sepsis of intraabdominal origin, between 2007 and 2008. We recorded demographic data, procalcitonin levels at days one, three and seven, and APACHE II and SOFA scores on admission, as well as SOFA score on days three and seven. RESULTS: 69 patients were included in the study. Mortality rate of our series was 23.19% (95%ic, 13.19-33.19%). Mean age of these patients was 64.94 (95%ic, 61;69y). More than 55% of patients had community acquired sepsis (p<0.05). Most frequent previous pathologies were hypertension (49.27%; 95%ci, 37.27;61.27%), followed by mellitus diabetes (24.63%; 95%ci, 14.43;34.83%). The most frequent focus of infection was colonic (40.57%; 95%ci, 28.57;52.57%). Mean APACHE II score on admission was 16.43 points (95%ci, 14.95;17.91points) and was higher in those patients who finally died (p<0.00001). Mean SOFA score on admission was 6.46 points (95%ci, 5.71;7.2points). In the binary regression logistic study, those factors identified as more related with outcome were age and the increase in SOFA score between days one and seven. Procalcitonin presented a different dynamic among Nonsurvivors (levels maintained or increased) and Survivors (whose levels decreased)(p<0.05). Procalcitonin levels on day seven identified better the outcome of these patients (AUC-ROC 0.768). Levels equal or higher than 3.5ng/mL identified mortality with 55% sensibility and 73% specificity. CONCLUSIONS: In our series of patients with severe sepsis of intraabdominal origin, procalcitonin does not identify outcome of patients on admission, but on day seven of observation. Increase on SOFA score between days one and seven and age were the factors that identified outcome in a more accurate way on patients with severe sepsis of intraabdominal origin.
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Smith, Laura Ann. "Effects of Bacterial Products on Human Blood Leukocytes." University of Toledo Health Science Campus / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=mco1164046331.

