Relevant bibliographies by topics / Septic shock

Contents

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

Academic literature on the topic 'Septic shock'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Septic shock"

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Hinshaw, Lerner B. "Sepsis/septic shock." Critical Care Medicine 24, no. 6 (June 1996): 1072–78. http://dx.doi.org/10.1097/00003246-199606000-00031.

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Ellrodt, A. Gray. "Sepsis and Septic Shock." Emergency Medicine Clinics of North America 4, no. 4 (November 1986): 809–40. http://dx.doi.org/10.1016/s0733-8627(20)31041-5.

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Kalil, Andre C. "Sepsis and Septic Shock." Seminars in Respiratory and Critical Care Medicine 42, no. 05 (September 20, 2021): 639–40. http://dx.doi.org/10.1055/s-0041-1735218.

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Chong, Josebelo, Tiffany Dumont, Lyndave Francis-Frank, and Marvin Balaan. "Sepsis and Septic Shock." Critical Care Nursing Quarterly 38, no. 2 (2015): 111–20. http://dx.doi.org/10.1097/cnq.0000000000000052.

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Dumont, Tiffany, Lyndave Francis-Frank, Josebelo Chong, and Marvin R. Balaan. "Sepsis and Septic Shock." Critical Care Nursing Quarterly 39, no. 1 (2016): 3–13. http://dx.doi.org/10.1097/cnq.0000000000000091.

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Murray, Michael J., and M. Kumar. "Sepsis and septic shock." Postgraduate Medicine 90, no. 1 (July 1991): 199–208. http://dx.doi.org/10.1080/00325481.1991.11700992.

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Mehta, Yatin, and Gaurav Kochhar. "Sepsis and Septic Shock." Journal of Cardiac Critical Care TSS 01, no. 01 (August 2017): 003–5. http://dx.doi.org/10.1055/s-0037-1604204.

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JAPARI, HAMID S., and GEORGE H. MCCRACKEN. "Sepsis and septic shock." Pediatric Infectious Disease Journal 11, no. 9 (September 1992): 739–49. http://dx.doi.org/10.1097/00006454-199209000-00014.

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Gobel, Barbara Holmes, and Glen J. Peterson. "Sepsis and Septic Shock." Clinical Journal of Oncology Nursing 14, no. 6 (November 26, 2010): 793–97. http://dx.doi.org/10.1188/10.cjon.793-797.

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Cecconi, Maurizio, Laura Evans, Mitchell Levy, and Andrew Rhodes. "Sepsis and septic shock." Lancet 392, no. 10141 (July 2018): 75–87. http://dx.doi.org/10.1016/s0140-6736(18)30696-2.

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Dissertations / Theses on the topic "Septic shock"

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Radhakrishnan, Jayachandran. "Functional genomics of severe sepsis and septic shock." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:2b2afd65-82e0-4847-b7ae-960635b7e884.

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Sepsis is the systemic inflammatory response to an infection. Severe sepsis with multi organ failure is one of the commonest causes of admission to intensive care units, and is associated with poor early and late outcomes. The pathophysiology of sepsis is complex, and poorly understood. This is reflected in the limited and contentious treatment options for sepsis. Genetic factors have been shown to be associated with the risk of and subsequent outcomes from infection. However, clear associations with bacterial sepsis are rare, and even when associations are present their functional effects are often unknown. Gene expression signatures in sepsis are investigated in this project using serial samples obtained from patients admitted to intensive care units with community-acquired pneumonia or faecal peritonitis. The evolving gene expression signatures that define the response to sepsis were identified with large changes seen in genes coding for ribosomal proteins RPS4Y1 and RPS26P54. The differences in the sepsis response between the two diagnostic classes were examined. The gene expression predictors of mortality in sepsis were determined and include genes from the class II MHC HLA-DRB4, HLA-DRB5 and the T cell differentiation protein MAL. The effects of important covariates on gene expression were investigated and their impact on survival related expression determined. The findings were confirmed in a validation cohort. A novel clustering of samples representing distinct inflammatory patterns in a clinically homogeneous population of sepsis patients was identified and related to differences in clinical behaviour. The biological relevance of the differentially expressed genes was ascertained by identifying enriched gene sets. The gene expression changes in sepsis were examined in the context of related clinically relevant immune phenomena: the sterile systemic inflammatory response in patients undergoing elective cardiac surgery and the phenomenon of endotoxin tolerance in PBMCs derived from healthy volunteers. The results highlight the complexities of clinical sepsis and identify hypotheses for future investigations.
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Furebring, Mia. "C5a Receptor Expression in Severe Sepsis and Septic Shock." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5832.

