Traumatic Lung Research Articles

Accurate identification of traumatic lung injury (TLI) by ATR-FTIR spectroscopy combined with chemometrics

Traumatic lung injury (TLI), which is a common mechanical injury, is receiving increasing attention because of its serious hazards. In forensic practices, accurately identifying TLI is of great importance for investigations and case trials. The main goal of this research was to identify TLI utilizing attenuated total reflection-Fourier transform infrared (ATR-FTIR) spectroscopy in combination with chemometrics. The macroscopic appearance of lung tissue showed that identifying TLI in lung tissue at the decomposition stage is not feasible by only visualization, and significant pulmonary hypostasis was observed in the lungs regardless of whether the lung tissue was injured. Average spectra and principal component analysis (PCA) suggested that the biochemical difference between injured lung tissue samples from the TLI group and noninjured lung tissue samples from the negative control group was mainly attributed to the different structures and contents of proteins. Partial least squares discriminant analysis (PLS-DA) was then utilized to identify TLI with an accuracy of 96.4% and 98.6% based on the training set and the test set, respectively. Next, we focused on samples that were misclassified in the model and proposed that the misclassification could be caused by the pulmonary hypostasis effect. Therefore, two additional PCA and PLS-DA models were created to identify the pulmonary hypostatic areas between the TLI group and the negative control group and the nonpulmonary hypostatic areas between the TLI group and the negative control group. The PCA results indicated that the biochemical difference between the two groups was still associated with proteins, and the two PLS-DA models achieved 100% accuracy based on both the training and test sets. This result indicated that when pulmonary hypostasis was considered and the lung tissue was divided into pulmonary hypostatic areas and nonpulmonary hypostatic areas for separate comparisons, TLI identification was achieved with a greater accuracy than that obtained when the two areas were combined. This research confirms that the combined application of ATR-FTIR spectroscopy and chemometrics can be utilized to accurately identify TLI.

Gastrointestinal consequences of lipopolysaccharide-induced lung inflammation

BackgroundRespiratory inflammation is the body’s response to lung infection, trauma or hypersensitivity and is often accompanied by comorbidities, including gastrointestinal (GI) symptoms. Why respiratory inflammation is accompanied by GI dysfunction remains unclear. Here, we investigate the effect of lipopolysaccharide (LPS)-induced lung inflammation on intestinal barrier integrity, tight-junctions, enteric neurons and inflammatory marker expression.MethodsFemale C57bl/6 mice (6–8 weeks) were intratracheally administered LPS (5 µg) or sterile saline, and assessed after either 24 or 72 h. Total and differential cell counts in bronchoalveolar lavage fluid (BALF) were used to evaluate lung inflammation. Intestinal barrier integrity was assessed via cross sectional immunohistochemistry of tight junction markers claudin-1, claudin-4 and EpCAM. Changes in the enteric nervous system (ENS) and inflammation in the intestine were quantified immunohistochemically using neuronal markers Hu + and nNOS, glial markers GFAP and S100β and pan leukocyte marker CD45.ResultsIntratracheal LPS significantly increased the number of neutrophils in BALF at 24 and 72 h. These changes were associated with an increase in CD45 + cells in the ileal mucosa at 24 and 72 h, increased goblet cell expression at 24 h, and increased expression of EpCAM at 72 h. LPS had no effect on the expression of GFAP, S100β, nor the number of Hu + neurons or proportion of nNOS neurons in the myenteric plexus.ConclusionsIntratracheal LPS administration induces inflammation in the ileum that is associated with enhanced expression of EpCAM, decreased claudin-4 expression and increased goblet cell density, these changes may contribute to systemic inflammation that is known to accompany many inflammatory diseases of the lung.

Applications of Ultrasonography in Respiratory Intensive Care

Emerging evidence suggests that ultrasonography of lung is a fast, inexpensive, widely available bed-side diagnostic tool which is useful for quick and early diagnosis of respiratory diseases. It is useful in the differential diagnosis of pulmonary infiltrates and has good accuracy in identifying consolidation and alveolar-interstitial syndrome. This technique can also be useful in the immediate evaluation of patients with dyspnoea or acute respiratory failure in the respiratory intensive care unit and helps in monitoring treatment response. Ultrasonography of lung has also been found to be useful in the diagnosis of pulmonary embolism, traumatic lung contusion and lung consolidation as well. There is a need for developing specific guidelines for establishing the standards of training and education regarding lung ultrasonography in India.

