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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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Malewicz, N. M., K. Walstein, T. Heine, A. Engler, A. Bick, L. Cox, A. Dötsch, et al. "Early suppression of peripheral mononuclear blood cells in sepsis in response to stimulation with cytomegalovirus, OKT3, and pokeweed mitogen." Journal of Applied Physiology 127, no. 6 (December 1, 2019): 1539–47. http://dx.doi.org/10.1152/japplphysiol.00438.2019.
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Critically ill patients are at risk for sepsis, and immunosuppressive mechanisms may prevail. Whether functional tests are helpful to detect immune alterations is largely unknown. Therefore, we tested the hypotheses that reactivity of peripheral blood mononuclear cells (PBMCs) to secrete interferon-γ (IFNγ) following stimulation in vitro is decreased in patients with early sepsis compared with postoperative patients. IFNγ secretion [enzyme-linked immunospot (ELISpot)] in response to stimulation with cytomegalovirus (CMV), pokeweed mitogen (PWM), muromonab-anti-CD3 (OKT3), and human leukocyte antigen (HLA)-DRA-mRNA expression and serum cytokine concentrations were repeatedly [ days 1, 3, 5, and 7 after intensive care unit (ICU) admission] determined in patients with sepsis ( n = 7) and patients undergoing major abdominal surgery (radical prostatectomy, cystectomy, n = 10). In a second cohort, HLA-DRA expression was assessed in 80 patients with sepsis, 30 postoperative patients, and 44 healthy volunteers (German clinical trials database no. 00007694). In patients with sepsis, IFNγ secretion (ELISpot) was decreased compared with controls after stimulation with CMV ( P = 0.01), OKT3 ( P = 0.02), and PWM ( P = 0.02 on day 5), whereas unstimulated IFNγ secretion did not differ. HLA-DRA expression was also significantly decreased in patients with sepsis at all time points ( P = 0.004) compared with postoperative surgical patients, a finding confirmed in the larger cohort. Reactivity of PBMCs to stimulation with CMV, PWM, and OKT3 as well as HLA-DRA expression was already decreased upon ICU admission in patients with sepsis when compared with postoperative controls, suggesting early depression of acquired immunity. ELISpot assays may help to clinically characterize the time course of immunocompetence in patients with sepsis. NEW & NOTEWORTHY We observed suppression of reactivity to stimulation with cytomegalovirus, muromonab-anti-CD3, and pokeweed mitogen in mononuclear blood cells of patients with early sepsis when compared with postoperative controls. Thus, there is early depression of acquired immunity in sepsis. Enzyme-linked immunospot assays may help to characterize immunocompetence in patients with sepsis.
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Diedrich, Stephan, Julia van der Linde, Michael Nielson, Pia Menges, Jens-Peter Kühn, Andre Käding, Dung Ngyuen Trung, Claus-Dieter Heidecke, Lars Ivo Partecke, and Wolfram Kessler. "The MRI Sepsis Score: An Innovative Tool for the Evaluation of Septic Peritonitis in Mice Using 7-Tesla Small Animal MRI." European Surgical Research 59, no. 3-4 (2018): 126–42. http://dx.doi.org/10.1159/000490663.
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Background: Magnetic resonance imaging (MRI) techniques are rarely used in the context of abdominal sepsis and in sepsis research. This study investigates the impact of MRI for monitoring septic peritonitis in an animal model (colon ascendens stent-induced peritonitis, CASP). The CASP model closely mimics that of human disease and is highly standardized. The most frequently employed readout parameter in mouse CASP studies is prolonged or decreased rate of survival. Monitoring the progression of peritonitis via MRI could provide a helpful tool in the evaluation of severity. The use of alternative readout systems could very well reduce the number of research animals. Perspectively, clinical improvement after certain treatment could be classified. Methods: This study describes for the first time MRI findings following the induction of septic peritonitis in mice using the CASP model. Two sublethal groups of mice with septic peritonitis were investigated. Each had received one of two differing stent diameters in order to control the leakage of feces into the abdominal cavity. Each mouse served as its own control. Imaging and analyses were performed blinded. Gut diameters, stomach volume, abdominal organ wall diameters, and volume of the adrenal glands were measured. Serum corticosterone levels were detected using ELISA. Serum IL-6, TNF-α, IL-1β, and IL-10 levels were screened by cytometric bead array. Statistical analysis was performed using the Mann-Whitney U test for nonparametric probes and the Kruskal-Wallis and t tests. Results: Using a 7-tesla MRI scanner 24 and 48 h after induction of septic peritonitis, interenteric fluid, organ swelling of spleen and adrenal glands, as well as dilatation of the stomach were compared to nonseptic conditions. Swelling of adrenal glands resulted in an increased serum corticosterone level. In addition, the wall of the intestine bowel was thickened. Based upon these findings, an MRI score (MRI sepsis score, MSS) for abdominal sepsis in mice was established. Reduced stent sizes led to reduced severity of the abdominal sepsis, which could be reproduced in the MSS, which is described here for the first time. Conclusions: Intraabdominal variations during septic peritonitis are detectable by MRI techniques. MRI methods should become a more important tool for the evaluation of abdominal peritonitis. MSS could provide an interesting tool for the evaluation of therapeutic strategies.
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Murando, Federica, Andrea Peloso, and Lorenzo Cobianchi. "Experimental Abdominal Sepsis: Sticking to an Awkward but Still Useful Translational Model." Mediators of Inflammation 2019 (December 5, 2019): 1–8. http://dx.doi.org/10.1155/2019/8971036.
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Animal models are widely used to replicate human intra-abdominal infections. Different methodologies have been described and proposed in the scientific literature, including injection and surgical models. The aim of this review is to recapitulate the advantages and disadvantages of each method to help choose the most appropriate model for individual experimental purposes.
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Young, John S., Sean F. Monaghan, Chun S. Chung, William G. Cioffi, Alfred Ayala, and Daithi S. Heffernan. "Divergent Invariant Natural Killer T-Cell Response to Sepsis of Abdominal vs. Non-Abdominal Origin in Human Beings." Surgical Infections 16, no. 1 (February 2015): 29–35. http://dx.doi.org/10.1089/sur.2014.057.
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SIMMS, H. HANK, and RONALD DʼAMICO. "Intra-abdominal sepsis alters tumor necrosis factor-α and interleukin-1β binding to human neutrophils." Critical Care Medicine 20, no. 1 (January 1992): 11–16. http://dx.doi.org/10.1097/00003246-199201000-00009.
