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dc.contributor.advisorMachado Romero, Carlos Alfonsospa
dc.contributor.advisorHiguera Cobos, Juan Diegospa
dc.contributor.advisorOchoa Vera, Miguel Enriquespa
dc.contributor.authorRueda Galvis, Myriam Vanessaspa
dc.date.accessioned2020-06-26T19:59:54Z
dc.date.available2020-06-26T19:59:54Z
dc.date.issued2018
dc.identifier.urihttp://hdl.handle.net/20.500.12749/1734
dc.description.abstractIntroducción: La sepsis representa una entidad que es generada por respuesta sistémica a la infección, inicialmente en 1992 se definió enfocada en el síndrome de respuesta inflamatoria sistémica(7), en el 2016 se modificó y ahora es considerada por The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) como una respuesta no regulada a la infección que causa disfunción orgánica múltiple y pone en peligro la vida. Los biomarcadores cardiacos (Troponina I, NT pro BNP) se demostraron útiles en la predicción de desenlaces adversos en sepsis, sin embargo con el advenimiento de la nueva definición esta relación no está probada. Métodos: Este es un estudio de evaluación de prueba diagnóstica en participantes del estudio ―Asociación entre la actividad de las Metaloproteinasas de matriz extracelular (MMPs) y la disfunción cardiovascular en pacientes con sepsis. Se calculó la asociación de NT pro BNP, troponina I y mortalidad, choque séptico, disfunción sistólica /diastólica e ingreso a UCI. Resultados: Se analizaron 289 registros. La mediana de edad de los pacientes fue de 63 años con un rango de edad entre 49-77 años. La mediana de NT-pro BNP fue 2099 (RIQ: 533-9051) y de la troponina I 0.1 (RIQ: 0.1-0.2). La mediana del SOFA de 4 (RIQ: 0-13), del APACHE II 13 (RIQ: 8-19) . El origen más frecuente de la sepsis fue tracto urinario (39.1%). El 28.37% (82) de los casos en la cohorte fallecieron. La disfunción sistólica estuvo presente en 39.83 %, la disfunción diastólica 69.11%. El 55.71% fueron manejados en unidad de cuidados intensivo, 47.06% presentaban sepsis. Se encontró una relación positiva estadísticamente significativa (p<0.001) entre niveles séricos de NT pro BNP, troponina I y mortalidad, disfunción sistólica y choque séptico, con AUC con capacidad predictiva pobre. No se halló asociación con NT pro BNP, troponina I y disfunción diastólica o ingreso a UCI. Conclusiones: Aún con criterios más específicos de clasificación de sepsis existe una asociación significativa entre biomarcadores de injuria miocárdica en sepsis y desenlaces adversos. Sus características psicométricas no son buenas, en este estudio son iguales a las de las escalas de riesgo conocidas a la fecha (SOFA-APACHE II)spa
dc.description.tableofcontentsRESUMEN Y PALABRAS CLAVE ............................................................................................... 8 SUMMARY AND KEYWORDS .................................................................................................. 9 INTRODUCCIÓN ................................................................................................................... 10 1. OBJETIVOS ................................................................................................................... 13 Objetivos Específicos .......................................................................................................................... 13 2. PLANTEAMIENTO DEL PROBLEMA .................................................................................... 14 3.MARCO TEÓRICO Y ESTADO DEL ARTE .............................................................................. 16 3.1 Fisiopatología de la sepsis: ........................................................................................................... 16 3.2 Disfunción cardiaca en sepsis, fisiopatología : ............................................................................ 17 3.3 Alteraciones hemodinámicas en miocardiopatía séptica: ........................................................... 21 3.4 Definición de cardiomiopatía séptica: .......................................................................................... 22 3.5 Ventilación mecánica y cardiomiopatía séptica : ......................................................................... 24 3.6 Métodos diagnósticos de cardiomiopatía séptica ....................................................................... 25 3.7 Biomarcadores de origen cardiogénico........................................................................................ 