Radiological examination of the skeletal system.
Diseases of bones and joints form a large proportion of the work seen in radiological practice. It is clearly impossible to give any but the briefest survey in a work such as this, and that only by omitting important sections. Trauma and fractures are adequately dealt with in standard surgical works and will not therefore be considered. This and the next chapter will be confined to illustrating the value of bone radiology in general medical and surgical problems.
PLAIN FILMS
Plain films still remain the mainstay of radiological investigation of the skeletal system. Views should always be obtained in two projections.
ISOTOPES
Technetium-99m phosphonate compounds accumulate in bone several hours after intravenous injection of the isotope; principally used for:
• detection of osteomyelitis and other musculoskeletal soft-tissue inflammatory changes;
• metastatic bone lesions: changes are seen much earlier than plain films;
• staging tumours such as breast carcinoma or bronchial carcinoma;
• functional bone abnormality: Paget’s disease.
Uptake of the isotope does occur, however, in many other conditions including osteoarthritis and inflammatory arthropathies.
ARTHROGRAPHY
In this procedure, contrast and air are injected into joints such as the knee, hip, elbow, shoulder, wrist and temporomandibular joints to diagnose loose bodies, ligamentous and cartilaginous abnormalities. The technique may be followed by computed tomography (CT arthrography). MRI is now the preferred modality in the majority of cases.
Fig.
ULTRASOUND
Ultrasound is utilized for the evaluation of:
• neonatal hip for congenital dislocation;
• soft-tissue lesions, abscesses and masses;
• joint effusions.
CT
CT aids:
• assessment of bone tumours prior to surgery;
• evaluation of certain fractures, such as the acetabulum and subtalar joint;
• study of the spinal column.
MRI
Although bone is not adequately visualized from lack of a signal, marrow in cancellous bone produces very clear images. MRI assists the investigation of bone tumours, soft tissue masses, the spinal column and joints. A common disorder of bone architecture, of unknown aetiology, which occurs with increasing frequency after middle age. It is characterized initially by bone resorption, followed by a reparative process in which increased bone deposition results in bone expansion and abnormal modeling.
Paget’s disease
A common disorder of bone architecture, of unknown aetiology, which occurs with increasing frequency after middle age. It is characterized initially by bone resorption, followed by a reparative process in which increased bone deposition results in bone expansion and abnormal modelling.
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Fig. Paget’s disease: calvarial thickening producing a ‘cotton wool’ appearance.
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Fig. Bowing of the tibia with pseudofracture in Paget’s disease.
RADIOLOGICAL FEATURES
Any bone may be affected.
• Skull. Initially a large area of well defined bone loss may be seen (osteoporosis circumscripta); later, generalized sclerosis with diploic thickening produces a characteristic ‘cotton wool’ appearance. There may be an increase in the size of the head.
• Spine. Most commonly involves a single vertebra with sclerosis, altered trabecular pattern and enlargement of the vertebral body.
• Pelvis. Frequently affected with coarsened trabecular pattern, cortical thickening and enlargement of the pubis and ischium.
• Long bones. Widening of bone with deformities, bowing of the tibia and incomplete fractures because of bone softening.
COMPLICATIONS
· Pathological fractures: tend to be sharply transverse.
· Pseudofractures: incomplete fractures found on the convex surfaces of bowed bones.
· Secondary degenerative changes: the hip joint is most frequently involved.
· Malignant degeneration: in widespread Paget’s disease there is an increased incidence of malignant bone tumours, especially osteogenic sarcoma.
· Neurological: nerve entrapment by bone expansion: deafness from Vlll-th nerve involvement, encroachment of the spinal exit foramina, etc.
· Cardiovascular: increased shunting of blood in involved bone may cause high output failure, although this is rare.
Benign bone tumours
Benign bone tumours are generally well defined and have a narrow zone of transition betweeormal and abnormal bone. They cause signs and symptoms by expansion and pressure on adjacent structures. If cystic, a pathological fracture may ensue.
CARTILAGE TUMOURS
Chondroma. A cartilaginous tumour, one of the most common benign tumours of bone, appears as a well-defined lytic lesion with small flecks of calcification. The hands and feet are most frequently affected, where expansion and thinning of the cortex may be a feature. Chondromas are often single but may be multiple in Oilier s disease.
Osteochondroma. Probably the commonest benign tumour, containing both bone and cartilage, often on a bony stalk with a bulbous broad distal end. The tumour is often found growing away from a joint, the most frequent site being the metaphyseal region of the lower femur and upper tibia. Hereditary multiple osteochondromas occur in diaphyseal aclasia, where a risk of malignant transformation to chondrosarcoma exists.
BONE FORMING TUMOURS
Osteoma. A benign tumour that contains only compact osseous tissue, most commonly found in the skull and sinuses. They are round, well defined and appear as a mass of amorphous dense bone with no cartilaginous component. Multiple osteomas are associated with colonic polyposis in
Osteoid osteoma. A small circular lucent area (nidus) under the cortex surrounded by thickened reactive bone and associated with periosteal reaction. Osteoid osteoma, a tumour of < I cm in diameter, is usually a lesion of young adults and presents with local pain. It may be cored out under radiological control.
