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dc.contributor | Machado Romero, Carlos Alfonso | |
dc.contributor | Higuera Cobos, Juan Diego | |
dc.contributor | Ochoa Vera, Miguel Enrique | |
dc.contributor | https://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0000898465 | |
dc.contributor | https://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0001543126 | |
dc.contributor | https://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0001692834 | |
dc.contributor | https://orcid.org/0000-0002-4552-3388 | |
dc.contributor | https://orcid.org/0000-0003-2622-9412 | |
dc.contributor | https://www.scopus.com/authid/detail.uri?authorId=36987156500 | |
dc.contributor | https://www.researchgate.net/profile/Miguel_Ochoa7 | |
dc.contributor | Grupo de Investigación en Ciencias y Educación en Salud | |
dc.creator | Rueda Galvis, Myriam Vanessa | |
dc.date | 2020-06-26T19:59:54Z | |
dc.date | 2020-06-26T19:59:54Z | |
dc.date | 2018 | |
dc.date.accessioned | 2022-03-14T20:09:37Z | |
dc.date.available | 2022-03-14T20:09:37Z | |
dc.identifier | http://hdl.handle.net/20.500.12749/1734 | |
dc.identifier | instname:Universidad Autónoma de Bucaramanga - UNAB | |
dc.identifier | reponame:Repositorio Institucional UNAB | |
dc.identifier.uri | http://biblioteca-repositorio.clacso.edu.ar/handle/CLACSO/22305 | |
dc.description | Introducción: 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) | |
dc.description | RESUMEN 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 .................................................................................................................... 88 | |
dc.description | Especialización | |
dc.description | Background: 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) | |
dc.format | application/pdf | |
dc.format | application/pdf | |
dc.format | application/pdf | |
dc.language | spa | |
dc.publisher | Universidad Autónoma de Bucaramanga UNAB | |
dc.publisher | Facultad Ciencias de la Salud | |
dc.publisher | Especialización en Medicina Interna | |
dc.relation | Rueda 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 UNAB | |
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dc.rights | http://creativecommons.org/licenses/by-nc-nd/2.5/co/ | |
dc.rights | Abierto (Texto Completo) | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.rights | http://purl.org/coar/access_right/c_abf2 | |
dc.rights | Atribución-NoComercial-SinDerivadas 2.5 Colombia | |
dc.subject | Systemic inflammatory response syndrome | |
dc.subject | Septic cardiomyopathy | |
dc.subject | Sepsis | |
dc.subject | Troponin I | |
dc.subject | Medicine | |
dc.subject | Internal medicine | |
dc.subject | Investigations | |
dc.subject | Complications | |
dc.subject | Patients | |
dc.subject | Prevention and control | |
dc.subject | Third consensus | |
dc.subject | Mortality | |
dc.subject | Systolic dysfunction | |
dc.subject | Diastolic dysfunction | |
dc.subject | Septic shock | |
dc.subject | Intensive care unit | |
dc.subject | Síndrome de respuesta inflamatoria sistémica | |
dc.subject | Miocardiopatía séptica | |
dc.subject | Sepsis | |
dc.subject | Troponina I | |
dc.subject | Medicina | |
dc.subject | Medicina interna | |
dc.subject | Investigaciones | |
dc.subject | Complicaciones | |
dc.subject | Pacientes | |
dc.subject | Prevención y control | |
dc.subject | Tercer consenso | |
dc.subject | NT pro BNP | |
dc.subject | Mortalidad | |
dc.subject | Disfunción sistólica | |
dc.subject | Disfunción diastólica | |
dc.subject | Choque séptico | |
dc.subject | Unidad de cuidados intensivos | |
dc.title | Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis | |
dc.title | Strength of association between Troponin I, NT-pro BNP and adverse outcomes in sepsis | |
dc.type | info:eu-repo/semantics/masterThesis | |
dc.type | Tesis | |
dc.type | http://purl.org/coar/resource_type/c_bdcc | |
dc.type | info:eu-repo/semantics/acceptedVersion | |
dc.type | http://purl.org/redcol/resource_type/TM | |
dc.coverage | Bucaramanga (Santander, Colombia) |
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