DOCSLIB.ORG

And Subpleural Fibrosis 1 Induces Progressive Pleural Scarring Β TGF

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
And Subpleural Fibrosis 1 Induces Progressive Pleural Scarring Β TGF TGF-β1 Induces Progressive Pleural Scarring and Subpleural Fibrosis Nathalie Decologne, Martin Kolb, Peter J. Margetts, Franck Menetrier, Yves Artur, Carmen Garrido, Jack Gauldie, This information is current as Philippe Camus and Philippe Bonniaud of September 29, 2021. J Immunol 2007; 179:6043-6051; ; doi: 10.4049/jimmunol.179.9.6043 http://www.jimmunol.org/content/179/9/6043 Downloaded from References This article cites 43 articles, 11 of which you can access for free at: http://www.jimmunol.org/content/179/9/6043.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 29, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2007 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology TGF-␤1 Induces Progressive Pleural Scarring and Subpleural Fibrosis1 Nathalie Decologne,* Martin Kolb,‡ Peter J. Margetts,‡ Franck Menetrier,* Yves Artur,† Carmen Garrido,* Jack Gauldie,‡ Philippe Camus,*§ and Philippe Bonniaud2*§ Pleural fibrosis is a misunderstood disorder which can cause severe restrictive lung disease with high morbidity and even mor- tality. The condition can develop in response to a large variety of diseases and tissue injury, among them infectious disease, asbestos, drugs, and radiation therapy. There is no efficient treatment to reverse established pleural fibrosis. TGF-␤1 is suspected, even if not proven, as a key cytokine in this process. In this study, we used adenoviral gene transfer of TGF-␤1 to the pleural mesothelium in rats. We show that local and transient TGF-␤1 overexpression induces homogenous, prolonged, and progressive pleural fibrosis without pleurodesis, associated with severe impairment of pulmonary function. We further demonstrate that pleural fibrosis can expand into the lung parenchyma from the visceral layer, but not into the muscle from the parietal layer. We Downloaded from provide evidence that matrix accumulation and fibrosis within the parenchyma evolved through a process involving “mesothelial- fibroblastoid transformation” and suggest that the pleural mesothelial cell may be an important player involved in the develop- ment of the subpleural distribution pattern known to be a hallmark of pulmonary fibrosis. This new model of pleural fibrosis will allow us to better understand the mechanisms of progressive fibrogenesis, and to explore novel antifibrotic therapies in the pleural cavity. The Journal of Immunology, 2007, 179: 6043–6051. http://www.jimmunol.org/ leural fibrosis can cause severe restrictive lung disease. It to pleural effusion and ultimately fibrosis (5, 6). Pleural fibrosis is usually considered as a complication of other disorders can be defined as excessive deposition of matrix components re- P involving the chest cavity. Pneumonia, with parapneumo- sulting in the destruction of regular pleural tissue architecture. The nic effusion and empyema, tuberculosis and asbestos are among disorder can manifest itself as discrete localized lesions (pleural the most common causes for pleural fibrosis (1). Furthermore, nu- plaques) or diffuse pleural thickening (5). Most research related to merous drugs can contribute to the development of pleural fibrosis, pleural scarring concerns the induction of pleurodesis as an ap- the best known being ergot drugs, cytostatic agents, and thoracic proach to treat chronic effusion associated with metastasized can- irradiation (Refs. 2 and 3, and www.pneumotox.com (“The drug- cer (7). Animal studies have shown that TGF-␤ plays an active role by guest on September 29, 2021 induced lung diseases”)). Other potential reasons are systemic con- in pleurodesis as well as in pleural fluid formation (8–12). nective tissue disease, hemothorax, and progressive postthoracot- TGF-␤ is a multifunctional cytokine critically involved in the omy scarring after coronary bypass (4). Depending on disease pathogenesis of fibrosis through its potent effects on fibroblast dif- severity, pleural