Localized Bone Lesions

75

Burgener, Kormano, Pudas, Differential Diagnosis in Conventional Radiology (ISBN 9783136561034), © 2007 Georg Thieme Verlag KG

5 Localized Bone Lesions

Conventional radiography remains the primary imagingmodality for the evaluation of skeletal lesions. The combina-tion of conventional radiography, which has a high speci-ficity but only an intermediate sensitivity, with radionuclidebone scanning, which has a high sensitivity but only a lowspecificity is still the most effective method for detectingand diagnosing bone lesions and differentiating betweenbenign and malignant conditions. Conventional radiography,is, however, limited in delineating the intramedullary extentof a bone lesion and even more so in demonstrating soft-tissue involvement. Although magnetic resonance imagingfrequently contributes to the characterization of a bone le-sion, its greatest value lies in the ability to accurately assessthe intramedullary and extraosseous extent of a skeletal le-sion.

A solitary bone lesion is often a tumor or a tumor-like ab-normality, but congenital, infectious, ischemic and traumaticdisorders can present in similar fashion. Differentiation be-tween a benign or malignant bone lesion is not alwayspossible. Signs of an aggressive or malignant osseous lesioninclude rapid growth, large size, poor demarcation, corticalviolation, interrupted periosteal reaction and soft tissue ex-tension. Signs of a nonaggressive or benign osseous lesioninclude slow growth, small size, sharp margination, corticalexpansion without cortical violation, solid periosteal reac-tion and no soft tissue extension. However these radiologicfeatures are not infallible and many exceptions occur indi-cating the need for histologic confirmation in the appro-priate setting.

In osteolytic lesions a geographic, moth-eaten and per-meative pattern of bone destruction are commonly dis-cerned. A geographic lesion (Figs. 5.1 and 5.2) has a well-de-fined margin separating it clearly from the surrounding nor-mal bone. The zone of transition of normal to abnormalbone is short and a sclerotic border of various thickness maysurround the lesion. Geographic lesions are usually benign,especially when they are marginated by a sclerotic rim.Multiple myeloma and metastases, however, frequently pre-sent as geographic lesions without sclerotic borders (Table5.1).

A moth-eaten lesion (Fig. 5.3) is a poorly demarcated focusof bone destruction with a long zone of transition from nor-mal to abnormal bone indicating its aggressive nature andrapid growth potential. Malignant bone tumors, osteomyeli-tis and eosinophilic granulomas frequently present with thispattern of bone destruction (Table 5.2).

A permeative lesion (Fig. 5.4) represents the most aggres-sive bone destruction pattern with rapid growth. The lesionmerges imperceptibly with the normal bone. Highly malig-nant tumors infiltrating the bone marrow such as round cellsarcomas (e.g. Ewing’s sarcomas and lymphomas) typicallyare associated with this pattern of bone destruction. It is,however, also found in acute osteomyelitis and rapidlydeveloping osteoporosis such as reflex sympathetic dystro-phy. Infiltration of the cortex may also be associated withthese conditions, presenting as cortical striation or tunnel-ing.

Fig. 5.1 Geographic lesion.A well-demarcated lesion withsclerotic border is seen in thedistal femur (nonossifyingfibroma).

Fig. 5.2 Geographic lesions. Multiple well-demarcated (punch-ed-out) purely lytic lesions are seen in the vault of the cranium(multiple myeloma).

Fig. 5.3 Moth-eaten lesion.A poorly demarcated osteo-lytic lesion (arrows) is seen inthe distal femur (non-Hodgkin lymphoma).

76


The cortex represents a barrier to nonaggressive lesions.Benign medullary processes may leave the endosteal surfaceintact or produce endosteal scalloping (Fig. 5.5). The latterfinding is, however, also frequently seen with multiple my-eloma and metastases. Progressive endosteal erosion as-sociated with solid new periosteal bone deposition createsan expanded osseous contour indicative of a nonaggressivebenign skeletal lesion. Aggressive skeletal lesions may pene-trate the entire thickness of the cortex (Fig. 5.6) and some-times induce a variety of interrupted periosteal reactions in-cluding onion-peel, sunburst and hair-on-end patterns or a

Table 5.1 Solitary well defined osteolytic lesion

Subchondral cyst (associated with arthritis, osteonecrosis, ortrauma)

