Pulmonary Infections: Imaging with CT
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Computed tomography (CT) plays a key role in various kinds of pulmonary infections especially in immunocompromised patients, owing to its much higher sensitivity and specificity than the traditionally performed chest X-ray. CT permits the detection of the main infectious pattern and associated findings with high confidence and allows for the precise assessment of all involved structures, to potentially guide a bronchoalveolar lavage or another diagnostic procedure, and to ensure a reliable follow-up. It may be performed at a carefully chosen dose, which may nearly reach that of a chest X-ray in specific situations. The importance of post-processing tools is undeniable in some conditions, in particular for the evaluation of micronodules in the immunocompromised population. The wide spectrum of features of specific organisms according to the immune status, such as in aspergillosis or tuberculosis, must be known, as well as the potential of atypical presentations in case of Pneumocystis jirovecii (PCP) pneumonia when occurring in non-HIV immunocompromised patients. In all cases, underlying disorders must be considered as well as all the differential diagnoses. Overall, CT definitely helps clinicians to diagnose pulmonary infections and to make treatment decisions, especially in vulnerable patients.
Imaging plays a crucial role in the diagnosis of respiratory infections that are a source of high morbidity and mortality especially regarding the increasing number of elderly and immunocompromised patients (Franquet 2006; Herold and Sailer 2004). Despite its much greater sensitivity and specificity than plain film radiography (Heussel et al. 1999), computed tomography (CT) has not been recommended for the initial assessment in most cases. It must be performed when there is a high clinical suspicion of infection with normal, ambiguous, or nonspecific chest X-ray findings, especially in immunocompromised patients (Beigelman-Aubry et al. 2012), in case of atypical clinical and/or radiological presentations, or when an empyema or abscess is suspected (Stigl and Marrie 2013). CT is able to detect even subtle lesions, while demonstrating them earlier than chest X-ray, as well as associated abnormalities or underlying conditions. In addition, it may suggest alternative diagnoses, and can guide interventions to take specimens for microbiology, regardless of the applied technique, either bronchoalveolar lavage (BAL) or percutaneous, transbronchial, or transthoracic needle biopsy. CT is also the imaging modality of choice to monitor response to specific treatment. Although the major CT patterns of pneumonia may be individualized, there is no specific one caused by one particular microorganism. Moreover, multiple CT patterns frequently coexist in the same patient with pulmonary infection. In addition, the radiological appearance of the organism-specific infection can change depending on the degree of the patients’ immunosuppression. The infective agents also vary with the type of immune deficiency. As the suggested diagnoses will very much depend on the individual setting, the conclusions drawn from the CT exam must always be integrated into the epidemiological, clinical data and laboratory tests and should result from a multidisciplinary approach. A first reminder of the most common types of pneumonias will be proposed before describing the technical approach and the main CT patterns encountered in routine practice.
1 Pneumonia Types
Community-acquired pneumonia (CAP), hospital-acquired pneumonia (HAP), ventilator-associated pneumonia (VAP), and healthcare-associated pneumonia (HCAP) are the main categories of pneumonias recognized by the currently accepted clinical classification of pneumonia (American Thoracic Society/Infectious Diseases Society of America 2005).
1.1 Community-Acquired Pneumonia (CAP)
Community-acquired pneumonia (CAP) is defined as an acute infection of the lung parenchyma acquired in the community, i.e., in outpatients or residents in long-term care facilities, >2 weeks before the onset of symptoms (Stigl and Marrie 2013). It can vary from a mild outpatient illness (Herold and Sailer 2004) to a more severe disease requiring hospital admission and, at times, intensive care (Niedemann 2015). The development of CAP may be related to either a defect in host defense, an exposure to an especially virulent pathogen, an overwhelming inoculum of microorganisms, or a combination of those factors (Stigl and Marrie 2013). Respiratory disorders, such as chronic obstructive pulmonary disease (COPD), cardiovascular disease, diabetes mellitus, chronic liver disease, HIV infection, and other forms of immune suppression, chronic kidney disease, old age, malignancy, any neurologic illness that predisposes to aspiration including seizures, alcoholic abuse, smoking, and splenectomy, are predisposing host conditions (Niedemann 2015). The diagnosis of CAP, usually based on the presence of cough, fever, sputum production, and/or pleuritic chest pain, is supported by infiltrates detected on the chest radiography in most cases. CT is therefore rarely required. Typical causative organisms of bacterial CAP include gram-positive bacteria such as Streptococcus pneumoniae (pneumococcus) that is responsible for approximately one-third of all cases of CAP, Haemophilus influenzae, and atypical pathogens, such as Mycoplasma pneumoniae, Chlamydophila pneumoniae (formally Chlamydia), and Legionella (Niedemann 2015). Viral agents, such as influenza A virus and respiratory syncytial virus, may also be involved, as well as fungi and parasites.