fibrosis can compromise respiratory function, ferentiation, extracellular matrix formation (13, 14), and epithelial- markedly impair quality of life, and can be associated with high to-mesenchymal transition (EMT)3 (15). Peritoneal mesothelial morbidity or even mortality. There is no effective therapy to re- cells may undergo mesenchymal conversion (16, 17) and TGF-␤1 verse established pleural fibrosis. gene transfer to the peritoneal mesothelium induces peritoneal fi- The pleura is a metabolically active membrane involved in brosis with evidence of mesothelial-to-mesenchymal transition or maintaining a dynamic homeostasis of fluid within the chest cav- “mesothelial-fibroblastoid transformation” (MFT) (18). ity. The homeostasis is important for the mechanical properties of In this study, we used transient transfer of the active TGF-␤1 chest wall and lungs, and a breakdown of the fluid balance can lead gene by adenoviral vectors to the pleural cavity and mesothelium. We demonstrate that this approach induces homogenous, pro- longed, and progressive pleural fibrosis without pleurodesis, asso- *Faculty of Medicine and Pharmacy, Institut National de la Sante´et de la Recherche Me´dicale (INSERM), Unite´Mixte de Recherche (UMR) 866, Dijon, France; †UMR ciated with severe impairment of pulmonary function. This new 1129, Flaveur, Vision et Comportement du Consommateur, Institut National de la model of pleural fibrosis will allow us to better understand the Recherche Agronomique, Etablissement National d’Enseignement Supe´rieur Agronomique de Dijon, University of Burgundy, Dijon, France; ‡Department of Pa- mechanisms of progressive fibrogenesis, and to explore novel an- thology and Molecular Medicine, Centre for Gene Therapeutics, McMaster Univer- tifibrotic therapies in the pleural cavity. We further show that pleu- sity, Hamilton, Ontario, Canada; and §Service de Pneumologie et Re´animation Res- ral fibrosis, through a process involving MFT, can expand into the piratoire, Centre Hospitalier Universitaire du Bocage, Dijon, France lung parenchyma from the visceral layer, but not into the muscle Received for publication June 12, 2007. Accepted for publication August 14, 2007. from the parietal layer, suggesting that a distinct local environment The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance is required for progressive fibrotic responses in the tissue. with 18 U.S.C. Section 1734 solely to indicate this fact. 1 N.D. was supported by the Comite´deCoˆte d’Or de la Ligue Contre le Cancer and by the Socie´te´ de Pneumologie de Langue Franc¸aise. P.B. was supported by Pneu- mologie De´veloppement. M.K. is a Parker B. Francis Fellow and was supported by a 3 Abbreviations used in this paper: EMT, epithelial-to-mesenchymal transition; MFT, Career Development Award of Department of Medicine, McMaster University. mesothelial-fibroblastoid transformation; PLF, pleural lavage fluid; BAL, bronchoal- P.J.M. is a Canadian Institutes for Health Research Clinician Scientist. veolar lavage; BALF, BAL fluid; HSP, heat shock protein; SMA, smooth muscle 2 Address correspondence and reprint requests to Dr. Philippe Bonniaud, Service de actin; MMP, matrix metalloproteinase. Pneumologie et Re´animation Respiratoire, Centre Hospitalier Universitaire du Bo- cage, 21079 Dijon, France. E-mail address: [email protected] Copyright © 2007 by The American Association of Immunologists, Inc. 0022-1767/07/$2.00 www.jimmunol.org 6044 TGF-␤1-INDUCED PLEURAL FIBROSIS Materials and Methods Recombinant adenovirus We used AdTGF-␤1223/225, an adenovirus construct with a mutant TGF-␤1 translated into spontaneously bioactive TGF-␤1, AdLacZ (coding for ␤-ga- lactosidase), and AdDL (control vectors) with no insert in the deleted E1 region for the experiments described. The construction of adenoviral vec- tors is described in detail elsewhere (19, 20). Animal treatment Female Sprague-Dawley rats (Charles River Laboratories) weighing 200– 225 g were housed in special pathogen-free conditions. Rodent laboratory food and water were provided ad libitum. The animals were treated in accordance to