Gout (intraosseous tophus)

Amyloidosis

Intraosseous ganglion

Simple (unicameral) bone cyst

Aneurysmal bone cyst

Epidermoid inclusion cyst

Glomus tumor

Intraosseous lipoma

Enchondroma

Chondroblastoma

Chondromyxoid fibroma

Nonossifying fibroma

Desmoplastic fibroma

Osteoblastoma

Giant cell tumor

Fibrosarcoma

Clear cell chondrosarcoma

Angiosarcoma

Plasmacytoma/multiple myeloma

Metastasis

Eosinophilic granuloma

Brown tumor (hyperparathyroidism)

Hemophilic pseudotumor

Osteonecrosis (bone infarct)

Brodie’s abscess/cystic osteomyelitis

Fibrous dysplasia

Sarcoidosis

Table 5.2 Solitary poorly defined osteolyticlesion

Hemangioma

Chondroblastoma

Osteoblastoma

Giant cell tumor

Fibrosarcoma

Malignant fibrous histiocytoma

Chondrosarcoma

Osteosarcoma

Ewing’s sarcoma

Angiosarcoma

Multiple myeloma

Metastasis

Lymphoma

Langerhans cell histiocytosis (eosinophilic granuloma)



Osteomyelitis

Brodie’s abscess

Sarcoidosis

Fig. 5.4 Permeative lesion.A poorly defined osteolyticlesion merging imperceptiblywith the normal bone is seenin the proximal femur. Notealso the beginning laminatedperiosteal reaction in thesubtrochanteric area (Ewingsarcoma).

Fig. 5.5 Endosteal scalloping.Sharply demarcated erosions of theinner cortex of the radius and ulnacaused by multiple osteolytic lesionsis seen (multiple myeloma).

Bone

77


Table 5.3 Bone lesions with calcification

Intraosseous lipoma

Osteochondroma

Enchondroma

Periosteal (juxtacortical) chondroma

Bizarre parosteal osteochondromatous proliferation (BPOP)

Chondroblastoma

Dysplasia epiphysealis hemimelica (Trevor’s disease)

Fibrocartilagenous mesenchymoma


Osteoid osteoma (nidus)

Osteoblastoma (nidus)

Ossifying fibroma

Gnathic tumors (see chapter 11)

Chordoma

Chondrosarcoma (all variants)

Metastasis (especially thyroid carcinoma)



Intraosseous hematoma

Osteogenesis imperfecta (popcorn calcifications in enlargedepimetaphyses)

Codman’s triangle. They are most commonly associated withosteosarcoma, Ewing’s sarcoma, and osteomyelitis and arediscussed in greater detail in chapter 3.

The matrix of a skeletal lesion may be inhomogeneous be-cause it contains areas of calcification or ossification. Calcifi-cations appear as ring-like, flocculent or fleck-like radio-dense areas (Figs. 5.7 and 5.8). Intramedullary matrix calcifi-cation is primarily associated with cartilaginous tumors andbone infarcts (Table 5.3). Foci of intramedullary ossificationsare more homogeneous and often ivory-like and are mostoften caused by bone islands, osteoblastic metastases andprimary bone forming neoplasms (Fig. 5.9). They are dis-cussed in detail in chapter 2.

Fig. 5.6 Corticalpenetration. A poorlydefined, mixed osteo-lytic and osteoblasticlesion is seen in thedistal femur penetrat-ing through the me-dial cortex. The lateralcortex is expandedand thinned but stillintact (osteosarcoma).

Fig. 5.7 Matrix calcifica-tion. A flocculent, ring-likecluster of calcification is seenin the distal femur (enchon-droma).

Fig. 5.8 Matrix calcifica-tion. An irregular, shell-likecalcification is seen in the dis-tal femur (bone infarct).

Fig. 5.9 Intramedul-lary ossification. Anirregular, ivory-likearea of sclerosis isseen in the proximalhumerus (enostosis orgiant bone island).


