Risk factors and the associated limit values for abnormal elevation of extravascular lung water in severely burned adults.

BACKGROUND: Increased extravascular lung water (EVLW) correlates with pulmonary morbidity and mortality in critical illness. The extravascular lung water index (EVLWI), which reflects the degree of EVLW in an individual, increases in the fluid reabsorption stage rather than the initial resuscitation stage in severe burn cases. While many factors contribute to EVLWI variation, the risk factors contributing to its abnormal elevation in severe burns remain unclear. The aim of this study was to identify the risk factors and associated limit values for abnormal elevation of EVLWI during the fluid reabsorption stage in a cohort of severely burned adults. METHOD: This prospective, single-center study included only adults with burn sizes≥50% of the total body surface area (TBSA) who were admitted within 24h after burn. Demographic data were collected, and transpulmonary thermodilution (TPTD) measurements and blood biochemistry tests were performed upon admission and up to day (PBD) 9. Risk factors for abnormal EVLWI were analyzed by logistic regression. Receiver operating characteristic (ROC) curves were constructed to determine the optimal cut-offs for each risk factor. RESULTS: Seventy-two patients were ultimately enrolled, with a mean age of 40.3 years and mean burn size of 69.4% TBSA. EVLWI began to abnormally increase (>7ml/kg) on day 3 and up to PBD 9, indicating that a supranormal EVLWI developed in the fluid reabsorption stage. Several relevant factors were considered, including patient age, burn size, intrathoracic blood volume index (ITBVI), pulmonary vascular permeability index (PVPI), cardiac index (CI), systemic vascular resistance index (SVRI), serum albumin, time of first excision and grafting, and number of operations and daily fluid administration. Among these factors, we found that only burn size and ITBVI were significantly correlated with EVLWI variation and were further identified as the independent risk factors for EVLWI abnormality. ROC analysis showed that the limits for predicting a supranormal EVLWI during the fluid reabsorption stage were 65.5% TBSA for burn size and 845ml/m2 for ITBVI. Patients with burn sizes or ITBVIs higher than the limit showed significantly longer mechanical ventilation time and substantially higher occurrences of acute respiratory distress syndrome (ARDS) and pneumonia within two weeks after burn. CONCLUSIONS: Burn size and ITBVI are the independent risk factors for EVLWI abnormality during the fluid reabsorption stage in severely burned adults. The limit values for predicting a supranormal EVLWI in those patients are 65.5% TBSA for burn size and 845ml/m2 for ITBVI.

Molecular Imaging of Smoke-Induced Changes in Nuclear Factor-Kappa B Expression in Murine Tissues Including the Lung.

Many inflammatory responses are mediated by activation of the transcription factor, nuclear factor-kappa B (NF-κB), and a wide variety of human diseases involve abnormal regulation of its expression. In this investigation, we evaluated the effect of smoke inhalation injury on NF-κB expression in lung using two strains of NF-κB reporter mice. Groups of reporter mice with viral thymidine kinase (TK) or "fire fly" luciferase (Luc) genes under control by the NF-κB promoter (TK/NF-κB mice and Luc/NF-κB mice) were subjected to nonlethal smoke inhalation injury. Sham-treated animals served as controls. Twenty-four hours (each animal was injected intravenously with either 9-(4-18F-fluoro-3-[hydroxymethyl]butyl)guanine (FHBG) (~ 1.0 mCi) or luciferin (1.0 mg). One hour later, the TK/NF-κB mice were studied by micro-positron emission tomography (µ-PET) imaging using a Concord P4 µ-PET camera, and the Luc/NF-κB mice were studied by bioluminescence imaging with a charge-coupled device camera. The µ-PET data demonstrated that smoke injury produced massive increases in NF-κB expression (FHBG-standardized uptake value: 3.1 vs 0.0) 24 hours after smoke inhalation, which was reduced 48 hours after smoke inhalation, but still significantly different than the control. Qualitative analysis of the bioluminescence data revealed a remarkably similar effect of burn NF-κB luciferase expression in vivo. Biodistribution studies of FHBG uptake and luciferase activity in lung tissue demonstrated a similar increase 24 hours after injury, which was reduced 48 hours later, but still significantly higher than the sham. The present data with these models providing longitudinal imaging data on the same mouse may prove useful in the examination of the factors producing lung injury by smoke inhalation, as well as the treatment(s) for the damage produced with and without burn injury.

