Pulmonary Medicine and Critical Care
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Chylothorax After Left Side Pneumothorax Surgery Managed by OK-432 Pleurodesis: an Effective Alternative
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Available online at www.sciencedirect.com ScienceDirect Journal of the Chinese Medical Association 77 (2014) 653e655 www.jcma-online.com Case Report Chylothorax after left side pneumothorax surgery managed by OK-432 pleurodesis: An effective alternative Sheng-Yang Huang a, Chou-Ming Yeh b, Chia-Man Chou a,c,*, Hou-Chuan Chen a a Division of Pediatric Surgery, Department of Surgery, Taichung Veterans General Hospital, Taichung, Taiwan, ROC b Taichung Hospital, Ministry of Health and Welfare, Taichung, Taiwan, ROC c National Yang-Ming University School of Medicine, Taipei, Taiwan, ROC Received June 13, 2013; accepted September 23, 2013 Abstract Chylothorax, a relatively rare complication of thoracic surgery, mostly occurs on the right side. We present a 16-year-old male who received thoracoscopic surgery for left spontaneous pneumothorax. Chylothorax developed on the postoperative 2nd day and resolved after diet control on the 4th day. Unfortunately, chylothorax recurred 2 weeks later. Chest drainage and nil per os with total parental nutrition were given but in vain. Thereafter, chemical pleurodesis with OK-432 was performed. Chylothorax resolved on the next day. The relevant literature is reviewed and possible pathogenesis clarified. Copyright © 2014 Elsevier Taiwan LLC and the Chinese Medical Association. All rights reserved. Keywords: chylothorax; pleurodesis; pneumothorax 1. Introduction 2. Case Report Postoperative chylothorax is infrequent but potentially A 16-year-old male patient had the history of left chest pain life-threatening and time-consuming to manage. Associated for 5 days. -
Section 8 Pulmonary Medicine
SECTION 8 PULMONARY MEDICINE 336425_ST08_286-311.indd6425_ST08_286-311.indd 228686 111/7/121/7/12 111:411:41 AAMM CHAPTER 66 EVALUATION OF CHRONIC COUGH 1. EPIDEMIOLOGY • Nearly all adult cases of chronic cough in nonsmokers who are not taking an ACEI can be attributed to the “Pathologic Triad of Chronic Cough” (asthma, GERD, upper airway cough syndrome [UACS; previously known as postnasal drip syndrome]). • ACEI cough is idiosyncratic, occurrence is higher in female than males 2. PATHOPHYSIOLOGY • Afferent (sensory) limb: chemical or mechanical stimulation of receptors on pharynx, larynx, airways, external auditory meatus, esophagus stimulates vagus and superior laryngeal nerves • Receptors upregulated in chronic cough • CNS: cough center in nucleus tractus solitarius • Efferent (motor) limb: expiratory and bronchial muscle contraction against adducted vocal cords increases positive intrathoracic pressure 3. DEFINITION • Subacute cough lasts between 3 and 8 weeks • Chronic cough duration is at least 8 weeks 4. DIFFERENTIAL DIAGNOSIS • Respiratory tract infection (viral or bacterial) • Asthma • Upper airway cough syndrome (postnasal drip syndrome) • CHF • Pertussis • COPD • GERD • Bronchiectasis • Eosinophilic bronchitis • Pulmonary tuberculosis • Interstitial lung disease • Bronchogenic carcinoma • Medication-induced cough 5. EVALUATION AND TREATMENT OF THE COMMON CAUSES OF CHRONIC COUGH • Upper airway cough syndrome: rhinitis, sinusitis, or postnasal drip syndrome • Presentation: symptoms of rhinitis, frequent throat clearing, itchy -
Allergic Bronchopulmonary Aspergillosis As a Cause of Bronchial Asthma in Children
Egypt J Pediatr Allergy Immunol 2012;10(2):95-100. Original article Allergic bronchopulmonary aspergillosis as a cause of bronchial asthma in children Background: Allergic bronchopulmonary aspergillosis (ABPA) occurs in Dina Shokry, patients with asthma and cystic fibrosis. When aspergillus fumigatus spores Ashgan A. are inhaled they grow in bronchial mucous as hyphae. It occurs in non Alghobashy, immunocompromised patients and belongs to the hypersensitivity disorders Heba H. Gawish*, induced by Aspergillus. Objective: To diagnose cases of allergic bronchopulmonary aspergillosis among asthmatic children and define the Manal M. El-Gerby* association between the clinical and laboratory findings of aspergillus fumigatus (AF) and bronchial asthma. Methods: Eighty asthmatic children were recruited in this study and divided into 50 atopic and 30 non-atopic Departments of children. The following were done: skin prick test for aspergillus fumigatus