Rev. méd. Chile v.133 n.4 Santiago abr. 2005
Infarto encefálico por embolia aérea. Caso clínico
Ischemic brain infarction after an air embolism. Case report
Patricio Mellado T1, Freddy Constanzo P1, Juan Francisco Miquel P2, Patricio Ibáñez L2.
1Departamentos de Neurología y 2Gastroenterología, Facultad de Medicina, Hospital Clínico de la Pontificia Universidad Católica de Chile. Santiago de Chile.
Dirección para correspondencia
Ischemic stroke due to embolic air is uncommon. There are few reports of patients with air embolic stroke as a complication of endoscopic procedures. The temporal relationship between the stroke and this procedure is the most important clue for the diagnosis. CT scan and MRI of the brain are confirmatory tests. The morbidity and mortality is high. Patients should be hospitalized in a critical care service and treated as soon as possible with oxygen in a pressure camera. We report a 52 years old woman with an ovarian cancer that, during an upper gastrointestinal endoscopy, had a severe alteration of consciousness that did not respond to the use of Flumazenil. A CT scan showed multiple areas of air embolism in the watershed area between anterior and middle right cerebral arteries. A conservative treatment was decided and the patients died 48 hours later.
(Key Words: Anterior cerebral artery; Brain infarction; Intracranial embolism; Middle cerebral artery)
La embolia aérea corresponde a la oclusión de un vaso sanguíneo por burbujas de aire. Es una complicación grave, aunque infrecuente, en algunos procedimientos clínicos, resultando en una alta morbilidad y eventualmente la muerte1,2. La embolia aérea debe ser considerada en el diagnóstico diferencial de cualquier accidente vascular, si se desarrolla durante o después de un procedimiento endoscópico3,4. Se debe considerar que los eventos cerebrovasculares no son comunes durante la endoscopia y que su diagnóstico debe ser efectuado precozmente para iniciar su tratamiento específico.
Describimos una paciente que presentó un accidente vascular encefálico debido a una embolia aérea arterial secundaria a un procedimiento endoscópico.
Caso clínico
Paciente mujer de 52 años con cáncer de ovario III C (adenocarcinoma mal diferenciado) diagnosticado 2 años antes. Su tratamiento consistió en una histerectomía total, salpingooforectomía bilateral, omentectomía y resección ileocólica, además de quimioterapia paliativa e ileostomía a permanencia por cuadros de obstrucción intestinal.
Debido a vómitos persistentes de dos semanas de duración, se realizó una endoscopia digestiva alta en forma ambulatoria. Se utilizó 4,5 mg de midazolam intravenoso como sedación. La endoscopia mostró una extensa esofagitis del tercio medio y distal, se tomó biopsias de estas zonas (Figura 1). Durante el procedimiento presentó compromiso de conciencia que no revirtió con flumazenil. En su examen físico general destacaba una frecuencia cardíaca de 100 por min e hipotensión arterial (90/50), que no respondió a la infusión de volumen. En el examen neurológico destacaba: coma y rigidez de descerebración bilateral, ojos desviados a derecha, reflejos oculocefálicos presentes, reflejo corneal abolido a izquierda, hipertonía de las cuatro extremidades, mayor en el hemicuerpo izquierdo, reflejos osteotendíneos aumentados simétricamente, clonus y Babinski bilateral (escala de NIHSS=27). Se decidió su traslado a la sala de reanimación del servicio de urgencias y se solicitó una tomografía computada de encéfalo (TC), la que mostró múltiples embolias aéreas en el territorio limítrofe superficial entre las arterias cerebral media y anterior derechas (Figura 2). La radiografía de tórax fue normal.
Figura 1. Fotografías del esófago de la paciente que muestran intensa esofagitis difusa del tercio medio y distal.
El equipo oncológico tratante decidió, en conjunto con la familia de la paciente, un manejo conservador, debido al mal pronóstico de la neoplasia de base, indicándose su traslado a sala y oxígeno al 100%. La paciente falleció a las 48 h sin recuperar conciencia ni sus déficits neurológicos. La biopsia del esófago mostró una esofagitis intensa y difusa del tercio medio y distal, la que fue interpretada como secundaria a quimioterapia.
Figura 2. Tomografía computada de encéfalo. Se observan burbujas de aire en el territorio limítrofe de las arterias cerebrales media y anterior derechas.
Discusión
El infarto encefálico debido a una embolia aérea es una condición infrecuente, se ha descrito asociada a: trauma, cirugía, cambios bruscos de presión, cateterismo venoso central, ventilación mecánica, biopsia pulmonar, hemodiálisis, angiografía y procedimientos endoscópicos y laparoscópicos1-13. La embolia puede ocluir una arteria o rara vez una vena, esto último se observa principalmente como una complicación infrecuente neuroquirúrgica1. Sus manifestaciones clínicas son variadas, desde cefalea hasta compromiso de conciencia, déficit focal, convulsiones y muerte1-3,6,13. Su morbimortalidad es elevada, una revisión de la literatura de 17 pacientes tratados con terapia hiperbárica mostró que 3 enfermos fallecieron (17,6%), 6 quedaron con un déficit neurológico invalidante (35,4%) y sólo 8 sin secuelas (47%)4,13.
El mecanismo por el cual una embolia aérea se localiza en el árbol arterial encefálico requiere de dos fenómenos: 1. Entrada de aire al sistema sanguíneo. 2. Paso del aire al circuito izquierdo, es decir, saltándose el pulmón que actúa como un filtro para estas burbujas. Estas burbujas de aire ocluyen arterias de pequeño diámetro (30 a 60 um) y sus consecuencias fisiopatológicas son una reducción en la perfusión distal a la obstrucción y una respuesta inflamatoria por daño endotelial1,3,5,13.
La presencia de aire en las arterias sistémicas ha sido explicada por los siguientes mecanismos: sobredistensión pulmonar y barotrauma secundario1-4,7,11,13, procedimientos quirúrgicos1-3,5,13, instalación de un catéter venoso central11-13, hemodiálisis12 o infrecuentemente debido a la presencia de fístulas duodeno-cava o esófago-venas pulmonares2,10.
El paso de estas burbujas al sistema izquierdo, saltándose el filtro pulmonar, ha sido explicado por embolia paradojal, es decir, el paso de la burbuja desde el sistema venoso al sistema arterial a través de una anomalía vascular, siendo la más frecuente el foramen oval permeable, presente hasta en 30% de la población1,11,13. Otra anomalía vascular que permite esta embolia paradojal es la presencia de un shunt intrapulmonar3,13. Por último, como se mencionó, existe la posibilidad del paso directo de aire al sistema izquierdo, por ejemplo en una fístula esófago-vena pulmonar.
Estudios en animales sugieren que grandes embolias aéreas venosas (20 ml) o pequeñas embolias aéreas continuas (11 ml por min) pueden causar embolias arteriales encefálicas1. Por otro lado, desde hace ya dos décadas, se utiliza, como un método diagnóstico validado y libre de riesgo, la prueba con microburbujas de aire disuelto en suero fisiológico e inyectadas por vía venosa para la detección de señales de embolia a través de la ecografía Doppler transcraneana, su presencia permite detectar un shunt derecha-izquierda. Así, las microburbujas de aire pueden ser utilizadas en la práctica clínica sin riesgo14.
En nuestra paciente, al igual que el caso descrito por Weber M et al2, el mecanismo que hemos postulado es el paso de aire directamente desde el esófago hacia el circuito izquierdo, probablemente hacia las venas pulmonares. Es probable que la esofagitis de la paciente haya facilitado el paso del aire que fue insuflado durante la endoscopia.
El diagnóstico de una embolia aérea encefálica se fundamenta en la presencia de un accidente cerebrovascular relacionado temporalmente con alguno de los factores de riesgo mencionados, siendo indistinguible desde el punto de vista del examen neurológico de otras etiologías del accidente cerebrovascular. La TC o la resonancia magnética de encéfalo son altamente sensibles y específicas para detectar burbujas de aire en el trayecto de los vasos, así como el infarto secundario1-4,6,11.
El tratamiento de la embolia aérea encefálica consiste en la estabilización hemodinámica del paciente en una unidad de cuidados intensivos y la oxigenoterapia como su tratamiento específico. Se debe utilizar oxígeno al 100%, o idealmente desde el inicio, cámara hiperbárica1-4,6,11-13. La administración de oxígeno no es sólo importante para tratar la hipoxia y la hipoxemia, sino también para eliminar las burbujas de aire en el encéfalo mediante una gradiente de difusión que favorezca su salida1. También se ha recomendado la posición supina horizontal, el uso de anticonvulsivantes en forma profiláctica y barbitúricos1. La terapia con anticoagulantes y esteroides es controvertida y la mayoría de los autores no la recomienda1.
El oxígeno hiperbárico ha sido recomendado como la terapia de primera línea en embolia aérea. Consiste en someter al paciente a presiones barométricas mayores a 760 mm de Hg, usualmente entre 2 y 3 atmósferas por 2 a 4 h, mientras se le administra oxígeno al 100%, lo que disminuye el tamaño de las burbujas por un mecanismo dual: la presión ambiental y la hiperoxia1,4,11-15. A 2,8 atmósferas de presión, las burbujas de aire son reducidas al menos en dos tercios de su diámetro inicial12,13. La hiperoxia produce una gradiente de difusión dentro de la burbuja de aire, con ingreso de oxígeno a ella y salida de nitrógeno1. Además, produce mejoría en el transporte plasmático y la entrega de O2 a los tejidos mal perfundidos1,12,13,15. Existen reportes de una rápida y completa mejoría neurológica en pacientes que han presentado una embolia aérea encefálica tratada con oxígeno en cámara hiperbárica4,12,13. Los mejores resultados se obtienen cuando se inicia la terapia antes de 5 h del evento, aunque su inicio después de 30 h puede ser beneficiosa13,16.
Nuestra paciente presentó una embolia aérea arterial asociada a una endoscopia digestiva alta, lo que está descrito como una rara complicación de este procedimiento, principalmente cuando es insuflado aire bajo presión por el gastroscopio o cuando se realizan procedimientos como biopsia, proponiéndose como mecanismos la embolia paradójica o la fístula esófago-vena pulmonar1-4,10,17. El mecanismo por el cual nuestra paciente presentó una embolia aérea arterial encefálica no fue estudiado debido a su manejo conservador.
Conclusión
El infarto encefálico debido a una embolia aérea es infrecuente, debe sospecharse en todo paciente que desarrolle un déficit neurológico durante o inmediatamente después de un procedimiento invasivo. Su diagnóstico oportuno con una TC o RM de encéfalo puede permitir su tratamiento con oxigenoterapia al 100% e idealmente en una cámara hiperbárica.
Referencias
1. Muth C, Shank E. Gas Embolism. N Engl J Med 2000; 342: 476-82.
[ Medline ]
2. Weber M, Fiebach J, Lichy M, Weber R, Schwark C, Grau A. Bilateral cerebral air embolism. J Neurol 2003; 250: 1115-7.
[ Medline ]
3. Akhtar N, Jafri W, Mozaffar T. Cerebral artery air embolism following an esophagogastroscopy: a case report. Neurology 2001; 56: 136-7.
[ Medline ]
4. Raju G, Bendixen B, Khan J, Summers R. Cerebrovascular accident during endoscopy: consider cerebral air embolism, a rapidly reversible event with hyperbaric oxygen therapy. Gastrointest Endosc 1998; 47: 70-3.
[ Medline ]
5. Mitchell S, Gorman D. The pathophysiology of cerebral arterial gas embolism. Extra Corpor Technol 2002; 34: 18-23.
6. Hodics T, Linfante I. Cerebral air embolism. Neurology 2003; 60: 112.
7. Foster P, Boriek A, Butler B, Gernhardt M, Bove A. Patent foramen ovale and paradoxical systemic embolism: a bibliographic review. Aviat Space Environ Med 2003; 74: B1-B64.
[ Medline ]
8. Katzgraber F, Glenewinkel F, Rittner C, Beule J. Fatal air embolism resulting from gastroscopy. Lancet 1995; 346: 1714-5.
9. Bou-Samra G, Darby P, Christensen G. Cerebral air em-bolism during endoscopy. Mo Med 1997; 94: 704-7.
10. Christl S, Scheppach W, Peters U, Kirchner T. Cerebral air embolism after gastroduodenoscopy: complication of a duodenocaval fistula. Gastrointest Endosc 1994; 40: 376-8.
[ Medline ]
11. Emaerel P, Gevers A, De Bruecker Y, Sunaert S, Wilms G. Stroke caused by cerebral air embolism during endoscopy. Gastrointest Endosc 2003; 57: 134-5.
12. Tibbles P, Edelsberg J. Hyperbaric-oxygen therapy. N Engl J Med 1996; 334: 1642-8.
[ Medline ]
13. Murphy B, Harford F, Cramer F. Cerebral air embolism resulting from invasive medical procedures. Treatment with hyperbaric oxygen. Ann Surg 1985; 210: 242-5.
14. Meairs S. Hennerici M, Mohr JP. Ultrasonography. En: Mohr JP, Choi DW, Grotta JC, Weir B, Wolf PA (eds). Stroke: Patophysiology, diagnosis, and management. Philadelphia. Churchill Livingstone 2004; 497-524.
15. Pomes J. Oxigenoterapia hiperbárica. En: Cubillos L, Espinoza R. Manual de Urgencias Médicas. Santiago. Mediterráneo 2002; 504-12.
16. Bitterman H, Melamed Y. Delayed hyperbaric treatment of cerebral air embolism. Israel J Med Sci 1993; 29: 22-6.
17. Katzgraber F, Glenewinkel F, Fischler S, Rittner C. Mechanism of fatal air embolism after gastrointestinal endoscopy. Int J legal Med 1998; 111: 154-6.
[ Medline ]
Correspondencia a: Dr. Patricio Mellado T. Marcoleta 347, Santiago, Chile. Fax: 56-2-632-6221. E-mail: pmellado@med.puc.cl
Recibido el 12 de agosto, 2004. Aceptado en versión corregida el 27 de enero, 2005.
martes, 16 de diciembre de 2008
Libros HBOT Dra.Nina Subotina
EDUCACIÓN
Dra Nina Subotina
Autora de los 2 libros
Doctora en Medicina graduada en el Primer Instituto de Medicina de Moscú (diploma de Honor).
Candidato en Ciencias Médicas (Comisión Superior de Certificación de U.R.S.S.).
Formación como especialista en medicina hiperbárica en el Barocentro de Moscú
Idiomas: ruso, inglés, francés, alemán, español.
VIDA LABORAL
Staff Servicio de Medicina Hiperbárica del Sanatorio Modelo Quilmes
(Pcia. de Buenos Aires) (1992-2000).
Directora del Centro de Medicina Hiperbárica Buenos Aires - Hipercámaras S.A. (desde 1998 hasta la fecha).
CARGOS Y MEMBRESÍAS
Vice-presidente de la Sociedad Argentina de Medicina Hiperbárica y Actividades Subacuáticas (SAMHAS).
Representante de la Red Nacional de Cámaras Hiperbáricas.
Miembro titular de la Undersea and Hyperbaric Medical Society (USA) (desde 1999).
Miembro titular de la Sociedad Argentina de Curación de las Heridas (SACH).
PUBLICACIONES
Autora de numerosos trabajos sobre los ritmos biológicos, rendimiento humano y aplicaciones clínicas de la oxigenoterapia hiperbárica.
Autora de Medicina Hiperbárica, 2006
Autora de La Cámara Hiperbárica: Ciencia, no milagro, 2007
CONTACTO
Hipercámaras Sociedad Anónima
Sanchez de Bustamante 1175
Buenos Aires, Argentina
Tel: 54-11-4963-0030
samhas@pccp.com.ar
Pie Diabetico Complicado
Mujer de 54 años;Diabetes Mellitus Insulino dependiente ,con Historia de Infecciones recurrentes en su pie Izquierdo con resultado de amputacion parcial y que presenta herida que complica la salvacion de dicho Miembro inferior ,se realizan tratamiento quirurgico con colgajo,antibioticos en conjunto con 37 sesiones de Oxigenacion Hiperbarica,logrando salvar el pie y mejorando la calidad de vida de la Paciente.h
DESHICENCIA DE SUTURA QUIRURGICA
Deshicencia de herida Quirurgica.
MUJER de 52 años de Edad presenta una Deshicencia de sutura Quirurgica como complicacion post-operatoria de Hernirrafia de rutina ,abriendose el sitio de sutura complicandose con Fasceitis Necrotizante .La herida inicialmente tenia las medidas de 5x20x4 de profundidad.Comenzo el tratamiento con HBOT en conjunto con curaciones y los antibioticos indicados y una sesion diaria de HBOT ,relizandose 30 sesiones de HBOT ,cicatrizandose la herida.
Dolor Muscular y HBOT
Agujetas
D
Se consideran un dolor muscular localizado debido a la práctica de ejercicio
Las agujetas (nombre médico mialgia diferida) es el nombre coloquial de un dolor muscular llamado "Dolor muscular de aparición tardía" (en inglés DOMS: Delayed Onset Muscular Soreness) acompañado de una inflamación muscular.[1] [2] Aparece como un dolor localizado después de un período de ejercicio intenso tras un período carente de ejercicio.[3] Su síntoma es un dolor intenso y localizado similar al de pequeñas agujas (de ahí el nombre) y suponen una disminución de la movilidad y la flexibilidad durante un periodo entre uno (24 h) y cinco días, dependiendo de la actividad y del historial previo de carencia deportiva. Existen numerosas teorías sobre el origen de las agujetas.[1]
Contenido
[ocultar]
* Fundamento de la mialgia diferida
La mialgia diferida (agujetas) aparece siempre en la práctica de un ejercicio en la que existe una contracción muscular excéntrica (contraria a la gravedad - un ejemplo puede ser cuando se corre cuesta arriba). Las investigaciones realizadas muestran que se produce igualmente en los músculos de animales que en los humanos.[1] El dolor proporciona sensación de rigidez al atleta y afecta tanto a atletas expertos como novatos, el factor importante es la "familiaridad" con el ejercicio realizado.[4] La intensidad de la mialgia es mayor cuanto más intenso ha sido el ejercicio realizado y menos habitual es en la rutina deportiva, aunque sobre este punto existe todavía una discusión en la comunidad científica.[5] Existen algunas teorías acerca del fundamento de la mialgia diferida:
* Microrrotura de fibras musculares - esta teoría es la más aceptada por la comunidad científica,[6] menciona que el dolor muscular y la inflamación se producen debido al número de microfibras rotas durante la práctica del ejercicio.
