eMedicine Specialties > Radiology > Chest

Emphysema

Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
Sarah Al Ghanem, MBBS, Consulting Staff, Department of Medical Imaging, King Fahad National Guard Hospital, Saudi Arabia; Klaus L Irion, MD, PhD, Consulting Staff, The Cardiothoracic Centre Liverpool NHS Trust, The Royal Liverpool University Hospital, UK; Chitra P Nagarajaiah, MBBS, MRCP, Acute Medicine Specialist Registrar, City Hospital of Birmingham, UK; Pablo Rydz Pinheiro Santana, MD, Staff Physician, Department of Radiology, Irion Radiologia, Brazil

Updated: Feb 17, 2009

Introduction

Background

Ballile and Laennec described the anatomopathology of the disease in 1793 and in 1826, respectively. After that, Lynne Reid published one of the landmark works in our understanding of emphysema, The Pathology of Emphysema (Reid, 1967) , which provided a detailed description of the anatomy of the lung units and of the anatomopathology and pathophysiology of emphysema, broadening the view of this complex disease.^{[1,2 ]}Various changes have happened since then, especially the advent of the high-resolution CT (HRCT) of the chest.

Pulmonary emphysema is defined as the permanent enlargement of airspaces distal to the terminal bronchioles and the destruction of the alveolar walls. Pathology reveals a marked increase in the size of the airspaces, resulting in labored breathing and an increased susceptibility to infection. It can be caused by irreversible expansion of the alveoli or by the destruction of alveolar walls. Fibrosis is not associated with this condition.

Chest radiograph of an emphysematous patient shows hyperinflated lungs with reduced vascular markings. Pulmonary hila are prominent, suggesting some degree of pulmonary hypertension (Corrêa da Silva, 2001).

CT densitovolumetry in a heavy smoker with emphysema revealed compromise of about 22% of the lung parenchyma (Corrêa da Silva, 2001).

CT densitovolumetry in a patient with lung cancer. Three-dimensional (3D) image shows that the cancer is in the portion of the right lung that was less affected by emphysema in a patient with poor pulmonary function (Corrêa da Silva, 2001).

Pathophysiology

The most important cause of pulmonary emphysema is cigarette smoking. Atmospheric pollution has also been implicated as a contributory cause, but to date no scientific data support this notion. Air pollution does contribute to acute exacerbations in patients with existing emphysema. Smoking and COPD are strongly related. For example, 90% of patients with COPD are smokers, though only about 20% of smokers develop COPD.

The pathogenesis of emphysema is based on the protease-protease-inhibitor theory. This theory dates back to 1897, when Camus and Gley recognized that serum had the capacity to inhibit the proteolytic enzyme trypsin. Later, alpha 1-antitrypsin was discovered as a specific protein that inhibits the proteolytic activity of trypsin. This protein is now often referred to as alpha 1-protease inhibitor (alpha 1-PI) or alpha 1-antitrypsin. The normal serum alpha 1-PI concentration is 20-50 mol/L (150-350 mg/dL). Serum levels of alpha 1-PI of less than 11 mol/L (<80 mg/dL) are considered deficient.^{[3 ]}

Leukocytes contain various proteolytic enzymes in their lysosomes. Alveolar macrophages, derived from monocytes, also contain proteolytic enzymes. The role of leukocytes and alveolar macrophages is to protect the terminal gas-exchange structures of the lungs from inhaled debris and infectious agents. In fighting inhaled foreign material, these phagocytic cells release large quantities of proteolytic enzymes and oxygen radicals, which have antimicrobial activity.

Although these large quantities of the proteolytic enzymes are responsible for the demise of microbes, the lungs normally remain unscathed. Alpha 1-PI and antioxidants in the serum, in cell membranes, and in the alveolar lining fluid layer prevent these toxic products at the cellular level from destroying the lungs.

Tobacco is a potent source of oxidants. The oxidants in cigarette smoke become involved in innumerable biochemical reactions, producing overwhelming numbers of free radicals. The alpha 1-PI molecule is susceptible to oxidative injury during smoking, making alpha 1-PI ineffective as a proteolytic enzyme. To take care of the clearing operation, large numbers of leukocytes are recruited at the site. This process unleashes other proteolytic enzymes, which are responsible for lung tissue damage. These events, triggered by cigarette smoke, damage the connective tissue of the lung and destroy the lung parenchyma, increasing pulmonary compliance and causing early airway closure during expiration and thus airtrapping.^{[4 ]}

Deficiency of alpha 1-PI is an autosomal dominant disorder associated with decreased levels of serum alpha 1-PI. This genetic disorder affects about 1 in 2000 people of European descent and approximately 2% of all cases of emphysema in the United States. Emphysema due to alpha 1-PI deficiency typically appears earlier than the emphysema caused by cigarette smoking. Cigarette smoking frequently accelerates the onset of emphysema associated with alpha 1-PI deficiency. The condition is often misdiagnosed as asthma, and correct diagnosis can be delayed for several years.