Pediatrics and and other allergens, measurement of serum total IgE, specific serum Clinical Pathology*, aspergillus fumigatus antibody titer IgG and IgE (AF specific IgG and IgE) Faculty of Medicine, and absolute eosinophilic count. Results: ABPA occurred only in atopic Zagazig University, asthmatics, it was more prevalent with decreased forced expiratory volume Egypt. at the first second (FEV1). Prolonged duration of asthma and steroid dependency were associated with ABPA. AF specific IgE and IgG were higher in the atopic group, they were higher in Aspergillus fumigatus skin Correspondence: prick test positive children than negative ones .Wheal diameter of skin prick Dina Shokry, test had a significant relation to the level of AF IgE titer. Skin prick test Department of positive cases for aspergillus fumigatus was observed in 32% of atopic Pediatrics, Faculty of asthmatic children. -
Khan CV 9-4-20
CURRICULUM VITAE DAVID A. KHAN, MD University of Texas Southwestern Medical Center 5323 Harry Hines Boulevard Dallas, TX 75390-8859 (214) 648-5659 (work) (214) 648-9102 (fax) [email protected] EDUCATION 1980 -1984 University of Illinois, Champaign IL; B.S. in Chemistry, Magna Cum Laude 1984 -1988 University of Illinois School of Medicine, Chicago IL; M.D. 1988 -1991 Good Samaritan Medical Center, Phoenix AZ; Internal Medicine internship & residency 1991-1994 Mayo Clinic, Rochester MN; Allergy & Immunology fellowship PROFESSIONAL EXPERIENCE 1994 -2001 Assistant Professor of Internal Medicine, UT Southwestern 1997 -1998 Co-Director, Allergy & Immunology Training Program 1998 - Director, Allergy & Immunology Training Program 2002- 2008 Associate Professor of Internal Medicine, UT Southwestern 2008-present Professor of Medicine, UT Southwestern AWARDS/HONORS 1993 Allen & Hanburys Respiratory Institute Allergy Fellowship Award 1993 Von Pirquet Award 2001 Outstanding Teacher 2000-2001 UTSW Class of 2003 2004 Outstanding Teacher 2003-2004 UTSW Class of 2006 2005 Outstanding Teacher 2004-2005 UTSW Class of 2007 2006 Daniel Goodman Lectureship, ACAAI meeting 2007 Most Entertaining Teacher 2006-2007 UTSW Class of 2009 2008 Stanislaus Jaros Lectureship, ACAAI meeting 2009 Outstanding Teacher 2007-2008 UTSW Class of 2010 2011 John L. McGovern Lectureship, ACAAI meeting 2012 I. Leonard Bernstein Lecture, ACAAI meeting 2014 Distinguished Fellow, ACAAI meeting 2015 Elliot F. Ellis Memorial Lectureship, AAAAI meeting 2015 Bernard Berman Lectureship, -
Hypersensitivity Pneumonitis: Challenges in Diagnosis and Management, Avoiding Surgical Lung Biopsy
395 Hypersensitivity Pneumonitis: Challenges in Diagnosis and Management, Avoiding Surgical Lung Biopsy Ferran Morell, MD1,2 Ana Villar, MD2,3 Iñigo Ojanguren, MD2,3 Xavier Muñoz, MD2,3 María-Jesús Cruz, PhD2,3 1 Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Catalonia, Spain Address for correspondence Ferran Morell, MD, Vall d’Hebron Institut 2 Ciber de Enfermedades Respiratorias (CIBERES), Barcelona, Spain de Recerca (VHIR), PasseigValld’Hebron, 119-129, 08035 Barcelona, 3 Servei de Pneumologia, Hospital Universitari Vall d’Hebron, Catalonia, Spain (e-mail: [email protected]). Barcelona, Spain Semin Respir Crit Care Med 2016;37:395–405. Abstract This review presents an update of the currently available information related to Keywords hypersensitivity pneumonitis, with a particular focus on the contribution of several ► hypersensitivity techniques in the diagnosis of this condition. The methods discussed include proper pneumonitis elaboration of a complete medical history, targeted auscultation, detection of specific ► bronchoalveolar immunoglobulin G antibodies against the most common antigens causing this disease, lavage skin tests, antigen-specific lymphocyte activation assays, bronchoalveolar lavage, and ► fi speci c inhalation cryobiopsy. Special emphasis is placed on the relevant contribution of specificinhalation challenge challenge (bronchial challenge test). Surgical lung biopsy is presented as the ultimate ► bronchial challenge recourse, to be used when the diagnosis cannot be reached through the other methods test covered. -
Chylothorax As Rare Manifestation of Pleural Involvement in Waldenström Macroglobulinemia: Mechanisms and Management
