Protection of laryngeal mucosa and function in laryngeal burns by heat absorption of perilaryngeal tissue.

OBJECTIVE: The laryngeal tissue carries most of the heat during inhalation injury. This study aims to explore the heat transfer process and the severity of injury inside laryngeal tissue by horizontally studying the temperature rise process at various anatomical layers of the larynx and observing the thermal damage in various parts of the upper respiratory tract. METHODS: The 12 healthy adult beagles were randomly divided into four groups, and inhaled room temperature air (control group), dry hot air of 80 °C (group I), 160 °C (group II), and 320 °C (group III) for 20 min, respectively. The temperature changes of the glottic mucosal surface, the inner surface of the thyroid cartilage, the external surface of the thyroid cartilage, and subcutaneous tissue were measured every minute. All animals were immediately sacrificed after injury, and pathological changes in various parts of laryngeal tissue were observed and evaluated under a microscope. RESULTS: After inhaling hot air of 80 °C, 160 °C and 320 °C, the increase of laryngeal temperature in each group was ΔT = 3.57 ± 0.25 °C, 7.83 ± 0.15 °C, 11.93 ± 0.21 °C. The tissue temperature was approximately uniformly distributed, and the difference was not statistically significant. The average laryngeal temperature-time curve showed that the laryngeal tissue temperature in group I and group II showed a trend of "first decrease and then increase", except that the temperature of group III directly increased with time. The prominent pathological changes after thermal burns mainly concluded necrosis of epithelial cells, loss of the mucosal layer, atrophy of submucosal glands, vasodilatation, erythrocytes exudation, and degeneration of chondrocytes. Mild degeneration of cartilage and muscle layers was also observed in mild thermal injury. Pathological scores indicated that the pathological severity of laryngeal burns increased significantly with the increase of temperature, and all layers of laryngeal tissue were seriously damaged by 320 °C hot air. CONCLUSIONS: The high efficiency of tissue heat conduction enabled the larynx to quickly transfer heat to the laryngeal periphery, and the heat-bearing capacity of perilaryngeal tissue has a certain degree of protective effect on laryngeal mucosa and function in mild to moderate inhalation injury. The laryngeal temperature distribution was in accordance with the pathological severity, and the pathological changes of laryngeal burns provided a theoretical basis for the early clinical manifestations and treatment of inhalation injury.

Incidental operating room fire from a breathing circuit warmer system: a case report.

BACKGROUND: An airway-associated fire in an operating room can have devastating consequences for patients. Breathing circuit warmers (BCWs) are widely used to provide heated and humidified anesthetic gases and eventually prevent hypothermia during general anesthesia. Herein, we describe a case of a BCW-related airway fire. CASE PRESENTATION: In this case, an electrical short within a BCW wire caused a fire inside the circuit. Simultaneously, the fire was extinguished, ventilation was stopped, and the endotracheal tube was disconnected from the BCW. The patient was exposed to the fire for less than 10 s, resulting in burns to the trachea and bronchi. Immediately after airway burn, bronchoscopy showed no edema or narrowing except for soot in the trachea and both main bronchus. After the inhalation burn event, prophylactic antibiotics, bronchodilator, mucolytics nebulizer, and corticosteroid nebulizer were started. On bronchoscopy 3 days after the inhalation burn, mucosal erythematous edema was observed and the inflammatory reaction worsened. The inflammatory reaction showed aggravation for up to 2 weeks, and then gradually recovered, and the epithelium and mucous membrane of the upper respiratory tract returned to normal after 4 weeks. Eventually, the patient recovered without long-term complications and was successfully discharged. CONCLUSIONS: This is the first report of a fire caused by BCW. We wanted to share our experience of how we responded to an airway-related fire in an OR and treated the patient. It cannot be overemphasized that the electrical medical appliance associated with the airways are fatal to the patient in the event of a fire, so caution should always be exercised.

Point-of-care endoscopic optical coherence tomography detects changes in mucosal thickness in ARDS due to smoke inhalation and burns.