* Temperatura incrementada localmente en los músculos - Esta teoría menciona que durante la práctica del ejercicio el músculo se calienta y en algunas zonas se producen "microlesiones". Posee cierta similitud con la teoría de las microrroturas musculares y la comunidad científica está pendiente de más investigaciones al respecto.
* Acumulación del ácido láctico - esta teoría, ya en desuso, acaba mencionando que el ácido láctico resultante de la actividad metabólica en las células musculares acaba "cristalizando" (de ahí viene su nombre) siendo esta la causa final del dolor muscular debido a la supuesta presencia de estos cristales intersticiales en el músculo.[7]
Existen otras teorías que aportan explicaciones a algunos efectos de la mialgia, quedando sin explicar otros.
Microrrotura de fibras musculares
La teoría de la microrrotura es clásica ya que en el año 1902 se formuló por primera vez,[8] en ella se menciona que la mialgia aparece tras la práctica deportiva se explica mediante alguna literatura científica como una rotura de fibras musculares en su mínima expresión, técnicamente es la rotura de los sarcómeros musculares.[9] Lo que acaba produciendo un efecto de inflamación ligero del músculo afectado.[10] Este dolor se debe a que la fibra muscular es débil y no es capaz de sostener el nivel de ejercicio, probablemente porque se está desentrenado y la fibra no es capaz de aguantarlo. Los patrones de rotura dentro del músculo son completamente aleatorios.[11] Existe alguna evidencia científica que menciona una mayor cantidad de microroturas en los músculos de contracción rápida.[12] [11] Esta teoría parece ser la más aceptada por la comunidad científica y se han realizado numerosos estudios en deportistas.[13]
Las zonas más afectadas por este dolor son las uniones musculares y los tendones cerca de las articulaciones, esto se debe a que la zona musculotendinosa es donde existen más fibras musculares débiles y más tensión. Existe un segundo supuesto: los receptores del dolor (nociceptores) se encuentran en mayor cantidad en estas regiones.[13] El dolor muscular suele tener un periodo que oscila entre los 5 y 7 días con un pico de dolor que se muestra a los 1-3 días tras el ejercicio. Por ejemplo, el dolor y la relajación de los músculos no contribuye a la pérdida de fuerza que aparece en los días de recuperación, no existen evidencias de una inhibición neuronal sobre los músculos[14] y una desactivación en las unidades motoras[15] El dolor y la debilidad muscular se deben prinicipalmente a los procesos inflamatorios más que al daño micromuscular producido.[16] Las investigaciones realizadas se han fundamentado en el desbalance sobre la homeostasis del calcio en los tejidos musculares debido a la microroturas musculares.[17]
Aumento de la temperatura
Durante un ejercicio intenso las células musculares pueden alcanzar temperaturas entre los 38º y los 48º, lo que supone una muerte celular o necrosis. Este proceso genera una desorganización estructural en los músculos que acaba generando un dolor generalizado en ciertos músculos.[18] Esta teoría se ha convertido en una derivación de la de microrotura de las fibras musculares, ya que puede considerarse como una causa más de la microrotura.
Acumulación de ácido láctico
La teoría fue establecida por primera vez por Assmussen en el año 1956[7] y desde entonces la teoría ha ido siendo cada vez más abandonada por la comunidad científica. En condiciones de anoxia (falta de oxígeno) como la que ocurre en las células musculares durante un ejercicio intenso el metabolismo cambia y las células fermentan los nutrientes para conseguir energía. La fermentación produce mucha menos energía que el metabolismo normal, que degrada la glucosa a dos ácidos pirúvicos y este se degrada completamente por otras rutas metabólicas. Sin embargo, en la fermentación el ácido pirúvico se transforma en ácido láctico que cristaliza en el músculo. El dolor producido, por tanto, sería el resultado de la acidez incrementada captada por los nervios y por las microrroturas del músculo debido a los cristales.[19]
Según mencionan algunos autores, esta teoría tiene pocos fundamentos, la observación muscular mediante biopsias musculares no ha podido mostrar la aparición de tales cristales. Tras formarse los cristales de ácido láctico muchos se degradan y una pequeña parte se recombina con otras sustancias para proporcionar moléculas energéticas (glucosa). Otra evidencia que niega tal cristalización es que el ácido láctico llega a cristalizar a temperaturas inferiores a -5ºC, cosa que hace que esta teoría pase a ser una "leyenda urbana" establecida por la transmisión de deportista a deportista sin llegar a un fundamento científico claro.
Espasmo muscular
Introducida en el año 1961 por Dvries,[20] esta teoría propone que el dolor sea resultado de pequeñas descargas eléctricas debido a la fatiga del músculo. Durante un periodo de actividad intensa las contracciones musculares reducen el flujo sanguíneo provocando daños a las células (isquemia) lo que produce un estímulo en las terminaciones nerviosas que vuelven a contraer la fibra muscular, con lo que se repite el ciclo. El aumento de la actividad eléctrica produce, además de la excitación de los nervios una gran fatiga muscular por la falta de flujo sanguíneo. La teoría ha sido criticada por algunos estudiosos de la fisiología y hoy en día se pone en duda.[21]
Tratamiento de la mialgia diferida
Se han investigado numerosos tratamientos contra la mialgia diferida tanto en situaciones previas como posteriores al ejercicio. Estas intervenciones se pueden clasificar en tres amplias categorías:[22]
* Farmacológicas que emplean tratamientos de productos no-esteroides y anti-inflamatorios (denominados en inglés: nonsteroidal anti-inflammatory drugs - NSAIDs). Estos métodos se centran básicamente en aliviar el dolor causado por las agujetas. No obstante los resultados acerca de sus beneficios son muy confusos, ya que existe abundante literatura que demuestra tanto sus efectos beneficiosos como los neutros.[16] Algunos medicamentos han sido ligeramente beneficiosos, como el ibuprofeno[23] [24] o el naproxeno.[25] Sin embargo hay estudios que mencionan el efecto nulo de la aspirina (a pesar de la creencia popular).[26]
* Terapéuticos que emplean modalidades físicas: diversas modalidades de masaje, ejercicios físicos específicos,[27] crioterapia,[28] ultrasonidos e incluso estimulación eléctrica.[29] Respecto a algunas terapias como la oxigenación hiperbárica (HBO, una terapia consistente en la inhalación de Oxígeno (O2) a altas dosis) se está produciendo un debate científico en la actualidad.[30]
* Dietéticas que emplean suplementos nutricionales tales como las isoflavonas (como pueden ser las isoflavonas de soja) y algunos aceites procedentes de pescados que se han mostrado eficaces en el tratamiento.[31] Se necesita todavía un "corpus" de investigación en esta área.
Prevención
No existe un método claro para prevenir y tratar las agujetas a pesar de las numerosas investigaciones.[16] Sin embargo se ha demostrado que los estiramientos musculares previos a la realización del ejercio así como posteriores disminuyen la intensidad del dolor. También tiene efectos positivos sacudirse los músculos durante la realización del ejercicio físico (favorece la circulación sanguínea) y tomarse una ducha caliente al concluirlo.[32] [33] Es conveniente un calentamiento previo así como el aumento progresivo del nivel de entrenamiento, empezando por ejercicios suaves hasta llegar a los más intensos,[34] de este modo las fibras musculares se preparan para una situación de esfuerzo.
Algunos suplementos dietéticos que parecen tener algún efecto en la mialgia diferida son la árnica, de origen homeopático;[35] la ubiquinona (coenzima-Q); y la L-carnitina, en ciertos trabajos científicos sobre corredores de maratón.[36]
Postratamiento
Se ha realizado una exhaustiva investigación acerca de como tratar las agujetas una vez se producen. Uno de los métodos más empleados en la medicina deportiva es el masaje muscular.[37] [38] El uso de antioxidantes (vitamina C y E) no ha dado resultados positivos para eliminar sus efectos.[39]
Una idea muy extendida y popular es que el consumo de agua con bicarbonato sódico o azúcar puede utilizarse para combatir las agujetas. Este remedio casero es el resultado de la aceptación masiva de la teoría referente al ácido láctico. Puesto que esta teoría está prácticamente descartada, este método probablemente no evita ni cura las agujetas ni sus síntomas, pero puede provocar basicidad y problemas gástricos. Por lo tanto no debe seguirse un tratamiento de este tipo. No obstante, podemos encontrar un pequeño alivio en la aplicación de frío. En caso de dolor muy intenso se puede tomar ibuprofeno, que aúna propiedades analgésicas y anti-inflamatorias.
Referencias
1. ↑ a b c "Acute inflammation: the underlying mechanism in delayed onset muscle soreness?", S. Lucille; Medicine & Science in Sports & Exercise. 23(5):542-551, May 1991
2. ↑ "Exercise-induced muscle damage and potential mechanisms for the repeated bout effect", MCHUGH, M.P., D.A.J. CONNOLLY, R.G. ESTON, AND G.W. GLEIM. Sports Med. 27:158–170. 1999.
3. ↑ "Abraham, WM: "Factors in delayed muscle soreness". Med Sci Sports Exerc 9:11
4. ↑ "Delayed Onset Muscle Soreness: Treatment Strategies and Performance Factors", Cheung, Karoline; Sports Medicine. 33(2):145-164, 2003
5. ↑ "Delayed-onset muscle soreness does not reflect the magnitude of eccentric exercise-induced muscle damage"; Kazunori Nosaka; Scandinavian Journal of Medicine & Science in Sports, Volume 12 Issue 6 Page 337-346, December 2002
6. ↑ "Morphologic and Mechanical Basis of Delayed-Onset Muscle Soreness", Richard L. Lieber, PhD and Jan Fridén, MD, PhD ; J Am Acad Orthop Surg, Vol 10, No 1, January/February 2002, 67-73.
7. ↑ a b "Observations on experimental muscle soreness". Asmussen E:, Acta Rheum Scand 1956; 2:109-116
8. ↑ "Ergographic studies in muscular soreness". Hough, T. (1902). American Journal of Physiology, 2, 76-92.
9. ↑ "Materials fatigue initiates eccentric contractioninduced injury in rat soleus muscle", WARREN, G.L., D.A. HAYES, D.A. LOWE, B.M. PRIOR, AND R.B. ARMSTRONG. J. Physiol. 464:477–489. 1993.
10. ↑ "Haematological and acute-phase responses associated with delayed-onset muscle soreness in humans"; GLEESON, M., J. ALMEY, S. BROOKS, R. CAVE, A. LEWIS, AND H. GRIFFITHS. Eur. J. Appl. Physiol. 71:137–142. 1995.
11. ↑ a b "Muscle damage induced by eccentric contractions of 25% strain", Lieber, R.L., And J. Fride´N, J. Appl. Physiol. 70:2498–2507. 1991
12. ↑ "Changes in human skeletal muscle induced by longterm eccentric exercise", Fridén, J. . Cell Tissue Res. 236:365–372. 1984.
13. ↑ a b "Exercise-induced muscle damage and potential mechanisms for the repeated bout effect", Mchugh, M.P., D.A.J. Connolly, R.G. Eston, And G.W. Gleim. Sports Med. 27:158–170. 1999.
14. ↑ . "Electromyographic analysis of exercise resulting in symptoms of muscle damage". Mchugh, M.P., D.A.J. Connolly, R.G. Eston, And G.W. Gleim, J. Sports Sci. 8:163–172. 2000.
15. ↑ . "Effect of ketoprofen on muscle function and EMG after eccentric exercise". Sayers, S.P., C.A. Knight, P.M. Clarkson, E.H. Van Wegen, And G. Kamen. Med. Sci. Sports Exerc., 33:702–710. 2001.
16. ↑ a b c "Treatment and Prevention of Delayed Onset Muscle Soreness", DECLAN A.J.; Journal of Strength and Conditioning Research, 2003, 17(1), 197–208
17. ↑ "Hydrogen peroxide disrupts calcium release from the sarcoplasmic reticulum of rat skeletal muscle fibers". Brotto, M., And T.M. Nosek, J. Appl. Physiol. 81:731–737. 1996.
18. ↑ "Response of the body to injury: Inflammation and repair. In: Pathophysiology: Clinical Concepts of Disease Processes". ABRAMS, G.D. S.A. Price and L.M. Wilson, eds. St. Louis, MO: Mosby, 1997. pp. 38–58.
19. ↑ "Traumatología y Medicina Deportiva: Bases de la Medicina del Deporte", Rafael Ballesteros Massó, Publicado en 2002, Thomson Learning Ibero
20. ↑ "Prevention of muscular stress after exercise". DeVries, H.A. Research Quarterly, 32, 177. (1961).
21. ↑ "Factors in delayed onset muscular soreness of man", Bobbert, M.F., Hollander A.P. & Huijing P.A. (1986). Medicine and Science in Sports and Exercise, 18(1), 75-81.
22. ↑ "Various Treatment Techniques on Signs and Symptoms of Delayed Onset Muscle Soreness", Gulick DT, Kimura IF, Sitler M, Paolone A, Kelly JD.; J Athl Train. 1996 Apr;31(2):145-152
23. ↑ "Effects of ibuprofen on exercise-induced muscle soreness and indices of muscle damage", Donnelly, A.E., R.J. Maughan, And P.H. Whiting. . Br. J. Sports Med. 24:191–195. 1990.
24. ↑ "Effect of ibuprofen use on muscle soreness, damage, and performance: A preliminary study", Hasson, S.M., J.C. Daniels, J.G. Divine, B.R. Niebuhr, S. Richmond, P.G. Stein, And J.H. Williams. . Med. Sci. Sports Exerc. 25:9–17. 1993.
25. ↑ "Efficacy of naproxen sodium for exercise-induced dysfunction muscle injury and soreness"; Dudley, G.A., J. Czerkawski, A.Meinrod, G.Gillis, A. Baldwin, And M. Scarpone. . Clin. J. Sport Med. 7:3–10. 1997.
26. ↑ "Effects of aspirin on delayed muscle soreness", Francis, K.T., And T. Hoobler. J. Sports Med. 27:333–337. 1987.
27. ↑ "Intermittent pneumatic compression effect on eccentric exercise-induced swelling, stiffness and strength loss", Chleboun, G.S., J.N. Howell, H.L. Baker, T.N. Ballard, J.L. Graham, H.L. Hallman, L.E. Perkins, J.H. Schauss, And R.R. Conaster. . Arch. Phys. Med. Rehabil. 76:744–749. 1995.
28. ↑ "Effects of cold water immersion on the symptoms of exercise-induced muscle damage", Eston, R., And D. Peters. J. Sports Sci. 17:231–238. 1999.
29. ↑ "Electroestimulación: Entrenamiento y periodización", Manuel Pombo Fernández, Publicado en 2004; ed. Paidotribo; ISBN 84-8019-776-5
30. ↑ "Hyperbaric oxygen therapy does not affect recovery from delayed onset muscle soreness". Mekjavic, I.B., J.A. Extner, P.A. Tesch, And O. Eiken. Med. Sci. Sports Exerc. 3:558–563. 2000.
31. ↑ "The effects of fish oil and isoflavones on delayed onset muscle soreness", Jon Lenn; Medicine & Science in Sports & Exercise. 34(10):1605-1613, October 2002.
32. ↑ "La guía completa de los estiramientos", Christopher M. Norris; Publicado en 2001, Ed.
33. ↑ "The effects of static stretching and warm-up on prevention of delayed-onset muscle soreness.", High DM, Howley ET, Franks BD; Res Q Exerc Sport. 1989 Dec;60(4):357-61.
34. ↑ "Science of Flexibility", Michael J. Alter; 2004, Ed. Human Kinetics
35. ↑ "Homoeopathic Arnica and Rhus toxicodendron for delayed onset muscle soreness A pilot for a randomized, double-blind, placebo-controlled trial"; N. Jawara, British Homoeopathic journal; Volume 86, Issue 1, January 1997, Pages 10-15
36. ↑ TVEITEN, D., S. BRUSET, C.F. BORCHGREVINK, AND J. NORSETH. "Effect of Arnica D 30 during hard physical exertion: A doubleblind randomized trial during the 1995 Oslo Marathon. Complement. Ther. Med. 6:71–74. 1998.correr a sprint durante 20 sg
37. ↑ "Does post-exercise massage treatment reduce delayed onset muscle soreness? A systematic review". E Ernst; British Journal of Sports Medicine, Vol 32, Issue 3 212-214; 1998
38. ↑ "The effects of massage on delayed onset muscle soreness", J E Hilbert, G A Sforzo, T Swensen; J Sports Med 2003;37:72-75
39. ↑ "An effect of ascorbic acid on delayed-onset muscle soreness Pain", Kaminski, M & Boal, R. (1992); 50(3), 327-321.
D
Se consideran un dolor muscular localizado debido a la práctica de ejercicio
Las agujetas (nombre médico mialgia diferida) es el nombre coloquial de un dolor muscular llamado "Dolor muscular de aparición tardía" (en inglés DOMS: Delayed Onset Muscular Soreness) acompañado de una inflamación muscular.[1] [2] Aparece como un dolor localizado después de un período de ejercicio intenso tras un período carente de ejercicio.[3] Su síntoma es un dolor intenso y localizado similar al de pequeñas agujas (de ahí el nombre) y suponen una disminución de la movilidad y la flexibilidad durante un periodo entre uno (24 h) y cinco días, dependiendo de la actividad y del historial previo de carencia deportiva. Existen numerosas teorías sobre el origen de las agujetas.[1]
Contenido
[ocultar]
* Fundamento de la mialgia diferida
La mialgia diferida (agujetas) aparece siempre en la práctica de un ejercicio en la que existe una contracción muscular excéntrica (contraria a la gravedad - un ejemplo puede ser cuando se corre cuesta arriba). Las investigaciones realizadas muestran que se produce igualmente en los músculos de animales que en los humanos.[1] El dolor proporciona sensación de rigidez al atleta y afecta tanto a atletas expertos como novatos, el factor importante es la "familiaridad" con el ejercicio realizado.[4] La intensidad de la mialgia es mayor cuanto más intenso ha sido el ejercicio realizado y menos habitual es en la rutina deportiva, aunque sobre este punto existe todavía una discusión en la comunidad científica.[5] Existen algunas teorías acerca del fundamento de la mialgia diferida:
* Microrrotura de fibras musculares - esta teoría es la más aceptada por la comunidad científica,[6] menciona que el dolor muscular y la inflamación se producen debido al número de microfibras rotas durante la práctica del ejercicio.
* Temperatura incrementada localmente en los músculos - Esta teoría menciona que durante la práctica del ejercicio el músculo se calienta y en algunas zonas se producen "microlesiones". Posee cierta similitud con la teoría de las microrroturas musculares y la comunidad científica está pendiente de más investigaciones al respecto.
