Airway Injury Research Articles

Clinical outcomes and complications of tracheal resection and anastomosis in dogs and cats: 20 cases (2009-2022).

To report clinical presentation, short-term outcome and complications of tracheal resection and anastomosis in dogs and cats. Clinical records of pets treated with tracheal resection and anastomosis in seven UK-based veterinaryreferral centres were retrospectively reviewed (2009 to 2022). Twenty client-owned pets (eight dogs; 12 cats) were included. Clinical signs comprised dyspnoea (n = 15), stridor (n = 5), subcutaneous emphysema (n = 3), pneumothorax and pneumomediastinum (n = 1), coughing (n = 3), regurgitation (n = 1) and exercise intolerance (n = 1). Indication for surgery was traumatic tracheal rupture (n = 5), tracheal avulsion (n = 7), neoplasia (n = 5) and stenosis (n = 3). Complications occurred in 15 patients (75%). Non-anastomotic complications occurred in nine patients and consisted of cough (n = 5), self-resolving laryngeal paralysis (n = 1), surgical site infection (n = 1) and septic shock (n = 2). Anastomotic complications occurred in seven patients and consisted of anastomotic dehiscence (n = 1), tracheal stenosis (n = 4) and fatal respiratory failure (n = 2). Revision surgery was performed in two dogs due to anastomotic dehiscence and stenosis, and tracheal stenting was performed in one cat due to stenosis. Sixteen patients survived to hospital discharge and 14 survived to latest follow-up (median: 119 days; range: 14 to 1744). Outcome was scored as excellent in five, good in seven, fair in two and poor in six patients. Tracheal resection and anastomosis is the surgical technique of choice to reconstruct tracheal defects. Although more than half of the patients recovered well, high morbidity and mortality rates were documented. This may be due to the severe comorbidities affecting most tracheal resection and anastomosis patients, as well as the client's decision against further treatment when facing serious post-operative complications.

Comparison of tissue reaction in primary tracheal repair using silk, monofilament absorbable (Polyglecaprone), and multifilament absorbable (Polyglactin 910) sutures (An experimental study on New Zealand rabbits)

Surgical interventions for tracheal trauma include repairing lacerations, reducing and closing cartilage fractures, and performing end-to-end anastomosis in cases of complete transection. One of the potential long-term complications following tracheal surgery is tracheal stenosis. The inflammatory reaction depends on the suture material used, the type of tissue being sutured, and the immune system. Several factors related to the suture material that influence the inflammatory reaction include suture absorbability, the number of filaments, suture size, and tissue reactivity to the suture. This study aimed to compare the inflammatory reaction (tissue reaction) caused by various suture materials in primary tracheal repair in male New Zealand rabbits. This experimental study employed a randomized controlled trial design, conducted on male New Zealand white rabbits. The rabbits were acclimatized for seven days, followed by permuted block randomization, dividing the samples into four groups. After the inflammatory phase (7 days), tissue reactions in the surgical area were examined post-tracheal reconstruction. Data analysis was performed using SPSS software. Each group consisted of six samples, demonstrating homogeneity in terms of age (p = 0.93), preoperative weight (p = 0.87), and postoperative weight (p = 0.88). Macroscopic evaluation showed no wound dehiscence, pus, or tracheal defects caused by suture displacement. Histopathological analysis revealed a significantly different degree of inflammation (p = 0.049) between the two treatment groups. Monofilament absorbable sutures (polyglecaprone) exhibited a lower inflammatory reaction than multifilament absorbable sutures (polyglactin 910) in primary tracheal repair, with silk sutures as the control.

23: Successful Use of Veno-venous extracorporeal membrane oxygenation (VV ECMO) for Retrieval and Peri-Operative Support for a Severe Traumatic Tracheobronchial Injury

23: Successful Use of Veno-venous extracorporeal membrane oxygenation (VV ECMO) for Retrieval and Peri-Operative Support for a Severe Traumatic Tracheobronchial Injury

Cardiac arrest after hanging: A scoping review.

