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Acute clinical manifestations in toxic smoke inhalation victims: systematic review of observational studies

Manifestações clínicas agudas em vítimas de inalação de fumaça tóxica: revisão sistemática de estudos observacionais

Manifestaciones clínicas agudas en víctimas de inhalación de humos: revisión sistemática de estudios observacionales

Abstract

Introduction:

Lung injuries from toxic smoke inhalation are the main causes of death in fire victims; however, information regarding the acute effects on the respiratory system after smoke inhalation and its constituents in closed environments are still scarce in literature.

Objective:

To investigate the acute clinical manifestations observed in victims of smoke inhalation during enclosed-space fires by means of systematic review.

Methods:

A systematic search was conducted in the following databases: MEDLINE (via PubMed), Lilacs, Scopus and Web of Science. There were no appliedrestrictions in terms of thepublication date. In addition, a manual search was performed on the references of published studies. Observational studies assessing the prevalence of acute clinical manifestations in victims of toxic smoke inhalation in closed environments were included.

Results:

Of the 4,603 articles identified, eight were included, comprising a total of 233 patients. The signs and symptoms were identified and ranked according to frequency. Dyspnea (58.80%, six studies), carbonaceous sputum (54.51%, four studies), hoarseness (39.91%, three studies), wheezing (34.33%, five studies) and sore throat (33.90%, two studies) were the most frequent acute clinical manifestations of smoke inhalation. Besides these, chest pain and pulmonary edema were observed, respectively in 13.30%, 5.15% of the studies.

Conclusion:

The results suggest that dyspnea, carbonaceous sputum, hoarseness, wheezing and sore throat were the most frequent acute clinical manifestations in victims of smoke inhalation. Further studies of a higher level of evidence and greater methodological rigor are required.

Keywords:
Smoke Inhalation Injury; Hydrogen Cyanide; Carbon Monoxide; Lung Injury

Resumo

Introdução:

As lesões pulmonares decorrentes da inalação de fumaça tóxica são as principais causas de morte em vítimas de incêndio; no entanto, informações a respeito das repercussões agudas no sistema respiratório decorrentes da inalação de fumaça e seus constituintes em ambientes fechados ainda são escassas na literatura.

Objetivo:

Investigar as manifestações clínicas agudas observadas em vítimas de inalação de fumaça tóxica em ambientes fechados através de uma revisão sistemática.

Métodos:

Uma pesquisa sistemática foi realizada nas seguintes bases de dados: MEDLINE (via PubMed), Lilacs, Scopus e Web of Science. Não houve restrições quanto ao ano de publicação. Além disso, realizou-se uma pesquisa em referências de estudos publicados. Foram incluídos estudos observacionais que avaliaram a prevalência das manifestações clínicas agudas em vítimas de inalação de fumaça tóxica em ambientes fechados.

Resultados:

Dos 4.603 artigos encontrados, oito foram incluídos, compreendendo um total de 233 pacientes. Os sinais e sintomas foram identificados e classificados de acordo com a frequência com que apareceram nos estudos incluídos. Dispneia (58,80%, seis estudos), escarro carbonáceo (54,51%, quatro estudos), disfonia (39,91%, três estudos), sibilância (34,33%, cinco estudos) e dor de garganta (33,90%, dois estudos) foram as manifestações clínicas agudas mais frequentes de inalação de fumaça. Além disso, dor torácica e edema pulmonar foram observados, respectivamente em 13,30% e 5,15% dos estudos.

Conclusão:

Os resultados sugerem que dispneia, escarro carbonáceo, disfonia, sibilância e dor de garganta foram as manifestações clínicas agudas mais frequentes nas vítimas de inalação de fumaça tóxica. São necessários novos estudos com alto nível de evidência e melhor rigor metodológico.

Palavras-chave:
Lesão por Inalação de Fumaça; Cianeto de Hidrogênio; Monóxido de Carbono; Lesão Pulmonar

Resumen

Introducción:

Las lesiones pulmonares producidas por la inhalación de humo son las principales causas de muerte entre las víctimas de fuego, sin embargo, informaciones con respeto de las repercusiones agudas en el sistema respiratorio derivadas de la inhalación de humo y sus constituyentes en ambientes cerrados siguen escasas en la literatura.

Objetivo:

Investigar las manifestaciones clínicas agudas observadas en víctimas de inhalación de humo en ambientes cerrados a través de una revisión sistemática.

Métodos:

Una pesquisa sistemática fue realizada en las siguientes bases de datos: MEDLINE (vía PubMed), Lilacs, Scopus y Web of Science. No hubo restricciones con relación al año de publicación. Además, se realizó una pesquisa en referencias de estudios publicados. Fueron incluidos estudios observacionales que evaluaron la prevalencia de las manifestaciones clínicas agudas en víctimas de inhalación de humo tóxico en ambientes cerrados.

Resultados:

De los 4.603 artículos encontrados, ocho fueron incluidos, comprendiendo un total de 233 pacientes. Los signos y síntomas fueron identificados y clasificados de acuerdo con la frecuencia con que aparecieron en los estudios incluidos. Disnea (58,80%, seis estudios), esputo carbonáceo (54,51%, cuatro estudios), disfonía (39,91%, tres estudios), sibilancia (34,33%, cinco estudios) y dolor de garganta (33,90%, de los estudios) han sido las manifestaciones clínicas agudas más frecuentes de la inhalación de humo. Además, dolor torácico y edema pulmonar han sido observados, respectivamente en 13,30% y 5,15% de los estudios.