Mucosal fluid evaporation is not the method of heat dissipation from fourth-degree laryngopharyngeal burns.

This study was designed to explore whether mucosal fluid evaporation represents a method of heat dissipation from thermal air inhalation injury and to assess laryngopharyngeal tissue damage according to heat quantity changes of dry air and vapour. Fifteen adult male beagles were divided into five groups to inhale heated air or vapour for 10 min as follows: control group (ordinary air), group I (91-110 °C heated air), group II (148-175 °C heated air), group III (209-227 °C heated air), and group IV (96 °C saturated vapour). The heat quantity changes of the dry air and vapour were calculated via thermodynamic formulas. The macroscopic and histological features of the laryngopharynxes were examined and assessed by various tissue damage grading systems. Group IV exhibited the most serious laryngopharyngeal damage, including cilia exfoliation, submucosal thrombosis, glandular atrophy, and chondrocyte degeneration, which is indicative of fourth-degree injury. The quality, heat quantity, and proportional reduction of heat quantity of vapour in group IV were all higher than those in the other groups. Furthermore, we found that mucosal fluid evaporation is not the method of heat dissipation from thermal air inhalation injury used by the airways. Laryngopharyngeal tissue damage depends chiefly on the heat quantity of vapour in the air.

Association between early airway damage-associated molecular patterns and subsequent bacterial infection in patients with inhalational and burn injury.

Bacterial infection is a major cause of morbidity affecting outcome following burn and inhalation injury. While experimental burn and inhalation injury animal models have suggested that mediators of cell damage and inflammation increase the risk of infection, few studies have been done on humans. This is a prospective, observational study of patients admitted to the North Carolina Jaycee Burn Center at the University of North Carolina who were intubated and on mechanical ventilation for treatment of burn and inhalational injury. Subjects were enrolled over a 2-yr period and followed till discharge or death. Serial bronchial washings from clinically indicated bronchoscopies were collected and analyzed for markers of tissue injury and inflammation. These include damage-associated molecular patterns (DAMPs) such as hyaluronic acid (HA), double-stranded DNA (dsDNA), heat-shock protein 70 (HSP-70), and high-mobility group protein B-1 (HMGB-1). The study population was comprised of 72 patients who had bacterial cultures obtained for clinical indications. Elevated HA, dsDNA, and IL-10 levels in bronchial washings obtained early (the first 72 h after injury) were significantly associated with positive bacterial respiratory cultures obtained during the first 14 days postinjury. Independent of initial inhalation injury severity and extent of surface burn, elevated levels of HA dsDNA and IL-10 in the central airways obtained early after injury are associated with subsequent positive bacterial respiratory cultures in patients intubated after acute burn/inhalation injury.

A comparative study of bronchoscopic microsample probe versus bronchoalveolar lavage in patients with burns-related inhalational injury, acute lung injury and chronic stable lung disease.

BACKGROUND AND OBJECTIVES: The bronchoscopic microsample (BMS) probe allows direct epithelial lining fluid (ELF) level measurement without saline lavage. We investigated whether cytokine levels in ELF from a BMS differed from those obtained by bronchoalveolar lavage (BAL) in stable and acute lung disease. METHODS: In a single-centre, prospective observational cohort study of 45 patients, a sequential BMS probe procedure and BAL were performed on patients with stable chronic obstructive lung disease, interstitial lung disease, acute lung injury (ALI), burns-related inhalational injury or controls. ELF samples were assayed for IL-1ß, IL-6, IL-8, TNF-α and G-CSF. RESULTS: Both bronchoscopic microsampling and BAL showed significantly higher cytokine levels in the ELF from patients with ALI and burns-related inhalational injury than from those with chronic stable lung disease. The BMS method detected cytokine levels approximately 20- to 80-fold higher than the corresponding BAL (uncorrected for dilution). The ratio of BMS and BAL cytokine levels was as follows: the ratio for IL-1ß [mean 55, 95% confidence interval (CI) 34-88] was higher than that for IL-6 (mean 16, 95% CI 10-23, p = 0.015) and IL-8 (mean 13, 95% CI -5 to 36, p = 0.03). The ratio for G-CSF (mean 43, 95% CI 24-75) was higher than that for IL-6 (mean 16, 95% CI 10-23, p = 0.008). CONCLUSIONS: The BMS probe safely collects ELF with higher equivalent inflammatory cytokine concentrations than via BAL from patients with both acute and chronic lung disease and can be an alternative to saline BAL. Variations in cytokine concentrations between BMS and BAL and sampling-site differences warrant further study.

