Respaldo de material de tanatología

El Síndrome de Burnout en Personal Psiquiátrico.

1. TÍTULO:
El Síndrome de Burnout en Personal Psiquiátrico.

2.  AUTOR:
Dr. Guillermo Rivera, Residente Psiquiatría II

3.  RESUMEN:

El síndrome de burnout es una situación que experimentan algunos profesionales de instituciones cuyo objeto de trabajo son personas, y que se caracteriza por un agotamiento emocional debido a una implicación excesiva en su trabajo, llegando a ser ineficaces para el desempeño adecuado de su actividad laboral. Definido como un síndrome de agotamiento emocional, despersonalización y bajos sentimientos de realización personal en el trabajo, que ocurre más frecuentemente a profesionales que trabajan frente al público.

Una de las poblaciones profesionales que, por el tipo de trabajo que desempeñan, provocan altos niveles de incidencia del síndrome de quemarse por el trabajo (“burnout”), es la profesión sanitaria. Nuestra investigación, basada en una muestra de profesionales de la salud mental, psiquiatras, enfermeras y cuidadores psiquiátricos comprende a 70 sujetos que trabajan en el Instituto Nacional de Psiquiatría ?Gregorio Pacheco?, pretende identificar el burnout entre el personal con mayor contacto con el paciente, así como su cuantificación y distribución por sexo y ocupación

Se encontraron diferencias en las puntuaciones en Burnout entre hombres y mujeres, puntuaron mas estas ultimas. Los cuidadores psiquiátricos son el colectivo más afectado en realización personal y despersonalización, y las enfermeras en cansancio emocional. Estos resultados tienen varias implicaciones en orden a la introducción de cambios organizacionales en las Unidades. En el trabajo se discuten también las implicaciones para la investigación que los resultados plantean.

Palabras Clave: Síndrome de Burnout, Personal psiquiátrico, MBI

4. INTRODUCCIÓN:

El síndrome burnout es un síndrome clínico descrito en 1974 por Herbert Freudenberger, psiquiatra que trabajaba como asistente voluntario en la Clínica Libre de Nueva York para toxicómanos, al igual que otros voluntarios jóvenes e idealistas. Observó que hacia el año de empezar a trabajar, la mayoría sufría una progresiva pérdida de energía, hasta llegar al agotamiento, así como desmotivación para el trabajo, junto con varios síntomas de ansiedad y de depresión. Freudenberger describió cómo estas personas se vuelven menos sensibles, poco comprensivas y hasta agresivas en relación con los pacientes, con un trato distanciado y cínico, con tendencia a culpar al paciente de los propios problemas que padece. Para describir este patrón conductual homogéneo Freudenberger eligió la misma palabra -burnout- que utilizaban también para referirse a los efectos del consumo crónico de las sustancias tóxicas de abuso (1).

Por aquel entonces (1976) la psicóloga social Cristina Maslach estudiaba las respuestas emocionales de los empleados de profesiones de ayuda a personas. Eligió también el mismo término que utilizaban de forma coloquial los abogados californianos para describir el proceso gradual de pérdida de responsabilidad profesional y desinterés cínico entre sus compañeros de trabajo. Maslach decidió emplear esta misma expresión por su gran aceptación social: los afectados se sentían fácilmente identificados con este feliz término descriptivo, no estigmatizador como los diagnósticos psiquiátricos (2).

Tras su introducción el término burnout hizo fortuna, y ha llegado a ser muy popular en el ámbito anglosajón, con el mérito de dar cuenta de una realidad sociolaboral, tanto en las publicaciones profesionales de médicos, enfermeras, trabajadores sociales, profesores, policías y directivos, como en los medios de comunicación. En estas primeras publicaciones de divulgación se destacaba más la importancia de las diferencias individuales, como de personalidad previa (perfeccionismo, idealismo, excesiva implicación en el trabajo), que la influencia de las condiciones objetivas de trabajo y se popularizaron los seminarios de prevención y de intervención dirigidos a su adecuado afrontamiento (1).

En principio se suponía que los ejecutivos eran los profesionales más estresados, pero las investigaciones sobre el estrés laboral revelaron que también estaban expuestos a estos problemas aquellas personas que tuviesen un contacto directo con pacientes, clientes, usuarios, cuyas exigencias desbordaban la capacidad de actuación de los profesionales. Éstos desarrollan en un periodo de tiempo más o menos variable el llamado ?síndrome de Burnout? (síndrome de estar quemado?, ?síndrome de quemarse por el trabajo?, ?síndrome del estrés crónico laboral asistencial?, ?síndrome del desgaste profesional?). Cuando se dice que el profesional está quemado se indica que la situación (familiar, social o laboral) le ha sobrepasado y ha quedado reducida su capacidad de adaptación. (3)

Aunque no existe una definición unánimemente aceptada, hay consenso al considerar que el síndrome de Burnout aparece en el individuo como una respuesta al estrés crónico, que surge al trabajar bajo ?condiciones difíciles? en contacto directo con los usuarios, clientes o pacientes, y que tiene consecuencias muy negativas para la persona y para la organización. Las consecuencias más visibles de la aparición del Burnout en las organizaciones son: absentismo laboral, abandono del puesto de trabajo, despidos, jubilaciones anticipadas, etc (4).
Para poder prevenir estas situaciones debemos conocer los síntomas y los factores que contribuyen a su aparición.

Actualmente, la conceptualización del síndrome de burnout más ampliamente aceptada es la propuesta por Maslach y Jackson (2), quienes señalan tres dimensiones constitutivas del mismo, a saber:

1. Cansancio emocional, sentimientos de estar emocionalmente agotado y exhausto debido al trabajo que el sujeto realiza.
2. Despersonalización, caracterizada por un cambio negativo en las actitudes y respuestas hacia los beneficiarios del propio trabajo, así como por incremento de la irritabilidad de la motivación laboral.
3. Sentimientos negativos de realización personal, que supone respuestas negativas hacia uno mismo y hacia el trabajo, evitación de las relaciones interpersonales y profesionales, baja productividad, incapacidad para soportar la presión y baja autoestima.

En conclusión, el burnout resulta de una discrepancia entre las expectativas e ideales individuales por una parte, y la dura realidad de la vida ocupacional cotidiana, por otra. El proceso de burning-out puede ser percibido conscientemente por la persona afectada, o bien puede negarse y mantenerse no reconocido durante mucho tiempo. Poco a poco, la persona se va sintiendo afectada, y va cambiando sus actitudes hacia el trabajo y hacia las personas con las que trabaja, hasta que el proceso cristaliza. Puede sentirlo a nivel emocional como una activación excesiva, por sus concomitantes somáticos (palpitaciones, dolores, cansancio, etc.) o por su conducta en el trabajo (impaciencia, olvidos, altanería, hipercriticismo, etc.). La técnica formal o estilo que utiliza cada persona para afrontar estas señales de alarma (ansiedad señal, estrés percibido o strain) va a ser crucial para que se desarrolle o no el burnout, para que resulte un rendimiento eficaz y satisfactorio, o bien deterioro, insatisfacción y burnout. No obstante, es preciso reconocer que no hay ninguna estrategia de afrontamiento que sea válida de forma universal e intemporal, inespecífica, pero suele ser adaptativo un estilo de afrontamiento orientado al conocimiento y resolución de los problemas, y que suele ser desadaptativo el afrontamiento de escape, salvo cuando, de verdad, no hay nada que hacer.

Se trata de una reacción a la tensión emocional crónica creada por el contacto continuo con otros seres humanos, en particular cuando éstos tienen problemas o motivos de sufrimiento. Es decir, se puede considerar un tipo de estrés ocupacional, pero, aunque tenga algunos efectos morbosos comunes con otras reacciones al estrés, el factor característico del burnout es que el estrés surge de la interacción social entre el operador y el destinatario de la ayuda. Por eso se dice, que este síndrome es “el precio de ayudar a los demás” (5). Así, cuando decimos o escuchamos que un funcionario u oficinista, por ejemplo, está “quemado”, se trata de otra cosa distinta

De ahora en adelante utilizaremos el término burnout. No se trata de seguir la actual y detestable moda de utilizar anglicismos, sino de querer diferenciar este síndrome específico de los profesionales que ayudan a los demás, con el “quemamiento” que otros trabajadores dicen tener cuando simplemente están hartos o cansados.

El núcleo del síndrome del burnout (5) es un esquema de sobrecarga emocional seguido de agotamiento emocional. La persona se implica excesivamente desde el punto de vista emocional y al final se verá desbordada por los requerimiento emocionales que le imponen los otros. La respuesta a tal situación (y por lo tanto uno de los aspectos del burnout) es el agotamiento emocional. El individuo se siente “vaciado” y le falta energía para afrontar un nuevo día, sus recursos emocionales se han agotado.

Cuando en la persona se ha instalado el agotamiento emocional, no se siente ya capaz de dar nada de sí a los demás. Un modo de librarse de la carga emocional es sustraerse a la implicación con los demás, intentando reducir el contacto con la gente al mínimo indispensable para llevar a término su trabajo. Como consecuencia, se transforma en un burócrata árido cuyas relaciones con los otros están sujetas estrechamente al reglamento. Esta rutina árida y burocrática es uno de los muchos sistemas con los que la gente se desconecta psicológicamente de cualquier implicación con los demás.

Esta desconexión emotiva, señala un segundo aspecto del síndrome del burnout: la despersonalización. Es como si el individuo viese a los otros a través de unos lentes manchados de herrumbre; se forma una mala opinión de ellos, siempre se espera lo peor y no tiene empacho en demostrarle cuanto les detesta. Esta reacción, cada vez más negativa hacia la gente, se manifiesta de varios modos, llegando a ignorarles y a ignorar sus necesidades y solicitudes y a no dar la ayuda, la asistencia o el servicio más idóneo para ellos.

Los sentimientos negativos hacia los demás, pueden progresar hasta terminar con sentimientos negativos hacia sí mismo. Los operadores de la ayuda pueden tener sentimientos de culpa o tormento por el modo con que han considerado o tratado a la gente: sienten que se están transformando en un tipo de persona fría e indiferente que a nadie gusta, ni siquiera a ellos mismos.

En este momento aparece el tercer aspecto del burnout: el sentimiento de una reducida realización personal. Quien se ocupa de los otros sufre un tormentoso sentimiento de inadaptación sobre su propia capacidad de establecer relaciones con los usuarios del servicio y que puede conducir a un auto-veredicto de “fracaso”. Con la caída de la autoestima, puede instaurarse la depresión(6). Algunos intentarán resolver lo que interpretan como problemas personales a través de psicoterapia, otros cambiarán de trabajo (evitando cualquier tarea que pueda implicar un contacto estresante con la gente).

El precio del burnout puede ser muy alto. Afecta negativamente, tanto al operador, como a su familia, al usuario y a la institución. Muchas veces, se trata de mecanismos de supervivencia del operador, que intenta reducir el estrés quizás con alcohol o con fármacos o bien alejándose de la gente.

Por fortuna existen métodos más constructivos para afrontar esta situación y que tienen como objetivo alguno o varios de los aspectos principales del síndrome: reducir la tensión emocional del trabajo con la gente, compensar la visión negativa despersonalizada de la gente y potenciar el sentido de realización personal y de autoestima del individuo (6).

Las diferencias fundamentales entre el estrés simple y el Síndrome de Burnout es que , mientras que el estrés puede desaparecer tras un período adecuado de descanso y reposo, el burnout no declina con las vacaciones ni con otras formas de descanso.

Existen una serie de síntomas asociados al síndrome de burnout (7). Se pueden clasificar en 4 grupos:

-Psicosomáticos:
? Fatiga crónica
? Dolores de cabeza frecuentes
? Problemas de sueño
? Úlceras u otros desórdenes gastrointestinales
? Pérdida de peso
? Hipertensión
? Asma
? Dolores musculares (espalda y cuello)
? Pérdida de ciclos menstruales

-Conductuales
? Absentismo laboral
? Abuso de drogas (alcohol y otras)
? Aumento de conducta violenta
? Comportamientos de alto riesgo (conducción violenta, etc.)

-Emocionales
? Distanciamiento afectivo
? Irritabilidad, recelos
? Incapacidad para concentrarse
? Baja autoestima y deseos de abandonar el trabajo
? Ideación suicida

-Defensivos
? Negación de las emociones
? Atención selectiva (sobre los clientes)
? Ironía, racionalización
? Desplazamiento de afectos

Aparte de estos síntomas que sufre el sujeto, también va a repercutir sobre la familia y sobre la calidad del trabajo(8).

Difícilmente van a desaparecer los efectos del burnout cuando el operador termina su jornada de trabajo y vuelve a casa. Es más que probable que el impacto repercuta en su familia. El individuo se quejará continuamente, hablará reiteradamente de su trabajo y se transformará en un problema para la familia. No es raro que los lamentos y agresividad se dirijan a otra persona (cónyuge) transformándose la situación en un riesgo de divorcio.

El operador afectado de burnout, incapaz de implicarse con sus familiares, ve cómo éstos reclaman más atención y dedicación y se quejan de que se hace más caso a los usuarios de su trabajo que a ellos mismos. Cuando el afectado por el síntoma cae en el ostracismo, manifiesta que es para proteger a su familia, aunque realmente casi siempre es porque no quiere revivir o rememorar los problemas del trabajo. Si bien puede ser bueno, en circunstancias normales, no compartir los asuntos o problemas del trabajo con el cónyuge, también puede ser la causa de una falta de comunicación a todos los niveles.

Es frecuente que los sentimientos cínicos y negativos hacia la gente que se generan en el burnout, termine afectando, no sólo a las personas relacionadas con el trabajo, sino a todo el mundo.

Por lo que respecta al trabajo, el resultado más evidente será una disminución del rendimiento que disminuye la motivación, aumenta la frustración y predomina una actitud de no participación. Sea cual sea el trabajo de la persona, se termina transformando en una “cadena de montaje”. Se trata a las persona como objetos, se cae en la rutina, lo que suele llevar implícito una menor atención a las necesidades humanas mostrando una menor sensibilidad hacia los sentimientos del usuario. Esta deshumanización en el trabajo puede traer como consecuencia el uso de medidas inapropiadas (por ejemplo, aumentado la cantidad de sedantes a los enfermos para que no molesten, o algo peor).

En fases precoces, el profesional se desconecta emocionalmente del trabajo (prefiere emplear el tiempo en rellenar fichas, cumplimentar papeles, etc. que estar con los usuarios), pero más adelante, también se desconecta físicamente (empieza marchándose antes, llegando tarde, y termina por faltar con frecuencia a su trabajo). si la situación se mantiene, pronto empezará a pensar en cambiar de oficio, generalmente más de tipo administrativo, donde no tenga apenas contacto con la gente.

Las variables pueden cambiar dependiendo de la profesión que se ejerza. Álvarez G. y Fernández R. (7) analizan un amplio número de estudios sobre el burnout en los profesionales de la salud y destacan los siguientes como los más relevantes:

? Los motivos ideológicos que les impulsaron a elegir esa profesión
? El hecho de que el trato directo con los pacientes y sus familiares suele ser emocionalmente exigente para el trabajador .
? La naturaleza de la enfermedad de los pacientes les hace enfrentarse en ocasiones con el “fracaso terapéutico” o con el volumen de trabajo y las presiones para realizarlo.
? La falta de información sobre el cometido que han de realizar y de cómo se hace. Este problema suele estar a menudo presente en el modelo médico jerarquizado.
? El apoyo laboral no parece suficiente con la sola colaboración de reuniones formales, sino que los encuentros han de cubrir algunas necesidades emocionales y de compañerismo.
? Los turnos rotativos que perturban el ritmo biológico de los trabajadores.
? Los trabajos nocturnos.
? El alto índice de contratación temporal.
? Las cargas de trabajo familiares, más del 80% de los profesionales son mujeres.
? En cuanto a las variables personales, aquellos que se sentían más responsables de la recuperación de sus pacientes, resultaban ser los sujetos más vulnerables al desarrollo de algún tipo de sintomatología, precisamente porque hacían recaer sobre sí el peso de los resultados.
? Variables de entrenamiento profesional. No cabe duda de que la falta de formación práctica en Escuelas y universidades se convierte en una trampa para los jóvenes que se inician en el ejercicio de sus labores. alguno de los errores más frecuentes son, según Wilder y Plutchik(9):

? Excesivos conocimientos teóricos
? Escasos entrenamientos en habilidades prácticas
? Inexistencia del aprendizaje de técnica de autocontrol emocional y de manejo de la propia ansiedad
? Falta de formación sobre el funcionamiento de las organizaciones en las que van a desarrollar su trabajo.

La  tarea psiquiátrica es particularmente dura Al comprobar que la actuación terapéutica es, cuando menos, incierta. Que buena parte de nuestros pacientes nos acompañan de por vida. Su cronicidad nos impregna. En muchos de ellos nos reconocemos. Sus pequeñas miserias, fobias, miedos, angustias, vicisitudes vitales son las nuestras: los que difícilmente sobrellevamos (con o sin análisis personal). La sociedad nos exige no solo controlar la locura, el acto psicótico imprevisible, sino remedios eficaces para el malestar cotidiano. Nos exige, una vez más, hacer frente a sus males: toxicomanía, delincuencia. Psiquiatrizar el mal: violadores, torturadores, psicópatas. Por lo que los niveles de Burnout en este colectivo son considerables.

Psiquiatria: Ansiedad

TRASTORNOS DE ANSIEDAD
(TOC y TAG)

TRASTORNO OBSESIVO COMPULSIVO (TOC).

Epidemiología.

Antes de 1980 el TOC era considerado como una rareza con mal pronóstico.  Esto podría explicarse porque la enfermedad es mantenida en secreto por los pacientes.(1)

Frecuencia en población psiquiátrica.

Del 0.1% al 4% de los pacientes psiquiátricos hospitalizados tienen este diagnostico.  El 10% de los pacientes ambulatorios lo tienen.(1)

Incidencia y prevalencia.

La prevalencia a 6 meses es de 1.6% y la prevalencia de vida de 2.5%.(1)

El 80% de los pacientes con txs de ansiedad consultan al médico de primer nivel.  Pasan 7.5 años entre el inicio de los síntomas de TOC y la primera consulta al siquiatra.(1)

Sexo.

En adultos: 1 hombre por cada 1.1 mujer. En niños predominan los hombres.(1)

En Colombia la prevalencia en la vida según el sexo es de 3.3% para los hombres y 3.9% para las mujeres para un total del 3.6% de la población.(2)

Edad de inicio.

+/- 6.8 años en hombres, 20.8 +/- 8.5 en mujeres.  Menos del 15% se inician luego de los 3 años.(1)

Estado civil.

Los pacientes más severamente enfermos tienen mas dificultades en el matrimonio.(1)

Edad.

Según la edad el grupo de mayor prevalencia de vida en Colombia es el de las edades entre los 50 y 60 años con un 6.2% seguido por el de 20 a 24 con un 4.6% (teniendo en cuenta que este último grupo comprende un rango menor de edades).(2).

Inteligencia.

Solo hay una pequeña y no significativa diferencia del IQ con grupos control.  De mucho interés es el hecho de que hay una pequeña pero consistente diferencia en la calificación verbal vs de desempeño, así como en las pruebas neurosicológicas de lóbulo frontal.(1)

Fenomenología.

Obsesiones. % Compulsiones %

Contaminación.
45
Revisión.
63

Duda patológica.
42
Lavado.
50

Somáticas
36
Conteo.
36

Simetría.
31
Preguntar o confesar.
31

Impulsos agresivos.
28
Simetría y precisión
28

Impulsos sexuales.
26
Atesorar.
18

Otros.
13
Múltiples.
48

Obsesiones múltiples.
60

(1)

Curso.

