key: cord-018134-k4vdqlgs
authors: Eisenberg, Ronald L.
title: Pneumonia
date: 2019-11-01
journal: What Radiology Residents Need to Know: Chest Radiology
DOI: 10.1007/978-3-030-16826-1_6
sha: 
doc_id: 18134
cord_uid: k4vdqlgs

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. ELECTRONIC SUPPLEMENTARY MATERIAL : The online version of this chapter (10.1007/978-3-030-16826-1_6) contains supplementary material, which is available to authorized users.

• Any pneumonia developing in a patient at least 48 hours after being hospitalized • Second most common nosocomial infection (after urinary tract infections) • Unlike community-acquired pneumonia, HAP is usually caused by a bacterial infection, rather than a virus • High morbidity and mortality rates and the primary cause of death in intensive care units

• Any pneumonia developing in a patient at least 48-72 hours after endotracheal tube intubation • 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%

Lobar Pneumonia

• Homogeneous consolidation of all or a substantial percentage of a single lobe • Sharply marginated by one or more fissures ( [1] • Silhouette sign when the consolidation is adjacent to the heart, aorta, or hemidiaphragm ( Fig. 6 

• Foreign material entering into the tracheobronchial tree secondary to gastroesophageal reflux, altered mental status (drug overdose, anesthesia), or neurologic disorder (stroke, traumatic brain injury) • Often develops in intubated patients, despite the presence of an inflatable cuff • Usually occurs in the most dependent portions of the lung ○ Supine -superior and posterior basal segments of the lower lobes or posterior segment of the upper lobes ( Fig. 6 .8) ○ Upright -lower lobes (typically on the right, because the right main bronchus runs more vertically and is wider) • Rapid appearance of air-space consolidation, especially in bedridden patients. • Noninfectious aspiration -usually clearance in less than 1 week ○ 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 ( 

• Radiographic clearance of pneumonia usually lags well behind clinical improvement • 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) • Failure of a pneumonia to resolve by 8 weeks suggests an inaccurate diagnosis or an endobronchial obstruction as a cause of postobstructive pneumonia ( Fig. 6 .11) • Especially in patients with smoking history or over age 40, CT should be considered to exclude an underlying bronchial lesion (see Fig. e6 .13) • Irregular infectious cavity containing necrotic debris or fluid.

• Often an air-fluid level, which usually has the same extent on both frontal and lateral views Thicker, often irregular wall Disparity in length of air-fluid levels Air-fluid levels of relatively equal lengths Split pleura sign on CT Empyema Necessitans (Fig. 6.16) • 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) • Loculated pleural fluid collection or mass with associated rib destruction and often bubbles of loculated gas in soft tissues

• 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 • Tends to form a voluminous exudate that produces a homogeneous parenchymal consolidation containing an air bronchogram • Lobar enlargement (especially the right upper) with the characteristic bulging fissure sign (Fig. 6 .17) ○ 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) • Most frequently result from infectious particles reaching the lung from an infected heart valve (especially the tricuspid), intravenous catheter, or injected debris • Persons at risk include drug abusers, immunocompromised patients, individuals with septal defects, and those with indwelling venous catheters, pacemakers, or prosthetic heart valves • 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) • Cavitary pulmonary nodules tend to develop rapidly (1-2 days) 

• Transient, rapidly changing, migrating, nonsegmental areas of parenchymal consolidation, which are associated with blood eosinophilia and minimal (or no) pulmonary symptoms • Bilateral patchy consolidations with ill-defined margins that are predominantly located in the periphery of the lung • May produce single or multiple air-space nodules with surrounding ground-glass opacities (Fig. 6 .20) • Unlike chronic eosinophilic pneumonia (see below), the transient air-space abnormalities resolve in some areas and reappear in others over days • 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)

• Classic appearance of multifocal areas of consolidation in both lungs, especially the upper lobes, reflecting inflammatory eosinophils filling alveoli and infiltrating the interstitium • Characteristic peripheral predominance ("reverse pulmonary edema pattern") • Rapid response to steroid therapy (clinical improvement within hours, radiographic clearing within a few days) Fig. 6 .20 Loeffler's syndrome. Peripheral air-space nodule with surrounding ground-glass opacity in the right lower lobe (arrow). Follow-up study showed that the nodule had disappeared [7] Fungal Pneumonia Aspergillosis • 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 • 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) • Central mass within a cavity in invasive aspergillosis is almost always necrotic lung (Fig. 6.22 ; see Figs. e6.27-e6.29) • 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) • 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) 