Hanging is a common cause of suicide and asphyxial cardiac arrest. There are few data to inform the treatment of cardiac arrest after hanging. We designed a scoping review to describe evidence relating to interventions and outcomes in patients with and without cardiac arrest after hanging. Medline, Embase and Cochrane were searched from inception to 05/12/2024. Titles and abstracts were screened, and duplicates were removed. Articles were eligible for inclusion if they studied non-judicial hanging in adults or children, included cardiac arrest patients and provided functional or survival outcomes. The search retrieved 855 articles. One hundred and nineteen references underwent full-text review. Forty-five studies were included in the review. Studies were mainly from high-income countries and were all observational. There was variation in the terminology for hanging and in the outcomes reported. Survival with favourable functional outcome was rare in patients with cardiac arrest after hanging but was very common in patients without cardiac arrest. Cervical spine, airway and vascular injuries were rare. No studies identified interventions that were associated with improved survival following return of spontaneous circulation. There are few data to inform treatment of patients with cardiac arrest after hanging. The available data suggest that cardiac arrest is a critical determinant of poor outcome following hanging. Further research should uniformly report outcomes of patients with cardiac arrest after hanging based on the Utstein template.

Tenascin-X deficiency causing classical-like Ehlers Danlos syndrome type 1 in humans is a significant risk factor for GI and tracheal ruptures.

Classical-like Ehlers Danlos Syndrome type 1 (clEDS1) is a very rare form of Ehlers Danlos Syndrome (EDS) caused by tenascin-X (TNX) deficiency, with only 56 individuals reported. TNX is an extracellular matrix protein needed for collagen stability. Previous publications propose that individuals with clEDS1 might be at risk for gastrointestinal (GI) tract perforations and/or tracheal ruptures. To characterize complications resulting from perforations of the GI tract and/or tracheal rupture in an international case series of individuals with clEDS1 due to disease-related tissue fragility. This case series includes individuals with confirmed clEDS1 and GI perforations and/or tracheal ruptures from participating centres. Researchers who previously reported such individuals were contacted for additional information. A retrospective assessment of clinical features was performed. Fifteen individuals were included. Ten had spontaneous GI perforations, seven of whom had multiple GI perforations. Almost all had severe diverticulosis. Three individuals experienced iatrogenic tracheal ruptures. Severe GI complications, such as perforation, and tracheal rupture were observed in a substantial number of individuals with clEDS1. As these features seem significantly more common in clEDS1 than in the average population, we advise vigilance during intubation and GI endoscopic interventions of individuals with clEDS1. Routine referrals to clinical geneticists are recommended for patients with symptoms indicative of clEDS1, especially with unexplained GI perforations and connective tissue symptoms. Our findings offer valuable insights for the clinical management of clEDS1 and underscore the importance of specialized care, providing a foundation for improved clinical guidelines and preventive strategies.

FATORES PREDITORES NA SÍNDROME DO DESCONFORTO RESPIRATÓRIO AGUDO EM PACIENTES COM A DOENÇA PULMONAR OBSTRUTIVA CRÔNICA: UMA REVISÃO INTEGRATIVA DE LITERATURA

Acute Respiratory Distress Syndrome (ARDS) is characterized by severe respiratory failure and represents a critical complication, often associated with the need for mechanical ventilation (MV). Chronic Obstructive Pulmonary Disease (COPD) is defined as a progressive condition that causes airway obstruction and injury to the lung parenchyma, often associated with smoking, and is one of the main causes of morbidity and mortality worldwide. Thus, patients with COPD are particularly susceptible to ARDS due to chronic impairment of the components of the respiratory system. This study addresses the relationship between COPD and ARDS, and aimed to identify the main predictors of ARDS in this population. Thus, this integrative literature review followed a methodological design that involved searching the PubMed, BVS and Scopus databases, with the selection of articles published in the last ten years. The research identified five relevant studies, which indicated factors such as COPD exacerbations, use of MV, advanced age, sepsis and environmental factors as predictors of ARDS in patients with COPD. Although the studies showed an association between these conditions, the scarcity of specific research on predictors of ARDS in patients with COPD was an important limitation, but among the studies of the qualitative analysis, 8,431 patients and 26 reviews were evaluated that comprised the 2024 meta-analysis evaluated, which strengthens the evidence on the subject.

Left main bronchial rupture: bronchoscopy and chest CT.

Left main bronchial rupture: bronchoscopy and chest CT.

Acute exposure to nitrogen mustard induces rapid nuclear component regulation and delayed stress to exogenous stimuli.