27 3.8 Manifestaciones ecocardiográficas .............................................................................................. 34 3.9 Puntajes de predicción de riesgo: ............................................................................................... 36 4. METODOLOGÍA ................................................................................................................ 39 4.1 Tipo de estudio ............................................................................................................................. 39 4.2 Población ...................................................................................................................................... 39 4.3 Muestra ........................................................................................................................................ 39 4.4 Recolección de la información ..................................................................................................... 40 4.5 Procesamiento y control de calidad ............................................................................................. 42 4.6 Procesamiento y Análisis estadístico ........................................................................................... 42 5. CONSIDERACIONES ÉTICAS .............................................................................................. 43 6. RESULTADOS ................................................................................................................... 45 6.1 Características de base ................................................................................................................. 45 6.2 Desenlaces primarios ................................................................................................................... 45 6.2.1 Exactitud diagnostica de la NT- pro BNP ................................................................................... 46 6.2.2 Exactitud diagnostica de la Troponina I .................................................................................... 48 6.2.3. Desenlace SOFA modificado ..................................................................................................... 49 6.2.4. Desenlace APACHE II modificado ............................................................................................. 50 7. DISCUSIÓN ...................................................................................................................... 51 8.LIMITACIONES Y FORTALEZAS ........................................................................................... 55 9. CONCLUSIONES................................................................................................................ 57 10. BIBLIOGRAFIA ................................................................................................................ 58 TABLAS ................................................................................................................................ 64 FIGURAS .............................................................................................................................. 66 ANEXOS............................................................................................................................... 74 CRONOGRAMA .................................................................................................................... 88spa
dc.format.mimetypeapplication/pdfspa
dc.language.isospaspa
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/2.5/co/*
dc.titleFuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsisspa
dc.title.translatedStrength of association between Troponin I, NT-pro BNP and adverse outcomes in sepsiseng
dc.degree.nameEspecialista en Medicina Internaspa
dc.coverageBucaramanga (Santander, Colombia)spa
dc.publisher.grantorUniversidad Autónoma de Bucaramanga UNABspa
dc.rights.localAbierto (Texto Completo)spa
dc.publisher.facultyFacultad Ciencias de la Saludspa
dc.publisher.programEspecialización en Medicina Internaspa
dc.description.degreelevelEspecializaciónspa
dc.type.driverinfo:eu-repo/semantics/masterThesis
dc.type.localTesisspa
dc.type.coarhttp://purl.org/coar/resource_type/c_bdcc
dc.subject.keywordsSystemic inflammatory response syndromeeng
dc.subject.keywordsSeptic cardiomyopathyeng
dc.subject.keywordsSepsiseng
dc.subject.keywordsTroponin Ieng
