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 Bone and Soft-Tissue Disorders

= JEUNE DISEASE

= autosomal recessive dysplasia characterized by short narrow thorax and short limbs

Prevalence: 1÷100,000 to 1÷130,000 live births

Associated with: renal anomalies (hydroureter), PDA

OB-US:

Prognosis: neonatal death in 80% (respiratory failure + infections)

DDx: Ellis-van Creveld syndrome

Avascular Necrosis  !!navigator!!

= AVN = OSTEONECROSIS = ASEPTIC NECROSIS

= consequence of reduced / completely interrupted blood supply to bone with death of cellular elements

Terminology (now often used interchangeably):

  1. Osteonecrosis = ischemic bone death ← sepsis
  2. Ischemic necrosis / avascular necrosis / aseptic necrosis = necrosis of epiphyseal + subarticular bone
  3. Bone infarction = necrosis of metaphyseal + diaphyseal bone

Cause: [common causes are underlined]

  • NO predisposing factors in 25%!
  1. Trauma / thermal injury → interruption of arteries
    • typically unilateral
    • Femoral head:
      1. Femoral neck fracture (60–75%)
      2. Dislocation of hip joint (25%)
      3. Slipped capital femoral epiphysis (15–40%)
    • Carpal scaphoid:
      • 4–6 months after fracture (in 10–15%), in 30–40% of nonunions of scaphoid fracture
      • Site: proximal fragment (most common)
    • humeral head (infrequent)
    • talus (after talar neck fracture)
  2. Nontraumatic
    • bilateral (in 70–80%)
    1. Occlusion / embolization of artery
      1. Thrombus: thromboembolic disease, sickle-cell disease (SS + SC hemoglobin), polycythemia rubra vera, pheochromocytoma (microscopic thrombotic disease)
      2. Nitrogen bubbles: Caisson disease, astronauts
      3. Fat: pancreatitis (intramedullary fat necrosis from circulating lipase), alcoholism
      4. Thromboembolism, arteriosclerosis
      5. Pregnancy
    2. Vessel wall disease:
      1. Collagen-vascular disease: SLE, rheumatoid arthritis, polyarteritis nodosa, sarcoidosis
      2. Infectious vasculitis
      3. Arteriosclerosis
    3. Vascular compression by abnormal deposition of:
      1. Fat: corticosteroid therapy (eg, renal transplant, Cushing disease), diabetes
      2. Blood: hemophilia, trauma (fractures, dislocations)
      3. Inflammatory cells: osteomyelitis, infection, Langerhans cell histiocytosis
      4. Tumor cells: leukemia, lymphoma
      5. Edema: radiation therapy, hypothyroidism, frostbite
      6. Substances: Gaucher disease (vascular compression by lipid-filled histiocytes), gout
    4. Direct cell toxicity
      1. Drug therapy: immunosuppressives, cytotoxics, biphosphonates
      2. Radiation therapy
    5. Idiopathic
      1. Spontaneous osteonecrosis of knee
      2. Legg-Calvé-Perthes disease
      3. Freiberg disease (repetitive microtrauma)
      4. Hypopituitarism

mnemonic: PLASTIC RAGS x 2

  • Pancreatitis, Pregnancy
  • Legg-Perthes disease, Lupus erythematosus
  • Alcoholism, Atherosclerosis
  • Steroids, Sickle-cell disease
  • Trauma, Thermal injury
  • Idiopathic (Legg-Perthes disease), Infection
  • Caisson disease, Collagen disease (SLE)
  • Rheumatoid arthritis, Radiation treatment
  • Alcoholism, Amyloid
  • Gaucher disease, Gout
  • Sickle cell disease, Spontaneous osteonecrosis of knee

mnemonic: GIVE INFARCTS

  • Gaucher disease
  • Idiopathic (Legg-Calvé-Perthes, Köhler, Chandler)
  • Vasculitis (SLE, polyarteritis nodosa, rheumatoid arthritis)
  • Environmental (frostbite, thermal injury)
  • Irradiation
  • Neoplasia (-associated coagulopathy)
  • Fat (prolonged corticosteroid use increases marrow)
  • Alcoholism
  • Renal failure + dialysis
  • Caisson disease
  • Trauma (femoral neck fracture, hip dislocation)
  • Sickle cell disease

Path:

  1. Stage of cell death: cellular ischemia / anoxia → death of hematopoietic cells (in 6–12 hours) >adipocytes >bone cells = osteoclasts and osteoblasts + osteocytes (in 12–48 hours)
    • Chondrocytes are adapted to relatively low oxygen tension and do not become devitalized!
  2. Stage of ↑ vascularity / reparative phase (osteoclasis): trabecular resorption ← inflammatory fibrovascular infiltration + proliferation ← hyperemia mixed with areas of relatively increased trabecular density ← osteonecrosis
  3. Stage of substitution / reactive phase (= osteogenesis): mesenchymal cells differentiate to osteoblasts on surface of dead trabeculae synthesizing new bone layer → trabecular thickening + osteoclastic resorption of devitalized bone (= creeping zone of substitution)
    • metadiaphyseal osteonecrosis: rim of sclerosis is frequently of undulating / serpentine morphology
    • epiphyseal osteonecrosis: increased bone resorption at junction of reactive zone and subchondral bone plate + weight-bearing → early fracture of overlying cartilage

Age: 4th–6th decades of life; M÷F = 4–8÷1

  • asymptomatic (majority of patients)
  • reduced range of motion; pain ← increase in intramedullary pressure ← medullary bone marrow edema

Location: femoral head (most common), humeral head, femoral condyles, proximal tibia, distal femoral metadiaphysis, distal tibial metadiaphysis, scaphoid, lunate, talus

Radiography (positive only after several months of symptoms):

  • preservation of joint space (DDx: arthritis)
  • patchy areas of lucency and sclerosis:
    • dense osteonecrotic bone ← lack of resorption relative to healthy osteopenic bone + new bone laid down over necrotic trabeculae:
      • sclerosis of serpentine / undulating morphology characteristically about lesion rim (more common in metadiaphyseal lesions)
      • early areas of articular collapse (in epiphyseal osteonecrosis) typically at junction of serpentine sclerotic rim and articular surface
    • radiolucent rim around area of osteonecrosis ← absorption around necrotic bone:
      • “crescent” sign = crescentic subchondral lucency = subchondral structural collapse of necrotic segment parallel to articular surface in weight-bearing portion with separation from overlying cartilage and attached subchondral bone plate (in epiphyseal osteonecrosis)
    • later findings:
      • flattening of articular surface ← articular fragmentation + progressive articular collapse, secondary osteoarthritis
      • increased bone density ← compression of osseous trabeculae ← microfracture of nonviable bone + calcification of dendritic marrow + creeping substitution = deposition of new bone

CT (less sensitive than MRI / NUC):

  • May be utilized for staging of known disease
  • staging upgrades in 30% compared with plain films
  • serpentine / undulating sclerotic margin (late stage)
  • useful for detecting location of articular collapse + extent in epiphyseal osteonecrosis!

NUC (80–85% sensitivity in early stages):

  • Bone marrow imaging (with radiocolloid) more sensitive than bone imaging (with diphosphonates)
  • More sensitive than plain films in early AVN ← evidence of ischemia seen as much as 1 year earlier
  • Less sensitive than MR except for SPECT

Technique: imaging improved with double counts, pinhole collimation

  • diffuse increased radionuclide activity in epiphyseal involvement with articular collapse + 2ndary osteoarthritis
  • very early: cold = photopenic defect on bone scan (blood flow, blood pool, static phase) + bone marrow scan ← interrupted blood supply
  • late: “doughnut” sign = cold spot surrounded by increased radionuclide uptake ← chronic reparative processes:
    1. capillary revascularization + new-bone synthesis
    2. degenerative osteoarthritis

MR:

MRI Classification of Aseptic Necrosis (Mitchell Classification)

StageT1T2Analogous to
Ahighintermediatefat
Bhighhighsubacute blood
Clowhighfluid/edema
Dlowlowfibrous tissue

Cx: Malignant transformation to sarcoma (exceedingly rare, exclusive to metaphysis / metadiaphysis): malignant fibrous histiocytoma (69%), osteosarcoma (17%), angiosarcoma (9%)

Cortical Infarction  !!navigator!!

  • Requires compromise of (a) nutrient artery and (b) periosteal vessels!

Age: particularly in childhood where periosteum is easily elevated by edema

  • avascular necrosis = osteonecrosis
  • osteochondrosis dissecans

Cx:

  1. Growth disturbances
    • cupped / triangular / coned epiphyses
    • “H-shaped” vertebral bodies
  2. Fibrosarcoma (most common), malignant fibrous histiocytoma, benign cysts
  3. Osteoarthritis

Medullary Infarction  !!navigator!!