the guidelines of the Ministe`re de la Recherche et de la Technologie (Paris, France). All animal procedures were performed with inhalation anesthesia with isoflurane (TEM). A total of 1.3 ϫ 109 PFU of AdTGF-␤1, AdLaCZ, or AdDL were administered in a volume of 800 ␮l of NaCl 0.9%, without any surgery, by intrapleural injection on the right side (sixth space) with a 20-G needle, animals in a left lateral decubitus position. For coadministration experiments, rats received, in 800 ␮lof 0.9% NaCl, 1 ϫ 109 PFU AdLacZ plus 1.3 ϫ 109 PFU AdTGF-␤1or1ϫ 9 ϫ 9 10 PFU AdLacZ plus 1.3 10 PFU AdDL. Rats were euthanized by Downloaded from abdominal aortic bleeding at days 4, 7, 14, 21, and 64 after adenoviral
Load more

Recommended publications
  • Pleural Effusion and Ventilation/Perfusion Scan Interpretation for Acute Pulmonary Embolus
    ventricular function by radionuclide angiography during exercise in normal subjects 33. Verani MS. Myocardial perfusion imaging versus two-dimensional echocardiography: and patients with chronic coronary heart disease. J Am Coll Cardiol 1983;1:1518- comparative value in the diagnosis of coronary artery disease. J NucíCardiol 1529. 1994;1:399-414. 29. Adam WE. Tarkowska A, Bitter F, Stauch M, Geffers H. Equilibrium (gated) 34. Foster T, McNeill AJ, Salustri A, et al. Simultaneous dobutamine stress echocardiog radionuclide ventriculography. Cardiovasc Radial 1979;2:161-173. raphy and technetium-99m SPECT in patients with suspected coronary artery disease. 30. Hurwitz RA, TrêvesS, Kuroc A. Right ventricular and left ventricular ejection fraction J Am Coll Cardiol I993;21:1591-I596. in pediatrie patients with normal hearts: first pass radionuclide angiography. Am 35. Marwick TH, D'Hondt AM, Mairesse GH, Baudhuin T, Wijins W, Detry JM, Meiin Heart J 1984;107:726-732. 31. Freeman ML, Palac R, Mason J, et al. A comparison of dobutamine infusion and JA. Comparative ability of dobutamine and exercise stress in inducing myocardial ischemia in active patients. Br Heart J 1994:72:31-38. supine bicycle exercise for radionuclide cardiac stress testing. Clin NucíMed 1984:9:251-255. 36. Senior R, Sridhara BS, Anagnostou E, Handler C, Raftery EB, Lahiri A. Synergistic 32. Cohen JL, Greene TO, Ottenweller J, Binebaum SZ, Wilchfort SD, Kim CS. value of simultaneous stress dobutamine sestamibi single-photon-emission computer Dobutamine digital echocardiography for detecting coronary artery disease. Am J ized tomography and echocardiography in the detection of coronary artery disease.
    [Show full text]
  • Pneumothorax Ex Vacuo in a Patient with Malignant Pleural Effusion After Pleurx Catheter Placement
    The Medicine Forum Volume 16 Article 20 2015 Pneumothorax ex vacuo in a Patient with Malignant Pleural Effusion After PleurX Catheter Placement Meera Bhardwaj, MS4 Thomas Jefferson University, [email protected] Loheetha Ragupathi, MD Thomas Jefferson University, [email protected] Follow this and additional works at: https://jdc.jefferson.edu/tmf Part of the Medicine and Health Sciences Commons Let us know how access to this document benefits ouy Recommended Citation Bhardwaj, MS4, Meera and Ragupathi, MD, Loheetha (2015) "Pneumothorax ex vacuo in a Patient with Malignant Pleural Effusion After PleurX Catheter Placement," The Medicine Forum: Vol. 16 , Article 20. DOI: https://doi.org/10.29046/TMF.016.1.019 Available at: https://jdc.jefferson.edu/tmf/vol16/iss1/20 This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of Thomas Jefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion in The Medicine Forum by an authorized administrator of the Jefferson Digital Commons. For more information, please contact: [email protected]. Bhardwaj, MS4 and Ragupathi, MD: Pneumothorax ex vacuo in a Patient with Malignant Pleural Effusion After PleurX Catheter Placement Pneumothorax ex vacuo in a Patient with Malignant Pleural Effusion After PleurX Catheter Placement Meera Bhardwaj, MS4 and Loheetha Ragupathi, MD INTRODUCTION Pneumothorax ex vacuo (“without vaccuum”) is a type of pneumothorax that can develop in patients with large pleural effusions.
