Pneumonia

Like all inflammatory processes, when pneumonia resolves it either results in restoration to the original state (restitutio ad integrum) without any perceptible morphologic damage to the lung parenchyma or gives rise to impaired healing (restitution cum defectu). Radiologically, the latter manifests as carnified pneumonia in which the original lung tissue is replaced by nonfunctional scar tissue.

Several pathologic types are distinguished, each with its own specific radiologic correlate:

Alveolar pneumonia: the inflammatory reaction is primarily confined to the airspaces and has three different manifestations:
- Lobar pneumonia: one entire lung lobe is evenly affected, attesting to microbial spread via the bronchial system and pores of Kohn. Lobar pneumonia follows a sequence of congestion → red hepatization → gray hepatization → yellow hepatization → resolution. Extensive consolidation of the affected lobe of lung is seen radiologically (▶Fig. 5.1).
- Bronchopneumonia: bronchogenic microbial spread results in inflammation of the peribronchial lung parenchyma, where there is less extensive spread than that seen in lobar pneumonia. This is the most common type of pneumonia. Imaging shows peribronchial ground-glass opacity and consolidation, which again are less extensive compared with lobar pneumonia. These opacities are not found throughout the entire lobe; often, they are seen simultaneously in several lobes (▶Fig. 5.2).
- Focal pneumonia: this manifests as a local focus of inflammation that does not spread further within the lung parenchyma. Often, focal pneumonia is asymptomatic or oligosymptomatic, making it difficult on differential diagnosis to distinguish this from lung carcinoma since both conditions manifest as consolidation or focal ground-glass opacity (▶Fig. 5.3).
  
  Fig. 5.1 Lobar pneumonia in the right upper lobe. Radiograph. The inferior margin of the consolidation is sharply bounded by the minor fissure (arrows); the middle lobe is not affected.
  
  Fig. 5.2 Bronchopneumonia in the middle lobe and in both lower lobes. CT image.
  
  Fig. 5.3 Focal pneumonia in the right upper lobe. CT image.
Interstitial pneumonia: the inflammatory reaction unfolds primarily in the lung interstitium, as characteristically observed for intracellular pathogens (e.g., viruses, chlamydiae). The predominant radiologic finding is ground-glass opacity (▶Fig. 5.4).

Depending on the number and virulence of the pathogens as well as on the patient’s immunocompetence status, the very same pathogen can cause different types of pneumonia (e.g., pneumococci: lobar pneumonia or focal pneumonia). Conversely, various pathogens give rise to identical radiologic findings; e.g., bronchopneumonia can be caused by, for example, Staphylococcus aureus, Klebsiella, Proteus, or Pseudomonas. It is not possible radiologically to pinpoint the causative organism. However, in general, the type of microorganism implicated in pneumonia can be identified (bacteria, viruses, or fungi). On the basis of characteristic findings, the presence of mycobacteriosis or pneumocystis pneumonia may at least be suspected. From other typical imaging patterns, limited conclusions can be drawn on the suspected microbial spectrum (▶Table 5.1 and ▶Fig. 5.5, ▶Fig. 5.6, ▶Fig. 5.7, ▶Fig. 5.8, ▶Fig. 5.9, ▶Fig. 5.10).

Table 5.1 Characteristic findings in pneumonia and typical microbial spectrum¹¹

Radiomorphology	Typical pathogens
Lobar consolidation (see ▶Fig. 5.1)	Mainly pneumococci
	Occasionally, Klebsiella (then often with increased volume of affected lung lobe)
	Staphylococcus aureus
	Legionella pneumophila
	Mycobacteria
Consolidation with cavitation (see ▶Fig. 5.5)	Staphylococcus aureus
	Gram-negative bacteria
	Klebsiella
	Proteus
	Pseudomonas
	Anaerobes
	Mycobacteria
	Small mycoplasma or viruses
Abscess (see ▶Fig. 5.6)	Mainly anaerobes
Focal pneumonia (see ▶Fig. 5.7)	Pneumococci
	Legionellae
	Coxiella burnetii
	As opportunistic infection: fungi
	Multiple nodules in hematogenous dissemination: Staphylococcus aureus
Reticulonodular pattern (see ▶Fig. 5.8)	Viruses
Reticulonodular pattern (see ▶Fig. 5.8)	Mycoplasma
Miliary pattern (see ▶Fig. 5.9)	Tuberculosis
Miliary pattern (see ▶Fig. 5.9)	Candida pneumonia
Pneumatoceles/cysts (see ▶Fig. 5.10)	Staphylococcus aureus
	Pneumococci
	Klebsiella
	Pneumocystis jirovecii