  • Nutrient artery is the sole blood supply for diaphysis!

Location: distal femur, proximal tibia, iliac wing, rib, humerus

  1. Acute phase:
    • NO radiographic changes without cortical involvement
    • area of rarefaction
    • infarcted area T1 hypointense + T2 hyperintense
    • bone marrow scan: diminished uptake in medullary RES for long period of time
    • bone scan: photon-deficient lesion within 24–48 hours; increased uptake after collateral circulation established
  2. Healing phase (complete healing / fibrosis / calcification):
    • demarcation by zone of serpiginous / linear calcification + ossification parallel to cortex
    • dense bone indicating revascularization
    • focal lesion with fatty marrow SI centrally + surrounding hypointense rim (= reactive / sclerotic bone)

Avascular Necrosis / Adult Osteonecrosis of Hip  !!navigator!!

Incidence: 10,000–20,000 new cases annually in USA

  • Involvement of one hip increases risk to contralateral hip to 70%!

Age: 20–50 years

Zonal anatomy (from articular surface to center of head):

  • zone of cell death
  • reactive interface / creeping zone of substitution
  • zone of reinforcing trabecular bone
  • zone of reactive marrow
  • zone of normal marrow

Classification (Steinberg):

  • Stage 0 = normal
  • Stage I = normal / barely detectable trabecular mottling; abnormal bone scan / MRI
  • Stage IIA = focal sclerosis + osteopenia
  • Stage IIB = distinct sclerosis + osteoporosis + early “crescent” sign
  • Stage IIIA = subchondral undermining (“crescent” sign) + cyst formation
  • Stage IIIB = mild alteration in femoral head contour / subchondral fracture + normal joint space
  • Stage IV = marked collapse of femoral head + significant acetabular involvement
  • Stage V = joint space narrowing + acetabular degenerative changes
  • hip / groin / thigh / knee pain; limited range of motion

MR (90–100% sensitive, 85% specific for symptomatic disease):

  • Prevalence of clinically occult disease: 6%
  • MR imaging changes reflect the death of marrow fat cells (not death of osteocytes with empty lacunae)!
  • Sagittal images particularly useful!

⇒EARLY AVN:

  • The early standard MRI may be normal ← lack of edema / hemorrhage / bone marrow response while Gd-enhancement shows devascularized areas
  • decreased Gd-enhancement on short-inversion-recovery (STIR) images (very early)
  • bone marrow edema: extensive even when area of infarction is small (early)
  • low-SI band with sharp inner interface + blurred outer margin on T1WI within 12–48 hours (= mesenchymal + fibrous repair tissue, amorphous cellular debris, thickened trabecular bone) seen as
    1. band extending to subchondral bone plate
    2. complete ring (less frequent)
  • “double-line” sign on T2WI (in 80%) [MORE SPECIFIC] = juxtaposition of inner hyperintense band (vascularized granulation tissue) + outer hypointense band (chemical shift artifact / fibrosis and sclerosis)

⇒ADVANCED AVN:

  • “pseudohomogeneous edema pattern” = large inhomogeneous areas of mostly decreased SI on T1WI
  • hypo- to hyperintense lesion on T2WI
  • contrast-enhancement of interface + surrounding marrow + within lesion

⇒SUBCHONDRAL FRACTURE:

  • predilection for anterosuperior portion of femoral head (SAG images!)
  • cleft of low SI running parallel to the subchondral bone plate within areas of fatlike SI on T1WI
  • hyperintense band (= fracture cleft filled with articular fluid / edema) within the intermediate- or low-signal-intensity of necrotic marrow on T2WI
  • lack of enhancement within + around fracture cleft

⇒COLLAPSE OF ARTICULAR SURFACE:

  • focal depression of subchondral bone with low SI on T2WI = fibrotic changes in infarcted bone marrow
  • loss of normal spherical contour of bone
  • incongruity of articular surfaces
  • Predisposition: increased thickness of reparative zone, increasing volume of joint effusion, presence of prominent surrounding edema, patient age >40 years, body mass index ≥24 kg/m2

Cx: early osteoarthritis through collapse of femoral head + joint incongruity in 3–5 years if left untreated

  • Best predictor: volume of femoral head involved; collapse in 43–87% with >25–50% + in 0–5% with <25–30% involvement of femoral head volume