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Cirioni, Oscar, Andrea Giacometti, Roberto Ghiselli, Cristina Bergnach, Fiorenza Orlando, Carmela Silvestri, Federico Mocchegiani, et al. "LL-37 Protects Rats against Lethal Sepsis Caused by Gram-Negative Bacteria." Antimicrobial Agents and Chemotherapy 50, no. 5 (May 2006): 1672–79. http://dx.doi.org/10.1128/aac.50.5.1672-1679.2006.
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ABSTRACT We investigated the efficacy of LL-37, the C-terminal part of the only cathelicidin in humans identified to date (termed human cationic antimicrobial protein), in three experimental rat models of gram-negative sepsis. Adult male Wistar rats (i) were given an intraperitoneal injection of 1 mg Escherichia coli 0111:B4 LPS, (ii) were given 2 × 1010 CFU of Escherichia coli ATCC 25922, or (iii) had intra-abdominal sepsis induced via cecal ligation and puncture. For each model, all animals were randomized to receive intravenously isotonic sodium chloride solution, 1-mg/kg LL-37, 1-mg/kg polymyxin B, 20-mg/kg imipenem, or 60-mg/kg piperacillin. Lethality; growth of bacteria in blood, peritoneum, spleen, liver, and mesenteric lymph nodes; and endotoxin and tumor necrosis factor alpha (TNF-α) concentrations in plasma were evaluated. All compounds reduced lethality compared to levels in controls. Endotoxin and TNF-α plasma levels were significantly higher in conventional antibiotic-treated rats than in LL-37- and polymyxin B-treated animals. All drugs tested significantly reduced bacterial growth compared to saline treatment. No statistically significant differences between LL-37 and polymyxin B were noted for antimicrobial and antiendotoxin activities. LL-37 and imipenem proved to be the most effective treatments in reducing all variables measured. Due to its multifunctional properties, LL-37 may become an important future consideration for the treatment of sepsis.
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Yin, Mei, Lei Si, Weidong Qin, Chen Li, Jianning Zhang, Hongna Yang, Hui Han, et al. "Predictive Value of Serum Albumin Level for the Prognosis of Severe Sepsis Without Exogenous Human Albumin Administration: A Prospective Cohort Study." Journal of Intensive Care Medicine 33, no. 12 (December 26, 2016): 687–94. http://dx.doi.org/10.1177/0885066616685300.
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Background: The prognostic significance of serum albumin levels in patients with sepsis has previously been reported; however, these studies have not excluded the potential confounding effect of exogenous albumin administration. In this study, we investigate the predictive value of serum albumin for the prognosis of severe sepsis without the interference of exogenous albumin administration. Methods: A prospective cohort study was conducted from April to November 2014 in the internal and surgical intensive care units of a tertiary care hospital. During the study period, due to a supply shortage, patients were not treated with human albumin. Serum albumin levels were measured, and laboratory and clinical data were collected at the onset of severe sepsis. Prognostic factors were analyzed using receiver operating characteristic curve and multivariate Cox proportional hazard regression analysis. Survival was assessed by Kaplan-Meier method. Results: One hundred sixteen patients were included in the study. The overall 28-day mortality was 26.7%. The most common infection sources were lower respiratory tract, abdomen/pelvis, and bloodstream. Compared to patients who survived, those who died had lower serum albumin levels and higher Acute Physiology and Chronic Health Evaluation II (APACHE II) and Sequential Organ Failure Assessment (SOFA) scores. Receiver operating characteristic curves demonstrate that albumin level is a strong predictor of 28-day mortality, and the optimal cutoff value maximizing sensitivity and specificity is 29.2 g/L. Through multivariate Cox regression analysis, low serum albumin levels (<29.2 g/L) and APACHE II scores are identified as independent risk factors for mortality. Patients with lower serum albumin levels more often had abdominal/pelvic sources of infection, acute kidney or liver injury, septic shock, and higher APACHE II and SOFA scores. The 28-day survival rate was lower for patients with serum albumin below 29.2 g/L than for patients with serum albumin at or above this level. Conclusion: Having excluded potential confounding effect of exogenous albumin administration, low serum albumin levels are associated with an increased risk of death in patients with severe sepsis.
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Papoff, Paola, Giancarlo Ceccarelli, Gabriella d'Ettorre, Carla Cerasaro, Elena Caresta, Fabio Midulla, and Corrado Moretti. "Gut Microbial Translocation in Critically Ill Children and Effects of Supplementation with Pre- and Pro Biotics." International Journal of Microbiology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/151393.
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Bacterial translocation as a direct cause of sepsis is an attractive hypothesis that presupposes that in specific situations bacteria cross the intestinal barrier, enter the systemic circulation, and cause a systemic inflammatory response syndrome. Critically ill children are at increased risk for bacterial translocation, particularly in the early postnatal age. Predisposing factors include intestinal obstruction, obstructive jaundice, intra-abdominal hypertension, intestinal ischemia/reperfusion injury and secondary ileus, and immaturity of the intestinal barrier per se. Despite good evidence from experimental studies to support the theory of bacterial translocation as a cause of sepsis, there is little evidence in human studies to confirm that translocation is directly correlated to bloodstream infections in critically ill children. This paper provides an overview of the gut microflora and its significance, a focus on the mechanisms employed by bacteria to gain access to the systemic circulation, and how critical illness creates a hostile environment in the gut and alters the microflora favoring the growth of pathogens that promote bacterial translocation. It also covers treatment with pre- and pro biotics during critical illness to restore the balance of microbial communities in a beneficial way with positive effects on intestinal permeability and bacterial translocation.
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Kaye, Sarrah. "Chronic uterine abscess in a Bolivian grey titi monkey (Plecturocebus donacophilus)." Veterinary Record Case Reports 8, no. 3 (August 2020): e001138. http://dx.doi.org/10.1136/vetreccr-2020-001138.
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An 11-year-old, reproductively active female Bolivian grey titi monkey (Plecturocebus donacophilus) in a zoological institution was presented for abdominal distension without concurrent clinical signs. Physical examination and imaging studies detected a uterine mass. Preoperative bloodwork revealed anaemia and hyperglobulinaemia. Hysterectomy was performed, but the patient died under anaesthesia. Histopathological examination found a chronic uterine abscess with effacement of the uterine wall and generalised inflammation consistent with sepsis. This case documents an uncommon reproductive tract lesion in a New World primate, and demonstrates the value of routine reproductive health monitoring in non-human primates, as not all pathologies will have clinical signs perceptible by caretakers. Earlier diagnosis may have resulted in an improved outcome in this case. Uterine abscess could be a differential diagnosis in cases of abdominal mass effect or distension in female titi monkeys.