210 Lymphology 49 (2016) 210-217 CHYLOTHORAX AS RARE MANIFESTATION OF PLEURAL INVOLVEMENT IN WALDENSTRÖM MACROGLOBULINEMIA: MECHANISMS AND MANAGEMENT G. Leoncini, C.C. Campisi, G. Fraternali Orcioni, F. Patrone, F. Ferrando, C. Campisi Unit of Thoracic Surgery (GL), Unit of General & Lymphatic Surgery - Microsurgery and Department of Surgical Sciences and Integrated Diagnostics (DISC) (CCC,CC), Unit of Pathology (GFO), Unit of Internal Medicine and Medical Oncology and Department of Internal Medicine (DIMI) (FP,FF), IRCCS San Martino University Hospital - National Institute for Cancer Research, and University School of Medicine and Pharmaceutics, Genoa, Italy ABSTRACT increase of IgM level. Pleuropulmonary involvement is reported to be rare (from 0 Here we report the clinical, pathological, to 5% of cases), and it usually occurs during and immunological features of a rare case of the late phase of the disease (3,4). In such a Waldenström macroglobulinemia (WM) with scenario, chylothorax is rarely observed in pleural infiltrations. An atypical chylothorax, WM patients; indeed only seven cases have successfully treated by videothoracoscopy, been reported in the literature (5-11). We represented the main clinical feature of this report the case of a 66-year old man with the case of low-grade lymphoplasmacytic main clinical presentation of pleural lymphoma. Pleuropulmonary manifestations infiltrations with right chylothorax following are rare (from 0 to 5% of cases) in WM, with immunochemotherapy. An extra-bone chylothorax observed in just seven patients marrow involvement was suggested by both worldwide. In addition to describing this pleural fluid examination and multiple uncommon clinical presentation, we investi- pleural biopsies in parallel with a marked gate hypothetical pathogenetic mechanisms decrease of bone marrow (BM) participation causing chylothorax and through an up-to- (tumor cells in BM from 70% to 8%). -
Workers' Compensation for Occupational Respiratory Diseases
ORIGINAL ARTICLE http://dx.doi.org/10.3346/jkms.2014.29.S.S47 • J Korean Med Sci 2014; 29: S47-51 Workers’ Compensation for Occupational Respiratory Diseases So-young Park,1 Hyoung-Ryoul Kim,2 The respiratory system is one of the most important body systems particularly from the and Jaechul Song3 viewpoint of occupational medicine because it is the major route of occupational exposure. In 2013, there were significant changes in the specific criteria for the recognition of 1Occupational Lung Diseases Institute, Korea Workers’ Compensation & Welfare Service, Ansan; occupational diseases, which were established by the Enforcement Decree of the Industrial 2Department of Occupational and Environmental Accident Compensation Insurance Act (IACIA). In this article, the authors deal with the Medicine, College of Medicine, the Catholic former criteria, implications of the revision, and changes in the specific criteria in Korea by University of Korea, Seoul; 3Department of focusing on the 2013 amendment to the IACIA. Before the 2013 amendment to the IACIA, Occupational and Environmental Medicine, Hanyang University College of Medicine, Seoul, occupational respiratory disease was not a category because the previous criteria were Korea based on specific hazardous agents and their health effects. Workers as well as clinicians were not familiar with the agent-based criteria. To improve these criteria, a system-based Received: 20 December 2013 structure was added. Through these changes, in the current criteria, 33 types of agents Accepted: 6 April 2014 and 11 types of respiratory diseases are listed under diseases of the respiratory system. In Address for Correspondence: the current criteria, there are no concrete guidelines for evaluating work-relatedness, such Hyoung-Ryoul Kim, MD as estimating the exposure level, latent period, and detailed examination methods. -
Asthma Exacerbation Management
CLINICAL PATHWAY ASTHMA EXACERBATION MANAGEMENT TABLE OF CONTENTS Figure 1. Algorithm for Asthma Exacerbation Management – Outpatient Clinic Figure 2. Algorithm for Asthma Management – Emergency Department Figure 3. Algorithm for Asthma Management – Inpatient Figure 4. Progression through the Bronchodilator Weaning Protocol Table 1. Pediatric Asthma Severity (PAS) Score Table 2. Bronchodilator Weaning Protocol Target Population Clinical Management Clinical Assessment Treatment Clinical Care Guidelines for Treatment of Asthma Exacerbations Children’s Hospital Colorado High Risk Asthma Program Table 3. Dosage of Daily Controller Medication for Asthma Control Table 4. Dosage of Medications for Asthma Exacerbations Table 5. Dexamethasone Dosing Guide for Asthma Figure 5. Algorithm for Dexamethasone