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- 1. SHOCK
- 2. CLASIFICACION DEL SHOCK Séptico Sx Shock Tóxico Anafiláctico Neurogénico Tóxico Nitroprusiato Bretililio Endocrinológico Crisis Adrenal T. Tiroidea Disfunción Diastólico Obstrucción V.C. Tumor Presión Intrator. PTx Tensión Complacencia Pericarditis CTx Taponamiento Disfunción Sisitólica V. Derecho TEP Masiva HTPulm Aguda V. Izq. TEP Saddle Disec. Aórtica Miopático IAM Izq/Der Contusión Miocarditis CMP Depresión Farmacológico Mecánico Valvulopatías CMP Hipertrófica CIV Arrítmias Bradicardia Sinusal (Vagal) Bloqueo A-V Taquicardia SVT/Ventricular Hemorrágico Trauma GI Retroperitoneal Depleción Líquidos Pérdida Externa DHE Diarrea/Vómitos Poliuria Redistribución Lesión Térmica Trauma Anafiláxis Venodilatación Sepsis Anafiláxis Toxinas/Drogas Distributivo Obstructivo Extracardiaco Cardiogénico Hipovolémico
- 3. CHOQUE SEPTICO EN EMBARAZO
- 5. Sepsis Severa: Un desafío creciente *Angus DC. Crit Care Med. 2001. Hoy >750,000 casos de sepsis severa / año en US * Futuro 200,000 400,000 600,000 800,000 1,000,000 1,200,000 1,400,000 1,600,000 1,800,000 2001 2025 2050 Año 100,000 200,000 300,000 400,000 500,000 600,000 Severe Sepsis Cases US Population Casos de Sepsis Total US Population/1,000
- 7. DEFINICIONES S. Séptico 60% (40-50% E. clínicos) S. Severa 40% (30-35% E. clínicos) Sepsis < 20%
- 8. Infección SIRS Shock Séptico Sepsis Severa Estas definiciones no implican una infección más severa, sino mas bien, un incremento en la severidad de la respuesta humana en contra de la infección (un continuum en la progresión de la misma enfermedad)
- 12. DISTRIBUCION POR SITIO DE INFECCION
- 17. PATOFISIOLOGIA INFLAMACION NEJM 1999;340:207-214
- 18. MODULADORES ENDOGENOS DE HOMEOSTASIS Anticoagulación/Antitrombosis Proteina C Activada (PCA) Anti-trombina III Inhibidor de la vía Factor Tisular (TFPI) Fibrinolísis Activador del Plasminógeno Tisular(t-PA) Proteina C Activada Inhibe PAI-1 y t-PA Anti-Inflamación Citoquinas anti-inflamatorias(IL-6 y IL-10) Inhibe prod FNT y fxn Lts/macrof acción de Ig Proteina C Activada Inhibe actividad anti-inflam mediada por trombina Inhibe adhesión de PMN al endotelio Prevenir coagulación generalizada Remover microtrombos formados y mantener fluides sanguínea Disminuir la respuesta inflamatoria
- 20. APOPTOSIS Células B (CD 20) Folículos Linfoideos Trauma Sepsis
- 21. APOPTOSIS CD 21, Trauma CD 21, Sepsis Células T, CD 4 , Trauma Células T, CD 4, Sepsis
- 24. EARLY GOAL DIRECTED THERAPY Rivers et al .NEJM 2001;345:1368-77
- 25. EGDT Rivers et al . NEJM 2001;345:1368-77
- 26. Rivers et al .NEJM 2001;345:1368-77
- 27. Rivers et al .NEJM 2001;345:1368-77
- 35. Van den Berghe et al. NEJM 2001;345:1359-1367
- 39. JAMA 2002; 288: 862-971
- 40. JAMA 2002; 288: 862-971 Mortalidad Uso de Vasopresores
- 44. Diseño del Estudio Infección con falla orgánica Comienzo infusión de droga (24 g/kg) Máximo 48 Horas - Consentimiento - Comenzar droga Fin de 96 horas infusión de droga en estudio Mortalidad a 28 días de cualquier causa Vivo o Muerto? Cuidado de rutina
- 47. Resultados Placebo (n-840) Drotrecogin alfa (activated) (n=850) 35 Mortality (%) 30 25 20 15 10 5 Bernard GR et al. N Engl J Med 2001; 344:699-709. Primary analysis results 0.005 19.4% 2-sided P -value Adjusted relative risk risk reduction 6.1% absolute reduction in mortality 30.8% 24.7% Increase in Odds of Survival 38.1%
- 48. Mortalidad Según Severidad APACHE II 30 to 53 25 to 29 20 to 24 3 to 19 Shock Shock No Shock Relative Risk (%) -50 -40 -30 -20 -10 0 10 20 30 Drotrecogin Alfa N (activado) Placebo 451 38.1% 49.0% 366 23.5% 35.8% 440 22.5% 25.7% 433 15.1% 12.1% 1200 26.3% 34.2% 490 21.0% 22.3% Total
- 50. Costos Hospitalarios a 28 Días P = 0.89 0.99 0.72 No- Sobrevivientes Sobrevivientes Todos Costos 0 10,000 20,000 30,000 40,000 50,000 60,000 Drotrecogin alfa (activated ) Placebo