78


Septation of the matrix represents another mechanism ofnew bone formation evoked by a neoplasm (Fig. 5.10). Inother instances intratumoral septations represent the rem-nants of the original bone matrix largely destroyed by theneoplasm (Fig. 5.11). Septation is associated with bothbenign and malignant lesions. Delicate thin trabeculae typi-cally are found in giant cell tumors and aneurysmal bonecysts, lobulated trabeculae in nonossifying fibromas, spicu-lated or radiating trabeculae in hemangiomas and irregularcoarse trabecula in a variety of benign and malignant lesions,often of fibrous connective tissue origin (Table 5.4). A uni-form hazy increase in radiodensity in an osteolytic lesion istermed ground glass appearance. It is most characteristic forfibrous dysplasia (Fig. 5.12), but is occasionally also found insimple (unicameral) bone cysts in the adult. The demonstra-tion of a sequestrum (Fig. 5.13) representing a segment of

Table 5.4 Osteolytic lesions with trabeculation/septation



Intraosseous lipoma

Hemangioma



Ossifying fibroma

Giant cell tumor

Gnathic tumors (see chapter 11)

Adamantinoma

Ameloblastoma

Fibrosarcoma


Osteosarcoma, teleangiectatic


Metastasis (e.g. blowout-metastases from kidney, thyroid orlung)



Fibrous dysplasia

Sarcoidosis

Fig. 5.10 Septation. A lyticlesion with extensive deli-cate trabeculation inducedby the tumor is seen in theiliac wing. Note also the lo-calized cortical violation(arrow) in the superolateralaspect of the lesion(aneurysmal bone cyst).

Fig. 5.11 Septation. A large expansile lytic lesion with remainingremnants of the original bone matrix producing a septated appear-ance, is seen in the ilium (plasmacytoma).

Fig. 5.12 Ground glass appearance . Aslightly expansile osteolytic lesion with ahazy increase in density is seen in theproximal tibia (fibrous dysplasia).

Fig. 5.13 Bone sequestrum. A lytic le-sion containing a small scleroticsequestrum in its center is surroundedby dense sclerosis and cortical thicken-ing in the tibia (chronic osteomyelitis).A healed fibula fracture is incidentallyalso seen.

Bone

79


Table 5.5 Osteolytic lesions containing asequestrum or bone fragment

Simple (unicameral) bone cyst with pathologic fracture (fallenfragment sign)

Fibrosarcoma (sequestered bone fragment)

Metastasis (sequestered bone fragment)

Bone lesion with pathologic fracture (fracture fragment)

Eosinophilic granuloma (sequestrum)

Comminuted fracture (intramedullary displaced cortical frag-ment)

Osteomyelitis (sequestrum)

Brodie’s abscess (sequestrum)

Infected pin tract (ring sequestrum)

Button sequestrum in skull (eosinophilic granuloma,metastases, epidermoid, osteoblastoma, osteomyelitis, radia-tion necrosis, bone flap undergoing avascular necrosis, burrhole and normal variants)

dense necrotic bone is indicative of chronic osteomyelitis(Table 5.5).

Bone expansion can be associated with both benign andmalignant lesions. In a slowly growing tumor the bone ero-sion on the inner cortex is compensated by bone appositionon the outer cortex (Fig. 5.14). In this instance the cortex re-mains intact at all times, but the thickness of this new corti-cal shell may be different when compared to the originalcortex. The interface between normal and expanded cortexmay be filled in with dense bone and often is referred to asbuttressing (Fig. 5.15). It is found, among others, with eosino-philic granulomas, aneurysmal bone cysts and osteoblas-tomas. In rapidly growing tumors the new bone formationcannot keep up with the bone breakdown resulting in corti-cal violation or frank destruction (Fig. 5.16) (Tables 5.6 and5.7).

Table 5.6 Expansile osteolytic lesion with intactcortex


Aneurysmal bone cyst (eccentric)

Enchondroma

Chondromyxoid fibroma (eccentric)

Nonossifying fibroma (eccentric)


Osteoblastoma

Giant cell tumor (eccentric)

Fibrosarcoma

Chondrosarcoma

Eosinophilic granuloma



Healing/healed fracture

Osteomyelitis (e.g. spina ventosa [phalanges or metacarpals]in tuberculosis)

Fibrous dysplasia

Fig. 5.14 Expansile lesion with in-tact cortex. An expansile, multilocu-lated lesion with intact, thinned orthickened cortex is seen in the distalhumerus (simple [unicameral] bonecyst).