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Jones, K. J. "Mediators of gram-positive septic shock." Thesis, Aston University, 2003. http://publications.aston.ac.uk/12349/.

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Gram-positive bacteria are increasingly becoming more prevalent especially Staphylococcus epidermidis in association with indwelling devices. Lipopolysaccaride (LPS) is the key Gram-negative component involved in this process, but it is not clear which components of Gram-positive bacteria are responsible for progression of this often fatal disease. The aim of this thesis was to investigate the effect of bacterial components on the immune systems. Lipid S, a short chain form of lipoteichoic acid (LTA) found to be excreted from bacteria during growth in culture medium was examined along with other Gram-positive cell wall components: LTA, peptidoglycan (PG) and wall teichoic acids (WTA) and LPS from Gram-negative bacteria. Lipid S, LTA, PG and LPS but not WTA all stimulated murine macrophages and cell lines to produce significant amounts of NO, TNF-a, IL-6 and IL-1 and would induce fever and tissue damage seen in inflammatory diseases. Lipid S proved to be the most potent out of the Gram-positive samples tested. IgG antibodies in patients serum were found to bind to and cross react with lipid S and LTA. Anti-inflammatory antibiotics, platelet activating factor (PAF), PAF receptor antagonists and monoclonal antibodies (mAbs) directed to LTA, CD14 and toll-like receptors were utilised to modulate cytokine and NO production. In cell culture the anti-LTA and the anti-CD14 mAbs failed to markedly attenuate the production of NO, TNF-a, IL-6 or IL-1, the anti-TLR4 antibody did greatly inhibit the ability of LPS to stimulate cytokine production but not lipid S. The tetracyclines proved to be the most effective compounds, many were active at low concentrations and showed efficacy to inhibit both lipid S and LPS stimulated macrophages to produce NO.
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Braga, D. "TRANSCRIPTOMIC ANALYSIS IN SEPTIC SHOCK PATIENTS." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/473670.

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Introduction Septic shock, also defined as distributive shock, is a complication of sepsis, characterized by pronounced hypotension, followed by anomalous distribution of blood at vessels, organs and tissues. The hemodynamic, cellular and metabolic alterations described in septic shock patients lead to a mortality that is at present around 40%. Septic shock patients develop dysfunctions or failure to multiple organs (MOF) but the molecular mechanisms triggering tissue injury remain largely undetermined and a specific treatment for septic shock is still not available. Aim This work is part of the European Project ShockOmics, a multicentric, prospective, observational study, whose aim is to identify with a multiscale approach, molecular biomarkers in septic shock patients who develop acute heart failure. The specific aim of the present Research project is to investigate the modifications induced by septic shock on transcriptional profile, using blood cells as RNA source. This investigation is performed at different timepoints starting from admission of the patient to the intensive care unit (ICU). Materials and Methods Septic shock patients were recruited in the ICUs of Geneva and Bruxelles University Hospitals, that are Partners of ShockOmics Project. Blood samples were collected in the acute phase of the disease at ICU admission (T1), after the appropriate pharmacological intervention (T2 ) and at steady state on day 7 of the ICU stay (T3). RNA was extracted from whole blood and RNA sequencing was used to evaluate the expression level of genes, long non coding RNAs and microRNAs. We explored the dataset using PCA and unsupervised hierarchical clustering and we identified differentially expressed genes and microRNAs across conditions. Gene Ontology analysis was used to identify relevant biological processes involved in shock. We identified microRNA regulatory targets with an in silico target prediction. Results We identified two main gene expression profiles corresponding to the acute phase of shock and to the condition of steady state. Between the acute phase of shock (day 1) and the steady state condition (day 7) we observed in patients at day 7 a downregulation of pathways of the innate immune response (Toll-like receptor and C-type lectin receptors pathways) and of acute inflammation (IL-1 receptor family and alarmins) and the upregulation in the same patients of genes of the adaptive immunity related to B and T lymphocytes activation. A transcriptional regulation was observed also for genes with antimicrobial function and protease activity and for genes involved in carbohydrate metabolism, lipid inflammatory pathway, transport of vesicles and protein synthesis. miR-125a-5p and miR-150-5p, with a predicted regulatory role in the MAPK pathway, and miR-193a-3p were differentially expressed in the acute and steady state condition. Conclusion We observed a significant modulation of multiple classes of genes involved in defense response to pathogens, immunity, inflammation and metabolism. From these results it appears that in septic shock a relevant change in the transcriptomic profile of blood cells is induced, in order to counteract the pathogens and as a consequence of the hemodynamic changes underlying the circulatory failure. The transcriptomic profile of septic shock patients showed inter patient variability reflecting the complexity of the shock condition and of the individual response to treatment. Specific signatures could turn out by combining clinical data and expression profile and could be used to better classify septic shock patients.
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Saha, Dhanonjoy C. "The effects of endotoxin and monophosphoryl lipid A on monocyte activity." Thesis, University of Surrey, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337003.