Conclusión:

Los resultados sugieren que la disnea, esputo carbonáceo, disfonía y dolor de garganta fueron las manifestaciones clínicas más frecuentes en las víctimas de inhalación de humo tóxico. Son necesarios nuevos estudios con alto nivel de evidencia y mejor rigor metodológico.

Palabras clave:
Lesión por Inhalación de Humo; Cianuro de Hidrógeno; Monóxido de Carbono; Lesión Pulmonar

Introduction 1 1 Clinical Trial Registration Information — URL: http://www.crd.york.ac.uk/PROSPERO. Unique identifier: CRD42016042728.

On January 27, 2013, Brazil experienced one of the biggest tragedies involving a fire in a closed environment, which killed 242 people and ended up with another one thousand injured. The fire at the Kiss nightclub in the city of Santa Maria, State of Rio Grande do Sul, in Southern Brazil, is worldwide considered the second biggest fire occurred in a nightclub, only exceeded by the Cocoanut Grove nightclub fire in Boston, Massachusetts, USA, in November 1942. Kiss nightclub’s was the second highest death toll due to fire in Brazilian history; the first one happened in 1961 in the city of Niterói, State of Rio de Janeiro, at the Gran Circus Norte-Americano, which killed 503 people 11. Pasqualoto AS, Albuquerque IM, Pereira MB, Bertolazi AN, Silva CSPR, Prado ALC, et al. Epidemiological profile, respiratory signs and symptoms of individuals who inhaled toxic smoke in Kiss nightclub fire, Santa Maria, RS, Brazil. ConScientiae Saude. 2015;14(2):229-35..

Smoke inhalation and its lung injury consequences are considered a leading cause of immediate death in fire victims 22. Anseeuw K, Delvau N, Burillo-Putze G, De Iaco F, Geldner G, Holmström P, et al. Cyanide poisoning by fire smoke inhalation: a European expert consensus. Eur J Emerg Med. 2013;20(1):2-9.),(33. O'Brien DJ, Walsh DW, Terriff CM, Hall AH. Empiric management of cyanide toxicity associated with smoke inhalation. Prehosp Disaster Med. 2011;26(5):374-82., and represent also a majority causes of mortality and morbidity related to exposure to smoke from fire 44. Klingsch WWF, Rogsch C, Schadschneider A, Schreckenberg M. Pedestrian and Evacuation Dynamics 2008. In: Löllgen H, Leyk D. Inhalation injury of lung and heart after inhalation of toxic substances. Springer: Berlin; 2010. p.781-9..

In a close environment, it is impossible to predict the pathophysiological interactions of all smoke toxins, especially if we consider the wide variety of pyrolysis components 22. Anseeuw K, Delvau N, Burillo-Putze G, De Iaco F, Geldner G, Holmström P, et al. Cyanide poisoning by fire smoke inhalation: a European expert consensus. Eur J Emerg Med. 2013;20(1):2-9.. In this sense, hydrogen cyanide (HCN) and carbon monoxide (CO) gases are commonly found at elevated concentrations in fire smoke and are associated with a high incidence of immediate death, severe morbidity and mortality 55. Hamel J. A review of acute cyanide poisoning with a treatment up date. Crit Care Nurse. 2011;31(1):72-81.)-(77. Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. Carbon monoxide poisoning - a public health perspective. Toxicology. 2000;145(1):1-14..

In this context, fire-related inhalation injury can result from direct local thermal and chemical exposures, immune responses to these factors, systemic effects of inhaled toxins, accrual of endobronchial debris, and secondary infection. The effect for individual patients is complex and unpredictable 88. Sheridan RL. Fire-Related Inhalation Injury. N Engl J Med. 2016;375(5):464-9..

Individuals who are accidentally exposed to toxic gases, as HCN and CO, usually present vague and nonspecific symptoms 99. Banauch GI, Brantly M, Izbicki G, Hall C, Shanske A, Chavko R, et al. Accelerated spirometric decline in New York city firefighters with a1-antitrypsin deficiency. Chest. 2010;138(5):1116-24.. In this sense, classically, the diagnosis of inhalation injury was subjective and made based on clinical findings 1010. Walker PF, Buehner MF, Wood LA, Boyer NL, Driscoll IR, Lundy JB, et al. Diagnosis and management of inhalation injury: na updated review. Crit Care. 2015;19:351.. Despite the fact, according to Sheridan 88. Sheridan RL. Fire-Related Inhalation Injury. N Engl J Med. 2016;375(5):464-9., the specific therapeutic interventions remain ineffective, the individual risk of death remains difficult to quantify, and the long-term implications for survivors remain ill-defined.