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Yuan, Yujie, Dongsheng Yan, Gang Han, Guosheng Gu, and Jianan Ren. "Complement C3 depletion compromises the outcomes of human abdominal sepsis: a link to the expansion of regulatory T cells." Journal of the American College of Surgeons 217, no. 3 (September 2013): S46—S47. http://dx.doi.org/10.1016/j.jamcollsurg.2013.07.095.
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Stasi, Alessandra, Giuseppe Castellano, Elena Ranieri, Barbara Infante, Giovanni Stallone, Loreto Gesualdo, and Giuseppe Stefano Netti. "SARS-CoV-2 and Viral Sepsis: Immune Dysfunction and Implications in Kidney Failure." Journal of Clinical Medicine 9, no. 12 (December 15, 2020): 4057. http://dx.doi.org/10.3390/jcm9124057.
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causal agent of coronavirus disease 2019 (COVID-19), first emerged in Wuhan, China. The clinical manifestations of patients infected with COVID-19 include fever, cough, and dyspnea, up to acute respiratory distress syndrome (ARDS) and acute cardiac injury. Thus, a lot of severe patients had to be admitted to intensive care units (ICU). The pathogenic mechanisms of SARS-CoV-2 infection are mediated by the binding of SARS-CoV-2 spikes to the human angiotensin-converting enzyme 2 (ACE-2) receptor. The overexpression of human ACE-2 is associated with the disease severity in SARS-CoV-2 infection, demonstrating that viral entry into cells is a pivotal step. Although the lung is the organ that is most commonly affected by SARS-CoV-2 infection, acute kidney injury (AKI), heart dysfunction and abdominal pain are the most commonly reported co-morbidities of COVID-19. The occurrence of AKI in COVID-19 patients might be explained by several mechanisms that include viral cytopathic effects in renal cells and the host hyperinflammatory response. In addition, kidney dysfunction could exacerbate the inflammatory response started in the lungs and might cause further renal impairment and multi-organ failure. Mounting recent evidence supports the involvement of cardiovascular complications and endothelial dysfunction in COVID-19 syndrome, in addition to respiratory disease. To date, there is no vaccine, and no specific antiviral medicine has been shown to be effective in preventing or treating COVID-19. The removal of pro-inflammatory cytokines and the shutdown of the cytokine storm could ameliorate the clinical outcome in severe COVID-19 cases. Therefore, several interventions that inhibit viral replication and the systemic inflammatory response could modulate the severity of the renal dysfunction and increase the probability of a favorable outcome.
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Newsome, Courtni T., Estefany Flores, Alfred Ayala, Stephen Gregory, and Jonathan S. Reichner. "Improved Antimicrobial Host Defense in Mice following Poly-(1,6)-β-d-Glucopyranosyl-(1,3)-β-d-Glucopyranose Glucan Treatment by a Gender-Dependent Immune Mechanism." Clinical and Vaccine Immunology 18, no. 12 (October 5, 2011): 2043–49. http://dx.doi.org/10.1128/cvi.05202-11.
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ABSTRACTClinical trials with biological modifiers targeting specific inflammatory mediators associated with severe sepsis have shown no or limited survival benefit. The approach taken in studies reported here was to limit the point source of intra-abdominal infection by potentiating innate immune function, thereby lessening the severity of sepsis and improving survival. Soluble beta-glucans, glucose polymers of the fungal cell wall, have been shown to stimulate innate immune host defense in animal and human studies when administered prior to an infectious challenge. We evaluated the effects of poly-(1,6)-β-d-glucopyranosyl-(1,3)-β-d-glucopyranose glucan (PGG glucan) on overall survival when administered intraperitoneally after the onset of polymicrobial infection by cecal ligation and puncture (CLP). Since gender-dependent differences in host immune response to infection have been reported, male and female mice were prospectively stratified for PGG glucan treatment. Outbred CD-1 mice were administered 10 mg/kg of body weight PGG glucan or the polysaccharide control, dextran, 1 h after CLP. Six hours after CLP, blood samples were obtained for cytokine measurements. Surprisingly, a gender-dependent effect on the response to PGG glucan was revealed. PGG glucan enhanced survival in female mice over a 10-day period, but survival in males was improved for only 24 h. In female mice, PGG glucan reduced interleukin-6 (IL-6) and IL-10 levels and reduced the bacterial burden in the liver. Ovariectomy abrogated the response to PGG glucan. Together, the translational potential of these findings is the indicated use of PGG glucan given locally, rather than intravenously, for improved source control during the management of sepsis. This therapy does not require prophylactic beta-glucan administration.
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Rabuel, Christophe, Estelle Renaud, David Brealey, Philippe Ratajczak, Thibaut Damy, Arnaud Alves, Aïda Habib, Mervyn Singer, Didier Payen, and Alexandre Mebazaa. "Human Septic Myopathy: Induction of Cyclooxygenase, Heme Oxygenase and Activation of the Ubiquitin Proteolytic Pathway." Anesthesiology 101, no. 3 (September 1, 2004): 583–90. http://dx.doi.org/10.1097/00000542-200409000-00006.
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Background Skeletal muscle failure and wasting are manifestations of sepsis in humans that leads to serious and prolonged complications. The authors investigated the role of the major proinflammatory and antiinflammatory pathways, namely the inducible isoforms cyclooxygenase (COX-2) and heme oxygenase (HO-1), and the ubiquitin proteolytic pathway in skeletal muscle of septic patients. Methods Protein expression was detected by Western blot techniques. Muscle biopsies were taken from two muscle groups, rectus abdominis and vastus lateralis, of septic and control patients. Results The study showed an increase in COX-2 and HO-1 proteins expression and an activation of the proteolytic ubiquitin pathway with a parallel increase in free ubiquitin and ubiquitinated proteins in skeletal muscle of septic but not of control patients. In addition, those patients who would die from septic shock expressed more COX-2 and HO-1 proteins in muscle biopsies than did those patients who would survive. Conclusions This study showed a marked involvement of local proinflammatory and antiinflammatory pathways and, more importantly, demonstrated the existence of an active ubiquitin proteolytic pathway in skeletal muscle of septic patients. Activation of ubiquitin pathway could be involved in sepsis-related muscle catabolism and wasting.
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Tucker, Erik I., Melani Helm, Owen JT McCarty, Sawan Hurst, David Gailani, and Andras Gruber. "Factor XI Inhibitor Antibody Treatment Improves Survival In a Murine Polymicrobial Sepsis Model." Blood 116, no. 21 (November 19, 2010): 820. http://dx.doi.org/10.1182/blood.v116.21.820.820.
