Inhalation Lung Injury Research Articles

Repair and regeneration of the alveolar epithelium in lung injury.

Considerable progress has been made in understanding the function of alveolar epithelial cells in a quiescent state and regeneration mechanism after lung injury. Lung injury occurs commonly from severe viral and bacterial infections, inhalation lung injury, and indirect injury sepsis. A series of pathological mechanisms caused by excessive injury, such as apoptosis, autophagy, senescence, and ferroptosis, have been studied. Recovery from lung injury requires the integrity of the alveolar epithelial cell barrier and the realization of gas exchange function. Regeneration mechanisms include the participation of epithelial progenitor cells and various niche cells involving several signaling pathways and proteins. While alveoli are damaged, alveolar type II (AT2) cells proliferate and differentiate into alveolar type I (AT1) cells to repair the damaged alveolar epithelial layer. Alveolar epithelial cells are surrounded by various cells, such as fibroblasts, endothelial cells, and various immune cells, which affect the proliferation and differentiation of AT2 cells through paracrine during alveolar regeneration. Besides, airway epithelial cells also contribute to the repair and regeneration process of alveolar epithelium. In this review, we mainly discuss the participation of epithelial progenitor cells and various niche cells involving several signaling pathways and transcription factors.

Synergistic Effects of Resistive Breathing on Endotoxin-Induced Lung Injury in Mice.

Resistive breathing (RB) is characterized by forceful contractions of the inspiratory muscles, mainly the diaphragm, resulting in large negative intrathoracic pressure and mechanical stress imposed on the lung. We have shown that RB induces lung injury in healthy animals. Whether RB exerts additional injurious effects when added to pulmonary or extrapulmonary lung injury is unknown. Our aim was to study the synergistic effect of RB on lipopolysaccharide (LPS)-induced lung injury. C57BL/6 mice inhaled an LPS aerosol (10mg/3mL) or received an intraperitoneal injection of LPS (10 mg/kg). Mice were then anaesthetized, the trachea was surgically exposed, and a nylon band of a specified length was sutured around the trachea, to provoke a reduction of the surface area at 50%. RB through tracheal banding was applied for 24 hours. Respiratory system mechanics were measured, BAL was performed, and lung sections were evaluated for histological features of lung injury. LPS inhalation increased BAL cellularity, mainly neutrophils (p < 0.001 to ctr), total protein and IL-6 in BAL (p < 0.001 and p < 0.001, respectively) and increased the lung injury score (p = 0.001). Lung mechanics were not altered. Adding RB to inhaled LPS further increased BAL cellularity (p < 0.001 to LPS inh.), total protein (p = 0.016), lung injury score (p = 0.001) and increased TNFa levels in BAL (p = 0.011). Intraperitoneal LPS increased BAL cellularity, mainly macrophages (p < 0.001 to ctr.), total protein levels (p = 0.017), decreased static compliance (p = 0.004) and increased lung injury score (p < 0.001). Adding RB further increased histological features of lung injury (p = 0.022 to LPS ip). Resistive breathing exerts synergistic injurious effects when combined with inhalational LPS-induced lung injury, while the additive effect on extrapulmonary lung injury is less prominent.

Sex-Based Disparities in Leukocyte Migration and Activation in Response to Inhalation Lung Injury: Role of SDF-1/CXCR4 Signaling.