dc.subject.keywordsMedicineeng
dc.subject.keywordsInternal medicineeng
dc.subject.keywordsInvestigationseng
dc.subject.keywordsComplicationseng
dc.subject.keywordsPatientseng
dc.subject.keywordsPrevention and controleng
dc.subject.keywordsThird consensuseng
dc.subject.keywordsMortalityeng
dc.subject.keywordsSystolic dysfunctioneng
dc.subject.keywordsDiastolic dysfunctioneng
dc.subject.keywordsSeptic shockeng
dc.subject.keywordsIntensive care uniteng
dc.identifier.instnameinstname:Universidad Autónoma de Bucaramanga - UNABspa
dc.identifier.reponamereponame:Repositorio Institucional UNABspa
dc.type.hasversioninfo:eu-repo/semantics/acceptedVersion
dc.rights.accessrightsinfo:eu-repo/semantics/openAccessspa
dc.rights.accessrightshttp://purl.org/coar/access_right/c_abf2spa
dc.relation.referencesRueda Galvis, Myriam Vanessa (2018). Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis. Bucaramanga (Santander, Colombia) : Universidad Autónoma de Bucaramanga UNABspa
dc.relation.references1. Torio, C.M, Andrews, R.M. (2013). National in patient hospital costs: the most expensive conditions by payer, Statistical Brief #160. Healthcare Cost and Utilization Project (HCUP) Statistical Briefs.. http://www.ncbi.nlm.nih.gov/books NBK169005/.spa
dc.relation.references2. Hotchkiss, R.S., Swanson, P.E., Freeman, B.D., et al. (2011) Apoptotic cell death in patients with sepsis, shock, and multiple organ dysfunction. Critical Care Medicine, 27(7), 1230-1251.spa
dc.relation.references3. Hotchkiss, R.S., Monneret, G., Payen,D. (2013). Sepsis-induced immunosuppression: from cellular dysfunctions to immunotherapy. Natural Reviews Immunology, 13(12), 862-874.spa
dc.relation.references4. Singer, M., Clifford S.D., Seymour W., et al. (2016). The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA, 315(8),801-810.spa
dc.relation.references5. Parrillo, J.E., Parker ,M.M., Natanson, C., et al. (1990). Septic shock in humans: advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. Annals of Internal Medicine, 113,227-42.spa
dc.relation.references6. Vincent, J.L., de Mendonça, A., Cantraine, F, et al. (1998). Working Group on ―Sepsis-Related Problems‖ of the European Society of Intensive Care Medicine. Use of the SOFA score to assess the incidence of organ dysfunction/failure in intensive care units: results of a multicenter, prospective study. Critical Care Medicine, 26(11), 1793-1800.spa
dc.relation.references7. Bone, R.C., Balk, R.A., Cerra, F.B., et al. (1992). American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Critical Care Medicine, 20(6), 864-874.spa
dc.relation.references8. Mervyn, S. (2016). The new sepsis consensus definitions (Sepsis-3): the good, the not so bad, and the actually quite pretty. Intensive Care Medicine. Publicado online 23 Diciembre 2016. DOI 10.1007/s00134-016-4600-4spa
dc.relation.references9. Gaieski, D.F., Edwards J.M., Kallan M.J., et al. (2013). Benchmarking the incidence and mortality of severe sepsis in the United States. Critical Care Medicine, 41(5),1167-1174.spa
dc.relation.references10. Vincent, J.L., Marshall J.C., Namendys-Silva S.A., et al. (2014). Assessment of the worldwide burden of critical illness: the Intensive Care Over Nations (ICON) audit. Lancet Respiratory Medicine, 2(5),380-386.spa
dc.relation.references11. Wang W., Sawicki G., Schulz R. (2002). Peroxynitrite-induced myocardial injury is mediated through matrix metalloproteinase-2. Cardiovascular Research, 53, 165–174spa
dc.relation.references12. Alvarez, S., Vico, T., Vanasco, V. (2016) Cardiac dysfunction, mitocondrial architecture, energy production, and inflammatory pathways: interrelated aspects in endotoxemia and sepsis. The International Journal of Biochemistry & Cell Biology, 81(Pt B), 307-314.spa
dc.relation.references13. De Angelo J. (1999) . Nitric oxide scavengers in the treatment of shock associated with systemic inflammatory response syndrome. Expert Opinion Pharmacotherapy, (1), 19-29.spa
dc.relation.references14. Cimolai, M.C., Alvarez, S., Bode C., et al.(2015). Mitochondrial Mechanisms in Septic Cardiomyopathy. Internal Journal of Molecular Scinces, (16), 17763-17778.spa
dc.relation.references15. Romero-Bermejo, F.J., Ruiz-Bailen, M., Gil-Cebrian, J., et al. (2011). Sepsis-induced cardiomyopathy. Current Cardiology Reviews, (7), 163-183.spa
dc.relation.references16. Ince, C., Mayeux, P.R., Nguyen, T, el al. (2016). The Endothelium in Sepsis. Shock, (45), 259-270spa
