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Background: Acute kidney injury (AKI) and multiple organ failure (MOF) are leading causes of mortality in trauma injuries. Early diagnosis of AKI and MOF is vital to improve outcomes, but current diagnostic criteria rely on laboratory markers that are delayed or unreliable. In this study, we investigated whether damage associated molecular patterns such as high-mobility group box 1 (HMGB1), syndecan-1 (SDC-1) and C3a correlate with the development of trauma-induced AKI and MOF., Methods: Thirty-nine swine underwent smoke inhalation and severe burns, then received critical care for 72 hours or until death. AKI was defined by the KDIGO (Kidney Disease: Improving Global Outcomes) criteria, which labels AKI when a 1.5-fold increase in blood creatinine levels from baseline or a urine output < 0.5 mL/kg/h for 6 hours or more occurs. MOF was defined by the presence of both AKI and acute respiratory distress syndrome (PaO 2 /FiO 2 <300 for 4 hours)., Results: Eight of 39 pigs developed AKI and seven of those developed MOF. Pathological analysis revealed that polytrauma induces significantly higher kidney injury scores compared to sham controls. The average time from injury to KDIGO AKI was 24 hours (interquartile range: 22.50-32.25). Twelve hours after injury, HMGB1 levels were significantly increased in animals that went on to develop AKI compared to those that did not (73.07 ± 18.66 ng/mL vs. 31.64 ± 4.15 ng/mL, p <0.01), as well as in animals that developed MOF compared to those that did not (81.52±19.68 ng/mL vs. 31.19 ± 3.972 ng/mL, p <0.05). SDC-1 and C3a levels were not significantly different at any time point between groups. ROC analysis revealed that HMGB1 levels at 12 hours post-injury were predictive of both AKI and MOF development (AKI: AUROC=0.81, cut-off value=36.41 ng/mL; MOF: AUROC=0.89, cut-off value=36.41 ng/mL). Spearman's correlation revealed that HMGB1 levels at 12 hours correlated with multiple parameters of AKI, including blood urea nitrogen, blood creatinine, and blood myoglobin., Conclusion: Twelve-hour post-injury HMGB1 levels predict AKI and MOF in a smoke inhalation and burn swine model. Further research is needed to validate this result in other polytrauma models and in critical combat causalities., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer GZ declared a shared affiliation with the author AM to the handling editor at the time of review., (Copyright © 2024 Yang, Cancio, Willis, Young, Kneifel, Salinas and Meyer.)

Smoke inhalation injury (SII) affects more than 50,000 people annually causing carbon monoxide (CO) poisoning. Although the increased blood level of carboxyhemoglobin (CO-Hb) is frequently used to confirm the diagnosis of SII, knowledge of its elimination in the acute phase is still limited. The aim of this study is to determine CO-Hb elimination rates and their differences in arterial (aCO-Hb) and mixed-venous (vCO-Hb) blood following severe SII in a clinically relevant ovine model. Forty-three chronically instrumented female sheep were subjected to SII (12 breaths, 4 sets) through tracheostomy tube under anesthesia and analgesia. After the SII, sheep were awakened and placed on a mechanical ventilator (FiO 2  = 1.0, tidal volume 12 mL/kg, and PEEP = 5cmH 2 O) and monitored. Arterial and mixed-venous blood samples were withdrawn simultaneously for blood gas analysis at various time points to determine CO-HB half-lifetime and an elimination curve. The mean of highest aCO-Hb level during SII was 70.8 ± 13.9%. The aCO-Hb elimination curve showed an approximated exponential decay during the first 60 min. Per mixed linear regression model analysis, aCO-Hb significantly (p < 0.001) declined (4.3%/minute) with a decay constant lambda of 0.044. With this lambda, mean lifetime and half-lifetime of aCO-Hb were 22.7 and 15.7 min, respectively. The aCO-Hb was significantly lower compared to vCO-Hb at all-time points (0-180 min). To our knowledge, this is the first report describing CO-Hb elimination curve in the acute phase after severe SII in the clinically relevant ovine model. Our data shows that CO-Hb is decreasing in linear manner with supportive mechanical ventilation (0-60 min). The results may help to understand CO-Hb elimination curve in the acute phase and improvement of pre-hospital and initial clinical care in patients with CO poisoning., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Background: Severely burned patients often suffer white blood cell and platelet drop following the injury. Though coagulopathy after burn injury have been reported, the association between leukopenia or thrombopenia and mortality is still unrevealed. To determine whether early drastic drops in white blood cells (WBCs) and platelets following injury can be prognostic markers in patients with major burns., Methods: This is a retrospective cohort study setting in a single Burn Center in Japan. Data comprising patients' characteristics and blood cell counts (red blood cells [RBCs], WBCs including neutrophils, monocytes, and lymphocytes, and platelets) over the first 30 days after burn injury were serially collected from patients suffering major burn injury (≥20% TBSA) from January 1, 2006 to December 31, 2015. To determine blood cell counts affecting 60-day mortality, we used multivariable Cox proportional hazard analysis to assess associations between each blood cell count and mortality, adjusting for age and %TBSA as covariates, and evaluated predicted value of the hazard ratio (HR) of death., Results: We enrolled 280 patients. Following burn injury, all blood cell counts were high at admission, then decreased. RBCs diminished progressively and plateaued 2 weeks after injury. WBCs decreased suddenly 2 days after injury, then increased and stabilized. Platelets decreased more rapidly than WBCs to their nadir at 3 days, then continually increased. After covariate adjustment, low RBCs from day 1 (HR: 0.566, 95% C.I. 0.423, 0.759) to day 5 (HR: 0.524, 95% C.I. 0.175, 0.576) were predictors of mortality. Neutrophil count was not a risk factor, but day 3 lymphocyte count (HR: 0.131, 95% C.I. 0.026, 0.646) and day 10 monocyte count (HR: 0.044, 95% C.I. 0.005, 0.396) were risk factors. Low platelet counts from day 3 (HR: 0.545, 95% C.I. 0.300, 0.981) to day 30 following injury were always a predictor of mortality., Conclusions: Early thrombopenia and lymphopenia were independent risk factors for 60-day mortality, and prolonged thrombopenia and monocytopenia were independent risk factors for mortality. These findings might shed light on mechanisms of immune response following severe burns., (Copyright © 2019 Elsevier Ltd and ISBI. All rights reserved.)

Smoke inhalation represents the leading cause of mortality and morbidity in burns patients. Given the injuries that can occur in the airway after this exposure, it is imperative to evaluate the need for orotracheal intubation in the emergency department and even in the place of first assistance by healthcare workers. Since the clinical signs are poor predictors of the severity of the lesion, in selected cases, it is advisable to perform a diagnostic fibroscopy. We present a case report of a patient with a smoke inhalation lesion in which the fibroscopy was determinant to proceed to intubation, and we propose an algorithm of action for the management of the airway in this type of patients., (Copyright © 2017 Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor. Publicado por Elsevier España, S.L.U. All rights reserved.)

Hexachloroethane (HC)/zinc chloride (ZnCl, smoke bomb) exposure in the military setting results in lung injury which is uncommon and has been rarely described in previous studies. The aim of this study is to investigate the correlation between the serum zinc in patients with HC/ZnCl smoke inhalation lung injury and disease severity. A total of 15 patients with HC/ZnCl-related conditions were recruited in this study. The serum zinc level and the pulmonary function tests and liver function tests including total lung capacity (TLC), forced vital capacity (FVC), forced expiratory pressure in 1 second (FEV1), alanine aminotransferase (ALT), and aspartate transaminase (AST) were analyzed. Eleven cases had mild clinical manifestations. Four cases rapidly developed features typical of severe adult respiratory distress syndrome. The level of serum zinc was increased, but FVC, FEV1, and TLC was decreased significantly in the moderate and severe cases. In addition, the serum zinc level correlated well with the TLC, FVC, and FEV1 (r = -0.587, -0.626, -0.617, respectively; P = .027, .017, .019, respectively). The 4 cases in moderate and severe group had delayed impairment of liver functions after the accident. This study suggested that the serum zinc level may be associated with the severity of lung and liver injuries after HC/ZnCl smoke inhalation.