Previous studies addressed the long-term effects of smoke inhalation on the respiratory system. These studies demonstrated a lung function decline and chronic respiratory symptoms 99. Banauch GI, Brantly M, Izbicki G, Hall C, Shanske A, Chavko R, et al. Accelerated spirometric decline in New York city firefighters with a1-antitrypsin deficiency. Chest. 2010;138(5):1116-24.),(1111. Fogarty PW, George PJ, Solomon M, Spiro SG, Armstrong RF. Long term effects of smoke inhalation in survivors of the King's Cross underground station fire. Thorax. 1991;46(12):914-8.),(1212. Greven F, Krop E, Spithoven J, Rooyackers J, Kerstjens H, Heederik D. Lung function, bronchial hyperresponsiveness, and atopy among firefighters. Scand J Work Environ Health. 2011;37(4):325-31.; however, studies evaluating initial clinical manifestations in the early phase of patients with smoke inhalation injuries are still scarce.

Based on this, we aimed to carry out, for the first time, a systematic review of the literature to investigate the acute clinical manifestations on the respiratory system observed in victims of smoke inhalation during enclosed-space fires.

Methods

This systematic review was performed following the recommendations proposed by Preferred Reporting Items for Systematic Review and Meta-analyses: The PRISMA Statement 1313. Moher D, Liberati A, Tetzlaff J, Altman DG. Preferred reporting items for systematic reviews and meta-analyses: The PRISMA statement. Ann Intern Med. 2009;151(4):264-9.. The protocol of systematic review was prospectively registered at International Prospective Register of Systematic Review database (PROSPERO) under the identification CRD42016042728.

Sources and search strategy

The investigators, who received formal training in systematic review, performed all searches. A systematic search was performed in the following electronic databases: MEDLINE (accessed via PubMed), Lilacs, Scopus, and Web of Science.

The search strategy used in PubMed is shown in Table 1. There were no appliedrestrictions in terms of the publication date. Articles in Portuguese, Spanish or English were included. A manual search was performed, but no unpublished study or conference abstract fulfilled the inclusion criteria. Thus, there was no need to contact authors for further information or to handle unpublished abstracts.

Table 1
Search strategy used in PubMed

Eligibility criteria

This review included observational studies (case study and case series) assessing the prevalence of acute clinical manifestations (in the first 24 hours) in victims of toxic smoke inhalation in closed environments. Experimental studies, postmortem analysis, comparison among diagnostic methods, comparison of preexisting chronic conditions, studies that have addressed long-term clinical manifestations or about the management of patients with smoke inhalation were excluded.

Data extraction

Two reviewers independently extracted the data from the eligible studies by using a standardized data extraction form. The following data were extracted: authors; year of publication; country of the research; study design; patient characteristics (demographics, sample size); fire location and acute clinical manifestations (clinical presentation, chest examination and radiologic findings).

Results

Description of studies

Of the 4,603 studies identified in the search, eight matched the eligibility criteria, yielding a total of 233 patients. Figure 1 shows the flowchart of the studies included in this review and Table 2 summarizes their characteristics.

Figure 1
Flowchart for the studies identified for analysis

Table 2
Characteristics of the included studies

According to their study design, four of the studies were case series 1515. Putman CE, Loke J, Matthay RA, Ravin CE. Radiographic manifestations of acute smoke inhalation. AJR Am J Roentgenol. 1977;129(5):865-70.),(1616. Lee MJ, O'Connell DJ. The plain chest radiograph after acute smoke inhalation. Clin Radiol. 1988;39(1):33-7.),(1818. Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5.),(1919. Cha SI, Kim CH, Lee JH, Park JY, Jung TH, Choi WI, et al. Isolated smoke inhalation injuries: acute respiratory dysfunction, clinical outcomes, and short-term evolution of pulmonary functions with the effects of steroids. Burns. 2007;33(2):200-8. and the other studies were case studies 1414. McArdle CS, Finlay WE. Pulmonary complications following smoke inhalation. Br J Anaesth. 1975;47(5):618-23.),(1717. Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Induction of bronchial hyperresponsiveness following smoke inhalation injury. Br J Dis Chest. 1988;82(4):436-8.),(2020. Dinh D, Rosini JM. Empiric treatment of cyanide toxicity in an enclosed-space fire survivor. J Emerg Nurs. 2014;40(3):282-5.),(2121. Tyagi R, Ramasethu R, Mohanty CS, Singhal A. Two cases of acute lung injury following closed space smoke inhalation. Med J Armed Forces India. 2015;71(Suppl 2): S538-41.. Most selected studies described two cases 1414. McArdle CS, Finlay WE. Pulmonary complications following smoke inhalation. Br J Anaesth. 1975;47(5):618-23.),(1717. Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Induction of bronchial hyperresponsiveness following smoke inhalation injury. Br J Dis Chest. 1988;82(4):436-8.),(2121. Tyagi R, Ramasethu R, Mohanty CS, Singhal A. Two cases of acute lung injury following closed space smoke inhalation. Med J Armed Forces India. 2015;71(Suppl 2): S538-41. and one of them only one case study 2020. Dinh D, Rosini JM. Empiric treatment of cyanide toxicity in an enclosed-space fire survivor. J Emerg Nurs. 2014;40(3):282-5..

