Dr. Koo and Dr. Yen are affiliated with the UC San
Diego Health System, San Diego, CA. This article is adapted from a
presentation delivered at the UC San Diego Post-Graduate Radiology
Course in October 2011.
High attenuation in the lungs is not
infrequently encountered on computed tomography (CT). Not all
significantly radiopaque lung findings are calcified. Iodine (a halogen)
as well as a variety of metals besides calcium cause high attenuation.
Pulmonary calcification may occur in two ways: dystrophic and
metastatic. The former denotes calcium deposition in damaged tissue
(caseation, necrosis, fibrosis) despite normocalcemia. Metastatic
calcification is defined later.
High attenuation is recognizable
on soft-tissue windows, but is easily missed if only lung windows are
assessed. The finding may be striking on maximum intensity projection
(MIP) images, if available. The literature offers assorted definitions
for high attenuation; for example, visually opaque as bone or > 200
HU.1,2 No single definition applies in every instance. In practice, however, these criteria may be useful in equivocal cases.
processed with high-spatial-frequency reconstruction algorithms for
lung analysis may cause the false appearance of high attenuation, such
as in tiny pulmonary nodules. This predisposes to the premature
conclusion of benignity. Therefore, we suggest that any suspicion of
high attenuation be confirmed on standard algorithm images.
in many cases the presence of high attenuation is ancillary and not
required for diagnosis, it can be helpful in the imaging interpretation
of some entities (eg, amiodarone). Mindful of the audience, we try to
cover the gamut of high attenuation specifically within the lungs on CT,
using intentional brevity and emphasizing features that lend themselves
to a diagnosis.
Airway and vascular processes
airway or vascular process is discernible on cross-sectional imaging,
whether purely by localization or by the presence of a tubular or
branching process. Airway processes may obstruct, causing any
combination of mucus plugging, bronchial dilation or bronchiectasis,
airway-centric opacities, atelectasis, consolidation, and air trapping.
Decreased perfusion due to hypoxic vasoconstriction or due to increased
pressures from air trapping is possible. In vascular processes,
decreased perfusion suggests oligemia or intrinsic vascular pathology.
respect to high attenuation alone, the presence of eccentric or
stippled calcifications within an airway-associated lesion should
trigger further investigation, as these patterns of calcification are
indeterminate for malignancy. On the other hand, popcorn calcification
is essentially diagnostic of a hamartoma and would preclude unnecessary
A calcified or ossified endobronchial lesion without an
associated soft-tissue component constitutes a broncholith, having
likely reached its location by erosion of a calcified lymph node through
an airway wall. The presence of calcified mediastinal/hilar lymph nodes
elsewhere may implicate sequela of histoplasmosis or tuberculosis.
Broncholithiasis does not have to be endobronchial. Its definition
includes calcified peribronchial lymph nodes that cause adjacent airway
distortion and/or obstruction.3 Less common causes of
broncholithiasis include aspiration of foreign bodies that either are
radiopaque or later calcify, and rarely endoluminal sequestration of
calcified bronchial cartilage.4
Ideally, distal airway
and airway-centric high-attenuating opacities are demonstrated in the
setting of oral contrast aspiration (Figure 1). Uniform high attenuation
makes infection unlikely. When confluent, the diagnosis becomes
challenging and relies more heavily on the sequence of events relative
to oral contrast administration as well as on history (eg, CNS
disorder). Ancillary findings of aspiration may include chemical
pneumonitis and secondary pneumonia.5 Aspiration of elemental mercury is considered in the appropriate setting.
asthmatics, moderate-to-severe central bronchiectasis affecting 3 or
more lobes, bronchial wall thickening, mucoid impaction, and
centrilobular lung nodules are suggestive of allergic bronchopulmonary
aspergillosis (ABPA) (Figure 2).6 The same features are less
useful in poorly controlled cystic fibrosis. High-attenuating mucus
relative to normal skeletal muscle adds specificity to the diagnosis in
asthmatics and may be the finding that elicits the diagnosis in cystic
fibrosis. The higher density is attributed to inspissation of mucus and
deposition of calcium salts and metals.7 Of note, persistent mucus plugging in general may calcify.