Tipo
%
Precipitante
%

Continuo.
85
sin precipitante.
71

Deteriorante.
10
con precipitante.
29

Episódico.
2

(1)

Los fenómenos obsesivos tienen como rasgos característicos, primero el carácter coercitivo con imposibilidad de control eficaz, segundo la tendencia a la repetición incesante, tercero lo absurdo del contenido y cuarto la vivencia angustiosa que provocan.(3)

En el plano del pensamiento se trata de ideas u ocurrencias que de forma reiterada se introducen en la conciencia del sujeto e interfieren el flujo normal del pensamiento y causan malestar y sufrimiento, puede tratarse de palabras, frases o rimas.  Frecuentemente el contenido es obsceno, blasfemo o absurdo.  Otras veces el sujeto vive atormentado por imágenes o representaciones obsesivas, escenas imaginadas con gran intensidad, comúnmente de naturaleza violenta o sexual que reiteradamente asedian su mente.  Los temas más frecuentes son: escrúpulos físicos (contaminación) o morales (pecado) y a la duda o imposibilidad de inclinarse por una opción (duda patológica).  Son también frecuentes las rumiaciones obsesivas consistentes en cavilaciones interminables y agobiantes sobre un tema concreto.  Son especialmente molestas las ideas de contraste como por ejemplo ideas obscenas o sacrílegos al observar imágenes religiosas.  En otros casos hay la necesidad de repetir mentalmente un contenido concreto de significado ilógico o banal como una fecha, una melodía o un slogan publicitario.(3)

Los contenidos de los temores obsesivos se corresponden con la temática de los escrúpulos como temor a la contaminación, a enfermedades (cáncer, SIDA, y venéreas) a gérmenes, a lesionar a alguien, a armas potenciales como cuchillos o tijeras, a la suciedad o a lo impuro.(3)

Las compulsiones son también apremiantes, reiterativas, ilógicas, ridículas y molestas, angustiosas o insoportables.  Las modalidades son numerosas como lavar, tocar, mirar, cantar, anotar, comprobar, ordenar, coleccionar, repetir un numero determinado de veces, etc.(3)

Comorbilidad.

El 10% de los pacientes con esquizofrenia tienen síntomas obsesivo compulsivos.(1)

No esta clara la  relación con la depresión y se acepta que hay depresión primaria y secundaria.  Hay estudios que apuntan a una vulnerabilidad genética y biológica para sufrir trastornos de ansiedad y depresión.  La mayoría de los pacientes reportan que los síntomas de depresión se iniciaron después de los síntomas obsesivos.(1)

Hay también un porcentaje variable de comorbilidad con fobias y pánico, trastornos alimenticios, abuso de alcohol y síndrome de Tourette.(1)

Etiología.

Hipótesis serotoninérgica.

La posibilidad del papel de la serotonina surgió con la observación de que la clorimipramina mejoraba a muchos pacientes.  Además se observó (Thoren et al 1980) que la mejoría clínica se asociaba a disminución cerebroespinal del ácido 5 hidroxiindolacético (5-HIAA).  El cual es un metabolito de la serotonina.(1).

Los IRSS actúan en la proteína transportadora de serotonina. Polimorfismo en el gen que codifica esta proteína afecta su expresión y estas diferencias en la proteína transportadora de serotonina debidas a estas variables genéticas se han asociado a TOC. (5)

Hipótesis del aprendizaje.

Las obsesiones y compulsiones son respuestas condicionadas que disminuyen la ansiedad.  Estas se establecen cuando una persona aprende que la ansiedad puede reducirse por este mecanismo.(1)

Estudios familiares y genéticos.

La mayoría de estudios concuerdan en que los parientes en primer grado de pacientes con TOC tienen más enfermedades psiquiátricas incluyendo TOC, lo mismo que una mayor frecuencia en gemelos

monocigotos.(1)

Tratamiento.

Terapia conductual.

Exposición con prevención de respuesta:  Se induce el paciente a que haga aquello que evoca los rituales (tocar suciedad, desordenar la casa, abandonar la casa) y se evita el lavado, orden o la verificación.  Por media hora, luego una hora y así paulatinamente.  Usando la persuasión y no la fuerza ya que los pacientes deben aprender a frenarse ellos mismos.(4)

Se explica al paciente que aunque el ritual le proporciona alivio inmediato esto lo convierte en una especie de adicto que solamente consigue que los síntomas se presenten más tarde.(4)

En los casos en que los rituales involucran a la familia estos deben actuar como cooterapeutas negándose gentil pero firmemente con frases como “en el hospital dijeron que…” cuando el paciente les solicite verificar, limpiarse o pregunte repetitivamente.(4)

En los obsesivos puros la eficacia del manejo conductual es menor pero también es útil.  Se usan básicamente la exposición imaginada evocando los pensamientos en situaciones que los provoquen, esto se hace reservando un periodo del día (15-30min) para pensar en la obsesión hasta que no se pueda continuar.(4)

En los obsesivos lentos se usa el establecimiento de horarios pero sin tanto éxito.(4).

Manejo farmacológico

Recomendaciones del comité de expertos para el manejo de primera línea con medicamentos.

Inhibidores selectivos de la recaptación de serotonina. (ISRS)

Fluvoxamina, fluoxetina, sertralina, paroxetina:

Solos o combinados con Terapia conductual (T.C) en adultos con síntomas de moderados a severos.

Adisionarlos cuando hay respuesta parcial o no hay respuesta a la T.C.

Usarlos antes de usar clorimipramina o cuando esta no se pueda usar debido a riesgos por los efectos anticolinérgicos, cardiovasculares, sexuales, sedantes o de ganancia de peso.

Cuando hay comorbilidad con otro trastorno en el que puedan ser útiles.

Clorimipramina.

Usar luego de dos fracasos con ISRS.

Como potenciador de los ISRS cuando hay respuesta parcial a estos.

Cuando hay efectos secundarios como insomnio, acatisia, nauseas o diarrea con los ISRS.

Cuando hay comorbilidad con otro trastorno para el cual los tricíclicos pueden ser útiles.

(6).

Recomendaciones del comité de expertos para el manejo del TOC complicado por comorbilidad.

Embarazo: T.C sola.

Enfermedad cardiovascular: T.C o TC+ISRS (Ej. sertralina)

Enfermedad renal: T.C o T.C+ISRS

Sd. De Tourette: T.C+Clorimipramina+antisicótico típico.

Pánico o Fobia social: T.C+ISRS.

Depresión: ISRS o Clorimipramina (según el perfil del paciente y hasta que                                       

                                                      pueda colaborar con la T:C), Luego T.C+Medicación.                           

(6).

TRASTORNO DE ANSIEDAD GENERALIZADA (TAG)

Las emociones son patrones innatos de reacción y respuesta que están involucrados en muchos aspectos de la vida debido a su papel funcional y adaptativo.  (Ej. El miedo nos prepara para huir de un peligro inminente(7).

La ansiedad es una preocupación excesiva o irreal que se manifiesta en dos esferas, a saber: componente somático (tensión motora, hiperactividad autonómica y vigilancia) el otro componente es el componente del pensamiento.(8).

Criterios para dx de TAG. (DSM IV)

Preocupación excesiva mayor de 6 meses.  (Ej. Económica, de salud propia o de conocidos, rendimiento laboral, reparación del automóvil, etc.)

Dificultad de control de la preocupación.

Preocupación asociada a 3 o más de los siguientes síntomas:

Inquietud o impaciencia.

Fatigabilidad.

Dificultad para concentrarse o poner la mente en blanco.

Irritabilidad.

Tensión muscular.

Alteraciones del sueño.

(9).

Varios aspectos distinguen el trastorno de ansiedad generalizada de la ansiedad no patológica (preocupación y miedo).  Las preocupaciones del TAG son difíciles de controlar e interfieren típica y significativamente en la actividad general del individuo, mientras que las preocupaciones normales de la vida diaria son más controlables e incluso pueden dejarse para otro momento.  En segundo lugar las preocupaciones del TAG son más permanentes, intensas, perturbadoras y duraderas, apareciendo a menudo en ausencia de factores desencadenantes.  Las preocupaciones normales de la vida diaria no suelen acompañarse de síntomas físicos.(9).

Etiología.

La etiología involucra claramente procesos psicológicos y fisiológicos.

Aspectos cognitivo comportamentales.

Distorsiones en el procesamiento de la información llevan a percibir peligro donde no lo hay y esto produce la ansiedad, además el paciente ansioso también percibe que su desempeño frente al peligro también es inadecuado.  La sensación de perdida de control con respecto al ambiente es fundamental para perpetuar la ansiedad.(10)

Aspectos biológicos.

Se ha sugerido al receptor cerebral de benzodiacepinas (BDZ) como un posible mecanismo biológico para la ansiedad.  Los sitios de unión de las BDZ son parte integral del receptor GABA, las BDZ se unen al receptor potenciando la acción del GABA el cual es el principal neurotransmisor inhibitorio cerebral.(10)

Dado que la mayor concentración de receptor de BDZ está en la región occipital se piensa que este es el sitio anatómico del TAG y algunos estudios funcionales han confirmado esto, pero este hallazgo no es especifico de TAG.  Otros estudios han implicado estructuras límbicas, los ganglios básales y la corteza prefrontal.(10)

La eficacia de las azaspironas (buspirona) las cuales actúan sobre la serotonina (5HT1A agonista) sugieren que este neurotransmisor también desempeña un importante papel en este trastorno.(10)

Otros neurotransmisores y péptidos que podrían estar implicados son la noradrenalina, el glutamato y la colesistokinina.(10)

En cuanto al aspecto genético se ha observado que el 20% de los familiares de pacientes con TAG tienen también este diagnostico.(10)

En estudios con PET se ha observado una activación bilateral de vías límbicas anteriores concomitantemente con una poderosa respuesta emocional y fenómenos autonómicos y endocrinos luego de inyección de procaina la cual se a usado como modelo farmacológico de ansiedad.(11).

Prevalencia.

La prevalensia a un año en población general es del 3% y la prevalencia para toda la vida es del 5%.  El sexo femenino es el más afectado con dos terceras partes de los casos.(12)

Clínica.

La mayoría de los pacientes son vistos inicialmente por el medico general o el internista y llevan sintomáticos varios años.  El cuadro clínico involucrando al menos dos sistemas diferentes debe hacer sospechar el diagnostico.(10)

Los síntomas pueden agruparse en tres áreas:

Tensión motora: con incapacidad para relajarse, fatiga, dolor de espalda o cervical.  La cefalea tensional es frecuente.(10)

El área de la hiperactividad autonómica la cual incluye acortamiento de la respiración, palpitaciones, diaforesis, sensación de calor o frío y poliuria.  Los síntomas gastrointestinales pueden incluir nauseas, flatulencia y diarrea .(10)

Los síntomas de hipervigilia son hiperatención al ambiente, irritabilidad, dificultad para conciliar el sueño .(10)

Se a reportado que el trastorno empeora en el periodo premestrual .(10)

Tratamiento.

Manejo farmacológico.

BENZODIACEPINAS.

Son el tratamiento de elección, son seguras y poco letales en caso de sobredosis.  La mayoría de los pacientes requieren tratamiento a largo plazo y el 63% han recaído al año de suspender la medicación, esto implica que en algunos pacientes se debe hacer tratamiento farmacológico más de seis meses .(13)

Entre los efectos secundarios se cuentan la sedación, poca coordinación y dificultades para aprender nueva información.  Durante las primeras semanas se desarrolla tolerancia a la sedación .(13)

Existe el temor a formular BDZ por temor a la dependencia y el síndrome de abstinencia.  El aumento de la dosis por el mismo paciente es raro en pacientes no farmacodependientes.  Las benzodiacepinas deben evitarse en pacientes alcohólicos o con farmacodependencia.  El síndrome de abstinencia ocurre cuando se suspenden las BDZ luego de varias semanas de uso, para disminuir el peligro del síndrome de abstinencia o de convulsiones por abstinencia las BDZ deben suspenderse lentamente (25% semanalmente) .(13)

El manejo generalmente requiere dosis equivalentes a 10 – 20 mg de diazepam. (1 a 6 mg de lorazepam o 0.5 a 6 mg de clonazepam repartidos en dos o tres tomas al día). Se debe iniciar a dosis bajas durante la primera semana mientras el paciente desarrolla tolerancia a los efectos de sedación y sicomotores (0.25 mg de clonazepam dos veces al día por ejemplo).  La primera dosis se debe tomar en un momento en que el paciente este en la casa y no necesite conducir o desempeñar alguna tarea .(13)

BUSPIRONA.

Es un ansiolitico que no interactúa con los receptores benzodiacepinicos sino que es un agonista parcial del receptor serotoninérgico 5HT1A, también puede incrementar la función adrenérgica y dopaminérgica centrales no tiene efecto sedante ni sobre la función motora tampoco produce síndrome de abstinencia.  Mientras que el efecto de las benzodiacepinas puede verse en la primera semana de tratamiento con la buspirona hay que esperar de 2 a 4 semanas.  La dosis inicial son 5 mg dos veces al día y se debe subir gradualmente la dosis hasta 20 o 30 mg al día.  Los pacientes que han recibido previamente benzodiacepinas tienen pobre respuesta a la buspirona.  Los efectos secundarios de la buspirona incluyen nauseas y cefalea .(13)

Manejo psicológico.

El manejo que se a mostrado efectivo corresponde al enfoque cognitivo conductual el cual incluye el reconocer y tratar ideas irracionales sobre perder el control o hacer el ridículo en público por ejemplo y aspectos conductuales como exposición gradual a las situaciones generadoras de ansiedad .(13)

Obsessive compulsive disorderes: theory and management. M A Jenike, L Baer, W E Minichiello.  Second edition Mosby year book inc. 1990.  Cap 2 S A Rasmussen, J L Eisen pg 10-27.

II estudio de salud mental y consumo de sustancias sicoactivas Colombia 1997. Y Torres I D Montoya, República de Colombia Ministerio de salud.

Manual de siquiatría. J L Ayuso, L S Carulla.  Interamericana Mc Graw Hill.  1993.

Miedos, fobias y rituales. Isaak M. Marks.  edi. Martínez roca 1991.

Evidence for linkage disequilibrium between serotonin transporter protein gene (SLC6A4) and obsessesive compulsive disorder.  McDougle CJ. Epperson CN. Price LH Gelerter J.  Mol Psychiatry 1998 May; 3(3):270-3.

The expert consensus guideline series, Treatment of obsesive compulsive disorder, E.d. J.S March, A Frances, D Carpenter, and D.A Kahn.  The Journal of clinical psychiatry, supplement 4, Vol 58 1997 pj 11-12.

Cronic anxiety. Ronald M. Rapee. David H. Barlow. The guilford press 1991 cap 1.

cap 5 paj 101.

Manual diagnóstico y estadístico de los trastornos mentales. DSM IV.edit. Masson, Barselona, 1995. Trastornos de ansiedad, pag 447-448.

Comprehensive textbook of psychiatry. Editors H. Kapkan B. Sadock. Chapter 17.5 Generalized Anxiety disorder L. Papp, J. Gorman. Pj 1238 1239

The journal of clinical psychiatry supplement 16, vol 58 1997 pg 13-15. functional brain alterations in depression and anxiety. 

Fundamentos de medicina, Psiquiatría, tercera edición editores R. Toro, L. Yepes. Cap 16 R. Toro. Pj 184.

Current psichiatric thrapy editor D. Dunner.  W.B saunders company 1993.  Chapter 43 Generalized anxiety disorder. D. Cowley. Pj 264 268.

Psiquiatria: Ansiedad y Depresion

ANSIEDAD Y DEPRESIÓN.
Dr. Rodrigo Escobar G.
Médico Cirujano. CES.
Especialista en Psiquiatría. Universidad de Barcelona (España).

Al abordar el problema de la depresión y la ansiedad es importante primero situarnos en el contexto de la magnitud del problema. Las cifras epidemiológicas en nuestro país son altas mostrando que en los estudios de Salud Mental de 1987,1993 y 1997 prevalencias vida de algún grado de depresión del 25.6%, 25.1% y 19.6% respectivamente, en todos los estudios la prevalencia vida fue mayor en el sexo femenino y en el último estudio se encontró una prevalencia más alta en el grupo de personas mayores de 61 años, así mismo encontró una prevalencia vida de ideación suicida del 4.7% y de algún intento de suicidio del 1.7% . En cuanto a la ansiedad la prevalencia vida reportada para algún trastorno de ansiedad fue del 10.5% en el estudio de 1993, encontrando también que el género femenino fue el más prevalente. En el estudio de 1997 se encontró que el trastorno de estrés pos – traumático fue el que alcanzó las tasas de prevalencia vida más elevadas dentro de este grupo de patologías llegando a un 4.3%, posiblemente relacionadas con el fenómeno de violencia de nuestro país.  Sorprendentemente el trastorno de pánico en este estudio se señala con una prevalencia muy baja del 0.3% a pesar de ser una patología que consulta en forma relativamente frecuente a los servicios de urgencias médicas sin que contemos con estadísticas en este campo.

Además de que las cifras de presentación de estas patologías son elevadas, se añade la falta de especialistas en el área de la psiquiatría en Colombia, llegando a tener 17 veces menos psiquiatras por 100.000 habitantes que en Los Estados Unidos y 10 veces menos que en Canadá. Este problema hace que la patología mental sea vista a menudo a profesionales de la salud primaria en donde encontramos que alrededor del 20% de los pacientes que se atienden tiene como diagnóstico único o como comorbilidad un diagnostico psiquiátrica, principalmente patología ansioso – depresiva.

Los estados depresivos pueden subdividirse de acuerdo al DSM-IV en Trastorno Depresivo Mayor y Trastorno Distímico, pero pueden encontrarse dentro del contexto de un Trastorno Bipolar, lo cual es importante descartar ya que tiene grandes implicaciones terapéuticas.

Todos los estados depresivos comparten la tristeza (hipotimia) y la pérdida del interés o de la capacidad de sentir placer (anhedonia) como los síntomas fundamentales y están acompañados de una serie de síntomas de acuerdo al tipo e intensidad del trastorno afectivo. En la depresión mayor aparecen frecuentemente alteraciones en el sueño, con insomnio ( o hipersomnia), pérdida del apetito (o aumento), disminución en la energía vital, fatiga, inquietud o lentitud psicomotora, sentimientos de culpa, inutilidad o preocupación excesiva, disminución de la concentración e indecisión. A medida que el cuadro empeora pueden aparecer ideas o actos de tipo suicida, y en ocasiones síntomas psicóticos. Afortunadamente la mayoría de las veces los cuadros son de características leves y si reciben tratamiento en forma temprana, la mayoría responde adecuadamente.  La distimia se trata de un cuadro de características depresivas pero su intensidad en menor y aparecen menos síntomas que en la depresión, pero la duración en de al menos 2 años por lo que se confunde muy frecuentemente con alguna alteración del carácter, más que una enfermedad con posibilidad de tratamiento. Los pacientes con síntomas depresivos pueden consultar inicialmente por síntomas somáticos de la depresión que incluyen dolores, síntomas cardiovasculares o gastrointestinales vagos e inespecíficos, que por supuesto obligan a su exploración pero que una vez descartada una patología diferente de base se pueden considerar parte del cuadro afectivo.
Siempre que nos encontramos frente a un paciente con un episodio depresivo debemos descartar un Trastorno Bipolar explorando los antecedentes de episodios maníacos en los que se presentan síntomas opuestos a la depresión como euforia, aumento de la energía vital, inquietud motora, aumento de la auto – estima, disminución de la necesidad de sueño, verborrea, desinhibición y en ocasiones síntomas psicóticos. En estos episodios depresivos, el tratamiento no se debe realizar con antidepresivos sino con reguladores del estado del ánimo como el Litio, la Carbamazepina o el Valproato para evitar una ciclación al estado de manía.

El mismo DSM IV subdivide los Trastornos de Ansiedad en Trastorno de Pánico con o sin agorafobia, Fobias específicas, Fobia social, Trastorno Obsesivo Compulsivo, Trastorno de Estrés postraumático, Trastorno de Estrés Agudo y Trastorno de Ansiedad Generalizada. En todos los trastornos de ansiedad se encuentran los típicos síntomas de la ansiedad que de acuerdo al trastorno específico se manifiestan en intensidad, frecuencia o situaciones diferentes. Estos síntomas se pueden dividir en somáticos o psíquicos así:  Los síntomas somáticos son palpitaciones, taquicardia, sudoración, temblor, disnea subjetiva, nausea, malestar abdominal, escalofríos y parestesias. Los síntomas psíquicos son angustia, miedo, sensación de desmayo, de perder el control, de enloquecer, desrealización ty despersonalización.

En el trastorno de Pánico estos síntomas ocurren de forma súbita sin que se observe un factor desencadenante (básicamente corresponden a una descarga adrenérgica) y rápidamente alcanzan un pico en un periodo de aproximadamente 10 minutos, estos episodios se repiten dando mucho malestar al paciente con temor a que se vuelvan a repetir. En algunos casos se puede desarrollar la Agorafobia en la que se experimenta miedo a estar en lugares donde resulte difícil escapar o pedir ayuda como son los espacios con mucha gente o los espacios abiertos, con la consiguiente evitación de estos lugares. Siempre que se sospecha un Trastorno de Pánico se debe descartar una patología orgánica como factor etiológico como las arritmias primarias o las alteraciones tiroideas.  En el Trastorno de Ansiedad Generalizada los síntomas aparecen en forma leve, poco intensa pero crónica, durando al menos 6 meses. Estas personas tienen dificultad para sentirse relajados y dificulta el funcionamiento del sujeto en su vida social, laboral y familiar. Las personas con Trastorno Obsesivo Compulsivo presentan una serie de pensamientos, imágenes o impulsos, llamados Obsesiones, que son recurrentes y persistentes, que generan ansiedad en el paciente y a pesar de que la persona los considera absurdos y no desea que se repitan, aparecen nuevamente. Además se acompañan de las denominadas Compulsiones que consisten en comportamientos o actos repetitivos que la persona realiza para disminuir la ansiedad generada por las obsesiones, sin embargo al poco tiempo de realizarlos nuevamente aparecen estas y la persona entra en un circulo vicioso que le consume mucho tiempo al día.

