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 Bone and Soft-Tissue Disorders

= inflammation of bone and marrow caused by bacteria (most commonly pyogenic bacteria + mycobacteria), fungi, parasites, viruses

Predisposed: immunosuppression, diabetes mellitus, sickle cell disease, intravenous drug abuse, alcoholism

Source of infection:

  1. direct inoculation: open fracture / direct trauma (commonly in young adults)
    • prominent local signs and symptoms
  2. hematogenous: bacteremia (commonly in elderly / child)
    • slow insidious progression of symptoms
    • positive blood culture (in 50%)
  3. extension from adjacent soft-tissue infection

Location: tibia, wrist, femur, rib, thoracolumbar spine

Dx: requires 2 out of 4 of the following criteria

  1. purulent material draining from site of osteomyelitis
  2. positive findings at bone tissue / blood culture
  3. localized classic physical findings of bone tenderness
  4. positive radiologic findings

Acute Pyogenic Osteomyelitis  !!navigator!!

Age: most commonly affects children

Organism:

  1. newborns: S. aureus, group B streptococcus, E. coli
  2. children: S. aureus (blood cultures in 50% positive)
  3. adults: S. aureus (60%), enteric species (29%), Streptococcus (8%)
  4. drug addicts: Pseudomonas (86%), Klebsiella, Enterobacteriae; (57 days average delay in diagnosis)
  5. sickle cell disease: S. aureus, Salmonella
  6. diabetics: often multiple organisms like S. aureus, Streptococcus, E. coli, Klebsiella, Clostridia, Pseudomonas (in soil + sole of shoes)
  7. HIV-infected patients: TB, atypical mycobacteria

Cause:

  1. genitourinary tract infection (72%)
  2. lung infection (14%)
  3. dermal infection (14%): direct contamination from a soft-tissue lesion in diabetic patient

Pathophysiology:

bacterial growth in bone → entrapped bone becomes necrotic within 48 hours → spread to shaft ± periosteum (large subperiosteal abscess in children) → lifted periosteum impedes blood supply → sequestrum (= dead bone) → rupture of periosteum → draining sinus + soft-tissue abscess; host response causes reactive sleeve of new bone deposition (= involucrum)

[involucrum, Latin = covering / sheath]

[sequestrum, Latin = deposit], [cloaca, Latin = sewer, canal]

Location:

  • Lower extremity (75%) over pressure points in diabetic foot
  • Vertebra (53%) = infectious spondylitis: lumbar (75%) >thoracic >cervical
  • Radial styloid (24%)
  • Sacroiliac joint (18%)
  • leukocytosis + fever (66%)

Conventional radiographs (insensitive):

  • radiographs normal in 95% at presentation (notoriously poor in early phase of infection for as long as 10–21 days)
    DDx: infarction (similar radiographic findings)
  • some abnormality in 90% 28 days after onset of infection:
    • localized soft-tissue swelling adjacent to metaphysis with obliteration of usual fat planes (after 3–10 days)
    • permeative metaphyseal osteolysis (lags 7–14 days behind pathologic changes)
    • endosteal erosion
    • intracortical fissuring
    • involucrum = cloak of laminated / spiculated periosteal reaction (develops after 20 days)
    • button sequestrum = detached necrotic cortical bone (develops after 30 days)
    • cloaca formation = space in which dead bone resides

US:

  • soft-tissue changes, fluid collection, periosteal reaction

CT:

  • overlying soft-tissue swelling
  • periosteal reaction
  • hypoattenuating marrow = density difference of >20 HU compared to healthy side indicates marrow infection
  • trabecular coarsening
  • focal cortical erosion
  • extramedullary fat-fluid level ← cortical breach

MR (82% sensitive, 80% specific in diabetics):

  • demonstrates extent of infection
  • normal marrow / low SI on T2WI excludes osteomyelitis!
  • bone marrow hypointense on T1WI in geographic confluent pattern ← infiltration by inflammatory cells + purulent material
  • hyperintense relative to normal fatty marrow on T2WI / STIR (= water-rich inflammatory tissue + edema fluid)
    • Periarticular bone marrow edema can be seen adjacent to joints involved by noninfectious inflammatory arthropathy / osteoarthritis and does not reliably indicate osteomyelitis!
      DDx: noninfectious inflammatory arthropathy (Charcot joint), osteoarthritis, cellulitis, normal hematopoietic marrow in children
  • variable enhancement after IV administration of Gd-chelate
  • focal / linear cortical involvement hyperintense on T2WI
  • subperiosteal infection = hyperintense halo surrounding cortex on T2WI
  • sinus tract (= communication of medullary fluid collection with soft-tissue fluid collection through cortical disruption) = hyperintense line on T2WI extending from bone to skin surface + enhancement of its borders
  • sequestrum = central hypointense area on T2WI

Abscess characteristics at MRI:

  • hyperintense enhancing rim (= hyperemic zone) around a central focus of low intensity (= necrotic / devitalized tissue) on contrast-enhanced T1WI
  • hyperintense fluid collection surrounded by hypointense pseudocapsule on T2WI + contrast enhancement of granulation tissue
  • adjacent hyperintense soft tissues on T2WI
  • fat-suppressed contrast-enhanced imaging (88% sensitive + 93% specific compared with 79% + 53% for nonenhanced MR imaging)

DDx: bone tumor (“no penumbra” sign = higher-SI layer of granulation tissue lining abscess cavity on T1WI)

NUC (~ 90% accurate):

Advantage: imaging of whole skeleton!