Fig. 5.15 Buttressing. Local-ized cortical thickening (ar-rows) is seen in the proximalfibula at the interface be-tween normal cortex and ex-panded cortex of the osteo-lytic lesion (aneurysmal bonecyst).

Fig. 5.16 Cortical destruc-tion. An eccentric, expansile,osteolytic lesion in the distalfemur metaphysis andepiphyses broke through thecortex with only a few corti-cal remnants remaining (giantcell tumor).


80


Table 5.7 Expansile osteolytic lesion withcortical violation

Aneurysmal bone cyst (eccentric)

Epidermoid inclusion cyst

Glomus tumor

Hemangioma (skull)

Chondromyxoid fibroma (eccentric)


Osteoblastoma

Giant cell tumor (eccentric)

Fibrosarcoma


Chondrosarcoma

Osteosarcoma

Angiosarcoma


Metastases (from kidney, thyroid, lung)


The location of a solitary lesion within a bone provides animportant clue to the correct diagnosis. In tubular bones theepiphysis is a common location for chondroblastomas, clearcell chondrosarcomas, metastases, lipomas, subchondralcysts, intraosseous ganglia and Brodie’s abscesses. Giant celltumors originate in the metaphysis, but quickly penetratethe closed growth plate and extend into the subchondralbone. Osteoid osteomas (intra-articular presentation), en-chondromas and eosinophilic granulomas occasionally arealso found in the epiphyses, but the diametaphysis is a morecharacteristic location for these tumors (Table 5.8). Lesionscommonly located in the epiphyses are also found about thejoints of flat bones, patella and carpal and tarsal bones.

Typical metaphyseal lesions include nonossifying fibromawhich characteristically develops a short distance from thegrowth plate, chondromyxoid fibroma which abuts thegrowth plate, simple (unicameral) bone cyst, aneurysmalbone cyst, osteochondroma, Brodie’s abscess, mesenchymalsarcomas such as osteosarcoma and chondrosarcoma andmetastases. Common diaphyseal lesions include round celltumors (e.g. Ewing’s sarcoma and lymphoma), metastases,nonossifying fibromas, simple (unicameral) bone cysts inadults, enchondromas, osteoid osteomas, osteoblastomas,and fibrous dysplasia.

The diagnosis of a tubular bone lesion is also facilitated bythe identification of its center with regard to the medullarycanal and cortex. Typical central lesions include simple (uni-cameral) bone cysts, enchondromas, fibrous dysplasia andbone infarcts. Eccentric lesions include aneurysmal bonecysts, giant cell tumors and chondromyxoid fibromas. Typi-cal cortical lesions are nonossifying fibromas and osteoidosteomas (Fig. 5.17). Surface lesions arise from the outer sur-face of the cortex (e.g. surface high-grade osteosarcoma).Juxtacortical lesions (Figs. 5.18 and 5.19) can be divided intothose originating from the deep layer of the periosteum (pe-riosteal lesions) and those derived from the outer layer of theperiosteum and growing in an exophytic pattern (parosteallesions). Typical examples of juxtacortical lesions includethe periosteal osteosarcoma and parosteal osteosarcoma(Table 5.9).

Bone

Table 5.8 Common location of tubular bonelesions

Epiphyses

Subchondral cyst (associated with arthritis, osteonecrosis ortrauma)


Amyloidosis

Intraosseous ganglion

Intraosseous lipoma

Chondroblastoma

Dysplasia epiphysealis hemimelica (Trevor’s disease)

Giant cell tumor (originates in metaphysis)

Clear cell chondrosarcoma

Metastasis

Brodie’s abscess

Metaphyses



Osteochondroma


Periosteal desmoid



Fibrosarcoma


Chondrosarcoma

Osteosarcoma

Metastasis

Osteomyelitis

Brodie’s abscess

Fibrous dysplasia

Diametaphysis

Simple (unicameral) bone cyst (in adults)

Intraosseous lipoma

Enchondroma

Periosteal chondroma


Bone island

Osteoid osteoma

Osteoblastoma

Adamantinoma (especially anterior tibia)

Fibrosarcoma


Ewing’s sarcoma

Angiosarcoma

Multiple myeloma

Metastasis

Lymphoma

Langerhans cell histiocytosis (eosinophilic granuloma)




Osteomyelitis

Fibrous dysplasia

Osteofibrous dysplasia (especially anterior tibia)

442


Table 17.2 Hilar and/or Mediastinal Lymph Node Enlargement

Disease Radiographic Findings Comments

Neoplastic diseases(malignant or benign)

Bronchogenic carci-noma (Fig. 17.11)

Unilateral hilar node enlargement involving bron-chopulmonary and tracheobronchial nodes, insome cases paratracheal and posterior mediastinalnodes.

