eMedicine Specialties > Pulmonology > Obstructive Airways Diseases

Emphysema

Author: Berj George Demirjian, MD, Fellow, Division of Pulmonary/Critical Care Medicine, Cedars-Sinai Medical Center
Coauthor(s): Nader Kamangar, MD, FACP, FCCP, FAASM, Associate Professor of Clinical Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Multi-campus Pulmonary and Critical Care Fellowship Program, University of California, Los Angeles, David Geffen School of Medicine; Medical Director, Hospitalist/Intensivist Program, Olive View-UCLA Medical Center; Associate Program Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA Medical Center/West Los Angeles Veterans Affairs Medical Center
Contributor Information and Disclosures

Updated: Oct 26, 2009

Introduction

Background

Emphysema is chronic obstructive pulmonary disease (COPD). Emphysema is defined pathologically as an abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of alveolar walls and without obvious fibrosis. Emphysema frequently occurs in association with chronic bronchitis. These 2 entities have been traditionally grouped under the umbrella term COPD. Patients have been classified as having COPD with either emphysema or chronic bronchitis predominance. The current definition of COPD put forth by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) does not distinguish between emphysema and chronic bronchitis.1

The 3 described morphological types of emphysema are centriacinar, panacinar, and paraseptal.

Centriacinar emphysema begins in the respiratory bronchioles and spreads peripherally. Also termed centrilobular emphysema, this form is associated with long-standing cigarette smoking and predominantly involves the upper half of the lungs.

Panacinar emphysema destroys the entire alveolus uniformly and is predominant in the lower half of the lungs. Panacinar emphysema generally is observed in patients with homozygous alpha1-antitrypsin (AAT) deficiency. In people who smoke, focal panacinar emphysema at the lung bases may accompany centriacinar emphysema.

Paraseptal emphysema, also known as distal acinar emphysema, preferentially involves the distal airway structures, alveolar ducts, and alveolar sacs. The process is localized around the septae of the lungs or pleura. Although airflow frequently is preserved, the apical bullae may lead to spontaneous pneumothorax. Giant bullae occasionally cause severe compression of adjacent lung tissue.

Gross pathology of bullous emphysema shows bullae...

Gross pathology of bullous emphysema shows bullae on the surface of the lungs.

[ CLOSE WINDOW ]
Gross pathology of bullous emphysema shows bullae...

Gross pathology of bullous emphysema shows bullae on the surface of the lungs.


Gross pathology of emphysema shows bullae on the ...

Gross pathology of emphysema shows bullae on the lung surface.

[ CLOSE WINDOW ]
Gross pathology of emphysema shows bullae on the ...

Gross pathology of emphysema shows bullae on the lung surface.


Pathophysiology

Emphysema is a pathological diagnosis defined by permanent enlargement of airspaces distal to the terminal bronchioles. This leads to a dramatic decline in the alveolar surface area available for gas exchange. Furthermore, loss of alveoli leads to airflow limitation by 2 mechanisms. First, loss of the alveolar walls results in a decrease in elastic recoil, which leads to airflow limitation. Second, loss of the alveolar supporting structure leads to airway narrowing, which further limits airflow.

Emphysema commonly presents with chronic bronchitis. Chronic bronchitis leads to obstruction by causing narrowing of both the large and small (<2 mm) airways. In the large airways, an increase in Goblet cells, squamous metaplasia of ciliary epithelial cells, and loss of serous acini can be seen. In the small airways, Goblet cell metaplasia, smooth muscle hyperplasia, and subepithelial fibrosis can be seen. In healthy individuals, small airways contribute little to airway resistance; however, in COPD patients, these become the main site of airflow limitation.

Pathogenesis

Most of cases of COPD are the result of exposure to noxious stimuli, most often cigarette smoke. The normal inflammatory response is amplified in persons prone to COPD development.1 Genetics are believed to play a role in this response because not all smokers develop the disease. The cellular composition of airway inflammation is predominantly mediated by neutrophils, macrophages, and lymphocytes. These cells release chemotactic factors to recruit more cells (proinflammatory cytokines that amplify the inflammation) and growth factors that promote structural change. The inflammation is further amplified by oxidative stress and protease production. Oxidants are produced from cigarette smoke and released from inflammatory cells. Proteases are produced by inflammatory and epithelial cells. This leads to a protease-antiprotease imbalance that leads to destruction of elastin and other structural elements. This is believed to be central in the development of emphysema.