* Acumulación del ácido láctico - esta teoría, ya en desuso, acaba mencionando que el ácido láctico resultante de la actividad metabólica en las células musculares acaba "cristalizando" (de ahí viene su nombre) siendo esta la causa final del dolor muscular debido a la supuesta presencia de estos cristales intersticiales en el músculo.[7]
Existen otras teorías que aportan explicaciones a algunos efectos de la mialgia, quedando sin explicar otros.
Microrrotura de fibras musculares
La teoría de la microrrotura es clásica ya que en el año 1902 se formuló por primera vez,[8] en ella se menciona que la mialgia aparece tras la práctica deportiva se explica mediante alguna literatura científica como una rotura de fibras musculares en su mínima expresión, técnicamente es la rotura de los sarcómeros musculares.[9] Lo que acaba produciendo un efecto de inflamación ligero del músculo afectado.[10] Este dolor se debe a que la fibra muscular es débil y no es capaz de sostener el nivel de ejercicio, probablemente porque se está desentrenado y la fibra no es capaz de aguantarlo. Los patrones de rotura dentro del músculo son completamente aleatorios.[11] Existe alguna evidencia científica que menciona una mayor cantidad de microroturas en los músculos de contracción rápida.[12] [11] Esta teoría parece ser la más aceptada por la comunidad científica y se han realizado numerosos estudios en deportistas.[13]
Las zonas más afectadas por este dolor son las uniones musculares y los tendones cerca de las articulaciones, esto se debe a que la zona musculotendinosa es donde existen más fibras musculares débiles y más tensión. Existe un segundo supuesto: los receptores del dolor (nociceptores) se encuentran en mayor cantidad en estas regiones.[13] El dolor muscular suele tener un periodo que oscila entre los 5 y 7 días con un pico de dolor que se muestra a los 1-3 días tras el ejercicio. Por ejemplo, el dolor y la relajación de los músculos no contribuye a la pérdida de fuerza que aparece en los días de recuperación, no existen evidencias de una inhibición neuronal sobre los músculos[14] y una desactivación en las unidades motoras[15] El dolor y la debilidad muscular se deben prinicipalmente a los procesos inflamatorios más que al daño micromuscular producido.[16] Las investigaciones realizadas se han fundamentado en el desbalance sobre la homeostasis del calcio en los tejidos musculares debido a la microroturas musculares.[17]
Aumento de la temperatura
Durante un ejercicio intenso las células musculares pueden alcanzar temperaturas entre los 38º y los 48º, lo que supone una muerte celular o necrosis. Este proceso genera una desorganización estructural en los músculos que acaba generando un dolor generalizado en ciertos músculos.[18] Esta teoría se ha convertido en una derivación de la de microrotura de las fibras musculares, ya que puede considerarse como una causa más de la microrotura.
Acumulación de ácido láctico
La teoría fue establecida por primera vez por Assmussen en el año 1956[7] y desde entonces la teoría ha ido siendo cada vez más abandonada por la comunidad científica. En condiciones de anoxia (falta de oxígeno) como la que ocurre en las células musculares durante un ejercicio intenso el metabolismo cambia y las células fermentan los nutrientes para conseguir energía. La fermentación produce mucha menos energía que el metabolismo normal, que degrada la glucosa a dos ácidos pirúvicos y este se degrada completamente por otras rutas metabólicas. Sin embargo, en la fermentación el ácido pirúvico se transforma en ácido láctico que cristaliza en el músculo. El dolor producido, por tanto, sería el resultado de la acidez incrementada captada por los nervios y por las microrroturas del músculo debido a los cristales.[19]
Según mencionan algunos autores, esta teoría tiene pocos fundamentos, la observación muscular mediante biopsias musculares no ha podido mostrar la aparición de tales cristales. Tras formarse los cristales de ácido láctico muchos se degradan y una pequeña parte se recombina con otras sustancias para proporcionar moléculas energéticas (glucosa). Otra evidencia que niega tal cristalización es que el ácido láctico llega a cristalizar a temperaturas inferiores a -5ºC, cosa que hace que esta teoría pase a ser una "leyenda urbana" establecida por la transmisión de deportista a deportista sin llegar a un fundamento científico claro.
Espasmo muscular
Introducida en el año 1961 por Dvries,[20] esta teoría propone que el dolor sea resultado de pequeñas descargas eléctricas debido a la fatiga del músculo. Durante un periodo de actividad intensa las contracciones musculares reducen el flujo sanguíneo provocando daños a las células (isquemia) lo que produce un estímulo en las terminaciones nerviosas que vuelven a contraer la fibra muscular, con lo que se repite el ciclo. El aumento de la actividad eléctrica produce, además de la excitación de los nervios una gran fatiga muscular por la falta de flujo sanguíneo. La teoría ha sido criticada por algunos estudiosos de la fisiología y hoy en día se pone en duda.[21]
Tratamiento de la mialgia diferida
Se han investigado numerosos tratamientos contra la mialgia diferida tanto en situaciones previas como posteriores al ejercicio. Estas intervenciones se pueden clasificar en tres amplias categorías:[22]
* Farmacológicas que emplean tratamientos de productos no-esteroides y anti-inflamatorios (denominados en inglés: nonsteroidal anti-inflammatory drugs - NSAIDs). Estos métodos se centran básicamente en aliviar el dolor causado por las agujetas. No obstante los resultados acerca de sus beneficios son muy confusos, ya que existe abundante literatura que demuestra tanto sus efectos beneficiosos como los neutros.[16] Algunos medicamentos han sido ligeramente beneficiosos, como el ibuprofeno[23] [24] o el naproxeno.[25] Sin embargo hay estudios que mencionan el efecto nulo de la aspirina (a pesar de la creencia popular).[26]
* Terapéuticos que emplean modalidades físicas: diversas modalidades de masaje, ejercicios físicos específicos,[27] crioterapia,[28] ultrasonidos e incluso estimulación eléctrica.[29] Respecto a algunas terapias como la oxigenación hiperbárica (HBO, una terapia consistente en la inhalación de Oxígeno (O2) a altas dosis) se está produciendo un debate científico en la actualidad.[30]
* Dietéticas que emplean suplementos nutricionales tales como las isoflavonas (como pueden ser las isoflavonas de soja) y algunos aceites procedentes de pescados que se han mostrado eficaces en el tratamiento.[31] Se necesita todavía un "corpus" de investigación en esta área.
Prevención
No existe un método claro para prevenir y tratar las agujetas a pesar de las numerosas investigaciones.[16] Sin embargo se ha demostrado que los estiramientos musculares previos a la realización del ejercio así como posteriores disminuyen la intensidad del dolor. También tiene efectos positivos sacudirse los músculos durante la realización del ejercicio físico (favorece la circulación sanguínea) y tomarse una ducha caliente al concluirlo.[32] [33] Es conveniente un calentamiento previo así como el aumento progresivo del nivel de entrenamiento, empezando por ejercicios suaves hasta llegar a los más intensos,[34] de este modo las fibras musculares se preparan para una situación de esfuerzo.
Algunos suplementos dietéticos que parecen tener algún efecto en la mialgia diferida son la árnica, de origen homeopático;[35] la ubiquinona (coenzima-Q); y la L-carnitina, en ciertos trabajos científicos sobre corredores de maratón.[36]
Postratamiento
Se ha realizado una exhaustiva investigación acerca de como tratar las agujetas una vez se producen. Uno de los métodos más empleados en la medicina deportiva es el masaje muscular.[37] [38] El uso de antioxidantes (vitamina C y E) no ha dado resultados positivos para eliminar sus efectos.[39]
Una idea muy extendida y popular es que el consumo de agua con bicarbonato sódico o azúcar puede utilizarse para combatir las agujetas. Este remedio casero es el resultado de la aceptación masiva de la teoría referente al ácido láctico. Puesto que esta teoría está prácticamente descartada, este método probablemente no evita ni cura las agujetas ni sus síntomas, pero puede provocar basicidad y problemas gástricos. Por lo tanto no debe seguirse un tratamiento de este tipo. No obstante, podemos encontrar un pequeño alivio en la aplicación de frío. En caso de dolor muy intenso se puede tomar ibuprofeno, que aúna propiedades analgésicas y anti-inflamatorias.
Referencias
1. ↑ a b c "Acute inflammation: the underlying mechanism in delayed onset muscle soreness?", S. Lucille; Medicine & Science in Sports & Exercise. 23(5):542-551, May 1991
2. ↑ "Exercise-induced muscle damage and potential mechanisms for the repeated bout effect", MCHUGH, M.P., D.A.J. CONNOLLY, R.G. ESTON, AND G.W. GLEIM. Sports Med. 27:158–170. 1999.
3. ↑ "Abraham, WM: "Factors in delayed muscle soreness". Med Sci Sports Exerc 9:11
4. ↑ "Delayed Onset Muscle Soreness: Treatment Strategies and Performance Factors", Cheung, Karoline; Sports Medicine. 33(2):145-164, 2003
5. ↑ "Delayed-onset muscle soreness does not reflect the magnitude of eccentric exercise-induced muscle damage"; Kazunori Nosaka; Scandinavian Journal of Medicine & Science in Sports, Volume 12 Issue 6 Page 337-346, December 2002
6. ↑ "Morphologic and Mechanical Basis of Delayed-Onset Muscle Soreness", Richard L. Lieber, PhD and Jan Fridén, MD, PhD ; J Am Acad Orthop Surg, Vol 10, No 1, January/February 2002, 67-73.
7. ↑ a b "Observations on experimental muscle soreness". Asmussen E:, Acta Rheum Scand 1956; 2:109-116
8. ↑ "Ergographic studies in muscular soreness". Hough, T. (1902). American Journal of Physiology, 2, 76-92.
9. ↑ "Materials fatigue initiates eccentric contractioninduced injury in rat soleus muscle", WARREN, G.L., D.A. HAYES, D.A. LOWE, B.M. PRIOR, AND R.B. ARMSTRONG. J. Physiol. 464:477–489. 1993.
10. ↑ "Haematological and acute-phase responses associated with delayed-onset muscle soreness in humans"; GLEESON, M., J. ALMEY, S. BROOKS, R. CAVE, A. LEWIS, AND H. GRIFFITHS. Eur. J. Appl. Physiol. 71:137–142. 1995.
11. ↑ a b "Muscle damage induced by eccentric contractions of 25% strain", Lieber, R.L., And J. Fride´N, J. Appl. Physiol. 70:2498–2507. 1991
12. ↑ "Changes in human skeletal muscle induced by longterm eccentric exercise", Fridén, J. . Cell Tissue Res. 236:365–372. 1984.
13. ↑ a b "Exercise-induced muscle damage and potential mechanisms for the repeated bout effect", Mchugh, M.P., D.A.J. Connolly, R.G. Eston, And G.W. Gleim. Sports Med. 27:158–170. 1999.
14. ↑ . "Electromyographic analysis of exercise resulting in symptoms of muscle damage". Mchugh, M.P., D.A.J. Connolly, R.G. Eston, And G.W. Gleim, J. Sports Sci. 8:163–172. 2000.
15. ↑ . "Effect of ketoprofen on muscle function and EMG after eccentric exercise". Sayers, S.P., C.A. Knight, P.M. Clarkson, E.H. Van Wegen, And G. Kamen. Med. Sci. Sports Exerc., 33:702–710. 2001.
16. ↑ a b c "Treatment and Prevention of Delayed Onset Muscle Soreness", DECLAN A.J.; Journal of Strength and Conditioning Research, 2003, 17(1), 197–208
17. ↑ "Hydrogen peroxide disrupts calcium release from the sarcoplasmic reticulum of rat skeletal muscle fibers". Brotto, M., And T.M. Nosek, J. Appl. Physiol. 81:731–737. 1996.
18. ↑ "Response of the body to injury: Inflammation and repair. In: Pathophysiology: Clinical Concepts of Disease Processes". ABRAMS, G.D. S.A. Price and L.M. Wilson, eds. St. Louis, MO: Mosby, 1997. pp. 38–58.
19. ↑ "Traumatología y Medicina Deportiva: Bases de la Medicina del Deporte", Rafael Ballesteros Massó, Publicado en 2002, Thomson Learning Ibero
20. ↑ "Prevention of muscular stress after exercise". DeVries, H.A. Research Quarterly, 32, 177. (1961).
21. ↑ "Factors in delayed onset muscular soreness of man", Bobbert, M.F., Hollander A.P. & Huijing P.A. (1986). Medicine and Science in Sports and Exercise, 18(1), 75-81.
22. ↑ "Various Treatment Techniques on Signs and Symptoms of Delayed Onset Muscle Soreness", Gulick DT, Kimura IF, Sitler M, Paolone A, Kelly JD.; J Athl Train. 1996 Apr;31(2):145-152
23. ↑ "Effects of ibuprofen on exercise-induced muscle soreness and indices of muscle damage", Donnelly, A.E., R.J. Maughan, And P.H. Whiting. . Br. J. Sports Med. 24:191–195. 1990.
24. ↑ "Effect of ibuprofen use on muscle soreness, damage, and performance: A preliminary study", Hasson, S.M., J.C. Daniels, J.G. Divine, B.R. Niebuhr, S. Richmond, P.G. Stein, And J.H. Williams. . Med. Sci. Sports Exerc. 25:9–17. 1993.
25. ↑ "Efficacy of naproxen sodium for exercise-induced dysfunction muscle injury and soreness"; Dudley, G.A., J. Czerkawski, A.Meinrod, G.Gillis, A. Baldwin, And M. Scarpone. . Clin. J. Sport Med. 7:3–10. 1997.
26. ↑ "Effects of aspirin on delayed muscle soreness", Francis, K.T., And T. Hoobler. J. Sports Med. 27:333–337. 1987.
27. ↑ "Intermittent pneumatic compression effect on eccentric exercise-induced swelling, stiffness and strength loss", Chleboun, G.S., J.N. Howell, H.L. Baker, T.N. Ballard, J.L. Graham, H.L. Hallman, L.E. Perkins, J.H. Schauss, And R.R. Conaster. . Arch. Phys. Med. Rehabil. 76:744–749. 1995.
28. ↑ "Effects of cold water immersion on the symptoms of exercise-induced muscle damage", Eston, R., And D. Peters. J. Sports Sci. 17:231–238. 1999.
29. ↑ "Electroestimulación: Entrenamiento y periodización", Manuel Pombo Fernández, Publicado en 2004; ed. Paidotribo; ISBN 84-8019-776-5
30. ↑ "Hyperbaric oxygen therapy does not affect recovery from delayed onset muscle soreness". Mekjavic, I.B., J.A. Extner, P.A. Tesch, And O. Eiken. Med. Sci. Sports Exerc. 3:558–563. 2000.
31. ↑ "The effects of fish oil and isoflavones on delayed onset muscle soreness", Jon Lenn; Medicine & Science in Sports & Exercise. 34(10):1605-1613, October 2002.
32. ↑ "La guía completa de los estiramientos", Christopher M. Norris; Publicado en 2001, Ed.
33. ↑ "The effects of static stretching and warm-up on prevention of delayed-onset muscle soreness.", High DM, Howley ET, Franks BD; Res Q Exerc Sport. 1989 Dec;60(4):357-61.
34. ↑ "Science of Flexibility", Michael J. Alter; 2004, Ed. Human Kinetics
35. ↑ "Homoeopathic Arnica and Rhus toxicodendron for delayed onset muscle soreness A pilot for a randomized, double-blind, placebo-controlled trial"; N. Jawara, British Homoeopathic journal; Volume 86, Issue 1, January 1997, Pages 10-15
36. ↑ TVEITEN, D., S. BRUSET, C.F. BORCHGREVINK, AND J. NORSETH. "Effect of Arnica D 30 during hard physical exertion: A doubleblind randomized trial during the 1995 Oslo Marathon. Complement. Ther. Med. 6:71–74. 1998.correr a sprint durante 20 sg
37. ↑ "Does post-exercise massage treatment reduce delayed onset muscle soreness? A systematic review". E Ernst; British Journal of Sports Medicine, Vol 32, Issue 3 212-214; 1998
38. ↑ "The effects of massage on delayed onset muscle soreness", J E Hilbert, G A Sforzo, T Swensen; J Sports Med 2003;37:72-75
39. ↑ "An effect of ascorbic acid on delayed-onset muscle soreness Pain", Kaminski, M & Boal, R. (1992); 50(3), 327-321.
Intoxicado con Monoxido de Carbono en HBOT
Fear this silent killer
Man in 40s recovering after exposure to deadly carbon monoxide
By ALYSSA NOEL, SUN MEDIA
*A man in his 40s is recovering from a serious bout of carbon monoxide poisoning after trying to warm an attached garage with a camping stove yesterday, a fire spokesman says.
Three others, including two children and a man in his 20s, were also taken to the Misericordia hospital from a home near 151 Avenue and 115 Street.
The man was initially listed in critical condition, but has stabilized after treatment in a hyperbaric chamber, a hospital spokesman said.
Every winter, senior respiratory therapist Grant Paulhus sees a handful of patients suffering from poisoning.
"We have to remind the public that carbon monoxide is dangerous and can kill you.
"You have to take appropriate precautions if you're using heating devices in your home or garage," Paulhus said.
The chambers, the only publicly funded machines of their kind in the province, work by exposing patients to 100% oxygen that's pressurized, which causes oxygen to move into their plasma quickly, removing the carbon monoxide from red blood cells.
The recent poisonings are a reminder for Edmontonians about the dangers of the so-called silent killer, said Jim Czelenski, a public education officer with fire services.
Carbon monoxide is odourless, tasteless and colourless.
Its symptoms - including headaches, dizziness, fatigue and nausea - resemble those of the flu.
And that's what sufferers often dismiss it as such.
Eventually, they pass out and, if no one notices, it could be fatal, he said.
Besides appliances like the camping stove in yesterday's incident, furnaces and cars are two other culprits.
"The two biggest messages are get your appliances checked regularly by a professional and obviously don't be running your vehicle in the garage, especially with the door closed," Czelenski said.
"That's a bad situation."
Although carbon monoxide detectors are mandatory for all buildings with fuel-burning appliances, some people still don't purchase them, Czelenski said.