dc.relation.references17. Dauphinee, S.M., Karsan, A., 2006. Lipopolysaccharide signaling in endothelial cells. Laboratory Investigation Journal , 86, 9-22.spa
dc.relation.references18. Morikawa, A., Koide, N., Kato, Y., et al. 2000. Augmentation of nitric oxide production by gamma interferon in a mouse vascular endothelial cell line and its modulation by tumor necrosis factor alpha and lipopolysaccharide. Infection and Immunity Journal. 68, 6209-6214.spa
dc.relation.references19. Liaudet, L., Soriano, F.G., Szabó, C. (2000) . Pathophysiological role of nitric oxide in inflammation, in: Nitric Oxide, biology and pathology. Critical Care Medicine, 28(4), 841-872.spa
dc.relation.references20. Thiemermann, C., Vane, J., (1990). Inhibition of nitric oxide synthesis reduces the hypotension induced by bacterial lipopolysaccharides in the rat in vivo. European Journal of Pharmacology, 182, 591-595.spa
dc.relation.references21. Blanco, J., Muriel-Bombin, A., Sagredo, V., Taboada, F., Gandia, F., Tamayo, L., Collado, J., Garcia-Labattut, A., Carriedo, D., Valledor, M., De Frutos, M., Lopez, M.J., Caballero, A., Guerra, J., Alvarez, B., Mayo, A., Villar, J., (2008). Incidence, organ dysfunction and mortality in severe sepsis: a Spanish multicentre study. Critical Care, 12(6), R158.spa
dc.relation.references22. McDonough, K.H., Virag, J.I., (2006). Sepsis-induced myocardial dysfunction and myocardial protection from ischemia/reperfusion injury. Frontiers Bioscience, 11, 23-32.spa
dc.relation.references23. Poelaert, J., Declerck, C., Vogelaers, D., et al, (1997). Left ventricular systolic and diastolic function in septic shock. Intensive Care Medicine, 23, 553-560.spa
dc.relation.references24. Smeding, L., Plotz, F.B., Groeneveld, A.B., et al. (2012). Structural changes of the heart during severe sepsis or septic shock. Shock, 37, 449-456.spa
dc.relation.references25. Larche, J., Lancel, S., Hassoun, S.M., et al. (2006). Inhibition of mitochondrial permeability transition prevents sepsis- induced myocardial dysfunction and mortality. Journal of the American College of Cardiology, 48, 377-385.spa
dc.relation.references26. Levy, R.J., Piel, D.A., Acton, P.D., et al. (2005). Evidence of myocardial hibernation in the septic heart. Critical Care Medicine, 33, 2752- 2756.spa
dc.relation.references27. Piantadosi, C.A., Suliman, H.B. (2012). Transcriptional control of mitochondrial biogenesis and its interface with inflammatory processes. Biochimica et Biophysica Acta, 1820, 532-541.spa
dc.relation.references28. Vanasco, V., Saez, T., Magnani, N.D., et al. (2014). Cardiac mitochondrial biogenesis in endotoxemia is not accompanied by mitochondrial function recovery. Free Radical Biology and Medicine, 77, 1-9.spa
dc.relation.references29. Vieillard-Baron A. (2001). Septic cardiomyopathy. Annals of Intensive Care, 1, 6–7.spa
dc.relation.references30. Hochstadt, A., Meroz, Y., Landesberg, G. (2011). Myocardial dysfunction in severe sepsis and septic shock: more questions than answers?. Journal of Cardiothoracic and Vasc Anesthesia, 25 (3), 526–35.spa
dc.relation.references31. dos Santos, C.C., Gattasm, D.J., Tsoporis, J.N., et al. (2010). Sepsis-induced myocardial depression is associated with transcriptional changes in energy metabolism and contractile related genes: a physiological and gene expression based approach. Critical Care Medicine, 38 (3), 894–902.spa
dc.relation.references32. Stengl, M., Bartak, F., Sykora, R., et al. (2010). Reduced L-type calcium current in ventricular myocytes from pigs with hyperdynamic septic shock. Critical Care of Medicine, 38(2), 580–7.spa
dc.relation.references33. Antonucci, E., Fiaccadori, E., Donadello, K., et al. (2013). Myocardial depression in sepsis: From pathogenesis to clinical manifestations and treatment. Journal of Critical Care, 29(4), 500-11.spa
dc.relation.references34. Repessé, X., Charron, C., Vieillard-Baron, A. (2013). Evaluation of left ventricular systolic function revisited in septic shock. Critical Care, 17(4), 164.spa
dc.relation.references35. Vieillard-Baron, A., Caille, V., Charron, C., et al. (2008). Actual incidence of global left ventricular hypokinesia in adult septic shock. Critical Care Medicine, 36(6), 1701-6spa
dc.relation.references36. Parker, M.M., Shelhamer, J.H., Bacharach, S.L., et al. (1984) Profound but reversible myocardial depression in patients with septic shock. Annals of Internal Medicine, 100:483–90.spa