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Fig Chondroma: a benign cartilaginous tumour.
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Fig. Chondromyxoid fibroma, a rare tumour but demonstrates the features of a benign tumour.
Fig. Osteochondroma
OTHER BENIGN LESIONS
Giant cell tumour. A benign tumour, with approximately half discovered in the vicinity of the knee joint. This is a lytic lesion of the epiphyseal region, with cortical thickening, expansion and the potential of turning into a malignant neoplasm.
Osteoblastoma; bone cyst; non-ossifying fibroma; aneurysmal bone cyst; chon-dromyxoid fibroma
MALIGNANT BONE TUMOURS
Primary malignant bone tumours are uncommon: they are destructive, often associated with periosteal reactions, and have a wide zone of transition betweeormal and abnormal bone. The most common malignant bone tumour is a metastasis and it is often solitary.
RADIOLOGICAL FEATURES
Plain films may show an area of bone destruction.
CT and MRI are the best imaging modalities to evaluate tumours and determine bone and soft tissue involvement; definitive diagnosis is by a biopsy. Features that may be verified by CT/MRI are: tumour vascularity; infiltration of surrounding tissues; relationship to nerves and vessels.
MALIGNANT BONE TUMOURS
Osteosarcoma. The second most common primary malignant tumour of bone after multiple myeloma, the classical features being:
• irregular medullary destruction;
• periosteal reaction;
• cortical destruction;
• soft-tissue mass;
• new bone formation.
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Fig. Osteogenic sarcoma extending into the soft tissues
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Fig. Osteogenic sarcoma. (A) Osteolytic type, at the upper end of the tibia. (B) Sclerosing type with calcification extending into the soft tissues around lower femur.
Fig. MRI studies of osteosarcoma of upper tibia. (A) Sagittal section showing tumour extending into soft tissues around cortex and into epiphysis. (B) Axial section showing tumour as high signal surrounding cortex (which appears black) and filling medulla.
Osteosarcoma presents between the ages of 10 and 25. Approximately half appear around the knee joint, involving the metaphysis of the distal femur and proximal tibia. The tumour may be lytic in nature, or sclerotic with neoplastic new bone formation and periosteal reaction. It erodes from its origins in the medulla through the cortex, with a resulting soft-tissue mass. Metastases often spread to the lungs and may form bone.
Chondrosarcoma. A slow-growing malignant tumour, derived from cartilage cells, which may contain areas of calcification within the tumour.
• Central type: usually arise from a tubular bone, is lytic and situated in the region of the metaphysis.
• Peripheral type: probably originate from the periosteum or evolve from a previous benign osteochondroma.
Fig. Chondrosarcoma of the right pubic ramus
Multiple myeloma occurs mainly in middle-aged and elderly patients and the diagnosis is often missed in the early stages. Clinically, bone pain and generalised weakness may be presenting features. The X-ray appearances are often diagnostic although marrow puncture and electrophoresis may be necessary to confirm the diagnosis. Myelomatous deposits appear as small punched-out holes in the bone. Characteristically these involve the inner surface of the cortex in the long bones. Sometimes, particularly in the spine, an appearance is produced resembling generalised osteoporosis. Small round punched-out deposits are also seen in the skull and are virtually diagnostic
Fig. Punched-out circular deposits of multiple myeloma in the skull vault.
Metastatic tumours
Bone metastases are the most common malignant bone tumours. Metastases disseminate mainly to marrow-containing bones, therefore they are more commonly found in the axial skeleton. Generally, spread distal to the knee and elbow is less likely than the proximal skeleton. Any primary tumour may metastasize to bone, but the most frequent to do so are:
• Breast: high incidence of bone deposits, usually lytic iature but may be sclerotic or mixed; the commonest cause of sclerotic deposits in females.
• Prostate: almost always sclerotic, lytic deposits being rare; the commonest cause of sclerotic deposits in a male.
• Lung: lytic deposits; peripheral deposits in the hands and feet are rare, but if present are likely to be from a bronchial carcinoma.
• Kidney, thyroid: lytic and can be highly vascular with bone expansion.
• Adrenal gland: predominantly lytic.
PRESENTATION
Bone pain; pathological fracture; soft-tissue swelling; staging or during follow-up of primary tumours.
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Fig. Lytic deposits in the cranial vault.
Fig. Sclerotic deposit in a vertebral body.
RADIOLOGICAL FEATURES
Bone metastases tend to be either lytic or sclerotic. On plain films:
• Lytic deposits. Destruction of bone detail with poor definition of margins and associated pathological fractures are the principal features. Periosteal reactions are rare compared to primary malignant tumours.
