Imaging Diagnosis
Imaging diagnosis is where pattern recognition meets patient safety. The board expects you to name a lesion from its radiographic hallmark (the sign, where it sits and which view shows it), and practice demands that you recognize the handful of findings that change everything: the unstable fracture, the missing pedicle, the destroyed disc space, the calcified aortic aneurysm. This chapter walks through congenital anomalies and trauma, the arthritides, tumors, metabolic and infectious disease, and the miscellaneous spinal, chest and abdominal findings that turn up on chiropractic films.
By the end of this chapter you can
- Distinguish a congenital block vertebra, os odontoideum, spina bifida occulta and transitional segments from acquired disease.
- Recognize the classic spinal fractures, including Jefferson, hangman, odontoid, clay shoveler, compression, burst and Chance fractures, and judge stability with the three column model.
- Describe spondylolysis and the types of spondylolisthesis.
- Separate degenerative, inflammatory and crystal arthritides by distribution, joint space pattern, bone density and erosions, including DISH, rheumatoid arthritis, ankylosing spondylitis, gout and CPPD.
- Analyze a bone lesion by age, location, margin, matrix and periosteal reaction, and recognize metastasis, multiple myeloma, hemangioma and the primary bone tumors.
- Identify the radiographic hallmarks of osteoporosis, osteomalacia, Paget disease, hyperparathyroidism, sickle cell disease and avascular necrosis.
- Distinguish pyogenic discitis, tuberculous spondylitis and tumor by what happens to the disc.
- Recognize Scheuermann disease, scoliosis types, pneumothorax, effusion, lung masses, abdominal aortic aneurysm and common calcifications, and know when to refer.
Section 1Congenital anomalies, normal variants and trauma
Congenital anomalies of the spine
Anomalies arise from failures of segmentation (the somites do not separate), failures of formation (part of a vertebra never forms) or failures of fusion (ossification centers do not unite). Most are incidental, but some alter mechanics, predispose to instability or mimic acquired disease.
| Anomaly | Radiographic hallmark | Significance |
|---|---|---|
| Congenital block vertebra (failure of segmentation) | Fused bodies with a rudimentary disc remnant and a concave anterior wasp waist at the fused disc level; total height equals two bodies plus a disc; posterior elements often fused too; C2 to C3 and C5 to C6 common | Increased stress and early degeneration at adjacent levels. Acquired fusion (surgery, infection, juvenile arthritis) lacks the wasp waist |
| Klippel Feil syndrome | Multiple cervical block vertebrae | Triad of short neck, low posterior hairline, limited motion; Sprengel deformity (high scapula) and omovertebral bone; renal and cardiac anomalies |
| Hemivertebra (failure of formation) | Wedge shaped half vertebra on the AP | Congenital scoliosis, often progressive |
| Butterfly vertebra | Central sagittal cleft with two triangular halves on the AP | Incidental; do not confuse with a fracture |
| Spina bifida occulta | Vertical lucent cleft between unfused laminae, most often L5 or S1 | Usually insignificant; spina bifida vera (with meningocele or myelomeningocele) is a different, clinical disease |
| Transitional lumbosacral segment | Enlarged transverse process of L5 forming a joint or fusion with the sacrum (sacralization), or a squared S1 with a disc (lumbarization) | Level counting errors; the disc above a transitional segment degenerates more readily; Bertolotti syndrome (pain at the pseudarthrosis) |
| Occipitalization of the atlas | Partial or complete fusion of C1 to the occiput | Associated with basilar impression and C1 to C2 instability |
| Agenesis of the posterior arch of C1 | Absent posterior arch with a hypertrophic, rounded anterior arch | Mimics fracture; the hypertrophic anterior arch indicates a longstanding condition |
| Cervical rib | Rib from C7, whose transverse process slopes down | Thoracic outlet syndrome |
Os odontoideum versus odontoid fracture
Os odontoideum is a smooth, round, well corticated ossicle separated from a shortened dens by a wide gap that lies above the level of the C1 superior articular facets. The anterior arch of C1 is often enlarged and rounded, which signals longstanding abnormal motion. It may be congenital or the result of an unrecognized childhood fracture. It is important because the transverse ligament no longer controls C1 relative to C2, so flexion extension films often show instability, and patients may present with myelopathy or vertebrobasilar symptoms. Upper cervical manipulation is contraindicated, and the patient should be referred for surgical evaluation if instability or neurologic signs are present. Contrast an acute type II odontoid fracture: a thin, irregular, non corticated lucency at the base of the dens with a normal sized anterior arch. The os terminale (ossicle at the tip of the dens) is a stable variant.
Upper cervical fractures
| Fracture | Mechanism | Hallmark and best view | Stability |
|---|---|---|---|
| Jefferson (C1 burst) | Axial load on the vertex (diving) | APOM: bilateral lateral offset of the C1 lateral masses over C2; combined overhang over about 7 mm (rule of Spence) implies transverse ligament rupture; CT confirms ring fractures in front and back | Unstable if the transverse ligament is torn |
| Posterior arch of C1 | Hyperextension compressing the arch between occiput and C2 | Lateral: vertical fracture through the posterior arch | Stable; must not be confused with a Jefferson fracture |
| Hangman (traumatic spondylolisthesis of C2) | Hyperextension with distraction or axial load (vehicle collisions) | Lateral: bilateral fractures through the C2 pars or pedicles, anterior slip of the C2 body on C3, broken spinolaminar line at C2 | Unstable, but the canal widens, so neurologic injury is often absent |
| Odontoid type I | Avulsion by the alar ligament | Oblique fracture through the tip | Usually stable; rare |
| Odontoid type II | Flexion or extension | APOM and lateral: fracture through the base of the dens | Most common; unstable; highest nonunion rate (poor blood supply) |
| Odontoid type III | Flexion or extension | Fracture extending into the body of C2 | Best healing (cancellous bone) |
Lower cervical fractures
- Clay shoveler fracture: an oblique avulsion of the spinous process of C7 (less often C6 or T1) from sudden flexion against contracted interspinous muscles. Lateral view shows the displaced tip; the AP shows a double spinous process (ghost) sign. Stable.