dc.relation.references37. Guarracino, F., Baldassarri, R., Pinsky, M.R. (2013). Ventriculo-arterial decoupling in acutely altered hemodynamic states. Critical Care, 17(2), 213–20.spa
dc.relation.references38. Landesberg, G., Gilon, D., Meroz, Y., et al. (2012). Diastolic dysfunction and mortality in severe sepsis and septic shock. European Heart Journal, 33(7), 895–903.spa
dc.relation.references39. Roosens, C.D., Ama, R., Leather, H.A., et al. (2006). Hemodynamic effects of different lung- protective ventilation strategies in closed-chest pigs with normal lungs. Critical Care of Medicine, 34(12), 2990–6.spa
dc.relation.references40. Pinsky, M.R. (2005). Cardiovascular issues in respiratory care. Chest, 128, 592–7.spa
dc.relation.references41. Latini, R., Caironi, R., Masson, S. (2016). Cardiac dysfunction and circulating cardiac markers during sepsis. Minerva anestesiologica , 82(6), 697-710spa
dc.relation.references42. Maeder, M,, Fehr, T., Rickli, H., et al. (2006). Sepsis associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and natriuretic peptides. Chest, 129:1349-66spa
dc.relation.references43. Rajaram, S.S., Desai, N.K., Kalra, A., et al.(2013). Pulmonary artery catheters for adult patients in intensive care. Cochrane Database Systematic Review, 28(2),1–59.spa
dc.relation.references44. Sandham, J.D, Hull, R.D., Brant, R.F., et al. (2003). A randomized, controlled trial of the use of pulmonary-artery catheters in high risk surgical patients. The New England Journal of Medicine,348(1), 5-14.spa
dc.relation.references45. Wheeler, A.P., Bernard, G.R, Thompson, B.T., et al. (2006). Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury. The New England Journal of Medicine, 354(41), 2213-24.spa
dc.relation.references46. Brett, J., Gerlach, H., Nawroth, P., et al. (1989). Tumor necrosis factor/cachectin increases permeability of endothelial cell monolayers by a mechanism involving regulatory G proteins. The Journal of Experimental Medicine, 169(6), 1977–91spa
dc.relation.references47. Landesberg, G., Jaffe A.S., Gilon D., et al. (2014). Troponin elevation in severe sepsis and septic shock: the role of left ventricular diastolic dysfunction and right ventricular dilatation. Critical Care Medicine, 42(4), 790-800.spa
dc.relation.references48. Markou, N., Gregorakos, L., Myrianthefs, P. (2011). Increased blood troponin levels in ICU patients. Current Opininon Critical Care, 1(5)7, 454–463.spa
dc.relation.references49. Brivet, F.G., Jacobs, F.M., Colin, P., et al. (2006). Cardiac troponin level is not an independent predictor of mortality in septic patients requiring medical intensive care unit admission. Critical Care, 10(1), 404.spa
dc.relation.references50. Bessiére, F., Khenifer, S., Dubourg, I., et al. (2013). Prognostic value of troponins in sepsis: a meta-analysis. Intensive Care Medicine , 39(7), 1181–1189spa
dc.relation.references51. Spies, C., Haude, V., Fitzner, R., Schroder, K., et al. (1998). Serum cardiac troponin T as a prognostic marker in early sepsis. Chest, 113, 1055–1063spa
dc.relation.references52. Bouhemad, B., Nicolas-Robin, A., Arbelot, C., et al. (2008). Isolated and reversible impairment of ventricular relaxation in patients with septic shock. Critical Care Medicine, 36(3) , 766–774spa
dc.relation.references53. Clerico, A. (2002). Pathophysiological and clinical relevance of circulating levels of cardiac natriuretic hormones: Are they merely markers of cardiac disease? Clinical Chemistry and Laboratory Medicine, 40(8), 752-60spa
dc.relation.references54. Ueda, S., Nishio, K., Akai, Y., et al. (2006). Prognostic value of increased plasma levels of brain natriuretic peptide in patients with septic shock. Shock, 26(2), 134-139spa
dc.relation.references55. Cuthbertson, B.H., Patel, R.R., Croal B.L., et al. (2005), B-type natriuretic peptide and the prediction of outcome in patients admitted to intensive care. Anaesthesia, 60(1), 16-21.spa
dc.relation.references56. Tomaru, K.K., Arai, M., Yokoyama, T., et al. (2002). Transcriptional activation of the BNP gene by lipopolysaccharide is mediated through GATA elements in neonatal rat cardiac myocytes. Journal of Mollecular and Cellular Cardiology, 34(6), 649-659.spa
dc.relation.references57. Turner, K.L., Moore, L.J., Todd, S.R., et al. (2011). Identification of cardiac dysfunction in sepsis with B-type natriuretic peptide. Journal of the American Collegues Surgeons, 213(1), 139–46.spa
