INDICACIONES OHBT

a siguiente lista de lesiones enfermedades y usos son aprobados mundialmente por la Asociación de Medicina Subacuática e Hiperbárica y que justifican su costo-beneficio:

* Enfermedad por descompresión
* Embolia gaseosa
* Intoxicación por monóxido de carbono
* Gangrena gaseosa
* Lesiones por radiación de tejidos blandos y óseos
* Heridas con problemas de cicatrización (Pie diabético)
* Injertos y colgajos de piel comprometidos
* Quemaduras térmicas
* Traumatismo por aplastamiento
* Reimplante de dedos y miembros
* Osteomielitis crónica
* Oclusión de arteria de la retina
* Sordera súbita
* Absceso cerebral
* Deporte
Enfermedad por descompresión:

La enfermedad de descompresión es aquella que se presenta en los buzos, posterior a estar respirando aire comprimido por largos periodos de tiempo y a profundidades mayores que las normadas. Este fenómeno se presenta al momento de subir a la superficie sin hacer las paradas de descompresión adecuadas. El motivo de dicha enfermedad es la formación de burbujas de nitrógeno en el interior de las vasos sanguíneos y tejidos que se han saturado con dicho gas (principalmente el sistema nervioso y articulaciones), por lo que esta enfermedad al final de cuentas es una enfermedad aeroembolica esto es, vasos sanguíneos ocluidos por burbujas como se ve en la fotografía electrónica

Existen clasificaciones de la enf. De descompresión, la más usual es la tipo I caracterizada por lesiones dérmicas, musculares, articulares, que pueden considerarse lesiones menores. La tipo II son aquellas que afectan el sistema nervioso, y sistema respiratorio, que potencialmente y en caso de no tratarlo rápida y adecuadamente en una cámara hiperbárica, el paciente tendrá secuelas graves que pueden ser desde complicaciones articulares, paraplejías, lesiones cerebro medulares que pueden llegar al estado de coma, o en el peor de los casos, la invalidez y muerte del paciente.

El único tratamiento etiológico para dicha patología es el uso de oxígeno hiperbático dentro de la cámara hiperbárica y utilizando tablas de descompresión comúnmente usados en todo el mundo, con ciertas modificaciones de la USA NAVY. El fundamento del tratamiento en cámara se basa en la ley de Boyle Mariotte la cual dice que al aumentar la presión sobre un gas, el volumen de el disminuirá, por lo que el tamaño de la burbuja disminuirá al someterla al incremento de presión.

Además de esta patología en paciente que bucean, existen otras que son candidatos prioritarios al tratamiento de medicina hiperbárica, como es la sobrexpansión pulmonar.

Podemos decir que estos pacientes que practican este deporte o trabajan realizando buceos, deberán tener todas las medidas de seguridad para ejercer dicha actividad, equipo adecuado, y tener en mente, dentro de la planeación del buceo, el sitio más cercano en donde se encuentre, un centro de medicina hiperbárica para en caso de presentarse alguna de estas patologías, que como muchas enfermedades, el tiempo de atención rápido determina la disminución de complicaciones severas (o hasta la muerte), ya que el único tratamiento efectivo es el uso de cámara hiperbárica.
La embolia gaseosa (enf. Aeroembólica),
Es muy parecida al mecanismo de lesión de la Enf. Por descompresión, ya que es la presencia de una burbuja de gas dentro del sistema vascular, con falta de circulación distal a la oclusión con la subsecuente falta de oxigeno tisular y muerte del tejido afectado. Se diferencia solo en que en la Enf. De descompresión la burbuja es de nitrógeno que el buzo respira dentro de la tanque de aire comprimido que lleva (compuesto por 79% nitrógeno y 21% oxigeno, misma concentración que nuestro aire del medio ambiente), y en la enf,. Aeromebolica el gas puede ser variado, como co2 (bióxido de carbono) como complicación en cirugías laparoscopicas, burbujas de aire de medio ambiente en procedimientos de acceso vascular y cirugía cardiaca, entre otras.
Intoxicación por monóxido de carbono:

El monóxido de carbono (co), es el producto de la combustión de varios materiales, por lo tanto, en todo incendio, fogata, estufa etc, el producto de dicha combustión será este producto, el cual es la causa principal de las defunciones en todo incendio mayor y no las quemadura en si como muchos piensan. Cuando el paciente sufre la quemadura muchas de las veces es por el estado de inconciencia que llego (o muerte) por la intoxación previa con el monóxido de carbono. El monóxido posterior a respirarlo se une firmemente a la hemoglobina formando un complejo denominado carboxihemoglobina , la cual desplaza al oxigeno, por lo que la capacidad de dicha proteína para transportar el oxigeno se ve comprometida, presentando datos de falta de oxigeno sistémico con los subsecuentes lesiones provocados por esto a todo nivel, pero principalmente en el sistema nervioso y cardiaco. Se estima que la mortalidad por intoxicación con monóxido de carbono es de 30-40% (casi la mitad de los pacientes). La unión de hemoglobina + monóxido de carbono se logra disociar naturalmente y a medio ambiente hasta 8 hrs. teniendo al paciente con oxigeno por mascarilla a medio ambiente hasta 2-3 hrs. y cuando se administra oxigeno 100% por tubo endotraqueal hasta 90 minutos. Ahora, se sabe que administrando oxigeno a presiones incrementadas por medio de cámara hiperbárica (oxigeno hiperbárico) esta disociación llega a ser de solo 25 a 30 minutos, con la recuperación subsecuente mas rápida y con menos lesiones tardías (como son las lesiones cerebrales tardías, muy temidas, ya que puede dejar secuelas con estados psicóticos, esquizofrénicos, neurológicos como vejigas neurogenicas, lagunas mentales, trastornos motores, etc.). Otra ventaja de la administración de oxigeno hiperbárico es que como este oxigeno se incrementa en forma diluida en el plasma y no requiere la hemoglobina para su transporte, todo nuestro cuerpo es saturado con oxigeno rápidamente sin necesidad de la hemoglobina que en ese momento esta ocupada por el monóxido de carbono, sin sufrir mayor lesión por la falta de oxigeno.

Hace 7 meses se tuvo el ejemplo mas claro de lo que hablamos, en argentina, se sufrió un incendio en una discoteca llena de muchachos, completamente sanos (caso de la discoteca del cromagnon, argentina), la mayoría de los que fallecieron fue por la intoxicación por monóxido de carbono, observamos por la televisión como varios de los socorristas sacaban los cuerpos no quemados, pero sin vida. Ahora se sabe que muchos de los que sobrevivieron sufrieron lesiones neurológicas tardías graves (visitar cualquier página de Internet en victimas del cromagnon) en donde se pone de manifiesto la angustia de las familias afectadas por la presencia de dichas complicaciones tardías en sus hijos afectados. También sabemos que 12 de ellos fueron atendidos adecuadamente con cámara hiperbárica por la Dr. Nina Sobbutina recuperándose íntegramente y sin complicaciones. Tan contundente son los datos científicos para el uso de oxigeno hiperbárico para esta enfermedad, que la ultima edición de cualquier libro o manual de emergencias medicas, dentro del capitulo de intoxación por monóxido de carbono, viene un apartado especial para esta tecnología, uno de ellos es el del autor Tintinnali.
angrena Gaseosa

La gangrena gaseosa es una forma severa de gangrena (muerte tisular) causada generalmente por el Clostridium perfringes. También puede provenir del grupo de estreptococos A , así como también por Staphylococcus aureus y Vibrio vulnificus que pueden causar infecciones similares.

La gangrena gaseosa ocurre como resultado de la infección por Clostridium, bacterias que bajo condiciones anaeróbicas (poco oxígeno), producen toxinas que causan la muerte tisular y síntomas asociados. La gangrena gaseosa no es común y sólo se presentan de 1.000 a 3.000 casos al año en los Estados Unidos.

Generalmente, la enfermedad se presenta en el sitio de un trauma o una herida quirúrgica reciente. Cerca de un tercio de los casos se presenta de manera espontánea y los pacientes a menudo tienen una enfermedad vascular subyacente (aterosclerosis o endurecimiento de las arterias), diabetes o cáncer de colon.

Esta enfermedad tiene un inicio súbito y dramático. La inflamación comienza en el sitio infectado con un tejido de aspecto entre pálido a rojo pardo, muy doloroso y edematizado. Al presionar el área edematizada con los dedos puede percibirse una sensación crepitante por la presencia de gas en el tejido. Es característica la manera como cambian rápidamente las márgenes del área infectada, con expansión del compromiso en tan sólo unos pocos minutos y destrucción completa del tejido afectado.

Cuadro Clínico
Incubación: 4 a 6 horas

Síntomas:

* Dolor
* Sensación herida tensa
* Taquicardia s/r con temperatura
* Intranquilidad
* Hipotensión
* Síntomas de shock
* Ictericia
* Coluria
* Oligoanuria

Examen Físico:

* Herida tensa o distensión abdominal.
* Secreción serosanguinolenta por la herida.
* Coloración bronceada de Belpau.
* Flictenas hemorrágicas
* Fetidez por herida.
* Edema marcado.
* Crepitación de partes blandas.

Lesiones por radiación a tejidos blandos y óseos.

La lesión por radiación podría clasificarse en aquellas que se presenta aguda, subaguda y crónicas. Las agudas son aquellas que se presentan inmediatamente posterior al uso de la radioterapia para tratar cualquier patología maligna(cáncer), el ejemplo mas clásico seria el sangrado de tubo digestivo por la lesión de la radiación al intestino; la subaguda a aquellas complicaciones que se presentan a las semanas de habérsele realizado el tratamiento con radiación, como son los procesos inflamatorios del pulmón Sec. A la radioterapia por cáncer broncogenico. Las lesiones crónicas o tardías son las que nos ocuparemos por ser las mas susceptibles de tratarse con este método y son aquellas que aparecen meses o años posterior al termino de la radioterapia.

Lesión a huesos:

Es una de las lesiones frecuentes como complicación al uso de la radioterapia en forma y tardía. Uno de los huesos mas afectados es la mandíbula, afectada posterior a la radioterapia por cáncer tanto área facial como en cuello. La lesión aparece posterior a la extracción dental o manipulación quirúrgica por cualquier motivo años después de haber recibido el tratamiento de la radiación. Se caracteriza por una lesión que no cicatriza, puede fracturar el tejido y es difícil de manejar. El éxito de la oxigenoterapia Hiperbárica se basa principalmente en la posibilidad de la angiogenesis en el sitio afectado y así poder sustituir los vasos lastimados con el procedimiento mencionado.

Lesión laringea:

Esta lesión es relativamente frecuente en los canceres de cuello, debido a la cercanía de sus estructuras, desgraciadamente, debido a la poca cura de estas lesiones con el tratamiento convencional, muchos de ellos sufren de cirugías tan agresivas como son la laringectomia (extirpación de la laringe—esencial para el habla--), este procedimiento se podría obviar al utilizar el oxigeno hiperbático en forma adjunta al tratamiento

Proctitis y enteritis por radiación (inflamación del recto e intestino):

La característica clínica es la presentación de pacientes que presentar sangrado frecuenté a través de recto, además de dolor en abdomen bajo, así como, en forma tardía, la estrechez de dichos conductos, con lo que el paciente requerirá muy posiblemente una cirugía electiva o de urgencia que será resectiva y costosa, además de la incomodidad del paciente de verse sometido a un procedimiento que lo hará obrar por medio de una colostomia en el abdomen. Existen muchos tratamientos para esta complicación, como es el uso de sustancias química, uso de láser, cirugías, etc, y así cuando existen varias técnicas para tratar alguna patología esto significa que no existe una 100% segura y adecuada. Además, estas técnicas tratan la mayoría de ellas solamente el sangrado, pero algunas veces las complicaciones por su uso pueden ser tan graves como la estenosis de estos sitios, ameritando posteriormente cirugías costosas y de alto riesgo. El uso de la oxigenoterapia Hiperbárica ataca la base de la causa que origino dicha complicación y es la lesión a la vascularización del tejido intestinal, regenerando nuevos vasos sanguíneos sanos.

