Acute dyspnea is a common presenting complaint in the Emergency Room (ER). Urgent identification of the underlying cause(s) for acute dyspnea is essential in guiding appropriate therapy and management, as patients can rapidly progress to acute respiratory failure (ARF), which confers a high morbidity and mortality.1,2 Evaluation with chest radiography is vital for initial assessment and may reveal diffuse parenchymal abnormalities that require further assessment with computed tomography (CT). Over the past decade, increased utilization of chest CT and, in particular, CT pulmonary angiography (CTPA) and aortic CT angiography in the ER3 has resulted in an upsurge of CT-detected pulmonary pathology.
The aim of this review is to outline a pattern-based approach for the analysis of diffuse pulmonary abnormalities in an acutely dyspneic patient with emphasis on CT appearances. Specific disease entities have characteristic radiologic findings and distributions in the lungs, and radiologists should analyze chest CTs by simultaneous evaluation of radiologic abnormalities and their distribution. Multiple abnormalities are usually present, which can be confusing. Recognition of the predominant finding and its distribution can generate an appropriate differential diagnosis that is further refined by the presence or absence of ancillary findings. Incorporation of the clinical history, laboratory data, and prior studies narrows the differential diagnosis, indicates the optimum modality for further evaluation, and, in some situations, provides important prognostic data. Acute presentation of malignancy, pulmonary emboli, drug reactions, and infections associated with immunosuppression will be covered elsewhere in this issue.
Acute dyspnea is often associated with fever, cough, hemoptysis, and/or chest pain, with a duration that can range from hours to days. Acute deterioration may be a precipitating event in a patient with previously occult underlying chronic lung disease. Patient history can provide valuable clues that may suggest a specific etiology such as an aspiration event, an inhalational exposure, a history of smoking, or an underlying chronic lung disease. A detailed physical examination may demonstrate signs of congestive heart failure or cutaneous manifestations of systemic vasculitis or rheumatologic disorders (Fig. 1). However, patient history in the ER may be limited to little more than “dyspnea,” and obtaining a chest CT is often the first step in evaluation, making the radiologist an integral part of the initial workup. Chest CT is especially useful when the chest radiograph demonstrates diffuse pulmonary findings, allowing accurate depiction of location and pattern of disease so that a more precise diagnosis may be given. The addition of laboratory testing can aid in further narrowing the differential diagnosis, and the selection of such tests should be individualized.
Distribution of Disease
Although diffuse pulmonary abnormalities on a chest radiograph or CT are often considered a nonspecific finding, careful evaluation of their distribution can provide valuable clues to the most likely etiology, as many diseases have a regional preference4,5 (Fig. 2). Distribution in the lung may be regional or zonal and are best appreciated on coronal multiplanar reformatted images. Zonal distribution has proven value in the diagnosis of chronic lung disease. For example, pathology due to smoking-related lung diseases predominates in the upper zone and mid zone, whereas the pattern of fibrosis from usual interstitial pneumonia (UIP) is seen predominantly in the lower zone. Regional distribution may be divided into central, dependent, multifocal, or peripheral (Fig. 3). Further determination of distribution relates to the anatomic location within a secondary pulmonary lobule, which is particularly helpful in the differential diagnosis of nodular and linear opacities.
CTPA is usually performed using 1 to 1.5 mm sections; these thin slices optimize accurate characterization of the radiographic findings and their localization within the secondary pulmonary lobule. CT findings may be divided into 4 main radiologic patterns: airspace (including ground-glass and consolidation), linear (including septal thickening and intralobular lines), nodular, and cystic/cavitary opacities6 (Fig. 4). Apparent airspace opacification can represent a normal finding. For example, a physiological alteration in lung attenuation is commonly noted when a CT scan, performed on a dyspneic patient, is obtained in expiration. The relative decrease in aerated lung causes an increase in attenuation of the lung parenchyma that mimics ground-glass opacity. Assessment of the posterior membrane of the trachea and major bronchi will confirm the expiratory nature of the CT scan, and apparent findings should be interpreted with caution. In addition, vessels, airway walls, and fissures can mimic bronchiectasis or lung nodules because of respiratory or cardiac motion artifacts.7,8
Patterns and Distribution: Airspace Opacities
Airspace opacities cause increased parenchymal opacification and may be divided into ground-glass opacity and consolidation. The increase in attenuation may obscure the underlying vessel pattern on CT (consolidation) or preserve the underlying vessel pattern (ground-glass opacity); both forms of airspace opacity usually occur together.
Central Distribution of Airspace Opacities
A central distribution of radiologic findings involves the parahilar regions with relative sparing of the lung periphery. Chest radiographic signs of a central parahilar distribution of airspace opacities include loss of silhouette of the heart and mediastinum, loss of the central intrapulmonary vascular pattern, and presence of air bronchograms radiating from the hila.
Hydrostatic (cardiogenic) pulmonary edema is a common cause for central airspace opacities, particularly when accumulation of fluid is rapid. The typical central “bat’s wing” appearance on a chest radiograph corresponds to central ground-glass opacity and consolidation on chest CT. Often, a dependent distribution is also present. Ancillary findings of smooth interlobular septal thickening and bronchial wall thickening reflect an increase in fluid in the lymphatics.9–11 Ill-defined centrilobular nodules occur but are not a prominent feature, and their presence usually suggests another etiology. The presence of pleural effusions, thickening of the fissures, and cardiomegaly are helpful in differentiating pulmonary edema from other conditions that cause central airspace opacity (Fig. 5A).
