Imaging in cardiomyopathies for nd radiology theory exam
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Imaging in Cardiomyopathies
Source: Grainger & Allison's Diagnostic Radiology, Braunwald's Heart Disease
Classification Overview
Cardiomyopathies are classified by phenotype (ESC approach) into:
| Phenotype | Main Types |
|---|---|
| Hypertrophic | HCM, Fabry disease, amyloidosis, athlete's heart |
| Dilated | DCM (ischaemic vs non-ischaemic), myocarditis |
| Restrictive | Amyloidosis, sarcoidosis, haemochromatosis, endomyocardial fibrosis |
| Arrhythmogenic | ARVC/ARVD |
| Unclassified | Takotsubo, LVNC (non-compaction) |
Imaging Modalities: Role Summary
| Modality | Key Roles |
|---|---|
| Chest X-ray | First-line; shows cardiomegaly, pulmonary congestion |
| Echocardiography | Workhorse; structure, function, wall thickness, Doppler |
| Cardiac MRI (CMR) | Gold standard for tissue characterisation; LGE fibrosis mapping |
| Cardiac CT | Wall thickness, coronary anatomy (rule out ischaemia), ARVC |
| Nuclear (MUGA/PET) | LV function, amyloid (pyrophosphate scan) |
1. Hypertrophic Cardiomyopathy (HCM)
Definition: Autosomal dominant sarcomere disease; septal thickness >15 mm in a non-dilated LV, unexplained by other causes.
Chest X-ray
- Often unhelpful in early disease
- Concentric hypertrophy may produce a rounded third left cardiac contour (different from aortic stenosis/hypertension which cause similar but distinguishable appearance)
Echocardiography (Primary Modality)
- M-mode: measures IVS and posterior wall thickness; IVS:posterior wall ratio >1.3 is diagnostic
- B-mode: asymmetric septal hypertrophy (ASH); apical/midventricular/mass-like variants
- Doppler: LVOT obstruction in 25% due to systolic anterior motion (SAM) of mitral valve (Venturi effect); rest gradient or provokable gradient; impaired diastolic function (reduced E wave, E/A equalisation)
- Limitation: apical forms near the low-frequency probe, poor acoustic window
Cardiac MRI (Gold Standard for Tissue Characterisation)
Key MRI features:
- Cine MRI: precise wall thickness measurement; all hypertrophy patterns visible; accurate LV mass quantification; RV involvement quantified
- Late gadolinium enhancement (LGE): PATHOGNOMONIC pattern = intramural fibrosis with selective septal enhancement and relative sparing of the subendocardial layer (distinguishes from MI where enhancement is subendocardial/transmural)
- Also: enhancement at anterior and inferior septal insertion points (RV insertion sites)
- Patchy large intramural foci in severe cases
- Prognostic value of LGE: Fibrosis on MRI predicts ventricular arrhythmias, sudden cardiac death (<40 years), and progression to HF (>40 years)
- T1/T2 mapping: quantitative tissue characterisation; can detect diffuse fibrosis not seen on LGE
Cardiac CT
- Accurate wall thickness information at very low dose (1-3 mSv)
- Useful when MRI is contraindicated (pacemaker, claustrophobia)
- Can exclude coronary artery disease simultaneously
Special Variants of Hypertrophic Phenotype
| Disease | Imaging Pearl |
|---|---|
| Anderson-Fabry disease (AFD) | T1 mapping shows markedly LOW native T1; LGE at infero-lateral wall |
| Amyloidosis | "Sparkling" appearance on echo; LGE shows diffuse global subendocardial enhancement ("zebra pattern"); T1 mapping shows high native T1 |
| Athlete's heart | Symmetric hypertrophy; normal diastolic function; LGE absent; regresses with detraining |
| Hypertension | Concentric LVH; no LGE in pure hypertensive disease |
2. Dilated Cardiomyopathy (DCM)
Definition: Dilated, poorly contracting LV (or both ventricles) in the absence of abnormal loading conditions or coronary artery disease sufficient to cause global dysfunction.
