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Isolated Diffuse Ground-Glass Opacity in Thoracic CT:
Causes and Clinical Presentations
Wallace T. Miller, Jr.1 and Rosita M. Shah
Miller WT, Shah R
round-glass opacity (GGO) is de- with simple clinical information. By isolated, developing dyspnea, and inpatients who are
1Both authors: Department of Radiology, University of Pennsylvania School of Medicine, 3400 Spruce St., Silverstein 1, Philadelphia, PA 19104. Address correspondence to W. T. Miller
(wallacejr.miller@uphs.upenn.edu).
TABLE 1 Causes of Isolated Diffuse Ground-Glass Opacity CMV disease in patients with AIDS is associ-
ated with greater levels of immunosuppres-
Categories Types of Diseases and Infections sion and greater mortality rates than in the
Opportunistic infections Pneumocystis pneumonia (PCP) general HIV-positive population [25].
Cytomegalovirus pneumonia (CMV) Many patients in whom CMV can be de-
Herpes simplex virus pneumonia (HSV) tected in blood, urine, and respiratory secre-
Respiratory syncytial virus bronchiolitis
Other tions clinically will be asymptomatic. In
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Fig. 1.—29-year-old HIV-positive man with Pneumocystis carinii pneumonia. High- Fig. 2.—36-year-old man with cytomegalovirus pneumonia following renal transplan-
resolution CT image through carina shows widespread ground-glass opacity uni- tation. High-resolution CT image through inferior hilum shows isolated diffuse
formly distributed across lungs. ground-glass opacity widely spread across both lungs.
late winter and early spring and commonly fections as a result of neutropenia but who many more. In a study of drug toxicity in pa-
causes fever, cough, dyspnea, and otalgia also are at risk for other causes of ID-GGO. tients with autologous bone marrow transplan-
with clinical signs of rales, rhonchi, or These patients frequently are thrombocy- tation, 65% of cases of drug toxicity manifested
wheezes. In immunocompetent adults, the topenic and are therefore at increased risk for as GGO [42].
course usually is self-limited and is treated diffuse aveolar hemorrhage, DAH. They also
on an outpatient basis. However, in immuno- may develop drug toxicity as a result of the Outpatients with Slowly
compromised adults, RSV infection may re- systemic chemotherapies they have received. Progressive Dyspnea
sult in a clinically significant pneumonia This leads to the differential of and drug tox- In this third scenario, an otherwise healthy
[37, 38]. icity. In our experience, drug toxicity is the outpatient will complain of mild chronic dysp-
The majority of patients with RSV pulmo- most difficult entity to diagnose and the most nea. Findings of the chest radiograph most of-
nary infection will have normal radiographic common cause of ID-GGO in this population. ten will appear normal or may show a faint
findings [39]. CT scans in 10 patients with In our study of the causes of ID-GGO, drug haze, which may be interpreted as diffuse
RSV infection following lung transplantation toxicity accounted for 4% of all pathology- GGO. In this situation, ID-GGO most often
revealed diffuse GGOs in seven patients, pul- proven cases and therefore represents an impor- will indicate one of the following chronic inter-
monary consolidation in five patients, and tree- tant cause of ID-GGO [9]. Because of the wide stitial diseases: HP, desquamative interstitial
in-bud opacities in four patients [40] (Fig. 3). variety of pharmacologic agents that can result pneumonia (DIP), respiratory bronchiolitis in-
Other viruses.—Many other viruses com- in ID-GGO, there are several histopathologic terstitial lung disease (RBILD), NSIP, acute in-
monly produce upper–respiratory tract illnesses patterns of drug-related damage to the pulmo- terstitial pneumonia (AIP), BOOP, and
and occasionally may produce a limited pneu- nary parenchyma. These include noncardio- sarcoidosis. Rarely, these patients will have
monia. It is likely that many of these will appear genic pulmonary edema, diffuse alveolar some of the unusual unclassified causes of ID-
as widespread or small focal regions of GGO, damage (DAD), nonspecific interstitial pneu- GGO such as pulmonary alveolar proteinosis
which are self-limited and radiographically re- monia (NSIP), DAH, bronchiolitis obliterans (PAP) or bronchoalveolar carcinoma (BAC). A
solve spontaneously. Because few of these pa- with organizing pneumonia (BOOP), hyper- history of smoking may be an important addi-
tients are definitively diagnosed, it is unknown sensitivity pneumonitis (HP), eosinophilic tional factor in this population. DIP and
how often ID-GGO is a manifestation of com- pneumonia, bronchiolitis obliterans, and ve- RBILD are seen almost exclusively among
munity-acquired viral pneumonias. noocclusive disease [41]. Note that the first six smokers and therefore would be unlikely diag-
patterns of damage listed here often will appear noses in patients who do not smoke.