Cistitis

Es la inflamación de la vejiga producida por la radiación, y se caracteriza principalmente por sangrado incohercibles, así como dolorosa, ameritando varios internamiento y no pocas hemotransfuciones. Al igual que en la lesión a intestino, el tratamiento se basa principalmente con sustancias químicas que “queman” los vaso sangrantes con los subsecuentes complicaciones de su uso. El fundamento del uso de la oxigenoterapia Hiperbárica se basa al igual, en la angiogenesis inducida. Existen varios reportes científicos y es unas las indicaciones aceptadas internacionalmente por su validez científica para tratarse con oxigeno hiperbárico.

Existen otras lesiones provocadas por la radioterapia que podrían ser susceptibles a tratarse con dicha tecnología, las cuales podrían discutirse científicamente.

Ahora, es necesario aclarar, el oxigeno hiperbárico no se usa para tratar el cáncer, la indicación es tratar las lesiones provocadas por la radioterapia y algunas provocadas por la quimioterapia, y al igual que varias de las indicaciones referidas, se usa en forma adjunta al tratamiento convencional (cirugías, curaciones, antibioticos, antiinflamatorios, etc.) Como parte fundamente en la asistencia de dichas complicaciones.
Pie diabético

El pie diabético constituye una causa importante de morbilidad en los pacientes afectos de diabetes mellitus llegando a ocasionar situaciones francamente invalidantes como consecuencia de las terapéuticas quirúrgicas que a veces son necesarias. No hay que olvidar la mortalidad que estos procedimientos y las estancias hospitalarias prolongadas pueden ocasionar.

Afecta del 4 a 10 % de la población diabética. Como tal, los problemas del pie representan una de las razones más comunes de la admisión a hospital entre pacientes diabéticos. Actualmente se reporta que la incidencia anual de ulceras del pie diabético varia de 1.2 a 3% por año. El índice de una amputación de las extremidades inferiores es 15 veces mayor en pacientes diabéticos comparado con los pacientes no diabéticos. Sin embargo, el 50% de las amputaciones en diabéticos pueden requerir una amputación del miembro contra lateral durante los primeros cuatro años después de una amputación del primer miembro.

Clasificación de pie diabético en hospitales

A Lesión pequeña, con menos de 2 cm de eritema, no incluye tejidos profundos.
B Lesión que puede llegar a hueso, con más de 2 cm eritema pero con lesión localizada.
C Lesión que llega hasta hueso, con mas de 2 cm de eritema, mal estado general.

A cada una de ellas se le anexa si es de origen neuropático, isquémico o mixto.

Clasificación de Wagner pie diabético

* Grado 0.- ninguna, pie riesgo
* Grado I.- ulceras superficiales
* Grado II.- ulcera profunda
* Grado III.- ulcera profunda mas abscesos
* Grado IV.- gangrena limitada
* Grado V.- gangrena extensa

La Medicina Hiperbárica en el pie diabético:
El incremento en la presión tisular de oxigeno inducido por la oxigenoterapia hiperbárica ha mostrado ser predictiva para el éxito en la curación aun en presencia de una presión tisular de oxigeno baja en el aire ambiente y una carencia del incremento del oxigeno normobarico.
uemaduras térmicas:

La quemadura es una lesión compleja y dinámica, caracterizada por una zona de coagulación, rodeada por áreas de estasis y circundada por un área de eritema. Se debe tratar las quemaduras para reducir al mínimo el edema, mantener la viabilidad del tejido marginal, favorecer las defensas del huésped y promover el cierre de la herida. En dichas fases actúa la oxigenoterapia Hiperbárica.

Una gran cantidad de trabajos apoyan la eficacia de la ohb en el tratamiento de quemaduras, Ikeda y Col. Observaron la reducción del edema en conejos quemados. Kelchum reporto mejora en el tiempo de curación y reducción de las infecciones en un modelo con animales, posteriormente los mismo autores demostraron mejoría en la microcirculacion, sugiriendo el uso de la ohb adjunto a la desbridación temprana de las lesiones.

Se considera que el uso de la ohb en forma temprana disminuye los costos de internamiento y de uso de quirófanos al reducir las estancias hospitalarias hasta la mitad del tiempo que normalmente utilizaría cualquier paciente con estas lesiones, y no sustituye ninguna de los métodos tradicionalmente utilizados, sugiriéndose adjuntar a ese tratamiento el uso de la ohb. En varios centros medicos de quemados, el uso de cámara Hiperbárica se encuentra adjunto a los servicios de quirófanos y unidad de cuidados intensivos para el traslado de estos pacientes sea mas rápida y eficiente, así como su rehabilitación.

Se sugiere que el uso de la ohb sea para las quemaduras consideradas graves o importantes en extensión debido que las pequeñas pueden ser tratadas convencionalmente con éxito.

raumatismo por aplastamiento (síndrome compartamental):

La isquemia aguda traumática se presenta cuando existe una lesión severa en una extremidad y la circulación de ésta se encuentra comprometida por el edema (hinchazón). Este compromiso puede ser tan severo que comprometa parte o toda la extremidad hasta el punto de presentarse muerte del tejido y necesidad de realización de amputaciones.

El problema inmediato que se presenta posterior a la agresión grave es la perfusión sanguínea deficiente para mantener viable el tejido distal, llegando a niveles de oxigeno tisular más bajo de lo considerado normal (30 mmhg), lográndose una disminución del poder bactericidad y de cicatrización de lesiones, por lo que los procesos infecciosos se perpetúan así como retardo en la cicatrización grave. Con el uso del oxigeno hiperbárico, el incremento del oxigeno sanguíneo puede llegar hasta los 2400 mmhg (normal de 90 a 100 mmhg) y a nivel de los tejidos dístales hasta 300-400 mmhg) con la subsecuente mejoría de las los tejidos hipoxico. Otro efecto importantísimo y primordial en estos casos es la disminución del edema Sec. Al trauma. La capacidad de la vasoconstricción proximal—capilares arteriales-- (no tiene ningún efecto en capilares venosos), hace que el volumen de sangre al la parte afectada disminuya, fenómeno que pudiera considerarse contraproducente, pero en realidad esto ayuda, ya que al disminuir el volumen de sangre que llega al tejido sin afectarse en la capacidad de salida de dicha sangre (capilares venosos) el edema tiende a disminuir. Afortunadamente, la disminución sanguínea a la parte afectada no se ve afectada gracias al incremento de oxigeno que va diluido en la poca sangre que le llega, esto es, le llega poca sangre pero ricamente oxigenada. Debido a este fenómeno, muchos autores se refieren al oxigeno hiperbárico como la bolsa de hielo mas efectiva que hay. Esto es aprovechado algunas de las lesiones deportivas.

El oxigeno hiperbárico reduce los índices de complicación asociados a lesiones por aplastamiento, síndrome compartamental y otras isquemias traumáticas agudas. Se ha reportado un índice de complicaciones que alcanzan el 50% en el manejo de fracturas abiertas con subsecuentes perdidas de tejido blando, los cuales podrían reducirse significativamente al ofrecerse este tratamiento en etapas iniciales

steomielitis Crónica Refractaria:

Es la infección crónica del hueso que frecuentemente ya han sido tratados médicamente por espacio de varios meses sin mejoría clínica ni radiográfica, caracterizándose por salida de material seropurulento de la lesión principal y falta de osificación adecuada del sitio óseo afectado. Normalmente el tratamiento convencional para esta enfermedad es la utilización de antibióticos por tiempos prolongados (meses), cirugía como es la llamada secuestrectomia (retiro de una porción relativamente grande de hueso desprendido), desbridaciones, curaciones, etc, que normalmente son llevadas en quirófano. No se exagera con el decir que son meses de tratamiento, así como costos elevados, sin mencionar las bajas posibilidades de curación adecuada, refiriéndose en estudios científicos que con este tratamiento el éxito seria aproximadamente de 60%. Adjuntando a este tratamiento convencional el uso de la oxigenoterapia Hiperbárica, esta posibilidad de cura se incrementa hasta el 85% y 90%. Ahora, si se toma en cuenta que dicho problema se tenga en huesos indispensables para la protección y cobertura de estructuras vitales, como son el esternon, costillas, cráneo, cara, pelvis, etc. Es obvio que la necesidad de cura es la prioridad numero uno. Como en muchos de los problemas médicos en donde se utiliza este tratamiento, deberá ser adjunto al tratamiento convencional. El fundamento de su utilización es que sabe que en el interior de la lesión ósea existe una presión parcial de oxigeno baja, por lo que las células encargadas de remodelar el hueso y osificarlo, no trabajan normalmente. Además, varios antibióticos necesitan aporte de oxigeno adecuado para cumplir su papel, como los aminoglucosidos , vancomicina y algunas sulfas.

Actualmente, se tienen reportes múltiples con base científica en donde se utiliza el oxigeno hiperbático para tratar estas complicaciones que ponen en peligro la vida del paciente y no solamente la estética de un segmento corporal, así tenemos que el Hosp. Central militar tiene una serie de casos de osteomielitis del esternon en pacientes postoperados de corazón, tratados con esta tecnología con bastante éxito
ordera Subita

La Pérdida de Audición Sensorioneural Súbita (SSHL, por su sigla en inglés), o sordera súbita, es una pérdida rápida de la audición. Puede ocurrirle a una persona de un momento a otro o dentro de un período de hasta 3 días. Debe considerarse una emergencia médica, por lo cual una persona que experimenta este tipo de desorden debe recurrir a un profesional de inmediato, el cual puede determinar si se trata de una SSHL haciendo una prueba de audición considerada de rutina. ¿Cuáles son los parámetros?

El sonido se mide en unidades llamadas decibeles. El nivel de decibeles es lo que llamamos volumen. Una conversación normal ronda un volumen de 60 decibeles. Otra manera de caracterizar el sonido es la frecuencia que presenta una onda sonora, y es lo que diferencia un tipo de sonido de otro. Si el profesional descubre una pérdida de al menos 30 decibeles (la mitad de una conversación normal) en tres frecuencias de las que nuestro oído puede captar, está en condiciones de diagnosticar una SSHL.

Mecanismos de acción de la Oxigenacion Hiperbárica

* Apoyo inmediato al tejido hipóxico y mal perfundido en áreas de compromiso circulatorio.
* Vasoconstricción sin hipoxia concomitante, lo que favorece la disminución del edema tisular.
* Atenúa la lesión por reperfusión posterior al evento isquémico.
* Activa los procesos bioenergéticos y bioreparativos.

Indicaciones de Oxigenación Hiperbárica en el deporte

I. Prevención, tratamiento y rehabilitación de aquellas lesiones o afecciones surgidas producto del ejercicio máximo sobre el organismo humano, incluyendo el overtrainig.