In 2005, a 53-year-old city woman died after a suspected leaky furnace released gas into her home. She and two others living in the house were discovered unconscious by a friend. In 2006, four people, including two children, were taken to hospital after an allegedly tampered furnace began to leak in an apartment building. Then, last January, eight seniors from an assisted living facility 260 km southeast of Edmonton in Linden were sent to the Misericordia with carbon monoxide poisoning.
lunes, 15 de diciembre de 2008
OXIGENO HIPERBARICO EN HERIDAS DE DIFICIL CICATRIZACION
Small World Wide Wounds Logo
Hyperbaric oxygen therapy for wound healing
Author(s)
James Wright
Staff Physician
Davis Hyperbaric Laboratory
USAFSAM/FEH, Brooks AFB, Texas, USA
Email: James.Wright@brooks.af.mil
Contents
* Introduction
* Effects of hypoxia
* Oxygen under pressure
* The HBO2 paradox
* Oxygen and infection
* HB02 and infection
* Side effects of HBO2
* Conclusion
* References
Published: May 2001
Last updated: May 2001
Revision: 1.0
Keywords: hyperbaric oxygen; wound healing; oxygen effects; infection.
Key Points
1.
Oxygen used under pressure or hyperbaric oxygen (HBO2) can assist wound healing.
2.
HBO2 is considered unnecessary in simple, well-perfused wounds, but can be used successfully in hypoxic or ischaemic wounds such as diabetic wounds, venous stasis ulcers, failing grafts and flaps, necrotising soft tissue infections and refractory osteomyelitis.
3.
In wound healing, hypoxia is an insufficient supply of oxygen which prevents normal healing processes. HBO2 provides the oxygen needed to stimulate and support wound healing.
4.
HBO2 is able to combat clinical infection such as gas gangrene by acting directly on anaerobic bacteria, enhancing leukocyte and macrophage activity and potentiating the effects of antibiotics.
5.
HBO2 is a relatively safe non-invasive therapy. Side effects include middle ear and pulmonary barotraumas and myopia. Contraindications include poor cardiac output and severe obstructive pulmonary disease.
Abstract
Oxygen is one of the most versatile and powerful agents available to the modern medical practitioner. The therapeutic use of oxygen under pressure is known as hyperbaric oxygen therapy (HBO2) and has been used to assist wound healing for almost 40 years. HBO2 has several specific biological actions which can enhance wound healing processes. Hyper-oxygenation of tissue, vasoconstriction, down regulation of inflammatory cytokines, up-regulation of growth factors, antibacterial effects, potentiation of antibiotics, and leukocyte effects of HBO2 are discussed in relation to wound healing problems. This article looks at how a greater understanding of the biological and physiological effects of using oxygen under pressure can benefit patients with problem wounds.
Introduction
HBO2 was first used to recompress divers by Behnke in the 1930s [1], and was developed to complement the effects of radiation in cancer treatment by Churchill-Davidson in the 1950s [2]. Within a few years HBO2 was being used to support patients undergoing cardiac surgery [3], and to treat clostridial gas gangrene [4] and carbon monoxide poisoning [5]. HBO2 was first used to assist wound healing when it was noted in 1965 that burns of the victims of a coal mine explosion, treated with HBO2 for their CO poisoning, healed faster [6]. In spite of this long history of therapeutic use, the mechanisms of action of HBO2 are still being discovered. As we learn more about how oxygen interacts with living organisms, new treatments and parameters of use are suggested. Today, the medical use of oxygen under pressure, or hyperbaric oxygen, is an evolving specialty.
Effects of hypoxia
Hypoxia can be defined as an insufficient supply of oxygen to support biological processes. It is possible to have hypoxia in one area of a wound and not in an adjacent area. Similarly hypoxia can be time-dependent with sufficient oxygen to support basal tissue maintenance at one time, but not enough to allow for growth or healing at another. Thus it is difficult to place an absolute number for PO2, which can be used to define hypoxia in all situations. Hypoxia in anaesthesia is defined as an oxygen saturation less than 90% or a PaO2 of < 60 mmHg [7]. This is clearly a higher level than the tissue oxygen pressure of 40 mmHg needed to reliably heal a leg wound [8][9]. In wound healing, hypoxia can be defined as an insufficient supply of oxygen to allow the healing process to proceed at a normal rate.
Not all effects of hypoxia are bad. In fact all wounds initially have areas of hypoxic tissue. Local hypoxia in the micro-environment of the wound causes several wound healing processes to occur such as leukocyte adherence, neovascularisation, collagen formation and bone formation. When hypoxia is severe, prolonged or widespread deleterious tissue effects can occur.
Ischaemia-reperfusion injury: When hypoxia extends beyond the local wound environment the effects of ischaemia-reperfusion injury can be seen. Reactive oxygen species are produced, including oxygen free radicals. Initially, these usually cause vasoconstriction followed by vasodilation, although the effects are dependent on vascular epithelial receptors in the tissue involved. Endothelial cell damage and release of prostaglandins, inflammatory cytokines (TNF-alpha and IL-6) and nitric oxide (NO) from the vascular endothelium occurs. Subsequent membrane peroxidation further increases the cellular damage.
As capillaries become leaky and interstitial oedema accumulates, circulation is further compromised with compounded injury. The surgical or medical re-establishment of interrupted circulation sends blood to the ischaemic area, providing new oxygen substrate for the formation of more free radicals, with the result that the injury temporarily worsens. In massive injury the release of inflammatory cytokines (and possibly free radicals) escapes the normal regulatory mechanisms and can lead to multiple organ failure. Hence a long and catastrophic chain of events can be initiated by oxygen deprivation.
Oxygen under pressure
HBO2 can provide pharmacological doses of oxygen to healing tissue. A typical wound care treatment dive consists of providing 90 minutes of 100% oxygen at 45 feet of sea water (fsw) - 13.7 m of sea water (msw) or 1.38 Bar. This is the equivalent of 2.36 (ATA) atmospheres of 100% oxygen. In recompression therapy for diving-related injuries a patient might be exposed to a minimum of four hours oxygen at depths varying from 60 fsw (18.3 meters, 2.8 atmospheres, 284 kilopascals) to the surface.
Hyperbaric chambers are either multiplace or monoplace. A multiplace chamber is able to treat several patients at one time with a medical attendant in the chamber Figure 1. The patients breathe oxygen through a mask or hood Figure 2. In a monoplace chamber one patient is treated in a small hyperbaric chamber filled with 100% oxygen Figure 3.
image
Figure 1 - Multiplace hyperbaric chamber at Davis Hyperbaric Laboratory, Brooks AFB, TX
image
Figure 2 - Patient breathing oxygen in multiplace chamber through a hood
image
Figure 3 - Sechrist Monoplace Chamber
In a typical wound care treatment dive hyperbaric oxygen is capable of providing tissue oxygen levels of greater than 11 times normal, or up to 620 mmHg. Most chronic wounds are hypoxic and HBO2 provides the oxygen needed to stimulate and support wound healing. Some examples of typical levels of oxygenation provided in a hyperbaric oxygen treatment are illustrated in Table 1
Table 1: Tissue PO2 values (tcpO2 = transcutaneous oxygen pressure). Adapted from Sheffield PJ. Measuring tissue oxygen tension: a review. Undersea Hyperb Ned 1998; 25: 179-88. PO2 values
ATAs 1.0 Air 1.0 O2 2.4 O2
air 159 760 1824
alveolar 104 673 1737
arterial 100 660 1700
venous 36 60 1650
muscle 29 59 250
subcutaneous 40 200-300 250-500
chronic wound 15 200-400 660
chest tcp02 67 450 1312
foot tcp02 63 280 919
When used in wound healing HBO2 provides a short pulse of oxygen - 90 minutes in a 24-hour day. Although, such a short time provision of elevated oxygen could not significantly effect wound healing, HBO2 acts in numerous ways that affect the wound after the treatment has stopped. There are eight principal methods in which HBO2 is capable of affecting tissue:
1. Pressure effects of oxygen
2. Vasoconstrictive effects of oxygen
3. 100% oxygen concentration effects on the diffusion gradient
4. Hyperoxygenation of ischaemic tissue
5. Down regulation of inflammatory cytokines
6. Up-regulation of growth factors
7. Leukocyte effects
8. Antibacterial effects.
Pressure effects of oxygen: The effect of elevating the ambient partial pressure of the inspired gas, usually to 2.38 ATAs, is unimportant in wound healing, but quite significant when dealing with the gas bubble diseases, decompression sickness and air gas embolism. At elevated pressures the harmful effects of gas bubbles in the tissue are minimised. Our research and that of others on wounds exposed to elevated pressures has demonstrated no evidence of an isolated pressure effect [10].
Vasoconstrictive effects of oxygen: The vasoconstrictive effects of HBO2 can be used to good effect to treat patients. HBO2 causes a significant reduction of oedema, which has been shown to be beneficial in reperfusion injury, crush injury, compartment syndrome, burns, wound healing, and failing flaps [11][12][13][14].
Oxygen diffusion effects: The diffusion of nitrogen out of the tissues in decompression sickness is facilitated by the use of 100% oxygen. In wound healing the beneficial effects of oxygen are primarily related to the concentration of oxygen molecules in the tissue, rather than by diffusion kinetics. However, the rate of oxygen entry into the wound environment is affected by the rate of diffusion from the capillaries. Oedema adversely affects the achievement of high oxygen concentrations in the wound and increases the intercapillary diffusion distance. Even a small increase in tissue oedema can dramatically slow the rate of entry of oxygen into the tissues and can cause tissue hypoxia.
Hyperoxygenation of tissue: The oxygenation of hypoxic tissue is one of the key mechanisms by which HBO2 accelerates wound healing. Numerous studies have shown a dose response curve for the provision of oxygen in the wound healing environment [10][14][15][16][17][18][19]. However, oxygen is a powerful drug and just like other drugs, it is possible to give too little or too much. Chronic wounds are frequently hypoxic and the provision of HBO2 corrects the hypoxia, albeit temporarily. It then allows for acceleration of the wound healing process through processes which continue long after the HBO2 session has ended and tissue oxygen levels have returned to pre-treatment values. Over time the oxygenation of the chronic wound improves with HBO2 therapy. Marx and Johnson demonstrated that for irradiated wounds, HBO2 induces neovascularisation, which becomes significant after about 14 treatments and continues for years after the HBO2 therapy has ceased [20] Figure 4. A typical chronic wound will usually require 20 to 30 HBO2 treatments. This probably represents the amount of neovascularisation needed to sustain wound healing.
image
Figure 4 - Increase in wound vascularisation with HBO2 treatment. tcpO2 = transcutaneous oxygen pressure; LSICS = left second intercostal space
Cytokine down regulation and growth factor up-regulation: HBO2 is capable of favourably influencing a number of cytokines and growth factors important to wound healing. When administered after wounding, HBO2 up-regulates collagen synthesis through pro-al(I) mRNA expression [21]. In rabbit ear wounds HBO2 has been shown to up-regulate mRNA for the platelet-derived growth factor (PDGF)-beta receptor [22]. In ischaemic flaps HBO2 up-regulates fibroblast growth factor (FGF) causing an increased effect over that seen with FGF alone [23]. In situations where FGF is ineffective, HBO2 can render it highly effective [24], although the effect is different from up-regulation. In patients with Crohn's disease interleukin-1 (IL-1), IL-6, and tumour necrosis factor (TNF)-alpha levels are diminished during HBO2 treatment [25]. TNF levels in normal rats become elevated after a single exposure to HBO2 [26]. For different physiological conditions HBO2 may cause up- or down regulation of cytokines. Vascular endothelial growth factor (VEGF) is up-regulated by hypoxia, yet the hyperoxia of HBO2 also up-regulates this factor [27]. The effects of transforming growth factor (TGF)-beta1 and platelet-derived growth factor (PDGF)-beta are synergistically enhanced by HBO2 [28].
The HBO2 paradox
Some biological processes and growth factors are stimulated or up-regulated by hypoxia and by HBO2. To date we have identified angiogenesis, collagen synthesis, osteoclastic activity, and release of VEGF. Other possible candidates are TNF-alpha and erythropoietin (EPO). However, it is unclear how oxygen is able to stimulate biological processes in both hypoxic and hyperoxic concentrations. I have called this paradoxical relation between oxygen and wound healing the 'Oxygen Paradox'.
One known mechanism is that by which fibroblasts are stimulated to make collagen through peroxides. These occur in the hypoxic wound and during HBO2 treatment [29]. Peroxides generated by HBO2 mimic one of the stimuli also found in hypoxia. Another mechanism is the stimulation of cytokines by hypoxia and further up-regulation of these cytokines by hyperoxia, which occurs during HBO2 treatment. This is the case for some interleukines and for TNF. There is some confusion on the exact timing of the release of growth factors and cytokines; in one study VEGF, TNF-alpha, and TGF-beta occurred in hypoxic wounds after they had been released in normoxia. VEGF, TGF-beta, and PDGF-beta have biphasic release patterns; their release is stimulated by hypoxia and hyperoxia, but is lowest during normoxia [29][30]. Furthermore, the activity of released VEGF is further enhanced during hyperoxia, especially in the presence of lactate [30].
It is clear that biologically active chemicals such as cytokines and growth factors have a complex array of stimuli to up and down regulate activity. Oxygen, cytokines and biologically active chemicals and metals appear to have key roles in wound healing processes. As we learn more about the role of oxygen, it appears to be much more detailed than in a simple mass-action equation.
Oxygen and infection
Oxygen is key to the phagocytosis and killing of bacteria by neutrophils or polymorphonuclear cells (PMNs). This process involves the production of oxygen radicals and superoxides and is directly influenced by the oxygen concentration in the tissue. As the oxygen tension falls below 30 mmHg the efficiency of bacteriocidal action of PMNs begins to drop off dramatically [31][32]. This was demonstrated by Knighton et al in 1984 where the phagocytic activity of neutrophils in ingesting Staph. aureus was compared to oxygen tension [33]. The activity level of phagocytosis is shown in Figure 5.
image
Figure 5 - Relationship of leukocyte killing of Staph. aureus and oxygen tension
PMN-mediated killing of several aerobic bacteria - Proteus vulgaris, Salmonella typhimurium, Klebsiella pneumoniae, Serratia marcescens, Pseudomonas aeruginosa and Staphylococcus species - is diminished in hypoxia [34]. Increasing the concentration of oxygen over ambient levels has been shown to reduce infection [35]. When supplemental oxygen was administered during a surgical operation and for two hours postoperatively, infection rates dropped by as much as 54% [36]. Thus, increasing tissue concentrations of oxygen has a beneficial effect on the ability of PMNs to combat bacteria and prevent infection.
HB02 and infection
HBO2 has six actions which have been used to combat clinical infection:
1. Tissue rendered hypoxic by infection is supported
2. Neutrophils are activated and rendered more efficient
3. Macrophage activity is enhanced
4. Bacterial growth is inhibited
5. Release of certain bacterial endotoxins is inhibited
6. The effect of antibiotics is potentiated.
Support of infected hypoxic tissue: Soft tissue and bone infections are frequently accompanied by localised areas of tissue hypoxia caused by the inflammatory processes accompanying infection and by subsequent vascular thrombosis [37]. As the infected tissue becomes infiltrated with inflammatory cells (PMNs and platelets) the PO2 falls [38]. In clostridial gas gangrene the production of phospholipase C has been associated with platelet and neutrophil aggregation and vascular thrombosis with subsequent hypoxia [37]. Administration of HBO2 can cause the PO2 to increase five-fold in infected tissue [39].
Neutrophil activation: As tissue PO2 rises, leukocyte killing of bacteria becomes much more efficient. Below a PO2 of 30 mmHg PMN killing is markedly reduced [40]. Because areas of hypoxia accompany serious tissue infections, HBO2 is an effective means of raising tissue PO2 to levels at which PMNs can function effectively. By raising tissue PO2 to levels higher than that achieved by breathing oxygen at ambient pressure, bacterial killing by PMNs is further enhanced [41]. Thus, by increasing tissue oxygen tension, a better than 'normal' antibacterial effect can be achieved. Hunt and colleagues have demonstrated that the clearance of bacteria from hypoxic tissue is enhanced by hyperoxic breathing mixtures [42][43]Figure 6.
image
Figure 6 - Wound bacterial growth and oxygen tension
Enhancement of macrophage activity: Macrophages, like PMNs, are affected by tissue oxygen tension. They perform a key role in combating infection by scavenging bacteria and foreign material. Under hypoxic conditions macrophages are unable to scavenge effectively and produce peroxides [44]. Hypoxia also induces macrophages to produce the inflammatory cytokines TNF-alpha, IL-1, IL-8, and intracellular adhesion molecule-1, which can adversely affect the response to infection [45]. While it is not yet known whether HBO2 can enhance macrophage function, it may be needed to bring the PO2 of hypoxic tissue up to normal levels so that macrophages can function normally.
Inhibition of bacterial growth: Anaerobic bacteria are particularly susceptible to increased concentrations of oxygen [46]. The more sensitive the anaerobic organism is to oxygen, the lower the level of superoxide dismutase, an enzyme that allows cells to defend themselves against oxygen free radicals [47]. With HBO2 large amounts of oxygen free radicals can be generated, making anaerobic bacteria particularly susceptible to oxidative killing. HBO2 treatment of anaerobic infections caused by Clostridial perfringens has increased patient survival, reduced the need for additional surgery, shortened hospital stay and improved outcome [4]. When used appropriately in Fournier's gangrene, a rapidly progressing necrotising infection of the perineum, HBO2 has reduced morbidity, extension of necrosis, and systemic toxicity [48].
Inhibition of endotoxin release: In C. perfringens infections the major source of tissue injury and death is caused by the alpha toxin. Secretion of this toxin is suppressed by HBO2 [49][50]. In rats exposed to E. coli peritonitis, HBO2 administration increased survival from 0% to 92% [51]. One of the mechanisms by which HBO2 appears to have worked is by antagonising some of the harmful effects of bacterial endotoxin release. However, to be optimally effective, HBO2 must be given early in the course of infection and combined with appropriate surgical debridement and antibiotics [52].
Potentiation of antibiotics: Both Knighton et al [35] and Hunt et al [53] have demonstrated that oxygen adds to the effectiveness of antibiotics; the greater the concentration of oxygen, the more pronounced the effect Figure 7. This has been demonstrated in experimental Staph. aureus osteomyelitis treated with cefazolin [54]. In Pseudomonas aeruginosa infections HBO2 has an additive effect with aminoglycoside antibiotics, reducing morbidity and mortality [55].
image
Figure 7 - Potentiation of antibiotic effects by HBO2
Side effects of HBO2
While HBO2 has an admirable safety record, those recommending HBO2 in wound care should be aware of potential side effects and complications.
Ear and sinus barotrauma: Middle ear barotrauma is the most common side effect of HBO2. Published reports indicate an incidence of 2-17%, and our experience with an elderly wound care population is consistent with this [56][57]. Fortunately most cases of barotrauma are minor and can be prevented by extra time spent in teaching the Valsalva manoeuver used on descent, slowing the descent rate, and trying other manoeuvers on descent such as drinking water with the nostrils occluded and head tilt during Valsalva. Those patients who cannot clear the middle ear during pressurisation will need to discontinue treatment and have pressure equalisation (PE) tubes inserted.