Patients Who Have Received Bone as ID-GGO on CT scans. Drugs, which can
Marrow–Suppressing Chemotherapy cause permeability edema, include cytosine ar- Chronic Interstitial Diseases Appearing as ID-GGO
In scenario two, a patient receiving bone abinoside (ara-C), gemcitabine, interleukin-2, An outpatient with chronic respiratory
marrow–suppressing chemotherapy, usually tumor necrosis factor, and all-transretinoic acid symptoms but without other clinically relevant
for metastatic carcinoma, presents with respi- (ATRA). Other chemotherapy medications that medical conditions who presents with ID-
ratory symptoms in the setting of thrombocy- have been shown to cause ID-GGO include GGO often will have a chronic interstitial lung
topenia and neutropenia. These patients are a daunorubicin, bleomycin, vincristine, carmus- disease. In our study of causes of ID-GGO,
special subset of immunocompromised indi- tine, methotrexate, topotecan, carboplatin, and chronic diffuse interstitial lung diseases ac-
viduals who are at risk for opportunistic in- vinorelbine [41] (Figs. 4 and 5). There likely are counted for 31% (10/32) of pathology-proven
Fig. 3.—65-year-old woman with respiratory syncytial virus pneumonia receiving Fig. 4.—75-year-old woman being treated for treated for promyelocytic leukemia and
chemotherapy for ovarian cancer. High-resolution CT image through carina shows presenting with all-transretinoic acid syndrome of noncardiogenic edema. Thick-
extensive ground-glass opacity across both lungs. There also is nonspecific intersti- section CT image through carina shows widespread ground-glass opacities and
tial thickening in more dependent lungs bilaterally; however, ground-glass opacity small bilateral pleural effusions.
remains dominant finding.
cases [9]. Those interstitial diseases that most are a variety of microorganisms that may re- monary edema secondary to an overwhelming
likely will present as ID-GGO include HP, DIP, side in decaying vegetable matter such as ther- allergic response. With lower-dose, chronic ex-
RBILD, and NSIP. Other interstitial diseases mophilic actinomycetes, the Penicillium posures, a granulomatous fibrosis develops in
that rarely may present as ID-GGO include species, the Aspergillus species, and the Myco- the interstitial spaces of the lungs [44].
sarcoidosis and BOOP. bacterium avium-intracellulare complex [43]. There are many of causes of HP, including
Hypersensitivity pneumonitis.—Inhalation A notable exception to this general rule is bird farmer’s lung, cotton worker’s lung (byssino-
of organic or inorganic particles by sensitized fancier’s disease in which the allergens are pro- sis), sugar cane worker’s lung (bagassosis),
individuals may result in the allergic phenom- teins contained in bird feathers, serum, or and mushroom worker’s diseases [43]. Urban
enon known as HP. In most cases, the allergens guano. Acute HP causes a capillary leak pul- populations can be exposed via contaminated
Fig. 5.—37-year-old woman with methotrexate lung toxicity being treated for rheu- Fig. 6.—29-year-old woman with hypersensitivity pneumonitis, slowly progressive
matoid arthritis. High-resolution CT image through carina shows widespread iso- dyspnea, and frequent exposure to birds. High-resolution CT scan of right upper lobe
lated ground-glass opacities with lobular distribution forming mosaic pattern. shows poorly defined centrilobular nodules of ground-glass opacity.
ventilation systems, especially humidifiers of subpleural reticulation may be seen in a mi- Acute interstitial pneumonia.—AIP is a
and air conditioners. Hobbies such as raising nority of patients. rapidly progressive interstitial fibrosis that re-
pigeons or parakeets can result in a form of Respiratory bronchiolitis interstitial lung sembles the organizing stage of DAD. It usually
HP called bird fancier’s disease. disease.—The histology of RBILD reveals ex- will present with progressive dyspnea leading to
CT examinations of HP result in a wide tensive infiltration of alveoli by macrophages as- respiratory failure over several weeks or
spectrum of findings including diffuse alveo- sociated with mild interstitial fibrosis in a months, and occasionally with an antecedent vi-
lar consolidation in acute HP, diffuse nodular peribronchiolar distribution [55]. Thus, it is histo- ral-like prodrome [55]. Chest CT may show al-
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interstitial lung disease in subacute and logically identical to DIP with the additional cri- veolar consolidation, GGOs, or both, often with
chronic HP, and irregular bands of fibrosis terion that it be most severe in the centrilobular associated traction bronchiectasis [55, 62].