Dosing – Inpatient Asthma Patient | Caregiver Education Materials Appendix A. Asthma Management – Outpatient Appendix B. Asthma Stepwise Approach (aka STEPs) Appendix C. Asthma Education Handout References Clinical Improvement Team Page 1 of 24 CLINICAL PATHWAY FIGURE 1. ALGORITHM FOR ASTHMA EXACERBATION MANAGEMENT – OUTPATIENT CLINIC Triage RN/MA: • Check HR, RR, temp, pulse ox. Triage level as appropriate • Notify attending physician if patient in severe distress (RR greater than 35, oxygen saturation less than 90%, speaks in single words/trouble breathing at rest) Primary RN: • Give oxygen to keep pulse oximetry greater than 90% Treatment Inclusion Criteria 1. Give nebulized or MDI3 albuterol up to 3 doses. Albuterol dosing is 0.15 to 0.3mg/kg per 2007 • 2 years or older NHLBI guidelines. • Treated for asthma or asthma • Less than 20 kg: 2.5 mg neb x 3 or 2 to 4 puffs MDI albuterol x 3 exacerbation • 20 kg or greater: 5 mg neb x 3 or 4 to 8 puffs MDI albuterol x 3 • First time wheeze with history consistent Note: For moderate (dyspnea interferes with activities)/severe (dyspnea at rest) exacerbations you with asthma can add atrovent to nebulized albuterol at 0.5mg/neb x 3. -
NUR 6325 Family Primary Care I Fall Semester 2021 Course Information
NUR 6325 Family Primary Care I Fall Semester 2021 Department of Nursing Instructor: Avis Johnson-Smith, DNP, APRN, FNP-BC, CPNP-PC, CPMHS, CNS, FAANP Email: [email protected] Phone: 229-431-2030 Office: Virtual Office Hours: By Appointment. If you have a question and an email response would suffice, then simply let me know this when you contact me. Time Zone: All due dates and times in this syllabus are Central Standard Time (CST) Course Information Course Description The course focus is on the transition from RN to Family Nurse Practitioner in the diagnosis and management of common acute and chronic conditions across the lifespan in a primary care setting. As a provider of family-centered care emphasis is placed on health promotion, risk reduction and evidence- based management of common symptoms and problems. Nursing’s unique contribution to patient care and collaboration with other health care professionals is emphasized. Course Credits Three semester credit hours (3-0-0) This course meets completely online using Blackboard as the delivery method Prerequisite / Co-requisite Courses NUR 6201, 6318, 6323, 6324, 6331, NUR 6327 Prerequisite Skills Accessing internet web sites, use of ASU Library resources, and proficiency with Microsoft Word and/or PowerPoint are expectations of the program name. Computer access requirements are further delineated in the graduate Handbook. Tutorials for ASU Library and for Blackboard are available through RamPort. The ASU Graduate Nursing Student Handbook1 should be reviewed before taking this course. Program Outcomes Upon completion of the program of study for the MSN Program, the graduate will be prepared to: 1. -
Silicosis: Pathogenesis and Changklan Muang Chiang Mai 50100 Thailand; Tel: 66 53 276364; Fax: 66 53 273590; E-Mail
Central Annals of Clinical Pathology Bringing Excellence in Open Access Review Article *Corresponding author Attapon Cheepsattayakorn, 10th Zonal Tuberculosis and Chest Disease Center, 143 Sridornchai Road Silicosis: Pathogenesis and Changklan Muang Chiang Mai 50100 Thailand; Tel: 66 53 276364; Fax: 66 53 273590; E-mail: Biomarkers Submitted: 04 October 2018 Accepted: 31 October 2018 1,2 3 Attapon Cheepsattayakorn * and Ruangrong Cheepsattayakorn Published: 31 October 2018 1 10 Zonal Tuberculosis and Chest Disease Center, Chiang Mai, Thailand ISSN: 2373-9282 2 Department of Disease Control, Ministry of Public Health, Thailand Copyright 3 Department of Pathology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand © 2018 Cheepsattayakorn et al. OPEN ACCESS Abstract Ramazzini first described this disease, namely “Pneumonoultramicroscopicsilicovolcanokoniosis” Keywords and then was changed according to the types of exposed dust. No reliable figures on the silica- • Silicosis inhalation exposed individuals are officially documented. How silica particles stimulate pulmonary • Biomarkers response and the exact path physiology of silicosis are still not known and urgently require further • Pathogenesis research. Nevertheless, many researchers hypothesized that pulmonary alveolar macrophages play a major role by secreting fibroblast-stimulating factor and re-ingesting these ingested silica particles by the pulmonary alveolar macrophage with progressive magnification. Finally, ending up of the death of the pulmonary alveolar macrophages and the development of pulmonary fibrosis appear. Various mediators, such as CTGF, FBRS, FGF2/bFGF, and TNFα play a major role in the development of silica-induced pulmonary fibrosis. A hypothesis of silicosis-associated abnormal immunoglobulins has been postulated. In conclusion, novel studies on pathogenesis and biomarkers of silicosis are urgently needed for precise prevention and control of this silently threaten disease of the world. -