The paranasal sinuses are also a possible site of barotrauma on descent. Because of this, patients with a cold, upper respiratory tract infection, or allergic rhinitis are not suitable candidates for HBO2. If a patient experiences sinus barotrauma during descent, the treatment dive is suspended and attention given to clearing the sinus. Oxymetazoline hydrochloride 0.05% (Afrin) nasal spray may be of help.
Myopia: Some patients receiving HBO2 will develop reversible myopia. The action of HBO2 on the ocular lens is as yet undefined, but may be due to oxidative change of the lens proteins [58][59][60]. After cessation of therapy, the refraction usually returns to the pretreatment state within a few weeks [61]. The amount of change in the lens is related to the dose and frequency of HBO2 sessions [58]. Patients with wound problems are usually given 20 to 50 HBO2 treatments, with most patients receiving 30 treatments or less. For most of our patients experiencing myopia it has been a temporary problem.
Aggravation of congestive heart failure: HBO2 causes increased peripheral vascular resistance from its vasoconstrictive effects. A decrease in heart rate, cardiac output, and cardiac load has been described in healthy dogs [62]. Blood flow to the left ventricle has been noted to decrease during HBO2 [63]. We have had patients with severe congestive heart failure suffer a precipitous decline in cardiac function after receiving HBO2. Because of this we generally do not accept patients with a cardiac ejection fraction of less than 35% for HBO2.
Oxygen seizures: Oxygen is capable of causing grand mal seizures if breathed under pressure for a long enough period of time. Some individuals are more sensitive to oxygen than others and the exact dose of oxygen needed to provoke a seizure is quite variable. The mechanism is unclear but may be due to increased delivery of oxygen free radicals to the brain [64]. Ionic calcium has also been implicated [65]. In our wound treatment dives, 2.4 ATA of oxygen is given for 90 minutes, broken up into three 30-minute periods with 10 minute air breaks between the oxygen periods. Using this procedure, the incidence of oxygen induced seizure is quite rare, 1:10,000 dives [66].
Pulmonary barotrauma: Pulmonary barotrauma is a potentially serious complication of HBO2. The injury is related to pressure changes and occurs only on ascent. For the lungs to be injured there must be an obstruction such as a closed glottis or bronchial obstruction after reaching depth. During ascent the trapped air will expand, injuring the lung. An ascent of 3.5 feet (1.07 meters) would cause a trapped air bubble to exert 80 mmHg (10.7 kilopascals) pressure, enough to rupture alveoli.
An untreated pneumothorax is an absolute contradiction to HBO2 therapy and patients with a pneumothorax must have a chest tube inserted prior to the treatment dive. If a pneumothorax occurs during the treatment, a chest tube must be inserted prior to ascent to prevent a marked deterioration in the condition of the patient.
Patients with severe obstructive pulmonary disease such as untreated asthma or severe chronic obstructive pulmonary disease (COPD), with air trapping or bleb formation, could be at risk of pneumothorax and should be excluded from diving. However, many of our patients have previously been cigarette smokers and have mild COPD, but dive without incident.
Conclusion
Hyperbaric oxygen is a powerful treatment for acute and chronic wounds, acting on injured and healing tissue in a number of ways. Hypoxic tissue, reperfusion injury, compartment syndrome, crush injury, failing flaps, chronic wounds, burns and necrotising infections have all been shown to respond favourably to HBO2. As we learn more about how HBO2 benefits wounds by up-regulating growth factors, down regulating cytokines, reducing oedema, and supporting angiogenesis and new tissue ingrowth, the potential benefits to wound healing become clearer.
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Last Modified: Monday, 21-May-2001 11:56:17 BST
Hyperbaric oxygen therapy for wound healing
Author(s)
James Wright
Staff Physician
Davis Hyperbaric Laboratory
USAFSAM/FEH, Brooks AFB, Texas, USA
Email: James.Wright@brooks.af.mil
Contents
* Introduction
* Effects of hypoxia
* Oxygen under pressure
* The HBO2 paradox
* Oxygen and infection
* HB02 and infection
* Side effects of HBO2
* Conclusion
* References
Published: May 2001
Last updated: May 2001
Revision: 1.0
Keywords: hyperbaric oxygen; wound healing; oxygen effects; infection.
Key Points
1.
Oxygen used under pressure or hyperbaric oxygen (HBO2) can assist wound healing.
2.
HBO2 is considered unnecessary in simple, well-perfused wounds, but can be used successfully in hypoxic or ischaemic wounds such as diabetic wounds, venous stasis ulcers, failing grafts and flaps, necrotising soft tissue infections and refractory osteomyelitis.
3.
In wound healing, hypoxia is an insufficient supply of oxygen which prevents normal healing processes. HBO2 provides the oxygen needed to stimulate and support wound healing.
4.
HBO2 is able to combat clinical infection such as gas gangrene by acting directly on anaerobic bacteria, enhancing leukocyte and macrophage activity and potentiating the effects of antibiotics.
5.
HBO2 is a relatively safe non-invasive therapy. Side effects include middle ear and pulmonary barotraumas and myopia. Contraindications include poor cardiac output and severe obstructive pulmonary disease.
Abstract
Oxygen is one of the most versatile and powerful agents available to the modern medical practitioner. The therapeutic use of oxygen under pressure is known as hyperbaric oxygen therapy (HBO2) and has been used to assist wound healing for almost 40 years. HBO2 has several specific biological actions which can enhance wound healing processes. Hyper-oxygenation of tissue, vasoconstriction, down regulation of inflammatory cytokines, up-regulation of growth factors, antibacterial effects, potentiation of antibiotics, and leukocyte effects of HBO2 are discussed in relation to wound healing problems. This article looks at how a greater understanding of the biological and physiological effects of using oxygen under pressure can benefit patients with problem wounds.
Introduction
HBO2 was first used to recompress divers by Behnke in the 1930s [1], and was developed to complement the effects of radiation in cancer treatment by Churchill-Davidson in the 1950s [2]. Within a few years HBO2 was being used to support patients undergoing cardiac surgery [3], and to treat clostridial gas gangrene [4] and carbon monoxide poisoning [5]. HBO2 was first used to assist wound healing when it was noted in 1965 that burns of the victims of a coal mine explosion, treated with HBO2 for their CO poisoning, healed faster [6]. In spite of this long history of therapeutic use, the mechanisms of action of HBO2 are still being discovered. As we learn more about how oxygen interacts with living organisms, new treatments and parameters of use are suggested. Today, the medical use of oxygen under pressure, or hyperbaric oxygen, is an evolving specialty.
Effects of hypoxia
Hypoxia can be defined as an insufficient supply of oxygen to support biological processes. It is possible to have hypoxia in one area of a wound and not in an adjacent area. Similarly hypoxia can be time-dependent with sufficient oxygen to support basal tissue maintenance at one time, but not enough to allow for growth or healing at another. Thus it is difficult to place an absolute number for PO2, which can be used to define hypoxia in all situations. Hypoxia in anaesthesia is defined as an oxygen saturation less than 90% or a PaO2 of < 60 mmHg [7]. This is clearly a higher level than the tissue oxygen pressure of 40 mmHg needed to reliably heal a leg wound [8][9]. In wound healing, hypoxia can be defined as an insufficient supply of oxygen to allow the healing process to proceed at a normal rate.
Not all effects of hypoxia are bad. In fact all wounds initially have areas of hypoxic tissue. Local hypoxia in the micro-environment of the wound causes several wound healing processes to occur such as leukocyte adherence, neovascularisation, collagen formation and bone formation. When hypoxia is severe, prolonged or widespread deleterious tissue effects can occur.
Ischaemia-reperfusion injury: When hypoxia extends beyond the local wound environment the effects of ischaemia-reperfusion injury can be seen. Reactive oxygen species are produced, including oxygen free radicals. Initially, these usually cause vasoconstriction followed by vasodilation, although the effects are dependent on vascular epithelial receptors in the tissue involved. Endothelial cell damage and release of prostaglandins, inflammatory cytokines (TNF-alpha and IL-6) and nitric oxide (NO) from the vascular endothelium occurs. Subsequent membrane peroxidation further increases the cellular damage.
As capillaries become leaky and interstitial oedema accumulates, circulation is further compromised with compounded injury. The surgical or medical re-establishment of interrupted circulation sends blood to the ischaemic area, providing new oxygen substrate for the formation of more free radicals, with the result that the injury temporarily worsens. In massive injury the release of inflammatory cytokines (and possibly free radicals) escapes the normal regulatory mechanisms and can lead to multiple organ failure. Hence a long and catastrophic chain of events can be initiated by oxygen deprivation.
Oxygen under pressure
HBO2 can provide pharmacological doses of oxygen to healing tissue. A typical wound care treatment dive consists of providing 90 minutes of 100% oxygen at 45 feet of sea water (fsw) - 13.7 m of sea water (msw) or 1.38 Bar. This is the equivalent of 2.36 (ATA) atmospheres of 100% oxygen. In recompression therapy for diving-related injuries a patient might be exposed to a minimum of four hours oxygen at depths varying from 60 fsw (18.3 meters, 2.8 atmospheres, 284 kilopascals) to the surface.
Hyperbaric chambers are either multiplace or monoplace. A multiplace chamber is able to treat several patients at one time with a medical attendant in the chamber Figure 1. The patients breathe oxygen through a mask or hood Figure 2. In a monoplace chamber one patient is treated in a small hyperbaric chamber filled with 100% oxygen Figure 3.
image
Figure 1 - Multiplace hyperbaric chamber at Davis Hyperbaric Laboratory, Brooks AFB, TX
image
Figure 2 - Patient breathing oxygen in multiplace chamber through a hood
image
Figure 3 - Sechrist Monoplace Chamber
In a typical wound care treatment dive hyperbaric oxygen is capable of providing tissue oxygen levels of greater than 11 times normal, or up to 620 mmHg. Most chronic wounds are hypoxic and HBO2 provides the oxygen needed to stimulate and support wound healing. Some examples of typical levels of oxygenation provided in a hyperbaric oxygen treatment are illustrated in Table 1
Table 1: Tissue PO2 values (tcpO2 = transcutaneous oxygen pressure). Adapted from Sheffield PJ. Measuring tissue oxygen tension: a review. Undersea Hyperb Ned 1998; 25: 179-88. PO2 values
ATAs 1.0 Air 1.0 O2 2.4 O2
air 159 760 1824
alveolar 104 673 1737
arterial 100 660 1700
venous 36 60 1650
muscle 29 59 250
subcutaneous 40 200-300 250-500
chronic wound 15 200-400 660
chest tcp02 67 450 1312
foot tcp02 63 280 919
When used in wound healing HBO2 provides a short pulse of oxygen - 90 minutes in a 24-hour day. Although, such a short time provision of elevated oxygen could not significantly effect wound healing, HBO2 acts in numerous ways that affect the wound after the treatment has stopped. There are eight principal methods in which HBO2 is capable of affecting tissue:
1. Pressure effects of oxygen
2. Vasoconstrictive effects of oxygen
3. 100% oxygen concentration effects on the diffusion gradient
4. Hyperoxygenation of ischaemic tissue
5. Down regulation of inflammatory cytokines
6. Up-regulation of growth factors
7. Leukocyte effects
8. Antibacterial effects.
Pressure effects of oxygen: The effect of elevating the ambient partial pressure of the inspired gas, usually to 2.38 ATAs, is unimportant in wound healing, but quite significant when dealing with the gas bubble diseases, decompression sickness and air gas embolism. At elevated pressures the harmful effects of gas bubbles in the tissue are minimised. Our research and that of others on wounds exposed to elevated pressures has demonstrated no evidence of an isolated pressure effect [10].
Vasoconstrictive effects of oxygen: The vasoconstrictive effects of HBO2 can be used to good effect to treat patients. HBO2 causes a significant reduction of oedema, which has been shown to be beneficial in reperfusion injury, crush injury, compartment syndrome, burns, wound healing, and failing flaps [11][12][13][14].
Oxygen diffusion effects: The diffusion of nitrogen out of the tissues in decompression sickness is facilitated by the use of 100% oxygen. In wound healing the beneficial effects of oxygen are primarily related to the concentration of oxygen molecules in the tissue, rather than by diffusion kinetics. However, the rate of oxygen entry into the wound environment is affected by the rate of diffusion from the capillaries. Oedema adversely affects the achievement of high oxygen concentrations in the wound and increases the intercapillary diffusion distance. Even a small increase in tissue oedema can dramatically slow the rate of entry of oxygen into the tissues and can cause tissue hypoxia.
Hyperoxygenation of tissue: The oxygenation of hypoxic tissue is one of the key mechanisms by which HBO2 accelerates wound healing. Numerous studies have shown a dose response curve for the provision of oxygen in the wound healing environment [10][14][15][16][17][18][19]. However, oxygen is a powerful drug and just like other drugs, it is possible to give too little or too much. Chronic wounds are frequently hypoxic and the provision of HBO2 corrects the hypoxia, albeit temporarily. It then allows for acceleration of the wound healing process through processes which continue long after the HBO2 session has ended and tissue oxygen levels have returned to pre-treatment values. Over time the oxygenation of the chronic wound improves with HBO2 therapy. Marx and Johnson demonstrated that for irradiated wounds, HBO2 induces neovascularisation, which becomes significant after about 14 treatments and continues for years after the HBO2 therapy has ceased [20] Figure 4. A typical chronic wound will usually require 20 to 30 HBO2 treatments. This probably represents the amount of neovascularisation needed to sustain wound healing.
image
Figure 4 - Increase in wound vascularisation with HBO2 treatment. tcpO2 = transcutaneous oxygen pressure; LSICS = left second intercostal space
Cytokine down regulation and growth factor up-regulation: HBO2 is capable of favourably influencing a number of cytokines and growth factors important to wound healing. When administered after wounding, HBO2 up-regulates collagen synthesis through pro-al(I) mRNA expression [21]. In rabbit ear wounds HBO2 has been shown to up-regulate mRNA for the platelet-derived growth factor (PDGF)-beta receptor [22]. In ischaemic flaps HBO2 up-regulates fibroblast growth factor (FGF) causing an increased effect over that seen with FGF alone [23]. In situations where FGF is ineffective, HBO2 can render it highly effective [24], although the effect is different from up-regulation. In patients with Crohn's disease interleukin-1 (IL-1), IL-6, and tumour necrosis factor (TNF)-alpha levels are diminished during HBO2 treatment [25]. TNF levels in normal rats become elevated after a single exposure to HBO2 [26]. For different physiological conditions HBO2 may cause up- or down regulation of cytokines. Vascular endothelial growth factor (VEGF) is up-regulated by hypoxia, yet the hyperoxia of HBO2 also up-regulates this factor [27]. The effects of transforming growth factor (TGF)-beta1 and platelet-derived growth factor (PDGF)-beta are synergistically enhanced by HBO2 [28].
The HBO2 paradox
Some biological processes and growth factors are stimulated or up-regulated by hypoxia and by HBO2. To date we have identified angiogenesis, collagen synthesis, osteoclastic activity, and release of VEGF. Other possible candidates are TNF-alpha and erythropoietin (EPO). However, it is unclear how oxygen is able to stimulate biological processes in both hypoxic and hyperoxic concentrations. I have called this paradoxical relation between oxygen and wound healing the 'Oxygen Paradox'.
One known mechanism is that by which fibroblasts are stimulated to make collagen through peroxides. These occur in the hypoxic wound and during HBO2 treatment [29]. Peroxides generated by HBO2 mimic one of the stimuli also found in hypoxia. Another mechanism is the stimulation of cytokines by hypoxia and further up-regulation of these cytokines by hyperoxia, which occurs during HBO2 treatment. This is the case for some interleukines and for TNF. There is some confusion on the exact timing of the release of growth factors and cytokines; in one study VEGF, TNF-alpha, and TGF-beta occurred in hypoxic wounds after they had been released in normoxia. VEGF, TGF-beta, and PDGF-beta have biphasic release patterns; their release is stimulated by hypoxia and hyperoxia, but is lowest during normoxia [29][30]. Furthermore, the activity of released VEGF is further enhanced during hyperoxia, especially in the presence of lactate [30].
It is clear that biologically active chemicals such as cytokines and growth factors have a complex array of stimuli to up and down regulate activity. Oxygen, cytokines and biologically active chemicals and metals appear to have key roles in wound healing processes. As we learn more about the role of oxygen, it appears to be much more detailed than in a simple mass-action equation.
Oxygen and infection
Oxygen is key to the phagocytosis and killing of bacteria by neutrophils or polymorphonuclear cells (PMNs). This process involves the production of oxygen radicals and superoxides and is directly influenced by the oxygen concentration in the tissue. As the oxygen tension falls below 30 mmHg the efficiency of bacteriocidal action of PMNs begins to drop off dramatically [31][32]. This was demonstrated by Knighton et al in 1984 where the phagocytic activity of neutrophils in ingesting Staph. aureus was compared to oxygen tension [33]. The activity level of phagocytosis is shown in Figure 5.
image
Figure 5 - Relationship of leukocyte killing of Staph. aureus and oxygen tension
PMN-mediated killing of several aerobic bacteria - Proteus vulgaris, Salmonella typhimurium, Klebsiella pneumoniae, Serratia marcescens, Pseudomonas aeruginosa and Staphylococcus species - is diminished in hypoxia [34]. Increasing the concentration of oxygen over ambient levels has been shown to reduce infection [35]. When supplemental oxygen was administered during a surgical operation and for two hours postoperatively, infection rates dropped by as much as 54% [36]. Thus, increasing tissue concentrations of oxygen has a beneficial effect on the ability of PMNs to combat bacteria and prevent infection.
HB02 and infection
HBO2 has six actions which have been used to combat clinical infection:
1. Tissue rendered hypoxic by infection is supported
2. Neutrophils are activated and rendered more efficient
3. Macrophage activity is enhanced
4. Bacterial growth is inhibited
5. Release of certain bacterial endotoxins is inhibited
6. The effect of antibiotics is potentiated.
Support of infected hypoxic tissue: Soft tissue and bone infections are frequently accompanied by localised areas of tissue hypoxia caused by the inflammatory processes accompanying infection and by subsequent vascular thrombosis [37]. As the infected tissue becomes infiltrated with inflammatory cells (PMNs and platelets) the PO2 falls [38]. In clostridial gas gangrene the production of phospholipase C has been associated with platelet and neutrophil aggregation and vascular thrombosis with subsequent hypoxia [37]. Administration of HBO2 can cause the PO2 to increase five-fold in infected tissue [39].
