Abstract
This chapter describes the imaging patterns of pneumonia (lobar, lobular, interstitial, round) and its complications (abscess, empyema, pneumatocele); bacterial, fungal, and viral infections; and the many manifestations of pulmonary tuberculosis.
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Caveats
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1.
You cannot interpret what you cannot see. On a supine AP image, enlargement of the cardiac silhouette, pulmonary edema, and layering pleural effusions make detection of a small pneumonia almost impossible. Indicate this limitation to the referring physician by stating something like: “In the appropriate clinical setting, it would be extremely difficult to exclude superimposed pneumonia.”
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2.
Especially in the retrocardiac area on the lateral view, it may be difficult to detect a subtle pneumonia. Normally, you should see discrete tubular structure representing pulmonary vessels. Opacification obscuring these vessels is the earliest sign of pneumonia (Fig. 6.1; see Fig. e6.1).
(All electronic images (Figs. e6.1–e6.54) can be found on this chapter’s website on SpringerLink: [https://doi.org/10.1007/978-3-030-16826-1_6])
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3.
Any asymmetry in the lungs on a frontal view may be the earliest sign of an area of consolidation (Fig. 6.2).
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4.
In hospitalized, bedridden patients, it often is impossible to determine whether a consolidation represents aspiration or infectious pneumonia. Consider using the term “aspiration/pneumonia” to indicate this to the referring physician.
Types of Pneumonia
Community-Acquired Pneumonia (CAP)
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A pneumonia contracted by a person who has little contact with the healthcare system
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Affects individuals of all ages and most commonly arises as a viral infection (though there may be bacterial superinfection)
Hospital-Acquired Pneumonia (HAP)
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Any pneumonia developing in a patient at least 48 hours after being hospitalized
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Second most common nosocomial infection (after urinary tract infections)
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Unlike community-acquired pneumonia, HAP is usually caused by a bacterial infection, rather than a virus
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High morbidity and mortality rates and the primary cause of death in intensive care units
Ventilator-Acquired Pneumonia (VAP)
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Any pneumonia developing in a patient at least 48–72 hours after endotracheal tube intubation
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Typically affecting critically ill patients in an intensive care unit, VAP develops in up to 30% of ventilated individuals and is associated with a mortality rate of up to 80%
Imaging Patterns
Lobar Pneumonia
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Homogeneous consolidation of all or a substantial percentage of a single lobe
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Sharply marginated by one or more fissures (Fig. 6.3)
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Air bronchograms (larger bronchi remain patent) (see Fig. e6.2)
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Silhouette sign when the consolidation is adjacent to the heart, aorta, or hemidiaphragm (Fig. 6.4)
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Most commonly bacterial, especially due to Streptococcus pneumoniae
Lobular Pneumonia (Bronchopneumonia) (Fig. 6.5; See Figs. e6.3–e6.7)
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Patchy, poorly defined, heterogeneous air-space consolidation that tends to involve the peripheral portions of the lungs
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Frequently multifocal, involving several areas at the same time
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Tends to have indistinct margins (unless touching a pleural fissure)
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Associated with exudate filling the bronchi, leading to associated atelectasis and absence of air bronchograms
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Patchy areas may coalesce to mimic lobar pneumonia
Interstitial Pneumonia
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Involvement of the walls of the alveoli and airways producing a fine, reticular pattern (Fig. 6.6)
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Diffuse or patchy ground-glass opacification on CT (see Fig. e6.8)
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Caused by viral pneumonias, mycoplasma, and chlamydia
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In immunosuppressed patients (CD4 counts under 200/mm2), likely to be Pneumocystis, with the classic pattern of bilateral prominence of reticular markings radiating outward from the hila (may mimic pulmonary edema)
Round Pneumonia (Fig. 6.7; See Figs. e6.9 and e6.10)
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Infectious mass-like opacity, usually seen in children who have a history of infectious symptoms and recent normal chest radiograph (making a neoplasm unlikely)
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Imaging appearance is due to underdeveloped pores of Kohn and the absence of canals of Lambert, which limit the centrifugal spread of early bacterial infection
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Most commonly due to Streptococcus pneumoniae or Haemophilus influenzae
Aspiration Pneumonia
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Foreign material entering into the tracheobronchial tree secondary to gastroesophageal reflux, altered mental status (drug overdose, anesthesia), or neurologic disorder (stroke, traumatic brain injury)
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Often develops in intubated patients, despite the presence of an inflatable cuff
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Usually occurs in the most dependent portions of the lung
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Supine – superior and posterior basal segments of the lower lobes or posterior segment of the upper lobes (Fig. 6.8)
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Upright – lower lobes (typically on the right, because the right main bronchus runs more vertically and is wider)
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Rapid appearance of air-space consolidation, especially in bedridden patients.