Background: Smoke inhalation and burn injury remain a major source of morbidity and mortality. There is known dysregulation of hemostasis in burn patients, but either hypercoagulation or hypocoagulation states are reported. Sheep are an established animal model for studying burn pathology and provide robust data on hemostatic function at baseline and after injury., Methods: After an IACUC-approved protocol, 15 sheep were anesthetized and subjected to a 40% full thickness burn with smoke inhalation. Blood was sampled at baseline, 1 day postinjury (early effects) and days 2, 3, and 4 (late effects) after injury. Assays at each timepoint assessed: hemostatic function by thromboelastography (TEG), platelet counts and function by flow cytometry and aggregometry, coagulation protein levels, and free hemoglobin. Data were analyzed by the Wilcoxon paired test (nonparametric) with significance set at less than 0.05., Results: By 24 hours postinjury, platelet counts had dropped, whereas the percent activated platelets increased. Absolute platelet functional response to the agonist adenosine diphosphate (ADP) decreased, whereas response to collagen showed no significant difference. On a per platelet basis, ADP response was unchanged, whereas the collagen response was elevated. Prothrombin time and activated partial thromboplastin time were prolonged. TEG parameters decreased significantly from baseline. Fibrinogen and factor V were trending up; coagulation proteins ATIII, factors IX and X were decreased.Late effects were followed in six animals. At day 4, platelet counts remained depressed compared with baseline with a nadir at day 2; responses to agonist on a per platelet basis remained the same for ADP and stayed elevated for collagen. Platelets continued to have elevated activation levels. Fibrinogen and factor V remained significantly elevated, whereas TEG parameters and prothrombin time, factors IX and X returned to near baseline levels., Conclusion: Coagulation parameters and hemostasis are dysregulated in sheep after smoke inhalation and burn. By 24 hours, sheep were hypocoagulable and subsequently became hypercoagulable by day 4. These results suggest a three-stage coagulopathy in burn injuries with a known early consumptive hypercoagulable state which is followed by a relatively hypocoagulable state with increased bleeding risk and then a return to a relatively unknown hypercoagulability with increased susceptibility to thrombotic disorders.

Pulmonary injury can be characterized by an increased need for fraction of inspired oxygen or inspired oxygen percentage (FiO2) to maintain arterial blood saturation of oxygenation (SaO2). We tested a smart oxygenation system (SOS) that uses the activity of a closed-loop control FiO2 algorithm (CLC-FiO2) to rapidly assess acute respiratory distress syndrome (ARDS) severity so that rescue ventilation (RscVent) can be initiated earlier. After baseline data, a pulse-oximeter (noninvasive saturation of peripheral oxygenation [SpO2]) was placed. Sheep were then subjected to burn and smoke inhalation injury and followed for 48 h. Initially, sheep were spontaneously ventilating and then randomized to standard of care (SOC) (n = 6), in which RscVent began when partial pressure of oxygen (PaO2) < 90 mmHg or FiO2 < 0.6, versus SOS (n = 7), software that incorporates and displays SpO2, CLC-FiO2, and SpO2/CLC-FiO2 ratio, at which RscVent was initiated when ratio threshold < 250. RscVent was achieved using a G5 Hamilton ventilator (Bonaduz, Switzerland) with adaptive pressure ventilation and adaptive support ventilation modes for SOC and SOS, respectively., Outcomes: the time difference from when SpO2/FiO2 < 250 to RscVent initiation was 4.7 ± 0.6 h and 0.2 ± 0.1 h, SOC and SOS, respectively (P < 0.001). Oxygen responsiveness after RscVent, defined as SpO2/FiO2 > 250 occurred in 4/7, SOS and 0/7, SOC. At 48 h the SpO2/FiO2 ratio was 104 ± 5 in SOC versus 228 ± 59 in SOS (P = 0.036). Ventilatory compliance and peak airway pressures were significantly improved with SOS versus SOC (P < 0.001). Data suggest that SOS software, e.g. SpO2/CLC-FiO2 ratio, after experimental ARDS can provide a novel continuous index of pulmonary function that is apparent before other clinical symptoms. Earlier initiation of RscVent translates into improved oxygenation (reduces ARDS severity) and ventilation.

Cyanide (CN) blood concentration is hardly considered during routine when evaluating smoke gas intoxications and fire victims, although some inflammable materials release a considerable amount of hydrogen cyanide. CN can be significant for the capacity to act and can in the end even be the cause of death. Systematic data concerning the influence of different fire conditions, especially those of various inflammable materials, on the CN-blood concentration of deceased persons do not exist. This study measured the CN level in 92 blood samples of corpses. All persons concerned were found dead in connection with fires and/or smoke gases. At the same time, the carboxyhemoglobin (COHb) level was determined, and the corpses were examined to detect pharmaceutical substances, alcohol and drugs. Furthermore, we analysed autopsy findings and the investigation files to determine the inflammable materials and other circumstances of the fires. Due to the inflammable materials, the highest concentration of CN in the victims was found after enclosed-space fires (n = 45) and after motor-vehicle fires (n = 8). The CN levels in these two groups (n = 53) were in 47 % of the cases toxic and in 13 % of the cases lethal. In victims of charcoal grills (n = 17) and exhaust gases (n = 6), no or only traces of CN were found. Only one case of the self-immolations (n = 12) displayed a toxic CN level. The results show that CN can have considerable significance when evaluating action ability and cause of death with enclosed-space fires and with motor-vehicle fires.

Cyanide toxicity is common after significant smoke inhalation. Two cases are presented that provide framework for the discussion of epidemiology, pathogenesis, presenting signs and symptoms, and treatment options of inhalational cyanide poisoning. An evidence-based algorithm is proposed that utilizes point-of-care testing to help physicians identify patients who benefit most from antidotal therapy.

Introduction: Host inflammatory response to any form of tissue injury, including burn, trauma, or shock, has been well documented. After significant burns, cytokines can increase substantially within the first 24 h after injury and may contribute to subsequent organ failure. Hemoadsorption by cytokine-adsorbing columns may attenuate this maladaptive response, thereby improving outcomes. The aim of this study was to investigate the feasibility, technical safety, and efficacy of cytokine and myoglobin removal by early use of a cytokine absorbing column (CytoSorb) in a porcine model of smoke inhalation and burn injury., Methods: Anesthetized female Yorkshire pigs (n = 15) were injured by wood bark smoke inhalation and a 40% total body surface area deep burn and observed for 72 h or death. The animals were randomized to hemoadsorption treatment (n = 9) or a sham group (n = 6) before injury. A 6-h hemoadsorption or sham session was performed on days one, two, and three. Serum cytokines (IL-1b, IL-6, IL-8, IL-10, TNF-alpha) and myoglobin were measured systemically, locally in bronchoalveolar lavage fluid and also in circulating blood before and after the adsorbing column to evaluate single pass clearance by the device., Results: Hemoadsorption caused significant removal of IL-1b, IL-6, IL-10, and myoglobin across the device mainly during the first run, ranging from 22% for IL-6 to 29% for IL-1b and 41% removal rates for myoglobin after 15  min of treatment. Systemic cytokine or myoglobin serum concentrations did not change., Conclusions: In a porcine model of smoke and burn injury, hemoadsorption using the CytoSorb cartridge did not result in significant systemic or pulmonary reductions in the measured cytokines or myoglobin despite efficient transmembrane reductions. Further investigations are needed to optimize the efficiency of mediator clearance to affect both circulating levels and clinically relevant outcomes.