Inhalation injury in burn patients: establishing the link between diagnosis and prognosis.

This study was to re-evaluate inhalation injury as a prognostic factor in burn patients and to determine the factors that should be considered when refining the definition of inhalation injury. A total of 192 burn patients (152 men, 40 women; mean age, 46.1±13.8 years) who were suspected to have an inhalation injury and underwent bronchoscopy between January 2010 and June 2012 were included in this prospective observational study. All patients underwent bronchoscopy within 24h of sustaining the burn. The bronchoscopic findings were classified as normal, mild, moderate, and severe. Mechanical ventilation was administered, when required. Age, percentage of TBSA burned, ABSI score, requirement of mechanical ventilation and PF ratio, but not inhalation injury, COHb level, and bronchoscopic grades, significantly differed between the survivors and non-survivors (p<0.05). Mechanical ventilation (adjusted odds ratio [OR]: 9.787) and severe inhalation injury on bronchoscopy (adjusted OR: 45.357) were independent predictors of mortality on multivariate logistic regression analysis. Inhalation injury diagnosed through history does not predict mortality from burns. Other components such as severity of inhalation injury determined using bronchoscopy, and administration of mechanical ventilation might help predict the morbidity and mortality of burn patients with inhalation injury and all of the factors should be considered when the definition of inhalation injury is refined.

Influence of inhalation injury on energy expenditure in severely burned children.

OBJECTIVE: Determine the effect of inhalation injury on burn-induced hypermetabolism in children. DESIGN: Prospective study comparing hypermetabolism (i.e., resting energy expenditure and oxygen consumption) in burned children with and without inhalation injury during acute hospitalization. SETTING: Single pediatric burn center. PATIENTS: Eighty-six children (1-18 years) with ≥40% total body surface area burns were stratified to two groups: no inhalation injury and inhalation injury. INTERVENTIONS: None. MAIN MEASUREMENTS AND RESULTS: Inhalation injury was diagnosed based on bronchoscopic evaluation. At admission, PaO2:FiO2 ratios (an index of respiratory distress) were significantly higher in patients with no inhalation injury than in patients with inhalation injury. No differences were detected in resting energy expenditure or percent of the predicted basal metabolic rate between groups. Additionally, oxygen consumption did not significantly differ between groups. CONCLUSIONS: Inhalation injury does not augment the burn-induced hypermetabolic stress response in children, as reflected by resting energy expenditure and oxygen consumption.

[Effect of dinitrosyl iron complexes on erythrocyte energy metabolism under thermal trauma conditions].

The effect of dinitrosyl iron complexes (DNIC) on the energy metabolism of erythrocytes under combined thermal trauma conditions has been studied on a group of 30 Wistar rats, which was divided into 3 groups: intact (n = 10), control (n = 10), and main (n = 10). Combined thermal trauma (skin burn + thermoinhalation damage) was modeled in animals of the control and main groups. Rats of control group received infusions of sodium chloride solution (n = 10) every day. Rats of the main group obtained infusions of DNIC solution in sodium chloride. Rat blood samples were characterized by the activity of lactate dehydrogenase in direct and reverse reaction, lactate level, and coefficients of the substrate provision and energy reactions balance. It was stated, that DNIC clearly normalized the energy metabolism of erythrocytes beginning with the third day after thermal trauma onset.

Infrared (IR) spectral markers of bronchial epithelia in victims of fatal burns.

Changes in the infrared spectra of bronchial epithelia in victims of fatal burns were investigated. The mechanism of spectral changes on the basis of cellular morphological changes was considered. The ability of spectral parameters to diagnose fatal burns was assessed. Ten cases of fatal burns and 20 control cases were selected. Their lung tissues were removed, and sections were cut and mounted on glass and barium fluoride slides. Spectra of polarized bronchial epithelia were obtained by microscopy based on their morphological changes. In the spectra, 16 major absorbance bands were evaluated to determine their ability to act as positive markers for exposure to fire. Compared with the control group, the bronchial epithelia of the fatal burn victims showed three spectral results. (1) The absorbance of 16 major bands from the spectra of polarized bronchial epithelia in fatal burn victims significantly increased. (2) For the same cell number, the absorbance at 2850, 2920, 2959, and 3084 cm(-1) decreased. (3) The degree of increased or decreased absorbance of bands is related to the degree of polarization. These spectral results suggest that there is a vital reaction induced by the inhalation of hot fumes that includes an increase in the number of bronchial epithelia and a polarization effect. Overall, Fourier transform infrared (FT-IR) microspectroscopy was shown to be a convenient and reliable method to provide objective spectral markers to assist the diagnosis of fatal burns by simultaneously monitoring several specific parameters, although these observations have yet to be applied at forensic scenes.