dc.relation.references58. Long, B., Koyfman, A. (2017). Ready for Prime Time? Biomarkers in Sepsis. Emergency Medicine Clinics of North America, 35, 109–122.spa
dc.relation.references59. Wang, F., Wu, Y., Tang, L., et al. (2012). Brain natriuretic peptide for prediction of mortality in patients with sepsis: a systematic review and meta-analysis . Critical Care, 16:R74.spa
dc.relation.references60. Post, F., Weilemann, L.S., Messow, C.M., et al. (2008). B-type natriuretic peptide as a marker for sepsis induced myocardial depression in intensive care patients. Critical Care Medicine, 36(11),3030-3037.spa
dc.relation.references61. Mokart, D., Sannini, A., Brun, J.P., et al. (2007). N- terminal pro-brain natriuretic peptide as an early prognostic factor in cancer patients developing septic shock. Critical Care , 11(2), R37.spa
dc.relation.references62. Seung, R., Kim, W.Y., Won, H.J., et al. (2015). Prognostic Value of B-type Natriuretic Peptide With the Sequential Organ Failure Assessment Score in Septic Shock . American Journal of medical sciencies, 349 (4), 287–291.spa
dc.relation.references63. Müller-Werdan, U., Werdan, K. (1999). Septic cardiomyopathy. Current Opinion in Critical Care, 5,415–421.spa
dc.relation.references64. Parker, M.M., Shelhamer, J.H., Natanson, C., el al. (1989). Serial cardiovascular variables in survivors and nonsurvivors of human septic shock: heart rate as an early predictor of prognosis. Critical Care Medicine, 15(10),923–929.spa
dc.relation.references65. Hestenes, S.M., Halvorsen P.S., Skulstad, H., et al.(2014). Advantages of Strain Echocardiography in Assessment of Myocardial Function in Severe Sepsis: An Experimental Study. Critical Care Medicine, 42(6), 432-440.spa
dc.relation.references66. Werdan, K., Oelke, A., Hettwer, S., et al. (2011). Septic cardiomyopathy: Hemodynamic quantification, occurrence, and prognostic implications. Clinical Research in Cardiology, 100(8), 661–668.spa
dc.relation.references67. Brown, S., Pittman, J., Hirshberg, E.L., et al. (2012) Diastolic dysfunction and mortality in early severe sepsis and septic shock: a prospective, observational echocardiography study. Critical Ultrasound Journal, 4(1), 8.spa
dc.relation.references68. Bouhemad, B., Nicolas-Robin, A., Benois, A., et al. (2003). Echocardiographic Doppler assessment of pulmonary capillary wedge pressure in surgical patients with postoperative circulatory shock and acute lung injury. Anesthesiology, 98(5), 1091–1100.spa
dc.relation.references69. Vicent, J.L, Moreno R., Takala., et al. (1996). The SOFA (Sepsis realted organ failure assessment) score to describe organ dysfunction/ failure. Intensive Care Medicine, 22(), 707-710.spa
dc.relation.references70. Ferreira, F.L., Bota, D.P., Bross, A., et al. (2001). Serial evaluation of the SOFA score to predict outcome in critically ill patients. JAMA, 286(14):1754-8spa
dc.relation.references71. 72. Knaus, W.A., Draper, E.A., Wagner , D.P., et al. (1985). APACHE II: everity of disease clasification system. Critical Care Medicine, 13(10), 818-820.spa
dc.relation.references72. Capuzzo, M., Valpondi, V., Sgarbi, A. (2000). Validation of severity scoring systems SAPS II and APACHE II in a single-center population.Intensive Care Medicine, 26(12), 1779.spa
dc.relation.references73. Zimmerman J.E., Kramer, A.A., McNair, D.S., et al. (2006) Acute Physiology and Chronic Health Evaluation (APACHE) IV: hospital mortality assessment for today's critically ill patients. Critical Care of Medicine, 34(5):1297-310.spa
dc.relation.references74. Swets J. (1988). Measuring the Accuracy of Diagnostic Systems. American Association for the Advancement of Science, 240 (4857), 1285- 1293.spa
dc.relation.references75. Mokart D, Brun JP, Faucher M., et al (2007) : N- terminal pro-brain natriuretic peptide as an early prognostic factor in cancer patients developing septic shock. Critical Care of Medicine, (11):37.spa
dc.relation.references76. Roch A., Alladet-Servent, J., Michelet P., et al. (2005): NH2 terminal pro- brain natriuretic peptide plasma level as an early marker of prognosis and cardiac dysfunction in septic shock patients Critical Care of Medicine, 33(5): 1001-1007.spa
dc.relation.references77. Chen Y., Li C. (2009) : Prognostic significance of brain natriuretic peptide obtained in the ED in patients with SIRS or sepsis. American Journal of Emergency Medicine, 27: 701-706.spa