- Flexion teardrop fracture: a triangular fragment from the anteroinferior body with the rest of the body displaced backward into the canal, from severe flexion and axial load (diving). It disrupts all three columns, is highly unstable and causes anterior cord syndrome.
- Extension teardrop fracture: a small avulsion from the anteroinferior corner of C2 (pulled by the anterior longitudinal ligament) in older patients; stable in flexion. The fragment is taller than wide.
- Facet dislocation: unilateral dislocation produces anterior slip of about 25 percent of the body width and a rotational bow tie appearance of the facets on the lateral; bilateral dislocation produces about 50 percent or more and is highly unstable.
Thoracolumbar fractures and the three column model
Denis divided the spine into three columns. The anterior column is the anterior longitudinal ligament and anterior two thirds of the body and disc; the middle column is the posterior third of the body and disc and the posterior longitudinal ligament; the posterior column is the neural arch, facets and posterior ligaments. Injury to two or more columns, and especially to the middle column, is considered unstable.
| Fracture | Mechanism | Radiographic hallmark | Columns and stability |
|---|---|---|---|
| Compression (wedge) | Flexion, often osteoporosis | Loss of anterior height with intact posterior height; step defect of the anterior cortex, a sclerotic zone of impaction below the endplate, paraspinal edema; most at the thoracolumbar junction | Anterior column only; stable unless over about 50 percent height loss |
| Burst | Axial load (fall from height) | Comminuted body with retropulsed fragment into the canal; widened interpediculate distance on the AP; posterior body height lost; CT required | Anterior and middle columns; unstable; risk of cord or cauda equina injury |
| Chance (flexion distraction) | Lap belt flexion over a fulcrum | Horizontal fracture through the spinous process, laminae, pedicles and body, usually T12 to L2; on the AP, horizontal lucency through the pedicles | All three columns; unstable; about half have abdominal visceral injury, especially in children |
| Transverse process | Direct blow or avulsion by psoas | Vertical or oblique lucency through the transverse process, most often L2 or L3 | Stable; check for renal injury (hematuria) |
Spondylolysis and spondylolisthesis
Spondylolysis is a defect in the pars interarticularis, most often a fatigue (stress) fracture from repetitive extension and rotation in children and adolescents (gymnasts, football linemen, divers). About 90 percent occur at L5. It is seen as a lucent collar across the neck of the Scotty dog on obliques, as a lucency through the pars on the lateral, and best on CT; SPECT bone scan or MRI (STIR) show an acute stress reaction before a defect appears. A unilateral defect may produce sclerosis and hypertrophy of the opposite pedicle (a stress response that can mimic osteoid osteoma).
| Wiltse type | Cause | Typical patient and level |
|---|---|---|
| I Dysplastic | Congenital dysplasia of the upper sacrum or L5 facets | Children, L5 to S1; high risk of progression and neurologic signs |
| II Isthmic | Pars lesion: lytic stress fracture (IIA), elongated intact pars (IIB) or acute fracture (IIC) | Most common in young people; L5 on S1 |
| III Degenerative | Facet and disc degeneration with intact pars | Women over 40 to 50, L4 on L5; rarely beyond grade 1; causes central and lateral recess stenosis |
| IV Traumatic | Acute fracture of the neural arch other than the pars | After major trauma |
| V Pathologic | Weakened bone (Paget disease, tumor, osteopetrosis) | Any level |
| VI Iatrogenic | After laminectomy or facetectomy | Postsurgical level |
Slip is graded by Meyerding (Chapter 7). A severe L5 slip produces the inverted Napoleon hat sign on the AP: the forward tilted L5 body is seen end on, superimposed over the sacrum. Flexion extension laterals show whether a slip moves.
Congenital anomalies are recognized by smooth, corticated, longstanding features (wasp waist, enlarged anterior arch of C1). Fractures are recognized by sharp, non corticated lines, soft tissue swelling and malalignment, and graded for stability by the columns injured. Any suspected unstable fracture, os odontoideum with motion, or neurologic sign means immobilization and referral, never manipulation.
Section 2Arthritides
Reading an arthritis film
Four questions separate most arthritides: Which joints are involved and in what distribution (symmetric or asymmetric, proximal or distal, axial or peripheral)? Is joint space loss uniform (inflammatory) or non uniform (degenerative)? Is there periarticular osteoporosis? Are there erosions, and what kind (marginal, punched out, central)? Bone production (osteophytes, syndesmophytes, periostitis) and soft tissue changes complete the picture.
| Feature | Degenerative (OA) | Rheumatoid arthritis | Seronegative spondyloarthropathy | Gout | CPPD |
|---|---|---|---|---|---|
| Joint space | Non uniform loss | Uniform loss | Uniform loss, then ankylosis | Preserved until late | Non uniform, like OA |
| Bone density | Normal | Periarticular osteoporosis | Normal early (osteoporosis in late AS) | Normal | Normal |
| Erosions | None (central in erosive OA) | Marginal (bare areas) | Marginal with fluffy new bone | Punched out with overhanging edge | Uncommon |
| Bone production | Osteophytes, sclerosis, subchondral cysts | Little | Syndesmophytes, periostitis, enthesitis | Overhanging edges | Large osteophytes, subchondral cysts |
| Distribution | Weight bearing joints, DIP, PIP, first CMC | Bilateral symmetric MCP, PIP, wrist; cervical C1 to C2 | SI joints and spine; asymmetric peripheral (psoriatic, reactive) | First MTP, asymmetric | Knee, wrist, second and third MCP |
Degenerative joint and disc disease
Osteoarthritis of synovial joints shows the four cardinal signs: non uniform joint space narrowing (greatest where load is greatest), subchondral sclerosis, osteophytes and subchondral cysts (geodes). There are no erosions and no osteoporosis. In the hip the femoral head typically migrates superolaterally; in the knee the medial compartment narrows first, producing varus. In the hand, osteophytes at the DIP (Heberden nodes) and PIP (Bouchard nodes) and the first carpometacarpal joint are typical. Erosive OA in middle aged women adds central erosions with a gull wing appearance at interphalangeal joints.