II. Tratamiento y rehabilitación de las lesiones traumáticas que los atletas reciben durante la práctica deportiva.

III. Preparación física del deportista, utilizando métodos científicos, para obtener altos rendimientos en cada disciplina.

Síndrome de Overtraining
La OH resuelve los trastornos Hipóxicos generales y revierte los signos isquémicos del ESG sin necesidad de interrumpir ni disminuir la carga de trabajo físico del entrenamiento.

OH En traumas deportivos
Desde 1989 en la escuela de medicina de la universidad de Dundee, Inglaterra, realizaron investigación tratando precozmente a jugadores de Foot-ball, con OH. En la mayoría de los casos las lesiones cicatrizaron en la mitad del tiempo estimado.

La mayoría de las lesiones de partes blandas reducen el aporte de sangre y producen edema, limitando la llegada de Oxígeno en un momento crítico para la reparación.

OH y aumento de la tolerancia al esfuerzo físico.
Durante altos niveles de ejercicio parece haber un metabolismo celular de tipo aeróbico, que usa las reservas de energía incrementada por la OH, cambiando esto en un metabolismo anaeróbico, solamente cuando están agotadas, resultando en un déficit de oxígeno. Se debe considerar el débito de oxígeno, como causa de incremento de la circulación sanguínea, necesaria para la función normal y para un esfuerzo cardiocirculatorio por largo tiempo.

Hyperbaric Oxygen Therapy

Hyperbaric Oxygen Therapy

Emi Latham, MD, FACEP, Assistant Clinical Professor of Emergency and Hyperbaric Medicine, University of California at San Diego
Marc A Hare, MD, Assistant Clinical Professor of Medicine, Department of Emergency Medicine, University of California San Diego Medical Center; Medical Director, Center for Wound Healing and Hyperbaric Medicine, Paradise Valley Hospital; Michael Neumeister, MD, FRCSC, FACS, Program Director, Assistant Professor, Department of Surgery, Division of Plastic Surgery, Southern Illinois University School of Medicine
Contributor Information and Disclosures

Updated: Nov 7, 2008

Introduction

Hyperbaric oxygen therapy (HBOT) is breathing 100% oxygen while under increased atmospheric pressure. HBOT is a treatment that can be traced back to the 1600s. The first well-known chamber was built and run by a British clergyman named Henshaw. He built a structure called the domicilium that was used to treat a multitude of diseases.1 The chamber was pressurized with air or unpressurized using bellows. The idea of treating patients under increased pressure was continued by the French surgeon Fontaine, who built a pressurized, mobile operating room in 1879.2 Dr. Orville Cunningham, a professor of anesthesia, ran what was known as the "SteelBall Hospital." The structure, erected in 1928, was 6 stories high and 64 feet in diameter. The hospital could reach 3 atmospheres of pressure.2 The hospital was closed in 1930 because of the lack of scientific evidence indicating that such treatment alleviated disease. It was deconstructed during World War II for scrap.

The military continued work with hyperbaric oxygen. The work of Paul Bert, who demonstrated the toxic effects of oxygen (producing grand mal seizures), as well as the work of J. Lorrain-Smith, who demonstrated pulmonary oxygen toxicity, were used with Navy divers. Exposure times to oxygen at different depths of water (and, hence, different levels of pressure) were quantified and tested based on time to convulsions.2
Oxygen Chambers

When a patient is given 100% oxygen under pressure, hemoglobin is saturated, but the blood can be hyperoxygenated by dissolving oxygen within the plasma. The patient can be administered systemic oxygen via 2 basic chambers: Type A, multiplace; and Type B, monoplace. Both types can be used for routine wound care, treatment of most dive injuries, and treatment of patients who are ventilated or in critical care.

Multiplace chamber

Multiplace chambers treat multiple patients at the same time, generally with a nurse or another inside observer who monitors the patients and assists with equipment manipulation or emergencies. Patients in a multiplace chamber breathe 100% oxygen via a mask or close-fitting plastic hood. Multiplace chambers can usually be pressurized to the equivalent of about 6 atmospheres of pressure.

If a different mixture of gas (nitrogen or helium mixture) is desired, the mixture can be given, via the mask, to only the patient, not the employee. All equipment used with patients, such as ventilators and intravenous lines, is put into the chamber with the patient. Since the employee is breathing air during the treatment (not using a mask), his or her nitrogen intake must be monitored, as this presents a risk for problems similar to those sometimes developed by scuba divers (eg, decompression sickness [DCS]).

Monoplace chamber

A monoplace chamber compresses one person at a time, usually in a reclining position. The gas used to pressurize the vessel is usually 100% oxygen. Some chambers have masks available to provide an alternate breathing gas (such as air). Employees tend to the patient from outside of the chamber and equipment remains outside the chamber; only certain intravenous lines and ventilation ducts penetrate through the hull. Newer Duoplace chambers can hold 2 people; their operation is similar to that of a monoplace chamber.


Other chambers

Two other types of chambers are worth mentioning, although they are not considered HBOT.

Topical oxygen, or Topox, is administered through a small chamber that is placed over an extremity and pressurized with oxygen. The patient does not breathe the oxygen, nor is the remainder of the body pressurized. Therefore, the patient cannot benefit from most of the positive effects of HBOT, which are systemic or occur at a level deeper than topical oxygen can penetrate (see Hyperbaric Physics and Physiology section below). Topox is based on the concept that oxygen diffuses through tissue at a depth of 30-50 microns.3 This method does not treat DCS, arterial gas emboli (AGE), or carbon monoxide (CO) poisoning.

Another problem with Topox is the design of the unit. A pressure differential must be created between the machine and open atmosphere to compress the machine. In order to keep the extremity from being pushed out of the pressurized machine, the cuff of the box must fit very tightly around the extremity, thereby creating a tourniquetlike effect. Topox is not covered by insurance, nor is it endorsed by the journal Diabetes Care for the treatment of foot ulcers.4

The other type of chamber is the portable "mild" hyperbaric chamber. These soft vessels can be pressurized to 1.5-1.7 atmospheres absolute (ATA). They are only approved by the FDA for the treatment of altitude illness. The number of these chambers has increased, as they are being used more commonly in off-label indications.
Hyperbaric Physics and Physiology

Physics of Hyperbaric Medicine

The physics behind hyperbaric oxygen therapy (HBOT) lies within the ideal gas laws.

* The application of Boyle’s law (p1 v1 = p2 v2) is seen in many aspects of HBOT. This can be useful with embolic phenomena such as decompression sickness (DCS) or arterial gas emboli (AGE). As the pressure is increased, the volume of the concerning bubble decreases. This also becomes important with chamber decompression; if a patient holds her breath, the volume of the gas trapped in the lungs overexpands and causes a pneumothorax.
* Charles’ law ([p1 v1]/T1 = [p2 v2]/T2) explains the temperature increase when the vessel is pressurized and the decrease in temperature with depressurization. This is important to remember when treating children or patients who are very sick or are intubated.
* Henry’s law states that the amount of gas dissolved in a liquid is equal to the partial pressure of the gas exerted on the surface of the liquid. By increasing the atmospheric pressure in the chamber, more oxygen can be dissolved into the plasma than would be seen at surface pressure.

The clinician must be able to calculate how much oxygen a patient is receiving. In order to standardize this amount, atmospheres absolute (ATA) are used. This can be calculated from the percentage of oxygen in the gas mixture (usually 100% in HBOT; 21% if using air) and multiplied by the pressure. The pressure is expressed in feet of seawater (fsw), which is the pressure experienced if one were descending to that depth while in seawater. Depth and pressure can be measured in many ways; some common conversions are 1 atmosphere (atm) = 33 feet of seawater (fsw) = 10 meters of sea water (msw) = 14.7 pounds per square inch (psi) = 1.01 bar.
Hyperbaric Physiology

Table 1 below summarizes the physiologic mechanisms of HBOT. Each of these is discussed in the context of the indications for HBOT later in this article.

Table 1. Physiologic Mechanisms of Hyperbaric Oxygen Therapy

CO poisoning
Crush injury/compartment syndrome
Compromised grafts and flaps
Severe blood loss anemia
Decrease gas bubble size Boyle's law Air or gas embolism
Vasoconstriction † Nylander G 8
Sukoff MH 9 Crush injury/compartment syndrome
Thermal burns
Angiogenesis Knighton DR 10 Problem wounds
Compromised grafts and flaps
Delayed radiation injury
Fibroblast proliferation/collagen synthesis Hunt TK 11 Problem wounds
Delayed radiation injury
Leukocyte oxidative killing ‡ Mader JT 12
Park MK 13
Mandell GL 14 Necrotizing soft tissue infections
Refractory osteomyelitis
Problem wounds
Reduces intravascular leukocyte adherence Zamboni WA 15
Thom SR 16, 17 Crush injury/compartment syndrome
Reduces lipid peroxidation Thom SR 18 CO poisoning
Crush injury/compartment syndrome
Toxin inhibition Van Unnik A 19 Clostridial myonecrosis
Antibiotic synergy Mirhij NJ 20
Keck PE 21
Mendel V 22
Muhvich KH 23 Necrotizing soft tissue infections
Refractory osteomyelitis
Mechanism References Clinical Application
Hyperoxygenation* Boerema I 5
Bassett BE 6
Bird AD 7 DCS/AGE
CO poisoning
Crush injury/compartment syndrome
Compromised grafts and flaps
Severe blood loss anemia
Decrease gas bubble size Boyle's law Air or gas embolism
Vasoconstriction † Nylander G 8
Sukoff MH 9 Crush injury/compartment syndrome
Thermal burns
Angiogenesis Knighton DR 10 Problem wounds
Compromised grafts and flaps
Delayed radiation injury
Fibroblast proliferation/collagen synthesis Hunt TK 11 Problem wounds
Delayed radiation injury
Leukocyte oxidative killing ‡ Mader JT 12
Park MK 13
Mandell GL 14 Necrotizing soft tissue infections
Refractory osteomyelitis
Problem wounds
Reduces intravascular leukocyte adherence Zamboni WA 15
Thom SR 16, 17 Crush injury/compartment syndrome
Reduces lipid peroxidation Thom SR 18 CO poisoning
Crush injury/compartment syndrome
Toxin inhibition Van Unnik A 19 Clostridial myonecrosis
Antibiotic synergy Mirhij NJ 20
Keck PE 21
Mendel V 22
Muhvich KH 23 Necrotizing soft tissue infections
Refractory osteomyelitis


*Most oxygen carried in the blood is bound to hemoglobin, which is 97% saturated at standard pressure. Some oxygen, however, is carried in solution, and this portion is increased under hyperbaric conditions due to Henry's law. Tissues at rest extract 5-6 mL of oxygen per deciliter of blood, assuming normal perfusion. Administering 100% oxygen at normobaric pressure increases the amount of oxygen dissolved in the blood to 1.5 mL/dL; at 3 atmospheres, the dissolved-oxygen content is approximately 6 mL/dL, which is more than enough to meet resting cellular requirements without any contribution from hemoglobin. Because the oxygen is in solution, it can reach areas where red blood cells may not be able to pass and can also provide tissue oxygenation in the setting of impaired hemoglobin concentration or function.

† Hyperoxia in normal tissues causes vasoconstriction, but this is compensated by increased plasma oxygen content and microvascular blood flow. This vasoconstrictive effect does, however, reduce posttraumatic tissue edema, which contributes to the treatment of crush injuries, compartment syndromes, and burns.