The most common acute clinical manifestations in victims of toxic smoke inhalation in closed environments were dyspnea (n = 137, 58.80%) 1515. Putman CE, Loke J, Matthay RA, Ravin CE. Radiographic manifestations of acute smoke inhalation. AJR Am J Roentgenol. 1977;129(5):865-70.)-(1717. Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Induction of bronchial hyperresponsiveness following smoke inhalation injury. Br J Dis Chest. 1988;82(4):436-8.),(1919. Cha SI, Kim CH, Lee JH, Park JY, Jung TH, Choi WI, et al. Isolated smoke inhalation injuries: acute respiratory dysfunction, clinical outcomes, and short-term evolution of pulmonary functions with the effects of steroids. Burns. 2007;33(2):200-8.)-(2121. Tyagi R, Ramasethu R, Mohanty CS, Singhal A. Two cases of acute lung injury following closed space smoke inhalation. Med J Armed Forces India. 2015;71(Suppl 2): S538-41., carbonaceous sputum (n = 127, 54.51%) 1515. Putman CE, Loke J, Matthay RA, Ravin CE. Radiographic manifestations of acute smoke inhalation. AJR Am J Roentgenol. 1977;129(5):865-70.),(1818. Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5.),(1919. Cha SI, Kim CH, Lee JH, Park JY, Jung TH, Choi WI, et al. Isolated smoke inhalation injuries: acute respiratory dysfunction, clinical outcomes, and short-term evolution of pulmonary functions with the effects of steroids. Burns. 2007;33(2):200-8.),(2121. Tyagi R, Ramasethu R, Mohanty CS, Singhal A. Two cases of acute lung injury following closed space smoke inhalation. Med J Armed Forces India. 2015;71(Suppl 2): S538-41., hoarseness (n = 93, 39.91%) 1515. Putman CE, Loke J, Matthay RA, Ravin CE. Radiographic manifestations of acute smoke inhalation. AJR Am J Roentgenol. 1977;129(5):865-70.),(1818. Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5.),(1919. Cha SI, Kim CH, Lee JH, Park JY, Jung TH, Choi WI, et al. Isolated smoke inhalation injuries: acute respiratory dysfunction, clinical outcomes, and short-term evolution of pulmonary functions with the effects of steroids. Burns. 2007;33(2):200-8., wheezing (n = 80, 34.33%) 1515. Putman CE, Loke J, Matthay RA, Ravin CE. Radiographic manifestations of acute smoke inhalation. AJR Am J Roentgenol. 1977;129(5):865-70.),(1717. Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Induction of bronchial hyperresponsiveness following smoke inhalation injury. Br J Dis Chest. 1988;82(4):436-8.)-(1919. Cha SI, Kim CH, Lee JH, Park JY, Jung TH, Choi WI, et al. Isolated smoke inhalation injuries: acute respiratory dysfunction, clinical outcomes, and short-term evolution of pulmonary functions with the effects of steroids. Burns. 2007;33(2):200-8.),(2121. Tyagi R, Ramasethu R, Mohanty CS, Singhal A. Two cases of acute lung injury following closed space smoke inhalation. Med J Armed Forces India. 2015;71(Suppl 2): S538-41. and sore throat (n = 79, 33.90%) 1919. Cha SI, Kim CH, Lee JH, Park JY, Jung TH, Choi WI, et al. Isolated smoke inhalation injuries: acute respiratory dysfunction, clinical outcomes, and short-term evolution of pulmonary functions with the effects of steroids. Burns. 2007;33(2):200-8.),(2121. Tyagi R, Ramasethu R, Mohanty CS, Singhal A. Two cases of acute lung injury following closed space smoke inhalation. Med J Armed Forces India. 2015;71(Suppl 2): S538-41.. Beside this, pulmonary edema and chest pain were reported with prevalence rates of 5.15% 1414. McArdle CS, Finlay WE. Pulmonary complications following smoke inhalation. Br J Anaesth. 1975;47(5):618-23.)-(1616. Lee MJ, O'Connell DJ. The plain chest radiograph after acute smoke inhalation. Clin Radiol. 1988;39(1):33-7. and 13.30% 1717. Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Induction of bronchial hyperresponsiveness following smoke inhalation injury. Br J Dis Chest. 1988;82(4):436-8.),(1919. Cha SI, Kim CH, Lee JH, Park JY, Jung TH, Choi WI, et al. Isolated smoke inhalation injuries: acute respiratory dysfunction, clinical outcomes, and short-term evolution of pulmonary functions with the effects of steroids. Burns. 2007;33(2):200-8.),(2121. Tyagi R, Ramasethu R, Mohanty CS, Singhal A. Two cases of acute lung injury following closed space smoke inhalation. Med J Armed Forces India. 2015;71(Suppl 2): S538-41., respectively. The lowest prevalence found in the included studies was of 5.15% and the highest was 58.80%.

The fire location differed among the studies. The study conducted by Cha et al. 1919. Cha SI, Kim CH, Lee JH, Park JY, Jung TH, Choi WI, et al. Isolated smoke inhalation injuries: acute respiratory dysfunction, clinical outcomes, and short-term evolution of pulmonary functions with the effects of steroids. Burns. 2007;33(2):200-8. reported a fire accident in a subway station in the city of Daegu, South Korea; another study 2121. Tyagi R, Ramasethu R, Mohanty CS, Singhal A. Two cases of acute lung injury following closed space smoke inhalation. Med J Armed Forces India. 2015;71(Suppl 2): S538-41. described a fire accident onboard India Naval Submarine; the study conducted by Lee and O’Connell 1616. Lee MJ, O'Connell DJ. The plain chest radiograph after acute smoke inhalation. Clin Radiol. 1988;39(1):33-7. reported an accident in a nightclub in the city of Dublin, Ireland. Another five studies 1414. McArdle CS, Finlay WE. Pulmonary complications following smoke inhalation. Br J Anaesth. 1975;47(5):618-23.),(1515. Putman CE, Loke J, Matthay RA, Ravin CE. Radiographic manifestations of acute smoke inhalation. AJR Am J Roentgenol. 1977;129(5):865-70.),(1717. Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Induction of bronchial hyperresponsiveness following smoke inhalation injury. Br J Dis Chest. 1988;82(4):436-8.),(1818. Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5.),(2020. Dinh D, Rosini JM. Empiric treatment of cyanide toxicity in an enclosed-space fire survivor. J Emerg Nurs. 2014;40(3):282-5. described a household fire accident.