    [Show full text]
  • Malignant Pleural Mesothelioma
    CLINICAL PRACTICE GUIDELINE LU-009 Version 2 MALIGNANT PLEURAL MESOTHELIOMA Effective Date: December, 2012 The recommendations contained in this guideline are a consensus of the Alberta Provincial Thoracic Malignancies Tumour Team synthesis of currently accepted approaches to management, derived from a review of relevant scientific literature. Clinicians applying these guidelines should, in consultation with the patient, use independent medical judgment in the context of individual clinical circumstances to direct care. CLINICAL PRACTICE GUIDELINE LU-009 Version 2 BACKGROUND Mesothelioma is a rare asbestos-related tumour that arises from mesenchymal cells that are found in the lining of the pleural cavity (Malignant Pleural Mesothelioma; MPM) in 70 to 90 percent of cases, and the peritoneal cavity in 10 to 30 percent of cases.1, 2 Due to the long latency period between exposure and disease, which has been reported to be between 30 and 50 years, most cases of mesothelioma being diagnosed today are the result of asbestos exposure in the 1960s and 1970s.3 Although safety measures for the use of asbestos were adopted in most countries several decades ago, the incidence rates, which are highly age-specific, are still rising, and are expected to peak over the next two decades.4-6 In Canada, the number of men diagnosed with mesothelioma has been steadily increasing over the past 20 years: there were 153 cases reported in 1984 versus 344 cases reported in 2003.3 Mesothelioma is less common in women: there were 78 Canadian women diagnosed with mesothelioma in 2003.3 In the United States, the peak mesothelioma incidence occurred in the early to mid-1990s and has possibly started to decline since then.
    [Show full text]
  • An Interesting Case of Undiagnosed Pleural Effusion Case Report
    Amit Panjwani, Thuraya Zaid [email protected] Pulmonary Medicine, Salmaniya Medical Complex, Manama, Bahrain. An interesting case of undiagnosed pleural effusion Case report Pleural effusions are commonly encountered in the Investigations revealed a haemoglobin level Cite as: Panjwani A, Zaid T. clinical practise of both respiratory and nonrespiratory of 16.4 g⋅dL−1, and total leukocyte count of An interesting case of specialists. An estimated 1–1.5 million new cases in 8870 cells⋅mm−3 with a differential count of 62% undiagnosed pleural effusion. the USA and 200 000–250 000 new cases of pleural neutrophils, 28% lymphocytes, 7% monocytes, 2% Breathe 2017; 13: e46–e52. effusions are reported from the UK each year [1]. eosinophils and 1% basophils. The platelet count Analysis of the relevant clinical history, physical was 160 000 cells⋅mm−3. Creatinine, electrolytes examination, chest radiography and diagnostic and liver function tests were normal. The ECG was thoracentesis is useful in identifying the cause of unremarkable and cardiac enzymes were within pleural effusion in majority of the cases [2]. In a few normal limits. Chest radiograph (figure 1) showed a cases, the aetiology may be unclear after the initial mild, right-sided pleural effusion, blunting of the left assessment. The list of diseases that may account for costophrenic angle, no shift of mediastinal position a persistent undiagnosed pleural effusion is long [3]. and no lung parenchymal opacities. We present an interesting case of undiagnosed pleural effusion that was encountered in our hospital. R Case presentation A 33-year-old male presented to our hospital with a history of sudden-onset, pleuritic, right-sided chest pain of 2 days’ duration.