Extensive or diffuse tracheobronchial high attenuation (eg, warfarin therapy, relapsing polychondritis) will not be discussed.
of the pulmonary circulation, characterized by vascular wall
calcification, is primarily seen with pulmonary hypertension and
congenital heart disease, but is not typically required for the
diagnosis of either entity. Increased wall shear stress and high flow
associated with elevated mean pulmonary arterial pressures probably
contribute to its development.8
The majority of
entities causing vascular high attenuation in the lungs are embolic in
nature. Calcified thrombus is a known association of chronic
thromboembolic disease (Figure 3), but is not integral to the diagnosis.
Chronic thromboembolic disease is confirmed by identifying an
appropriate filling defect pattern in the pulmonary arteries (eg, webs,
bands, eccentric thrombus) with or without pulmonary hypertension,
collateral systemic supply, parenchymal scarring from prior infarction,
mosaic attenuation, and bronchial dilation.9 Occasionally, acute thromboembolic disease is detectable on unenhanced chest CT as high attenuating clot.10
rarely reported, predominantly intravascular calcifications have been
described in the setting of fat embolism and ARDS, thought to be related
to vascular injury and subsequent thrombosis.11
cement embolism, the pulmonary arterial filling defects are purely high
attenuating and tubular in configuration, occasionally straddling
bifurcation points (Figure 4). The presence of post-vertebroplasty
change with or without perivertebral venous leakage of acrylic cement is
confirmatory. The caliber of the perivertebral veins is such that the
pulmonary emboli are typically segmental or subsegmental in location.12
contacting circulating blood through accidental or intentional
administration, elemental mercury becomes spherical owing to interface
tension. This is unlike iodinated contrast, which readily intermixes
with blood. Mercury embolizes to dependent locations within lung due to
its higher density than water. The droplets may coalesce and become
tubular within vessels. The diagnosis is based on pure high-attenuating
material in a generally symmetric and bilateral vascular distribution,
arborized, if extensive, and supported by the presence of droplets in
the right side of the heart or in other vascular beds. If fortuitous,
images will show subcutaneous deposits in the injected extremity.13 History and clinical findings secure the diagnosis.
foreign body emboli (eg, glue from treatment of an arteriovenous
malformation) may be diagnosed by clinical history and sequence of
events. Central venous catheters occasionally break spontaneously and
migrate into the lungs. The shearing of catheters by introducing needles
is said to have been more common prior to the Seldinger technique.14
in pulmonary artery sarcomas may initially conjure the diagnosis of
calcified chronic pulmonary thromboembolic disease, but the imaging
appearances are dissimilar. The filling defects associated with sarcomas
tend to span the entire lumen of proximal pulmonary arteries, unusual
in chronic thromboembolic disease. Other suggestive features include
luminal expansion, tissue invasion, and heterogeneous contrast
enhancement. Finally, ossification in pulmonary artery sarcomas is more
peripheral and nodular or stippled compared to chronic thromboembolic
disease and is more often seen with osteo- or chondrosarcoma subtypes.15
Parenchymal processesSolitary pulmonary nodule
The workup of a solitary
pulmonary nodule has been well described in the literature, with
diagnosis/management depending on nodule characteristics, stability, and
risk factors for malignancy.16,17 With exceptions, diffuse,
central, lamellar, and popcorn type calcifications are indicative of
benign etiologies, while stippled and eccentric patterns are
indeterminate. The most common causes of solitary pulmonary nodules are
hamartomas, granulomas, and malignancy. As above, the diagnosis of a
hamartoma (or even multiple hamartomas) is made simple by the infrequent
occurrence of popcorn calcification.