Chest X-ray
- Cardiomegaly - cardiothoracic ratio >0.5
- Pulmonary venous congestion / pulmonary oedema in advanced disease
- Pleural effusions
Echocardiography
- Dilated LV with reduced EF (globally hypokinetic)
- Spherical LV shape
- Functional mitral regurgitation (dilated annulus)
- Diastolic dysfunction pattern
- LV thrombus detection (especially at apex)
Cardiac MRI
Key feature: Differentiating ischaemic from non-ischaemic DCM by LGE pattern
| Parameter | Ischaemic DCM | Non-ischaemic DCM |
|---|---|---|
| LGE pattern | Subendocardial or transmural; coronary territory distribution | Mid-wall/intramural striae (patchy fibrosis); subepicardial; may be absent |
| LGE distribution | Follows coronary artery territory | Non-territorial, often septal mid-wall |
| Coronaries on CTA | Atherosclerosis/occlusion | Normal |
| Clinical relevance | Guides revascularisation | Predicts arrhythmia risk |
Cardiac CT
- Coronary CT angiography to exclude ischaemic cause (now first-line in many centres)
- LV dilatation on 4-chamber views
- Myocardial thinning at infero-apical segments in ischaemic DCM
3. Restrictive Cardiomyopathy (RCM)
Definition: Increased wall stiffness causing rapid pressure rise with small volume increase; both ventricles normal/reduced in size with normal wall thickness (usually); diastolic dysfunction predominates.
Causes: Amyloidosis, sarcoidosis, haemochromatosis, Anderson-Fabry disease, endomyocardial fibrosis (Loeffler syndrome), radiation, carcinoid.
Chest X-ray
- Frequently unremarkable in early stages
- Advanced: left atrial enlargement, signs of elevated pulmonary venous pressure (similar to mitral stenosis)
Echocardiography
- Normal-sized or minimally enlarged ventricles with enlarged atria
- Normal or mildly decreased EF
- In Loeffler/endomyocardial fibroelastosis/carcinoid: endocardial thickening visible
- Doppler: elevated early diastolic velocity (E wave), short deceleration time, low atrial velocity (A wave) = restrictive filling pattern
- KEY challenge: must differentiate from constrictive pericarditis - similar Doppler findings
Key differentiating features (RCM vs Constrictive Pericarditis):
| Feature | RCM | Constrictive Pericarditis |
|---|---|---|
| Pericardial thickness | Normal (<4 mm) | Thickened (>4 mm) |
| IVS kinetics | Normal | Septal bounce |
| IVC on inspiration | No significant change | Collapses (>50%) |
| Myocardial LGE | Present (amyloid, sarcoid) | Absent |
| Pericardial enhancement | Absent | May be present |
Cardiac MRI
- Gold standard for pericardial thickness measurement: >4 mm predicts constriction
- T1 and T2 weighted: tissue characterisation of infiltrative diseases
- LGE patterns by specific diseases:
- Amyloidosis: diffuse global subendocardial enhancement; classic "zebra" or "leopard" pattern; rest T1 elevated; early blood-pool nulling
- Sarcoidosis: patchy, non-coronary territory LGE; predilection for basal septum and lateral wall; T2 high in active disease
- Haemochromatosis: LOW T2* signal (iron deposition causes susceptibility effect - myocardium appears dark on T2*)
- T1/T2 mapping: promising for differential diagnosis of infiltrative forms
4. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
Definition: Progressive replacement of RV myocardium by fibrofatty tissue; leads to RV dysfunction, ventricular arrhythmias, and sudden death in young athletes.
Chest X-ray
- May be normal or show mild cardiomegaly
- RV enlargement in advanced disease
Echocardiography
- RV dilatation and dysfunction (reduced RVEF)
- RV wall motion abnormalities (focal akinesis, dyskinesis)
- RVOT dilatation
- Limitation: poor RV acoustic window
Cardiac MRI (Modality of Choice)
- Gold standard for ARVC diagnosis
- Key findings:
- RV fatty infiltration: T1 high signal (fat) in RV free wall; however fat is also present in normal subjects, so presence alone is non-specific
- RV dilatation and dysfunction: reduced RVEF, increased RVEDV
- Regional wall motion abnormalities: focal akinesia, dyskinesia, or aneurysm of the RV free wall (triangle of dysplasia: RV inflow, outflow, and apex)
- LGE: fibrosis in RV wall; LV involvement in advanced cases
- Task Force Criteria (2010): structural/functional abnormalities on MRI are part of major and minor diagnostic criteria
Cardiac CT
- Can detect fatty infiltration in RV wall
- Structural assessment if MRI contraindicated
5. Myocarditis (Inflammatory Cardiomyopathy)
Echocardiography
- LV systolic dysfunction (regional or global)
- Pericardial effusion suggests inflammatory process
- Non-specific; cannot provide tissue diagnosis
Cardiac MRI - Lake Louise Criteria (Cornerstone)
Three-sequence protocol (must meet ≥2 criteria for diagnosis):
| Sequence | Finding | Meaning |
|---|---|---|
| T2-weighted (STIR) | Regional/global T2 signal increase | Myocardial oedema |
| Early gadolinium enhancement (EGE) | Global relative enhancement ratio >4 (blood pool vs myocardium) | Inflammatory hyperaemia/capillary leak |
| Late gadolinium enhancement (LGE) | Non-ischaemic distribution enhancement | Myocyte necrosis/fibrosis |
LGE pattern in myocarditis: classically subepicardial, most frequently in lateral and/or inferior wall.