- 52. 0 1m 2m 3m Meses Mortalidad Log rank P = 0.048 Placebo Drotrecogin alfa Mortalidad a 3 Meses (Todos los Pacientes) 37.6% 33.9% 30.8% 24.7% 0.0 0.1 0.2 0.3 0.4
- 53. 0.0 0.1 0.2 0.3 0.4 0.5 0 3m 6m 1yr 1.5yrs 2yrs 2.5yrs Tiempo Rata Mortalidad Beneficio Sostenido Drotrecogín (Todos los Pacientes) Placebo Drotrecogín Alfa Log rank P = 0.097 Placebo Mediana Sobrevida = 846 days Drotrecogín Mediana Sobrevida = 1113 days 50.7% 47.4%
Notas del editor
- In the study by Angus et al described on the previous slide, the national estimate of severe sepsis was 750,000 cases. Since this figure was based on 1995 data, it is estimated that there will be more than 750,000 cases this year. Based on data from the US census, Angus et al estimate that the number of cases of severe sepsis will increase steadily at 1.5% per annum. This increase in the incidence of severe sepsis is greater than the anticipated population growth. The disproportionate growth is due to the high incidence of sepsis in older patients and a disproportionate increase in the number of elderly Americans (“graying” of America). Angus DC, Linde-Zwirble WT, Lidicker J, et al. Incidence, cost, outcome of severe sepsis in the United States. Crit Care Med. 2001 (In Press).
- The prospectively defined primary analysis quoted p-value for the effect of drotrecogin alfa (activated) on 28-day all-cause mortality compared with placebo was based on a Cochran-Mantel-Haenszel test stratified by three baseline covariates that were highly predictive of outcome in the placebo treatment group: Pre-infusion APACHE II score, a commonly used measure of baseline disease severity in sepsis trials Age class (<60 years, 60 years) Pre-infusion Protein C activity level 259 of the 840 patients in the placebo group (30.8%) and 210 of the 850 patients in the drotrecogin alfa (activated) group (24.7%) had died 28 days after the start of the study agent infusion (p=0.005 in the non-stratified analysis). The absolute reduction in mortality in the drotrecogin alfa (activated) group was 6.1%. The relative risk reduction and odds ratio were calculated using the logit-adjusted method with adjustments for the same three baseline covariates described above. The results of the prospectively defined primary analysis represent a reduction in the adjusted relative risk of death of 19.4% (95% confidence interval, 6.6 to 30.5) in the drotrecogin alfa (activated) group. Bernard GR, Vincent JL, Laterre PF, et al. Efficacy and safety of recombinant human activated Protein C for severe sepsis. N Engl J Med 2001;344:699-709.
- Drotrecogin alfa (activated) also produced a mortality benefit irrespective of the degree of organ dysfunction. Data on file, Eli Lilly and Company
- Statement: Xigris treated patients had significantly lower mortality rates over the 90 day study period compared to Placebo. Xigris significantly improved survival over the first 90 days. The mortality benefit for Xigris treated patients observed in PROWESS is persistent beyond just the 28 day study period. Interpretation: More Xigris patients survive the acute severe sepsis episode and go onto show better survival rates through 90 days compared to Placebo. Note: The p-Value represents survival analysis over the entire 90 days. Reference: DEREK ANGUS, CHEST 2002
- Statement: Xigris treated patients demonstrated lower long term mortality rates compared to Placebo. Interpretation: The Placebo and Xigris treatment arms never cross, showing that the Xigris survival benefit is not lost over the longer-term. It is important to note that the PROWESS trial was not powered (not enough patients enrolled) to determine long-term mortality benefit to 2.5 years. Note: Xigris improved median survival by 9 months compared to Placebo. Half of the Xigris treated patients survived for more than 1113. Half of the Placebo patients survived for 846 days. Reference: DEREK ANGUS, CHEST 2002