ANESTESIA EN EL TRASPLANTE

PULMONAR

Ana González Román

Sº Anestesia y Reanimación

Hospital Universitario Puerta de Hierro Majadahonda

RECUERDO HISTORICO

"El milagro de San Cosme y San Damián“ S. XII-XIII

RECUERDO HISTORICO

• 1963 → Hardy realiza 1er Tx pulmonar en humanos.

• 1968 → Denton Cooley

Fritz Derom

• 1983 → Cooper (Toronto, Canadá)

• 1990 → Ramón Arcas (Hospital Gregorio Marañón, España)

• INMUNOSUPRESION??

• 1990-2006 España → 1641 Tx pulmonares (36% EPOC).

ACTIVIDAD tx pulmon españa

El equipo de Coordinación…

EPIDEMIOLOGIA

EPIDEMIOLOGIA

JAMA 2010; 304:2620-2627

Donante

• 12 UCIs

• FR y Fi02 para CO2 40-45 mmHg y O2 >90 mmHg

• Válidos 6 h post MC: 95% en V protección y 54% en V conv

(p<0,001)

• Superv receptor a 6m: 75% V prot vs 69% V conv

• << IL-6 y TNF tras 6h de VM en V protección (p<0,05)

Mascia L, Pasero D, Slusky AS, et al. Effect of lung protective strategy

for organ donors on eligibility and availability of lungs for transplantation.

JAMA 2010; 304:2620–2627.

V convencional

• VT 10-12 ml/k + PEEP 3-5cmH2O

• Circ abierto de aspiración

• Test apnea en T

V protección

• VT 6-8 ml/k + PEEP 8-10cmH2O

• Circ cerrado de aspiración

• Test de apnea en CPAP

• Reclutamiento tras desconex

¿Cuándo está indicado el trasplante?

• ¿La gravedad de la enfermedad justifica la consideración del trasplante?

• Clase funcional NYHA III-IV.

• Expectativa de vida limitada 1-2 a.

• Deterioro progresivo a pesar de tto médico optimizado.

• Limite edad:

• Tx unipulmonar → 65 a.

• Tx bipulmonar → 60 a.

• ¿Existe enfermedad de otro órgano que contraindique el procedimiento?

INDICACIONES SEGUN PATOLOGIA

SUPERVIVENCIA MENOR DEL 50% A LOS 2 AÑOS

INDICACIONES SEGUN PATOLOGIA

CONTRAINDICACIONES

ELECCION DEL PROCEDIMIENTO

QUIRURGICO

• UNIPULMONAR

• EPOC

• PATOLOGIA INTERSTICIAL

• BIPULMONAR

• PATOLOGIA SEPTICA: FQ, Bronquiectasias

• ENFERMEDAD VASCULAR PULMONAR

• CARDIOPULMONAR

• ENFERMEDAD VASCULAR PULMONAR

VALORACION PREOPERATORIA

• RUTINA → HEMOGRAMA, COAGULACION, BIOQUIMICA

• RESPIRATORIO → RX TORAX, TAC , GAMMAGRAFIA PERFUSION PULMONAR

• CARDIOLOGICO → ECG, ECOCARDIOGRAMA, CORONARIOGRAFIA

• INFECCIOSO → SEROLOGIA, CULTIVOS, MANTOUX

• ESTADO NUTRICIONAL, PSICOLOGICO

Valoración preoperatoria

• Fisiopatología de la enfermedad de base

• Patología asociada

• Valoración cardiológica completa

( ECG, Eco , Coronariografía ( HTP, FE biventricular)

• Estado nutricional

• Rehabilitación con fisioterapia

• Valoración psiquiátrica

Fisiopatología

• EPOC: Disminución de flujos espiratorios, atrapamiento aéreo,

↑ volumen residual y espacio muerto.

• Enf. bronquiectasica ( patrón mixto).

• Enf. intersticiales : Restricción de todos los volúmenes

pulmonares, disminución de la elasticidad y complianza.

• Enf. vascular pulmonar: Primaria o secundaria a enf. cardiaca o

extracardiaca.

Ventilacion MecaNica no invasiva

Indicaciones

Fallo respiratorio hipercápnico

• IRCA

• Fallo respiratorio postextubación

• En lista de espera de TX PULMONAR

• Pacientes no candidatos a IOT

Fallo respiratorio hipoxémico

. Edema cardiogénico sin inestabilidad HD

. Fallo respiratorio postoperatorio

. Pacientes no candidatos a intubación

VMNI

Ventajas

• Aplicación de forma intermitente

• Fácil de retirar y reinstaurar

• Mayor confort ?

• Reduce necesidad de sedación

• Reduce la necesidad de SNG

• Evita complicaciones asociadas a la IOT ( menor nº de infecciones nosocomiales)

• Menor incidencia de atrofia muscular

• Instauración precoz

• Reducción de tiempo de estancia en UCPQ

MANEJO INTRAOPERATORIO

Monitorización

• Paciente despierto

• Premedicación ligera

• ECG 5 derivaciones

• SatO2

• ETCO2

• PAI

• Catéter Swan-Ganz

(PAP,PVC,GC,SVO2,RVP,RVS)

• ECO Transesofágico

• Tª,TOF,BIS,INVOS

• Monitorización respiratoria y

gasometrías seriadas

SWAN-GANZ

Inducción

• Lenta y progresiva ( ↓↓brusca de catecolaminas endógenas: hipotensión)

• Farmacos poco depresores

• Inotrópicos cargados

• Parámetros ventilatorios prefijados.

EVITAR VENTILACION MANUAL

• Tubo doble luz (fibrobroncoscopio)

En BQ y FQ tubo de una luz previo para limpieza de secreciones

IOT

• DE ELECCION: • TDL Robertshaw izquierdo.