Frequency

United States

As a component of COPD, pulmonary emphysema is a major health problem worldwide. An estimated 14 million persons in the United States have COPD. Of these, about 1.5 million have emphysema, and 12.5 million have chronic bronchitis.^{[5 ]}The American Lung Association American Lung Data and Statistics ranks emphysema 15th among chronic conditions contributing to activity limitations, and 44% of patients with emphysema claim to have limitations in their daily living activities resulting from their disease. More than 17,800 deaths are attributable to emphysema in the United States each year.^{[6,7 ]}

International

• The World Health Organization estimated that COPD is currently the seventh leading cause of death and disability worldwide, but it is expected to be fifth by 2020 and third by 2030.
• In 2001, the estimated prevalence of COPD worldwide was 1013 cases per 100,000 population; it was highest in the western Pacific region and lowest in Africa.
• According to the latest WHO estimates (2007), currently 210 million people have COPD and 3 million people died of COPD in 2005.^{[8 ]}

Mortality/Morbidity

In 2001, estimated prevalence of COPD worldwide was 1013 cases per 100,000 population; rates were highest in the Western Pacific Region and lowest in Africa. Smoking cigarettes is the leading cause of COPD. Smoking is the cause of 80-90% of COPD deaths.^{[7 ]}Though the prevalence of smoking is decreasing in the industrialized world, the prevalence is rising in Asia and Africa. Other important risk factors for COPD in developing countries are indoor air pollution from combustion of biomass or traditional fuels and coal, previous tuberculous infection, outdoor air pollution, and childhood respiratory infections. The rise in morbidity and mortality from COPD is expected to be dramatic in Asian and African countries in the next 2 decades, mostly because of an increasing prevalence of smoking.^{[9 ]}

• In Taiwan, mortality rates for COPD decreased from 1981 to 1993 and increased thereafter. This change was largely attributable to increased rates in men. COPD is increasingly important and a leading cause of death in Taiwan.^{[10 ]}
• In the United States, COPD is the fourth most common cause of death, accounting for nearly 4.5% of all deaths. Furthermore, COPD may be a contributory factor in another 4.3% of deaths.
• In the United Kingdom, current trends in COPD differ from those in many other countries because COPD had been more common than in other countries undergoing a smoking epidemic at the same time, and cigarette consumption in men and women peaked more than 25 years ago. Male mortality from COPD has been decreasing for 30 years, whereas female mortality has risen steadily during the same period. A strong socioeconomic gradient in morbidity and mortality persists. Emergency hospital admissions for exacerbations and home oxygenation account for a large proportion of health care costs.^{[11 ]}
• In Canada, COPD affects 5% of all adults and is the fourth leading cause of death. Of interest, the leading causes of hospitalizations and mortality among patients with COPD are cardiovascular events. Increasing evidence suggests that COPD is a risk factor for cardiovascular events.^{[12 ]}

Race

In an extensive review of data from the National Center for Health Statistics and from population-based studies, Gillum confirmed that African Americans had lower overall COPD rates but higher asthma mortality rates than whites and that compared with whites, African Americans had lower rates of chronic bronchitis and emphysema but had similar or higher asthma prevalence rates. He suggested that the disproportionate and excessive asthma-related mortality and hospitalization rates are out of proportion in African Americans and may be due to increased disease severity, poorer outcomes of outpatient treatment in African Americans than in whites, or both.^{[13,14 ]}

Sex

Estimates show that 4-6% of white men and 1-3% of white women have emphysema or COPD. Mortality rate in men is higher than that in women.^{[7,8,14 ]}

Age

• Clinically manifested emphysema usually occurs in people aged 50 years or older, with the peak at about 70 years of age, after decades of smoking.
• Emphysema before 50 years of age may be seen in people born with alpha 1-PI deficiency.

Anatomy

A secondary pulmonary lobule is an anatomic unit of lung structure. It is composed of a terminal bronchiole and 5-15 acini. The acini are the units of lung where gas exchange takes place. Each acinus is composed of 1-3 respiratory bronchioles that lead to the alveolar ducts and sacs. The terminal bronchioles are the last of purely conducting ciliated airways, but the respiratory bronchioles are nonciliated, partially alveolated structures.

A secondary pulmonary lobule is polyhedral and measures approximately 1-2.5 cm on each side. After the terminal bronchioles enter the center of the lobule, they begin to branch at short intervals (1-3 mm). The alveoli and pulmonary capillary bed fill the space between these 2 structures. Proximal to this level, the airway branches at 1-cm intervals.

The secondary pulmonary lobule can be further subdivided into core and septal structures. The core structures include the pulmonary arteriole, terminal bronchiole, and accompanying lymphatics. The septal structures include the pulmonary veins, lymphatics, and the fibrous septum itself. The pulmonary arteriole accompanies the terminal bronchiole into the center of the lobule, supplying blood to the alveolar capillary bed.

Venous drainage is toward the periphery of the lobule, forming pulmonary veins that travel in the interlobular septa. The interlobular septa are composed of connective tissues that form the boundaries of the secondary lobule. In the human lung, the secondary pulmonary lobule is incompletely surrounded by interlobular septa. The septa are well developed in the apex and periphery of the lung and are rather poorly developed in the posterior aspects of both the upper and lower lobes. At the lung bases, these septa are oriented perpendicular to the pleura, accounting for the appearance of Kerley B lines.

Besides the interlobular septa, pulmonary lymphatics are also found in the bronchovascular bundles as they drain from the pleural surface to the hila.

High-resolution CT (HRCT) allows visualization of abnormalities of the interlobular septa and components of the secondary pulmonary lobule, even when the chest radiograph is normal. When the pulmonary acinus is opacified, it measures approximately 6 mm and is roughly spherical. Some experts believe that the acinus is the most important functional unit in the lung. However, an acinar pattern of small nodules on chest radiography has little pathologic specificity.