- Easily distinguishable from MI (subendocardial/transmural, follows coronary territory)
- In Takotsubo CMP: LGE is typically absent - key differentiator
Important: Negative LGE does NOT exclude myocarditis - early/hyperaemic phase may show abnormality only on T2 and EGE without LGE.
6. Takotsubo (Stress) Cardiomyopathy
- Echo/CMR: Apical LV ballooning with hypercontractile basal segments (reverse apical ballooning pattern in atypical forms)
- LGE: Characteristically absent (no necrosis - distinguishes from STEMI and myocarditis)
- CMR: T2 elevation in apical segments (oedema); resolves with recovery
- Coronary angiography: normal coronaries
7. LV Non-Compaction (LVNC)
- Echo/CMR: Excessive trabeculation in LV; ratio of non-compacted to compacted layer >2.3 (MRI criterion); typically apical
- CMR is superior for trabeculation quantification
- LGE may be present in trabeculated segments
LGE Pattern Summary Table (High-Yield for Exam)
| Disease | LGE Location | Pattern |
|---|---|---|
| MI (ischaemic) | Subendocardial → transmural | Coronary territory |
| HCM | Intramural septum; RV insertion | Patchy, spares subendocardium |
| DCM (non-ischaemic) | Mid-wall septum | Linear/striae |
| Myocarditis | Subepicardial lateral/inferior | Non-territorial |
| Amyloidosis | Global subendocardial | "Zebra/leopard" pattern |
| Sarcoidosis | Basal septum, lateral wall | Patchy, non-territorial |
| ARVC | RV free wall | Fibrofatty |
| Haemochromatosis | Low T2* (dark) | Not LGE; T2* mapping |
| Takotsubo | Absent | - |
Key MRI Sequences and What They Show
| Sequence | Information |
|---|---|
| Cine (SSFP) | Morphology, function, volumes, EF, wall motion |
| T1-weighted | Anatomy; fat (bright); delayed enhancement (fibrosis) |
| T2-weighted (STIR) | Oedema detection; active inflammation |
| LGE (10-15 min post Gd) | Fibrosis, necrosis, infiltration |
| T1 mapping (native) | Elevated in amyloid/oedema; low in haemochromatosis/fat |
| T2 mapping | Oedema quantification |
| T2 mapping* | Iron overload (haemochromatosis - low T2*) |
| EGE (early gadolinium) | Hyperaemia/capillary leak (myocarditis) |
Exam Pearls
- CMR is the gold standard for tissue characterisation in all cardiomyopathies
- LGE spares subendocardium in HCM - key distinction from MI
- Myocarditis = subepicardial LGE laterally; Takotsubo = no LGE
- Amyloidosis: global subendocardial LGE + high native T1 + early blood-pool nulling + "sparkling" echo
- Haemochromatosis: low T2* (iron causes susceptibility artefact making myocardium dark)
- ARVC: RV fatty infiltration + RV dilatation/dysfunction + CMR Task Force Criteria
- Constrictive pericarditis vs RCM: pericardial thickness >4 mm on CT/MRI favours constriction
- DCM ischaemic vs non-ischaemic: subendocardial LGE in coronary territory = ischaemic; mid-wall septal LGE = non-ischaemic
- Cardiac CT provides coronary anatomy + wall thickness at low dose; used when MRI contraindicated or to exclude ischaemic cause in DCM
- Lake Louise Criteria require ≥2 of 3 (T2, EGE, LGE) for CMR diagnosis of myocarditis
Sources: Grainger & Allison's Diagnostic Radiology, Chapter 14 (Cardiomyopathies) | Braunwald's Heart Disease, 12th Ed.
Imaging in bone tumors in detail
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Imaging in Bone Tumours - Detailed Notes for ND Radiology Theory Exam
Source: Grainger & Allison's Diagnostic Radiology, Chapters 40 & 41
PART 1: RADIOLOGICAL ASSESSMENT - THE SYSTEMATIC APPROACH
When analysing any bone lesion, six key radiological parameters must be assessed before making a diagnosis.