Bacterial respiratory tract infections are promoted by systemic hyperglycemia after severe burn injury in pediatric patients.

BACKGROUND: Burns are associated with hyperglycemia leading to increased incidence of infections with pneumonia being one of the most prominent and adverse complications. Recently, various studies in critically ill patients indicated that increased pulmonary glucose levels with airway/blood glucose threshold over 150 mg/dl lead to an overwhelming growth of bacteria in the broncho-pulmonary system, subsequently resulting in an increased risk of pulmonary infections. The aim of the present study was to determine whether a similar cutoff value exists for severely burned pediatric patients. METHODS: One-hundred six severely burned pediatric patients were enrolled in the study. Patients were divided in two groups: high (H) defined as daily average glucose levels >75% of LOS >150 mg/dl), and low (L) with daily average glucose levels >75% of the LOS <150 mg/dl). Incidences of pneumonia, atelectasis, and acute respiratory distress syndrome (ARDS) were assessed. Incidence of infections, sepsis, and respiratory parameters were recorded. Blood was analyzed for glucose and insulin levels. Statistical analysis was performed using Student's t-test and chi-square test. Significance was set at p<0.05. RESULTS: Patient groups were similar in demographics and injury characteristics. Pneumonia in patients on the mechanical ventilation (L: 21%, H: 32%) and off mechanical ventilation (L: 5%, H: 15%), as well as ARDS were significantly higher in the high group (L: 3%, H: 19%), p<0.05, while atelectasis was not different. Patients in the high group required significantly longer ventilation compared to low patients (p<0.05). Furthermore, incidence of infection and sepsis were significantly higher in the high group, p<0.05. CONCLUSION: Our results indicate that systemic glucose levels over 150 mg/dl are associated with a higher incidence of pneumonia confirming the previous studies in critically ill patients.

[Comparing the effect of high frequency oscillatory ventilation and conventional mandatory ventilation on the myocardial function of rabbit with inhalation injury].

OBJECTIVE: To compare the effect of high frequency oscillatory ventilation (HFOV) and conventional mandatory ventilation (CMV) on the myocardial function of rabbits with inhalation injury. METHODS: Steam inhalation injury model was reproduced in 16 New Zealand albino rabbits. They were randomly divided into CMV group (n = 8) and HFOV group (n = 8) by drawing lots, and they received ventilation in metered volume and HFOV treatment respectively. Heart blood was drawn from rabbits before they were sacrificed 4 hours after treatment to determine the plasma activity of lactate dehydrogenase 1 (LDH1) and creatine phosphorylated kinase (CPK-MB). Myocardial tissue from left ventricle was harvested and homogenized to determine the concentration of TNF-α and IL-8, the activity of caspase-1, and the activity of myosin-light-chain kinase (MLCK) and the ATPase of myosin light chain (MLC-ATPase) by enzyme-linked immunosorbent assay, spectrophotometry, and the nuclide liquid scintillation technique respectively. Part of the myocardial tissue sample was examined pathologically. Data were processed with analysis of variance. RESULTS: (1) The activities of LDH1 and CPK-MB in plasma were obviously higher in CMV group than in HFOV group [(643 ± 108), (342 ± 48) U vs. (233 ± 92), (186 ± 36) U, with F value respectively 10.326 and 9.846, P values all below 0.01]. (2) The contents of TNF-α, IL-8 and the activity of caspase-1 in myocardial tissue homogenate were obviously higher in CMV group than in HFOV group [(181 ± 35), (89 ± 19) pg/g, and (0.56 ± 0.27) g/g protein vs. (94 ± 21), (43 ± 11) pg/g, and (0.24 ± 0.12) g/g protein, with F value respectively 8.239, 7.826, 5.716, P values all below 0.01]. (3) The activities of MLC-ATPase and MLCK were lower in CMV group than in HFOV group [(0.24 ± 0.12) µmol×mg(-1)×min(-1), (3.3 ± 1.1) mmol×mg(-1)×min(-1) vs. (0.48 ± 0.16) µmol×mg(-1)×min(-1), (7.7 ± 1.7) mmol×mg(-1)×min(-1), with F value respectively 4.125, 4.766, P values all below 0.01]. (4) No obvious necrosis, degeneration or inflammatory cell infiltration was observed in myocardial tissue of rabbits in 2 groups under light microscope; but the myocardial fiber was slightly swollen, and it was less marked in the HFOV group. CONCLUSIONS: The influence of HFOV on myocardial myosin phosphorylation system of rabbits with inhalation injury is less than that of CMV.