‡ HBOT increases the generation of oxygen free radicals, which oxidize proteins and membrane lipids, damage DNA, and inhibit bacterial metabolic functions. HBO is particularly effective against anaerobes and facilitates the oxygen-dependent peroxidase system by which leukocytes kill bacteria.

Additionally, evidence is growing that HBOT alters the levels of proinflammatory mediators and may blunt the inflammatory cascade. More studies are needed to further elucidate this complex interaction.

As HBOT is known to decrease heart rate while maintaining stroke volume, it has the potential to decrease cardiac output. At the same time, through systemic vasoconstriction, HBOT increases afterload. This combined effect can exacerbate congestive heart failure in patients with severe disease; however, clinically significant worsening of congestive heart failure is rare.
Contraindications

As with most medical treatments, absolute and relative contraindications exist with the use of hyperbaric oxygen therapy (HBOT).2

Table 2. Absolute Contraindications to Hyperbaric Oxygen Therapy

Absolute Contraindications Reason Contraindicated Necessary Conditions Prior to HBOT
Untreated pneumothorax Gas emboli
Tension pneumothorax
Pneumomediastinum Thoracostomy
Bleomycin Interstitial pneumonitis No treatment for extended time from use of medication
Cisplatin Impaired wound healing No treatment for extended time from use of medication
Disulfiram Blocks superoxide dismutase, which is protective against oxygen toxicity Discontinue medication
Doxorubicin Cardiotoxicity Discontinue medication
Sulfamylon Impaired wound healing Discontinue and remove medication
Absolute Contraindications Reason Contraindicated Necessary Conditions Prior to HBOT
Untreated pneumothorax Gas emboli
Tension pneumothorax
Pneumomediastinum Thoracostomy
Bleomycin Interstitial pneumonitis No treatment for extended time from use of medication
Cisplatin Impaired wound healing No treatment for extended time from use of medication
Disulfiram Blocks superoxide dismutase, which is protective against oxygen toxicity Discontinue medication
Doxorubicin Cardiotoxicity Discontinue medication
Sulfamylon Impaired wound healing Discontinue and remove medication


Relative Contraindications Reason Contraindicated Necessary Conditions Prior to HBOT
Asthma Air trapping upon ascent leading to pneumothorax Must be well controlled with medications
Claustrophobia Anxiety Treatment with benzodiazepines
Congenital spherocytosis Severe hemolysis None; HBOT for emergencies only
Chronic obstructive pulmonary disease (COPD) Loss of hypoxic drive to breathe Observation in chamber
Eustachian tube dysfunction Barotrauma to tympanic membrane Training, PE tubes
High fever Higher risk of seizures Provide antipyretic
Pacemakers or epidural pain pump Malfunction or deformation of device under pressure Ensure company has pressure-tested device and learn to what depth
Pregnancy Unknown effect on fetus (Previous studies from Russia suggest HBOT is safe.) None, but HBOT may be used in emergencies
Seizures May have lower seizure threshold Should be stable on medications; may be treated with benzodiazepines
Upper respiratory infection (URI) Barotrauma Resolution of symptoms or decongestants
Relative Contraindications Reason Contraindicated Necessary Conditions Prior to HBOT
Asthma Air trapping upon ascent leading to pneumothorax Must be well controlled with medications
Claustrophobia Anxiety Treatment with benzodiazepines
Congenital spherocytosis Severe hemolysis None; HBOT for emergencies only
Chronic obstructive pulmonary disease (COPD) Loss of hypoxic drive to breathe Observation in chamber
Eustachian tube dysfunction Barotrauma to tympanic membrane Training, PE tubes
High fever Higher risk of seizures Provide antipyretic
Pacemakers or epidural pain pump Malfunction or deformation of device under pressure Ensure company has pressure-tested device and learn to what depth
Pregnancy Unknown effect on fetus (Previous studies from Russia suggest HBOT is safe.) None, but HBOT may be used in emergencies
Seizures May have lower seizure threshold Should be stable on medications; may be treated with benzodiazepines
Upper respiratory infection (URI) Barotrauma Resolution of symptoms or decongestants
Decompression Sickness and Air Embolism

Decompression Sickness
Decompression sickness (DCS) refers to symptoms caused by blocked blood supply, damage from direct mechanical effects, or later biochemical actions from suspected bubbles evolving from inert gas dissolved in blood or tissues when atmospheric pressure decreases too rapidly.24, 25 DCS can occur after scuba diving, ascent with flying, or hypobaric or hyperbaric exposure.

DCS can be broken down into the following 3 types:

* Type I involves musculoskeletal, skin, and lymphatic tissue, and often has accompanying fatigue.
* Type II includes neurologic systems (either CNS or peripheral), cardiorespiratory, audiovestibular, and shock.25
* Type III DCS describes a syndrome that presents with symptoms that progress to a spinal deficit that may be refractory to recompression.

The bubbles causing DCS also can injure vessel endothelium, which leads to platelet aggregation, denatured lipoproteins, and activation of leukocytes, causing capillary leaks and proinflammatory events.26, 27

Hyperbaric oxygen therapy (HBOT) is used to diminish the size of the bubbles, not simply through pressure, but also by using an oxygen gradient. According to Boyle’s law, the volume of the bubble becomes smaller as pressure increases. With a change in 1.8 ATA, this is only about 30%. The bubble causing DCS is thought to be composed of nitrogen. When a tissue compartment is at equilibrium and then ascends to a decreased atmospheric pressure, nitrogen seeps out of blood, tissue, or both, causing a bubble. During HBOT, the patient breathes 100% oxygen, creating oxygen-rich, nitrogen-poor blood. This creates a gradient of nitrogen between the blood and the bubble, causing nitrogen to efflux from the bubble into the bloodstream, which, in effect, makes the bubble smaller.25

The treatment of choice is recompression. Although treatment as soon as possible has the greatest success, recompression is still the definitive treatment, and no exclusionary time from symptom onset has been established.25, 26 DCS Type I can be treated using the US Navy Treatment Table 5: 60 fsw for two 20-min periods, with a slow decompression to 30 fsw for another 20 minutes. For DCS types I, II, and III, the US Navy Treatment Table 6 is a recommended treatment protocol. Patients are placed at 60 fsw (2.4 ATA) for at least three 20-min intervals and then are slowly decompressed to 30 fsw. They remain there for at least another 2.5 hours. The time a patient is kept at 60 or 30 fsw can be extended depending on the patient’s symptom response to therapy.28
Air Embolism
Air embolism refers to bubbles in the arterial or venous circulation. Venous bubbles can result from compressed gas diving (such as scuba)29 but are often filtered through the pulmonary capillary bed. If a large volume of bubbles is noted, they may overwhelm the pulmonary filter and enter the arterial circulation.30 Arterial gas emboli (AGE) can also result from pulmonary barotrauma25 or accidental intravenous air injection or some surgical procedures.31, 32, 33, 34, 35 Symptoms usually occur within seconds to minutes of the event and can include loss of consciousness, confusion, neurological deficits, cardiac arrhythmias, or cardiac arrest.

The treatment of choice is recompression therapy. Gas embolism used to be treated with US Navy Treatment Table 6A, which required a pressure of 6 ATA. The rationale was that the larger volume of gas warranted increased pressure to force bubble redistribution or elimination. No conclusive evidence shows that this offers superior treatment to the US Navy Treatment Table 6 for most cases; however, if complete relief is not achieved after initial recompression, deeper recompression may be needed.25
Carbon Monoxide Poisoning

Carbon monoxide (CO) poisoning, whether intentional or accidental, occurs when one inhales the colorless and odorless carbon monoxide gas. Despite improved awareness and sensory alarms, multiple deaths occur each year.

CO binds to hemoglobin with 200 times the affinity of oxygen. CO also shifts the oxygen dissociation curve to the left (the Haldane effect), which decreases oxygen release to tissues. CO can also bind cytochrome oxidase aa3/C and myoglobin. Reperfusion injury can occur when free radicals and lipid peroxidation are produced.

The treatment of CO poisoning with hyperbaric oxygen therapy (HBOT) is based upon the theory that oxygen competitively displaces CO from hemoglobin. While breathing room air, this process takes about 300 minutes. While on a 100% oxygen nonrebreather mask, this time is reduced to about 90 minutes; with HBOT, the time is shortened to 32 minutes. HBOT (but not normobaric oxygen) restores cytochrome oxidase aa3/C36 and helps to prevent lipid peroxidation.37 HBOT is also used to help prevent the delayed neurologic sequelae (DNS); treatment instituted sooner is more effective.38 Multiple papers describe controversial methods and conclusions about the use of HBOT for CO poisoning.39, 37, 40, 41, 42

Patients with CO poisoning can present with myriad symptoms that they may not initially attribute to CO poisoning, as CO is considered the “great imitator” of other illnesses.18, 43, 44 Presentation can include flulike symptoms such as headache, visual changes, dizziness, and nausea. More serious manifestations include loss of consciousness, seizures, chest pain, ECG changes, tachycardia, and mild to severe acidosis.

Candidates for HBOT are those who present with morbidity and mortality risks that include pregnancy and cardiovascular dysfunction and those who manifest signs of serious intoxication, such as unconsciousness (no matter how long a period), neurologic signs, or severe acidosis. CO-hemoglobin (Hgb) level usually does not correlate well with symptoms or outcome;45, 37, 46 many patients with CO-Hgb levels of 25-30% are treated.

Pregnant females often have a CO level that is 10-15% lower than the fetus. Fetal Hgb not only has a higher affinity for CO but also has a left-shifted oxygen dissociation curve compared with adult hemoglobin. Exposure to CO causes an even farther leftward shift, in both adult and fetal hemoglobin, and decreased oxygen release from maternal blood to fetal blood and from fetal blood to fetal tissues. Pregnant patients with CO-Hgb levels greater than 10% should be treated with HBOT.2

HBOT is administered at 2.5-3 ATA for periods of 60-100 minutes. Depending on patient presentation and response, 1-5 treatments are recommended.3
Enhancement of Healing in Selected Problem Wounds

Normal wound healing proceeds through stages of hemostasis, removal of infectious agents, resolution of the inflammatory response, reestablishment of a connective tissue matrix, angiogenesis, and resurfacing. Problem (or chronic) wounds are those which do not proceed completely through this process because of any number of local and systemic host factors. For this reason, chronic wounds are often categorized as diabetic wounds, venous stasis ulcers, arterial ulcers, or pressure ulcers.

Wounds that fail to heal are typically hypoxic.47 Multiple components of the wound healing process are affected by oxygen concentration or gradients, which explains why hyperbaric oxygen therapy (HBOT) can be an effective therapy to treat chronic wounds. Angiogenesis occurs in response to high oxygen concentration.10 This is likely a multifactorial effect of HBOT. First, fibroblast proliferation and collagen synthesis are oxygen dependent,11 and collagen is the foundational matrix for angiogenesis. In addition, HBOT likely stimulates growth factors involving angiogenesis and other mediators of the wound healing process.48 Hyperbaric oxygen also has been shown to have direct and indirect antimicrobial activity; in particular, it increases intracellular leukocyte killing.13, 14, 12

Diabetic lower extremity ulcers have been the focus of most wound research in hyperbaric medicine, since the etiology of these wounds is multifactorial, and HBOT can address many of these factors. Several randomized controlled clinical trials have studied HBOT for the treatment of diabetic lower extremity wounds.49, 50, 51, 52 Additionally, many more prospective, noncontrolled clinical trials and retrospective trials have been completed. Based on the body of evidence, major insurance carriers around the world now endorse the use of HBOT for the treatment of diabetic lower extremity wounds that show evidence of deep soft tissue infection, osteomyelitis, or gangrene. HBOT has been shown to reduce the amputation rate in patients with diabetic ulcers as well.49, 50, 52

In an effort to select patients appropriately for HBOT, various objective vascular evaluation methods have been used, including transcutaneous oximetry, capillary perfusion pressure, laser Doppler, and other types of vascular studies. Debate is ongoing regarding which method provides the most reliable data and whether these methods are more useful than other clinical markers of wound failure.