Complications arising in association with pneumonia can result in delayed, or no, clinical improvement during antibiotic treatment or lead to relapse after initial successful treatment. The most common complications include:

Pleural empyema: pleural empyema generally manifests as a rather large pleural effusion that is often multiloculated rather than free-flowing. It is not possible radiologically to make a reliable distinction between parapneumonic pleural empyema and noninfected, sympathetic pleural
effusion (see criteria below suggestive of pleural empyema). In cases of justified clinical suspicion (no improvement, deterioration of general condition, or persistently high inflammatory laboratory results), differentiation can be made between pleural empyema and noninfected pleural effusion through thoracocentesis. This procedure is recommended for hospitalized patients whose lateral upright chest radiograph shows a pleural effusion of more than 5 cm.¹

Fig. 5.4 Interstitial pneumonia. CT image. Diffuse, bilateral ground-glass opacity.

Fig. 5.5 Pneumonia in the right upper lobe. CT image. Central cavitation in consolidations.

Fig. 5.6 Lung abscess in the left lower lobe. CT images. (a) Soft-tissue window: relatively thin-walled cavitation. (b) Lung window: air-fluid level in abscess.

Fig. 5.7 Focal pneumonia in the left upper lobe. CT image
Abscess formation: early abscess formation is seen on CT as rounded, largely water-isodense areas in lung regions affected by pneumonia. Later, following bronchial drainage of the liquid portions, abscess formation can be identified as cavitation on radiographs, too (see ▶Fig. 5.5). That antibiotics rarely penetrate into the inside of abscesses gives rise to a delayed treatment response and the need for a prolonged treatment course. CT examination is indicated if a lung abscess is suspected¹ to rule out any mass, foreign body, infarction pneumonia, or superinfection caused by bronchial obstruction. If conservative antibiotic treatment fails, CT- or fluoroscopy-guided drainage may be useful.²

Fig. 5.8 Bilateral reticulonodular pattern in viral pneumonia. CT image.

Fig. 5.9 Miliary pattern in miliary tuberculosis. CT image.

Fig. 5.10 Cysts and ground-glass opacities in Pneumocystis jirovecii pneumonia. CT image.

Fig. 5.11 Community-acquired pneumonia in the right upper lobe (arrows). Radiograph.

5.1 Community-Acquired Pneumonia

Community-acquired pneumonia is defined as acute infection of the lower respiratory tract with evidence of pulmonary opacity on radiographs, even in the absence of auscultation findings (▶Fig. 5.11).¹

In clinical terms, a distinction is generally made between typical and atypical pneumonia, each involving a different spectrum of microorganisms. This distinction is illustrated in ▶Table 5.2 and can also be inferred from the radiologic image of pneumonia.

Community-acquired atypical pneumonia includes viral pneumonia which regularly causes epidemic outbreaks. In addition to seasonal influenza epidemics caused by influenza A and B viruses, in the recent past viral severe acute respiratory syndrome (SARS) as well as bird and swine flu has drawn attention. The radiologic findings for the various types of viral pneumonia are so similar as to preclude identification of the causative virus.

Risk stratification to determine the necessity for admission to the hospital or, possibly, for intensive medical therapy can be decided on the basis of the following clinical criteria (CRB-65 index⁴):

Respiratory rate: at least 30/min.
Diastolic blood pressure: maximum 60 mm Hg.
Systolic blood pressure: maximum 90 mm Hg.
Clouding of consciousness: present.
Age: at least 65 years.

One point is assigned for each criterion met; the CRB-65 index is the sum of all points.