• Sclerotic deposits. Show as an area of ill-defined increased density with subsequent loss of bone architecture. Vertebral secondaries may feature sclerotic pedicles. With multiple lesions, a diagnosis of metastases is almost certain. Isotope bone scanning is more sensitive than plain films (localized areas of increased uptake: hot spots).
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Fig. Isotope bone scan showing multiple bone deposits.
In cases where the primary tumour is unknown, an image-guided biopsy of the bone lesion may reveal the site of the primary carcinoma.
DIFFERENTIAL DIAGNOSIS
• Paget’s disease (sclerotic areas).
• Multiple myeloma (lytic areas).
• Primary malignant tumour.
• Infection or osteomyelitis.
Multiple myeloma
Multiple myeloma is a primary malignant tumour of bone marrow, in which there is infiltration of the marrow-producing areas of the skeleton by a malignant proliferation of plasma cells. The skull, spine, pelvis, ribs, scapulae and the proximal axial skeleton are primarily involved with destruction of marrow and erosion of bony trabeculae; the distal skeleton is rarely involved. The disease may occur in a disseminated form, or as a localized solitary enlarging mass (plasmacytoma). Multiple myeloma is the most common primary malignant tumour of bone and tends to be confined to the skeletal system.
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Fig. 7.16 Lateral skull in multiple myeloma showing widespread well-defined ‘punched out’ lytic lesions in the cranial vault.
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Fig. Myeloma deposits in the humerus producing lytic areas and ‘endosteal scalloping’: compare the appearances with a normal humerus.
PRESENTATION
A male predominance, usually in the over-40 age group; weight loss; malaise; bone pain; backache; vertebral body collapse; pathological fracture; Bence-Jones proteinuria.
RADIOLOGICAL FEATURES
At time of presentation 80-90% have skeletal abnormalities. Plain films feature:
• Generalized osteoporosis with a prominence of the bony trabecular pattern, especially in the spine, resulting from marrow involvement with myeloma tissue. Loss of spinal bone density may be the only radiological sign in multiple myeloma. Pathological fractures are common.
• Compression fractures of the vertebral bodies, indistinguishable from those of senile osteoporosis.
• Scattered ‘punched-out’ lytic lesions with well-defined margins, those lying near the cortex produce internal scalloping.
• Bone expansion with extension through the cortex, producing soft-tissue masses.
COMPLICATIONS
• Pathological fractures that heal with abundant callus.
• Hypercalcaemia secondary to excessive bone destruction.
• Renal failure may result from a combination of amyloid deposition, hypercalcaemia and tubular precipitation of abnormal proteins.
• Increased incidence of infections such as pneumonia.
Hyperuricaemia and secondary gout
Osteoporosis
Osteoporosis is a condition in which there is a reduction of bone mass.
PRESENTATION
• Asymptomatic.
• Bone pain.
• Skeletal fractures.
• Vertebral compression fractures.
RADIOLOGICAL INVESTIGATIONS
• Plain films.
• Bone densitometry either by CT, X-ray or isotope bone absorptiometry.
Fig. Osteoporotic lower thoracic and lumbar spine showing loss of bone density with vertebral collapse.
RADIOLOGICAL FEATURES
Detection of osteoporosis on plain films requires a reduction in bone mass of at least 25-30%. Osteoporosis results in a loss of bone density, a decrease in the number of trabeculae and coarse striations.
The condition manifests itself most prominently in the spine. The vertebral bodies appear lucent with thin cortical lines, often with a biconcave appearance (‘cod fish’ vertebrae), vertebral wedging and collapse; this subsequently leads to a kyphosis. Fractures of the peripheral skeleton, including femoral neck fractures, commonly occur even after minor trauma.
CAUSES OF LOCAL OSTEOPOROSIS
• Disuse of a particular part (tumours, fracture).
• Inflammatory conditions such as rheumatoid arthritis and osteomyelitis.
• Sudeck’s atrophy (neural or muscle paralysis). Development of pain and osteoporosis often after slight trauma; it may have a neurovascular aetiology.
CAUSES OF GENERALIZED OSTEOPOROSIS
• Senile osteoporosis..
• Postmenopause.
• Steroid therapy.
• Immobility (prolonged bed rest).
• Endocrine: Cushing’s disease.
• Multiple myeloma.
• Nutritional deficiency syndromes: scurvy, malnutrition, chronic liver disease, malabsorption syndromes.
Osteoarthritis
Osteoarthritis is characterized by degeneration of articular cartilage and is part of the normal ageing process due to wear and tear of the articular surface. Secondary osteoarthitis results from previous trauma with malalignment of articular surfaces, joint infection and rheumatoid arthritis.
RADIOLOGICAL FEATURES
Any joint, particularly weight-bearing, may be affected. The hips, knees, shoulders, hands, wrists and spine are frequently involved. Features of osteoarthritis include:
• Osteophyte formation: osteophytes are spurs of compact bone which form at joint margins.
