egdt and egdt and inflammationinflammation management of ... sa borges... · egdt and egdt and...
TRANSCRIPT
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EGDT and EGDT and InflammationInflammation
Management of Management of SepsisSepsis
Dr. Márcio Borges SáCoordinator of Multidisciplinary Sepsis UnitIntensive Care Medicine.Hospital Son Llàtzer. Palma de Mallorca. Spain.
UPDATEUPDATE--SUMMIT DE ENFERMEDADES INFECCIOSAS, Valenci a, 23/03/2007SUMMIT DE ENFERMEDADES INFECCIOSAS, Valencia, 23/03 /2007 ..
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Is it important EGDT?
-- Management change
- Higher incidence- Higher incidence
- Higher mortality
PIMIS PROYECT
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SEPSISSEPSIS
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COMPLICADA FISIOPATOLOGÍA: INTERACCIÓN COMPLEJAP
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ENDOTELIO ES LA BASE FUNDAMENTALENDOTELIO ES LA BASE FUNDAMENTAL
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TIC
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SEPSIS: NUEVOS y “ANTIGUOS CONCEPTOS”
• CASCADA INFLAMATORIA
• SEPSIS y SISTEMA INMUNE
• MEC. INMUNOSUPRESIÓN
1. Citoquinas: PRO/ANTI-Inflam.
2. Anergia
3. Apoptosis3. Apoptosis
4. Muerte de células sistema inmune
• SEPSIS Y COAGULACIÓN
• SEPSIS Y ENDOTELIO
• FACTORES GENÉTICOS
• HIBERNACIÓN CELULAR
• MUERTE y SEPSIS
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CASCADA INFLAMATORIA
TNFIL-1IL-8IL-6 Y IL-10Radicales O2PAFProteasasProstaglandinas
TNF
IL-1
ProstaglandinasLeucotrienosBradiquininas
MICROTROMBOSIS
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MECANISMOS INMUNOSUPRESIÓN
* CD4 activadas secretan Citoquinas
- Inflamatorias (Th1): TNFα; Intef.γ;
- Anti-Inflam. (Th2): IL-4; IL-10
* Anergia: no respuesta a un Ag.
Cels. T. Incapaz proliferar o secretar Cels. T. Incapaz proliferar o secretar citoquinas frente Antígenos
• Apoptosis: muerte genetic. prog.
1. Cel Necrotica: ↑ Th1
2. Cel. Apoptotica: ↑ Th2 y Anergia
• Muerte Células Inmunes
Th2 Th1
CD4
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Lesión VascularActiva V y VIIIActiva XIFibronógeno: fibrinaFactor XIII: coáguloActiva Plaquetas“ Cels. EndotelialesAdhesión leucos/endot.↑Permeab. Vascular↑ citoquinas/proteasas
SEPSIS y COAGULACIÓN: TROMBINA
↑ citoquinas/proteasas↑Unión trombomodulina↑ APC y TAFI
1. Procoagulante2. Proinflamatoria3. Antifibrinolítica
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SEPSIS Y ENDOTELIO
heterogeneidad
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HOMEOSTASIS Y SEPSIS
↓ Fibrinolisis
• mediadores proinflamatorios
• lesión endotelial
• expresión factor tisular
• producción trombina
↑Coagulación↑Inflamación
• ↑↑↑↑ PAI-1• ↑↑↑↑ TAFI• ↓↓↓↓ Proteína C
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FACTORES GENÉTICOS
• Determinantes susceptib.
• Polimorfismos identificados:
- Recept. TNF, IL-1, Fcγ y TLRs.
• Polimorfismo y Citoquinas:Polimorfismo y Citoquinas:
- Determinar Inflam/Anti-Inflamat.
- Hiper/Hipo respuesta a Infección
• Riesgo Muerte y Polimorfismo:
- TNF-α y TNF-β en SEPSIS
• Trat. Inmuno-Modulador!!
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MUERTE y SEPSIS
• Autopsias en SEPSIS¿?¿?
• Shock refractario¿?
• Depresión miocárdica!¿?
• Arritmias!¿?
• SDRA: Hipoxemia Refract.
SEPSIS
• SDRA: Hipoxemia Refract.
• F. Renal Agudo: poco!!!!
