An unusual cause of “traumatic” hemothorax: perforation of the lung parenchyma by a bifid rib

2019 ◽  
Vol 120 (1) ◽  
pp. 76-77
Author(s):  
Sander Ovaere ◽  
Anneleen Peeters ◽  
Lieven Depypere
Keyword(s):  
Lung Parenchyma ◽  
Bifid Rib

Quantitative Microscopic Comparison of the Organization of the Lung in Transgenic Mice Expressing Transforming Growth Factor-α (TGF-α)

1996 ◽  
Vol 54 ◽  
pp. 14-15
Author(s):  
C. G. Plopper ◽  
C. Helton ◽  
A. J. Weir ◽  
J. A. Whitsett ◽  
T. R. Korfhagen
Keyword(s):  
Growth Factor ◽  
Pulmonary Fibrosis ◽  
Transgenic Mice ◽  
Blood Vessels ◽  
Lung Parenchyma ◽  
Lung Maturation ◽  
Alveolar Air ◽  
Parenchymal Tissue ◽  
Air Space ◽  
Conducting Airways

A wide variety of growth factors are thought to be involved in the regulation of pre- and postnatal lung maturation, including factors which bind to the epidermal growth factor receptor. Marked pulmonary fibrosis and enlarged alveolar air spaces have been observed in lungs of transgenic mice expressing human TGF-α under control of the 3.7 KB human SP-C promoter. To test whether TGF-α alters lung morphogenesis and cellular differentiation, we examined morphometrically the lungs of adult (6-10 months) mice derived from line 28, which expresses the highest level of human TGF-α transcripts among transgenic lines. Total volume of lungs (LV) fixed by airway infusion at standard pressure was similar in transgenics and aged-matched non-transgenic mice (Fig. 1). Intrapulmonary bronchi and bronchioles made up a smaller percentage of LV in transgenics than in non-transgenics (Fig. 2). Pulmonary arteries and pulmonary veins were a smaller percentage of LV in transgenic mice than in non-transgenics (Fig. 3). Lung parenchyma (lung tissue free of large vessels and conducting airways) occupied a larger percentage of LV in transgenics than in non-transgenics (Fig. 4). The number of generations of branching in conducting airways was significantly reduced in transgenics as compared to non-transgenic mice. Alveolar air space size, as measured by mean linear intercept, was almost twice as large in transgenic mice as in non-transgenics, especially when different zones within the lung were compared (Fig. 5). Alveolar air space occupied a larger percentage of the lung parenchyma in transgenic mice than in non-transgenic mice (Fig. 6). Collagen abundance was estimated in histological sections as picro-Sirius red positive material by previously-published methods. In intrapulmonary conducting airways, collagen was 4.8% of the wall in transgenics and 4.5% of the wall in non-transgenic mice. Since airways represented a smaller percentage of the lung in transgenics, the volume of interstitial collagen associated with airway wall was significantly less. In intrapulmonary blood vessels, collagen was 8.9% of the wall in transgenics and 0.7% of the wall in non-transgenics. Since blood vessels were a smaller percentage of the lungs in transgenics, the volume of collagen associated with the walls of blood vessels was five times greater. In the lung parenchyma, collagen was 51.5% of the tissue volume in transgenics and 21.2% in non-transgenics. Since parenchyma was a larger percentage of lung volume in transgenics, but the parenchymal tissue was a smaller percent of the volume, the volume of collagen associated with parenchymal tissue was only slightly greater. We conclude that overexpression of TGF-α during lung maturation alters many aspects of lung development, including branching morphogenesis of the airways and vessels and alveolarization in the parenchyma. Further, the increases in visible collagen previously associated with pulmonary fibrosis due to the overexpression of TGF-α are a result of actual increases in amounts of collagen and in a redistribution of collagen within compartments which results from morphogenetic changes. These morphogenetic changes vary by lung compartment. Supported by HL20748, ES06700 and the Cystic Fibrosis Foundation.