Aspiration pneumonitis is a result of chemical injury to the lungs from massive aspiration of acidic gastric contents and is a cause of acute dyspnea and central airspace opacities that mimics pulmonary edema.12 The pneumonitis appears initially as a ground-glass abnormality but may evolve into consolidation. When central airspace opacities are seen, the concomitant presence of centrilobular nodules or dependent tree-in-bud opacities should favor the diagnosis of aspiration pneumonitis over hydrostatic pulmonary edema. Aspiration pneumonitis often resolves in 4 to 5 days unless complicated by secondary bacterial pneumonia or development of acute respiratory distress syndrome (ARDS). Altered mental status, seizures, and recent intoxication are all relevant risk factors in the clinical history.
Diffuse pulmonary hemorrhage (DPH) typically presents as central ground-glass opacity and consolidation (Fig. 5B). Multifocal distribution can be seen in some cases. In most cases there are associated ill-defined centrilobular nodules that differentiate DPH from other causes of central airspace opacity. Within 24 to 48 hours of intra-alveolar hemorrhage, interlobular septal thickening and intralobular lines develop in a central distribution, reflecting deposition of hemosiderin in the interstitium. The combination of ground-glass opacity, interlobular septal thickening, and intralobular lines creates a crazy-paving appearance on CT.13–15 Crazy-paving is more commonly seen in DPH than in cardiogenic edema or aspiration pneumonitis.
DPH does not cause hemoptysis in up to one third of patients and may, therefore, be unsuspected clinically.16 DPH is most commonly seen in the setting of pulmonary capillaritis14 associated with vasculitic disorders such as granulomatosis with polyangiitis (GPA, formerly Wegener granulomatosis), Goodpasture syndrome, collagen vascular disease,17,18 and antiphospholipid antibody syndrome. DPH may also be seen in the absence of pulmonary capillaritis in patients with coagulation disorders, pulmonary venoocclusive disease, elevated pulmonary venous pressures, and diffuse alveolar damage (DAD). Bronchoalveolar lavage (BAL) with the return of increasing amounts of red blood cells on serial lavage can confirm the diagnosis. BAL can also exclude other alveolar-filling diseases such as infection and alveolar proteinosis but cannot identify the underlying lung disease responsible for the bleeding.
Dependent Distribution of Airspace Opacities
A dependent distribution refers to posterior opacities on a chest radiograph or chest CT and relative sparing of nondependent peripheral regions of the lung.19,20
Aspiration pneumonia may develop secondary to aspiration of colonized oropharyngeal contents and is a common cause of dependent airspace opacities in an acutely dyspneic patient. Consolidation and ground-glass opacity involve the superior and basal segments of the lower lobes and dependent aspects of the upper lobes (Fig. 6). The right lung is more commonly involved than the left because of the more vertical orientation of the right main stem bronchus. An atypical distribution may be seen if aspiration occurs when the patient is on his or her stomach or side, leading to anterior or lateral “dependent” opacities, respectively. Decreased enhancement on contrast-enhanced CT indicates secondary infection or necrosis within the consolidation. Aspirated fluid often fills dependent segmental airways, and atelectasis can complicate airway obstruction.21,22 Ancillary findings include tree-in-bud opacities, bronchial wall thickening, and fluid within dependent sub-segmental airways.
Permeability (noncardiogenic) edema causes a dependent distribution of multiple, confluent consolidative opacities and associated dependent atelectasis.20 Injury to the respiratory epithelium corresponds to a clinical diagnosis of ARDS and pathologic diagnosis of DAD. The combination of multifocal extensive ground-glass opacity with dependent consolidation is typical of a DAD pattern. DAD can progress within a few days of symptoms from the proliferative to the fibrotic phase of DAD. CT demonstration of traction bronchiectasis indicates a poor prognosis with a high mortality rate.23 The dependent distribution of consolidative airspace opacities in permeability edema can be differentiated from the central ground-glass opacity of hydrostatic (cardiogenic) edema despite similar symptoms and presentation. Septal thickening is rare in permeability edema but is a significant feature of hydrostatic edema. Bronchial wall thickening, tree-in-bud opacities, and airway obstruction are not seen in permeability edema but are commonly present with aspiration pneumonia, that also causes dependent consolidation.
Acute interstitial pneumonia (AIP) is often referred to as idiopathic ARDS and is seen in previously healthy patients who develop fulminant respiratory failure over 1 to 3 weeks with no identifiable precipitating event. A short viral-like prodrome is usually reported. Consolidation is frequent and is usually symmetric in the dependent lung.24–26 In the acute phase, bilateral multifocal ground-glass opacities are also seen, with areas of lobular sparing (Fig. 7). These features are often associated with small pleural effusions and mild mediastinal lymphadenopathy. Traction bronchiectasis and architectural distortion develop in the organizing phase of the disease (within a week of onset) and indicate a poor prognosis if seen at presentation in patients with AIP.25–27 When compared with other causes of DAD, AIP has more symmetric lower lobe predominance of consolidation and more extensive honeycombing in the fibrotic phase.28 Prognosis is extremely poor as no effective treatment exists; mortality exceeds 70%.29 Lung biopsy should be considered for the patient without prior lung disease in whom the cause of persistent respiratory failure is unknown despite a thorough microbiological and rheumatologic evaluation.30
Multifocal Distribution of Airspace Opacities
A multifocal distribution refers to opacities that involve multiple regions of the lung and may appear patchy, random, and often asymmetric. Affected and unaffected secondary pulmonary lobules may lie adjacent to one another, resulting in a geographic appearance that is often termed lobular.