Alpha1-antitrypsin deficiency

AAT is a glycoprotein member of the serine protease inhibitor family that is synthesized in the liver and is secreted into the blood stream. The main purpose of this 394–amino acid, single-chain protein is to neutralize neutrophil elastase in the lung interstitium and to protect the lung parenchyma from elastolytic breakdown. Severe AAT deficiency predisposes to unopposed elastolysis with the clinical sequela of an early onset of panacinar emphysema.

Deficiency of AAT is inherited as an autosomal codominant condition. The gene is located on the long arm of chromosome 14 and has been sequenced and cloned. The most common type of severe AAT deficiency occurs in individuals who are homozygous for the Z-type protein. Homozygous individuals (PIZZ) have serum levels well below the reference range levels (reference range, 20-53 mmol/L). The risk of emphysema occurs below a threshold of 11 mmol/L.

Frequency

United States

The National Health Interview Survey reports the prevalence of emphysema at 18 cases per 1000 persons and chronic bronchitis at 34 cases per 1000 persons.2 While the rate of emphysema has stayed largely unchanged since 2000, the rate of chronic bronchitis has decreased. This prevalence is based on the number of adults who have ever been told by any health care provider that they have emphysema or chronic bronchitis. This is felt to be an underestimate because most patients do not present for medical care until the disease is in a late stage.

International

The Burden of Obstructive Lung Disease (BOLD) study showed that the worldwide prevalence of COPD (stage II or higher) was 10.1%.3 This figure varied by geographic location and by sex. Pooled prevalence among men was 11.8% (8.6-22.2%) and among women was 8.5% (5.1-16.7%). The differences can, in part, be explained by site and sex differences in the prevalence of smoking. These rates are similar to rates observed in the Proyecto Latino Americano de Investigacion en Obstruccion Pulmonar (PLATINO study), which studied 5 countries in Latin America.4

Mortality/Morbidity

A US Centers for Disease Control and Prevention (CDC) Morbidity Mortality Weekly Report study of the National Vital Statistics System reported an age-standardized death rate from COPD in the United States for adults older than 25 years of 64.3 deaths per 100,000 population.5 This rate varied by location, with the lowest rate in Hawaii (27.1 deaths per 100,000 population) and the highest rate in Oklahoma (93.6 deaths per 100,000 population).

Sex

In the past, COPD was more prevalent among men. This was attributed to the difference in smoking rates in men versus women. With the increase in smoking among women, the difference has declined. Some studies have suggested women may be more susceptible to COPD.6

Clinical

History

Most patients seek medical attention late in the course of their disease. Patients often ignore the symptoms because they start gradually and progress over the course of years. Patients often modify their lifestyle to minimize dyspnea and ignore cough and phlegm production. With retroactive questioning, a multiyear history can be elicited.

  • Commonly, patients present in their fifth decade of life with productive cough or acute chest illness. The cough usually is worse in the morning and produces small amounts of colorless sputum from concomitant chronic bronchitis.
  • Breathlessness, the most significant symptom, does not occur until the sixth decade of life. By the time the forced expiratory volume in 1 second (FEV1) has fallen to 50% of predicted, the patient is breathless upon minimal exertion.
  • Wheezing may occur in some patients, particularly during exertion and exacerbations.
AAT-deficient patients present earlier than other COPD patients. Severe AAT deficiency mainly affects the lungs and the liver. Liver dysfunction dominates the clinical picture in the first decade of life. The patients who are homozygous (ie, PIZZ) develop emphysema with the following distinctive features: early presentation (<50 y), predilection for the lung bases, and panacinar morphological pattern.

Physical

The sensitivity of the physical evaluation in mild-to-moderate disease is relatively poor. However, the physical signs are quite sensitive and specific for severe disease. Patients with severe disease experience tachypnea and respiratory distress with simple activities.

  • The respiratory rate increases in proportion to disease severity. The use of accessory respiratory muscles and paradoxical indrawing of lower intercostal spaces are evident.
  • In advanced disease, cyanosis, elevated jugular venous pressure, and peripheral edema can be observed.
  • Measurement of the forced expiratory time maneuver is a simple bedside test; a forced expiratory time greater than 6 seconds indicates severe expiratory airflow obstruction.
  • Thoracic examination reveals hyperinflation (ie, barrel chest), wheezing, diffusely decreased breath sounds, hyperresonance upon percussion, and prolonged expiration.