Degenerative disc disease (intervertebral osteochondrosis) produces disc space narrowing, endplate sclerosis, the vacuum phenomenon (nitrogen gas in fissured disc, essentially excluding infection at that level), marginal osteophytes and retrolisthesis. Traction spurs project horizontally a few millimeters from the endplate margin and suggest instability; claw spurs curve toward the disc. In the cervical spine, uncovertebral arthrosis (osteophytes from the uncinate processes) narrows the intervertebral foramina, best seen on obliques, and is the main cause of cervical foraminal stenosis. Degeneration is most common at C5 to C6 and C6 to C7, and at L4 to L5 and L5 to S1. Facet arthrosis (sclerosis, hypertrophy and osteophytes of the zygapophyseal joints) contributes to lateral recess and foraminal stenosis and to degenerative spondylolisthesis.
DISH and OPLL
Diffuse idiopathic skeletal hyperostosis (DISH, Forestier disease) is an enthesopathy of older adults, more common in men and associated with diabetes and obesity. Its criteria are flowing ossification along the anterolateral aspect of at least four contiguous vertebral bodies, with preserved disc height, and no facet ankylosis or SI joint erosion. It favors the right side of the thoracic spine (the pulsating aorta on the left seems to inhibit it), may show a thin lucent line between the ossification and the anterior body, and looks like dripping candle wax. Peripheral enthesophytes (whiskering of the pelvis, large heel and olecranon spurs) are common. Large anterior cervical ossification can cause dysphagia. A fused DISH segment acts like a long bone and fractures easily after minor trauma.
Ossification of the posterior longitudinal ligament (OPLL) is a dense linear strip behind the cervical vertebral bodies on the lateral, most common in people of East Asian descent, and causes canal stenosis and myelopathy. It coexists with DISH in a substantial minority of patients.
Rheumatoid arthritis
RA is a symmetric inflammatory synovitis. In the hands and wrists it shows fusiform soft tissue swelling, periarticular osteoporosis, uniform joint space loss and marginal erosions at the bare areas, in a bilateral symmetric pattern at the MCP, PIP and carpal joints, while largely sparing the DIP joints. Early erosion of the ulnar styloid is characteristic. Late deformities include ulnar deviation at the MCPs, swan neck and boutonniere fingers, and carpal fusion. Large joints show uniform narrowing: axial migration and protrusio acetabuli at the hip, tricompartmental loss at the knee.
The cervical spine is involved in most long standing cases and is what matters most for chiropractors:
- Atlantoaxial instability: synovitis around the dens weakens the transverse ligament, so the ADI widens beyond 3 mm, often only on flexion.
- Erosion of the dens (a pencil or apple core dens).
- Cranial settling (atlantoaxial impaction): erosion of the lateral masses lets the dens rise toward the foramen magnum.
- Subaxial stair step subluxations at multiple levels with facet erosion and disc narrowing without large osteophytes.
Ankylosing spondylitis and the other seronegatives
The seronegative spondyloarthropathies are rheumatoid factor negative, associated with HLA-B27, and attack the SI joints, spine and entheses. Ankylosing spondylitis (AS) typically begins in young men with inflammatory back pain. Its radiographic sequence is:
- Bilateral symmetric sacroiliitis, the earliest finding: erosions first on the iliac side (thinner cartilage) give a ragged, pseudo widened joint, followed by sclerosis and finally bony ankylosis.
- Romanus lesions (erosions at the anterior vertebral corners) that heal with sclerosis (shiny corners), producing squared vertebral bodies.
- Marginal syndesmophytes: thin, vertical ossification of the outer annulus bridging adjacent bodies, starting at the thoracolumbar and lumbosacral junctions and ascending.
- Bamboo spine when syndesmophytes are continuous; facet ankylosis and ossified interspinous ligaments make the trolley track sign on the AP (central dagger sign plus two facet lines).
The ankylosed spine is brittle and osteoporotic; a minor fall can cause a transverse carrot stick fracture through the fused column, often with neurologic injury. Andersson lesions (destructive discovertebral lesions) can mimic infection. Hip involvement is bilateral, concentric and may ankylose.
| Disease | SI joints | Spine | Peripheral hallmark |
|---|---|---|---|
| Ankylosing spondylitis | Bilateral symmetric | Marginal syndesmophytes, ascending, continuous; bamboo spine | Hips and shoulders; enthesitis |
| Enteropathic (inflammatory bowel disease) | Bilateral symmetric | Same as AS | Nonerosive arthritis of large lower limb joints |
| Psoriatic arthritis | Bilateral asymmetric (or unilateral) | Nonmarginal, bulky, comma shaped syndesmophytes with skip levels | DIP erosions, pencil in cup, sausage digit, fluffy periostitis, acro-osteolysis, ivory phalanx, no osteoporosis |
| Reactive arthritis | Bilateral asymmetric (or unilateral) | Nonmarginal syndesmophytes, like psoriatic | Lower extremity: feet, fluffy calcaneal spurs and periostitis at the Achilles and plantar fascia insertion |
Gout, CPPD and related crystal disease
Gout is deposition of monosodium urate. Bony changes appear only after years of recurrent attacks. The hallmarks are well defined punched out erosions with sclerotic margins and an overhanging edge (the Martel sign), often slightly away from the joint margin, with joint space preserved until late and normal bone density. Lumpy soft tissue tophi (sometimes faintly calcified) sit next to the erosions. Distribution is asymmetric, favoring the first MTP joint (podagra), the feet, ankles, knees and olecranon bursa.
Calcium pyrophosphate dihydrate deposition (CPPD) produces chondrocalcinosis: thin linear calcification of hyaline cartilage parallel to the subchondral bone, and of fibrocartilage, classically the knee menisci, the triangular fibrocartilage of the wrist and the pubic symphysis. Its arthropathy looks like OA but in unusual places: isolated patellofemoral disease, the radiocarpal joint with scapholunate widening, the second and third MCP joints with hook like osteophytes, and the glenohumeral joint, with large subchondral cysts. Calcification around the dens (crowned dens syndrome) can cause acute neck pain and fever. Look for associated hyperparathyroidism and hemochromatosis (which also favors second and third MCP hook osteophytes).
Hydroxyapatite deposition disease causes amorphous calcific tendinitis, most often in the supraspinatus tendon above the greater tuberosity, and occasionally in the longus colli (prevertebral calcification at C1 to C2 with acute painful dysphagia). The neuropathic (Charcot) joint shows the six Ds: distension, increased density, debris, disorganization, dislocation and destruction; diabetes affects the foot, syringomyelia the shoulder and tabes dorsalis the knee and spine.