Pulmonary hair embolism in a rescued free-ranging Eurasian otter Lutra lutra in Kinmen, Taiwan

2020 ◽  
Vol 142 ◽  
pp. 55-61
Author(s):  
WT Li ◽  
YL Chiang ◽  
TY Chen ◽  
CL Lai
Keyword(s):  
Foreign Body ◽  
Traumatic Injury ◽  
Lung Parenchyma ◽  
Giant Cells ◽  
Hair Shaft ◽  
Lutra Lutra ◽  
Lung Lobe ◽  
Eurasian Otter ◽  
Foreign Body Giant Cells ◽  
Free Ranging

Eurasian otters Lutra lutra are listed as Near Threatened on the IUCN Red List and are imperiled by habitat loss, water pollution, and poaching. Harassment and attacks by stray animals are also recognized threats to the health of wild Eurasian otters. Pulmonary hair embolism is a possible complication in animals with deep traumatic injury, but to date no cases have been reported in wildlife. A free-ranging, adult male Eurasian otter was rescued due to severe emaciation and multiple bite wounds. The otter died 3 d after rescue and was necropsied. Grossly, a 1.5 × 1.5 × 1.5 cm firm nodule was observed in the left cranial lung lobe. Histologically, a fragment of hair shaft surrounded by multinucleated foreign body giant cells was observed in a medium-sized vein, and extensive eosinophilic infiltration was noted in the adjacent vascular wall and lung parenchyma. Based on the gross and histological findings, the pulmonary lesion was consistent with eosinophilic pneumonia and vasculitis induced by hair embolism. The presence of well-formed multinucleated foreign body giant cells and eosinophils may imply a late stage of foreign body reaction, and thus the presumptive source of hair embolism is an animal bite. This is the first report of pulmonary hair embolism associated with animal bite in a rescued free-ranging Eurasian otter.

Pentoxifylline and Oxypurinol: Potential Drugs to Prevent the “Cytokine Release (Storm) Syndrome” Caused by SARS-CoV-2?

2020 ◽  
Vol 26 (35) ◽  
pp. 4515-4521
Author(s):  
Francisco J. López-Iranzo ◽  
Ana M. López-Rodas ◽  
Luis Franco ◽  
Gerardo López-Rodas
Keyword(s):  
Lung Parenchyma ◽  
Interstitial Tissue ◽  
Cytokine Release ◽  
Phase I Clinical Trials ◽  
Infected People ◽  
Tnf Α ◽  
Transient Loss ◽  
Anti Inflammatory ◽  
And Control ◽  
Inflammatory Action

Background: COVID-19, caused by SARS-CoV-2, is a potentially lethal, rapidly-expanding pandemic and many efforts are being carried out worldwide to understand and control the disease. COVID-19 patients may display a cytokine release syndrome, which causes severe lung inflammation, leading, in many instances, to death. Objective: This paper is intended to explore the possibilities of controlling the COVID-19-associated hyperinflammation by using licensed drugs with anti-inflammatory effects. Hypothesis: We have previously described that pentoxifylline alone, or in combination with oxypurinol, reduces the systemic inflammation caused by experimentally-induced pancreatitis in rats. Pentoxifylline is an inhibitor of TNF-α production and oxypurinol inhibits xanthine oxidase. TNF-α, in turn, activates other inflammatory genes such as Nos2, Icam or IL-6, which regulate migration and infiltration of neutrophils into the pulmonary interstitial tissue, causing injury to the lung parenchyma. In acute pancreatitis, the anti-inflammatory action of pentoxifylline seems to be mediated by the prevention of the rapid and presumably transient loss of PP2A activity. This may also occur in the hyperinflammatory -cytokine releasing phase- of SARS-CoV-2 infection. Therefore, it may be hypothesized that early treatment of COVID-19 patients with pentoxifylline, alone or in combination with oxypurinol, would prevent the potentially lethal acute respiratory distress syndrome. Conclusion: Pentoxifylline and oxypurinol are licensed drugs used for diseases other than COVID-19 and, therefore, phase I clinical trials would not be necessary for the administration to SARS-CoV-2- infected people. It would be worth investigating their potential effects against the hyperinflammatory response to SARS-CoV-2 infection.