The aim of the study was to determine whether sex-related differences exist in immune response to inhalation lung injury. C57BL/6 mice were exposed to Cl2 gas (500 ppm for 15, 20, or 30 min). Results showed that male mice have higher rates of mortality and lung injury than females. The binding of the chemokine ligand C-X-C motif chemokine 12 (CXCL12), also called stromal-derived-factor-1 (SDF-1), to the C-X-C chemokine receptor type 4 (CXCR4) on lung cells promotes the migration of leukocytes from circulation to lungs. Therefore, the hypothesis was that elevated SDF-1/CXCR4 signaling mediates exaggerated immune response in males. Plasma, blood leukocytes, and lung cells were collected from mice post-Cl2 exposure. Plasma levels of SDF-1 and peripheral levels of CXCR4 in lung cells were higher in male vs. female mice post-Cl2 exposure. Myeloperoxidase (MPO) and elastase activity was significantly increased in leukocytes of male mice exposed to Cl2. Lung cells were then ex vivo treated with SDF-1 (100 ng/mL) in the presence or absence of the CXCR4 inhibitor, AMD3100 (100 nM). SDF-1 significantly increased migration, MPO, and elastase activity in cells obtained from male vs. female mice post-Cl2 exposure. AMD3100 attenuated these effects, suggesting that differential SDF-1/CXCR4 signaling may be responsible for sex-based disparities in the immune response to inhalation lung injury.

First-day computed tomography: does it has a role in the assessment of patients with inhalation lung injury?

BackgroundInhalation lung injury occurs in almost one-third of all serious burns and is responsible for a considerable proportion of burn patient fatalities each year. History of closed space fire or unconsciousness at the accident site, occurrence of pharyngeal or facial burns, hoarseness, and wheezing, and laboratory tests that include blood gas abnormalities or Carboxyhemoglobin levels in blood ˃ 10% are used to diagnose inhalation lung injury. It is also characterized by radiological findings of alveolar or interstitial edema, atelectasis, and/or consolidations, as well as the presence of erythema with laryngeal or tracheal edema in the bronchoscope.ObjectivesTo study the diagnostic and prognostic efficacy of radiologist score and bronchial wall thickening as radiological CT findings in inhalation lung injury.MethodsThis prospective case–control study included 48 patients with inhalation lung injury (ILI) as a case group and 10 patients without ILI were selected as the control group, all recruited from the burn and plastic department. Within the first 12 h of suspected ILI, a fiberoptic bronchoscope was done to confirm the diagnosis. An initial chest X-ray was done followed by computed tomography through which the radiologist score (RADS) together with bronchial wall thickening (BWT) was done.ResultsDuration of ventilation was higher in cases than in controls (8.50 ± 3.94 vs 3.25 ± 0.50). The hospital duration was higher in cases than in controls (13.6 ± 4.68 vs9.50 ± 4.52). The BWT was 2.12 ± 0.66 (mean ± SD) in the ILI group while the control group was 1.32 ± 0.48 (mean ± SD). Correlating between baseline PaO2 and RADS score and BWT, it was found that there was a highly significant negative correlation between PaO2 and RADS score and BWT among inhalation lung injury patients (P value 0.001). The sensitivity of BWT in the detection of the need for mechanical ventilation was 83% at a cut-off point of 1.65. Its specificity was 78% and accuracy 75%.ConclusionCT done within 24 h of burn patients has a good role in the diagnosis and management of ILI from the burn.

927: DABBING LUNG INJURY MANAGED BY VV ECMO

Introduction: E-cigarette or vaping-associated lung injury (EVALI) is an uncommon complication of e-cigarettes or vaping. Most cases are associated with tetrahydrocannabinol (THC) containing products. “Dabbing” refers to the process of ingesting high concentrations of THC-containing oils or waxes with butane solvents to vaporize cannabinoids for inhalation. Another distinction is the presence of impurities and unpurged butane in the vapors inhaled by the users. Description: A 29-year-old male presented with cough, dyspnea, and fever seven days prior to admission. He reported smoking marijuana but denied vaping. Initial chest radiograph demonstrated multifocal pneumonia. PCR for SARS-CoV-2 was negative. He required four liters of supplemental oxygen. Physical exam was remarkable for diffuse pulmonary crackles. Broad spectrum antibiotics for pneumonia were initiated. Oxygen requirements rapidly increased, prompting intubation 48 hours from presentation. Ventilator settings escalated to a positive end-expiratory pressure of 18 cm H2O with 100% FiO2. Computed tomography angiography ruled out pulmonary embolism, however showed diffuse patchy nodular and confluent opacities. Respiratory cultures grew commensal flora and blood cultures were negative. Comprehensive laboratory investigations for an infectious etiology and autoimmune vasculitis were negative. In further discussion with the patient’s wife, he has been “dabbing” for the past six months. High dose intravenous steroids were initiated. The patient continued to have refractory hypoxemic and hypercapnic respiratory failure with ARDS requiring prone positioning. The patient ultimately required transition to veno-venous extracorporeal membrane oxygenation (VV-ECMO). The patient received 12 days of VV-ECMO and was eventually liberated after 19 days of ventilator support. At discharge he was asymptomatic, at his baseline level of function, and required no supplemental oxygen. He was discharged on daily steroids with a taper and outpatient follow-up. Discussion: The necessity of VV-ECMO utilization in “dabbing” associated acute lung injury represents a rare severe presentation. Dabbing is emerging as a trend among young adults and represents an under-investigated cause of severe inhalational lung injury.