    [Show full text]
  • Nasal Cavity Trachea Right Main (Primary) Bronchus Left Main (Primary) Bronchus Nostril Oral Cavity Pharynx Larynx Right Lung
    Nasal cavity Oral cavity Nostril Pharynx Larynx Trachea Left main Right main (primary) (primary) bronchus bronchus Left lung Right lung Diaphragm © 2018 Pearson Education, Inc. 1 Cribriform plate of ethmoid bone Sphenoidal sinus Frontal sinus Posterior nasal aperture Nasal cavity • Nasal conchae (superior, Nasopharynx middle, and inferior) • Pharyngeal tonsil • Nasal meatuses (superior, middle, and inferior) • Opening of pharyngotympanic • Nasal vestibule tube • Nostril • Uvula Hard palate Oropharynx • Palatine tonsil Soft palate • Lingual tonsil Tongue Laryngopharynx Hyoid bone Larynx Esophagus • Epiglottis • Thyroid cartilage Trachea • Vocal fold • Cricoid cartilage (b) Detailed anatomy of the upper respiratory tract © 2018 Pearson Education, Inc. 2 Pharynx • Nasopharynx • Oropharynx • Laryngopharynx (a) Regions of the pharynx © 2018 Pearson Education, Inc. 3 Posterior Mucosa Esophagus Submucosa Trachealis Lumen of Seromucous muscle trachea gland in submucosa Hyaline cartilage Adventitia (a) Anterior © 2018 Pearson Education, Inc. 4 Intercostal muscle Rib Parietal pleura Lung Pleural cavity Trachea Visceral pleura Thymus Apex of lung Left superior lobe Right superior lobe Oblique Horizontal fissure fissure Right middle lobe Left inferior lobe Oblique fissure Right inferior lobe Heart (in pericardial cavity of mediastinum) Diaphragm Base of lung (a) Anterior view. The lungs flank mediastinal structures laterally. © 2018 Pearson Education, Inc. 5 Posterior Vertebra Esophagus (in posterior mediastinum) Root of lung at hilum Right lung • Left main bronchus Parietal pleura • Left pulmonary artery • Left pulmonary vein Visceral pleura Pleural cavity Left lung Thoracic wall Pulmonary trunk Pericardial membranes Heart (in mediastinum) Sternum Anterior mediastinum Anterior (b) Transverse section through the thorax, viewed from above © 2018 Pearson Education, Inc. 6 Alveolar duct Alveoli Respiratory bronchioles Alveolar duct Terminal bronchiole Alveolar sac (a) Diagrammatic view of respiratory bronchioles, alveolar ducts, and alveoli © 2018 Pearson Education, Inc.
    [Show full text]
  • Allergic Bronchopulmonary Aspergillosis: a Perplexing Clinical Entity Ashok Shah,1* Chandramani Panjabi2
    Review Allergy Asthma Immunol Res. 2016 July;8(4):282-297. http://dx.doi.org/10.4168/aair.2016.8.4.282 pISSN 2092-7355 • eISSN 2092-7363 Allergic Bronchopulmonary Aspergillosis: A Perplexing Clinical Entity Ashok Shah,1* Chandramani Panjabi2 1Department of Pulmonary Medicine, Vallabhbhai Patel Chest Institute, University of Delhi, Delhi, India 2Department of Respiratory Medicine, Mata Chanan Devi Hospital, New Delhi, India This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. In susceptible individuals, inhalation of Aspergillus spores can affect the respiratory tract in many ways. These spores get trapped in the viscid spu- tum of asthmatic subjects which triggers a cascade of inflammatory reactions that can result in Aspergillus-induced asthma, allergic bronchopulmo- nary aspergillosis (ABPA), and allergic Aspergillus sinusitis (AAS). An immunologically mediated disease, ABPA, occurs predominantly in patients with asthma and cystic fibrosis (CF). A set of criteria, which is still evolving, is required for diagnosis. Imaging plays a compelling role in the diagno- sis and monitoring of the disease. Demonstration of central bronchiectasis with normal tapering bronchi is still considered pathognomonic in pa- tients without CF. Elevated serum IgE levels and Aspergillus-specific IgE and/or IgG are also vital for the diagnosis. Mucoid impaction occurring in the paranasal sinuses results in AAS, which also requires a set of diagnostic criteria. Demonstration of fungal elements in sinus material is the hall- mark of AAS.