• Joint space narrowing: cartilage loss eventually leads to non-uniform joint space narrowing.
• Loose bodies: result from separation of cartilage and osteophytes.
• Subchondral cysts and sclerosis: increased bone density around joints with degenerative cyst formation.
COMMON SITES OF INVOLVEMENT
Knee. The most common joint involved, with femorotibial compartment loss of joint space. The medial compartment is the weight-bearing part under greatest stress, and so almost always shows the earliest narrowing. Severe changes may require total knee joint replacement.
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Fig. Degenerative changes at the knee joint with loss of medial compartment joint space.
Spine. Degenerative changes are present iearly all elderly patients. Features include:
• narrowing of disc space;
• new bone formation (spurring) between adjacent vertebrae may cause nerve root impingement or spinal cord compression;
• sclerosis and osteophytes at intervertebral apophyseal joints.
Degenerative changes in the cervical spine with mid and lower cervical loss of disc space.
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Fig. 7.22 Degenerative changes in the cervical spine with mid and lower cervical loss of disc space.
Hips. Joint space narrowing is seen initially at the superior maximum weight-bearing aspect, with femoral and acetabular osteophytes. Other findings may include sclerosis and subchondral cyst formation. Severe changes ofteecessitate total hip joint replacement.
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Fig. Degenerative changes in the left hip with loss of joint space and osteophyte formation.
Hands. Typically affects:
• base of first metacarpal;
• proximal interphalangeal joints (Bouchard’s nodes);
• distal interphalangeal joints (Heberden’s nodes).
Rheumatoid arthritis
Rheumatoid arthritis is defined as a chronic polyarthritis due to inflammation, congestion and proliferation of synovium, leading to bone erosion with cartilage destruction.
Fig. Rheumatoid arthritis: erosive changes, predominantly at the metacarpophalangeal joints and wrists.
RADIOLOGICAL FEATURES .
Radiological changes lag behind clinical symptoms. Rheumatoid arthritis tends to have a symmetrical distribution, most commonly affecting the hands and feet. Any synovial joint may be involved, the most significant and frequent findings in rheumatoid arthritis being uniform narrowing of joint space, marginal erosions and periarticular osteoporosis. The following features may be found:
• Joint swelling: from synovial membrane proliferation and joint effusions.
• Erosions: initially located in the periarticular area along the joint margins, where no protective layer exists. Erosions eventually spread across the articular surface.
• Osteoporosis: periarticular at first, but later generalized from disuse and hyperaemia.
• Joint-space narrowing: widening of joint spaces at the outset of disease, but eventually a significant narrowing from erosions and cartilage deformity. Obliteration and complete destruction of joint space eventually leads to ankylosis.
SPECIFIC SITES OF INVOLVEMENT
• Hands: the MCP and PIP joints are commonly affected, with distal inter-
phalangeal joint involvement less marked. Abnormalities include soft-
tissue swelling and subluxation at the MCP joints:
‘Boutonniere’ deformity: flexion deformity at proximal interphalangeal joint and extension at distal interphalangeal joint;
‘Swan neck’ deformity: hyperextension at proximal interphalangeal joint and flexion at distal interphalangeal joint.
• Feet: broadly similar changes to hands.
• Wrists: erosions with fusion of the carpal bones.
• Elbows: common site for soft-tissue rheumatoid nodules.
• Shoulders: erosion of humeral head and acromio-clavicular joints.
• Knees: uniform joint-space narrowing with osteoporosis. Baker’s cyst is a complication, with rupture producing symptoms and signs similar to those of a deep-vein thrombosis.
• Cervical spine: subluxation, erosion and fusion. Subluxation is most common at the atlanto-axial joint.
Gout
Gout is characterized by a raised plasma uric acid level with recurrent attacks of arthritis. It is due to an inborn error of metabolism and predominantly affects males.
PRESENTATION
• Hot swollen joint, usually the first metatarso-phalangeal (MTP) joint.
• Asymptomatic hyperuricaemia.
RADIOLOGICAL FEATURES
Radiological changes only occur many years after clinical symptoms.There exists a predilection for the first MTP joint, but ankles, knees, elbows and other joints may also be involved. Plain films may reveal:
• Joint effusions and swellings.
• Erosions: These tend to have a ‘punched-out’ appearance, lying separately from the articular surface. Bone density is preserved.
• Tophi: Composed of sodium urate and deposited in bone, soft tissues and around joints. Calcification in the tophi may be found, and intraosseous tophi may enlarge to produce erosions with joint destruction.
Fig. Gout: soft tissue swelling with sharply defined erosions. Involvement is asymmetrical.
Fig. Gout affecting the first metarso-phalangeal joints. Soft tissue swelling is present with large erosions.
COMPLICATIONS
Renal calculi: non-opaque on plain films; renal failure.
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Ankylosing spondylitis
Ankylosing spondylitis, a progressive inflammatory disease, usually affects young adult males, often with a family history of the disease; 95% of patients carry the human leukocyte antigen (HLA-B27 antigen).