Arthritides are sorted by distribution, joint space pattern, bone density, erosion type and new bone formation. Degenerative disease narrows non uniformly and builds osteophytes; RA narrows uniformly with osteoporosis and threatens the atlantoaxial joint; the seronegatives attack the SI joints and form syndesmophytes; crystal diseases leave punched out erosions (gout) or cartilage calcification (CPPD).
Section 3Tumors and tumor-like lesions
Analyzing a bone lesion
Radiographs cannot give a histologic diagnosis, but a disciplined analysis narrows the differential and, more importantly, tells you whether a lesion looks aggressive or nonaggressive. Work through these variables:
- Age: the single most useful clue. Over 40, the most likely malignant lesions in bone are metastasis and multiple myeloma. Primary malignant bone tumors are rare and cluster in adolescents (osteosarcoma, Ewing sarcoma) or older adults (chondrosarcoma).
- Number: multiple lesions in an older adult suggest metastasis or myeloma.
- Location: which bone, and epiphysis, metaphysis or diaphysis; central, eccentric or cortical. In the spine, body versus posterior elements.
- Margin and zone of transition: a geographic lesion with a narrow, sclerotic margin is slow growing; a moth eaten pattern (multiple coalescing holes) or a permeative pattern (innumerable tiny holes with a wide zone of transition) is aggressive.
- Matrix: osteoid matrix is cloud like or fluffy (osteosarcoma); chondroid matrix forms rings and arcs or popcorn calcification (enchondroma, chondrosarcoma); ground glass suggests fibrous dysplasia.
- Periosteal reaction: solid, thick, uniform new bone means a slow process. Laminated (onion skin), spiculated (sunburst or hair on end) and the Codman triangle (periosteum lifted at the edge of a fast growing lesion) mean aggression.
- Cortex and soft tissue: cortical destruction with a soft tissue mass suggests malignancy; expansion with a thin intact shell suggests a slower process.
Metastatic disease
Skeletal metastasis is the most common malignant tumor of bone. Spread is usually hematogenous, often through the valveless vertebral venous plexus (Batson plexus), so deposits favor red marrow: the spine (lumbar and thoracic most), pelvis, ribs, skull, and proximal femur and humerus. Lesions distal to the elbow and knee are uncommon (acral metastases suggest lung primary). The five primaries most likely to seed bone are breast, lung, thyroid, kidney and prostate.
- Osteolytic (most common overall): lung, kidney and thyroid (often expansile, blown out), breast.
- Osteoblastic: prostate in men, breast in women (often mixed); also carcinoid and some bladder cancers. Diffuse blastic disease can produce an ivory vertebra.
The classic plain film sign is the missing pedicle (the winking owl sign) on the AP: tumor destroys the cortical ring of one pedicle, so one of the owl's eyes disappears. The body is usually involved first, but cancellous destruction is hard to see until 30 to 50 percent of the bone mineral is gone, whereas the cortical pedicle outline shows loss earlier on the AP. Other findings are vertebral collapse, an ivory vertebra and a paraspinal mass. Crucially, metastasis spares the disc: the disc space is preserved, which separates it from infection. MRI (T1 marrow replacement, convex posterior border, pedicle involvement) and bone scan are far more sensitive than radiographs.
Multiple myeloma and plasmacytoma
Multiple myeloma is the most common primary malignant bone tumor in adults, a malignancy of plasma cells in patients usually over 50. Radiographic patterns are multiple well defined punched out lytic lesions without sclerotic rims (the raindrop skull), diffuse osteopenia with vertebral collapse, or rarely sclerosis. Because the pedicles contain less red marrow, myeloma tends to spare the pedicles early, the opposite of metastasis, though this is a tendency rather than a rule. The bone scan is often normal (cold) because the lesions provoke little osteoblastic response, so a skeletal survey, MRI, low dose whole body CT or PET is used. Laboratory clues are the CRAB features (hypercalcemia, renal insufficiency, anemia, bone lesions), a very high ESR, rouleaux, a monoclonal M spike on serum protein electrophoresis and Bence Jones proteinuria. A solitary plasmacytoma is an expansile, often bubbly lytic lesion of a vertebral body or pelvis that frequently progresses to myeloma.
Benign spinal tumors
Vertebral hemangioma is the most common benign tumor of the spine, found incidentally in about 10 percent of adults, mostly in the thoracic and lumbar bodies. Thickened vertical trabeculae separated by fat and vessels give the classic vertical striations (corduroy cloth or jailhouse appearance) on the radiograph, a polka dot pattern on axial CT, and bright signal on both T1 and T2 MRI because of fat. The body is not expanded and does not collapse in the usual case. It needs no treatment and is not by itself a contraindication to adjusting; rare aggressive hemangiomas extend into the canal and cause cord compression.
Osteoid osteoma affects people aged about 10 to 25 (male predominance). A small lucent nidus under about 1.5 cm is surrounded by dense reactive sclerosis, typically in the cortex of the femur or tibia. The classic history is night pain relieved by aspirin or NSAIDs (the nidus produces prostaglandins). In the spine it arises in the posterior elements and causes a painful scoliosis concave toward the lesion. CT shows the nidus best; bone scan shows intense focal uptake (double density sign). Osteoblastoma is histologically similar but larger (over 1.5 to 2 cm), expansile, also favors the posterior elements, and is not reliably relieved by aspirin.
Aneurysmal bone cyst (under age 20) is an expansile, blown out lytic lesion of the posterior elements or long bone metaphysis with fluid fluid levels on MRI. Langerhans cell histiocytosis (eosinophilic granuloma) in a child is the classic cause of vertebra plana (uniform collapse of a body into a thin wafer with preserved discs) and of skull lesions with beveled edges (hole within a hole).
