Toracotomía de Resucitación: Una Opción Vital en Trauma Crítico
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Emergency Department Thoracotomy Toracotomia en pacientes con trauma, con signos de vida.
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Toracotomía de Resucitación: Una Opción Vital en Trauma Crítico
- 1. TORACOTOMÍA DE RESUCITACIÓN ANA SANTOS ARRIETA ESTUDIANTE I NIVEL, CIRUGÍA GENERAL UNIVERSIDAD DE CARTAGENA
- 2. Historia Toracotomía de Resucitación • Inicia el concepto de toracotomía como medida de resucitación -masaje cardíaco abierto 1874 Promulgacion de Schift: • Sugirió por primera vez la posible aplicación de esta técnica para las heridas penetrantes de tórax y laceraciones del corazón 1882 Block: • Primera reparación cardiaca exitosa por herida en VD 1896 Rehn: • Describió el éxito de la reanimación abierta en un paciente en paro cardíaco durante un procedimiento quirúrgico mediante toracotomía abierta emergente 1901 Igelsrund: American Journal of Surgery, 1988. 156(6); 430–436. Arch Surg 13:205, 1926. Ann Thorac Surg 39:492, 1985
- 3. Historia Toracotomía de Resucitación Inicialmente, colapso cardiovascular por causas médicas fue la razón más común para la toracotomía en el año 1900 1960 La eficacia de compresiones torácicas cerradas – 1965 Introducción de desfibrilación externa: eliminaron la reanimación abierta en paro cardiaco medico Las indicaciones para la emergente toracotomía después de un trauma también se hicieron más limitadas 1943 Blalock y Ravitch: Uso de la pericardiocentesis en lugar de toracotomía como el tratamiento preferido para taponamiento cardiaca después de una lesión JAMA 173:1064, 1960. NEJM 254:541, 1956. Surgery 14:157, 1943.
- 4. Historia Toracotomía de Resucitación Finales 1960, Mejoras en técnicas quirúrgicas cardiotorácicas: Restablecimiento de la toracotomía inmediata para heridas en tórax que amenazaran la vida de los pacientes El uso de la oclusión temporal de la aorta torácica en pacientes con hemorragia abdominal exsanguinante amplió las indicaciones En la última década , los análisis de los resultados críticos del paciente de trauma pos EDT ha atemperado el entusiasmo desenfrenado para esta técnica J Surg , 1966; 112:686. J Trauma 1976; 16:610. J Trauma 1984; 24:387 JACS 2004;199: 211
- 5. Toracotomía de Resucitación Toracotomía de Resucitación Toracotomía en el Servicio de Urgencias (“EDT”) Parte Integral del manejo inicial del paciente in extremis – Maniobra salvadora Toracotomía Pre-hospitalaria ◦ Londres ◦ Hampshire ◦ España ◦ Brasil ◦ Australia ◦ USA Cohn, S. Acute Care Surgery and Trauma. 1 Ed. UK: Informa; 2009
- 6. Signos de Vida Toracotomía de Resucitación Respuesta Pupilar Ventilación espontanea Presencia de pulso carotideo TA medible o palpable Movimiento de extremidad Actividad cardiaca eléctrica J Am Coll Surg. 2001;193:303-309. World J of Emer Sur 2006, 1: 1-13 Indicaciones: • Trauma penetrante <15 m RCP • Trauma Cerrado < 5 min RCP • HipoTA persistente Postrauma (<60mmHg) Contraindicaciones: • Trauma penetrante >15 m RCP + No SdeV • Trauma Cerrado > 5 min RCP + No SdV o Asistolia
- 7. Objetivos Toracotomía de Resucitación Control de la Hemorragia Liberar el Taponamiento Cardiaco Facilitar el masaje cardiaco interno/abierto Prevenir el embolismo aéreo Exponer la aorta torácica descendente para su pinzamiento Reparar lesiones cardiacas, pulmonares o grandes vasos Can J Surg. 2008; 51 (1): 57-69
- 8. Complicaciones Toracotomía de Resucitación Top Emerg Med 2000;22(3):55–6 Otras Sangrado Intercostal o mamaria interna Pericarditis o sind pericardiotomia Defectos del septo, daño valvular, alteración conducción eléctrica, isquemia miocardica Hipoxia Cerebral Renal Medula espinal Infecciosas Iatrogénicas Lesión mamaria Laceración del pulmón Lesión del N frénico Ruptura cardiaca Lesión esofágica
- 9. Cuando parar? Toracotomía de Resucitación Top Emerg Med 2000;22(3):55–6 Daño irreparable Ausencia de S de V después de 10 min de reanimación Ausencia de ritmo cardiaco compatible con la vida después de 15 min de reanimacion Imposibilidad para recuperar TAS >60 mmHg después de 30 min
- 10. La Controversia Toracotomía de Resucitación Ultima oportunidad de supervivencia Costos Exposición de personal Medico VS J Trauma Acute Care Surg. 2015;79: 159-173 Encefalopatía Anoxia Severa
- 12. Ausencia de pulso - Presencia de Signos de Vida Lesión Torácica Penetrante Toracotomía de Resucitación J Trauma Acute Care Surg. 2015;79: 159-173 Valoración de Calidad Conclusión de Hallazgos Participantes Calidad de Evidencia Tasas de eventos Efecto Absoluto anticipado Sin EDT Con EDT RR Sin EDT Con EDT Supervivencia 853 (32) Moderada 2.8% 21.3% 7.6 28/1000 185/1000 Neurológico 454 (16) Moderada 2.5% 11.7% 4.7 25/1000 92/1000
- 13. Tipo de Trauma Toracotomía de Resucitación J Trauma Acute Care Surg. 2015;79: 159-173