The age of the patients with inhalation injuries ranged from 2 years to 81 years. Considering the gender of the patients, there was male predominance in five studies 1414. McArdle CS, Finlay WE. Pulmonary complications following smoke inhalation. Br J Anaesth. 1975;47(5):618-23.),(1515. Putman CE, Loke J, Matthay RA, Ravin CE. Radiographic manifestations of acute smoke inhalation. AJR Am J Roentgenol. 1977;129(5):865-70.),(1717. Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Induction of bronchial hyperresponsiveness following smoke inhalation injury. Br J Dis Chest. 1988;82(4):436-8.),(1818. Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5.),(2121. Tyagi R, Ramasethu R, Mohanty CS, Singhal A. Two cases of acute lung injury following closed space smoke inhalation. Med J Armed Forces India. 2015;71(Suppl 2): S538-41.. One study did not report the gender of the sample 1616. Lee MJ, O'Connell DJ. The plain chest radiograph after acute smoke inhalation. Clin Radiol. 1988;39(1):33-7..

Discussion

To the best of our knowledge, this is the first systematic review to describe the acute clinical manifestations observed in victims of smoke inhalation during enclosed-space fires. The most common acute clinical manifestations were dyspnea, carbonaceous sputum, hoarseness, wheezing and sore throat. Besides this, pulmonary edema and chest pain have also been reported. Because of the heterogeneity between studies, it was not possible to perform a meta-analysis.

In fires, oxygen is either consumed by combustion or displaced by other gases and its concentration reduction in ambient results in decreased oxygen delivery and it may contribute to asphyxiation and mortality. In this context, the low arterial partial pressure of oxygen and the low pH of acidosis are sensed by chemoreceptors of the carotid bodies and neural signals are transmitted to centers of the brain stem, where they are integrated and result in the sensation of dyspnea 2222. Schleiffenbaum B. Reduced oxygen transport capacity as a cause of dyspnea. Schweiz Med Wochenschr. 1994;124(26):1177-82.. In addition, dyspnea may occur due to various reasons that vary depending on the gas that was inhaled as well as due to the decreased ambient oxygen concentration 2323. Young CJ, Moss J. Smoke inhalation: diagnosis and treatment. J Clin Anesth. 1989;1(5):377-86., the decrease of oxygen supply through binding to hemoglobin 2424. Haponik EF. Clinical smoke inhalation injury: pulmonary effects. Occup Med. 1993;8(3):430-68. or by the inhibition of cellular oxygenation, which causes tissue anoxia by inhibition of cytochrome oxidase enzymes 2525. Mayes RW. ACP Broadsheet No 142: November 1993. Measurement of carbon monoxide and cyanide in blood. J Clin Pathol. 1993;46(11):982-8.. Of the eight included studies, six presented dyspnea 1515. Putman CE, Loke J, Matthay RA, Ravin CE. Radiographic manifestations of acute smoke inhalation. AJR Am J Roentgenol. 1977;129(5):865-70.)-(1717. Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Induction of bronchial hyperresponsiveness following smoke inhalation injury. Br J Dis Chest. 1988;82(4):436-8.),(1919. Cha SI, Kim CH, Lee JH, Park JY, Jung TH, Choi WI, et al. Isolated smoke inhalation injuries: acute respiratory dysfunction, clinical outcomes, and short-term evolution of pulmonary functions with the effects of steroids. Burns. 2007;33(2):200-8.)-(2121. Tyagi R, Ramasethu R, Mohanty CS, Singhal A. Two cases of acute lung injury following closed space smoke inhalation. Med J Armed Forces India. 2015;71(Suppl 2): S538-41.. Only two did not demonstrate this manifestation 1414. McArdle CS, Finlay WE. Pulmonary complications following smoke inhalation. Br J Anaesth. 1975;47(5):618-23.),(1818. Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5.. We believe that it may have occurred because the study conducted by McArdle and Finlay 1414. McArdle CS, Finlay WE. Pulmonary complications following smoke inhalation. Br J Anaesth. 1975;47(5):618-23. was a two-case study and consequently, has less chance to present this manifestation. Moreover, the study conducted by Hantson et al. 1818. Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5. was a retrospective study, which may have risk of selection bias and consequently justify the absence of findings related to this manifestation. Besides this, from the 64 subjects included in their analyses 1818. Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5., loss of consciousness was presented in 21 subjects and 18 of these were intubated at the scene of the fire. Based on the above, we suppose the lack of this manifestation may be a bias considering that it is unlikely that from 64 subjects, no one has presented this symptom, which was observed in 137 subjects of the other included studies.