Neutrophil activation: As tissue PO2 rises, leukocyte killing of bacteria becomes much more efficient. Below a PO2 of 30 mmHg PMN killing is markedly reduced [40]. Because areas of hypoxia accompany serious tissue infections, HBO2 is an effective means of raising tissue PO2 to levels at which PMNs can function effectively. By raising tissue PO2 to levels higher than that achieved by breathing oxygen at ambient pressure, bacterial killing by PMNs is further enhanced [41]. Thus, by increasing tissue oxygen tension, a better than 'normal' antibacterial effect can be achieved. Hunt and colleagues have demonstrated that the clearance of bacteria from hypoxic tissue is enhanced by hyperoxic breathing mixtures [42][43]Figure 6.
image
Figure 6 - Wound bacterial growth and oxygen tension
Enhancement of macrophage activity: Macrophages, like PMNs, are affected by tissue oxygen tension. They perform a key role in combating infection by scavenging bacteria and foreign material. Under hypoxic conditions macrophages are unable to scavenge effectively and produce peroxides [44]. Hypoxia also induces macrophages to produce the inflammatory cytokines TNF-alpha, IL-1, IL-8, and intracellular adhesion molecule-1, which can adversely affect the response to infection [45]. While it is not yet known whether HBO2 can enhance macrophage function, it may be needed to bring the PO2 of hypoxic tissue up to normal levels so that macrophages can function normally.
Inhibition of bacterial growth: Anaerobic bacteria are particularly susceptible to increased concentrations of oxygen [46]. The more sensitive the anaerobic organism is to oxygen, the lower the level of superoxide dismutase, an enzyme that allows cells to defend themselves against oxygen free radicals [47]. With HBO2 large amounts of oxygen free radicals can be generated, making anaerobic bacteria particularly susceptible to oxidative killing. HBO2 treatment of anaerobic infections caused by Clostridial perfringens has increased patient survival, reduced the need for additional surgery, shortened hospital stay and improved outcome [4]. When used appropriately in Fournier's gangrene, a rapidly progressing necrotising infection of the perineum, HBO2 has reduced morbidity, extension of necrosis, and systemic toxicity [48].
Inhibition of endotoxin release: In C. perfringens infections the major source of tissue injury and death is caused by the alpha toxin. Secretion of this toxin is suppressed by HBO2 [49][50]. In rats exposed to E. coli peritonitis, HBO2 administration increased survival from 0% to 92% [51]. One of the mechanisms by which HBO2 appears to have worked is by antagonising some of the harmful effects of bacterial endotoxin release. However, to be optimally effective, HBO2 must be given early in the course of infection and combined with appropriate surgical debridement and antibiotics [52].
Potentiation of antibiotics: Both Knighton et al [35] and Hunt et al [53] have demonstrated that oxygen adds to the effectiveness of antibiotics; the greater the concentration of oxygen, the more pronounced the effect Figure 7. This has been demonstrated in experimental Staph. aureus osteomyelitis treated with cefazolin [54]. In Pseudomonas aeruginosa infections HBO2 has an additive effect with aminoglycoside antibiotics, reducing morbidity and mortality [55].
image
Figure 7 - Potentiation of antibiotic effects by HBO2
Side effects of HBO2
While HBO2 has an admirable safety record, those recommending HBO2 in wound care should be aware of potential side effects and complications.
Ear and sinus barotrauma: Middle ear barotrauma is the most common side effect of HBO2. Published reports indicate an incidence of 2-17%, and our experience with an elderly wound care population is consistent with this [56][57]. Fortunately most cases of barotrauma are minor and can be prevented by extra time spent in teaching the Valsalva manoeuver used on descent, slowing the descent rate, and trying other manoeuvers on descent such as drinking water with the nostrils occluded and head tilt during Valsalva. Those patients who cannot clear the middle ear during pressurisation will need to discontinue treatment and have pressure equalisation (PE) tubes inserted.
The paranasal sinuses are also a possible site of barotrauma on descent. Because of this, patients with a cold, upper respiratory tract infection, or allergic rhinitis are not suitable candidates for HBO2. If a patient experiences sinus barotrauma during descent, the treatment dive is suspended and attention given to clearing the sinus. Oxymetazoline hydrochloride 0.05% (Afrin) nasal spray may be of help.
Myopia: Some patients receiving HBO2 will develop reversible myopia. The action of HBO2 on the ocular lens is as yet undefined, but may be due to oxidative change of the lens proteins [58][59][60]. After cessation of therapy, the refraction usually returns to the pretreatment state within a few weeks [61]. The amount of change in the lens is related to the dose and frequency of HBO2 sessions [58]. Patients with wound problems are usually given 20 to 50 HBO2 treatments, with most patients receiving 30 treatments or less. For most of our patients experiencing myopia it has been a temporary problem.
Aggravation of congestive heart failure: HBO2 causes increased peripheral vascular resistance from its vasoconstrictive effects. A decrease in heart rate, cardiac output, and cardiac load has been described in healthy dogs [62]. Blood flow to the left ventricle has been noted to decrease during HBO2 [63]. We have had patients with severe congestive heart failure suffer a precipitous decline in cardiac function after receiving HBO2. Because of this we generally do not accept patients with a cardiac ejection fraction of less than 35% for HBO2.
Oxygen seizures: Oxygen is capable of causing grand mal seizures if breathed under pressure for a long enough period of time. Some individuals are more sensitive to oxygen than others and the exact dose of oxygen needed to provoke a seizure is quite variable. The mechanism is unclear but may be due to increased delivery of oxygen free radicals to the brain [64]. Ionic calcium has also been implicated [65]. In our wound treatment dives, 2.4 ATA of oxygen is given for 90 minutes, broken up into three 30-minute periods with 10 minute air breaks between the oxygen periods. Using this procedure, the incidence of oxygen induced seizure is quite rare, 1:10,000 dives [66].
Pulmonary barotrauma: Pulmonary barotrauma is a potentially serious complication of HBO2. The injury is related to pressure changes and occurs only on ascent. For the lungs to be injured there must be an obstruction such as a closed glottis or bronchial obstruction after reaching depth. During ascent the trapped air will expand, injuring the lung. An ascent of 3.5 feet (1.07 meters) would cause a trapped air bubble to exert 80 mmHg (10.7 kilopascals) pressure, enough to rupture alveoli.
An untreated pneumothorax is an absolute contradiction to HBO2 therapy and patients with a pneumothorax must have a chest tube inserted prior to the treatment dive. If a pneumothorax occurs during the treatment, a chest tube must be inserted prior to ascent to prevent a marked deterioration in the condition of the patient.
Patients with severe obstructive pulmonary disease such as untreated asthma or severe chronic obstructive pulmonary disease (COPD), with air trapping or bleb formation, could be at risk of pneumothorax and should be excluded from diving. However, many of our patients have previously been cigarette smokers and have mild COPD, but dive without incident.
Conclusion
Hyperbaric oxygen is a powerful treatment for acute and chronic wounds, acting on injured and healing tissue in a number of ways. Hypoxic tissue, reperfusion injury, compartment syndrome, crush injury, failing flaps, chronic wounds, burns and necrotising infections have all been shown to respond favourably to HBO2. As we learn more about how HBO2 benefits wounds by up-regulating growth factors, down regulating cytokines, reducing oedema, and supporting angiogenesis and new tissue ingrowth, the potential benefits to wound healing become clearer.
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34. Hohn DC. Host resistance of infection: Established and emerging concepts. In: Hunt TK, editor. Wound Healing and Wound Infection. New York: Appleton-Century-Crofts, 1980; 264-280.
35. Knighton DR, Halliday B, Hunt TK. Oxygen as an antibiotic. A comparison of the effects of inspired oxygen concentration and antibiotic administration on in vivo bacterial clearance. Arch Surg 1986; 121(2): 191-5.
36. Greif R, Akca O, Horn EP, Kurz A, Sessler DI. Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection. Outcomes Research Group. N Engl J Med 2000; 342(3): 161-7.
37. Bryant AE, Chen RY, Nagata Y, Wang Y, Lee CH, Finegold S, Guth PH, Stevens DL. Clostridial gas gangrene. II. Phospholipase C-induced activation of platelet gpIIbIIIa mediates vascular occlusion and myonecrosis in Clostridium perfringens gas gangrene. J Infect Dis 2000; 182(3): 808-15.
38. Silver IA. Tissue PO2 changes in acute inflammation. Adv Exp Med Biol 1978; 94: 769-74.
39. Korhonen K, Kuttila K, Niinikoski J. Tissue gas tensions in patients with necrotising fasciitis and healthy controls during treatment with hyperbaric oxygen: a clinical study. Eur J Surg 2000; 166(7): 530-4.
40. Hohn DC, MacKay RD, Halliday B, Hunt TK. Effect of O2 tension on microbicidal function of leukocytes in wounds and in vitro. Surg Forum 1976; 27(62): 18-20.
41. Mader JT, Adams KR, Sutton TE. Infectious diseases: Pathophysiology and mechanisms of hyperbaric oxygen. J Hyperbar Med 1987; 2: 133-40.
42. Conolly WB, Hunt TK, Sonne M, Dunphy JE. Influence of distant trauma on local wound infection. Surg Gynecol Obstet 1969; 128(4): 713-8.
43. Hunt TK, Linsey M, Grislis H, Sonne M, Jawetz E. The effect of differing ambient oxygen tensions on wound infection. Ann Surg 1975; 181(1): 35-9.
44. Mrotek JJ, Henderson R, Kiel J, et al. Normobaric oxygen concentrations affect cultured mouse macrophage responses. Fed Proc 1986; 45: A958.
45. Scannell G. Leukocyte responses to hypoxic/ischemic conditions. New Horiz 1996; 4(2): 179-83.
46. Gottlieb SF. Effect of hyperbaric oxygen on microorganisms. Annu Rev Microbiol 1971; 25: 111-52.
47. Tally FP, Goldin BR, Jacobus NV, Gorbach SL. Superoxide dismutase in anaerobic bacteria of clinical significance. Infect Immun 1977; 16(1): 20-5.
48. Korhonen K, Hirn M, Niinikoski J. Hyperbaric oxygen in the treatment of Fournier's gangrene. Eur J Surg 1998; 164(4): 251-5.
49. Van Unnick A. Inhibition of toxin production in Clostridium perfringens in vitro by hyperbaric oxygen. Antonie Leewenhoek Microbiol 1965; 31: 181-6.
50. Hill GB, Osterhout S. Experimental effects of hyperbaric oxygen on selected clostridial species: II. In vivo studies in mice. J Infect Dis 1972; 125: 26.
51. Thom SR. Hyperbaric oxygen therapy in septicemia. J Hyperb Med 1987; 2: 141-6.
52. Korhonen K, Klossner J, Hirn M, Niinikoski J. Management of clostridial gas gangrene and the role of hyperbaric oxygen. Ann Chir Gynaecol 1999; 88(2): 139-42.
53. Hunt TK, Linsey M, Grislis HJ, et al. The effect of differing ambient oxygen tensions on wound infection. Ann Surg 1975; 181: 35-9.
54. Mendel V, Reichert B, Simanowski HJ, Scholz HC. Therapy with hyperbaric oxygen and cefazolin for experimental osteomyelitis due to Staphylococcus aureus in rats. Undersea Hyperb Med 1999; 26(3): 169-74.
55. Luongo C, Imperatore F, Matera MG, Mangoni G, Marmo M, Baroni A, Catalanotti P, Rossi F, Filippelli A. Effect of hyperbaric oxygen therapy in experimental subcutaneous and pulmonary infections due to Pseudomonas aeruginosa. Undersea Hyperb Med 1999; 26(1): 21-5.
56. Plafki C, Peters P, Almeling M, Welslau W, Busch R. Complications and side effects of hyperbaric oxygen therapy. Aviat Space Environ Med 2000; 71(2): 119-24.
57. Stone JA, Loar H, Rudge FW. An eleven year review of hyperbaric oxygenation in a military clinical setting. Undersea Biomed Res 1991; 18: 80.
58. Palmquist BM, Philipson B, Barr PO. Nuclear cataract and myopia during hyperbaric oxygen therapy. Br J Ophthalmol 1984; 68(2): 113-7.
59. Ross ME, Yolton DP, Yolton RL, Hyde KD. Myopia associated with hyperbaric oxygen therapy. Optom Vis Sci 1996; 73(7): 487-94.
60. Anderson B, Jr, Shelton DL. Axial length in hyperopic myopia. In: Bove AA, Bachrach AJ, Greenbaum LI, Jr, editors. Underwater and Hyperbaric Physiology IX. Proceedings of the Ninth International Symposium on Underwater and Hyperbaric Physiology. Bethesda, MD: Undersea and Hyperbaric Medical Society, 1987.
61. Lyne AJ. Ocular effects of hyperbaric oxygen. Trans Ophthalmol Soc UK 1978; 98(1): 66-8.
62. Abel FL, McNamee JE, Cone DL, Clarke D, Tao J. Effects of hyperbaric oxygen on ventricular performance, pulmonary blood volume, and systemic and pulmonary vascular resistance. Undersea Hyperb Med 2000; 27(2): 67-73.
63. Bergo GW, Risberg J, Tyssebotn I. Effect of 5 bar oxygen on cardiac output and organ blood flow in conscious rats. Undersea Biomed Res 1988; 15(6): 457-70.
64. Chavko M, Harabin AL. Regional lipid peroxidation and protein oxidation in rat brain after hyperbaric oxygen exposure. Free Radic Biol Med 1996; 20(7): 973-8.
65. Wang WJ, Ho XP, Yan YL, Yan TH, Li CL. Intrasynaptosomal free calcium and nitric oxide metabolism in central nervous system oxygen toxicity. Aviat Space Environ Med 1998; 69(6): 551-5.
66. Davis JC, Dunn JM, Heimbach RD. Hyperbaric medicine: Patient selection, treatment procedures and side effects. In: Davis JC, Hunt TK, editors. Problem Wounds - the role of oxygen. New York: Elsevier, 1988.
All materials copyright © 1992-Feb 2001 by SMTL, March 2001 et seq by SMTL and MEP unless otherwise stated.
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Last Modified: Monday, 21-May-2001 11:56:17 BST
HBOT EN QUEMADOS
Hyperbaric Oxygen Therapy Heals Burns Faster With Less Scars
Serious burns which can be caused by chemical and electricity as well as by fire, can be among the most painful of injuries, and among the most difficult to treat. There are burn victims who don't need skin transplants but who do need medical assistance. Long term physical and emotional disabilities occur when burns go on to heal leaving tissue scars. HBOT can help burn patients heal faster with fewer complications and less scarring.
Peak damage occurs within 3-4 days after the initial burn and can be up to 10 times worse than the initial burn injury. These injuries can result in life long difficulties, physical limitation, and significant disfigurement as the body heals from the injury.
Adjunctive hyperbaric oxygen therapy has been shown to limit the progression of the burn injury, reduce swelling, may reduce the need for surgical intervention, diminish lung damage and shorten the time of hospitalization. When burn victims are not hospitalized with non life threatening burns, HBOT can be carried out at private facilities when first or second degree burns are involved.
In order for a burn to heal properly, it is very important for the burned area to develop new tissue cover quickly. Viable cells from healthy areas migrate into the wound and start to reproduce given the appropriate conditions with help from HBOT. Oxygen is very important to wound healing. When the environment of the fibroblast has an oxygen tension of less than 10mmHg, the cell can divide, but it can no longer synthesize collagen. It cannot migrate to where it is needed for healing. When the oxygen tension is increased, the fibroblast can again carry out these wound healing function. The collagen produced by these cells for a protective fibrous matrix and new capillaries grow into this matrix. Wound healing is a dynamic process and an adequate oxygen tension is mandatory for this process to proceed successfully.
HBOT inhibits wound infection by helping to support the body's infection fighting white blood cells and by helping to increase the effectiveness of any antibiotics that are used when an infection occurs. HBOT aids the survival of skin grafts and flaps when it is necessary to use them in more severe burns. (See compromised grafts and flaps)
HBOT is a useful part of an overall treatment program for burns, whether the burn is serious or not. Prevention of scarring especially facial scarring may be cosmetic in some cases but victims need not carry the physical scar as well as the emotional scar burns leave with them.
Serious burns which can be caused by chemical and electricity as well as by fire, can be among the most painful of injuries, and among the most difficult to treat. There are burn victims who don't need skin transplants but who do need medical assistance. Long term physical and emotional disabilities occur when burns go on to heal leaving tissue scars. HBOT can help burn patients heal faster with fewer complications and less scarring.
Peak damage occurs within 3-4 days after the initial burn and can be up to 10 times worse than the initial burn injury. These injuries can result in life long difficulties, physical limitation, and significant disfigurement as the body heals from the injury.
Adjunctive hyperbaric oxygen therapy has been shown to limit the progression of the burn injury, reduce swelling, may reduce the need for surgical intervention, diminish lung damage and shorten the time of hospitalization. When burn victims are not hospitalized with non life threatening burns, HBOT can be carried out at private facilities when first or second degree burns are involved.
In order for a burn to heal properly, it is very important for the burned area to develop new tissue cover quickly. Viable cells from healthy areas migrate into the wound and start to reproduce given the appropriate conditions with help from HBOT. Oxygen is very important to wound healing. When the environment of the fibroblast has an oxygen tension of less than 10mmHg, the cell can divide, but it can no longer synthesize collagen. It cannot migrate to where it is needed for healing. When the oxygen tension is increased, the fibroblast can again carry out these wound healing function. The collagen produced by these cells for a protective fibrous matrix and new capillaries grow into this matrix. Wound healing is a dynamic process and an adequate oxygen tension is mandatory for this process to proceed successfully.
HBOT inhibits wound infection by helping to support the body's infection fighting white blood cells and by helping to increase the effectiveness of any antibiotics that are used when an infection occurs. HBOT aids the survival of skin grafts and flaps when it is necessary to use them in more severe burns. (See compromised grafts and flaps)
HBOT is a useful part of an overall treatment program for burns, whether the burn is serious or not. Prevention of scarring especially facial scarring may be cosmetic in some cases but victims need not carry the physical scar as well as the emotional scar burns leave with them.
INTOXICACION MONOXIDO DE CARBONO E INHALACION HUMO
CARBON MONOXIDE POISONING
AND SMOKE INHALATION
Hyperbaric oxygen (HBO2) treatment is indicated for the following signs and symptoms:
* Alteration in Mental Status
* Neurological Signs
* Cardiovascular Dysfunction
* Pulmonary Edema
* Severe Acidosis
* Carboxyhemoglobin Levels in Excess of 25%
Patients who manifest any of the first five signs listed above should be referred for HBO2 treatment irrespective of their carboxyhemoglobin level. Treatment is most effective when initiated within six hours of exposure.
