Smoke Inhalation Injury*

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Smoke Inhalation Injury* Jornal Brasileiro de Pneumologia 30(6) - Nov/Dez de 2004 Lesão por inalação de fumaça* Smoke inhalation injury ROGÉRIO SOUZA(TE SBPT), CARLOS JARDIM, JOÃO MARCOS SALGE(TE SBPT), CARLOS ROBERTO RIBEIRO CARVALHO(TE SBPT) A lesão inalatória é hoje a principal causa de morte nos Inhalation injury is the main cause of death in burn pacientes queimados, motivo pelo qual se justifica o grande patients and has therefore, understandably, been the número de estudos publicados sobre o assunto. Os mecanismos subject of numerous published studies. The pathogenesis envolvidos na gênese da lesão inalatória envolvem tanto os of inhalation injury involves both local and systemic fatores de ação local quanto os de ação sistêmica, o que mechanisms, thereby increasing the repercussions of the acaba por aumentar muito as repercussões da lesão. injury. The search for tools that would allow earlier Atualmente, buscam-se ferramentas que permitam o diagnosis of inhalation injury and for treatment strategies diagnóstico cada vez mais precoce da lesão inalatória e ainda to lessen its deleterious effects is ongoing. In this review, estratégias de tratamento que minimizem as conseqüências we describe the physiopathological mechanisms of da lesão já instalada. Esta revisão aborda os mecanismos inhalation injury, as well as the current diagnostic tools fisiopatológicos, os métodos diagnósticos e as estratégias de and treatment strategies used in patients suffering from tratamento dos pacientes vítimas de lesão inalatória. Ressalta inhalation injury. We also attempt to put experimental ainda as perspectivas terapêuticas em desenvolvimento. therapeutic approaches into perspective. J Bras Pneumol 2004; 30(5) 557-65. Descritores: Lesão por inalação de fumaça/diagnóstico. Key words: Smoke inhalation injury/diagnosis. Smoke Lesão por inalação de fumaça/fisiopatologia. Lesão por inhalation injury/pathophysiology. Smoke inhalation injury/ inalação de fumaça/complicações. Queimaduras por complications. Burns, inhalation/therapy. Review literature. inalação/terapia. Literatura de revisão. Intoxicação por Carbon monoxide. Poisoning/complications. monóxido de carbono/complicações. * Trabalho realizado na Disciplina de Pneumologia da Faculdade de Medicina da Universidade de São Paulo, FMUSP, São Paulo, SP. Endereço para correspondência: Rogério Souza. R. Afonso de Freitas 556, CEP 04006-052 – São Paulo, SP. Tel: 55-11-3889 7426. Email: [email protected] Recebido para publicação, em 28/4/03. Aprovado, após revisão, em 20/2/04. 557 Souza, Rogério et al. Lesão por inalação de fumaça INTRODUÇÃO superiores, enquanto que partículas com menos A lesão inalatória é o resultado do processo de um micrômetro podem atingir os sacos inflamatório das vias aéreas após a inalação de alveolares. O aumento do fluxo aéreo determinado produtos incompletos da combustão e é a principal pela taquipnéia também pode levar ao aumento responsável pela mortalidade (até 77%) dos da taxa de deposição de partículas nas vias aéreas pacientes vítimas de queimaduras(1, 2). Cerca de mais distais(6). 33% dos pacientes com queimaduras extensas Os gases são divididos em duas categorias, de apresentam lesão inalatória e o risco aumenta acordo com o mecanismo de lesão: irritantes e progressivamente com o aumento da superfície asfixiantes. Os gases irritantes causam lesão na corpórea queimada. A presença de lesão inalatória, mucosa através de reações de desnaturação ou por si, aumenta em 20% a mortalidade associada oxidação. Podem causar broncoespasmo, à extensão da queimadura(3). Nos últimos anos traqueobronquite química e até mesmo edema houve um crescente entendimento dos mecanismos pulmonar. O local de ação dos gases irritantes depende fisiopatológicos relacionados à lesão inalatória, o em grande parte de sua solubilidade em água. Os que vem permitindo abordagens cada vez mais gases mais solúveis como a amônia e o dióxido de particularizadas. enxofre geralmente provocam reações nas vias aéreas superiores, provocando sensação dolorosa na boca, nariz, faringe ou mesmo nos olhos. De modo PRODUÇÃO E CONSTITUIÇÃO DA contrário, os gases pouco solúveis são responsáveis FUMAÇA pelas lesões mais distais nas vias aéreas e, por serem A fumaça é a mistura de gases e partículas em pouco irritantes para as vias aéreas superiores, podem suspensão resultantes da queima de qualquer permitir exposição oligossintomática, aumentando a combustível. A produção de fumaça depende de chance e a extensão da lesão parenquimatosa. Os dois processos: pirólise e oxidação. A pirólise é o gases asfixiantes são definidos como aqueles que fenômeno de liberação de elementos do retiram oxigênio do ambiente. A retirada de oxigênio combustível causada exclusivamente pela ação do ocorre tanto pela diminuição