Note that HBOT should be used in conjunction with a complete wound healing care plan. As with all chronic wounds, other underlying host factors (eg, large vessel disease, glycemic control, nutrition, infection, presence of necrotic tissue, offloading) must be simultaneously addressed in order to have the highest chance of successful healing and functional capacity.

Because the goals of HBOT for wound healing include cellular proliferation and angiogenesis, HBOT is generally performed daily for a minimum of 30 treatments. Treatment is generally at 2 to 2.4 ATA for a total of 90 minutes of 100% oxygen breathing time. Based on the response to therapy, extended courses of therapy may be indicated.
Compromised Skin Grafts and Flaps

Most skin grafts and flaps in normal hosts heal well. In patients with compromised circulation, this may not be the case. Patients with diabetes or vasculopathy from another etiology and patients who have irradiated tissue are particularly subject to flap or graft compromise. In these patients, hyperbaric oxygen therapy (HBOT) has been shown to be useful. Unfortunately, if patients are not identified early, the initial flap or graft may be lost. Even in such cases, patients can significantly benefit from HBOT to prepare the wound bed for another graft or flap procedure; the procedure then has a higher chance of success following HBOT.

Over 30 animal studies have shown efficacy of HBOT in preserving both pedicled and free flaps in multiple models. These models looked at arterial, venous, and combined insults in addition to irradiated tissues. While improvement was observed regardless of the type of vascular defect, those with arterial insufficiency and radiation injury showed the greatest improvement.

Human case studies showing benefit of hyperbaric treatment for flap survival were first reported in 1966. A controlled clinical trial showing improved survival of split skin grafts followed shortly thereafter.53 This was corroborated by a later clinical trial.54 Additionally, evidence exists of benefit for flaps in post-irradiated tissue in human subjects.55

As the underlying pathophysiology of all compromised grafts and flaps is hypoxia, HBOT benefits patients by reducing the oxygen deficit. A unique mechanism of action of HBOT for preserving compromised flaps is the possibility of closing arteriovenous shunts.56 Additionally, the same mechanisms of action that improve wound healing, namely, improved fibroblast and collagen synthesis11 and angiogenesis,10 also are likely to benefit a compromised graft or flap.

The current standard for HBOT to treat a compromised graft or flap includes twice daily treatment until the graft or flap appears viable and then once per day until completely healed. The initiation of HBOT should be expedited. In general, benefit should be seen by 20 treatments; if it is not, continuation of therapy should be reviewed. However, the cost of creating a complex flap is high, which makes HBOT cost-effective for this diagnosis. Of course, patients with compromised flaps need surgical attention to the arterial and venous supply, appropriate local management, and maximization of medical support.
Crush Injury and Compartment Syndrome

Acute peripheral traumatic ischemia includes those injuries that are caused by trauma that leads to ischemia and edema; a gradient of injury exists. This category contains crush injuries as well as compartment syndrome. Crush injuries often result in poor outcome because of the body’s attempt to manage the primary injury. The body then develops more injury due to the reperfusion response. Injuries are graded using definite points on a severity scale. The commonly referenced system is the Gustilo classification,57 but other classification scales are available.

The benefits of hyperbaric oxygen therapy (HBOT) for this indication include hyperoxygenation by increasing oxygen within the plasma. HBOT also induces a reduction in blood flow58, 59 that allows capillaries to resorb extra fluid, resulting in decreased edema. As a gradient of oxygenation is based on blood flow, oxygen tissue tensions can be returned, allowing for the host defenses to properly function.11 Animal studies suggest that a decreased neutrophil adherence to ischemic venules is observed with elevated oxygen pressures (2.5 ATA).15, 16 Reperfusion injury is diminished, as HBOT generates scavengers to destroy oxygen radicals.60

Compartment syndrome also is a continuum of injury that occurs when compartment pressures exceed the capillary perfusion pressures. The extent to which the injury has affected tissues is unclear, even after surgical intervention.61, 58, 62 HBOT is not recommended during the “suspected” stage of injury, when compartment syndrome is not yet present but may be impending. HBOT is beneficial during the impending stage, when objective signs are noted (pain, weakness, pain with passive stretch, tense compartment). With these signs, even if surgery is not elected because of compartment pressures or patient stability, HBOT is indicated. Once the patient has undergone fasciotomy, HBOT can be used to help decrease morbidity.3

HBOT should be started as soon as is feasible, ideally within 4-6 hours from time of injury. After emergent surgical intervention, the patient should undergo HBOT at 2-2.5 ATA for 60-90 minutes. For the next 2-3 days, perform HBOT 3 times daily, then twice daily for 2-3 days, and then daily for the next 2-3 days.2
Necrotizing Soft Tissue Infections

These infections may be single aerobic or anaerobic but are more often mixed infections that often occur as a result of trauma, surgical wounds, or foreign bodies, including subcutaneous and muscular injection of contaminated street drugs. They are often seen in compromised hosts who have diabetes or a vasculopathy of another type. These infections are named based on their clinical presentation and include necrotizing fasciitis, clostridial and nonclostridial myonecrosis, and Fournier gangrene.

Regardless of the depth of the tissue invasion, these infections have similar pathophysiology that includes local tissue hypoxia, which is exacerbated by a secondary occlusive endarteritis.63 Intravascular sequestration of leukocytes is common in these types of infections, mediated by toxins from specific organisms.64 Clostridial theta toxin appears to be one such mediator. All of these factors together foster an environment for facultative organisms to continue to consume remaining oxygen, and this promotes growth of anaerobes.

The cornerstones of therapy are wide surgical debridement and aggressive antibiotic therapy. Hyperbaric oxygen therapy (HBOT) is used adjunctively with these measures, as it offers several mechanisms of action to control the infection and reduce tissue loss. First, HBOT is toxic to anaerobic bacteria.65 Next, HBOT improves polymorphonuclear function and bacterial clearance.12, 66 Based on results of work related to CO poisoning, HBOT may decrease neutrophil adherence based on inhibition of beta-2 integrin function.17, 16 Further investigation is needed to see if this mechanism is at work in necrotizing infections as well. In the case of clostridial myonecrosis, HBOT can stop the production of the alpha toxin.19, 67 Finally, limited evidence indicates that HBOT may facilitate antibiotic penetration or action in several classes of antibiotics, including aminoglycosides,20 cephalosporins,22 sulfonamides21 and amphotericin.23

Multiple clinical studies suggest that HBOT is efficacious in the treatment of necrotizing soft tissue infections. These include case series, retrospective and prospective studies, and non-randomized clinical trials. They suggest significant reductions in mortality and morbidity. The reduction in mortality was remarkably similar in 2 studies: 34% (untreated) vs. 11.9% (treated) in one study;68 38% (untreated) vs. 12.5% (treated) in the other.69 In another study,70 the treated group had more patients with diabetes and more patients in shock and still had significantly less mortality (23%) than the untreated group (66%). Clinical studies involving patients with Fournier gangrene treated with HBOT bear similar results.

Initial HBOT is aggressively performed at least twice per day in coordination with surgical debridement. Typically, a treatment pressure ranging from 2.0-2.5 ATA is adequate. However, in the specific case of clostridial myonecrosis, 3 ATA is often used to ensure adequate tissue oxygen tensions to stop alpha toxin production. For the same reason, HBOT should be initiated as quickly as possible in this circumstance and performed 3 times in the first 24 h if at all feasible.
Intracranial Abscess
The disorders considered in treatment of intracranial abscesses (ICA) include subdural and epidural empyema as well as cerebral abscess.2 Studies from around the world have reviewed mortality from ICA with a resulting mortality of about 20%.71 HBOT has multiple mechanisms that make it useful as an adjunctive therapy for ICA.

HBOT induces high oxygen tensions in tissue, which helps to prevent anaerobic bacterial growth, including organisms commonly found in ICA.72, 73, 74, 75 HBOT can also help reduce increased intracranial pressure (ICP) and its effects are proposed to be more pronounced with perifocal brain swelling.9, 76, 77 As discussed earlier, HBOT can enhance host immune systems and the treatment of osteomyelitis.78 Candidates for adjunctive HBOT are patients who have multiple abscesses, who have an abscess that is in a deep or dominant location, whose immune systems are compromised, in whom surgery is contraindicated, who are poor candidates for surgery, and who exhibit inadequate response despite standard surgical and antibiotic treatment.3

HBOT is administered at 2.0-2.5 ATA for 60-90 minutes per treatment. HBOT may be 1-2 sessions per day. The optimized number of treatments has not been determined.3
Delayed Radiation Injury

Radiation therapy causes acute, subacute, and delayed injuries. Acute and subacute injuries are generally self-limited. However, delayed injuries are often much more difficult to treat and may appear anywhere from 6 months to years after treatment. They generally are seen after a minimum dose of 6000 cGy. While uncommon, these injuries can cause devastating chronic debilitation to patients. Notably, they can be quiescent until an invasive procedure is performed in the radiation field. Injuries are generally divided into soft tissue versus hard tissue injury (osteoradionecrosis [ORN]).

While the exact mechanism of delayed radiation injury is still being elucidated, the generally accepted explanation is that an obliterative endarteritis and tissue hypoxia lead to secondary fibrosis.79 Hyperbaric oxygen therapy (HBOT) was first used to treat ORN of the mandible. Based on the foundational clinical research of Marx,80 multiple subsequent studies supported its use. The success of HBOT in treating ORN then led to its use in soft tissue radionecrosis as well.
Osteoradionecrosis

Marx demonstrated conclusively that ORN is primarily an avascular aseptic necrosis rather than the result of infection.80 He developed a staging system for classifying and planning treatment,81 which is largely accepted throughout the oromaxillofacial surgery community.

* Stage I - Exposed alveolar bone: The patient receives 30 HBOT treatments and then is reassessed for bone exposure, granulation, and resorption of nonviable bone. If response is favorable, an additional 10 treatments may be considered.
* Stage II - A patient who formerly was Stage I with incomplete response or failure to respond: Perform transoral sequestrectomy with primary wound closure followed by an additional 10 treatments.
* Stage III - A patient who fails stage II or has an orocutaneous fistula, pathologic fracture, or resorption to the inferior border of the mandible: The patient receives 30 treatments, transcutaneous mandibular resection, wound closure, and mandibular fixation, followed by an additional 10 postoperative treatments.
* Stage IIIR - Mandibular reconstruction 10 weeks after successful resolution of mandibular ORN: The patient receives 10 additional postoperative HBOT treatments.