• PATOLOGIA SEPTICA:

• 1º TET Unilumen → Aspiración secreciones → TDL

• Auscultación + Fibrobroncoscopio

• ALTERNATIVAS:

• TCB UNIVENT

• Bloqueador bronquial ARNDT

• Intubación selectiva bronquial TET simple

• CEC

• Fin intervención: TDL → TET Simple

Ventilación en paciente

con EPOC

Objetivos:

- Evitar atrapamiento aéreo

- Preservar tiempo espiratorio

Métodos:

- Evitar VT elevados

- Evitar Frecuencias Respiratorias elevadas

- Acortar la relación I:E ( 1:3-1:4- 1:5). Desconexiones intermitentes

- Flujos inspiratorios elevados

Mantener Pplateau < 25-30 cmH2O

EPOC DESPIERTO

EPOC ANESTESIA

Enfisema severo

MONITORIZACION

. Vía central yugular ipsilateral abordaje alto

. Paciente despierto : dtco clínico de neumotorax

PATRON VENTILATORIO

Evitar P intratorácicas altas

• VT bajos

• FR normales→ HIPERCAPNIA PERMISIVA

• Relación I/E : 1/4, 1/5, desconexiones intermitentes

OJO!! NEUMOTORAX PULMON DEPENDIENTE

Enfermedad de base

Hipercapnia permisiva

• Vasodilatación cerebral.

• Aumento de la PIC

• Narcosis

• Convulsiones

• Depresor miocárdico. Disminuye la contractilidad

• Incremento de la actividad simpática

Paso de respiración espontánea

a ventilación mecánica

• -↑ P.intratorácica media-↓ Retorno venoso ( En obstructivos- autopeep; restrictivos-disminución distensibilidad)

• -Hiperinsuflación en pacientes enfisematosos( Atrapamiento- neumotaponamiento- test de apnea)

• Fenómeno de interdependencia ventricular( la disfunción del VD reduce la complianza diastólica del VI por desviación del tabique IV)

Interacción con el V.I.

• Interdependencia ventricular

– Crecimiento en espacio pericárdico limitado

– Comparten septo interventricular

– Llenado izquierdo comprometido: GC reducido

Fases del Tx

PRIMER PULMON

-Peor relación V/Q

-Disfunción precoz del

injerto con > frecuencia

• Clampaje bronquial

• Clampaje arterial

• Reperfusión

SEGUNDO PULMON

. Clampaje bronquial

• Clampaje arterial

• Reperfusión

CLAMPAJE BRONQUIAL

Ventilación unipulmonar→SHUNT→HIPOXIA

- Reclutamiento

- FiO2 100%

- CPAP

- PEEP

- Ventilación intermitente

VENTILACION EN EL Tx UNIPULMONAR

• EPOC

• Vt 4-5ml/kg + flujos inspiratorios altos + ↑T espiratorio + ↓ I:E 1:5 + FR con hipercapnia permisiva (Ph> 7.30)

• FQ/Bronquiectasias

• Vt 8-10 ml/kg + I:E 1:1 + tiempos inspiratorios 5sg + aspiraciones frecuentes

• Restrictivos

• Vt 8-10 ml/kg + I:E elevada + P meseta < 35 cm H20 + PEEP

• HTP

• Vt 6-8 ml/kg + FR para normocapnia + FIO2 80-100%

VENTILACION EN EL Tx BIPULMONAR SECUENCIAL

• Toracotomía bilateral

• Inicio pulmón con peor V/Q

• Clampaje arteria 2º pulmón:

¡↑RIESGO EDEMA REPERFUSION + ENTRADA EN CEC!

• MANEJO

• Vt 6-8ml/kg + I:E 1:2 - 1:3 + PEEP 5-10 cm H2O + FIO2 ↑

CLAMPAJE ARTERIA PULMONAR

-Aumento RVP ↑ PAP

EVITAR FVD

- Vasodilatadores pulmonares ( NO, PGs)

- Inodilatadores ( dobutamina, milrinona)

- Noradrenalina para mantener PAM ¡PRESION DE PERFUSION!

ECO TRANSESOFAGICO

Valoración disfunción VD, anastomosis vasculares, detección

precoz de trombosis

Sobrecarga Presión VD Sobrecarga Volumen VD

Contractilidad VD

Triada del Fracaso de VD

Respuesta adaptativa en HP

El pronóstico de la HAP está determinado por cómo se

adapta el VD al ↑ de postcarga

Reversible (TEA, TxPulmonar)

HIPERTROFIA ADAPTATIVA DILATACIÓN + IªC

Isquemia

Cambios

estruct

Inflamación

Apoptosis

fibrosis

NeuroHormonas

Señales ICels

Control de la PAP

Aumentan Disminuyen

Hipoxia FiO2 ↑

Hipercapnia Hiperventilar

Acidosis Alcalosis

Hipotermia Normotermia

Anestesia superficial. Dolor Anestesia adecuada

↑ P. intratorácica: PEEP, atelectasias Volúmenes tidal normales

Vasodilatadores pulmonares

Vasodilatadores pulmonares

inhalados

↓ RVP

Poca repercusión TAS

Mejoran

ventilación/perfusión

Mejoran oxigenación arterial

iNO

( 10 – 40 ppm)

t½ = 2 – 6 sg

Admón. contínua

HP de rebote

Toxicidad clínica ( metaHb, N02

)

Técnicamente complejo

Iloprost

(10-20 µg)

t½ = 20 -30

min

Admón. 15 – 30 min.

Fácil aplicación.

Nebulizador ultrasónica r.inspir

Milrinona

NTG

De elección

HEMODINAMICA EN EL Tx PULMONAR

NPS, NTG y la PGI2, producen una vasodilatación indiscriminada en todo el parénquima pulmonar. El resultado es un efecto favorable sobre la resistencia venosa pulmonar (RVP) y la resistencia venosa sistémica (RVS), pero por otro lado aumenta el cortocircuito arteriovenoso (Qs/Qt), con lo que disminuye la tensión parcial de oxígeno arterial (PaO2). En contrapartida, el •NO reduce la RVP, no modifica la RVS y, muy importante, aumenta la PaO2 y reduce el Qs/Qt

CAUSAS DE CEC

•Hipoxia

•HTP

•FVD

•Dificultades técnicas

•Cirugía cardíaca asociada

¿CUANDO ENTRAR EN CEC?