- 14. Toracotomía de Resucitación Inter CardioVasc and Thor Sur 200;. 7: 845–849
- 15. Toracotomía de Resucitación Inter CardioVasc and Thor Sur 200;. 7: 845–849
- 16. Ausencia de pulso - Ausencia de Signos de Vida Lesión Torácica Penetrante Toracotomía de Resucitación J Trauma Acute Care Surg. 2015;79: 159-173 Valoración de Calidad Conclusión de Hallazgos Participantes Calidad de Evidencia Tasas de eventos Efecto Absoluto anticipado Sin EDT Con EDT RR Sin EDT Con EDT Supervivencia 920 (32) Moderada 0.2% 8.3% 4.3 2/1000 81/1000 Neurológico 641 (16) Moderada 0.18% 3.9% 19.5 2/1000 37/1000
- 17. Predictores Funcionales Toracotomía de Resucitación J Trauma Acute Care Surg. 2015;79: 159-173
- 18. Ausencia de pulso - Presencia de Signos de Vida Lesión ExtraTorácica Penetrante Toracotomía de Resucitación J Trauma Acute Care Surg. 2015;79: 159-173 Valoración de Calidad Conclusión de Hallazgos Participantes Calidad de Evidencia Tasas de eventos Efecto Absoluto anticipado Sin EDT Con EDT RR Sin EDT Con EDT Supervivencia 160 (11) Moderada 1.7% 15.6% 9.2 17/1000 139/1000 Neurológico 85 (6) Moderada 1,5% 16.5% 11 15/1000 150/1000
- 19. Ausencia de pulso - Ausencia de Signos de Vida Lesión ExtraTorácica Penetrante Toracotomía de Resucitación J Trauma Acute Care Surg. 2015;79: 159-173 Valoración de Calidad Conclusión de Hallazgos Participantes Calidad de Evidencia Tasas de eventos Efecto Absoluto anticipado Sin EDT Con EDT RR Sin EDT Con EDT Supervivencia 139 (8) Bajo 0.1% 2.9% 28.8 1/1000 28/1000 Neurológico 60 (4) Bajo 0.09% 5% 55 1/1000 49/1000
- 20. Toracotomía de Resucitación Ann Emerg Med. 2015;65:297-307
- 21. Toracotomía de Resucitación Acute Care Surg. 2013;74: 1315-1320 • 21/1369 Desenlace neurológico favorable • Todos reportaban SV en la escena o a su llegada a Urg Buen pronostico pos EDT • 2/500 (no SV o SdeV en escena o Urg) Sobrevivieron, con pobre desenlace neurologico Pobre Resultado pos EDT • 5 Pacientes neurológicamente intactos. • El mayor tiempo 11-15 min Duración de RCP
- 22. Toracotomía de Resucitación Amer, Surg. 2013; 79:982
- 23. Toracotomía de Resucitación Amer, Surg. 2013; 79:982 87 Pacientes pos EDT Edad 30.89 Hombres 86% Mujeres14% Cerrado 32% Penetrante (68%) PAF 23% Arma Blanca 45% Accidente Trans 29% ISS 46.9 (Cerrado = Penetrante) Mortalidad Cerrado 92% Penetrante 81% No sobrevivientes mueren Urg 64% y Qx 24% Complicaciones -Neumonia, re-intervención, hernias ventrales grandes, bacteremia-fungemia
- 24. Ausencia de pulso - Presencia de Signos de Vida Trauma Cerrado Toracotomía de Resucitación J Trauma Acute Care Surg. 2015;79: 159-173 Valoración de Calidad Conclusión de Hallazgos Participantes Calidad de Evidencia Tasas de eventos Efecto Absoluto anticipado Sin EDT Con EDT RR Sin EDT Con EDT Supervivencia 454 (22) Moderado 0.5% 4.6% 9.3 5/1000 41/1000 Neurológico 298 (10) Moderado 0.3% 2,4% 7.8 3/1000 21/1000
- 25. Ausencia de pulso - Ausencia de Signos de Vida Trauma Cerrado Toracotomía de Resucitación J Trauma Acute Care Surg. 2015;79: 159-173 Valoración de Calidad Conclusión de Hallazgos Participantes Calidad de Evidencia Tasas de eventos Efecto Absoluto anticipado Sin EDT Con EDT RR Sin EDT Con EDT Supervivencia 995 (24) Bajo 0.001% 0.7% 704 0/1000 7/1000 Neurológico 825 (11) Bajo 0.0006% 0.1% 202 0/1000 1/1000
- 26. Recomendaciones Toracotomía de Resucitación J Trauma Acute Care Surg. 2015;79: 159-173
- 27. Infección por Patógenos de Transmisión Hemática Toracotomía de Resucitación • HIV 3.7 (2.6-5,2%) • VHB NA • VHC 12,3 (10,4-14,5) Trauma Cerrado • HIV 1.9% (1,1-3-3%) • VHB 0,6% (0,2-2,1) • VHC 9,9 (8-12,2%) Trauma Penetrante • HIV 0,3% • VHB 6-30% • VHC 1,8% Tasa de Transmisión J Trauma Acute Care Surg. 2015;79: 159-173
- 28. Toracotomía de Resucitación Interactive CardioVascular and Thoracic Surgery 16 (2013) 509–516
- 29. Toracotomía de Resucitación Acute Care Surg. 2013;74: 1315-1320
- 30. Toracotomía de Resucitación Acute Care Surg. 2013;74: 1315-1320
- 31. Técnicas en Paro Cardiaco Traumático: Toracotomía, Soporte extracorpóreo e Hipotermia Papel cada vez mayor de Circulación Extracorporea y la utilización de sistemas de heparina para evitar anticoagulación sistémica El desarrollo de hipotermia se asocia a pobres resultados en trauma Hipotensión leve (34°C) mejora la supervivencia en choque hemorrágico grave Preservación de órganos el suficiente tiempo para realizar hemostasia quirúrgica seguida de reanimación con Bypass Curr Opin Crit Care 2013 19(6):594-8 Toracotomía de Resucitación
- 32. Incisiones Toracotomía de Resucitación • Acceso rápido con instrumentos simples • Posibilidad de realización en pacientes en posición supino • Fácil extensión a Hemitorax derecho • Cumplimiento de objetivos • Pericardiotomia • Masaje Cardiaco Abierto • Pinzamiento Aorta Toracica Toracotomía Anterolateral • Heridas torácicas penetrantes derechas Toracotomía Bilateral – Incisión de Clamshell Feliciano, D. Mattox, K. Moore, E. Emergency Department Thoracotomy En Trauma. 6 Ed. McGraw-Hill, 2008 Top Emerg Med 2000;22(3):55–6
