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Approach to Diffuse Lung Disease: Anatomic Basis and High-Resolution Computed Tomography


Introduction

Diffuse lung diseases are often detected and initially evaluated on chest radiographs (CXR). A CXR can provide valuable clues regarding pulmonary pathology such as the lung volume, distribution, and characterization of abnormalities. Radiographs assess lung volumes and distribution of disease. Whereas low volumes suggest the presence of a restrictive defect such as pulmonary fibrosis, large lung volumes suggest hyperinflation or obstructive lung disease. Ancillary findings such as lymphadenopathy, pleural effusions, and pleural plaques can assist in determining the cause of the pulmonary abnormality. Serial radiographs allow assessment of the acuity of abnormalities; those that persist for more than 4 weeks often indicate a chronic etiology. Findings on a CXR are often nonspecific, and necessitate further evaluation with thin-section chest computed tomography (CT) or high-resolution CT (HRCT).

High-resolution CT is a noninvasive cross-sectional examination of the whole lung. The distribution and characteristics of HRCT findings can indicate which group of differential diagnoses to consider or point to a specific disease without the need for biopsy. HRCT can suggest further tests for a definitive diagnosis or, if tissue sampling is required, can direct the site of biopsy. After diagnosis, follow-up HRCT scans monitor disease activity, the response to treatment, or the development of complications. Evolution of abnormalities over time may have prognostic implications.

High-Resolution Computed Tomography Protocol

The protocol for an HRCT scan is described in detail in Chapter 1 . The principle of HRCT is acquisition of thin transverse sections (1–1.5-mm thickness) with a high spatial resolution technique and lung kernel algorithms to visualize the lung parenchyma ( Fig. 17.1 ). Multiplanar reformatting in the coronal and sagittal planes facilitates evaluation of the distribution of parenchymal abnormalities. Maximum-intensity projection (MIP) and minimum-intensity projection (MinIP) images aid detection of multiple nodules and decreased attenuation, respectively. Prone images are routinely included in the HRCT protocol to differentiate early reticular abnormalities in the dependent peripheral portions of the lower lobes that persist from gravity-dependent density that resolves on prone imaging ( Figs. 17.2 and 17.3 ).

FIGURE 17.1, Effects of slice thickness. A, A 5-mm axial section through the middle lobe. B, A 1.5-mm axial section through the same region. The thinner slice results in less partial volume averaging and creates a sharper image. There is improved definition of the walls of the vessels and airways and the fissures. Subcentimeter cystic lucencies in the middle lobe are also more clearly visualized in this patient with lymphangioleiomyomatosis.

FIGURE 17.2, Effects of technique: supine versus prone. A, A 1.25-mm axial section in the supine position demonstrates lower lobe posterior ground-glass opacities representing dependent atelectasis. B, Axial image that is flipped but was obtained in the prone position at the same level shows clearing of the posterior ground-glass opacities that now lie anteriorly as this is now the dependent position. Gravity-dependent changes can increase attenuation of the posterior lung parenchyma by up to 100 Hounsfield units.

FIGURE 17.3, Effects of technique: supine versus prone. A, Supine 1.25-mm axial section demonstrates posterior lower lobe–dependent ground-glass opacities. B, Axial image that is flipped but was obtained in the prone position at the same level does not show resolution of the ground-glass opacities that represent changes of interstitial lung disease.

Expiratory HRCT images are performed either dynamically (during expiration) or on static images (after end-expiration) ( Fig. 17.4 ). The attenuation of the lung parenchyma on expiratory images is compared with inspiratory images at equivalent levels in the thorax. During normal expiration, the lung parenchyma decreases in volume and increases in attenuation. Areas of air trapping can be easily visualized on expiratory HRCT images as regions that remain similar in volume and attenuation when compared with the inspiratory images. Adequate expiration is confirmed if the posterior membrane of the trachea and main bronchi becomes flat or concave. It is important to consider normal expiration as the cause for increased parenchymal attenuation before suggesting a diagnosis of lung pathology. Respiratory motion can result in artifacts that mimic bronchiectasis, pulmonary embolism, and pulmonary nodules ( Fig. 17.5 ).

FIGURE 17.4, Effects of technique: inspiration versus expiration. A, Axial 1.5-mm computed tomography scan through the upper zones in inspiration demonstrates posterior gravity-dependent changes that can increase the attenuation of the lung by up to 100 Hounsfield units. B, Expiration images at the same level show decrease in volume of the lung parenchyma, crowding of the vasculature, and a diffuse increase in attenuation throughout the lung parenchyma. There is concavity of the posterior membranous wall of the trachea.

FIGURE 17.5, Respiratory motion artifact. The patient is breathing during acquisition of the scan, which caused a diffuse increase in attenuation and created a double exposure of the fissures and vessels. Artifacts seen adjacent to the vessels and airways mimic lung nodules and bronchiectasis as seen in the right upper lobe.

