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Inhalation injury in severely burned children does not augment the systemic inflammatory response

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Inhalation injury in combination with a severe thermal injury increases mortality. Alterations in inflammatory mediators, such as cytokines, contribute to the incidence of multi-organ failure and mortality. The aim of the present study was to determine the effect of inhalation injury on cytokine expression in severely burned children. Methods Thirty severely burned pediatric patients with inhalation injury and 42 severely burned children without inhalation injury were enrolled in the study. Inhalation injury was diagnosed by bronchoscopy during the first operation. Blood was collected within 24 hours of admission and again at five to seven days following admission. Cytokine expression was profiled using multi-plex antibody-coated beads. Significance was accepted at a p value of less than 0.05. Results The mean percentages of total body surface area burned were 67% ± 4% (56% ± 6%, third-degree burns) in the inhalation injury group and 60% ± 3% (45% ± 3%, third-degree burns) in the non-inhalation injury group ( p value not significant [NS]). Mean age was 9 ± 1 years in the inhalation injury group and 8 ± 1 years in the non-inhalation injury group ( p value NS). Time from burn to admission in the inhalation injury group was 2 ± 1 days compared to 3 ± 1 days in the non-inhalation injury group ( p value NS). Mortalities were 40% in the inhalation injury group and 12% in the non-inhalation injury group ( p < 0.05). At the time of admission, serum interleukin (IL)-7 was significantly increased in the non-inhalation injury group, whereas IL-12p70 was significantly increased in the inhalation injury group compared to the non-inhalation injury group ( p < 0.05). There were no other significant differences between groups. Five to seven days following admission, all cytokines decreased with no differences between the inhalation injury and non-inhalation injury cohorts. Conclusion In the present study, we show that an inhalation injury causes alterations in IL-7 and IL-12p70. There were no increased levels of pro-inflammatory cytokines, indicating that an inhalation injury in addition to a burn injury does not augment the systemic inflammatory response early after burn.

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Published 01 January 2007
Reads 8
Language English
Available onlinehttp://ccforum.com/content/11/1/R22
Vol 11 No 1 Open Access Research Inhalation injury in severely burned children does not augment the systemic inflammatory response Celeste C Finnerty, David N Herndon and Marc G Jeschke
Shriners Hospitals for Children and Department of Surgery, University of Texas Medical Branch, 815 Market Street, Galveston, TX, USA
Corresponding author: Marc G Jeschke, majeschk@utmb.edu
Received: 9 Nov 2006 Revisions requested: 30 Dec 2006 Revisions received: 5 Jan 2007 Accepted: 16 Feb 2007
Published: 16 Feb 2007
Critical Care2007,11:R22 (doi:10.1186/cc5698) This article is online at: http://ccforum.com/content/11/1/R22 © 2007 Finnertyet al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Introductioninjury in combination with a severe Inhalation thermal injury increases mortality. Alterations in inflammatory mediators, such as cytokines, contribute to the incidence of multiorgan failure and mortality. The aim of the present study was to determine the effect of inhalation injury on cytokine expression in severely burned children.
Methods Thirty severely burned pediatric patients with inhalation injury and 42 severely burned children without inhalation injury were enrolled in the study. Inhalation injury was diagnosed by bronchoscopy during the first operation. Blood was collected within 24 hours of admission and again at five to seven days following admission. Cytokine expression was profiled using multiplex antibodycoated beads. Significance was accepted at apvalue of less than 0.05.
Resultsmean percentages of total body surface area The burned were 67% ± 4% (56% ± 6%, thirddegree burns) in the inhalation injury group and 60% ± 3% (45% ± 3%, thirddegree burns) in the noninhalation injury group (pvalue not significant
Introduction During the past 20 years, mortality from major burns has decreased due to improved intensive care unit care, improve ments in wound management, better control of sepsis, and control of hemodynamic disorders [1,2]. Of the injuries now associated with burns, the single most important contributor to mortality is inhalation injury. Twenty to thirty percent of all major burns are associated with a concomitant inhalation injury and a mortality of 25% to 50% when patients required ventilator support for more than one week following injury [2].
[NS]). Mean age was 9 ± 1 years in the inhalation injury group and 8 ± 1 years in the noninhalation injury group (pvalue NS). Time from burn to admission in the inhalation injury group was 2 ± 1 days compared to 3 ± 1 days in the noninhalation injury group (pvalue NS). Mortalities were 40% in the inhalation injury group and 12% in the noninhalation injury group (p< 0.05). At the time of admission, serum interleukin (IL)7 was significantly increased in the noninhalation injury group, whereas IL12p70 was significantly increased in the inhalation injury group compared to the noninhalation injury group (p< 0.05). There were no other significant differences between groups. Five to seven days following admission, all cytokines decreased with no differences between the inhalation injury and noninhalation injury cohorts.
Conclusion In the present study, we show that an inhalation injury causes alterations in IL7 and IL12p70. There were no increased levels of proinflammatory cytokines, indicating that an inhalation injury in addition to a burn injury does not augment the systemic inflammatory response early after burn.
Lung injury from smoke inhalation is associated with tracheo bronchial hyperemic sloughing of ciliated epithelium, formation of copious tracheal exudates, and pulmonary capillary perme ability changes that result in a pulmonary edema [3]. Further studies show a progressive increase in lung permeability soon after thermal injury [4]. The inhalation of toxic smoke causes the release of thromboxane and other mediators, which increases pulmonary artery pressure and causes secondary damage to the respiratory epithelium and release of chemotac tic factors [3]. Neutrophils subsequently undergo diapedeses from the pulmonary microvasculature and release enzymes such as elastase and free oxygen radicals, disrupting endothe lial junctions and the epithelial integrity, thus permitting an exu date of proteinrich plasma to enter the lung [3]. A
DC = dendritic cell; GMCSF = granulocytemacrophage colonystimulating factor; IFNγ= interferongamma; IL = interleukin; MIP1β= macrophage inflammatory protein1beta; TBSA = total body surface area; TNF = tumor necrosis factor.
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