• INDICACIONES:

• IC< 2 l/min/m

• SVO2 < 60%

• PAM < 50-60 mm Hg

• Sat < 85%

• Ph < 7

• EFECTOS SECUNDARIOS

• Disfunción de injerto

• ↑ tiempo quirúrgico

• Sobrecarga líquidos

• ↑ Necesidades transfusión

Manejo de CEC

• Heparinización: 3mg/K inicial; 1mg/k/h. ACT>450

• Normotermia→ PAM 50-60

• Ultrafiltración para evitar hemodilución y politransfusión

• Antifibrinolíticos ( tranexámico)

• Reversión heparina con protamina 1/1,5

• En perfusiones largas coagulopatía (hemoderivados: plasma,plaquetas, fibrinogeno)

• TROMBOELASTOGRAMA

Objetivos en la desconexión CEC

INICIAR LA VENTILACIÓN ANTES DE PERFUNDIR

- Prevención del FRACASO VENTRICULO DCHO

- Corrección de la COAGULACION

- Mantenimiento de la NORMOTERMIA

Sobrecarga Presión VD Sobrecarga Volumen VD

Contractilidad VD

Triada del Fracaso de VD

REPERFUSIÓN

- Reexpansión del pulmón implantado

(VT 6- 8 ml/kg , PEEP 6-10, Gasometrías seriadas)

- Desclampaje progresivo REPERFUSIÓN CONTROLADA

( compresión digital→ Hiperaflujo : aumento brusco de ETCO2)

- Arritmias

- Desviación del GC por ↓↓ brusca de RVP (

normovolemia)

HEMODINAMICA EN EL Tx PULMONAR

• REPERFUSION PULMON IMPLANTADO

• ↓ PAP + ↓ RVP + ↑ GC

¡EDEMA DE REPERFUSION!

• ↑ Ppulmonares + repercusión VD

• Etiología:

• Tiempo de isquemia

• Edema neurógeno donante

• Traumatismo quirúrgico, HTP, CEC

• MANEJO:

• Vasodilatadores, NO, O2

• ↓ POSTCARGA VD + MEJORAR LLENADO VI

Mantenimiento

• O2/AIRE

• FiO2 para mantener SAT O2>90

• Farmacos anestésicos según arte

• Inotrópicos para optimizar estado hemodinámico

• Manta térmica e infusores de sueros calientes

• Protección postural

• Cambio tubo una luz (fibrobroncoscopio: limpieza de secreciones, toma de muestras, comprobación suturas) y Traslado a la U. de Recuperación

Momentos críticos

• RESPIRACION ESPONTANEA → VM

• VENTILACION UNIPULMONAR

• CLAMPAJE ARTERIA PULMONAR

• REPERFUSION PULMON TX

• TRASLADO

POSTOPERATORIO

CONTROL HD Y RESPIRATORIO

• HEMODINAMICO

• PRIORIZAR ESTABILIDAD HD A BALANCE NEGATIVO

• RESTRICCION LIQUIDOS + PAM 50-60 mm Hg

• FLUIDOTERAPIA si:

• IC < 2.5 l/min/m, PCP < 6 mm Hg, PVC < 5 mm Hg

• RESPIRATORIO

• PO2 > 90 con < FIO2

• Ventilación protección pulmonar

• Intentar desconexión lo antes posible

• PULMON ANÓMALO* PULMON NORMAl

• Factores de riesgo ALI** No factores riesgo ALI

VT= 6ml/Kg de PBW VT< 10 ml/Kg de PBW

Ppl <15-20 cmH2O Ppl<15-20cm H2O

PEEP>=5cm H2O PEEP >=5 cm H2O

*Enfermedad pulmonar intersticial, resección pulmonar, neumonía severa, edema

**Sepsis, aspiración, Transfusión

Shultz MJ. Anesthesiology 2007; 106:1226-31

Parámetros para la ventilación

pulmonar selectiva

• “Intentar” FiO2 < 0,8-1

• Disminuir VT

• Pplat < 25 cmH2O VT<= 10 ml/Kg PBW

• Pplat 25-30 cmH2O VT 6-8 ml/Kg PBW

• Pplat > 30 cmH2O VT < 6ML/kg

PEEP>=5 cmH2O

• Ajustar FR para mantener VE

• Reclutamiento

Steinberg K, Kacmarek R

Respiratory Care 2007; 52: 556-567

Anesthesiology 2011; 114: 1102-10

“PEEP should be utilized in the same fashion as any

potent drug, ie dose should be tailored to each patient

according to his needs and response. Since the degree of

parenchymal injury varies from patient to patient the

requeriment for a specific level of PEEP may be

expected to vary. Arbitary selection of an upper (or

lower) limit prevents optimal utilitation of this

potentially live-saving technique”

Kirby 1975

Current opinion in anesthesiology 2012; 25 ,121-122

Receptor

• Grado variable de DPI: 90%

Causa más frecuente de muerte en el postoperatorio inmediato

•Edema, hipoxemia, infiltrados, < complianza, HTP, fracaso VD

•Rechazo agudo

•ECMO / Novalung

• Hiperinsuflación dinámica del nativo

•Hipoxemia, hipercapnia, hipoTA

•Vent para enfisematoso desconexión V independiente

PCV

VT< 6 ml/kg

PEEP moderada

Pinsp <20 cmH2O

Hipercapnia

permisiva

Receptor

• Fracaso de la extubación:

• CEC, DPI, IMC < 17 kg/m2…

• VMNI

• Traqueo percutánea precoz

• Disfunción frénica

• Broncoscopias

VMNI

CoNTRAINDICACIONES

• Inestabilidad hemodinámica

• Fallo multiorgánico

• Inestabilidad ECG con evidencia de isquemia o

arritmias ventriculares

• Necesidad de proteger la vía aérea ó manejo de

secreciones

• Hipoxemia severa

Criterios de suspension VMNI

• Intolerancia a la mascarilla por disconfort o dolor

• Disnea persistente

• No mejoría en la gasometría ( acidosis o hipoxemia

severas)

• Inestabilidad HD ó ECG

• Encefalopatía hipercápnica que no mejora en los

primeros minutos

Conclusiones

V protección

• VT 6-8 ml/k + PEEP 8-10cmH2O

• Circ cerrado de aspiración

• Test de apnea en CPAP, no en T

• Reclutamiento tras desconex

PCV

VT< 6 ml/kg

PEEP moderada

Pinsp <20 cmH2O

Hipercapnia

permisiva

DONANTE.