Las personas que presencian o son víctimas de una situación traumática severa y la han vivido con un miedo intenso o gran terror pueden desarrollar un Trastorno de Estrés Postraumático que consiste en que esta situación es revivida en una forma recurrente con pesadillas, pensamientos, imágenes o ?flashback? (imágenes muy nítidas que dan la sensación de volver a vivir la situación). La persona con esta enfermedad desarrolla evitaciones de situaciones, lugares, conversaciones o actividades que estén asociadas con el trauma y genera síntomas de tipo ansioso que no estaban presentes antes de este, como irritabilidad, hipervigilancia, insomnio y disminución en la concentración.

El tratamiento de los Trastornos Depresivos y los Trastornos de Ansiedad se basa en  los antidepresivos y los ansiolíticos. En Colombia tenemos los Antidepresivos Tricíclicos (ADT), los Inhibidores Selectivos de la Recaptación de la Serotonina (ISRS), un Inhibidor Reversible de la Monoaminoxidasa A (IRMA) llamado Moclobemida y un Inhibidor de la Recaptación de la Serotonina y Noradrenalina (IRSN) denominado Venlafaxina. En general se considera que todos los antidepresivos son eficaces a pesar de tener acciones neurobioquímicas diferentes sin embargo los perfiles de seguridad y tolerancia son diferentes. Estos medicamentos NO tienen potencial de adicción ni de tolerancia a diferencia de las benzodiazepinas por lo que pueden darse a largo plazo sin necesidad de estar variando las dosis. Los ADT son los medicamentos antidepresivos clásicos e incluyen la Imipramina, la Amitriptilina, la Clomipramina  y la Butriptilina. Este grupo de medicamentos ejerce su acción terapéutica  por medio del aumento de la serotonina y noradrenalina en la hendidura sináptica. Sin embargo producen bloqueo a nivel de los receptores ?1 adrenérgicos, histaminérgicos tipo 1 y muscarínicos de acetilcolina que están relacionados con los efectos secundarios de estos fármacos. Estos son la hipotensión ortostática, las palpitaciones, la boca seca, el estreñimiento, la dificultad en la micción, la visión borrosa, el sedación, etc. Estos efectos hacen necesario que la dosis se realice en forma ascendente lenta equivalente a 25 mg de Imipramina cada 2 o 3 días hasta llegar al equivalente de 150 a 200 mg/día. Todos los medicamentos antidepresivos tardan 2 a 3 semanas para comenzar a ejercer su acción terapéutica pero los efectos adversos se pueden presentar desde el inicio del tratamiento. Los ISRS son la fluoxetina, la sertralina, la fluvoxamina, la paroxetina y el citalopram. Estos tienen un perfil de mayor seguridad pues su acción es básicamente aumentando la serotonina a nivel sináptico sin efectos sobre los otros neurotrasmisores, además la dosis de inicio es en una gran cantidad de pacientes la dosis terapéutica sin necesidad de hacer un ascenso gradual. También tienen en su mayoría (excepto la fluvoxamina) vidas medias largas que posibilitan la dosis única diaria. Los efectos secundarios más frecuentes son nausea, dispepsia, diarrea, sudoración, cefalea, insomnio, disminución en la libido y eyaculación retrasada. Estos medicamentos son inhibidores de algunas isoenzimas del citocromo P-450, principalmente la 2D6 la cual metaboliza una gran cantidad de medicamentos incluyendo otros medicamentos psiquiátricos y antiarrítmicos, lo que hace necesario vigilar las interacciones farmacológicas para evitar los aumentos en los niveles plasmáticos de otros medicamentos. El tratamiento para una depresión debe hacerse durante un año si la persona solamente ha tenido un episodio depresivo en su vida sin embargo cuando la depresión es recurrente el tiempo puede ser mayor, manteniendo la dosis a la cual ha respondido al tratamiento.

Las benzodiazepinas son los medicamentos ansiolíticos más utilizados en la actualidad. Estos medicamentos tienen una acción rápida y producen disminución de los niveles de ansiedad en forma temprana. Se incluyen en este grupo el diazepam, el lorazepam, el alprazolam, el clonazepam, el bromazepam, etc. Estos medicamentos tienen el potencial de producir dependencia y tolerancia que depende de la dosis, el tiempo del tratamiento, la vida media y la potencia relativa de la sustancia. En general se deben utilizar por tiempos cortos y conjuntamente con algún antidepresivo para luego hacer un descenso lento para evitar los síntomas de abstinencia. Las benzodiazepinas con efecto antipánico son el alprazolam y el clonazepam, las otras benzodiazepinas no se recomiendan para el Trastorno de Pánico a pesar de ser excelentes ansiolíticos.

Ventilación Mecánica en casa

Reprinted from Respiratory Care [Respir Care 1995;40(12):1313-1320]
AARC Clinical Practice Guideline
Long-Term Invasive Mechanical Ventilation in the Home
HIMV 1.0 PROCEDURE:
The application of invasive mechanical ventilation and care of the patient-ventilator system in the home, as ordered by a physician.
HIMV 2.0 DESCRIPTION/DEFINITION:
Mechanical ventilation may be defined as a life support system designed to replace or support normal ventilatory lung function.(1) Ventilator dependence is caused by an imbalance between ventilatory capacity and demand.(2) “A ventilator-assisted individual (VAI) may require mechanical aid for breathing to augment or replace spontaneous ventilatory efforts to achieve medical stability” or to maintain life.(3) The patient eligible for invasive long term mechanical ventilation in the home (HIMV) requires a tracheostomy tube(4-6) for ventilatory support but no longer requires intensive medical and monitoring services.(7-9) This guideline refers to patients ventilated by positive pressure via a tracheostomy tube in the home.
The goals of HIMV are
2.1 to sustain and extend life;(8,10-19)
2.2 to enhance the quality of life;(10-15,17-29)
2.3 to reduce morbidity;(8,10,11,13,16,20,30)
2.4 to improve or sustain physical and psychological function of all VAIs(7,8,10,13,15,16,18,20,31,32) and to enhance growth and development in pediatric VAIs;(5,7,8,12,17-19,23,28,33-36)
2.5 to provide cost-effective care.(7,8,10,11,13-19,22, 23,27,28,32,36-45)
HIMV 3.0 SETTING:
The setting is the home, which for the purposes of this guideline may be the patient’s home,(4,5,10,18,19,22, 27,32,34,38,40,41,46-53) a foster home,(10,17) or a group-living environment.(10,51)
HIMV 4.0 INDICATIONS:
4.1 Patients requiring invasive long-term ventilatory support have demonstrated:
4.1.1 an inability to be completely weaned from invasive ventilatory support or
4.1.2 a progression of disease etiology that requires increasing ventilatory support.
4.2.Conditions that met these criteria may include but are not limited to ventilatory muscle disorders,(4,5,10,11,14,16-19,21,26,27,33,35,38,42,43,46,52,54-62) alveolar hypoventilation syndrome,(4,5,10,17,18, 19,23,33,34,42,43,46,47,59,60) primary respiratory disorders,(4,10,17,18,19,23,42,46,59,60) obstructive diseases,(5,10,57,58) restrictive diseases,(5,10,16,43,46,56) and cardiac disorders including congenital anomalies.(17,23,19,42,46,59)
HIMV 5.0 CONTRAINDICATIONS
Contraindications to HIMV include:
5.1 The presence of a physiologically unstable medical condition requiring higher level of care or resources than available in the home.(4-7,10, 14,16,17,19,20,21,23,26,29,33,52,59) Examples of indicators of a medical condition too unstable for the home and long term care setting are:
5.1.1 FIO2 requirement > 0.40(4,5,10,16,35)
5.1.2 PEEP > 10 cm H2O(4,5,10,12,16,35)
5.1.3 Need for continuous invasive monitoring in adult patients(4,6,16)
5.1.4 Lack of mature tracheostomy
5.2 Patient’s choice not to receive home mechanical ventilation(5,10,16,19,23,26,39,42,52,56,58,63,64)
5.3 Lack of an appropriate discharge plan(4,5,8,11, 13,18,33,34,38,39,46,48,51,65)
5.4 Unsafe physical environment as determined by the patient’s discharge planning team.(10,13,66)
5.4.1 Presence of fire, health or safety hazards including unsanitary conditions.(39,51)
5.4.2 Inadequate basic utilities (such as heat, air conditioning, electricity).(4,5,10, 19,22,33,38,39,52,67)
5.5 Inadequate resources for care in the home:
5.5.1 Financial(9,10,13,14,16,18,19,23,25,26,33,35,38-40,44,52,55,56,59,68,69)
5.5.2 Personnel
5.5.2.1 Inadequate medical follow-up(13,14,16,18,29,33,36,38,39,50,61)
5.5.2.2 Inability of VAI to care for self, if no caregiver is available(5,16)
5.5.2.3 Inadequate respite care for caregivers(17,19,26)
5.5.2.4 Inadequate numbers of competent caregivers(5,13,21,23,25,26,30,38,39,52,68)
HIMV 6.0 HAZARDS AND COMPLICATIONS
6.1 Deterioration or acute change in clinical status of VAI. Although ventilator-associated complications in the home are poorly documented, experience in other sites can be extrapolated. The following may cause death or require rehospitalization for acute treatment.
6.1.1 Medical: Hypocapnia, respiratory alkalosis,(70) hypercapnia, respiratory acidosis,(70) hypoxemia, barotrauma,(5,64,70) seizures, hemodynamic instability,(21) airway complications (stomal or tracheal infection, mucus plugging, tracheal erosion or stenosis),(5) respiratory infection (tracheobronchitis, pneumonia),(57,70,71) bronchospasm,(5) exacerbation of underlying disease, or natural course of the disease
6.1.2 Equipment-related: Failure of the ventilator, malfunction of equipment,(10) inadequate warming and humidification of the inspired gases, inadvertent changes in ventilator settings, accidental disconnection from ventilator,(27) accidental decannulation
6.1.3 Psychosocial: Depression,(5,10,43) anxiety,(4,10,43) loss of resources–caregiver or financial,(10,19,25,40,43) detrimental change in family structure or coping capacity(5,10,19,25, 34,38,54,55,56,71,72)
HIMV 7.0 LIMITATIONS
In the home care setting, making and implementing changes in the plan of care may take longer than in a health care facility.
HIMV 8.0 ASSESSMENT OF NEED
8.1 Determination that indications are present and contraindications are absent.
8.2 Determination that the goals listed in 2.1 can be met in the home.
8.3 Determination that no continued need exists for higher level of services.
8.4 Determination that frequent changes in the plan of care will not be needed.
HIMV 9.0 ASSESSMENT OF OUTCOME
At least the following aspects of patient management and condition should be evaluated periodically as long as the patient receives HIMV
9.1 Implementation and adherence to the plan of care
9.2 Quality of life
9.3 Patient satisfaction
9.4 Resource utilization
9.5 Growth and development in the pediatric patient
9.6 Unanticipated morbidity, including need for higher level site of care.
9.7 Unanticipated mortality
HIMV 10.0 RESOURCES
10.1 Equipment
10.1.1 Ventilator(s)–Choice should be based on patient’s clinical need.(5,10,14,22,23, 35,38,67,73) Patient’s medical needs may dictate that more than one ventilator be provided.
10.1.1.1 Ventilators chosen for home care must be dependable and easy for the intended caregivers to operate; small size and lightweight are desirable
10.1.1.2 Mobility is frequently an essential element of the plan of care of the patient. The mechanical ventilator system chosen for such a patient should allow mobility.
10.1.2 With portable, volume-cycled ventilators, use of the SIMV mode increases work of breathing, and the addition of an external continuous-flow system reduces portability.(1,10,74-76)
10.1.3 Complex and nonportable components are not recommended for HIMV but may be used to meet the needs of certain pediatric patients.(10,13,22,35,75)
10.1.3.1 Ventilators powered by external compressed gas sources are less desirable.(10,22)
10.1.3.2 A second ventilator should be provided for
10.1.3.2.1 patients who cannot maintain spontaneous ventilation for 4 or more consecutive hours;(4,10,13,67)
10.1.3.2.2 patients who live in an area where a replacement ventilator cannot be provided within 2 hours;(4,13,39,67)
10.1.3.2.3 patients who require mechanical ventilation during mobility as prescribed in their plan of care.
10.1.4 An adequate power source must be available to operate the ventilator consistent with patient needs.(4,5,10,13,14,39,67) This may be supplied by one or more of the following methods:
10.1.4.1 Alternating current (AC) is the primary power source for most long-term care ventilators. Emergency AC power should be available in the long-term care facility.
10.1.4.2 Direct current (DC) by external battery may be used to allow mobility and as an emergency power source. The internal battery of the ventilator should be used only for short-term, emergency use. It should not be used as a primary source of power.
10.1.5 Alarms
10.1.5.1 A patient-disconnect (eg, low-pressure10 or low-exhaled-volume) and a high-pressure alarm are essential.
10.1.5.2 If patient disconnection is likely to produce a serious adverse effect, a remote alarm and a secondary alarm may be indicated. A secondary alarm may be based on chest-wall impedance and cardiac activity, exhaled volume, end-tidal CO2, or pulse oximetry with alarm capabilities.(42)
10.1.6 Humidification system(s) are essential for invasive mechanical ventilation. The type of system used is determined by the patient’s medical needs(77) and the patient’s need for mobility.(10,13,35) It may be appropriate for the patient to use more than one type of system, based on those needs.(1,15,78,79-81)
10.1.6.1 Heated humidifier (temperature probes should be provided).
10.1.6.2 Heat and moisture exchanger can be used during transport and to enhance mobility.(1,77,81)
10.1.7 Ventilator circuit and accessories as medically indicated.
10.1.8 Self-inflating resuscitation bag with tracheostomy attachments and mask of appropriate size(5,10,21-23,39,67)
10.1.9 Replacement tracheostomy tube of appropriate size plus a tube one size smaller should be available at all times.
10.1.10 Suction equipment(5,10,13,21-23,39,62,67) including a battery-powered aspirator for patients who leave the home or when indicated as an alternate source in the event of a power failure
10.1.11 Supplemental oxygen as medically indicated(10,13,39,67).
10.1.12 Patients must have an adequate means of communicating their needs and desires and to summon help in the case of emergency.(10)
10.2 Personnel:
10.2.1 Lay caregivers (eg, family members, personal care attendants, and non-credentialed health care personnel such as nurse’s aides) can be taught skills and techniques of care for a specific VAI. Appropriately trained lay caregivers must demonstrate competency in
10.2.1.1 proper set up, use, troubleshooting, and maintenance of the equipment and supplies;(10,23,32,33,39,40,50,65)
10.2.1.2 patient assessment and ongoing response to invasive mechanical ventilation;(10,23,32,33,35,40,65)
10.2.1.3 responding to the hazards of invasive mechanical ventilation;(22,23,26,33)
10.2.1.4 responding to emergencies;(10,23,32,39,40) in the case of
10.2.1.4.1 power failure;
10.2.1.4.2 acute life threatening events such as accidental decannulation(22) or other need for tracheostomy tube replacement,(10) other unexpected events, or medical deterioration of the patient
10.2.1.4.3 failure of equipment or supplies;
10.2.1.5 complying with appropriate infection control procedures;(10,39,65)
10.2.1.6 providing appropriate return demonstrations in the use and application of any additional techniques required for the ongoing care of the VAI, such as suctioning and use of ancillary equipment;(10,39,40,50,65)
10.2.2 Level-II practitioners are health-care professionals capable not only of providing direct patient care but also possessing demonstrated competencies to monitor and assess both the patient and equipment. Level-II practitioners are capable of training and evaluating lay caregivers. Level-II practitioners should be credentialed health care professionals (eg, RRT, CRTT, RN) with documented knowledge and demonstrated competencies to:
10.2.2.1 provide knowledge and understanding of the patient’s disease, goals and limitations of invasive mechanical ventilation;(32,33,39)
10.2.2.2 assess patient’s response to invasive mechanical ventilation;
10.2.2.3 make recommendations for changes in respiratory management of patient, including weaning as necessary;(10,33)
10.2.2.4 train and monitor caregivers;(4,5,10,32,33,40,50)
10.2.2.5 monitor patient’s ongoing ventilatory status;
10.2.2.6 communicate results of assessment to the health care team.(5,39)
10.3 Finances: HIMV can only be instituted and maintained with adequate financial resources to provide the necessary equipment and personnel to manage the patient’s care.(10,13,35,43)
HIMV 11.0 MONITORING
The frequency of monitoring should be determined by the ongoing individualized care plan and be based upon the patient’s current medical condition. The ventilator settings, proper function of equipment, and the patient’s physical condition should be monitored and verified: (1) with each initiation of invasive ventilation to the patient, including altering the source of ventilation, as from one ventilator or resuscitation bag to another ventilator; (2) with each ventilator setting change; (3) on a regular basis as specified by individualized plan of care.(35)
All appropriately trained caregivers should follow the care plan and implement the monitoring that has been prescribed. These caregivers may operate, maintain and monitor all equipment and perform all aspects of care required by the VAI after having been trained and evaluated on their level of knowledge for that equipment and the VAI’s clinical response to each of the interventions.
11.1 Lay caregivers should monitor the following regularly:
11.1.1 Patient’s physical condition: respiratory rate, heart rate, color changes, chest excursion, diaphoresis, and lethargy, blood pressure, body temperature.
11.1.2 Ventilator settings: The frequency at which alarms and settings are to be checked should be specified in the plan of care.
11.1.2.1 Peak pressures
11.1.2.2 Preset tidal volume
11.1.2.3 Frequency of ventilator breaths
11.1.2.4 Verification of oxygen concentration setting
11.1.2.5 PEEP level (if applicable)
11.1.2.6 Appropriate humidification of inspired gases
11.1.2.7 Temperature of inspired gases (if applicable)
11.1.2.8 Heat and moisture exchanger function
11.1.3 Equipment function:(10,13)
11.1.3.1 Appropriate configuration of ventilator circuit(82)
11.1.3.2 Alarm function
11.1.3.3 Cleanliness of filter(s)–according to manufacturer’s recommendation
11.1.3.4 Battery power level(s)–both internal and external
11.1.3.5 Overall condition of all equipment
11.1.3.6 Self-inflating manual resuscitator–cleanliness and function
11.2 A Level-II practitioner should perform a thorough, comprehensive assessment of the patient and the patient-ventilator system on a regular basis as prescribed by the plan of care. In addition to the variables listed in 11.1.1-11.1.3. the Level-II practitioner should implement, monitor, and assess results of other interventions as indicated by the clinical situation and anticipated in the care plan.
11.2.1 Pulse oximetry–should be used in patients requiring a change in prescribed oxygen levels or in patients with a suspected change in condition.(10,35)
11.2.2 End-tidal CO2–may be useful for establishing trends in CO2 levels during weaning.(10,23,33,35,59,83,84)
11.2.3 Specimen collection (and analysis as applicable) as prescribed by physician–including but not limited to sputum and blood work (eg, arterial blood gas analysis and complete blood counts).(5,10,32,37)
11.2.4 Cardiorespiratory monitoring (electrocardiogram, heart-rate trending)(10)
11.2.5 Pulmonary function testing
11.2.6 Ventilator settings
11.2.7 Exhaled tidal volume
11.2.8 Analysis of fraction of inspired oxygen
11.3 Level-II personnel are also responsible for maintaining interdisciplinary communication concerning the plan of care
11.4 Level-II personnel should integrate respiratory plan of care into the patient’s total care plan.(10) Plan of care should include
11.4.1 all aspects of patient’s respiratory care(66) and
11.4.2 ongoing assessment and education of the caregivers involved.
HIMV 12.0 FREQUENCY:
12.1 The frequency of ventilation (and the patient’s ventilator-free time) is dictated by the patient’s physiologic needs and is determined in consultation with the patient’s physician.
12.2 The frequency of assessment of the VAI and the patient-ventilator system must be noted in the evolving total care plan as determined by the health care team, in conjunction with the VAI and their caregivers.
HIMV 13.0 INFECTION CONTROL
13.1 Both professional and lay caregivers should be aware of the potential for transmission of both chronic and acute infection from patient to caregiver and from caregiver to patient and should take the steps necessary to avoid that transmission. Aspects of avoidance include:
13.1.1 careful handwashing and barrier protection when appropriate
13.1.2 careful disposal of medical waste
13.1.3 adequate environmental air exchange
13.1.4 maximizing protection of patient, family, and caregivers (eg, influenza immunization) and minimizing exposure to persons with acute infections (eg, limiting visitors with upper respiratory infections).
13.2 Evidence is lacking to support an optimal plan for changing and processing ventilator circuits and ancillary equipment in the home. However, studies from institutional settings(85,86) suggest that ventilator circuits need not be changed more often than once each week. Further, it appears that the less often a circuit is entered, the less likely contamination is to occur.
Respiratory Home Care Focus Group:
Peggi Robart RRT RCP, Chairman, Boston MA
Barry J Make MD, Denver CO
Susan L McInturff RRT RCP, Bremerton WA
Dennis W Tureson Sr RRT CRTT, Minneapolis MN
Melissa P Weimer, RRT, McKeesport PA
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27. Splaingard ML, Frates RC Jr, Harrison GM, Carter E, Jefferson LS. Home positive-pressure ventilation: twenty years’ experience. Chest 1983;84(4):376-382.
28. Downes JJ, Pilmer SL. Chronic respiratory failure–controversies in management. Crit Care Med 1993;21 (9, Suppl):S363-S364.
29. Purtilo RB. Ethical issues in the treatment of chronic ventilator-dependent patients. Arch Phys Med Rehabil 1986;67:718-721.
30. Dunkin LJ. Home ventilatory assistance. Anaesthesia 1983;38:644-649.
31. Affeldt JE, Bower AG, Dail CW, Aratan N. Prognosis for recovery in severe poliomyelitis. Arch Phys Med Rehabil 1957;38:290-295.
32. Make BJ. Long-term management of ventilator-assisted individuals: the Boston University experience. Respir Care 1986;31(4):303-310.
33. American Thoracic Society Ad Hoc Committee of the Scientific Assembly on Pediatrics. Home mechanical ventilation of pediatric patients. Am Rev Respir Dis 1990;141:258-259.
34. Massachusetts Department of Public Health, Burr BH, Guyer B, Todres ID, Abrahams B, Chiodo T. Home care for children on respirators. N Engl J Med 1983;309 (21):1319-1323.
35. Kacmarek RM, Thompson JE. Respiratory care of the ventilator-assisted infant in the home. Respir Care 1986;31(7):605-614.
36. Whitcomb ME. Care of the ventilator-dependent patient: public policy considerations. Respir Care 1986;31 (4):283-287.
37. Clark K. Psychosocial aspects of prolonged ventilator dependency. Respir Care 1986;31(4):329-333.
38. Dunne P. Demographics and financial impact of home respiratory care. Respir Care 1994;39(4):309-320.
39. Feldman J, Tuteur PG. Mechanical ventilation: from hospital intensive care to home. Heart Lung 1982; 11(2):162-165.
40. Fields AI, Rosenblatt A, Pollack MM, Kaufman J. Home care cost-effectiveness for respiratory technology-dependent children. AJDC 1991;145:729-733.
41. Fischer DA, Prentice WS. Feasibility of home care for certain respiratory-dependent restrictive or obstructive lung disease patients. Chest 1982;82(6):739-743.
42. Frates RC Jr, Splaingard ML, Smith EO, Harrison GM. Outcome of home mechanical ventilation in children. J Pediatr 1985;106(5):850-856.
43. Sivak ED, Cordasco EM, Gipson WT. Pulmonary mechanical ventilation at home: a reasonable and less expensive alternative. Respir Care 1983;28(1):42-49.
44. Goldberg AI, Frownfelter D. The ventilator-assisted individuals study. Chest 1990;98(2):428-433.
45. Goldberg AI, Faure EA. Home care for life supported persons in England: the Responaut approach. Chest 1984;86:910-914.
46. Goldberg A. Children on ventilators: breathing easier at home. Cont Pediatr Vol. 59-79.
47. Oren J, Kelly DH, Shannon DC. Long-term follow-up of children with congenital central hypoventilation syndrome. Pediatrics 1987;80(3):375-380.
48. Goldberg AI. Mechanical ventilation and respiratory care in the home in the 1990s: some personal observations. Respir Care 1990;35(3):247-259.
49. Peters SG, Viggiano RW. Home mechanical ventilation. Mayo Clin Proc 1988;63:1208-1213.
50. Thompson CL, Richmond M. Teaching home care for ventilator-dependent patients: the patients’ perception. Heart Lung 1990;19(1):79-83.
51. Prentice WS. Transition from hospital to home. In: Gilmartin ME, Make BJ, (editors). Prob Respir Care 1988;1(2):174-191.
52. Nochomovitz ML, Montenegro HD, Parran S, Daly B. Placement alternatives for ventilator-dependent patients outside the intensive care unit. Respir Care 1991; 36(3):199-204.
53. American Medical Association Home Care Advisory Panel. Guidelines for the medical management of the home care patient, 1992.
54. Miller JR, Colbert AP, Schock NC. Ventilator use in progressive neuromuscular disease: impact on patients and their families. Dev Med Child Neurol 1988;30 (2):200-207.
55. Moss AH, Casey P, Stocking CB, Roos RP, Brooks BR, Siegler M. Home ventilation for amyotrophic lateral sclerosis patients: outcomes, costs, and patient, family, and physician attitudes. Neurology 1993;43:438-443.
56. Sivak ED, Cordasco EM, Gipson WT, Mehta A. Home care ventilation: the Cleveland Clinic experience from 1977 to 1985. Respir Care 1986;31(4):294-302.
57. Hänninen P, Wendelin H, Räsänen O, Panelius M. Chronic respiratory paralysis. Acta Paediatr 1972; 228(Suppl):1-32.
58. Gilgoff I, Prentice W, Baydur A. Patient and family participation in the management of respiratory failure in Duchenne’s muscular dystrophy. Chest 1989;95(3): 519-524.
59. Schreiner MS, Downes JJ, Kettrick RG, Ise C, Voit R. Chronic respiratory failure in infants with prolonged ventilator dependency. JAMA 1987;258(23):3398-3404.
60. Strumpf DA, Millman RP, Hill NS. The management of chronic hypoventilation. Chest 1990;98(2):474-480.
61. Pierson DJ. Home respiratory care in different countries. Eur Respir J 1989;2(7, Suppl):630S-636S.
62. Adams AB, Whitman J, Marcy T. Surveys of long-term ventilatory support in Minnesota: 1986 and 1992. Chest 1993;103(5):1463-69.
63. Silverstein MD, Stocking CB, Antel JP. Amyotrophic lateral sclerosis and life-sustaining therapy: patient’s desires for information, participation in decision making, and life-sustaining therapy. Mayo Clin Proc 1991;66:906-913.
64. Snider GL. Thirty years of mechanical ventilation: changing implications (commentary). Arch Intern Med 1983;143:745-749.
65. Daley White K, Walsh Perez P. Your ventilator patient can go home again. Nursing 1986;12:54-56.
66. American Association for Respiratory Care. AARC clinical practice guideline: discharge planning for the respiratory care patient. Respir Care 1995;40(12): 1308-1312.
67. Kacmarek RM, Spearman CB. Equipment used for ventilatory support in the home. Respir Care 1986;31 (4):311-328.
68. Hodgkin JE. Non-ventilator aspects of care for ventilator-assisted patients. Respir Care 1986;31(4):334-337
69. DeWitt PK, Jansen MT, Davidson Ward SL, Keens TG. Obstacles to discharge of ventilator-assisted children from the hospital to home. Chest 1993;103(5):1560-1565.
70. Pierson DJ. Complications associated with mechanical ventilation. Crit Care Clin 1990;6(3):711-724.
71. Harrison GM Jr, Mitchell MB. The medical and social outcome of 200 respirator and former respirator patients on home care. Arch Phys Med Rehabil 1961;42: 590-598.
72. Quint RD, Chesterman E, Crain LS, Winkleby M, Boyce WT. Home care for ventilator-dependent children. AJDC 1990;144:1238-1241.
73. Drinker P, McKhann CF. The use of a new apparatus for the prolonged administration of artificial ventilation: a fatal case of poliomyelitis. JAMA 1929;255(11):1473-1475, 1658-1660.
74. Kacmarek RM, Stanek KS, McMahon K, Wilson RS. Imposed work of breathing during synchronized intermittent mandatory ventilation (SIMV) provided by five home care ventilators. Respir Care 1990;35(5):405-414.
75. Kacmarek RM. Essential gas delivery features of mechanical ventilators. Respir Care 1992;37(9):1045-1055.
76. Robart P, Hirsch C, Barker S, Kacmarek R. Work of breathing imposed during spontaneous breathing in the SIMV mode of home care ventilators (abstract). Respir Care 1992;37(11):1358-1360.
77. American Association for Respiratory Care. AARC clinical practice guideline: humidification during mechanical ventilation. Respir Care 1992;37(8):887-890.
78. Branson RD, Chatburn RL. Humidification of inspired gases during mechanical ventilation (editorial). Respir Care 1993;38(5):461-468.
79. Shelly MP. Inspired gas conditioning. Respir Care 1992;37(9):1070-1080.
80. Misset B, Escudier B, Rivara D, Leclercq B, Nitenberg G. Heat and moisture exchanger vs heated humidifier during long-term mechanical ventilation. Chest 1991; 100(1):160-163.
81. Branson RD, Hurst JM, Laboratory evaluation of moisture output of seven airway heat and moisture exchangers. Respir Care 1987;32(9):741-747.
82. Gietzen JW, Lund JA, Swegarden JL. Effect of PEEP-valve placement on function of a home-care ventilator. Respir Care 1991;36(10):1093-1098.
83. Carlon GC, Ray C, Miodownik S, Kopec I, Groeger JS. Capnography in mechanically ventilated patients. Crit Care Med 88;16(5):550-556.
84. Stock MC. Capnography for adults. Crit Care Clin 1995;11(1):219-232.
85. Hess DR, Burns EC, Romagnoli DM, Kacmarek RM. Weekly ventilator circuit changes. A strategy to reduce costs without affecting pneumonia rates. Anesthesiology 1995;82(4):903-911.
86. Kollef MG, Shapiro SD, Fraser VJ, Silver, P, Murphy DM, Trovillion E, et al. Mechanical ventilation with or without 7-day circuit changes. A randomized controlled trial. Ann Intern Med 1995;123(3):168-174.
Additional Bibliography
Goldberg AI, Monahan CA. Home health care for children assisted by mechanical ventilation: the physician’s perspective. J Pedriatr 1989;114(3):378-383.
Bone RC. Long-term ventilator care: a Chicago problem and a national problem. Chest 1987;92(3):536-539.
Indihar FJ, Forsberg DP. Experience with a prolonged respiratory care unit. Chest 1982;81(2):189-192.
Indihar FJ, Walker NE. Experience with a prolonged respiratory care unit: revisited. Chest 1984;86(4):616-620.
Wagner DP. Economics of prolonged mechanical ventilation. Am Rev Respir Dis 1989;140(Suppl):S14-S18.
Gracey DR, Viggiano RW, Naessens JM, Hubmayr RD, Silverstein MD, Koenig GE. Outcomes of patients admitted to a chronic ventilator-dependent unit in an acute-care hospital. Mayo Clin Proc 1992;67:131-136.
American Association of Respiratory Care. Guidelines for disinfection of respiratory care equipment used in the home. Respir Care 1988;33(9):801-808.
Chatburn RL. Decontamination of respiratory care equipment: what can be done, what should be done. Respir Care 1989;34(2):98-109.
Davis PB, di Sant’Agnese PA. Assisted ventilation for patients with cystic fibrosis. JAMA 1978;239(18):1851-1854.
Zwillich CW, Pierson DJ, Creagh CE, Sutton FD, Schatz E, Petty TL. Complications of assisted ventilation: a prospective study of 354 consecutive episodes. Am J Med 1974;57:161-170.
Stauffer JL, Olson DE, Petty TL. Complications and consequences of endotracheal intubation and tracheotomy: a prospective study of 150 critically ill adult patients. Am J Med 1981;70:65-76.
Craven DE, Kunches LM, Kilinsky V, Lichtenberg DA, Make BJ, McCabe WR. Risk factors for pneumonia and fatality in patients receiving continuous mechanical ventilation. Am Rev Respir Dis 1986;133:792-796.
Dreyfuss D, Djedaini K, Weber P, Brun P, Lanore JJ, Rahmani J, Boussougant Y, Coste F. Prospective study of nosocomial pneumonia and of patient and circuit colonization during mechanical ventilation with circuit changes every 48 hours versus no change. Am Rev Respir Dis 1991; 143:738-743.
Craven DE, Goularte TA, Make BJ. Contaminated condensate in mechanical ventilator circuits: a risk factor for nosocomial pneumonia? Am Rev Respir Dis 1984;129:625-628.
Pierson DJ, George RB. Mechanical ventilation in the home: possibilities and prerequisites. Respir Care 1986;31 (4):266-270.
Interested persons may copy these Guidelines for noncommercial purposes of scientific or educational advancement. Please credit AARC and Respiratory Care Journal.