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Abstract Abstract 820 Sepsis results in a systemic inflammatory state that is frequently accompanied by intravascular coagulation and fibrinolysis, resulting in a coagulopathy with thrombotic and hemorrhagic components (disseminated intravascular coagulation– DIC). We have shown that the plasma coagulation protease factor XI (FXI) contributes substantially to experimental thrombus formation in baboons and mice, but does not appear to be essential for hemostasis. These results are supported by studies in human populations that show FXI deficiency confers a decreased risk of thrombotic ischemic stroke and deep venous thrombosis, while the associated bleeding diathesis is often mild. FXI appears to contribute to lethal consumptive coagulopathy in protein C deficient mice, while FXI deficiency reduces DIC and prolongs survival of surgical cecal-ligation and puncture (CLP)-induced abdominal sepsis in mice. Taken together, these data suggest that FXI may be an important contributor to the response leading to DIC in sepsis, and that inhibiting FXI may be a safer therapeutic alternative in this setting to activated protein C (APC), which can exacerbate hemorrhage. To investigate the contribution of FXI to consumptive coagulopathy and mortality in sepsis we used the standard CLP polymicrobial sepsis model. To inhibit FXI in the mouse, we developed a new murine anti-mouse FXI monoclonal antibody (14E11) that targets the Apple 2 domain of FXI, and has been shown in vitro to inhibit the activation of FXI by factor XIIa, while not significantly inhibiting activation by thrombin. A single injection of 14E11 (4 mg/kg, SC) prolonged the aPTT of mice up to 3-fold for 48 hrs. Following CLP, the abdomen was closed and mice were treated with vehicle (PBS, SC), APC (6 mg/kg, SC), or 14E11 (4 mg/kg, SC) (n=20 for each group). Overall survival was 45% for vehicle, 15% for APC, and 80% for 14E11 treated mice (P<0.001 for 14E11 vs. both APC and vehicle). 24 hrs after CLP, platelet count in vehicle, APC, and 14E11 treated mice (n=8 each) were lower by 24±7%, 25±5%, and 12±6%, and leukocyte counts were lower by 51±15%, 42±14%, and 43±13% respectively, compared with baseline. Thrombin/antithrombin complex levels were higher in the vehicle treated group 24 hrs after CLP (5.0±1.2 μg/L) compared with 2.2±0.2 μg/L in normal healthy mice (P<0.05), while APC and 14E11 treated groups showed only moderately elevated TAT levels (2.6±0.2 and 2.7±0.4 μg/L, respectively). The pharmacological effects of 14E11 later in the course of sepsis and the apparent poor outcome of early APC treatment remain to be evaluated. In a separate cohort (n=12 each), tail-clip bleeding times were 12.8±1.0, 17.9±1.8, and 12.1±1.7 min for vehicle, APC, and 14E11 treated animals respectively (P<0.05 for APC vs. vehicle and 14E11) 30min after injection. In summary, the outcome was better for 14E11 treated mice in CLP-induced sepsis compared to vehicle or APC treatment, and the data indicate that consumptive coagulopathy may be less severe following FXI inhibition. Furthermore, mice treated with 14E11 showed no increase in bleeding compared with vehicle treatment, while APC significantly prolonged the tail bleeding time. The results suggest that therapeutic inhibition of FXI, by specifically inhibiting FXI activation by FXIIa, could be beneficial in treating sepsis-related DIC. It is also possible that inhibition of FXI may limit DIC with a lower risk of exacerbating bleeding when compared to anticoagulant therapies such as heparin or APC. Disclosures: Tucker: Aronora,LLC: Employment, Equity Ownership, Patents & Royalties. Helm:Aronora,LLC: Employment. Gruber:Aronora,LLC: Consultancy, Equity Ownership, Patents & Royalties.
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Deng, X., X. Wang, and R. Andersson. "Endothelial barrier resistance in multiple organs after septic and nonseptic challenges in the rat." Journal of Applied Physiology 78, no. 6 (June 1, 1995): 2052–61. http://dx.doi.org/10.1152/jappl.1995.78.6.2052.
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Local variations in endothelial permeability, hypothesized to play a role in the development of multiple-organ injury, were measured by 125I-labeled human serum albumin flux and leakage index in rats with a variety of challenges. The albumin flux significantly increased in the peritoneum, pancreas, stomach, and liver in acute pancreatitis; in the peritoneum and liver in abdominal sepsis; in the spleen, proximal small intestine, colon, liver, lungs, heart, and muscle in bacteremia; in the kidneys, liver, lungs, heart, brain, and muscle in endotoxemia; and in the peritoneum, proximal small intestine, colon, kidneys, liver, and heart after bradykinin administration. A redistribution of the tissue blood content, measured by 51Cr-labeled red blood cells, was noted. An increased albumin leakage index, assaying endothelial permeability considering local hemodynamic alterations, was noted in various organs in the different experimental groups. Thus septic and nonseptic challenges induce endothelial barrier injury. The endothelial resistance appears to be organ and/or tissue dependent and associated with a redistribution of blood.
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Yuan, Yujie, Dongsheng Yan, Gang Han, Guosheng Gu, and Jianan Ren. "Complement C3 depletion links to the expansion of regulatory T cells and compromises T-cell immunity in human abdominal sepsis: A prospective pilot study." Journal of Critical Care 28, no. 6 (December 2013): 1032–38. http://dx.doi.org/10.1016/j.jcrc.2013.09.007.
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Schietroma, Mario, Federica Piccione, Francesco Carlei, Marco Clementi, Zuleyka Bianchi, Fabiola De Vita, and Gianfranco Amicucci. "Peritonitis from Perforated Appendicitis: Stress Response after Laparoscopic or Open Treatment." American Surgeon 78, no. 5 (May 2012): 582–90. http://dx.doi.org/10.1177/000313481207800541.