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Noninfectious aspiration – usually clearance in less than 1 week
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Mendelson syndrome – large-volume aspiration of gastric acid, which produces a chemical pneumonitis and acute lung injury (even ARDS) and a diffuse radiographic pattern simulating pulmonary edema (Fig. 6.9; see Fig. e6.11)
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Lipoid pneumonia – chronic aspiration of ingested exogenous lipid material (such as mineral oil for chronic constipation); appears radiographically as chronic consolidation or mass, which has low attenuation on CT (Fig. 6.10; see Fig. e6.12)
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Follow-up of Pneumonia
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Radiographic clearance of pneumonia usually lags well behind clinical improvement
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Follow-up chest radiographs are recommended in approximately 4–6 weeks to ensure complete resolution of the consolidation and to assess persistent abnormality of the lung parenchyma (scarring, bronchiectasis)
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Failure of a pneumonia to resolve by 8 weeks suggests an inaccurate diagnosis or an endobronchial obstruction as a cause of post-obstructive pneumonia (Fig. 6.11)
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Especially in patients with smoking history or over age 40, CT should be considered to exclude an underlying bronchial lesion (see Fig. e6.13)
Complications of Pneumonia
Pneumatocele
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Thin-walled, gas-filled cyst in the lung parenchyma that is most frequently caused by pneumonia (especially in children following staphylococcal pneumonia), trauma, or the inhalation of hydrocarbon fluid (Fig. 6.12; see Fig. e6.14)
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Single or multiple thin-walled cystic spaces (may be thick-walled in the acute phase and mimic a lung abscess)
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CT may show scattered thin-walled cysts interspersed with normal lung in areas previously affected by pneumonia or trauma (see Fig. e6.15)
Lung abscess (Fig. 6.13; See Figs. e6.16–e6.19)
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Irregular infectious cavity containing necrotic debris or fluid.
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Often an air-fluid level, which usually has the same extent on both frontal and lateral views
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The wall of the abscess may be smooth or ragged, with an unusual nodular appearance suggesting a cavitating malignancy
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If it extends to the pleural surface, a lung abscess forms an acute angle (unlike the obtuse angle formed by an empyema)
Empyema (Figs. 6.14 and 6.15; See Figs. e6.20 and e6.21)
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Loculated infection within the pleural space
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Stages of parapneumonic effusions:
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Initially sterile (exudative stage) with normal glucose levels
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As white blood cells and bacteria accumulate in the fluid collection (fibropurulent stage), the glucose level and pH decrease
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Finally, in the chronic organizing stage, the fluid is thick and purulent, and there is the development of a fibrin peel
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Initially, may appear as a typical pleural effusion (usually unilateral)
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As it reaches the fibropurulent stage, an empyema may become loculated with a characteristic lenticular shape and smooth border that is convex to the lung and forms an obtuse angle with the chest wall
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Disparity in the lengths of air-fluid levels on PA and lateral projections
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Presence of an air-fluid level or pockets of air within a pleural collection suggests a bronchopleural fistula
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CT – Classic split pleura sign (smooth thickening and contrast enhancement of the visceral and parietal pleura surrounding the loculated collection of fluid in the pleural space)
Empyema Necessitans (Fig. 6.16)
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Chronic empyema draining via a sinus tract into the subcutaneous tissues of the chest wall, most commonly related to tuberculosis or fungal infection (actinomycosis, aspergillosis, blastomycosis, mucormycosis)
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Loculated pleural fluid collection or mass with associated rib destruction and often bubbles of loculated gas in soft tissues
Special Types of Bacterial Pneumonia
Klebsiella
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Gram-negative bacterial pneumonia that is most common in debilitated middle-aged and older men with alcoholism (about two-thirds of cases); high mortality rate
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Tends to form a voluminous exudate that produces a homogeneous parenchymal consolidation containing an air bronchogram
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Lobar enlargement (especially the right upper) with the characteristic bulging fissure sign (Fig. 6.17)
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Bulging fissure sign also in Haemophilus influenzae pneumonia (predominantly in compromised hosts, such as chronic pulmonary disease, immune deficiency, alcoholism, diabetes) (see Fig. e6.22)
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High frequency of abscess and cavity formation (ischemic necrosis and death of a portion of the lung may result in sloughed lung within a thick-walled cavity, known as “pulmonary gangrene”)
Septic emboli (Figs. 6.18 and 6.19; See Figs. e6.23–e6.25)
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Most frequently result from infectious particles reaching the lung from an infected heart valve (especially the tricuspid), intravenous catheter, or injected debris
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Persons at risk include drug abusers, immunocompromised patients, individuals with septal defects, and those with indwelling venous catheters, pacemakers, or prosthetic heart valves