Nitrogen mustard (NM) is a vesicant agent with potent toxic effects on various tissues. Numerous theories have been proposed to explain its toxic mechanisms, yet research on the interconnections among these theories is lacking. This study focuses on analyzing the characteristics of genes involved in NM-induced bronchial injury within the Comparative Toxicogenomics Database (CTD). Subsequently, based on the CTD, we compared and analyzed the acute exposure and delayed changes following exposure in 16HBE cells. The injury processes caused by NM to bronchial and skin tissues are similar, primarily involving metabolism and regulation of nuclear constituents and inflammatory responses within the cellular matrix. During the acute exposure phase, NM rapidly induces nuclear stress, with the JUN family at the core of regulating metabolic and nucleic acid activities, and various nuclear binding proteins exhibit abnormalities. Delayed reactions following acute exposure are primarily centered in the cytoplasmic region, with diverse reaction types, including oxidative stress and responses to exogenous stimuli. Abnormalities in the activity of multiple cellular matrix enzymes are observed, with a relatively even involvement of various stress responses. Communication between the nucleus and cytoplasm is extreme active during the injury, and the content of the communication changes over time. These results suggest a temporal sequence in which NM causes chromatin damage and mediates cytoplasmic stress responses. In prevention and first aid, rapid DNA repair should be the primary focus, while subsequent treatment after acute exposure should focus more on delayed inflammatory and oxidative stress responses.

Combating COVID-19 and its co-infection by Aspergillus tamarii SP73-EGY using in vitro and in silico Studies

The COVID-19 pandemic has caused significant mortality and morbidity for millions of people. Severe Acute Respiratory Syndrome-2 (SARS-CoV-2) virus is capable of causing severe and fatal diseases. We evaluated the antiviral properties of Aspergillus tamarii SP73-EGY isolate extract against low pathogenic coronavirus (229E), Adeno-7- and Herpes-2 viruses. The extract showed a high selectivity index (SI = 43.4) and a significant inhibition of 229E (IC50 = 8.205 μg/ml). It was stronger than the drug control, remdesivir (IC50 = 38.2 μg/ml, SI = 7.29). However, the extract showed minimal efficacy against Adeno-7- and Herpes-2-Viruses (IC50 = 22.52, 47.79 μg/ml, and SI = 6.75, 5.08, respectively). It exhibited profound efficacy against the highly pathogenic SARS-CoV-2 (IC50 = 8.306 μg/ml, SI = 42.2). Kojic acid, the primary component of the extract, showed substantial antiviral activity against SARS-CoV-2 (IC50 = 23.4 μg/ml, SI = 5.6), Remdesivir (IC50 = 4.55 μg/ml, SI = 61.45). Therefore, the extract demonstrated the most notable antiviral characteristics against coronavirus infection. Co-infecting microorganisms may contribute to immune system deterioration and airway injury caused by SARS-CoV-2. The extract showed significant efficacy against E. coli and P. aeruginosa, with an inhibition range of 3.5–10 mm at a concentration of 200 mg/ml. A molecular docking study showed that hexadecanoic, Kojic, octanoic acids, and 4(4-Methylbenzylidene)cyclohexane-1,3-dione have stronger binding affinity to the SARS-CoV-2 Mpro than Remdesivir. Molecular dynamics simulations were employed to examine the structural stability and flexibility of these complexes. This confirmed the high binding affinities of Kojic acid and 4(4-Methylbenzylidene)cyclohexane-1,3-dione, thereby proving their potential as novel anti-SARS-CoV-2.

Cold stimulated bronchial epithelial cells derived exosomes HMGB1 aggravates bronchial epithelial cells injury.

The aim of this study was to reveal the mechanism of cold stimulation (CS)-bronchial epithelial cells (BECs) derived exosomes (CS-BECs-exo) aggravated sepsis induced acute lung injury (SALI). CS-BECs-exo were separated by differential centrifugation and were characterized. Proteomics, immunoprecipitation, and RAGE knockout (RAGE) mice were used to investigate the mechanism of CS-BECs-exo aggravated SALI. The results of transmission electron microscope (TEM) showed that CS-BECs-exo showed a double-layer membrane structure like a saucer. Nanoparticle tracking analysis (NTA) particle size analysis showed that the average particle size of CS-BECs-exo was 123.6 nm. The results of proteomics showed that the expression level HMGB1 was significantly increased in CS-BECs-exo compared with BECs-exo. CS-BECs-exo significantly increased oxidative stress and inflammatory reaction of SALI. In addition, CS-BECs-exo significantly increased RAGE and decreased the levels of Nrf-2 and OH-1. RAGE knockout (RAGE KO) and silence of RAGE (RAGE siRNA) significantly canceled the effects of CS-BECs-exo on SALI. HMGB1 knockout (HMGB1) and silence of HMGB1 also significantly (HMGB1 siRNA) canceled the effects of CS-BECs-exo on SALI. In conclusion, CS-BECs-exo aggravated ALI in sepsis via HMGB1/RAGE/Nrf-2/OH-1 signal pathway.