A man who became breathless after tiling a bathroom

Inhalational lung injury should be considered in patients presenting with acute respiratory symptoms and a history of occupational or recreational exposure to toxic substances. We present the case of a 29-year-old patient who developed pneumonitis following usage of waterproofing sealant spray in an enclosed space, despite the use of a dust mask. The patient was managed with oxygen therapy, corticosteroids and bronchodilators. He made a complete clinical recovery with resolution of almost all changes seen on computerised tomography (CT) imaging within 7 days.

Evaluation of an Injectable, Solid-State, Oxygen-Delivering Compound (Ox66) in a Rodent Model of Pulmonary Dysfunction-Induced Hypoxia.

Pulmonary dysfunction (PD) and its associated hypoxia present a complication to the care of many service members and can arise intrinsically via comorbidities or extrinsically by infection or combat-related trauma (burn, smoke inhalation, and traumatic acute lung injury). Current supportive treatments (e.g., ventilation and supplemental oxygen) relieve hypoxia but carry a significant risk of further lung injury that drives mortality. Ox66 is a novel, solid-state oxygenating compound capable of delivering oxygen via intravenous infusion. Male Sprague Dawley rats (N = 21; 250-300 g) were surgically prepared for cardiovascular monitoring, fluid infusion, mechanical ventilation, and intravital and phosphorescence quenching microscopy (interstitial oxygen tension; PISFO2) of the spinotrapezius muscle. Baselines (BL) were collected under anesthesia and spontaneous respiration. PD was simulated via hypoventilation (50% tidal volume reduction) and was maintained for 3 hours. Groups were randomized to receive Ox66, normal saline (NS; vehicle control), or Sham (no treatment) and were treated immediately following PD onset. Arterial blood samples (65 µL) and intravital images were taken hourly to assess blood gases and chemistry and changes in arteriolar diameter, respectively. Significance was taken at P < .05. PD reduced PISFO2 for all groups; however, by 75 minutes, both NS and Sham were significantly lower than Ox66 and remained so until the end of PD. Serum lactate levels were lowest in the Ox66 group-even decreasing relative to BL-but only significant versus Sham. Furthermore, all Ox66 animals survived the full PD challenge, while one NS and two Sham animals died. No significant vasoconstrictive or vasodilative effect was noted within or between experimental groups. Treatment with intravenous Ox66 improved interstitial oxygenation in the spinotrapezius muscle-a recognized bellwether for systemic capillary function-suggesting an improvement in oxygen delivery. Ox66 offers a novel approach to supplemental oxygenation that bypasses lung injury and dysfunction.