In our institutes, we perform a quantitative evaluation of volatile hydrocarbons in post-mortem blood in all fatal fire-related cases using headspace gas chromatography mass spectrometry. We previously reported that benzene concentrations in the blood were positively correlated with carbon monoxide-hemoglobin (CO-Hb) concentrations in fire-related deaths. Here, we present 3 cases in which benzene concentrations in the blood were not correlated with CO-Hb concentrations. A high CO-Hb concentration without a hydrocarbon component, such as benzene, indicates that the deceased inhaled carbon monoxide that was not related to the smoke from the fire. Comparing volatile hydrocarbons with CO-Hb concentrations can provide more information about the circumstances surrounding fire-related deaths. We are currently convinced that this is the best method to detect if carbon monoxide poisoning occurred before a house fire started., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Inhalation injury seriously threatens the survival and quality of life in burn and trauma patients. So far there is no breakthrough in the treatment of inhalation injury. A significant advance has been witnessed in the experimental study of the use of stem cells in the treatment of lung injury in recent years. In this paper, according to the results of our study in the systemic transplantation of bone marrow mesenchymal stem cells for the treatment of inhalation injury, the effect of mesenchymal stem cells on anti-inflammatory process and repair of lung tissues in inhalation injury, and its possible mechanisms are reviewed.

Background: Several biological markers of lung injury are predictors of morbidity and mortality in patients with acute respiratory distress syndrome (ARDS). Some lung-protective ventilation strategies, such as low tidal volume, are associated with a significant decrease in plasma biomarker levels compared to the high tidal volume ventilation strategy. The primary objective of this study was to test whether the institution of high-frequency percussive ventilation (HFPV) to patients with respiratory distress after smoke inhalation injury influenced initial biomarker levels of lung injury (just before and after using percussive ventilation)., Materials and Methods: A prospective observational cohort study was conducted in the intensive care unit of the Brussels Burn Center. Fifteen intubated, mechanically ventilated patients with minor burns and ARDS following smoke inhalation were enrolled in our study. Physiologic data and serum samples were collected before intubation and at four different time points within the first 48h after intubation to measure the concentration of interleukin (IL)-6, IL-8, and tumor necrosis factor-α (TNF alpha). The differences in biomarker levels before and after starting HFPV were analyzed using repeated measure analysis of variance and a paired t test with correction for multiple comparisons., Results: Before starting HFPV under endotracheal intubation, all biological markers (IL-6, IL-8, and TNF alpha) were elevated in the spontaneously breathing patients with acute lung injury (ALI). After intubation and institution of a positive pressure ventilation with HFPV (tidal volume 5.6-6.6ml/kg per ideal body weight), none of the biological markers were increased significantly at either an early (3±2h) or a later point in time. However, the levels of IL-8 had decreased significantly after intubation at a later point in time. During the post-intubation period, the PaO2/FiO2 (partial pressure of arterial oxygen/fraction of the inspired oxygen) ratio increased significantly and the plateau airway pressure decreased significantly., Conclusion: Levels of IL-6, IL-8, and TNF alpha are elevated in spontaneously ventilating patients with minor burns and ARDS following smoke exposition prior to endotracheal intubation. The institution of HFPV with percussive positive pressure ventilation enhances blood oxygenation and could not further increase the initial levels of these biological markers of lung injury after smoke inhalation injury., (Copyright © 2014 Elsevier Ltd and ISBI. All rights reserved.)

Objective: To explore the protective effects of hydrogen-rich saline on rats with smoke inhalation injury., Methods: 36 healthy male Sprague-Dawley rats were randomly divided into 3 groups (n = 12 per group): sham group (S), inhalation injury plus normal saline treatment group (I+NS), and inhalation injury plus hydrogen-rich saline treatment group (I+HS). 30 min after injury, normal saline and hydrogen-rich saline were injected intraperitoneally (5 mL/kg) in I+NS group and I+HS group, respectively. All rats were euthanized and blood and organ specimens were collected for determination 24 h after inhalation injury., Results: Tumor necrosis factor-alpha (TNF-α) levels, malondialdehyde (MDA) concentrations, nuclear factor kappa B (NF-κB) p65 expression, and apoptosis index (AI) in I+HS group were significantly decreased (P < 0.05), while superoxide dismutase (SOD) activities were increased compared with those in I+NS group; and a marked improvement in alveolar structure was also found after hydrogen-rich saline treatment., Conclusions: Hydrogen-rich saline treatment exerts protective effects in acute lung injury induced by inhalation injury, at least in part through the activation of anti-inflammatory and antioxidant pathways and inhibition of apoptosis.

Introduction: Fire smoke inhalation a recognized etiologic factor of airway injuries. The objective of this study was evaluation of serum high-mobility group box 1 (HMGB1) protein concentration in subjects exposed to fire smoke (SEFS)., Material and Methods: The study group consisted of 40 consecutive patients admitted to the Toxicology Unit, Lodz, Poland after exposure to fire smoke. Serum HMGB1 concentrations were measured upon admission to hospital and rechecked on the 2nd and on the day of discharge. Patients also underwent routine toxicological diagnostic procedures applied in case of those exposures, such as carboxyhaemoglobin (COHb) levels and urinary thiocyanate concentrations. The same diagnostic tests were performed in 10 healthy volunteers not exposed to smoke of the control group., Results: The average serum SEFS concentration of HMGB1 protein was not significantly higher on admission in comparison with the respective values recorded on the 2nd day and on the day of discharge. The mean serum level of HMGB1 protein of exposed group was higher than that one in the control group, however the difference was not statistically significant. The highest concentration of HMGB1 protein was noted in serum of 28 subjects exposed to fire smoke reporting at least one symptom and the difference was statistically significant in a comparison with the control group., Conclusion: As indicated, an acute exposure to smoke may lead to transient increase of HMGB1 in serum in exposed subjects. Further studies are necessary in order to confirm the importance of this protein in pathogenesis of acute airway injury due to exposure to fire smoke.

Background: Myocardial infarction is the leading cause of death in fire fighters and has been linked with exposure to air pollution and fire suppression duties. We therefore investigated the effects of wood smoke exposure on vascular vasomotor and fibrinolytic function, and thrombus formation in healthy fire fighters., Methods: In a double-blind randomized cross-over study, 16 healthy male fire fighters were exposed to wood smoke (~1 mg/m³ particulate matter concentration) or filtered air for one hour during intermittent exercise. Arterial pressure and stiffness were measured before and immediately after exposure, and forearm blood flow was measured during intra-brachial infusion of endothelium-dependent and -independent vasodilators 4-6 hours after exposure. Thrombus formation was assessed using the ex vivo Badimon chamber at 2 hours, and platelet activation was measured using flow cytometry for up to 24 hours after the exposure., Results: Compared to filtered air, exposure to wood smoke increased blood carboxyhaemoglobin concentrations (1.3% versus 0.8%; P < 0.001), but had no effect on arterial pressure, augmentation index or pulse wave velocity (P > 0.05 for all). Whilst there was a dose-dependent increase in forearm blood flow with each vasodilator (P < 0.01 for all), there were no differences in blood flow responses to acetylcholine, sodium nitroprusside or verapamil between exposures (P > 0.05 for all). Following exposure to wood smoke, vasodilatation to bradykinin increased (P = 0.003), but there was no effect on bradykinin-induced tissue-plasminogen activator release, thrombus area or markers of platelet activation (P > 0.05 for all)., Conclusions: Wood smoke exposure does not impair vascular vasomotor or fibrinolytic function, or increase thrombus formation in fire fighters. Acute cardiovascular events following fire suppression may be precipitated by exposure to other air pollutants or through other mechanisms, such as strenuous physical exertion and dehydration.

