Blood carboxyhemoglobin elimination curve, half-lifetime, and arterial-venous differences in acute phase of carbon monoxide poisoning in ovine smoke inhalation injury model.

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 (FiO2 = 1.0, tidal volume 12 mL/kg, and PEEP = 5cmH2O) 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 Arterial and mixed-venous blood samples were withdrawn simultaneously for blood gas analysis at various time points to determine CO-HB half-lifetime and an elimination curve.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.

Natural kinetics of blood cells following major burn: Impact of early decreases in white blood cells and platelets as prognostic markers of mortality.

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.

Proposal for an algorithm for the management of the patient's airway after smoke inhalation. / Propuesta de algoritmo para el manejo de la vía aérea del paciente tras inhalación de humo.

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.

Prognostic value of serum zinc levels in patients with acute HC/zinc chloride smoke inhalation.

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.

Platelet and coagulation function before and after burn and smoke inhalation injury in sheep.

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.

Concentrations of cyanide in blood samples of corpses after smoke inhalation of varying origin.

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.

Closed-Loop Control of FiO2 Rapidly Identifies Need For Rescue Ventilation and Reduces ARDS Severity in a Conscious Sheep Model of Burn and Smoke Inhalation Injury.

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 ±â€Š0.6 h and 0.2 ±â€Š0.1 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 ±â€Š5 in SOC versus 228 ±â€Š59 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.

Case Files of the University of Massachusetts Toxicology Fellowship: Does This Smoke Inhalation Victim Require Treatment with Cyanide Antidote?

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.

[Advances in the experimental study of the use of mesenchy- mal stem cells for the treatment of inhalation injury].

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.

Evaluation of the Cytosorb™ Hemoadsorptive Column in a Pig Model of Severe Smoke and Burn Injury.

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.

High-mobility group box 1 protein levels in serum of subjects after exposure to fire smoke--short communication.

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.

Protective Effects of Hydrogen-Rich Saline on Rats with Smoke Inhalation Injury.

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.

Detection of carbon monoxide poisoning that occurred before a house fire in three cases.

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.

High-frequency percussive ventilation and initial biomarker levels of lung injury in patients with minor burns after smoke inhalation injury.

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.

Effect of wood smoke exposure on vascular function and thrombus formation in healthy fire fighters.

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.

No correlation between initial arterial carboxyhemoglobin level and degree of lung injury following ovine burn and smoke inhalation.

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.

Report on a study of fires with smoke gas development : determination of blood cyanide levels, clinical signs and laboratory values in victims.

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.

Noninvasive carbon dioxide monitoring in a porcine model of acute lung injury due to smoke inhalation and burns.

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.

Destructive pulmonary effects of smoke inhalation and simultaneous alterations in circulating IL-6, TNF-α, and IFN-γ levels at different burn depths: an experimental study on rats.

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.