- 33. Toracotomía Anterolateral izquierda Toracotomía de Resucitación Bisturi Hoja #10 Retractor torácico Finochietto Pinzas dentadas Tijeras curvas Pinzas vasculares Satinsky Cuchillo de Lebsche Palas desfibriladoras internas Suturas •Prolene CT 2-0 •Seda 2-0 •Compresas de teflon Feliciano, D. Mattox, K. Moore, E. Emergency Department Thoracotomy En Trauma. 6 Ed. McGraw-Hill, 2008 Top Emerg Med 2000;22(3):55–6
- 34. Taponamiento Pericárdico y Hemorragia Cardiaca Toracotomía de Resucitación Incremento de presión pericárdica Restricción ventricular diastólica GC: Taquicardia y RVS Caída de Volumen sistólico y perfusión coronaria Disminución GC Presión Pericárdica = Presión de Llenado Ventricular Hipoperfusión coronaria La Tasa mas alta de supervivencia pos EDT es en pacientes con heridas cardiacas penetrantes, especialmente si están asociadas a Taponamiento pericárdico. Feliciano, D. Mattox, K. Moore, E. Emergency Department Thoracotomy En Trauma. 6 Ed. McGraw-Hill, 2008 Top Emerg Med 2000;22(3):55–6
- 35. Hemorragia Intratoracica Toracotomía de Resucitación Menos del 5% en lesiones penetrantes y porcentaje inferior en trauma cerrado Heridas penetrantes al Hilio pulmonar y grandes vasos Ruptura de Aorta torácica Alta tasa de mortalidad en lesiones vasculares debido a la falta de contención de hemorragia en tórax ◦ Taponamiento del tejido adyacente ◦ Espasmo de los vasos Feliciano, D. Mattox, K. Moore, E. Emergency Department Thoracotomy En Trauma. 6 Ed. McGraw-Hill, 2008 Top Emerg Med 2000;22(3):55–6
- 36. Masaje Cardiaco Abierto Toracotomía de Resucitación La única posibilidad de salvar el paciente lesionado en Paro Cardiorrespiratorio es una EDT 20-25% del GC basal 10-20% Perfusión cerebral normal Feliciano, D. Mattox, K. Moore, E. Emergency Department Thoracotomy En Trauma. 6 Ed. McGraw-Hill, 2008 Top Emerg Med 2000;22(3):55–6
- 37. Pinzamiento Aorta Torácica Toracotomía de Resucitación Incrementa el retorno a circulación espontanea posRCP Reposición del volumen sanguíneo circulante Fin del pinzamiento El pinzamiento aorta torácica o el cambio a la aorta infrarenal: 30 minutos Aplicación cuidadosa: ◦ Costo metabólico ◦ Riesgo de paraplejia Redistribución de volumen sanguíneo a Miocardio y Cerebro Reducción de perdida sanguínea subdiafragmatica Feliciano, D. Mattox, K. Moore, E. Emergency Department Thoracotomy En Trauma. 6 Ed. McGraw-Hill, 2008 Top Emerg Med 2000;22(3):55–6
- 38. Embolismo Aereo Toracotomía de Resucitación Lesión Torácica Penetrante IOT y Ventilación con presión positiva Hipotensión y Paro Cardiaco Comunicación Alvelo-Venosa Embolo Aéreo Isquemia Miocardica EDT con pinzamiento de Hilio pulmonar Feliciano, D. Mattox, K. Moore, E. Emergency Department Thoracotomy En Trauma. 6 Ed. McGraw-Hill, 2008 Top Emerg Med 2000;22(3):55–6
- 40. Julio 28 Testamento En 1890, en carta a su hermano Theo, Vincent van Gogh escribió: Que sean Mis cuadros los que digan Se mato al día siguiente. Sus cuadros siguen diciendo. Los Hijos de los Días, Eduardo Galeano
- 41. Toracotomía de Resucitación Acute Care Surg. 2013;74: 1315-1320
- 42. Toracotomía de Resucitación Acute Care Surg. 2013;74: 1315-1320
Notas del editor
- Since its introduction in 1900, the emergency department thoracotomy (EDT) has been a subject of intense debate. It is a drastic, last-ditch effort to save the life of a patient in extremis due to chest injury.[1] Although some studies boast a 60% survival rate, others have argued that EDT is a futile and expensive procedure that only places health care providers at significant personal risk. Further, indications for EDT have widely varied. For these reasons, the EDT remains a controversial but potentially lifesaving procedure in a select group of patients.[2, 3]
- Emergency department thoracotomy (EDT) is used as a life-saving maneuver in an attempt to facilitate resuscitation of patients in cardiovascular collapse following trauma. Despite the aggressive nature of this operation, it has been difficult to effectively evaluate the impact that EDT has on outcomes and resource utilization. Additionally, the definition of “signs of life” and specific indications and protocols for EDT are inconsistent across trauma centers and in the published literature
- Finalizar: Asistolia sin lesión cardiaca Lesión cardiaca y asistolia: reparar, masaje, adrenalina intra cardiaca… min (capacidad de salvamento= tas >70)
- ED thoracotomy permits (1) release of pericardial tamponade, (2) control of intrathoracic blood loss, (3) internal cardiac massage, and (4) cross-clamping of the descending thoracic aorta to enhance coronary and cerebral perfusion and to reduce subdiaphragmatic bleeding.