Infection often results in a multifocal distribution of ground-glass opacities and consolidation. Common symptoms at presentation include productive cough, fevers, chills, pleuritic pain, hemoptysis, and dyspnea. Laboratory data often reveal a leukocytosis with a neutrophilic predominance. Selected laboratory abnormalities may raise suspicion for specific microbiological organisms. For example, hyponatremia and lymphopenia have been associated with Legionella pneumonia and H1N1 influenza, respectively.31,32 Associated CT findings that may confirm the diagnosis of infection include tree-in-bud opacity or decreased enhancement or cavitation within consolidation. Although many patients who present with multifocal airspace opacities have bacterial pneumonia, viral pneumonias such as influenza, parainfluenza, and severe acute respiratory syndrome can be indistinguishable and may also cause a rapid decline in respiratory function.33 Ground-glass opacities in immunocompetent patients are more indicative of atypical pneumonias such as viral and Mycoplasma pneumonia, and segmental consolidation is more suggestive of bacterial pneumonia, although overlap exists.34 When multifocal ground-glass opacities are associated with sparing of secondary pulmonary lobules, Mycoplasma pneumonia should be considered. Bronchial wall thickening, air trapping, interlobular septal thickening, and centrilobular nodules are also associated with Mycoplasma pneumonias.34,35
Hypersensitivity pneumonitis (HP) is a diffuse granulomatous interstitial lung disease (ILD) that most frequently presents after repeated inhalation of organic antigens.36 Multifocal ground-glass opacities are reported in most subacute cases. Ground-glass opacities are combined with ill-defined multifocal centrilobular nodules of mid to lower lung zone predominance that reflect peribronchiolar and perivascular inflammation with granuloma formation.25,37–39 Mosaic attenuation of the lungs with lobular areas of air trapping, due to bronchiolitis, is present in most cases and is an important clue for the diagnosis of HP.40,41 Air trapping is better depicted on expiratory images and can be the predominant or only feature of HP (Fig. 8). The combination of scattered areas of ground-glass opacities, air trapping, and normal lung is a classic radiologic sign called “head cheese sign.”42,43 A subset of patients present after a large, single exposure of antigens which results in ARF with central consolidation and nodular airspace opacities on chest radiograph and CT. Acute dyspnea may also be secondary to subacute changes superimposed on chronic fibrotic changes related to HP. Fibrosis tends to be central rather than peripheral with relative sparing of the lung bases, allowing distinction from UIP or idiopathic pulmonary fibrosis.44 The differential diagnosis of subacute HP includes desquamative interstitial pneumonia (DIP) that can be indistinguishable on CT; however, as 80% to 95% of patients affected by HP are nonsmokers, the 2 conditions can usually be distinguished through knowledge of the patient’s smoking history.45
Acute eosinophilic pneumonia (AEP) is a rare, febrile illness with rapid onset of 1 to 5 days.46 It is thought to be a hypersensitivity reaction to inhaled agents and is often seen after recent onset of binge cigarette smoking or intense exposure to dust or fumes. Pulmonary eosinophilia induces DAD, and patients are highly symptomatic with ARF and hypoxemia.
On the radiographs, AEP mimics cardiogenic pulmonary edema with the earliest finding of septal lines and reticular opacities that rapidly progress to extensive bilateral ground-glass opacities and confluent consolidations with small bilateral pleural effusions. Absence of cardiomegaly and absence of response to diuresis distinguish AEP from cardiogenic edema. On CT, ground-glass opacities and consolidation are seen in the majority of cases and are multifocal in distribution47,48 (Fig. 9). The majority of cases are associated with interlobular septal thickening, bronchovascular thickening, and small pleural effusions that may mimic pulmonary edema.47,49 Ill-defined centrilobular nodules and crazy-paving features are also described.
When AEP is suspected, BAL should be performed to assess for an elevated eosinophil count in the lavage fluid. AEP usually resolves rapidly with corticosteroids treatment, and no relapse occurs after cessation.
Acute exacerbation of ILD (AE-ILD) refers to an accelerated decline in lung function in patients with UIP, nonspecific interstitial pneumonia, HP, or rheumatoid arthritis–associated ILD. CT features of AE-ILD include multifocal ground-glass opacities on a background of chronic ILD (Fig. 10). This diagnosis should be considered if CT chest imaging demonstrates traction bronchiectasis and/or honeycombing. AE-ILD, especially in the setting of idiopathic pulmonary fibrosis, can progress rapidly to ARF and carries a high morbidity and mortality.29,50 Rarely, AE-ILD can be the initial presentation of an undiagnosed ILD. In most cases, AE-ILD is a diagnosis of exclusion after alternative etiologies of respiratory failure, such as infection and cardiogenic pulmonary edema, have been excluded.51
Peripheral Distribution of Airspace Opacities
A peripheral distribution of radiologic findings refers to abnormalities seen in the peripheral third of the lungs on a chest radiograph and in the subpleural space on CT. Abnormalities in the subpleural space are readily detected, as this area is typically devoid of normal structures. In the acute setting, peripheral airspace opacities may be secondary to aspiration pneumonia or pulmonary infarcts. A subacute presentation of peripheral opacities occurs with chronic eosinophilic pneumonia.52 Organizing pneumonia also demonstrates peripheral airspace opacities but tends to have a more indolent presentation. Peripheral nodules may be secondary to septic emboli.
Chronic eosinophilic pneumonia presents in most cases with a classic imaging pattern that appears as a photographic negative of pulmonary edema with peripheral multifocal consolidation and ground-glass opacity of upper lung zone predominance (Fig. 3D). Crazy-paving features may be seen in some cases.52–54 Patients often have a history of asthma and may present with several weeks of cough with sputum production, fever, night sweats, weight loss, wheezing, and dyspnea.55,56
Patterns and Distribution: Nodular Opacities
CT-detected pulmonary nodules may be categorized by size, distribution, and attenuation. When nodules are multiple, diffuse, and small (usually <1 cm in size), it is useful to report their distribution in relation to the secondary pulmonary lobule to narrow the differential diagnosis.