1. Age of Patient
| Age Group | Most Likely Lesion |
|---|---|
| <5 years | Metastatic neuroblastoma, leukaemia |
| 5-15 years | Ewing sarcoma, osteosarcoma |
| 10-25 years | Osteosarcoma, Ewing sarcoma, osteoblastoma |
| 20-40 years | GCT, fibrosarcoma/UPS |
| >40 years | Metastases (commonest!), myeloma, chondrosarcoma, Paget sarcoma |
2. Location within Skeleton & Bone
Skeletal site:
- Axial > appendicular (metastases, myeloma prefer red marrow)
- Long bones: osteosarcoma (distal femur, proximal tibia, proximal humerus)
- Flat bones / diaphysis: Ewing sarcoma (pelvis, ribs)
Location within the bone:
| Position | Tumours |
|---|---|
| Epiphysis | GCT (mature skeleton), chondroblastoma (open physis), clear cell chondrosarcoma |
| Metaphysis | Osteosarcoma, chondrosarcoma, NOF, ABC, SBC |
| Diaphysis | Ewing sarcoma, fibrous dysplasia, adamantinoma (tibia), myeloma |
| Epiphysis + Metaphysis | GCT (crosses physis in adults) |
| Intramedullary | Most primary bone tumours |
| Intracortical | Osteoid osteoma, adamantinoma |
| Surface/juxtacortical | Parosteal osteosarcoma, periosteal chondroma |
3. Rate of Growth - Lodwick Classification (Zone of Transition)
| Type | Description | Significance |
|---|---|---|
| Type 1A | Sharp, geographic, sclerotic margin | Slow growth; benign |
| Type 1B | Well-defined lytic, no marginal sclerosis | Slow growth; benign/low-grade |
| Type 1C | Slightly less sharp, non-sclerotic | Transitional |
| Type 2 | Moth-eaten - multiple lucent areas 2-5 mm, separated by intact bone | More aggressive |
| Type 3 | Permeative - multiple coalescing tiny (<1 mm) ill-defined lesions, zone of transition >several cm | Most aggressive; Ewing, lymphoma, myeloma |
- Benign/low-grade tumours: remain in medullary cavity, endosteal scalloping + expansion without cortical destruction
- High-grade malignant: cortical destruction + extra-osseous soft-tissue mass by presentation
4. Periosteal Reaction Types
| Type | Description | Significance |
|---|---|---|
| Solid/thick | Well-formed, uniform | Slow growth; NOT necessarily benign (can see in grade 2 chondrosarcoma) |
| Laminated ("onion skin") | Multiple parallel layers | Subperiosteal tumour extension, infection, haematoma; CLASSIC in Ewing sarcoma |
| Codman triangle | Interrupted periosteal reaction at edge of tumour | Marks limit of subperiosteal tumour in longitudinal direction; indicates aggressive lesion |
| Sunburst/hair-on-end (spiculated) | Radiating perpendicular spicules | Most aggressive; CLASSIC in osteosarcoma; also Ewing |
| Multilaminated | Periodic growth pattern | Repeated episodes of tumour growth |
Exam Pearl: No periosteal reaction is pathognomonic for any tumour - it indicates aggressiveness, not histological type.
5. Matrix Mineralisation
| Matrix Type | Appearance | Tumour |
|---|---|---|
| Osteoid/tumour bone | Dense, fluffy, cloud-like, "ivory" | Osteosarcoma |
| Chondroid | Rings, arcs, C-shapes, "pop-corn" calcification | Chondrosarcoma, enchondroma, osteochondroma |
| No matrix | Purely lytic | GCT, myeloma, metastases (renal, thyroid), fibrosarcoma |
| Ground glass | Hazy, "smoke-filled" | Fibrous dysplasia |
6. CT and MRI Role
CT:
- Best for: cortical detail, matrix mineralisation characterisation, periosteal reaction details
- Identifies subtle endosteal scalloping, cortical destruction
- CT-guided biopsy
MRI (Gold Standard for Local Staging):
- T1W: anatomy, medullary extent (normal marrow = bright; tumour = dark, intermediate)
- T2W/STIR: tumour extent, oedema, soft-tissue component (tumour = bright); identifies skip lesions
- Contrast (Gd): tumour enhancement pattern; solid vs cystic components; vascular supply
- Key MRI roles:
- Defines intramedullary extent - always underestimated on X-ray
- Cortical saucerisation by Ewing sarcoma visible
- Soft-tissue extension and neurovascular bundle proximity (surgical planning)
- Skip lesions (transarticular/intramedullary discontinuous foci)
- Response to chemotherapy assessment
PART 2: CLASSIFICATION OF BONE TUMOURS
WHO Classification - Key Benign Tumours (Table 40.1, Grainger & Allison)
| Origin | Benign | Intermediate/Locally Aggressive |
|---|---|---|
| Chondrogenic | Osteochondroma, enchondroma | ACT/grade 1 chondrosarcoma, chondroblastoma |
| Osteogenic | Osteoma, osteoid osteoma | Osteoblastoma |
| Giant cell-rich | GCL small bones | Giant cell tumour |
| Fibrogenic | NOF, benign fibrous histiocytoma | Desmoplastic fibroma |
| Undefined | Simple bone cyst, FD, ABC | - |
WHO Classification - Malignant Bone Tumours
| Origin | Malignant Tumour |
|---|---|
| Chondrogenic | Chondrosarcoma (grade 1-3), dedifferentiated |
| Osteogenic | Osteosarcoma (7 subtypes) |
| Fibrogenic | Fibrosarcoma, UPS (undifferentiated pleomorphic sarcoma) |
| Marrow | Ewing sarcoma, myeloma, lymphoma |
| Notochordal | Chordoma |
| Metastatic | (Most common overall >40 yrs) |
PART 3: INDIVIDUAL TUMOURS IN DETAIL
A. OSTEOSARCOMA
Epidemiology: Commonest non-haematological primary bone malignancy; 4/million/year; bimodal - peak at 10-14 years (adolescent growth spurt), second peak in elderly (Paget-related). Male:female = 1.35:1.