• FMO (es vago!!!!)
• Disociación en necropsias!
• Porque Mueren!!!
enfermo
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SEPSIS“RESPOSTA INFLAMATORIA DESCONTROLADA”
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SEPSISSEPSIS
Vincent et al, Am J Resp Crit Care Med. 2006.
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MOF and MORTALITY: SOAP STUDYMOF and MORTALITY: SOAP STUDY
Vincent et al. SOAP study. CCM. 2006
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EPIDEMIOLOGÍA SEPSIS EN USAEPIDEMIOLOGÍA SEPSIS EN USAAngus et al; Crit Care Med; 2001Angus et al; Crit Care Med; 2001
45,8
30
35
40
45
50%
Nº=192.980 pts
Incidencia de DMOIncidencia de DMO
24,4 22 20,6
9,31,3
0
5
10
15
20
25
30
RESP CARDVASC RENAL HEMAT SNC HEPAT
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EPIDEMIOLOGÍA SEPSIS EN USAEPIDEMIOLOGÍA SEPSIS EN USAAngus et al; Crit Care MedAngus et al; Crit Care Med; 2001; 2001
40,1 38,2
54,3
40
50
60%
Nº=192.980 pts
Mortalidad de DMOMortalidad de DMO
40,1
32,438,2
22,8 24,4
0
10
20
30
RESP CARDVASC RENAL HEMAT SNC HEPAT
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Disfunción de órganos y mortalidad:Cambios evolutivos en las primeras 24 horas
Levy M. Early changes in organ function predict eventual survival in severe sepsis. Crit Care Med 2005; 33: 2194-2201.
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¡¿PODRÍA SER PEOR!?
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SEPSISSEPSIS
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ESTEROIDES Y SEPSISESTEROIDES Y SEPSIS
CORTICUS TRIAL Annane et al
Vasopresores 1 h (TAS)Vasopresores 1 h (TAS) TAS < 90 TAS < 90 mmHmmH > 1 h con Vs> 1 h con Vs
Quirúrgicos: 65%Quirúrgicos: 65% Médicos: 60%Médicos: 60%Quirúrgicos: 65%Quirúrgicos: 65% Médicos: 60%Médicos: 60%
Abdomen 36%, Pulmón 30%Abdomen 36%, Pulmón 30% Abdomen 16%, Pulmón 44%Abdomen 16%, Pulmón 44%
NoNo--resp: 45%resp: 45% No resp: 77%No resp: 77%
Mort. Cruda: 32,4%Mort. Cruda: 32,4% Mort. Cruda: 58%Mort. Cruda: 58%
Annane et al, JAMA, 2002.Sprung, NEJM.2008
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Estudios de Estudios de PCArPCAr Y SEPSISY SEPSIS
Mortalidad PCAr Placebo P
PROWESS 24,7 30,8 0,05
ENHANCE * 25,3 NO -ENHANCE * 25,3 NO -
ADDRESS 18,5 17 NS
*: Si inicio de PCA < 24 hs menor mortalidad: 22,9% vs 27,4%, p=0,01ENHANCE ↑↑↑↑ hemorragias graves que PROWESS (6,5% vs 3,5%).