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Initially, multiple ill-defined round or wedge-shaped opacities with a swirling pattern that are usually peripheral and tend to involve the lower lobes (starry night sign – mimicking the brush strokes in van Gogh’s painting of that name)
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Cavitary pulmonary nodules tend to develop rapidly (1–2 days)
Loeffler’s syndrome
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Transient, rapidly changing, migrating, nonsegmental areas of parenchymal consolidation, which are associated with blood eosinophilia and minimal (or no) pulmonary symptoms
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Bilateral patchy consolidations with ill-defined margins that are predominantly located in the periphery of the lung
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May produce single or multiple air-space nodules with surrounding ground-glass opacities (Fig. 6.20)
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Unlike chronic eosinophilic pneumonia (see below), the transient air-space abnormalities resolve in some areas and reappear in others over days
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Loeffler’s syndrome (also known as simple pulmonary eosinophilia) is applied to idiopathic cases; a similar imaging pattern can occur in response to parasitic infection or be drug-induced
Chronic eosinophilic pneumonia (Fig. 6.21; See Fig. e6.26)
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Classic appearance of multifocal areas of consolidation in both lungs, especially the upper lobes, reflecting inflammatory eosinophils filling alveoli and infiltrating the interstitium
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Characteristic peripheral predominance (“reverse pulmonary edema pattern”)
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Rapid response to steroid therapy (clinical improvement within hours, radiographic clearing within a few days)
Fungal Pneumonia
Aspergillosis
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Common fungus found in soil, on plants, and in decaying matter, as well as in household dust and building materials, which does not harm persons with normal immune systems and no allergic hypersensitivity
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Invasive aspergillosis (most aggressive form) is essentially limited to debilitated patients, diabetics, and neutropenic individuals with severely compromised immune systems (organ or bone marrow transplants, high-dose steroids or chemotherapy, lymphoma, leukemia)
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Central mass within a cavity in invasive aspergillosis is almost always necrotic lung (Fig. 6.22; see Figs. e6.27–e6.29)
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CT halo sign – early finding of a zone of ground-glass opacity (usually related to hemorrhage) surrounding a nodule or mass is strongly suggestive of invasive aspergillosis in an immunocompromised patient (Fig. 6.23; see Fig. e6.30)
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Aspergilloma – solid homogeneous, rounded, mobile mycetoma that develops in a pre-existing cyst or cavity (primarily upper lobe) in a patient with underlying lung disease and is separated from its wall by a crescentic air space (air crescent sign) (see Fig. e6.31)
Other Fungal Diseases
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Histoplasmosis – central United States; nodules often calcify (Fig. 6.24)
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Coccidioidomycosis – southwestern United States (also northern Mexico and Central and South America)
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Actinomycosis , Nocardia – pleural effusion and extension to the chest wall are common (may develop empyema) (see Fig. e6.32)
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Candidiasis , aspergillosis , sporotrichosis , and mucormycosis – essentially limited to debilitated patients and those with underlying diseases (diabetes mellitus, lymphoma, leukemia) (see Fig. e6.33)
Pneumocystis jirovecii (formerly carinii) pneumonia (Figs. 6.25 and 6.26; See Figs. e6.34–e6.36)
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Caused by a yeast-like fungus and almost exclusively seen in immunosuppressed patients (especially AIDS, lymphoproliferative diseases, or renal transplants)
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Initially, bilateral diffuse interstitial opacities spreading outward from the hila
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If untreated, this soon progresses to a homogeneous diffuse alveolar consolidation that may simulate pulmonary edema
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Thin-walled, air-filled lung cysts (especially apical and subpleural) occur in about 40% of patients and may cause a pneumothorax
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Thick-walled cavities usually indicate superinfection
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Hilar adenopathy and significant pleural effusions are rare (their presence should raise the possibility of an alternate diagnosis)
Viral Pneumonia
Infectious Mononucleosis (Epstein-Barr Virus)
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Although a clinical diagnosis, may appear on chest radiographs as bilateral hilar enlargement due to lymphadenopathy (see Fig. e6.37)
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Important to look for medial displacement of gas within the stomach and splenic flexure caused by splenomegaly
Varicella (Chickenpox) pneumonia (Fig. 6.27; See Fig. e6.38)
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Diffuse distribution of small (1–10 mm), poorly defined nodules, which may coalesce to produce extensive bilateral fluffy infiltrates that tend to develop near the hilum and lung bases
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Healed varicella pneumonia classically appears as tiny military calcifications scattered widely throughout both lungs (develops several years after the pulmonary infection)
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No calcification of hilar lymph nodes (unlike histoplasmosis or tuberculosis, the two other major causes of diffuse pulmonary calcifications)
Tree-in-Bud Pattern in Other Viral Pneumonias
Tuberculosis
Primary