BACKGROUND: The prevalence of acute respiratory distress syndrome (ARDS) in mechanically ventilated burn patients is 33%, with mortality varying from 11-46% depending on ARDS severity. Despite the new Berlin definition for ARDS, prompt bedside diagnosis is lacking. We developed and tested a bedside technique of fiberoptic-bronchoscopy-based optical coherence tomography (OCT) measurement of airway mucosal thickness (MT) for diagnosis of ARDS following smoke inhalation injury (SII) and burns. METHODS: 16 female Yorkshire pigs received SII and 40% thermal burns. OCT MT and PaO2-to-FiO2 ratio (PFR) measurements were taken at baseline, after injury, and at 24, 48, and 72h after injury. RESULTS: Injury led to thickening of MT which was sustained in animals that developed ARDS. Significant correlations were found between MT, PFR, peak inspiratory pressure (PIP), and total infused fluid volume. CONCLUSIONS: OCT is a useful tool to quantify MT changes in the airway following SII and burns. OCT may be effective as a diagnostic tool in the early stages of SII-induced ARDS and should be tested in humans.

Investigating the potential to assess severe lung inhalation injuries using computed tomography.

PURPOSE: The purpose of this study is to investigate the potential use of computed tomography (CT) in assessing inhalation injuries at various levels by studying the changes in lung imaging of rabbits with severe inhalation injury. METHODS: The sham, serious, critical, and extremely critical lung inhalation injury models were established by the New Zealand white rabbits' inhalation of steam for 0s, 0.25s, 0.50s, and 1.00s, respectively. Lung CT scans were performed at 1, 4, and 12h after the administration of steam and a radiologist's scores (RADS) were collected for each CT scan. Lung tissues were later collected to measure the lung wet/dry weight (W/D) ratio and to determine pathological scores. The correlation of the RADS with the lung-tissue pathological scores and W/D changes was investigated. RESULTS: The RADS and lung-tissue pathological scores are dependent on the time after injury and the level of injury. W/D ratios are dependent on the level of injury. The W/D ratio showed an increasing trend from 1h to 4h for the 0.25s, 0.50s, and 1s inhalation injury groups, while the W/D ratio decreased from 4h to 12h for the 0.25s and 0.50s inhalation injury groups. Further analysis indicates that, at the same time point, the lung RADS positively correlates with both the lung pathological scores and W/D ratios. CONCLUSION: A lung CT scan is able to reflect the early-stage lung injuries of rabbits with different levels of severe inhalation injury.

[Morphological and pathological changes of larynx after severe laryngeal burn in dogs and their relationship with laryngostenosis].