PRESENTATION
• Repeated attacks of backache and stiffness.
• Anorexia and weight loss.
RADIOLOGICAL FEATURES
On plain films the following features may be seen:
• Sacroiliac joints. The earliest changes begin in the sacroiliac joints with symmetrical blurring and poor definition of joint margins. Later, erosion and bony sclerosis lead to a tendency for complete sacroiliac joint fusion. Both joints are commonly affected; a unilateral sacroiliitis should raise the suspicion of a bacterial infection, commonly tuberculous. Sacroiliitis is usually evident on bone scanning before any radiographic change.
• Spinal changes. The entire spine may be involved but changes usually commence in the lumbar region and progress upwards to involve the thoracic and cervical spine. The features most commonly noted are: squaring of the vertebral bodies due to new bone formation in the anterior vertebral bodies, and filling in of the normal anterior concavity by longitudinal ligamentous calcification; calcification of the lateral and anterior spinal ligaments to produce the classical ‘bamboo spine’.
• Peripheral joint involvement. An erosive arthropathy may accompany ankylosing spondylitis, the hips being the commonest joints involved.
Fig. Typical ‘bamboo spine’ with paraspinal ligament calcification. The right sacroiliac joint appears ill defined and the left fused.
COMPLICATIONS/ASSOCIATIONS
• Upper-lobe lung fibrosis.
• Aortic incompetence: from an aortitis of the ascending aorta.
• Inflammatory bowel disease: a colitis resembling Crohn’s disease or ulcerative colitis.
• Atlanto-axial subluxation.
• Fractures: spinal rigidity causes increased susceptibility to trauma.
• Ventilatory failure: due to restrictive chest movements and ankylosis of the costovertebral joints.
• Iritis
Rickets
Vitamin D deficiency in children can cause rickets. Deficiency may be nutritional, due to malabsorption, chronic renal disease or prolonged anticonvulsant therapy.
PRESENTATION
Failure to thrive; bone pain; bone deformities.
RADIOLOGICAL FEATURES
The principal pathological change is a lack of calcification of osteoid tissue in the growing epiphysis. The whole skeleton is affected, especially rapidly growing areas: wrists, knees and proximal humeri. Greenstick fractures are common.
The following features may be seen on plain films.
• Widening of the growth plate and epiphysis, with delayed appearance of epiphyses.
• Fraying and indistinct margins of the metaphysis producing a cupped appearance.
• Periosteal reactions, especially during the healing stage.
• Bowing and curvature of bones.
• Bulbous enlargement of the anterior ends of the ribs producing a ‘rickety rosary.
Fig. Looser’s zone’ in the femur (arrow).
OSTEOMALACIA
Vitamin D deficiency in the mature skeleton can lead to osteomalacia, the adult counterpart of rickets.
PRESENTATION
Bone pain; muscular weakness; elevated serum alkaline phosphatase; pathological fractures.
RADIOLOGICAL FEATURES
• Generalized reduction in bone density.
• Looser’s zones (pseudofractures) are narrow translucent bands, at the cortical margins, and are diagnostic of osteomalacia. They are seen most frequently in the ribs, scapulae, pubic rami and medial aspects of the proximal femora.
• Biconcave vertebrae (‘cod fish’ vertebrae).
• Bone softening leading to triradiate pelvis.
OSTEOMYELITIS
Osteomyelitis is an infection of bone. Staphylococcus aureus being responsible for the majority of cases; other causes include tuberculosis and Salmonella infection in sickle cell disease. The inflammatory process can be either acute or chronic, the latter leading to bone necrosis and pus formation, which sometimes discharges through to the skin to form a sinus communication with bone. Necrotic bone may separate from living tissue to produce a sequestrum. Sources of infection may be:
• haematogenous: usually in children;
• direct traumatic implantation, e.g. compound fracture or surgery;
• extension from adjacent soft tissues, e.g. a foot ulcer in diabetes.
Fig. Acute osteomyelitis of the radius with patchy bone destruction
PRESENTATION
• Pain.
• Pyrexia.
RADIOLOGICAL FEATURES
• Plain films: may be normal for up to 10 days but the earliest sign is soft-tissue swelling. Infected bone initially loses detail and becomes ill-defined with periosteal reaction and eventually bone destruction.
• Isotope bone scanning: uses technetium, gallium or labelled white cells. All indicate increased activity but are non-specific as conditions such as Paget’s disease or neoplasia may also show increased uptake. The findings have to be interpreted in the clinical setting.
• CT: detects associated soft-tissue mass and sequestra. Their presence may need surgical removal.
• MRI: a sensitive technique in detecting infection.
Chronic osteomyelitis
Organisms responsible for the infection persist in dead bone, and exacerbations may ensue periodically. The bone appears thickened and sclerotic with a central radiolucent destructive area, often with a chronic draining sinus. An abscess with a sclerotic margin, sometimes containing a sequestrum, may follow (Brodie’s abscess).