Fire victims often suffer from burn injury and concomitant inhalation trauma, the latter significantly contributing to the morbidity and mortality in these patients. Measurement of blood carboxyhemoglobin levels has been proposed as a diagnostic marker to verify and, perhaps, quantify the degree of lung injury following inhalation trauma. However, this correlation has not yet been sufficiently validated. A total of 77 chronically instrumented sheep received sham injury, smoke inhalation injury, or combined burn and inhalation trauma following an established protocol. Arterial carboxyhemoglobin concentrations were determined directly after injury and correlated to several clinical and histopathological determinants of lung injury that were detected 48 hours post-injury. The injury induced severe impairment of pulmonary gas exchange and increases in transvascular fluid flux, lung water content, and airway obstruction scores. No significant correlations were detected between initial carboxyhemoglobin levels and all measured clinical and histopathological determinants of lung injury. In conclusion, the amount of arterial carboxyhemoglobin concentration cannot predict the degree of lung injury at 48 hours after ovine burn and smoke inhalation trauma.

Background: This is a report on an international non-interventional study of patients exposed to fires with smoke development in closed rooms. The objective of the study was to document clinical symptoms, relevant laboratory values and blood cyanide concentrations from fire victims in order to confirm or rule out presumptive correlations between the individual parameters., Materials and Methods: The study was conducted in five European countries with patients being included if they presented with the characteristic clinical signs, such as soot deposits and altered neurological status. Venous blood samples were taken from victims prior to administration of an antidote in all cases and determination of cyanide concentration was performed in a central laboratory using high performance liquid chromatography., Results: Data from 102 patients (62 % male, average age 49 years) were included in the evaluation with no blood samples being available for analysis from 2 patients. In 25 patients the blood cyanide concentration was below the limit of detection of 1.2 μmol/l. Cyanide levels between 1.2 and 10 μmol/l were measured in 54 patients, 7 patients had values between 10 and 20 μmol/l, 4 patients between 20 and 40 μmol/l while levels above 40 μmol/l were determined in 10 patients. The results of the study could not demonstrate that the cyanide level was influenced either by the interval between smoke exposure and blood sampling or the duration presence at the fire scene. The following clinical signs or laboratory values were recorded as relevant for increased and possibly toxic cyanide levels: respiratory arrest, dyspnea, resuscitation requirement, tracheal intubation, respiratory support measures, low Glasgow coma scale (GCS) score and respiratory frequency. A correlation between cyanide concentration and the total amount of soot deposits on the face and neck, in the oral cavity and in expectoration was confirmed. A correlation between cyanide and carboxyhemoglobin (COHb) levels in the blood of fire victims was also confirmed., Conclusions: As long as it is not possible to immediately determine the blood cyanide concentration in patients exposed to fire with smoke development, a decreased GCS score, soot deposits particularly in expectoration, dyspnea and convulsions are to be regarded as risk markers for intoxication. In their presence immediate administration of hydroxocobalamin as an antidote is recommended.

In critically ill intubated patients, assessment of adequacy of ventilation relies on measuring partial pressure of arterial carbon dioxide (PaCO2), which requires invasive arterial blood gas analysis. Alternative noninvasive technologies include transcutaneous CO2 (tPCO2) and end-tidal CO2 (EtCO2) monitoring. We evaluated accuracy of tPCO2 and EtCO2 monitoring in a porcine model of acute lung injury (ALI) due to smoke inhalation and burns. Eight anesthetized Yorkshire pigs underwent mechanical ventilation, wood-bark smoke inhalation injury, and 40% total body surface area thermal injury. tPCO2 was measured with a SenTec system (SenTec AG, Therwil, Switzerland) and EtCO2 with a Capnostream-20 (Oridion Medical, Jerusalem, Israel). These values were compared with PaCO2 measurements from an arterial blood gas analyzer. Paired measurements of EtCO2-PaCO2 (n = 276) and tPCO2-PaCO2 (n = 250) were recorded in the PaCO2 range of 25 to 85 mmHg. Overlapping data sets were analyzed based on respiratory and hemodynamic status of animals. Acute lung injury was defined as PaO2/FIO2 ≤ 300 mmHg; hemodynamic instability was defined as mean arterial pressure ≤ 60 mmHg. Before ALI, EtCO2 demonstrated moderate correlation with PaCO2 (R = 0.45; P < 0.0001), which deteriorated after onset of ALI (R = 0.12; P < 0.0001). Before ALI, tPCO2 demonstrated moderate correlation (R = 0.51, P < 0.0001), which was sustained after onset of ALI (R = 0.78; P < 0.0001). During hemodynamic stability, EtCO2 demonstrated moderate correlation with PaCO2 (R = 0.44; P < 0.0001). During hemodynamic instability, EtCO2 did not correlate with PaCO2 (R = 0.03; P = 0.29). tPCO2 monitoring demonstrated strong correlation with PaCO2 during hemodynamic stability (R = 0.80, P < 0.0001), which deteriorated under hemodynamically unstable conditions (R = 0.39; P < 0.0001). Noninvasive carbon dioxide monitors are acceptable for monitoring trends in PaCO2 under conditions of hemodynamic and pulmonary stability. Under unstable conditions, reevaluation of patient status and increased caution in the interpretation of results are required.

The current study sought to examine the interactions between inflammatory and immune events in the lung and circulating interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) levels at different burn depths with concomitant smoke inhalation in the rat model. Forty-eight female Sprague-Dawley rats were divided into six groups: S, sham; P, partial-thickness burns; F, full-thickness burns; I, inhalation; Pi, partial-thickness burns + inhalation; and Fi, full-thickness burns + inhalation. Blood samples and lung biopsies were obtained 24 hours later. Blood levels of IL-6, TNF-α, and IF-γ were measured with enzyme-linked immunosorbent assay. The proportions of CD3+ lymphocytes and CD68+ macrophages in the biopsies were studied immunohistochemically. The most severe inflammatory changes, except the neutrophil sequestration, were observed in the Fi group. A dense amount of neutrophils was observed in the F group. Edema and massive alveolar bleeding were seen in the I, Pi, and Fi groups. The amount of CD3+ lymphocytes were dense in the P, F, and Pi groups. The amount of CD68+ macrophages were significantly dense in Pi, F, I, and Fi groups. IL-6, TNF-α, and IF-γ increased in all groups when compared to the S group. The highest IL-6 level was seen in the Fi group. TNF-α significantly increased in the F, Pi, I, and Fi groups. Increase in IFN-γ levels in the Pi and Fi groups was significantly higher than in the P and F groups. In concomitant smoke inhalation and skin burns, pulmonary damage and systemic inflammatory response are related and may be evaluated by blood levels of IL-6, TNF-α, and IFN-γ cytokines.