Associations: Li-Fraumeni syndrome, Rothmund-Thomson syndrome, familial retinoblastoma, Paget disease, prior radiotherapy, bone infarction, fibrous dysplasia.
WHO Subtypes (7):
- Conventional (75%) - high-grade intramedullary
- Telangiectatic
- Low-grade central
- Small cell
- Parosteal - surface, low grade
- Periosteal - surface, intermediate grade
- High-grade surface
Conventional Osteosarcoma:
Conventional osteosarcoma - X-ray appearances: (A) early normal appearing; (B) lytic permeative metaphyseal; (C) sclerotic with sunburst periosteal reaction - distal femur/proximal tibia (most common site = around knee)
| Feature | Detail |
|---|---|
| Site | Metaphysis of long bones; distal femur (40%), proximal tibia (20%), proximal humerus (10%) - around the knee in 60% |
| X-ray | Mixed sclerotic-lytic lesion; permeative/moth-eaten destruction; sunburst periosteal reaction (most aggressive); Codman triangle; soft-tissue mass with tumour bone formation (fluffy/cloud-like density) |
| Matrix | Osteoid matrix - dense, fluffy, amorphous sclerosis (differentiate from reactive host bone!) |
| MRI T1 | Low-intermediate SI tumour; dark on T1; medullary extent clearly shown |
| MRI T2/STIR | Heterogeneous high SI; soft-tissue extension; skip lesions |
| Key MRI features | Defines extent for limb salvage surgery; neurovascular bundle proximity; skip lesions (intramedullary discontinuous foci within same bone or transarticular) |
| CT | Matrix mineralisation detail; periosteal reaction characterisation |
Telangiectatic Osteosarcoma:
- Purely lytic, large, expansile; no matrix mineralisation
- Multiple fluid-fluid levels (FFLs) on MRI - mimics ABC!
- Key distinction: solid nodular tissue in walls + Gd enhancement = malignant
- DDx: ABC has no solid enhancing component
Parosteal Osteosarcoma:
- Surface lesion; posterior distal femur most common
- Dense ossified surface mass; may encircle bone; normal medullary cavity (until late)
- X-ray: densely ossified lobulated surface lesion
- MRI: low SI ossified centre; cleavage plane between lesion and cortex useful prognostically
Periosteal Osteosarcoma:
- Surface, intermediate grade (chondroblastic)
- X-ray: spiculated periosteal reaction + ossified soft-tissue component
- MRI: confirms extensive surface lesion + intramedullary signal change
B. EWING SARCOMA
Epidemiology: 2nd most common bone sarcoma in children; 6-8% primary malignant bone tumours; 75% under age 20 (peak 5-15 yrs); male:female = 1.4:1; rare in non-Caucasians. Translocation t(11;22).
Family includes: Ewing sarcoma, PNET, adult neuroblastoma, Askin tumour (chest wall).
| Feature | Detail |
|---|---|
| Site | Diaphysis (35%) or metadiaphysis (60%) - classic diaphyseal unlike osteosarcoma (metaphyseal); femur + humerus (31%), pelvis (21%, ilium), ribs (<8%) |
| X-ray | Permeative/moth-eaten destruction; wide zone of transition; "onion-skin" (multilamellar) periosteal reaction; soft-tissue mass in 80% |
| Codman triangle | Present |
| Sunburst | Can occur but less typical than in osteosarcoma |
| MRI | Large soft-tissue mass (often disproportionate to bone destruction); may show "cortical saucerisation"; T2 bright; intermediate T1 |
| Mimics infection | Systemic features (fever, raised ESR) + diaphyseal lytic lesion - DDx osteomyelitis |
| Pelvic Ewing | Large soft-tissue mass; can be very large with iliac bone destruction |
C. CHONDROSARCOMA
Epidemiology: 2nd most common primary bone malignancy; 4th-5th decade (unlike osteosarcoma); male predominance.