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Wilson, Susan. "Lipopolysaccharide-activated signal transduction in cardiac and vascular smooth cells." Thesis, University of Strathclyde, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367047.

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Darwiche, Aiman A. "Machine Learning Methods for Septic Shock Prediction." Diss., NSUWorks, 2018. https://nsuworks.nova.edu/gscis_etd/1051.

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Sepsis is an organ dysfunction life-threatening disease that is caused by a dysregulated body response to infection. Sepsis is difficult to detect at an early stage, and when not detected early, is difficult to treat and results in high mortality rates. Developing improved methods for identifying patients in high risk of suffering septic shock has been the focus of much research in recent years. Building on this body of literature, this dissertation develops an improved method for septic shock prediction. Using the data from the MMIC-III database, an ensemble classifier is trained to identify high-risk patients. A robust prediction model is built by obtaining a risk score from fitting the Cox Hazard model on multiple input features. The score is added to the list of features and the Random Forest ensemble classifier is trained to produce the model. The Cox Enhanced Random Forest (CERF) proposed method is evaluated by comparing its predictive accuracy to those of extant methods.
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MacKenzie, Iain M. J. "Nitric oxide synthesis and human septic shock." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301763.

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Bagley, John Sorrell. "The beta adrenergic receptor in septic shock." Thesis, University of Aberdeen, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305466.

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The myocardial depression found during septic shock has been a subject of intense study for many years. Many theories exist as to the precise cause of this condition but in this thesis the role of the β-adrenergic receptor is examined. Some investigators have found reduced response to β-adrenergic stimulation in models of septic shock in animals. This is of interest to the clinician since adrenergic stimulation is a key manipulation in the management of septic shock. An animal model of septic shock was established using a comparatively small dose of Escherichia coli endotoxin infused into the male Sprague-Dawley rat. Heart function and response to isoprenaline, a β1-agonist, were measured in an in vitro organ bath. A reduction in the force of contraction was found together with a shift in the response curve to the right. These findings were associated with an increase in the number of β-receptors in the ventricular tissue from the same hearts, a measurement made using radioligand binding with I125-(-)-Iodocyanopindolol, a β1-antagonist. The finding of more β-receptors in the context of septic shock raises interesting questions discussed in the thesis. When forskolin, a plant alkaloid that stimulates the adenyl cyclase enzyme, was used to stimulate the atria in vitro the same response was found in the endotoxin treated and the normal groups. This is strong evidence that endotoxin causes a myocardial depressant effect mediated prior to adenylcyclase in the β-receptor transduction cascade.
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Barrett, L. K. "Mechanisms of vasopressin hypersensitivity in septic shock." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1445995/.