Adoptively Transferred in vitro-Generated Myeloid-Derived Suppressor Cells Improve T-Cell Function and Antigen-Specific Immunity after Traumatic Lung Injury

Immune reactions after trauma are characterized by immediate activation of innate immunity and simultaneously downregulation of adaptive immunity leading to a misbalanced immunohomeostasis and immunosuppression of the injured host. Therefore, the susceptibility to secondary infections is strongly increased after trauma. Immune responses are regulated by a network of immune cells influencing each other and at the same time modifying their functions dependent on the inflammatory environment. Although myeloid-derived suppressor cells (MDSCs) are initially described as T-cell suppressors, their immunomodulatory capacity after trauma is mostly undefined. Therefore, in vitro-generated MDSCs were adoptively transferred into mice after blunt chest trauma (TxT). A single MDSC treatment-induced splenic T-cell expansion decreased apoptosis sensitivity and improved proliferation in the absence of T-cell exhaustion until 2 weeks after trauma. MDSC treatment had a long-lasting effect on the genomic landscape of CD4+ T cells by upregulating primarily Th2-associated genes. Remarkably, immune-activating functions of MDSCs supported the ability of TxT mice to respond to post-traumatic secondary antigen challenge. Secondary insults were mimicked by immunizing MDSC-treated TxT mice with ovalbumin (OVA), followed by OVA restimulation in vitro. MDSC treatment significantly increased the frequency of OVA-specific T cells, enhanced their Th1/Th2 cytokine expression, and induced upregulation of cytolytic molecules finally improving OVA-specific cytotoxicity. Overall, we could show that therapeutic MDSC treatment after TxT improves post-traumatic T-cell functions, which might enable the traumatic host to counterbalance trauma-induced immunoparalysis.

ECMO for paediatric cardiac arrest caused by bronchial rupture and severe lung injury: a case report about life-threatening rescue at an adult ECMO centre

BackgroundBronchial rupture in children is a rare but dangerous complication after chest trauma and is associated with increased mortality. Veno-venous (V-V) extracorporeal membrane oxygenation (ECMO) is reported as one of the treatments for this life-threatening complication.Case presentationA 4-year-old boy with bronchial rupture and traumatic wet lung complicated by cardiac arrest after chest trauma was admitted to an adult ECMO centre. He experienced two cardiac arrests, one before and one during the operation. The total duration of cardiac arrest was 30 min. V-V ECMO was initiated because of severe hypoxia and hypercapnia during the operation. ECMO was performed for 6 days, and mechanical ventilation lasted 11 days. On the 31st day after surgery, he had recovered completely and was discharged without neurological deficit.ConclusionV-V ECMO can be considered for supportive care in children with severe acute respiratory failure after bronchial rupture. In an emergency, V-V ECMO can be carried out effectively in a qualified and experienced adult ECMO centre. However, the application of ECMO in children is different from that in adults and requires more refined management.

Acute respiratory distress syndrome

There are several medical conditions that directly or indirectly lead to pulmonary destruction or acute lung injury or Acute Respiratory Distress Syndrome e.g. Sepsis, Inhalation of harmful substances, severe pneumonia, Head, chest, or another major injury, Pancreatitis (inflammation of the pancreas), massive blood transfusions and burns. Due to some incidences involved in the etiology of ARDS and limited information about the epidemiology, recognition, management, and less significant results regarding patients with acute respiratory distress syndrome (ARDS), shows intense research on ARDS is needed. From an earlier time, this syndrome has been given many names, including congestive atelectasis, traumatic adult respiratory distress syndrome and shock lung. Recently, the new definition of ARDS has been published, and this definition suggested severity-oriented respiratory treatment by introducing three levels of severity consistent with PaO2/FiO2 and positive end-expiratory pressure. Lung-protective ventilation is still the key to a better outcome in ARDS. ARDS is said to a selection of etiologies, carries high morbidity, mortality (10to 90%), and financial cost. This review is an attempt to compile all aspects of the management of ARDS.

A Rationale for Safe Ventilation with Inhalation Injury: An Editorial Review.