Causes

  • Cigarette smoking: Smoking is by far the single most clearly established environmental risk factor for emphysema and chronic bronchitis. One in 5 persons who smoke develops COPD, and 80-90% of COPD patients have a smoking history.
  • AAT deficiency syndrome: This syndrome leads to protease-antiprotease imbalance and unopposed action of neutrophil elastases.
  • Persons who use intravenous drugs
    • Emphysema occurs in approximately 2% of persons who use intravenous drugs and is attributed to pulmonary vascular damage that results from the insoluble filler (eg, cornstarch, cotton fibers, cellulose, talc) contained in methadone or methylphenidate.
    • The bullous cysts found in association with intravenous use of cocaine or heroin occur predominantly in the upper lobes. In contrast, methadone and methylphenidate injections are associated with basilar and panacinar emphysema.
  • Immune deficiency syndromes
    • Human immunodeficiency virus (HIV) infection was found to be an independent risk factor for COPD, even after controlling for confounding variables such as smoking, intravenous drug use, race, and age.7
    • Apical and cortical bullous lung damage occurs in patients who have autoimmune deficiency syndrome and Pneumocystis carinii infection. Reversible pneumatoceles are observed in 10-20% of patients with this infection.
  • Vasculitis syndrome
    • Hypocomplementemic vasculitis urticaria syndrome (HVUS) may be associated with obstructive lung disease.
    • Other symptoms include angioedema, nondeforming arthritis, sinusitis, conjunctivitis, and pericarditis.
  • Connective-tissue disorders
    • Cutis laxa is a disorder of elastin that is characterized most prominently by the appearance of premature aging. The disease usually is congenital, with various forms of inheritance (ie, dominant, recessive). Precocious emphysema has been described in association with cutis laxa as early as the neonatal period or infancy. The pathogenesis of this disorder includes a defect in the synthesis of elastin or tropoelastin.
    • Marfan syndrome is an autosomal dominant inherited disease of type I collagen characterized by abnormal length of the extremities, subluxation of the lenses, and cardiovascular abnormality. Pulmonary abnormalities, including emphysema, have been described in approximately 10% of patients.
    • Ehlers-Danlos syndrome refers to a group of inherited connective-tissue disorders with manifestations that include hyperextensibility of the skin and joints, easy bruisability, and pseudotumors.
  • Salla disease
    • Salla disease is an autosomal recessive storage disorder described in Scandinavia; the disease is characterized by intralysosomal accumulation of sialic acid in various tissues.
    • The most important clinical manifestations are severe mental retardation, ataxia, and nystagmus.
    • Precocious emphysema has been described and likely is secondary to impaired inhibitory activity of serum trypsin.

More on Emphysema

Overview: Emphysema
Differential Diagnoses & Workup: Emphysema
Treatment & Medication: Emphysema
Follow-up: Emphysema
Multimedia: Emphysema
References
[ CLOSE WINDOW ]

References

  1. Global Initiative for Chronic Obstructive Pulmonary Disease. Caverley P, Augusti A, Anzueto, et al, eds. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Medical Communications Resources; 2008.

  2. Adams PF, Barnes PM, Vickerie JL. Summary health statistics for the U.S. population: National Health Interview Survey, 2007. Vital Health Stat 10. Nov 2008;1-104. [Medline].

  3. Buist AS, McBurnie MA, Vollmer WM, et al. International variation in the prevalence of COPD (the BOLD Study): a population-based prevalence study. Lancet. Sep 1 2007;370(9589):741-50. [Medline].

  4. Menezes AM, Perez-Padilla R, Jardim JR, et al. Chronic obstructive pulmonary disease in five Latin American cities (the PLATINO study): a prevalence study. Lancet. Nov 26 2005;366(9500):1875-81. [Medline].

  5. Centers for Disease Control and Prevention. Deaths from chronic obstructive pulmonary disease--United States, 2000-2005. MMWR Morb Mortal Wkly Rep. Nov 14 2008;57(45):1229-32. [Medline].

  6. Silverman EK, Weiss ST, Drazen JM, et al. Gender-related differences in severe, early-onset chronic obstructive pulmonary disease. Am J Respir Crit Care Med. Dec 2000;162(6):2152-8. [Medline].

  7. Crothers K, Butt AA, Gibert CL, Rodriguez-Barradas MC, Crystal S, Justice AC. Increased COPD among HIV-positive compared to HIV-negative veterans. Chest. Nov 2006;130(5):1326-33. [Medline].