Rx:

  1. core decompression (for grade 0–II): most successful with <25% involvement of femoral head
  2. osteotomy (for grade 0–II)
  3. arthroplasty / arthrodesis / total hip replacement (for grade >III)

DDx:

  1. Transient osteoporosis of the hip = bone marrow edema syndrome (marked diffuse increased SI on long repetition time images + diffuse contrast enhancement, no reactive interface)
  2. Subchondral epiphyseal insufficiency fracture (low SI band in superolateral femoral head convex toward articular surface; speckled / linear hypointense areas, focal depression of epiphyseal contour)
  3. Spondyloarthropathy

Blount Disease  !!navigator!!

[Walter Putnam Blount (1900–1992), professor of orthopedics at Marquette Medical School, Milwaukee, Wisconsin]

= TIBIA VARA

= avascular necrosis of medial tibial condyle

Age:>6 years

  • limping, lateral bowing of leg
  • medial tibial condyle enlarged + deformed (DDx: Turner syndrome)
  • irregularity of metaphysis (medially + posteriorly prolonged with beak)

Calvé-Kümmel-Verneuil Disease  !!navigator!!

= VERTEBRAL OSTEOCHONDROSIS = VERTEBRA PLANA

= avascular necrosis of vertebral body

Age: 2–15 years

  • uniform collapse of vertebral body into flat thin disk
  • increased density of vertebra
  • neural arches NOT affected
  • disks are normal with normal intervertebral disk space
  • intravertebral “vacuum cleft” sign (PATHOGNOMONIC)

DDx: eosinophilic granuloma, metastatic disease

Freiberg Disease  !!navigator!!

[Albert Henry Freiberg (1868–1940), orthopedic surgeon in Cincinnati, Ohio]

= osteochondrosis of head of 2nd (3rd / 4th) metatarsal

Age: 10–18 years; M÷F = 1÷3

  • metatarsalgia, swelling, tenderness

Early:

  • flattening, increased density, cystic lesions of metatarsal head
  • widening of metatarsophalangeal joint

Late:

  • osteochondral fragment
  • sclerosis + flattening of metatarsal head
  • increased cortical thickening

Kienböck Disease  !!navigator!!

= LUNATOMALACIA

[Robert Kienböck (1871–1953), radiologist in Vienna, Austria]

= avascular necrosis of lunate bone

Predisposed: individuals engaged in manual labor with repeated / single episode of trauma

Age: 20–40 year old males

Associated with: ulna minus variant (short ulna) in 75%

  • progressive pain + soft-tissue swelling of wrist

Location: uni- >bilateral (usually right hand)

Classification (Lichtman):

  • Stage I = normal radiographs + abnormal MRI
  • Stage II = increased radiographic density with preservation of normal lunate shape
  • Stage IIIA = lunate sclerosis + collapse on radiographs
  • Stage IIIB = + diminished carpal height and flexion of scaphoid
  • Stage IV = + extensive carpal degenerative changes

Radiographs:

  • initially normal radiograph
  • osteonecrotic fracture of carpal lunate
  • increased density + altered shape + collapse of lunate

CT:

  • coronal fracture creating a dorsal and volar half
  • multiple lunate fragments

MR:

  • diffusely decreased T1 SI involving entire lunate
  • variable T2 / STIR signal intensity

Cx: scapholunate dissociation, ulnar deviation of triquetrum, degenerative joint disease in radiocarpal / midcarpal compartments

Rx: ulnar lengthening / radial shortening, lunate replacement

Köhler Disease  !!navigator!!

[Alban Köhler (1874–1947), radiologist in Wiesbaden, Germany and co-founder of Deutsche Röntgengesellschaft in Berlin]

= avascular necrosis of tarsal scaphoid

Age: 3–10 years; boys

  • irregular outline
  • fragmentation
  • disklike compression in AP direction
  • increased density
  • joint space maintained
  • decreased / increased uptake on radionuclide study

Legg-Calvé-Perthes Disease  !!navigator!!