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ICNARCICNARC: : DrotrecoginDrotrecogin alfaalfa (activated): (activated): RealReal--life use and outcomes for the UKlife use and outcomes for the UK11
• The aims of this audit were to monitor the real-life use of DrotAA and subsequent outcomes;to undertake a rigorous, nonrandomized evaluation of the effectiveness of DrotAA, by linkingthe data on DrotAA to the ongoing outcome audit for all admissions to adult, general criticalcare units; and to compare our results with those from the PROWESS study
197 unitsinvited to participate
1:Adapted from Rowan KM et al. Crit Care. 2008,12:R58
133 unitsagreed to participate
13 unitswithdrew
or were lapsed
8 unitswere excluded
112 unitsactively participated
Recorded 1292 infusions of DrotAA
1079 admitted with severe sepsis and ≥2 organ failing (receiving DrotAA)
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Primary results of matched cohort analysis on acute hospitalmortality compared with PROWESS on 28-days
ICNARC: ICNARC: DrotrecoginDrotrecogin alfaalfa (activated): (activated): RealReal--life use and outcomes for the UKlife use and outcomes for the UK 11
Individual Matching
Historic, same unit 287/609 332/609 0.008 7.4%
Contemporaneous, same unit 353/764 406/764 0.002 6.9%
Contemporaneous, non-DrotAA unit 285/666 362/666 <0.001 11.5%
DrotAA (n/N)
Control (n/N) p ARR
27
1: Adapted from Rowan KM et al. Crit Care. 2008,12:R58
0.6 0.7 0.8 0.9 1.0 1.2Relative Risk
Favors DrotAA Favors control
Propensity Matching
Contemporaneous, non-DrotAA unit 285/666 362/666 <0.001 11.5%
Contemporaneous, DrotAA unit prior to first use 422/922 486/922 0.001 6.9%
Historic, same unit 436/929 494/929 0.003 6.3%
Contemporaneous, same unit 480/1049 516/1049 0.11 3.4%
Contemporaneous, non-DrotAA unit 364/818 476/818 <0.001 13.7%
Contemporaneous, DrotAA unit prior to first use 479/1053 561/1053 <0.001 7.8%
PROWESS 210/850 259/840 0.005 6.1%
ARR: Absolute Risk Reduction
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Subgroup results: acute hospital mortality for individual matching toc o n t r o l p o o l 4 . P o o l 4 i n c l u d e s p a t i e n t s f r o m acontemporaneous DrotAA unit but before the first use in that unit
ICNARC: ICNARC: DrotrecoginDrotrecogin alfaalfa (activated): (activated): RealReal--life use and outcomes for the UKlife use and outcomes for the UK 11
DrotAA (n/N)
Control (n/N) p
67/260 77/226<5399/209 122/22653-63110/213 106/21564-71146/240 181/25572+
422/922 486/922 0.001All patients0.30Age (years)
0.17Sex
28
1: Adapted from Rowan KM et al. Crit Care. 2008,12:R58
201/454 223/425Female221/468 263/497Male
0.17Sex
74/185 62/1852147/389 184/3893201/348 240/3484 or 5
0.024Organs failing (n)
107/331 97/305<20121/259 149/27020-24117/205 141/21025-2977/127 99/13730+
0.36APACHE II score
79/236 64/242<2581/206 112/22725-30102/210 129/20331-35160/270 181/25036+
0.031ICNARC physiology score
0.6 0.7 0.8 1.0 1.2
Relative RiskFavors DrotAA Favors control
0.50.4 1.4 1.6
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Estudios de GEstudios de G--CSF Y SEPSISCSF Y SEPSIS
Autor/Año
-Tipo
Diseño Nº pacientes Mortalidad Efectos2º#
Nelson/2000
-NAC
DC Filg=237
Plac=243
NS* NS
Wunderlink/2001
-NAC/Nosoc
DC Filg=12
Plac=6
Filg: 4/12
Plac: 6/6
NS
-NAC/Nosoc Plac=6 Plac: 6/6
Root/2003
-NAC/Nosoc
DC NS NS
Hartmann/2005
-Nosoc
DC Filg=12
Plac=16
NS** NS
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ATB Y SEPSIS: PRECOCIDADATB Y SEPSIS: PRECOCIDAD
Retraso desde inicio hipoTa Mortalidad
00--29 min29 min 17,3%17,3%
3030--59 min59 min 22,8%22,8%3030--59 min59 min 22,8%22,8%
11--2 hs2 hs 29,5%29,5%
6 hs6 hs 58%58%
99--12 hs12 hs 74,6%74,6%
Kumar et al, CCM, 2006;34.
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Clin Inf Dis. 2008..