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Elevated intra-abdominal pressure during laparoscopy may promote systemic inflammatory response. In patients with generalized peritonitis from perforated appendicitis, we sought to compare acute phase response and immunologic status from laparoscopic and open approach. One hundred and forty-seven consecutive patients underwent appendectomy for perforated appendicitis (73 patients had laparoscopic appendectomy and 74 patients had open appendectomy. Bacteremia, endotoxemia, white blood cells, peripheral lymphocytes subpopulation, human leukocyte antigen-DR (HLA-DR), neutrophil-elastase, interleukin-1 and 6 (IL-1 and 6), and C-reactive protein were investigated. One hour after intervention, bacteremia was significantly higher in the open group compared with the laparoscopic group ( P < 0.05). A significantly higher concentration of systemic endotoxin was detected intraoperatively in the open group of patients in comparison with the laparoscopic group ( P < 0.05). Laparotomy caused a significant increase in neutrophil concentration, neutrophil-elastase, IL-1 and 6, and C-reactive protein and a decrease of HLA-DR. We recorded 6 cases (8.1%) of intra-abdominal abscess in the open group and one (1.3%) in the laparoscopic group ( P < 0.05). Open appendectomy, in case of peritonitis, increased the incidence of bacteremia, endotoxemia, and systemic inflammation compared with laparoscopic appendectomy. Early enhanced postoperative systemic inflammation may cause lower transient immunologic defense after laparotomy (decrease of HLA-DR), leading to enhanced sepsis in these patients.
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Shrestha, Prakash, Sean E. O’Neil, Barbara S. Taylor, Olaoluwa Bode-Omoleye, and Gregory M. Anstead. "Hemoptysis in the Immunocompromised Patient: Do Not Forget Strongyloidiasis." Tropical Medicine and Infectious Disease 4, no. 1 (February 12, 2019): 35. http://dx.doi.org/10.3390/tropicalmed4010035.
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Strongyloidiasis, due to infection with the nematode Strongyloides stercoralis, affects millions of people in the tropics and subtropics. Strongyloides has a unique auto-infective lifecycle such that it can persist in the human host for decades. In immunosuppressed patients, especially those on corticosteroids, potentially fatal disseminated strongyloidiasis can occur, often with concurrent secondary infections. Herein, we present two immunocompromised patients with severe strongyloidiasis who presented with pneumonia, hemoptysis, and sepsis. Both patients were immigrants from developing countries and had received prolonged courses of corticosteroids prior to admission. Patient 1 also presented with a diffuse abdominal rash; a skin biopsy showed multiple intradermal Strongyloides larvae. Patient 1 had concurrent pneumonic nocardiosis and bacteremia with Klebsiella pneumoniae and Enterococcus faecalis. Patient 2 had concurrent Aspergillus and Candida pneumonia and developed an Aerococcus meningitis. Both patients had negative serologic tests for Strongyloides; patient 2 manifested intermittent eosinophilia. In both patients, the diagnosis was afforded by bronchoscopy with lavage. The patients were successfully treated with broad-spectrum antibiotics and ivermectin. Patient 1 also received albendazole. Strongyloidiasis should be considered in the differential diagnosis of hemoptysis in immunocompromised patients with possible prior exposure to S. stercoralis.
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Binti Kamilen, Khalilah Alhuda, and Mohd Yusran Othman. "Intrauterine Intussusception Presenting as Fetal Ascites and Meconium Peritonitis." International Journal of Human and Health Sciences (IJHHS) 5, no. 0-2 (September 23, 2021): 18. http://dx.doi.org/10.31344/ijhhs.v5i0-2.336.
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Intussusception is a well-known cause of intestinal obstruction in children. Its occurrence in fetus as an intrauterine incidence is extremely rare and poses a diagnostic difficulty. Intrauterine intussusception may result in intestinal atresia once the gangrenous segment resorbed. However, a very late occurrence of intussusception just prior to delivery may present as meconium peritonitis. We are reporting a case of premature baby who was born at 35 weeks gestation via emergency caesarean for breech in labour. Routine scan 4 days prior to the delivery showed evidence of fetal ascites. She was born with good Apgar Score and weighed 2.5kg. Subsequently she developed respiratory distress syndrome requiring mechanical ventilation. She passed minimal meconium once after birth then developed progressive abdominal distension and vomiting. Abdominal radiograph on day 4 of life revealed gross pneumoperitoneum and bedside percutaneous drain was inserted to ease the ventilation. Upon exploratory laparotomy, a single ileal perforation was seen 20cm from ileocecal junction with an intussusceptum was seen in the distal bowel. Gross meconium contamination and bowel edema did not favour the option of primary anastomosis, thus stoma was created. Reversal of stoma was performed a month later and she recovered well. Fetus with a complicated intrauterine intussusception may present with fetal ascites and their postnatal clinical and radiological findings need to be carefully assessed for evidence of meconium peritonitis; in which a timely surgical intervention is required to prevent the sequelae of prolonged intraabdominal sepsis in this premature baby.International Journal of Human and Health Sciences Supplementary Issue-2: 2021 Page: S18
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Arnold, J., D. Leinhardt, G. Carlson, P. Gray, R. A. Little, and M. H. Irving. "Thermogenic and hormonal responses to amino acid infusion in septic humans." American Journal of Physiology-Endocrinology and Metabolism 263, no. 1 (July 1, 1992): E129—E135. http://dx.doi.org/10.1152/ajpendo.1992.263.1.e129.
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Metabolic effects of a commercially available amino acid infusate were investigated in five preoperative patients with abdominal sepsis and five healthy subjects. Oxygen consumption (VO2) was measured continuously during the 3-h study, and blood samples were taken regularly for hormone and metabolite analyses. During 1 h of preinfusion measurements, VO2 was 15% higher (P less than 0.05) in the septic patients. Preinfusion plasma cortisol, glucagon, and catecholamines were also significantly elevated in the septic group. The amino acid solution (9 g nitrogen; 950 kJ; 227 kcal) was infused into each subject through their central venous catheter during the 2nd and 3rd h of the study. VO2 increased similarly in both groups by approximately 21% during the infusion (P less than 0.05), whereas respiratory quotient increased significantly in only the controls (P less than 0.05). Plasma insulin and glucagon concentrations rose significantly in both groups during the infusion, despite little change in glucose levels. Plasma norepinephrine increased in both groups, although the response was significant in only the control subjects. In summary, the amino acid infusate stimulated metabolic rate similarly in the septic and nonseptic subjects.
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Boldingh, Quirine J. J., Fleur E. E. de Vries, and Marja A. Boermeester. "Abdominal sepsis." Current Opinion in Critical Care 23, no. 2 (April 2017): 159–66. http://dx.doi.org/10.1097/mcc.0000000000000388.
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Peetermans, W. E., and M. Hiele. "Abdominal Sepsis." Acta Clinica Belgica 53, no. 4 (January 1998): 251–54. http://dx.doi.org/10.1080/17843286.1998.11754170.
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Nychytailo, M. Yu. "Abdominal sepsis." Infusion & Chemotherapy, no. 3.2 (December 15, 2020): 231–33. http://dx.doi.org/10.32902/2663-0338-2020-3.2-231-233.