  8. [Guideline] US Preventive Services Task Force. Counseling and interventions to prevent tobacco use and tobacco-caused disease in adults and pregnant women: US Preventive Services Task Force Reaffirmation Recommendation Statement. Ann Int Med. Apr 21 2009;150(8):551-555. [Full Text].

  9. COMBIVENT Inhalation Aerosol Study Group. In chronic obstructive pulmonary disease, a combination of ipratropium and albuterol is more effective than either agent alone. An 85-day multicenter trial. COMBIVENT Inhalation Aerosol Study Group. Chest. May 1994;105(5):1411-9. [Medline].

  10. Calverley PM, Anderson JA, Celli B, et al. Salmeterol and fluticasone propionate and survival in chronic obstructive pulmonary disease. N Engl J Med. Feb 22 2007;356(8):775-89. [Medline].

  11. O'Donnell DE, Flüge T, Gerken F, et al. Effects of tiotropium on lung hyperinflation, dyspnoea and exercise tolerance in COPD. Eur Respir J. Jun 2004;23(6):832-40. [Medline].

  12. Tashkin DP, Celli B, Senn S, et al. A 4-year trial of tiotropium in chronic obstructive pulmonary disease. N Engl J Med. Oct 9 2008;359(15):1543-54. [Medline].

  13. Brusasco V, Hodder R, Miravitlles M, Korducki L, Towse L, Kesten S. Health outcomes following treatment for six months with once daily tiotropium compared with twice daily salmeterol in patients with COPD. Thorax. May 2003;58(5):399-404. [Medline].

  14. Donohue JF, van Noord JA, Bateman ED, et al. A 6-month, placebo-controlled study comparing lung function and health status changes in COPD patients treated with tiotropium or salmeterol. Chest. Jul 2002;122(1):47-55. [Medline].

  15. [Best Evidence] Calverley PM, Rabe KF, Goehring UM, Kristiansen S, Fabbri LM, Martinez FJ. Roflumilast in symptomatic chronic obstructive pulmonary disease: two randomised clinical trials. Lancet. Aug 29 2009;374(9691):685-94. [Medline].

  16. Spencer S, Calverley PM, Burge PS, Jones PW. Impact of preventing exacerbations on deterioration of health status in COPD. Eur Respir J. May 2004;23(5):698-702. [Medline].

  17. Wood-Baker RR, Gibson PG, Hannay M, Walters EH, Walters JA. Systemic corticosteroids for acute exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. Jan 25 2005;CD001288. [Medline].

  18. Walters JA, Walters EH, Wood-Baker R. Oral corticosteroids for stable chronic obstructive pulmonary disease. Cochrane Database Syst Rev. Jul 20 2005;CD005374. [Medline].

  19. [Best Evidence] Sin DD, Tashkin D, Zhang X, et al. Budesonide and the risk of pneumonia: a meta-analysis of individual patient data. Lancet. Aug 29 2009;374(9691):712-9. [Medline].

  20. Petty TL. The National Mucolytic Study. Results of a randomized, double-blind, placebo-controlled study of iodinated glycerol in chronic obstructive bronchitis. Chest. Jan 1990;97(1):75-83. [Medline].

  21. [Best Evidence] Sasaki T, Nakayama K, Yasuda H, et al. A randomized, single-blind study of lansoprazole for the prevention of exacerbations of chronic obstructive pulmonary disease in older patients. J Am Geriatr Soc. Aug 2009;57(8):1453-7. [Medline].

  22. Hubbard RC, Crystal RG. Augmentation therapy of alpha 1-antitrypsin deficiency. Eur Respir J Suppl. Mar 1990;9:44s-52s. [Medline].

  23. Naunheim KS, Wood DE, Mohsenifar Z, et al. Long-term follow-up of patients receiving lung-volume-reduction surgery versus medical therapy for severe emphysema by the National Emphysema Treatment Trial Research Group. Ann Thorac Surg. Aug 2006;82(2):431-43. [Medline].

  24. [Guideline] Orens JB, Estenne M, Arcasoy S, et al. International guidelines for the selection of lung transplant candidates: 2006 update--a consensus report from the Pulmonary Scientific Council of the International Society for Heart and Lung Transplantation. J Heart Lung Transplant. Jul 2006;25(7):745-55. [Medline].

  25. Hurst JR, Donaldson GC, Quint JK, Goldring JJ, Baghai-Ravary R, Wedzicha JA. Temporal clustering of exacerbations in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. Mar 1 2009;179(5):369-74. [Medline].