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Although traditionally considered a disease of children and young adults, with the dramatic decrease in the prevalence of tuberculosis (especially in children and young adults), primary pulmonary disease can develop at any age
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Primary tuberculosis may affect any lobe, so that the diagnosis cannot be excluded because the infection is not in the upper lobe
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“Latent” TB refers to someone who has a positive TST with no history of tuberculous infection or imaging evidence of active or old disease (most often detected when undergoing routine screening for employment or school)
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“Inactive” TB refers to someone with imaging evidence of prior tuberculosis but no sign of active disease
Imaging
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One or more foci of lobar or segmental air-space consolidation that is usually homogeneous, dense, and well defined (Fig. 6.29)
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If multiple, randomly distributed throughout the lungs
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Cavitation is infrequent.
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Associated enlargement of hilar or mediastinal lymph nodes (usually unilateral) is seen in about one-third of patients (may be the only imaging finding, especially in children and immunocompromised adults with AIDS) (Fig. 6.30; see Fig. e6.40)
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Unilateral pleural effusion often occurs, especially in adults, and is usually associated with pulmonary parenchymal abnormalities (see Fig. e6.41)
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In patients with an adequate host immune response, the consolidation slowly decreases in size and may form a well-circumscribed nodule that may eventually calcify (Ghon lesion) and be associated with an ipsilateral calcified lymph node (Ranke complex) (see Figs. e6.42 and e6.43)
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Characteristic apical pleural thickening and fibronodular appearance in one or both upper lungs (Fig. 6.31; see Fig. e6.44)
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CT – enlarged lymph nodes typically have a low-density center (due to caseous necrosis) with rim enhancement (reflecting granulomatous tissue); may demonstrate subtle cavitation that is not visible on chest radiographs (see Fig. e6.45)
Postprimary (Reactivation/Active)
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Results from either activation of a latent primary infection or, less commonly, from a repeat infection in a previously sensitized host
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About 10% of all infected patients with tuberculosis develop reactivation (highest risk within the first 2 years or during periods of immunosuppression)
Imaging
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Initially, a nonspecific hazy, poorly marginated alveolar infiltrate that most commonly affects the upper lobes, especially the apical and posterior segments (Figs. 6.32; see Fig. e6.46)
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Bilateral (though often asymmetric) upper lobe disease is common and is almost diagnostic of postprimary tuberculosis
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Because an apical lesion may be obscured by overlying clavicle or ribs, an apical lordotic view is often of value
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Cavitation is common (about 50%) and characteristic of postprimary disease (Figs. 6.33 and 6.34; see Fig. e6.47)
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The presence of cavitation indicates that the disease is highly contagious, and this finding alone warrants putting the patient in respiratory isolation
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Air-fluid levels in cavities are uncommon and usually a manifestation of superinfection (see Fig. e6.48)
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Tuberculous cavities may result in endobronchial spread and the classic “tree-in-bud” pattern of centrilobular bronchial dilatation and filling by mucus, pus, or fluid, associated with a linear branching pattern that resembles a budding tree and is generally more pronounced in the lung periphery (see Figs. e6.49–e6.51)
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Other complications of cavitation include rupture into the pleural space (leading to empyema or bronchopleural fistula) and the development of a pseudoaneurysm of the pulmonary artery (Rasmussen aneurysm)
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Pleural effusion and lymph node enlargement are rare in postprimary tuberculous disease (though common and sometimes the only finding in primary disease)
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As the disease heals, fibrotic changes develop in the surrounding lung, which cause volume loss in the affected segment with displacement of the fissures and hilar structures (see Fig. e6.52)
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CT – because the diagnosis of typical postprimary tuberculosis is generally evident on chest radiographs, CT is primarily used to assess the extent and nature of the disease (more sensitive for demonstrating cavitation and such complications as vascular erosion, rupture into the pleural space, and miliary and endobronchial spread)
Miliary
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Hematogenous dissemination that usually occurs in patients with altered host resistance to the primary infection
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Almost invariably leads to a dramatic febrile response with night sweats and chills
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There may be minimal symptoms in severely debilitated patients, especially elderly persons and those receiving steroids
Imaging
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Diffuse pattern of innumerable tiny (1–2 mm), discrete, relatively well-defined pulmonary nodules distributed uniformly throughout both lungs (Fig. 6.35; see Figs. e6.53 and e6.54)
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CT – may detect the presence of diffuse lung involvement when corresponding chest radiographs are normal or show only minimal or limited disease
References
Eisenberg RL. Clinical Imaging: An Atlas of Differential Diagnosis. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2010.