= COXA PLANA

[Arthur Thornton Legg (1874–1939), orthopedic surgeon in Boston]

[Jacques Calvé (1875–1954), orthopedic surgeon at Fondation Franco-Americaine de Berck, France]

[Georg Clemens Perthes (1869–1927), head of the surgical clinic in Tübingen, Germany]

= idiopathic avascular necrosis of femoral head in children; one of the most common sites of AVN; in 10–15% almost always metachronously bilateral

Incidence: 1÷10,000 children; increased with lower socioeconomic status, low birth weight, delayed skeletal maturation

Age:

  1. 2–12 (peak, 5–6) years: M÷F = 3–5÷1
  2. adulthood: Chandler disease

Cause: trauma in 30% (subcapital fracture, epiphyseolysis, esp. posterior dislocation), closed reduction of congenital hip dislocation, prolonged interval between injury and reduction

Pathophysiology:

  • insufficient femoral head blood supply (epiphyseal plate acts as a barrier in ages 4–10; ligamentum teres vessels become nonfunctional; blood supply is from medial circumflex artery + lateral epiphyseal artery only); articular cartilage continues to grow ← supplied with nutrients from synovium

Stages:

  • I = histologic + clinical diagnosis without radiographic findings
  • II = sclerosis ± cystic changes with preservation of contour + surface of femoral head
  • III = loss of structural integrity of femoral head
  • IV = in addition loss of structural integrity of acetabulum

Radiographic Findings in Legg-Calvé-Perthes Disease (Catterall Classification)

GroupRadiographic FindingsEpiphyseal Involvement
I
  • anterior portion of epiphysis involved
  • NO metaphyseal reaction / sequestrum / subchondral fracture
<25%
II
  • more extensive involvement of anterior portion of epiphysis
  • sequestrum
  • anterolateral metaphyseal reaction
  • subchondral fracture line NOT extending to apex of epiphysis
<50%
III
  • entire epiphysis dense
  • diffuse metaphyseal reaction + widening of neck
  • subchondral fracture line posteriorly
most
IV
  • epiphyseal flattening / mushrooming / collapse
  • extensive metaphyseal reaction
  • posterior remodeling of posterior head
total
  • 1 week–6 months (mean 2.7 months) duration of symptoms prior to initial presentation: limp, knee pain
  • decreased range of hip motion concerning abduction and internal rotation

NUC (may assist in early diagnosis):

  • decreased uptake (early) in femoral head = interruption of blood supply
  • increased uptake (late) in femoral head
    1. revascularization + bone repair
    2. degenerative osteoarthritis
  • increased acetabular activity associated with degenerative joint disease

X-RAY:

  • Early signs:
    • femoral epiphysis smaller than on contralateral side (96%) = epiphyseal growth deficit
    • sclerosis of femoral head epiphysis ← sequestration + compression (82%)
    • slight widening of joint space ← thickening of cartilage, failure of epiphyseal growth, presence of joint fluid, joint laxity (60%)
    • ipsilateral bone demineralization (46%)
    • alteration of pericapsular soft-tissue outline ← atrophy of ipsilateral periarticular soft tissues (73%)
    • radiolucency of lateral + medial metaphyseal areas of femoral neck
    • N.B.: NEVER destruction of articular cortex as in bacterial arthritis
  • Late signs:
    • delayed osseous maturation of a mild degree
    • “radiolucent crescent line” of subchondral fracture = small archlike subcortical lucency (32%)
    • subcortical fracture on anterior articular surface (best seen on FROG LEG view)
    • lateral subluxation of femoral head = lateral collapse of ossific nucleus
    • femoral head fragmentation
    • femoral neck cysts (from intramedullary hemorrhage in response to stress fractures)
    • loose bodies (only found in males)
  • Regenerative signs:
    • coxa plana = flattened collection of sclerotic fragments (over 18 months)
    • coxa magna = remodeling of femoral head to become wider + flatter in mushroom configuration to match widened metaphysis + epiphyseal plate

CT:

  • loss of “asterisk” sign (= starlike pattern of crossing trabeculae in center of femoral head) with distortion of asterisk and extension to surface of femoral head

MR (gold standard):

  • “asterisk” sign of marrow edema = normal marrow SI of femoral epiphysis replaced by low T1-SI + high T2-SI
  • low signal intensity on T1WI and T2WI = necrotic portion of superior epiphysis
  • “double-line” sign (80%) = sclerotic nonsignal rim between necrotic + viable bone edged by a hyperintense rim of granulation tissue
  • “crescent” sign ← subchondral fracture
  • prominent involvement of anterosuperior + lateral femoral head (often best seen on SAG images)
  • thickening of epiphyseal cartilage
  • synovial hypertrophy, joint effusion
  • fluid within fracture plane
  • absent enhancement of femoral head epiphysis
  • early increased diffusivity in affected femoral epiphysis
  • hip joint incongruity: lateral femoral head uncovering, labral inversion, femoral head deformity