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“La mayor oportunidad de mejorar el pronóstico de nuestros pacientes en los próximos 25 años
no va a venir del descubrimiento de nuevas terapias, sino del uso mas efectivo de
“Hacia donde va la práctica clínica en la sepsis“
terapias, sino del uso mas efectivo de las ya existentes“
Pronovost P.J. Lancet 2004;363:1061-67
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Ley de los BorgiasLey de los Borgias
“Dos venenos matan más que uno...”(César Borgia)
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TERAPIA INICIAL
TRATAMIENTO SOPORTE
Control foco
SEPSIS
TRATAMIENTOSSEPSIS: PCA-r, EsteroidesNUEVAS PERSPECTVAS
MULTIDISCIPLINAR
ATBATB
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Early goal-directed therapy ((resuscitationresuscitation byby objetives)objetives)
Rivers E. N Engl J Med 2001; 345:1368-77
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EARLY-GOAL DIRECT THERAPY
46,540
50
p=0,009
30,5
0
10
20
30
MortalityEGDT CT Rivers E, et al. NEJM. 2001
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SEPSIS INICIATIVES: EGDTSEPSIS INICIATIVES: EGDT
NºPREPts
(mort%)
POSTPts
(Mort%)p/OR/NNT
Trzeciak,USA, 06Trzeciak,USA, 06
URGURG3838
1616
(43,8)(43,8)
2222
(18,2)(18,2)
0,090,09; OR 0,4; OR 0,4
NNT=6NNT=6
Gaisky,USA, 06*Gaisky,USA, 06*
URGURG3838
2222
(55)(55)
1616
(25)(25)
0,10,1: 0R 0,27: 0R 0,27
NNT=3NNT=3
Micek, USA; 06Micek, USA; 06
URGURG120120
6060
(48,3)(48,3)
6060
(30)(30)
0,04; OR 0,460,04; OR 0,46
NNT=6NNT=6
Stentom, CAN,06*Stentom, CAN,06*
URGURG--UCIUCI9696
5151
(46,)(46,)
4545
(23,2)(23,2)
0,01; OR 0,340,01; OR 0,34
NNT=4NNT=4
GlobalGlobal 12981298671671
(44,8)(44,8)
627627
(24,5)(24,5)
RRR 45%;ARR 20,3%RRR 45%;ARR 20,3%
NNT=5NNT=5
Otero et al, Chest, 2006.
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SEPSIS SEPSIS
Prospective, 2 years, Emergence Dpt, 330 ptsProspective, 2 years, Emergence Dpt, 330 pts
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SEPSIS SEPSIS
Nguyen. CRIT CARE MED, 2007.
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MANEJO SEPSISMANEJO SEPSIS
Micek S et al, Crit Care Med. 2006, 34;2707Micek S et al, Crit Care Med. 2006, 34;2707--2713.2713.
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SEPSIS MANAGEMENTSEPSIS MANAGEMENT
Variables Before After p
LOS (LOS (daysdays))
MicekMicek CCM, 2006CCM, 2006 12,112,1±±9,29,2 8,98,9±±7,27,2 0,030,03
2828--day day MortalityMortality
Micek S et al, Crit Care Med. 2006.
* Shorr et al, Crit Care Med. 2007.
2828--day day MortalityMortality
MicekMicek, CCM, 2006, CCM, 200648,3%48,3% 30,0%30,0% 0,040,04
CostsCosts **
ShorrShorr, CCM, 2007, CCM, 2007$21,985$21,985 $16,103$16,103 0,0080,008
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MANEJO SEPSISMANEJO SEPSIS
Micek S et al, Crit Care Med. 2006.
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IMPACT OF BUNDLES IMPLEMENTATION IN THE FIRST 6 HOURS
4 BUNDLES
Gao et al, Crit Care; 2005; Micek, CCM, 2006; Shapiro, CCM, 2007.
SAVE 1 LIFE
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PLASMATIC LACTATE: PLASMATIC LACTATE:
Dellinger and SSC. Intensive Crit Care. 2008..
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SEPSIS MANAGEMENTSEPSIS MANAGEMENT
Dellinger and SSC. Intensive Crit Care. 2008..
The goals of initial resuscitation
Should be include Lactate in the first hours of res uscitation
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SurvivingSurviving SepsisSepsis CampaignCampaign: 2007: 2007
Variable Comentarios Grado
Resucitación Inicial (< 6hs)
Iniciar inmediatamente si hipoTA o Lactato > 4 mmolUsar parámetros HD (PVC, TAM, diuresis, SATvO2)
I-C
Diagnóstico Obtener cultivos antes de ATB, pero no retrasarlosObtener estudios de imagen
I-C
Antibioticoterapia Inicio intravenoso primera hora: sepsis grave y shock sépticoAmplio espectro y parámetros PK-PDReevaluar diariamente ATB
I-D/I-BI-BI-C
Dellinger et al, Crit Care Med. 2007.