Franquet E. Pneumonia. Semin Roentg. 2017;52:27–34.
Nemec SF, Bankier AA, Eisenberg RL. Lower lobe-predominant diseases of the lung. AJR. 2013;200:712–28.
Ridge CA, Bankier AA, Eisenberg RL. Mosaic attenuation. AJR. 2011;197:W970–7.
Cantin L. Multiple cystlike lung lesions in the adult. AJR. 2010;194:W1–W11.
Nachiappan AC, Rahbar K, Xiao S, et al. Pulmonary tuberculosis: role of radiology in diagnosis and management. Radiographics. 2017;37:52–72.
Jeong JJ, Kim K-I, Seo IJ, et al. Eosinophilic lung diseases: a clinical, radiologic, and pathologic overview. Radiographics. 2007;27:617–37.
Nemec SF, Bankier AA, Eisenberg RL. Upper lobe-predominant diseases of the lung. AJR. 2013;200:W222–37.
Gosset N, Bankier AA, Eisenberg RL. Tree-in-bud pattern. AJR. 2009;193:W472–7.
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Electronic Supplementary Material
Fig. e6.1
Subtle retrocardiac pneumonia. (a) Frontal view shows normal discrete tubular vessels behind the heart (TIF 3129 kb)
Fig. e6.1
Subtle retrocardiac pneumonia. (b) Obscuration of the vessels behind the heart (arrows) indicates pneumonia (TIF 511 kb)
Fig. e6.2
Lobar pneumonia (right upper lobe). Homogeneous consolidation of the right upper lobe and the medial and posterior segments of the right lower lobe. Note the associated air bronchograms (arrows) [1] (TIF 795 kb)
Fig. e6.3
Lobular pneumonia (right middle lobe). (a) Increased opacification at the right base medially silhouettes the right heart border (TIF 1725 kb)
Fig. e6.3
Lobular pneumonia (right middle lobe). (b) Lateral view shows that the opacification projects over the cardiac shadow (arrows), consistent with a right middle lobe pneumonia (TIF 2078 kb)
Fig. e6.4
Lobular pneumonia (lingula). (A) An area of consolidation silhouettes the left heart border (TIF 1400 kb)
Fig. e6.4
Lobular pneumonia (lingula). (B) Lateral view shows that the opacification projects over the cardiac shadow (arrow), confirming its location in the lingula (TIF 1792 kb)
Fig. e6.5
Lobular pneumonia (multifocal). (A) Heterogeneous areas of opacification in the lower lungs on the right (back arrow) and left (white arrow) (TIF 2110 kb)
Fig. e6.5
Lobular pneumonia (multifocal). (B) On the lateral view, the anterior opacification (black arrow) is in the right middle lobe, with a sharp posterior margin at the major fissure. The posterior opacification (white arrow) is in the left lower lobe, silhouetting the left hemidiaphragm and producing a positive spine sign (TIF 2010 kb)
Fig. e6.6
Lobular pneumonia (lingula). Focal consolidation with air bronchograms (arrow) [2] (TIF 581 kb)
Fig. e6.7
Lobular pneumonia (multifocal). Ill-defined areas of mixed interstitial-alveolar infiltrates in the right upper lobe, along with a segmental ground-glass opacity in the superior segment of the left lower lobe [2] (TIF 441 kb)
Fig. e6.8
Interstitial pneumonia (Pneumocystis jirovecii). Diffuse, bilateral ground-glass opacities with minimal peripheral sparing in a patient with AIDS [1] (TIF 532 kb)
Fig. e6.9
Round pneumonia. Soft-tissue opacifications in the posterolateral aspects of both lower lobes (arrows) with mild bilateral hilar prominence [1] (TIF 646 kb)
Fig. e6.10
Round pneumonia. (a) Radiographs demonstrate a mass-like lesion in the right lower lobe (arrows) (TIF 1776 kb)
Fig. e6.10
Round pneumonia. (b) Radiographs demonstrate a mass-like lesion in the right lower lobe (arrows) (TIF 2085 kb)
Fig. e6.10
Round pneumonia. (c) CT image shows an irregular cavitary mass with air bronchograms (TIF 1123 kb)
Fig. e6.10