Objective: To investigate the morphological and pathological changes of the larynx after severe laryngeal burn in dogs and their relationship with laryngostenosis. Methods: Eighteen healthy, male beagle dogs were assigned into control group, immediately after injury group, and 2, 4, 6, and 8 weeks after injury groups according to the random number table, with 3 dogs in each group. Dogs of injury group inhaled saturated steam through mouth for 5 seconds to reproduce severe laryngeal burn. Tracheotomy and intubation were performed immediately after injury, and 400 000 U/d penicillin was intravenously infused for 1 week. The feeding, activity, and vocalization of dogs in each group after injury were observed until they were sacrificed. Immediately after injury and 2, 4, 6, and 8 weeks after injury, the laryngeal morphology of the dogs in corresponding time point groups were observed by endoscope. After the observation, the dogs in each injury group were sacrificed, and the laryngeal tissue was taken. The epiglottis, glottis, and cricoid cartilage were collected to make full-thickness tissue slice, respectively, and their pathological changes were observed with hematoxylin and eosin staining. The dogs of control group were not specially treated, and their life activities, laryngeal morphological and pathological changes were observed. Results: (1) The dogs of control group had normal feeding, activities, and vocalization. All the dogs in injury group survived until they were sacrificed, and their feeding, activities, and vocalization were obviously reduced after injury compared with those of control group. The dogs of 2, 4, 6 and 8 weeks after injury groups ate and moved normally 2 weeks after injury but vocalized abnormally in frequency and volume compared with those of control group, which lasted until they were sacrificed. (2) The dog's laryngeal mucosa in control group was complete and pink, without obvious exudation. The laryngeal mucosa of the dog in immediately after injury group was pale and edematous, with obvious exudation, local ulceration, necrosis, and exfoliation, and dilated microvessels on the surface. The laryngeal mucosa of the dogs in 2 weeks after injury group was pale, edematous, and oozed less than that of immediately after injury group, and the glottis was blocked by an obviously extruding mass. The paleness and edema of laryngeal mucosa were significantly reduced in the dogs of 4 weeks after injury group compared with those of 2 weeks after injury group, without dilated microvessel, and the glottic extruding mass was obviously smaller than that of 2 weeks after injury group. The sizes of glottic mass were similar between the dogs of 6 and 8 weeks after injury groups, which were obviously smaller than that in 4 weeks after injury group. (3) In the dogs of control group, the epithelial cells of epiglottis, glottis, and cricoid cartilage were normal in morphology, the proper glands were visible in the intrinsic layer, and the muscle fibers and the chondrocytes were normal in morphology. In the dogs of immediately after injury group, large sheets of epiglottis epidermis exfoliated, the epithelial cells were swollen and necrotic, the intrinsic glands were atrophic and necrotic, and the chondrocytes were degenerated and necrotic. The epidermis of the glottis partially exfoliated, the epithelial cells were swollen and necrotic, the intrinsic glands were atrophic and necrotic, the muscle fibers were partially atrophic and fractured, and the vacuolar chondrocytes were visible. The cricoid cartilage epidermis was ablated, the epithelial cells were swollen, the intrinsic layer and submucosal layer were slightly edematous, and the morphological structure of glands, chondrocytes, and muscle fibers were normal. In the dogs of 2 weeks after injury group, the epiglottis epidermis was completely restored, a small amount of glands in the intrinsic layer were repaired, and obsolete necrotic chondrocytes and new chondrocytes could be seen. A large number of fibroblasts, new capillaries, and inflammatory cells infiltration were observed in the epidermis of glottis, and intrinsic layer glands were repaired. The cricoid cartilage epidermis was repaired intactly, and there was no edema in the intrinsic layer. In the dogs of 4 weeks after injury group, the epiglottis intrinsic layer glands were further repaired compared with those of 2 weeks after injury group, and new chondrocytes were seen in the submucosa of the glottis. The condition of cricoid cartilage was consistent with that of control group. The dog's epiglottis, glottis, and cricoid cartilage were similar between the 6 and 8 weeks after injury groups, and no significant change was observed compared with those of 4 weeks after injury group. Conclusions: The morphological changes of larynx after severe laryngeal burn in dogs include mucosa detachment and necrosis, and mass blocking glottis. Pathological changes include epidermis shedding and necrosis, gland atrophy and necrosis, vascular congestion and embolism, chondrocytes degeneration, necrosis and proliferation, even local granulation tissue formation and cartilaginous metaplasia. These results may be the cause of laryngostenosis after laryngeal burn.

Inhalation Injury in the Burned Patient.