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Patients in prolonged, catecholamine-refractory septic shock have plasma vasopressin levels inappropriately low for their hypotension, yet show enhanced responses to exogenously administered hormone. I hypothesised that altered vasopressin signalling within vascular smooth muscle is responsible for this heightened sensitivity. Both vasopressin and the catecholamine, norepinephrine vasoconstrict via sarcolemmal G protein- coupled receptors. Diversity in the calcium signalling pathways downstream of these receptors may explain the differential effect of sepsis on vascular reactivity to the two hormones. To investigate this, I characterised a long-term fluid-resuscitated, rat model of faecal peritonitis, and examined in-vivo reactivity to these vasopressors. In subsequent ex-vivo studies performed on mesenteric resistance arteries taken from these animals, I compared concentration-response characteristics, calcium mobilisation pathways, and calcium-tension relationships for the two agonists, using wire myography and fluorescence microscopy. I also measured hormone levels in a cohort of septic and non-septic intensive care patients and undertook preliminary myography studies on human small mesenteric arteries. In prolonged illness, vasopressin levels were not elevated in either the septic rats or in septic patients, despite hypotension and organ dysfunction. Pressor responses to norepinephrine, but not vasopressin, were diminished in septic rats. This pattern of reactivity was mirrored ex-vivo, with decreased efficacy of norepinephrine, but increased potency of vasopressin. Differences were apparent in the calcium mobilisation pathways contributing to norepinephrine- and vasopressin-induced responses in septic vessels, with a greater reliance on store-operated calcium channels with vasopressin, compared to voltage- gated calcium channels with norepinephrine. The norepinephrine calcium- tension relationship was similar in sham and septic vessels but, for vasopressin, there was evidence of agonist-specific increased calcium sensitivity of the contractile apparatus in the septic tissues. In conclusion, my long-term septic model was able to satisfactorily mimic the clinical scenario. I demonstrated increased vasoconstriction to vasopressin suggesting enhanced receptor coupling to calcium signalling. Vasopressin, but not norepinephrine, may be able to both effectively mobilise calcium in septic vascular smooth muscle and sensitise the contractile apparatus to its effect. In addition to providing insight into the phenomenon of vasopressin hypersensitivity in septic shock, this work supports modulation of calcium mobilisation channels and/or sensitisation pathways as a potential new therapeutic paradigm.
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Books on the topic "Septic shock"

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Vincent, Jean Louis, and Lambertus G. Thijs, eds. Septic Shock. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-83108-9.

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K, Root Richard, Sande Merle A. 1939-, and University of California, San Francisco. Dept. of Medicine. Continuing Medical Education Division., eds. Septic shock. New York: Churchill Livingstone, 1985.

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J, Sibbald William, and Sprung Charles L, eds. Perspectives on sepsis and septic shock. Fullerton, Calif: Society of Critical Care Medicine, 1986.

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Rietschel, E. T., and Hermann Wagner, eds. Pathology of Septic Shock. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80186-0.

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L, Vincent J., and Thijs L. G. 1938-, eds. Septic shock: European view. Berlin: Springer-Verlag, 1987.

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Eichacker, Peter Q., and Jérôme Pugin, eds. Evolving Concepts in Sepsis and Septic Shock. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1581-4.

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Redl, Heinz, and Günther Schlag, eds. Cytokines in Severe Sepsis and Septic Shock. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8755-7.

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Heinz, Redl, and Schlag Günther, eds. Cytokines in severe sepsis and septic shock. Basel: Birkhäuser Verlag, 1998.

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Evans, Thomas J. Septic Shock Methods and Protocols. New Jersey: Humana Press, 1999. http://dx.doi.org/10.1385/1592592163.

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Sakorafas, George H. Septic shock: Current pathogenetic concepts, optimal management, and future perspectives. New York: Nova Biomedical Books, 2004.

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Book chapters on the topic "Septic shock"

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Theisler, Charles. "Sepsis/Septic Shock." In Adjuvant Medical Care, 315–17. New York: CRC Press, 2022. http://dx.doi.org/10.1201/b22898-309.

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Aydin, Ani, Daniel Joseph, and Melissa Joseph. "Sepsis, Septic Shock." In Simulation in EMS and Critical Care Transport, 325–37. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-40090-2_29.

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Cohen, Jonathan. "Septic Shock." In Critical Care Infectious Diseases Textbook, 407–19. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1679-8_23.

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Kashani, John, Richard D. Shih, Thomas H. Cogbill, David H. Jang, Lewis S. Nelson, Mitchell M. Levy, Margaret M. Parker, et al. "Septic Shock." In Encyclopedia of Intensive Care Medicine, 2060. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_3297.

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Norwitz, Errol R., and Hee Joong Lee. "Septic Shock." In Critical Care Obstetrics, 571–95. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444316780.ch41.