Introduction: Fire smoke inhalation is a well-recognized aetiological factor of airway injuries. The objective of this study was evaluation of Clara cell protein (CC16) and myeloperoxidase (MPO) concentrations in serum of patients after exposure to uncontrolled fire smoke., Methods: The study group consisted of 40 consecutive patients admitted to the Toxicology Unit after exposure to fire smoke. CC16 and MPO concentrations in their serum samples was measured on the day of admission to hospital and rechecked at the 2nd day and on the day of discharge. Patients also underwent routine toxicological diagnostic procedures applied in case of exposures, such as carboxyhaemoglobin (COHb) levels and blood lactate and urinary thiocyanate concentrations. The same diagnostic tests were performed in the control group consisting of 10 healthy subjects not exposed to fire smoke., Results: The average concentration of CC16 in the serum of subjects exposed to toxic factors was significantly higher at the day of admission in comparison with the respective values recorded on the 2nd day and on the day of discharge. The mean level of CC16 in the serum of the exposed group was also significantly higher than that in the control group. Tests for MPO concentrations in the serum did not reveal any significant changes in patients exposed to fire smoke., Conclusions: As indicated, acute exposure to smoke induces injury at the alveolar level, which results in a transient increase of CC16 in serum of exposed subjects.

Patients with chronic obstructive pulmonary disease (COPD) respond poorly to corticosteroids. Histone deacetylase-2 (HDAC-2) plays a pivotal role in many cases of steroid insensitivity. The main aim of this study was to restore the smoking-induced reduction in corticosteroid sensitivity by increasing HDAC-2 activity using low-dose theophylline. Rats were exposed to cigarette smoke (CS) and treated with budesonide and two doses of theophylline. Besides the pathologic examination and cell counting in the bronchoalveolar lavage fluid (BALF), the expression of HDAC-2 and CXC chemokine ligand-8 (CXCL-8) were measured. Airway inflammation induced by CS was demonstrated by pathologic changes of lung tissue and increased level of CXCL-8. CS exposure also markedly decreased HDAC-2 expression. Moreover, a negative correlation was found between HDAC-2 activity and a lung destruction index. The index was restored to control levels with inhaled corticosteroid treatment in combination with a low, not a high, dose of theophylline. These results indicate that low-dose theophylline might provide protection from smoke damage and improve the anti-inflammatory effects of steroids by increasing HDAC-2 activity.

Objective: To evaluate physical examination findings and their association with carboxyhemoglobin (COHb) concentrations in 21 dogs that were exposed to smoke during a kennel fire., Series Summary: Twenty-one dogs were exposed to a kennel fire. Physical exam findings, presenting, and posttherapy COHb concentrations as well as therapeutic interventions were evaluated. COHb concentrations upon presentation were increased in all smoke inhalation exposed dogs. These dogs were compared to a small set of clinically normal staff-owned dogs who were not exposed to fire. Physical parameters significantly associated with higher COHb concentrations included lower body temperature, increased respiratory effort, abnormal respiratory auscultation, altered neurologic status, and length of hospital stay. Oxygen therapy resulted in a more rapid decline in COHb concentrations although 5 dogs still had mildly increased COHb concentrations 24-hour postadmission., Unique Information Provided: This study describes the relationship of admitting clinical findings of dogs exposed to a kennel fire with their initial blood COHb concentrations. It also describes the resolution of increased COHb concentrations with use of oxygen therapy and hospitalization. Additionally, COHb concentrations for a control group of dogs was evaluated and compared to the dogs exposed to smoke inhalation., (© Veterinary Emergency and Critical Care Society 2012.)

Background: Associations between acute respiratory inflammatory responses, changes in bronchial hyperresponsiveness, serum pneumoprotein levels, and exposure to fire smoke were studied., Methods: The study comprised 51 firefighters. Blood samples were taken within 24 hr following exposure to fire smoke, and after a week and 3 months. Sputum was induced within 5 days post-exposure and subjects underwent spirometry and methacholine provocation one week post-exposure. Exposure was registered by a questionnaire., Results: No changes were observed following smoke exposure in bronchial hyperresponsiveness and serum pneumoprotein levels. Nevertheless, in a sizable proportion of the firefighters (44%) elevated sputum neutrophil levels (≥60%) were found. Serum IL-8 concentrations were higher 24 hr post-exposure compared to pre-exposure. Elevated neutrophil levels in sputum were associated with elevated serum IL-8 (β = 0.010, P = 0.004) and TNFα (β = 0.005, P = 0.034) levels within 24 hr post-exposure and IL-8 elevation lasted up to 3 months., Conclusions: Acute exposure to fire smoke induces acute neutrophilic airway and long-lasting systemic inflammation in healthy firefighters in the absence of bronchial hyperresponsiveness., (Copyright © 2011 Wiley Periodicals, Inc.)

Background: Carbon monoxide toxicity in infants and children, like adults, produce nonspecific symptoms with normal vital signs necessitating the serum measurement of carboxyhemoglobin (COHb). In infants, the COHb may be falsely elevated., Objectives: Our goal was to report a case of suspected carbon monoxide toxicity in an infant and the likely cause of the falsely elevated serum COHb., Case: A previously healthy 3-month-old girl presented to the pediatric emergency department (ED) with smoke inhalation from a defective furnace. She was asymptomatic. On examination, she was alert, with Glasgow Coma Scale of 15 and normal vital signs. Cardiorespiratory and neurological examinations were completely normal. Because of concern regarding carbon monoxide poisoning, she was treated with normobaric oxygen therapy. Initial and subsequent serum COHb levels were persistently elevated, despite treatment and the infant appearing clinically well. As such, she had a prolonged stay in the ED. Further investigations found that fetal hemoglobin interferes with the spectrophotometric method used to analyze serum COHb levels., Conclusions: Carboxyhemoglobin serum level, in infants, may be falsely elevated due to the fetal hemoglobin interfering with standard methods of analysis. Knowledge of the false elevation using standard spectrophotometric methods of COHb in clinically well-appearing infants can decrease unnecessary oxygen therapy and monitoring time in the ED.

Introduction: Soluble 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., Methods: suPAR 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., Results: Systemic 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., Conclusions: Pulmonary 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.

Objective: To study the effect of bone marrow-derived mesenchymal stem cells (MSC) transplantation on the major inflammatory cytokines content in peripheral blood, lung water mass fraction, and lung tissue injury in rabbits with smoke inhalation injury., Methods: Sixteen adult New Zealand big ear rabbits were subjected to smoke inhalation injury and then were divided into pure injury group (PI, n = 8) and MSC transplantation group (MT, n = 8) according to the random number table. Via ear marginal vein, rabbits in PI group were injected with 10 mL phosphate buffered saline (PBS); rabbits in MT group were injected with 10 mL PBS containing the third passage MSC (1 x 10⁷ cell) isolated from marrow of healthy young New Zealand big ear rabbit. Another 8 rabbits were enrolled as normal control group (NC). Rabbits in NC group were injected with 10 mL PBS via ear marginal vein without smoke inhalation injury. Blood was harvested from rabbits in PI and MT groups at post injury hour (PIH) 2, 4, 6. Contents of TNF-α, IL-1β, IL-6, and IL-10 in serum were determined with ELISA. At PIH 24, left lung was harvested for morphology and histopathology observation; the right lung tissue was obtained to measure and calculate lung water mass fraction. Blood and lung tissue of rabbits in NC group were harvested and determined in the same way. Data were processed with t test., Results: (1) Serum contents of TNF-α in PI and MT groups at each time point were obviously higher than that in NC group (t = 2.43 - 9.57, P < 0.05 or P < 0.01). Serum contents of IL-1β and IL-6 in PI group at each time point were obviously higher than those in NC group (t = 8.49 - 19.80, P values all below 0.01). Serum content of IL-1β in MT group at each time point was close to that in NC group (t = 0.11 - 0.92, P values all above 0.05). Serum content of IL-6 in MT group at PIH 2 was close to that in NC group (t = 2.12, P > 0.05), but that of MT group increased significantly at PIH 4 and 6 (t = 2.83, P values all below 0.05). Serum contents of TNF-α, IL-1β, and IL-6 in MT group at each time point were obviously lower than those in PI group (t = 2.35 - 12.45, P < 0.05 or P < 0.01). (2) Serum content of IL-10 in MT group at PIH 2, 4, and 6 was respectively (13.0 ± 3.6), (11.6 ± 8.5), (15.2 ± 4.4) pg/mL, and they were higher than those in PI group [(5.5 ± 3.4), (5.0 ± 1.7), (7.9 ± 3.5) pg/mL, with t value respectively 4.28, 2.15, 3.67, P values all below 0.01]. Serum contents of IL-10 in PI and MT groups were obviously higher than that in NC group (t = 2.46-8.14, P < 0.05 or P < 0.01). (3) Lung tissue injury in MT group was alleviated markedly as compared with that in PI group. (4) At PIH 24, lung water mass fraction in MT group was (69 ± 7)%, which was obviously lower than that in PI group [(87 ± 6)%, t = 5.49, P < 0.01]. Compared with that in NC group [(48 ± 3)%], lung water mass fraction in PI and MT groups were increased obviously (with t value respectively 16.93 and 7.22, P values all below 0.01)., Conclusions: MSC transplantation can decrease pro-inflammatory cytokines, increase anti-inflammatory cytokines, decrease lung water mass fraction, ameliorate systemic inflammatory response, and protect lung tissue in rabbits with smoke inhalation injury.