Centrilobular Distribution of Nodules
Centrilobular nodules preside in the center of the secondary pulmonary lobule and typically spare the fissures and the subpleural space to within 5 mm of the pleural surface unless large, when they may touch the pleura. Centrilobular nodules are subdivided into branching or nonbranching categories. Nonbranching centrilobular nodules are usually ill-defined, have ground-glass attenuation, and are evenly spaced.57–59 They are often associated with ground-glass opacities and septal thickening. They occur with inflammatory causes of bronchiolitis or vasculitis. The most common causes of nonbranching nodules include infection, HP, DPH, pulmonary edema, and smoking-related ILD (SR-ILD). Branching centrilobular nodules have soft tissue attenuation and can be well or ill defined. They are referred to as tree-in-bud opacities and represent inflammation and impaction of the distal airways with fluid, pus, or mucus. The most common causes for tree-in-bud opacities, in a patient with acute dyspnea, are infection and aspiration. Tree-in-bud opacities represent small airways disease and are associated with bronchial wall thickening, fluid within distal airways, mosaic attenuation, and air trapping on expiration studies.
Nonbranching Centrilobular Nodules
Infection due to viral, fungal, and Mycoplasma pneumonia are more frequently associated with centrilobular nodules than bacterial infection.34,60 They are reported in the majority of patients with Mycoplasma pneumonia.61
HP in the subacute phase commonly demonstrates ill-defined diffuse centrilobular nodules of mid to lower lung zone predominance that reflect peribronchiolar and perivascular inflammation with granuloma formation25,37,38 (Fig. 8).
SR-ILD is a spectrum of pathologic changes including respiratory bronchiolitis and DIP that may present with acute dyspnea. CT most commonly demonstrates centrilobular ground-glass nodules due to bronchiolitis and peribronchiolar deposition of hemosiderin-laden macrophages and ground-glass opacity secondary to intra-alveolar macrophages. A multifocal, upper zone–predominant, lobular, or peripheral distribution is commonly seen in SR-ILD.
DPH can present with diffuse centrilobular nonbranching nodules.62 There are associated ground-glass opacities, interlobular septal thickening, and intralobular lines. The absence of lobular areas of low attenuation and air trapping in DPH allows distinction from HP, DIP, or infections associated with centrilobular nodules.
Branching Centrilobular Nodules
Bronchopneumonia is associated with inflammation of the walls and fluid filling in distal airways, resulting in a tree-in-bud pattern. Organisms that are commonly associated with this pattern include Staphylococcus aureus and Mycoplasma pneumoniae, along with gram-negative bacteria, viruses such as respiratory syncytial virus, adenovirus, influenza, parainfluenza, and fungi, particularly Aspergillus.63–65 Chest CT demonstrates tree-in-bud opacities and larger centrilobular nodules, often referred to as acinar nodules (Fig. 11A). There is progression in multifocal areas to more confluent consolidation. S. aureus infection is associated with cavitation within confluent nodules and resultant abscess formation.66
Aspiration pneumonia is associated with tree-in-bud opacities due to chemical bronchiolitis22 (Fig. 11B). Tree-in-bud opacities are particularly common after chronic aspiration of small volumes of material in patients with impaired swallowing mechanisms, depressed level of consciousness, or esophageal abnormalities. Patients with chronic aspiration may present acutely to the ER with pneumonia, and the diagnosis should be suspected in the presence of migratory opacities67 or tree-in-bud opacities.68 Dependent consolidation, basal-predominant bronchiectasis, and fluid in distal airways are commonly seen, and bronchial wall thickening, mosaic attenuation, and air trapping may also be present, secondary to airway inflammation.21,22,69
Variants of this condition include granulomatous pneumonitis due to chronic aspiration of legumes such as lentils and lipoid pneumonia caused by chronic lipoid aspiration. They present, respectively, with poorly defined nodules and consolidation of low attenuation on CT.
Mycobacterial infection is a common cause for tree-in-bud opacities. The detection of tree-in-bud opacities is of importance in the diagnosis of endobronchial spread of tuberculosis in both the primary and reactivation phases.70–72 The combination of peribronchiolar consolidation, bronchial wall thickening, branching, nonbranching centrilobular nodules, and thick-walled and thin-walled cavities should raise suspicion for active tuberculosis (Fig. 11C). With treatment, consolidation and centrilobular nodules resolve, but healed cavitary nodules may persist.72 On the basis of the distribution and pattern of CT findings, an accurate diagnosis of tuberculosis can be made in almost all cases of active infection and can also be excluded in the majority of cases.71,73 The presence of consolidation, cavitation, and bronchial wall thickening is more common in patients with smear-positive sputum than those with smear-negative sputum, although centrilobular nodules occur in both forms of active disease.74
Small Miliary Nodules
The term “miliary” refers to randomly distributed, well-defined, soft tissue attenuation nodules that are 1 to 5 mm in diameter. The nodules are symmetrically and uniformly distributed but tend to predominate at the bases and in the periphery of the lungs. Miliary nodules are found in close relation to small vessels because of the hematogenous nature of spread, but they do not show any predilection for centrilobular structures, fissures, or the subpleural space. In the setting of acute dyspnea without known malignancy, miliary nodules are most likely secondary to tuberculosis or fungal infection.57,65,75–78
Miliary tuberculosis rarely may present with ARF.79 Random, miliary nodules are often associated with ground-glass opacities, septal and intralobular lines, and lymphadenopathy. Hilar and mediastinal lymph nodes may show central low attenuation after intravenous contrast enhancement80 (Fig. 12).