da fração de oxigênio calor, através do derretimento ou fervura. A do ar inspirado, como por qualquer outro mecanismo oxidação é o processo em que o oxigênio reage que impeça a captação e distribuição de oxigênio quimicamente com moléculas do combustível pelo sistema cardiovascular. Assim, são considerados quebrando-as em compostos menores que asfixiantes tanto o dióxido de carbono, que diminui resultam na produção de luz e calor. Como a fração de oxigênio do ambiente, quanto o monóxido produtos resultantes da oxidação podemos citar de carbono, cuja ligação com a hemoglobina diminui o monóxido de carbono (CO), dióxido de a oferta de oxigênio aos tecidos(6, 7). nitrogênio (NO2) e dióxido de enxofre (SO2), além do carbono elementar. A predominância de um ou outro processo, além da temperatura, ventilação, MECANISMOS DE LESÃO e do tipo de material queimado no ambiente levam Para facilitar a compreensão, tanto do quadro à produção de uma grande quantidade de clínico, quanto do tratamento, após o elementos constituintes da fumaça, cada qual com esclarecimento dos componentes da fumaça, são sua toxicidade e mecanismo de lesão peculiar(4, 5). apresentados os quatro mecanismos responsáveis Os constituintes da fumaça podem ser divididos pela lesão inalatória: em dois grupos: material particulado e gases. Tanto um como o outro produzem lesões nas vias aéreas, LESÃO TÉRMICA DIRETA mas por mecanismos e em territórios diferentes. A ação decorrente da temperatura da fumaça O material particulado pode levar à obstrução inalada raramente provoca lesões nos territórios das vias aéreas por efeito direto de deposição e abaixo da laringe. Apesar de ter alta temperatura, pela indução de broncoespasmo. De acordo com a fumaça tende a ser seca, o que diminui muito o o tamanho da partícula, a região de depósito é potencial de troca de calor. Além disso, as regiões diferente: partículas maiores que cinco supralaríngeas têm grande capacidade de troca de micrômetros tendem a se depositar nas vias aéreas calor, já que as mucosas encerram grande 558 Jornal Brasileiro de Pneumologia 30(6) - Nov/Dez de 2004 quantidade relativa de água. As lesões em vias 250 vezes maior que a do oxigênio. A produção de aéreas superiores são caracterizadas pela presença carboxihemoglobina, complexo extremamente de eritema, edema e ulcerações de mucosa, estável, além de causar um decréscimo na saturação podendo haver sangramento local ou mesmo de oxihemoglobina, causa um desvio da curva de obstrução da área acometida(8-10). dissociação para a esquerda, diminuindo a liberação de oxigênio aos tecidos. Além disso, a inibição competitiva com os sistemas da citocromo oxidase, INALAÇÃO DO GÁS HIPÓXICO principalmente a do P-450, impede o uso do Durante a combustão, a concentração de oxigênio para geração de energia. O monóxido de oxigênio cai progressivamente até o momento em carbono liga-se também à mioglobina, prejudicando que o fogo se extingue, pelo próprio consumo o armazenamento de oxigênio nos músculos(14-16). gerado pela combustão. Dependendo do tipo de A toxicidade do cianeto é causada pela inibição da combustível, o momento de extinção do fogo oxigenação celular, o que causa anóxia tecidual pela varia. A maior parte do fogo decorrente da inibição reversível das enzimas citocromo oxidase (Fe3+). combustão de derivados de petróleo se extingue A inibição da via glicolítica aeróbia desvia o metabolismo em frações de oxigênio entre 13% e 15%, para a via anaeróbia alternativa, produzindo então o enquanto componentes que contenham oxigênio acúmulo de sub-produtos ácidos(17, 18). podem permitir a combustão até frações inspiradas O tipo de exposição, o tempo, ou ainda a menores que 10%. Essa diminuição da fração predominância de um ou mais desses mecanismos inspirada de oxigênio faz com que as vítimas determinam diferentes evoluções da lesão passem a referir dispnéia e tontura, que podem inalatória. Na Figura 1 podemos observar a evoluir para confusão mental, torpor, coma e até evolução dos fenômenos relacionados à lesão mesmo óbito, em frações ao redor de 5%, inalatória nos diferentes territórios do sistema (11) consideradas incompatíveis com a vida . respiratório frente a diferentes exposições. TOXINAS LOCAIS DIAGNÓSTICO DA LESÃO INALATÓRIA Dentre os vários componentes da fumaça, Apresentação clínica podem causar lesão direta nas vias aéreas a acroleína, formaldeídos, dióxido de enxofre e Além da história de exposição à fumaça em dióxido de nitrogênio. A ação lesiva decorre de ambiente fechado, vários sinais e sintomas devem (19) um processo inflamatório agudo, mediado por levar à suspeita clínica de lesão inalatória . Os polimorfonucleares, principalmente neutrófilos. mais importantes são listados na Tabela 1. Esse processo pode gerar sintomas, apenas 24 Alguns achados devem levar à suspeita
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