Edaravone combined with dexamethasone exhibits synergic effects on attenuating smoke-induced inhalation lung injury in rats

Inhalational lung injury often leads to morbidity and mortality during fire disasters. In this study, we aimed to evaluate the protective effects of edaravone combined with dexamethasone on smoke-induced inhalational lung injury. Sprague-Dawley rats were divided into five groups, namely, the control, model (inhalation), and three treatment groups (edaravone, dexamethasone, and edaravone combined with dexamethasone). After drug intervention in the acute lung injury model, arterial blood gas, wet:dry weight ratio of the lung tissue, bronchoalveolar lavage fluid, and pulmonary histopathology were determined. The production of reactive oxygen species (ROS), mitochondrial membrane potential (MMP), inflammatory cytokines, peroxidase and apoptosis were further analyzed to explore the underlying mechanisms. The results of blood gas and inflammatory cytokine analysis and the histopathological data demonstrated that edaravone combined with dexamethasone had obvious protective effects on smoke infiltration and tissue injury. Moreover, after the co-administration of edaravone and dexamethasone, malondialdehyde and myeloperoxidase levels in the lung tissue decreased, whereas those of glutathione peroxidase and superoxide dismutase were elevated. In addition, this drug combination could inhibit smoke-induced apoptosis in lung tissues by reducing the cleavage of caspase-3, caspase-9, and poly ADP-ribose polymerase (PARP), and also reverse smoke-mediated mitochondrial dysfunction, including ROS generation, loss of MMP, early release of cytochrome C, second mitochondrial activator of caspases, and apoptosis-inducing factor. In conclusion, edaravone combined with dexamethasone had a protective effect on smoke-induced inhalational lung injury in rats and can be further explored as an attractive therapeutic option for the treatment of smoke inhalation-induced pulmonary dysfunction.

Time to Start Up: CT-Basted Radiomics in Children’s Lung Diseases

Time to Start Up: CT-Basted Radiomics in Children’s Lung Diseases

Development of novel nanofibers targeted to smoke-injured lungs

Smoke inhalation injury is associated with significant mortality and current therapies remain supportive. The purpose of our study was to identify proteins upregulated in the lung after smoke inhalation injury and develop peptide amphiphile nanofibers that target these proteins. We hypothesize that nanofibers targeted to angiotensin-converting enzyme or receptor for advanced glycation end products will localize to smoke-injured lungs. MethodsFive targeting sequences were incorporated into peptide amphiphile monomers methodically to optimize nanofiber formation. Nanofiber formation was assessed by conventional transmission electron microscopy. Rats received 8 min of wood smoke. Levels of angiotensin-converting enzyme and receptor for advanced glycation end products were evaluated by immunofluorescence. Rats received the targeted nanofiber 23 h after injury via tail vein injection. Nanofiber localization was determined by fluorescence quantification. ResultsPeptide amphiphile purity (>95%) and nanofiber formation were confirmed. Target proteins were increased in smoke inhalation versus sham (p < 0.001). After smoke inhalation and injection of targeted nanofibers, we found a 10-fold increase in angiotensin-converting enzyme-targeted nanofiber localization to lung (p < 0.001) versus sham with minimal localization of non-targeted nanofiber (p < 0.001). ConclusionsWe synthesized, characterized, and evaluated systemically delivered targeted nanofibers that localized to the site of smoke inhalation injury in vivo. Angiotensin-converting enzyme-targeted nanofibers serve as the foundation for developing a novel nanotherapeutic that treats smoke inhalation lung injury.

ATS Core Curriculum 2020. Pediatric Pulmonary Medicine.

The American Thoracic Society Core Curriculum updates clinicians annually in adult and pediatric pulmonary disease, medical critical care, and sleep medicine, in a 3- to 4-year recurring cycle of topics. These topics will be presented at the 2020 International Conference. Below is the pediatric pulmonary medicine core, including pediatric hypoxemic respiratory failure; modalities in noninvasive management of chronic respiratory failure in childhood; surgical and nonsurgical management of congenital lung malformations; an update on smoke inhalation lung injury; an update on vaporizers, e-cigarettes, and other electronic delivery systems; pulmonary complications of sarcoidosis; pulmonary complications of congenital heart disease; and updates on the management of congenital diaphragmatic hernia.