Lung injury from smoke inhalation manifests as airway and parenchymal damage, at times leading to the acute respiratory distress syndrome. From the beginning of this millennium, the approach to mechanical ventilation in the patient with ARDS was based on reduction of tidal volume to 6 milliliters/kilogram of ideal body weight, maintaining a ceiling of plateau pressure, and titration of driving pressure (plateau pressure minus PEEP). Beyond these broad constraints, there is little specification for the mechanics of ventilator settings, consideration of the metabolic impact of the disease process on the patient, or interaction of patient disease and ventilator settings. Various studies suggest that inhomogeneity of lung injury, which increases the risk of regional lung trauma from mechanical ventilation, may be found in the patient with smoke inhalation. We now appreciate that energy transfer principles may affect optimal ventilator management and come into play in damaged heterogenous lungs. Mechanical ventilation in the patient with inhalation injury should consider various factors. Self-injurious respiratory demand by the patient can be reduced using analgesia and sedation. Dynamic factors beginning with rate management can reduce the incidence of potentially damaging ventilation. Moreover, preclinical study is underway to examine the flow of gas based on the ventilator mode selected, which may also be a factor triggering regional lung injury.

N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-κB pathways

ABSTRACT Lung ischemia/reperfusion (I/R) injury (LIRI) is a common complication after lung transplantation, embolism, and trauma. N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of I/R injury. However, there are no or few reports of m6A-related regulators in LIRI till now. In this text, dysregulated genes in lung tissues of LIRI rats versus the sham group were identified by RNA sequencing (RNA-seq). RNA-seq outcomes revealed that only YTH N6-methyladenosine RNA binding protein 3 (YTHDF3) and insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) were differentially expressed in the LIRI versus sham group among 20 m6A-related regulators. Next, the functions and molecular mechanisms of YTHDF3 and IGF2BP2 in LIRI were investigated in a hypoxia/reoxygenation-induced BEAS-2B cell injury model in vitro. Results showed that YTHDF3 or IGF2BP2 knockdown attenuated hypoxia/reoxygenation-mediated inhibitory effects on cell survival and cell cycle progression and inhibited hypoxia/reoxygenation-induced cell apoptosis and pro-inflammatory cytokine secretion in BEAS-2B cells. Genes that could be directly regulated by YTHDF3 or IGF2BP2 were identified based on prior experimental data and bioinformatics analysis. Moreover, multiple potential downstream pathways of YTHDF3 and IGF2BP2 were identified by the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analysis of the above-mentioned genes. Among these potential pathways, we demonstrated that YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-κB pathways in BEAS-2B cells. In conclusion, YTHDF3 or IGF2BP2 knockdown weakened hypoxia/reoxygenation-induced human lung bronchial epithelial cell injury by inactivating p38, AKT, ERK1/2, and NF-κB pathways.

The Reaction Pathway of miR-30c-5p Activates Lipopolysaccharide Promoting the Course of Traumatic and Hemorrhagic Shock Acute Lung Injury.

Acute lung injury (ALI) is an acute hypoxic respiratory failure caused by diffuse inflammatory injury in alveolar epithelial cells during severe infection, trauma, and shock. Among them, trauma/hemorrhagic shock (T/HS) is the main type of indirect lung injury. Despite a great number of clinical studies, indirect factor trauma/hemorrhagic shock to the function and the mechanism in acute lung injury is not clear yet. Therefore, it is still necessary to carry on relevant analysis in order to thoroughly explore its molecular and cellular mechanisms and the pathway of disease function. In our research, we aimed to identify potential pathogenic genes and do modular analysis by downloading disease-related gene expression profile data. And our dataset is from the NCBI-GEO database. Then, we used the Clusterprofiler R package, GO function, and KEGG pathway enrichment analysis to analyze the core module genes. In addition, we also identified key transcription factors and noncoding RNAs. Based on the high degree of interaction of potential pathogenic genes and their involved functions and pathways, we identified 17 dysfunction modules. Among them, up to 9 modules significantly regulate the response to bacterial-derived molecules, and the response to lipopolysaccharide and other related functional pathways that mediate disease development. In addition, miR-290, miR-30c-5p, miR-195-5p, and miR-1-3p-based ncRNA and Jun, Atf1, and Atf3-based transcription factors have a total of 80 transcription drivers for functional modules. In summary, this study confirmed that miR-30c-5p activates lipopolysaccharide response pathway to promote the pathogenesis of ALI induced by hemorrhagic shock. This result can be an important direction for further research on related deepening diseases such as acute respiratory distress syndrome (ARDS). It further provides a piece of scientific medical evidence for revealing the pathogenic principle and cure difficulty of acute lung injury and also provides important guidance for the design of therapeutic strategies and drug development.

Evaluating the Limits in the Biomechanics of Blunt Lung Injury.