Types:
- Central (conventional) - most common; arises in medullary cavity
- Secondary - from osteochondroma or enchondroma
- Dedifferentiated - high-grade component within low-grade; worst prognosis
- Clear cell - epiphyseal; low grade
- Mesenchymal - young patients; highly malignant
Imaging:
| Feature | Detail |
|---|---|
| Site | Pelvis, proximal femur, proximal humerus, ribs (unlike osteosarcoma = distal femur) |
| X-ray | Lytic lesion with chondroid matrix (rings and arcs calcification, "popcorn"); endosteal scalloping; slow-growing; no aggressive periosteal reaction in low-grade |
| Size | Mean 8 cm (vs enchondroma 5 cm) |
| Endosteal scalloping >2/3 cortical thickness | Seen in 67% chondrosarcomas vs 11% enchondromas - key imaging sign |
| Bone scintigraphy | >80% chondrosarcomas show increased uptake; normal activity favours enchondroma |
| MRI | Lobulated; T2 very bright (high water content cartilage); septal enhancement post-contrast; dynamic CE-MRI for dedifferentiation foci |
| CT | Best for calcification pattern and cortical erosion |
| Cartilage cap (secondary from osteochondroma) | Cap >2 cm on US/CT/MRI = malignant transformation likely; <2 cm = unlikely |
| FDG-PET | Low SUVmax = benign; elevated SUVmax = higher-grade; not yet routine |
D. GIANT CELL TUMOUR (GCT) OF BONE
Epidemiology: Locally aggressive (intermediate); 20-40 years; rare in skeletally immature; female preponderance. ~1-2% metastasise to lung.
| Feature | Detail |
|---|---|
| Site | Epiphysis (closed physis required); distal femur, proximal tibia, distal radius; extends to subchondral bone |
| X-ray | Purely lytic ("soap bubble" appearance); eccentric, epiphyseal/subchondral; no matrix; no periosteal reaction in uncomplicated cases; type 1B/1C zone of transition; cortical expansion; may break cortex |
| MRI T1 | Low-intermediate SI |
| MRI T2 | Heterogeneous; areas of low SI (haemosiderin); fluid-fluid levels (25%) |
| MRI Gd | Solid enhancement (distinguishes from ABC) |
| CT | No internal calcification (distinguishes from chondroid lesions); cortical thinning; soft-tissue extension |
| Recurrence | High local recurrence rate after curettage |
E. OSTEOID OSTEOMA
Epidemiology: Young adults (10-35 years); male:female = 3:1; night pain relieved by aspirin/NSAIDs (classic clinical feature from prostaglandin production).
| Feature | Detail |
|---|---|
| Site | Cortex of long bone diaphysis/metaphysis (femur, tibia); posterior elements of spine (scoliosis) |
| X-ray | Small (<1.5 cm) radiolucent nidus surrounded by dense reactive sclerosis; nidus may be hard to see |
| CT | Modality of choice - shows nidus precisely; central calcification in 50% of nidus; surrounding sclerosis; localises lesion for radiofrequency ablation guidance |
| MRI | Marked surrounding reactive marrow oedema (can be confusing - overestimates lesion); nidus T1 iso, T2 high; Gd enhancement |
| Bone scan | Intense "double density" hot spot |
F. OSTEOBLASTOMA
- Similar to osteoid osteoma but >2 cm in diameter
- Posterior spinal elements (common site)
- Less reactive sclerosis; more expansile
- No aspirin-relief (typically)
- May be locally aggressive
G. ENCHONDROMA
| Feature | Detail |
|---|---|
| Site | Short tubular bones of hands/feet (>50%); metaphysis |
| X-ray | Lytic lesion with chondroid calcification (rings/arcs/stippled); expansion in small bones; minimal or no endosteal scalloping |
| DDx Chondrosarcoma | Size >5 cm; deep endosteal scalloping (>2/3 cortical thickness); pain; soft-tissue mass |
| Syndromes | Ollier disease (multiple enchondromatosis - non-hereditary; increased risk of malignancy); Maffucci syndrome (enchondromas + soft-tissue haemangiomas; high malignancy risk) |
H. OSTEOCHONDROMA (MOST COMMON BENIGN BONE TUMOUR)
| Feature | Detail |
|---|---|
| Site | Metaphysis of long bones (distal femur, proximal tibia, proximal humerus); may be pedunculated or sessile |
| X-ray | Bony excrescence with cortex and medullary cavity continuous with parent bone (pathognomonic); grows away from physis; cartilage cap not visible on X-ray |
| MRI | Cartilage cap: T2 bright; measure cap thickness perpendicular to bony component: cap >2 cm = suspicious for secondary chondrosarcoma |
| US | Can measure cap thickness |
| Malignant change | Pain after skeletal maturity; continued growth; cap >2 cm; dispersal of calcifications in soft-tissue mass |
| Multiple hereditary | Multiple hereditary exostoses (MHE) - autosomal dominant; higher risk of malignancy |
I. BONE METASTASES
Most common bone malignancy in >40 years. Bone is 3rd commonest site of metastatic spread (after lung and liver).
