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Sindrome de distress respiratorio

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Sindrome de distress respiratorio

  1. 1. SINDROME DE DISTRESS RESPIRATORIO AGUDO<br />DraMaria Gloria Agreda Vedia<br />
  2. 2. “Insuficiencia respiratoria aguda debida a un demapulmonar no cardiogénico”.<br />Alta Mortalidad: 40 - 70 %<br />Insuficiencia respiratoria “Incapacidad del aparato respiratorio para mantener los niveles arteriales de oxígeno y dióxido de carbono CO2adecuados para satisfacer las demandas del Organismo. Diagnóstico gasométrico; PaO2 < 60 mmHg y PCO2 > 49 mmHg.<br />
  3. 3.
  4. 4. SDRACriterios de Diagnóstico<br />INICIO AGUDO<br />INFILTRADOS BILATERALES RX<br />PRESION CAPILAR PULMONAR < 18 mm Hg.No signos clínicos de ICC<br />PaO2 / FIO2 < 200<br />
  5. 5. SDRA<br />
  6. 6. Criterios de IPA y SDRA<br />Injuria Pulmonar Aguda (IPA):<br />PaO2/FiO2 < 300<br />Rxtorax con Infiltrado Bilateral<br />PCCP < 18 mm Hg ó No evidenciaclínica de hipertensión auricularizquierda.<br />Inicio Agudo<br />Síndrome Distrés Respiratorio Agudo (SDRA):<br />PaO2/FiO2 < 200 y resto igual. <br />
  7. 7. ETIOLOGIA<br />INJURIA PULMONAR DIRECTA<br /> - CAUSAS COMUNES: <br /> NEUMONIA<br /> ASPIRACION CONTENIDO GASTRICO <br /> - CAUSAS MENOS COMUNES:<br />CONTUSION PULMONAR EMBOLIA GRASA INJURIA INHALATORIA CASI AHOGAMIENTO POST CIRUGIA PULMONAR<br />
  8. 8. ETIOLOGIA<br />INJURIA PULMONAR INDIRECTA<br />CAUSAS COMUNES :<br />SEPSIS SEVERA TRAUMA SEVERO CON SHOCK TRANSFUSIONES MULTIPLES<br />CAUSAS MENOS COMUNES :<br />BY PASS CARDIO PULMONAR SOBREDOSIS DE DROGAS PANCREATITIS AGUDA<br />
  9. 9. SRDAFISIOPATOLOGIA<br />Edema pulmonar agudo por aumento de la permeabilidad producto de la inflamación (Perdida de la integridad de la barrera alveolo capilar, con salida de líquido rico en proteínas )<br />Proceso inflamatorio difuso del pulmón<br />( Injuria pulmonar dependiente de neutrófilos y otros mecanismos Pro - Inflamatorios: Citoquinas)<br />
  10. 10. Patogenia <br />PMN se adhiere al endotelio capilar injuriado y migran a través del intersticio hacia el espacio aéreo.<br />El espacio aéreo es llenado con fluido rico en proteínas. <br />En el alveolo los macrófagos secretan citoquinas (IL-1, IL-6, IL-8 e IL-10, TNF)<br />
  11. 11. estímulo<br />TNF<br />IL-1,6,8,10<br />FR<br />PAF<br />PROTEASAS<br />PG<br />LT<br />BRADIQUININA<br />TNF<br />IL-1<br />adhesión<br />Microtrombosis<br />
  12. 12. Patogenia<br />Las citoquinas actúan localmente estimulando quimiotaxisy activando PMN.<br />Macrófago también secreta otras citoquinas.<br />La IL-1 puede estimular al fibroblasto para la producción de matriz celular. <br />
  13. 13. Patogenia<br />Los PMN en el alveolo liberan: proteasas, leucotrienos y otras moléculas proinflamatorias como ; PAFelastasa, colagenasa, FR, citoquinasetc<br />El edema rico en proteína en el alveolo inactiva el surfactante. (Atelectasias)<br />
  14. 14. Patogenia <br />Algunas enzimas como la elastasa podrían ser importantes mediadores del daño del epitelio alveolar y la progresión a la fibrosis.<br />Otras células inflamatorias (macrófagos, linfocitos, plaquetas) están involucradas en el daño<br />
  15. 15. EPITELIO ALVEOLAR NORMAL<br />Células tipo I: Neumocitos I<br />90% de la superficie, aplanadas.<br />Poca tolerancia a la injuria.<br />Células tipo II: Neumocitos II<br />10% de la superficie, cuboideas.<br />Mayor tolerancia a la injuria, proliferan y se diferencian a tipo I luego de la injuria.<br />Producción de surfactante, transporte agua y iones.<br />