Tobacco smoking is the primary risk factor for chronic obstructive pulmonary disease (COPD). However, recent epidemiological studies have established domestic exposure to wood smoke and other biomass fuels as additional important risk factors, characteristic in developing countries. Oxidative stress is one of the mechanisms concerned with pathogenesis of COPD. However, the molecular mechanisms involved in the onset and progress of COPD associated with biomass and specifically that derived from wood smoke exposure remain unknown. We analyzed the relationship between forced expiratory volume in first second (FEV(1)) with plasma malondialdehyde (MDA) concentration and activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione-S-transferase (GST) in COPD patients associated with wood smoke (WSG; n = 30), tobacco smoking (TSG; n = 30), and healthy control subjects (HCG; n = 30). Differences between FEV(1) from WSG and TSG (58 +/- 22% and 51 +/- 24%, respectively) with HCG (100 +/- 6%) were observed (P < 0.01). Plasma MDA concentration was higher in both WSG and TSG (1.87 +/- 0.81 and 1.68 +/- 0.82 nmol/mL, respectively) compared with HCG (0.42 +/- 0.17 nmol/mL; P < 0.01). SOD activity showed a significant increase in both WSG and TSG (0.36 +/- 0.12 and 0.37 +/- 0.13 U/mL) compared with HCG (0.19 +/- 0.04 U/mL; P < 0.01). No differences were shown regarding GPx, GR, and GST activities between COPD and control groups. Inverse correlations were founded between MDA and SOD with FEV(1) in both COPD patients and control subjects (P < 0.001). These results indicate a role for oxidative stress in COPD associated with wood smoke similar to that observed with tobacco smoking in subjects who ceased at least 10 years previous to this study.

Background: Hydrogen cyanide (HCN) and carbon monoxide (CO) may be important components of smoke from fire accidents. Accordingly, patients admitted to hospital from fire accidents may have been exposed to both HCN and CO. Cyanide (CN) intoxication results in cytotoxic hypoxia leading to organ dysfunction and possibly death. While several reports support the use of hyperbaric oxygen therapy (HBO) for the treatment of severe CO poisoning, limited data exist on the effect of HBO during CN poisoning. HBO increases the elimination rate of CO haemoglobin in proportion to the increased oxygen partial pressure and animal experiments have shown that in rats exposed to CN intoxication, HBO can increase the concentration of CN in whole blood., Objective: The purpose of the present study was to determine whole blood CN concentrations in fire victims before and after HBO treatment., Materials and Methods: The patients included were those admitted to the hospital because of CO intoxication, either as fire victims with smoke inhalation injuries or from other exposures to CO. In thirty-seven of these patients we measured CN concentrations in blood samples, using a Conway/microdiffusion technique, before and after HBO. The blood samples consisted of the remaining 2 mL from the arterial blood gas analysis. CN concentration in blood from fire victims was compared to 12 patients from non-fire accidents but otherwise also exposed to CO intoxication., Results: The mean WB-CN concentration before patients received HBO did not differ significantly between the two groups of patients (p = 0.42). The difference between WB-CN before and after HBO did not differ significantly between the two groups of patients (p = 0.7). Lactate in plasma before and after did not differ significantly between the two groups of patients. Twelve of the 25 fire patients and one of the non-fire patients had been given a dose of hydroxycobalamin before HBO., Discussion and Conclusion: CN concentrations in blood from patients admitted to hospital with CO intoxication and smoke inhalation exposure did not differ significantly from controls. Accordingly, we were not able to detect any changes in CN concentrations in blood after treatment with HBO., Trial Registration: ClinicalTrials.gov identifier: NCT00280579.

Objective: The aims of this study were to clarify changes in total ghrelin within the somatotropic axis in severe burn subjects with or without inhalation injury as well as the responsiveness of GH, IGF-1, and IGFBP-3 to the different severity of burn injuries., Design: Twenty-three patients with severe burn injuries (>30% of 2nd degree burns or >10% of 3rd degree burns) were classified into 2 groups according to inhalation injury: group I with inhalation injury (n=9) and group II without inhalation injury (n=14). The evaluations of serum GH, IGF-1, IGFBP-3, and total ghrelin were done on post-burn injury days 3, 7, 14, 21, and 40. Cortisol levels were measured from 24-h urine collections on post-burn injury days 7 and 21., Results: In all subjects, the levels of GH fluctuated throughout the observation period whereas IGF-1 showed an initial decline with nadir on day 7 and a subsequent increase through day 40. The levels of IGFBP-3 and total ghrelin showed a progressive increase with nadir on day 3. Compared with the group II, the GH levels were increased in the group I on post-burn days 3, 7, and 14, of which day 7 showed statistical significance (p<0.05). The levels of IGF-1 (days 7 and 21; p<0.05) and IGFBP-3 (days 7, 14, 21, and 40; p<0.05, p<0.01, p<0.05, p<0.05, respectively) were lower in the group I than in the group II throughout the study period. On post-burn injury days 3, 7, 14, and 21, total ghrelin levels were lower in the group I than in the group II with statistical significance on post-burn day 7 (p<0.001)., Conclusions: Our present data show a concurrence of elevated GH levels and decreased IGF-I, IGFBP-3, and total ghrelin levels during the early burn injury period, in addition to more GH burst amplitude as well as greater falling of IGF-I, IGFBP-3 and total ghrelin levels proportional to the severity of burn injury. Further studies are needed to ascertain whether acyl- and desacyl-ghrelin instead of total ghrelin are completely independent of increased GH or other stress mediators, and whether GH-releasing hormone (GHRH) mainly stimulates the production and release of GH in acute critical conditions.