Miliary fungal infection is indistinguishable from tuberculosis and can present with acute dyspnea in patients who have disseminated histoplasmosis, blastomycosis, and coccidioidomycosis, particularly in immunocompromised patients.81–83
Larger Random Nodules
Septic pulmonary emboli can present as multiple bilateral nodules that are usually >1 cm in diameter and random in distribution, although they often have a peripheral predilection. The nodules demonstrate varying degrees of cavitation due to intermittent deposition of infected foci within the lung parenchyma from a source such as tricuspid or pulmonic valve endocarditis, Lemierre syndrome, infection of indwelling catheters or prosthetic devices, or dental infections.84,85 Ground-glass opacities surrounding the nodules (halo sign) are often present and likely to represent perilesional hemorrhage. Initial reports of a central “feeding vessel” leading to the septic emboli was postulated to be due to occlusion of a pulmonary artery, but thin-section CT has demonstrated that these vessels actually pass around the nodules and represent pulmonary veins rather than arteries.86 Associated features include wedge-shaped peripheral consolidations secondary to pulmonary infarcts (Fig. 13).
GPA, formerly called Wegener granulomatosis, is a multisystem necrotizing vasculitis affecting small-sized to medium-sized vessels.87 The nodules of GPA are random in distribution, seen in all zones, measure up to 10 cm in diameter, and often have irregular margins. Cavitation is common in nodules >2 cm, and their thick shaggy walls become smooth and thin after treatment. Multifocal consolidation and ground-glass opacities are often present, resulting from pulmonary hemorrhage due to small vessel vasculitis or capillaritis. A rim of consolidation reflecting organizing pneumonia may be detected surrounding the areas of pulmonary hemorrhage, resulting in a “reverse halo” sign.88–91
Patterns and Distribution: Linear Opacities
Linear opacities may be secondary to interlobular septal thickening or intralobular lines. In an acutely dyspneic patient, they are rarely seen as an isolated finding but occur in combination with ground-glass opacities. A combination of ground-glass opacity, interlobular septal thickening, and intralobular lines can result in a crazy-paving appearance. In the acute setting, a crazy-paving appearance is most likely to reflect an underlying diagnosis of AIP, DAD, or atypical infection. If the predominant linear opacity is due to intralobular lines and there is associated traction bronchiectasis or honeycomb cystic change, underlying chronic ILD, and possible acute exacerbation or superimposed pneumonia, should be considered in the differential.
Central Distribution of Linear Opacities
Hydrostatic (cardiogenic) pulmonary edema is frequently associated with smooth interlobular septal thickening due to engorgement of the lymphatics from edema9–11 (Fig. 14). On a chest radiograph, septal thickening is most easily seen in the periphery of the lung, but CT often shows a diffuse distribution associated with ground-glass opacity. The septal thickening may be more prominent than central ground-glass opacity and is often most pronounced at the lung apices and bases. Bronchial wall thickening, pleural effusions, and fissural thickening are associated features that provide clues to the diagnosis. In permeability edema, airspace opacities, septal lines and crazy-paving are frequently seen together. When all causes for crazy-paving are evaluated, DAD and its many etiologies are the commonest pathologic diagnoses.92
DPH initially presents with ill-defined, ground-glass attenuation centrilobular nodules, and, within 24 to 48 hours, accumulation of hemosiderin in the interstitium results in prominent interlobular and intralobular lines.13–15 The combination of ground-glass opacities, centrilobular nodules, and interlobular and intralobular lines may also be seen in subacute HP and DIP, but these conditions are associated with bronchiolitis and, as such, also show lobular lucencies and air trapping, which are not features of DPH. Infection may be indistinguishable from DPH, particularly viral or Mycoplasma pneumonia. However, DPH is not associated with tree-in-bud opacities, which are commonly seen in infection.
Multifocal Distribution of Linear Opacities
Atypical pneumonias, particularly Mycoplasma pneumonia, may result in septal thickening in combination with multifocal ground-glass opacities, lobular sparing, and bronchial wall thickening.35
Patterns and Distribution: Cystic Opacities
Cysts are common findings of chronic lung disease but may be present with a subacute presentation. Causes can include infection, septic emboli, vasculitides, complications of preexisting cavitary or cystic lung disease, or apparent cystic lucencies due to diffuse parenchymal opacification sparing underlying cystic lung disease such as emphysema.
Multifocal Distribution of Cystic Opacities
Infection may be associated with thin-walled spherical cysts or pneumatoceles (Fig. 15A). S. aureus is a common cause in an immunocompetent patient.93 Thick-walled cavities are an important feature of endobronchial spread of tuberculosis and are associated with tree-in-bud opacities and consolidation.
Patients may also present with acute dyspnea when preexisting emphysema or cystic lung disease is complicated by secondary infection. In these cases, increased cyst wall thickness, air-fluid levels, and adjacent consolidation are apparent (Fig. 15B).
Vasculitis such as GPA may present with cavitary nodules due to a necrotizing vasculitis involving medium-sized arteries.94 Cavitation is common, particularly if the nodules are >2 cm in diameter.
Peripheral Distribution of Cystic Opacities
Septic emboli result in multiple, peripheral nodules that are in varying stages of evolution, with some solid, others cavitary or cystic84,95 (Fig. 13). Associated features include peripheral wedge-shaped consolidation secondary to infarction and pleural effusions.
An acutely dyspneic patient with diffuse parenchymal abnormalities on a chest radiograph presents a challenging scenario for the radiologist. Chest CT allows greater anatomic correlation and characterization when compared with chest radiography. Analysis of the distribution of radiographic findings and identification of the predominant radiographic abnormality on chest CT are essential to providing a limited differential diagnosis of the underlying etiology. This pattern-based approach, when combined with the patient’s clinical symptoms, laboratory data, and evaluation of prior studies to determine chronicity of the findings, can be extremely helpful in directing further clinical management. This article has described a practical approach to differentiating the main parenchymal conditions that cause acute dyspnea in a patient with no known malignancy or immune compromise.