Putative role of TNF-alpha, interleukin-8 and ICAM-1 as indicators of an early inflammatory reaction after burn: a morphological and immunohistochemical study of lung tissue of fire victims.

AIMS: To investigate incipient inflammatory changes as first steps in the development of a systematic inflammatory response syndrome in the lungs of burn victims. METHODS: At the Institute of Legal Medicine of the University Hospital of Freiburg a collection of 40 forensic autopsy cases of burn victims was established that had died within 1 h after fire exposure. This group was compared with a total of 48 autopsy cases in three control groups (postmortem burns vs deaths from haemorrhagic shock vs railway suicide deaths). In all cases, immunohistochemical studies of lung tissue probes were performed to detect the presence of pro-inflammatory mediators using antibodies against tumour necrosis factor α (TNF-α), interleukin-8 (IL-8) and inter-cellular adhesion molecule 1 (ICAM-1). RESULTS: The lungs of burn victims showed a significantly higher extent of intra-alveolar oedema than the other groups. Immunohistochemically, macrophages in all groups mostly showed a distinct expression of TNF-α, but not of IL-8 or ICAM-1. Interestingly, intravascular erythrocytes often showed a positivity of TNF-α that was strongest in the group of burn victims and differed significantly from all the control groups. CONCLUSIONS: In burn victims with short survival times of ≤1 h after fire exposure, the immunohistochemical expression profiles of TNF-α, IL-8 and ICAM-1 in the lungs were not altered enough to prove an instant inflammatory reaction in these cases. Nevertheless, the positive reaction of TNF-α in erythrocytes of burn victims may indicate the beginning of a non-specific immune response to fire-induced inhalation trauma.

Steroids and extubation: the potential for clinical trials.

Intubation and mechanical ventilation are necessary adjuncts to airway management of the patient with inhalation injury. However, the ultimate goal of intubation is ultimate removal from mechanical ventilation. Extubation of the inhalation injury patient is often challenging due to the increased work of breathing, multiple operative interventions, and increased metabolic rate that often accompanies inhalation injury. The next two papers in the compendium describe two very different, yet potentially applicable, adjuncts to extubation of the burn patient: steroids and noninvasive positive pressure ventilation.

[Effect of high frequency oscillatory ventilation combined with exogenous pulmonary surfactant on apoptosis of lung tissue in rabbit with acute respiratory failure induced by steam inhalation injury].

OBJECTIVE: To investigate the effect of high frequency oscillatory ventilation (HFOV) combined with exogenous pulmonary surfactant (PS) on apoptosis of lung tissue in rabbit suffering from steam inhalation injury. METHODS: Thirty-two New Zealand rabbits were randomly divided into four groups, and acute respiratory failure model was reproduced by severe steam inhalation injury. Then they were ventilated and treated by controlled mandatory ventilation (CMV), HFOV, CMV+PS or HFOV+PS, respectively. After the animals were euthanized at 4 hours treatment time point, the right middle lobe of rabbit lung was harvested for the examination of caspase-3 and p73 contents and relative values, as well as mRNA expression of caspase-3 and p73. RESULTS: (1)Contents of caspase-3 and p73 in lung tissue homogenates in HFOV group and HFOV+PS group were significantly lower than those in CMV group and CMV+PS group (P<0.05 or P<0.01), and also contents of caspase-3 and p73 in lung tissue homogenates in groups with exogenous PS were significantly lower than those of groups without exogenous PS (all P<0.05). (2) Caspase-3, p73 mRNA expressions in lung tissue in HFOV group and HFOV+PS group were significantly lower than those of CMV group and CMV+PS group (all P<0.01). Caspase-3 and p73 mRNA expression in lung tissue in groups with exogenous PS group were significantly lower than those of the corresponding group without exogenous PS (all P<0.05). CONCLUSION: Compared with CMV or CMV+PS, HFOV or HFOV+PS can decrease the concentration of caspase-3 and p73, reduce the mRNA expression of caspase-3 and p73 in the lung homogenates, as a result lung tissue apoptosis in inhalation injury may be suppressed.