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Lima, Erica Silva. "Efeito da suplementação dietética com L-glutamina na sepse abdominal induzida em rato." Universidade do Estado do Rio de Janeiro, 2012. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5869.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Após o estímulo deflagrador de um trauma ou infecção, a liberação de citocinas na circulação sanguínea desempenha um importante papel efetor e também modulador da resposta imune sistêmica. Essas citocinas podem ser pró-inflamatórias, que estimulam a liberação de diversos tipos celulares e de outras citocinas, como fator de necrose tumoral-alfa (TNF-α), interleucina 1 (IL-1), IL-2, IL-6, IL-8, IL-12 e interferon-gama (INF-); ou citocinas com efeitos antiinflamatórios, que inibem o processo inflamatório, em parte pela redução da produção de diversas citocinas que regulam positivamente a resposta, minimizando o comprometimento orgânico resultante, como IL-4, IL-10, IL-13. A L-glutamina é o aminoácido mais abundante no organismo, com importante papel no metabolismo protéico. Sua ação trófica sobre a mucosa do intestino delgado é bastante conhecida, o que o torna componente essencial para a manutenção estrutural e funcional do intestino. O objetivo deste trabalho foi avaliar o efeito da suplementação dietética com L-glutamina na modulação da resposta inflamatória em animais submetidos a sepse abdominal induzida por ligadura e perfuração cecal. Foram utilizados 24 ratos Wistar machos adultos, com peso inicial entre 200 e 230 g, distribuídos em três grupos, cada um com oito animais, da seguinte forma: grupo I (controle) submetidos a operação simulada (laparotomia e manipulação de alças intestinais); grupo II submetidos a laparotomia, com indução de sepse abdominal; e grupo III receberam suplementação dietética com L-glutamina por sete dias e, após, foram submetidos a indução de sepse abdominal. Foram coletadas amostras sanguíneas de todos os animais antes (tempo 0) e duas e quatro horas (tempos 1 e 2) após a indução da sepse abdominal. Foram verificados o número de leucócitos, a dosagem da concentração plasmática de citocinas pró- e antiinflamatórias (INF-γ, IL-6 e IL-10) e análise microbiológica de líquido peritoneal. A glicemia apresentou aumento significativo em todos os grupos, comparando-os ao início e ao final do experimento (p<0,05). No que concerne à IL-10, observou-se aumento significativo nos animais do grupo III entre os tempos 0 e 2, e entre os tempos 1 e 2 (p=0,0331 e p=0,0155, respectivamente). Não se observou qualquer outra diferença ao serem analisadas as demais citocinas (IFN- e IL-6), em todos os grupos e em todos os momentos analisados. Nossos achados sugerem que a suplementação dietética com L-glutamina em animais submetidos à indução de sepse abdominal com modelo CLP parece potencializar a resposta antiinflamatória, aumentando a concentração plasmática de IL-10, enquanto as concentrações de INF-γ e IL-6 não apresentaram variação significativa.
After the triggering stimulus of trauma or infection, the release of cytokines into the bloodstream plays an important effector and modulator role on the systemic immune response. These cytokines may be pro-inflammatory, stimulating the release of several cell types and other cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin 1 (IL-1), IL-2, IL-6, IL-8, IL-12 and interferon-gamma (IFN-); or cytokines with anti-inflammatory effects that inhibit the inflammatory process, in part by reducing the production of several cytokines that positively regulate the response, minimizing the resulting organic damages, such as IL-4 , IL-10, IL-13. L-Glutamine is the most abundant amino acid in the body, with an important role in protein metabolism, acting as a vehicle for nitrogen transport. Its trophic action on the small intestinal mucosa is well known, which makes it an essential component in the maintenance of the bowel structure and function. This study aimed at evaluating the effect of the dietary supplementation with L-glutamine in modulating the inflammatory response in animals submitted to the induction of abdominal sepsis by cecal ligation and puncture (CLP). We used 24 adult male Wistar rats, initially weighing between 200 and 230 g, divided into three groups, each with eight animals as follows: group I (control) sham operation (laparotomy and manipulation of the bowel); group II laparotomy with induction of abdominal sepsis; and group III dietary supplementation with L-glutamine for seven days and after submitted to the induction of abdominal sepsis. Blood samples were collected from all animals before (time 0) and two and four hours (times 1 and 2) after the induction of abdominal sepsis. We verified white blood cell (WBC) count, the plasmatic concentration of pro- and anti-inflammatory cytokines (INF-γ, IL-6 and IL-10), and the microbiological analysis of peritoneal fluid. Blood glucose increased significantly in all groups, comparing them in the beginning and in the end of the experiment (p<0.05). Concerning to IL-10, we observed a significant increase in the animals of group III between times 0 and 2, and times 1 and 2 (p=0.0331 and p=0.0155, respectively). We did not observe any difference in the analysis of the other cytokines (IFN- and IL-6) in all groups and at all times. Our findings suggest that dietary supplementation with L-glutamine in animals submitted to the induction of abdominal sepsis with CLP model seems to enhance the anti-inflammatory response, increasing the plasmatic concentration of IL-10, while the concentration of INF-γ and IL-6 did not present significant change.
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Books on the topic "Human abdominal sepsis][Sepsis"

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Sartelli, Massimo, Matteo Bassetti, and Ignacio Martin-Loeches, eds. Abdominal Sepsis. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-59704-1.

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Sartelli, Massimo, Matteo Bassetti, and Ignacio Martin-Loeches. Abdominal Sepsis: A Multidisciplinary Approach. Springer, 2018.

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Sartelli, Massimo, Matteo Bassetti, and Ignacio Martin-Loeches. Abdominal Sepsis: A Multidisciplinary Approach. Springer, 2019.

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Evans, Charlotte, Anne Creaton, Marcus Kennedy, and Terry Martin, eds. Sepsis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198722168.003.0011.

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Sepsis is common and has been the focus of recent large-scale, multi-centre trials internationally. Mortality rates have improved, largely due to a focus on early identification, key interventions, and close monitoring. Setting goals and resuscitation targets coupled with frequent reassessment is the essence of modern sepsis care. Retrieval services bring the intensive care unit to the patient. Specific conditions such as infective endocarditis, central nervous system infections, respiratory, gastrointestinal, abdominal, obstetric, and necrotizing soft tissue sepsis require special consideration. With newly emerging infections and increasing air travel, the importance of a travel history is emphasized. Sepsis in the immunocompromised host gets a special mention due to the complexity of patient, organism, and drug interactions. The chapter is completed by a table to guide empirical antibiotic choice.
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Doyle, Jeffrey D., and John C. Marshall. Intra-abdominal sepsis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0187.