COMPLICATIONS
• Soft-tissue abscess.
• Fistulae.
• Premature fusion of epiphyses.
• Deformity.
Pyogenic arthritis leading to bony ankylosis (e.g. hip fusion)
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Fig. Chronic osteomyelitis of the tibia with extensive sclerosis
FRACTURE
Plain films are the principal method of initial evaluation of a patient with suspected skeletal trauma. Any bone may fracture but some are particularly susceptible. Typical signs and features of a fracture are:
• Fracture line: the fracture line may traverse the whole diameter of the bone or minor fractures may cause a break in the continuity of the normal cortical outline.
• Soft tissue swelling: usually accompanies a fracture.
• Cortical irregularity: a slight bulge or step in the cortex.
TYPES OF FRACTURES
• Greenstick: in children bone tends to be flexible, so a fracture may occur with buckling or bending of bone or a break only on one side of the cortex.
• Comminuted: a fracture with multiple fragments.
• Avulsion: a fragment of bone becomes detached from the site of a ligamentous or tendon insertion.
• Pathological: a fracture through diseased bone, often after trivial trauma, e.g. Paget’s disease, osteoporosis or tumour.
• Stress or fatigue fracture: results from chronic repetitive minor trauma. Susceptible areas include the second and third metatarsals (march fracture), proximal tibial shaft and the base of the fifth metatarsal.
Impacted fracture: the fragments are compressed into each other
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Fig. Secondary deposit in the humerus; pathological fracture
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Fig. Greenstick fractures of the distal forearm (arrows).
Shoulder dislocation
Shoulder dislocation commonly results from an athletic injury or fall. Dislocation almost always occurs anteriorly with the humeral head lying in front of, and below, the glenoid cavity; posterior dislocation is rare. Avulsion of the glenoid labrum or avulsion of the greater tuberosity may be associated with the dislocation. Complications include damage to the radial and axillary nerves or rotator cuff muscles
Supracondylar fracture
Usually occur in children; brachial artery njury is a recognized complication.
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Fig. Severe supracondylar fracture in a young child, AP and lateral projections
Elbow fractures
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Fig. Dislocation at the elbow.
These can be classified as: intercondylar T and Y fractures; lateral and medial condylar fracture; radial head fracture; olecranon fracture; and elbow dislocation
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Fig. Olecranon fracture.
Colles‘ fracture
May follow a fall on the outstretched hand, resulting in a fracture of the lower end of the radius with posterior displacement of the distal fragment.
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Fig. Colles‘ fracture.
Scaphoid fracture
Fig. Scaphoid fracture (arrow).
The fracture is often difficult to identify and if there is clinical suspicion, a further X-ray after 10 days is required, when it may be more easily visualized. Complications include non-union and avascular necrosis of the proximal fragment.
Hip fracture
Fractures can be classified into femoral neck, trochanteric and subtrochanteric types
Fig. Intertrochanteric fracture.
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Fig. Femoral neck fracture
Ankle fracture
Fig. Fracture of the medial malleolus, seen only on the lateral view showing the importance of two projections.
CONGENITAL LESIONS
There are large numbers of congenital bone lesions and dystrophies and many of these show characteristic radiological appearances. Some are very rare and are of little concern to the student, though they are of considerable interest to the radiologist. A full review of the rarer conditions will be found in monographs or in larger radiology textbooks.
Some bone dystrophies are associated with other lesions and can be diagnosed or suspected on clinical examination as readily as by radiology.
Achondroplasia. People with achondroplasia with a large head and trunk and relatively small limbs are easily recognised and used to be a familiar sight in circuses. Gargoylism, or Hurler’s syndrome, in its more severe manifestations is also readily diagnosed on clinical inspection. Osteogenesis imperfecta can be recognised by the clinician from the characteristic blue sclerotics.
Craniostenosis with premature fusion of the cranial sutures gives rise to characteristic deformity of the skull. The most common variety results in oxycephaly, or turricephaly.
Congenital anomalies of the spine are not rare and may be associated with neurological lesions. In the cervical region, fusion of vertebrae (Klippel-Feil syndrome) can occur and fusion of the atlas and occiput (atlanto-occipital fusion) is also encountered. In the dorsal region hemivertebrae are encountered with associated spinal scoliosis and kyphoscoliosis. Severe cases may give rise to kinking of the spinal cord with cord compression. This develops in adolescence as the spine elongates relative to the cord. Spina bifida is commonest in the lumbosacral region. The gross degrees associated with syringomyelocele– and meningomyelocele are self-evident. In minor degrees the diagnosis can only be made on X-ray, and such minor lesions are often encountered at X-ray as a symptomless chance finding (spina bifida occulta).
Fig. Klippel-Feil syndrome: congenital partial fusion of cervical vertebrae. Rudimentary discs are still present.