Exercise Performed Concomitantly with Particulate Matter Exposure Inhibits Lung Injury

2017 ◽  
Vol 39 (02) ◽  
pp. 133-140 ◽  
Author(s):  
Adriano Silva-Renno ◽  
Guilherme Baldivia ◽  
Manoel Oliveira-Junior ◽  
Maysa Brandao-Rangel ◽  
Elias El-Mafarjeh ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Systemic Inflammation ◽  
Air Pollutants ◽  
Lung Parenchyma ◽  
Treadmill Training ◽  
Tnf Alpha ◽  
Systemic Response ◽  
Pm 2.5 ◽  
Pm 10 ◽  
Particulate Matter Exposure

AbstractAir pollution is a growing problem worldwide, inducing and exacerbating several diseases. Among the several components of air pollutants, particulate matter (PM), especially thick (10–2.5 µm; PM 10) and thin (≤2.5 µm; PM 2.5), are breathable particles that easily can be deposited within the lungs, resulting in pulmonary and systemic inflammation. Although physical activity is strongly recommended, its effects when practiced in polluted environments are questionable. Therefore, the present study evaluated the pulmonary and systemic response of concomitant treadmill training with PM 2.5 and PM 10 exposure. Treadmill training inhibited PM 2.5- and PM 10-induced accumulation of total leukocytes (p<0.001), neutrophils (p<0.001), macrophages (p<0.001) and lymphocytes (p<0.001) in bronchoalveolar lavage (BAL), as well as the BAL levels of IL-1beta (p<0.001), CXCL1/KC (p<0.001) and TNF-alpha (p<0.001), whereas it increased IL-10 levels (p<0.05). Similar effects were observed on accumulation of polymorphonuclear (p<0.01) and mononuclear (p<0.01) cells in the lung parenchyma and in the peribronchial space. Treadmill training also inhibited PM 2.5- and PM 10-induced systemic inflammation, as observed in the number of total leukocytes (p<0.001) and in the plasma levels of IL-1beta (p<0.001), CXCL1/KC (p<0.001) and TNF-alpha (p<0.001), whereas it increased IL-10 levels (p<0.001). Treadmill training inhibits lung and systemic inflammation induced by particulate matter.

Lung ultrasound in blunt chest trauma: A clinical review

Ultrasound ◽  
2021 ◽  
pp. 1742271X2199460
Author(s):  
Serena Rovida ◽  
Daniele Orso ◽  
Salman Naeem ◽  
Luigi Vetrugno ◽  
Giovanni Volpicelli
Keyword(s):  
Blunt Chest Trauma ◽  
Chest Trauma ◽  
Lung Ultrasound ◽  
Lung Parenchyma ◽  
Trauma Patients ◽  
Minor Trauma ◽  
Major Life ◽  
Diagnostic Modality ◽  
Life Threatening ◽  
Sternal Fractures

Introduction Bedside lung sonography is recognized as a reliable diagnostic modality in trauma settings due to its ability to detect alterations both in lung parenchyma and in pleural cavities. In severe blunt chest trauma, lung ultrasound can identify promptly life-threatening conditions which may need direct intervention, whereas in minor trauma, lung ultrasound contributes to detection of acute pathologies which are often initially radio-occult and helps in the selection of those patients that might need further investigation. Topic Description We did a literature search on databases EMBASE, PubMed, SCOPUS and Google Scholar using the terms ‘trauma’, ‘lung contusion’, ‘pneumothorax’, ‘hemothorax’ and ‘lung ultrasound’. The latest articles were reviewed and this article was written using the most current and validated information. Discussion Lung ultrasound is quite accurate in diagnosing pneumothorax by using a combination of four sonographic signs; absence of lung sliding, B-lines, lung pulse and presence of lung point. It provides a rapid diagnosis in hemodynamically unstable patients. Lung contusions and hemothorax can be diagnosed and assessed with lung ultrasound. Ultrasound is also very useful for evaluating rib and sternal fractures and for imaging the pericardium for effusion and tamponade. Conclusion Bedside lung ultrasound can lead to rapid and accurate diagnosis of major life-threatening pathologies in blunt chest trauma patients.