Influence of cell type:1 A hilar mass as the sole roentgenographic ab-

normality is characteristic of an undifferen-tiated small-cell carcinoma;

2 Generalized mediastinal widening almost cer-tainly indicates spread from an undifferentiatedcarcinoma;

3 Hilar or mediastinal lymph node enlargement israre in alveolar cell (bronchiolar) carcinoma.

Hodgkin’s disease(Fig. 17.12)

Bilateral but asymmetric enlargement, especially ofparatracheal and tracheobronchial nodes,frequently also anterior mediastinal and retroster-nal nodes. Bronchopulmonary nodes are lessfrequently enlarged than the more central ones.Unilateral involvement is very rare.

Mediastinal lymph node enlargement is seen onthe initial chest roentgenogram in approximately50 % of patients. May be associated with pulmo-nary involvement or pleural effusion in advancedcases.

Non-Hodgkin’s lym-phoma

Bilateral, asymmetric node enlargement similar toHodgkin’s disease.

May occasionally present as parenchymal con-solidation without associated lymph node enlarge-ment.

Leukemia Usually symmetric enlargement of mediastinal andbronchopulmonary nodes.

Occurs in 25 % of patients, more commonly in lym-phocytic than in myelocytic leukemia. Pleural effu-sion and parenchymal involvement may be as-sociated.

Fig. 17.11 Small cell carcinoma with mediastinal lymph nodemetastases and lymphangitis carcinomatosa. Enlarged right tra-cheobronchial lymph nodes (asterisk) and subtle obliteration ofthe notch between aorta and main pulmonary artery by metastaticlymph nodes (arrow).

Fig. 17.12 Hodgkin’s disease. Enlarged anterior mediastinal andhilar lymph nodes. Intrapulmonary mass lesion in the left lung.

Fig. 17.13 a−d Bronchopulmonary amyloidosis. a, b Hilar and �azygos nodes are enlarged, with a pattern similar to sarcoidosis.Even small pulmonary densities occur, c, d The same patient, 6years later. Unlike sarcoidosis, the hilar and mediastinal lymphnodes continually grow. Miliary parenchymal changes have also in-creased.

Chest

443


Table 17.2 (Cont.) Hilar and/or Mediastinal Lymph Node Enlargement


Immunoblastic lymph-adenopathy(a hyperimmune dis-order of B lympho-cytes)

Bilateral, asymmetric node enlargement similar toHodgkin’s disease.

Lungs are occasionally affected in a pattern similarto Hodgkin’s disease.

Heavy-chain disease(a plasma cell dyscrasia)

Symmetric enlargement of mediastinal lymphnodes.

Hepatosplenomegaly is common, lung involvementrare.

Bronchopulmonaryamyloidosis (a plasmacell dyscrasia)(Fig. 17.13)

Symmetric hilar and mediastinal lymph node en-largement. Enlarged nodes may be densely cal-cified.

Sometimes associated with diffuse pulmonary in-volvement.

(continues on page 444)

a

c

b

d

17 Mediastinal or Hilar Enlargement

444


Table 17.2 (Cont.) Hilar and/or Mediastinal Lymph Node Enlargement


Lymph nodemetastases (Fig. 17.14)

Unilateral or bilateral enlargement of either hilar ormediastinal nodes or both.

May be associated with lymphangitic changes inthe lungs (see Table 17.3).

Post-transplantationlymphoproliferativedisorder (PTLD)

Hilar and mediastinal lymph node enlargementoften associated with pulmonary nodules measur-ing up to 5 cm in diameter. Rarely pleural and/orpericardial effusion/thickening is also evident.

Lymphocyte proliferation developing 1 month to1 year after transplant. Histologic range frombenign hyperplastic proliferation to malignant lym-phoma. Related to Epstein-Barr virus-infectedB-cells.

Castleman’s disease(giant lymph nodehyperplasia)

Hilar or mediastinal nodes or both.Large circumscribed mediastinal mass is the mostcommon presentation.