Aim: To evaluate early and late complications among victims exposed to indoor fire and smoke inhalation., Method: An observational, descriptive and prospective longitudinal study of 15 victims of smoke inhalation admitted to the intensive care unit., Results: Although without significant burns, 13 of the victims were unconscious, with airway injury, abnormal temperature and hypokalaemia, and underwent mechanical ventilation. Initial carbon monoxide concentration averaged 20.4+/-8.3%, dropping to 3.9+/-3.3% 4h later. On the 1st day, two victims recovered and were transferred, and another two died. Creatine kinase levels (2594+/-2455 U/l) correlated with duration of intensive care. Of the remaining 11 patients, 10 had early pneumonia. Steroid treatment was initiated for four patients receiving prolonged mechanical ventilation, because of persistent fever and dry cough without evidence of infection., Conclusions: Mortality and systemic involvement were related to burn of the upper airway and contact with combustion products. Initial creatine kinase levels emerged as a prognostic marker of injury severity. Bronchoscopy was useful in grading airway injury and obtaining bronchoalveolar culture. Corticosteroids were effective, after the acute phase, in treating non-infectious pulmonary complications.

Study Objective: To assess outcomes in patients treated with hydroxocobalamin at the fire scene or in the ICU for suspected smoke inhalation-associated cyanide poisoning., Methods: Adult smoke inhalation victims with suspected cyanide poisoning as determined by soot in the face, mouth, or nose or expectorations and neurologic impairment received an intravenous infusion of hydroxocobalamin 5 g (maximum 15 g) at the fire scene or in the ICU in this observational case series conducted from 1987 to 1994. Blood cyanide specimens were collected before administration of hydroxocobalamin. The threshold for cyanide toxicity was predefined as greater than or equal to 39 micromol/L., Results: The sample included 69 patients (mean age 49.6 years; 33 men), of whom 39 were comatose. Out-of-hospital deaths were excluded. Fifty of the 69 patients (72%) admitted to the ICU survived after administration of hydroxocobalamin. In the group in which cyanide poisoning was confirmed a posteriori (n=42), 67% (28/42) survived after administration of hydroxocobalamin. The most common adverse events were chromaturia (n=6), pink or red skin discoloration (n=4), hypertension (n=3), erythema (n=2), and increased blood pressure (n=2). No serious adverse events were attributed to hydroxocobalamin. Laboratory tests revealed transient alterations in renal and hepatic function consistent with the critical condition of the patients and mild anemia consistent with progressive hemodilution., Conclusion: Empiric administration of hydroxocobalamin was associated with survival among 67% of patients confirmed a posteriori to have had cyanide poisoning. Hydroxocobalamin was well tolerated irrespective of the presence of cyanide poisoning. Hydroxocobalamin appears to be safe for the out-of-hospital treatment of presumptive cyanide poisoning from smoke inhalation.

Objective: We describe a modified triage system used in managing a smoke inhalation mass casualty incident that we recently encountered at our community hospital., Materials and Methods: The patients were triaged as priority 1, 2 or 3 on the basis of their symptoms, signs and circumstances at scene. In addition, the use of fibre-optic examinations of the upper airway, chest radiography and carboxyhaemoglobin levels with arterial blood gas analyses were used to aid in disposal plans., Results: Of the 22 patients evacuated, 15 were triaged as priority 2 and the remaining seven as priority 3. None of the patients was identified as priority 1. All the priority 2 patients underwent further investigations. Those with mild upper airway oedema (four patients) or raised carboxyhaemoglobin levels (two patients) were admitted. Only one patient had both. Another patient who was a known asthmatic developed bronchospasm and was admitted as well. All six were admitted to the general ward with subsequent good recovery and were discharged within 3 days. The remaining nine priority 2 and seven priority 3 patients were discharged from the emergency department., Conclusions: These modified triage criteria, with selective use of fibre-optic examinations, chest radiography and arterial blood gas analyses with carboxyhaemoglobin levels, are useful in smoke inhalation mass casualty incidents without dermal burns. Systemic injury and poisoning by toxic fumes often coexist with airway burns and should not be overlooked. Lastly, disaster planning and frequent drills at both local and national levels will optimize the response to future mass casualty incidents.

This prospective, randomized, controlled experimental study looks at the effects on global and regional microvascular blood flow (RMBF) in an ovine model of septic shock after severe smoke inhalation injury. Sixteen sheep were randomized into two groups, a control group (no injury, n = 8) and a smoke/sepsis (SS) group (n = 8), which received an insufflation of 4 sets of 12 breaths of cotton smoke (<40 degrees C) followed by instillation of live Pseudomonas aeruginosa into both lung lobes, according to an established protocol. All sheep were mechanically ventilated with 100% oxygen, and fluid resuscitated with lactated Ringer's solution for the entire duration of the 24-h experimental period to maintain hematocrit at baseline (BL) levels. Healthy control animals were not subjected to the injury and received only 4 x 12 breaths of room air and instillation of the vehicle (normal saline). Blood flow was analyzed using colored microspheres. Control animals remained hemodynamically stable and had no statistical changes from BL in visceral or cerebral blood flow during the entire experimental period. All SS animals developed a hypotensive, hyperdynamic circulation, characterized by a significant increase in heart rate and cardiac output with a simultaneous significant fall in mean arterial pressure, which, in combination, led to a fall in systemic vascular resistance index versus BL (P < 0.001, each). In visceral organs, the trachea showed a significant increase in RMBF (P < 0.001). In addition, skeletal muscle significantly increased versus BL and versus controls over time (P < 0.01). Whereas the pancreas displayed a significant drop in RMBF versus BL and controls (P < 0.05), no statistical differences occurred in the renal cortex, spleen, and ileum. All investigated cerebral structures, such as the cortex cerebri, basal ganglia, thalamus, hippocampus, pons, medulla oblongata, and cerebellum showed a significant increase in RMBF versus BL and versus control animals (P < 0.05, each). These data differ in areas of normal, increased, and decreased RMBF during septic shock after smoke inhalation injury and show differences to former studies of our group investigating RMBF in ovine models of either smoke inhalation or P. aeruginosa infusion. The results of this study reflect the complex pathophysiological variances of the combined injury and may provide a basis for future investigations for the treatment of this kind of injury.

A severe burn leads to hypermetabolism and catabolism resulting in compromised function and structure of essential organs. The massive release of cytokines is implicated in this hypermetabolic response. The aim of the present study was to compare cytokine expression profiles from severely burned children without signs of infections or inhalation injury (n = 19) to the cytokine profiles from normal, noninfected, nonburned children (n = 14). The Bio-Plex suspension array system was used to measure the concentration of 17 cytokines. The expression of proinflammatory and anti-inflammatory cytokines was maximal during the first week after thermal injury. Significant increases were measured for 15 mediators during the first week after thermal injury: interleukin (IL) 1beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12 p70, IL-13, IL-17, interferon gamma, monocyte chemoattractant protein 1, macrophage inflammatory protein 1beta, and granulocyte colony-stimulating factor (P < 0.05). Granulocyte-macrophage colony-stimulating factor was significantly increased during the second week after burn (P < 0.05). Within 5 weeks, the serum concentrations of most cytokines decreased, approaching normal levels. When compared with the cytokine levels measured in normal children, a total of 16 cytokines were significantly altered (P < 0.05). After severe burn, a specific cytokine expression profile is observed in patients without complications such as inhalation injury or sepsis. The cytokine concentrations decrease during 5 weeks after burn but remain elevated over nonburned values. Furthermore, the elevation in most serum cytokine levels during the first week after burn may indicate a potential window of opportunity for therapeutic intervention.

A total of 230 cases of deaths in burning spaces dating from the years 1995-2003 were investigated in Forensic Medicine Department, Silesian University of Medicine, Katowice. HbCO and HCN found in 177 blood samples ranged from 4-95 % (mean, 31,5 %) and 0,5-40,3 microg/ml (mean, 9,98 microg/ml), respectively. Moreover, ethanol was found in 122 blood samples. Its concentration ranged from 0,89-5,0 per thousand (mean, 1,45 per thousand). A comparative analysis of HbCO and HCN levels in the groups with and without ethanol showed that the range and the mean concentration of both these xenobiotics were higher in the group with no alcohol. It was also shown that the increased ethanol caused a drop in HbCO and HCN levels. To evaluate HbCO and HCN levels, the regression and correlation analysis was used.