Thoracic blunt trauma is evident in up to one-fifth of all hospital admissions, and is second only to head trauma in motor vehicle crashes. One of the most problematic injury mechanisms associated with blunt thoracic trauma is pulmonary contusion, occurring in up to 75% of blunt thoracic trauma cases. The source and effects of pulmonary contusion caused by blunt lung injury are not well defined, especially within the field of continuum biomechanics. This, paired with unreliable diagnostics for pulmonary contusion, leads to uncertainty in both the clinical entity and mechanics of how to predict the presence of injury. There is a distinct need to combine the clinical aspects with mechanical insights through the identification and mitigation of blunt lung trauma and material testing and modeling. This is achieved through using the mechanical insights of lung tissue behavior in order to better understand the injurious mechanisms and courses of treatment of blunt-caused pulmonary contusion. This paper hopes to act as a step forward in connecting two perspectives of blunt lung injury, the clinical entity, and mechanical testing and modeling, by reviewing the known literature and identifying the unknowns within the two related fields. Through a review of related literature, clinical evidence is correlated to mechanical data to gain a better understanding of what is being missed in identification and response to blunt lung injury as a whole.

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.

Posttraumatic pneumonectomy and management of severely contaminated pleural space.

Posttraumatic pneumonectomy and management of severely contaminated pleural space.

Lung hemorrhage in trauma: Technical tricks and tips

At some point as the on-call trauma surgeon, you may need to operate on a bleeding lung. This concise review addresses preoperative and intraoperative considerations for traumatic lung injuries, including how to deal with specific findings at the time of surgery.

Traumatic lung pathologies confused with COVID-19

Traumatic lung pathologies confused with COVID-19

Retraction for Li et al., volume 316, 2019, p. L1107-L1117.

RetractionRetraction for Li et al., volume 316, 2019, p. L1107–L1117Published Online:09 Dec 2021https://doi.org/10.1152/ajplung.00391.2018_RETRetracted articleMoreSectionsPDF (98 KB)Download PDFDownload PDFPlus ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmail Li QC, Liang Y, Su ZB. Prophylactic treatment with MSC-derived exosomes attenuates traumatic acute lung injury in rats. Am J Physiol Lung Cell Mol Physiol 316: L1107–L1117, 2019. First published March 20, 2019; doi:10.1152/ajplung.00391.2018.The American Physiological Society is retracting this article at the request of the authors. The authors were unable to replicate the findings when attempting to repeat the study. The authors apologize for the inconvenience caused by the retraction of this article.This article has no references to display. Previous Back to Top FiguresReferencesRelatedInformationRelated articlesProphylactic treatment with MSC-derived exosomes attenuates traumatic acute lung injury in rats 29 May 2019American Journal of Physiology-Lung Cellular and Molecular Physiology More from this issue > Volume 321Issue 6December 2021Pages L1215-L1215 Crossmark Copyright & PermissionsCopyright © 2021 the American Physiological Society.https://doi.org/10.1152/ajplung.00391.2018_RETPubMed34882504History Published online 9 December 2021 Published in print 1 December 2021 PDF download Metrics Downloaded 287 times

Ventilation-induced epithelial injury drives biological onset of lung trauma in vitro and is mitigated with prophylactic anti-inflammatory therapeutics.

Mortality rates among patients suffering from acute respiratory failure remain perplexingly high despite the maintenance of blood oxygen homeostasis during ventilatory support. The biotrauma hypothesis advocates that mechanical forces from invasive ventilation trigger immunological mediators that spread systemically. Yet, how these forces elicit an immune response remains unclear. Here, a biomimetic in vitro three‐dimensional (3D) upper airways model allows to recapitulate lung injury and immune responses induced during invasive mechanical ventilation in neonates. Under such ventilatory support, flow‐induced stresses injure the bronchial epithelium of the intubated airways model and directly modulate epithelial cell inflammatory cytokine secretion associated with pulmonary injury. Fluorescence microscopy and biochemical analyses reveal site‐specific susceptibility to epithelial erosion in airways from jet‐flow impaction and are linked to increases in cell apoptosis and modulated secretions of cytokines IL‐6, ‐8, and ‐10. In an effort to mitigate the onset of biotrauma, prophylactic pharmacological treatment with Montelukast, a leukotriene receptor antagonist, reduces apoptosis and pro‐inflammatory signaling during invasive ventilation of the in vitro model. This 3D airway platform points to a previously overlooked origin of lung injury and showcases translational opportunities in preclinical pulmonary research toward protective therapies and improved protocols for patient care.