with distortion of the hila in chronic HP [45– regions of the secondary pulmonary lobule. This Lymphocytic interstitial pneumonia.—
49]. However, ID-GGO is among the more similarity has led some authors to suggest that Lymphocytic interstitial pneumonia (LIP) is
common manifestations of subacute HP and, DIP and RBILD are two manifestations of the an idiopathic interstitial abnormality charac-
other than pulmonary edema, HP is probably same disease [55, 56]. On CT, RBILD often will terized by diffuse lymphocytic infiltration of
the most common cause of ID-GGOs in nor- appear as ID-GGO. Very fine, often centrilobular, the interstitium of the lung [63]. It usually is
mal hosts [45, 47, 49] (Fig. 6). These ID- nodules also may be apparent on chest CT [56]. associated with Sjögren’s syndrome in adults
GGOs often will appear as a mosaic pattern. Nonspecific interstitial pneumonia.—NSIP and HIV infection in children. Some reports
Desquamative interstitial pneumonia.— represents an interstitial pneumonia that does have suggested that LIP may represent a pre-
DIP is characterized pathologically by infil- not meet criteria for UIP, DIP, AIP, or BOOP cursor to lymphoma or a low-grade lym-
tration of alveoli by macrophages associated and thus has a variable histologic and radiologic phoma; however, others suggest that LIP
with mild interstitial fibrosis. In the past, appearance [57, 58]. It has been associated with represents a variant of lymphoid hyperplasia
many individuals believed that DIP was an collagen vascular disorders, chronic passive and is not a premalignant condition [64–66].
early phase of usual interstitial pneumonia congestion, and drug toxicity but is most often Diffuse GGO appears to be the most common
(UIP). Currently, DIP is believed to be a direct an idiopathic disorder. When idiopathic, NSIP CT finding in LIP and is present in nearly all
result of smoking-related lung toxicity. Pa- most often affects patients in their 40s, 50s, and patients [66–71]. Bronchovascular and septal
tients with DIP typically are between ages of 60s and presents with an insidious onset of thickening also have been reported [70, 71].
30 to 50 years and present with chronic pro- cough and dyspnea [55]. Thin-walled cysts also may be present in
gressive dyspnea, with or without fevers [50]. ID-GGOs are the most common radio- some cases. Serial CT examinations show re-
Most patients will improve clinically and ra- graphic findings in NSIP and are found in nearly versibility of all findings except cysts [70].
diographically with corticosteroid therapy or 100% of cases. GGO often is found in a sub- Cryptogenic organizing pneumonia and
smoking cessation [6, 51]. pleural distribution but may also show a random bronchiolitis obliterans with organizing
CT scans show ID-GGO in many patients or diffuse distribution [56, 57, 59, 60] (Fig. 8). pneumonia.—BOOP is a histologic pattern of
with DIP. Some studies have found that the Reticulation, either randomly or in a subpleural lung injury. This often is due to a variety of
GGOs predominantly are distributed in the distribution, also is a common finding in one pulmonary insults such as infectious pneumo-
periphery of the lung [52–54]. However, in half to four fifths of cases [56, 57, 60, 61]. Irreg- nia, connective tissue disorders, and bone
many other cases, GGOs also may show a dif- ular linear opacities and traction bronchiectasis marrow transplantation. However, in some
fuse or random distribution (Fig. 7). A pattern also may be seen [56, 59, 60]. cases it may have no recognizable cause. The
Fig. 7.—72-year-old woman with desquamative interstitial pneumonia, slowly pro- Fig. 8.—26-year-old woman with nonspecific interstitial pneumonia, progressive
gressive dyspnea, and 40-pack-year history of smoking. High-resolution CT reveals dyspnea, and positive antinuclear antibodies. High-resolution CT of upper lobes
uniform ground-glass opacity. reveals subpleural areas of ground-glass opacity.