About 10–20 % of all adult patients hospitalized with CAP require admission to an intensive care unit. Severe CAP, usually defined by respiratory and/or circulatory failure, requires mechanical ventilation in 40–80 % of cases, with concomitant septic shock in up to 50 % of cases and a high mortality rate (Stigl and Marrie 2013). Usual complications observed in severe CAP include empyema, lung abscess, pneumothorax, acute respiratory distress syndrome (ARDS), chronic respiratory failure requiring tracheostomy, major cardiac events such as acute coronary syndrome, and multisystem organ failure (Stigl and Marrie 2013).
1.2 Hospital-Acquired or Nosocomial Pneumonia (HAP), Ventilator-Associated Pneumonia (VAP), and Healthcare-Associated Pneumonia (HCAP) (American Thoracic Society/Infectious Diseases Society of America 2005)
HAP or nosocomial pneumonia occurs 48 h or more after admission and does not appear to be incubating at the time of admission. Nosocomial pneumonia is the leading cause of death from hospital-acquired infections and most commonly affects intensive care unit (ICU) patients, particularly individuals requiring mechanical ventilation (Franquet 2008). VAP is a type of HAP that develops more than 48–72 h after endotracheal intubation. HCAP is defined as pneumonia that occurs in settings of a nonhospitalized patient with extensive healthcare contact, such as wound care, residency in a nursing home, or hemodialysis. The latter pneumonia is increasingly caused by multidrug-resistant (MDR) pathogens. Common pathogens of HAP, VAP, and HCAP are found in both the Proteobacteria and the Firmicutes phylum and include aerobic gram-negative bacilli (e.g., Escherichia coli, Klebsiella pneumoniae, Enterobacter spp., Pseudomonas aeruginosa, Acinetobacter spp.) and gram-positive cocci (e.g., Staphylococcus aureus, including methicillin-resistant S. aureus [MRSA], Streptococcus spp.) (Jones 2010). Nosocomial pneumonia due to viruses or fungi is significantly less common, except in the immunocompromised patient.
2 Technical Aspects of CT Procedures
3 Main CT Patterns
Although an overlap may be observed among the different patterns, with several patterns potentially occurring in various infectious disorders, the type of pneumonia may be suggested according to the predominant CT feature.
3.1 Alveolar Consolidation
Alveolar consolidation, which refers to an exudate or another product of disease replacing alveolar air and rendering the lung solid, appears as a homogeneous increase in pulmonary parenchymal attenuation obscuring the margins of vessels and airway walls. It may be associated with an air bronchogram, a pattern of air-filled bronchi on a background of high-attenuation airless lung (Hansell et al. 2008) that argues against the presence of a central obstructing lesion (Walker et al. 2014). Alveolar consolidation can be differentiated from atelectasis by the absence of direct and indirect signs of volume loss, such as fissural displacement, mediastinal shift, and diaphragmatic elevation. Alveolar consolidation is a major feature of infectious pneumonia as well as the predominant CT pattern of lobar pneumonia, bronchopneumonia, or diffuse alveolar consolidation.
3.1.1 Lobar Pneumonia
3.1.2 Bronchopneumonia or Lobular Pneumonia
Differential diagnoses include organizing pneumonia, lymphoma, adenocarcinoma, radiation pneumonitis, acute hypereosinophilic syndrome, pulmonary alveolar proteinosis, granulomatous or inflammatory conditions, or lipoid pneumonia (Kjeldsberg et al. 2002).
3.1.3 Diffuse Alveolar Consolidation
The differential diagnoses of infectious causes in case of diffuse involvement are pulmonary edema, noninfectious causes of DAD, and acute interstitial pneumonia.
3.2 Ground-Glass Opacity and Interstitial Pneumonia
Ground-glass opacity, a common but nonspecific finding, which refers to a hazy increased opacity of lung with preservation of bronchial and vascular margins (Hansell et al. 2008), is a major feature of interstitial pneumonia. Pathologically, it is characterized by a mononuclear inflammatory cellular infiltrate in the alveolar septa and the distal peribronchovascular interstitium (Muller 2003). This interstitial inflammatory reaction results from epithelial damage, with thickening of the peribronchial area and interlobular septa. Initially applied to different clinical and radiographic findings from those caused by S. pneumoniae, atypical pneumonia refers to an interstitial pattern that can be associated with dense consolidation.
