CHRONIC OSTEOMYELITIS
NUR AINA BINTI AB KADIR
CONTENTS
Pathology
Intro-
duction
Investigation
Treatment
Clinical
features
Staging
INTRODUCTION
 Chronic pyogenic osteomyelitis
 Incidence is decline
 Other causes: tuberculosis, fungal infections
Types Chronic osteomyelitis
secondary to acute
osteomyelitis
Garre’s osteomyelitis
Brodie’s abscess
CHRONIC OSTEOMYELITIS
 Open fracture/operation
 Staphylococcus aureus
 Escherichia coli
 Streptococcus pyogenes
 Proteus mirabilis
 Pseudomonas aeruginosa
 Staphylococcus epidermidis (foreign implants )
PREDISPOSING FACTORS
 COMMONEST: local trauma eg: open fracture/
prolonged bone operation, foreign implant
 Host defences:
 Scar formation
 Dead bone
 Blood vessel
 Bacteria covered in a protein-polysaccharides
slime (glycocalyx)
PREDISPOSING FACTORS
 Delayed and inadequate treatment
 Patient’s condition:
 Very old/debilitated
 Suffering from substance abuse
 Diabetes
 Peripheral vascular disease
PATHOLOGY
 Bone is destroyed or devitalized
 Cavities containing pus and pieces of dead
bone (sequestra)
 the result of chronic reactive new bone
formation – which may take the form of a
distinct bony sheath (involucrum).
 Sequestra act as substrates for bacterial
adhesion
 A sinus may seal off for weeks/ even months
healing
CLINICAL FEATURES
 Pain,Pyrexia,Redness,Tenderness
 Discharging sinus
 Longstanding cases the tissues are thickened
and puckered or folded inwards where a scar
or sinus adheres to the underlying bone.
 Seropurulent discharge and excoriation of the
surrounding skin.
 Post-traumatic osteomyelitis: the bone may
be deformed or ununited
IMAGING
X- ray
Radio
Isotope
scintigraphy
CT scan MRI
IMAGING
 X-ray examination: bone resorption patchy
loss of density/frank excavation around an
implant & thickening & sclerosis of the
surrounding bone
 Crudely thickened & mishappentumour
 Sinogram: help
IMAGING
 Radioisotope
scintigraphy
 Sensitive,not
specific.
 99mTc-HDP scans:
increased activity
 67Ga-citrate or
111In-labelled
leucocytes: specific
for osteomyelitis
hidden foci of
infection.
 CT and MRI  the
extent of bone
destruction and
reactive oedema,
hidden abscesses
sequestra.
Technetium
Indium
INVESTIGATIONS
 Elevated CSR,ESR and WBC levels.
 Cultures of organisms- antibiotic sensitivity-
deep tissue
 Molecular technique- amplication of bacterial
DNA/RNA fragments(PCR), by gel
electrophoresis
STAGING-ADULT
LESION TYPE
STAGE 1 MEDULLARY
STAGE 2 SUPERFICIAL
STAGE 3 LOCALIZED
STAGE 4 DIFFUSE
TYPE A NORMAL
TYPE B COMPROMISED BY LOCAL/SYSTEMIC CONDITION
TYPE C SEVERELY COMPROMISED BY LOCAL AND SYSTEMIC
CONDITIONS
CATEGORY INTERPRETATION
Stage 1 or 2, Type A Least serious
Stage 1,2,3, Type B Have chance of recover
Type C Poor prognosis
Stage 4 Long term palliative care
TREATMENT
Antibiotic
Local
treatment
Operation
ANTIBIOTIC
 To suppress the infection, prevent its spread to
healthy bone
 Control acute flares
 Choices:
 Microbiological studies
 Capable of penetration
 Non toxic for long-term use
ANTIBIOTIC
 Fusidic acid, clindamycin, cephalosporins
 Meticillin-resistant Stapyhlococcus aureus
infection (MRSA): vancomycin and teicoplanin
 4-6 weeks –serum antibiotic concentration
measurement
 Surgical clearance failed continue for
another 4w
 Continuous collaboration with a microbiologist.
LOCAL TREATMENT
 Simple dressing
 Colostomy paste
 Acute abscess urgent incision & drainage
OPERATION
 INDICATIONS
 chronic haematogenous infection
 intrusive symptoms
 failure of adequate antibiotic treatment
 evidence of a sequestrum
 post-traumatic and postoperative infections
 intractable wound and/or an infected ununited
fracture
 Presence of foreign implant
 Debridement
 Dealing with the ‘dead space’
 Soft tissue cover
 After care
Dealing with the ‘dead space’
 Porous antibiotic-impregnated beads can be
laid in the cavityleft for 2/3 weeksreplaced
with cancellous bone grafts.