In centriacinar or centrilobular emphysema, enlargement and destruction are centered in the first- and second-order respiratory bronchioles. In panacinar emphysema, enlargement and destruction are relatively uniform throughout the acinus. In paraseptal emphysema, the enlargement and destruction occur in the periphery of the secondary pulmonary lobule along the interlobular septa.

Presentation

Patient presentation

Patients with advanced-stage emphysema typically present with shortness of breath, which occurs when they perform ordinary daily chores, such as climbing a flight of stairs. They have no associated cough; however, if they have a cough, it tends to be minor and nonproductive of sputum.

On physical examination, the patient appears tachypneic, expiratory time is lengthened, and use of accessory muscles of ventilation is observed during inspiration and exhalation, as is pursed-lip breathing, increased heart rate, and increased anteroposterior chest-wall diameter (barrel chest). Patients with emphysema frequently attempt to increase the vertical dimension of their thorax to achieve a mechanical advantage for the muscles of ventilation. For example, when sitting, they place both of their elbows on the arms of the chair and lean forward. The thorax is hyperresonant to percussion, and auscultation reveals diminished or distant breath sounds.

Spirometry reveals a pattern of chronic airflow obstruction. Measurements of forced vital capacity (FVC), forced expiratory volume in 1 second (FEV₁), and FEV₁/FVC ratio are used to assess the pattern. Carbon-monoxide diffusing capacity is usually performed with spirometry to differentiate emphysema from asthma and chronic bronchitis. In emphysema, the carbon-monoxide diffusing capacity is usually depressed. The combination of a decreased FVC, a decreased FEV₁, and a decreased carbon-monoxide diffusing capacity is generally diagnostic of emphysema.

Arterial blood gases vary with the severity of emphysema. In mild and moderate disease, PaO₂ and PaCO₂ may remain normal, or PaCO₂ can be decreased (respiratory alkalosis) while PaO₂ stays normal. In moderately severe and severe emphysema, the patient is likely to be hypoxemic and hypercarbic (respiratory acidosis).

Causes

Although cigarette smoking is the single most important cause of emphysema, other factors are implicated in rare cases. For instance, 2% of intravenous drug abusers develop emphysema attributed to pulmonary vascular injury secondary to the embolization of cornstarch, cotton fibers, cellulose, or talc. Bullous cysts found in association with intravenous abuse of cocaine or heroin predominantly affects the upper lobes. In contrast, methadone and methylphenidate injections are associated with basilar and panacinar emphysema.

A combination of HIV and Pneumocystis carinii infection may cause apical and peripheral bullous lung damage. Reversible pneumatoceles also are observed in patients with these conditions. An emphysema-like disease is associated with HIV, probably as a result of a combination of factors, including malnutrition, direct cytotoxicity, and enhanced cytokine or elastase release. HIV is a risk factor for the premature development of emphysema. HIV patients are often heavy smokers and generally present in the fifth decade of life with the clinical symptoms of emphysema.

Hypocomplementemic vasculitis urticaria syndrome may be associated with obstructive lung disease in more than one half of patients.

Several connective tissue disorders due to defective synthesis of elastin or tropoelastin are associated with emphysema. Precocious emphysema has been described in association with cutis laxa as early as the neonatal period or infancy. Marfan syndrome is associated with several pulmonary abnormalities, including emphysema. Salla disease is a rare genetic disorder characterized by intralysosomal accumulation of sialic acid in various tissues. Precocious emphysema has been described with Salla disease and likely is secondary to impaired inhibitory activity of serum trypsin.

Irregular emphysema (paracicatricial emphysema) affects patients with pulmonary fibrosis, such as those with lung parenchymal scars, diffuse lung fibrosis, and pneumoconiosis. Irregular emphysema is recognized on HRCT as areas of low attenuation associated with lung fibrosis. When fibrosis is only microscopic, radiologic distinction between irregular and centrilobular emphysema may become impossible.

Preferred Examination

Conventional chest radiography is generally the first imaging procedure performed in patients with respiratory symptoms. Frontal and lateral chest radiographs may reveal changes of emphysema. A chest radiograph is universally available, noninvasive, and inexpensive, and it poses an acceptable radiation exposure.

High-resolution CT (HRCT) is more sensitive than chest radiography in diagnosing emphysema and in determining its type and extent of disease. HRCT also has a high specificity for diagnosing emphysema with virtually no false-positive diagnoses. However, in clinical practice, more reliance is placed on patient history, lung function tests, and abnormal chest radiographs to diagnose emphysema. However, some patients with early emphysema, particularly those with early disease, may present with atypical symptoms, and it is in these patients that an HRCT is most rewarding. If significant emphysema is found on HRCT, no further workup is necessary; specifically, lung biopsy is not needed.

Studies are under way to assess the role of CT in the early detection of lung cancer in patients with COPD and in predicting response to lung-volume–reduction surgery (LVRS). Radionuclide scanning and MRI have a potential role in patients being assessed for LVRS.