Primary bone tumors outside the spine
| Tumor | Age | Classic site | Radiographic hallmark |
|---|---|---|---|
| Giant cell tumor | 20 to 40, skeletally mature | Epiphysis and metaphysis around the knee (distal femur, proximal tibia), distal radius; sacrum in the spine | Eccentric lytic lesion extending to the subarticular bone, no sclerotic rim, soap bubble expansion; locally aggressive, occasional lung metastases |
| Osteosarcoma | 10 to 25 (second peak in elderly with Paget disease or prior radiation) | Metaphysis around the knee, proximal humerus | Mixed lytic and sclerotic, cloud like osteoid matrix, sunburst spiculation, Codman triangle, soft tissue mass; raised alkaline phosphatase; lung metastases |
| Ewing sarcoma | 5 to 20 | Diaphysis or metadiaphysis of long bones; pelvis, ribs | Permeative destruction, onion skin laminated periostitis, large soft tissue mass; fever, leukocytosis and raised ESR mimic osteomyelitis |
| Chondrosarcoma | 40 to 60 | Pelvis, proximal femur, proximal humerus, ribs | Lytic lesion with rings and arcs chondroid calcification, deep endosteal scalloping (over two thirds of the cortex), cortical thickening, pain; may arise from an enchondroma or osteochondroma |
| Chordoma | Older adults | Sacrum and clivus (notochord remnants) | Destructive midline lytic mass with a soft tissue component and amorphous calcification |
| Lymphoma of bone | Adults | Long bones, spine | Permeative lysis; Hodgkin disease may cause an ivory vertebra or anterior scalloping from adjacent nodes |
Benign lesions not to touch
Some lesions are so characteristic that biopsy is unnecessary and can even mislead the pathologist, because healing tissue looks aggressive under the microscope. Recognize and leave them alone:
- Bone island (enostosis): a small dense focus of compact bone in cancellous bone with brush border or thorny radiating spicules that blend with surrounding trabeculae; cold or only mildly warm on bone scan.
- Fibrous cortical defect and nonossifying fibroma: eccentric, cortical, metaphyseal lucency with a scalloped sclerotic border in children, especially around the knee; heals spontaneously.
- Simple (unicameral) bone cyst: central metaphyseal lucency in the proximal humerus or femur of a child; a fallen fragment sign after fracture is diagnostic.
- Fibrous dysplasia: expansile ground glass lesion; the shepherd's crook deformity of the proximal femur.
- Enchondroma: central lucent lesion of the hand phalanges with stippled chondroid calcification; multiple in Ollier disease, with soft tissue hemangiomas in Maffucci syndrome (higher malignant risk).
- Osteochondroma: a bony outgrowth whose cortex and medulla are continuous with the parent bone, pointing away from the joint; a cartilage cap over about 1.5 to 2 cm in an adult or new pain suggests malignant change.
- Myositis ossificans: post traumatic ossification in muscle that matures from the periphery inward (zonal pattern) and is separated from the cortex by a lucent cleft, the reverse of osteosarcoma.
- Cortical desmoid (avulsive cortical irregularity) at the posteromedial distal femoral metaphysis of adolescents.
Analyze a bone lesion by age, number, location, margin, matrix and periosteal reaction. In adults over 40, metastasis and myeloma dominate; the missing pedicle with a preserved disc is the classic sign of metastasis. Recognize the benign don't touch lesions (bone island, nonossifying fibroma, hemangioma, osteochondroma, myositis ossificans) so they are not biopsied or overtreated.
Section 4Metabolic, endocrine, hematologic and infectious disease
Osteoporosis
Osteoporosis is reduced bone quantity with normal mineralization of the bone that remains. Causes include postmenopausal estrogen loss and aging (the most common), corticosteroids (and Cushing syndrome), disuse, heparin, hyperthyroidism, alcohol and malabsorption. Plain films are insensitive: about 30 to 50 percent of bone mineral must be lost before radiolucency is visible, so diagnosis rests on DEXA. Radiographic signs in the spine:
- Increased radiolucency with thin but sharply outlined cortices, so the bodies look penciled in or like empty boxes.
- Loss of horizontal trabeculae with relative prominence of vertical trabeculae (which can mimic hemangioma, though the body is not striated throughout).
- Insufficiency fractures: wedge fractures (mid and lower thoracic, increasing kyphosis, the dowager hump), biconcave (codfish) vertebrae from the disc pressing into weakened endplates (more typical of the lumbar spine), and vertebra plana.
- Steroid induced osteoporosis adds dense marginal condensation of the endplates from exuberant callus.
Elsewhere, fragility fractures of the hip, distal radius (Colles), proximal humerus and pelvis are typical, as are sacral insufficiency fractures (an H shaped uptake on bone scan). A new compression fracture with trivial trauma in an older patient still requires a search for myeloma or metastasis; MRI distinguishes them (pathologic fractures show a convex posterior border, pedicle involvement and complete marrow replacement).
Osteomalacia and rickets
Osteomalacia is inadequate mineralization of osteoid in adults, usually from vitamin D deficiency (poor intake or sunlight, malabsorption, liver or renal disease) or phosphate wasting. Bone looks diffusely osteopenic with indistinct, smudged trabeculae. The hallmark is the Looser zone (pseudofracture): a lucent band perpendicular to the cortex, often bilateral and symmetric, on the compressive (concave) side of bones: the medial femoral neck, pubic and ischial rami, the axillary border of the scapula, ribs and the ulna. Multiple symmetric Looser zones are called Milkman syndrome. Softened bone also produces bowing, protrusio acetabuli, biconcave vertebrae and basilar impression. In children, rickets affects the growth plates: widened physes and cupped, frayed metaphyses, bowed legs and the rachitic rosary at the costochondral junctions. Labs show low or normal calcium, low phosphate and high alkaline phosphatase.
Paget disease
Paget disease (osteitis deformans) is disordered remodeling in older adults (usually over 55, slight male predominance), with excessive osteoclastic resorption followed by chaotic osteoblastic repair. The pelvis is most often affected, followed by the spine, skull, femur and tibia. Three phases occur, sometimes together:
- Lytic: osteoporosis circumscripta of the skull (a large sharply marginated lucency) and a blade of grass or flame shaped advancing edge in a long bone, beginning at the end of the bone.
- Mixed: the cotton wool skull with thickened diploe.
- Blastic: dense, enlarged bone.