This rare benign condition may be associated withfever, anemia and gammaglobulinemia. Two typescan be differentiated.Type 1: the hyaline vascular type (90 %), almost al-ways local, with no systemic symptoms;Type 2 the plasma-cell type, which may be multi-centric and associated with systemic symptoms.

Bacterial and myco-plasma infections

Primary tuberculosis(Fig. 17.15)

Mostly unilateral hilar (60 %) or hilar and paratra-cheal (40 %) lymph node enlargement. Bilateralnode enlargement is a rare presentation.

Hilar node enlargement differentiates primaryfrom secondary (reunification) tuberculosis. In thelatter, there is no observable lymphadenopathy.

Tularemia (Francisellatularensis)

Unilateral hilar node enlargement with characteris-tically oval pneumonic consolidations and pleuraleffusion.

Ipsilateral hilar node enlargement occurs in 25−50 % of tularemic pneumonias. Is a potentialbioterrorism agent.

Pertussis (whoopingcough)

Unilateral hilar node enlargement. Often associated with ipsilateral segmental pneu-monia and atelectasis.

Anthrax (Bacillus an-thracis)

Symmetric enlargement of all lymph nodes orgeneralized mediastinal widening.

Often associated with pleural effusion, rarely withpulmonary hemorrhages. Has been used as abioterrorism weapon

Plague pneumonia(caused by Yersiniapestis)

Symmetric hilar and paratracheal node enlarge-ment.

Nonsegmental homogeneous consolidations mayoccur in lungs mimicking alveolar edema. May beused as a bioterrorism weapon.

Mycoplasma pneu-moniae

Unilateral or bilateral hilar lymph node enlarge-ment associated with segmental pneumonia, pre-dominantly in lower lobes.

Most common in children. Together withparenchymal disease.

Viral, rickettsial infec-tions

Unilateral or bilateral hilar node enlargement.

Rubeola Bilateral hilar node enlargement may be associatedwith diffuse interstitial pneumonia.

If pneumonia in rubeola is segmental, it is due tosecondary bacterial infection.

Echovirus pneumonia Bilateral hilar node enlargement and associated in-crease of bronchovascular markings.

Respiratory infections occur predominantly ininfants.

Varicella pneumonia Bilateral hilar node enlargement associated withpatchy, diffuse air-space consolidation.

Pulmonary consolidation may mask hilar node re-action. Mainly occurs in adults with varicella.

Psittacosis(ornithosis)

Unilateral or bilateral hilar node enlargement as-sociated with variable radiographic presentationsof pneumonia.

Roentgenographic resolution of pneumonia isslow.

Epstein-Barr(infectious mononu-cleosis) (Fig. 17.16)

Bilateral, symmetric, predominantly hilar lymphnode enlargement.

Splenomegaly. Roentgenographic changes in thelungs are rare.

AIDS (acquired im-munodeficiency syn-drome) (Figs. 17.15and 17.17)

Bilateral lymph node enlargement. Lymphadenopathy is common in AIDS patients(up to 80 %); most often related to chest infec-tions, less commonly caused by AIDS-associatedlymphoma.


Chest

445


Fig. 17.14 Metastatic melanoma with lymphangitis carcinoma-tosa and bilateral hilar lymph node enlargement.

Fig. 17.15 Primary tuberculosis in a patient with AIDS. Righthilar lymph node enlargement.

Fig. 17.16 Infectious mononucleosis. Enlargement of bron-chopulmonary nodes and the azygos node—a pattern characteris-tic of sarcoidosis.

Fig. 17.17 Benign mediastinal lymphadenopathy in AIDS. Lymphnodes on the right side are predominantly enlarged, both in thehilar and the upper mediastinal regions.

17 Mediastinal or Hilar Enlargement

642


Table 27.1 (Cont.) Differential Diagnosis of Abdominal Calcifications

Site and Pattern ofCalcification

Common Causes Radiographic Findings and Comments

E. Focal parenchymalcalcification of thekidney

Tuberculosis(Fig. 27.19)

May appear as a single nodular or irregular calcification (seeabove).

Adenocarcinoma(Fig. 27.20)

About 10 % of renal adenocarcinomas calcify. If a renal masscontains calcium in a nonperipheral location, it is very likelymalignant. Even a curvilinear cystic peripheral calcificationof a mass does not exclude malignancy.