Limitations of Techniques

Chest radiographic findings are not good indicators of the severity of disease and do not help in identifying patients with COPD without clinically significant emphysema. Imaging information from HRCT does not alter the management of emphysema; therefore, HRCT has no place in the day-to-day care of patients with COPD. In their early stages, the 3 forms of emphysema can be distinguished morphologically by using HRCT. However, as the disease becomes more extensive, the distinction becomes difficult or impossible, both radiographically and pathologically.

Differential Diagnoses

Asthma
Bronchiectasis
Bronchiolitis Obliterans Organizing Pneumonia
Congestive Heart Failure

Other Problems to Be Considered

Bronchitis
Other causes of small airway disease

Radiography

Chest radiograph of an emphysematous patient shows hyperinflated lungs with reduced vascular markings. Pulmonary hila are prominent, suggesting some degree of pulmonary hypertension (Corrêa da Silva, 2001).

Schematic representation of 1 criterion for defining flattening of the diaphragm on the lateral chest radiograph: drawing a line from the posterior to anterior costophrenic angles and measuring the distance from this line to the apex of the diaphragm. If the height is less than 1.5 cm, the criterion of flattening is fulfilled (Corrêa da Silva, 2001).

Schematic representation of another criterion for defining flattening of the diaphragm on the lateral chest radiograph. When the angle formed by the contact point between the diaphragm and the anterior thoracic wall is more than or equal to 90°, the criterion is fulfilled (Corrêa da Silva, 2001).

Schematic representation of another sign of emphysema on the lateral chest radiograph. When the retrosternal space (defined as the space between the posterior border of the sternum and the anterior wall of the mediastinum) is larger than 2.5 cm, it is highly suggestive of overinflated lungs. This radiograph is from a patient with pectus carinatum, an important differential diagnosis to consider when this space is measured (Corrêa da Silva, 2001).

Close-up image shows emphysematous bullae in the left upper lobe. Note the subpleural, thin-walled, cystlike appearance (Corrêa da Silva, 2001).

A, Frontal posteroanterior (PA) chest radiograph shows no abnormality of the pulmonary vasculature, with normal intercostal spaces and a diaphragmatic dome between the 6th and 7th anterior ribs on both sides. B, Image in a patient with emphysema demonstrating reduced pulmonary vasculature resulting in hyperlucent lungs. The intercostal spaces are mildly enlarged, and the diaphragmatic domes are straightened and below the extremity of the seventh rib (Corrêa da Silva, 2001).

A, Lateral radiograph of the chest shows normal pulmonary vasculature, a retrosternal space within normal limits (<2.5 cm), and a normal angle between the diaphragm and the anterior thoracic wall. B, Lateral view of the chest shows increased pulmonary transparency, increased retrosternal space (>2.5 cm), and an angle between the thoracic wall and the diaphragm >90°. Straightening of the diaphragm can be more evident in this projection than on others (Corrêa da Silva, 2001).

Findings

In moderate-to-severe emphysema, chest radiographic findings include bilaterally hyperlucent lungs of large volume, flattened hemidiaphragms with widened costophrenic angles, horizontal ribs, and a narrow mediastinum. The peripheral vascular markings are attenuated, but the markings become prominent when the patient has pulmonary hypertension and right-sided heart failure. A lateral view shows increased retrosternal airspace and flattening of the anterior diaphragmatic angle. In addition, bullae and an irregular distribution of the lung vasculature may be present. When pulmonary hypertension develops, the hilar vascular shadows become prominent, with filling of the lower retrosternal airspace due to right ventricular enlargement.

Degree of Confidence

In clinical practice, reliance is placed on the patient's history, lung function, and abnormal chest radiographs to diagnose emphysema. Chest radiographic findings generally cannot establish the diagnosis of mild emphysema; however, when emphysema is fully established, classic radiographic findings are typically observed. Findings on routine chest radiographs can suggest emphysema, but this is not a sensitive technique for diagnosis. However, chest radiography is useful to look for complications during acute exacerbations and to exclude other pathologies, such as superadded infection or lung cancer.

False Positives/Negatives

The chest radiograph is not a good indicator of the severity of disease and does not help in identifying patients with COPD without significant emphysema. Thurlbeck and Simon found that only 41% of those with moderately severe emphysema and two thirds of those with severe emphysema had evidence of disease on chest radiography.^{[15 ]}

Computed Tomography

Findings

High-resolution CT

CT of the chest, especially HRCT, has a much greater sensitivity and specificity than those of plain chest radiography in diagnosing and assessing the severity of emphysema. CT can depict surgically treatable areas of bullous disease that are not evident on plain chest radiography. CT is also useful in predicting the outcome of surgery. HRCT may be useful in diagnosing subclinical or mild emphysema, and HRCT can be used to differentiate the pathologic types of emphysema. However, CT scanning is not yet used to routinely evaluate patients with COPD. Instead, it is being reserved for patients in whom the diagnosis is in doubt, to look for coexistent pathologies, and to assess their suitability for surgical intervention.^{[16,17,18 ]}

High-resolution CT (HRCT) in a patient after viral bronchiolitis obliterans demonstrates areas of airtrapping, which is predominant in the inferior lobes and associated with bronchiectasis in the left lower lobe. Note that the decreased attenuation caused by the airtrapping can simulate emphysema (Corrêa da Silva, 2001).

Pediatric high-resolution CT (HRCT) shows a hyperinflated right lung with large pulmonary bullae due to congenital lobar emphysema (Corrêa da Silva, 2001).