American Thoracic Society/European Respi- ally along the bronchovascular bundles but oc- sandblasters [79]. When found in association
ratory Society International Multidisciplinary casionally as randomly distributed interstitial with silica or other exposures, PAP typically
Consensus Classification Conference has nodules [73–75]. Irregular linear bands of fibro- will present with an acute onset of symptoms.
identified cryptogenic organizing pneumonia sis, traction bronchiectasis, and coarse cystic Leukemia and lymphoma also may predis-
(COP) as the preferred term for idiopathic spaces may develop in stage IV sarcoidosis. pose patients to PAP [80, 81]. PAP was fatal
BOOP [66]. COP is a rare inflammatory con- GGOs are among the least common presenta- in approximately one third of patients before
dition presenting with progressive dyspnea tions of sarcoidosis (Fig. 9). When GGOs do oc- the availability of therapy involving high-vol-
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and often with fever and constitutional symp- cur in patients with sarcoidosis, careful ume bronchoalveolar lavage; since the intro-
toms that are unresponsive to standard pneu- inspection of the CT image often will reveal a duction of this therapy, many patients can be
monia therapies. It is persistent and can lead fine stippled appearance to the GGO, as if it cured of the disorder and others may be
to serious illness if not treated with corticos- were composed of innumerable, tiny, 1- to 2- treated successfully with repeated episodes of
teroids, a therapy that in most cases will result mm, ill-defined nodules. Sarcoidosis, HP, and bronchoalveolar lavage [82].
in a complete cure of the disease. BOOP, re- RBILD are the causes of GGO most likely to Thin-section CT characteristically will
gardless of cause, most often will appear as give this fine stippled appearance. Rarely, sar- show GGOs in association with thickening of
multifocal alveolar opacities scattered coidosis may appear as multiple large ground- the interlobular septa of the secondary pulmo-
throughout the lungs [72]. Rarely, BOOP may glass masses. This pattern is known as alveolar nary lobules [83–85] (Fig. 10). This combina-
appear as ID-GGO. sarcoid. This appearance is virtually pathogno- tion of findings has been termed the “crazy
Sarcoidosis.—Sarcoidosis is an idiopathic monic of sarcoidosis. paving appearance” and, when present, is
granulomatous disorder with multisystemic quite suggestive of PAP. However, occasion-
ramifications including changes in the Other Diseases Appearing as ID-GGO ally PAP will present as ID-GGO.
meninges, bone, eyes, heart, and skin. Racial PAP.—Other disorders that present as ID- Bronchoalveolar carcinoma.—A form of
predilections include African American and GGO include PAP and BAC. PAP is a rare, id- well-differentiated pulmonary adenocarci-
Puerto Rican residents of the United States iopathic disorder of middle-aged adults. Ac- noma, BAC, has a wide variety of radio-
and West Indians in the United Kingdom. It cumulation of protein and lipid-rich material graphic appearances including solitary
characteristically presents in patients be- within the lung alveoli results in the subacute pulmonary nodules, focal alveolar opacities
tween the ages of 20 and 40 years but may be onset of slowly progressive and often inca- resembling pneumonia, ground-glass nod-
encountered at nearly any age. pacitating dyspnea [76–78]. This accumula- ules, diffuse alveolar consolidation, and ID-
There are a wide variety of CT manifesta- tion appears to be a result of an abnormality of GGOs. Most diffuse BACs will have a domi-
tions of sarcoidosis. Hilar and mediastinal ade- surfactant production, metabolism, or clear- nant mass, nodule, or area of consolidation
nopathy is present in the early and middle stages ance. Occasionally PAP may be associated with associated ID-GGO. Rarely, there will
of the disease. The interstitial lung disease most with exposure to a variety of inorganic dusts, be no such sentinel patch and only ID-GGOs
commonly appears as many small nodules, usu- most commonly silica, such as is seen in will be present [86].
Fig. 9.—46-year-old woman with sarcoidosis who presented with dyspnea and had Fig. 10.—53-year-old man with pulmonary alveolar proteinosis. Slowly progressive
restrictive pulmonary function tests. High-resolution CT image through carina high-resolution CT image through carina shows presence of ground-glass opacities
reveals ground-glass opacities composed of many faint centrilobular nodules widely with slight fine intralobular interstitial thickening. This combination of ground-glass
distributed throughout lungs. opacities and interstitial thickening has been termed “crazy paving.”
Patients with Acute Development of Pulmonary Edema most often is a result of ARDS but has a number
Dyspnea Pulmonary edema is a result of imbalances in of other causes.