Reevaluar diariamente ATBDuración general: 7-10 dias, pero excepciones Considerar tratamiento combinado P. aeruginosa
Considerar “ “ en neutropenicos
Trat ATB combinado no más de 3-5 días y luego desescalada
según ATBiograma
I-CI-D2-D2-D2-D
Esteroides Test ACTH no recomendado para diagnóstico de ISRR
Considerar hidrocortisona i.v. Si hipoTA refractaria a fluidos/Vs
2-B2-C
PCA recombinante Considerar pacientes graves (APACHE II ≥ 25; DMO ≥ 2) sin CISG y bajo riesgo (APACHE < 20 y DMO= 1) no administrarla
2-B/2-CI-A
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SEPSIS MANAGEMENTSEPSIS MANAGEMENT
FEW
Nguyen et al, Ann Emerg Med. 2006.
FEWMINUTES
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RECOMENDACIONES DEL MANEJO DIAGNOSTICO-TERAPEUTICO INICIAL YDIAGNOSTICO-TERAPEUTICO INICIAL Y
MULTIDISCIPLINARIO DE LA SEPSIS GRAVE EN EL AMBITO HOSPITALARIO
GTEI. SEMICYUC.07Leon C. Med Intensiva. 2007
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Detección precoz y estratificación de pacientes con sepsis
¿Tiene historia de infección aguda?
¿Tiene el paciente dos o más signos o síntomas de infección? SRIS
si
si
Sepsis
Obtención de lactato
¿Hay evidencia de disfunción orgánica o hipo perfusión tisular durante la infección?
si
Hipoperfusión tisular presente*
Hipoperfusión tisular no presente
Sepsis
Sepsis Grave
Shock Séptico
si
Avisar Equipo de Sepsis
* TAS ≤ 90 mm Hg, TAM ≤ 65 mm Hg ó Lactato ≥ 3 mmol/l
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SEPSIS SEPSIS
Ferrer R. JAMA. 2008;299(19):2294-2303
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BIOMARCADORESBIOMARCADORES
Biomarcadores seriados : 72 hs
RiversRivers E, E, CritCrit CareCare MedMed. 2007. 35.. 2007. 35.
Biomarcadores seriados : 72 hs
Relación biomarcadores :-Tipo estrategia terapéutica-Grado hipoxemia tisular:1. Lactato plasmático2. SvcO2-Disfunción Orgánica (DO)-Mortalidad
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BIOMARCADORESBIOMARCADORES
NS
Rivers E, Crit Care Med. 2007. 35.
NS
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BIOMARCADORESBIOMARCADORES
NIVELES PICO BIOMARCADORES: EGDT x CONTROLES
Rivers E, Crit Care Med. 2007. 35.
Pico BM: significativamente menores EGDT
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BIOMARCADORESBIOMARCADORES
NIVELES PICO BIOMARCADORES 72 hs: según grado hipox ia tisular
Rivers E, Crit Care Med. 2007. 35.
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BIOMARCADORESBIOMARCADORES
Biomarcador pIL-1ra <0,001
Media niveles BM eran significativamente mayores en no supervivientes que supervivientes intra-hospital ario
Rivers E, Crit Care Med. 2007. 35.
ICAM-1 =0,001
TNF-α =0,007
Casp-3 <0.01
IL-8 <0,001
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BIOMARCADORESBIOMARCADORES
Antagonista receptor IL-1 (IL-1ra)
Rivers E, Crit Care Med. 2007. 35.
p=0,026: 0-72 hs p<0,006: 12-72 hs
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BIOMARCADORESBIOMARCADORES
Rivers E, Crit Care Med. 2007. 35.
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SEPSIS MANEJO: MUSTSEPSIS MANEJO: MUST
Shapiro et al, CCM, 2006;34:2707Shapiro et al, CCM, 2006;34:2707--2713.2713.
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MultidisciplinaryMultidisciplinary SepsisSepsis UnitUnitSon Son Llàtzer`sLlàtzer`s experienceexperience
UPDATEUPDATE--SUMMIT DE ENFERMEDADES INFECCIOSAS, Valenci a, 23/03/2007SUMMIT DE ENFERMEDADES INFECCIOSAS, Valencia, 23/03 /2007 ..