scholarly journals Organizing Pneumonia and Microvascular Fibrosis as Late Sequelae after a COVID-19 Infection. A Case Report

Surgeries ◽  
2021 ◽  
Vol 2 (2) ◽  
pp. 190-198
Author(s):  
Johan L. Dikken ◽  
Alexander P. W. M. Maat ◽  
Janina L. Wolf ◽  
Henrik Endeman ◽  
Rogier A. S. Hoek ◽  
...  
Keyword(s):  
Interstitial Fibrosis ◽  
Pleural Empyema ◽  
Lung Parenchyma ◽  
Endothelial Damage ◽  
Low Grade ◽  
Organizing Pneumonia ◽  
Microvascular Damage ◽  
Pulmonary Changes ◽  
Trapped Lung ◽  
Low Grade Inflammation

We report a patient with COVID-19 requiring hospitalization for two weeks, complicated by multiple segmental pulmonary embolisms for which dabigatran was initiated. After clearing the infection, the patient remained asymptomatic for 5 months. He was then readmitted with a spontaneous haemothorax, most likely related to the use of dabigatran, which progressed to a pleural empyema with a trapped lung. The patient underwent a video assisted thoracoscopy (VATS) with decortication. Because of focal abnormalities, biopsies for histopathology were taken from the lung parenchyma. These showed an organizing pneumonia with progression towards fibrosis and arteries with intimal fibrosis. So far, no histopathological reports exist on late pulmonary changes after a COVID-19 infection. The unusual combined presence of microvascular damage and interstitial fibrosis may reflect a pathophysiological concept in which early endothelial damage by SARS-CoV-2 can lead to a chronic state of microvascular damage, low grade inflammation, and early progression towards pulmonary fibrosis.

scholarly journals Cellular Senescence in Lung Fibrosis

2021 ◽  
Vol 22 (13) ◽  
pp. 7012
Author(s):  
Fernanda Hernandez-Gonzalez ◽  
Rosa Faner ◽  
Mauricio Rojas ◽  
Alvar Agustí ◽  
Manuel Serrano ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cellular Senescence ◽  
Lung Fibrosis ◽  
Lung Diseases ◽  
Physiological Mechanism ◽  
Lung Parenchyma ◽  
Scar Tissue ◽  
Interstitial Lung Diseases ◽  
Cellular Damage ◽  
Age Related

Fibrosing interstitial lung diseases (ILDs) are chronic and ultimately fatal age-related lung diseases characterized by the progressive and irreversible accumulation of scar tissue in the lung parenchyma. Over the past years, significant progress has been made in our incomplete understanding of the pathobiology underlying fibrosing ILDs, in particular in relation to diverse age-related processes and cell perturbations that seem to lead to maladaptation to stress and susceptibility to lung fibrosis. Growing evidence suggests that a specific biological phenomenon known as cellular senescence plays an important role in the initiation and progression of pulmonary fibrosis. Cellular senescence is defined as a cell fate decision caused by the accumulation of unrepairable cellular damage and is characterized by an abundant pro-inflammatory and pro-fibrotic secretome. The senescence response has been widely recognized as a beneficial physiological mechanism during development and in tumour suppression. However, recent evidence strengthens the idea that it also drives degenerative processes such as lung fibrosis, most likely by promoting molecular and cellular changes in chronic fibrosing processes. Here, we review how cellular senescence may contribute to lung fibrosis pathobiology, and we highlight current and emerging therapeutic approaches to treat fibrosing ILDs by targeting cellular senescence.

scholarly journals Mechanical power at a glance: a simple surrogate for volume-controlled ventilation

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Lorenzo Giosa ◽  
Mattia Busana ◽  
Iacopo Pasticci ◽  
Matteo Bonifazi ◽  
Matteo Maria Macrì ◽  
...  
Keyword(s):  
Peak Pressure ◽  
Minute Ventilation ◽  
Clinical Intervention ◽  
Lung Parenchyma ◽  
Mechanical Power ◽  
Icu Patients ◽  
Controlled Ventilation ◽  
Volume Controlled Ventilation ◽  
New Equation ◽  
Volume Controlled