and ossified metastases are uncommon, but should be entertained if the
calcification pattern is indeterminate or if certain primary
malignancies are known. Osteosarcoma and chondrosarcoma occur more
frequently. Less common are other sarcomas (eg, synovial sarcoma),
mucinous adenocarcinomas (eg, breast, colon, ovary), and thyroid
malignancies (eg, medullary carcinoma) (Figure 5). Lesions that newly
calcify may represent treated metastases in the appropriate setting (eg,
choriocarcinoma). Carney’s triad is rare and difficult to diagnose
prospectively. The triad includes benign pulmonary chondroma (commonly
calcified), gastrointestinal stromal tumor, and extra-adrenal
When considering calcified/ossified
metastatic disease, the differential may include nodular amyloid,
hyalinizing granulomas, and rheumatoid nodules (Figure 6). In practice,
these are difficult to differentiate on CT, having in common
well-marginated solitary or multiple pulmonary nodules/masses that can
cavitate and calcify. In addition, imaging findings may precede or occur
in the absence of clinical findings. For amyloid, chronic inflammatory
diseases and multiple myeloma are predisposing conditions and may raise
the possibility.18,19 Thin-walled air cysts also help distinguish amyloid but may be seen with metastases from the aforementioned primaries.20-22
Although Histoplasma and Mycobacterium are possible causative agents of
hyalinizing granulomas, calcified lymph nodes have not been described
in association.12,23 The bias of necrobiotic lung nodules for
peripheral or pleural locations and their ascribed waxing and waning
course are of limited diagnostic value, even with known rheumatoid
arthritis and subcutaneous necrobiotic nodules.24
attenuating lung nodules on the order of 2 to 5 mm are frequently
labeled calcified granulomas. Doing so is not always accurate. It is
appropriate in the presence of calcified mediastinal/hilar lymph nodes,
which typically implicate disseminated histoplasmosis, less commonly
miliary tuberculosis, as the culprit. Splenic and/or liver
calcifications are more suggestive of the former.12,25
the absence of calcified lymph nodes and splenic or liver
calcifications, the late sequelae of a viral pneumonia, particularly
varicella (chickenpox), is entertained. The calcified lung nodules are
said to be on the order of 1-2 mm.25
calcifications occur in other infectious settings, but are less integral
to the diagnosis. Examples include apical tuberculous fibronodular
changes, symmetric bilateral ground glass opacities in pneumocystis
jiroveci pneumonia, cavitary filling defects of aspergillomas, hepatic
and pulmonary hydatid cysts, and pleuroparenchymal changes in
paragonimiasis, all of which may calcify, rarely in some cases.1,2,8,25,26
Keep in mind that while calcification is often taken to mean healing, the underlying infection could still be active.1
evidence of chronic pulmonary venous hypertension, a distinctively
lower-lung-predominant distribution of high-attenuating nodules
anywhere from 1-8 mm in size) is highly suggestive of diffuse pulmonary
ossification, nodular type (Figure 7).
The nodules may be misinterpreted as calcified granulomas. The classic
example of diffuse pulmonary ossification is chronic mitral stenosis. In
the case of rheumatic heart disease, findings often comprise a
calcified mitral valve, an
enlarged left atrium with or without atrial wall calcifications, and
Nodular ossification also occurs in the setting of
pulmonary fibrosis and may be similarly misconstrued as calcified
granulomatous disease. Its occurrence only in areas of fibrosis aids in
the diagnosis. Dendriform ossification, however, is more commonly
described in this setting (Figure 8). This second type of diffuse
pulmonary ossification reflects linear/branching high attenuation along
the interstitium and is more reminiscent of bony trabeculation. Chronic
or repeated lung injury is thought to be the substrate for diffuse
pulmonary ossification. In fact, ossification may occur in a number of
entities (eg, amyloid, tuberculosis). Suffice it to say that any
longstanding calcification is transformable to bone.8,27-30
differential for bilateral centrilobular ground glass lung opacities is
considerably broad. If high attenuation is felt to be associated,
however, then recurrent alveolar hemorrhage resulting in deposition of
iron and variably of calcium is possible, whether from idiopathic or
secondary pulmonary hemosiderosis (Figure 9). Support for a secondary
cause may come from evidence of increased pulmonary capillary/venous
pressures, collagen vascular disease, or hemorrhagic disease.
Hemosiderosis from mitral stenosis tends to distribute in the lower
Unilateral or bilateral 3- to 10-mm
fluffy centrilobular lung nodules with variably perceptible high
attenuation are a common manifestation of metastatic calcification
(Figure 10) and may resemble hemosiderosis. These nodules can densely
calcify or densely consolidate. The absence of upper-lung involvement
does not exclude the diagnosis despite a predilection for more alkaline
environments. Development requires a derangement in calcium or phosphate
metabolism leading to hypercalcemia and subsequent calcium deposition
in normal tissues. Knowledge of a predisposing benign or malignant
condition aids in the diagnosis (eg, chronic renal failure, multiple
myeloma). Vascular calcifications in the chest wall and uptake on bone
scan are also supportive.12,32,33
Bilateral mid- to
upper-lung predominant < 5 mm perilymphatic nodules with or without
mass-like conglomeration in both upper lungs elicits a differential of
inorganic dust exposure and sarcoidosis (Figure 11). Added calcification
or ossification contributes little to the diagnosis, although it is
exceedingly rare in sarcoid lung nodules.25 Silicosis and
coal workers’ pneumoconiosis are largely indistinguishable despite
slight differences in nodule margins and calcification pattern.