Pulmonary injury as a predictor of cerebral hypoxia in traumatic brain injury: from physiology to physiopathology.

Traumatic brain injury is caused by mechanical forces impacting the skull and its internal structures and constitutes one of the main causes of morbidity and mortality in the world. Clinically, severe traumatic brain injury is associated with the development of acute lung injury and so far, few studies have evaluated the cellular, molecular and immunological mechanisms involved in this pathophysiological process. Knowing and investigating these mechanisms allows us to correlate pulmonary injury as a predictor of cerebral hypoxia in traumatic brain injury and to use this finding in decision making during clinical practice. This review aims to provide evidence on the importance of the pathophysiology of traumatic brain injury-acute lung injury, and thus confirm its role as a predictor of cerebral hypoxia, helping to establish an appropriate therapeutic strategy to improve functional outcomes and reduce mortality.

FOLLICULIN GENE MUTATION IN A YOUNG WOMAN WITH RECURRENT PNEUMOTHORAX

TOPIC: Genetic and Developmental Disorders TYPE: Medical Student/Resident Case Reports INTRODUCTION: Folliculin (FLCN) gene mutation, commonly linked with Birt-Hogg-Dube (BHD) syndrome, is associated with primary spontaneous pneumothorax (PSP). PSP is defined by air in the pleural space in those without a history of lung disease or trauma. A pneumothorax (PTX) can be a life-threatening condition that requires immediate tube thoracostomy placement. Here, we present a case of recurrent PSP in a woman presenting with dyspnea. CASE PRESENTATION: A 36-year-old woman non-smoker with a history of unclassified bullous lung disease and recurrent PTX status post right video assisted thoracoscopic surgery (VATS) with mechanical pleurodesis and left VATS with talc pleurodesis presented to the emergency department (ED) with progressive dyspnea. Family history was notable for bullous lung disease and PTX in her maternal grandfather and mother. Days prior to ED, she developed right sided pleuritic chest pain after yoga that self-resolved. Chest radiography revealed right sided pleural effusion without signs of PTX. A day prior to the ED, she developed dyspnea with exertion. On admission, she was at 100% saturation on room air, normotensive and had decreased breath sounds in her right lower lung field. Computed tomography (CT) revealed a new large right basilar, anterior, medial PTX and redemonstration of multiple bilateral bullae unchanged from prior imaging. VATS was recommended but refused. A 10.3 French chest tube was placed to wall suction overnight. Repeat CT revealed near complete resolution of the PTX with unchanged bullae. Genetics workup revealed an FLCN mutation c.1584del; p.Glu530Argfs*7 suggesting the cause of recurrent PTX. DISCUSSION: A diagnosis of PSP requires the exclusion of lung diseases such as cystic fibrosis and alpha-1-antitrypsin, connective tissue disorders such sjogren's and marfan syndromes, rare conditions such as lymphangioleiomyomatosis and tuberous sclerosis. PSP commonly occurs due to rupture of subpleural bullae and can be a complication of BHD syndrome. BHD syndrome is a hereditary cancer disorder characterized by renal cell cancer, colonic polyps, hair follicle hamartomas, lung cysts and PTX. It is associated with a FLCN gene mutation, which is expressed in type I pneumocytes that form the structure of alveoli. FLCN mutation lung cysts are hypothesized to be due to a defect in cell-cell adhesion resulting in expansion of alveolar spaces. FLCN mutation patients can rarely present with a purely spontaneous PTX. PSP treatment options include a chest tube (recurrence rate (RR) 26.4%), VATS pleurectomy (RR 0.4%), VATS abrasion (RR 2.3%) and lung transplantation. CONCLUSIONS: A FLCN gene mutation should be excluded in those with recurrent PTX. Genetic testing should be considered as well as appropriate cancer screening with renal ultrasound and colonoscopy given its association with BHD. REFERENCE #1: Boone, P. M. et al. (2019). The genetics of pneumothorax. AJRCCM, 199(11), 1344-1357. REFERENCE #2: Daccord, C. et al. (2020). Birt–Hogg–Dubé syndrome. European Respiratory Review, 29(157), 200042. REFERENCE #3: Frohlich, B. et al. (2008). Novel mutations in the folliculin gene associated with spontaneous pneumothorax. European Respiratory Journal, 32(5), 1316-1320. DISCLOSURES: No relevant relationships by George Moran, source=Web Response No relevant relationships by Hekmat Nasiri, source=Web Response No relevant relationships by Sudhir Rajan, source=Web Response