Protective role of mesenchymal stem cells transfected with miRNA-378a-5p in phosgene inhalation lung injury

Phosgene-induced lung injury is an important type of acute lung injury (ALI). Currently, no effective clinical treatment has been developed yet. Our previous study revealed that expressions of 6 miRNAs were significantly increased in phosgene-induced lung injury. The screened miRNA with the most significant effect on hepatocyte growth factor (HGF) expression by mesenchymal stem cells (MSCs) was transfected into MSCs. This study aimed to investigate whether the transfected MSCs had better therapeutic effects than MSCs alone. MSCs were co-cultured with miRNA mimics for 24h and 48h. HGF expression in culture supernatant was detected by ELISA. HGF expression in MSCs was detected by Western blot after being co-cultured with the selected miRNA inhibitor. The transfected MSCs were given to rats suffering from phosgene-induced lung injury. Expressions of TNF-α, IL-6, IL-1β and IL-10, were assayed by ELISA. SP-C mRNA level was tested by RT-PCR. VE-CAD expression was tested by Western blot. We found that miRNA-378a-5p most increased HGF expression among the six miRNAs. After transfection of MSCs with miRNA-378a-5p inhibitor, HGF expression was decreased. Compared with untreated MSCs, MSCs transfected with miRNA-378a-5p exhibited more significant decreases in lung injury score, white blood cell count and protein content while restoring respiratory indexes. Meanwhile, expressions of TNF-α, IL-6, IL-1β were decreased while those of IL-10, SP-C and VE-cadherin were increased. In conclusion, MSCs transfected with miRNA-378a-5p were more effective in treating phosgene-induced lung injury by repairing the secretion of alveolar epithelial cells and improving the permeability of vascular endothelial cells compared with MSCs alone.

Multidrug Resistant Organism Burden in Critically-Ill Burn Patients

<h3>Background</h3> The National Burn Repository 2019 reports burn-related data from July 2017- June 2018 of 1,101 hospitals and 221,519 patients. Large total body surface area (TBSA) burns and inhalational lung injury (ILI) are major risks for a complicated course requiring critical care support and infections are the most serious and most common complications of burns. The aim of this study is to evaluate the burden of multidrug resistant organisms (MDRO) in critically-ill burn patients. <h3>Methods</h3> Our burn center receives 3,000 visits and provides treatment for around 1300 patients annually. In 2018, 225 patients were admitted to the hospital's 9-bed critical-care burn unit. Patients who had burns more than 10% TBSA and/or ILI were included in the study if they survived more than 48 hours. The records were reviewed for length of stay (LOS), mortality, as well as MDRO clinical as well surveillance cultures. <h3>Results</h3> 55 patients were included in the study with 39 (71%) male and with an average LOS of 11 days. Inhalational lung injury was found to be present in 58% of patients. 8 patients died who had an average TBSA burn of 60%. While patients who were discharged alive had average TBSA burns of 29% and average LOS of 26 days. 22% of discharged patients were found to have MDRO acquisition detected by clinical cultures and 14% of patients had MRSA detected by follow-up nasal screening. <h3>Conclusions</h3> MDRO colonization is common in severely-ill burn patients. This highlights the importance of more aggressive MDRO surveillance in this population for early detection and prevention of hospital-associated infections and outbreaks.

BMSC-derived exosomes alleviate smoke inhalation lung injury through blockade of the HMGB1/NF-κB pathway