- Finalizar: Asistolia sin lesión cardiaca Lesión cardiaca y asistolia: reparar, masaje, adrenalina intra cardiaca… min (capacidad de salvamento= tas >70)
- Finalizar: Asistolia sin lesión cardiaca Lesión cardiaca y asistolia: reparar, masaje, adrenalina intra cardiaca… min (capacidad de salvamento= tas >70)
- When treating moribund trauma victims presenting in extremis, clinicians are forced to make immediate life-or-death decisions for their patients decisions that attempt to balance the last chance of survival with the risk of salvaging patients with severe anoxic encephalopathy or exposing health care providers to blood-borne pathogens. Limited salvage rates in conjunction with considerable potential risks associated with EDT have been central to the controversy.
- Overall, 853 patients in 32 studies met these criteria, and 182 (21.3% [18.7Y24.2%]) survived their hospitalization after EDT. As the subcommittee estimated hospital survival without EDT in this population to be 2.8% (range, 2Y5%), patients presenting pulseless to the emergency department with signs of life after penetrating thoracic injury were nearly eight times (relative risk [RR], 7.6) more likely to survive their hospitalization after EDT than without EDT by group estimates. Neurologic outcome after EDT in this population was reported in 16 studies involving 454 patients. Of these, 53 patients (11.7% [9.0Y15.0%]) survived EDT neurologically intact, whereas the subcommittee estimated hospital survival without EDT in this population to be 2.5% (2.8% 90% [90% of penetrating EDT survivors are neurologically intact]). When compared with the estimated neurologically intact survival of patients resuscitated without EDT, patients who underwent EDT were nearly five times (RR, 4.7) more likely to survive neurologically intact.
- An analysis of all available evidence revealed that EDT improves both survival and neurologically intact survival in patients presenting pulseless to the emergency department with signs of life after penetrating thoracic injury. Injury mechanism is a well-recognized predictor of survival after EDT. Although those who sustain penetrating injuries clearly have more favorable outcomes than those who sustain blunt injuries the specific type of penetrating injuries also impacts EDT survival. Branney et al. reported their 23-year experience with EDT in 1998, revealing that 14.6% survived EDT after cardiac stab wounds whereas only 1.8% survived after cardiac gunshot wounds. In a contemporary series evaluating 283 patients sustaining penetrating cardiac or great vessel injuries,57 this author determined that 24% survived EDT after stab wounds as compared with 3% surviving gunshot wounds. Although few would argue that single cardiac stab wounds are the injury associated with the best EDT survival,other physiologic survival predictors such as the presence or absence of signs of life are also essentialto predict EDT outcomes.
- Hospital survival and neurologic outcome were evaluated with respect to injury mechanism and anatomic injury location in patients without signs of life on presentation. Of 920 patients in 32 studies, 76 (8.3% [6.6-10.2%]) survived their hospitalization. As the subcommittee estimated hospital survival without EDT in this population to be 0.2% (range, 0-2%), patients presenting pulseless to the emergency department without signs of life after penetrating thoracic injury were 41 times (RR, 41.3) more likely to survive their hospitalization after EDT than without EDT. Neurologic outcome after EDT in this population was reported in 16 studies involving 641 patients. Of these, 25 patients (3.9% [2.6-5.6%]) survived EDT neurologically intact, whereas the subcommittee estimated hospital survival without EDT in this population to be 0.18% (0.2% 90% [90% of penetrating EDT survivors are neurologically intact]). When compared with the estimated neurologically intact survival of these patients resuscitated without EDT, patients who underwent EDT were nearly 20 times (RR, 19.5) more likely to survive neurologically intact.
- Complete review of available data revealed that EDT improves both survival and neurologically intact survival in patients presenting pulseless to the emergency department with absent signs of life after penetrating thoracic injury. In the three largest series during the past 20 years,39,52,57 0 of 80, 3 of 79, and 5 of 107 (3 of 107 neurologically intact) survived their hospitalization after EDT when presenting without signs of life after a penetrating thoracic wound. Not only is the presence or absence of signs of life important, but the duration without signs of life is also vital to the decision-making process. Once again, accurate nomenclature is essential because this phenomenon has been labeled arrest time, CPR time, duration of absent vital signs, and duration of absent signs of life. Although we recognize the importance of the duration without a perfusing rhythm in patients who have sustained a traumatic cardiopulmonary arrest, the above current evidence limitations prevent its incorporation into our evidencebased guidelines. Clearly, patients who require prehospital CPR before EDT survive less often than those who do not. After careful analysis of all available pertinent data and its shortcomings though, we are unable to offer any alteration to the commonly held dictum: EDT is likely futile after 15 minutes of arrest time after penetrating injury. Furthermore, both survival and neurologically intact survival are rare after more than 15 minutes of CPR regardless of injury mechanism or anatomic location
- The combination of three EDT survival predictors-injury mechanism, anatomic injury location, and the presence of signs of life on presentation -was evaluated with respect to hospital survival and neurologic outcome. Overall, 160 patients in 11 studies met these criteria, and 25 (15.6% [10.6Y21.9%]) survived their hospitalization after EDT in this group. As the subcommittee estimated hospital survival without EDT in this population to be 1.7% (range, 1-5%), patients presenting pulseless to the emergency department with signs of life after penetrating extrathoracic injury were nine times (RR, 9.2) more likely to survive their hospitalization after EDT than without EDT. Neurologic outcome after EDT in this population was reported in six studies involving 85 patients. Of these, 14 patients (16.5% [9.7-25.5%]) survived EDT neurologically intact, whereas the subcommittee estimated hospital survival without EDT to be 1.5% (1.7% 90% [90% of penetrating EDT survivors are neurologically intact]) in this population. When compared with the estimated neurologically intact survival of these patients resuscitated without EDT, patients who underwent EDT were 11 times (RR, 11.0) more likely to survive neurologically intact. Analysis reveals that EDT improves both hospital survival and neurologically intact hospital survival in patients presenting pulseless to the emergency department with signs of life after penetrating extrathoracic injury. The present study did not include patients with isolated cranial injuries nor did it consider organ preservation for transplantation as a measured outcome. Our penetrating extrathoracic data included neck, abdominal, and extremity injuries and were grouped together both to provide adequate sample size and to simplify the clinician’s decision-making algorithm. Importantly though, all extrathoracic injury sites likely do not have equivalent salvage rates after EDT. Recent data do suggest a role for EDT after penetrating abdominal, neck, or extremity injury however. This author reviewed 50 consecutive patients who underwent EDT for abdominal exsanguination. Of 39 patients who presented with signs of life after penetrating abdominal injury, 7 survived their hospitalization, all neurologically intact. Sheppard et al. reported outcomes after EDT for penetrating nontorso injuries. Of 27 patients, 3 survived (2 neck, 1 extremity) of which 1 had a poor neurologic outcome. These data suggest that EDT is another potentially useful maneuver in the physician’s armamentarium when confronted with an exsanguinating extrathoracic wound.