This determines the scope of diagnosis as presented in ▶Table 5.3. Radiography examination should in principle be performed in two planes at the time of diagnosis. There is no good evidence to support the use of follow-up X-ray examination on completion of treatment. It may be considered for risk patients at the earliest 2 weeks after ending treatment. CT examination is not indicated at the time of diagnosis.

Table 5.2 Characteristics of typical and atypical pneumonia

Parameters	Typical pneumonia	Atypical pneumonia
Microbial spectrum	Bacteria: Pneumococci Staphylococci	Obligate intracellular bacteria: Chlamydiae Mycoplasma Legionellae Viruses
Clinical presentation	Acute picture: Fever Shaking chills Cough Purulent sputum Reduced general state	Less acute picture: Moderate fever Headache Joint pain
Inflammation site	Alveolar spaces	Interstitium
Radiologic image	Consolidation	Ground-glass opacity

Table 5.3 Risk stratification and diagnostic scope for community-acquired pneumonia¹

Treatment	CRB-65 index	Radiograph needed for diagnosis	Radiograph for follow-up examination
Outpatient	0-1 No risk factors^a	Recommended	Optional in the presence of risk factors for tumor disease At the earliest, 2 weeks after ending treatment
Outpatient	0-1 With risk factors^a	Obligatory
Normal hospital ward or outpatient setting^b	2	Obligatory	Recommended for active smokers
Intensive care unit	≥3	Obligatory	Age >65 years, severe concomitant diseases, at the earliest 2 weeks after ending treatment
^aRisk factors: • Antibiotic treatment in past 3 months. • Residents of care homes. • Severe concomitant diseases (congestive heart failure, liver cirrhosis, end-stage kidney disease, stroke with neurologic deficits). ^bThe CRB-65 index is intended merely as a guide and is not a substitute for clinical decision-making in a particular case.

Note

CT indications which may apply in the course of treatment of community-acquired pneumonia¹:

Treatment failure:
- Progressive pneumonia:
  - Deterioration of clinical state (respiratory insufficiency, severe sepsis, or septic shock).
  - Radiologic progression seen only coincident with clinical deterioration.
- Delayed-response pneumonia: no clinical stability observed within 72 h of starting treatment (stability criteria: heart rate, maximum 100/min; respiratory rate, maximum 24/min; systolic blood pressure, at least 90 mm Hg; body temperature, maximum 37.8°C; oxygen partial pressure, at least 60 mm Hg; and oxygen saturation, at least 90%).
Suspected lung abscess.

Treatment failure can manifest as progressive pneumonia or as nonprogressive, delayed-response pneumonia:

Progressive pneumonia: any increase in pulmonary opacities seen on radiographs within the first 72 h may be interpreted as progressive pneumonia only in the setting of coincident clinical deterioration.
Delayed-response pneumonia: if there is no evidence of clinical stability within 72 h, other causes, also nonmicrobial, for the pulmonary opacities must be considered.

In both situations, a CT examination is usually indicated.⁵^,⁶

5.2 Hospital-Acquired/Nosocomial Pneumonia

Hospital-acquired (nosocomial) pneumonia is defined as pneumonia presenting at least 48 h after the patient’s admission to the hospital and which was not incubating at the time of admission.⁷ It is the second most common hospital-acquired infection and causes considerable morbidity and mortality, in particular, in intensive care units. It often constitutes a limiting factor in immunosuppressant therapies, for example, in chemotherapy. The types of hospital-acquired pneumonia presenting during such treatment courses are caused by opportunistic pathogens and will be discussed in Section 5.3.

The microbial spectrum of hospital-acquired pneumonia differs from that implicated in community-acquired pneumonia. In the case of intensive care patients on long-term ventilation, infection is mainly attributed to hospital-specific bacterial pathogens. Due to the myriad forms of bacterial
resistance, together with new types emerging during treatment, the clinical and radiologic course is more challenging compared with community-acquired pneumonia. Multifocal infiltrates and changing courses alternating between regressive and progressive findings are common (▶Fig. 5.12).

