Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2693_Библиотеки_им_академика_М_И_Перельмана.pdf
272
• They most often are discovered on either plain chest x-ray or CT scan of the
chest.
• Primary cardiac lesions may be found on echocardiogram
C. J. Rees et al.
Special Populations
Age
• Chest neoplasms may occur in any age group.
Co-morbidities
• There are many potential co-morbidities to consider depending on the specic
type of neoplasm. COPD is often present in patients with bronchogenic
carcinoma.
• Thymus mass (thymoma) is associated with myasthenia gravis in about onehalf of cases.
17 Chest Neoplasms
a, b Stage II thymoma (WHO type B1) in a 33-year-old woman who presented with
myasthenia gravis. Frontal chest radiograph shows a hilum overlay sign (arrow) of
a suggestive anterior mediastinal mass. Contrast-enhanced CT scan conrms the
presence of a low-heterogeneous anterior mediastinal mass (arrow). Note the indentation of the arterial trunk pulmonary by the mass. c, d Stage III thymoma (WHO
type B2) in a 54-year-old woman. Frontal chest radiograph reveals a lobulated
mediastinal mass (arrow) on the right side. Contrast-enhanced CT scan demonstrates an enhanced anterior mediastinal mass (arrow) with inltration of surrounding fat (open arrow) [From article: A diagnostic approach to the mediastinal masses.
Insights into Imaging. 2013 Feb;4(1):29–52.
0201-0, at http://link.springer.com/article/10.1007%2Fs13244-012-0201-0/fulltext.
html; by Sergi Juanpere, Noemí Cañete, Pedro Ortuño, Sandra Martínez, Gloria
Sanchez, Lluis Bernado, © The Author(s) 2012; licensed under Creative Commons
Attribution License BY 2.0
from original
http://creativecommons.org/licenses/by/2.0] Caption
https://doi.org/10.1007/s13244-012-
273
Pitfalls inDiagnosis
Critical Steps Not toMiss
• A thorough medical history and chest imaging are essential early in the evaluation of a chest tumor
Mimics
• Infection is the primary mimic of neoplasms in the chest
Time-Dependent Interventions
• Ensuring adequate oxygenation
• Imaging to establish likely etiology
Overall Principles ofTreatment
• Treatment depends on the type of neoplasm and whether any symptomatic
obstruction or compression exists.
274
C. J. Rees et al.
Disease Course
• Disease course depends on the specic diagnosis.
Related Evidence
Papers of particular interest have been highlighted as:
** Of key importance
Practice Guideline
Rivera MP, Mehta AC, Wahidi MM. Establishing the diagnosis of lung cancer:
Diagnosis and management of lung cancer, 3rd ed: American College of Chest
Physicians evidence-based clinical practice guidelines. Chest. 2013 May;143(5
Suppl):e142S-65S. https://doi.org/10.1378/chest.12-2353. PMID: 23649436.
http://www.ncbi.nlm.nih.gov/pubmed/23649436 **
Moreau P, San Miguel J, Ludwig H, Schouten H, Mohty M, Dimopoulos M,
Dreyling M; ESMO Guidelines Working Group. Multiple myeloma: ESMO
Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol.
2013 Oct;24 Suppl 6:vi133-7. https://doi.org/10.1093/annonc/mdt297. PMID:
23956208. http://www.ncbi.nlm.nih.gov/pubmed/23956208 **
Senkus E, Kyriakides S, Penault-Llorca F, Poortmans P, Thompson A, Zackrisson S,
Cardoso F; ESMO Guidelines Working Group. Primary breast cancer: ESMO
Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol.
2013 Oct;24 Suppl 6:vi7-23. https://doi.org/10.1093/annonc/mdt284. PMID:
23970019. http://www.ncbi.nlm.nih.gov/pubmed/23970019 **
Ettinger DS, Akerley W, Borghaei H, Chang A, Cheney RT, Chirieac LR, D'Amico
TA, Demmy TL, Ganti AK, Govindan R, Grannis FW, Horn L, Jahan TM,
Jahanzeb M, Kessinger A, Komaki R, Kong FM, Kris MG, Krug LM, Lennes IT,
Loo BW, Martins R, O'Malley J, Osarogiagbon RU, Otterson GA, Patel JD,
Schenck MP, Pisters KM, Reckamp K, Riely GJ, Rohren E, Swanson SJ, Wood
DE, Yang SC; National Comprehensive Cancer Network. Malignant pleural
mesothelioma. J Natl Compr Canc Netw. 2012 Jan;10(1):26-41. PMID:
22223867.