  26. Lightowler JV, Wedzicha JA, Elliott MW, Ram FS. Non-invasive positive pressure ventilation to treat respiratory failure resulting from exacerbations of chronic obstructive pulmonary disease: Cochrane systematic review and meta-analysis. BMJ. Jan 25 2003;326(7382):185. [Medline].

  27. Ries AL, Bauldoff GS, Carlin BW, et al. Pulmonary Rehabilitation: Joint ACCP/AACVPR Evidence-Based Clinical Practice Guidelines. Chest. May 2007;131(5 Suppl):4S-42S. [Medline].

  28. Celli BR, Cote CG, Marin JM, et al. The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease. N Engl J Med. Mar 4 2004;350(10):1005-12. [Medline].

  29. Anthonisen NR. Prognosis in chronic obstructive pulmonary disease: results from multicenter clinical trials. Am Rev Respir Dis. Sep 1989;140(3 Pt 2):S95-9. [Medline].

  30. Anthonisen NR, Connett JE, Kiley JP, et al. Effects of smoking intervention and the use of an inhaled anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study. JAMA. Nov 16 1994;272(19):1497-505. [Medline].

  31. Brenes GA. Anxiety and chronic obstructive pulmonary disease: prevalence, impact, and treatment. Psychosom Med. Nov-Dec 2003;65(6):963-70. [Medline].

  32. Burrows B, Bloom JW, Traver GA, Cline MG. The course and prognosis of different forms of chronic airways obstruction in a sample from the general population. N Engl J Med. Nov 19 1987;317(21):1309-14. [Medline].

  33. Chapman KR. Therapeutic algorithm for chronic obstructive pulmonary disease. Am J Med. Oct 21 1991;91(4A):17S-23S. [Medline].

  34. Davis RM, Novotny TE. The epidemiology of cigarette smoking and its impact on chronic obstructive pulmonary disease. Am Rev Respir Dis. Sep 1989;140(3 Pt 2):S82-4. [Medline].

  35. Dunn WF, Nelson SB, Hubmayr RD. Oxygen-induced hypercarbia in obstructive pulmonary disease. Am Rev Respir Dis. Sep 1991;144(3 Pt 1):526-30. [Medline].

  36. Fabbri LM, Luppi F, Beghé B, Rabe KF. Update in chronic obstructive pulmonary disease 2005. Am J Respir Crit Care Med. May 15 2006;173(10):1056-65. [Medline].

  37. Ferguson GT, Cherniack RM. Management of chronic obstructive pulmonary disease. N Engl J Med. Apr 8 1993;328(14):1017-22. [Medline].

  38. Fletcher C, Peto R. The natural history of chronic airflow obstruction. Br Med J. Jun 25 1977;1(6077):1645-8. [Medline].

  39. Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM. Global burden of COPD: systematic review and meta-analysis. Eur Respir J. Sep 2006;28(3):523-32. [Medline].

  40. Karpel JP, Kotch A, Zinny M, Pesin J, Alleyne W. A comparison of inhaled ipratropium, oral theophylline plus inhaled beta-agonist, and the combination of all three in patients with COPD. Chest. Apr 1994;105(4):1089-94. [Medline].

  41. Lopez-Majano V, Dutton RE. Regulation of respiration during oxygen breathing in chronic obstructive lung disease. Am Rev Respir Dis. Aug 1973;108(2):232-40. [Medline].

  42. Mannino DM, Watt G, Hole D, Gillis C, Hart C, McConnachie A. The natural history of chronic obstructive pulmonary disease. Eur Respir J. Mar 2006;27(3):627-43. [Medline].

  43. McKay SE, Howie CA, Thomson AH, Whiting B, Addis GJ. Value of theophylline treatment in patients handicapped by chronic obstructive lung disease. Thorax. Mar 1993;48(3):227-32. [Medline].

  44. Medical Research Council Working Party. Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Report of the Medical Research Council Working Party. Lancet. Mar 28 1981;1(8222):681-6. [Medline].

  45. Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease: a clinical trial. Nocturnal Oxygen Therapy Trial Group. Ann Intern Med. Sep 1980;93(3):391-8. [Medline].

  46. O'Donnell DE, Parker CM. COPD exacerbations . 3: Pathophysiology. Thorax. Apr 2006;61(4):354-61.

  47. O'Donnell DE, Sanii R, Anthonisen NR, Younes M. Effect of dynamic airway compression on breathing pattern and respiratory sensation in severe chronic obstructive pulmonary disease. Am Rev Respir Dis. Apr 1987;135(4):912-8. [Medline].