- Overall, 139 patients in eight studies met these criteria, and four (2.9% [0.9Y6.8%]) survived their hospitalization after EDT in this group Compared with an estimated hospital survival of 0.1% (range, 0Y1%) without EDT in this population, patients presenting pulseless to the emergency department without signs of life after penetrating extrathoracic injury were nearly 29 times (RR, 28.8) more likely to survive their hospitalization after EDT than without EDT. Neurologic outcome after EDT in this population was reported in four studies involving 60 patients. Of these, three patients (5.0% [1.3Y13.0%]) survived EDT neurologically intact. As the baseline neurologically intact survival for patients presenting pulseless to the emergency department without signs of life after penetrating extrathoracic injury is unreported in prior literature, the subcommittee estimated hospital survival without EDT in this population to be 0.09% (0.1% 90% [90% of penetrating EDT survivors are neurologically intact]). When compared with the estimated neurologically intact survival of these patients resuscitated without EDT, patients who underwent EDT were nearly 56 times (RR, 55.7) more likely to survive neurologically intact. Data suggest a role for EDT in patients presenting pulseless to the emergency department without signs of life after penetrating extrathoracic injury. We recognize that evidence is limited regarding this clinical scenario. Eight cohort studies without controls or case series contributed dataVeach with less than 40 patients contributed and either 0 or 1 survivor per study. These sample size limitations then in turn create less reliable RR survival calculations. mportantly, the limitations reflect not only a difference in outcomes when compared with thoracic injuries but also hesitation of the practitioner to perform the procedure under these circumstances. Of the several functions of EDT (relieve pericardial tamponade, temporize thoracic bleeding, open-chest cardiac massage, maximize cerebral and coronary blood flow while limiting infradiaphragmatic exsanguination, prevention of air embolism), open-chest cardiac massage, and placement of a descending thoracic aortic cross clamp may offer an improved, albeit small, chance of survival for these critically injured patients
- Overall, 454 patients in 22 studies met these criteria, and 21 (4.6% [3.0Y6.9%]) survived their hospitalization after EDT When compared with a subcommittee estimated hospital survival of 0.5% (range, 0Y3%) without EDT in this population, patients presenting pulseless to the emergency department with signs of life after blunt injury were nine times (RR, 9.3) more likely to survive their hospitalization after EDT than without EDT. Neurologic outcome after EDT in this population was reported in 10 studies involving 298 patients. Of these, seven patients (2.4% [1.0Y4.6%]) survived EDT neurologically intact. As the subcommittee estimated hospital survivalwithout EDTin this population to be 0.3% (0.5% 60% [60% of blunt EDT survivors are neurologically intact]) when compared with the estimated neurologically intact survival of these patients resuscitated without EDT, patients who underwent EDT were nearly eight times (RR, 7.8) more likely to survive neurologically intact. In patients presenting pulseless to the emergency department with signs of life after blunt injury, EDT improves both hospital survival and neurologically intact hospital. Pointing to the importance of EDT survival predictors, EDT salvage rates after blunt injury have been unfavorable. Rhee et al compiled 25 years of EDT literature in a 2000 meta-analysis, revealing that 1.4% of blunt injury patients survived EDT. many series contributed no survivors despite the presence of signs of life on presentation. Importantly, both hospital survival rates and neurologic outcome are poor after EDT for blunt injury. Although 90% of EDT survivors after penetrating injury survive neurologically intact only 59% of blunt EDT survivors are neurologically intact . This association may reflect the absence of wounds to rapidly temporize in blunt trauma victims or concomitant traumatic brain injury in multi-injured blunt trauma patients. Thus, not only are patients less likely to survive after EDT for blunt injury but also, when they do survive, blunt injury patients are more likely to be neurologically impaired.
- Overall, 995 patients in 24 studies met these criteria, and seven (0.7% [0.3Y1.4%]) survived their hospitalization after EDT in this group As the subcommittee estimated hospital survival without EDT in this population to be 0.001% (range, 0Y0.01%),despite limited survival after EDT, patients presenting pulseless to the emergency department without signs of life after blunt injury were more likely (RR, 704) to survive their hospitalization after EDT than without EDT. Neurologic outcome after EDT in this population was reported in 11 studies involving 825 patients. Of these, only one patient (0.1% [G0.01Y0.6%]) survived EDT neurologically intact. When compared with the estimated neurologically intact survival of 0.0006% (0.001% 60% [60% of blunt EDT survivors are neurologically intact]) without EDT, patients who underwent EDT were more likely (RR, 202) to survive neurologically intact. In patients presenting pulseless to the emergency department without signs of life after blunt injury, EDT did not improve either hospital survival or neurologically intact hospital survival. Although survival was universally poor in this group, outcomes were yet more dismal when neurologic outcomes were considered. Of seven hospital survivors, only one survived neurologically intact. Overall, a single patient of 825 who underwent EDT for blunt injury without signs of life survived without neurologic impairment. For these reasons, this subcommittee recommends against the performance of EDT in this clinical situation. Highlighting the importance of both injury mechanism and the physiologic signs of life, clinicians should be equipped to make rapid evidence-based life-ordeath decisions using this framework.
