Osteomyelitis
by: wadeea Al-Asad
Superfision by
Prof. Khaled Alnozaily
prof. Essam Alnajash
•Etiology
•Diagnosis
•Treatment
•Classification
•What is infection?
• is a condition in which pathogenic microorganisms multiply and
spread within the body tissues.
•What is Osteomyelitis?
• Osteomyelitis is the infection of bone characterized by
progressive inflammatory destruction and apposition of new
bone.
•Microorganisms may reach the musculoskeletal
tissues by:
• Direct Introduction through the skin
• Direct spread from a contiguous focus of infection
• Indirect spread via the bloodstream from a distant site
Etiology
• Osteomyelitis occurs when an adequate number of a sufficiently
virulent organism overcomes the host’s natural defenses
(inflammatory and immune responses) and establishes a focus of
infection.
• it is much easier to prevent an infection than it is to treat it.
Etiology
• Patient dependent factors:
Nutrition
immunologic status,
alcohol abuse,
smoking,
infection at a remote site,
congestive heart failure,
depression, and other comorbidities
Etiology
• Surgeon dependent factors:
prophylactic antibiotics, (golden hours)
skin and wound care, (CDC guidelines for skin preparation)
operating environment,
surgical technique,
treatment of impending infections, such as in open fractures.
Duration of hospital stay
Diagnosis
• Symptoms and Signs (classical triad)
• Laboratory Studies:
•CBC WBC
Diagnosis
ESR
False positive
False negative
Peak 3-5days
• Returns 3 weeks
Diagnosis
•CRP
• Better
• increases within 6 hours of infection, reaches a peak elevation 2 days
after infection, and returns to normal within 1 week after adequate
treatment has begun.
• Can misleading
Diagnosis
•D-dimer
• Better than CRP, ESR
• Specificity of 93% and a sensitivity of 89%.
• D-dimer can return to normal levels after 2 days postoperatively.
Diagnosis
•Imaging Studies
•Plane Radiography
• Soft tissue swelling and bone distraction
• 30% to 50% of the bone matrix must be lost to show a lytic lesion on
radiographs
• Initial image less than 5%
• After one week around 30%
• 2-3 weeks 90%
Diagnosis
•CT
• Can show soft-tissue abscess easly
• Acute osteomyelitis (based on detection of intraosseous gas,
osteolysis, soft-tissue masses, abscesses, or foreign bodies)
• Identifies sequestra in chronic osteomyelitis.
Diagnosis
•Ultrasonography
• Localize abscess cavity
• Guide for aspiration
Diagnosis
•Radionuclide scanning
• Does not detect the presence of infection but, instead, reflects
inflammatory changes or the reaction of bone to the infection.
Diagnosis
•MRI
• MRI is the most appropriate tool to rule out cartilaginous epiphyseal
infection.
• Detect changes much earlier than radiograph
Diagnosis
•Culture studies
• Isolating and identifying the offending organism and determining
antibiotic susceptibility.
• Antibiotics should be stopped 14 days before culture
• 3-5 different site
• Cultures of superficial wounds or sinus tracks should not be relied on
because they are poor indicators of deep infection and usually are
polymicrobial.
Treatment
• Identify the infecting organism and administer effective antibiotic
treatment or chemotherapy.
• Provide analgesia and general supportive measures, including rest of
the affected part or splintage of the affected joint.
• Release pus as soon as it is detected.
• Eradicate avascular and necrotic tissue.
• Stabilize the bone if it has fractured and restore continuity if there is a
gap in the bone.
• Maintain or regain soft-tissue and skin cover.
ACUTE HAEMATOGENOUS OSTEOMYELITIS
• Mainly a disease of children
• Adults also affected
• Incidence of Surgery is decreased
• Staphylococcus aureus (found in over 70% of cases)
• Group B Strep is most common organism in neonates
• Metaphysis of long bone the commonest site in children
Etiology and pathogens
Etiology and pathogens
Pathology
Inflammation
Suppuration
Bone necrosis
Reactive bone
formation
Resolution
Or
Chronisity
Acute
Inflammation
Increase
intraossious
pressure
Obstruction
of blood flow
Intravascular
thrombosis
Pus
formation
Sub-
periosteal
abscess
Spread
through the
shaft
Reenter or to
soft tissue Bone death
Clinical features
•History and examination
• History of recent disease
• Symptoms
• Signs
• Redness, hotness, Edema and
Swelling are late signs
Diagnosis
• PLAN X-RAY
• First week : no
abnormality
• Second week: faint
extracortical outline due
to periosteal new bone
formation
• Later periosteal
thickening becomes
more obvious.