LUNG HERNIATION: A RARE RESULT OF CPR

TOPIC: Lung Pathology TYPE: Medical Student/Resident Case Reports INTRODUCTION: Lung herniation as a result of cardiopulmonary resuscitation (CPR) is a rare condition whereby the pleura-covered lung parenchyma protrudes through a defect in the chest wall. CASE PRESENTATION: A 70-year-old male with a history of end stage renal disease on dialysis and heart failure presented to the hospital with three weeks of progressive dyspnea and diagnosed with pulmonary edema. He was started on hemodialysis for volume removal. On hospital day four, the patient developed cardiac arrest, and was found to be in hemorrhagic shock, with massive hemorrhage from his dialysis fistula. The patient underwent high quality chest compressions while receiving standard advanced cardiac life support and a massive transfusion protocol. After return of spontaneous circulation and control of the bleeding, a right chest mass was palpated. Imaging demonstrated multiple consecutive right anterior rib and costochondral junction fractures resulting in flail chest and a large anterior herniation of the lung with an associated moderate hemothorax. A thoracostomy tube was offered as was surgical fixation; however, the patient's family decided to pursue comfort measures. DISCUSSION: Lung herniation is an extremely rare entity first described in association with CPR in 1986. Since then, there have been only seven cases of lung herniation after CPR reported in the literature. Furthermore, an occurrence with chondrosternal disruption is even more uncommon, such as our patient with flail chest. When providing high-quality chest compressions, traumatic injuries to the sternum and ribs is often unavoidable and rate of injury does not vary based on medical training of compressor nor patient factors such as age and gender. However, certain comorbidities place patients at increased risk for traumatic lung herniation including COPD and obesity. Chest tube drainage of associated hemothorax may result in spontaneous reduction of the herniated lung. Otherwise, early surgical fixation should be pursued as it is associated with low morbidity and excellent prognosis. There is no consensus on management with concurrent flail chest. Clinicians should include lung herniation in the differential of a patient with recent chest trauma from CPR, when confronted with worsening respiratory symptoms or worsening ventilatory mechanics, as intervention is necessary. CONCLUSIONS: Lung herniation is a rare phenomenon that may be the result of high-quality CPR, especially in patients with the aforementioned risk factors. We believe the incidence of this thoracic pathology will increase as the at-risk population continues to rise thus emphasizing the importance of clinician recognition of this condition as early surgical fixation may provide a definitive treatment. REFERENCE #1: Batra AK. Lung herniation after CPR. Crit Care Med. 1986;14(6):595-6. doi: 10.1097/00003246-198606000-00022. PMID: 3709206. REFERENCE #2: Deliliga, A., Chatzinikolaou, F., Koutsoukis, D. et al. Cardiopulmonary resuscitation (CPR) complications encountered in forensic autopsy cases. BMC Emerg Med 19, 23 (2019). https://doi.org/10.1186/s12873-019-0234-5 REFERENCE #3: Allen GS, Fischer RP. Traumatic lung herniation. Annal Thoracic Surg. 1997;63(5):1455–6. doi: 10.1016/s0003-4975(97)00109-4. DISCLOSURES: No relevant relationships by Andrew Deitchman, source=Web Response No relevant relationships by Jesse Liou, source=Web Response No relevant relationships by John Nawrocki, source=Web Response

The role of extracellular vesicles in traumatic brain injury-induced acute lung injury.

Acute lung injury (ALI), a common complication after traumatic brain injury (TBI), can evolve into acute respiratory distress syndrome (ARDS) and has a mortality rate of 30%-40%. Secondary ALI after TBI exhibits the following typical pathological features: infiltration of neutrophils into the alveolar and interstitial space, alveolar septal thickening, alveolar edema, and hemorrhage. Extracellular vesicles (EVs) were recently identified as key mediators in TBI-induced ALI. Due to their small size and lipid bilayer, they can pass through the disrupted blood-brain barrier (BBB) into the peripheral circulation and deliver their contents, such as genetic material and proteins, to target cells through processes such as fusion, receptor-mediated interactions, and uptake. Acting as messengers, EVs contribute to mediating brain-lung cross talk after TBI. In this review, we aim to summarize the mechanism of EVs in TBI-induced ALI, which may provide new ideas for clinical treatment.