- In patients presenting pulseless to the emergency department with signs of life after penetrating thoracic injury, we strongly recommend that patients undergo EDT. This recommendation is based on moderate quality of evidence and places emphasis on patient preference for improved survival and neurologically intact survival after EDT. In patients presenting pulseless to the emergency department without signs of life after penetrating thoracic injury, we conditionally recommend that patients undergo EDT. This recommendation is based on moderate quality of evidence and places emphasis on patient preference for improved survival and neurologically intact survival after EDT but also acknowledges that elapsed time without signs of life is an important component In patients presenting pulseless to the emergency department with signs of life after penetrating extrathoracic injury, we conditionally recommend that patients undergo EDT. This recommendation does not pertain to patients with isolated cranial injuries. This recommendation is based on moderate quality of evidence and places emphasis on patient preference for improved survival and neurologically intact survival after EDT but also acknowledges that penetrating injuries to all extrathoracic anatomic areas will not have equivalent salvage rates after EDT. In patients presenting pulseless to the emergency department without signs of life after penetrating extrathoracic injury, we conditionally recommend that patients undergo EDT. This recommendation does not pertain to patients with isolated cranial injuries and is based on low quality of evidence. The majority of subcommittee members believed that most patients would prefer undergoing EDT in hopes of improved survival and neurologically intact survival. With a moderate overall quality of evidence for both critical outcomes, subcommittee panelists believed that most patients would favor undergoing EDT in this clinical scenario because of the improvements in both survival and neurologically intact survival over patients resuscitated without EDT. However, the subcommittee recognizes that many patients would not want to undergo EDT after blunt injury because of the possibility of concomitant severe traumatic brain injury and poor neurologic outcome in survivors. In patients presenting pulseless to the emergency department without signs of life after blunt injury, we conditionally recommend against the performance of EDT. This recommendation is based on low quality of evidence and re- flects subcommittee group disagreement regarding the strength of the unanimous recommendation against EDT.
- Since 1990, eight reports have assessed the prevalence of blood-borne pathogens in trauma victims of which four studies have prospectively tested for all serum markers (anti-HIV, HBsAg, antiYhepatitis C virus [antiHCV]). Contrary to assumptions, HIV and hepatitis prevalence rates are greater in blunt (HIV, 3.7% [2.6Y5.2%]; hepatitis B virus [HBV], NA; HCV, 12.3% [10.4Y14.5%]) than penetrating (HIV, 1.9% [1.1Y3.3%]; HBV, 0.6% [0.2Y2.1%]; HCV, 9.9% [8Y12.2%]) trauma victims. Regardless, when needlestick or cut exposure transmission rates (HIV, 0.3%; HBV, 6Y30%; HCV, 1.8% [0Y7%]) from known seropositive blood are considered, it is imperative that universal precautions are maintained for all resuscitations
- Criterio de selección. Trauma y perdida de signos de vida 15 min en heridas penetrantes y paro presenciado en trauma cerrado
- A left anterolateral thoracotomy incision is preferred for EDT. Advantages of this incision in the critically injured patient include (a) rapid access with simple instruments, (b) the ability to perform this procedure on a patient in the supine position, and (c) easy extension into the right hemithorax, a clamshell thoracotomy, for exposure of both pleural spaces as well as anterior and posterior mediastinal structures. The key resuscitative maneuvers of EDT, namely, pericardiotomy, open cardiac massage, and thoracic aortic cross clamping are readily accomplished via this approach. The initial execution of a clamshell thoracotomy should be done in hypotensive patients with penetrating wounds to the right chest. This provides immediate, direct access to a right-sided pulmonary or vascular injury while still allowing access to the pericardium from the left side for open cardiac massage. Clamshell thoracotomy may also be considered in patients with presumed air embolism, providing access to the cardiac chambers for aspiration, coronary vessels for massage, and bilateral lungs for obliteration of the source.
- Preparation for EDT should be performed well ahead of the patient's arrival. Set-up should include a 10-blade scalpel, Finochietto's chest retractor, toothed forceps, curved Mayo's scissors, Satinsky's vascular clamps (large and small), long needle holder, Lebsche's knife and mallet, and internal defibrillator paddles. Sterile suction, skin stapler, and access to a variety of sutures should be available (specifically 2-0 prolene on a CT-1 needle, 2-0 silk ties, and teflon pledgets). Upon patient arrival and determination of the need for EDT, the patient's left arm should be placed above the head to provide unimpeded access to the left chest. The anterolateral thoracotomy is initiated with an incision at the level of the fifth intercostal space (Fig. 15-2). Clinically, this level for incision corresponds to the inferior border of the pectoralis major muscle, just below the patient's nipple. In women, the breast should be retracted superiorly to gain access to this interspace, and the incision is made at the inframammary fold. The incision should start on the right side of the sternum; if sternal transection is required, this saves the time-consuming step of performing an additional skin incision. As the initial incision is carried transversely across the chest, and one passes beneath the nipple, a gentle curve in the incision toward the patient's axilla rather than direct extension to the bed should be performed; this curvature in the skin correlates with the natural curvature of the rib cage. The skin, subcutaneous fat, and chest wall musculature are incised with a knife to expose the ribs and associated intercostal space. Intercostal muscles and the parietal pleura are then divided in one layer with either curved Mayo scissors or sharply with the scalpel; the intercostal muscle should be divided along the superior margin of the rib to avoid the intercostal neurovascular bundle. Once the incision is completed and the chest entered, a standard Finochietto's rib retractor is inserted, with the handle directed inferiorly toward the axilla (Fig. 15-3). Placement of the handle toward the bed rather than the sternum allows extension of the left thoracotomy into a clamshell thoracotomy with crossing of the sternum without replacing the rib retractor.