Son Son Llàtzer`sLlàtzer`s experienceexperience
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Adult patients attending the Hospital with:
Suspected infectionSuspected infection+
> 2 SIRS criteria+
≥ 1 Organ disfunction
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SIRS:SIRS:SIRS:SIRS:TemperatureTemperature >38ºC>38ºCTemperatureTemperature <36ºC<36ºCHeartHeart raterate >> 90bpm90bpmRespìratoryRespìratory raterate >> 20 rpm20 rpmPaCO2 < 32 PaCO2 < 32 mmHgmmHgLeukocytesLeukocytes > > 1200012000LeukocytesLeukocytes < < 4000 4000 oror >10% >10% immatureimmature formsforms
Levy MM et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions
Conference. Crit Care Med. 2003;31:1250-6.
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53,6
86
73
5660
70
80
90
100
SIRS
12,612
0
10
20
30
40
50
Fever HipoT TaquiC TRF LeucoC LeucP
%
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Organ disfunction:Organ disfunction:Arterial hypotension (SBP <90 mmHg or MAP < 70 mmHg or decrease > 40 mmHg)
Levy MM et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions
Conference. Crit Care Med. 2003;31:1250-6.
70 mmHg or decrease > 40 mmHg)PaO2/FiO2 <300 or SpO2 < 90%Urine output <0.5 ml/Kg/h or < 45 ml/ 2hAltered mental statusCreatinine increase >0.5 mg/dl o doubledINR >1.5 or aPTT>60 secsPlatelet < 100000 Bilirubin >4 mg /dlC-reactive protein > 2 SD above normal valueLactate > 3 mmol/l
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58,150,5
36,940
50
60
70
Organ Failure IOrgan Failure I
20,3
0
10
20
30
HypoTA Hypoxe Oliguria Concien
%
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SIRS and MORTALITYSIRS and MORTALITY
Alive n(%) Dead n(%) OR (IC95%) p
Fever 177 (77,3) 52 (22,7) 0,68 (0,50-0,91) 0,008
Hypothermia 40 (63) 23 (36,5) 1,34 (0,94-1,93) 0,125
HR > 90 291 (72,4) 111 (27,6) 0,85 (0,59-1,22) 0,387
RR > 24 249 (70,5) 104 (29,5) 1,16 (0,83-1,63) 0,385
paCO2< 32 103 (70,5) 43 (29,5) 1,05 (0,78-1,43) 0,733
Leuk> 12.000 196 (73,4) 71 (26,6) 0,87 (0,06-1,15) 0,327
Leuk< 4.000 35 (63,6) 20 (36,4) 1,33 (0,91-1,95) 0,163
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MOF and MORTALITYMOF and MORTALITY
Organ Failure Alive n (%) Dead n (%) OR (IC95%) p
MAP < 70 mmHg 176 (68.8) 80 (31.3) 1.24 (0.93-1.66) 0.137
paO2/FiO2 <300 189 (72.1) 73 (27.9) 0.96 (0.72-1.28) 0.777
Oliguria 73 (52.9) 65 (47.1) 2.26 (1.72-2.97) <0.001Oliguria 73 (52.9) 65 (47.1) 2.26 (1.72-2.97) <0.001
Impaired mental 72 (63.7) 41 (36.3) 1.40 (1.04-1.89) 0.033
Creatinine x 2 68 (54) 58 (46) 2.08 (1.59-2.74) <0.001
Coagulopaty 52 (59.8) 35 (40.2) 1.56 (.15-2.12) 0.007
Bilirubin >4 16 (50) 16 (50) 1.86 (1.28-2.72) 0.005
CRP x 2 78 (80.4) 19 (19.6) 0.64 (0.42-0.99) 0.031
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60
80
100
RELACIÓN DMO Y MORTALIDAD INTRAHOSPITALARIARELACIÓN DMO Y MORTALIDAD INTRAHOSPITALARIA
0
20
40
1 2 3 >4
Vivo Exitus*: p<0,001
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Intensive Care Med. 2007 Nov; 33 (11)
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LACTATO: PREDICTOR LACTATO: PREDICTOR
Trzeciak et al, Intensive Care Med. 2007.