Round pneumonia. (d) After appropriate antibiotic therapy, a repeat scan demonstrates clearing of the pneumonia and a residual pneumatocele (arrow) (TIF 1271 kb)
Fig. e6.11
Aspiration pneumonia. Bilateral air-space opacities (open arrows), predominantly in the posterior and lower lung, in a patient with gastroesophageal reflux disease. Note right-sided position of a dilated esophagus (solid arrow) [3] (TIF 1463 kb)
Fig. e6.12
Lipoid pneumonia after laxative aspiration. Ovoid opacity with virtually pathognomonic central fat attenuation (arrow) in the medial segment of the middle lobe [3] (TIF 1122 kb)
Fig. e6.13
Post-obstructive pneumonia (failure of pneumonia to clear). (a) Initial image shows an area of opacification in the left mid-lung (arrow) (TIF 1582 kb)
Fig. e6.13
Post-obstructive pneumonia (failure of pneumonia to clear). (b) After a course of antibiotics, a repeat study 6 weeks later shows no improvement and prompted the ordering of a CT scan (TIF 1434 kb)
Fig. e6.13
Post-obstructive pneumonia (failure of pneumonia to clear). (c) This demonstrates an irregular mass (arrow) that proved to be a bronchogenic carcinoma (TIF 737 kb)
Fig. e6.14
Pneumatocele. (a) Following hydrocarbon poisoning, there has been the development of a large, thin-walled cystic space (arrow) (TIF 578 kb)
Fig. e6.14
Pneumatocele. (b) In another patient, there are multiple thin-walled pneumatoceles bilaterally, more prominent on the right [1] (TIF 631 kb)
Fig. e6.15
Pneumatoceles. In this fire eater, there is a dramatic change (arrows) before (a) and after (b) treatment (TIF 2212 kb)
Fig. e6.15
Pneumatoceles. In this fire eater, there is a dramatic change (arrows) before (a) and after (b) treatment (TIF 2138 kb)
Fig. e6.15
Pneumatoceles. (c) Multiple pneumatoceles (arrows) after recurrent infections in a patient with AIDS [5] (TIF 2424 kb)
Fig. e6.16
Lung abscess (Proteus pneumonia). Large, thick-walled left upper lobe cavity with an air-fluid level (arrow) and associated consolidation [1] (TIF 873 kb)
Fig. e6.17
Lung abscess (staphylococcal pneumonia). Multiple cavities with air-fluid levels (arrows) associated with diffuse air-space consolidation and a large pleural effusion [1] (TIF 883 kb)
Fig. e6.18
Lung abscess (Pneumocystis jirovecii pneumonia). (a) Left upper lobe consolidation with an air-fluid level (arrows) in a young male with AIDS (TIF 881 kb)
Fig. e6.18
Lung abscess (Pneumocystis jirovecii pneumonia). (b) CT scan confirms a large abscess in the superior segment of the left lower lobe, with thick nodular walls and an air-fluid level (arrow) [2] (TIF 588 kb)
Fig. e6.19
Lung abscess. (a) Irregular-walled cavity in the right apex posteriorly (arrows), representing a lung abscess that developed following surgery for a non-small-cell lung cancer (TIF 622 kb)
Fig. e6.19
Lung abscess. (b) Irregular-walled cavity in the right apex posteriorly (arrows), representing a lung abscess that developed following surgery for a non-small-cell lung cancer (TIF 996 kb)
Fig. e6.20
Empyema. Large soft-tissue mass fills much of the left hemithorax [1] (TIF 823 kb)
Fig. e6.21
Empyema. Large mottled opacity over the right upper hemithorax represents an extensive empyema that obscures the underlying parenchymal streptococcal pneumonia. The patchy air densities within the empyema indicate communication with the bronchial tree [1] (TIF 991 kb)
Fig. e6.22
Bulging fissure sign (Haemophilus influenzae pneumonia) [1] (TIF 773 kb)
Fig. e6.23
Septic emboli. Multiple nodular opacifications throughout both lungs in a patient with endocarditis (TIF 1283 kb)