3.3 Nodular Pattern
- Bronchogenic distribution presents as nonhomogeneous centrilobular micronodules that spare the subpleural space with a location at least 3 mm from the pleura and that are associated with a tree-in-bud pattern, defined as centrilobular branching structures that resemble a budding tree (Hansell et al. 2008). This presentation may be seen in bacterial, fungal, viral, mycobacterial, or mycoplasma (Fig. 7) infections. In postprimary (reactivation) tuberculosis, centrilobular micronodules and linear branching opacities have a dense attenuation and distinct margins. These features are readily associated with cavitation, predominantly localized in the apical and posterior segments of the superior lobes and the superior segment of the lower lobes in this setting (Fig. 32). Aspergillus bronchiolitis and/or bronchopneumonia must be considered in immunocompromised patients (Logan et al. 1994).
The differential diagnosis of infectious micronodules is miliary metastatic disease in case of micronodules with a random distribution. Uncommonly, multiple centrilobular nodules may be related to vascular lesions as embolized tumor or foreign material (Walker et al. 2014). Other differential diagnoses of centrilobular nodules include hypersensitivity pneumonitis or vasculitis.
Other causes of cavitated nodules include granulomatosis with polyangiitis and cavitated metastases.
Cavities may be observed in case of necrotizing pneumonia or pulmonary gangrene, abscesses, or pneumatoceles.
3.4.1 Necrotizing Pneumonia or Pulmonary Gangrene
Cavitation may occur in other conditions including malignancy and lung infarction (Walker et al. 2014).
3.4.2 Pulmonary Abscess
A pulmonary abscess may be single or multiple, with a characteristic spherical shape. It measures between 2 and 6 cm in diameter, demonstrates a central hypoattenuation (Fig. 9) or cavitation representing localized necrotic cavity, contains pus, and demonstrates peripheral enhancement after intravenous contrast medium injection, without or with an air-fluid level (Fig. 5). It usually displays an acute angle when it intersects with an adjacent pleural surface. Consolidation in the adjacent parenchyma occurs in half of all cases (Muller 2003). Bronchopulmonary fistula may be observed. As the most frequent cause of lung abscess is aspiration, the most common localizations are the posterior segment of an upper lobe or the superior segment of a lower lobe (Muller 2003). Bilateral involvement that predominantly affects the lung bases with abscess formation suggests a P. aeruginosa infection. Infections caused by anaerobic bacteria are commonly encountered, abscesses caused by S. aureus, K. pneumoniae, and P. aeruginosa being associated with higher mortality (Francis et al. 2005).
3.4.3 Air-Crescent Sign
3.4.4 Septic Emboli
Septic embolism may appear as cavitated nodules (see cavitated nodules).
Pneumatoceles manifest as single or multiple approximately round thin-walled and gas-filled spaces in the lung (Hansell et al. 2008) (Fig. 10). These lucencies are associated with a recent infection and usually transient, progressively increasing in size over the following days and weeks and then resolving after weeks or months. They are most likely due to bronchial drainage of necrotic parenchymal tissue, followed by a check-valve airway obstruction. They usually occur in P. jirovecii infections occurring in patients with acquired immune deficiency syndrome (AIDS) (Fig. 26) or in case of previous S. aureus pneumonia, but they can also be seen with other infections including E. coli and S. pneumoniae (Beigelman-Aubry et al. 2012).
Numerous noninfectious disorders may also manifest with pneumatoceles/cysts, including cavitary metastases.
3.4.6 Meniscus, Cumbo, and Water Lily Signs
Meniscus, cumbo, and water lily signs are related to air dissecting the different layers of an echinococcal cyst secondary to bronchial erosion (Walker et al. 2014).
While a pericystic emphysema or meniscus sign refers to air between the outer pericyst and ectocyst, the cumbo sign is related to air penetrating the endocyst with an air-fluid level capped with air between pericyst and endocyst. The water lily sign relates to the ruptured hydatid cyst with the endocyst membrane floating on surface fluid (Walker et al. 2014).
3.5 Associated Abnormalities
3.5.1 Mediastinal and Hilar Abnormalities
- The most common mediastinal and hilar abnormality is lymphadenopathy (Fig. 45). Right paratracheal, hilar, and subcarinal regions and/or hilar lymph node enlargement with associated homolateral small focal infiltrate or parenchymal consolidation, which is commonly sublobar and subpleural in location in the middle lobe, basal segments of lower lobes, and anterior segments of upper lobes, is the usual hallmark of primary TB (Beigelman et al. 2000). Necrotic components with peripheral rim enhancement (rim sign) mainly suggest tuberculosis, but they can also correspond to fungal infection, atypical mycobacteria, histoplasmosis, metastases (Fig. 46) from head/neck and testicular malignancy, and lymphoma (Bhalla et al. 2015). Bronchonodal fistula can be observed as a complication of active pulmonary TB with TB lymphadenitis especially in the elderly. The fistulas usually involve the right lobar bronchus and the main bronchus on the left side (Park et al. 2015).