 Papineau technique: the entire cavity is
packed with small cancellous chips mixed with
an antibiotic and a fibrin sealantarea is
covered by adjacent muscle & the skin wound
is sutured without tension
Dealing with the ‘dead space’
 Radical excision of all avascular and infected
tissue followed by closed irrigation and suction
drainage of the bed using double-lumen tubes
and an appropriate antibiotic solution in high
concentration.
 The spaces is gradually filled by vascular
granulation tissue
 Tubes is removedculture negative
 Refractory caseexcise the infected and/or
devitalized segment of bone completely and
then close the gap by the Ilizarov method
DIFFERENTIAL DIAGNOSIS
Tubercular
osteomyelitis
• Thin& watery discharge
• Often multifocal
Soft tissue
infection
• Absence of thickening of underlying bone
• Absence of sinus fixed to the bone
Ewing’s
sarcoma
• Sudden onset of pain & swelling
• Biopsy
GARRE’S SCLEROSING
OSTEOMYELITIS
GARRE’S SCLEROSING
OTEOMYELITIS
 Rare form of non-suppurative osteomyelitis
 Marked sclerosis, cortical thickening
 No abscess, diffuse enlargement of the bone
at the affected site
 Adolescent and young adult
 Long history of aching and slight swelling over
the bone
 Recurrent attack of acute pain with malaise
and slight fever
X-RAY
 increased bone density and cortical thickening
 some cases the marrow cavity is completelly
obliterated.
 There is no abscess cavity.
 Diaphysis and mandible
DIAGNOSIS
 If a small segment of bone is
involvedosteoid osteoma.
 If there is marked periosteal layering of new
boneEwing’s sarcoma.
 Biopsy: low-grade inflammatory lesion with
reactive bone formation
 Micro-organism culture: staphylococal
infection
TREATMENT
 Operation:
 the abnormal area is excised and the exposed
surface thoroughly curetted.
 Bone grafts, bone transport or free bone
transfer may be needed.
Also know as SUBACUTE
HAEMATOGENOUS OSTEOMYELITIS
BRODIE’S ABSCESS
PATHOLOGY
 well-defined cavity in cancellous bone –
usually in the tibial metaphysis – containing
glairy seropurulent fluid (rarely pus).
 The cavity is lined by granulation tissue
containing a mixture of acute and chronic
inflammatory cells.
 The surrounding bone trabeculae are often
thickened.
 The lesion sometimes encroaches on and
erodes the bony cortex.
CLINICAL FEATURES
 child or adolescent
 had pain near one of the larger joints for
several weeks or even months.
 Limp,slight swelling, muscle wasting and local
tenderness.
 The temperature is usually normal and there
 is little to suggest an infection.
 The WBC count and blood cultures usually
show no abnormality but the ESR is
sometimes elevated
IMAGING
 lesion is a circumscribed,
 round or oval radiolucent ‘cavity’ 1–2 cm in
diameter.
 tibial or femoral metaphysis, but it may occur in
the epiphysis or in one of the cuboidal bones (e.g.
the calcaneum).
 Sometimes the ‘cavity’ is surrounded by a halo of
sclerosis extending into the diaphysis.
 Metaphyseal lesions cause little or no periosteal
reaction; diaphyseal lesions may be associated
with periosteal new bone formation and marked
cortical thickening.
 If the cortex malignant tumour.
DIAGNOSIS
 Clinical and x ray appearances may resembles
osteoid osteoma,cystic tuberculosis,
eosinophilic granuloma
 Biopsy
 If fluid is encountered: bacteriological culture
TREATMENT
 Conservative
 Immobilization
 Antibiotic (flucloxacillin & fusidic acid)
 IV for 4-5 days
 Oral 6 weeks
 Diagnosis in doubt: open biopsy + curettage
 Curettage: x-ray shows no healing after
conservative treatment
 Apley’s System of Orthopaedics and Fracture
,11th edition, page 36-41
 Essential orthopaedics by Maheshwari
 http://reference.medscape.com/features/slides
how/osteomyelitis#page=7
 http://radiopaedia.org/articles/osteomyelitis
REFERENCES

Chronic osteomyeliti sby aina

  • 1.
  • 2.