Inhalation injury causes a heterogeneous cascade of insults that increase morbidity and mortality among the burn population. Despite major advancements in burn care for the past several decades, there remains a significant burden of disease attributable to inhalation injury. For this reason, effort has been devoted to finding new therapeutic approaches to improve outcomes for patients who sustain inhalation injuries.The three major injury classes are the following: supraglottic, subglottic, and systemic. Treatment options for these three subtypes differ based on the pathophysiologic changes that each one elicits.Currently, no consensus exists for diagnosis or grading of the injury, and there are large variations in treatment worldwide, ranging from observation and conservative management to advanced therapies with nebulization of different pharmacologic agents.The main pathophysiologic change after a subglottic inhalation injury is an increase in the bronchial blood flow. An induced mucosal hyperemia leads to edema, increases mucus secretion and plasma transudation into the airways, disables the mucociliary escalator, and inactivates hypoxic vasocontriction. Collectively, these insults potentiate airway obstruction with casts formed from epithelial debris, fibrin clots, and inspissated mucus, resulting in impaired ventilation. Prompt bronchoscopic diagnosis and multimodal treatment improve outcomes. Despite the lack of globally accepted standard treatments, data exist to support the use of bronchoscopy and suctioning to remove debris, nebulized heparin for fibrin casts, nebulized N-acetylcysteine for mucus casts, and bronchodilators.Systemic effects of inhalation injury occur both indirectly from hypoxia or hypercapnia resulting from loss of pulmonary function and systemic effects of proinflammatory cytokines, as well as directly from metabolic poisons such as carbon monoxide and cyanide. Both present with nonspecific clinical symptoms including cardiovascular collapse. Carbon monoxide intoxication should be treated with oxygen and cyanide with hydroxocobalamin.Inhalation injury remains a great challenge for clinicians and an area of opportunity for scientists. Management of this concomitant injury lags behind other aspects of burn care. More clinical research is required to improve the outcome of inhalation injury.The goal of this review is to comprehensively summarize the diagnoses, treatment options, and current research.

Inhalation injury caused by cornstarch dust explosion in intubated patients-A single center experience.

BACKGROUND: Around 10%-20% of burned patients have inhalation injuries, and the severity of these injuries is correlated with mortality. Fiberoptic bronchoscopy is an important tool for the early diagnosis of inhalation injury. This study investigated correlations between the severity of inhalation injury and outcomes of patients involved in a cornstarch dust explosion in northern Taiwan in 2015. METHODS: Patients with burns who were intubated after the explosion were enrolled. Their medical records were reviewed, and data including patient characteristics, percentage of total body surface area (%TBSA) burned, severity of the inhalation injury, mechanical ventilation settings, and outcomes were collected and analyzed. RESULTS: Twenty patients underwent fiberoptic bronchoscopy during the first 24h to evaluate an inhalation injury. Their mean age was 22.4±5.5 years and the mean %TBSA burned was 55.7±19.4%. Fourteen patients had a grade 1 inhalation injury and six had a grade 2 injury. There was a higher %TBSA burned in the grade 1 group than in the grade 2 group, although the difference did not reach statistical significance (60.0±20.3% versus 45.5±13.5%, p=0.129). Compared to the grade 2 group, the grade 1 group had a significantly higher white blood cell count (29.4±9.3 versus 18.6±4.6, p=0.015) and frequency of facial burns (85.7% versus 33.3%, p=0.037). The overall intensive care unit mortality rate was 10% (n=2), with no significant intergroup difference (grade 1, 14.3% versus grade 2, 0%, p=0.192). CONCLUSION: Although the explosion resulted in a high rate of inhalation injuries in critically ill patients, there was no significant correlation between mortality and the severity of the inhalation injuries.

Development of an in vivo model of laryngeal burn injury.

OBJECTIVES/HYPOTHESIS: Inhalation injury significantly increases morbidity and mortality in burn patients. Approximately one in five burn patients have acute injury to the larynx, trachea, and/or lungs-and as many as 70% have long-term laryngeal abnormalities. Although inhalation injury to the lung has been studied extensively, no models exist to study these insults to the larynx. As such, we developed an in vivo rabbit model to create precise and reproducible laryngeal burn with resultant tissue damage as a foundation for interventional studies. METHODS: Following tubeless tracheotomy, a custom temperature-control device was employed to apply heated air (70°C-80°C, 150°C-160°C, or 310°C-320°C) ± smoke derived from unbleached cotton to the larynx, endoscopically, minimizing adjacent tissue damage in six rabbits. Pain, nutrition, and level of activity were monitored. Direct laryngoscopy and histological examination were performed 24 hours following insult. RESULTS: All animals survived injury with appropriate pain control; oral intake was initiated and all were adequately ventilating via tracheostomy. Burn sequelae were noted under direct visualization 24 hours after injury, and graded levels of edema and tissue damage were observed as a function of temperature. Edema obstructed true vocal fold visualization at increased temperatures. These injury patterns correlated with graded tissue damage on histology. CONCLUSION: We created an in vivo model of laryngeal burn injury employing a custom burn device resulting in graded tissue injury. This model is critical for investigation of the mechanisms underlying burn injury, and ultimately, the development and evaluation of therapies for this challenging population. LEVEL OF EVIDENCE: NA Laryngoscope, 127:186-190, 2017.