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Intra-abdominal infection encompasses a broad group of infections arising both within the peritoneal cavity and the retroperitoneum. The probable bacteriology reflects patterns of normal and pathological colonization of the gastrointestinal tract. Anaerobic bacteria are found in the distal small bowel and colon. The abdomen is the second most common site of infection leading to sepsis in critically-ill patients. Intra-abdominal infections can be complex to manage and require excellent collaboration between intensivists, diagnostic and interventional radiologists, surgeons, and sometimes gastroenterologists and infectious disease specialists. Prompt diagnosis, appropriate antimicrobial coverage and timely source control are the cornerstones of successful management. The spectrum of pathologic conditions responsible for intra-abdominal infection is broad, although some common biological features facilitate an understanding of their diagnosis and management.
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Thomson, D., and M. W. Wuechler. Abdominal Sepsis (Digestive Surgery, Vol. 13, No.4-5, 1996). S Karger Pub, 1996.

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Waldmann, Carl, Neil Soni, and Andrew Rhodes. Gastrointestinal disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0020.

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Vomiting and gastric stasis/gastroparesis 318Gastric erosions 320Diarrhoea 322Upper gastrointestinal haemorrhage (non-variceal) 324Bleeding varices 326Intestinal perforation 328Intestinal obstruction 330Lower gastrointestinal bleeding 332Colitis 334Intra-abdominal sepsis 336Pancreatitis 338Acute acalculous cholecystitis 340Splanchnic ischaemia 342Abdominal hypertension (IAH) and abdominal compartment syndrome ...
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Moshe, Schein, and Wise Leslie, eds. Cytokines and the abdominal surgeon. Austin: R.G. Landes, 1998.

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Gardiner, Matthew D., and Neil R. Borley. Emergency surgery. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199204755.003.0008.

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This chapter begins by discussing the basic principles of Advanced Trauma Life Support, care of the critically ill surgical patient, shock, SIRS and sepsis, and blood products and transfusion, before focusing on the key areas of knowledge, namely traumatic head injury, spine and spinal cord trauma, maxillofacial trauma, cardiothoracic trauma, abdominal trauma, urological trauma, vascular trauma, assessment of the acute abdomen, acute appendicitis, acute upper gastrointestinal haemorrhage, lower gastrointestinal haemorrhage, gastrointestinal obstruction, gastrointestinal perforation, acute pancreatitis, and superficial sepsis. The chapter concludes with relevant case-based discussions.
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Johnson, Steven B. Pathophysiology and management of abdominal injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0334.

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Abdominal injuries are common following blunt and penetrating trauma. They can result in a spectrum of severity from benign to potentially life-threatening conditions. Soon after injury, haemorrhage is the predominant concern, and leading cause of morbidity and mortality. Active haemorrhage resulting in shock requires emergent operative intervention and aggressive haemostatic resuscitation. However haemodynamically-stable patients benefit from non-operative management of solid organ injuries with or without angiographic embolization. Sepsis usually occurs as a result of intra-abdominal infections from missed bowel perforations or anastomotic leaks. Sterile systemic hyperinflammatory conditions can result from major hepatic necrosis or pancreatic injuries, and closely mimic infectious conditions. Damage control surgery is a valuable adjunct to the operative management of major abdominal trauma. This concept recognizes that the time and procedures required to perform definitive operative repair may be detrimental when physiological derangements are excessive. By limiting operations to controlling haemorrhage and enteric contamination, further deterioration, and the ‘vicious bloody cycle of trauma’ can be avoided. The operative and critical care management of patients with abdominal trauma should be closely integrated to correct physiological derangements with rapid stabilization and reversal of hypoperfusion. Abdominal compartment syndrome, characterized by intra-abdominal hypertension and resultant remote organ dysfunction, is a risk in patients undergoing high-volume fluid resuscitation. Emergent decompressive laparotomy is indicated in patients with abdominal compartment syndrome and results in rapid reversal of physiological compromise. Paramount to optimal management of abdominal injuries is the close integration of operative and critical care approaches.
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Book chapters on the topic "Human abdominal sepsis][Sepsis"

1

Champion, Howard R., Nova L. Panebianco, Jan J. De Waele, Lewis J. Kaplan, Manu L. N. G. Malbrain, Annie L. Slaughter, Walter L. Biffl, et al. "Abdominal Sepsis." In Encyclopedia of Intensive Care Medicine, 25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1024.