Regarding other acute clinical manifestation, hoarseness was observed in 93 subjects of the 233 included in this systematic review. This finding is relevant because the presence of hoarseness indicates the necessity of mechanical ventilation and prolonged ICU stay 1818. Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5.. On the other hand, the presence of carbonaceous sputum, the second most common found manifestation, does not predict the severity of airway injury 2626. Heimbach DM, Waeckerle JF. Inhalation injuries. Ann Emerg Med. 1988;17(12):1316-20.. An overall synthesis of the other included studies has not been possible, because only the frequency of the clinical manifestations was presented. Also, they have poor generalizability due to variations in confounding effect modifiers and different selection biases operating at specialist treatment centers.

In relation to the male predominance in the present systematic review, it is known that this group is more prone to be involved in accidents that result in death 2727. Zabeu JLA, Zovico JRR, Pereira Jr WN, Tucci Neto PF. Profile of motorcycle victims from the emergency service of a university hospital. Rev Bras Ortop. 2013;48(3):242-5.),(2828. Martins CBG, Jorge MHP. Deaths from external causes in Cuiabá, 0 a 24 years: Profile of victims and families according to intentionality. Rev Bras Epidemiol. 2013;16(2):454-68.. Earlier studies also demonstrated a greater male involvement among victims of smoke inhalation during enclosed-space fires 2929. Chen MC, Chen MH, Wen BS, Lee MH, Ma H. The impact of inhalation injury in patients with small and moderate burns. Burns. 2014;40(8):1481-6.)-(3232. Rech TH, Boniatti MM, Franke CA, Lisboa T, Wawrzeniak IC, Teixeira C, et al. Inhalation injury after exposure to indoor fire and smoke: The Brazilian disaster experience. Burns. 2016;42(4):884-90.. On the other hand, regarding the fire location, most studies described a household fire accident 1414. McArdle CS, Finlay WE. Pulmonary complications following smoke inhalation. Br J Anaesth. 1975;47(5):618-23.),(1515. Putman CE, Loke J, Matthay RA, Ravin CE. Radiographic manifestations of acute smoke inhalation. AJR Am J Roentgenol. 1977;129(5):865-70.),(1717. Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Induction of bronchial hyperresponsiveness following smoke inhalation injury. Br J Dis Chest. 1988;82(4):436-8.),(1818. Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5.),(2020. Dinh D, Rosini JM. Empiric treatment of cyanide toxicity in an enclosed-space fire survivor. J Emerg Nurs. 2014;40(3):282-5.. This finding is consistent with what was previously reported in two studies, which showed that the majority of fire accidents occur in a domestic environment 3333. Montes SF, Barbosa MH, Sousa Neto AL. Clinical and epidemiological aspects of burned patients hospitalized in a Teaching Hospital. Rev Esc Enferm USP. 2011;45(2):369-73.),(3434. Cruz BF, Cordovil PBL, Batista KNM. Epidemiological profile of patients who suffered burns in Brazil: literature review. Rev Bras Queimaduras. 2012;11(4):246-50..

It should also be considered that the severity of inhalation injuries can be influenced by the component materials of the structures. Due to the increasing use of synthetic materials in interior furnishings and building construction, the toxic constituents of modern structural fires began to be associated with a higher degree of toxicity, potentially resulting in more severe inhalation injuries and worse clinical outcomes 3535. Barillo DJ, Goode R, Rush BF Jr, Lin RL, Freda A, Anderson EJ Jr. Lack of correlation between carboxyhemoglobin and cyanide in smoke inhalation injury. Curr Surg. 1986;43(5):421-3.),(3636. Sheridan R. Specific therapies for inhalation injury. Crit Care Med. 2002;30(3):718-9.. The different materials and components of constructions used in the past may be a potential reason for the distinct clinical manifestations found in the present study, since from the eight included studies, five of them are older studies 1414. McArdle CS, Finlay WE. Pulmonary complications following smoke inhalation. Br J Anaesth. 1975;47(5):618-23.)-(1616. Lee MJ, O'Connell DJ. The plain chest radiograph after acute smoke inhalation. Clin Radiol. 1988;39(1):33-7.),(1717. Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Induction of bronchial hyperresponsiveness following smoke inhalation injury. Br J Dis Chest. 1988;82(4):436-8.),(1818. Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5..

In relation to radiological findings, the presence of pulmonary infiltrates at initial evaluation has been indicated as a marker of severe injury and a poor prognosis 1414. McArdle CS, Finlay WE. Pulmonary complications following smoke inhalation. Br J Anaesth. 1975;47(5):618-23.. Lee and O’Connell 1616. Lee MJ, O'Connell DJ. The plain chest radiograph after acute smoke inhalation. Clin Radiol. 1988;39(1):33-7. demonstrated that the initial chest radiography is an important predictor of significant smoke inhalation injuries, enabling the selection of patients likely to need ventilatory support.