Berylliosis and pulmonary sarcoidosis mimic one another on imaging and
pathology and have more of a tendency for interstitial thickening.
Unilateral mass-like consolidation should prompt consideration for
malignancy.34 Egg-shell calcifications make berylliosis unlikely.
is an acute form of silicosis. The alveolar proteinaceous filling that
is characteristic of this process may manifest with nonspecific
consolidation and nodular or patchy ground glass, but the diagnosis is
perhaps most suggested by crazy paving associated with calcification in
areas of consolidation.33
Baritosis (barium), stannosis (tin), and siderosis (iron) are radiopaque dust exposures that cause small lung nodules.1,12
These are very rare conditions and difficult to diagnose prospectively
without a contributory history. Fibrotic changes in the lungs argue
against pure radiopaque dust exposure, unlike in inorganic dusts,
combined exposures (eg, silicosiderosis), and sarcoid.34
parenchymal (or alveolar septal) amyloidosis is in the differential of
perilymphatic nodularity but has no zonal predilection and is not
associated with bilateral mass-like consolidation.12,35 As with nodular amyloidosis, thin-walled air cysts would support the diagnosis.36
whether inhalational or intravenous, is in the differential of
bilateral mass-like consolidation but has no zonal predilection. The
diagnosis may be considered if the consolidation is seen with a
background of ground glass, diffuse centrilobular nodules (≤ 4 mm), or
profuse micronodules (< 1 mm), all without zonal predominance. High
attenuation, if perceptible within the masses, can be diffuse. The
addition of lower-lung-predominant panlobular emphysma suggests
methylphenidate (Ritalin) abuse associated with intravenous talcosis.37
Without bilateral conglomerate masses, the diagnosis of talcosis
becomes more difficult but may be considered for diffuse bilateral small
centrilobular or tree-in-bud lung nodules.38,39
inconsistently seen, a crazy-paving pattern predominating in the mid-
to lower-lung zones with extensive high-attenuating “interstitial”
opacities suggests pulmonary alveolar microlithiasis. A genetic mutation
in the lung’s phosphate transporter results in accumulation of alveolar
calcium-phosphate microliths that tend to align along the septa, giving
the illusion of interlobular septal thickening. Unresolved microliths
create the ground glass appearance. Larger concretions may produce a
sandstorm appearance of calcified micronodules, and confluence leads to
diffusely high-attenuating consolidation, often posteriorly and along
heart borders. Subpleural cysts and apical bullae may be seen.40-42
and iodinated oil embolism are in the differential of single or
multiple high-attenuating areas of consolidation without associated lung
nodules (Figure 12). Amiodarone is typically peripheral. The iodine
moieties of the antiarrhythmic drug are responsible for the high
attenuation, ranging from 82-174 HU according to one series. The
presence of interstitial opacities or fibrosis would favor amiodarone,
as would a high-attenuating liver or spleen (90-110 HU). Amiodarone
toxicity versus simple lung accumulation cannot be differentiated on
imaging alone.1,43 The diagnosis of iodinated oil embolism relies on knowledge of prior lymphangiography or transcatheter oil chemoembolization.12 In either case, history is integral to the diagnosis.
material or staple lines are linear or curvilinear. They skirt the
outer margins of the lung and may invaginate. Volume loss is invariably
present due to partial lung resection. Fine detail of the material is
not always appreciable using different windowing. Nonrecognition may
cause confusion with one or more of the above entities, particularly if
lung opacities are superimposed (eg, in the postoperative setting). On
the other hand, these regions should be closely monitored for tumor
recurrence in the appropriate setting.44
certain metallic opacities cause significant streak artifact and may
require scout tomography and clinical history for elucidation (eg,
bullets, fiducial markers).
attenuation in the lungs is more than calcification. Acknowledging this
adds complexity to its interpretation. At times, its presence is a
welcome clue to otherwise nonspecific lung opacities. In many cases,
however, the diagnosis will remain uncertain. Nevertheless, we hope this
article leads to more confident interpretation.
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