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

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

Late consequences of respiratory system burns.

Burn inhalation has negative effects on pulmonary function and may result in whole airway damage. The consequences of a methane explosion are thermal injury of the respiratory tract, shock wave, and carbon monoxide intoxication. The aim of this study was to determine changes in the pulmonary function tests (PFTs) after six years of follow-up in miners who survived a methane explosion. Two groups were examined: 41 miners who fell victims to a methane explosion and had a documented thermal injury of the respiratory tract and 25 healthy miners who served as controls. Pulmonary function studies were repeated after six months and six years from the time of injury in 33 study subjects and at the same time intervals in 16 control subjects. The study included static and dynamic lung volumes and diffusing capacity for carbon monoxide (DLCO). The mean values of PFTs were within normal ranges in both groups examined six months and six years after the injury. A significant decrease in DLCO was observed in the victims (98.4% vs. 85.4%), but not in the control group, after a six years' observation. The decrease may be one of the reasons for a breathing discomfort emerging in these patients. In the control subjects we observed a significant decrease in FEV1 (96.4% vs. 83.4%)--over a six years' period. This finding is due likely to smoking and heavy pollution of the working environment.

[Findings in bronchial lavage in patients with burns of the upper respiratory tract]. / Nálezy v bronchiálních lavázích u pacientu s popálením horních dýchacích cest.

The study is focused on cytologic and biochemical changes in bronchoalveolar lavage (BAL) at the group of patients from the Clinic of Burns Medicine at the University Hospital Královské Vinohrady in Prague. Only patients with inhalation trauma were involved in the study. The obtained data are from BAL measurements collected between intubation and extubation. There was the greater number of polymorphonuclears in the first two weeks in all patients. After 2-3 weeks there was a gradual increase in the number of macrophages at four patients and three patients had still the greater number of polymorphonuclears. There was a positive findings of PCNA at one patient and other markers (bcl-2, p53) were negative. The cytoflowmetry proved the increase in number of CD3 cells by 20% in one patient. The amount of proteins in the last BAL just before extubation was lower than 22 g/l. Serin proteinase activity was lower than 50 ncat/l at five patients and the ratio of MMP-8/TIMP-2 was higher than one in all analysed samples. There was no development of lung inflammation into chronic stadium. Two patients died.

Inducibility of HBD-2 in acute burns and chronic conditions of the lung.

The respiratory tract produces a number of molecules that act in the first line of host defense to protect against pathogenic colonization and tissue invasion. Most of the innate antimicrobial activity can be attributed to airway fluid proteins, such as lysozyme, lactoferrin, and secretory leukoproteinase inhibitor, and peptides, such as defensins. Human beta-defensins are cationic antimicrobial peptides with broad and potent microbicidal activity that have been shown to play a role in protecting the healthy lung from infection. To determine the effect of thermal injury on the production of the inducible beta-defensin, human beta-defensin-2 (HBD-2), we measured the concentration of HBD-2 by Western blot analysis in bronchoalveolar lavage samples from the lungs of burned patients with and without inhalation injury. Our data demonstrates an increased amount of HBD-2 in the pulmonary airways with thermal injury compared to normal lung. A further substantial increase in levels was noted in chronic lung conditions.

[The change in tissue oxygenation after severe steam inhalation injury].

Tissue oxygenation was observed in dogs inflicted with steam inhalation injury in this study. Main findings were as follows: there was significant decrease in cardiac output (CO), oxygen delivery (DO2), alveolar oxygen partial pressure (PAO2), arterial oxygen partial pressure (PaO2), mixed venous oxygen partial pressure (PVO2), arterial oxygen saturation (SaO2), mixed venous oxygen saturation (SVO2), and pH (P < 0.01), and marked increase in P(A-a)O2, oxygen extraction ratio (ERO2), and arterial carbon dioxide partial pressure (PaCO2) (P < 0.01 and P < 0.05). However there was no obvious change in oxygen consumption rate (VO2) within four hours after inhalation injury. The results indicated that the tissue hypoxia was caused directly by insufficient blood perfusion and oxygen supply as well.