The cornerstone of therapy is to begin and complete (if possible) HBOT prior to any surgical intervention and then to resume HBOT as soon as possible after surgery. Only in this way is adequate time allowed for angiogenesis to support postoperative healing. For patients with a history of significant radiation exposure, but no exposed bone, who require oral surgery, many practitioners suggest 20 HBOT treatments prior to surgery and 10 treatments immediately following surgery. Feldmeier has published an excellent review of this literature.82
Soft Tissue Radionecrosis

While soft tissue radionecrosis also is rare, it causes significant morbidity, depending on the site of injury. All of these injuries lead to significant local pain. Both radiation cystitis and radiation proctitis can result in severe blood loss with symptomatic anemia, and radiation cystitis may cause obstructive uropathy secondary to fibrosis and blood clot formation. Radionecrosis of the neck and larynx can lead to dysphagia and respiratory obstruction. Irradiated skin develops painful, necrotic wounds that do not heal with standard wound healing care plans.

For each of these subpopulations of soft tissue radionecrosis, published case series and prospective, nonrandomized clinical trials corroborate one another, providing a degree of external validity. Larger studies are warranted. A national registry is currently being evaluated, from which more powerful conclusions may be forthcoming. Currently, the largest group of reported patients treated with HBOT for soft tissue radionecrosis are those with radiation cystitis. At least 15 publications, representing almost 200 patients, report a combined success rate in the 80% range. The 2 largest studies were published by Bevers83 and Chong.84
HBOT and Carcinogenesis

Practitioners and patients are often concerned that HBOT may foster recurrence of malignancy or promote the growth of an existing tumor. This is largely because of the known angiogenic effective of HBOT. Feldmeier has reviewed this subject extensively. Malignant angiogenesis appears to follow a different pathway than angiogenesis related to wound healing. His review of the literature suggests that the risk is low.85
Refractory Osteomyelitis

Refractory osteomyelitis is defined as acute or chronic osteomyelitis that is not cured after appropriate interventions. More often than not, refractory osteomyelitis is seen in patients whose systems are compromised. This condition often results in nonhealing wounds, sinus tracts, and, in the worst case, more aggressive infections that require amputation.

Mader and Niinikoski showed that hyperbaric oxygen therapy (HBOT) is capable of elevating oxygen tension in infected bone to normal or above normal levels.86, 12 Since polymorphonuclear (PMN) function requires adequate oxygen concentration, this is a significant mechanism by which HBOT helps to control osteomyelitis, as demonstrated by Mader in the same study.12

A unique mechanism by which HBOT is beneficial in osteomyelitis is in promoting osteoclast function. The resorption of necrotic bone by osteoclasts is oxygen-dependent. This has best been demonstrated in animal models of osteomyelitis.87

Additionally, as previously mentioned, HBOT facilitates the penetration or function of antibiotic drugs. Other properties of HBOT previously discussed, such as neovascularization and blunting the inflammatory response, likely provide additional benefit.

Convincing animal evidence supports the use of HBOT in the treatment of osteomyelitis. Clinical studies are somewhat problematic, however, because osteomyelitis has so many different presentations that comparisons become difficult. This is compounded by the small study sizes found in the literature; however, these do suggest benefit of HBOT for refractory osteomyelitis in humans.

One specific subset of osteomyelitis that merits special attention is malignant otitis externa. This progressive pseudomonal osteomyelitis of the ear canal can spread to the skull base and become fatal. Davis et al published a study of 17 patients with malignant otitis externa, all of whom showed dramatic improvement with the addition of HBOT to standard surgical debridement and antibiotic therapy.88
Thermal Burns

Thermal burns present a multifactorial tissue injury that culminates in a marked inflammatory response with vascular derangement from activated platelets and white cell adhesion with resultant edema, hypoxia, and vulnerability to severe infection. Poor white cell function caused by the local environment exacerbates this problem. Hyperbaric oxygen therapy (HBOT) addresses each of these pathophysiological derangements, and can, therefore, make a significant difference in patient outcomes. These mechanisms of action have been discussed above.

Multiple animal studies support the utility of HBOT for treatment of thermal burns. Human studies ranging from case series to randomized clinical trials have supported the potential benefit of HBOT in burn treatment. These include a small randomized study by Hart89 that demonstrated improved healing and decreased mortality. Niezgoda90 showed increased healing in a standardized human burn model. In a series of publications, Cianci91, 92 suggests significant reduction in length of hospital stay, need for surgery, and cost.

Because of the goals of therapy, HBOT is begun as soon as possible after injury, with a goal of 3 treatments within the first 24 hours and then twice daily. Length of treatment depends on the clinical impairment of the patient and the extent of and response to grafting. Special attention must be given to fluid management and chamber and patient temperature to avoid undue physiologic stress to the patient as well as potential complications of treatment (ie, oxygen toxicity).
Exceptional Anemia

Patients who develop exceptional anemia have lost significant oxygen carrying capacity in the blood. These patients become candidates for hyperbaric oxygen therapy (HBOT) when they are unable to receive blood products because of religious or medical reasons. The major oxygen carrier in human blood is hemoglobin, transporting 1.34 mL of oxygen per gram. Borema performed an experiment in the 1960s in which exsanguinated pigs (who had only plasma in their vasculature) were able to sustain life under hyperbaric conditions.5

The body generally uses 5-6 vol% (mL of O2 per 100 mL of blood);93 under 3 ATA, 6 vol% of molecular oxygen can be dissolved into the plasma.94 The CNS and cardiovascular systems are the two most oxygen-sensitive systems in the human body.93, 95 Oxygen debt is one way of determining a patient’s need to start or continue HBOT. A cumulative oxygen debt is the time integral of the volume of oxygen consumption (VO2) measured during and after shock insult minus the baseline VO2 required during the same time interval.3 Patients who have a debt >33 L/m2 do not survive, whereas patients with debts ≤9 usually recover.2

HBOT is administered at 2-3 ATA for periods of up to 4 hours per treatment. As many as 3-4 sessions a day may be necessary, depending on a patient’s clinical picture. Treatments should continue until the patient can receive blood products, no longer demonstrates end stage organ failure, or no longer has a calculated oxygen debt.3

Complications and Special Concerns

As with any medical therapy, treatment brings both risks and benefits. One of the more frequently seen injuries caused by hyperbaric oxygen therapy (HBOT) is barotrauma (ie, injuries caused by pressure as a result of an inability to equalize pressure from an air-containing space and the surrounding environment).2, 3

Table 4. Complications to Hyperbaric Oxygen Therapy

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Table
Complication Presentation Treatment
Barotrauma
Middle ear (URI, Eustachian tube dysfunction) Ear pain, fullness
Muffled hearing Autoinflation technique
Pseudoephedrine/oxymetazoline
Tympanostomy tubes
Wait for URI resolution
Sinus Sinus pain or bleeding Oxymetazoline/pseudoephedrine
Antihistamines
Steroid nasal spray
Dental Tooth pain Replacement of filling or crown (allows trapped air bubble to escape)
Pulmonary Dry cough
Chest pain or burning
Decreased vital capacity No breath-holding
Thoracostomy (if pneumothorax)
Increase decompression time
Round or oval window blowout Immediate deafness
Tinnitus
Nystagmus, vertigo, or both Discontinue Valsalva
Refer to ENT
Visual refraction change
Lens morphology Progressive myopia with prolonged number of treatments Most resolve spontaneously when treatment finished
Cataracts Clouding of vision Prescreen for existing cataracts
HBOT does not influence cataract formation
Oxygen toxicity
CNS (Incidence 0.7 per 10,000 treatments at 2.4 ATA) Seizure Removal from oxygen source
Resume HBOT with shorter oxygen treatment periods
Does not require medication
Treat hypoglycemia if present
Treat fever if present
Pulmonary Dry cough
Chest pain or burning
Decreased vital capacity Decrease total oxygen exposure time (including outside HBOT)
Complication Presentation Treatment
Barotrauma
Middle ear (URI, Eustachian tube dysfunction) Ear pain, fullness
Muffled hearing Autoinflation technique
Pseudoephedrine/oxymetazoline
Tympanostomy tubes
Wait for URI resolution
Sinus Sinus pain or bleeding Oxymetazoline/pseudoephedrine
Antihistamines
Steroid nasal spray
Dental Tooth pain Replacement of filling or crown (allows trapped air bubble to escape)
Pulmonary Dry cough
Chest pain or burning
Decreased vital capacity No breath-holding
Thoracostomy (if pneumothorax)
Increase decompression time
Round or oval window blowout Immediate deafness
Tinnitus
Nystagmus, vertigo, or both Discontinue Valsalva
Refer to ENT
Visual refraction change
Lens morphology Progressive myopia with prolonged number of treatments Most resolve spontaneously when treatment finished
Cataracts Clouding of vision Prescreen for existing cataracts
HBOT does not influence cataract formation
Oxygen toxicity
CNS (Incidence 0.7 per 10,000 treatments at 2.4 ATA) Seizure Removal from oxygen source
Resume HBOT with shorter oxygen treatment periods
Does not require medication
Treat hypoglycemia if present
Treat fever if present
Pulmonary Dry cough
Chest pain or burning
Decreased vital capacity Decrease total oxygen exposure time (including outside HBOT)

Pediatric Considerations
Pediatric patients also have special concerns. The proportion of surface area to body mass is much greater in children than in adults. As temperature in the chamber can fluctuate, care must be taken to ensure the child remains warm without causing hyperthermia. This can be more difficult in a monoplace chamber because the patient cannot be physically reached from outside the chamber to provide blankets or warmed water as heat sources. Unless children can focus and equalize their ears, consideration for placement of tympanostomy tubes should be discussed with the parents to prevent middle ear barotrauma.

Oxygen administration is easy in a monoplace chamber because the chamber is pressurized with oxygen. Multiplace chambers can fashion equipment to fit the child. A neck ring can be fitted over the child’s torso, or, if the child is small enough, 2 hoods can be placed together to form a capsule around the child. Care must be taken when treating patients with ductal dependent lesions, as oxygen is a signal for ductus arteriosus closure. This has not been a documented problem in pregnancy. Bronchopulmonary dysplasia in a preterm infant, as is associated with mechanical ventilation and elevated oxygen tensions, can be accelerated with HBOT.2
Potential New Indications for Hyperbaric Oxygen Therapy

Central Retinal Vein Occlusion

Central retinal vein occlusion is a relatively common cause of visual loss. The main risk factors include diabetes, glaucoma, hypertension, and hypercoagulable conditions. Hyperbaric oxygen therapy (HBOT) provides oxygenation to the ischemic retina and diminishes retinal edema, allowing the retina to revascularize. The effect is sometimes rapid, and visual acuity may be significantly improved or nearly restored in a few treatments.

Multiple case reports, series, and retrospective analyses now show potential benefit.96, 97 Given the lack of other consistently efficacious treatments for this devastating condition, and the relative safety of HBOT, HBOT will likely be officially recommended for use by the Undersea and Hyperbaric Medical Society (UHMS) in late 2008.
Sudden Deafness
Sudden sensorineural hearing loss (SSHL) is a relatively rare cause of total sensorineural hearing loss cases. SSHL has many causes, but idiopathic SSHL still predominates. The condition is thought to be related to inner ear hypoxia, and HBOT increases the partial pressure of oxygen (pO2) in the inner ear.