Ray CE Jr, English B, Funaki BS, Burke CT, Fidelman N, Ginsburg ME, Kinney
TB, Kostelic JK, Kouri BE, Lorenz JM, Nair AV, Nemcek AA Jr, Owens CA,
Saleh AG, Vatakencherry G, Mohammed TL. ACR appropriateness criteria®
radiologic management of thoracic nodules and masses. J Am Coll Radiol. 2012
Jan;9(1):13-9.
http://www.ncbi.nlm.nih.gov/pubmed/22221631 **
http://www.ncbi.nlm.nih.gov/pubmed/22223867 **
https://doi.org/10.1016/j.jacr.2011.09.013. PMID 22221631.
17 Chest Neoplasms
275
Zelenetz AD, Abramson JS, Advani RH, Andreadis CB, Bartlett N, Bellam N, Byrd
JC, Czuczman MS, Fayad LE, Glenn MJ, Gockerman JP, Gordon LI, Harris NL,
Hoppe RT, Horwitz SM, Kelsey CR, Kim YH, LaCasce AS, Nademanee A,
Porcu P, Press O, Pro B, Reddy N, Sokol L, Swinnen LJ, Tsien C, Vose JM,
Wierda WG, Yahalom J, Zafar N.Non-Hodgkin's lymphomas. J Natl Compr
Canc Netw. 2011 May;9(5):484-560. PMID: 21550968.
http://www.ncbi.nlm.
nih.gov/pubmed/21550968 **
Demetri GD, Antonia S, Benjamin RS, Bui MM, Casper ES, Conrad EU 3rd,
DeLaney TF, Ganjoo KN, Heslin MJ, Hutchinson RJ, Kane JM 3rd, Letson GD,
McGarry SV, O'Donnell RJ, Paz IB, Pfeifer JD, Pollock RE, Randall RL, Riedel
RF, Schupak KD, Schwartz HS, Thornton K, von Mehren M, Wayne J; National
Comprehensive Cancer Network Soft Tissue Sarcoma Panel. Soft tissue sarcoma. J Natl Compr Canc Netw. 2010 Jun;8(6):630-74. PMID: 20581298.
http://
www.ncbi.nlm.nih.gov/pubmed/20581298 **
Stahl M, Budach W, Meyer HJ, Cervantes A; ESMO Guidelines Working Group.
Esophageal cancer: Clinical Practice Guidelines for diagnosis, treatment and
follow- up. Ann Oncol. 2010 May;21 Suppl 5:v46-9.
https://doi.org/10.1093/
annonc/mdq163. PMID: 20555101. http://www.ncbi.nlm.nih.gov/pubmed/
20555101 **
Review
Mirrielees JA, Kapur JH, Szalkucki LM, Harter JM, Salkowski LR, Strigel RM,
Traynor AM, Wilke LG.Metastasis of primary lung carcinoma to the breast: a
systematic review of the literature. J Surg Res. 2014 May 15;188(2):419-31.
https://doi.org/10.1016/j.jss.2014.01.024. PMID: 24560348. http://www.ncbi.
nlm.nih.gov/pubmed/24560348 **
Kurihara Y, Matsuoka S, Yamashiro T, Fujikawa A, Matsushita S, Yagihashi K,
Nakajima Y. MRI of pulmonary nodules. AJR Am J Roentgenol. 2014
Mar;202(3):W210-6.
https://doi.org/10.2214/AJR.13.11618. PMID: 24555616.
http://www.ncbi.nlm.nih.gov/pubmed/24555616
Mechtler LL, Nandigam K.Spinal cord tumors: new views and future directions.
Neurol Clin. 2013 Feb;31(1):241-68. https://doi.org/10.1016/j.ncl.2012.09.011.
PMID: 23186903. http://www.ncbi.nlm.nih.gov/pubmed/23186903 **
Lamba G, Frishman WH.Cardiac and pericardial tumors. Cardiol Rev. 2012 Sep-
Oct;20(5):237-52. https://doi.org/10.1097/CRD.0b013e31825603e7. PMID:
22447042. http://www.ncbi.nlm.nih.gov/pubmed/22447042 **
Restrepo CS, Chen MM, Martinez-Jimenez S, Carrillo J, Restrepo C.Chest neo-
plasms with infectious etiologies. World J Radiol. 2011 Dec 28;3(12):279-88.
https://doi.org/10.4329/wjr.v3.i12.279. PMID: 22224176. http://www.ncbi.nlm.
nih.gov/pubmed/22224176 **
276
C. J. Rees et al.
Leja MJ, Shah DJ, Reardon MJ. Primary cardiac tumors. Tex Heart Inst J.