Earlier studies have explained the role of early recognition and prompt management in the presence of smoke inhalation injury 3737. Souza R, Jardim C, Salge JM, Carvalho CRR. Smoke inhalation injury. J Bras Pneumol. 2004;30(6):557-65.),(3838. Gill P, Martin RV. Smoke inhalation injury. Br J Anaesth. 2015;15(3):143-8.. Another study included 2020. Dinh D, Rosini JM. Empiric treatment of cyanide toxicity in an enclosed-space fire survivor. J Emerg Nurs. 2014;40(3):282-5. in this systematic review also demonstrated that early identification and intervention are vital in cyanide toxicity, and that empire antidotal treatment should not be delayed. Furthermore, it is also known that pulmonary effects of smoke inhalation injury may vary from cough and dyspnea, within minutes to hours of exposure 3939. Park GY, Park JW, Jeong DH, Jeong SH. Prolonged airway and systemic inflammatory reactions after smoke inhalation. Chest. 2003;123(2):475-80. to acute lung injury, acute respiratory distress syndrome 4040. Enkhbaatar P, Traber DL. Pathophysiology of acute lung injury in combined burn and smoke inhalation injury. Clin Sci (Lond). 2004;107(2):137-43. and long-term pulmonary dysfunction 3939. Park GY, Park JW, Jeong DH, Jeong SH. Prolonged airway and systemic inflammatory reactions after smoke inhalation. Chest. 2003;123(2):475-80..

Although this is the first systematic review to describe the acute clinical manifestations observed in victims of toxic smoke inhalation during enclosed-space fires, based on a comprehensive and systematic bibliographic search, that employed an explicit methodology and reproducible eligibility criteria, unrestricted by date or language and performed independently by two reviewers, some limitations merit discussion. First, because of the methodological heterogeneity between studies, it was not possible to perform a meta-analysis. Second, the impossibility of methodological assessment using the Newcastle-Ottawa scale. This scale was designed to evaluate the quality of case-control and cohort studies, although in the present study, four of the studies were case series and the other studies were case studies. Finally, deficits in the design and different ways of reporting data in the included studies. Therefore, it is possible that this systematic review is subject to bias through the inclusion of low-quality studies.

In this way, the present systematic review allows the conclusion that dyspnea, carbonaceous sputum, hoarseness, wheezing, and sore throat were the most frequent acute clinical manifestations of smoke inhalation. These findings have potential clinical implications on early identification of signs and symptoms, and improvement of early physiotherapy intervention for patients with inhalation injury, which in turn may lead to increased survival and reduce the risk of mortality and treatment of long-term effects of smoke inhalation.

Conclusion

Dyspnea, carbonaceous sputum, hoarseness, wheezing and sore throat were the most frequent acute clinical manifestations observed in victims of toxic smoke inhalation in closed environments. Further studies of higher level of evidence and greater methodological rigor are required.