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Kim, Kyuseok, Han Sung Choi, Sung Phil Chung, and Woon Young Kwon. "Septic Shock." In Essentials of Shock Management, 55–79. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-5406-8_5.

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Bone, Roger C. "Septic Shock." In Anesthesia and the Lung, 239–51. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0899-4_26.

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De Backer, Daniel, and Antoine Vieillard-Baron. "Septic Shock." In Hemodynamic Monitoring Using Echocardiography in the Critically Ill, 109–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-87956-5_11.

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Ramasubban, Suresh. "Septic Shock." In ICU Protocols, 511–18. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-0898-1_52.

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Mayo, Paul H. "Septic Shock." In Echocardiography in ICU, 159. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-32219-9_16.

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Conference papers on the topic "Septic shock"

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Martínez-Brotóns, F., J. R. Oncins, J. Mestres, V. Amargós, and C. Reynaldo. "KALLIKREIN-KININ SYSTEM IN PATIENTS WITH SHOCK. COMPARISON BETWEEN SEPTIC AND CARDIOGENIC SHOCK." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644335.

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Alterations of the kallikrein-kinin system (KKS) consistent with activation and increased consumption have been reported in septic patients and it has been suggested that this activation could contribute to the development of septic shock. As similar alterations have been found in other critically ill patients, many of them prone to shock, we wonder if activation of the KKS could be a consequence rather than a cause of the hemodynamic instability. To answer this question we compared 12 patients with septic shock (8 fatal) with 10 cases of cardiogenic shock secondary to myocardial infarction (8 fatal) as a model of non septic shock. In adition 25 episodes of uncomplicated sepsis and 10 intra-intensive care unit controls were studied. A functional measure of factor XII, high molecular weight kininogen (HMWK) (coagulative methods), prekallikrein (PK), Cl-inhibitor (Cl-INH), α2-macroglobulin (α2-M)- Antithrombin III (AT-III) and kallikrein inhibitor activity (KIA) (chromogenic methods) was performedRESULTS: Patients with septic shock, specially in fatal cases, showed a highly significant decrease in activities of factor XII (P<0.001), PK (P<0.0001), HMWK (P<0.005), α2-M (P<0.001), AT-III (P<0.0001) and KIA (P<0.005). Cl-INH activity was increased in uncomplicated sepsis (P<0.001) but came back to normal or was slightly decreased in septic shock. Components and inhibitors of the KKS were within normal limits in all patients with cardiogenic shock.Our findings support the idea of a contribution of the KKS to the development of septic shock but this system neither seems to play a role in the pathogenesis of cardiogenic shock nor to be altered as a consequence of it.
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Schuh, Ch J. "Sepsis and Septic Shock Analysis using Neural Networks." In NAFIPS 2007 - 2007 Annual Meeting of the North American Fuzzy Information Processing Society. IEEE, 2007. http://dx.doi.org/10.1109/nafips.2007.383917.

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Fernandes, A., S. Sharma, C. Bendor-Grynbaum, P. Soni, O. Lamikanra, S. S. Gupta, and Y. Kupfer. "Mycobacterium Tuberculosis Associated Septic Shock." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6926.

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Holder, A., K. Uppal, D. P. Jones, and A. M. Esper. "Metabolomics-Based Differentiation Between Severe Sepsis and Septic Shock." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2602.

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Rogers, R. S., K. Hibbert, R. Sharma, S. Calvo, K. L. Brait, N. A. Pulido, B. T. T. Thompson, and V. K. Mootha. "The Proteomic Signature of Septic Shock Differs from Cardiogenic Shock or Bacteremia Without Sepsis or Shock." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6507.

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Margraf, A., C. Liu, and A. Zarbock. "Thrombopoietin levels in sepsis and septic shock - a meta-analysis." In 65th Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1728178.

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MIHO TANI, VANESSA, Erich De Paula, THAMIRES BRANCO DA SILVA, GUILHERME ROSSI ASSIS DE MENDONÇA, and FABIO ROGERIO. "Microvascular thrombosis in sepsis and septic shock: an autopsy study." In XXIV Congresso de Iniciação Científica da UNICAMP - 2016. Campinas - SP, Brazil: Galoa, 2016. http://dx.doi.org/10.19146/pibic-2016-50621.