2011;38(3):261-2. PMID: 21720466. http://www.ncbi.nlm.nih.gov/
pubmed/21720466 **
Smith SE, Keshavjee S. Primary chest wall tumors. Thorac Surg Clin. 2010
Nov;20(4):495-507.
https://doi.org/10.1016/j.thorsurg.2010.07.003. PMID:
20974433. http://www.ncbi.nlm.nih.gov/pubmed/20974433 **
Cohort Study
Sakellaridis T, Gaitanakis S, Piyis A.Rib tumors: a 15-year experience. Gen Thorac
Cardiovasc Surg. 2014 Jul;62(7):434-40.
0387-9. PMID: 24615297. http://www.ncbi.nlm.nih.gov/pubmed/24615297 **
Use PubMed Clinical Queries to nd the most recent evidence. Use this search
strategy:
“Thoracic Neoplasms”[Mesh] OR “Breast Neoplasms”[Mesh] OR “Esophageal
Neoplasms”[Mesh] OR “Spinal Neoplasms”[Mesh] OR “Sarcoma”[Mesh] OR
“Mesothelioma”[Mesh] OR “Multiple Myeloma”[Mesh] OR “Lymphoma”
[Mesh]
https://doi.org/10.1007/s11748-014-
Chapter 18
Chronic Obstructive Pulmonary Disease
ChristopherJ.Rees, CharlesV.Pollack,Jr., andVictoriaG.Riese
Name andSynonyms
Chronic Obstructive Pulmonary Disease; COPD; Emphysema
Incidence/Epidemiology
• COPD affects about 5 % of the U.S. population.
• COPD is reported as the third- or fourth-leading cause of death in the U.S,
depending upon the survey. COPD is directly responsible for about 120,000
deaths per year in the U.S.
• COPD is associated with a very high rate of medical resource utilization.
The majority of these costs are for hospitalization of acute exacerbations of
COPD.
• In the U.S., nearly 2 % of all hospital admissions are directly attributable to
COPD.It is considered a major contributing factor in another 9 % of hospital
admissions. In patients older than 65, the percentage of all hospital admission
related to COPD approaches 20 %.
• COPD is the only major cause of death that is increasing in the U.S.
C. J. Rees
Emergency Department, Pennsylvania Hospital, Philadelphia, PA, USA
C. V. Pollack,
Department of Emergency Medicine, Thomas Jefferson University,
Philadelphia, PA, USA
V. G. Riese
Librarian Consultant, Eldersburg, MD, USA
C. V. Pollack, Jr. (ed.), Differential Diagnosis of Cardiopulmonary Disease,
https://doi.org/10.1007/978-3-319-63895-9_18
Jr. ()
277© Springer Nature Switzerland AG 2019
278
C. J. Rees et al.
• The incidence and mortality of COPD in women is increasing worldwide.
This is likely related to the increased incidence of smoking among women
during the last 50 years.
• Tobacco smoke is the major risk factor for developing COPD, but only 15 %
of smokers will develop COPD.
• Alpha-1 antitrypsin deciency accounts for less than 1 % of COPD cases.
Worldwide prevalence of chronic obstructive pulmonary disease (COPD). The prevalence of COPD (in 2007) in different geographic regions based on the Burden of
Obstructive Lung Disease data [Buist AS, McBurnie MA, Vollmer WM, et al.
International variation in the prevalence of COPD (the BOLD Study): a populationbased prevalence study. Lancet. 2007; 370:741 -750.] is presented based on results for
specic cities within the countries listed. The reasons for these regional differences are
not entirely clear and may be due to different environmental exposures (smoking, biomass, occupation), as well as possibly genetic factors. [Cho M, Silverman E.Genetics
and Racial, Ethnic, and Gender Characteristics of COPD.In: Crapo JD, editor. Atlas of
Chronic Obstructive Pulmonary Disease. Philadelphia, PA: Current Medicine Group;
2009. 160 p. ISBN: 978-1-57340-294-1] Caption from original
Differential Diagnosis
• The primary symptoms of COPD are dyspnea (usually exertional early in the
disease course), cough, and sputum production.
18 Chronic Obstructive Pulmonary Disease
• The differential diagnosis of these symptoms is broad, and includes many
diseases and organ symptoms.
• Patients may present with worsening fatigue, exercise or activity intolerance,
and often complain of daily cough for many months.