High-Resolution Computed Tomography Evaluation

Many lung diseases involve the lung parenchyma, interstitium, or both. The key to diagnosis is recognition of the distribution of disease in relation to various anatomic regions ( Table 17.1 ). Craniocaudal distribution refers to the preference of a disease process for the upper, mid, or lower zones ( Fig. 17.6 ). Inhalational diseases, including smoking-related lung disease, have a predilection for the upper zones. This is because of the relative paucity of lymphatic drainage in the upper zones clearing inhaled pathogens. Hematogenous diseases, such as miliary metastases, have a predilection for the lower zones, where blood flow is greatest. Axial distribution refers to distribution on a single transverse image; certain diseases are central in distribution, and others predominantly involve the peripheral third of the lung ( Fig. 17.7 ). A dependent distribution of disease involves the posterior portion of the lung in supine patients and anterior portion in the prone position. Most importantly, thin-section CT permits evaluation of the distribution of disease at the level of the secondary pulmonary lobule (SPL), a key step in the accurate assessment and diagnosis of diffuse lung disease.

TABLE 17.1
Differentiation of Diseases by Distribution
Distribution Disease
Upper zone Pulmonary Langerhans cell histiocytosis
Emphysema
Respiratory bronchiolitis
Cystic fibrosis
Hypersensitivity pneumonitis
Sarcoidosis
Reactivation tuberculosis
Pneumoconioses (silicosis, coal worker's pneumoconiosis, berylliosis)
Ankylosing spondylitis, neurofibromatosis 1
Lower zone Hematogenous metastases
Aspiration
Usual interstitial pneumonitis
Nonspecific interstitial pneumonitis
Asbestosis
Central Pulmonary edema
Pulmonary hemorrhage
Pneumocystis pneumonia
Lymphoma
Kaposi sarcoma
Peripheral Organizing pneumonia
Chronic eosinophilic pneumonia
Aspiration pneumonia
Pulmonary infarction
Septic emboli
Sarcoidosis
Adenocarcinoma
Lymphoma
IgG4-related lung disease
Dependent Aspiration
Diffuse alveolar damage (noncardiogenic pulmonary edema or acute lung injury)

FIGURE 17.6, Distribution of disease in separate patients. A, Coronal image shows upper and mid-zone–predominant nodules in this patient with sarcoidosis. B, Sagittal image shows volume loss in the upper lobes associated with bronchiectasis and mosaic attenuation secondary to cystic fibrosis. C, Axial image shows dependent consolidation in this patient with aspiration pneumonia. Aspiration may cause peripheral and dependent distribution of changes. D, Coronal image shows lower zone honeycomb cysts and traction bronchiolectasis in this patient with a usual interstitial pneumonitis pattern of pulmonary fibrosis and a clinical syndrome of idiopathic pulmonary fibrosis.

FIGURE 17.7, Distribution of disease in four separate patients: central versus peripheral. A, A 1.25-mm axial section in the upper lobes demonstrates central ground-glass opacities representing pulmonary edema in this patient with cardiac failure awaiting heart transplant. B, Axial sections in a patient with Kaposi sarcoma show central peribronchovascular nodules and flame-shaped opacities. C, Axial section in a patient with septic emboli secondary to endocarditis of the tricuspid valve shows multiple solid and cavitary peripheral nodules of variable size. D, Axial image through the mid zone in this patient with organizing pneumonia demonstrates multiple peripheral and peribronchiolar consolidative opacities with air bronchograms. This appearance is typical of organizing pneumonia.

Anatomy of the Secondary Pulmonary Lobule

The SPL is the functional unit of lung where gaseous exchange occurs. The SPL contains bronchioles, branches of the pulmonary artery and veins, lymphatics, and interstitial tissue. The SPL measures approximately 1 to 2.5 cm in diameter, is roughly polyhedral in shape, and is outlined by an interlobular septum ( Fig. 17.8 ). The structures in the center of the SPL, the centrilobular structures, consist of a lobular bronchiole and pulmonary artery that course and divide together. The pulmonary artery forms a dot approximately 0.5 to 1 mm in diameter, visible on HRCT in the center of the SPL. The wall of the bronchiole is 0.05 to 0.15 mm and beyond the resolution of HRCT to be normally visible unless thickened or fluid filled. Lobular bronchioles divide into terminal bronchioles, the most distal conducting airways that then divide into several respiratory bronchioles in the center of the SPL. Respiratory bronchioles open into several alveolar ducts to form an acinus. The 10 to 15 acini in each SPL participate in gas exchange and surround the centrilobular bronchovascular structures. Deoxygenated blood in the pulmonary artery passes through the rich capillary network surrounding the acini, where gas exchange occurs. The SPL is outlined by a connective tissue septum, the interlobular septum, within which course pulmonary veins and pulmonary lymphatics. Interlobular septa measure 0.1 cm and are often identified on HRCT by the pulmonary veins that course through the septa and measure 0.5 cm in diameter. The capillary network connects the centrilobular structures to the septal pulmonary veins that carry oxygenated blood back to the heart .