Semiautomated assessment of emphysema by using HRCT data is possible and can help eliminate interobserver and intraobserver variability and provide a reproducible assessment of the percentage of lung affected. Gould et al^{[21 ]}measured the mean density in vivo of the lowest fifth percentile of the distribution of pixels and compared it with a computed quantification of emphysema on the subsequently excised lungs and showed a strong correlation between lung attenuation and distal airspace size.

Müller et al^{[22 ]}and Kinsella et al^{[23 ]}used a CT attenuation mask to highlight voxels in a given attenuation range to quantitate emphysema and define areas of abnormally low attenuation. They compared different masks, mean lung attenuations, and visual appearances and pathologic grades of emphysema in 28 patients undergoing lung resection for tumor. In each patient, a single representative CT image was compared with corresponding pathologic specimens. They found good correlation between the extent of emphysema as assessed by using the attenuation mask and the pathologic grade. Such methods not only eliminate interobserver and intraobserver variability but also enable reproducible assessment of the percentage of lung that is affected. Although quantitative CT measurements have problems, these methods hold real promise for improving our understanding of lung function.

High-resolution CT (HRCT) demonstrates areas of centriacinar emphysema. Note the low attenuation areas without walls due to destruction of the alveoli septae centrally in the acini. Red element shows the size of a normal acinus (Corrêa da Silva, 2001).

High-resolution CT (HRCT) shows large bullae in both inferior lobes due to uniform enlargement and destruction of the alveoli walls causing distortion of the pulmonary architecture (Corrêa da Silva, 2001).

Miller et al^{[25 ]}found that CT can cause underestimation of the extent of emphysema when lesions are less than 0.5 cm. However, in their study, the inflation pressures of the fixed lung specimens were not controlled, and a number of their patients had only thick-section (10 mm) studies.

Mild-to-moderate degrees of centrilobular emphysema are depicted on HRCT as small, round areas of low attenuation, several millimeters in diameter, grouped near the center of secondary pulmonary lobules, with no discernible walls in many cases. Although the centrilobular location of these lucencies cannot always be appreciated on HRCT, lung parenchymal changes are diagnostic of emphysema.

Alpha 1-PI deficiency is classically associated with panlobular emphysema, though panlobular emphysema may also be seen in smokers without alpha 1-PI deficiency, in the elderly, and in people with distal bronchial and bronchiolar obliteration. It is almost always most severe in the lower lobes. In severe panlobular emphysema, the characteristic HRCT appearance is that of decreased lung attenuation, with few visible pulmonary vessels in the abnormal regions; bullae or cysts are characteristically absent. Mild and even moderately severe panlobular emphysema can be subtle and difficult to detect.^{[26 ]}

Paraseptal emphysema usually involves the distal part of the secondary lobule and is therefore most obvious in subpleural regions. Paraseptal emphysema may be seen in isolation or in combination with centrilobular emphysema. It is often asymptomatic, but it can be associated with spontaneous pneumothorax in young adults. HRCT shows the bullae or air cysts associated with paraseptal emphysema well despite their thin walls.

High-resolution CT (HRCT) shows subpleural bullae consistent with paraseptal emphysema. Red mark shows the size of a normal acinus (Corrêa da Silva, 2001).

Helical CT

Because of the great variability of the machines, with single helical scanners and several models of multisection CT scanners, no technique has been standardized, and the detection rate of emphysema varies with the technique. Even with thick sections, the detection and quantification of emphysema is better than it is with conventional radiography and pulmonary function tests. The great advantage of helical CT is that the whole chest can be scanned in a single acquisition of less than 20 seconds.

For the visual detection of emphysema, use of a high-definition algorithm (bone or lung settings) is helpful. However, for the automatic detection of emphysema by computer, the standard algorithm is probably best. High-definition filters affect the attenuation measured by the computer, deviating from the values from the real Hounsfield scale and generally increasing the attenuation to variable degrees depending on the air-lung-tissue proportion. This effect is even more important when the attenuation of the lungs is compared for high-definition processing with scanners from different suppliers.

CT densitovolumetry of a nonsmoker, healthy young patient shows normal lungs. Less than 0.35% of lungs have attenuations below -950 HU (Corrêa da Silva, 2001).

CT densitovolumetry in a patient with lung cancer. Three-dimensional (3D) image shows that the cancer is in the portion of the right lung that was less affected by emphysema in a patient with poor pulmonary function (Corrêa da Silva, 2001).

CT densitovolumetry shows the attenuation mask. Green areas are those with attenuation below the selected threshold (here, -950 HU to evaluate emphysema), and pink areas are those with attenuations above the threshold. Area outside the patient is highlighted in green because of air (Corrêa da Silva, 2001).

Various authors have been investigating volumetric quantification of emphysema based on the Hounsfield scale by using CT pulmonary densitovolumetry. Some have suggested that precocious detection with quantification and 3-dimensional (3D) demonstration of the extension and distribution of emphysema could be helpful in smoking cessation programs or in risk assessments for occupational exposures.

Degree of Confidence

HRCT is more sensitive than standard chest radiography.

In healthy nonsmokers aged 19-40 years, a maximum of 0.35% of the area of emphysema can be detected by means of CT quantification.^{[27 ]}

HRCT is useful in the workup of smokers with new-onset or progressive dyspnea. The severity of emphysematous change may be underestimated on conventional radiography, whereas HRCT depicts combined fibrosis and emphysema. Patients with these conditions may have relatively normal lung volumes and spirometric results, but they may have severe dyspnea and a reduced diffusing capacity.