• In patients without a current diagnosis of COPD, the differential includes:
• Congestive heart failure
• Interstitial lung disease
• Thromboembolic Disease (pulmonary embolism)
• Asthma
• Bronchiectasis
• Tuberculosis
• Bronchiolitis
• Airway obstruction from bronchogenic or metastatic cancer, lymphadenopathy (sarcoidosis), and tracheal stenosis/scarring.
• It is important to remember that many of these disorders can occur together.
• In patients with an existing diagnosis of COPD, who present with acute dyspnea (exacerbation of COPD), the cause of the exacerbation needs to be
investigated. The differential for acute dyspnea in these patients is also broad,
and includes:
• CHF/pulmonary edema
• Acute coronary syndrome
• Pneumonia
• Viral respiratory infection
• Pulmonary embolism
• Pleural effusion
• Pneumothorax
• Pericardial effusion
• Mucous plugging of bronchi
• Rib fracture from severe coughing
• Electrolyte imbalance (especially hypokalemia and hypocalcemia)
279
Pathophysiology andEtiology
• Chronic obstructive pulmonary disease (COPD) is a disease characterized by
chronic, progressive airow obstruction.
• The Global Initiative for Chronic Obstructive Lung Disease (GOLD), sponsored by the National Heart, Lung, and Blood Institute (NHLBI) and the
World Health Organization (WHO), denes COPD as follows: “Chronic
obstructive pulmonary disease (COPD), a common preventable and treatable
disease, is characterized by airow limitation that is usually progressive and
associated with an enhanced chronic inammatory response in the airways
and the lung to noxious particles or gases. Exacerbations and comorbidities
contribute to the overall severity in individual patients.”
280
C. J. Rees et al.
Severity criteria of COPD. [3] BTS: BTS guidelines for the management of chronic
obstructive pulmonary disease. The COPD Guidelines Group of the Standards of
Care Committee of the BTS. Thorax 1997, 52:S1-28. [2] Pauwels RA, Buist AS,
Calverley PMA, Jenkins CR, Hurd SS: Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: NHLBI and WHO
Global Initiative for Chronic Obstructive Lung Disease (GOLD): executive summary.
Respiratory Care 2001, 46:798-825. [From article: Health-related quality of life is
related to COPD disease severity. Health and Quality of Life Outcomes. 2005 Sep
9;3(1):56.
https://doi.org/10.1186/1477-7525-3-56, at http://link.springer.com/article
/10.1186%2F1477-7525-3-56/fulltext.html; by Elisabeth Ståhl, Anne Lindberg,
Sven-Arne Jansson, Eva Rönmark, Klas Svensson, Fredrik Andersson, Claes-Göran
Löfdahl, Bo Lundbäck, © Ståhl etal; licensee BioMed Central Ltd. 2005; licensed
under Creative Commons Attribution License BY 2.0
http://creativecommons.org/
licenses/by/2.0]
• The pathophysiology of COPD involves the airways, lung parenchyma, and
pulmonary vasculature.
• Airways: The most signicant pathologic change in the airways involves
chronic inammation from exposure to cigarette smoke and other pollutants, which leads to several permanent anatomic changes such as:
• Mucous gland hyperplasia and increased numbers of goblet cells,
resulting in increased mucous secretion. Increased mucous secretion
and stasis leads to pathogenic bacterial colonization.
• Increased mucous-secreting and goblet cells replace surfactant-secreting
cells, which augments collapse and destruction of the small airways.
• Increased induction of inammatory cells with increased local protease
production, accelerating tissue damage and breakdown.
• Fibrosis with loss of elastic recoil, narrowing, collapse, and subsequent
destruction and reduction in the number of small airways.
• There is also squamous metaplasia within the airways resulting in an
increased risk for cancer.
18 Chronic Obstructive Pulmonary Disease
281
Overview of small airways in COPD: schematic view [Barnes PJ.Pathophysiology
of COPD.In: Crapo JD, editor. Atlas of Chronic Obstructive Pulmonary Disease.
Philadelphia, PA: Current Medicine Group; 2009. 160 p. ISBN: 978-1-57340-294-1]
Caption adapted from original
Link between inammation and airway obstruction in chronic obstructive pulmonary disease (COPD). Chronic exposure to inhaled cigarette smoke and biomass particles (wood smoke) results in chronic inammation of the lungs.
Genetic and other unknown factors are responsible for the increased susceptibility to inhaled irritants. Inammation generates reactive oxygen species (oxidative stress), which is normally counteracted by endogenous antioxidant
mechanisms, but these may be defective in COPD.Inammation also activates
proteinases, which result in connective tissue destruction. This may be countered
by antiproteinases and repair mechanisms that may also be defective in COPD.