O2 terapia en casa u hospicio

Reprinted from RESPIRATORY CARE (Respir Care 1992;37:918-922)
AARC Clinical Practice Guideline
Oxygen Therapy in the Home or Extended Care Facility
OT-CC 1.0 PROCEDURE:
The procedure addressed is the administration of oxygen therapy in the home or in the extended care facility other than by mechanical ventilator.
OT-CC 2.0 DESCRIPTION/DEFINITION:
Oxygen therapy is the administration of oxygen at concentrations greater than that in ambient air with the intent of treating or preventing the symptoms and manifestations of hypoxia.(1)
OT-CC 3.0 SETTING:
This Guideline is confined to oxygen administration in the home or extended care facility.
OT-CC 4.0 INDICATIONS:
Documented hypoxemia: In adults, children and infants older than 28 days: (1) PaO2 < or = 55 torr or SaO2 < or = 88% in subjects breathing room air,1,2 or (2) PaO2 of 56-59 torr or SaO2 or SpO2 < or = 89% in association with specific clinical conditions (eg, cor pulmonale, congestive heart failure, or erythro-cythemia with hematocrit > 56).(3,4)
Some patients may not qualify for oxygen therapy at rest but will qualify for oxygen during ambulation, sleep, or exercise. Oxygen therapy is indicated during these specific activities when SaO2 is demonstrated to fall to < or = 88%.(5) OT-CC 5.0 CONTRAINDICATIONS: No absolute contraindications to oxygen therapy exist when indications are present. OT-CC 6.0 PRECAUTIONS AND/OR POSSIBLE COMPLICATIONS: 6.1 In spontaneously breathing hypoxemic patients with chronic obstructive pulmonary disease, oxygen administration may lead to an increase in PaCO2.(6-8) 6.2 Undesirable results or events may result from noncompliance with physician's orders or inadequate instruction in home oxygen therapy. 6.3 Complications may result from use of nasal cannulae9 or transtracheal catheters.(10) 6.4 Fire hazard is increased in the presence of increased oxygen concentrations. 6.5 Bacterial contamination associated with certain nebulizers and humidification systems is a possible hazard.(11-13) 6.6 Possible physical hazards can be posed by unsecured cylinders, ungrounded equipment, or mishandling of liquid oxygen (resulting in burns). Power or equipment failure can lead to an inadequate oxygen supply. OT-CC 7.0 LIMITATIONS OF PROCEDURE: Oxygen therapy has only limited benefit for the treatment of hypoxia due to anemia and benefit may be limited when circulatory disturbances are present. OT-CC 8.0 ASSESSMENT OF NEED: 8.1 Initial assessment: Need is determined by the presence of clinical indicators as previously described and the presence of inadequate oxygen tension and/or saturation as demonstrated by the analysis of arterial blood. Concurrent pulse oximetry values must be documented and reconciled with the results of the baseline blood gas analysis if future assessment is to involve pulse oximetry. 8.2 Ongoing evaluation or reassessment: Additional arterial blood gas analysis is indicated whenever there is a major change in clinical status that may be cardiopulmonary related. Arterial blood gas measurements should be repeated in 1-3 months when oxygen therapy is begun in the hospital in a clinically unstable patient to determine the need for long-term oxygen therapy (LTOT).(14) Once the need for LTOT has been documented, repeat arterial blood gas analysis or oxygen saturation measurements are unnecessary other than to follow the course of the disease, to assess changes in clinical status, or to facilitate changes in the oxygen prescription.(14,15) OT-CC 9.0 ASSESSMENT OF OUTCOME: Outcome is determined by clinical and physiologic assessment to establish adequacy of patient res-ponse to therapy. OT-CC 10.0 RESOURCES: 10.1 Equipment 10.1.1 Low-flow oxygen systems: Such devices supply oxygen at flows that are less than the patient's inspiratory demand (ie, the delivered oxygen is diluted with room air). These devices may supply either a low or high FIO2 depending upon the specific design.(16,17) Reservoir masks or other devices designed to provide for a high FIO2 are usually not appropriate for long-term oxygen therapy outside of the hospital. 10.1.1.1 Nasal cannulae can provide 24-40% oxygen (depending on patient's inspiratory flowrate) with flowrates up to 6 L/min in adults;1 infant flows should be limited to a maximum of 2 L/min.(18,19) Oxygen supplied to adults by nasal cannulae at flows < or = to 4 L/min need not be humidified.(20,21) 10.1.1.2 Transtracheal oxygen catheters can provide continuous oxygen therapy with oxygen consumption compared to nasal cannulas of only about one half of that used at rest and two thirds of that used with exercise. Transtracheal catheters may require greater patient supervision and have an increased risk for complication.(10) 10.1.1.3 Oxygen-conserving devices: Oxygen reservoir cannulae (nasal or pendant), demand oxygen delivery devices, and transtracheal catheters are currently being utilized for oxygen conservation. Each of these devices may have advantages or disadvantages that are related to specific design. 10.1.2 High-flow oxygen delivery systems: Such devices can provide a prescribed gas mixture of high or low oxygen concentration at flows that exceed patient demand; however, they are impractical for home use except for humidifying devices that are compressor-driven with supplemental oxygen bled in at low flows. Tracheostomy collars and T-tube adapters may be used with high-flow supplemental oxygen systems. The gas should be humidified by a continuous aerosol generator or a heated humidifier.(22,23) The humidifier is preferable because of the greater likelihood for the transmission of contagion via nebulizer. 10.1.3 Oxygen supply systems 10.1.3.1 Oxygen concentrators: Concentrators extract oxygen from ambient air and should deliver oxygen at concentrations of 85% or greater at up to 4 L/min.(24) Membrane oxygen concentra-tors typically provide oxygen at a lower FDO2, and higher flows are required to 'compensate' for the reduced FDO2. 10.1.3.2 Liquid oxygen systems: Liquid oxygen is provided in large reser-voir cannisters with smaller portable units that can be transfilled by the patient. There is evaporation loss from the cannisters when they are not in use. Many of the portable liquid oxygen units are appropriate for ambulatory therapy and can be utilized with oxygen-conserving devices to extend their functional time. 10.1.3.3 Compressed gas cylinders: Oxygen may be supplied in large cylinders (eg, G or H cylinders) as stationary units for home oxygen therapy. Smaller cylinders (eg, D and E cylinders) may be equipped with wheels and used as portable oxygen units (strollers). E cylinders may also be used as a backup for oxygen concentrators in the event of a power or equipment failure. Smaller cylinders coupled with oxygen conserving devices may be used as ambulatory units. 10.2 Personnel: Credentialed respiratory care practitioners (RRT or CRTT) or other credentialed persons with equivalent training and documented ability to perform the tasks may assess patients, initiate and monitor oxygen delivery systems, recommend changes in therapy, and instruct caregivers. Caregivers may operate and maintain oxygen delivery devices and assess a specific patient after they have been instructed by credentialed practitioners and have demonstrated the appropriate level of skill. OT-CC 11.0 MONITORING: 11.1 Patient 11.1.1 Clinical assessment should routinely be performed by the patient and/or the caregiver to determine changes in clinical status (eg, use of dyspnea scales and diary cards). Patients should be visited/monitored at least once a month by credentialed personnel unless conditions warrant more frequent visits. 11.1.2 Measurement of baseline oxygen tension and saturation is essential before oxygen therapy is begun.(5,15) These measurements should be repeated when clinically indicated or to follow the course of the disease. Measurements of SO2 also may be made to determine appropriate oxygen flow for ambulation, exercise, or sleep. 11.2 Equipment Maintenance and Supervision: All oxygen delivery equipment should be checked at least once daily by the patient or caregiver. Facets to be assessed include proper function of the equipment, prescribed flowrates, FDO2, remaining liquid or compressed gas content, and backup supply. A respiratory care practitioner or equivalent should during monthly visits reinforce appropriate practices and performance by the patient and caregivers and assure that the oxygen equipment is being maintained in accordance with manufacturers' recommendations. Liquid systems need to be checked to assure adequate delivery.(25) Oxygen concentrators should be checked regularly to assure that they are delivering 85% oxygen or greater at 4 L/min.(24) OT-CC 12.0 FREQUENCY: Oxygen therapy should be administered continuously unless the need has been shown to be associated only with specific situations (eg, exercise and sleep). OT-CC 13.0 INFECTION CONTROL: Under normal circumstances low-flow oxygen systems without humidifiers do not present a clinically important risk of infection and need not be routinely replaced. High-flow systems that employ heated humidifiers or aerosol generators, particularly when applied to subjects with artificial airways, can be important sources of infection and should be cleaned and disinfected on a regular basis. (Although studies have suggested that tubing should be changed every 48 hours in the hospital, there are no definitive studies regarding the frequency of tube changes at home or in long-term care facilities.) Oxygen Therapy Guidelines Committee: Dianne Lewis MS RRT, Chairman, Naples FL Thomas A Barnes EdD RRT, Boston MA Kay Beattie BA RRT, Columbus OH Laura J Reisman Beytas MPH RRT, Peoria IL Walter J O'Donohue Jr MD, Omaha NE Noah Perlman BS RRT, Boston MA Ray H Ritz BA RRT, Boston MA John Salyer RRT, Salt Lake City UT REFERENCES 1. American College of Chest Physicians, National Heart, Lung and Blood Institute. National Conference on Oxygen Therapy. Chest 1984;86:234-247. Published concurrently in Respir Care 1984;29:922-935. 2. American Academy of Pediatrics, American College of Obstetricians and Gynecologists. Guidelines for peri-natal care, 2nd ed. 1988:246-247. 3. Weitzenblum E, Sautegeau A, Ehrhart M, Mammosser M, Pelletier A. Long-term oxygen therapy can reverse the progression of pulmonary hypertension in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1985;131:493-498. 4. Report of the Medical Research Council Working Party. Long-term domiciliary oxygen therapy in chronic cor pulmonale complicating chronic bronchitis and emphysema. Lancet 1981;1:681-685. 5. Criteria for Medicare coverage of oxygen services in the home. Federal Register 1985;50(66):3-4. 6. Sassoon CSH, Hassell KT, Mahutte CK. Hyperoxic-induced hypercapnia in stable chronic obstructive pulmonary disease. Am Rev Respir Dis 1987;135:907-911. 7. Fisher AB. Oxygen therapy: side effects and toxicity. Am Rev Respir Dis 1980;122(5, Part 2):61-69. [4 or 5?] 8. Aubier M, Murciano D, Milic-Emili J, Touaty E, Daghfous J, Pariente R. Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure. Am Rev Respir Dis 1980;122:747-754. 9. Toome B. Allergic contact dermatitis to a nasal cannula (letter). Arch Dermatology 1989;125:571. 10. Christopher KL, Spofford BT, Petrun MD, McCarty DC, Goodman JR, Petty TL. A program for transtracheal oxygen delivery. Ann Intern Med 1987;107: 802-808. 11. U.S. Department of Health and Human Services, Public Health Services, Centers for Disease Control. Guideline for prevention of nosocomial pneumonia and guideline ranking scheme. Atlanta: CDC, 1982. 12. Pierce AK, Sanford JP. Bacterial contamination of aerosols. Arch Intern Med 1973;131:156-159. 13. Wexler MR, Rhame FR, Blumenthal MN, Cameron SB, Juni BA, Fish LA. Transmission of gram-negative bacilli to asthmatic children via home nebulizers. Ann Allergy 1991;66:267-271. 14. Conference Report. New problems in supply, reimbursement and certification of medical necessity for long-term oxygen therapy. Am Rev Respir Dis 1990;142: 721-724. 15. O'Donohue WJ Jr. Effect of oxygen therapy on increasing arterial oxygen tension in hypoxemic patients with stable chronic obstructive pulmonary disease while breathing ambient air. Chest 1991;100:968-972. 16. Redding JS, McAlfie DD, Parham AM. Oxygen concentrations received from commonly used delivery systems. South Med J 1978;71:169-172. 17. Goldstein RS, Young J, Rebuck AS. Effect of breathing pattern on oxygen concentration received from standard face masks. Lancet 1982;2:1188-1190. 18. Vain NE, Prudent LM, Stevens DP, Weeter MM, Maisels J. Regulation of oxygen concentration delivered to infants via nasal cannula. Am J Dis Child 1989;143: 1458-1460. 19. Fan LL, Voyles JB. Determination of inspired oxygen delivered by nasal cannula in infants with chronic lung disease. J Pediatr 1983;103:923-925. 20. Estey W. Subjective effects of dry versus humidified low-flow oxygen. Respir Care 1980;25:1143-1144. 21. Campbell E, Baker D, Crites-Silver P. Subjective effects of oxygen for delivery by nasal cannula: a prospective study. Chest 1988;86:241-247. 22. Dahlby RW, Hogg JC. Effect of breathing dry air on structure and function of airways. J Appl Physiol 1980;61(1):312-317. 23. Chatburn RL, Primiano FP Jr. A rational basis for humidity therapy. Respir Care 1987;32:249-253. 24. Conference Report. Problems in prescribing and supplying oxygen for Medicare patients. Am Rev Respir Dis 1986;134:340-341. 25. Massey LW, Hussey JD, Albert RK. Inaccurate oxygen delivery in some portable liquid oxygen devices. Am Rev Respir Dis 1988;137:204-205. ADDITIONAL BIBLIOGRAPHY Conference Report. Further recommendations for prescribing and supplying long-term oxygen therapy. Am Rev Respir Dis 1988;138:745-747. Neff TA, Petty TL. Long-term continuous oxygen therapy in chronic airway obstruction: mortality in relation to cor pulmonale, hypoxemia and hypercapnia. Ann Intern Med 1970; 72:621-626. Nocturnal Oxygen Therapy Trial Group. Continuous and nocturnal oxygen therapy in hypoxemic chronic obstructive lungdisease: a clinical trial. Ann Intern Med 1980;93:391-398. Heaton RK, Grant I, McSweeny AJ, Adams KM, Petty TL. Psychologic effects of continuous and nocturnal oxygen therapy in hypoxemic chronic obstructive pulmonary disease. Arch Intern Med 1983;143:1941-1947. Anthonisen NR, Wright BC, Hodgkin JE. Prognosis in chronic obstructive pulmonary disease. Am Rev Respir Dis 1986;133: 14-20. O'Donohue WJ Jr. The future of home oxygen therapy. Respir Care 1988;33:1125-1130. U.S. Department of Health and Human Services, Office of Inspector General, Office of Audit. Review of medical necessity for oxygen concentrators. Blue Cross and Blue Shield of Alabama, 1988. Common identification No. A-04-87-002000. Levine BE, Bigelow DB, Hemstra RD, Beckwitt JH, Mitchell RS, Nett LM, et al. The role of long-term continuous oxygen administration in patients with chronic airway obstruction and hypoxemia. Ann Intern Med 1967;66:639-650. Abraham AS, Cole RC, Bishop JM. Reversal of pulmonary hypertension by prolonged oxygen administration to patients with chronic bronchitis. Circ Res 1968;23:147-157. Selinger SR, Kennedy TP, Buescher P, Terry P, Parham W, Gofreed D, et al. Effects of removing oxygen from patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1987;136:85-91. Interested persons may copy these Guidelines for noncommercial purposes of scientific or educational advancement. Please credit AARC and Respiratory Care Journal.

Manejo de Emergencias de la Vía aérea

Reprinted from Respiratory Care (Respir Care 1995;40(7):749-760)
AARC Clinical Practice Guideline
Management of Airway Emergencies
MAE 1.0 PROCEDURE:
Recognition of signs of an impending or actual airway emergency. Initial treatment and continued management of airway emergencies to minimize the likelihood of adverse outcomes, in adults, children, and infants.
MAE 2.0 DESCRIPTION/DEFINITION:
Management of airway emergencies (MAE) for the purpose of this guideline encompasses all care necessary to deal with sudden and often life-threatening events affecting natural and artificial airways and involves the identification, assessment, and treatment of patients in danger of losing or not being able to maintain an adequate airway, including the newborn. This includes (1) identification of the causes of airway emergencies; (2) management of airway emergencies prior to tracheal intubation; (3) use of adjunctive equipment and special techniques for establishing, maintaining, and monitoring effective ventilation; (4) translaryngeal tracheal intubation, including nasal and oral tracheal intubation; (5) transtracheal catheter ventilation, (6) percutaneous dilational cricothyrotomy, and; (7) surgical cricothyrotomy.
MAE 3.0 SETTING:
The guideline applies to a variety of settings including but not limited to hospitals and pre- or interhospital transport.
MAE 4.0 INDICATIONS:
4.1 Conditions requiring management of the airway, in general, are impending or actual (1) airway compromise, (2) respiratory failure, and (3) need to protect the airway. Specific conditions include but are not limited to
4.1.1 Airway emergency prior to endotracheal intubation
4.1.2 Obstruction of the artificial airway
4.1.3 Apnea
4.1.4 Acute traumatic coma(1)
4.1.5 Penetrating neck trauma(2)
4.1.6 Cardiopulmonary arrest and unstable dysrhythmias(3)
4.1.7 Severe bronchospasm(4-8)
4.1.8 Severe allergic reactions with cardiopulmonary compromise(9,10)
4.1.9 Pulmonary edema(11,12)
4.1.10 Sedative or narcotic drug effect(13)
4.1.11 Foreign body airway obstruction(3)
4.1.12 Choanal atresia in neonates(14)
4.1.13 Aspiration
4.1.14 Risk of aspiration
4.1.15 Severe laryngospasm(15)
4.1.16 Self-extubation(16,17)
4.2 Conditions requiring emergency tracheal intubation include, but are not limited to
4.2.1 Persistent apnea
4.2.2 Traumatic upper airway obstruction (partial or complete)(18-20)
4.2.3 Accidental extubation of the patient unable to maintain adequate spontaneous ventilation(16,17)
4.2.4 Obstructive angioedema (edema involving the deeper layers of the skin, subcutaneous tissue, and mucosa)(21-23)
4.2.5 Massive uncontrolled upper airway bleeding(2,24)
4.2.6 Coma with potential for increased intracranial pressure(25)
4.2.7 Infection-related upper airway obstruction (partial or complete)
4.2.7.1 Epiglottitis in children or adults(26,27)
4.2.7.2 Acute uvular edema(28)
4.2.7.3 Tonsillopharyngitis or retropharyngeal abscess(29)
4.2.7.4 Suppurative parotitis(30)
4.2.8 Laryngeal and upper airway edema(31)
4.2.9 Neonatal- or pediatric-specific
4.2.9.1 Perinatal asphyxia(32,33)
4.2.9.2 Severe adenotonsillar hypertrophy(34,35)
4.2.9.3 Severe laryngomalacia(36,37)
4.2.9.4 Bacterial tracheitis(38-40)
4.2.9.5 Neonatal epignathus(41,42)
4.2.9.6 Obstruction from abnormal laryngeal closure due to arytenoid masses(43)
4.2.9.7 Mediastinal tumors(44)
4.2.9.8 Congenital diaphragmatic hernia(45)