  48. O'Donnell R, Breen D, Wilson S, Djukanovic R. Inflammatory cells in the airways in COPD. Thorax. May 2006;61(5):448-54. [Medline].

  49. Papi A, Luppi F, Franco F, Fabbri LM. Pathophysiology of exacerbations of chronic obstructive pulmonary disease. Proc Am Thorac Soc. May 2006;3(3):245-51. [Medline].

  50. Peto R, Speizer FE, Cochrane AL, et al. The relevance in adults of air-flow obstruction, but not of mucus hypersecretion, to mortality from chronic lung disease. Results from 20 years of prospective observation. Am Rev Respir Dis. Sep 1983;128(3):491-500. [Medline].

  51. Petty TL, Finigan MM. Clinical evaluation of prolonged ambulatory oxygen therapy in chronic airway obstruction. Am J Med. Aug 1968;45(2):242-52. [Medline].

  52. Postma DS, Sluiter HJ. Prognosis of chronic obstructive pulmonary disease: the Dutch experience. Am Rev Respir Dis. Sep 1989;140(3 Pt 2):S100-5. [Medline].

  53. Prigmore S. End-of-life decisions and respiratory disease. Nurs Times. Feb 14-20 2006;102(7):56, 59, 61. [Medline].

  54. Ram FS, Rodriguez-Roisin R, Granados-Navarrete A. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2006;CD004403.

  55. Rutten FH, Cramer MJ, Lammers JW, Grobbee DE, Hoes AW. Heart failure and chronic obstructive pulmonary disease: An ignored combination?. Eur J Heart Fail. Nov 2006;8(7):706-11. [Medline].

  56. Sanders C. The radiographic diagnosis of emphysema. Radiol Clin North Am. Sep 1991;29(5):1019-30. [Medline].

  57. Schachter EN. Cilomilast. Drugs Today (Barc). Apr 2006;42(4):237-47.

  58. Sutherland ER, Martin RJ. Airway inflammation in chronic obstructive pulmonary disease: comparisons with asthma. J Allergy Clin Immunol. Nov 2003;112(5):819-27; quiz 828. [Medline].

  59. Thurlbeck WM. Overview of the pathology of pulmonary emphysema in the human. Clin Chest Med. Sep 1983;4(3):337-50. [Medline].

  60. Thurlbeck WM. Pathophysiology of chronic obstructive pulmonary disease. Clin Chest Med. Sep 1990;11(3):389-403. [Medline].

  61. Tsoumakidou M, Siafakas NM. Novel insights into the aetiology and pathophysiology of increased airway inflammation during COPD exacerbations. Respir Res. May 22 2006;7(1):80.

  62. Vestbo J. Clinical assessment, staging, and epidemiology of chronic obstructive pulmonary disease exacerbations. Proc Am Thorac Soc. May 2006;3(3):252-6. [Medline].

  63. Weitzenblum E, Sautegeau A, Ehrhart M, Mammosser M, Pelletier A. Long-term oxygen therapy can reverse the progression of pulmonary hypertension in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis. Apr 1985;131(4):493-8. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

emphysema, chronic obstructive pulmonary disease, COPD, chronic obstructive lung disease, chronic lung, chronic bronchitis, airflow obstruction, centriacinar emphysema, centrilobular emphysema, panacinar emphysema, paraseptal emphysema, distal acinar emphysema, alpha1-antitrypsin deficiency, AAT

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Berj George Demirjian, MD, Fellow, Division of Pulmonary/Critical Care Medicine, Cedars-Sinai Medical Center
Berj George Demirjian, MD is a member of the following medical societies: American College of Chest Physicians, American Medical Association, California Medical Association, California Thoracic Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Nader Kamangar, MD, FACP, FCCP, FAASM, Associate Professor of Clinical Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Multi-campus Pulmonary and Critical Care Fellowship Program, University of California, Los Angeles, David Geffen School of Medicine; Medical Director, Hospitalist/Intensivist Program, Olive View-UCLA Medical Center; Associate Program Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA Medical Center/West Los Angeles Veterans Affairs Medical Center
Nader Kamangar, MD, FACP, FCCP, FAASM is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

Helen M Hollingsworth, MD, Director, Adult Asthma and Allergy Services, Associate Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Boston Medical Center
Helen M Hollingsworth, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American Thoracic Society, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.