The effectiveness of HBOT in SSHL as either primary or adjunctive therapy has not been conclusively established. Although some studies have shown improvement in hearing after HBOT, others have not. Because two thirds or more of these patients have spontaneous recovery, selection of patients and evaluation of results is easily confounded. HBOT has been adopted for treatment of SSHL in some countries but has not gained widespread acceptance in the United States and is not an approved indication by the UHMS.
Bisphosphonate-Associated Osteonecrosis
Bisphosphonates are used widely for the management of metastatic cancer in bone, osteoporosis, Paget disease of bone, and acute hypercalcemia. The exact mechanism of the pathophysiology that lead to osteonecrosis is unknown. However, bisphosphonates bind to bone and incorporate in the osseous matrix. During bone remodeling, they are taken up by osteoclasts, which induces cell death. They also inhibit osteoblast-mediated osteoclastic resorption and have antiangiogenic properties. As a result, bone turnover is suppressed; therefore, little physiologic remodeling occurs. The most vulnerable site appears to be the jaw.

No reliable treatment for this condition is currently available. Case studies using HBOT to treat bisphosphonate-associated osteonecrosis prompted a pilot study with favorable results. Therefore, a randomized clinical trial is currently underway to evaluate the efficacy of HBOT for this condition.
FURTHER READING

Jain KK, Neubauer RA. Textbook of Hyperbaric Medicine. 4th ed., revised. Seattle, Wash: Hogrefe and Huber Publishing; 2004.

Neuman T, Thom S, eds. Physiology and Medicine of Hyperbaric Oxygen Therapy. Philadelphia, Pa: Saunders/Elsevier; 2008.
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Media file 1: Rectangular hyperbaric chamber.
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Rectangular hyperbaric chamber.

Rectangular hyperbaric chamber.
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Media file 2: Interior of rectangular chamber.
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Interior of rectangular chamber.

Interior of rectangular chamber.
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Media file 3: Cylindrical multiplace chamber.
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Cylindrical multiplace chamber.

Cylindrical multiplace chamber.
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Media file 4: Monoplace chamber.
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Monoplace chamber.

Monoplace chamber.
Keywords

hyperbaric oxygen, HBO, HBOT, oxygen therapy, hyperbaric oxygen chamber, HBO therapy, HBO treatment, hyperbaric medicine, hyperbaric therapy, diving medicine, decompression sickness, arterial gas embolism, diving accidents, radiation-damaged tissue, radionecrosis, osteoradionecrosis, radiation necrosis, soft tissue infections, necrotizing fasciitis, osteomyelitis, clostridial myonecrosis, non-healing wound, chronic wound, carbon monoxide poisoning, CO poisoning, compromised graft, compromised flap, crush injury, compartment syndrome, reperfusion injury

References

Acknowledgments

Multiplace hyperbaric chamber photos courtesy of OxyHeal Health Group, Inc.

Monoplace hyperbaric chamber photos courtesy of Sechrist Industries, Inc.


Further Reading

Further Reading

Jain KK, Neubauer RA. Textbook of Hyperbaric Medicine. 4th ed., revised. Seattle, Wash: Hogrefe and Huber Publishing; 2004.

Neuman T, Thom S, eds. Physiology and Medicine of Hyperbaric Oxygen Therapy. Philadelphia, Pa: Saunders/Elsevier; 2008.

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Kiryu J, Ogura Y. Hyperbaric oxygen treatment for macular edema in retinal vein occlusion: relation to severity of retinal leakage. Ophthalmologica. 1996;210(3):168-70. [Medline].
97.

Krott R, Heller R, Aisenbrey S, et al. Adjunctive hyperbaric oxygenation in macular edema of vascular origin. Undersea Hyperb Med. Winter 2000;27(4):195-204. [Medline].

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Further Reading
Further Reading

Further Reading

Jain KK, Neubauer RA. Textbook of Hyperbaric Medicine. 4th ed., revised. Seattle, Wash: Hogrefe and Huber Publishing; 2004.

Neuman T, Thom S, eds. Physiology and Medicine of Hyperbaric Oxygen Therapy. Philadelphia, Pa: Saunders/Elsevier; 2008.
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Keywords

hyperbaric oxygen, HBO, HBOT, oxygen therapy, hyperbaric oxygen chamber, HBO therapy, HBO treatment, hyperbaric medicine, hyperbaric therapy, diving medicine, decompression sickness, arterial gas embolism, diving accidents, radiation-damaged tissue, radionecrosis, osteoradionecrosis, radiation necrosis, soft tissue infections, necrotizing fasciitis, osteomyelitis, clostridial myonecrosis, non-healing wound, chronic wound, carbon monoxide poisoning, CO poisoning, compromised graft, compromised flap, crush injury, compartment syndrome, reperfusion injury
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Contributor Information and Disclosures
Author

Emi Latham, MD, FACEP, Assistant Clinical Professor of Emergency and Hyperbaric Medicine, University of California at San Diego
Emi Latham, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose
Coauthor

Marc A Hare, MD, Assistant Clinical Professor of Medicine, Department of Emergency Medicine, University of California San Diego Medical Center; Medical Director, Center for Wound Healing and Hyperbaric Medicine, Paradise Valley Hospital
Marc A Hare, MD is a member of the following medical societies: American College of Emergency Physicians and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose

Michael Neumeister, MD, FRCSC, FACS, Program Director, Assistant Professor, Department of Surgery, Division of Plastic Surgery, Southern Illinois University School of Medicine
Michael Neumeister, MD, FRCSC, FACS is a member of the following medical societies: American Academy of Dermatology, American Association for Hand Surgery, American Burn Association, American Medical Association, American Society of Plastic Surgeons, Canadian Medical Association, College of Physicians and Surgeons of Alberta, College of Physicians and Surgeons of Ontario, Pacific Dermatologic Association, Royal College of Physicians and Surgeons of Canada, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose
Medical Editor

Erik D Schraga, MD, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Disclosure: Nothing to disclose
Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock for Investment from broker recommendation; Avanir Pharma Stock for Investment from broker recommendation
Chief Editor

Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary for Employment

¿Que tratamiento estaría indicado en la necrobiosis lipoidica diabeticorum?

¿Que tratamiento estaría indicado en la necrobiosis lipoidica diabeticorum?
Respuesta
La búsqueda sobre necrobiosis lipoidica, ha localizado tán solo 8 ensayos clínicos, de los cuales 4 están realizados con un grupo control y todos realizados con un número pequeño de casos. La mayoría de artículos publicados, están basados en pequeñas series de casos (en muchas ocasiones de uno a cinco) con diferentes terapias. Reproducimos la revisión realizada en UpToDate 1 sobre el tratamiento de esta entidad clínica: “Habitualmente, el tratamiento de la necrobiosis lipoidica no es óptimo y debe ser mantenido de forma crónica. Para el tratamiento inicial valore la administración de un corticoide tópico de potencia moderado (por ejemplo crema de acetónido de triamcinolona al 0,1% tres veces al día). Si no hay mejoría en dos semanas, considere la utilización de dipropionato de betometasona dos veces al día, monitorizando la presencia de atrofia de piel. La inyección intralesional de triamcinolona (5 á 10 mg/ml de triamcinolona diluido con lidocaína hasta reducir a 2.5 a 5mg /ml) puede ser realizada con precaución si no hay úlceras y el riesgo percibido es bajo. Evite la utilización de corticoides tópicos o inyectables si existe cualquier tipo de ulceración y reduzca la potencia y la duración del corticoide a la más baja que pueda controlar la inflamación. La interconsulta o referencia del paciente están a menudo indicadas. Un informe basado en un caso informa de la posibilidad de que la crema de tacrolimus pueda ser de algún beneficio en etapas precoces de la enfermedad”. “Para enfermedad ulcerativa, un número de casos con tratamiento exitoso con agentes como ciclosporina, factor estimulante de la colonia granulocitos-macrófagos, altas dosis de nicotinamida, oxígeno hiperbárico, corticoides sistémicos, e infliximab han sido informados. Sin embargo no se ha identificado una terapia consistente y beneficiosa“. No incluidos en la revisión de Up todate, destacan: *Una serie de 30 pacientes tratados con psoralen más radiaciones ultravioleta A (PUVA) 2,muestran mejoría o desaparición de los síntomas en 16 pacientes, 10 no mejoraron y en cuatro la evolución fue mala. *Un ensayo clinico controlado (16 pacientes) con bajas dosis de acido acetil salicilico 3 o con dipiridamol (14 pacientes) 4 no mostraron mejoría en relación al placebo. La revisión publicada por e-medicine 5 concluye que no hay una definida una terapìa efectiva. Además del tratamiento con corticoides, informa de publicaciones de casos clínicos con mejoría mediante terapia con: nicotinamida, pentoxifilina, aspirina, dipiridamol, ticlopidina, clofazimina, tretinoina ,colágeno bovino tópicamente e inyecciones intralesionales con heparina. Referencias:1. Goldstein BG.Metabolic and inherited diseases affecting the skin. In: UpToDate, Rose, BD (Ed), UpToDate, Wellesley, MA, 2005. 2.De Rie MA, Sommer A, Hoekzema R, Neumann HA.Treatment of necrobiosis lipoidica with topical psoralen plus ultraviolet A.Br J Dermatol. 2002 Oct;147(4):743-7 3.Beck HI, Bjerring P, Rasmussen I, Zachariae H, Stenbjerg S.Treatment of necrobiosis lipoidica with low-dose acetylsalicylic acid. A randomized double-blind trial.Acta Derm Venereol. 1985;65(3):230-4. 4. Statham B, Finlay AY, Marks R.A randomized double blind comparison of an aspirin dipyridamole combination versus a placebo in the treatment of necrobiosis lipoidica.Acta Derm Venereol. 1981;61(3):270-1 5.Barnes Ch J.Necrobiosis Lipoidica.Last Updated: October 8, 2001 e-medicine . Total de artículos localizados e incluidos:5 I: Metaanálisis y/o revisiones sistemáticas:0 II: Ensayos clínicos:2 III: Cohortes, casos controles, serie de casos clínicos:1 IV: Consenso de profesionales:0 GU: Guías de práctica clínica:0 Otros:Revisión narrativa:2 Advertencia sobre la utilización de las respuestas. Las contestaciones a las preguntas formuladas, se elaboran con una finalidad exclusivamente formativa. Lo que se pretende, es contribuir con información al enriquecimiento y actualización del proceso deliberativo de los profesionales de la Medicina y de la Enfermería.Nunca deberán ser usadas como criterio único o fundamental para el establecimiento de un determinado diagnóstico o la adopción de una pauta terapéutica concreta. De ningún modo se pretende sustituir, avalar o tutelar la responsabilidad del médico. Esta deriva de sus propias decisiones y solo por él debe ser asumida, no pudiendo ser compartida por quienes solo le han informado. La Consejeria de Sanidad y el Servicio Murciano de Salud, rechazan a priori toda responsabilidad respecto de cualquier daño o perjuicio que se pueda imputar a la utilización total o parcial de la información aportada y que fue solicitada previamente por el profesional médico ó de enfermería.

FFECT OF HYPERBARIC OXYGEN ON THE REGENERATION OF EXPERIMENTAL CRUSH INJURIES OF NERVES

Revista do Hospital das Clínicas
Print ISSN 0041-8781
Rev. Hosp. Clin. vol.54 n.3 São Paulo Jun. 1999


EFFECT OF HYPERBARIC OXYGEN ON THE REGENERATION OF EXPERIMENTAL CRUSH INJURIES OF NERVES

Paulo Tuma Jr., Mariza D'Agostino Dias, Gino Arrunátegui, Gustavo Gibin Duarte, Alexandre Wada, Armando Santos Cunha and Marcus Castro Ferreira

RHCFAP/2967

TUMA Jr. P et al. - Effect of hyperbaric oxygen on the regeneration of experimental crush injuries of nerves . Rev. Hosp. Clín. Fac. Med. S. Paulo 54 (3): 81 - 84,1999.