  16. 16. Alveolo injuriado<br />Fase aguda<br />Alveolo normal <br />Desprendimiento<br /> epitelio bronquial<br />Surfactante inactivado<br />Sistema<br />surfactante<br />NeumocitoI<br />Necrótico o apoptótico<br />M. Basal <br />epitelial<br />Macrófago<br /> alveolar<br />M. Basal denudada<br />Lt<br />FR<br />PAF<br />Pr-<br />Fluído rico en pr-<br />Neumocito<br />I<br />NeumocitoII<br />intacto<br />Intersticio <br />Detritus<br />celulares<br />Mem. hialina<br />TNF<br />IL1<br />Fibrina <br />Neumocito<br />II<br />Neutrófilo migrando<br />IL6<br />IL10<br />Proteasas <br />Eritrocito <br />Intersticio <br />edematoso<br />TNF<br />IL8<br />MIF<br />Procolágeno <br />Célula<br />Endotelial <br />IL8<br />IL8<br />Capilar <br />M. Basal <br />endotelial<br />Plaquetas <br />Neutrófilo <br />Fibroblasto <br />C. endotelial injuriada<br />edematosa<br />Fibroblasto <br />
  17. 17. EPITELIO ALVEOLAR INJURIADO<br />Pérdida de la integridad e inundación alveolar.<br />Poca capacidad para remover el fluido, producir o recambiar surfactante.<br />Pérdida de la barrera.<br />Si la injuria es severa la reparación epitelial es insuficiente o desorganizada, y puede conducir a fibrosis. <br />
  18. 18. FASES del SDRA<br />Fase Exudativa: Después del inicio de los síntomas. Hay daño alveolar difuso, Edema.<br />Fase Proliferativa: Hay organización del exudado y fibrosis.<br />Fase Fibrótica: Fase de cicatrización. <br />
  19. 19. Resumen de cambios histopatológicos en ARDSG J Bellingan. Thorax2002<br />Fase exudativa Fase proliferativaFase fibrótica<br />Membranas hialinas Ruptura de la barrera Fibrosis<br />Edema Edema Macrófagos<br />Neutrófilos Proliferación de cél. Linfocitos<br />alveolares tipo II<br />Daño epitelial infiltración miofibrobl. Organización de la matriz<br /> Colapso alveolar Cambios enfisematosos<br />en parche<br />Apoptosis epitelial Fibroproliferación<br />
  20. 20. REPOBLACIÓN DEL EPITELIO ALVEOLAR<br />Células tipo II pasan a tipo I<br />Resorción del edema alveolar; clarificación de la proteína soluble por transporte paracelular; endocitosis de células I<br />Macrófagos remueven proteína insoluble y PMN apoptóticos.<br />Remodelación y fibrosis. <br />
  21. 21. SDRACLINICA<br />TIEMPO DE INICIO ES VARIABLE.<br /><ul><li>HALLAZGOS INESPECIFICOS:</li></ul> - DISNEA<br /> - TAQUIPNEA<br /> - TAQUICARDIA<br /> - CIANOSIS<br /> - ALTERACION MENTAL<br /> - OTROS SINTOMAS RELACIONADOS A LA <br /> CONDICION PREDISPONENTE<br />
  22. 22. SDRADIAGNOSTICO DIFERENCIAL<br /><ul><li>INSUFICIENCIA CARDIACA CONGESTIVA
  23. 23. NEUMONIA BACTERIANA
  24. 24. NEUMONIA ASPIRATIVA
  25. 25. NEUMONIA VIRAL
  26. 26. INHALACION DE HUMOS</li></li></ul><li>SDRAEXAMENES<br /><ul><li>EXAMENES BACTERIOLOGICOS
  27. 27. TAC
  28. 28. ECOCARDIOGRAFIA
  29. 29. BRONCOFIBROSCOPIA
  30. 30. CATETERISMO ARTERIAL PULMONAR</li></ul> (SwanGanz)<br />
  31. 31. SDRA<br />
  32. 32. SDRAMANEJO<br /><ul><li>MONITOREO EN UCI
  33. 33. LINEAS ENDOVENOSAS. FLUIDOTERAPIA
  34. 34. VENTILACION MECANICA
  35. 35. TRATAMIENTO DE LA ENFERMEDAD DE FONDO
  36. 36. OTRAS TERAPIAS</li></li></ul><li>Ventilación mecánica<br />
  37. 37. SDRAOTRAS TERAPIAS<br /><ul><li>OXIDO NITRICO INHALADO: TRATAMIENTO DE RESCATE EN HIPOXEMIA REFRACTARIA.
  38. 38. CORTICOIDES: CONTROVERSIA PUEDEN SER UTILES EN LA FASE FIBROPROLIFERATIVA.
  39. 39. B2 AGONISTAS INHALADOS: REMOCION DEL EDEMA PULMONAR.
  40. 40. FACTOR DE CRECIMIENTO ESPECIFICO DEL ENDOTELIO: ACELERAR RESOLUCION. FUTURO</li>

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