4.2.9.9 Presence of thick and/or particulate meconium in amniotic fluid(46-48)
4.2.10 Absence of airway protective reflexes
4.2.11 Cardiopulmonary arrest
4.2.12 Massive hemoptysis(49)
4.3 The patient in whom airway control is not possible by other methods may require surgical placement of an airway (needle or surgical cricothyrotomy).(20,50,51)
4.4 Conditions in which endotracheal intubation may not be possible and in which alternative techniques may be used include but are not limited to
4.4.1 restriction of endotracheal intubation by policy or statute;
4.4.2 difficult or failed intubation in the presence of risk factors associated with difficult tracheal intubations(52) such as
4.4.2.1 Short neck,(53) or bull neck(54)
4.4.2.2 Protruding maxillary incisors(53)
4.4.2.3 Receding mandible(53)
4.4.2.4 Reduced mobility of the atlanto-occipital joint(55)
4.4.2.5 Temporomandibular ankylosis(55)
4.4.2.6 Congenital oropharyngeal wall stenosis(56)
4.4.2.7 Anterior osteophytes of the cervical vertebrae, associated with diffuse idiopathic skeletal hyperostosis(57)
4.4.2.8 Large substernal and/or cancerous goiters(58)
4.4.2.9 Treacher-Collins syndrome(59)
4.4.2.10 Morquio-Brailsford syndrome(60)
4.4.2.11 Endolaryngeal tumors(61)
4.4.3 when endotracheal intubation is not immediately possible
MAE 5.0 CONTRAINDICATIONS:
Aggressive airway management (intubation or establishment of a surgical airway) may be contraindicated when the patient’s desire not to be resuscitated has been clearly expressed and documented in the patient’s medical record or other valid legal document.(62-64)
MAE 6.0 PRECAUTIONS/HAZARDS AND/OR COMPLICATIONS:
The following represent possible hazards or complications related to the major facets of management of airway emergencies:
6.1 Translaryngeal intubation or cricothyrotomy is usually the route of choice. It may be necessary occasionally to use a surgical airway. Controversy exists as to whether intubation is hazardous in the presence of an unstable injury to the cervical spine. In one series the incidence of serious cervical spine injury in a severely injured population of blunt trauma patients was relatively low, and commonly used methods of precautionary airway management rarely led to neurologic deterioration.(65-67)
6.1.1 Failure to establish a patent airway(68-70)
6.1.2 Failure to intubate the trachea(68,69)
6.1.3 Failure to recognize intubation of esophagus(25,68,71-81)
6.1.4 Upper airway trauma, laryngeal, and esophageal damage(82)
6.1.5 Aspiration(70,74,82,83)
6.1.6 Cervical spine trauma(67,84,85)
6.1.7 Unrecognized bronchial intubation(25,68,72,82,86,87)
6.1.8 Eye injury(70)
6.1.9 Vocal cord paralysis(88)
6.1.10 Problems with ETT tubes
6.1.10.1 Cuff perforation(89)
6.1.10.2 Cuff herniation(89)
6.1.10.3 Pilot-tube-valve incompetence(90)
6.1.10.4 Tube kinking during biting(70,89)
6.1.10.5 Inadvertent extubation(17,25,68,72,86,91-93)
6.1.10.6 Tube occlusion(17,72,82,89,93,94)
6.1.11 Bronchospasm(68,70,74)
6.1.12 Laryngospasm(72)
6.1.13 Dental accidents(70)
6.1.14 Dysrhythmias(94)
6.1.15 Hypotension and bradycardia due to vagal stimulation(94)
6.1.16 Hypertension and tachycardia(94,95)
6.1.17 Inappropriate tube size(89,96-99)
6.1.18 Bleeding
6.1.19 Mouth ulceration(82)
6.1.20 Nasal-intubation specific
6.1.20.1 Nasal damage including epistaxis
6.1.20.2 Tube kinking in pharynx
6.1.20.3 Sinusitis(100-102) and otitis media
6.1.21 Tongue ulceration
6.1.22 Tracheal damage including tracheoesophageal fistula, tracheal innominate fistula, tracheal stenosis, and tracheomalacia(103-107)
6.1.23 Pneumonia(108)
6.1.24 Laryngeal damage with consequent laryngeal stenosis,(82,101,107,109,110) laryngeal ulcer, granuloma, polyps, synechia
6.1.25 Surgical cricothyrotomy or tracheostomy specific(111,112)
6.1.25.1 Stomal stenosis(82,113)
6.1.25.2 Innominate erosion(113)
6.1.26 Needle cricothyrotomy specific(114-118)
6.1.26.1 Bleeding at insertion site with hematoma formation
6.1.26.2 Subcutaneous and mediastinal emphysema(117)
6.1.26.3 Esophageal perforation
6.2 Emergency ventilation
6.2.1 Inadequate oxygen delivery(119-121)
6.2.2 Hypo- or hyperventilation(122-124)
6.2.3 Gastric insufflation and/or rupture(125,126)
6.2.4 Barotrauma(127-129)
6.2.5 Hypotension due to reduced venous return secondary to high mean intrathoracic pressure(130-132)
6.2.6 Vomiting and aspiration(125)
6.2.7 Prolonged interruption of ventilation for intubation(3,126)
6.2.8 Failure to establish adequate functional residual capacity in the newborn(133-135)
6.2.9 Movement of unstable cervical spine (more than by any commonly used method of endotracheal intubation).(136)
6.2.10 Failure to exhale due to upper airway obstruction during percutaneous transtracheal ventilation.(118,136)
MAE 7.0 LIMITATIONS OF PROCEDURE:
Despite adequate management of airway emergencies, desired outcome may not be achieved because of the patient’s underlying condition and progression of the process leading to the need for emergency airway management.
MAE 8.0 ASSESSMENT OF NEED:
The need for management of airway emergencies is dictated by the patient’s clinical condition. Careful observation, the implementation of basic airway management techniques, and laboratory and clinical data should help determine the need for more aggressive measures. Specific conditions requiring intervention include
8.1 Inability to adequately protect airway (eg, coma, lack of gag reflex, inability to cough) with or without other signs of respiratory distress.
8.2 Partially obstructed airway. Signs of a partially obstructed upper airway include ineffective patient efforts to ventilate, paradoxical respiration, stridor, use of accessory muscles, patient’s pointing to neck, choking motions, cyanosis, and distress. Signs of lower airway obstruction may include the above and wheezing.
8.3 Complete airway obstruction. Respiratory efforts with no breath sounds or suggestion of air movement are indicative of complete obstruction.
8.4 Apnea. No respiratory efforts are seen. May be associated with cardiac arrest.
8.5 Hypoxemia, hypercarbia, and/or acidemia seen on arterial blood gas analysis, oximetry or exhaled gas analysis.
8.6 Respiratory distress. Elevated respiratory rate, high or low ventilatory volumes, and signs of sympathetic nervous system hyperactivity may be associated with respiratory distress.
MAE 9.0 ASSESSMENT OF PROCESS AND OUTCOME:
Timely intervention to maintain the patient’s airway can improve outcome in terms of survival and level of function. Under rare circumstances, maintenance of an airway by nonsurgical means may not be possible. Despite optimal maintenance of the airway, patient outcomes are affected by patient-specific factors. Lack of availability of appropriate equipment and personnel may adversely affect patient outcome. Monitoring and recording are important to the improvement of the process of emergency airway management. Some aspects (eg, frequency of complications of tracheal intubation or time to establishment of a definitive airway) are easy to quantitate and can lead to improvement in hospitalwide systems. Patient condition following the emergency should be evaluated from this perspective.
MAE 10.0 RESOURCES:
10.1 Personnel: All health professionals should be trained, evaluated at frequent intervals, and retrained as necessary in the skills of emergency clearance of foreign body airway obstruction and airway secretions. Health professionals who are primary members of resuscitation teams in acute care hospitals should be skilled in advanced management of airway emergencies, emergency cardiac care (ECC), and advanced cardiac life support (ACLS).(137)
Emergency response system-a designated resuscitation team should be continuously available (24 hours/day, 7 days/week) to assist with the management of airway emergencies. Team members should be notified simultaneously. All hospital workers must know how to activate the hospital’s emergency response system.(137)
10.1.1 Level I
10.1.1.1 Training-all Level I personnel should be trained, evaluated by performance, and retrained as necessary in clearance of foreign-body airway obstruction, emergency airway-secretion evacuation techniques, and basic life support (BLS) at frequent intervals that do not exceed one year. Retraining should focus on identified deficiencies.
10.1.1.2 Responsibilities-Level I personnel are health professionals who assist the primary (Level II) members of the health-care team. They should be capable of assisting Level II personnel by (1) assessing patients for airway emergencies, respiratory, and/or cardiac arrest, (2) activating the resuscitation team, (3) administering BLS, (4) clearing the airway of foreign-body obstruction or material with the potential for obstruction, (5) providing mouth-to-mask ventilation, (6) assisting with tracheal intubation, (7) attaching pulse oximeter and capnograph, (8) moving adjunct airway equipment to the scene, (9) collecting arterial blood for analysis, (10) making a written record of resuscitation efforts.
10.1.1.3 Credentials-Level I health professionals should hold one or more of the following or equivalent credentials: RRT, CRTT, RN, MD, or DO; and have current BLS health-care provider-course completion card from the American Heart Association or a similar equivalent organization. Health professionals and hospital personnel not holding one of these Level I credentials should at a minimum be capable of assessing the patient for foreign-body airway obstruction, activating the resuscitation team, and administering BLS until the team arrives.
10.1.2 Level II
10.1.2.1 Training-Level II personnel should be trained, evaluated by performance, and retrained as necessary in advanced management of airway emergencies-ACLS and/or pediatric advanced life support (PALS) and/or neonatal resuscitation program (NRP)-as appropriate at intervals that should not exceed 1 year. To maintain operator competence, certain procedures (eg, endotracheal intubation) need to be reinforced as often as every 3 months. Retraining should focus on identified deficiencies.
10.1.2.2 Responsibilities-Level II health professionals should be capable of serving as primary members of the resuscitation team. They may respond not only to airway emergency calls in their work areas but also to other areas of the hospital. They are skilled in the use of all adjunctive equipment and special techniques for ECC/ACLS, eg, establishing, maintaining, and monitoring effective ventilation and circulation as described in more detail in the AARC Clinical Practice Guideline: Resuscitation in the Acute Care Hospital.137 They have the skills of Level I personnel and also the following capabilities: (1) advanced ECG monitoring and dysrhythmia recognition, (2) tracheal intubation and airway stabilization; (3) establishing ventilation via transtracheal catheter and cricothyrotomy; (4) emergency treatment of tension pneumothorax or hemothorax with large bore needle; (5) preparing patients for emergency transport; (6) use of continuous and transport mechanical ventilators, (7) evaluating oxygenation, ventilation and acid-base balance from blood gas reports.(138-141)
10.1.2.3 Credentials-Level II health professionals should hold one or more of the following credentials: RRT, RN, MD, or DO; and current ACLS, PALS, and/or NRP course-completion card from the American Heart Association or a similar equivalent association.
10.2 Equipment should be rapidly available and functional. Durability, portability, reliability, and cost should be considered
10.2.1 Ventilation devices should comply with the recommendations made in the AARC Guideline: Resuscitation in the Acute Care Hospital.(137)
10.2.2 Airway management devices should comply with the recommendations made in the AARC Guideline: Resuscitation in the Acute Care Hospital.137 Some other airway devices are available (eg, laryngeal mask airway, esophageal obturator airway, combination esophageal-tracheal tubes) and may be acceptable and useful although they do not provide the airway control and protection afforded by an endotracheal tube.(142)
10.2.2.1 The laryngeal mask airway (LMA) provides a low-pressure seal around the glottis. Although its size effectively prohibits its being inserted into either the trachea or the esophagus, it does not reliably protect the airway from aspirated gastric contents. It may cause less airway trauma than the endotracheal tube and less cardiovascular instability. Available in sizes 1-4, it works in children as well as adults. It may be easier to insert in patients with higher Mallampati classifications.(69,143-151)
10.2.2.2 The esophageal obturator airway/esophageal gastric tube airway (EOA/EGTA) are considered together. Although researchers originally claimed it required less time for training than the endotracheal tube, this may not be the case. It is still widely used, primarily in prehospital care of adults. There have been several reports of the effectiveness of the EOA, but comparison is difficult due to variability in patients and in the medical supervision of the systems. Complications have been reported in many studies. While some believe it to be a useful second-line airway adjunct (for keeping gas out of the stomach and stomach contents out of the pharynx), others feel that the time used for training in EOA insertion would be better spent in training for endotracheal intubation or, failing that, placing more emphasis on basic airway maintenance and ventilation.(152-163)
10.2.2.3 The pharyngeotracheal lumen airway (PTL) is a double-lumen tube that is inserted blindly into the pharynx. After the position of the tube has been assessed, the patient is ventilated through the appropriate lumen. A large pharyngeal balloon seals the airway and a smaller secondary balloon is then inflated. The published complication rate is low, but there has been relatively little evaluation of this device.(164,165)
10.2.2.4 The esophageal tracheal Combitube (ETC) is the newest airway device to be developed. It is similar to the PTL in that it is a double-lumen tube that is inserted blindly into the oropharynx; the position of the tube is assessed; and the patient is ventilated through the appropriate lumen. It has both a low reported rate of complications and few published evaluations.(24,166-172)
10.2.2.5 A 12-16 gauge intravenous catheter-over-the-needle device is used to initiate transtracheal catheter ventilation with the breathing mixture supplied at high pressure (30-50 psi). Because exhalation with this device must occur passively through the upper airway, CO2 excretion is usually inadequate. This technique has potential for providing oxygen to the patient with a partially obstructed airway.
10.2.2.6 Percutaneous dilational cricothyrotomy is performed by making a small vertical incision and advancing a cricothyrotomy tube over a guidewire and dilator.(173) If the catheter is improperly placed or becomes dislodged, ventilation and oxygenation will fail and barotrauma will occur (eg, massive subcutaneous emphysema, pneumomediastinum, pneumothorax, bleeding).
10.2.2.7 Surgical cricothyrotomy requires experience, skill, and specialized equipment and may be facilitated by a tracheal dilator or tracheal hook and a standard tracheostomy or endotracheal tube.
MAE 11.0 MONITORING:
11.1 Patient
11.1.1 Clinical signs-continuous observation of the patient and repeated clinical assessment by a trained observer provide optimal monitoring of the airway. Special consideration should be given to the following:(174)
11.1.1.1 Level of consciousness
11.1.1.2 Presence and character of breath sounds
11.1.1.3 Ease of ventilation
11.1.1.4 Symmetry and amount of chest movement
11.1.1.5 Skin color and character (temperature and presence or absence of diaphoresis)
11.1.1.6 Presence of upper airway sounds (crowing, snoring, stridor)
11.1.1.7 Presence of excessive secretions, blood, vomitus, or foreign objects in the airway
11.1.1.8 Presence of epigastric sounds
11.1.1.9 Presence of retractions
11.1.1.10 Presence of nasal flaring
11.1.2 Physiologic variables-Repeated assessment of physiologic data by trained professionals supplements clinical assessment in managing patients with airway difficulties. Monitoring devices should be available, accessible, functional, and periodically evaluated for function. These data include but are not limited to:(142,175)
11.1.2.1 Ventilatory frequency, tidal volume, and airway pressure
11.1.2.2 Presence of CO2 in exhaled gas
11.1.2.3 Heart rate and rhythm
11.1.2.4 Pulse oximetry
11.1.2.5 Arterial blood gas values
11.1.2.6 Chest radiograph
11.2 Endotracheal tube position-Regardless of the method of ventilation used, the most important consideration is detection of esophageal intubation.
11.2.1 Tracheal intubation is suggested but may not be confirmed bY
11.2.1.1 bilateral breath sounds over the chest, symmetrical chest movement, and absence of ventilation sounds over the epigastrium;(174,175,177)
11.2.1.2 presence of condensate inside the tube, corresponding with exhalation;(174,176,177)
11.2.1.3 visualization of the tip of the tube passing through the vocal cords;
11.2.1.4 Esophageal detector devices may be useful in differentiating esopha-geal from tracheal intubation.(178,179)
11.2.2 Tracheal intubation is confirmed by detection of CO2 in the exhaled gas,(180-182) although cases of transient CO2 excretion from the stomach have been reported.(183)
11.2.3 Tracheal intubation is confirmed by endoscopic visualization of the carina or tracheal rings through the tube.
11.2.4 The position of the endotracheal tube (ie, depth of insertion) should be appropriate on chest radiograph.
11.3 Airway Management Process-a properly managed airway may improve patient outcome. Continuous evaluation of the process will identify components needing improvement. These include response time, equipment function, equipment availability, practitioner performance, complication rate, and patient survival and functional status.
MAE 12.0 FREQUENCY/AVAILABILITY/ DURATION:
Because the need for management of airway emergencies occurs unpredictably, personnel need to be able to respond with the appropriate equipment within 3 minutes, 24 hours/day, 7 days/week.(184) Additionally, a person capable of airway management in the infant should be present at every delivery. A Level-II practitioner should be present at every high-risk delivery.
MAE 13.0 INFECTION CONTROL:
13.1 Implement Universal Precautions including mouth-to-barrier devices and recommendations related to avoidance of the transmission of tuberculosis and other airborne diseases.(185,186)
13.2 Observe all infection control guidelines posted for the patient.
13.3 Disinfect all equipment to be reused on other patients.
Airway Emergencies Guidelines Committee:
Thomas A Barnes EdD RRT, Chairman, Boston MA
Karen M Boudin MA RRT, Stanford CA
Charles G Durbin Jr MD, Charlottesville VA
Robert R Fluck Jr MS RRT, Syracuse NY
Cynthia Malinowski MA RRT, Loma Linda CA