SUMMARY: Hyperbaric oxygen has been successfully used on treatment of acute ischemic injuries involving soft tissues and chronic injuries. In nerve crush injuries, the mechanisms involved are very similar to those found in ischemic injuries. Consequently, it is logical to hypothesize that hyperbaric oxygen should improve nerve repair, which is a critical step on functional recovery. In the present study, we created standard nerve crush injuries on sciatic nerves of rats, which underwent treatment with hyperbaric oxygen. Results were assessed by functional evaluation using walking-track analysis. The functional recovery indexes observed did not differ from control group. We concluded that hyperbaric oxygen therapy, in the schedule used, had no influence on functional recovery after nerve crush injuries.


DESCRIPTORS: Hyperbaric oxygen. Nerve regeneration. Nerve injury. Sciatic function index. Experimental study.

Therapy with hyperbaric oxygen (HBO) is an adjuvant treatment in some cases of acute trauma with ischemia, such as crush injuries of extremities, compartmental syndrome, poorly healing injuries, ischemic flaps, and radionecrosis of bone1.

Crush injuries and section of nerves may manifest a physiopathology similar to that associated with ischemia of muscle and skin flaps. In the initial period after the nerve damage, swelling and edema occur, as indicated by higher nerve weight caused by increase of water1.

Previous studies showed improvement in functional recovery when therapy with hyperbaric oxygen is used either after transection and suture2 or when autologous nerve grafting is interposed3 in rat the sciatic nerve model. However, the same results were not seen with nerve tubulization after transection1, and in crush injuries of rat fibular nerves4.

Fibular nerve has better vascularization, compared to sciatic nerve, due to its smaller transverse section area4. The present study was designed to evaluate the influence of HBO in the functional recovery after crush injury in rats, using the sciatic nerve, which is theoretically more susceptible to ischemia than the fibular nerve.

MATERIAL AND METHODS

Surgical Procedure

Twenty Wistar male rats, weighting from 300 to 350 g, with ages of around 8 weeks, were operated on under anesthesia using chloral hydrate in a concentration of 10%, 400 mg/kg, intra-peritoneal injection. An incision was made dorsally on the right thigh. Through a muscle splitting incision, the sciatic nerve was exposed from the notch to its first division (Figure 1).

The crush injury of 1.5 mm was performed on the nerve, using a hemostatic "mosquito" forceps (Figure 2). As described by Dash5, the nerve was crushed 1 cm proximally to the bifurcation, for 5 seconds, with the instrument closed to the first notch (Figure 3). After the procedure, the muscle and skin were closed, and the animals were placed in separated cages, with water and food ad libitum.

Hyperbaric Oxygen Therapy

Animals were randomized into two groups, A and B (Table 1). In the first group (A), animals received oxygen in a 100% concentration in an individual hyperbaric chamber, model Seechrist®, under a 2.8 atmospheres pressure for 30 minutes, twice a day, during three consecutive days. Therapy started at the first hour after the operation. The other group (B) did not receive hyperbaric oxygen after the injuries.

Functional Evaluation

Functional recovery was assessed using the walking-track analysis, according to the method previously described by Medinaceli et al.6 and modified by Bain et al7. The analyses were made before the surgery, and 2, 15 and 30 days after.

In order to create foot prints on paper, animals had their posterior foot painted in blue ink and were placed on white paper in a track. Afterwards, the prints were measured, and the following measurements were taken: the distance between first and fifth toes (toe spread - TS), distance between second and fourth toes (intermediate toe spread - ITS), and the total length of the footprint (print length - PL).

The measures were used to calculate the Sciatic Function Index for each animal, as proposed by Bain7:

SFI= [-38.3 x (PLO - PLN)¸ PLN] +

[109.5 x (TSO - TSN)¸TSN] +

[13.3 x (ITSO - ITSN)¸ITSN] - 8,8

PLO = length of the operated print

PLN = length of the normal print

TSO = operated toe spread

TSN = normal toe spread

ITSO = intermediate operated toe spread

ITSN = intermediate normal toe spread

Using this formula, the Sciatic Function Index (SFI) was calculated, and the values were classified as follows::

SFI = 0 +/- ® normal sciatic function

SFI = -100 +/- ®12 Æ complete dysfunction

Statistical Analysis

The variable SFI was presented descriptively in a table containing mean, standard deviation, median, minimal values, and maximal values, for each group and evaluation condition.

The two factors, group and evaluation condition, were studied through the mean profile analysis, and the following hypotheses were tested:

• H01: the mean profiles are parallels and the groups have the same behaviour during the studied conditions.

• H02: the mean profiles are the same, and there is no difference between the means of the two groups on the conditions studied.

• H03: there is no influence of the condition factor, and the means are constant during the different conditions.


Significance level in this study was <0.05.

RESULTS

A SFI near 0 was observed in the measures made before the injuries, demonstrating normal function. Two days after the injury, the SFI decreased in both groups. After 15 days, the SFI was half-way towards zero, and in 30 days, the SFI was nearest to zero of the three measurements taken after injury (Table 2 and Graph 1).

There was no statistically significant difference between the HBO and control groups (Table 3).

DISCUSSION

Some nerve injuries are followed by hypoperfusion and edema. These changes can be detected almost immediately after a nerve injury1.

In any acute ischemic tissue, cellular changes occur, and they disturb the regulation of flow through the capillary membranes, leading to edema. This edema seems to be important in maintaining ischemia, because it compresses the microcirculation and decreases tissue perfusion. When the circulation is restored after long ischemic periods, physiologic shunts are opened, increasing the edema, resulting in a paradoxic ischemia (no-reflow phenomenon)8. HBO used early might interfere with this sequence by promoting vessel constriction, decreasing the flow and thus the edema. Hyperoxygenation would compensate for the decrease of flow, maintaining tissue oxygenation in suitable level8. Another possible mechanism of action associated with HBO is the decrease in the neutrophil linkage to the endothelial wall, which minimizes the delivery of free radicals produced by the reperfusion phenomenon8,9.

The intensity of these harmful factors on the neural structures, however, has not been established. Other possible actions of HBO would consist of increasing production of vascular and neural growth factors, which improves the tissue perfusion1. In spite of all these possible mechanisms, the exact cellular mechanism of action of HBO is not still completely understood1,9,10.

Several schedules for treatment with HBO have been proposed, but there is not a standardized model that would be adequate for use in experimental animals. Pressures of more than three atmospheres during more than three hours, more than twice a day, are considered to have potential toxicity11. In this study, HBO was used an hour after the operation, and during three consecutive days, with a pressure of 2.8 atmospheres, for 30 minutes, twice a day. This proposed schedule seems to be adequate for this experimental model, and morbidity or death associated to the HBO was not observed.

Previous reports showed improve on functional recovery after rat sciatic nerve transection and autologous graft with the use of HBO2,3. On the other hand, the same was not observed in transections treated with tubulization1, and in crush injuries of rat fibular nerves4.

The crush injury differs from the transection injury because it produces axonotmesis, a functional impairment that returns to normal almost completely after three weeks from the injury, as observed in our control group, confirming the data by Dash et al5. Transection causes a injury in which spontaneous regeneration occurs only rarely. Consequently, HBO might have a more significant influence on nerve injuries with complete interruption by regulating the nerve environment, than it does with crush injuries, for which the external factors are less critical.

Results observed in this study agreed with the experiment performed by Santos et al.4 using crush injury, although the authors had used the fibular nerve and a different HBO schedule. Fibular nerve has better vascularization, compared to sciatic nerve. Although both have perineurial circulation, the fibular nerve has better vascularization because of its smaller transverse section area4. This difference seems not to interfere with functional evaluation after crush injuries of nerves in animals exposed to HBO.



RHCFAP/2967

TUMA Jr. P e col. - Efeito da oxigenioterapia hiperbárica na regeneração de lesões experimentais de nervos. Rev. Hosp. Clín. Fac. Med. S. Paulo 54 (3): 81 - 84, 1999.
O oxigênio hiperbárico exerce efeitos comprovadamente benéficos no tratamento de lesões isquêmicas agudas de partes moles e em feridas de difícil cicatrização. Nas lesões neurais por esmagamento, os mecanismos fisiopatológicos assemelham-se aos efeitos dependentes da isquemia tissular. Portanto, a terapia com oxigênio hiperbárico teria participação nos processos de reparação neural, que constitui um dos pontos críticos para a recuperação funcional após as lesões por esmagamento de nervos periféricos. Neste estudo, foram realizadas lesões por esmagamento em nervo ciático de ratos, submetidos à terapia com oxigênio hiperbárico no pós-operatório. Os resultados foram quantificados através de avaliação funcional pelo método de "walking-track analysis". Os índices de recuperação funcional observados não diferiram dos observados no grupo controle. Portanto, verificou-se que a terapia com oxigênio hiperbárico, no esquema proposto, não teve influência na recuperação funcional após lesões neurais por esmagamento.



DESCRITORES: Oxigênio hiperbárico. Regeneração neural. Lesão neural. Índice de função ciática. Estudo experimental.

REFERENCES

1. SANTOS PM, ZAMBONI WA, WILLIAMS SL et al. - Hyperbaric oxygen treatment after rat peroneal nerve transection and entubation. Otolaringol Head Neck Surg, 1996; 114: 424-434.

2. ZAMBONI WA, BROWN RE, ROTH AC, et al. - Functional evaluation of peripheral nerve repair and the effect of hyperbaric oxygen. J Reconstr Microsurg, 1995; 11: 27-29.

3. GINGRASS M, ZAMBONI WA, BROWN RE, et al. - The effect of high tension oxygen on nerve regeneration in a nerve graft model. J Reconstr Microsurg, 1993; 9: 158.

4. SANTOS PM, WILLIAMS SL & COVEY J - Peroneal motor nerve crush injury and hyperbaric oxygen effect . Laryngoscope, 1995; 105: 1061-1065.

5. DASH H, KONONOV A, PRAYSON RA, et al. - Evaluation of nerve recovery from minimal-duration crush injury. Ann Plast Surg, 1996; 37: 526-531.

6. DE MEDINACELI L FREED WJ & WYATT RJ. - An index of the functional condition of rat sciatic nerve based on measurements made from walking tracks. Exp Neurol, 1982; 77: 634-643.

7. BAIN JR, MACKINNON SE & HUNTER DA. - Functional evaluation of complete sciatic, peroneal, and posterior tibial nerve injuries in the rat. Plast Reconstr Surg, 1989; 83: 129-138.

8. NYLANDER G, LEWIS D, NORDSTROM H, et al. - Reduction of postischemic edema with hyperbaric oxygen. Plast Reconstr Surg, 1985; 76 : 596-601.

9. ELLIS FR & DEWAR KM - Effect of hyperbaric oxygen on nerve tissue. Br J Anesth, 1970; 42: 800.

10. MUKOYAMA M, IIDA M & SOBUE I - Hyperbaric oxygen therapy for peripheral nerve damage induced in rabbits with Clioquinol. Exp Neurol, 1975; 47: 371-380.

11. DAVIS JC - Hyperbaric oxygen therapy: a committee report. Bethesda, Undersea Medical Society, 1983.


Division of Plastic Surgery, University of São Paulo School of Medicine - São Paulo, Brazil.