PREOPERATORIO

RECEPTOR.

POSTOPERATORIO

INMUNOSUPRESION

• SIMULECT (Baxilisimab)

• SOLUMODERIN (Metilprednisolona)

• CICLOSPORINA

• IMUREL (Azatioprina)

• En casos de retrasplante

• Se mantienen mismos fármacos: • FK (Prograf)

• Mofetilmicofenolato (Cellcept)

• Esteroides a las mismas dosis

PROFILAXIS ANTIINFECCIOSA

• PROFILAXIS ANTIBACTERIANA • Amoxicilina-clavulánico o según cultivos previos.

• PROFILAXIS ANTIVÍRICA • En todos (excepto Receptor - / Donante +):

• Ganciclovir

• Si Receptor -/ Donante +: • + Citotec

• PROFILAXIS ANTINEUMOCISTIS CARINI • A partir día 14 del po:

• Septrim forte

• PROFILAXIS ANTIFÚNGICA • Ambisome nebulizado

COMPLICACIONES HD

• SANGRADO

• FR:

• Qx Torácica previa

• Pleurodesis química

• CEC

• Hipotermia

• Manipulación quirúrgica

• TTO

• Medidas conservadoras

• Reintervención:

• Sangrado > 200 ml/h

• Inestabilidad HD

• ARRITMIAS

• Frecuente (80%)

• Supraventriculares:

• FA

• Flutter

• FR:

• Hipoxia, acidosis

• Tx bipulmonar

• > 60 a

COMPLICACIONES HD

• SINDROME BAJO GC

• Se define por:

• IC < 2.5 ml/min/m

• PAM <65 mmHg

• PCP > 18 mmHg

• Oliguria

• Signos de mala perfusión periférica o cerebral

• TTO:

• Optimizar FC, precarga

• DVA

• BCIAo

• DISFUNCION VD

• Se define:

• ↓ GC, PA

• ↑ PTDVD

• TTO:

• ↓ Postcarga: VD

• Precarga: Fluidoterapia

• ↑ Contractilidad:

• Dobutamina

• Adrena, NA → ↑ RVP (mant. PA)

• - PDE: RVS ↑

• Levosimendan, BCIAo

COMPLICACIONES HD

• ESTENOSIS VV. PULMONARES

• Poco frecuente

• Pronóstico fatal

• DESCARTAR SI EDEMA PERSISTENTE

• Dx: ETE, Arteriografía, TC

• Dx Diferencial:

• DPI

• Rechazo

• Infección

• TTO: Reqx

• ESTENOSIS ARTERIA PULMONAR

• Poco frecuente

• Clínica:

• Asintomático

• Persistencia HTP, fracaso VD

• Dx : ETE, Arteriografía

• TTO:

• Conservador

• Angioplastia con balón

• Stent

• Corrección quirúrgica

COMPLICACIONES HD

• HTP (PAPm > 25 mm Hg)

• > Frecuencia:

• Tx unipulmonar

• HTP primaria

• Causas:

• DPI

• Estenosis vv. Pulmonares

• Hipoxia, acidosis, hipercapnia

• TTO:

• NO

• NTP, NTG, - PDE

• PGE1

• PGI2: Iloprost, Beraprost

• TEP

• Infrecuente

• Mortalidad 43 %

• Dx

• Si sospecha: ETE

• Eco- Dopler EEII

• Rx Tx, Gammagrafía

• TTPA 1.5-2

COMPLICACIONES RESPIRATORIAS

• DISFUNCION PRECOZ DE INJERTO (DPI)

• RECHAZO AGUDO

• COMPLICACIONES ANASTOMOTICAS

• INFECCIONES

• NEUMOTORAX

DPI • Inducido por ISQUEMIA-REPERFUSION

• Etiologia • Donante: Edad, Sexo, cifras pO2, tiempo intubación

• Preservación órgano: Líquido preservación, Tª

• Procedimeinto quirúrgico: CEC, tipo trasplante

GRADO 0: PO2/FiO2 >300 + no infiltrados radiológicos

PO2/FiO2 < 300 + no infiltrados radiológicos

Cánula nasal o FiO2 < 0,3 + no infiltrados radiológicos

GRADO 1: PO2/FiO2 >300 + infiltrados radiológicos

Cánula nasal o FiO2 < 0,3 + infiltrados radiológicos

GRADO 2: PO2/FiO2 200- 300 + infiltrados radiológicos

GRADO 3: PO2/FiO2 < 200 + infiltrados radiológicos

Oxigenación extracorporea + infiltrados

VM con FiO2 >0,5 + NO a partir de 48h + infiltrados

DPI

Dx DIFERENCIAL

TRATAMIENTO

- Rechazo hiperagudo humoral

- Obstrucción venas pulmonares

- Edema Cardiogénico

- Neumonía

- TRALI

MANEJO HD

•Restricción fluidos Hto 25-30 %

•Vasopresores sistémicos +/- VD

pulmonares

•Uso preventivo de UF o diálisis”

MANEJO RESPIRATORIO

•Bajos Vt (6-8 ml/kg)

•P. meseta < o = 25-30cm H2O

•PEEP

• FR para mantener adecuada PCO2

. PCV

PREVENCION DE DISFUNCIÓN DEL INJERTO

- VT 6-8ml/k

- PEEP 5-10

- I/E : 1/2-1/3

- NO, PGs, Acetilcisteina??