Nephroblastoma(Wilms’ tumor)(Fig. 27.21)

Cystic, streaky, or amorphous calcification of the tumor isuncommon, but may occur in older children and adultswith nephroblastoma.

Xanthogranulomatous pyelonephritis(Fig. 27.22)

Simulates carcinoma, but inflammatory masses may bemultiple and diffusely calcified. A large pelvic calculus ispresent in the majority of cases, causing pelvocaliceal ob-struction.


Fig. 27.19 Renal tuberculosis of the left kidney with focal calcifi-cation. The calcification appears cystic but internal calcificationsare also present.

Fig. 27.20 Adenocarcinoma of the left kidney with calcification—a thick-walled, somewhat cystic calcification with irregular internalcalcific deposits.

Fig. 27.21 A large Wilms’ tumor in the right kidney of a three-year-old boy, seen as an enlarged, nonexcreting kidney containingtiny flecks of calcification.

Fig. 27.22 Xanthogranulomatous pyelonephritis. Scout filmshows pelvic stones and parenchymal calcifications.

Abdomen

643





F. Cystic (curvilinear)renal calcification

Simple renal cyst(Fig. 27.23)

A thin curvilinear calcification can be demonstrated in 3 %.

Adenocarcinoma(Fig. 27.24)

20 % of thin curvilinear calcifications are due to a calcifiedfibrous pseudocapsule of a renal adenocarcinoma.

Polycystic or multicystic disease(Fig. 27.25)

Curvilinear calcifications similar to that of a simple cyst mayoccur.

Echinococcal cyst The majority are calcified. Complete circumferential ring ofcalcium is characteristic but not always present.

Organized perirenal hematoma(Fig. 27.26)Old perirenal abscess

May appear as large cystlike calcification.

Nephroblastoma (Wilms’ tumor) May appear cystic due to peripheral calcification.


Fig. 27.23 Two calcified simple renal cysts in the right kidney(arrows) are seen.

Fig. 27.24 Adenocarcinoma of the kidney. Curvilinear calcifica-tion (with possible internal calcifications) in a large tumor of thelower pole of the right kidney.

Fig. 27.25 Polycystic kidneys with renal failure and calcificationof the cyst walls bilaterally.

Fig. 27.26 Calcification of an organized perirenal hematomaon the left.

27 Abdominal Calcifications

644





Renal artery aneurysm A cracked eggshell-like circular calcification at the renalhilus is seen in about one third of renal artery aneurysms.

Renal milk of calciumDD: Residual Pantopaque from prior cystpuncture and Pantopaque injection

Calcium-containing sediment in a cyst, caliceal diver-ticulum, or obstructed renal pelvis. Mimics calculus insupine films. In upright position calcific material gravitatesto the bottom of the cyst.

Ureteral calcification Ureteral calculus:Mostly idiopathic but the following condi-tions predispose:− Decreased mobility− Pre-existing ureteral obstruction− Metabolic diseases (see nephrocalcino-

sis)− Pre-existing infection− Postoperative ureteral stump

DD: Phleboliths (round, located laterally,and commonly below the interspinousline)

Characteristically irregular, often oval, lodged at threelevels:Ureteropelvic junction (large calculi)Pelvic brimUreterovesical junction (small calculi)Stones less than 4 mm will eventually pass spontaneously inover 80 %.4−6 mm stones will be passed spontaneously in 50 %, butoften cause renal obstruction.Stones larger than 6 mm rarely pass spontaneously andhave a high incidence of serious complications.

Schistosomiasis Tubular calcification of the distal ureter occurs in about15 % of patients.

Tuberculosis(Fig. 27.27)

Ureter calcifies less frequently than the kidney and its ap-pearance is variable. Ipsilateral renal calcification is oftenpresent.

Adrenal and retroperi-toneal calcification

A. Triangular Neonatal adrenal hemorrhage Occurs in infants born to mothers with diabetes and/orwith an abnormal obstetric history. The periphery of theadrenal calcifies a few weeks after hemorrhage. Can be anincidental finding.

Adrenal tuberculosis(Addison’s disease)

In about a quarter of patients discrete, stippled densitiesoutline the entire adrenal. Calcification can also be con-fluent and dense.