  • 3.
    INTRODUCTION  Chronic pyogenicosteomyelitis  Incidence is decline  Other causes: tuberculosis, fungal infections Types Chronic osteomyelitis secondary to acute osteomyelitis Garre’s osteomyelitis Brodie’s abscess
  • 4.
    CHRONIC OSTEOMYELITIS  Openfracture/operation  Staphylococcus aureus  Escherichia coli  Streptococcus pyogenes  Proteus mirabilis  Pseudomonas aeruginosa  Staphylococcus epidermidis (foreign implants )
  • 5.
    PREDISPOSING FACTORS  COMMONEST:local trauma eg: open fracture/ prolonged bone operation, foreign implant  Host defences:  Scar formation  Dead bone  Blood vessel  Bacteria covered in a protein-polysaccharides slime (glycocalyx)
  • 6.
    PREDISPOSING FACTORS  Delayedand inadequate treatment  Patient’s condition:  Very old/debilitated  Suffering from substance abuse  Diabetes  Peripheral vascular disease
  • 7.
    PATHOLOGY  Bone isdestroyed or devitalized  Cavities containing pus and pieces of dead bone (sequestra)  the result of chronic reactive new bone formation – which may take the form of a distinct bony sheath (involucrum).  Sequestra act as substrates for bacterial adhesion  A sinus may seal off for weeks/ even months healing
  • 9.
    CLINICAL FEATURES  Pain,Pyrexia,Redness,Tenderness Discharging sinus  Longstanding cases the tissues are thickened and puckered or folded inwards where a scar or sinus adheres to the underlying bone.  Seropurulent discharge and excoriation of the surrounding skin.  Post-traumatic osteomyelitis: the bone may be deformed or ununited
  • 10.
  • 11.
    IMAGING  X-ray examination:bone resorption patchy loss of density/frank excavation around an implant & thickening & sclerosis of the surrounding bone  Crudely thickened & mishappentumour  Sinogram: help
  • 13.
    IMAGING  Radioisotope scintigraphy  Sensitive,not specific. 99mTc-HDP scans: increased activity  67Ga-citrate or 111In-labelled leucocytes: specific for osteomyelitis hidden foci of infection.  CT and MRI  the extent of bone destruction and reactive oedema, hidden abscesses sequestra.
  • 14.
  • 15.
    INVESTIGATIONS  Elevated CSR,ESRand WBC levels.  Cultures of organisms- antibiotic sensitivity- deep tissue  Molecular technique- amplication of bacterial DNA/RNA fragments(PCR), by gel electrophoresis
  • 16.
    STAGING-ADULT LESION TYPE STAGE 1MEDULLARY STAGE 2 SUPERFICIAL STAGE 3 LOCALIZED STAGE 4 DIFFUSE TYPE A NORMAL TYPE B COMPROMISED BY LOCAL/SYSTEMIC CONDITION TYPE C SEVERELY COMPROMISED BY LOCAL AND SYSTEMIC CONDITIONS CATEGORY INTERPRETATION Stage 1 or 2, Type A Least serious Stage 1,2,3, Type B Have chance of recover Type C Poor prognosis Stage 4 Long term palliative care
  • 17.
  • 18.
    ANTIBIOTIC  To suppressthe infection, prevent its spread to healthy bone  Control acute flares  Choices:  Microbiological studies  Capable of penetration  Non toxic for long-term use
  • 19.
    ANTIBIOTIC  Fusidic acid,clindamycin, cephalosporins  Meticillin-resistant Stapyhlococcus aureus infection (MRSA): vancomycin and teicoplanin  4-6 weeks –serum antibiotic concentration measurement  Surgical clearance failed continue for another 4w  Continuous collaboration with a microbiologist.
  • 20.
    LOCAL TREATMENT  Simpledressing  Colostomy paste  Acute abscess urgent incision & drainage
  • 21.
    OPERATION  INDICATIONS  chronichaematogenous infection  intrusive symptoms  failure of adequate antibiotic treatment  evidence of a sequestrum  post-traumatic and postoperative infections  intractable wound and/or an infected ununited fracture  Presence of foreign implant
  • 22.
     Debridement  Dealingwith the ‘dead space’  Soft tissue cover  After care
  • 23.
    Dealing with the‘dead space’  Porous antibiotic-impregnated beads can be laid in the cavityleft for 2/3 weeksreplaced with cancellous bone grafts.  Papineau technique: the entire cavity is packed with small cancellous chips mixed with an antibiotic and a fibrin sealantarea is covered by adjacent muscle & the skin wound is sutured without tension
  • 24.