Fig. e6.24
Septic emboli. Multiple nodular lesions. Note the peripheral location of the nodules and the numerous cavitations (TIF 594 kb)
Fig. e6.25
Septic emboli. (a) Scattered, mostly peripheral, poorly defined foci of air-space consolidation, many of which contain varying degrees of cavitation. Note that a number of these appear to be associated with “feeding” vessels (arrows), suggesting a hematogenous origin [1] (TIF 605 kb)
Fig. e6.25
Septic emboli. (b) Scattered, mostly peripheral, poorly defined foci of air-space consolidation, many of which contain varying degrees of cavitation. Note that a number of these appear to be associated with “feeding” vessels (arrows), suggesting a hematogenous origin [1] (TIF 594 kb)
Fig. e6.26
Chronic eosinophilic pneumonia. Air-space consolidation confined mainly to the periphery of the lung (reverse pulmonary edema pattern) [7] (TIF 774 kb)
Fig. e6.27
Aspergillosis. Multiple cavities of various sizes are superimposed on a diffuse pulmonary infiltrate. A fungus ball almost fills the large cavity in the right upper lobe (arrows). A right pleural effusion also is seen in this patient with chronic lymphocytic leukemia [1] (TIF 703 kb)
Fig. e6.28
Aspergillosis. Thin-walled cavitary nodule in the right lung of a patient with leukemia [1] (TIF 1792 kb)
Fig. e6.29
Aspergillosis. Bilateral large upper lobe cavities containing fungus balls of different sizes in an elderly man with residual tuberculosis [1] (TIF 484 kb)
Fig. e6.30
Invasive pulmonary aspergillosis. Nodule in the posterior segment of the right upper lobe is surrounded by a “halo” of ground-glass opacity (arrows) in this young neutropenic male [2] (TIF 817 kb)
Fig. e6.31
Aspergilloma. (a) Soft-tissue mass within a cavity (air crescent sign) in the right upper lobe (TIF 636 kb)
Fig. e6.31
Aspergilloma. (b) Supine and (c) prone axial CT images show that the curvilinear air moves to the nondependent position (TIF 545 kb)
Fig. e6.31
Aspergilloma. (b) Supine and (c) prone axial CT images show that the curvilinear air moves to the nondependent position (TIF 1535 kb)
Fig. e6.32
Fungal lung abscess. Large right apical, thick-walled cavitary lesion in an acutely ill patient with actinomycosis [1] (TIF 598 kb)
Fig. e6.33
Fungal lung abscess. Large thin-walled cavity at the right base (arrow) containing a smooth, elliptical homogeneous mass (arrowheads), representing a mucormycosis fungus ball in a diabetic patient [1] (TIF 589 kb)
Fig. e6.34
Pneumocystis jiroveci pneumonia. Severe, bilateral air-space consolidation with air bronchograms. The patient was undergoing immunosuppressive therapy for lymphoma and died shortly after this radiograph was made [1] (TIF 619 kb)
Fig. e6.35
Pneumocystis jiroveci pneumonia. (a) Bilateral, symmetric, mostly perihilar opacities (TIF 1674 kb)
Fig. e6.35
Pneumocystis jiroveci pneumonia. (b) CT image confirms the bilateral, widespread ground-glass opacities and also shows scattered lung cysts (arrow) [5] (TIF 1118 kb)
Fig. e6.36
Pneumocystis jirovecii pneumonia. Bilateral ground-glass opacities containing multiple cysts in a young HIV-positive male [2] (TIF 824 kb)
Fig. e6.37
Infectious mononucleosis. (a) Bilateral hilar lymphadenopathy [1] (TIF 795 kb)
Fig. e6.37
Infectious mononucleosis. (b) Bilateral hilar lymphadenopathy [1] (TIF 1027 kb)
Fig. e6.38
Varicella pneumonia. Multiple calcified nodules [1] (TIF 681 kb)
Fig. e6.39
Tree-in-bud pattern (respiratory syncytial virus). Peripheral, poorly defined centrilobular nodules and “tree-in-bud” opacities bilaterally in a patient with leukemia. Note the scattered lung nodules surrounded by halos of ground-glass attenuation [1] (TIF 1572 kb)