AimsTo investigate the role of bone marrow mesenchymal stem cell (BMSC)-derived exosomes in smoke inhalation lung injury. Main methodsIn this study, we initially isolated exosomes from BMSCs and identified them by western blot and transmission electron microscopy. BMSC-derived exosomes were then used to treat in vitro and in vivo models of smoke inhalation lung injury. Pathologic alterations in lung tissue, the levels of inflammatory factors and apoptosis-related factors, and the expression of HMGB1 and NF-κB were determined to evaluate the therapeutic effect of BMSC-derived exosomes. Key findingsWe found that BMSC-derived exosomes could alleviate the injury caused by smoke inhalation. Smoke inhalation increased the levels of inflammatory factors and apoptosis-related factors and the expression of HMGB1 and NF-κB, and these increases were reversed by BMSC-derived exosomes. HMGB1 overexpression abrogated the exosome-induced decreases in inflammatory factors, apoptosis-related factors and NF-κB. SignificanceCollectively, these results indicate that BMSC-derived exosomes can effectively alleviate smoke inhalation lung injury by inhibiting the HMGB1/NF-κB pathway, suggesting that exosome, a noncellular therapy, is a potential therapeutic strategy for inhalation lung injury.

Effect of sivelestat sodium on early inflammatory reaction and pulmonary edema in rats with smoke inhalation induced lung injury

Objective To investigate the effects of sivelestat sodium on early inflammatory response and pulmonary edema in rats with smoke inhalation-induced lung injury. Methods Seventy-five Sprague-Dawley rats were randomly divided into control group, model group, low-dose group, middle-dose group and high-dose group. The smoke inhalation model was continued except for the control group. The rats were given intraperitoneal injection of normal saline, cevicell sodium 10 mg/kg, 20 mg/kg and 30 mg/kg. The general condition and lung tissue were observed after 24 hours. Results Compared with the control group, rats in each group had a certain degree of lung injury, alveolar wall thickening, alveolar interstitial hyperemia, etc. The alveolar septal thickness, lung tissue wet-dry (W/D) level, the incidence of edema and the levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), neutrophil elastase (NE) and myeloperoxidase (MPO) in the model group were significantly higher than those of the other 4 groups. The lung function recovery was highest in the low dose group and the alveolar septal thickness was the highest among the dose group. The alveolar wall thickening incidence of W/D level and pulmonary edema in lung tissue in the low dose group were (6.76±0.40)μm, (5.18±0.13) and 40.00%, respectively, and the levels of TNF-α, IL-6, NE and MPO were (19.62±0.83)pg/L, (9.41±0.25)pg/L, (6.23±0.18)μg/L and (30.64±0.87)pg/L, significantly better than the middle dose group and high dose group (P<0.05). Conclusions Sivelestat sodium can significantly affect the smoke inhalation lung injury, and improve the recovery of liver function, which can significantly reduce the incidence of inflammation and pulmonary ede-ma in the lung, but its therapeutic effect and drug delivery. There was a significant association between doses and therapeutic effect, in the case of rats, a dose of 10 mg/kg was the best for treatment. Key words: Lung injury; Smoke inhalation injury; Sivelestat sodium; Inflammation; Pulmonary edema; Rats

Perfluorochemical-facilitated plasminogen activator delivery to the airways: A novel treatment for inhalational smoke-induced acute lung injury.

BackgroundEffective clinical management of airway clot and fibrinous cast formation of severe inhalational smoke‐induced acute lung injury (ISALI) is lacking. Aerosolized delivery of tissue plasminogen activator (tPA) is confounded by airway bleeding; single‐chain urokinase plasminogen activator (scuPA) moderated this adverse effect and supported transient improvement in gas exchange and lung mechanics. However, neither aerosolized plasminogen activator (PA) yielded durable improvements in physiologic responses or reduction in cast burden. Here, we hypothesized that perfluorochemical (PFC) liquids would facilitate PA distribution and sustain improvements in physiologic outcomes in ISALI.MethodsSpontaneously breathing adult sheep (n = 36) received anesthesia and analgesia and were instrumented, exposed to cotton smoke inhalation, and supported by mechanical ventilation for 48 h. Groups (n = 6/group) were studied without supplemental treatment, or, starting 4 h post injury, they received intratracheal low volume (8 mL) PFC liquid alone or a dose range of tPA/PFC or scuPA/PFC suspensions (4 or 8 mg in 8 mL PFC) every 8 h. Outcomes were evaluated by sequential measurements of cardiopulmonary parameters, lung histomorphology, and biochemical analyses of bronchoalveolar lavage fluid.ResultsDose‐response and PA‐type comparisons of outcomes demonstrated sustained superiority with low‐volume PFC suspensions of scuPA over tPA or PFC alone, favoring the highest dose of scuPA/PFC suspension over lower doses, without airway bleeding.ConclusionsWe propose that this improved profile over previously reported aerosolized delivery is likely related to improved dose distribution. Sustained salutary responses to scuPA/PFC suspension delivery in this translational model are encouraging and support the possibility that the observed outcomes could be of clinical importance.