False Positives/Negatives

Using 1.5- and 10-mm collimation scans, Miller et al^{[25 ]}showed that the extent of centriacinar and panacinar emphysema was consistently underestimated with CT because it missed most lesions less than 0.5 cm in diameter. They concluded that CT is insensitive in detecting the earliest lesions of emphysema. However, the inflation pressures of the fixed lung specimens were not controlled, and a number of their patients had only thick-section (10 mm) studies.

Magnetic Resonance Imaging

Findings

Hyperpolarized gases are contrast agents that, when inhaled, provide images of the lung airspaces with high temporal and spatial resolution. The availability of these gases has great potential in the study of diffuse lung disease, particularly emphysema.

Ley et al assessed emphysematous enlargement of distal airspaces and concomitant large- and small-airway disease by using diffusion-weighted helium MRI, HRCT, and lung function tests. Helium MRI and HRCT results agreed better than did HRCT results and functional characterizations of emphysema in terms of hyperinflation and large- and small-airway disease, as assessed on lung function tests.^{[28 ]}

Sergiacomi et al^{[29 ]}used lung-perfusion 2-dimensional (2D) dynamic breath-hold technique in patients with severe emphysema and found a high sensitivity (86.7%) and good specificity (80.0%) in detecting perfusion defects. They observed low peak signal intensities in emphysematous regions and concluded that lung perfusion MRI is a potential alternative to nuclear medicine study in the evaluation of severe pulmonary emphysema.

Degree of Confidence

Sergiacomi et al used a lung-perfusion 2D dynamic breath-hold technique in patients with severe emphysema and showed a high sensitivity (86.7%) and good specificity (80.0%) in detecting perfusion defects.^{[29 ]}

False Positives/Negatives

No false-positive or false-negative findings have been established.

Nuclear Imaging

Findings

Functional evaluation of the lungs can be carried out by using xenon-133 (¹³³ Xe) lung ventilation scintigraphy before and after lung-volume–reduction surgery (LVRS) in patients with pulmonary emphysema.¹³³ Xe washout curves during lung scintigraphy exhibit a biphasic pattern: The first component of the washout curve, m(r), corresponds to an initial rapid phase in washout that reflects emptying of the large airways, and the second component, m(s), reflects a slower phase of washout that is attributed to gas elimination in the small airways.^{[30 ]}

Radionuclide ventilation scans enable a useful assessment of lung function before and after LVRS. Travaline et al^{[31 ]}demonstrated that small-airway ventilation in lung regions that were surgically treated and also in those areas that were not surgically treated in the same patient were associated with increased improvement in lung function after LVRS.

Intervention

The major goal in treating emphysema is improving the patient's quality of life. Quitting smoking in the early phase is the single most important factor for maintaining healthy lungs. Avoidance of exposure to polluted atmosphere, including passive smoke, is emphasized to lessen the deterioration of lung function. Early detection with 3D graphic demonstration of the extension of the disease in comparison with more advanced cases can be an additional tool in smoking cessation programs.

Many medications are available for emphysema. Pharmacologic mainstays are bronchodilators and anti-inflammatory agents. Bronchodilators may be prescribed to treat emphysema if the patient has a tendency to have bronchospasm. These drugs may be inhaled as aerosol sprays or taken orally. The bronchodilators primarily used are beta2-agonists and anticholinergics. Not all patients with emphysema derive clinical benefit from bronchodilators; however, some believe that patients with emphysema, especially those who have an FEV₁ of less than 2 L, should be given a 1-week trial of a bronchodilator.

Inhaled glucocorticosteroids does not alter long-term deterioration in FEV₁ in patients with COPD. Some clinicians prescribe a 2-week trial of an oral glucocorticosteroid to identify patients who respond favorably to these anti-inflammatory agents. These patients are then prescribed an inhaled glucocorticosteroid to minimize adverse reactions related to long-term steroid use.

Prompt and appropriate antibiotic therapy is indicated in patients with superadded bacterial infections.

Prolonged use of oxygen for 15 hr/day increases the life expectancy of patients with chronic respiratory failure. In patients who have a PaO₂ of 55 mm Hg or less, oxygen therapy is indicated. Oxygen is usually administered by means of standard nasal cannula or an oxygen-conserving device. For these patients, oxygen therapy generally improves gas exchange, decreases the work of the heart, reduces pulmonary vascular resistance, and improves the ability to perform activities of daily living.

Lung-volume–reduction surgery (LVRS) has been used to treat emphysema to reduce lung volume. A small lung is better accommodated inside the thorax than a large lung, and this enables the ventilatory muscles to work more efficiently than before. However, no data from randomized, controlled trials support the therapeutic benefit of LVRS compared with nonsurgical intervention. HRCT and 3D CT densitovolumetry are frequently used for preoperative investigation and for accessing the anatomic results.

Single-lung transplantation is an option for patients with COPD. Its success rate among COPD, compared with other diseases, is favorable. However, patients with emphysema have the worst survival rate among patients with chronic airflow limitation.