  1. 67Ga scan: 100% sensitivity; increased uptake 1 day earlier than for 99mTc-MDP
    ◊ Gallium also helpful for chronic osteomyelitis!
  2. Static 99mTc-diphosphonate: 83% sensitive with 5–60% false-negative rate in neonates + children because of
    1. masking effect of epiphyseal plates
    2. early diminished blood flow with infection
    3. spectrum of uptake pattern from hot to cold
  3. Triple-phase skeletal scintigraphy:
    92% sensitive + 87% specific
    ◊Positive within 1–2 days after onset of symptoms!
    Phase 1: Radionuclide angiography = increased perfusion phase of regional blood flow
    Phase 2: “blood pool” images ← hyperemia = tissue phase
    Phase 3: “bone uptake” ←
    • increased osteoblastic activity = delayed phase
    • increased activity in all 3 phases (HALLMARK)
    • photopenia (rare) = “cold” osteomyelitis (due to vascular thrombosis + bone infarct) → may become “hot” at subsequent imaging (esp. TB)
    • No uptake during delayed phase = NO osteomyelitis!
    • Obtain SPECT whenever possible!

    Limitations: diagnostic difficulties in children (motion), in posttraumatic / postoperative state, diabetic neuropathy (poor blood supply), neoplasia, septic arthritis, Paget disease, healed osteomyelitis, noninfectious inflammatory process
  4. WBC-scan:
    1. 111In-labeled leukocytes: best agent for acute infections
    2. 99mTc-hexamethylpropyleneamine oxime labeled leukocytes: preferred over 111In-leukocyte imaging especially in extremities
    • WBC scans have largely replaced gallium imaging for acute osteomyelitis ← faster imaging + greater resolution ← improved photon flux and improved dosimetry (higher dose allowed relative to 111In)
  5. Bone marrow imaging (99mTc-sulfur colloid) in combination with WBC-scan
  • “cold” area in early osteomyelitis subsequently becoming “hot” if localized to long bones / pelvis (not seen in vertebral bodies)
  • local increase in radiopharmaceutical uptake (positive within 24–72 hours)

Scintigraphy is more useful than MR imaging in a child when the suspected site of osteomyelitis is not clinically evident (+ bacteremia / limping / refusing to bear weight)

Cx:

  1. Abscess of soft-tissue / bone
  2. Fistula formation
  3. Pathologic fracture
  4. Septic arthritis (← extension into joint)
  5. Growth disturbance due to epiphyseal involvement
  6. Neoplasm
  7. Amyloidosis
  8. Severe deformity with delayed treatment

Acute Pyogenic Neonatal Osteomyelitis

Age: onset <30 days of age

Prevalence: 1–3÷1000 admissions to nursery

Risk factors: prematurity, low birth weight, complicated delivery, antecedent illness, umbilical artery catheterization, invasive procedure

Anatomy: metaphyseal vessels penetrate growth plate (= physis) crossing into epiphysis

Site:metaphysis + epiphysis of long bones

  • little / no systemic disturbance
  • multicentric involvement more common
  • often joint involvement (transphyseal / subperiosteal route)
  • bone scan falsely negative / equivocal in 70%

Acute Pyogenic Osteomyelitis in Infancy

Age:<18 months of age

Anatomy: metaphyseal vessels penetrate growth plate (= physis) crossing into epiphysis

Pathomechanism: spread from metaphysis to epiphysis

  • striking soft-tissue component
  • subperiosteal abscess with extensive periosteal new bone

Cx: frequent infection of epiphysis + joint ← transphyseal blood flow

◊osteomyelitis of proximal femur is usually associated with septic arthritis in children <1 year of age.

Prognosis: rapid healing

Acute Pyogenic Osteomyelitis in Childhood

Cause: hematogenous spread ← bacteremia

Organism: Staphylococcus aureus, β-hemolytic Streptococcus, Streptococcus pneumoniae, Escherichia coli, Pseudomonas aeruginosa; increasing incidence of methicillin-resistant S. aureus (MRSA) and Kingella kingae

Age: 2–16 years of age

Anatomy: transphyseal vessels closed; metaphyseal vessels adjacent to growth plate loop back toward metaphysis

Site: primary focus of infection located in metaphysis via nutrient artery; abscess formation in medulla with spread to cortex

Pathophysiology: metaphyseal capillaries lack phagocytic lining cells → uninhibited growth of microorganisms

Location: femur, tibia

  • sequestration frequent
  • periosteal elevation → disruption of periosteal blood supply
  • small single / multiple osteolytic areas in metaphysis
  • extensive periosteal reaction parallel to shaft (after 3–6 weeks); may be “lamellar nodular” (DDx: osteoblastoma, eosinophilic granuloma)
  • shortening of bone ← destruction of epiphyseal cartilage
  • growth stimulation ← hyperemia + premature maturation of adjacent epiphysis
  • midshaft osteomyelitis less frequent site
  • serpiginous tract with small sclerotic rim (PATHOGNOMONIC)

CAVE:

  1. Increased uptake in contralateral limb in patient with a limp
  2. Diffuse hyperemia in normal bones of an extremity involved with focal osteomyelitis should not be mistaken for multifocal osteomyelitis / septic arthritis.