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Background. Sepsis is a life-threatening acute organ dysfunction that occurs as a result of dysregulation of the macroorganism’s response to infection. Septic shock is a variant of sepsis characterized by the circulatory failure, manifested by hypotension and increased lactate levels >2 mmol/L despite adequate infusion, which requires the administration of vasopressors to maintain average blood pressure >65 mm Hg.
Objective. To describe the management of patients with abdominal sepsis.
Materials and methods. Analysis of literature data on this topic.
Results and discussion. Complicated intra-abdominal infection (IAI) is the growth of pathogenic microorganisms in a usually sterile abdominal cavity, usually due to the perforation of the hollow organs. Uncomplicated IAI involves transmural inflammation of the digestive tract, which does not spread beyond the hollow organ. If uncomplicated IAI are not treated, there is a possibility that they will progress to complicated ones. Measures to control the source of infection include the drainage of abscesses or places of accumulation of infected fluid, removal of necrotic infected tissues and restoration of the anatomy and functions of the affected area. Several multivariate studies have found that failure to adequately control the source of infection is a risk factor for adverse outcomes and death in patients with IAI. Surviving sepsis and other recommendations also support the need for early control of the source of infection. In a study by B. Tellor et al. (2012) mortality was 9.5 % among individuals with adequate control of the infection source and 33.3 % among patients who failed to achieve such control. In some situations, it is advisable to manage patients conservatively. Thus, in appendicular infiltration, most studies have demonstrated the benefits of conservative management (Andersson R.E., Petzold M.G., 2007). Management of IAI without final control of the primary source is possible in cases where the organism has already overcome the infection, and surgery can only increase the number of complications. In general, patients with localized infections may need less invasive management. Thus, percutaneous drainage can be used for localized accumulations of fluid in the abdominal cavity. 80-92 % of drainage procedures are successful on the first attempt. <5 % of patients require surgical treatment. Such drainage procedures are used in infected pancreatic necrosis, and the final debridement of the infection source may be delayed. In critically ill patients, damage control laparotomy and limited intervention (resection without reanastomosis or stoma formation, temporary drainage and tamponade of the abdominal cavity if necessary, temporary closure of the abdominal cavity) are performed to control the infection. Indications for damage control laparotomy include inability to achieve adequate control of the source of IAI during primary laparotomy, hemodynamic instability, the need to re-evaluate the condition of the problematic anastomosis, and diffuse peritonitis. A prospective study of staged laparotomies revealed a shorter length of stay in the intensive care unit, a lower incidence of complications and lower treatment costs using this method compared to the standard one. Antibacterial support of surgical interventions is an important aspect of treatment. In conditions of increasing antibiotic resistance, antibiotics should be prescribed strictly in accordance with the recommendations and for as short effective period as possible.
Conclusions. 1. Despite the fact that approaches are changing, control of the IAI source remains the main method of treatment of most patients with IAI. 2. The choice of empirical antibacterial therapy should be based on the risk assessment and potential of resistant bacteria. 3. The duration of antimicrobial therapy can be significantly reduced (4 days).
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Rajput, Ibrahim, Peter Lodge, and Geoffrey I. Sandle. "Mo1959 Basolateral IKCA Channel Inhibition by Octreotide Prevents the Increase in Mucosal Permeability Induced by Chemical Hypoxia in Human Colon: Implications for Preventing Sepsis After Major Abdominal Surgery." Gastroenterology 146, no. 5 (May 2014): S—702. http://dx.doi.org/10.1016/s0016-5085(14)62549-x.
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Jacobson, Richard A., Kiedo Wienholts, Ashley J. Williamson, Sara Gaines, Sanjiv Hyoju, Harry van Goor, Alexander Zaborin, Benjamin D. Shogan, Olga Zaborina, and John C. Alverdy. "Enterococcus faecalis exploits the human fibrinolytic system to drive excess collagenolysis: implications in gut healing and identification of druggable targets." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 1 (January 1, 2020): G1—G9. http://dx.doi.org/10.1152/ajpgi.00236.2019.
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Perforations, anastomotic leak, and subsequent intra-abdominal sepsis are among the most common and feared complications of invasive interventions in the colon and remaining intestinal tract. During physiological healing, tissue protease activity is finely orchestrated to maintain the strength and integrity of the submucosa collagen layer in the wound. We (Shogan, BD et al. Sci Trans Med 7: 286ra68, 2015.) have previously demonstrated in both mice and humans that the commensal microbe Enterococcus faecalis selectively colonizes wounded colonic tissues and disrupts the healing process by amplifying collagenolytic matrix-metalloprotease activity toward excessive degradation. Here, we demonstrate for the first time, to our knowledge, a novel collagenolytic virulence mechanism by which E. faecalis is able to bind and locally activate the human fibrinolytic protease plasminogen (PLG), a protein present in high concentrations in healing colonic tissue. E. faecalis-mediated PLG activation leads to supraphysiological collagen degradation; in this study, we demonstrate this concept both in vitro and in vivo. This pathoadaptive response can be mitigated with the PLG inhibitor tranexamic acid (TXA) in a fashion that prevents clinically significant complications in validated murine models of both E. faecalis- and Pseudomonas aeruginosa-mediated colonic perforation. TXA has a proven clinical safety record and is Food and Drug Administration approved for topical application in invasive procedures, albeit for the prevention of bleeding rather than infection. As such, the novel pharmacological effect described in this study may be translatable to clinical trials for the prevention of infectious complications in colonic healing. NEW & NOTEWORTHY This paper presents a novel mechanism for virulence in a commensal gut microbe that exploits the human fibrinolytic system and its principle protease, plasminogen. This mechanism is targetable by safe and effective nonantibiotic small molecules for the prevention of infectious complications in the healing gut.
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Nikiforov, Ivan, John Goldman, Pramil Cheriyath, Anix Vyas, and Vinod Nookala. "Aeromonas hydrophilaSepsis Associated with Consumption of Raw Oysters." Case Reports in Infectious Diseases 2014 (2014): 1–3. http://dx.doi.org/10.1155/2014/163040.