Pediatric bronchial rupture: outcomes in four cases.

Pediatric bronchial rupture: outcomes in four cases.

Successful Management of Delayed Left Main Bronchus Rupture with End-to-End Anastomosis

Successful Management of Delayed Left Main Bronchus Rupture with End-to-End Anastomosis

Traumatic bronchial injury management

Traumatic bronchial injury management

Endoscopic treatment of intermediate bronchus rupture in a 4-year-old child with polytrauma

BACKGROUND: In the structure of childhood traumatism, thoracic trauma occurs in less than 10% of cases, but it is the second most likely cause of death in children. A bronchial rupture that disrupts adequate ventilation of the lungs can be the culprit of the fatal outcome. The purpose of our publication is to demonstrate a rare clinical observation of successful endoscopic treatment of an intermediate bronchus rupture in a 4-year-old child with polytrauma. CLINICAL CASE DESCRIPTION: A 4-year-old boy was injured in a traffic accident as a pedestrian. During the first three days, he was treated for multiple injuries (Injury Severity Score 41) in a local hospital where, because of emergency indications, drainage of the right pleural cavity with two drains for tension pneumothorax and laparotomy for intra-abdominal bleeding due to liver rupture were done. Because of patient’s relative stabilization by the 3rd post-trauma day, he was transferred to our clinic (level 1 trauma center). We could stabilize his hemodynamics; however, air blowing through the drains was maintained, complete straightening of the parenchyma of the right lung was not reached, and blood gas composition remained subcompensated. On day 5 of the post-traumatic period, laryngotracheobronchoscopy was performed, and the rupture of intermediate bronchus measuring 3×9 mm was diagnosed. Its occlusion with a positive effect was done. After 7 days, laryngotracheobronchoscopy was repeated, and blockers were removed. After that, complete straightening of the right lung was reached; no recurrence of bronchopulmonary fistula. Long mechanical ventilation and long hospital stay were results of severe traumatic brain injury. At the follow-up visit in a year, no pathology in respiratory organs was detected at clinical laboratory, radiological and endoscopic examination. CONCLUSION: Bronchial rupture may be a cause of inadequate ventilation and aggravation of the post-traumatic period in a polytrauma patient. The present observation demonstrates that intraluminal endoscopy allows to timely detect the rupture of the large bronchus and to perform a minimally invasive surgical treatment. Such a tactics ensured further positive dynamics in child's condition and favorable outcomes after polytrauma, as a whole.

Hemoptysis caused by bronchial artery-pulmonary artery fistula complicated with Dieulafoy disease: A case report.

Bronchial artery-pulmonary artery fistula (BPF) is a rare vascular malformation of the bronchial arteries, associated with congenital heart disease, pulmonary hypertension, or pulmonary infections. It typically presents in adulthood and has a low incidence. Another rare vascular anomaly, bronchial Dieulafoy disease (BDD), is characterized by an abnormally developed artery within the submucosa of the bronchial tree. This condition is thought to arise from a combination of congenital dysplasia and chronic airway inflammation or injury. Both BPF and BDD are uncommon causes of hemoptysis, and their simultaneous occurrence is exceptionally rare. This report discusses a case of BPF complicated by BDD in a patient who presented with recurrent hemoptysis. The diagnosis was established through bronchial artery angiography, bronchoscopy, and surgical pathology. By examining the clinical features, imaging findings, and diagnostic criteria of these conditions, this case report aims to enhance clinicians' understanding of cryptogenic hemoptysis and provide valuable insights for clinical practice.

A Case of Posterior Tracheal Wall Rupture During Tracheostomy Treated With Sternocleidomastoid Muscle Reinforcement

A posterior tracheal wall rupture is a rare but life-threatening complication of tracheostomy. Several flaps based on the sternocleidomastoid (SCM) muscle, which has sufficient length and abundant blood supply, are utilized for the reconstruction of tracheal defects. We discuss here a case of a 71-year-old male with multiple organ failure and mental retardation, with posterior tracheal wall damage that had occurred during tracheostomy tube insertion. When planning the repair of the wound, additional reinforcement was necessary due to saliva leakage secondary to decreased consciousness. Direct suturing was followed by the reinforcement of SCM muscle transposition, which was conducted through cervical and endoscopic approach.

