Tracheobronchial Cytologic Changes Following Lower Airway Thermal Injury

Ambiavagar, M.; Chalon, Jack; I, Zargham

doi:10.1097/00005373-197404000-00002

Cited by 13 publications

(5 citation statements)

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“…Unfortunately, early bronchoscopic examination does not predict the severity of pulmonary injury, as inhalation injury is rarely limited to the upper airways. 5 Patients with smoke inhalation injury, for the purposes of the study, were identified as those thermally injured patients who also had a strong prehospital history of smoke exposure. This was typically from flame burn in a confined space.…”

Section: Discussionmentioning

confidence: 99%

“…11 Smoke denatures alveolar surfactant, resulting in atelectasis, decreased compliance, and increasing shunt as the inhalation injury evolves. 5 Although severe upper airway injury usually becomes apparent within 24 hours, alveolar edema may not be maximal until 2 to 3 days postinjury. 6 Pulmonary arterial hypertension and severe systemic capillary permeability ("capillary leak") exacerbate alveolar edema.…”

Section: Discussionmentioning

confidence: 99%

“…The alveolar microenvironment is significantly altered by smoke inhalation, with lung damage occurring because of surfactant denaturation, loss of endothelial and epithelial barrier functions, and influx of inflammatory cells. 3,4 A rapid, postinhalation influx of polymorphonuclear neutrophils (PMNs) into the lungs, 5 combined with diminished alveolar macrophage phagocytotic and bactericidal functions, 6,7 contribute to parenchymal injury and pulmonary immune dysfunction, predisposing to the rapid development of ARDS and infection. As the alveolar macrophages coordinate the local immune response to infection by means of cytokine production, 8 the effect of smoke inhalation on the ability of these cells to produce an appropriate cytokine response may be compromised.…”

mentioning

confidence: 99%

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Smoke Inhalation Enhances Early Alveolar Leukocyte Responsiveness to Endotoxin

Wright

Murphy

2005

The Journal of Trauma: Injury, Infection, and Critical Care

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Smoke Inhalation Enhances Early Alveolar Leukocyte Responsiveness to Endotoxin

Wright

Murphy

2005

The Journal of Trauma: Injury, Infection, and Critical Care

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“…Although the diagnosis of inhalation trauma is preferably based on fiberoptic observations, bronchoscopy is an invasive procedure with risk of serious complications [18]. Furthermore, frequently bronchoscopy does not adequately inform on the severity of pulmonary injury [19,20]. …”

Section: Introductionmentioning

confidence: 99%

Soluble urokinase-type plasminogen activator receptor levels in patients with burn injuries and inhalation trauma requiring mechanical ventilation: an observational cohort study

et al. 2011

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IntroductionSoluble urokinase-type plasminogen activator receptor (suPAR) has been proposed as a biologic marker of fibrinolysis and inflammation. The aim of this study was to investigate the diagnostic and prognostic value of systemic and pulmonary levels of suPAR in burn patients with inhalation trauma who need mechanical ventilation.MethodssuPAR was measured in plasma and nondirected lung-lavage fluid of mechanically ventilated burn patients with inhalation trauma. The samples were obtained on the day of inhalation trauma and on alternate days thereafter until patients were completely weaned from the mechanical ventilator. Mechanically ventilated patients without burns and without pulmonary disease served as controls.ResultsSystemic levels of suPAR in burn patients with inhalation trauma were not different from those in control patients. On admission and follow up, pulmonary levels of suPAR in patients with inhalation trauma were significantly higher compared with controls. Pulmonary levels of suPAR highly correlated with pulmonary levels of interleukin 6, a marker of inflammation, and thrombin-antithrombin complexes, markers of coagulation, but not plasminogen activator activity, a marker of fibrinolysis. Systemic levels of suPAR were predictive of the duration of mechanical ventilation and length of intensive care unit (ICU) stay. Duration of mechanical ventilation and length of ICU stay were significantly longer in burn-injury patients with systemic suPAR levels > 9.5 ng/ml.ConclusionsPulmonary levels of suPAR are elevated in burn patients with inhalation trauma, and they correlate with pulmonary inflammation and coagulation. Although pulmonary levels of suPAR may have diagnostic value in burn-injury patients, systemic levels of suPAR have prognostic value.

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“…Hay sitios críticos que son blanco de esta lesión , como lo son la interrupción de la respiración aerobia mitocondrial, daño de membranas celulares, el ácido desoxirribonucleico(ADN)y las vías sintéticas de proteínas y citoesqueleto. (8) Al interrumpirse el proceso de fosforilación oxidativa, lleva a una reducción de adenosin trifosfato (ATP), lo que desencadena una serie de procesos, inicialmente hay una disminución de la actividad de la bomba de sodio-potasio en la membrana celular, esto lleva a cambios celulares del equilibrio osmótico produciendo edema celular. (9) Al continuar en déficit de ATP se altera la producción de proteínas y la homeostasis del calcio intracelular ya que este es controlado por enzimas dependientes de ATP, al haber una reducción de este el calcio intracelular aumenta lo que lleva a activación de fosfolípidos que desintegran la membrana, y lesionan otros componentes del citosol.…”

Section: Mecanismo De Lesiónunclassified