1. Vincent J-L, Akça S, De Mendonça A, et al.. The epidemiology of acute respiratory failure in critically ill patients(*). Chest. 2002;121:1602–1609.
2. Pierrakos C, Vincent J-L. The changing pattern of acute respiratory distress syndrome over time: a comparison of two periods. Eur Respir J. 2012;40:589–595.
3. Mamlouk MD, vanSonnenberg E, Gosalia R, et al.. Pulmonary embolism at CT angiography: implications for appropriateness, cost, and radiation exposure in 2003 patients. Radiology. 2010;256:625–632.
4. Webb WR. High-resolution CT of the lung parenchyma. Radiol Clin North Am. 1989;27:1085–1097.
5. Seely JM, Jones LT, Wallace C, et al.. Systemic sclerosis: using high-resolution CT to detect lung disease in children. Am J Roentgenol. 1998;170:691–697.
6. Hansell DM, Bankier AA, MacMahon H, et al.. Fleischner Society: glossary of terms for thoracic imaging. Radiology. 2008;246:697–722.
7. Primack SL, Remy-Jardin M, Remy J, et al.. High-resolution CT of the lung: pitfalls in the diagnosis of infiltrative lung disease. Am J Roentgenol. 1996;167:413–418.
8. Tarver RD, Conces DJ, Godwin JD. Motion artifacts on CT simulate bronchiectasis. Am J Roentgenol. 1988;151:1117–1119.
9. Forster BB, Müller NL, Mayo JR, et al.. High-resolution computed tomography of experimental hydrostatic pulmonary edema. Chest. 1992;101:1434–1437.
10. Scillia P, Delcroix M, Lejeune P, et al.. Hydrostatic pulmonary edema: evaluation with thin-section CT in dogs. Radiology. 1999;211:161–168.
11. Storto ML, Kee ST, Golden JA, et al.. Hydrostatic pulmonary edema: high-resolution CT findings. Am J Roentgenol. 1995;165:817–820.
12. Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med. 2001;344:665–671.
13. Cheah FK, Sheppard MN, Hansell DM. Computed tomography of diffuse pulmonary haemorrhage with pathological correlation. Clin Radiol. 1993;48:89–93.
14. Travis WD, Colby TV, Lombard C, et al.. A clinicopathologic study of 34 cases of diffuse pulmonary hemorrhage with lung biopsy confirmation. Am J Surg Pathol. 1990;14:1112–1125.
15. Hisada T, Ishizuka T, Tomizawa Y, et al.. “Crazy-paving” appearance in systemic lupus erythematosus. Intern Med. 2006;45:29–30.
16. Zamora MR, Warner ML, Tuder R, et al.. Diffuse alveolar hemorrhage and systemic lupus erythematosus. Clinical presentation, histology, survival, and outcome. Medicine (Baltimore). 1997;76:192–202.
17. Schwarz MI, Zamora MR, Hodges TN, et al.. Isolated pulmonary capillaritis and diffuse alveolar hemorrhage in rheumatoid arthritis and mixed connective tissue disease. Chest. 1998;113:1609–1615.
18. Martínez-Martínez MU, Abud-Mendoza C. Diffuse alveolar hemorrhage in patients with systemic lupus erythematosus. Clinical manifestations, treatment, and prognosis. Rheumatol Clin. 2014;10:248–253.
19. Hedlund LW, Vock P, Effmann EL, et al.. Hydrostatic pulmonary edema. An analysis of lung density changes by computed tomography. Invest Radiol. 1984;19:254–262.
20. Tagliabue M, Casella TC, Zincone GE, et al.. CT and chest radiography in the evaluation of adult respiratory distress syndrome. Acta Radiol. 1994;35:230–234.
21. Giménez A, Franquet T, Erasmus JJ, et al.. Thoracic complications of esophageal disorders. Radiographics. 2002;22:S247–S258.
22. Franquet T, Giménez A, Rosón N, et al.. Aspiration diseases: findings, pitfalls, and differential diagnosis. Radiographics. 2000;20:673–685.
23. Ichikado K, Suga M, Muranaka H, et al.. Prediction of prognosis for acute respiratory distress syndrome with thin-section CT: validation in 44 cases. Radiology. 2006;238:321–329.
24. Primack SL, Hartman TE, Ikezoe J, et al.. Acute interstitial pneumonia: radiographic and CT findings in nine patients. Radiology. 1993;188:817–820.
25. Akira M. Computed tomography and pathologic findings in fulminant forms of idiopathic interstitial pneumonia. J Thorac Imaging. 1999;14:76–84.
26. Ichikado K, Johkoh T, Ikezoe J, et al.. Acute interstitial pneumonia: high-resolution CT findings correlated with pathology. Am J Roentgenol. 1997;168:333–338.
27. Ichikado K, Suga M, Müller NL, et al.. Acute interstitial pneumonia: comparison of high-resolution computed tomography findings between survivors and nonsurvivors. Am J Respir Crit Care Med. 2002;165:1551–1556.
28. Tomiyama N, Müller NL, Johkoh T, et al.. Acute respiratory distress syndrome and acute interstitial pneumonia: comparison of thin-section CT findings. J Comput Assist Tomogr. 2001;25:28–33.
29. Bouros D, Nicholson AC, Polychronopoulos V, et al.. Acute interstitial pneumonia. Eur Respir J. 2000;15:412–418.
30. Warner DO, Warner MA, Divertie MB. Open lung biopsy in patients with diffuse pulmonary infiltrates and acute respiratory failure. Am Rev Respir Dis. 1988;137:90–94.
31. Schuetz P, Haubitz S, Christ-Crain M, et al.. Hyponatremia and anti-diuretic hormone in Legionnaires’ disease. BMC Infect Dis. 2013;13:585.