The essential triad is bone enlargement, cortical thickening and coarsened trabeculae. In the spine look for the picture frame vertebra (thick peripheral cortex around a less dense center) and an enlarged ivory vertebra (enlargement separates it from blastic metastasis and lymphoma). In the pelvis, thickening of the iliopectineal line (the brim sign) and protrusio. In the tibia, anterior bowing (saber shin). Alkaline phosphatase is strikingly raised with normal calcium. Complications include pathologic transverse (banana) fractures, basilar impression, spinal stenosis, deafness, high output heart failure and sarcomatous degeneration (under 1 percent, signaled by new pain and a destructive lesion).
Hyperparathyroidism and renal osteodystrophy
Excess parathyroid hormone drives osteoclastic resorption. The pathognomonic finding is subperiosteal resorption along the radial aspect of the middle phalanges of the second and third fingers, best seen on a fine detail PA hand film. Other findings are acro-osteolysis of the tufts, resorption of the distal clavicles, the salt and pepper skull, loss of the lamina dura around the teeth, subchondral resorption that widens the SI joints and symphysis, and brown tumors (expansile lytic lesions of osteoclasts and hemorrhage). Primary hyperparathyroidism (usually an adenoma) is associated with chondrocalcinosis and renal stones. Secondary hyperparathyroidism of chronic renal failure (renal osteodystrophy) combines resorption with osteomalacia and osteosclerosis; its classic spinal sign is the rugger jersey spine: dense bands under each endplate with a lucent middle, like the stripes on a rugby shirt. Soft tissue and vascular calcification are common.
Sickle cell disease and avascular necrosis
In sickle cell disease, sickled cells occlude small vessels. Infarction of the central endplate (supplied by end arteries) produces the H shaped (Lincoln log) vertebra with step like central depressions, distinct from the smooth curve of a codfish vertebra. Marrow hyperplasia widens the diploe of the skull (hair on end appearance, also seen in thalassemia) and causes generalized osteopenia. Other findings are medullary bone infarcts (serpiginous calcification), avascular necrosis of the femoral and humeral heads, dactylitis (hand foot syndrome) in infants, and osteomyelitis, for which Salmonella is characteristically more common than in other populations (though Staphylococcus aureus remains frequent).
Avascular necrosis (osteonecrosis) is bone death from interrupted blood supply. Causes include corticosteroids, alcoholism, trauma (femoral neck fracture, hip dislocation, scaphoid waist fracture), sickle cell disease, Gaucher disease, caisson disease (dysbaric), lupus, pancreatitis and radiation. In the femoral head, radiographs are normal early; then patchy sclerosis appears, followed by the crescent sign (a subchondral lucent line indicating collapse), flattening and finally secondary osteoarthritis. The joint space is preserved until late. MRI is the most sensitive test, showing a serpiginous band (the double line sign on T2). Named osteonecroses include Legg Calve Perthes disease (femoral head, boys about 4 to 8, with fragmentation and flattening), Kienbock disease (lunate, associated with negative ulnar variance), Freiberg infraction (second metatarsal head), Preiser disease (scaphoid) and Kohler disease (tarsal navicular in children).
Osteomyelitis
Hematogenous osteomyelitis in children seeds the metaphysis, where slow flow in looping vessels favors bacterial settling; Staphylococcus aureus is the most common organism. Radiographs lag 10 to 14 days behind symptoms. The earliest signs are deep soft tissue swelling and loss of fat planes; then a poorly defined lytic area with periosteal reaction appears. Chronic infection produces a sequestrum (a dense fragment of dead bone), an involucrum (a shell of new periosteal bone around it) and a cloaca (an opening through which pus drains). A Brodie abscess is a subacute, walled off metaphyseal lucency with a thick sclerotic rim. MRI (marrow edema, abscess) and three phase bone scan detect infection days to weeks before radiographs.
Pyogenic discitis and vertebral osteomyelitis
In adults, bacteria reach the vertebral endplate through the arterial supply (from urinary tract, skin or dental sources, injection drug use, endocarditis, or after spinal procedures), then spread into the disc and to the adjacent endplate. In children the disc is vascular and may be infected directly. Risk factors are diabetes, immunosuppression, injection drug use, dialysis and recent instrumentation. The lumbar spine is most often affected, and patients have severe constant pain, often fever and raised ESR and CRP.
The radiographic sequence is the key board fact: the earliest plain film sign is loss of disc height, followed within weeks by loss of the sharp white cortical endplate line and erosion of the endplates on both sides of the disc, then paraspinal soft tissue swelling. Healing produces sclerosis and eventually bony fusion across the disc. MRI with gadolinium is the test of choice: low T1 signal in the disc and both adjacent bodies, high T2 signal in the disc, enhancement, and epidural or paraspinal abscess.
Tuberculous spondylitis
Tuberculosis of the spine (Pott disease) is the most common skeletal form of tuberculosis and favors the lower thoracic and upper lumbar spine. It begins in the anterior vertebral body and spreads beneath the anterior longitudinal ligament to involve several contiguous levels, sometimes with skip lesions, producing anterior scalloping (gouge defects) of the bodies. Because mycobacteria lack proteolytic enzymes, the disc is relatively preserved early compared with pyogenic infection. Collapse of the anterior bodies produces a sharp angular kyphosis, the gibbus deformity. Large paraspinal and psoas (cold) abscesses, which may calcify, are characteristic. Neurologic deficit (Pott paraplegia) may follow.
| Feature | Pyogenic discitis | Tuberculous spondylitis | Metastasis |
|---|---|---|---|
| Disc | Narrowed early, destroyed | Relatively spared early, lost late | Preserved |
| Endplates | Eroded on both sides of the disc | Anterior body destruction and scalloping | Body and pedicle destruction |
| Levels | Usually one disc and two bodies | Multiple contiguous levels, skip lesions | Multiple scattered levels |
| Soft tissue | Moderate paraspinal swelling | Large, often calcified paraspinal and psoas abscess | Paraspinal mass possible |
| Deformity | Mild | Gibbus (sharp angular kyphosis) | Collapse, pathologic fracture |
| Tempo | Weeks; fever, high ESR and CRP | Months; weight loss, night sweats | Weeks to months; history of cancer |
Systemic bone disease leaves recognizable signatures: thin penciled cortices and codfish vertebrae (osteoporosis), Looser zones (osteomalacia), an enlarged bone with a thick cortex (Paget disease), radial phalangeal resorption and rugger jersey spine (hyperparathyroidism), H vertebrae (sickle cell) and the crescent sign (avascular necrosis). In the spine, a narrowing disc with eroded endplates on both sides is infection until proven otherwise and needs urgent referral.