A circumferential thickening of the esophagus may be related to a cytomegalovirus (CMV) infection, esophagitis being the second most common gastrointestinal manifestation of this organism after colitis (Wang et al. 2015), or Candida (Kuyumcu 2015) infection in immunocompromised patients.
- In case of a circumferential thickening of the trachea or main bronchi occurring in the same context, the possibility of invasive aspergillosis of the respiratory tract should always be considered (Fig. 47) with the specific risk of tracheal rupture. Acute tuberculous tracheobronchial involvement may also be seen with circumferential narrowing associated with smooth or irregular wall thickening (Bhalla et al. 2015). Sequelar fibrotic bronchostenosis predominating on the left main bronchus and post-obstructive bronchiectasis may occur in this setting (Bhalla et al. 2015).
Acute infectious mediastinitis may rarely be observed. It appears as increased soft tissue attenuation of mediastinal fat with fluid collections, air bubbles, air-fluid levels, and pneumomediastinum, with pericardial/pleural effusion. Regarding chronic or fibrosing mediastinitis, especially related to tuberculosis and fungal infections, including histoplasmosis, aspergillosis, mucormycosis, cryptococcosis, and blastomycosis, CT may display focal or diffuse involvement with calcifications as well as stenosis/obstruction of the vessels, airways, or esophagus (Akman et al. 2004).
3.5.2 Pleural Abnormalities
Pleural effusions, sometimes loculated, are encountered in 20–60 % of acute bacterial pneumonias. Most of the parapneumonic effusions without pleural thickening resolve under adequate medical treatment.
Empyema, which occurs in less than 5 % of pulmonary infections, typically displays obtuse angles along its interface with adjacent pleura. It appears as a smooth and thin enhancement of the visceral and parietal pleura that surrounds the fluid collection and that is referred as the split pleura sign (Walker et al. 2014) (Figs. 10 and 11). It is commonly associated with a hyperattenuation of the extra-pleural fat. The pathogens traditionally involved in empyema are S. pneumoniae, Streptococcus pyogenes, and S. aureus. The same findings may be seen in case of TB.
In this setting, an air-fluid level suggests a bronchopleural fistula (Walker et al. 2014), which is a sinus tract between a bronchus and the pleural space that most often results from a necrotizing pneumonia. CT features of bronchopleural fistula include an intrapleural airspace of various sizes, a new or changed air-fluid level, and, possibly, a fistulous communication, which may be become visible after the use of mIP post-processing. The air-fluid level within the pleura usually exhibits a length disparity when comparing posterior and lateral chest radiographs or between coronal and sagittal reformats unlike an air-fluid level associated with a pulmonary abscess typically displaying a spherical shape (Walker et al. 2014).
3.5.3 Other Features
Spondylodiscitis and/or an intramuscular cold abscess firstly suggests tuberculosis. A wavy periosteal reaction highly suggests thoracic actinomycosis.
Concomitant small hypodense lesions in the liver and/or spleen may suggest pyogenic abscesses or fungal infections, in particular candidiasis.
A worsening of CT findings may be encountered in case of “immune reconstitution inflammatory syndrome” (IRIS). This syndrome is related to paradoxical worsening of preexisting infectious processes such as mycobacterial, viral, and Pneumocystis jirovecii infection following the initiation of highly active antiretroviral therapy (HAART) in HIV-infected individuals, a low CD4+ T-cell count being a major risk factor (Huis in ‘t Veld et al. 2012). IRIS syndrome may also be encountered in HIV-negative patients in conditions such as following corticosteroid withdrawal, discontinuation of antitumor necrosis factor-alpha therapy or recovery of neutropenia after cytotoxic chemotherapy, and engraftment of stem cell transplantation. It may be then observed in case of aspergillosis, candidiasis, and viral pneumonitis (Cheng et al. 2000).
Calcified peribronchial lymph nodes can erode into adjacent bronchi or cause distortion of the latter and can generate a broncholithiasis (Bhalla et al. 2015).
In conclusion, the recognition of the main CT pattern in association with the knowledge of the underlying disorders and the clinical context permits to strongly narrow the differential diagnosis. The application of a good technique is crucial for patients’ management. In all cases, a multidisciplinary approach ensures the best outcome for the patient.
Thanks to Pr Laurent Nicod, Pr John-David Aubert, Dr Frederic Tissot, Dr Francesco Doentz and Dr Khalid Alfudhili for their help.
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