Differential diagnosis of hospital-acquired pneumonia from other pulmonary opacities is difficult, in particular, in ventilated patients. A summary of the various underlying causes is given in ▶Table 5.4. The suggestive effect of clinical data can make it harder to reach a correct diagnosis. For example, purulent sputum or tracheal secretion is often caused by infection of the upper airways, while elevated inflammatory laboratory results can have many causes in intensive care patients. It is therefore important to conduct meticulous image analysis and have access to comprehensive information on the clinical course. Ideally, the radiologic findings should be discussed with the treating clinicians.

Fig. 5.12 Hospital-acquired pneumonia. Radiograph, supine position. Bilateral pulmonary opacities. Besides, cardiomegaly. Tracheal cannula, central venous catheter with catheter tip relatively peripherally in the left brachiocephalic vein.

Table 5.4 Differential diagnosis of hospital-acquired (nosocomial) pneumonia in intensive care patients with pulmonary opacity on radiograph⁸

Differential diagnosis	Remarks
Atelectasis	Common, displacement of other anatomic structures indicates loss of lung volume
Pleural effusion	Basal predominant homogenous grading increase of opacity on supine image, possibly lateral pleural fluid layer
Pulmonary edema	Mainly symmetrical, possibly cardiomegaly suggestive of congestive heart failure or clinical signs of another cause (e.g., kidney failure, sepsis)
Lung infarction	As sequela of pulmonary embolism; pleural-based triangular opacity (so-called Hampton hump), may be multiple
Adult respiratory distress syndrome	Diffuse bilateral opacities; no laboratory results suggestive of bacterial inflammation, severe respiratory insufficiency
Alveolar hemorrhage	Treatment-induced (drug toxicity) or caused by an underlying disease
Drug toxicity	This should also be taken into consideration in case of persistent bilateral pulmonary opacities; no pathognomonic radiologic findings for drug-induced lung disease; at times, the temporal coincidence between radiologic findings and administration or discontinuation of certain drugs can afford insights
Postoperative changes	Secondary to thoracic surgery: intrapulmonary hematomas, impaired lymph drainage, impaired pulmonary venous drainage

5.3 Opportunistic Pneumonia

Opportunistic pneumonias are pulmonary infections that may arise because of the patient’s compromised immune system. The microbial spectrum implicated in opportunistic pneumonia differs from that identified for community-acquired pneumonia as well as for other common forms of hospital-acquired pneumonia in immunocompetent patients. ▶Table 5.5 gives a summary of the various mechanisms of the immune system, typical diseases or forms of immunosuppressant treatment, and the resultant typical spectrum of opportunistic pathogens.

A number of typical clinical constellations can be identified⁹:

Aplasia: this is defined as a decline in the neutrophil count to below 500/µL or in the leukocyte count to below 1,000/µL, often secondary to aplasiogenic chemo- or radiotherapy. This leads to diminished phagocytosis. The lung infections presenting during the initial days of onset of aplasia are often imputed to gram-positive cocci, especially S. aureus, and gram-negative bacteria, such as Pseudomonas aeruginosa. If aplasia persists for at least 5 days, fungal infections are identified additionally. In Europe, these are typically caused by Aspergillus and Candida species.⁹
AIDS (acquired immunodeficiency syndrome): this leads to a reduction in the T helper cells (CD4-positive T lymphocytes) and, in turn, to reduced specific cellular immunity. The most common pulmonary infection is Pneumocystis jirovecii pneumonia, which is frequently the first manifestation of AIDS disease. Less commonly, tuberculosis and pulmonary toxoplasmosis are observed.⁹
Organ transplantations: organ transplant results in reduced lymphocyte function due to immunosuppression, putting patients at risk for pneumonia caused by intracellular pathogens, such as Legionella pneumophila, and viruses (especially cytomegalovirus), as well as for mycobacteriosis, nocardiosis, and aspergillosis. Aspergillus and Nocardia account for two-thirds of infections in heart transplant patients. Lung transplant recipients are at higher risk for cytomegalovirus infection.⁹

Stem cell transplant: in the conditioning phase, the patient’s diseased bone marrow is destroyed by means of high-dose
chemotherapy and whole-body irradiation, making the patient particularly susceptible to pneumococcal pneumonia during this phase. In the wake of conditioning and stem cell transplant, the risk of opportunistic pneumonia is similar to that faced by aplastic patients.