- Inodilatadores

Objetivo HD→ Disminuir postcarga del VD

→ Mejorar contractilidad VD

→Mejorar llenado de VI

DPI • NO

• 10-20 ppm

• NO USO PROFILACTICO

• Efectos 2º:

• HTP rebote

• MetaHb

• > lesion oxidativa

• ECMO (2.7-5-5%)

• USO PRECOZ (<24 hrs)

• RETRASPLANTE

Novalung como puente al Tx

en HAP

Dispositivo extracorporeo

de asistencia pulmonar

87 87

ECMO (extracorporeal membrane oxygenation)

Acceso percutáneo (Cirugía Vascular): 15-23 Fr

Soporte respiratorio y circulatorio

Flujo máximo 7l/min

Precisa anticoagulación (ACT 180-200 seg)

Duración hasta 14 días

ASISTENCIAS DE CORTA DURACIÓN

DIFERENCIAS ENTRE novalung Y ecmo

ECMO

• Normalmente por disección

• 180 s

• Si

• No

• Con bomba

• Veno-venoso/Veno-arterial

• Oxigenar y eliminar CO2

• 1,9 m2 o mayor

• 1-7 L/min-1

• Mayor de 1,4 L

• Normalmente 1-10 L/min-1

Novalung

• Percutanea

• 150 s

• No

• Si

• Sin bomba

• Arterio/venoso

• Eliminar CO2

• 1,3 m2

• 0,5-4,5 L/min-1

• 0,24 L

• 1-15 L/min-1

Canulación

TCA

Intercambiador

de calor

Pulsatilidad

Bomba

Modalidad

Acción

Superf de membrana

V de flujo sanguineo

V de cebado

Flujo de O2

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Sciurba FC, Hunninghake GM, San Jose Estepar R, Silverman EK,

et al. Identification of early interstitial lung disease in smokers from

the COPDGene study. Acad Radiol 2010;17:48–53.

Copyright ª 2012 by the American Thoracic Society

DOI: 10.1164/ rccm.201202-0222ED

Ext racorporeal Membrane Oxygenat ion as “ Br idge”t o Lung Transplant at ion: What Remains in Ordert o Make It St andard of Care?

Since its introduction into clinical practice, lung transplantation

(LTx) isgradually becoming a worldwide standard treatment forpatients with a broad spectrum of end-stage respiratory diseases(1–3). From 1995 to 2010, more than 30,000 LTx have beenperformed, and it is worth noting that in recent years the num-ber of LTx has been progressively increasing to more than3,000/year in 2010, with a post-transplant graft half-life that

went from 4.7 in the 1990s to 5.9 in the new millennium (4).However, the crude mortality rate of patients awaiting LTx ishigher than mortality for other solid organs. Mortality rate in2009 for patients on the waiting list for LTx was about 14.1% inNorth A merica (www.srtr.org) and 14.7% in Italy (www.airt.it).What are the reasons for these unacceptable mortality rates?

First, patients have to wait for the graft longer than patientswaiting for other organs because of the small number of lungssuitable for transplantation (5). Second is the lack of supportivetherapies that are able to replace respiratory function when

the primary pulmonary diseases evolve from “ respiratory in-sufficiency” to “ respiratory failure,” characterized by refrac-tory hypoxemia and hypercapnia.

HOW TO MANAGE SHORTAGE OF GRAFTS FOR LUNGTRANSPLANTATION

Different linesof investigation have been developed with the goalof increasing lung suitability from the multiorgan donor. In par-ticular, a recent study demonstrated that a lung-protective me-chanical ventilation strategy applied in potential donors mightsignificantly increase the eligibility of the lungs for transplant(6). Moreover, a very innovative technique of ex vivo lung per-

fusion has been shown effective in a clinical trial examining re-conditioning human lungs from high-risk donors, which wouldhave been declined according to conventional criteria (7).

HOW TO “ BRIDGE” PATIENTS TO LUNGTRANSPLANTATION

Invasive mechanical ventilation (IMV), which is usually appliedin these cases, may not fulfill the goals of an optimal bridge toLTx. In fact, IMV is a potential cause of ventilator-associatedpneumonia and ventilator-induced lung injury, which can furtherenhance the initial lung damage and lead to multiorgan dysfunc-

tion, resulting in clinical unsuitability for LTx (“ too sick to betransplanted” ).

Extracorporeal life support (ECLS), such as extracorporealmembrane oxygenation (ECMO), after initially discouraging

experiences, is being progressively recognized as an optimal

strategy to bridge patientswith lung failure to LTx. In fact, ECLS

can potentially provide an adequate level of respiratory supportfor the patient’s requirements, thereby minimizing the clinicalimpact of mechanical ventilation and increasing the chance to

receive a successful LTx (8, 9). A lthough suggested by a number

of case reports (10–12), this hypothesis has never been system-

atically investigated.In this issue of the Journal (pp. 763–768), the article pub-

lished by Dr. Fuehner and colleagues is a welcome next step in

this line of study (13). The authors reported on the outcome of

26 patients awaiting LTx, who developed end-stage respiratory

failure and were supported with ECMO while awake, as bridge

to definitive treatment. These data were compared with those of

34 historical control patients, who were supported traditionally

with IMV as a bridging treatment to LTx. The results of this

study confirmed that ECMO isa very efficient strategy to bridge

patients to LTx and, furthermore, suggested that for this pur-

pose ECMO may be even more efficacious than IMV. In fact,

although both groups were comparable in terms of duration of

support (9 d vs. 15 d) and percentage of patients that received

LTx (23% vs. 29%), survival at six months after LTx was sig-

nificantly higher in the ECMO group (80% vs. 50%, P ¼ 0.02).

Therefore, ECMO wasaseffective as IMV in extending the pre-

transplant life expectancy to increase the chances to receive an

organ, but probably more effective than IMV in preserving

physiological homeostasis, thus preserving the post-transplant

life expectancy, more closely approaching the ideal “ bridge”

to LTx.

Remarkably, in this experience ECMO was applied as an

alternative to IMV with the declared purpose of avoiding its in-

jurious effects, and not asrescue treatment in patients refractory

to conventional therapy. Therefore, it was applied in extubated,

awake patients at an earlier stage of their progression to respi-

ratory failure. Thisstrategy may also allow patients to ambulate,

receive active physiotherapy, and thus potentially be in better

physical condition to ultimately benefit the most from LTx

(14). However, in 27% of cases in the ECMO group, IMV could

not be avoided. Interestingly, these patients had a post-LTx

survival rate of only 43%. From this data stems the ultimate

need to define the optimal timing and clinical criteria to apply

ECLS as bridge to LTx. Starting ECLS too early might increase

the chance of developing ECLS-related complications, whereas

starting too late may not be optimal to prevent multiorgan

dysfunction.The study by Dr. Fuehner and colleagues is particularly pro-

vocative as it is the first attempt, as far asbridging to LTx iscon-

cerned, to systematically compare ECMO and IMV. Previously,

only case series have generally been published (10–12), demon-

strating bridging feasibility but without the chance to measureSupported by the Italian Ministry of University and Research PRIN 2007 and

Fondazione per la Ricerca sulla Fibrosi Cistica–onlus 2008.