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.

[Advances in the research of pathogenesis and treatment of severe smoke inhalation injury].

Among the fire victims, respiratory tract injury resulted from smoke inhalation is the major cause of death. Particulate substances in smoke, toxic and harmful gas, and chemical substances act together would rapidly induce the occurrence of dramatic pathophysiologic reaction in the respiratory tract, resulting in acute injury to the respiratory tract, thus inducing serious injury to it and acute respiratory distress syndrome, leading to death of the victims. In recent years, the pathophysiologic mechanism of severe smoke inhalation injury has been gradually clarified, thus appreciable advances in its treatment have been achieved. This paper is a brief review of above-mentioned aspects.

Early leukocyte gene expression associated with age, burn size, and inhalation injury in severely burned adults.

BACKGROUND: In the patient with burn injury, older age, larger percentage of total body surface area (TBS) burned, and inhalation injury are established risk factors for death, which typically results from multisystem organ failure and sepsis, implicating burn-induced immune dysregulation as a contributory mechanism. We sought to identify early transcriptomic changes in circulating leukocytes underlying increased mortality associated with these three risk factors. METHODS: We performed a retrospective analysis of the Glue Grant database. From 2003 to 2010, 324 adults with 20% or greater TBS burned were prospectively enrolled at five US burn centers, and 112 provided blood samples within 1 week after burn. RNA was extracted from pooled leukocytes for hybridization onto Affymetrix HU133 Plus 2.0 GeneChips. A multivariate regression model was constructed to determine risk factors for mortality. Testing for differential gene association associated with age, burn size, and inhalation injury was based on linear models using a fold change threshold of 1.5 and false discovery rate of 0.05. RESULTS: After adjusting for potential confounders, age greater than 60 years (relative risk [RR], 4.53; 95% confidence interval [CI], 2.93-6.99), burn size greater than 40% TBS (RR, 4.24; 95% CI, 2.61-6.91), and inhalation injury (RR, 2.08; 95% CI, 1.35-3.21) were independently associated with mortality. No genes were differentially expressed in association with age greater than 60 years or inhalation injury. Fifty-one probe sets representing 39 unique genes were differentially expressed in leukocytes from patients with burn size greater than 40% TBS; these genes were associated with platelet activation and degranulation/exocytosis, and gene-set enrichment analysis suggested increased cellular proliferation and down-regulation of proinflammatory cytokines. CONCLUSION: Among adults with large burns, older age, increasing burn size, and inhalation injury have a modest effect on the leukocyte transcriptome in the context of the "genomic storm" induced by a 20% or greater than TBS burned. The 39-gene signature we identified may provide novel targets for the development of therapies to reduce morbidity and mortality associated with burns greater than 40% TBS. LEVEL OF EVIDENCE: Epidemiologic study, level III.

Laryngeal morphologic changes and epidemiology in patients with inhalation injury: a retrospective study.