Abstract Background Mechanical power is a summary variable including all the components which can possibly cause VILI (pressures, volume, flow, respiratory rate). Since the complexity of its mathematical computation is one of the major factors that delay its clinical use, we propose here a simple and easy to remember equation to estimate mechanical power under volume-controlled ventilation: $$ \mathrm{Mechanical}\ \mathrm{Power}=\frac{\mathrm{VE}\times \left(\mathrm{Peak}\ \mathrm{Pressure}+\mathrm{PEEP}+F/6\right)}{20} $$Mechanical Power=VE×Peak Pressure+PEEP+F/620 where the mechanical power is expressed in Joules/minute, the minute ventilation (VE) in liters/minute, the inspiratory flow (F) in liters/minute, and peak pressure and positive end-expiratory pressure (PEEP) in centimeter of water. All the components of this equation are continuously displayed by any ventilator under volume-controlled ventilation without the need for clinician intervention. To test the accuracy of this new equation, we compared it with the reference formula of mechanical power that we proposed for volume-controlled ventilation in the past. The comparisons were made in a cohort of mechanically ventilated pigs (485 observations) and in a cohort of ICU patients (265 observations). Results Both in pigs and in ICU patients, the correlation between our equation and the reference one was close to the identity. Indeed, the R2 ranged from 0.97 to 0.99 and the Bland-Altman showed small biases (ranging from + 0.35 to − 0.53 J/min) and proportional errors (ranging from + 0.02 to − 0.05). Conclusions Our new equation of mechanical power for volume-controlled ventilation represents a simple and accurate alternative to the more complex ones available to date. This equation does not need any clinical intervention on the ventilator (such as an inspiratory hold) and could be easily implemented in the software of any ventilator in volume-controlled mode. This would allow the clinician to have an estimation of mechanical power at a simple glance and thus increase the clinical consciousness of this variable which is still far from being used at the bedside. Our equation carries the same limitations of all other formulas of mechanical power, the most important of which, as far as it concerns VILI prevention, are the lack of normalization and its application to the whole respiratory system (including the chest wall) and not only to the lung parenchyma.

scholarly journals Cardiothoracic imaging findings of Proteus syndrome

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
S. Mojdeh Mirmomen ◽  
Andrew E. Arai ◽  
Evrim B. Turkbey ◽  
Andrew J. Bradley ◽  
Julie C. Sapp ◽  
...  
Keyword(s):  
Cardiac Mri ◽  
Lung Parenchyma ◽  
Nonparametric Tests ◽  
Pulmonary Angiography ◽  
Left Ventricular ◽  
Proteus Syndrome ◽  
Imaging Findings ◽  
Septal Wall ◽  
Significant Difference ◽  
Hyperlucent Lung

AbstractIn this work, we sought to delineate the prevalence of cardiothoracic imaging findings of Proteus syndrome in a large cohort at our institution. Of 53 individuals with a confirmed diagnosis of Proteus syndrome at our institution from 10/2001 to 10/2019, 38 individuals (men, n = 23; average age = 24 years) underwent cardiothoracic imaging (routine chest CT, CT pulmonary angiography and/or cardiac MRI). All studies were retrospectively and independently reviewed by two fellowship-trained cardiothoracic readers. Disagreements were resolved by consensus. Differences between variables were analyzed via parametric and nonparametric tests based on the normality of the distribution. The cardiothoracic findings of Proteus syndrome were diverse, but several were much more common and included: scoliosis from bony overgrowth (94%), pulmonary venous dilation (62%), band-like areas of lung scarring (56%), and hyperlucent lung parenchyma (50%). In addition, of 20 individuals who underwent cardiac MRI, 9/20 (45%) had intramyocardial fat, mostly involving the endocardial surface of the left ventricular septal wall. There was no statistically significant difference among the functional cardiac parameters between individuals with and without intramyocardial fat. Only one individual with intramyocardial fat had mildly decreased function (LVEF = 53%), while all others had normal ejection fraction.

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