NUC (3-phase bone scan):

  • initially NO uptake of radiopharmaceutical on early dynamic images
  • increased activity in lateral pillar ← revascularization phase
  • increased activity at epiphyseal base near physis ← transphyseal neovascularization

US:

  • joint effusion, synovitis

Cx: severe degenerative joint disease in early adulthood

Rx: bed rest, abduction bracing (to reduce stress on infarcted head), physical therapy

Metadiaphyseal Osteonecrosis  !!navigator!!

  • well-defined serpentine hypointense rim surrounding a central region of fat SI on T1WI
  • “double line” sign = bands of low + high SI that course together in parallel surrounding a central region of low SI (= necrotic bone) on T2WI (virtually PATHOGNOMONIC)

Panner Disease  !!navigator!!

[Hans Jessen Panner (1871–1930), head of roentgenological clinic at Rikshospitalet, Copenhagen, Denmark]

(NOT osteonecrosis)

= benign self-limited disorder of fragmented ossification in epiphysis of humeral capitellum

Age: children 7–12 years of age

Preiser Disease  !!navigator!!

[Georg Karl Felix Preiser (1876–1913), orthopedic surgeon in Hamburg, Germany]

= nontraumatic spontaneous osteonecrosis of entire scaphoid

Scaphoid Osteonecrosis  !!navigator!!

= OSTEONECROSIS OF PROXIMAL POLE OF SCAPHOID

Cause: fracture through waist / proximal pole and nonunion

Incidence of proximal pole osteonecrosis:

  1. in >60% of fracture nonunions of proximal ¹/³ of scaphoid
  2. in ~ 20% of midscaphoid fractures

X-RAY:

  • increased density of proximal scaphoid fracture fragment compared with distal scaphoid / adjacent carpal bones
  • often sclerotic rounded fracture margins (= nonunion)
  • frequently surrounding lucencies (= cysts)

NUC (bone scan):

  • decreased uptake in proximal pole

CT:

  • increased sclerosis + lack of normal trabeculae in proximal third of scaphoid

MR:

  • homogeneously decreased SI (≤SI of skeletal muscle) at T1WI in proximal pole of scaphoid (71% sensitive, 74% specific)
  • <20% enhancement in proximal pole (86% sensitive, 96% specific)
  • complete absence of enhancement in proximal pole (54–76% sensitive)

Cx: scaphoid nonunion advanced collapse (= persistent fracture nonunion, radioscaphoid joint space narrowing, sclerosis, osteophytes, potentially proximal pole collapse)

Spontaneous Osteonecrosis of Knee  !!navigator!!

= SONK

Cause: ? meniscal tear (78%), trauma with resultant microfractures, vascular insufficiency, degenerative joint disease, severe chondromalacia, gout, rheumatoid arthritis, joint bodies, intraarticular steroid injection (45–85%)

Age: 7th decade (range, 13–83 years)

  • acute onset of pain

Location: weight-bearing medial condyle more toward epicondylus (95%), lateral condyle (5%), may involve tibial plateau

  • radiographs usually normal (within 3 months after onset)
  • positive bone scan within 5 weeks (most sensitive)
  • flattening of weight-bearing segment of medial femoral epicondyle
  • radiolucent focus in subchondral bone + peripheral zone of osteosclerosis
  • horizontal subchondral fracture (within 6–9 months) + osteochondral fragment
  • periosteal reaction along medial side of femoral shaft (30–50%)

Cx: osteoarthritis

Talar Avascular Necrosis  !!navigator!!

  • Fractures involving the talar body have a higher prevalence of AVN

Risk of AVN:

  1. nondisplaced fracture
    • talar neck fracture (Hawkins type I) 0–15%
  2. fracture with dislocation / subluxation of:
    • subtalar joint (Hawkins type II) 20–50%
    • ankle + subtalar joints (Hawkins type III) almost 100%
    • subtalar + tibiotalar + talonavicular joints (Hawkins type IV fracture) 100%
  • increase in talar dome opacity / sclerosis
  • deformity + articular collapse + bone fragmentation
  • absent Hawkins sign = thin subchondral radiolucent line along talar dome (← disuse osteopenia) indicates an adequate blood supply

 Outline