Utility of fiberoptic bronchoscopy in the critical care unit: how far-reaching are the complications and outcomes?

Background Fiberoptic bronchoscopy (FOB) is standard as a pre-eminent technique for diagnostic, palliative, and curative purposes in variable pulmonary insults. Objectives The objectives of this study were to identify the causation, technical aspects, pathophysiological impacts, and complications of FOB in critically ill patients, to discover the correlation between FOB outcomes and independent risk factors, and ultimately to anticipate predictors of mortality in critically ill patients who underwent FOB. Patients and methods This prospective cohort study was carried out in ICUs on 52 critically ill patients who were subjected to FOB for diagnostic or therapeutic purposes. They were grouped into the mechanical ventilation (MV) (28/52) and non-MV (24/52) groups. FOB outcomes and complications were encountered. Results Diagnostic indication of FOB was seen in 40/52 (77%) cases, while the therapeutic purposes of FOB were seen in 12/52 (23%) cases. FOB had a particular indication in the management of 12/52 cases (13.6%) for both pneumonic and inhalation lung injury cases, 10/52 (19.2%) cases for underlining focal lung lesion, 8/52 (15.4%) cases for hemoptysis, and 5/52 (9.6%) cases for either acute respiratory distress syndrome or atelectasis condition. There was a highly considerable variation between the MV and non-MV groups. Hypoxemia, bleeding, arrhythmia, bronchospasm, and laryngospasm were the most prevalent side effects of FOB, with unremarkable differences between both groups. FOB outcomes were as follows: 31/52 (59.6%) cases improved, 11/52 (21.2%) died, and 10/52 (19.2%) were referred to a tertiary health unit. There were significant negative correlations between outcomes and reasons for admission, time of onset of FOB, and radiological pattern. Older age, respiratory insult, immune-compromised state, nonventilatory assessment, and less frequency of FOB performance were predictors of mortality among critically ill patients who underwent FOB. Conclusion Flexible bronchoscopy is a safe and effective procedure for the diagnosis and treatment of pulmonary pathology in critically ill patients.

The Construction of A Sheep Acute Respiratory Distress Syndrome Model Induced by Smoke Inhalation Injury

Objective To establish a model of acute respiratory distress syndrome induced by sheep smoke inhalation lung injury. Methods Nine healthy, 12-24 month old, non-pregnant female sheep were randomly selected, the sheep were divided into three groups, through the internal control of smoke generator device components (CO, CO2, O2, particle concentration and smoke temperature, etc.) to adjust the exposure time of the sheep model construction of smoke. The chest CT were examined before and after exposure to smoke at 6h, 12h, 24h and 48h, respectively. From the smoke exposure 12h endotracheal intubation and mechanical ventilation, by adjusting the ventilator parameters of hypoxemia and hypercapnia, statistical analysis of PaO2/FiO2, PEEP and other indicators, according to the ARDS definition of diagnosis in Berlin definition. Results The CT showed mild inflammation of the lungs in first group, oxygen index of 95% confidence interval [331.13, 353.53]; In second groups, oxygenation index 95% confidence interval [220.09, 383.90]; CT showed airway edema, pulmonary inflammatory exudation and lung injury in third group. Oxygenation index 95% confidence interval of [195.16, 244.84], PEEP&gt;5cm. There was significant difference between the two groups (P&lt;0.05). Conclusions The severity of lung injury can be changed by adjusting the exposure time of smoke inhalation; when the smoke exposure time up to 45 minutes, a stable model of smoke inhalation lung injury in sheep ARDS can be successfully established.