• Histoplasmosis -central United States; nodules often calcify ( Fig. 6 .24) • Coccidioidomycosis -southwestern United States (also northern Mexico and Central and South America) • Actinomycosis, Nocardia -pleural effusion and extension to the chest wall are common (may develop empyema) (see Fig. e6 .32) • Candidiasis, aspergillosis, sporotrichosis, and mucormycosisessentially limited to debilitated patients and those with underlying diseases (diabetes mellitus, lymphoma, leukemia) (see Fig. e6 .33) • Caused by a yeast-like fungus and almost exclusively seen in immunosuppressed patients (especially AIDS, lymphoproliferative diseases, or renal transplants) • Initially, bilateral diffuse interstitial opacities spreading outward from the hila • If untreated, this soon progresses to a homogeneous diffuse alveolar consolidation that may simulate pulmonary edema • Thin-walled, air-filled lung cysts (especially apical and subpleural) occur in about 40% of patients and may cause a pneumothorax • Thick-walled cavities usually indicate superinfection • Hilar adenopathy and significant pleural effusions are rare (their presence should raise the possibility of an alternate diagnosis)

• Although a clinical diagnosis, may appear on chest radiographs as bilateral hilar enlargement due to lymphadenopathy (see Fig. e6 .37) • 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) • 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 • Healed varicella pneumonia classically appears as tiny military calcifications scattered widely throughout both lungs (develops several years after the pulmonary infection) • No calcification of hilar lymph nodes (unlike histoplasmosis or tuberculosis, the two other major causes of diffuse pulmonary calcifications) 

• Cytomegalovirus, which typically occurs in immunosuppressed individuals (especially after transplantation) (Fig. 6 .28) • Respiratory syncytial virus in infants and young children (see Fig.  e6 .39)

• 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 • Primary tuberculosis may affect any lobe, so that the diagnosis cannot be excluded because the infection is not in the upper lobe Fig. 6 .28 Tree-in-bud pattern (cytomegalovirus). Centrilobular groundglass opacities in addition to nodules and "tree-in-bud" opacities in a patient with chronic myelogenous leukemia who underwent bone marrow transplantation [1] • "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) • "Inactive" TB refers to someone with imaging evidence of prior tuberculosis but no sign of active disease Imaging • One or more foci of lobar or segmental air-space consolidation that is usually homogeneous, dense, and well defined (Fig. 6 .29) • If multiple, randomly distributed throughout the lungs • Cavitation is infrequent. • Characteristic apical pleural thickening and fibronodular appearance in one or both upper lungs (Fig. 6 .31; see Fig. e6 .44) • 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 and is almost diagnostic of postprimary tuberculosis • Because an apical lesion may be obscured by overlying clavicle or ribs, an apical lordotic view is often of value • Cavitation is common (about 50%) and characteristic of postprimary disease (Figs. 6.33 and 6.34; see Fig. e6 .47) • The presence of cavitation indicates that the disease is highly contagious, and this finding alone warrants putting the patient in respiratory isolation • Air-fluid levels in cavities are uncommon and usually a manifestation of superinfection (see Fig. e6 .48) • 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 a b Note the thickening of bronchial walls (white arrow) [1] branching pattern that resembles a budding tree and is generally more pronounced in the lung periphery (see Figs. e6.49-e6.51) • 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) • Pleural effusion and lymph node enlargement are rare in postprimary tuberculous disease (though common and sometimes the only finding in primary disease) • 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) • 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)

• Hematogenous dissemination that usually occurs in patients with altered host resistance to the primary infection • Almost invariably leads to a dramatic febrile response with night sweats and chills • There may be minimal symptoms in severely debilitated patients, especially elderly persons and those receiving steroids Imaging • 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) • CT -may detect the presence of diffuse lung involvement when corresponding chest radiographs are normal or show only minimal or limited disease

Clinical Imaging: An Atlas of Differential Diagnosis

Lower lobe-predominant diseases of the lung

Mosaic attenuation

Multiple cystlike lung lesions in the adult

Pulmonary tuberculosis: role of radiology in diagnosis and management

Eosinophilic lung diseases: a clinical, radiologic, and pathologic overview

Upper lobe-predominant diseases of the lung

Tree-in-bud pattern