Drenaje Postural

Reprinted from RESPIRATORY CARE (Respir Care 1991;36:1418-1426)
AARC Clinical Practice Guideline
Postural Drainage Therapy
PDT 1.0 PROCEDURE:
Postural drainage therapy (PDT) is a component of bronchial hygiene therapy. It consists of postural drainage, positioning, and turning and is sometimes accompanied by chest percussion and/or vibration.
Cough or airway clearance techniques are essential components of therapy when postural drainage is intended to mobilize secretions.(1-6) Postural drainage therapy is often used in conjunction with aerosol administration and other respiratory care procedures.
This procedure has been commonly referred to as(7-12)
chest physiotherapy,
chest physical therapy,
postural drainage and percussion, and
percussion and vibration.
PDT 2.0 DESCRIPTION/DEFINITION:
Postural drainage therapy is designed to improve the mobilization of bronchial secretions(2,4,5,8-10,13-18) and the matching of ventilation and perfusion,(19-23) and to normalize functional residual capacity (FRC)(17,24-30) based on the effects of gravity and external manipulation of the thorax. This includes turning, postural drainage, percussion, vibration, and cough.
2.1 Turning
Turning is the rotation of the body around the longitudinal axis to promote unilateral or bilateral lung expansion(19,22) and improve arterial oxygenation.(19-21,31) Regular turning can be to either side or the prone position,(32) with the bed at any degree of inclination (as indicated and tolerated). Patients may turn themselves or they may turned by the caregiver or by a special bed or device.(21,22,33-35)
2.2 Postural Drainage
Postural drainage is the drainage of secretions, by the effect of gravity, from one or more lung segments to the central airways (where they can be removed by cough or mechanical aspiration).(2,4,5,11,13,15-18,26,29,36,37) Each position consists of placing the target lung segment(s) superior to the carina. Positions should generally be held for 3 to 15 minutes (longer in special situations).(4,6,13,16,18,20,29,38-40) Standard positions are modified as the patient’s condition and tolerance warrant.
2.3 External Manipulation of the Thorax
2.3.1 Percussion
Percussion is also referred to as cupping, clapping, and tapotement. The purpose of percussion is to intermittently apply kinetic energy to the chest wall and lung. This is accomplished by rhythmically striking the thorax with cupped hand or mechanical device directly over the lung segment(s) being drained. No convincing evidence demonstrates the superiority of one method over the other.(4,18,41-44)
2.3.2 Vibration
Vibration involves the application of a fine tremorous action (manually performed by pressing in the direction that the ribs and soft tissue of the chest move during expiration) over the draining area. No conclusive evidence supports the efficacy of vibration, the superiority of either manual or mechanical methods, or an optimum frequency.(2,4,13,27,28,30,36,38,39,45-47)
PDT 3.0 SETTING:
Although PDT can be used with neonates, infants, childrens, and adults, this Guideline applies primarily to older children and adults. PDT can be performed in a wide variety of settings.
3.1 Critical care
3.2 In-patient acute care
3.3 Extended care and skilled nursing facility care
3.4 Home care
3.5 Outpatient/ambulatory care
3.6 Pulmonary diagnostic (bronchoscopy) laboratory
PDT 4.0 INDICATIONS:
4.1 Turning
4.1.1 inability or reluctance of patient to change body position. (eg, mechanical ventilation, neuromuscular disease, drug-induced paralysis)
4.1.2 poor oxygenation associated with position(20,22,48-50) (eg, unilateral lung disease)
4.1.3 potential for or presence of atelectasis(24,26,30)
4.1.4 presence of artificial airway
4.2 Postural Drainage
4.2.1 evidence or suggestion of difficulty with secretion clearance
4.2.1.1 difficulty clearing secretions with expectorated sputum production greater than 25-30 mL/day (adult)(3,7,9,11,12,27,38,40, 46,51-53)
4.2.1.2 evidence or suggestion of re-tained secretions in the presence of an artificial airway
4.2.2 presence of atelectasis caused by or suspected of being caused by mucus plugging(24,26,29,30,54)
4.2.3 diagnosis of diseases such as cystic fibrosis,(1,5,6,13-15,18,36,55) bronchiectasis,(4,5,14) or cavitating lung disease
4.2.4 presence of foreign body in airway(56-58)
4.3 External Manipulation of the Thorax
4.3.1 sputum volume or consistency suggesting a need for additional manipulation (eg, percussion and/or vibration) to assist movement of secretions by gravity, in a patient receiving postural drainage
PDT 5.0 CONTRAINDICATIONS:
The decision to use postural drainage therapy requires assessment of potential benefits versus potential risks. Therapy should be provided for no longer than necessary to obtain the desired therapeutic results. Listed contraindications are relative unless marked as absolute (A).
5.1 Positioning
5.1.1 All positions are contraindicated for
5.1.1.1 intracranial pressure (ICP) > 20 mm Hg(59,60)
5.1.1.2 head and neck injury until stabilized (A)
5.1.1.3 active hemorrhage with hemodynamic instability (A)
5.1.1.4 recent spinal surgery (eg, laminectomy) or acute spinal injury
5.1.1.5 acute spinal injury or active hemoptysis
5.1.1.6 empyema
5.1.1.7 bronchopleural fistula
5.1.1.8 pulmonary edema associated with congestive heart failure
5.1.1.9 large pleural effusions
5.1.1.10 pulmonary embolism
5.1.1.11 aged, confused, or anxious patients who do not tolerate position changes
5.1.1.12 rib fracture, with or without flail chest
5.1.1.13 surgical wound or healing tissue
5.1.2 Trendelenburg position is contraindicated for
5.1.2.1 intracranial pressure (ICP) > 20 mm Hg(59,60)
5.1.2.2 patients in whom increased intracranial pressure is to be avoided (eg, neurosurgery, aneurysms, eye surgery)
5.1.2.3 uncontrolled hypertension
5.1.2.4 distended abdome
5.1.2.5 esophageal surgerY
5.1.2.6 recent gross hemoptysis re-lated to recent lung carcinoma treated surgically or with radiation therapy(59)
5.1.2.7 uncontrolled airway at risk for aspiration (tube feeding or recent meal)
5.1.3 Reverse Trendelenburg is contraindicated in the presence of hypotension or vasoactive medication
5.2 External Manipulation of the Thorax
In addition to contraindications previously listed
5.2.1subcutaneous emphysema
5.2.2 recent epidural spinal infusion or spinal anesthesia
5.2.3 recent skin grafts, or flaps, on the thorax
5.2.4 burns, open wounds, and skin infections of the thorax
5.2.5 recently placed transvenous pacemaker or subcutaneous pacemaker (particularly if mechanical devices are to be used)
5.2.6 suspected pulmonary tuberculosis
5.2.7 lung contusion
5.2.8 bronchospasm
5.2.9 osteomyelitis of the ribs
5.2.10 osteoporosis
5.2.11 coagulopathy
5.2.12 complaint of chest-wall pain
PDT 6.0 HAZARDS/COMPLICATIONS:
6.1 Hypoxemia
Action To Be Taken/Possible Intervention: Administer higher oxygen concentrations during procedure if potential for or observed hypoxemia exists. If patient becomes hypoxemic during treatment, administer 100% oxygen, stop therapy immediately, return patient to original resting position, and consult physician. Ensure adequate ventilation. Hypoxemia during postural drainage may be avoided in unilateral lung disease by placing the involved lung up-permost with patient on his or her side.(20,22,48-50)
6.2 Increased Intracranial Pressure
Action To Be Taken/Possible Intervention: Stop therapy, return patient to original resting position, and consult physician.
6.3 Acute Hypotension during Procedure
Action To Be Taken/Possible Intervention: Stop therapy, return patient to original resting position, and consult physician.
6.4 Pulmonary Hemorrhage
Action To Be Taken/Possible Intervention: Stop therapy, return patient to original resting position, call physician immediately. Administer oxygen and maintain an airway until
physician responds.
6.5 Pain or Injury to Muscles, Ribs, or Spine
Action To Be Taken/Possible Intervention: Stop therapy that appears directly associated with pain or problem, exercise care in moving patient, and consult physician.
6.6 Vomiting and Aspiration
Action To Be Taken/Possible Intervention: Stop therapy, clear airway and suction as needed, administer oxygen, maintain airway, return patient to previous resting position, and contact physician immediately.
6.7 Bronchospasm
Action To Be Taken/Possible Intervention: Stop therapy, return patient to previous resting position, administer or increase oxygen delivery while contacting physician. Administer physician-ordered bronchodilators.
6.8 Dysrhythmias
Action To Be Taken/Possible Intervention: Stop therapy, return patient to previous resting position, administer or increase oxygen delivery while contacting physician.
PDT 7.0 LIMITATIONS OF METHOD:
7.1 Presumed effectiveness of PDT and its application may be based more on tradition and anecdotal report than on scientific evidence. The procedure has been used excessively and in patients in whom it is not indicated.(11,40,61-63)
7.2 Airway clearance may be less than optimal in patients with ineffective cough.
7.3 Optimal positioning is difficult in critically ill patients.
PDT 8.0 ASSESSMENT OF NEED:
The following should be assessed together to establish a need for postural drainage therapy
8.1 excessive sputum production
8.2 effectiveness of cough
8.3 history of pulmonary problems treated successfully with PDT (eg, bronchiectasis, cystic fibrosis, lung abscess)
8.4 decreased breath sounds or crackles or rhonchi suggesting secretions in the airway
8.5 change in vital signs
8.6 Abnormal chest x-ray consistent with atelectasis, mucus plugging, or infiltrates
8.7 deterioration in arterial blood gas values or oxygen saturation
PDT 9.0 ASSESSMENT OF OUTCOME:
These represent individual criteria that indicate a positive response to therapy (and support continuation of therapy). Not all criteria are required to justify continuation of therapy (eg, a ventilated patient may not have sputum production > 30 mL/day, but have improvement in breath sounds, chest x-ray, or increased compliance or decreased resistance).
9.1 Change in sputum production
If sputum production in an optimally hydrated patient is less than 25 mL/day with PDT the procedure is not justified.(3,5,7,9,11,12,38,40,46,51-53) Some patients have productive coughs with sputum production from 15 to 30 mL/day (occasionally as high as 70 or 100 mL/day) without postural drainage. If postural drainage does not increase sputum in a patient who produces > 30 mL/day of sputum without postural drainage, the continuation of the therapy is not indicated. Because sputum production is affected by systemic hydration, apparently ineffective PDT probably should be continued for at least 24 hours after optimal hydration has been judged to be present.
9.2 Change in breath sounds of lung fields being drained
With effective therapy, breath sounds may ‘worsen’ following the therapy as secretions move into the larger airways and increase rhonchi. An increase in adventitious breath sounds can be a marked improvement over absent or diminished breath sounds. Note any effect that coughing may have on breath sounds. One of the favorable effects of coughing is clearing of adventitious breath sounds.
9.3 Patient subjective response to therapy
The caregiver should ask patient how he or she feels before, during, and after therapy. Feelings of pain, discomfort, shortness of breath, dizziness, and nausea should be considered in decisions to modify or stop therapy. Easier clearance of secretions and increased volume of secretions during and after treatments support continuation.
9.4 Change in vital signs
Moderate changes in respiratory rate and/or pulse rate are expected. Bradycardia, tachycardia, or an increase in irregularity of pulse, or fall or dramatic increase in blood pressure are indications for stopping therapy.
9.5 Change in chest x-ray
Resolution or improvement of atelectasis may be slow or dramatic.
9.6 Change in arterial blood gas values or oxygen saturation
Oxygenation should improve as atelectasis resolves.
9.7 Change in ventilator variables
Resolution of atelectasis and plugging reduces resistance and increases compliance.
PDT 10.0 RESOURCES:
10.1 Equipment
10.1.1 bed or table that can be adjusted for a range of positions from Trendelen-burg to Reverse Trendelenburg position
10.1.2 pillows for supporting patient
10.1.3 light towel for covering area of chest during percussion
10.1.4 tissues and/or basin for collecting expectorated sputum
10.1.5 suction equipment for patients unable to clear secretion
10.1.6 gloves, goggles, gown, and mask as indicated for caregiver protection
10.1.7 optional: hand-held and mechanical percussor or vibrator
10.1.8 oxygen delivery device
10.1.9 recent chest x-ray, if available
10.1.10 stethoscope for auscultation
10.2 Personnel
A spectrum of education and skill levels is required for personnel who administer postural drainage therapy. Different clinical situations warrant the degree of training necessary to provide optimal respiratory care.
10.2.1. The Level I care provider who provides routine maintenance therapy to the stable patient should possess the following skills and knowledge
10.2.1.1 proper technique for administration of PDT
10.2.1.2 proper use of equipment
10.2.1.3 breathing patterns and cough techniques
10.2.1.4 technique modification in re-sponse to adverse reactions
10.2.1.5 position or frequency modification in response to severity of symptoms
10.2.1.6 ability to assess patient condition and patient response to therapy including physical exam (auscultation and vital signs) and tests of expiratory flow or ventilator mechanics
10.2.1.7 ability to recognize and respond to adverse reactions to and complications of procedure
10.2.1.8 understanding of and compliance with Universal Precautions
10.2.2 For initial assessments and care of the unstable patient, the Level II care provider should possess
10.2.2.1 knowledge of proper use and limitations of equipment
10.2.2.2 ability to assess patient condition and patient response to therapy
10.2.2.3 ability to perform physical exam auscultation and vital signs
10.2.2.4 knowledge of effects of gravity and body position on ventilation, perfusion, and sputum mobilization
10.2.2.5 knowledge of procedures, indications, contraindications, and hazards for turning
10.2.2.6 knowledge of standard drainage positions, techniques for percussion and vibration, segmental and airway anatomy
10.2.2.7 ability to teach diaphragmatic breathing, relaxation, huff cough, forced expiration technique (FET), suctioning
10.2.2.8 ability to monitor effects and patient response to changes in position and other postural drainage therapy techniques
10.2.2.9 understanding of and ability to comply with Universal Precautions and infection control issues related to cleaning and maintaining equipment
10.2.2.10 ability to instruct patient/family/caregiver in goals of therapy and proper technique for administration of PDT and associated therapies
10.2.2.11 knowledge of proper use of equipment, including suction if re-quired
10.2.2.12 ability to prepare, measure, and mix medications if required
10.2.2.13 ability to clean equipment
10.2.2.14 knowledge of breathing patterns and cough techniques
10.2.2.15 abilty to modify techniques in response to adverse reactions
10.2.2.16 ability to modify dosage or frequency in response to severity of symptoms
10.2.3 The subject providing self administration of postural drainage should possess knowledge and skills related to
10.2.3.1 proper technique for administration
10.2.3.2 proper use of equipment
10.2.3.3 breathing patterns and cough techniques
10.2.3.4 technique modification in re-sponse to adverse reactions
10.2.3.5 position or frequency modification in response to severity of symptoms
PDT 11.0 MONITORING:
The following should be chosen as appropriate for monitoring a patient’s response to postural drainage therapy, before, during, and after therapy.
11.1 Subjective response–pain, discomfort, dyspnea, response to therapy
11.2 Pulse rate, dysrhythmia, and EKG if available
11.3 Breathing pattern and rate, symmetrical chest expansion, synchronous thoracoabdom-inal movement, flail chest
11.4 Sputum production (quantity, color, consistency, odor) and cough effectiveness
11.5 Mental function
11.6 Skin color
11.7 Breath sounds
11.8 blood pressure
11.9 oxygen saturation by pulse oximetry (if hypoxemia is suspected)
11.10 intracranial pressure (ICP)
PDT 12.0 FREQUENCY:
The frequencies suggested are recommendations from group experience and apply to patients in whom the therapy is indicated. Careful assessment and prudent clinical judgment must be exercised by the caregiver.
12.1 Turning
Ventilated and critically ill patients: as necessary with goal of once each hour or every other hour as tolerated, around the clock. Less acute patients should be turned every 2 hours as tolerated.
12.2 Postural Drainage Therapy
12.2.1 In critical care patients, including those on mechanical ventilation, PDT should be performed from every 4 to every 6 hours as indicated. PDT order should be re-evaluated at least every 48 hours based on assessments from individual treatments.
12.2.2 In spontaneously breathing pa-tients, frequency should be determined by assessing patient response to therapy.
12.2.3 Acute care patient orders should be re-evaluated based on patient response to therapy at least every 72 hours or with change of patient status.
12.2.4 Domiciliary patients should be re-evaluated every 3 months and with change of status.
PDT 13.0 INFECTION CONTROL:
13.1 Implement Universal Precautions.(64)
13.2 Observe all infection control guidelines posted for patient.
13.3 Disinfect all equipment used between patients.
Bronchial Hygiene Guidelines Committee:
Lana Hilling RCP CRTT, Chairman,Concord CA
Eric Bakow RRT, Pittsburg PA
Jim Fink RCP RRT, San Francisco CA
Chris Kelly BS RRT, Oakland CA
Dennis Sobush MA PT, Milwaukee WI
Peter A Southorn MD, Rochester MN
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51. Anthonisen P, Riis P, Sigaard-Anderson T. The value of lung physiotherapy in the treatment of acute exacerbations in chronic bronchitis. Act Med Scand 1964; 175:715-719.
52. Murray JF. The ketchup-bottle method. N Engl J Med 1979;300(20):1155-1157.
53. Sutton PP, Pavia D, Bateman JRM, Clarke SW. Chest physiotherapy: a review. Eur J Respir Dis 1982;63:188-201.
54. Peters RM, Turnier E,. Physical therapy: indications for and effects in surgical patients. Am Rev Respir Dis 1980;122:147-154.
55. Tecklin J, Holsclaw D. Evaluation of bronchial drainage in patients with cystic fibrosis. Phys Ther 1975; 55:1081-1084.
56. Cotton EK, Abrams G, Van Houtte J, Burrington J. Removal of aspirated foreign bodies by percussion and postural drainage. Clin Pediatr 1973;12:270-276.
57. Law D, Kosloske AM. Management of tracheobronchial foreign bodies in children: a reevaluation of postural drainage and bronchoscopy. Pediatrics 1976;58:362-367.
58. Raghu G, Pierson DJ. Successful removal of an aspirated tooth by chest physiotherapy. Respir Care 1986; 31:1099-1101.