Section 5Miscellaneous skeletal, thoracic and abdominal findings
Scheuermann disease and scoliosis
Scheuermann disease (juvenile kyphosis) appears in adolescents, more often boys, as a rigid thoracic kyphosis. The commonly taught radiographic criteria are anterior wedging of 5 degrees or more in at least three contiguous vertebrae, with endplate irregularity, multiple Schmorl nodes, mild disc narrowing and a thoracic kyphosis over about 40 to 45 degrees. Limbus bones may accompany it. A lumbar form produces endplate irregularity and Schmorl nodes without much wedging, often in young athletes.
Scoliosis is a lateral curve of 10 degrees or more by Cobb measurement, with vertebral rotation. Curves are named by the side of the convexity and the region of the apex. On the AP, the vertebral bodies rotate toward the convexity, so the spinous processes rotate toward the concavity and the convex side pedicles move toward the midline; the convex side ribs are pushed backward, producing the rib hump on the Adams forward bending test.
| Type | Features | Imaging note |
|---|---|---|
| Adolescent idiopathic | About 80 percent of structural scoliosis; girls; typically right thoracic convexity; painless | Progression risk rises with larger Cobb angle and a low Risser grade; commonly observation under about 25 degrees, bracing about 25 to 40 degrees in a growing child, surgical referral over about 45 to 50 degrees |
| Atypical curve | Left thoracic curve, painful curve, rapid progression, neurologic signs | MRI to exclude syrinx, Chiari malformation, tethered cord or tumor |
| Painful scoliosis in a teen | Night pain, relieved by NSAIDs | Osteoid osteoma of the posterior elements on the concave side |
| Congenital | Hemivertebra, butterfly vertebra, unsegmented bar | Screen for renal and cardiac anomalies |
| Neuromuscular | Long C shaped curve (cerebral palsy, muscular dystrophy) | Often progressive |
| Degenerative (de novo) | Adults over 50, lumbar, with disc and facet degeneration and lateral listhesis | Associated stenosis |
| Functional (nonstructural) | Leg length inequality, antalgic posture, muscle spasm | Corrects on side bending or recumbency; no fixed rotation |
Chest film findings
Chiropractors take chest films less often than spinal films, but cervical, thoracic and full spine films include the lung apices, the mediastinum and sometimes the bases, and the reader is responsible for everything on the film.
- Pneumothorax: a thin white visceral pleural line with no lung markings beyond it, usually at the apex on an upright film. An expiratory film makes a small one easier to see. On a supine film air collects anteriorly and inferiorly, producing the deep sulcus sign. Primary spontaneous pneumothorax occurs in tall, thin young men (and smokers). Tension pneumothorax shifts the mediastinum away from the affected side and depresses the hemidiaphragm; it is a clinical emergency.
- Pleural effusion: fluid collects first in the posterior costophrenic sulcus, visible on the lateral film with about 50 to 75 mL; blunting of the lateral costophrenic angle on the PA needs about 200 mL or more. Larger effusions form a meniscus curving up the lateral chest wall; massive effusion shifts the mediastinum away. A lateral decubitus film is the most sensitive plain film and shows whether fluid layers freely.
- Consolidation (pneumonia): air space opacity with air bronchograms, localized by the silhouette sign.
- Atelectasis: opacity with volume loss: shift of fissures, trachea or mediastinum toward the collapse and elevation of the hemidiaphragm.
- Congestive heart failure: cardiomegaly (CTR over 0.5), upper lobe vascular redistribution (cephalization), Kerley B lines (short horizontal septal lines at the lateral bases), perihilar bat wing edema and bilateral effusions.
- COPD: hyperinflation with flattened hemidiaphragms, more than 10 posterior ribs visible, a long narrow heart and an enlarged retrosternal space.
Lung masses and mediastinal masses
A solitary pulmonary nodule is a rounded opacity up to 3 cm; larger lesions are masses and are presumed malignant. Features favoring benignity are benign calcification patterns (central, laminated, diffuse or popcorn, the last typical of hamartoma) and stability for two years on comparison films. Features favoring malignancy are size over 3 cm, spiculated margins, upper lobe location, growth and a smoking history. Every new nodule needs comparison with old films or referral for CT. The Pancoast (superior sulcus) tumor is a lung cancer at the apex that invades the lower brachial plexus and sympathetic chain: shoulder and medial arm pain in a C8 to T1 distribution, hand weakness and Horner syndrome. On cervical and thoracic films it appears as asymmetric apical opacity or destruction of the first or second posterior rib or an adjacent transverse process. Mediastinal masses are classified by compartment: anterior (the four Ts: thymoma, teratoma, thyroid, terrible lymphoma), middle (lymph nodes, bronchogenic cyst, bilateral hilar adenopathy of sarcoidosis) and posterior (neurogenic tumors such as schwannoma and neurofibroma, which may enlarge a foramen).
Abdominal aortic aneurysm
An abdominal aortic aneurysm (AAA) is a focal dilation of the abdominal aorta to 3 cm or more in diameter, usually infrarenal. Risk factors are age over 65, male sex, smoking, family history, hypertension and atherosclerosis. On the lateral lumbar film, a calcified aortic wall appears as a curvilinear line anterior to the L1 to L4 bodies; an aneurysm shows as an anterior wall bowed away from a posterior wall, with a diameter of 3 cm or more measured outer wall to outer wall. On the AP film, curvilinear calcification may lie lateral to the vertebral margin. Many aneurysms are not calcified enough to see, so a normal film does not exclude AAA, and ultrasound is the diagnostic and screening test (screening is recommended for men 65 to 75 who have ever smoked).
Management depends on size and symptoms. An AAA found incidentally should be confirmed by ultrasound and referred to the patient's physician or a vascular specialist; the rupture risk rises steeply above about 5.5 cm (about 5.0 cm in women), which is the usual threshold for repair, and rapid growth (over about 0.5 cm in six months or 1 cm a year) also prompts repair. A pulsatile abdominal mass with sudden severe back, flank or abdominal pain, hypotension or syncope suggests rupture or impending rupture and requires an ambulance. Avoid forceful lumbar and abdominal procedures in a patient with a known large aneurysm.