RATIONALE: HBO2 treatment must be predicated more on the clinical picture than the carboxyhemoglobin levels. HBO2 hastens the disassociation of carbon monoxide from hemoglobin, myoglobin, cytochromes and other hemoproteins. At sea level, oxygen has not been shown to antagonize lipid peroxide while HBO2 does. HBO2 also provides tissue oxygenation via saturated plasma.
Source: Hyperbaric Oxygen Therapy: A Committee Report. Undersea and Hyperbaric Medical Society. 1996 Revision.
AND SMOKE INHALATION
Hyperbaric oxygen (HBO2) treatment is indicated for the following signs and symptoms:
* Alteration in Mental Status
* Neurological Signs
* Cardiovascular Dysfunction
* Pulmonary Edema
* Severe Acidosis
* Carboxyhemoglobin Levels in Excess of 25%
Patients who manifest any of the first five signs listed above should be referred for HBO2 treatment irrespective of their carboxyhemoglobin level. Treatment is most effective when initiated within six hours of exposure.
RATIONALE: HBO2 treatment must be predicated more on the clinical picture than the carboxyhemoglobin levels. HBO2 hastens the disassociation of carbon monoxide from hemoglobin, myoglobin, cytochromes and other hemoproteins. At sea level, oxygen has not been shown to antagonize lipid peroxide while HBO2 does. HBO2 also provides tissue oxygenation via saturated plasma.
Source: Hyperbaric Oxygen Therapy: A Committee Report. Undersea and Hyperbaric Medical Society. 1996 Revision.
INTOXICACION MONOXIDO DE CARBONO E INHALACION HUMO
CARBON MONOXIDE POISONING
AND SMOKE INHALATION
Hyperbaric oxygen (HBO2) treatment is indicated for the following signs and symptoms:
* Alteration in Mental Status
* Neurological Signs
* Cardiovascular Dysfunction
* Pulmonary Edema
* Severe Acidosis
* Carboxyhemoglobin Levels in Excess of 25%
Patients who manifest any of the first five signs listed above should be referred for HBO2 treatment irrespective of their carboxyhemoglobin level. Treatment is most effective when initiated within six hours of exposure.
RATIONALE: HBO2 treatment must be predicated more on the clinical picture than the carboxyhemoglobin levels. HBO2 hastens the disassociation of carbon monoxide from hemoglobin, myoglobin, cytochromes and other hemoproteins. At sea level, oxygen has not been shown to antagonize lipid peroxide while HBO2 does. HBO2 also provides tissue oxygenation via saturated plasma.
Source: Hyperbaric Oxygen Therapy: A Committee Report. Undersea and Hyperbaric Medical Society. 1996 Revision.
AND SMOKE INHALATION
Hyperbaric oxygen (HBO2) treatment is indicated for the following signs and symptoms:
* Alteration in Mental Status
* Neurological Signs
* Cardiovascular Dysfunction
* Pulmonary Edema
* Severe Acidosis
* Carboxyhemoglobin Levels in Excess of 25%
Patients who manifest any of the first five signs listed above should be referred for HBO2 treatment irrespective of their carboxyhemoglobin level. Treatment is most effective when initiated within six hours of exposure.
RATIONALE: HBO2 treatment must be predicated more on the clinical picture than the carboxyhemoglobin levels. HBO2 hastens the disassociation of carbon monoxide from hemoglobin, myoglobin, cytochromes and other hemoproteins. At sea level, oxygen has not been shown to antagonize lipid peroxide while HBO2 does. HBO2 also provides tissue oxygenation via saturated plasma.
Source: Hyperbaric Oxygen Therapy: A Committee Report. Undersea and Hyperbaric Medical Society. 1996 Revision.
EMBOLISMO AEREO Y HBOT
AIR OR GAS EMBOLISM
The treatment of choice for air or gas embolism of the arterial or venous system is recompression in a hyperbaric chamber. Recompression is indicated for the following types of air emboli:
* Surgical
* Diagnostic Procedures
* Renal Dialysis
* Pulmonary Over-Pressure During Scuba Diving
* Cardiovascular Surgery
When gases enter the vasculature in sufficient volume to compromise the function of an organ or body part, the process can create varying degrees of ischemia to the affected areas. Treatment is most effective when initiated within minutes of the incident. However, evidence has shown that delayed and repeat treatment has demonstrated a means to a more expedient recovery.
RATIONALE: Recompression of gas bubbles as well as the rescue of hypoxic tissue by way of HBO2 treatment is the only form of treatment known. HBO2 reduces the mortality rate and remedies the development of permanent neurological damage. Repeated HBO2 treatments after the initial recompression hastens the resolution of residual signs in some cases.
Source: Hyperbaric Oxygen Therapy: A Committee Report. Undersea and Hyperbaric Medical Society. 1996 Revision.
The treatment of choice for air or gas embolism of the arterial or venous system is recompression in a hyperbaric chamber. Recompression is indicated for the following types of air emboli:
* Surgical
* Diagnostic Procedures
* Renal Dialysis
* Pulmonary Over-Pressure During Scuba Diving
* Cardiovascular Surgery
When gases enter the vasculature in sufficient volume to compromise the function of an organ or body part, the process can create varying degrees of ischemia to the affected areas. Treatment is most effective when initiated within minutes of the incident. However, evidence has shown that delayed and repeat treatment has demonstrated a means to a more expedient recovery.
RATIONALE: Recompression of gas bubbles as well as the rescue of hypoxic tissue by way of HBO2 treatment is the only form of treatment known. HBO2 reduces the mortality rate and remedies the development of permanent neurological damage. Repeated HBO2 treatments after the initial recompression hastens the resolution of residual signs in some cases.
Source: Hyperbaric Oxygen Therapy: A Committee Report. Undersea and Hyperbaric Medical Society. 1996 Revision.
Quemaduras y HBOT
THERMAL BURNS
The burn wound is a complex and dynamic pathophysiologic process characterized by a zone of coagulation, surrounded by a region of stasis, and bounded by an area of hyperemia. An intense inflammatory reaction leading to rapid edema formation, increased microvascular permeability, and sluggish blood flow results in thrombosis, ischemia, and advancing necrosis. The basic problems in repair of burns include susceptibility to infection, prolonged healing, and excessive scarring. These problems are greatly increased due to the loss of the integumentary barrier to bacterial invasion and compromised or obstructed microvasculature. These problems further prevent humeral and cellular elements from reaching the burned tissue as well as delayed regeneration and healing. The therapy of burns must be directed at minimizing edema, preserving marginally viable tissue, enhancing host defenses, and promoting wound closure. Adjunctive hyperbaric oxygen (HBO2) therapy can attack these problems, directly maintaining microvascular integrity, minimizing edema, and providing the substrate necessary to maintain viability.
RATIONALE: A significant body of data clearly supports the efficacy of HBO2 in the treatment of thermal injury. A reduction in fluid requirements, less conversion of partial to full thickness injury, preservation of marginally viable tissue, improved microcirculation, reduction in edema, faster epithelialization, less inflammatory response, enhancement of PMN killing, preservation of tissue creatine phosphate, adenosine triphosphate, and decreased wound lactate have all been reported. Infection remains the leading cause of death from burn injuries that are treated at burn centers. Therefore, control of infection is a major goal of therapy. Present evidence indicates that brief HBO2 exposures (2 ATA for 2 hrs) inhibit Pseudomonas aeruginosa both in vitro and in vivo. An intact microvasculature is a critical factor in the ability to provide cellular and humeral elements to the site of the injury. Any improvement in the microvasculature, whether it be preservation of intact capillaries or control of interstitial edema, would favorably influence the burn outcome. In human studies, HBO2 therapy has been shown to exert a positive, beneficial effect on the burn wound by: (1) reducing edema and plasma extravasation, (2) preserving the microcirculation, (3) preventing the conversion of partial to full thickness injury, and (4) maintaining the viability of the dermal elements which lead to a more rapid epithelialization. This has lead to a reduced need for surgery, a reduced length of hospital stay, and a reduced mortality rate. HBO2 therapy, used as an adjunct to traditional burn care, demonstrates greatest effects when initiated within the first 4 hours following the injury, or as quickly as possible.
Source: Hyperbaric Oxygen Therapy: A Committee Report. Undersea and Hyperbaric Medical Society. 1996 Revision.
The burn wound is a complex and dynamic pathophysiologic process characterized by a zone of coagulation, surrounded by a region of stasis, and bounded by an area of hyperemia. An intense inflammatory reaction leading to rapid edema formation, increased microvascular permeability, and sluggish blood flow results in thrombosis, ischemia, and advancing necrosis. The basic problems in repair of burns include susceptibility to infection, prolonged healing, and excessive scarring. These problems are greatly increased due to the loss of the integumentary barrier to bacterial invasion and compromised or obstructed microvasculature. These problems further prevent humeral and cellular elements from reaching the burned tissue as well as delayed regeneration and healing. The therapy of burns must be directed at minimizing edema, preserving marginally viable tissue, enhancing host defenses, and promoting wound closure. Adjunctive hyperbaric oxygen (HBO2) therapy can attack these problems, directly maintaining microvascular integrity, minimizing edema, and providing the substrate necessary to maintain viability.
RATIONALE: A significant body of data clearly supports the efficacy of HBO2 in the treatment of thermal injury. A reduction in fluid requirements, less conversion of partial to full thickness injury, preservation of marginally viable tissue, improved microcirculation, reduction in edema, faster epithelialization, less inflammatory response, enhancement of PMN killing, preservation of tissue creatine phosphate, adenosine triphosphate, and decreased wound lactate have all been reported. Infection remains the leading cause of death from burn injuries that are treated at burn centers. Therefore, control of infection is a major goal of therapy. Present evidence indicates that brief HBO2 exposures (2 ATA for 2 hrs) inhibit Pseudomonas aeruginosa both in vitro and in vivo. An intact microvasculature is a critical factor in the ability to provide cellular and humeral elements to the site of the injury. Any improvement in the microvasculature, whether it be preservation of intact capillaries or control of interstitial edema, would favorably influence the burn outcome. In human studies, HBO2 therapy has been shown to exert a positive, beneficial effect on the burn wound by: (1) reducing edema and plasma extravasation, (2) preserving the microcirculation, (3) preventing the conversion of partial to full thickness injury, and (4) maintaining the viability of the dermal elements which lead to a more rapid epithelialization. This has lead to a reduced need for surgery, a reduced length of hospital stay, and a reduced mortality rate. HBO2 therapy, used as an adjunct to traditional burn care, demonstrates greatest effects when initiated within the first 4 hours following the injury, or as quickly as possible.
Source: Hyperbaric Oxygen Therapy: A Committee Report. Undersea and Hyperbaric Medical Society. 1996 Revision.
caso clinico de heridas,quemaduras y HBOT
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Del Rio veteran shaped by adversity of the worst kind, love of the best
December 15, 2008
By Bill Sontag
Feature Writer
At the family dining room table, Bobby Barrera reflects on and recounts the injuries that changed his life forever during a very brief tour in Vietnam. As the shirt suggests, Barrera is an unswerving spokesman for Disabled American Veterans. (LIVE! photo/Bill Sontag) (click image to enlarge)
A hazy, 39-year-old black-and-white photo is a snapshot of a robust Marine with a cigarette dangling from his right hand, and a determined – if somewhat menacing – countenance. Today, the hand is gone, along with the left arm, and so is the intimidation, replaced respectively by prosthesis and surpassing understanding.
Pfc. Bobby Barrera was no seasoned veteran of combat in Vietnam – only six weeks “in country” with Company C, 1st Battalion, 7th Marines – when a command-detonated 500-pound bomb exploded beneath the rumbling amphibious tractor (“amtrac”) on which he rode. The bomb was triggered by enemy in the jungle, waiting for the amtrac bearing one man – sniper Staff Sgt. Carlos Hathcock – to ride above the bomb, the third of five vehicles in the convoy.
Hathcock, with his 93 “confirmed kills,” wore a daredevil symbol of his reputation in his headgear, making him an easily identified, marked man with an enemy’s lucrative bounty on his head. “White Feather” Hathcock flaunted his status at his enemies and they got him. “They were watching us,” Barrera said, Thursday (Nov. 13, 2008).
[BARRERA_FAMILY]
The Barrera family – closely knit and supportive – demonstrate great pride in each other’s accomplishments. They are, from left, son Aldo, daughter Karla, Maricelia and Bobby. In front is grandson Alejandro, 5. (LIVE! photo/Bill Sontag) (click image to enlarge)
The huge bomb ruptured and ignited the amtrac’s fuel cells, enveloping and sending Barrera, Hathcock and six other Marines into sheets of flame in which their uniforms and flesh became part of the inferno.
“All of us got burned over 40-57 percent of our bodies. But we all walked to the helicopter that came to pick us up, landing just about 60 yards from the burning track,” Barrera recalled. He looked at his fellow Marines and was struck by the ghastly appearance of their exposed skin, hanging, sagging away from charred uniforms, like ill-fitting latex gloves.
“The enemy had started shooting at us, and the other Marines returned fire while we boarded the helicopter, and were flown to the USS Repose, a hospital ship in Da Nang Harbor,” Barrera said. From the Repose, things went from horrific to worse, to better again for Barrera, and now he’s in a position to pave a similar path for American veterans everywhere.
[BARRERA_BEFORE]
A tough-looking Marine taking a snapshot break from infantry training at Camp Pendleton, Calif., June 1969, is the “before” image of Bobby Barrera. Three months later, Barrera was critically burned over 40 percent of his once-robust body, and in for years of excruciating treatments and surgical repairs. (Contributed photo/Bobby Barrera) (click image to enlarge)
He passed the 60-year milestone in June, and is reflective upon a lifetime of opportunity that has unfolded beneath his drive and determination since that horrific day, September 16 (Dieciseis de septiembre), 1960. Then, as his life was momentarily reduced to char, on the other side of the world, friends and family back in Del Rio were lifting cold ones to commemorate Padre Hidalgo’s 1810 “Grito” for Mexico’s independence from Spain.
Fellow Del Rio Marine Pat Dugan calls the area where Barrera nearly lost his life “one of the toughest areas of combat in Vietnam. It was called ‘the Arizona Territory’ because it was very dangerous, a free fire zone with no rules,” said Dugan, Thursday (Nov. 26).
Barrera’s arrival in Vietnam had followed a quickie wedding to the Marine Corps with no honeymoon, completing infantry training at Camp Pendleton, Calif., then advanced infantry training. “Graduation was at 6 p.m., and by midnight I was on a plane – the Flying Tigers – enroute to Alaska, Okinawa, Japan, and then on Continental to Da Nang. On Continental they treated us like royalty, like it might be our last trip, and, for some, I’m sure it was.”
Plunked down at Da Nang Air Base, the young Marine was undaunted. “Not until I got to where my unit was, and that was when it hit me. The armory was closed for the night, so I wasn’t issued a weapon, so we went to bunkers as we were told to when we heard firing. Finally, a sergeant came around and told us it was friendly artillery, not incoming rounds.”
Capable of plowing through ocean surfs for beach landings, the amphibious tracked vehicle was the transportation of choice and necessity when Charley Company, 1st Battalion, 7th Marines came ashore at Da Nang during the Vietnam War. Barrera was in a convoy of five similar “amtracs” when a 500-pound bomb blew up, spewing fire from fuel tanks over the eight men riding atop the vehicle. (Contributed photo/Bobby Barrera) (click image to enlarge)
Only six weeks later, in unspeakable pain aboard the Repose, Barrera began his first round of narcotics to dull the agony, then was airlifted to a two-day hospital visit for more stabilization in Japan. “They had us pretty drugged up, so I don’t remember much about Japan except a nurse holding a cigarette for me to smoke at the airport,” Barrera said.
Next, a C-130 Hercules cargo and transport ship launched from Wright-Patterson Air Force Base, Ohio, stopping off in San Antonio long enough to pick up a team of physicians, nurses and technicians from the prestigious burn unit of Brooke Army Medical Center. (For more perspectives on this world-renowned facility, listen to this 2006 National Public Radio broadcast report, at http://www.npr.org/templates/story/story.php?storyId=5570807)
[BARRERA_DRESS-BLUESIII]
Col. Phil Torres, representing the Marine Corps commandant, presents Barrera with his first set of dress uniform components, Tuesday (Nov. 9, 1999), as the veteran received the Leaders in Furthering Education (LIFE) Presidential Unsung Hero Award. The “blues” were a motivating factor in Barrera’s enlistment, but they had to be purchased. His private first class salary prohibited it. “Bobby, here’s your blues,” thundered Torres, 30 years later. (Contributed photo/DAV Magazine) (click image to enlarge)
Despite the life-saving treatments of physicians, compassionate care by superlative staff and surgeries that restored his face and use of one arm, his arrival at BAMC marked the beginning of levels of pain that not even the bomb explosion in Vietnam could match. Comparing his pain level aboard the Repose with his months of therapy at BAMC, Barrera commented, “The Navy was much more generous with their drugs for pain than the Army – a big, big difference.”
In the burn center, he and others with similar injuries were introduced – and reintroduced daily – to the Hubbard Tank, a T-shaped stainless steel tub much like a whirlpool bath. Unlike the whirlpool that eases stiff muscles of athletes, the Hubbard tank was a therapeutic form of torture. Technicians and nurses submerged him and “they hold you down and scrub your wounds, and then, back in bed they applied what they called ‘the butter,’” said Barrera, an ointment with restorative and therapeutic qualities, but little relief from the ever-present pain.
The tank-and-butter treatments continued daily for about 40 days, Barrera remembered, followed by three or four flights – twice a day, each day and still in great pain – to Brooke Army Medical Center for hyperbaric chamber sessions to infuse the wounds with oxygen, accelerating their healing.
Amid veterans, families, and members of all U.S. armed forces, Barrera delivers the keynote address at the Veterans Day Program at Forest Lawn Memorial Park, Hollywood Hills, Calif. The 2006 program also featured the Aztec Skydiving Team and the Notre Dame Irish Knight Marching Band. (Contributed photo/Bobby Barrera) (click image to enlarge)
Then he sustained surgeries to amputate his left arm because of infection by phycomycoses, water molds that infected wounds and could not be treated. “It’s like gangrene, only much faster, and all they can do is amputate,” Barrera explained. More amputations followed when the infections spread, then more surgeries created ears and lips, both burned off his face by the flames, and finally fittings for his right “arm” prosthesis. “I call it my hook, and sometimes, like some people who lose their glasses, I forget where I took it off, and have to go looking,” Barrera said, chuckling.