Editorials 699

the impact of the results against a control group. This concern

has been, at least in part, addressed in this report by identifying

historical control patients treated with IMV as bridge to LTx.

It isrecognized that the comparison islimited in that the historical

control patients were nonmatched, and the investigation was only

a retrospective observational analysis of few patients, treated in a

single center. A lthough these are relevant methodological issues,

the study by Dr. Fuehner and colleagues has the merit of provid-

ing a solid background and enticing data for the basis of a multi-

center randomized controlled trial (RCT), which is, at this point,

strongly warranted. A n RCT would ultimately clarify an under-

standing of whether the potential increased incidence of ECLS-

related complications outweighs the injuriouseffectsof IMV, asa

bridge to LTx. This step will be key in defining ECLS as the

standard of care in patientswith lung failure waiting for transplant.A re these data sufficient to propose ECLS as standard bridge

procedure for patients waiting for lung transplant? In the lastdecade, there has been a progressive increase in the literatureof publicationson ECLS(seeFigure 1), including ECLSasbridge

to LTx. Interestingly, a relevant increase in publications is gen-erally observed in coincidence with two episodes: (1) the H1N1epidemics (15), and (2) coincident technological advances inECLS (12, 16). This may explain why only very few RCTs have

been published on ECLSfor patientswith respiratory failure, andno RCTs have been performed on strategies to bridge to LTx.

In our view, thecurrent extensiveclinical effortsto improvetheefficacy of the supportive treatments bridging patients to LTxshould adopt the methodological challenges taken by the studies

that have tested strategiesaimingat increasing thenumber of suit-able lungs for transplant from multiorgan donors (6). We ac-knowledge the difficulties of randomizing patients in end-stagerespiratory failure waiting for a transplant, but ultimately clini-cians need to have more solid evidence than that provided byFuehner and colleagues. A lternative methods, including prag-

matic study design and cluster randomization procedure, mayprovide information about ECLS. The technology of mechanicalventilation has evolved and continued to improve over time, andstrategies of protective lung ventilation have improved the per-

formance of mechanical ventilation to support critically il lpatients. A lso, ECLS, which washistorically a costly and imperfecttechnology with significant morbidity, has advanced technologi-cally and come of age—with better performance and an improved

morbidity profile. It is now theoretically truly conceivable to con-sider that ECLS may be more effective and have less overallmorbidity in patients with advanced lung failure. It is time tocompare these two technologies head to head in an RCT.

Author disclosures are available with the text of this article at www.atsjournals.org.

Lor enzo Del Sor bo, M.D.

V. Mar co Ranier i, M.D.

Dipartimento di Anestesiologia e Medicina degli Stati CriticiUniversita di TorinoTorino, I taly

Shaf Keshavjee, M.D.

Toronto L ung Transplant ProgramUniversity of TorontoToronto, Canada

References

1. Cooper JD, Pearson FG, Patterson GA, Todd TR, Ginsberg RJ,

Goldberg M, DeMajo WA. Technique of successful lung transplan-

tation in humans. J Thorac Cardiovasc Surg 1987;93:173–181.

2. Kotloff RM, Thabut G. Lung transplantation. Am J Respir Crit CareMed

2011;184:159–171.

3. Pierre AF, Keshavjee S. Lung transplantation: donor and recipient

critical care aspects. Curr Opin Crit Care 2005;11:339–344.

4. Christie JD, Edwards LB, Kucheryavaya AY, Benden C, Dobbels F,

Kirk R, Rahmel AO, Stehlik J, Hertz MI. The Registry of the Inter-

national Society for Heart and Lung Transplantation: twenty-eighth

adult lung and heart-lung transplant report–2011. J Heart L ung

Transplant 2011;30:1104–1122.

5. Punch JD, Hayes DH, LaPorte FB, McBride V, Seely MS. Organ do-

nation and utilization in the United States, 1996–2005. Am J Trans-

plant 2007;7:1327–1338.

6. Mascia L, Pasero D, Slutsky AS, ArguisMJ, Berardino M, Grasso S, Munari

M, Boifava S, Cornara G, Della Corte F, et al. Effect of a lung protective

strategy for organ donors on eligibility and availability of lungs for

transplantation: a randomized controlled trial. JAMA 2010;304:2620–2627.

7. Cypel M, Yeung JC, Liu M, A nraku M, Chen F, Karolak W, Sato M,

Laratta J, Azad S, Madonik M, et al. Normothermic ex vivo lung per-

fusion in clinical lung transplantation. N Engl J Med 2011;364:1431–1440.

8. Cypel M, Keshavjee S. Extracorporeal life support as a bridge to lung

transplantation. Clin Chest Med 2011;32:245–251.

9. Del Sorbo L, Boffini M, Rinaldi M, Ranieri VM. Bridging to lung trans-

plantation by extracorporeal support. Minerva Anestesiol 2012;78:243–250.

Figure 1. Number of articles on extracorporeal

life support (ECLS) (gray line, left vertical axis)

and ECLS as bridge to LTx (black line, right vertical

axis), published on PubMed for each year from

2000 until 2011.

700 AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 185 2012

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11. Doyle TW, Washko GR, Fernandez IE, Nishino M, Okajima Y,

Yamashiro T, Divo MJ, Celli BR, Sciurba FC, Silverman EK, et al.

Interstitial lung abnormalities and reduced exercise capacity. Am

J Respir Crit Care Med 2012;185:756–762.

12. du Bois RM, Weycker D, Albera C, Bradford WZ, Costabel U, Kartashov

A, Lancaster L, NoblePW, Sahn SA, SzwarcbergJ, et al. Six-minute-walk

test in idiopathic pulmonary fibrosis: test validation and minimal clinically

important difference. Am J Respir Crit CareMed 2011;183:1231–1237.