- The highest survival rate following EDT is in patients with penetrating cardiac wounds, especially when associated with pericardial tamponade.7 Early recognition of cardiac tamponade, prompt pericardial decompression, and control of cardiac hemorrhage are the key components to successful EDT and patient survival following penetrating wounds to the heart (see Chap. 28).13 The egress of blood from the injured heart, regardless of mechanism, results in tamponade physiology. Rising intrapericardial pressure produces abnormalities in hemodynamic and cardiac perfusion that can be divided into three phases.14 Initially, increased pericardial pressure restricts ventricular diastolic filling and reduces subendocardial blood flow.15 Cardiac output under these conditions is maintained by compensatory tachycardia, increased systemic vascular resistance, and elevated central pressure (i.e., ventricular filling pressure). In the intermediate phase of tamponade, rising pericardial pressure further compromises diastolic filling, resulting in diminished cardiac output. Although blood pressure may be maintained deceptively well, subtle signs of shock (e.g., anxiety, diaphoresis, and pallor) become evident. During the final phase of tamponade, compensatory mechanisms fail as the intrapericardial pressure approaches the ventricular filling pressure. Cardiac arrest ensues as profound coronary hypoperfusion occurs. The classic description of clinical findings, Beck's triad, is rarely observed in the ED; therefore, a high index of suspicion in the at-risk patient sustaining penetrating torso trauma is crucial, with prompt intervention essential. In the first two phases of cardiac tamponade, patients may be aggressively managed with definitive airway control, volume resuscitation to increase preload, and pericardiocentesis. The patient in the third phase of tamponade, with profound hypotension (SBP < 60), should undergo EDT rather than pericardiocentesis as the management for evacuation of pericardial blood.16,17 Following release of tamponade, the source of tamponade can be directly controlled with appropriate interventions based on the underlying injury (see Technical Considerations). The pericardium is incised widely, starting at the cardiac apex and extending toward the sternal notch, anterior and parallel to the phrenic nerve (Fig. 15-3). If the pericardium is not tense with blood it may be picked up at the apex with toothed forceps and sharply opened with scissors. If tense pericardial tamponade exists, a knife or the sharp point of a scissors is often required to initiate the pericardiotomy incision. Blood and blood clots should be completely evacuated from the pericardium. The heart should be delivered from the pericardium by placing the right hand through the pericardial incision, encircling the left side of the heart and pulling it into the left chest. This effectively places the left side of the pericardium behind the heart allowing access to the cardiac chambers for repair of cardiac wounds and access for effective open cardiac massage. Prompt hemorrhage control is paramount for a cardiac injury. In the beating heart, cardiac bleeding sites should be controlled immediately with digital pressure on the surface of the ventricle and partially occluding vascular clamps on the atrium or great vessels. Efforts at definitive cardiorrhaphy may be delayed until initial resuscitative measures have been completed. In the nonbeating heart, cardiac repair is done prior to defibrillation and cardiac massage. Cardiac wounds in the thin walled right ventricle are best repaired with 3-0 nonabsorbable running or horizontal mattress sutures. Buttressing the suture repair with Teflon pledgets is ideal for the thinner right ventricle, but not essential. When suturing a ventricular laceration, care must be taken not to incorporate a coronary vessel into the repair. In these instances, vertical mattress sutures should be used to exclude the coronary and prevent cardiac ischemia. In the more muscular left ventricle, particularly with a linear stab wound, control of bleeding can often be achieved with a skin-stapling device. Low-pressure venous, atrial, and atrial appendage lacerations can be repaired with simple running or pursestring sutures. Posterior cardiac wounds may be particularly treacherous when they require elevation of the heart for their exposure; closure of these wounds is best accomplished in the OR with optimal lighting and equipment. For a destructive wound of the ventricle, or for inaccessible posterior wounds, temporary inflow occlusion of the superior and inferior vena cava may be employed to facilitate repair (see Chap. 29). Use of a foley catheter for temporary occlusion of cardiac injuries has been suggested; in our experience this may inadvertently extend the injury due to traction forces.
- Life-threatening intrathoracic hemorrhage occurs in less than 5% of patients following penetrating injury presenting to the ED, and in even lower percentage of patients sustaining blunt trauma.18 The most common injuries include penetrating wounds to the pulmonary hilum and great vessels; less commonly seen are torn descending thoracic aortic injuries with frank rupture or penetrating cardiac wounds exsanguinating into the thorax through a traumatic pericardial window. There is a high mortality rate in injuries to the pulmonary or thoracic great-vessel lacerations due to the lack of hemorrhage containment by adjacent tissue tamponade or vessel spasm (see Chaps. 26 and 29). Either hemithorax can rapidly accommodate more than half of a patient's total blood volume before overt physical signs of hemorrhagic shock occur. Therefore, a high clinical suspicion is warranted in patients with penetrating torso trauma, particularly in those with hemodynamic decompensation. Patients with exsanguinating wounds require EDT with rapid control of the source of hemorrhage if they are to be salvaged.