References

  • 1
    Pasqualoto AS, Albuquerque IM, Pereira MB, Bertolazi AN, Silva CSPR, Prado ALC, et al. Epidemiological profile, respiratory signs and symptoms of individuals who inhaled toxic smoke in Kiss nightclub fire, Santa Maria, RS, Brazil. ConScientiae Saude. 2015;14(2):229-35.
  • 2
    Anseeuw K, Delvau N, Burillo-Putze G, De Iaco F, Geldner G, Holmström P, et al. Cyanide poisoning by fire smoke inhalation: a European expert consensus. Eur J Emerg Med. 2013;20(1):2-9.
  • 3
    O'Brien DJ, Walsh DW, Terriff CM, Hall AH. Empiric management of cyanide toxicity associated with smoke inhalation. Prehosp Disaster Med. 2011;26(5):374-82.
  • 4
    Klingsch WWF, Rogsch C, Schadschneider A, Schreckenberg M. Pedestrian and Evacuation Dynamics 2008. In: Löllgen H, Leyk D. Inhalation injury of lung and heart after inhalation of toxic substances. Springer: Berlin; 2010. p.781-9.
  • 5
    Hamel J. A review of acute cyanide poisoning with a treatment up date. Crit Care Nurse. 2011;31(1):72-81.
  • 6
    Huzar TF, George T, Cross JM. Carbon monoxide and cyanide toxicity: etiology, pathophysiology and treatment in inhalation injury. Expert Rev Respir Med. 2013;7(2):159-70.
  • 7
    Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. Carbon monoxide poisoning - a public health perspective. Toxicology. 2000;145(1):1-14.
  • 8
    Sheridan RL. Fire-Related Inhalation Injury. N Engl J Med. 2016;375(5):464-9.
  • 9
    Banauch GI, Brantly M, Izbicki G, Hall C, Shanske A, Chavko R, et al. Accelerated spirometric decline in New York city firefighters with a1-antitrypsin deficiency. Chest. 2010;138(5):1116-24.
  • 10
    Walker PF, Buehner MF, Wood LA, Boyer NL, Driscoll IR, Lundy JB, et al. Diagnosis and management of inhalation injury: na updated review. Crit Care. 2015;19:351.
  • 11
    Fogarty PW, George PJ, Solomon M, Spiro SG, Armstrong RF. Long term effects of smoke inhalation in survivors of the King's Cross underground station fire. Thorax. 1991;46(12):914-8.
  • 12
    Greven F, Krop E, Spithoven J, Rooyackers J, Kerstjens H, Heederik D. Lung function, bronchial hyperresponsiveness, and atopy among firefighters. Scand J Work Environ Health. 2011;37(4):325-31.
  • 13
    Moher D, Liberati A, Tetzlaff J, Altman DG. Preferred reporting items for systematic reviews and meta-analyses: The PRISMA statement. Ann Intern Med. 2009;151(4):264-9.
  • 14
    McArdle CS, Finlay WE. Pulmonary complications following smoke inhalation. Br J Anaesth. 1975;47(5):618-23.
  • 15
    Putman CE, Loke J, Matthay RA, Ravin CE. Radiographic manifestations of acute smoke inhalation. AJR Am J Roentgenol. 1977;129(5):865-70.
  • 16
    Lee MJ, O'Connell DJ. The plain chest radiograph after acute smoke inhalation. Clin Radiol. 1988;39(1):33-7.
  • 17
    Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Induction of bronchial hyperresponsiveness following smoke inhalation injury. Br J Dis Chest. 1988;82(4):436-8.
  • 18
    Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest. 1997;111(3):671-5.
  • 19
    Cha SI, Kim CH, Lee JH, Park JY, Jung TH, Choi WI, et al. Isolated smoke inhalation injuries: acute respiratory dysfunction, clinical outcomes, and short-term evolution of pulmonary functions with the effects of steroids. Burns. 2007;33(2):200-8.
  • 20
    Dinh D, Rosini JM. Empiric treatment of cyanide toxicity in an enclosed-space fire survivor. J Emerg Nurs. 2014;40(3):282-5.
  • 21
    Tyagi R, Ramasethu R, Mohanty CS, Singhal A. Two cases of acute lung injury following closed space smoke inhalation. Med J Armed Forces India. 2015;71(Suppl 2): S538-41.
  • 22
    Schleiffenbaum B. Reduced oxygen transport capacity as a cause of dyspnea. Schweiz Med Wochenschr. 1994;124(26):1177-82.
  • 23
    Young CJ, Moss J. Smoke inhalation: diagnosis and treatment. J Clin Anesth. 1989;1(5):377-86.
  • 24
    Haponik EF. Clinical smoke inhalation injury: pulmonary effects. Occup Med. 1993;8(3):430-68.
  • 25
    Mayes RW. ACP Broadsheet No 142: November 1993. Measurement of carbon monoxide and cyanide in blood. J Clin Pathol. 1993;46(11):982-8.
  • 26
    Heimbach DM, Waeckerle JF. Inhalation injuries. Ann Emerg Med. 1988;17(12):1316-20.
  • 27
    Zabeu JLA, Zovico JRR, Pereira Jr WN, Tucci Neto PF. Profile of motorcycle victims from the emergency service of a university hospital. Rev Bras Ortop. 2013;48(3):242-5.
  • 28
    Martins CBG, Jorge MHP. Deaths from external causes in Cuiabá, 0 a 24 years: Profile of victims and families according to intentionality. Rev Bras Epidemiol. 2013;16(2):454-68.
  • 29
    Chen MC, Chen MH, Wen BS, Lee MH, Ma H. The impact of inhalation injury in patients with small and moderate burns. Burns. 2014;40(8):1481-6.
  • 30
    Davis CS, Albright JM, Carter SR, Ramirez L, Kim H, Gamelli RL, et al. Early pulmonary immune hyporesponsiveness is associated with mortality after burn and smoke inhalation injury. J Burn Care Res. 2012;33(1):26-35.
  • 31
    Hassan Z, Wong JK, Bush J, Bayat A, Dunn KW. Assessing the severity of inhalation injuries in adults. Burns. 2012;36(2):212-6.
  • 32
    Rech TH, Boniatti MM, Franke CA, Lisboa T, Wawrzeniak IC, Teixeira C, et al. Inhalation injury after exposure to indoor fire and smoke: The Brazilian disaster experience. Burns. 2016;42(4):884-90.
  • 33
    Montes SF, Barbosa MH, Sousa Neto AL. Clinical and epidemiological aspects of burned patients hospitalized in a Teaching Hospital. Rev Esc Enferm USP. 2011;45(2):369-73.
  • 34
    Cruz BF, Cordovil PBL, Batista KNM. Epidemiological profile of patients who suffered burns in Brazil: literature review. Rev Bras Queimaduras. 2012;11(4):246-50.
  • 35
    Barillo DJ, Goode R, Rush BF Jr, Lin RL, Freda A, Anderson EJ Jr. Lack of correlation between carboxyhemoglobin and cyanide in smoke inhalation injury. Curr Surg. 1986;43(5):421-3.
  • 36
    Sheridan R. Specific therapies for inhalation injury. Crit Care Med. 2002;30(3):718-9.
  • 37
    Souza R, Jardim C, Salge JM, Carvalho CRR. Smoke inhalation injury. J Bras Pneumol. 2004;30(6):557-65.
  • 38
    Gill P, Martin RV. Smoke inhalation injury. Br J Anaesth. 2015;15(3):143-8.
  • 39
    Park GY, Park JW, Jeong DH, Jeong SH. Prolonged airway and systemic inflammatory reactions after smoke inhalation. Chest. 2003;123(2):475-80.
  • 40
    Enkhbaatar P, Traber DL. Pathophysiology of acute lung injury in combined burn and smoke inhalation injury. Clin Sci (Lond). 2004;107(2):137-43.

Publication Dates

  • Publication in this collection
    2018

History

  • Received
    26 July 2017
  • Accepted
    16 Feb 2018
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