32. Cao B, Li X-W, Mao Y, et al.. Clinical features of the initial cases of 2009 pandemic influenza A (H1N1) virus infection in China. N Engl J Med. 2009;361:2507–2517.
33. Agarwal PP, Cinti S, Kazerooni EA. Chest radiographic and CT findings in novel swine-origin influenza A (H1N1) virus (S-OIV) infection. Am J Roentgenol. 2009;193:1488–1493.
34. Tanaka N, Matsumoto T, Kuramitsu T, et al.. High resolution CT findings in community-acquired pneumonia. J Comput Assist Tomogr. 1996;20:600–608.
35. Lee I, Kim TS, Yoon H-K. Mycoplasma pneumoniae
pneumonia: CT features in 16 patients. Eur Radiol. 2006;16:719–725.
36. Patel AM, Ryu JH, Reed CE. Hypersensitivity pneumonitis: current concepts and future questions. J Allergy Clin Immunol. 2001;108:661–670.
37. Silver SF, Müller NL, Miller RR, et al.. Hypersensitivity pneumonitis: evaluation with CT. Radiology. 1989;173:441–445.
38. Lynch DA, Rose CS, Way D. Hypersensitivity pneumonitis: sensitivity of high-resolution CT in a population-based study. Am J Roentgenol. 1992;159:469–472.
39. Remy-Jardin M, Remy J, Wallaert B, et al.. Subacute and chronic bird breeder hypersensitivity pneumonitis: sequential evaluation with CT and correlation with lung function tests and bronchoalveolar lavage. Radiology. 1993;189:111–118.
40. Hansell DM, Wells AU, Padley SP, et al.. Hypersensitivity pneumonitis: correlation of individual CT patterns with functional abnormalities. Radiology. 1996;199:123–128.
41. Small JH, Flower CD, Traill ZC, et al.. Air-trapping in extrinsic allergic alveolitis on computed tomography. Clin Radiol. 1996;51:684–688.
42. Webb WR, Thin-section CT. of the secondary pulmonary lobule: anatomy and the image—the 2004 Fleischner lecture. Radiology. 2006;239:322–338.
43. Chung MH, Edinburgh KJ, Webb EM, et al.. Mixed infiltrative and obstructive disease on high-resolution CT: differential diagnosis and functional correlates in a consecutive series. J Thorac Imaging. 2001;16:69–75.
44. Lynch DA, Newell JD, Logan PM, et al.. Can CT distinguish hypersensitivity pneumonitis from idiopathic pulmonary fibrosis? Am J Roentgenol. 1995;165:807–811.
45. Yi ES. Hypersensitivity pneumonitis. Crit Rev Clin Lab Sci. 2002;39:581–629.
46. Allen J. Acute eosinophilic pneumonia. Semin Respir Crit Care Med. 2006;27:142–147.
47. Johkoh T, Müller NL, Akira M, et al.. Eosinophilic lung diseases: diagnostic accuracy of thin-section CT in 111 patients. Radiology. 2000;216:773–780.
48. Cheon JE, Lee KS, Jung GS, et al.. Acute eosinophilic pneumonia: radiographic and CT findings in six patients. Am J Roentgenol. 1996;167:1195–1199.
49. Daimon T, Johkoh T, Sumikawa H, et al.. Acute eosinophilic pneumonia: thin-section CT findings in 29 patients. Eur J Radiol. 2008;65:462–467.
50. Blivet S, Philit F, Sab JM, et al.. Outcome of patients with idiopathic pulmonary fibrosis admitted to the ICU for respiratory failure. Chest. 2001;120:209–212.
51. Collard HR, Moore BB, Flaherty KR, et al.. Acute exacerbations of idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 2007;176:636–643.
52. Mayo JR, Müller NL, Road J, et al.. Chronic eosinophilic pneumonia: CT findings in six cases. Am J Roentgenol. 1989;153:727–730.
53. Gaensler EA, Carrington CB. Peripheral opacities in chronic eosinophilic pneumonia: the photographic negative of pulmonary edema. Am J Roentgenol. 1977;128:1–13.
54. Ebara H, Ikezoe J, Johkoh T, et al.. Chronic eosinophilic pneumonia: evolution of chest radiograms and CT features. J Comput Assist Tomogr. 1994;18:737–744.
55. Alam M, Burki NK. Chronic eosinophilic pneumonia: a review. South Med J. 2007;100:49–53.
56. Marchand E, Cordier JF. Idiopathic chronic eosinophilic pneumonia. Orphanet J Rare Dis. 2006;1:11.
57. Murata K, Itoh H, Todo G, et al.. Centrilobular lesions of the lung: demonstration by high-resolution CT and pathologic correlation. Radiology. 1986;161:641–645.
58. Naidich DP, Zerhouni EA, Hutchins GM, et al.. Computed tomography of the pulmonary parenchyma. Part 1: distal air-space disease. J Thorac Imaging. 1985;1:39–53.
59. Itoh H, Tokunaga S, Asamoto H, et al.. Radiologic-pathologic correlations of small lung nodules with special reference to peribronchiolar nodules. Am J Roentgenol. 1978;130:223–231.
60. Reittner P, Ward S, Heyneman L, et al.. Pneumonia: high-resolution CT findings in 114 patients. Eur Radiol. 2003;13:515–521.
61. Okada F, Ando Y, Wakisaka M. Chlamydia pneumoniae
pneumonia and Mycoplasma pneumoniae
pneumonia: comparison of clinical findings and CT findings. J Comput Assist Tomogr. 2005;29:626–632.
62. Lichtenberger JP, Digumarthy SR, Abbott GF, et al.. Diffuse pulmonary hemorrhage: clues to the diagnosis. Curr Probl Diagn Radiol. 2014;43:128–139.