59. Tyler ML. Complications of positioning and chest physiotherapy. Respir Care 1982;27:458-466.
60. MacKenzie CF, Ciesla N, Imle PC, et al. In: Chest physiotherapy in the intensive care unit. Baltimore: Williams & Wilkins, 1990.
61. van der Schans CP, Piers DA, Postma DS. Effects of manual percussion on tracheobronchial clearance in patients with chronic airflow obstruction and excessive tracheobronchial secretions. Thorax 1986;41:448-452.
62. Shapiro BA, Cane RD, Peterson J, Weber D. Authoritative medical direction can assure cost-beneficial bronchial hygiene therapy. Chest 1988;93:1038-1042.
63. Eid N, Bucheit J, Neuling M, Phelps H. Chest physiotherapy in review. Respir Care 1991;36:270-282.
64. Centers for Disease Control. Update: universal precautions for prevention of transmission of human immunodeficiency virus, hepatitis B virus, and other bloodborne pathogens in health care settings. MMWR 1988;37:377-388.
ADDITIONAL BIBLIOGRAPHY
Denton R. Bronchial secretions on cystic fibrosis: the effects of treatment with mechanical percussion vibration. Am Rev Respir Dis 1962;86:141-146.
Committee on Therapy, American Thoracic Society. Physical adjuncts in the treatment of pulmonary diseases. Am Rev Respir Dis 1968;97:725-736.
Barach AL, Dulfano MJ. Effect of chest vibration in pulmonary emphysema: a preliminary report. Ann Allergy 1968; 26:10-17.
March H. Appraisal of postural drainage for chronic obstruction pulmonary disease. Arch Phys Med Rehab 1972;52:528-530.Lefcoe NM, Paterson NAM. Adjunct therapy in chronic obstructive pulmonary disease. Am J Med 1973;54:343-350.
Schlenker JD, Hubay CA. The pathogenesis of post-operative atelectasis. Arch Surg 1973;107:846-850.
Laszlo G, Archer GG, Darrell JH, Dawson JM, Fletcher CM. The diagnosis and prophylaxis of pulmonary complications of surgical operation. Br J Surg 1973;60:129-134.
Ray JF, Yost L, Moallen S. Immobility, hypoxemia, and pulmonary arteriovenous shunting. Arch Surg 1974;109:537-541.
Martin CJ, Ripley H, Reynolds J, Best F. Chest physiotherapy and the distribution of ventilation. Chest 1976;69(2):174-178.
Chopra SK, Taplin GV, Simmons DH, Robinson GD Jr, Coulson A. Effects of hydration and physical therapy on tracheal transport velocity. Am Rev Respir Dis 1977;115:1009-1014.
Winning TJ, Brock-Utne JG, Goodwin NM. Bronchodilators and physiotherapy during long term mechanical ventilation of the lungs. Anaesth Intens Care 1977;5:48-50.
Newton DAG, Bevans HG. Physiotherapy and intermittent positive pressure ventilation of chronic bronchitis. Br Med J 1978;2:1525-1528.
Hedstrand U, Liw M, Rooth G, Lindgren CH. Effects of respiratory physiotherapy on arterial oxygen tension. Acta Anaesth Scand 1978;22:349-352.
Moody LE, Martindale CL. Effect of pulmonary hygiene measures on levels of arterial oxygen saturation in adults with chronic lung disease. Heart Lung 1978;7(2):315-319.
West JB. Regional differences in the lung. Chest 1978;74:426.
Seaton D, Lapp NL, Morgan WKG. Effect of body position on gas exchange after thoracotomy. Thorax 1979;34:518.
Barnes CA, Asonye UO, Vidyasagar D. The effects of bronchopulmonary hygiene on PtcCO2 values in critically ill neonates. Crit Care Med 1981;9:819-822
Remolina C, Khan AU, Santiago TV, Edelman NH. Positional hypoxemia in unilateral lung disease. N Engl J Med 1981;304:523.
Rossman CM, Waldes R, Sampson D, Newhouse MT. Effect of chest physiotherapy on the removal of mucus in patients with cystic fibrosis. Am Rev Respir Dis 1982;126:131-135.
Reines HD, Sade RM, Bradford BF, Marshall J. Chest physiotherapy fails to prevent post-operative atelectasis in children after cardiac surgery. Ann Surg 1982;195:451-455.
White DJ, Mawdsley RH. Effects of selected bronchial drainage positions and percussion on blood pressure of healthy human subjects. Phys Ther 1983;63:325-330.
Ford GT, Whitelaw WA, Rosenal TW, Cruse PJ, Guenter CA. Diaphragm function after upper abdominal surgery in humans. Am Rev Respir Dis 1983;127:431-436.
King M. Mucus and mucociliary clearance. Respir Care 1983;28:335-344.
Buscaglia AJ, St Marie MS. Oxygen saturation during chest physiotherapy for acute exacerbation of severe chronic obstructive pulmonary disease. Respir Care 1983;28:1009-1013.
King M, Phillips DM, Gross D, Vartian V, Changhk Eidulka A, et al. Enhanced tracheal mucus clearance with high frequency chest wall compression. Am Rev Respir Dis 1983; 128:511-515.
Mazzocco M, Kirilloff L, Owens G, Rogers R. Physiologic effects of chest percussion and postural drainage in patients with bronchiectasis (abstract). Am Rev Respir Dis 1984;129 (4, Part 2):A52.
Torrington KG, Sorenson DE, Sherwood LM. Postoperative chest percussion with postural drainage in obese patients following gastric stapling. Chest 1984;86:891-895.
King M, Phillips DM, Zidulka A, Chang HK. Tracheal mucus clearance in high-frequency oscillation. Am Rev Respir Dis 1984;130:703-706.
Rivington-Law BA, Epstein SW, Thompson GL, et al. Effect of chest wall vibrations on pulmonary function in chronic bronchitis. Chest 1984;85(3):378-381.
Britton S, Bejstedt M, Vedin L. Chest physiotherapy in primary pneumonia. Br Med J 1985;290:1703-1704.
Mackenzie CF, Shin B. Cardiorespiratory function before and after chest physiotherapy in mechanically ventilated patients with post-traumatic respiratory failure. Crit Care Med 1985;13:483-486.
McDonnell T, McNicholas WT, Fitzgerald MX. Hypoxemia during chest physiotherapy in patients with septic fibrosis. Ir J Med Sci 1986;155:345-348.
Johnson NT, Marini JJ, Pierson DJ, Hudson LD. Acute lobar atelectasis: effect of chest percussion and postural drainage (CPPL) on resolution (abstract). Am Rev Respir Dis 1987;135(4, Part 2):433.
Biddle CJ, Holland MS, Schreiber TR, Mathewson HS. Prevention of hypoxemia in good risk patients during postoperative transport by positioning and deep breathing. Respir Care 1987;32(1):24-28.
Bozynski MEA, Naglie RA, Nicks JJ, Burpee B, Johnson RV. Lateral positioning of the stable ventilated very low birth weight infant. AJDC 1988;142:200-202.
Kaminska TM, Pearson SB. A comparison of postural drainage and positive expiratory pressure in the domiciliary management of patients with chronic bronchial sepsis. Physiotherapy 1988;74(5):251-254.
Prasad A, Tasker R. Guidelines for the physiotherapy management of critically ill children with acutely raised intracranial pressure. Physiotherapy 1990;76(4):248-250
Ersson U, Carlson H, Mellström A, Ponten U, Hedstrand U, Jakobsson S. Observation on intracranial dynamics during respiratory physiotherapy in unconscious neurosurgical patients. Acta Anaesthesiol Scand 1990;34:99-103.
Interested persons may copy these Guidelines for noncommercial purposes of scientific or educational advancement. Please credit AARC and Respiratory Care Journal.

Aspiración Nasotraqueal

Reprinted from RESPIRATORY CARE (Respir Care 1992;37:898-901)
AARC Clinical Practice Guideline
Nasotracheal Suctioning
NTS 1.0 PROCEDURE:
Nasotracheal suctioning (NTS) is a component of bronchial hygiene therapy.
NTS 2.0 DESCRIPTION/DEFINITION:
NTS is intended to remove accumulated secretions, blood, vomitus, and other foreign material from the trachea that cannot be removed by the patient’s spontaneous cough or other less invasive procedures. NTS has been used to avoid intubation that was solely intended for the removal of secretions.(1-4)
NTS refers to the insertion of a suction catheter through the nasal passage and pharynx into the trachea in order to aspirate accumulated secretions or foreign material.(3)
The clearance of secretions is accomplished by application of subatmospheric pressure.(5)
NTS 3.0 SETTINGS:
NTS is performed in a wide variety of settings, and this guideline applies to patients of all ages.
3.1 Critical care
3.2 Emergency room or department
3.3 Inpatient acute care
3.4 Extended care and skilled nursing facility care
3.5 Home care
3.6 Outpatient or ambulatory care
NTS 4.0 INDICATIONS:
The need to maintain a patent airway and remove secretions or foreign material from the trachea in the presence of
4.1 inability to clear secretions;(6)
4.2 audible evidence of secretions in the large/central airways that persist in spite of patient’s best cough effort.(4,7,8-10)
NTS 5.0 CONTRAINDICATIONS:
Listed contraindications are relative unless marked as absolute.
5.1 Occluded nasal passages
5.2 Nasal bleeding
5.3 Epiglottitis or croup (absolute)
5.4 Acute head, facial, or neck injury
5.5 Coagulopathy or bleeding disorder(2)
5.6 Laryngospasm(2)
5.7 Irritable airway
5.8 Upper respiratory tract infection
NTS 6.0 HAZARDS/COMPLICATIONS:
6.1 Mechanical trauma(10-15)
6.1.1 Laceration of nasal turbinates(5,7,16)
6.1.2 Perforation of the pharynx(17)
6.1.3 Nasal irritation/bleeding(16,18)
6.1.4 Tracheitis
6.1.5 Mucosal hemorrhage(13)
6.2 Hypoxia/hypoxemia(1,14,19-21)
6.3 Cardiac dysrhythmias/arrest(3,7,14,15)
6.4 Bradycardia(1,19,22-24)
6.5 Increase in blood pressure(1,19,21)
6.6 Hypotension(1,19)
6.7 Respiratory arrest(7)
6.8 Uncontrolled coughing(1,15,18)
6.9 Gagging/vomiting(18,25)
6.10 Laryngospasm(1,2,7)
6.11 Bronchoconstriction/bronchospasm(1,14,15)
6.12 Pain(18)
6.13 Nosocomial infection(15,16,23)
6.14 Atelectasis(5,14)
6.15 Misdirection of catheter((15,18)
6.16 Increased intracranial pressure (ICP)(21,26,27)
6.16.1 Intraventricular hemorrhage(21)
6.16.2 Exacerbation of cerebral edema
NTS 7.0 LIMITATIONS OF METHOD:
7.1 NTS is a blind, high-risk procedure with uncertain outcome.(18,24)
7.2 NTS should not be used to stimulate a cough.
7.3 Risks are increased in a combative or uncooperative patient.
7.4 Duration of application of subatmospheric pressure, or suction, should be limited to < or = 15 seconds.(20,28) 7.5 Controversy exists concerning possible overuse of this procedure.(5,8,10) NTS 8.0 ASSESSMENT OF NEED: 8.1 Personnel should auscultate chest for indications for NT suctioning.(1,29) 8.2 Personnel should assess effectiveness of cough. NTS 9.0 ASSESSMENT OF OUTCOME: 9.1 Effectiveness of NTS should be reflected by improved breath sounds. 9.2 Effectiveness of NTS should be reflected by removal of secretions. NTS 10.0 RESOURCES: 10.1 Equipment: 10.1.1 Vacuum source(1) 10.1.2 Calibrated, adjustable regulator(30 ) 10.1.3 Collection vessel and connecting tubing(1) 10.1.4 Sterile suction catheter of appropriate caliber(1,8,29) 10.1.5 Sterile disposable gloves(1,8) 10.1.6 Sterile water and cup(1,8) 10.1.7 Sterile normal saline--amount adequate for irrigation (5-10 mL for adults)(1,8,31) 10.1.8 Water-based lubricant(1,8) 10.1.9 Local anesthetic is sometimes used to reduce discomfort.(1) 10.1.10 Nasopharyngeal airway when frequent NTS is required(1,18,29) 10.1.11 Resuscitation bag with mask(1,23,29,31) In the acute care setting, with initiation of NTS, or when working with the unstable patient, the following are recommended. 10.1.12 EKG monitor 10.1.13 Oxygen(1,20,28,32,33) 10.1.14 Personnel protective equipment for Universal Precautions(34,35) 10.2 Personnel: 10.2.1 Level I caregiver may be the provider of service after Level II personnel have established need by patient assessment and the first NTS episode has been completed. Level I personnel must demonstrate 10.2.1.1 knowledge of proper assembly and use of equipment;(7) 10.2.1.2 knowledge of upper airway anatomy and physiology;(7,23) 10.2.1.3 ability to recognize secretion retention on auscultation;(1) 10.2.1.4 ability to monitor vital signs and assess patient's condition and response to procedure; 10.2.1.5 ability to recognize and re-spond to adverse reactions and compli-cations of procedures; 10.2.1.6 ability to employ technique of cardiopulmonary resuscitation when indicated; 10.2.1.7 ability to evaluate and document procedure effectiveness and patient response. 10.2.2 Level II provider initially assesses the patient, determines the need for NTS, and evaluates response to and effectiveness of first episode.Level II personnel have all the skills of Level I providers plus: 10.2.2.1 knowledge and understanding of patient's disease, goals, and limitation of NTS;(23) 10.2.2.2 recognition and understanding of basis of pathophysiology; 10.2.2.3 ability to perform initial treatment and be available to troubleshoot the procedure; 10.2.2.4 ability to modify techniques and equipment and take definitive action in response to adverse reaction; 10.2.2.5 ability to detect adverse reactions and avoid patient harm by em-ploying techniques of cardiopulmonary resuscitation with mechanical airway adjuncts and bag-mask devices; 10.2.2.6 knowledge of basic EKG and dysrhythmia recognition; 10.2.2.7 knowledge of signs and symptoms of decreased cardiac output, oxygenation, and perfusion; 10.2.2.8 ability to teach Level I and lay personnel providing home care. 10.2.3 Home care should be provided by lay personnel trained and knowledgeable in 10.2.3.1 proper assembly and use of equipment; 10.2.3.2 correct positioning of patient; 10.2.3.3 proper suctioning technique; 10.2.3.4 assessment of patient response to procedure; 10.2.3.5 response to adverse reaction; 10.2.3.6 care and cleaning of equipment. NTS 11.0 MONITORING: The following should be monitored during and following the procedure. 11.1 Breath sounds 11.2 Skin color(36) 11.3 Breathing pattern and rate 11.4 Pulse rate, dysrhythmia, EKG if available 11.5 Color, consistency, and volume of secretions 11.6 Presence of bleeding or evidence of physical trauma 11.7 Subjective response including pain(25) 11.8 Cough 11.9 Oxygenation (pulse oximeter if available) 11.10 Intracranial pressure (ICP), if equipment is available NTS 12.0 FREQUENCY: Nasotracheal suctioning should be performed only when absolutely necessary and other methods to remove secretions from airway have failed.(4,5,8,10,29) NTS 13.0 INFECTION CONTROL: 13.1 CDC Guidelines for Universal Precautions should be adhered to.(35) 13.2 All equipment and supplies should be appropriately disposed of or disinfected. Bronchial Hygiene Guidelines Committee: Lana Hilling RCP CRTT, Chairman, Concord CA Eric Bakow MA RRT, Pittsburgh PA James Fink MS RCP RRT, San Francisco CA Chris Kelly BA RCP RRT, Oakland CA Dennis Sobush MA PT, Milwaukee WI Peter A Southorn MD, Rochester MN REFERENCES 1. Burton GG, Hodgkin JE, Ward JJ, eds. Respiratory care: a guide to clinical practice, 3rd ed. Philadelphia: JB Lippincott, 1991:498-502. 2. Fuchs PL. Streamlining your suctioning techniques. Part I. Nasotracheal suctioning. Nursing 1984;14:55-61. 3. Demers RR. Management of the airway in the perioperative period. Respir Care 1984;29:529-536. 4. Vender JS, Shapiro BA. Essentials of artificial airway management in critical care. Acute Care 1987;13:97-124. 5. Demers RR, Saklad M. Minimizing harmful effects of mechanical aspiration. Heart Lung 1973;2:542. 6. Stiller K, Geake T, Taylor J, Grant R, Hall B. Acute lobar atelectasis: a comparison of two chest physiotherapy regimens. Chest 1990;98:1336-1340. 7. Demers RR, Saklad M. Mechanical aspiration: a reappraisal of its hazards. Respir Care 1975;20:661-666. 8. Hoffman LA, Maszkiewicz RC. Airway management for the critically ill patient. Am J Nurs 1987;87:39-53. 9. Lough MD, Doershuk CF, Stern RC. Pediatric respira-tory therapy, 3rd ed. Chicago: Year Book Medical Publishers, 1985:125. 10. Carroll P. Safe suctioning. Nursing 1989;19:49-51. 11. Jung RC, Gottlieb LS. Comparison of tracheobronchial suction catheters in humans. Chest 1976;69:179-181. 12. Landa J, Kwoka M, Chapman G, Brito M, Sackner M. Effects of suctioning on mucociliary transport. Chest 1980;77:202-207. 13. Sackner MA, Landa JF, Greeneltch N, Robinson MJ. Pathogenesis and prevention of tracheobronchial damage with suction procedures. Chest 1973;64:284-290. 14. Riegel B, Forshee T. A review and critique on preoxygenation for endotracheal suctioning. Heart Lung 1985; 14:507-518. 15. Demers RR. Complications of endotracheal suctioning procedures. Respir Care 1982;27:453-457. 16. LeFrock JL, Klainer AS, Wu H-W, Turndorf H. Transient bacteremia associated with nasotracheal suction-ing. JAMA 1976;236:1610-1611. 17. Touloukian RJ, Beardsley GP, Ablow RC, Effman EL. Traumatic perforation of the pharynx in the newborn. Pediatrics 1977;59:1019-1022. 18. Wanner A, Zighelboim A, Sackner MA. Nasopharyn-geal airway: a facilitated access to the trachea. Ann Intern Med 1971;75:593. 19. Simbruner G, Coradello H, Fodor M, Havelec L, Lubec G, Pollak A. Effect of tracheal suction on oxygenation, circulation and lung mechanics in newborn infants. Arch Dis Child 1981;56:326-330. 20. Naigow D, Powaser MM. The effect of different endotracheal suction procedures on arterial blood gases in a controlled experimental model. Heart Lung 1977;6:808-816. 21. Perlman JM, Volpe JJ. Suctioning in the pre-term: effects on cerebral blood flow velocity, intracranial pressure, and arterial blood pressure. Pediatrics 1983;72:329-334. 22. Fox WW, Schwartz BS, Shaffer TH. Pulmonary physiotherapy in neonates: physiologic changes and respira-tory management. J Pediatr 1978;92:977-981. 23. Scanlon CL, Spearman CB, Sheldon RL, Egan DF, eds. Egan's fundamentals of respiratory care, 5th edition. St Louis: CV Mosby, 1990:483-486. 24. Cordero L, Hon EH. Neonatal bradycardia following nasopharyngeal simulation. J Pediatr 1971;78:441-447. 25. Larson RP, Ingalls-Severn KJ, Wright JR, Kiviat NC, Maunder RJ. Diagnosis of Pneumocystis carinii pneumonia by respiratory care practitioners: advantages of a nasotracheal suctioning method over sputum induction. Respir Care 1989;34:249-253. 26. Fisher DM, Frewen T, Swedlow DB. Increase in intracranial pressure during suctioning stimulation vs rise io PaCO2. Anesthesiology 1982;57:416-417. 27. Parsons LC, Shogan JS. The effects of the endotracheal tube suctioning/manual hyperinflation procedure on patients with severe closed head injuries. Heart Lung 1984;13:372-380. 28. Peterson GM, Pierson DJ, Hunter PM. Arterial oxygen saturation during nasotracheal suctioning. Chest 1979; 76:283-287. 29. Petty TL. Intensive and rehabilitative respiratory care, 3rd ed. Philadelphia: Lea & Febiger, 1982:30-33,154. 30. Curran JF, Stanek KS, Kacmarek RM. Portable airway-suction systems: a comparison of performance. Respir Care 1991;36:259-266. 31. Bostick J, Wendelgass ST. Normal saline instillation as part of the suctioning procedure: effects on PaO2 and amount of secretions. Heart Lung 1987;16:532-537. 32. Langrehr EA, Woodburn SC, Guthrie MP. Oxygen insufflation during endotracheal suctioning. Heart Lung 1981;10:1028-1036. 33. Jacquette G. To reduce hazards of tracheal suction. Am J Nurs 1971;71:2362-2364. 34. Occupational exposure to bloodborne pathogens. Final Rule. Federal Register 1991;56:64175-64182. 35. Centers for Disease Control. Update: Universal Precautions for prevention of transmission of human immunodeficiency virus, hepatitis B virus, and other blood-borne pathogens in health care 36. settings. MMWR 1988; 37:377-399. 37. McFadden R. Decreasing respiratory compromise during infant suctioning. Am J Nurs 1981;81:2158-2161. Interested persons may copy these Guidelines for noncommercial purposes of scientific or educational advancement. Please credit AARC and Respiratory Care Journal.