    [Show full text]
  • The Spectrum of Computed Tomography Appearances
    RESPIRATORY MEDICIXE (1997) 91, 213-219 Allergic bronchopulmonary aspergillosis: the spectrum of computed tomography appearances N. PANCHAL",R. BHAGAT",C. PANT+AND A. SHAH" “Department of Clinical Research, Vallabhbhai Pate1 Chest Institute, University of Delhi, Delhi, lndia ‘Imaging Division, Institute of Nuclear Medicine and Allied Sciences, Timaupuv, Delhi, India Although computed tomography (CT) of the thorax has been compared to plain chest radiography and bronchography for demonstration of central bronchiectasis (CB) in allergic bronchopulmonary aspergil- losis (ABPA), the CT presentation of the disease is yet to be highlighted. With this in view, the CT appearances in 23 patients with ABPA were evaluated. The scans were assessed for bronchial, parenchymal and pleural abnormalities. Central bronchiectasis was identified in all patients, involving 114 (85%) of the 134 lobes and 210 (52%) of the 406 segments studied. Other bronchial abnormalities such as dilated and totally occluded bronchi (11 patients), air-fluid levels within dilated bronchi (five patients), bronchial wall thickening (10 patients) and parallel-line shadows (seven patients) were also observed. Parenchymal abnormalities, which had a predilection for upper lobes, included consolidation in 10 (43%) patients, collapse in four (17%) patients and parenchymal scarring in 19 (83%) patients. A total of six cavities were seen in three (13%) patients, and an emphysematous bullae was detected in one (4%) patient. The pleura was involved in 10 (43%) patients. Ipsilateral pleural effusion with collapse was observed in one patient, while in nine other patients, parenchymal lesions extended up to the pleura. Concomitant allergic Aspergillus sinusitis (AAS) was also detected in three (13%) of the 23 patients.
    [Show full text]
  • Case Report Cryptogenic Organising Pneumonia: Clinical, Pathological, and Prognostic Analysis of 27 Cases
    Int J Clin Exp Med 2016;9(3):6911-6919 www.ijcem.com /ISSN:1940-5901/IJCEM0019752 Case Report Cryptogenic organising pneumonia: clinical, pathological, and prognostic analysis of 27 cases Yanli Li1*, Yan Li1*, Fengfeng Han1, Haiyang Yu1, Tianyun Yang1, Huimin Li2, Wenbin Guan3, Xuejun Guo1 Departments of 1Respiratory Medicine, 2Radiology, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, China; 3Department of Pathology, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, China. *Equal contributors and co-first authors. Received November 14, 2015; Accepted November 29, 2015; Epub March 15, 2016; Published March 30, 2016 Abstract: Background: Buds of granulation tissue within the lumen of distal pulmonary airspaces characterises organising pneumonia (OP). This study aimed to analyse the clinical and pathological features and prognosis of pa- tients with cryptogenic OP. Methods: Twenty-seven patients were retrospectively analysed. A multidisciplinary team (a clinician, radiologist, and pathologist) diagnosed all patients. Clinical features, laboratory data, chest radiology, treatment and prognosis, pulmonary function, and haematoxylin-eosin and immunohistochemical staining were assessed. Results: Symptoms (in decreasing prevalence) were cough, dyspnoea, fever, and chest tightness. The erythrocyte sedimentation rate (in most patients) and C-reactive protein level were increased. Radiologic findings (in decreasing prevalence) were consolidation, nodules, and band-like opacities. The lung function results were ‘normal’ and ‘restrictive’ in 30.8% and 38.5% of patients, respectively. Most patients responded to corticosteroids. The prognosis of the patients was excellent in 77.8% and poor in 22.2%. Organised polypoid granulation inflamma- tory tissue was in the distal bronchiole airways, respiratory bronchioles, alveolar ducts, and alveoli.