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Introduction. Aeromonas hydrophilais a gram negative bacillus that is native to aquatic environments that is increasingly reported in humans. This case is remarkable forA. hydrophilawith an initial presentation of acute pancreatitis.Case Presentation.A 61-year-old male presented to the emergency department with nausea, vomiting, and abdominal pain for two days. His past medical history was significant for alcohol abuse. Initial laboratory examination showed an elevated white blood cell count, elevated lipase, and elevated liver function tests (LFT). Computer tomography (CT) showed peripancreatic inflammatory changes and retroperitoneal free fluid, suggestive of acute pancreatitis. The patient was treated with intravenous (IV) fluids and IV meropenem. After two days, the patient developed sepsis and respiratory failure and was intubated. Blood cultures were positive forAeromonas hydrophilasensitive to ciprofloxacin which was added to his treatment. Additionally, it was discovered that this patient had recently vacationed in Florida where he consumed raw oysters. He was discharged home on the eighth day of the hospital admission.Conclusion.This is a rare case ofA. hydrophilasepsis in an elderly patient with acute pancreatitis and a history of consumption of raw oysters. This case suggests thatA. hydrophilacan cause disseminated infection in immunocompetent individuals.
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Bartlett, John G. "Intra-abdominal sepsis." Medical Clinics of North America 79, no. 3 (1995): 599–617. http://dx.doi.org/10.1016/s0025-7125(16)30059-1.
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Loganathan, Arun. "Intra-abdominal sepsis." Surgery (Oxford) 33, no. 11 (November 2015): 553–58. http://dx.doi.org/10.1016/j.mpsur.2015.08.007.
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Russell, R. C. G. "Intra-Abdominal Sepsis." Journal of the Royal Society of Medicine 80, no. 8 (August 1987): 471–72. http://dx.doi.org/10.1177/014107688708000801.
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Bretland, P. M. "Intra-Abdominal Sepsis." Journal of the Royal Society of Medicine 80, no. 8 (August 1987): 528–30. http://dx.doi.org/10.1177/014107688708000823.
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Foitzik, Thomas, and Norbert Runkel. "Intra-abdominal sepsis." Current Opinion in Infectious Diseases 9, no. 5 (October 1996): 353–58. http://dx.doi.org/10.1097/00001432-199610000-00012.
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Krukowski, Z. H. "Postoperative abdominal sepsis." British Journal of Surgery 75, no. 12 (December 1988): 1153–54. http://dx.doi.org/10.1002/bjs.1800751202.
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Leaper, D. J., M. Irving, J. Bancewicz, and M. Mughal. "Server abdominal sepsis." British Journal of Surgery 73, no. 8 (August 1986): 682–83. http://dx.doi.org/10.1002/bjs.1800730839.
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Pendela, Venkata Satish, Anisleidys Munoz, JulieAnn Warner, and Roopa Yarlagadda. "Case Report: Germ cell tumor presenting as cecal mass." F1000Research 8 (October 10, 2019): 1737. http://dx.doi.org/10.12688/f1000research.20774.1.
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Extra gonadal germ cell tumors most frequently occur in the anterior mediastinum, retro-peritoneum, and pineal and suprasellar regions. The infrequency of its occurrence inside gastrointestinal tract makes it an arduous diagnostic challenge. A 23 year old male with no significant past medical history presented to the emergency department with increasing abdominal pain, diarrhea, episodic vomiting for 3 weeks. Review of systems was positive for melena and shortness of breath on exertion. Fullness and irregularity along with tenderness was noted around the right iliac region. CT scan (computed tomography) of the abdomen revealed a cecal mass with multiple metastases to liver, lungs and abdominal lymph nodes. Colonic endoscope was performed but it could not be advanced beyond the cecal mass. Biopsies from the mass were reported as poorly differentiated metastatic carcinoma. During the course of hospitalization, he developed symptomatic small bowel obstruction with perforation. Colonic resection was performed and histology showed Germ-Cell Tumor. Beta HCG level was 118789 IU/L suggestive of a non-seminomatous germ cell tumor. Ultrasound of the scrotum, MRI brain (magnetic resonance imaging) and CT scan of the chest did not reveal a primary tumor. Chemotherapy was started with Bleomycin, Etoposide and Cisplatin after which beta human chorionic gonadotropin (HCG) levels dropped dramatically. His hospital course got complicated with neutropenic sepsis with shock which progressed to multi-organ dysfunction and unfortunately, he succumbed to the disease burden. This case demonstrates one of the rare presentations of extragonadal germ cell tumors and the diagnostic challenges associated with it. Very few cases have been reported in the literature, and none of them presented as a cecal mass. Early recognition of this presentation will help in reducing the tumor burden and the mortality associated with it, as germ cell tumors are highly susceptible to chemotherapy.
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Kim, Janice, Hilary Rosen, Kristen Angel, Azarnoush Maroufi, Samantha Tweeten, Jacqueline Lui, John Crandall, Tracy Lanier, Jane Siegel, and Akiko Kimura. "Transmission of Listeriosis in a Neonatal Intensive Care Unit Supported by Whole-Genome Sequencing." Infection Control & Hospital Epidemiology 41, S1 (October 2020): s53. http://dx.doi.org/10.1017/ice.2020.536.
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Background: Listeriosis is a rare but serious infectious disease caused by Listeria monocytogenes (LM) and predominantly transmitted through contaminated food. Moreover, 15% of listeriosis cases in the United States are pregnancy associated; nosocomial neonatal transmission in hospitals is extremely rare. In July 2018, the California Department of Public Health (CDPH) was notified of 4 patients, a mother–neonate pair and twin neonates, with listeriosis at the same hospital. The CDPH and San Diego County Health and Human Services Agency initiated an investigation to determine transmission and prevent additional infections. Methods: We reviewed medical records of the neonates and their mothers, interviewed the mothers with a detailed food exposure questionnaire, interviewed healthcare personnel (HCP), and performed an infection control assessment of the neonatal intensive care unit (NICU). CDPH performed whole-genome sequencing (WGS) on LM isolates that were then analyzed by whole-genome multilocus sequence typing (wgMLST) by the Centers for Diseases Control and Prevention (CDC) to assess relatedness in PulseNet, a public health laboratory database. The CDC also performed testing for LM on formalin-fixed placentas from the mother of the twins. Results: During a 1-week period, 4 patients with LM were identified at the hospital. A mother was admitted at 31 weeks gestation with acute abdominal and back pain that progressed with precipitous vaginal delivery and postpartum sepsis. Her neonate was resuscitated, transported to the NICU, underwent a sepsis evaluation, received antibiotics, and was transferred to another hospital within 6 hours. Maternal blood, placenta, and neonatal blood cultures grew LM. Twin neonates, born to an asymptomatic mother and present in the NICU during the index neonate’s stay, developed acute infection 4 and 6 days after the index neonate’s transfer; blood cultures confirmed LM. The LM isolates from the 4 patients were indistinguishable by wgMLST and were not related to other PulseNet isolates. LM was not detected in the twin placentas. There were no common food exposures between the mothers. At least 1 common HCP cared for all 3 neonates. Infection control lapses included lack of proper hand hygiene during the index neonate’s resuscitation and potentially after cleaning and disinfection of the neonate’s incubator. Conclusions: This report provides supportive evidence that nosocomial transmission of LM can occur during a brief NICU stay due to lapses in infection control practices. Strict adherence to standard precautions in the delivery room and NICU is imperative to prevent cross transmission.Disclosures: NoneFunding: None
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Flax, Sherri. "ADAMTS13 Immunohistochemical Expression in Normal and Diseased Equine Tissues." Blood 134, Supplement_1 (November 13, 2019): 4925. http://dx.doi.org/10.1182/blood-2019-127407.