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Colon Hidalgo, D., S. Rao, D. Masic, and M. Rech. "Racial Disparities and Septic Shock Outcomes." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1632.

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Ramanathan, R., R. Wu, and D. Datta. "Procalcitonin and Outcomes in Septic Shock." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1634.

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Ramanathan, R., R. Wu, and D. Datta. "Troponins and Outcomes in Septic Shock." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1637.

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Reports on the topic "Septic shock"

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Neodo, Anna, Fiona Augsburger, Jan Waskowski, Joerg C. Schefold, and Thibaud Spinetti. Monocytic HLA-DR expression and clinical outcomes in adult ICU patients with sepsis – a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0119.

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Review question / Objective: The scope of this review was defined using PICOTS framework where 1) population: adult critically ill patients with sepsis or septic shock; 2) index prognostic factor: cell surface protein expression of mHLA-DR in blood; 3) comparative factor: none; 4) outcomes to be predicted: mortality, secondary infections, length of stay, and organ dysfunction score (sequential organ failure assessment [SOFA], multiple organ dysfunction score [MODS], logistic organ dysfunction score [LODS]), composite outcomes where component endpoints consist of at least one of the outcomes stated above (e.g., “adverse outcome” defined as death or secondary infection), 5) timing (of the prediction horizon and the moment of prognosis): any; and 6) setting: ICU. Condition being studied: Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to severe infections. It can further progress to septic shock, which includes hemodynamic failure and increased mortality rates. A recent worldwide epidemiological study estimated 48.9 million sepsis cases and 11 million of sepsis-related deaths (~20% of global deaths in 2017). Although its management has advanced considerably, sepsis remains deadly and challenging to treat. The 28/30-day mortality averages around 25% for sepsis and 38% for septic shock in high-income countries. Current models describe the underlying pathophysiologic mechanisms of sepsis as an interplay between concurrent dysfunctional pro- and anti-inflammatory immune response.
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Du, Xinxin, Tingting Shi, Chunbo Yang, and Xiangyou Yu. Effect of glycocalyx biomarker syndecan-1 on prognosis in adult patients with sepsis/septic shock: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2023. http://dx.doi.org/10.37766/inplasy2023.6.0043.

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Zeng, Yiqian, Zhao Liu, Fei Xu, and Zhanhong Tang. Intravenous high-dose vitamin C monotherapy for sepsis and septic shock: a meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0097.

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Chen, Chi-Hsin, Edward Pei-Chuan Huang, James d’Etienne, Eric H. Chou, Yen-Hsing Liu, Yu-Sheng Huang, Jia-How Chang, Pei-Chun Lai, and Yen-Ta Huang. Triple Combination of Hydrocortisone, Ascorbic Acid, and Thiamine (HAT) for Sepsis/Septic Shock: Meta-analysis and Trial Sequential Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2020. http://dx.doi.org/10.37766/inplasy2020.9.0097.

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Huang, Hui-Bin, Hua Zhou, Xiang-Jun Zhang, Yuan Xu, and Bin Du. Outcomes of septic shock adult patients receiving extracorporeal membrane oxygenation: A pooled experience of 1,895 cases. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2020. http://dx.doi.org/10.37766/inplasy2020.7.0040.

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Zhu, Huiyan, Xiaoya Xu, Kai Zhang, and Qiaoping Ye. The effect of intravenous vitamin C on clinical outcomes in patients with sepsis or septic shock: a meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0013.

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Belenska-Todorova, Lyudmila Filipova, Valeriya Gyurkovska, and Nina Dimitrova Ivanovska. Neutralization of Tumour Necrosis Factor-related Apoptosis-inducing Ligand Ameliorates the Symptoms of Zymosan-induced Septic Shock. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, November 2021. http://dx.doi.org/10.7546/crabs.2021.11.15.

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Lin, Leqing, Wei Cao, Baixue Yao, Wenxue Tang, Baiyong Wang, and Bin Wang. Application Secure Medical Imaging and value of blood perfusion index monitoring guidance in fluid resuscitation treatment of septic shock. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0010.