The Efficacy of Autologous Nebulized Platelet Rich Plasma (PRP) As an Early Adjuvant Therapeutic and Prognostic Treatment Modality in the Management of Inhalation Lung Injury

Background: Despite considerable advances in our knowledgeof the pathophysiology of inhalation injury, there arefew specific therapeutic options, and patient care is mainlysupportive. Platelets release growth factors and other immunesystem components to start healing process. By using nebulizedPlatelet Rich Plasma (PRP), platelets may reduce inflammationand stimulates bronchial tree healing. However, there are noclear data supporting or refuting the use of inhaled PRP ininhalation injury.Objective: To evaluate the role of nebulized autologousPlatelet Rich Plasma (PRP) in management of Smoke InhalationInjury (SII) as early adjuvant therapeutic and prognosticmodality.Methods: This is prospective study that included 40patients with burns 25-50% TBSA and have inhalation lunginjury. They were divided into 2 groups; 20 patients receivedaerosolized particles of nebulized PRP beside regular regimen.The other control group included 20 patients and receivedregular treatment regimen only.Results: There was a statistical significant difference(p<0.01) of biologic changes in upper airway with smokeinjury in study group patients compared to control grouppatients who received regular protocol measured at the samefollow-up time interval, relatively same TBSA and initialbronchoscopy scoring. The mean extubation time was 7±1days in study group compared to 14±1 days in control group.Study group less showed shorter hospital stay and less mortalityrate.Conclusion: The application of aerosolize the PRP solutionin the nebulizer with regular treatment protocol of inhalationburn patients could be a beneficial therapeutic tool for regeneratingof post burn damaged tracheo-broncho-pulmonarytree. Further studies on larger patient population with clinicaland pathological evidences are warranted

Inhalation lung injury induced by smoke bombs in children: CT manifestations, dynamic evolution features and quantitative analysis.

This retrospective study aimed to investigate the computed tomography (CT) manifestations, short-term dynamic evolution features and quantitative lung CT analysis of inhalation lung injury induced by smoke bomb flare. Eleven pediatric patients (aged 11 to 13) who inhaled the smoke of smoke bombs underwent several low-dose chest CT scans. The image characteristics and their dynamic changes were observed and quantitative CT values were analyzed. The quantitative CT indicators included lung injury CT score (LICTS), lung fibrosis CT score (LFCTS), mean lung density (MLD), normally aerated volume ratio (NAVR) and reductively aerated volume ratio (RAVR). Box-plot was used to analyze the dynamic changes of each indicator and Spearman statistical method was used to analyze the correlation between any two indicators. (I) In most cases, there were multiple consolidation and massive ground-glass opacities (GGOs) in the two lungs, which aggravated in the early stage and then gradually dissoluted in the later stage. LICTS was positively correlated with MLD (r=0.811, P=0.000), while it was negatively correlated with NAVR (r=-0.712, P=0.000). There existed interstitial fibrosis in the later stage, and LFCTS was positively correlated with RAVR (r=0.382, P=0.028). (II) In one case, the patterns were like layered cake, i.e., consolidation with air bronchus signs in the accumulation area, GGOs in the aforementioned area and normal lung in the top area. The patterns aggravated in the early stage and quickly dissolved in the later stage, and only a few residual fibrotic lesions existed on the final scan. (III) For severe cases, pneumomediastinum and subcutaneous emphysema aggravated in the early stage and then gradually dissolved in the later stage. The chest CT manifestations of inhalation lung injury induced by smoke bombs are predominantly GGOs and consolidation. They aggravate in the early stage and gradual dissolute in the later stage. CT quantitative values can contribute to evaluating the extent of this disease, and NAVR and RAVR can be used to assess pulmonary function.