Congenital anomalies of the limbs are fairly common and include syndactyly, poldactyly and brachdactyly. Phocomelia (absence of the proximal parts of the limb) and other severe deformities have been well publicised since the tragic thalidomide cases. Attention was focused on these deformities and it was realised that they could be produced by toxic effects in utero resulting from drugs taken by the mother. In most of these severe cases radiology does little more than emphasise the bony features of an obvious congenital lesion.
Down’s syndrome may show characteristic X-ray changes which can be helpful in assessing clinically doubtful cases in infancy. In the hand the middle phalanx of the fifth finger is short and curved and there may be epiphyses at both ends of the metacarpals and metatarsals. The pelvis shows a characteristic appearance with large iliac blades and flat acetabular roofs. There are often only II ribs present instead of the normal.
Congenital dislocations. The hip-joint is the only joint at which a congenital dislocation is commonly seen. The diagnosis in infancy was often missed until the child began walking but careful clinical examination will permit the diagnosis of most cases soon after birth. Once the diagnosis is suspected it can readily be proved or disproved by ultrasound examination. With early diagnosis soon after birth, the results of treatment have been excellent, and the morbidity of this condition much reduced.
Fig. Congenital dislocation of the right hip – note sloping acetabular roof, delayed ossification of the femoral capital epiphysis and false acetabulum formation.
Metabolic and endocrine disorders
Hyperparathyroidism of the primary type is characterised by true osteoporosis, i.e. there is a quantitative abnormality of the bone in which all the elements including the osteoid are diminished. This is in contrast to osteomalacia in which there is a qualitative defect, i.e. osteoid is present but it is not normally mineralised. The osteoporosis of hyperparathyroidism is due to widespread pathological resorption of bone stimulated by overactivity of the parathyroid. An important point is that although the radiological changes can be very severe they are relatively uncommon, occurring in less than 30% of patients. Thus the majority of cases may show no detectable bone changes. When present, however, such changes are fairly characteristic. Apart from the generalised porosis, specific appearances may be seen in the hands where cortical erosions are shown in the phalanges. These are best seen on the radial side of the phalanges and are very characteristic. The skull may also show marked osteoporosis with a diagnostic fine granular appearance (‘pepper-pot’ skull). There is also some loss of definition between the inner and outer tables and the diploe. An X-ray of the teeth may show loss of the lamina dura or dense cortical line of their surrounding bone . Bone cysts due to osteoclastic proliferation may develop late in the disease and deformities of the bone may occur.
Fig. Osteomalacia with biconvex discs herniating into vertebrae.
Fig. Hyperparathyroidism showing subperiosteal erosion of the lateral aspect of middle phalanges and digital terminal tufts.
In advanced cases deposits of calcium in the kidney substance may occur (nephrocalcinosis) and frank renal calculi may develop. All patients with renal calculi and especially patients with recurrent bilateral calculi should be investigated to exclude parathyroid tumours. A single normal serum calcium level should not be accepted as excluding hyperparathyroidism, and several readings at intervals are now regarded as essential. Estimates of the percentage of patients with renal calculi who are suffering from hyperparathyroidism vary between 5 and 20%.
Secondary hyperparathyroidism may result from chronic renal insufficiency. The consequent disturbance to the normal serum phosphorus and calcium results in parathyroid disturbance. The resulting radiological picture may be very similar to that of primary hyperparathyroidism though cyst formation is unusual.
Hypothyroidism. This gives rise to characteristic changes in infants.
Children with cretinism have short thick bones. The epiphyses are late in appearing and tend to be irregular and deformed and may be fragmented. There is often a metaphysial band of increased density at the growing ends of the bones.
Cushing’s syndrome. Most spontaneous cases are associated with adrenal hyperplasia or tumour. Bone changes consist of osteoporosis affecting mainly the axial skeleton and not the limbs. Painless fractures may occur in the osteoporotic spine and in the ribs and pelvis and these may be discovered by the radiologist though unsuspected clinically. With osteoporosis of the spine there may be collapse and wedging of the vertebral bodies. The characteristic round-shoulder appearance and loss of height in Cushing’s syndrome is due to the resulting dorsal kyphosis. With the wide spread use of corticosteroids in the treatment of rheumatic and other disorders, it is important to realise that prolonged steroid therapy can induce bone changes identical with those of Cushing’s syndrome, even including spinal deformities and spontaneous fractures. Destructive joint changes, particularly in the hips, may also follow steroid therapy.