    Dealing with the‘dead space’  Radical excision of all avascular and infected tissue followed by closed irrigation and suction drainage of the bed using double-lumen tubes and an appropriate antibiotic solution in high concentration.  The spaces is gradually filled by vascular granulation tissue  Tubes is removedculture negative  Refractory caseexcise the infected and/or devitalized segment of bone completely and then close the gap by the Ilizarov method
  • 25.
    DIFFERENTIAL DIAGNOSIS Tubercular osteomyelitis • Thin&watery discharge • Often multifocal Soft tissue infection • Absence of thickening of underlying bone • Absence of sinus fixed to the bone Ewing’s sarcoma • Sudden onset of pain & swelling • Biopsy
  • 26.
  • 27.
    GARRE’S SCLEROSING OTEOMYELITIS  Rareform of non-suppurative osteomyelitis  Marked sclerosis, cortical thickening  No abscess, diffuse enlargement of the bone at the affected site  Adolescent and young adult  Long history of aching and slight swelling over the bone  Recurrent attack of acute pain with malaise and slight fever
  • 28.
    X-RAY  increased bonedensity and cortical thickening  some cases the marrow cavity is completelly obliterated.  There is no abscess cavity.  Diaphysis and mandible
  • 29.
    DIAGNOSIS  If asmall segment of bone is involvedosteoid osteoma.  If there is marked periosteal layering of new boneEwing’s sarcoma.  Biopsy: low-grade inflammatory lesion with reactive bone formation  Micro-organism culture: staphylococal infection
  • 30.
    TREATMENT  Operation:  theabnormal area is excised and the exposed surface thoroughly curetted.  Bone grafts, bone transport or free bone transfer may be needed.
  • 31.
    Also know asSUBACUTE HAEMATOGENOUS OSTEOMYELITIS BRODIE’S ABSCESS
  • 32.
    PATHOLOGY  well-defined cavityin cancellous bone – usually in the tibial metaphysis – containing glairy seropurulent fluid (rarely pus).  The cavity is lined by granulation tissue containing a mixture of acute and chronic inflammatory cells.  The surrounding bone trabeculae are often thickened.  The lesion sometimes encroaches on and erodes the bony cortex.
  • 33.
    CLINICAL FEATURES  childor adolescent  had pain near one of the larger joints for several weeks or even months.  Limp,slight swelling, muscle wasting and local tenderness.  The temperature is usually normal and there  is little to suggest an infection.  The WBC count and blood cultures usually show no abnormality but the ESR is sometimes elevated
  • 34.
    IMAGING  lesion isa circumscribed,  round or oval radiolucent ‘cavity’ 1–2 cm in diameter.  tibial or femoral metaphysis, but it may occur in the epiphysis or in one of the cuboidal bones (e.g. the calcaneum).  Sometimes the ‘cavity’ is surrounded by a halo of sclerosis extending into the diaphysis.  Metaphyseal lesions cause little or no periosteal reaction; diaphyseal lesions may be associated with periosteal new bone formation and marked cortical thickening.  If the cortex malignant tumour.
  • 35.
    DIAGNOSIS  Clinical andx ray appearances may resembles osteoid osteoma,cystic tuberculosis, eosinophilic granuloma  Biopsy  If fluid is encountered: bacteriological culture
  • 36.
    TREATMENT  Conservative  Immobilization Antibiotic (flucloxacillin & fusidic acid)  IV for 4-5 days  Oral 6 weeks  Diagnosis in doubt: open biopsy + curettage  Curettage: x-ray shows no healing after conservative treatment
  • 37.
     Apley’s Systemof Orthopaedics and Fracture ,11th edition, page 36-41  Essential orthopaedics by Maheshwari  http://reference.medscape.com/features/slides how/osteomyelitis#page=7  http://radiopaedia.org/articles/osteomyelitis REFERENCES

Editor's Notes

  • #6 presence of scar formation, dead and dying bone around the focus of infection, poor penetration of new blood vessels and non-collapsing cavities in which microbes can thrive. Bacteria covered in a protein–polysaccharide slime (glycocalyx) that protects them from both the host defences and antibiotics
  • #22 Collaboration with plastic surgeon
  • #29 Fully sclerosis,diaphysis no medullary n cortical differentiation
  • #30 Micro-organisms are seldom cultured but the condition is usually ascribed to a staphylococcal infection.