Replacement therapy restores alpha 1-protease inhibitor (alpha 1-PI) serum levels to normal in patients with alpha 1-PI deficiency. Treatment with alpha 1-PI is given only to patients with emphysema related to alpha 1-PI deficiency, and it is not recommended for those who develop emphysema as a result of cigarette smoking or other environmental factors. Purified human alpha 1-PI is delivered intravenously at a dose of 60 mg/kg every 2 weeks. The yearly cost is approximately $30,000.

Medicolegal Pitfalls

• A thorough history must be obtained from the patient, particularly with regard to his or her social circumstances, cigarette smoking, occupational and environmental exposure, and family history of emphysema.
  • Alpha 1-protease inhibitor (alpha 1-PI) deficiency should be diagnosed early.
  • Any patient presenting with emphysema in their 40s should be evaluated for alpha 1-PI deficiency, and radiologists reporting about the radiographs of such patients must raise the question of such deficiency.
• Differentiating COPD from asthma is sometimes difficult on conventional radiology, but efforts must be made to make this differentiation with clinical correlation because approaches to treatment and prognosis differ.
• The role of various treatment regimens in the management of emphysema is not clear.
  • The natural history of alpha 1-antitrypsin deficiency is unknown.
  • The effect of replacement therapy has not been determined in controlled, randomized trials.
  • Lung-volume–reduction surgery (LVRS) is currently being studied in controlled clinical trials.

Special Concerns

• Air travel is a special concern in patients with emphysema.
  • Many airlines fly planes at altitudes of 30,000-40,000 feet, but the cabin is pressurized to an altitude of 5000-8000 feet. At these altitudes, atmospheric partial pressure of oxygen (PO₂) falls to 132-109 mm Hg. Healthy individuals can tolerate these pressures, but patients with moderate-to-severe emphysema may have problems.
  • Furthermore, patients with COPD may develop substantial decrease in nocturnal PaO₂ during sleep. A predicted PaO₂ of 50 mm Hg or less at an altitude of 8000 feet is an indication for supplemental oxygen. Therefore, supplemental oxygen must be made available for these patients before their flights.

Multimedia

Media file 1: Chest radiograph of an emphysematous patient shows hyperinflated lungs with reduced vascular markings. Pulmonary hila are prominent, suggesting some degree of pulmonary hypertension (Corrêa da Silva, 2001).

Media file 2: Schematic representation of 1 criterion for defining flattening of the diaphragm on the lateral chest radiograph: drawing a line from the posterior to anterior costophrenic angles and measuring the distance from this line to the apex of the diaphragm. If the height is less than 1.5 cm, the criterion of flattening is fulfilled (Corrêa da Silva, 2001).

Media file 3: Schematic representation of another criterion for defining flattening of the diaphragm on the lateral chest radiograph. When the angle formed by the contact point between the diaphragm and the anterior thoracic wall is more than or equal to 90°, the criterion is fulfilled (Corrêa da Silva, 2001).

Media file 4: Schematic representation of another sign of emphysema on the lateral chest radiograph. When the retrosternal space (defined as the space between the posterior border of the sternum and the anterior wall of the mediastinum) is larger than 2.5 cm, it is highly suggestive of overinflated lungs. This radiograph is from a patient with pectus carinatum, an important differential diagnosis to consider when this space is measured (Corrêa da Silva, 2001).

Media file 5: Close-up image shows emphysematous bullae in the left upper lobe. Note the subpleural, thin-walled, cystlike appearance (Corrêa da Silva, 2001).

Media file 6: A, Frontal posteroanterior (PA) chest radiograph shows no abnormality of the pulmonary vasculature, with normal intercostal spaces and a diaphragmatic dome between the 6th and 7th anterior ribs on both sides. B, Image in a patient with emphysema demonstrating reduced pulmonary vasculature resulting in hyperlucent lungs. The intercostal spaces are mildly enlarged, and the diaphragmatic domes are straightened and below the extremity of the seventh rib (Corrêa da Silva, 2001).

Media file 7: A, Lateral radiograph of the chest shows normal pulmonary vasculature, a retrosternal space within normal limits (<2.5 cm), and a normal angle between the diaphragm and the anterior thoracic wall. B, Lateral view of the chest shows increased pulmonary transparency, increased retrosternal space (>2.5 cm), and an angle between the thoracic wall and the diaphragm >90°. Straightening of the diaphragm can be more evident in this projection than on others (Corrêa da Silva, 2001).

Media file 8: High-resolution CT (HRCT) in a patient after viral bronchiolitis obliterans demonstrates areas of airtrapping, which is predominant in the inferior lobes and associated with bronchiectasis in the left lower lobe. Note that the decreased attenuation caused by the airtrapping can simulate emphysema (Corrêa da Silva, 2001).

Media file 9: Pediatric high-resolution CT (HRCT) shows a hyperinflated right lung with large pulmonary bullae due to congenital lobar emphysema (Corrêa da Silva, 2001).

Media file 10: Algorithmic representation of emphysema that Reid proposed in 1956.

Media file 11: Pulmonary acinus measures 6-10 mm (red or blue). When normal, the distal terminal bronchiole used to define the acinus cannot be resolved on high-resolution CT (HRCT). Image represents the proportion of acini in relation to the lung image. One lobule, as Reid defined it, can have 3-5 acini (red groups). A secondary pulmonary lobule described by the interstitial septa can have as many as 100 acini (blue groups, the biggest one showing a pulmonary lobule containing about 35 acini) (Corrêa da Silva, 2001).