Acute Pyogenic Osteomyelitis in Adulthood

Associated with: soft-tissue abscess, pathological fracture

Risk factors: IV drug use, previous trauma, immunosuppressed state, diabetes

Site: epiphysis + subchondral region (after growth plate closure)

  • delicate periosteal new bone
  • joint involvement common

Chronic Osteomyelitis  !!navigator!!

  • 67Ga citrate more useful than 111In-labeled leukocytes ← lymphocytes are predominant cell type
  • CT considered superior to MR for chronic osteomyelitis
  • cortical destruction and gas
  • thick irregular sclerotic bone with radiolucencies, elevated periosteum, chronic draining sinus

Sclerosing Osteomyelitis of Garré

= STERILE OSTEOMYELITIS

= low-grade nonnecrotic nonpurulent infection

Location: mandible (most commonly)

  • focal bulge of thickened cortex ← sclerosing periosteal reaction)

DDx: osteoid osteoma, stress fracture

Chronic Recurrent Multifocal Osteomyelitis

= benign self-limited disease of genetic etiology

◊May be identical to chronic sclerosing osteomyelitis of Garré; childhood equivalent to SAPHO syndrome

Age: children + adolescents; M÷F = 1÷2

Histo: nonspecific subacute / chronic osteomyelitis

  • pain, tenderness soft-tissue swelling
  • limited range of motion
  • elevated ESR + C-reactive protein; normal WBC

Associated with: psoriasis, palmoplantar pustulosis, inflammatory bowel disease

Location: tibia >femur >clavicle >fibula

◊Whole-body imaging (99mTc bone scintigraphy, MRI) usually shows additional unsuspected locations

Site: metaphyses of long bones (75%); often symmetric

  • No abscess formation, fistula, sequestra

Early:

  • small areas of bone lysis, often confluent
  • progressive sclerosis surrounding osteolytic foci

MRI:

  • bone marrow edema, periostitis, soft-tissue inflammation, transphyseal disease
  • joint effusion (30%), synovial thickening, cartilage destruction, destruction of subchondral bone

Late:

  • sclerosis + hyperostosis

Prognosis: delayed spontaneous resolution

DDx: subacute + chronic infectious osteomyelitis; histiocytosis; hypophosphatasia; malignancy (leukemia, lymphoma, Ewing sarcoma)

Brodie Abscess

= small intraosseous abscess involving cortex surrounded by reactive bone (in smoldering indolent infection of subacute pyogenic osteomyelitis / inadequate treatment of acute osteomyelitis)

Organism: S. aureus (most common); cultures often negative

Histo: granulation tissue + eburnation

Age: more common in children; M >F

Location: predilection for ends of tubular bones (proximal / distal tibial metaphysis most common); carpal + tarsal bones

Site: metaphysis, rarely traversing the open growth plate; epiphysis (in children + infants)

  • lytic lesion often in an oval configuration that is oriented along the long axis of the bone
  • surrounded by thick dense rim of reactive sclerosis that fades imperceptibly into surrounding bone
  • lucent tortuous channel extending toward growth plate prior to physeal closure (PATHOGNOMONIC)
  • periosteal new-bone formation
  • ± adjacent soft-tissue swelling
  • may persist for many months

MR:

  • “double line” effect = high SI of granulation tissue surrounded by low SI of bone sclerosis on T2WI
  • well-defined lesion of low- to intermediate SI outlined by low-signal rim on T1WI
  • generally surrounded by marrow edema
  • no / rim enhancement after IV Gd-chelate

DDx: Osteoid osteoma

Epidermoid Carcinoma  !!navigator!!

Etiology: complication of chronic osteomyelitis (0.2–1.7%)

Histo: squamous cell carcinoma (90%); occasionally: basal cell carcinoma, adenocarcinoma, fibro-sarcoma, angiosarcoma, reticulum cell sarcoma, spindle cell sarcoma, rhabdomyosarcoma, parosteal osteosarcoma, plasmacytoma

Age: 30–80 (mean 55) years; M >>F

Latent period: 20–30 (range of 1.5–72) years

  • history of childhood osteomyelitis
  • exacerbation of symptoms with increasing pain, enlarging mass
  • change in character / amount of sinus drainage

Location: at site of chronically / intermittently draining sinus; tibia (50%), femur (21%)

  • lytic lesion superimposed on changes of chronic osteomyelitis
  • soft-tissue mass
  • pathologic fracture

Prognosis:

  1. Early metastases in 14–20–40% (within 18 months)
  2. No recurrence in 80%

 Outline