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ADAMTS13 is a metallopeptidase primarily synthesized in the liver. Its main function is to cleave von Willebrand factor (VWF) on the endothelial surface, and thus regulate platelet adhesion at the sites of vascular injury; VWF acts as a scaffold at the site of injury for platelet activation, platelet binding, and clot formation. Platelet activation also results in the release of platelet-dense granule components (such as cytokines, pro- and anti-inflammatory factors and other bioactive molecules) that are essential regulators of coagulation, but are also associated with inflammation. Reduced activity of ADAMTS13 is found in human patients with acquired thrombotic thrombocytopenic purpura (TPP), sepsis, and DIC. Both human TTP and equine colic are histologically characterized by the presence of microthrombi. Cleavage of VWF is dependent upon allosteric activation of ADAMTS13, which is broadly conserved in many animals, including horses. Human TTP and equine idiopathic colic share several interesting clinical similarities. Both have seasonal variations, typically in summer, can be associated with viral and bacterial infections, may be hereditary, have autoimmune associations, and recur. Both TTP and equine colic are clinically characterized by fever, abdominal pain renal failure, and neurologic symptoms. Microangiopathy is the predominant pathology in both TTP and equine colic. Using tissues obtained from thirteen horses euthanized for non-thrombotic conditions, immunohistochemical stains indicate the presence of ADAMTS13 in equine liver and colon. Furthermore, in one horse with colic, immunohistochemical staining of the resected colon indicates the presence of ADAMTS13 in the aboral margin (Figure 1) and the absence ADAMTS13 staining in the diseased tissue. These findings suggest that equine colic may be an animal model of thrombotic microangiopathy, very similar to TTP. Future studies will investigate immunohistochemical detection of ADAMTS13 in human tissues. Figure 1 Disclosures No relevant conflicts of interest to declare.
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Nazareth, Helen, Stacy A. Genagon, and Thomas A. Russo. "Extraintestinal Pathogenic Escherichia coli Survives within Neutrophils." Infection and Immunity 75, no. 6 (February 12, 2007): 2776–85. http://dx.doi.org/10.1128/iai.01095-06.
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ABSTRACT Extracellular pathogenic Escherichia coli (ExPEC) strains are common causes of a variety of clinical syndromes, including urinary tract infections, abdominal infections, nosocomial pneumonia, neonatal meningitis, and sepsis. ExPEC strains are extracellular bacterial pathogens; therefore, the innate immune response (e.g., professional phagocytes) plays a crucial role in the host defense against them. Studies using the model ExPEC strain CP9 demonstrated that it is relatively resistant to neutrophil-mediated bactericidal activity. Although this could be due to resistance to phagocytosis, the ability of CP9 to survive the intracellular killing mechanisms of neutrophils is another possibility. Using a variation of the intracellular invasion assay, we studied the survival of CP9 within peripheral blood-derived human neutrophils. Our results indicated that CP9 did survive within human neutrophils, but we were unable to demonstrate that intracellular replication occurred. This finding was not unique to CP9, since when a conservative assessment of survival was used, four of six additional ExPEC strains, but not an E. coli laboratory strain, were also capable of survival within neutrophils. Initial studies in which we began to decipher the mechanisms by which CP9 is able to successfully survive intracellular neutrophil-mediated bactericidal activity demonstrated that CP9 was at least partially susceptible to the neutrophil oxidative burst. Therefore, absolute resistance to the oxidative burst is not a mechanism by which ExPEC survives within neutrophils. In addition, electron microscopy studies showed that CP9 appeared to be present in phagosomes within neutrophils. Therefore, avoidance of phagosomal uptake or subsequent escape from the phagosome does not appear to be a mechanism that contributes to CP9's survival. These findings suggest that survival of ExPEC within neutrophils may be an important virulence mechanism.
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Potapov, A. F., T. M. Tyaptirgyanova, and A. N. Kirillin. "Detoxification in Abdominal Sepsis." General Reanimatology 1, no. 3 (June 20, 2005): 32. http://dx.doi.org/10.15360/1813-9779-2005-3-32-35.
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Mureșan, Mircea Gabriel, Ioan Alexandru Balmoș, Iudita Badea, and Ario Santini. "Abdominal Sepsis: An Update." Journal of Critical Care Medicine 4, no. 4 (October 1, 2018): 120–25. http://dx.doi.org/10.2478/jccm-2018-0023.
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Abstract Despite the significant development and advancement in antibiotic therapy, life-threatening complication of infective diseases cause hundreds of thousands of deaths world. This paper updates some of the issues regarding the etiology and treatment of abdominal sepsis and summaries the latest guidelines as recommended by the Intra-abdominal Infection (IAI) Consensus (2017). Prognostic scores are currently used to assess the course of peritonitis. Irrespective of the initial cause, there are several measures universally accepted as contributing to an improved survival rate, with the early recognition of IAI being the critical matter in this respect. Immediate correction of fluid balance should be undertaken with the use of vasoactive agents being prescribed, if necessary, to augment and assist fluid resuscitation. The WISS study showed that mortality was significantly affected by sepsis irrespective of any medical and surgical measures. A significant issue is the prevalence of extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae in the clinical setting, and the reported prevalence of ESBLs intra-abdominal infections has steadily increased in Asia. Europe, Latin America, Middle East, North America, and South Pacific. Abdominal cavity pathology is second only to sepsis occurring in a pulmonary site. Following IAI (2017) guidelines, antibiotic therapy should be initiated as soon as possible after a diagnosis has been verified.
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&NA;. "UNTREATED INTRA-ABDOMINAL SEPSIS." Journal of Trauma: Injury, Infection, and Critical Care 29, no. 7 (July 1989): 1037. http://dx.doi.org/10.1097/00005373-198907000-00068.
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