BACKGROUND AND OBJECTIVES: Laryngeal morphologic changes are important in risk assessment of upper airway obstruction (UAO) after inhalation injury. This retrospective study evaluates the clinical application of laryngeal burn classification system. MATERIALS AND METHODS: Clinical data from January 1999 to June 2013 were analyzed retrospectively. The following data collected: age, gender, total burned surface area (TBSA), third-degree burn surface area, co-morbid injuries and complications, proportion of patients with tracheotomy, interval between tracheotomy and injury, incidence and mortality of UAO, and reasons for death. RESULTS: Four hundred and forty-three patients were included; 405 patients underwent multiple fibro-laryngoscopic observation, of which I, II and III types of laryngeal burns were present in 49.9, 38.0, and 12.1% patients, respectively. Laryngeal burn severity was related to TBSA and third-degree burn surface area. Overall tracheotomy rate (n=443) was 37.02%. The mean interval between tracheotomy and injury was 10.0±12.17h. Over 75% patients underwent tracheotomy within 12h. Compared with moderate inhalation burn group, the severe inhalation burn group showed a significantly higher tracheotomy rate within 12h and a significantly shorter interval between tracheotomy and injury. Patient mortality was significantly related to the severity of inhalation injury. CONCLUSION: The classification system of the morphologic laryngeal changes in laryngeal burn patients could effectively evaluate the UAO risk, enable earlier prophylactic tracheotomy after UAO onset, reduce surgical difficulties and risks, decrease clinical pressure of doctors, and prevent UAO. Laryngeal burn severity was related to TBSA and mortality and may be an important severity and prognosis indicator of inhalation injury.

[Frostbite injuries causing compromised airway after inhalation of propane]. / Forfrysninger som årsag til truet luftvej efter inhalation af flaskegas.

We describe a case report of a 23-year-old man with acute pharyngeal injuries due to frostbite subsequent to inhalation of propane. He was fiber-optically intubated on admission to hospital since his airways were considered acutely compromised. He was subsequently kept intubated for 11 days due to persistent pharyngeal oedema and frostbite injuries. The latter is caused by low temperature of propane upon release from a pressurized container. Injuries caused by frostbite often gradually progress and thus caution should be exerted in regards to airway management.

[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.

Airway obstruction and bacterial invasion in autopsy tissue of pediatric burn victims.

This study measured airway obstruction and bacterial invasion in systematically sampled lung tissue of burn victims at autopsy. Lung tissue from victims of combined smoke inhalation and burn injury (n = 5) and burn injury alone (n = 9) was examined histologically and the degree of bronchial and bronchiolar obstruction was measured. The walls of both bronchi and bronchioles were examined for bacterial invasion. Correlation analysis was performed for the association of airway obstruction with TBSA burn, number of ventilatory days, maximum inspiratory pressure, and days after injury. There was no significant difference in the mean degree of airway obstruction in smoke inhalation and burn victims compared with victims of burn-only injury (P > .05). Increased bronchiolar obstruction scores were detected in victims with pneumonia (55.3 ± 24.2%) compared with victims without pneumonia (9.3 ± 0.2%; P = .03). Bacterial invasion of the bronchial wall was present in one case, and invasion into the walls of bronchioles was seen in five cases. Burned children who died had extensive bronchiolar obstruction whether or not they had smoke inhalation injury. There was bacterial invasion into the airway wall in six of 14 cases (43%). Improved understanding of the mechanisms of airway obstruction is important for improved care of burned children.

Pathological changes of the three clinical types of laryngeal burns based on a canine model.

OBJECTIVE: The study was designed to examine pathological changes of inhalational laryngeal burns of three clinical types: congestive, oedematous and obstructive. METHODS: A total of 18 healthy, male, adult Beagle dogs were randomly assigned to inhale hot dry air at room temperature (group C), 80°C (Group 1), 160°C (Group 2) or 320°C (Group 3) for 20min to induce inhalation injury. Each larynx was evaluated and scored based on the 'clinical scoring and typing system of laryngeal burns at early stage'. Tissue samples of the epiglottis, laryngeal vestibule, vocal folds and infraglottic cavity of the larynx were observed microscopically and evaluated based on a 'pathological scoring system'. RESULTS: Pathological changes of the larynxes of groups 1 and 2 were primarily characterised by slight atrophy of the mucosa and mild oedema of the submucosal tissues. Group 3 larynxes showed two distinct pathological changes: oedematous and atrophic types. The larynxes of the atrophic type showed lower clinical scores (29.5±0.7 vs. 44.3±2.1) but higher pathological scores (18.6±3.2 vs. 13.7±1.8) than the larynxes of the oedematous type. CONCLUSION: Severe laryngeal burns could manifest as severe laryngeal oedema or atrophic change. The laryngeal burns of the atrophic type might suggest an unsatisfactory prognosis, although it had less risk of laryngeal obstruction at an early stage.

