Emphysema 

  • Author: Berj George Demirjian, MD; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: Sep 16, 2011
 

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.

Note the images below.

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 lGross pathology of emphysema shows bullae on the lung surface.
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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.

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Epidemiology

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]

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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, FCCM  Associate Professor of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, University of California, Los Angeles, David Geffen School of Medicine, Olive View-UCLA Medical Center; Associate Program Director, Pulmonary and Critical Care Multi-Campus Fellowship Program, Cedars-Sinai/West Los Angeles Veterans Affairs/Los Angeles Kaiser Permanente/Olive View-UCLA Medical Center; Site Director, Pulmonary/Critical Care Fellowship Program, Olive View-UCLA Medical Center

Nader Kamangar, MD, FACP, FCCP, FCCM 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.

Specialty Editor Board

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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Timothy D Rice, MD  Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, St 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, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

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.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Sat Sharma, MD, FRCPC, to the development and writing of this article.

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Gross pathology of bullous emphysema shows bullae on the surface of the lungs.
Gross pathology of emphysema shows bullae on the lung surface.
At high magnification, loss of airway walls and dilated airspaces are observed in emphysema.
Chest radiograph shows hyperinflation, flattened diaphragms, increased retrosternal space, and hyperlucency of the lung parenchyma in emphysema.
A CT scan shows emphysematous bullae in upper lobes.
Diffuse emphysema secondary to cigarette smoking.
Pressure-volume curve is drawn for a patient with restrictive lung disease and obstructive disease and is compared to healthy lungs.
Flow-volume curve of lungs with emphysema shows marked decrease in expiratory flows, hyperinflation, and air trapping (patient B) compared to a patient with restrictive lung disease, who has reduced lung volumes and preserved flows (patient A).
Forced expiratory volume in 1 second (FEV1) can be used to evaluate the prognosis in patients with emphysema. The benefit of smoking cessation is shown here because the deterioration in lung function parallels that of a nonsmoker, even in late stages of the disease.
A CT scan showing severe emphysema and bullous disease.
An emphysematous lung shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on posteroanterior (PA) film.
An emphysematous lung shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on lateral chest radiograph.
The differential diagnosis of unilateral hyperlucent lung includes pulmonary arterial hypoplasia and Swyer-James syndrome. The expiratory chest radiograph exhibits evidence of air trapping and is helpful in making the diagnosis. Swyer-James syndrome is unilateral bronchiolitis obliterans, which develops during early childhood.
Lateral chest radiograph of Swyer-James syndrome may demonstrate some of the features of emphysema.
 
 
 
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