Calcifications and stones
| Finding | Appearance and location | Significance |
|---|---|---|
| Phleboliths | Small round pelvic calcifications with a lucent center, below the interspinous line | Calcified venous thrombi; benign; often mistaken for ureteral stones |
| Renal calculi | Dense opacities over the renal shadow; a staghorn calculus fills the collecting system | Most stones (calcium) are radiopaque; uric acid stones are radiolucent; staghorns are usually struvite from urease producing infection |
| Ureteral calculi | Small opacity along the course of the ureter (near the transverse processes, over the SI joint, at the bladder) | Lodge at the ureteropelvic junction, the pelvic brim (iliac vessel crossing) and the ureterovesical junction; colicky flank pain |
| Gallstones | Right upper quadrant, often faceted and laminated, in clusters | Only about 10 to 20 percent are radiopaque; ultrasound is the test |
| Porcelain gallbladder | Calcified gallbladder wall | Associated with gallbladder carcinoma; refer |
| Pancreatic calcification | Speckled calcification crossing the upper lumbar spine (about L1 to L2) | Chronic pancreatitis, usually alcohol related |
| Splenic artery | Tortuous ring or tram track calcification in the left upper quadrant | Atherosclerosis; aneurysm if a ring is large |
| Calcified mesenteric lymph nodes | Mottled, mulberry like, mobile between films | Old granulomatous infection; benign |
| Uterine fibroid (leiomyoma) | Popcorn like calcified pelvic mass | Benign |
| Costal cartilage | Marginal (parallel lines) in men, central tongue like in women | Normal aging |
Every spinal film is also a chest or abdominal film. Know Scheuermann criteria and the scoliosis patterns that need MRI, recognize pneumothorax, effusion, lung and apical masses, and search every lumbar lateral for aortic calcification. An AAA of 3 cm or more is referred, and a symptomatic pulsatile mass is an emergency.
The chapter in one breath
- A block vertebra has a wasp waist; os odontoideum is a smooth ossicle with a big rounded C1 anterior arch and often instability.
- Jefferson: C1 lateral mass overhang on the APOM; hangman: bilateral C2 pars fractures; type II odontoid: base of dens, worst healing; clay shoveler: C7 spinous avulsion.
- Compression fractures involve the anterior column; burst fractures add the middle column and widen the interpediculate distance; Chance fractures split all three columns.
- Isthmic spondylolisthesis is an L5 pars defect; degenerative is L4 with an intact pars.
- OA narrows non uniformly with osteophytes; RA narrows uniformly with osteoporosis, marginal erosions and atlantoaxial instability; DISH flows over four levels with normal discs.
- AS starts with bilateral symmetric sacroiliitis and builds marginal syndesmophytes; psoriatic and reactive arthritis form nonmarginal syndesmophytes; gout has overhanging edges; CPPD calcifies cartilage.
- Metastasis causes the missing pedicle and spares the disc; myeloma gives punched out lesions and a cold bone scan; hemangioma shows vertical striations.
- Paget disease enlarges bone and thickens cortex; Looser zones mean osteomalacia; radial phalangeal resorption means hyperparathyroidism; H vertebrae mean sickle cell.
- Infection destroys the disc and both endplates; TB spreads under the ALL, spares the disc early and forms a gibbus and cold abscess.
- Scheuermann: 5 degrees of wedging in 3 levels; left thoracic scoliosis needs MRI; AAA is 3 cm or more and is referred.
Words worth knowing
| Term | What it means |
|---|---|
| Wasp waist | Anterior concavity at the fused disc level of a congenital block vertebra. |
| Os odontoideum | A separate, corticated ossicle above a shortened dens, often with atlantoaxial instability. |
| Rule of Spence | Combined C1 lateral mass overhang over about 7 mm on the APOM implies transverse ligament rupture. |
| Hangman fracture | Bilateral fractures of the C2 pars or pedicles with anterior slip of C2. |
| Clay shoveler fracture | Avulsion fracture of a lower cervical or upper thoracic spinous process, usually C7. |
| Burst fracture | Axial load fracture of the anterior and middle columns with a retropulsed fragment. |
| Chance fracture | Horizontal flexion distraction fracture through all three columns, often from a lap belt. |
| Spondylolysis | A defect of the pars interarticularis, most often at L5. |
| Inverted Napoleon hat sign | AP appearance of a severely slipped, forward tilted L5 over the sacrum. |
| Vacuum phenomenon | Nitrogen gas within a degenerated disc or joint, which argues against infection. |
| DISH | Flowing anterolateral ossification over at least four vertebrae with preserved discs and normal SI joints. |
| Syndesmophyte | Vertical ossification of the outer annulus bridging vertebrae in spondyloarthropathy. |
| Romanus lesion | Erosion of an anterior vertebral corner in ankylosing spondylitis that heals as a shiny corner. |
| Martel sign | Overhanging edge of bone at a gouty erosion. |
| Chondrocalcinosis | Calcification of hyaline or fibrocartilage, typical of CPPD. |
| Winking owl sign | Loss of one pedicle outline on the AP film, classic for metastasis. |
| Batson plexus | Valveless vertebral venous plexus through which tumors spread to the spine. |
| Codman triangle | Triangle of periosteal new bone at the edge of an aggressive lesion lifting the periosteum. |
| Vertebra plana | Uniform flattening of a vertebral body, classically from eosinophilic granuloma in a child. |
| Looser zone | Lucent pseudofracture perpendicular to the cortex in osteomalacia. |
| Picture frame vertebra | Enlarged vertebra with thickened cortex, typical of Paget disease. |
| Rugger jersey spine | Dense subendplate bands of renal osteodystrophy. |
| Crescent sign | Subchondral lucent line in avascular necrosis indicating collapse. |
| Sequestrum | A fragment of dead bone in chronic osteomyelitis. |
| Gibbus | Sharp angular kyphosis from anterior collapse, classic for spinal tuberculosis. |
| Pancoast tumor | Apical lung cancer invading the lower brachial plexus and sympathetic chain. |