Table 5.5 Immune system mechanisms, disease-mediated deficiencies, and resultant opportunistic pneumonia¹¹^,¹²

Immune mechanism	Mediators	Damage	Spectrum of opportunistic microorganisms
Adaptive cellular response	T cell system	Organ transplant Stem cell transplant Cortisone treatment AIDS Hodgkin lymphoma Chronic lymphatic leukemia	Pneumocystis jirovecii Viruses (cytomegalovirus, herpes simplex virus) Mycobacteria Legionellae
Adaptive humoral response	Immunoglobulins	Chemotherapy Malignant melanoma Chronic lymphatic leukemia AIDS Hypogammaglobulinemia	Pneumococci Gram-negative bacteria Mycobacteria Candida Pneumocystis jirovecii Viruses (cytomegalovirus, herpes simplex virus)
Innate cellular response	Macrophages/monocytes Granulocytes NK cells	Chemotherapy Radiotherapy Stem cell transplant Blood system disease Bone marrow carcinosis (e.g., small cell lung carcinoma)	Staphylococcus aureus Gram-negative bacteria Fungi
Innate humoral response	Complement system Properdin system Monokines/lymphokines	Multiple myeloma Non-Hodgkin lymphoma Chronic lymphatic leukemia	Streptococcus pneumoniae Haemophilus influenzae
Abbreviations: AIDS, acquired immunodeficiency syndrome; NK cells, natural killer cells.

High-dose corticosteroid treatment: this results in impairment of granulocyte function, thus compromising chemotactic activity. Patients are at increased risk for P. jirovecii pneumonia. Preexisting tuberculosis may be reactivated.⁹

Radiographic images of opportunistic infections may be normal or show only uncharacteristic changes.¹⁰ CT is indicated if opportunistic pneumonia is suspected but no evidence of pneumonia is seen on the radiograph. Aplastic patients with certain risk constellations, e.g., receiving aplasiogenic chemotherapy or following stem cell transplant, often become febrile. In such settings, there is virtually always an indication for CT. It is precisely for this cohort of patients that all efforts must be made to exploit the CT dose reduction potentials and opt for low-dose CT scans.

5.3.1 Fungal Pneumonia

By virtue of their ubiquitous nature, Aspergillus and Candida are the main opportunistic causal agents of fungal pneumonia.

Aspergillus spp. are molds that give rise to infections with extremely varied characteristics depending on their invasiveness. A distinction is made between noninvasive aspergillomas, invasive pulmonary aspergillosis, and semi-invasive chronic necrotizing aspergillosis.¹³ Another disease caused by Aspergillus spp., allergic bronchopulmonary aspergillosis, is discussed in the section on allergic pulmonary diseases.

Fig. 5.13 Aspergilloma (arrow) in a preformed cavity in the right upper lobe. CT image, coronal.

Aspergilloma

Aspergilloma is a mycetoma composed of Aspergillus hyphae; in other words, it is like a round fungus ball. This grows in a preformed cavern, often in association with longstanding tuberculosis or sarcoidosis (▶Fig. 5.13). When the patient changes position, the fungus ball can move within the cavern in line
with the force of gravity and this can serve as a diagnostic criterion. At times, the aspergilloma may fill the entire cavern and can no longer be distinguished from the cavern wall; instead, the entire lesion appears as a relatively homogeneous area of consolidation (▶Fig. 5.14). Noninvasive aspergilloma can progress to an invasive form of Aspergillus infection in immunocompromised patients.

Fig. 5.14 Aspergilloma in the right upper lobe. CT image. The fungus ball cannot be distinguished from the cavern wall; the entire lesion manifests as a homogeneous nodule.

Fig. 5.15 Invasive pulmonary aspergillosis in the right upper lobe. CT images. Course over 2 weeks. (a) Baseline findings in aplastic patient: rounded consolidation in the right upper lobe, surrounded by ground-glass opacity, i.e., halo sign. (b) Two weeks later, patient is no longer aplastic: newly emerged air crescent sign (arrows), slight increase in nodule size.

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