Oxidative Injury to Lung Mitochondrial DNA is a Key Contributor for the Development of Chemical Lung Injury.

The mechanisms and extent to which inhalation of oxidant gases damage the mitochondrial genome contributing to the development of acute and chronic lung injury have not been investigated. C57BL/6 mice exposed to chlorine (Cl 2 ) gas and returned to room air, developed progressive loss of lung DNA glycosylase OGG1, significant oxidative injury to mtDNA, decreased intact lung mitochondrial (mt) DNA, generation of inflammatory pathway by DAMPs causing airway and alveolar injury with significant mortality. Global proteomics identified over 1400 lung proteins with alteration of key mitochondrial proteins at 24 h post Cl 2 exposure. Intranasal instillation of a recombinant protein containing mitochondrial targeted OGG1 (mitoOGG1) post exposure, decreased oxidative injury to mtDNA, lung mitochondrial proteome, severity of the acute and chronic lung injury and increased survival. These data show that injury to the mt-genome is a key contributor to the development of acute and chronic lung injury.

Identification of Nicotinic Acetylcholine Receptor for N-Acetylcysteine to Rescue Nicotine-induced Injury Using BeatingCilia in Primary Tissue Derived Airway Organoids.

Smoking is one of the major contributors to airway injuries. N-acetylcysteine (NAC) has been proposed as a treatment or preventive measure for such injuries. However, the exact nature of the smoking-induced injury and the protective mechanism of NAC are not yet fully understood. Here, patient tissue-derived airway organoids for modeling smoking-induced injury, therapeutic investigation, and mechanism studies are developed. Airway organoids consist mainly of ciliated cells, together with basal cells, goblet cells, and myofibroblast-like cells. The organoids display apical-out and basal-in polarity and are enriched in beating cilia, which are sensitive to smoking challenge and NAC treatment. An algorithm is developed to measure ciliary beating activity by analyzing the altered beating pattern of cilia in response to nicotine challenge and NAC treatment. Nicotinic acetylcholine receptors (nAChRs) expressed by airway organoids are involved in the mechanisms of nicotine-induced injury through the nicotine-nAChR pathway. In contrast to the common understanding that NAC has an antioxidative effect that mitigates airway damage, it is elucidated that NAC binding to nicotine can abolish the binding capacity of nicotine to nAChRs and thus prevent nicotine-induced injury. This study focuses on the advances and potential of humanized organoids in understanding biological processes, mechanisms, and identifying therapeutic targets.

Tips and tricks in the operative management of esophageal, trachea, and bronchial injuries: What you need to know.

Tracheal injuries can be immediately life-threatening. Fiberoptic bronchoscopy in the operating room can make the diagnosis and satisfy the principle of achieving an airway distal to the injury. Repair is performed with a single layer of absorbable suture. Esophageal injuries are diagnosed with imaging, endoscopy, or intraoperatively. In the chest, esophageal injuries are best repaired through posterolateral incisions. Repairs are performed in one or two layers, and drains are routinely used. For a damage-control approach to esophageal injuries, wide drainage can be considered. For both tracheal and esophageal injuries, the operative approach is based on the anatomic location of the injury and muscle flap buttressing of the repairs is routinely employed.

The Role of Gastroesophageal Reflux in Airway Inflammation.

Gastroesophageal reflux disease occurs when the barrier at the esophagogastric junction is weakened, allowing for transient relaxations of the lower esophageal sphincter or disruption of the esophagogastric junction. This leads to the refluxate traveling up the esophagus, and potentially into the pharynx, where it can be aspirated into the airway. The refluxate can cause a range of symptoms, including sore throat, coughing, wheezing, and shortness of breath, which may occur with or without visible airway inflammation. Both experimental and clinical studies have shown that aspirated refluxate can directly damage the airway lining and trigger immune responses that contribute to airway injury and inflammation. While traditional diagnostic tests for gastroesophageal reflux disease can identify abnormal reflux patterns, there is a need for more specific methods to predict airway inflammation or therapeutic outcomes related to reflux aspiration.