13. Washko GR, Lynch DA, Matsuoka S, Ross JC, Umeoka S, Diaz A,

Sciurba FC, Hunninghake GM, San Jose Estepar R, Silverman EK,

et al. Identification of early interstitial lung disease in smokers from

the COPDGene study. Acad Radiol 2010;17:48–53.

Copyright ª 2012 by the American Thoracic Society

DOI: 10.1164/ rccm.201202-0222ED

Ext racorporeal Membrane Oxygenat ion as “ Bridge”t o Lung Transplant at ion: What Remains in Ordert o Make It St andard of Care?

Since its introduction into clinical practice, lung transplantation(LTx) isgradually becoming aworldwide standard treatment forpatientswith a broad spectrum of end-stage respiratory diseases(1–3). From 1995 to 2010, more than 30,000 LTx have beenperformed, and it is worth noting that in recent years the num-

ber of LTx has been progressively increasing to more than3,000/year in 2010, with a post-transplant graft half-life thatwent from 4.7 in the 1990s to 5.9 in the new millennium (4).

However, the crude mortality rate of patients awaiting LTx ishigher than mortality for other solid organs. Mortality rate in2009 for patientson the waiting list for LTx wasabout 14.1% in

North America (www.srtr.org) and 14.7% in Italy (www.airt.it).What are the reasons for these unacceptable mortality rates?

First, patients have to wait for the graft longer than patientswaiting for other organs because of the small number of lungs

suitable for transplantation (5). Second isthe lack of supportivetherapies that are able to replace respiratory function whenthe primary pulmonary diseases evolve from “ respiratory in-

sufficiency” to “ respiratory failure,” characterized by refrac-tory hypoxemia and hypercapnia.

HOW TO MANAGE SHORTAGE OF GRAFTS FOR LUNG

TRANSPLANTATION

Different linesof investigation havebeen developed with thegoalof increasing lung suitability from the multiorgan donor. In par-ticular, a recent study demonstrated that a lung-protective me-chanical ventilation strategy applied in potential donors might

significantly increase the eligibility of the lungs for transplant(6). Moreover, a very innovative technique of ex vivo lung per-fusion has been shown effective in a clinical trial examining re-conditioning human lungs from high-risk donors, which wouldhave been declined according to conventional criteria (7).

HOW TO “BRIDGE” PATIENTS TO LUNG

TRANSPLANTATION

Invasive mechanical ventilation (IMV), which isusually appliedin these cases, may not fulfill the goals of an optimal bridge toLTx. In fact, IMV is a potential cause of ventilator-associatedpneumonia and ventilator-induced lung injury, which can further

enhance the initial lung damage and lead to multiorgan dysfunc-tion, resulting in clinical unsuitability for LTx (“ too sick to betransplanted” ).

Extracorporeal life support (ECLS), such as extracorporealmembrane oxygenation (ECMO), after initially discouragingexperiences, is being progressively recognized as an optimal

strategy tobridgepatientswith lungfailure toLTx. In fact, ECLScan potentially provide an adequate level of respiratory supportfor the patient’s requirements, thereby minimizing the clinicalimpact of mechanical ventilation and increasing the chance to

receive asuccessful LTx (8, 9). A lthough suggested by anumber

of case reports (10–12), this hypothesis has never been system-

atically investigated.

In this issue of the Journal (pp. 763–768), the article pub-

lished by Dr. Fuehner and colleagues is a welcome next step in

this line of study (13). The authors reported on the outcome of

26 patients awaiting LTx, who developed end-stage respiratory

failure and were supported with ECMO while awake, asbridge

to definitive treatment. These data were compared with those of

34 historical control patients, who were supported traditionally

with IMV as a bridging treatment to LTx. The results of this

study confirmed that ECMO isavery efficient strategy to bridge

patients to LTx and, furthermore, suggested that for this pur-

pose ECMO may be even more efficacious than IMV. In fact,

although both groups were comparable in terms of duration of

support (9 d vs. 15 d) and percentage of patients that received

LTx (23% vs. 29%), survival at six months after LTx was sig-

nificantly higher in the ECMO group (80% vs. 50%, P ¼ 0.02).

Therefore, ECMO wasaseffective asIMV in extending thepre-

transplant life expectancy to increase the chances to receive an

organ, but probably more effective than IMV in preserving

physiological homeostasis, thus preserving the post-transplant

life expectancy, more closely approaching the ideal “bridge”

to LTx.Remarkably, in this experience ECMO was applied as an

alternative to IMV with the declared purpose of avoiding its in-

juriouseffects, and not asrescue treatment in patientsrefractory

to conventional therapy. Therefore, it wasapplied in extubated,

awake patients at an earlier stage of their progression to respi-

ratory failure. Thisstrategy may also allow patientsto ambulate,

receive active physiotherapy, and thus potentially be in better

physical condition to ultimately benefit the most from LTx

(14). However, in 27% of cases in the ECMO group, IMV could

not be avoided. Interestingly, these patients had a post-LTx

survival rate of only 43%. From this data stems the ultimate

need to define the optimal timing and clinical criteria to apply

ECLSasbridge to LTx. Starting ECLStoo early might increase

the chance of developing ECLS-related complications, whereas

starting too late may not be optimal to prevent multiorgan

dysfunction.The study by Dr. Fuehner and colleagues isparticularly pro-

vocative asit isthe first attempt, asfar asbridging to LTx iscon-

cerned, to systematically compare ECMO and IMV. Previously,

only case series have generally been published (10–12), demon-

strating bridging feasibility but without the chance to measureSupported by the Italian Ministry of University and Research PRIN 2007 and

Fondazione per la Ricerca sulla Fibrosi Cistica–onlus 2008.

Editorials 699

the impact of the results against a control group. This concern

hasbeen, at least in part, addressed in this report by identifying

historical control patients treated with IMV as bridge to LTx.