"BLT Kidney Thyroid" (Breast, Lung, Thyroid, Kidney, Prostate) = 80% of all bone metastases.
Prevalence at death: Breast + Prostate = 80-85%; Lung = 40-80%; Thyroid = 50-60%; Renal = 20-35%.
Distribution: Axial skeleton (red marrow sites): spine (thoracic > lumbar > cervical), pelvis, proximal femur/humerus, ribs, sternum, skull.
Batson venous plexus = valveless vertebral venous plexus explains spinal predilection.
| Type | Primary Tumour | X-ray Appearance |
|---|---|---|
| Lytic | Kidney, thyroid, lung, breast, GI | Destructive, permeative; no matrix |
| Sclerotic | Prostate (most common), breast (some), carcinoid, medulloblastoma | Dense, "ivory" vertebrae; diffuse sclerosis |
| Mixed | Breast (most common), lung | Both lytic and sclerotic |
Ivory vertebra: Prostate >> lymphoma, Paget disease (common causes); dense sclerotic vertebral body.
Imaging Modalities for Metastases:
| Modality | Role |
|---|---|
| X-ray | First-line; insensitive (requires 30-50% bone loss) |
| Bone scintigraphy (Tc-99m MDP) | Sensitive screening tool; detects osteoblastic activity; false-negative in lytic mets (renal, thyroid, myeloma) |
| CT | Cortical detail; pathological fracture risk; biopsy guidance |
| MRI | Most sensitive for marrow involvement; STIR/T1 for diffuse marrow disease; whole-body MRI replacing bone scan |
| FDG-PET-CT | Functional + anatomical; excellent for lytic mets; less sensitive for purely sclerotic |
| Specific tracers | NaF-PET (bone); PSMA-PET (prostate); I-131 (thyroid) |
Superscan: Diffuse, uniformly increased uptake on bone scan with absent renal activity and absent soft-tissue background - seen with widespread diffuse sclerotic metastases (prostate, breast).
J. MULTIPLE MYELOMA
| Feature | Detail |
|---|---|
| Age | >40 years (97% present after 40) |
| X-ray | "Punched out" lytic lesions (no reactive sclerosis); skull ("pepper-pot" skull); diffuse osteoporosis; vertebral compression fractures |
| Bone scan | Often FALSE NEGATIVE (no osteoblastic reaction) - bone scan not useful! |
| MRI | Modality of choice; focal or diffuse marrow involvement; T1 low SI, T2/STIR high SI |
| Whole-body MRI | Now recommended for staging in guidelines |
| FDG-PET-CT | Detects active disease; used for treatment response |
| X-ray skeletal survey | Traditional staging method |
K. SIMPLE BONE CYST (SBC) / UNICAMERAL BONE CYST
| Feature | Detail |
|---|---|
| Age | Children/adolescents |
| Site | Proximal humerus (most common), proximal femur; metaphyseal; central |
| X-ray | Central lytic lesion, slightly expansile, well-defined margins; thin cortex; may have "fallen fragment" sign (fallen cortical fragment inside cyst after pathological fracture) |
| MRI | Homogeneous fluid signal; T1 low, T2 high; no solid component |
L. ANEURYSMAL BONE CYST (ABC)
| Feature | Detail |
|---|---|
| Age | <20 years |
| Site | Metaphysis long bones; posterior spinal elements |
| X-ray | Eccentric, expansile, "blown out" lytic lesion; thin cortical shell; "soap bubble" |
| MRI | Multiple fluid-fluid levels (FFLs) - blood products of different ages; thin septa; T1 and T2 components from haemorrhage |
| DDx | Telangiectatic osteosarcoma (has solid enhancing nodules); GCT (older age, epiphysis) |
| Primary vs Secondary | Secondary ABC arises in GCT, chondroblastoma, fibrous dysplasia, osteoblastoma |
M. NON-OSSIFYING FIBROMA (NOF)
| Feature | Detail |
|---|---|
| Site | Metaphysis/metadiaphysis; cortically based; distal femur, tibia |
| X-ray | Eccentric, cortically based lytic lesion with sclerotic margin (type 1A); no matrix; multilobulated; "bubbly" |
| MRI | T1/T2 low-intermediate SI (fibrous tissue); no oedema |