“I don’t know if I could go through this again. It was the worst thing that’s ever happened to me, obviously,” Barrera said. “Most of the survivors – including me – said we’d always carry a gun, and if we ever got burned another time, we would just shoot ourselves, rather than ever go through that again.”
Discharged from the Marine Corps in September 1970, Barrera became a patient of the U.S. Department of Veterans Affairs. Late that month, the doctors gave him leave to come home for first time for from BAMC for the holiday season. His dad, Indalecio Barrera, Del Rio’s police chief, and his mom, Elia Barrera were his support system.
“It was overwhelming relief for my parents to know that I was going to survive, but, for me, coming home was a terrible experience. I was coming home a different person. I didn’t want anyone to see me that way,” Barrera said. His lips had not been reconstructed with grafts yet, and his amputations worsened the matter. He wanted to remain cloistered, but friends and family ignored his fears and came to visit anyway. “That was the first major hurdle I had to overcome, and they made that happen for me.”
In 1973, Barrera had been through 32 surgeries, and he opted out of any more. “I came back to Del Rio … stayed here, and said, ‘No more of this,’” Barrera said. Only four blocks from his uncle’s house on West 6th Street, Barrera saw a beautiful young woman he wanted to meet, so he struggled for an opening line. Maricelia Marin owned a pet Capuchin, native to Central and South America, so Barrera struggled for an opening line, one that still makes the couple blush: “Can you show me your monkey?”
“We started going steady in November 1973. Despite my injuries, she made me feel very comfortable, so we got married in April 1974 at Saint Joseph’s Church. The turning point in my life was when I married Maricelia. She gave direction to my life,” Barrera said.
[BARRERA_KERRY]
Barrera receives a warm hug, Feb. 23, from Sen. John Kerry (D-Mass.) following Barrera’s introduction during Kerry’s visit to Sul Ross University while campaigning for now-President-elect Barrack Obama. The audience in the packed campus auditorium gave both Barrera and Kerry a standing ovation as the senator approached the podium, pausing for the moment. (LIVE! file photo/Bill Sontag) (click image to enlarge)
Two years later, his sister-in-law, Vangie, graduated from Del Rio High School and was headed for college, provoking Barrera to consider another chance for a degree from Saint Mary’s University. With his single, prosthetic arm, Barrera knew he’d not be able to turn book pages, hold notebooks still for writing. Maricelia attended classes with him – carrying his books, turning their pages, and steadying the notepaper – and she helped her husband study. “When I got my bachelor’s degree [1978, psychology], under my name I had hers written there, too,” Barrera said. “She has always given me the right balance of her love, support, and a swift kick in the butt when I most need it.”
For five years, Barrera taught Spanish and English at Del Rio High School, eventually pestering administrators long enough to add psychology to the curriculum, with him as instructor, of course. “By that time, I earned a Master of Education at Sul Ross [Alpine], in guidance and counseling, and was working part time with the Juvenile Probation Department of the 63rd Judicial District under Judge George Thurmond.” His work with youthful offenders began as a volunteer, then part time, and finally full time during which time he created the community service program for the department.
When Laughlin Air Force Base opened a Family Support Center, Barrera became its first director within the Mission Support Squadron, commanded by Col. Sidney Hirschberg. Beginning with an office of three in 1989, and ending his career there in October 1997 with a staff of 13, Barrera built the services to military personnel and their families to include financial management, answering needs before and after deployments, vocational counseling and an employment program for spouses, transition services from active duty to civilian life upon separation from service, and a base relocation program for transferees.
Barrera got involved with the Disabled American Veterans (DAV) organization while working at Laughlin, and, in 1997, he was accorded the Air Force Outstanding Federal Employee with Disabilities award, followed the next year with the DAV award, Outstanding Disabled Veteran of the Year. Since then, Barrera has acquired leadership opportunities as both educator and mentor, traveling often, and addressing hundreds of youth groups, civic clubs, military audiences and veterans organizations across the United States.
His theme for most of those is “The Four S’s of Life,” composed in Barrera’s private moments of reflection, and refined with his training and experience in psychology. They elaborate, he says, on the need within each individual facing any of life’s challenges to seek support, keep a sense of humor, maintain a spiritual relationship with God, and nourish a keen sense of self. Since the 1998 DAV award, Barrera has taught the lessons each year at “Leadership V.A..” “They’re usually 70 or 80 people from the top leadership positions – the cream of the crop, really – of the Veterans Administration: physicians, financial officers, medical division chiefs, researchers and research administrators.
Now Barrera serves as DAV senior vice commander, and is in line to be nominated for the national commander’s position at the DAV National Convention in Denver, August 2009. “If I get it, that will mean almost non-stop traveling,” Barrera said, notwithstanding the pleasure and privilege of gaining the slot. For more about the DAV, see www.dav.org.
Barrera sees abundant opportunity to continue improvements in respect accorded to veterans and treatments afforded to the wounded. “In the past, especially with World War II and Korean War veterans, there was a lot of need for improvement in health care. But in the last 10 years, there have been dramatic improvements. Now our veterans usually rate their satisfaction with VA hospitals above private for-profit institutions,” Barrera said. For more about the Department of Veterans Affairs, see www.va.gov.
He also sees important progress in how returning veterans are perceived by the American public. “I’m always emphasizing that when the Vietnam veteran returned, they didn’t receive a welcome home or the respect and gratitude of their country. Now, I see that kind of treatment not happening – thankfully – to our veterans returning from Iraq and Afghanistan. People must learn how to separate their feelings about the war from their feelings about the warrior!”
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Del Rio veteran shaped by adversity of the worst kind, love of the best
December 15, 2008
By Bill Sontag
Feature Writer
At the family dining room table, Bobby Barrera reflects on and recounts the injuries that changed his life forever during a very brief tour in Vietnam. As the shirt suggests, Barrera is an unswerving spokesman for Disabled American Veterans. (LIVE! photo/Bill Sontag) (click image to enlarge)
A hazy, 39-year-old black-and-white photo is a snapshot of a robust Marine with a cigarette dangling from his right hand, and a determined – if somewhat menacing – countenance. Today, the hand is gone, along with the left arm, and so is the intimidation, replaced respectively by prosthesis and surpassing understanding.
Pfc. Bobby Barrera was no seasoned veteran of combat in Vietnam – only six weeks “in country” with Company C, 1st Battalion, 7th Marines – when a command-detonated 500-pound bomb exploded beneath the rumbling amphibious tractor (“amtrac”) on which he rode. The bomb was triggered by enemy in the jungle, waiting for the amtrac bearing one man – sniper Staff Sgt. Carlos Hathcock – to ride above the bomb, the third of five vehicles in the convoy.
Hathcock, with his 93 “confirmed kills,” wore a daredevil symbol of his reputation in his headgear, making him an easily identified, marked man with an enemy’s lucrative bounty on his head. “White Feather” Hathcock flaunted his status at his enemies and they got him. “They were watching us,” Barrera said, Thursday (Nov. 13, 2008).
[BARRERA_FAMILY]
The Barrera family – closely knit and supportive – demonstrate great pride in each other’s accomplishments. They are, from left, son Aldo, daughter Karla, Maricelia and Bobby. In front is grandson Alejandro, 5. (LIVE! photo/Bill Sontag) (click image to enlarge)
The huge bomb ruptured and ignited the amtrac’s fuel cells, enveloping and sending Barrera, Hathcock and six other Marines into sheets of flame in which their uniforms and flesh became part of the inferno.
“All of us got burned over 40-57 percent of our bodies. But we all walked to the helicopter that came to pick us up, landing just about 60 yards from the burning track,” Barrera recalled. He looked at his fellow Marines and was struck by the ghastly appearance of their exposed skin, hanging, sagging away from charred uniforms, like ill-fitting latex gloves.
“The enemy had started shooting at us, and the other Marines returned fire while we boarded the helicopter, and were flown to the USS Repose, a hospital ship in Da Nang Harbor,” Barrera said. From the Repose, things went from horrific to worse, to better again for Barrera, and now he’s in a position to pave a similar path for American veterans everywhere.
[BARRERA_BEFORE]
A tough-looking Marine taking a snapshot break from infantry training at Camp Pendleton, Calif., June 1969, is the “before” image of Bobby Barrera. Three months later, Barrera was critically burned over 40 percent of his once-robust body, and in for years of excruciating treatments and surgical repairs. (Contributed photo/Bobby Barrera) (click image to enlarge)
He passed the 60-year milestone in June, and is reflective upon a lifetime of opportunity that has unfolded beneath his drive and determination since that horrific day, September 16 (Dieciseis de septiembre), 1960. Then, as his life was momentarily reduced to char, on the other side of the world, friends and family back in Del Rio were lifting cold ones to commemorate Padre Hidalgo’s 1810 “Grito” for Mexico’s independence from Spain.
Fellow Del Rio Marine Pat Dugan calls the area where Barrera nearly lost his life “one of the toughest areas of combat in Vietnam. It was called ‘the Arizona Territory’ because it was very dangerous, a free fire zone with no rules,” said Dugan, Thursday (Nov. 26).
Barrera’s arrival in Vietnam had followed a quickie wedding to the Marine Corps with no honeymoon, completing infantry training at Camp Pendleton, Calif., then advanced infantry training. “Graduation was at 6 p.m., and by midnight I was on a plane – the Flying Tigers – enroute to Alaska, Okinawa, Japan, and then on Continental to Da Nang. On Continental they treated us like royalty, like it might be our last trip, and, for some, I’m sure it was.”
Plunked down at Da Nang Air Base, the young Marine was undaunted. “Not until I got to where my unit was, and that was when it hit me. The armory was closed for the night, so I wasn’t issued a weapon, so we went to bunkers as we were told to when we heard firing. Finally, a sergeant came around and told us it was friendly artillery, not incoming rounds.”
Capable of plowing through ocean surfs for beach landings, the amphibious tracked vehicle was the transportation of choice and necessity when Charley Company, 1st Battalion, 7th Marines came ashore at Da Nang during the Vietnam War. Barrera was in a convoy of five similar “amtracs” when a 500-pound bomb blew up, spewing fire from fuel tanks over the eight men riding atop the vehicle. (Contributed photo/Bobby Barrera) (click image to enlarge)
Only six weeks later, in unspeakable pain aboard the Repose, Barrera began his first round of narcotics to dull the agony, then was airlifted to a two-day hospital visit for more stabilization in Japan. “They had us pretty drugged up, so I don’t remember much about Japan except a nurse holding a cigarette for me to smoke at the airport,” Barrera said.
Next, a C-130 Hercules cargo and transport ship launched from Wright-Patterson Air Force Base, Ohio, stopping off in San Antonio long enough to pick up a team of physicians, nurses and technicians from the prestigious burn unit of Brooke Army Medical Center. (For more perspectives on this world-renowned facility, listen to this 2006 National Public Radio broadcast report, at http://www.npr.org/templates/story/story.php?storyId=5570807)
[BARRERA_DRESS-BLUESIII]
Col. Phil Torres, representing the Marine Corps commandant, presents Barrera with his first set of dress uniform components, Tuesday (Nov. 9, 1999), as the veteran received the Leaders in Furthering Education (LIFE) Presidential Unsung Hero Award. The “blues” were a motivating factor in Barrera’s enlistment, but they had to be purchased. His private first class salary prohibited it. “Bobby, here’s your blues,” thundered Torres, 30 years later. (Contributed photo/DAV Magazine) (click image to enlarge)
Despite the life-saving treatments of physicians, compassionate care by superlative staff and surgeries that restored his face and use of one arm, his arrival at BAMC marked the beginning of levels of pain that not even the bomb explosion in Vietnam could match. Comparing his pain level aboard the Repose with his months of therapy at BAMC, Barrera commented, “The Navy was much more generous with their drugs for pain than the Army – a big, big difference.”
In the burn center, he and others with similar injuries were introduced – and reintroduced daily – to the Hubbard Tank, a T-shaped stainless steel tub much like a whirlpool bath. Unlike the whirlpool that eases stiff muscles of athletes, the Hubbard tank was a therapeutic form of torture. Technicians and nurses submerged him and “they hold you down and scrub your wounds, and then, back in bed they applied what they called ‘the butter,’” said Barrera, an ointment with restorative and therapeutic qualities, but little relief from the ever-present pain.
The tank-and-butter treatments continued daily for about 40 days, Barrera remembered, followed by three or four flights – twice a day, each day and still in great pain – to Brooke Army Medical Center for hyperbaric chamber sessions to infuse the wounds with oxygen, accelerating their healing.
Amid veterans, families, and members of all U.S. armed forces, Barrera delivers the keynote address at the Veterans Day Program at Forest Lawn Memorial Park, Hollywood Hills, Calif. The 2006 program also featured the Aztec Skydiving Team and the Notre Dame Irish Knight Marching Band. (Contributed photo/Bobby Barrera) (click image to enlarge)
Then he sustained surgeries to amputate his left arm because of infection by phycomycoses, water molds that infected wounds and could not be treated. “It’s like gangrene, only much faster, and all they can do is amputate,” Barrera explained. More amputations followed when the infections spread, then more surgeries created ears and lips, both burned off his face by the flames, and finally fittings for his right “arm” prosthesis. “I call it my hook, and sometimes, like some people who lose their glasses, I forget where I took it off, and have to go looking,” Barrera said, chuckling.
“I don’t know if I could go through this again. It was the worst thing that’s ever happened to me, obviously,” Barrera said. “Most of the survivors – including me – said we’d always carry a gun, and if we ever got burned another time, we would just shoot ourselves, rather than ever go through that again.”
Discharged from the Marine Corps in September 1970, Barrera became a patient of the U.S. Department of Veterans Affairs. Late that month, the doctors gave him leave to come home for first time for from BAMC for the holiday season. His dad, Indalecio Barrera, Del Rio’s police chief, and his mom, Elia Barrera were his support system.
“It was overwhelming relief for my parents to know that I was going to survive, but, for me, coming home was a terrible experience. I was coming home a different person. I didn’t want anyone to see me that way,” Barrera said. His lips had not been reconstructed with grafts yet, and his amputations worsened the matter. He wanted to remain cloistered, but friends and family ignored his fears and came to visit anyway. “That was the first major hurdle I had to overcome, and they made that happen for me.”
In 1973, Barrera had been through 32 surgeries, and he opted out of any more. “I came back to Del Rio … stayed here, and said, ‘No more of this,’” Barrera said. Only four blocks from his uncle’s house on West 6th Street, Barrera saw a beautiful young woman he wanted to meet, so he struggled for an opening line. Maricelia Marin owned a pet Capuchin, native to Central and South America, so Barrera struggled for an opening line, one that still makes the couple blush: “Can you show me your monkey?”
“We started going steady in November 1973. Despite my injuries, she made me feel very comfortable, so we got married in April 1974 at Saint Joseph’s Church. The turning point in my life was when I married Maricelia. She gave direction to my life,” Barrera said.
[BARRERA_KERRY]
Barrera receives a warm hug, Feb. 23, from Sen. John Kerry (D-Mass.) following Barrera’s introduction during Kerry’s visit to Sul Ross University while campaigning for now-President-elect Barrack Obama. The audience in the packed campus auditorium gave both Barrera and Kerry a standing ovation as the senator approached the podium, pausing for the moment. (LIVE! file photo/Bill Sontag) (click image to enlarge)
Two years later, his sister-in-law, Vangie, graduated from Del Rio High School and was headed for college, provoking Barrera to consider another chance for a degree from Saint Mary’s University. With his single, prosthetic arm, Barrera knew he’d not be able to turn book pages, hold notebooks still for writing. Maricelia attended classes with him – carrying his books, turning their pages, and steadying the notepaper – and she helped her husband study. “When I got my bachelor’s degree [1978, psychology], under my name I had hers written there, too,” Barrera said. “She has always given me the right balance of her love, support, and a swift kick in the butt when I most need it.”
For five years, Barrera taught Spanish and English at Del Rio High School, eventually pestering administrators long enough to add psychology to the curriculum, with him as instructor, of course. “By that time, I earned a Master of Education at Sul Ross [Alpine], in guidance and counseling, and was working part time with the Juvenile Probation Department of the 63rd Judicial District under Judge George Thurmond.” His work with youthful offenders began as a volunteer, then part time, and finally full time during which time he created the community service program for the department.
When Laughlin Air Force Base opened a Family Support Center, Barrera became its first director within the Mission Support Squadron, commanded by Col. Sidney Hirschberg. Beginning with an office of three in 1989, and ending his career there in October 1997 with a staff of 13, Barrera built the services to military personnel and their families to include financial management, answering needs before and after deployments, vocational counseling and an employment program for spouses, transition services from active duty to civilian life upon separation from service, and a base relocation program for transferees.
Barrera got involved with the Disabled American Veterans (DAV) organization while working at Laughlin, and, in 1997, he was accorded the Air Force Outstanding Federal Employee with Disabilities award, followed the next year with the DAV award, Outstanding Disabled Veteran of the Year. Since then, Barrera has acquired leadership opportunities as both educator and mentor, traveling often, and addressing hundreds of youth groups, civic clubs, military audiences and veterans organizations across the United States.
His theme for most of those is “The Four S’s of Life,” composed in Barrera’s private moments of reflection, and refined with his training and experience in psychology. They elaborate, he says, on the need within each individual facing any of life’s challenges to seek support, keep a sense of humor, maintain a spiritual relationship with God, and nourish a keen sense of self. Since the 1998 DAV award, Barrera has taught the lessons each year at “Leadership V.A..” “They’re usually 70 or 80 people from the top leadership positions – the cream of the crop, really – of the Veterans Administration: physicians, financial officers, medical division chiefs, researchers and research administrators.
Now Barrera serves as DAV senior vice commander, and is in line to be nominated for the national commander’s position at the DAV National Convention in Denver, August 2009. “If I get it, that will mean almost non-stop traveling,” Barrera said, notwithstanding the pleasure and privilege of gaining the slot. For more about the DAV, see www.dav.org.
Barrera sees abundant opportunity to continue improvements in respect accorded to veterans and treatments afforded to the wounded. “In the past, especially with World War II and Korean War veterans, there was a lot of need for improvement in health care. But in the last 10 years, there have been dramatic improvements. Now our veterans usually rate their satisfaction with VA hospitals above private for-profit institutions,” Barrera said. For more about the Department of Veterans Affairs, see www.va.gov.
He also sees important progress in how returning veterans are perceived by the American public. “I’m always emphasizing that when the Vietnam veteran returned, they didn’t receive a welcome home or the respect and gratitude of their country. Now, I see that kind of treatment not happening – thankfully – to our veterans returning from Iraq and Afghanistan. People must learn how to separate their feelings about the war from their feelings about the warrior!”
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