Mortalidad intra-hosp: 15%, 25% y 38% según interva lo lactato
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Nguyen H al, Crit Care Med. 2004
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OCCULT SHOCK: LACTATEOCCULT SHOCK: LACTATE
28-day Mortality: predictors of risk: SBP and Serum Lactate
After adjust SBP: Lactate independent factor associated with mortality: p<0,001
Howell M et al, ICM, 2007.
AUC: 0,87
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PIMIS: LACTATEPIMIS: LACTATE
InitialInitial 6h6h 12 h12 h pp
SevereSevere sepsissepsis 2.2 (1.6) 1.7 (1.3) 1.5 (0.8)In-6h: 0,02In-12h: 0,0016h-12h: 0,03
In-6h: 0,01
Socias A, Borges M, ICM (abst), 2007.
SepticSeptic shockshock** 3.3 (2.7) 2.9 (2.6) 2.6 (2.6)In-6h: 0,01In-12h: 0,0016h-12h: 0,04
p p ** <0.0001 <0.0001 <0.0001 ///////
NO DIFFERENCES MEDIAN LACTATE BETWEEN MED NO DIFFERENCES MEDIAN LACTATE BETWEEN MED -- SURGSURG
500 first episodies
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PIMIS: LACTATEPIMIS: LACTATE
FactorFactor Lactate 0h Lactate 0h Lactate 6h Lactate 6h Lactate 12h Lactate 12h
SOFA 0SOFA 0pRho Spearman
<0,00010.269
<0,00010.282
0,0020.242
SOFA 1dSOFA 1dpRho Spearman
0,0010.220
<0,00010.277
<0,00010.285
Borges M, ICM, abst 2007.
SOFA 2dSOFA 2d pRho Spearman
0,0450.141
0,0120.206
0,0010.282
SOFA 3dSOFA 3dpRho Spearman
0,0690.131
0,0680,151
0,0060.228
SOFA 5dSOFA 5d pRho Spearman
0,3420,071
0,7960.022
0,0030.255
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OrganOrgan disfunctiondisfunction and and mortalitymortality
25
30
35
40%
Present
*
*
* p<0.05* p<0.05
0
5
10
15
20
MAP<70
PaO2/FiO
2<300
Oligur ia
Impaired consciousness
Creatinine x 2Im
paired coagulation
Bilir rubin>4C protein x 2Initial lactate>3
Present Absent*
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SERUMSERUM LACTATE MEAN andLACTATE MEAN andMORTALITYMORTALITY
Value DE p
Lactate 0Lactate 0 3,963,96 0,570,57 0,00010,0001Lactate 0Lactate 0 3,963,96 0,570,57 0,00010,0001
LactateLactate 6 h6 h 3,863,86 0,690,69 0,00010,0001
LactateLactate 12 h12 h 3,823,82 0,740,74 0,00010,0001
Borges M, Socias A, ICM (abst), 2007.
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54
40
50
60 OR IC 95%%
5,755,75 2,652,65--12,4612,46
LACTATE “0” - MORTALITY
p=0,001
Age, sex, nº OD, Vasoactive
20
0
10
20
30
<3,5 >=3,5%
OR IC 95%%
3,073,07 1,241,24--7,557,55
Age, sex, nº OD, VasoactiveDegree sepsis, hypoxemia
Borges M, Med Intensiva, 2007
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47,7
30
40
50 OR IC 95%%
4,484,48 1,861,86--10,7710,77
Δ LACTATE “0-6 hs” and MORTALITY
p=0,001Age, sex, nº OF, Vasoactive
16,9
0
10
20
>Basal <=Basal%
p=0,001
OR IC 95%%
4,514,51 1,701,70--11,9811,98
Age, sex, nº OF, VasoactiveDegree Sepsis, hypoxemia
Borges M, Med Intensiva, 2007
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56
40
50
60 OR IC 95%%
4,664,66 1,811,81--12,0612,06
LACTATE CLEARANCE (0-6 hs) and MORTALITY
p=0,001 Age, sex, nº OF, Vasoactive
21,4
0
10
20
30
<(-15%) >=(-15%)%
p=0,001
OR IC 95%%
4,584,58 1,451,45--14,4414,44
Age, sex, nº OF, VasoactiveDegree Sepsis, hypoxemia
Borges M, Med Intensiva, 2007
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62
40
50
60 OR IC 95%%
5,455,45 1,991,99--15,6615,66
LACTATE CLEARANCE (6-12 hs) and MORTALITY
p=0,0001 Age, sex, nº OF, Vasoactive
23
0
10
20
30
<(-15%) >=(-15%)%
p=0,0001
OR IC 95%%
4,954,95 1,891,89--16,5416,54
Age, sex, nº OF, VasoactiveDegree Sepsis, hypoxemia
Borges M, Med Intensiva, 2007
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PIMIS: LACTATEPIMIS: LACTATE
AUC 95% CI pLactate 0 h 0,617 0,536-0,699 0,003
Lactate 6 hs 0,602 0,504-0,700 0,032
Lactate 12 hs 0,721 0,633-0,809 <0,0001
Borges M, ICM (abst), 2007.