Media file 12: High-resolution CT (HRCT) demonstrates areas of centriacinar emphysema. Note the low attenuation areas without walls due to destruction of the alveoli septae centrally in the acini. Red element shows the size of a normal acinus (Corrêa da Silva, 2001).

Media file 13: High-resolution CT (HRCT) shows large bullae in both inferior lobes due to uniform enlargement and destruction of the alveoli walls causing distortion of the pulmonary architecture (Corrêa da Silva, 2001).

Media file 14: Panacinar emphysema of the left lung in a patient with a right lung transplant. Note the red element showing the size of a normal acinus and its discrepancy with the destroyed and enlarged airspaces of the left lower lobe (Corrêa da Silva, 2001).

Media file 15: High-resolution CT (HRCT) shows bullae distributed in the subpleural spaces including the fissures; this is characteristic of paraseptal emphysema (Corrêa da Silva, 2001).

Media file 16: High-resolution CT (HRCT) shows subpleural bullae consistent with paraseptal emphysema. Red mark shows the size of a normal acinus (Corrêa da Silva, 2001).

Media file 17: High-resolution CT (HRCT) shows enlarged air-spaces or bullae adjoining pulmonary scars, consistent with paracicatricial emphysema. Red mark shows the size of a normal acinus (Corrêa da Silva, 2001).

Media file 18: CT densitovolumetry of a nonsmoker, healthy young patient shows normal lungs. Less than 0.35% of lungs have attenuations below -950 HU (Corrêa da Silva, 2001).

Media file 19: Expiratory CT densitovolumetry in the same patient as in Image 20 shows no areas of airtrapping (Corrêa da Silva, 2001).

Media file 20: CT densitovolumetry in a heavy smoker with emphysema revealed compromise of about 22% of the lung parenchyma (Corrêa da Silva, 2001).

Media file 21: CT densitovolumetry in a patient with lung cancer. Three-dimensional (3D) image shows that the cancer is in the portion of the right lung that was less affected by emphysema in a patient with poor pulmonary function (Corrêa da Silva, 2001).

Media file 22: CT densitovolumetry shows the attenuation mask. Green areas are those with attenuation below the selected threshold (here, -950 HU to evaluate emphysema), and pink areas are those with attenuations above the threshold. Area outside the patient is highlighted in green because of air (Corrêa da Silva, 2001).

Media file 23: CT densitovolumetry demonstrates irregular distribution of the emphysema, with substantial predominance in the left lung (Corrêa da Silva, 2001).

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Keywords

emphysema, chronic obstructive pulmonary disease, COPD, chronic obstructive lung disease, dyspnea on exertion, air trapping, airtrapping, barrel chest, panlobular emphysema, panacinar emphysema, centrilobular emphysema, centriacinar emphysema, paracicatricial emphysema, paraseptal emphysema, bullous emphysema, pulmonary emphysema

Contributor Information and Disclosures

Author

Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP is a member of the following medical societies: American Institute of Ultrasound in Medicine, Royal College of Physicians, Royal College of Physicians and Surgeons of the United States, Royal College of Radiologists, and Royal College of Surgeons of England
Disclosure: Nothing to disclose.

Coauthor(s)

Sarah Al Ghanem, MBBS, Consulting Staff, Department of Medical Imaging, King Fahad National Guard Hospital, Saudi Arabia
Disclosure: Nothing to disclose.

Klaus L Irion, MD, PhD, Consulting Staff, The Cardiothoracic Centre Liverpool NHS Trust, The Royal Liverpool University Hospital, UK
Klaus L Irion, MD, PhD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chitra P Nagarajaiah, MBBS, MRCP, Acute Medicine Specialist Registrar, City Hospital of Birmingham, UK
Chitra P Nagarajaiah, MBBS, MRCP is a member of the following medical societies: Royal College of Physicians of the United Kingdom
Disclosure: Nothing to disclose.

Pablo Rydz Pinheiro Santana, MD, Staff Physician, Department of Radiology, Irion Radiologia, Brazil
Disclosure: Nothing to disclose.

Medical Editor

Judith K Amorosa, MD, FACR, Clinical Professor and Program Director, Department of Radiology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School; Consulting Staff, Department of Radiology, Robert Wood Johnson University Hospital
Judith K Amorosa, MD, FACR is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America, and Society of Thoracic Radiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

John D Newell, Jr, MD, FACR, FCCP, FASER, Co-Director of Thoracic Imaging, UCDHSC; Director of Lung Imaging Center, Professor of Radiology and Professor of Medicine, Department of Radiology, University of Colorado Health Sciences Center, National Jewish Medical and Research Center; Univ. Colorado Hospital
John D Newell, Jr, MD, FACR, FCCP, FASER is a member of the following medical societies: American College of Chest Physicians, American College of Radiology, American Roentgen Ray Society, American Thoracic Society, Association of University Radiologists, Radiological Society of North America, and Society of Thoracic Radiology
Disclosure: Siemens Medical Grant/research funds Consulting; Forevision Technologies Ownership interest Consulting; Vida Corporation Ownership interest Board membership; TeraRecon Grant/research funds Consulting; eMedicine Honoraria Consulting

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
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Chief Editor

Kavita Garg, MD, Professor, Department of Radiology, University of Colorado Health Sciences Center
Kavita Garg, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Radiological Society of North America, and Society of Thoracic Radiology
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