Markedly elevated levels of plasma atrial natriuretic peptide (ANP), which exhibit potent diuretic and vasoactive properties, has been well documented in patients with acute lung injury. We examined the physiological effects of additional smoke inhalation on plasma ANP concentrations in an ovine burn model. Seventeen sheep were instrumented to receive fluid and have physiological measurements taken. The burn group (n=8) received 40% body surface area third degree burn and the burn+smoke group (n=9) received the same burn plus 48 breaths of cotton smoke insufflation. The animals were resuscitated according to the Parkland formula with Ringer's lactate in the following 72 h period. Hemodynamic, oxygenation, fluid balance, and plasma ANP levels were serially determined. The effects of smoke inhalation manifested as deteriorated oxygenation, and increased fluid accumulation after a sustained initial shock period of more than 12 h. Plasma ANP levels in the burn+smoke group showed a biphasic elevation, whereas the burn group showed no appreciable changes throughout the whole experimental period. The initial increase in plasma ANP concentrations occurred immediately after injury (from 96+/-10 at baseline to 136+/-17 pg/mL at 3h after injury); thereafter, it decreased towards baseline value, followed by a second increase in the post resuscitation period (183+/-43 pg/mL at 72 h after injury). Decreased urine output and accentuated pulmonary vascular resistance in the combined injury group was observed between the two ANP level peaks, indicating that ANP release modified physiological responses to the burn+smoke injury.

Carbon monoxide is a toxic gas with potentially lethal action, which forms as a result of incomplete combustion in conditions where there is a lack of oxygen and which, therefore, is present in varying percentages in environments where fire develops. In addition to carbon monoxide, other factors such as cyanide may contribute or might actually be the primary cause of a subject's demise. In cases of exposure to both substances, the role of cyanide as a toxic/lethal agent in death by asphyxiation is still not clear: some authors attribute a primary action to such a gas in causing the demise, others consider carbon monoxide to be the only cause of the lethal event. For this reason it is in the interest of forensic medicine to study all lethal cases of exposure to toxic substances originating from fires of various types of materials, in order to determine information regarding kinetic action and the possible strengthening of the effect of the two substances. Two case studies are presented here, in which the results of the toxicological examinations are quite different, and the contributions of CO and HCN in a fire asphyxiation are considered.

Objectives: Smoke inhalation has become the principal cause of death in burns patients. There are few guidelines for the management of smoke inhalation in the accident and emergency department. The aim was to identify what factors influence immediate management., Methods: A retrospective case note review using data from three west of Scotland accident and emergency departments in 1999. Computerized record systems were used to identify suitable patients., Results: Of 120 patients, 63 patients had incomplete data and were excluded. A total of 57 patients were classified into one of five categories: no burns, normal vital signs and examination (group 1, n=23); no burns, abnormal vital signs or examination (group 2, n=26); minor burns (<15% total body surface area) with or without abnormal vital signs or examination (group 3, n=5); major burns (>15% total body surface area) (group 4, n=2); in cardiac arrest on arrival (group 5, n=1). In groups 1 and 3, the result of two investigations significantly influenced management. In group 2, arterial blood gases and carboxyhaemoglobin levels were abnormal in 25% of cases, but only on one occasion did it influence an admission decision., Conclusion: Arterial blood gases, chest radiography and carboxyhaemoglobin estimation rarely influence immediate management. Patients presenting with normal vital signs and examination and short smoke exposure may be safe to discharge from the accident and emergency department without further investigation.

Lead-containing paint is common in structures built before 1977. Heated lead in burning paint can be aerosolized and absorbed directly into the bloodstream through the lungs. Acute lead intoxication has been reported in this setting. The objective of this study was to determine if victims of severe smoke inhalation secondary to closed-space fires have clinically important elevated blood lead levels. A case-control study, with a 2:1 ratio of cases to controls, was matched for age and sex. Cases were drawn from a prospective convenience sample of intubated victims of closed-space fires presenting to the ED of an urban tertiary burn center. Cases had blood lead levels obtained 24 hours postexposure. Matched control subjects had blood lead levels obtained during ED evaluation for a complaint unrelated to smoke inhalation. The difference between mean lead levels for cases and control subjects was expressed with a 95% confidence interval (CI). Among 22 cases, the mean lead level was 6.64 mug/dL (standard deviation [SD], 4.14 mug/dL). Among the 44 matched control subjects, mean lead level was 2.89 mug/dL (SD, 1.65 mug/dL). The mean difference between cases and control subjects was 3.75 mug/dL (95% confidence interval, 1.86-5.64). Although severe smoke inhalation is associated with a more than 2-fold statistically significant increase in blood lead levels, there is no evidence to suggest that these elevations are clinically important.

The combination of burn injury with smoke inhalation from fires significantly increases mortality. The mechanism of increased mortality is poorly understood but has been associated with multiple organ dysfunction syndrome, including cardiac dysfunction. Impaired cardiac function correlates with decreased survival in burn patients. We investigated smoke inhalation from burning cotton combined with a 40% body surface area, third-degree burn during the first 4 hours after injury in rats. In the early phase after injury, burn caused a significant rise in lung neutrophil infiltration but no increase in lung water. Smoke led to a rise in lung water but only a mild increase in neutrophil infiltration. Combined smoke and burn did not increase neutrophil accumulation or lung water above that which occurred with either injury alone. Only in combined smoke and burn was there a drop in cardiac output and stroke volume with pulmonary edema and lung neutrophil influx.

Objective: To investigate the beneficial effects of exogenous surfactant supplementation (ESS) and partial liquid ventilation (PLV) in treating acute lung injury induced by wood smoke inhalation., Design: A prospective, randomized, controlled, multigroup study., Setting: An animal research laboratory at a medical center., Subjects: Newborn piglets (n = 29; 1.80 +/- 0.06 kg) of either sex., Interventions: Animals were ventilated with a tidal volume of 15 mL/kg, a rate of 30 breaths/min, a positive end-expiratory pressure of 5 cm H(2)O, and an Fio(2) of 1.0. After the induction of acute lung injury by wood smoke inhalation, animals were randomly assigned to receive either conventional mechanical ventilation (CMV) or PLV with or without ESS pretreatment. Animals were grouped as CMV, ESS-CMV, PLV, and ESS-PLV., Measurements and Main Results: Arterial blood gases, cardiovascular hemodynamics, dynamic lung compliance, and total lung injury scores were measured. After smoke inhalation, all four groups displayed similar high arterial carboxyhemoglobin levels, low Pao(2) (<150 mm Hg), and low dynamic lung compliance (<66% of its baseline). In the CMV group, these deleterious conditions remained during the 4-hr observation period, and severe lung injury was noted histologically. All treatment groups demonstrated a significant increase in Pao(2) compared with the CMV group. In addition, both the PLV and ESS-PLV groups displayed significant improvements in dynamic lung compliance and in their histologic outcomes. Nevertheless, none of the variables measured in the PLV group differed from those measured in the ESS-PLV group., Conclusions: In a newborn piglet model of smoke inhalation injury, PLV or ESS improved oxygenation. PLV compared favorably with ESS in its greater improvements in lung compliance and lung pathology. However, the combined therapy of ESS and PLV was not clearly superior to PLV alone during the observation period.