Lactate clearance0-6 hs
0,648 0,553-0,743 0,003
Lactate clearance6-12 hs
0,83 0,775-0,905 <0,0001
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Shock oculto
El 20% de los pacientes con shock séptico no tratado tienen hiperlactacidemia sin hipotensión
La importancia del shock oculto
El 50% de los pacientes resucitados del shock tienen hipoxia tisular oculta, a pesar de mantener constantes vitales normales y PVC normal (ScO2 baja, lactato elevado)
Rivers EP. Central venous oxygen saturation monitoring in the critically ill patient. Curr Opin Crit Care 2001; 7: 204-211.
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58,1
74,360
70
80
90
100
Occult hypoperfusion = Shock
Lactate 0: initial
Lactate 1: 6 hs
Lactate 2: 12 hs
58,1
48,6
30,1
0
10
20
30
40
50
HypoTA Lact0 Lact1 Lact2
% LactateLactate > 2,2> 2,2
Borges M, SEIMC, 2007
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OCCULT SHOCK
Relationship between MBP < 70 mmHg and mortality:-In the moment of protocol activation: 31,4%-At 6 hours: 45,7%.
Variable RR IC 95%MBP>70mmHg 1,985 (1.31-2.99)MBP<70mmHg 1,989 (1.25-3.16)
Relative risk(RR) of deaths in pts with normo or hy potensive was the same
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OCCULT SHOCK
PL < 3 < 3 ≥ 3 ≥ 3 p
PL-0 20,8% 40,3% 0,002
Relationship between Plasmatic Lactate (PL) and Mortality with MBP ≥70 mmHg:
PL-0 20,8% 40,3% 0,002
PL-6h 25,3% 52,2% 0,008
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PLASMATIC LACTATE: Value PLASMATIC LACTATE: Value
Jansen et al, Crit Care. 2008.
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5,3 5,46
8
10
LACTATE OUTLACTATE OUT--SIDE HOSPITALSIDE HOSPITAL
p<0,02
LACTATE LEVELS AND OUTCOME
3,7 3,2
0
2
4
TI T2
Dead AliveJansen et al, Crit Care. 2008.
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PLASMATIC LACTATE: Value PLASMATIC LACTATE: Value
Jansen et al, Crit Care. 2008.
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PLASMATIC LACTATE: Value PLASMATIC LACTATE: Value
Jansen et al, Crit Care. 2008.
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�Inflammation: complex system�EGDT: ↓ mortality, resource`s use�EGDT: “gold standart”(¿?)�Complicated implemmentation�Diagnosis -“simultaneuos” therapies
UPDATEUPDATE--SUMMIT DE ENFERMEDADES INFECCIOSAS, Valenci a, 23/03/2007SUMMIT DE ENFERMEDADES INFECCIOSAS, Valencia, 23/03 /2007 ..EGDTEGDT--InflammationInflammation
�Diagnosis -“simultaneuos” therapies�Clasical SIRS: few role�OF: main objetive�Tissue Hypoxia: Inflammation (BM)�Individualized each case/hospital
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Muito obrigado!
UPDATEUPDATE--SUMMIT DE ENFERMEDADES INFECCIOSAS, Valenci a, 23/03/2007SUMMIT DE ENFERMEDADES INFECCIOSAS, Valencia, 23/03 /2007 ..EGDTEGDT--InflammationInflammation