dc.relation.references78. Klouche, K., Pommet, S., Amigues, L., et al (2014) Plasma Brain Natriuretic Peptide and Troponin Levels in Severe Sepsis and Septic Shock : Relationships With Systolic Myocardial Dysfunction and Intensive Care Unit Mortality. Journal or Intensive Care Medicine, 29(4):229-37spa
dc.relation.references79. Charpentier J, Luyt CE, Fulla Y, et al. (2004) Brain natriuretic peptide: a marker of myocardial dysfunction and prognosis during severe sepsis. Critical Care of Medicine. 32(3):660-665.spa
dc.relation.references80. Maeder M, Ammann P, Kiowski W, Rickli H. (2005) B-type natriuretic peptide in patients with sepsis and preserved left ventricular ejection fraction. European Journal of Heart Failure. 2005;7(7):1164-1167.spa
dc.relation.references81. Landesber, G., Jaffe, A., Gilon, Dan., et al. (2014) Troponin Elevation in Severe Sepsis and Septic Shock: The Role of Left Ventricular Diastolic Dysfunction and Right Ventricular Dilatation. Critical Care of Medicine. 42:790–800.spa
dc.relation.references82. Redfield MM, Jacobsen SJ, Burnett JC Jr, et al.(2003) Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JaMa. 289:194-202.spa
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dc.subject.lembSíndrome de respuesta inflamatoria sistémicaspa
dc.subject.lembMiocardiopatía sépticaspa
dc.subject.lembSepsisspa
dc.subject.lembTroponina Ispa
dc.subject.lembMedicinaspa
dc.subject.lembMedicina internaspa
dc.subject.lembInvestigacionesspa
dc.subject.lembComplicacionesspa
dc.subject.lembPacientesspa
dc.subject.lembPrevención y controlspa
dc.description.abstractenglishBackground: Sepsis represents an entity that is generated by a systemic response to infection. In1992 was defined based on the systemic inflammatory response syndrome (7), in 2016 it was modified and is now considered by The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) as an unregulated response to infection, that causes multiple organ dysfunction and endangers life. The cardiac biomarkers (Troponin I, NT pro BNP) was useful in the prediction of adverse outcomes in sepsis, however with the new definition this relationship is not proven. Methods: This study is an evaluation study of the diagnostic test in participants of the study "Association between the activity of extracellular matrix metalloproteinases (MMPs) and cardiovascular dysfunction in patients with sepsis. The association of NT pro BNP, troponin I and mortality, septic shock, systolic / diastolic dysfunction and admission to the ICU was calculated. Results: We analyzed 289 records. The median age of the patients was 63 years with an age range between 49-77 years. The median NT-pro BNP was 2099 (RIQ: 533-9051) and troponin I 0.1 (RIQ: 0.1-0.2). The SOFA median of 4 (RIQ: 0-13), of the APACHE II 13 (RIQ: 8-19). The most frequent origin of sepsis was the urinary tract (39.1%). 28.37% (82) of the cases in the cohort died. Systolic dysfunction was present in 39.83%, diastolic dysfunction 69.11%. 55.71% were managed in intensive care unit, 47.06% had sepsis. A statistically significant positive relationship (p <0.001) was found between serum levels of NT pro BNP, troponin I and mortality, systolic dysfunction and septic shock, with AUC with poor predictive capacity. No association was found with NT pro BNP, troponin I and diastolic dysfunction or admission to the ICU. Conclusions: Even with more specific criteria for the classification of sepsis, there is a significant association between biomarkers of myocardial injury in sepsis and adverse outcomes. Its psychometric characteristics are not the best, but in this study are similar to the risk scales known to date (SOFA-APACHE II)eng
dc.subject.proposalTercer consenso
dc.subject.proposalNT pro BNP
dc.subject.proposalMortalidad
dc.subject.proposalDisfunción sistólica
dc.subject.proposalDisfunción diastólica
dc.subject.proposalChoque séptico
dc.subject.proposalUnidad de cuidados intensivos
dc.type.redcolhttp://purl.org/redcol/resource_type/TM
dc.rights.creativecommonsAtribución-NoComercial-SinDerivadas 2.5 Colombia*
dc.contributor.researchgroupGrupo de Investigación en Ciencias y Educación en Saludspa
dc.contributor.researchgroupGrupo de Investigaciones Clínicasspa
dc.coverage.campusUNAB Campus Bucaramangaspa
dc.description.learningmodalityModalidad Presencialspa


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Atribución-NoComercial-SinDerivadas 2.5 Colombia
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