Aspiración de secreciones (manejo en casa)

Reprinted from Respiratory Care (Respir Care 1999;44(1):99-104)
AARC Clinical Practice Guideline
Suctioning of the Patient in the Home
HCS 1.0 PROCEDURE
Suctioning of the patient (with or without an artificial airway) cared for in the home. This includes nasal, oropharyngeal, and endotracheal suctioning.
HCS 2.0 DESCRIPTION
Suctioning is a component of bronchial hygiene that involves the mechanical aspiration of secretions from the nasopharynx, oropharynx, and trachea. The airway may be in its natural state or artificial (as with a tracheostomy) or surgically altered (as with a laryngectomy). The patient may or may not be receiving mechanical ventilation. The procedure includes patient preparation, the actual suctioning event, and follow-up care and observation of the patient.
2.1 Patient preparation.
2.1.1 Whenever possible, the patient should be encouraged to clear the airway by directed cough or other airway clearance techniques.(1-5)
2.1.2 Whenever possible, the patient should be taught to perform this procedure for himself.(4-7)
2.1.3 Preoxygenation or hyperinflation prior to the suctioning event may not be routinely indicated for all patients cared for in the home. Whenever possible the patient’s response to suctioning during his stay in the acute care or long-term care facility should be made a part of the discharge summary, and the health care professional establishing the patient in the home should request this information.
Experience with neuromuscular patients suggests that hyperinflation when the vital capacity of such patients is < 1.5L makes tracheal suctioning unnecessary.(5,8) Other patients for whom preoxygenation or hyperinflation may not be necessary or advisable include those 2.1.1.1 requiring only nasal or oropharyngeal suctioning;(9) 2.1.1.2 without an endotracheal airway, whose vital capacity and muscle strength are adequate to produce an effective cough; 2.1.1.3 whose ventilatory drive has been demonstrated to stem from hypoxia;(10) 2.1.1.4 with a demonstrated tolerance for the procedure with no adverse reactions. 2.1.4 Preoxygenation and/or hyperinflation may be indicated in: 2.1.4.1 pediatric patients with decreased respiratory reserve; 2.1.4.2 patients who have been documented to experience oxygen desaturation during the suctioning event as evidenced by pulse oximetry; 2.1.4.3 patients who exhibit cardiac dysrhythmias during the suctioning event; 2.1.4.4 patients who are receiving continuous supplemental oxygen. 2.1.5 When preoxygenation and/or hyperinflation are indicated, it is recommended that this be done manually using a resuscitation bag with supplemental oxygen, as appropriate. All caregivers should receive thorough instruction in the use of resuscitation bags and manual hyperventilation techniques; improper or imprecise use of resuscitation bags for hyperinflation can cause lung injury and respiratory alkalosis. If hyperoxygenation or hyperventilation are not required, tidal volume may be conserved by passing the suction catheter through the port cap on the swivel adapter of the ventilator circuit. 2.1.6 Normal saline solution should not be instilled routinely but only when specifically medically indicated(11-15) (for example, to stimulate cough(14,15)). 2.2 The suctioning event: Actual introduction of the suction device (catheter or oral suction tip) into the naso- or oropharynx, or into the trachea via the laryngostoma or artificial airway should be in accordance with existing Clinical Practice Guidelines.(9,16) 2.2.1 It is common and accepted practice to use 'clean' rather than sterile technique during suctioning in the home environment, although scientific evidence to support or discount either technique in home care is lacking.(17) 2.2.2 Clean (non-sterile) gloves should be used when endotracheal suctioning is performed. Gloves reduce the risk of introduction of inoculant to the patient's airway,(15) the risk of cutaneous infection in the caregiver, and transmission of organisms to others.(18,19) Gloves may not be necessary when oropharyngeal suctioning is performed. 2.2.3 At the conclusion of the suctioning event, the catheter or tonsil tip should be flushed by suctioning recently boiled or distilled water to rinse away mucus, followed by the suctioning of air through the device to dry the internal surface and, thus, discourage microbial growth. The outer surface of the device may be wiped with alcohol or hydrogen peroxide. The suction catheter or tonsil tip should be allowed to air dry and then be stored in a clean, dry area. 2.2.4 Suction catheters treated in the manner described may be reused. We recommend that the catheters be discarded after 24 hours although no evidence for or against this can be found. Tonsil tips may be cleaned, boiled, and reused indefinitely. If it is feasible to clean the suction device and subject it to high level disinfection, it may be reused until its integrity is lost.(20) The importance of mechanical cleaning cannot be overemphasized (ie, removal of mucus and other organic material). 2.3 Follow-up care: Following the suctioning event 2.3.1 the patient should be monitored for adverse reactions;(9,16) 2.3.2 the patient in whom pre-procedure hyperoxygenation and/or hyperinflation was indicated should be treated by the same method(s) post-procedure.(16,21) HCS 3.0 SETTING This guideline applies only to the home care setting. Alternate care sites such as subacute, rehabilitation, or skilled nursing facilities should use Guidelines for suctioning in the acute care setting.(9,16) HCS 4.0 INDICATIONS The primary indication for suctioning the patient cared for at home is the patient's inability to adequately clear the airway by cough. The need for airway clearance is evidenced by: 4.1 more frequent or congested-sounding cough; 4.2 coarse rhonchi and expiratory wheezing audible to the patient and/or caregiver with or without auscultation; 4.3 visible secretions; 4.4 increased peak pressures during volume-cycled mechanical ventilation; 4.5 decreased tidal volumes during pressure-cycled ventilation; 4.6 indication by the patient that suctioning is necessary; 4.7 suspected aspiration of gastric or upper airway secretions; 4.8 otherwise unexplained increase in shortness of breath, respiratory rate, or heart rate; 4.9 decreases in vital capacity and/or oxygen saturation (as indicated by pulse oximetry), thought to be related to mucus plugging.(22) HCS 5.0 CONTRAINDICATIONS When suctioning is indicated, no absolute contraindications exist and failure to suction can prove to be more detrimental than potential adverse reactions. Routine or 'scheduled' suctioning, with no indication of need is not recommended. HCS 6.0 HAZARDS/COMPLICATIONS Because the suctioning event is inherently the same in the home as in the critical care setting, the possible hazards and complications are the same. Dislodgement and introduction into the lower airway of bacteria colonizing the tracheal tube has been demonstrated. Further, the bacterial count introduced may be increased when saline is instilled.(12,13) The home care patient is not monitored by any except the most basic methods, and the patient must be closely observed for all of the following: 6.1 oxygen desaturation as indicated by pulse oximetry if such monitoring has been prescribed; 6.2 trauma to the oral, tracheal, or bronchial mucosa; 6.3 cardiac arrest; 6.4 respiratory arrest; 6.5 cardiac dysrhythmias; 6.6 pulmonary atelectasis; 6.7 bronchospasm or bronchoconstriction; 6.8 airway infection; 6.9 bleeding or hemorrhage from the airway; 6.10 hypertension; 6.11 hypotension. HCS 7.0 LIMITATIONS OF PROCEDURE Endotracheal suctioning is not a benign procedure, and the caregiver should remain sensitive to possible hazards and complications, taking all necessary precautions to ensure patient safety. Secretions in the peripheral airways cannot be removed by suctioning. Optimal humidification of inspired gases and appropriate systemic hydration is important to the maintenance of airway integrity. HCS 8.0 ASSESSMENT OF NEED The patient should be periodically assessed by the caregiver to determine the need for suctioning when the need does not obviously present itself. For patients on long-term mechanical ventilation, this assessment should be included in the patient/ventilator system check.(23) HCS 9.0 ASSESSMENT OF OUTCOME Results and observations related to suctioning should be recorded to inform and alert other caregivers. The suctioning procedure can be considered successful and the need for suctioning affirmed by one or more of the following: 9.1 removal of secretions; 9.2 improvement in breath sounds; 9.3 decreased peak inspiratory pressure during volume-cycled mechanical ventilation; 9.4 increased tidal volume delivery during pressure-cycled mechanical ventilation; 9.5 clearing of cough; 9.6 improvement in oxyhemoglobin saturation as reflected by pulse oximetry; 9.7 subjective improvement as reported by patient; 9.8 a decrease in respiratory and heart rate and decreased shortness of breath. HCS 10.0 RESOURCES 10.1 Equipment: Equipment and supplies to used for suctioning the home care patient may include: 10.1.1 electrically powered aspirator with a calibrated, adjustable regulator and collection bottle with overflow protection. A battery-powered aspirator may be needed for the patient who leaves the home or lives in an environment subject to frequent power failures; 10.1.2 suction catheters, sized appropriately. Open suction systems are used most frequently. (The use of closed systems has not been demonstrated to be medically indicated in the patient who is not immunosuppressed(18)); 10.1.3 tap water that has been boiled, stored in a closed, clean container, and used within 24 hours of boiling to flush the catheter. (Water directly from the tap should not be used because of the possibility of contamination.(18)) 10.1.4 clean or sterile gloves as indicated; barrier protection when active infection is present or suspected; 10.1.5 manual resuscitator when hyperinflation is medically indicated; 10.1.6 oxygen source when preoxygenation is medically indicated; 10.1.7 sterile normal saline for instillation when medically indicated; 10.1.8 oral suction device (eg, tonsil tip); 10.1.9 sterile distilled and/or recently boiled water and cleaning solution. 10.2 Personnel: As stated previously, the patient should be trained in self-care whenever possible. In the event that the patient is unable to perform the procedure, the bedside caregivers (family members, personal care attendants, other designated care givers) should be thoroughly trained and demonstrate their ability to perform the procedure and clean and care for equipment.(24) 10.2.1 Only credentialed or licensed professional staff with documented specialized training and experience in airway management procedures and patient assessment should be specified as trainers (eg, licensed and credentialed respiratory care practitioners and registered nurses). These trainers should also observe, on a regular basis, performance of the procedure by the patient and caregivers to determine the need for reinforcement and remediation.(24) 10.2.2 All caregivers should demonstrate a good understanding of the procedure and the ability to perform the procedure competently, including: 10.2.2.1 knowledge of proper use and assembly of all necessary equipment and supplies; 10.2.2.2 ability to recognize that suctioning is indicated; 10.2.2.3 ability to assess effectiveness of the procedure; 10.2.2.4 ability to monitor vital signs, assess the patient's condition, and appropriately respond to complications or adverse reactions; 10.2.2.5 ability to perform the procedure with the least amount of risk of introducing inoculant into the patient's airway; 10.2.2.6 knowledge of infection control procedures and demonstrated ability to effectively wash hands and clean, disinfect, and properly store equipment and supplies. HCS 11.0 MONITORING The patient should be monitored to ascertain effectiveness of the procedure and to detect any adverse reaction. Variables to be monitored include: 11.1 breath sounds, 11.2 skin color--including the presence or absence of cyanosis, 11.3 respiratory rate and characteristics, 11.4 heart rate, 11.5 sputum characteristics (color, volume, consistency, odor) 11.6 blood pressure, 11.7 ventilator variables (including tidal volume, peak inspiratory pressure, respiratory rate, expiratory pressure), 11.8 oxygen saturation by pulse oximetry when medically indicated. HCS 12.0 FREQUENCY The suctioning procedure should be undertaken only when indications are clearly present (Sections 4, 5, & 8). HCS 13.0 INFECTION CONTROL All caregivers should practice infection control procedures appropriate to the home environment.(25) To the extent feasible, patients should be protected from visitors and caregivers with active viral and bacterial infections that are airborne or spread by direct contact. Immunizations recommended by the Centers for Disease Control and Prevention should be current in both caregivers and patient. When HIV and/or hepatitis or other bloodborne infection are known to be present or when the patient's status is unknown and when infection with organisms spread by droplet infection is known or suspected, specific precautions should be instituted.(25) With all patients the steps undertaken are 13.1 proper handwashing before and after performing the procedure; 13.2 clean or sterile suctioning technique as indicated; 13.3 cleaning and disinfection of all equipment and supplies beginning with thorough mechanical cleaning with detergent and water and followed by one of the following 13.3.2 a 60-minute soak in a solution of vinegar and water with an acetic acid content > or = 1.25% (The vinegar solution should not be reused.);(26,27)
13.3.3 quaternary ammonium compound (prepared and reused according to manufacturer’s instructions);(26,27)
13.3.4 glutaraldehyde;(28)
13.3.5 boiling when equipment withstands such procedures;
13.4 proper storage of equipment and supplies between use;
13.5 proper disposal of spent supplies and infectious waste.(29)
Respiratory Home Care Working Group
Susan L McInturff RRT RCP, Chairman, Bremerton WA
Barry J Make MD, Denver CO
Peggi Robart MA RRT,RCP, Boston MA
Allan B Saposnick MS RRT, Sharon Hill PA
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23. American Association for Respiratory Care. AARC Clinical Practice Guideline: long-term invasive mechanical ventilation in the home. Respir Care 1995;40(12):1313-1320
24. American Association for Respiratory Care. AARC Clinical Practice Guideline: providing patient and caregiver training. Respir Care 1996;41(7):658-663.
25. Garner JS, Hospital Infection Control Practices Advisory Committee, Centers for Disease Control and Prevention. Guidelines for Isolation Precautions in Hospitals. Atlanta GA: Centers for Disease Control and Prevention, 1-01-1996. www.cdc.gov
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27. Chatburn RL, Kallstrom TJ, Bajaksouzian S. A comparison of acetic acid with a quaternary ammonium compound for disinfection of hand-held nebulizers. Respir Care 1988;3:179-187.
28. Working Group,. American Respiratory Care Foundation. Guidelines for disinfection of respiratory care equipment used in the home. Respir Care 1988;33(9):801-808.
29. Ralph IG. Infectious waste management: a home care responsibility. Home Healthcare Nurse 1993;11:25-33.
Interested persons may copy these Guidelines for noncommercial purposes of scientific or educational advancement. Please credit AARC and RESPIRATORY CARE Journal.