Fig. e6.40
Primary tuberculosis. Combination of a focal parenchymal lesion (arrows) and enlarged right hilar lymph nodes [1] (TIF 554 kb)
Fig. e6.41
Primary tuberculosis. Unilateral right tuberculous pleural effusion without parenchymal or lymph node involvement [1] (TIF 739 kb)
Fig e6.42
Inactive tuberculosis. (a) Calcified peripheral granuloma (Ghon lesion, black arrow) and calcified hilar lymph nodes (white arrows), combining to form a Ranke complex [8] (TIF 1681 kb)
Fig e6.42
Inactive tuberculosis. (b) Calcified peripheral granuloma (Ghon lesion, black arrow) and calcified hilar lymph nodes (white arrows), combining to form a Ranke complex [8] (TIF 1521 kb)
Fig e6.43
Inactive tuberculosis. Densely calcified hilar nodes and enlarged calcified node in the aorticopulmonary window (arrow) (TIF 1776 kb)
Fig e6.44
Inactive tuberculosis. Apical pleural thickening (arrows) (TIF 1174 kb)
Fig e6.45
Mediastinal tuberculous adenopathy. Multiple enlarged mediastinal lymph nodes with central areas of low attenuation and peripheral enhancement (arrows) [1] (TIF 608 kb)
Fig. e6.46
Recurrent active tuberculosis. (a) Years after clearing of the process in Fig. 6.23, thee is the development of a new opacity in the left perihilar region (arrow) (TIF 1711 kb)
Fig. e6.46
Recurrent active tuberculosis. (b) CT image confirms the changes as cavitation (black arrows) and also demonstrates a surrounding tree-in-bud pattern (white arrow) [3] (TIF 1282 kb)
Fig. e6.47
Active tuberculosis. Large cavitary lesion with surrounding consolidation involving the apical posterior segment of the right upper lobe. (Courtesy of Diana Litmanovich, MD, Boston) (TIF 1496 kb)
Fig e6.48
Active tuberculosis. Multiple large cavities with air-fluid levels in both upper lobes. Note the chronic fibrotic changes and upward retraction of the hila [1] (TIF 916 kb)
Fig e6.49
Active tuberculosis. (a) Multiple areas of the “tree-in-bud” pattern (arrows) (TIF 519 kb)
Fig e6.49
Active tuberculosis. (b) More inferior image shows larger nodular opacities (arrows), representing extension of the granulomatous infection into adjacent alveoli [1] (TIF 520 kb)
Fig e6.50
Active tuberculosis with endobronchial spread. Typical appearance of numerous, diffuse, poorly defined nodules, some of which are perivascular and centrilobular [1] (TIF 845 kb)
Fig. e6.51
Active tuberculosis with endobronchial spread. (a) Maximum intensity projections (MIPS) show generalized tree-in-bud opacities [9] (TIF 1346 kb)
Fig. e6.51
Active tuberculosis with endobronchial spread. (b) Maximum intensity projections (MIPS) show generalized tree-in-bud opacities [9] (TIF 1889 kb)
Fig e6.52
Healed active tuberculosis. Diffuse interstitial fibrosis pattern [1] (TIF 665 kb)
Fig e6.53
Miliary tuberculosis. Numerous, well-defined, 1–2 mm nodules diffusely distributed through the right lower lobe. Some nodules appear septal (arrows) or subpleural, whereas others appear to be associated with small feeding vessels, suggesting a hematogenous origin [1] (TIF 928 kb)
Fig e6.54
Miliary tuberculosis. Image at the level of the aortic arch shows numerous, 1–2 mm nodules randomly distributed throughout both lungs [2] (TIF 577 kb)
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Eisenberg, R.L. (2020). Pneumonia. In: What Radiology Residents Need to Know: Chest Radiology . Springer, Cham. https://doi.org/10.1007/978-3-030-16826-1_6
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