It isrecognized that thecomparison islimited in that thehistorical

control patientswere nonmatched, and the investigation wasonly

a retrospective observational analysisof few patients, treated in a

single center. A lthough these are relevant methodological issues,

the study by Dr. Fuehner and colleagues hasthe merit of provid-

ing a solid background and enticing data for the basis of a multi-

center randomized controlled trial (RCT), which is, at this point,

strongly warranted. An RCT would ultimately clarify an under-

standing of whether the potential increased incidence of ECLS-

related complicationsoutweighsthe injuriouseffectsof IMV, asa

bridge to LTx. This step will be key in defining ECLS as the

standard of care in patientswith lung failurewaitingfor transplant.Are these data sufficient to propose ECLSasstandard bridge

procedure for patients waiting for lung transplant? In the last

decade, there has been a progressive increase in the literatureof publicationson ECLS(seeFigure1), includingECLSasbridge

to LTx. Interestingly, a relevant increase in publications is gen-erally observed in coincidence with two episodes: (1) the H1N1

epidemics (15), and (2) coincident technological advances inECLS(12, 16). This may explain why only very few RCTs havebeen published on ECLSfor patientswith respiratory failure, andno RCTs have been performed on strategies to bridge to LTx.

Inour view, thecurrent extensiveclinical effortsto improvetheefficacy of the supportive treatments bridging patients to LTx

should adopt the methodological challengestaken by the studiesthat havetestedstrategiesaimingat increasingthenumber of suit-able lungs for transplant from multiorgan donors (6). We ac-knowledge the difficulties of randomizing patients in end-stagerespiratory failure waiting for a transplant, but ultimately clini-

cians need to have more solid evidence than that provided byFuehner and colleagues. Alternative methods, including prag-matic study design and cluster randomization procedure, mayprovide information about ECLS. The technology of mechanical

ventilation hasevolved and continued to improve over time, andstrategies of protective lung ventilation have improved the per-formance of mechanical ventilation to support critically ill

patients. Also, ECLS, which washistorically acostly and imperfecttechnology with significant morbidity, has advanced technologi-cally and come of age—with better performance and an improved

morbidity profile. It is now theoretically truly conceivable to con-sider that ECLS may be more effective and have less overallmorbidity in patients with advanced lung failure. It is time to

compare these two technologies head to head in an RCT.

Author disclosures are available with the text of thisarticle at www.atsjournals.org.

Lorenzo Del Sorbo, M.D.

V. Marco Ranier i, M.D.

Dipartimento di Anestesiologia e Medicina degli Stati CriticiUniversita di TorinoTorino, Italy

Shaf Keshavjee, M.D.

Toronto Lung Transplant ProgramUniversity of TorontoToronto, Canada

References

1. Cooper JD, Pearson FG, Patterson GA, Todd TR, Ginsberg RJ,

Goldberg M, DeMajo WA. Technique of successful lung transplan-

tation in humans. J Thorac Cardiovasc Surg 1987;93:173–181.

2. Kotloff RM, Thabut G. Lung transplantation. Am JRespir Crit CareMed

2011;184:159–171.

3. Pierre AF, Keshavjee S. Lung transplantation: donor and recipient

critical care aspects. Curr Opin Crit Care 2005;11:339–344.

4. Christie JD, Edwards LB, Kucheryavaya AY, Benden C, Dobbels F,

Kirk R, Rahmel AO, Stehlik J, Hertz MI. The Registry of the Inter-

national Society for Heart and Lung Transplantation: twenty-eighth

adult lung and heart-lung transplant report–2011. J Heart Lung

Transplant 2011;30:1104–1122.

5. Punch JD, Hayes DH, LaPorte FB, McBride V, Seely MS. Organ do-

nation and utilization in the United States, 1996–2005. Am J Trans-

plant 2007;7:1327–1338.

6. MasciaL, Pasero D, Slutsky AS, ArguisMJ, Berardino M, Grasso S, Munari

M, Boifava S, Cornara G, Della Corte F, et al. Effect of a lung protective

strategy for organ donors on eligibility and availability of lungs for

transplantation: arandomizedcontrolled trial. JAMA 2010;304:2620–2627.

7. Cypel M, Yeung JC, Liu M, Anraku M, Chen F, Karolak W, Sato M,

Laratta J, Azad S, Madonik M, et al. Normothermic ex vivo lung per-

fusion in clinical lung transplantation. N Engl JMed 2011;364:1431–1440.

8. Cypel M, Keshavjee S. Extracorporeal life support as a bridge to lung

transplantation. Clin Chest Med 2011;32:245–251.

9. Del Sorbo L, Boffini M, Rinaldi M, Ranieri VM. Bridging to lung trans-

plantation by extracorporeal support. MinervaAnestesiol 2012;78:243–250.

Figure 1. Number of articles on extracorporeal

life support (ECLS) (gray line, left vertical axis)

and ECLSas bridge to LTx (black line, right vertical

axis), published on PubMed for each year from

2000 until 2011.

700 AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CAREMEDICINE VOL 185 2012

Extracorporeal Membrane Oxygenation as "Bridge" to Lung Transplantation: What R… Abrir con el lector de PDF

Dispositivos de Asistencia Respiratoria Extracorpóreos. CPH

Nº. Indicación. Tipo de

Asistencia. Desconexión. Evolución.

1 D.P.I. Novalung-

centrifuga Si Exitus

2 Fuga aérea Novalung Si Alta

3 F.Q. Puente Tx Novalung Si Exitus

4 Enfisema. Puente

Tx Novalung Si Alta

5 D.P.I Novalung-

Centrífuga x 2 No Exitus

6 D.P.I ECMO VA No Exitus

7 D.P.I ECMO VA No Exitus

8 D.P.I ECMO VV Si Alta

RECHAZO AGUDO

• 0-3 meses (> frec. 5-15 d)

• CLINICA:

• Malestar general

• Superponible a DPI

• Dx: BIOPSIA TRANSBRONQUIAL

• SOSPECHA:

1.DESCARTAR INFECCION: ATB

2.RESPUESTA A CORTICOIDES (metilprednisolona)

3.Inmunosupresión?

OTRAS COMPLICACIONES

• ANASTOMOSIS BRONQUIAL

• INFECCIONES

Preacondicionamiento EX VIVO