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Shin, Reuben D., and Peter W. Marcello. "Intra-abdominal Sepsis." In Surgical Intensive Care Medicine, 427–36. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-19668-8_31.

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Metze, Dieter, Tam Nguyen, Birgit Haack, Alexander K. C. Leung, Noriko Miyake, Naomichi Matsumoto, A. J. Larner, et al. "Diffuse Abdominal Sepsis." In Encyclopedia of Molecular Mechanisms of Disease, 532. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6560.

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Brozovich, Marc E., and Peter W. Marcello. "Intra-abdominal Sepsis." In Surgical Intensive Care Medicine, 343–48. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-0-387-77893-8_30.

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Clarke, D. P., and J. R. Buscombe. "Imaging Abdominal Sepsis." In The Imaging of Infection and Inflammation, 183–97. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-4990-7_9.

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Marcello, Peter W. "Intra-Abdominal Sepsis." In Surgical Intensive Care Medicine, 461–70. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4757-6645-5_28.

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De Waele, Jan J., and Inneke De laet. "Intra-Abdominal Hypertension and MODS." In Sepsis Management, 59–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-03519-7_6.

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Preiser, Jean-Charles, and Jean-Louis Vincent. "Sepsis." In Metabolism of Human Diseases, 319–22. Vienna: Springer Vienna, 2014. http://dx.doi.org/10.1007/978-3-7091-0715-7_46.

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May, Addison K. "Treatment of Abdominal Sepsis." In Intensivist Should Know, 175–79. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003042136-30.

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Ryan, Thomas, and John D. Coakley. "Adjunctive Therapies in Abdominal Sepsis." In Hot Topics in Acute Care Surgery and Trauma, 359–68. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-59704-1_23.

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Conference papers on the topic "Human abdominal sepsis][Sepsis"

1

Hedenstierna, G., M. Lattuada, and E. Maripuu. "Mechanical Ventilation Worsens Abdominal Edema in Experimental Sepsis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4665.

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Gutsche, Markus, Vikram Sahni, Daya Upadhyay, Frank T. Kagawa, and Sharmila Pramanik. "Eosinopenia With Abdominal Pain And Sepsis In HIV." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6181.

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Fuss, Yu O., A. O. Voloboyeva, and V. P. Polovyj. "Signs of abdominal sepsis in patients with generalized peritonitis." In SCIENTIFIC PROGRESS OF MEDICINE AND PHARMACY OF THE EU COUNTRIES. Baltija Publishing, 2021. http://dx.doi.org/10.30525/978-9934-26-075-9-27.

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Bustamante, A. C., K. Opron, T. J. Standiford, and B. Singer. "Transcriptomic Profiles of Sepsis in the Human Brain." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2387.

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Li, Yumei, Wenli Zhou, Jiantao Zhang, and Chaoying Yan. "Clinical analyses of neonatal sepsis caused by Listeria monocytogene." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027980.

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Doerschug, K., A. Delsing, G. Schmidt, and A. Ashare. "Renin-Angiotensin System Activation Correlates with Microvascular Dysfunction in Human Sepsis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1139.

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Xu, Jianqiao, and Lixin Xie. "Dynamic changes of monocyte human leukocyte antigen-DR and T cell subsets in sepsis." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa2926.

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Urooj, F., P. Flinders, J. Paul, and B. Padmakumar. "G167(P) A case series of human parechovirus associated sepsis and meningitis in young children." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.162.

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Fang, Yen-Ling, Wen-Bin Lee, Chih-Hung Wang, Chun-Chih Chien, Huey-Ling You, Mel S. Lee, and Gwo-Bin Lee. "An Integrated Microfluidic System for Fast Isolation of Bacteria in Human Whole Blood for Diagnosis of Sepsis." In 2020 IEEE 33rd International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2020. http://dx.doi.org/10.1109/mems46641.2020.9056344.

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Parekh, Dhruv, Jaimin Patel, Sian Lax, Aaron Scott, Rachel Dancer, Gavin Perkins, and David Thickett. "LSC Abstract – Vitamin D deficiency is associated with and influences the severity of human and murine sepsis." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pp240.

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