B. Cystic (curvilinear) Adrenal cyst:− Lymphatic− Necrotic pseudocyst (Fig. 27.28)− Cystic adenoma− Echinococcal− Old hemorrhage (Fig. 27.29)

A thin rim of curvilinear calcification above the kidney.

C. Mottled mass calci-fication

Adrenal cortical carcinomaPheochromocytoma (rare)Adrenal cortical adenoma (rare)Adrenal myelolipoma (a small mass ofbone marrow and fat) (very rare)

Scattered flecks of calcification throughout the mass.

Neuroblastoma Calcification that is fine granular or stippled, rarely massive,occurs in about 50 % of neuroblastomas. It is the secondmost common malignancy in children (after Wilms’ tumor).

Retroperitoneal teratoma Calcified spicules of cartilage or bone are seen near themidline of the upper abdomen. Teeth inclusions may beidentifiable.

Retroperitoneal cavernous hemangioma(Fig. 27.30)

A large mass with multiple phleboliths.


Abdomen

645


Fig. 27.27 Tuberculosis of the right distal ureter with charac-teristic ribbon-like calcifications (arrows).

Fig. 27.28 Necrotic pseudocyst of the right adrenal. A largecystic calcified mass, separate from the kidney, is seen.

Fig. 27.29 Calcified old adrenal hemorrhage above the left kid-ney.

Fig. 27.30 Retroperitoneal cavernous hemangioma. Multiple �phleboliths superimposed on the calcified and ectatic abdominalaorta and anterior to it are seen.


646





Other retroperitoneal tumors(Fig. 27.31)

Calcification is extremely rare.

Calcified lymph node(s) One or more 1 to 1.5 cm dense, often coarse calcifications.

Retroperitoneal hematomaTuberculous psoas abscess

May present as a large calcification.

D. Longitudinal tubu-lar calcification

Atherosclerosis Sclerotic plaques of the aortic wall are common in theelderly. The aorta characteristically narrows toward the bi-furcation. It may be curved and simulate an aneurysm.

Abdominal aortic aneurysm(Fig. 27.32)

The walls of the aneurysm tend to calcify more than thenormal aorta. Calcified plaques outline the aneurysm thatmost commonly occurs below the renal arteries, Obliquefilms can be used to avoid superimposition of the spine.


Fig. 27.31 Retroperitoneal teratoma. A large calcified massoriginating in the right retroperitoneum with extension into thesubhepatic space is seen.

Fig. 27.32 Calcified abdominal aortic aneurysm.

Abdomen

647





Pelvic calcification

A. Tubular calcification Arteriosclerosis The aorta and the iliac arteries are frequently calcified andseen as irregular plaque-like densities. May be seen inyoung persons with diabetes.

Vas deferensAssociated conditions:Diabetes mellitusTuberculosisDegenerative change(Fig. 27.33)

Bilaterally symmetric tubular densities that run mediallyand caudally to enter the base of the prostate, somewhatmimicking a medium-sized arteriosclerotic artery.Vas deferens calcification due to chronic inflammation(tuberculosis, syphilis) is intraluminal and has an irregularpattern.

B. Calcified bladderwall

Schistosomiasis(Fig. 27.34)

About 50 % of patients with schistosomiasis of the bladderhave visible calcifications of the bladder, most apparent atthe base. A linear opaque shadow may surround a relativelynormal-sized bladder. A disruption in the continuity of thehomogenous line of calcification is suggestive of asquamous cell carcinoma of the bladder, a common compli-cation.

Tuberculous cystitis A rare cause of bladder wall calcification. Usually a faint cal-cified rim is seen in a contracted bladder, associated withcalcifications in a kidney and ureter.

Encrusted cystitis:nonspecific infectionpost-irradiation

A very rare cause of calcification of the bladder wall.


Fig. 27.33 Calcified vas deferens in a 65-year-old patient, anincidental finding.

Fig. 27.34 a, b a Schis-tosomiasis of the uri-nary bladder. A linearcalcified ring representsthe bladder wall. b Thesame patient, two yearslater. The disruption ofthe right bladder wallcalcification is virtuallydiagnostic for a compli-cating squamous carci-noma.

a b


Localized Bone Lesions

Documents

Transcript of Localized Bone Lesions