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Cherian, Jerald, Jodi Segal, Ritu Sharma, Allen Zhang, Eric Bass, and Michael Rosen. Patient Safety Practices Focused on Sepsis Prediction and Recognition. Agency for Healthcare Research and Quality (AHRQ), April 2024. http://dx.doi.org/10.23970/ahrqepc_mhs4sepsis.

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Objectives. Patient safety practices (PSPs) focused on sepsis prediction and recognition, encompass interventions designed to identify patients with sepsis early and improve timely adherence to guidelines. Our objectives were to review the evidence published after the previous Making Healthcare Safer (MHS) report to determine the effectiveness of sepsis prediction and recognition PSPs on patient safety related outcomes. Methods. We searched PubMed and the Cochrane library for systematic reviews and primary studies published from January 2018 through August 2023, supplemented by gray literature searches. We included reviews and primary studies of sepsis prediction and recognition PSPs reporting measures of clinical process (time to diagnosis or treatment, adherence to guidelines, Severe Sepsis and Septic Shock Early Management Bundle), patient outcomes (hospital or intensive care unit (ICU) length of stay, mortality), implementation (use, barriers, and facilitators), or costs. Findings. We focused on 7 systematic reviews and 8 primary studies that were eligible for full review, and briefly summarized 36 pre-post studies that lacked a separate comparison group. All the sepsis prediction and recognition PSPs were multi-component interventions. Across the systematic reviews and primary studies of neonates, the PSPs improved clinical process measures (low strength of evidence), but evidence was insufficient about length of stay or mortality outcomes. Across the systematic reviews and primary studies of adults, the PSPs did not demonstrate an effect on clinical process, length of stay, or mortality outcomes. In primary studies of adults, evidence was insufficient in the prehospital setting for mortality, length of stay, and clinical process measures. In the emergency department setting, strength of evidence was low for mortality and clinical process measures and insufficient for length of stay. In ward or hospitalwide settings, strength of evidence was low across all three outcome types. The secondary outcome of alerting system performance (e.g., positive predictive value) could not be meaningfully compared across studies due to diversity in populations and interventions. Conclusions. This review finds that recent primary studies and systematic reviews do not support that specific PSPs for sepsis prediction and recognition are effective at reducing mortality or length of stay or improve clinical processes in adults in pre-hospital, emergency department, or hospitalwide settings as compared to usual care. Sepsis prediction and recognition PSPs may improve clinical process outcomes in neonates in ICUs.
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Zerbib, Olivier, Yaniv Hadi, Daniel Kovarsky, Gal Sahaf Levin, Tamar Gottesman, Mor Darkhovsky, and Shaul Lev. Multiple Recurrent Pneumothoraces and Thoracic Drain Insertion in a Mechanically Ventilated Patient Suffering from Methadone Induced Cardiomyopathy. Science Repository, January 2023. http://dx.doi.org/10.31487/j.jcmcr.2022.01.02.

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Objective: To describe the experience of a multimodal therapeutic approach in a patient with methadone-induced dilated cardiomyopathy who developed recurrent bilateral tension pneumothorax. Setting: Department of Intensive Care. Patient: A patient with methadone-induced cardiomyopathy and severe left ventricular dysfunction who after mechanical ventilation underwent bilateral tension pneumothorax and prolonged cardiovascular resuscitation (CPR). Interventions: Cardiac Angiography, Multiple counter–shock (defibrillator dose), Multiple Thoracic Drains. Case Report: A 56-year-old man with past IV drug abuse and severe left ventricular dysfunction was transferred from the intensive cardiac care unit (ICCU) to our intensive care unit (ICU) ward due to suspected aspiration pneumonia. Multiple attempts of weaning off mechanical ventilation were unsuccessful, followed by development of septic shock. Following cardiothoracic consultation, two thoracic drains were placed. Due to repeated events of bilateral tension pneumothorax and CPR attempts, a total of seven thoracic drains were placed, permitting rapid control and improvement in the patient status. The possibility of Extracorporeal Membrane Oxygenation (ECMO) was not considered as supportive care due to methadone use and severe secondary cardiomyopathy. In the following days, control and stabilization of the patient status was obtained. Vasopressor treatment withdrawal, cessation of drainage and removal of five thoracic access points were successfully performed prior to percutaneous tracheostomy. The two remaining drains were removed later on during hospitalization. After 29 days in the ICU, the patient was discharged to a step down ward.
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