FIGURE 17.8, Diagram depicting the anatomy of the secondary pulmonary lobule (SPL). A, Airways. An SPL is surrounded by interlobular septa (S). Within the SPL, a lobular bronchiole (LB) divides into several terminal bronchioles (TBs) that in turn divide into multiple respiratory bronchioles (RBs). Several alveolar sacs (ASs) communicate with the RBs. This is the site of gaseous exchange within the lungs. B, Lobular pulmonary vessels. The pulmonary artery (PA in blue ) branches course into the SPL alongside the bronchioles. The PA carries deoxygenated blood into the SPL and divides into a rich capillary network that surrounds the alveolar sacs. The capillary network transfers oxygenated blood to the periphery of the SPL. Pulmonary veins (PV in red ) lie within the interlobular septa and transmit blood back to the heart. C, Interstitium. The lymphatics (L in green ) course within a sheath that surrounds the bronchovascular bundle and course within the interlobular septa together with the pulmonary veins. There is an internal framework of connective tissue within the SPL that surrounds the alveolar sacs, known as the intralobular interstitium (ILI in gray ).

Lung Interstitium

The lung interstitium forms a support system of connective tissue surrounding the lung parenchyma. The interstitium is divided into a central, peripheral, and intralobular interstitium. The central (axial) interstitium extends from the hila into the lung parenchyma, enveloping the bronchovascular bundles like a sheath and dividing as the bronchovascular bundles branch and arborize. The axial interstitium eventually reaches and terminates in the center of the SPL, surrounding the centrilobular pulmonary artery and bronchiole. The peripheral interstitium forms a subpleural cloak around the lung and extends along the fissures and forms the interlobular septa that outline the SPL. Between the central, centrilobular interstitium and the peripheral interlobular interstitium runs a fine meshwork of interstitial lines, the intralobular interstitium, that supports the structures within the SPL. The septa are most easily identified on CT in the subpleural region, along the fissures, and at the lung apices and bases.

Lymphatics are present in the interstitium. They course along the bronchovascular bundles surrounding the bronchiole and pulmonary artery that supply each lobule and within the interlobular septa. Lymphatic obstruction from tumor or edema can result in thickening of the bronchovascular interstitium and interlobular septa. Because the interlobular septa are best developed in the subpleural region and along the fissures, these areas are often involved with perilymphatic diseases, but centrilobular diseases involve structures in the center of the SPL; do not extend to the pleura, fissures, or interlobular septa; and are located approximately 5 to 10 mm from those surfaces. This distinction is helpful in localizing the site of abnormality on HRCT and directing the differential diagnosis.

High-Resolution Computed Tomography Patterns

Most abnormalities identified on thin-section CT can be categorized into one of four main patterns: nodular, reticular, increased, or decreased attenuation. The predominant pattern as well as its anatomic location are extremely helpful in determining the imaging differential diagnosis. Diseases may show a craniocaudal and axial distribution as well as a predisposition to particular areas at the level of the SPL.

Nodular Pattern ( Table 17.2 )

A nodular pattern consists of multiple well-defined rounded soft tissue or ground-glass nodules. The nodules usually measure between 2 and 10 mm in diameter, and their distribution can be related to the structures of the SPL ( Fig. 17.9 ).

TABLE 17.2
Causes of Multiple Nodular Opacities
Type Causes
Perilymphatic Sarcoidosis
Lymphangitic carcinomatosis, lymphoma
Silicosis, coal worker's pneumoconiosis
Rare Berylliosis
Amyloidosis
Lymphocytic interstitial pneumonia
Random Metastases
Miliary infection: tuberculosis, fungal
Centrilobular: nonbranching Respiratory bronchiolitis
Hypersensitivity pneumonitis
Pulmonary hemorrhage
Infection
Pulmonary edema
PLCH
Rare Follicular bronchiolitis
Pulmonary arterial hypertension
Invasive mucinous adenocarcinoma
Organizing pneumonia
Capillary hemangioendotheliosis
Metastatic calcification, talcosis
Pneumoconiosis (coal worker's pneumoconiosis, silicosis)
Centrilobular: branching (tree-in-bud) Infection: bacterial, mycobacterial, viral, fungal, ABPA, panbronchiolitis
Aspiration
Bronchiectasis, cystic fibrosis
Rare Invasive adenocarcinoma
Follicular bronchiolitis
Organizing pneumonia
ABPA, Allergic Bronchopulmonary Aspergillasis; PLCH, pulmonary Langerhans cell histiocytosis.

FIGURE 17.9, Diagram depicting the different nodular patterns at the level of the secondary pulmonary lobule (SPL). A, Perilymphatic pattern. Multiple nodules course along the bronchovascular bundle, interlobular septa, adjacent subpleural or fissural visceral pleura (VP in pink ). B, Random pattern. Nodules do not correspond to any anatomic structure and vary in size. Some may abut the fissure and subpleural region C, Centrilobular nonbranching pattern. These nodules lie in the center of the SPL. They are most frequently of ground-glass attenuation but occasionally are solid or cavitary. They do not extend into the interlobular septa, the subpleural, or fissural regions. D, Centrilobular branching nodules. These are also known as tree-in-bud opacities. The opacity is the result of inflammation and fluid filling of the small airways.

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