In scenario four, the interstitial causes of the Starling forces, which govern the transport Cardiogenic pulmonary edema.—Left-
ID-GGO usually will have a prolonged clini- of fluids between the vascular and interstitial sided heart failure is by far the most common
cal presentation, and chest radiographs most spaces of the lung. During homeostasis, there is cause of hydrostatic edema and thus com-
often will be normal in appearance or show a near balance between these forces, and the monly is known as cardiogenic pulmonary
nonspecific interstitial abnormalities. The al- small net transfer of fluid into the interstitium is edema. On thin-section CT, the most common
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veolar causes of ID-GGO usually will present removed via the pulmonary lymphatics. How- manifestation of cardiogenic pulmonary
acutely and chest radiographs often will show ever, a disturbance of this equilibrium will lead edema is ID-GGO (Fig. 11). CT also may
diffuse alveolar consolidation. ID-GGO in to excessive transport of water and solutes into show thickening of the interlobular septa. The
this setting most often will be secondary to the interstitial space. If the process continues, GGOs associated with hydrostatic edema of-
one of the acute alveolar causes of ID-GGO: the interstitial lymphatics become overwhelmed ten will have a central, perihilar distribution
cardiogenic pulmonary edema, acute respira- and fluid overflows into the alveoli, leading to and be associated with enlarged pulmonary
tory distress syndrome (ARDS), other causes alveolar edema [87]. vessels and an enlarged heart.
of permeability edema, or DAH. Typically, pulmonary edema is subdivided Adult respiratory distress syndrome.—
into two major etiologic subcategories: hydro- ARDS is the most common cause of noncardio-
Acute Alveolar Diseases Appearing as ID-GGO static pulmonary edema and increased perme- genic pulmonary edema and is a common phys-
In our study of the causes of ID-GGO, acute ability pulmonary edema. In hydrostatic edema, iologic response to a wide variety of insults
alveolar diseases such as DAH, cardiogenic there is increased intravascular hydrostatic pres- including sepsis, aspiration of gastric contents,
edema, and noncardiogenic pulmonary edema sure, which results in a net force driving water overwhelming pneumonia, severe trauma, mul-
accounted for 19% (6/32) of pathology-proven and solutes into the interstitial and, subsequently, tiple fractures, major burns, pancreatitis, pro-
causes of ID-GGO [9]. Because of the need for alveolar spaces of the lung. Hydrostatic edema longed hypotension, disseminated intravascular
pathologic proof, pulmonary edema as a cause most often is a manifestation of left-sided heart coagulation, drug overdose, and thoracic sur-
of ID-GGO is probably underrepresented in this failure. Increased permeability edema usually is gery [88, 89].
series and pulmonary edema likely represents a result of disruption of the capillary epithelial CT scans of ARDS most often will show
the single most common cause of ID-GGO. membrane, which allows plasma proteins to pass bilateral GGO, pulmonary consolidation, or
Thus, an acute clinical presentation of respira- into the interstitial space. These proteins exert an a combination of both [90, 91]. ID-GGO is
tory symptoms in a patient with ID-GGO osmotic force drawing water into the interstitial most often a manifestation of the earlier ex-
should raise the possibility of hydrostatic and space, and if of sufficient volume, they spill into udative phase of disease [90, 91]. Pulmonary
capillary leak pulmonary edema and DAH. the alveolar spaces [87]. Permeability edema opacities often will be most severe in the
Fig. 11.—44-year-old man with cardiogenic edema and with acute onset of dyspnea Fig. 12.—60-year-old man with diffuse alveolar hemorrhage and with acute onset of
and history of mitral stenosis. High-resolution CT image through great vessels shows dyspnea and history of Wegener’s granulomatosis. High-resolution CT image through
geographic ground-glass opacity. right upper lobe bronchus reveals randomly distributed ground-glass opacities.
Clinical Scenarios and Differential Diagnoses of Patients with scenarios: patients who are immunocompro-
TABLE 2 mised, patients who are receiving bone marrow–
Isolated Diffuse Ground-Glass Opacity
suppressing medications, outpatients who have
Scenario Disease Category Differential Diagnoses
slowly progressive dyspnea, inpatients and out-
Immunosuppressed Opportunistic infections PCP, CMV, HSV, RSV, other viruses patients who have acutely developing dyspnea,
(HIV, transplant) and inpatients who are acutely ill. These clinical
Bone marrow suppression Opportunistic infections PCP, CMV, HSV, RSV, other viruses scenarios engender limited differential diagnoses
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