    [Show full text]
  • Penetrating Injuries of the Pleural Cavity
    Thorax: first published as 10.1136/thx.39.10.789 on 1 October 1984. Downloaded from Thorax 1984;39: 789-793 Penetrating injuries of the pleural cavity DAVID JJ MUCKART, FRED M LUVUNO, LYNNE W BAKER From the Department ofSurgery, King Edward VIII Hospital, Durban, South Africa ABSTRACT Two hundred and fifty one cases of penetrating wounds of the chest were studied prospectively. Clinical evidence is presented to show that: (1) basal intercostal drains are ade- quate to remove both air and fluid from within the pleural cavity; (2) frequent chest radio- graphs are unnecessary and intercostal drains may be removed on clinical grounds alone; (3) long term antibiotic prophylaxis is unnecessary; (4) eight per cent of those undergoing initial observation will develop a delayed haemothorax or pneumothorax of sufficient size to require drainage; (5) subcutaneous emphysema is of no prognostic significance in the symptom- less patient with minimal intrapleural damage on admission; and (6) outpatient follow up is not required. Intercostal tube drainage after penetrating chest absence of the following was documented: trauma not affecting the heart or great vessels has (1) shock as defined by a systolic blood pressure of been the standard method of treatment for many less than 100 mm Hg and a pulse rate greater than years at the King Edward VIII Hospital in Durban. 100 beats/min; (2) multiple stab wounds; Several questions concerning this approach, how- (3) severe associated head, limb or abdominal ever, remain unanswered. The use of serial chest injury; (4) respiratory distress; (5) subcutaneous radiographs and long term antibiotics, the outcome emphysema.
    [Show full text]
  • Icd-9-Cm (2010)
    ICD-9-CM (2010) PROCEDURE CODE LONG DESCRIPTION SHORT DESCRIPTION 0001 Therapeutic ultrasound of vessels of head and neck Ther ult head & neck ves 0002 Therapeutic ultrasound of heart Ther ultrasound of heart 0003 Therapeutic ultrasound of peripheral vascular vessels Ther ult peripheral ves 0009 Other therapeutic ultrasound Other therapeutic ultsnd 0010 Implantation of chemotherapeutic agent Implant chemothera agent 0011 Infusion of drotrecogin alfa (activated) Infus drotrecogin alfa 0012 Administration of inhaled nitric oxide Adm inhal nitric oxide 0013 Injection or infusion of nesiritide Inject/infus nesiritide 0014 Injection or infusion of oxazolidinone class of antibiotics Injection oxazolidinone 0015 High-dose infusion interleukin-2 [IL-2] High-dose infusion IL-2 0016 Pressurized treatment of venous bypass graft [conduit] with pharmaceutical substance Pressurized treat graft 0017 Infusion of vasopressor agent Infusion of vasopressor 0018 Infusion of immunosuppressive antibody therapy Infus immunosup antibody 0019 Disruption of blood brain barrier via infusion [BBBD] BBBD via infusion 0021 Intravascular imaging of extracranial cerebral vessels IVUS extracran cereb ves 0022 Intravascular imaging of intrathoracic vessels IVUS intrathoracic ves 0023 Intravascular imaging of peripheral vessels IVUS peripheral vessels 0024 Intravascular imaging of coronary vessels IVUS coronary vessels 0025 Intravascular imaging of renal vessels IVUS renal vessels 0028 Intravascular imaging, other specified vessel(s) Intravascul imaging NEC 0029 Intravascular
    [Show full text]
  • Modern Management of Traumatic Hemothorax