63. Logan PM, Primack SL, Miller RR, et al.. Invasive aspergillosis of the airways: radiographic, CT, and pathologic findings. Radiology. 1994;193:383–388.
64. Tanaka H, Shibusa T, Sugaya F, et al.. A case of influenza B viral bronchopneumonia followed by CT. Nihon Kyobu Shikkan Gakkai Zasshi. 1992;30:947–951.
65. Lee KS, Kim TS, Han J, et al.. Diffuse micronodular lung disease: HRCT and pathologic findings. J Comput Assist Tomogr. 1999;23:99–106.
66. Macfarlane J, Rose D. Radiographic features of staphylococcal pneumonia in adults and children. Thorax. 1996;51:539–540.
67. Friedlander AL, Fessler MB. A 70-year-old man with migratory pulmonary infiltrates. Chest. 2006;130:1269–1274.
68. Rossi SE, Franquet T, Volpacchio M, et al.. Tree-in-bud pattern at thin-section CT of the lungs: radiologic-pathologic overview. Radiographics. 2005;25:789–801.
69. Harding SM, Schan CA, Guzzo MR, et al.. Gastroesophageal reflux-induced bronchoconstriction. Is microaspiration a factor? Chest. 1995;108:1220–1227.
70. Im JG, Itoh H, Shim YS, et al.. Pulmonary tuberculosis: CT findings--early active disease and sequential change with antituberculous therapy. Radiology. 1993;186:653–660.
71. Hatipoğlu ON, Osma E, Manisali M, et al.. High resolution computed tomographic findings in pulmonary tuberculosis. Thorax. 1996;51:397–402.
72. Poey C, Verhaegen F, Giron J, et al.. High resolution chest CT in tuberculosis: evolutive patterns and signs of activity. J Comput Assist Tomogr. 1997;21:601–607.
73. Lee KS, Hwang JW, Chung MP. Utility of CT in the evaluation of pulmonary tuberculosis in patients without AIDS. Chest. 1996;110:977–984.
74. Kosaka N, Sakai T, Uematsu H, et al.. Specific high-resolution computed tomography findings associated with sputum smear-positive pulmonary tuberculosis. J Comput Assist Tomogr. 2005;29:801–804.
75. Neeld DA, Goodman LR, Gurney JW, et al.. Computerized tomography in the evaluation of allergic bronchopulmonary aspergillosis. Am Rev Respir Dis. 1990;142:1200–1205.
76. Lee KS, Im JG. CT in adults with tuberculosis of the chest: characteristic findings and role in management. Am J Roentgenol. 1995;164:1361–1367.
77. Im JG, Itoh H, Han MC. CT of pulmonary tuberculosis. Semin Ultrasound CT MR. 1995;16:420–434.
78. Hong SH, Im JG, Lee JS, et al.. High resolution CT findings of miliary tuberculosis. J Comput Assist Tomogr. 1998;22:220–224.
79. Choi D, Lee KS, Suh GY, et al.. Pulmonary tuberculosis presenting as acute respiratory failure: radiologic findings. J Comput Assist Tomogr. 1999;23:107–113.
80. Im JG, Song KS, Kang HS, et al.. Mediastinal tuberculous lymphadenitis: CT manifestations. Radiology. 1987;164:115–119.
81. Stelling CB, Woodring JH, Rehm SR, et al.. Miliary pulmonary blastomycosis. Radiology. 1984;150:7–13.
82. Goodwin RA, Shapiro JL, Thurman GH, et al.. Disseminated histoplasmosis: clinical and pathologic correlations. Medicine (Baltimore). 1980;59:1–33.
83. Arsura EL, Kilgore WB. Miliary coccidioidomycosis in the immunocompetent. Chest. 2000;117:404–409.
84. Huang RM, Naidich DP, Lubat E, et al.. Septic pulmonary emboli: CT-radiographic correlation. Am J Roentgenol. 1989;153:41–45.
85. Stawicki SP, Firstenberg MS, Lyaker MR, et al.. Septic embolism in the intensive care unit. Int J Crit Illn Inj Sci. 2013;3:58–63.
86. Dodd JD, Souza CA, Müller NL. High-resolution MDCT of pulmonary septic embolism: evaluation of the feeding vessel sign. Am J Roentgenol. 2006;187:623–629.
87. Jennette JC, Falk RJ, Andrassy K, et al.. Nomenclature of systemic vasculitides. Proposal of an international consensus conference. Arthritis Rheum. 1994;37:187–192.
88. Aberle DR, Gamsu G, Lynch D. Thoracic manifestations of Wegener granulomatosis: diagnosis and course. Radiology. 1990;174pt 1703–709.
89. Hoffman GS, Kerr GS, Leavitt RY. Wegener granulomatosis: an analysis of 158 patients. Ann Intern Med. 1992;116:488–498.
90. Weir IH, Müller NL, Chiles C, et al.. Wegener’s granulomatosis: findings from computed tomography of the chest in 10 patients. Can Assoc Radiol J. 1992;43:31–34.
91. Lee KS, Kim TS, Fujimoto K, et al.. Thoracic manifestation of Wegener’s granulomatosis: CT findings in 30 patients. Eur Radiol. 2003;13:43–51.
92. Johkoh T, Itoh H, Müller NL, et al.. Crazy-paving appearance at thin-section CT: spectrum of disease and pathologic findings. Radiology. 1999;211:155–160.
93. Dines DE. Diagnostic significance of pneumatocele of the lung. JAMA. 1968;204:1169–1172.
94. Hansell DM. Small-vessel diseases of the lung: CT-pathologic correlates. Radiology. 2002;225:639–653.
95. Kwon WJ, Jeong YJ, Kim K-I, et al.. Computed tomographic features of pulmonary septic emboli: comparison of causative microorganisms. J Comput Assist Tomogr. 2007;31:390–394.