| Natural history | Usually involutes spontaneously (fills in with bone) |
| Jaffe-Campanacci | Multiple NOFs + café-au-lait spots |
N. FIBROUS DYSPLASIA
| Feature | Detail |
|---|---|
| Site | Rib (most common overall), proximal femur, skull/facial bones; mono or polyostotic |
| X-ray | "Ground-glass" matrix (hazy, "smoke-filled"); geographic lytic lesion with "rind" of sclerosis (thick sclerotic margin); bone expansion; NO periosteal reaction (unless fractured); "shepherd's crook" deformity (varus proximal femur - late) |
| CT | Best demonstrates ground-glass matrix |
| MRI T1 | Iso-intermediate SI; areas of hyperintensity from haemorrhage |
| MRI T2 | Variable (intermediate-low if fibrous; high if cystic change); FFLs possible |
| Bone scan/Whole body MRI | Polyostotic disease mapping |
| McCune-Albright | Polyostotic FD + café-au-lait spots + precocious puberty (GnRH-independent) |
PART 4: STAGING & BIOPSY IMAGING
Enneking Staging System (Musculoskeletal Tumour Society)
| Stage | Grade | Site | Metastasis |
|---|---|---|---|
| IA | Low grade (G1) | Intracompartmental (T1) | None (M0) |
| IB | Low grade (G1) | Extracompartmental (T2) | None |
| IIA | High grade (G2) | Intracompartmental (T1) | None |
| IIB | High grade (G2) | Extracompartmental (T2) | None |
| III | Any grade | Any | Regional/distant mets |
MRI is essential for Enneking staging - defines compartmental involvement.
Biopsy Planning
- MRI guides biopsy site (viable, non-necrotic, non-haemorrhagic tissue)
- Biopsy tract must lie in the planned surgical resection field
- CT-guided for axial/deep lesions
- US-guided for soft-tissue component
PART 5: RESPONSE TO TREATMENT
Post-chemotherapy MRI assessment:
- Decrease in T2 SI = good response
- Decrease in soft-tissue mass size
- Peripheral ossification around soft-tissue component
- Dynamic contrast-enhanced MRI: reduced enhancement = tumour necrosis
- Histological necrosis >90% = good response (Huvos grading)
EXAM SUMMARY: HIGH-YIELD IMAGING PEARLS
| Feature | Tumour |
|---|---|
| Sunburst periosteal reaction | Osteosarcoma (most classic) |
| Onion-skin periosteal reaction | Ewing sarcoma |
| Codman triangle | Any aggressive tumour (non-specific) |
| Fluid-fluid levels on MRI | ABC (primary), telangiectatic osteosarcoma, GCT |
| "Popcorn" calcification | Enchondroma, chondrosarcoma (chondroid matrix) |
| Ground-glass matrix | Fibrous dysplasia |
| "Sunray" spiculation + metaphyseal mixed lesion around knee | Conventional osteosarcoma |
| Purely lytic + epiphyseal + subchondral + no sclerosis | GCT |
| Punched-out lytic + no reactive sclerosis + false -ve bone scan | Myeloma |
| Diaphyseal lytic + fever + elevated ESR + periosteal reaction | Ewing sarcoma (DDx osteomyelitis) |
| Posterior distal femur surface mass + ossified + middle-aged | Parosteal osteosarcoma |
| Cortical based + small nidus + dense sclerosis + night pain | Osteoid osteoma |
| Endosteal scalloping >2/3 cortical thickness | Chondrosarcoma (not enchondroma) |
| Cartilage cap >2 cm on MRI | Secondary chondrosarcoma from osteochondroma |
| "Fallen fragment" sign | Simple bone cyst |
| Shepherd's crook deformity | Fibrous dysplasia (proximal femur) |
| Ivory vertebra | Prostate metastasis, Paget, lymphoma |
| Superscan on bone scan | Diffuse sclerotic metastases |
| False-negative bone scan | Myeloma, lytic metastases (renal, thyroid) |
Source: Grainger & Allison's Diagnostic Radiology, Chapters 40 (Benign Bone Tumours) & 41 (Malignant Bone Tumours), 6th/current edition
Retroperitoneal lesions in detail
Finding Sources
Finding Sources
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