    rauma & f T T o re l a t a m n r e u n o t J Mahoozi, et al., J Trauma Treat 2016, 5:3 Journal of Trauma & Treatment DOI: 10.4172/2167-1222.1000326 ISSN: 2167-1222 Review Article Open Access Modern Management of Traumatic Hemothorax Hamid Reza Mahoozi, Jan Volmerig and Erich Hecker* Thoraxzentrum Ruhrgebiet, Department of Thoracic Surgery, Evangelisches Krankenhaus, Herne, Germany *Corresponding author: Erich Hecker, Thoraxzentrum Ruhrgebiet, Department of Thoracic Surgery, Evangelisches Krankenhaus, Herne, Germany, Tel: 0232349892212; Fax: 0232349892229; E-mail: [email protected] Rec date: Jun 28, 2016; Acc date: Aug 17, 2016; Pub date: Aug 19, 2016 Copyright: © 2016 Mahoozi HR. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Hemothorax is defined as a bleeding into pleural cavity. Hemothorax is a frequent manifestation of blunt chest trauma. Some authors suggested a hematocrit value more than 50% for differentiation of a hemothorax from a sanguineous pleural effusion. Hemothorax is also often associated with penetrating chest injury or chest wall blunt chest wall trauma with skeletal injury. Much less common, it may be related to pleural diseases, induced iatrogenic or develop spontaneously. In the vast majority of blunt and penetrating trauma cases, hemothoraces can be managed by relatively simple means in the course of care. Keywords: Traumatic hemothorax; Internal chest wall; Cardiac Hemodynamic response injury; Clinical manifestation; Blunt chest-wall injuries; Blunt As above mentioned the hemodynamic response is a multifactorial intrathoracic injuries; Penetrating thoracic trauma response and depends on severity of hemothorax according to its classification.
    [Show full text]
  • Treatment of Hemothorax in the Era Of€The€Minimaly Invasive Surgery
    Mil. Med. Sci. Lett. (Voj. Zdrav. Listy) 2019, 88(4), 180-187 ISSN 0372-7025 (Print) ISSN 2571-113X (Online) DOI: 10.31482/mmsl.2019.011 Since 1925 REVIEW ARTICLE TREATMENT OF HEMOTHORAX IN THE ERA OF THE MINIMALY INVASIVE SURGERY Radek Pohnán 1,2 , Šárka Blažková 2, Vladislav Hytych 2, Petr Svoboda 1, Michal Makeľ 1, Iva Holmquist 3,4 and Miroslav Ryska 1 1 Department of Surgery, Central Military Hospital – Faculty Military Hospital, 2nd Faculty of Medicine, Charles University, Prague, Czech Republic 2 Department of Thoracic Surgery, Thomayer's Hospital, 140 59 Prague, Czech Republic 3 Emory University Hospital Midtown, Maternity Center, Atlanta, Georgia, USA 4 Department of Epidemiology, Faculty of Health Sciences, University of Defence, Hradec Kralove, Czech Republic Received 19th July 2018. Accepted 13th May 2019. On-line 6th December 2019. Summary Hemothorax is a frequent clinical situation often associated with chest injury or with iatrogenic lesions. Spontaneous hemothorax is uncommon and among its cause may include coagulation disorders, pleural, pulmonary or vascular pathology. Diagnostics is based on radiography or ultrasound and thoracentesis which may be also therapeutic solution. The majority of hemothoraxes can be managed non-operatively but hemodynamic instability, the volume of evacuated blood and persisting blood loss or persisting hemothorax require surgery. A surgical approach may vary from open thoracotomy to rapidly developing minimally invasive methods - video-assisted thoracoscopic surgery (VATS) and videothoracoscopy (VTS). Key words: hemothorax; surgery; VATS; thoracotomy Introduction Hemothorax is a pathological collection of the blood within the pleural cavity. Hemothorax most frequently origin in a thoracic injury but the exact incidence is not known.
    [Show full text]