Application of flexible bronchoscopy in inhalation lung injury.

BACKGROUND: As acute inhalational injury is an uncommon presentation to most institutions, a standard approach to its assessment and management, especially using flexible bronchoscopy, has not received significant attention. METHODS: The objective of this study is to evaluate the value of using flexible bronchoscopy as part of the evaluation and management of patients with inhalational lung injury. Twenty-three cases of inhalational lung injury were treated in our three hospitals after a fire in a residential building. The twenty cases that underwent bronchoscopy as part of their management are included in this analysis. After admission, the first bronchoscopy was conducted within 18-72 hours post inhalational injury. G2-level patients were reexamined 24 hours after the first bronchoscopy, while G1-level patients were reexamined 72 hours later. Subsequently, all patients were re-examined every 2-3 days until recovered or until only tunica mucosa bronchi congestion was identified by bronchoscopy. RESULTS: Twenty patients had airway injury diagnosed by bronchoscopy including burns to the larynx and glottis or large airways. Bronchoscopic classification of the inhalation injury was performed, identifying 12 cases of grade G1 changes and 8 cases of grade G2. The airway injury in the 12 cases of grade G1 patients demonstrated recovery in 2-8 days, in the airway injury of the 8 cases of grade G2 patients had a prolonged recovery with airway injury improving in 6-21 days averaged. The difference in recovery time between the two groups was significant (P <0.05). CONCLUSIONS: The use of flexible bronchoscopy has great value in the diagnosis of inhalational injury without any complications. Its use should be incorporated into clinical practice. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1476676925108926.

Intussusception technique of intrabronchial silicone stents: description of technique and a case report.

Respiratory tract infection with human papillomavirus has been associated with major airway complications, including tracheal stenosis. We report a case of recurrent respiratory papillomatosis infection complicated with iatrogenic airway fire injury causing airway stenosis. This was treated with reconstruction and a silicone Y stent placement. Three years after the stent placement, the patient presented with wheezing and shortness of breath. Bronchoscopy revealed tracheal narrowing proximal to the tracheal limb of the Y stent. The stenosis was treated with a stent intussusception technique with satisfactory results.

DNA and inflammatory mediators in bronchoalveolar lavage fluid from children with acute inhalational injuries.

The aim of this study was to assess the feasibility of using serial bronchoalveolar lavage fluids (BALFs) to characterize the course of cell damage and inflammation in the airways of pediatric patients with acute burn or inhalation injury. This was a prospective, longitudinal, descriptive pilot study conducted at the Burn and Pediatric Intensive Care Units in a tertiary care medical center. Six consecutively intubated and mechanically ventilated pediatric patients with acute inhalational injuries were studied. Serial BALF specimens from clinically indicated bronchoscopies were used to measure DNA and cytokine levels. BALF DNA levels for the six pediatric burn subjects were the highest within the first 72 hours after burn injury and declined thereafter. At the early stages after injury, BALF DNA levels (median [min, max] 3789 [1170, 11,917] ng/ml) were similar to those in adult burn patients and pediatric cystic fibrosis or bronchiectasis patients and was higher than those in pediatric recurrent pneumonia patients. BALF DNA levels in children and adults with inhalation injury correlated significantly with BALF interleukin-6, interleukin-8, and transforming growth factor-ß1 levels. The patient with the most severe early visible airway mucosal damage and soot pattern at bronchoscopy, as well as the most extensive burns, also had the highest average early BALF DNA level (11,917 ng/ml) and the longest ventilator course and hospital stay. Procedures were well tolerated. In children with acute burn and inhalational injury, airway cellular damage and inflammation (reflected in high BALF DNA levels) appear to peak during the first 72 hours after burn or inhalation injury followed by a slow decline. Serial analysis of factors in airway secretions is feasible and has the potential to reveal important pathophyisiologic pathways and therapeutic targets for the treatment of acute inhalational injuries.