Pulmonary dysfunction after smoke inhalation and thermal injury is associated with excessive morbidity and mortality. The purpose of this study was to evaluate alveolar leukocyte function after thermal injury and smoke inhalation.
Twenty-one patients with thermal injury only (n = 8); thermal injury and smoke inhalation injury (n = 8); and nonburned controls (n = 5) were assessed by means of bronchoscopically directed lavage (bronchoalveolar lavage [BAL]) on the first and fourth days postinjury. BAL-isolated pulmonary leukocytes were assessed for number, composition, viability, and production of tumor necrosis factor (TNF)alpha, interleukin (IL)-8, and IL-6 in response to 100 ng/mL of lipopolysaccharide (LPS) (mean +/- SEM; significance at p < 0.05).
Six of eight Smoke patients had gross evidence of lung injury. On day 1, Smoke and Burn BAL isolates yielded greater cell counts than Control (10.6 vs. 4.5 vs. 2.4 x 10(6)/mL). Smoke macrophages on day 1 produced more TNFalpha (1.2 vs. 0.2 ng/mL), IL-6 (8.0 vs. 1.9 ng/mL), and IL-8 (85 vs. 32 ng/mL) after LPS stimulation compared with respective unstimulated (0 ng/mL of LPS) day-1 Smoke cells. LPS-stimulated Burn cells on day 1 produced more IL-8 (150 vs. 62 ng/mL) but not TNFalpha (0.4 vs. 0.25 ng/mL) or IL-6 (1.8 vs. 0.69 ng/mL), when compared with respective unstimulated Burn cells. By day 4, LPS-stimulated Smoke and Burn cells produced significantly more TNFalpha (Smoke, 0.41 vs. 0.16 ng/mL; Burn, 0.87 vs. 0.51 ng/mL) and IL-6 (Smoke, 2.5 vs. 0.47 ng/mL; Burn, 4.1 vs. 1.47 ng/mL), but not IL-8 (Smoke, 51.1 vs. 51.1 ng/mL; Burn, 54.4 vs. 55.6 ng/mL), compared with respective unstimulated day-4 cells.
Smoke inhalation induces a massive influx of alveolar leukocytes that are primed for an early, enhanced LPS-activated cytokine response compared with alveolar leukocytes isolated after burn injury alone or normal controls.
"Smoke inhalation may lead to release of mediators that increase pulmonary artery pressure and cause secondary damage to the respiratory epithelium and the release of additional inflammatory molecules [3,8]. Lung injury resulting from smoke inhalation is associated with significant increases in the incidence of pneumonia and ARDS in thermally injured patients . These may be exacerbated by early hemodynamic instability and massive burn edema, both of which are commonly observed in burn injury patients with smoke inhalation. "
[Show abstract][Hide abstract] ABSTRACT: Severely burned patients suffering from inhalation injury have a significantly increased risk for mortality compared with burned patients without inhalation injury. Severe burn is associated with a distinct serum cytokine profile and alterations in cytokines that contribute to morbidity and mortality. The aim of the present study was therefore to determine whether severely burned pediatric patients with concomitant inhalation injury who had a fatal outcome exhibited a different serum cytokine profile compared with burn patients with inhalation injury who survived. Early identification followed by appropriate management of these high-risk patients may lead to improved clinical outcome.
Thirteen severely burned children with inhalation injury who did not survive and 15 severely burned pediatric patients with inhalation injury who survived were enrolled in the study. Blood was collected within 24 hours of admission and 5 to 7 days later. Cytokine levels were profiled using multiplex antibody coated beads. Inhalation injury was diagnosed by bronchoscopy during the initial surgery. The number of days on the ventilator, peak inspiratory pressure rates, arterial oxygen tension (PaO2)/fraction of inspired oxygen (FiO2) ratio and incidence of acute respiratory distress syndrome were recorded for those patients.
Significantly altered levels of IL-4, IL-6, IL-7, IL-10, and IL-13 were detected within the first 7 days after admission in serum from burn pediatric patients with concomitant inhalation injury who did not survive when compared with similar patients who did (P < 0.05). Alterations in these cytokines were associated with increased incidence of acute respiratory distress syndrome, number of days under ventilation, increased peak inspiratory pressure, and lower PaO2/FiO2 ratio in this patient population. Multiple logistic regression analysis revealed that patients with increased IL-6 and IL-10 as well as decreased IL-7 serum levels had a significantly greater risk for mortality (P < 0.05).
Early alterations in serum levels of IL-6, IL-7 and IL-10 may constitute useful predictive markers for identifying patients those who have sustained a burn with concomitant inhalation injury and who have high mortality.
[Show abstract][Hide abstract] ABSTRACT: This prospective study aims to address mortality in the context of the early pulmonary immune response to burn and inhalation injury. The authors collected bronchoalveolar lavage fluid from 60 burn patients within 14 hours of their injury when smoke inhalation was suspected. Clinical and laboratory parameters and immune mediator profiles were compared with patient outcomes. Patients who succumbed to their injuries were older (P = .005), had a larger % TBSA burn (P < .001), and required greater 24-hour resuscitative fluids (P = .002). Nonsurvivors had lower bronchoalveolar lavage fluid concentrations of numerous immunomodulators, including C5a, interleukin (IL)-1β, IL-1RA, IL-8, IL-10, and IL-13 (P < .05 for all). Comparing only those with the highest Baux scores to account for the effects of age and % TBSA burn on mortality, nonsurvivors also had reduced levels of IL-2, IL-4, granulocyte colony-stimulating factor, interferon-γ, macrophage inflammatory protein-1β, and tumor necrosis factor-α (P < .05 for all). The apparent pulmonary immune hyporesponsiveness in those who died was confirmed by in vitro culture, which revealed that pulmonary leukocytes from nonsurvivors had a blunted production of numerous immune mediators. This study demonstrates that the early pulmonary immune response to burn and smoke inhalation may be attenuated in patients who succumb to their injuries.
Journal of burn care & research: official publication of the American Burn Association 01/2012; 33(1):26-35. DOI:10.1097/BCR.0b013e318234d903 · 1.43 Impact Factor
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