- External chest compression provides approximately 20 to 25% of baseline cardiac output, with 10 to 20% of normal cerebral perfusion.19,20 This degree of vital organ perfusion can provide reasonable salvage rates for 15 minutes, but few normothermic patients survive 30 minutes of closed-chest compression. Moreover, in models of inadequate intravascular volume (hypovolemic shock) or restricted ventricular filling (pericardial tamponade), external chest compression fails to augment arterial pressure or provide adequate systemic perfusion; the associated low diastolic volume and pressure result in inadequate coronary perfusion.21 Therefore, closed cardiac massage is ineffective for postinjury cardiopulmonary arrest. The only potential to salvage the injured patient with ineffective circulatory status is immediate EDT Early defibrillation for ventricular fibrillation or pulseless ventricular tachycardia has proven benefit, and evidence supports the use of amiodarone (with lidocaine as an alternative) following epinephrine in patients refractory to defibrillation. Magnesium may be beneficial for torsades de pointes; other dysrhythmias should be treated according to current guidelines.50 Internal defibrillation may also be required, with similar indications as closed chest CPR. Familiarity with the internal cardiac paddles and appropriate charging dosages in joules is required (Fig. 15-6). In the event of cardiac arrest, bimanual internal massage of the heart should be instituted promptly (Fig. 15-7). We prefer to do this with a hinged clapping motion of the hands, with the wrists apposed, sequentially closing from palms to fingers. The ventricular compression should proceed from the cardiac apex to the base of the heart. The two-handed technique is strongly recommended, as the one-handed massage technique poses the risk of myocardial perforation with the thumb. Pharmocologic adjuncts to increase coronary and cerebral perfusion pressure may be needed. The first agent in resuscitation at this juncture is intracardiac epinephrine. Epinephrine should be administered using a specialized syringe, which resembles a spinal needle, directly into the left ventricle. Typically, the heart is lifted up slightly to expose the more posterior left ventricle, and care is taken to avoid the circumflex coronary during injection. Although epinephrine continues to be advocated during resuscitation, there is a growing body of data suggesting that vasopressin may be superior to epinephrine in augmenting cerebral perfusion and other vital organ blood flow
- The rationale for temporary thoracic aortic occlusion in the patient with massive hemorrhage is two-fold. First, in patients with hemorrhagic shock, aortic cross clamping redistributes the patient's limited blood volume to the myocardium and brain.9 Second, patients sustaining intraabdominal injury may benefit from aortic cross clamping due to reduction in subdiaphragmatic blood loss.8 Temporary thoracic aortic occlusion augments aortic diastolic and carotid systolic blood pressure, enhancing coronary as well as cerebral perfusion.22,23 Canine studies have shown that the left ventricular stroke-work index and myocardial contractility increase in response to thoracic aortic occlusion during hypovolemic shock.24 These improvements in myocardial function occur without an increase in the pulmonary capillary wedge pressure or a significant change in systemic vascular resistance. Thus, improved coronary perfusion resulting from an increased aortic diastolic pressure presumably accounts for the observed enhancement in contractility.25 These experimental observations suggest that temporary aortic occlusion is valuable in the patient either with shock due to non-thoracic trauma or in patients with continued shock following the repair of cardiac or other exsanguinating wounds. Indeed, occlusion of the descending thoracic aorta appears to increase the return of spontaneous circulation following cardiopulmonary resuscitation.26,27 Reports of successful resuscitation using EDT in patients in hemorrhagic shock and even sustaining cardiac arrest following extremity and cervical injuries exist.28 In these situations, EDT P.247 may be a temporizing measure until the patient's circulating blood volume can be replaced by blood product transfusion. However, once the patient's blood volume has been restored, the aortic cross clamp should be removed. Thoracic cross clamping in the normovolemic patient may be deleterious because of increased myocardial oxygen demands resulting from the increased systemic vascular resistance.29 Careful application of this technique is warranted as there is substantial metabolic cost and a finite risk of paraplegia associated with the procedure.30, 31, 32 However, in carefully selected patients, aortic cross clamping may effectively redistribute the patient's blood volume until external replacement and control of the hemorrhagic source is possible. Typically, complete removal of the aortic cross clamp or replacement of the clamp below the renal vessel should be performed within 30 minutes; the gut's tolerance to normothermic ischemia is 30-45 minutes. Following thoracotomy and pericardiotomy with evaluation of the heart, the descending thoracic aorta should be occluded to maximize coronary perfusion if hypotension (SBP < 70 mmHg) persists. We prefer to cross-clamp the thoracic aorta inferior to the left pulmonary hilum (Fig. 15-8). Exposure of this area is best provided by elevating the left lung anteriorly and superiorly. Although some advocate taking down the inferior pulmonary ligament to better mobilize the lung, this is unnecessary and risks injury to the inferior pulmonary vein. Dissection of the thoracic aorta is optimally performed under direct vision by incising the mediastinal pleura and bluntly separating the aorta from the esophagus anteriorly and from the prevertebral fascia posteriorly. Care should be taken in dissecting the aorta, and completely encircling it may avulse thoracic and other small vascular branches. Alternatively, if excessive hemorrhage limits direct visualization, which is the more realistic clinical scenario, blunt dissection with one's thumb and fingertips can be done to isolate the descending aorta. Once identified and isolated, the thoracic aorta is occluded with a large Satinsky or DeBakey's vascular clamp. If the aorta cannot be easily isolated from the surrounding tissue, digitally occlude the aorta against the spine to affect aortic occlusion. Although occlusion of the thoracic aorta is typically performed after pericardiotomy, this may be the first maneuver upon entry into the chest in patients sustaining extrathoracic injury and associated major blood loss.
- Bronchovenous air embolism can be a subtle entity following thoracic trauma, and is likely to be much more common than is recognized.33, 34, 35 The clinical scenario typically involves a patient sustaining penetrating chest injury who precipitously develops profound hypotension or cardiac arrest following endotracheal intubation and positive-pressure ventilation. Traumatic alveolovenous communications produce air emboli that migrate to the coronary arterial systems; any impedance in coronary blood flow causes global myocardial ischemia and resultant shock. The production of air emboli is enhanced by the underlying physiology—there is relatively low intrinsic pulmonary venous pressure due to associated intrathoracic blood loss and high bronchoalveolar pressure from assisted positive pressure ventilation. This combination increases the gradient for air transfer across bronchovenous channels.36 Although more often observed in penetrating trauma, a similar process may occur in patients with blunt lacerations of the lung parenchyma (see Chap. 26). Immediate thoracotomy with pulmonary hilar cross clamping prevents further propagation of pulmonary venous air embolism. Thoracotomy with opening of the pericardium also provides access to the cardiac ventricles; with the patient in the Trendelenburg's position (done to trap to air in the apex of the ventricle), needle aspiration is performed to remove air from the cardiac chambers. Additionally, vigorous cardiac massage may promote dissolution of air already present in the coronary arteries.35 Aspiration of the aortic root is done to alleviate any accumulated air pocket, and direct needle aspiration of the right coronary artery may be attempted Control of the pulmonary hilum has two indications. First, if coronary or systemic air embolism is present, further embolism is prevented by placing a vascular clamp across the pulmonary hilum (Fig. 15-9). Associated maneuvers such as vigorous cardiac massage to move air through the coronary arteries and needle aspiration of air from the left ventricular apex and the aortic root are also performed (Fig. 15-10). Second, if the patient has a pulmonary hilar injury or marked hemorrhage from the lung parenchyma, control of the hilum may prevent exsanguination. Hilar control can be performed by a Satinsky's clamp, the pulmonary hilar twist, or temporarily with digital control (see Chaps. 26 and 27).