Etiology and Aggravation in Thoracic Medicine
DePaul Law Review Volume 21 Issue 1 Fall 1971: Medico-Legal Symposium II Article 6 Etiology and Aggravation in Thoracic Medicine W. B. Buckingham Follow this and additional works at: https://via.library.depaul.edu/law-review Recommended Citation W. B. Buckingham, Etiology and Aggravation in Thoracic Medicine, 21 DePaul L. Rev. 103 (1971) Available at: https://via.library.depaul.edu/law-review/vol21/iss1/6 This Article is brought to you for free and open access by the College of Law at Via Sapientiae. It has been accepted for inclusion in DePaul Law Review by an authorized editor of Via Sapientiae. For more information, please contact [email protected]. ETIOLOGY AND AGGRAVATION IN THORACIC MEDICINE W. B. BUCKINGHAM* INTRODUCTION N THE practice of thoracic medicine, misconceptions about the etiology and/or the aggravation of thoracic diseases are common- place. These errors are frequently perpetuated by patients and occasionally by well-meaning lawyers and well-trained physicians. Superficial analysis indicates that most of these misconceptions arise from the concept of post hoc ergo propter hoc. In diseases affecting the thorax, multiple etiological factors commonly operate over pro- longed periods of time. Under such circumstances it is extremely difficult to sort out cause and effect. Thus, in light of the imperfec- tions in diagnosis, misconceptions about etiology and aggravation of disease can be appreciated. There are substantial limitations and uncertainties to any medical diagnosis. The semantic derivation of the word "diagnosis" comes through the Greek words whose meaning is "to know through" or "to understand by means of the manifestations of." A complete diagnosis in the modem sense of the term is a disease entity in which the causative mechanisms are clearly understood, and the man- ifestations readily appreciated both in clinical signs and symptoms and in laboratory findings. -
Management of Acute Exacerbation of Asthma and Chronic Obstructive Pulmonary Disease in the Emergency Department
Management of Acute Exacerbation of Asthma and Chronic Obstructive Pulmonary Disease in the Emergency Department Salvador J. Suau, MD*, Peter M.C. DeBlieux, MD KEYWORDS Asthma Asthmatic crisis COPD AECOPD KEY POINTS Management of severe asthma and chronic obstructive pulmonary disease (COPD) exac- erbations require similar medical interventions in the acute care setting. Capnography, electrocardiography, chest x-ray, and ultrasonography are important diag- nostic tools in patients with undifferentiated shortness of breath. Bronchodilators and corticosteroids are first-line therapies for both asthma and COPD exacerbations. Noninvasive ventilation, magnesium, and ketamine should be considered in patients with severe symptoms and in those not responding to first-line therapy. A detailed plan reviewed with the patient before discharge can decrease the number of future exacerbations. INTRODUCTION Acute asthma and chronic obstructive pulmonary disease (COPD) exacerbations are the most common respiratory diseases requiring emergent medical evaluation and treatment. Asthma accounts for more than 2 million visits to emergency departments (EDs), and approximately 4000 annual deaths in the United States.1 In a similar fashion, COPD is a major cause of morbidity and mortality. It affects more than 14.2 million Americans (Æ9.8 million who may be undiagnosed).2 COPD accounts for more than 1.5 million yearly ED visits and is the fourth leading cause of death Disclosures: None. Louisiana State University, University Medical Center of New Orleans, 2000 Canal Street, D&T 2nd Floor - Suite 2720, New Orleans, LA 70112, USA * Corresponding author. E-mail address: [email protected] Emerg Med Clin N Am 34 (2016) 15–37 http://dx.doi.org/10.1016/j.emc.2015.08.002 emed.theclinics.com 0733-8627/16/$ – see front matter Ó 2016 Elsevier Inc.