Acromegaly. This condition shows characteristic radiological as well as characteristic clinical changes. The skull vault is thickened and the paranasal sinuses are enlarged. The sella is also enlarged in a high proportion of cases. The prognathous mandible is as obvious at X-ray as it is clinically. In bones the muscular attachments are accentuated. The vertebrae become enlarged and kyphosis commonly develops. In the hands the tufts of the terminal phalanges are expanded. Osteoporosis. The distinction between osteoporosis and osteomalacia has already been emphasised and some of the rare causes such as osteogenesis imperfecta, hyperparathyroidism and Cushing’s syndrome have been mentioned. A common form of osteoporosis encountered in clinical practice is so-called senile osteoporosis. The exact aetiology of this common and often painful disorder remains obscure. Occasionally this type of generalised osteoporosis is seen in younger patients (presenile or idiopathic osteoporosis). As the osteoporosis progresses, pathological fractures and wedging of the vertebrae are seen, with kyphosis and loss of stature. Since the aetiology of senile osteoporosis is controversial, treatment is unsatisfactory, and there is as yet no effective therapy for the condition. Postmenopausal osteoporosis is seen mainly in females above the age of 50. It is related to reduced oestrogen levels and is commoner in females of slender build.
Paget’s disease. The clinical features of the advanced case have been widely recognised since Paget’s classic description but the cause of this mysterious and not uncommon disease of bone remains unknown. It is of great interest to the radiologist who often encounters it as a chance finding on routine X-ray of an elderly patient. The pelvis, skull and lumbar spine are perhaps the commonest areas to be involved. The essential bone change is a resorption of the normal bone whilst at the same time new bone is laid down in an abnormal irregular manner. Radiologically, two forms of Paget’s disease are recognised and these have been termed the spongy and the amorphous. The former is the commoner and results in replacement of the normal bone trabeculae by coarse irregular striae. The amorphous type of bone replacement results in a hazy opaque mottled appearance in the bone. Sometimes both processes are seen in the same area. A common feature of Paget’s disease is an increase in size and thickness of bone which is very characteristic. When the skull is involved the bone may be three or four times its normal thickness. The skull may also be affected by an unusual type of Paget’s disease in which large areas of bone resorption occur (so called osteoporosis circumscripta). The femur and tibia are also common sites for Paget’s disease but it is rare in the hands or feet. A rare complication of Paget’s disease is sarcoma developing in an area of affected bone. Most cases of bone sarcoma in elderly patients usually arise in pre-existing Paget’s disease.
Inflammatory diseases of bone
With the widespread use of antibiotics, pyogenic infection of bone has become relatively rare except as a result of compound fractures. Further, acute haematogenous osteomyelitis when seen presents a completely different pathological picture from that seen before the advent of antibiotics. Treatment by antibiotics has also profoundly influenced prognosis. Gross destruction of bone with sequestration and chronic sinus formation, which was formerly a major problem, is now rarely seen. In the well-treated case radiological changes may be negligible. In any case it should be remembered that radiological abnormalities in acute osteomyelitis are not detectable for the first week or two of the disease. When antibiotics have been administered from the start and disease is well controlled no bone changes at all may be seen by the radiologist. When treatment has been delayed a periosteal reaction will be demonstrated at the site of the infection together with some osteoporosis of the involved area.
Subacute and chronic osteomyelitis due to invasion with organisms of low-grade virulence may occur in older children and in adults. These can produce destructive bone lesions and give rise to difficulty in differential diagnosis from neoplasm.
Tuberculosis of bone. Tuberculous infection of bones and joints was usually of the bovine type. With the control of bovine tuberculosis now achieved in this country infection of bones and joints has become increasingly rare. There has, however, been some recent increase in the incidence and this has been mainly accounted for by immigrants, particularly from the Indian subcontinent. Nevertheless, it is true that cases of tuberculosis of bone and joint which used to be common in X-ray practice are now rarely seen by a general radiologist.
Tuberculous infections of long bones generally produce destructive lesions or can present with so-called ‘cystic’ manifestations which can cause considerable difficulty in radiological diagnosis. Tuberculosis of the spine was one of the commonest forms of bone tuberculosis and its onset is usually in infancy or childhood. Characteristically, there was bone destruction and destruction of the intervertebral disc with a resulting fusion of two or more vertebrae and angular kyphosis. Paravertebral cold abscess which may track well away from the bone focus is common. Cord compression may occur from collapse of the vertebrae, or from protrusion of a cold abscess or granulation tissue into the spinal canal.
Syphilis of bone. Like osseous tuberculosis, syphilis of bone is now more commonly seen in radiological museums than in clinical practice. In congenital syphilis radiological evidence of osteochondritis, periostitis, and osteitis is frequent. The metaphysitis is involved in the first months of life, producing a ‘saw tooth’ or disorganised appearance on X-ray. The metaphysis shows increased density with a zone of osteoporosis beneath and metaphysial fracture may occur. These changes are best seen at the knee and wrist.
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Fig. Pott’s disease of the spine with fusion of several vertebrae, angular kyphosis and calcified cold abscess. several vertebrae, angular kyphosis and calcified cold abscess. |
Skeletal changes may also occur in acquired syphilis, though these are now rarely encountered. In its most characteristic form tertiary syphilis produces a so-called ‘lace-work’ periostitis, but osteitis with destructive changes is also seen. In the days when it was common tertiary syphilis had the reputation of being the great simulator of other forms of bone disease, so protean were its manifestations.
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