Diagnosis
• Ultrasonography: fluid collection
• CT
• RADIONUCLIDE SCANNING
• MRI: best method of demonstrating bone marrow inflammation.
It is extremely sensitive.
Diagnosis
• Laboratory Studies
• The most certain way to confirm the clinical diagnosis is to aspirate
pus or fluid from the metaphyseal subperiosteal abscess, the
extraosseous soft tissues or an adjacent joint.
• Aspiration will give a positive result in over 60% of cases
• Blood cultures should be obtained if fever above 38 °C is detected
• CBC CRP ESR
Differential diagnosis
• Cellulitis
• Acute arthritis
• Necrotic myositis
• Acute rheumatism
• Sickle cell crisis
Treatment
Treatment
Non-operative
Antibiotics
Early with no abscess
Typically broad-spectrum
IV antibiotic for 4-6 weeks
Operative
Drainage, detriment with
antibiotic
Abscess or no response to
antibiotic
Complications
• Epiphyseal damage and altered bone growth
• Suppurative arthritis.
• Metastatic infection
• Pathological fracture.
• Chronic osteomyelitis.
Chronic Osteomyelitis
• Sequel to acute haematogenous osteomyelitis
• The usual organisms are Staphylococcus aureus, Escherichia coli,
Streptococcus pyogenes, Proteus mirabilis and Pseudomonas
aeruginosa
• In the presence of foreign implants Staphylococcus , is the
commonest of all.
• The commonest predisposing factors is local trauma, such as an open
fracture or a prolonged bone operation
Clinical factors
• Pain, pyrexia, Redness and tenderness with sinus
• X-ray examination will usually show bone resorption with thickening
and sclerosis of the surrounding bone.
• CT and MRI they will show the extent of bone destruction and
reactive oedema, hidden abscesses and sequestra.
• CRP, ESR and WBC levels may be increased.
• Organisms cultured from discharging sinuses should be tested
repeatedly for antibiotic sensitivity.
• Superficial swab sample may not reflect the really persistent infection
in the deeper tissue
Staging
Treatment
• Antibiotic:Chronic infection is seldom eradicated
To suppress the infection and prevent its spread to healthy bone and to
control acute flares.
• Operation :
The presence of a foreign implant may prompt surgical intervention to
remove the implant
• Depridement: all infected soft tissue
and dead or devitalized bone, as well as any infected
implant, must be excised
• Dealing with the ‘dead space
Porous antibiotic- impregnated
beads can be laid in the cavity and
left for 2 or 3 weeks and then
replaced with cancellous bone
graft
• The local concentrations of
antibiotic achieved are 200 times
higher than levels achieved with
systemic antibiotic administration
Thank you

osteomyelitis.ppt bone infection OM 12 lec

  • 1.
    Osteomyelitis by: wadeea Al-Asad Superfisionby Prof. Khaled Alnozaily prof. Essam Alnajash
  • 2.
  • 3.
    •What is infection? •is a condition in which pathogenic microorganisms multiply and spread within the body tissues. •What is Osteomyelitis? • Osteomyelitis is the infection of bone characterized by progressive inflammatory destruction and apposition of new bone.
  • 4.
    •Microorganisms may reachthe musculoskeletal tissues by: • Direct Introduction through the skin • Direct spread from a contiguous focus of infection • Indirect spread via the bloodstream from a distant site
  • 5.
    Etiology • Osteomyelitis occurswhen an adequate number of a sufficiently virulent organism overcomes the host’s natural defenses (inflammatory and immune responses) and establishes a focus of infection. • it is much easier to prevent an infection than it is to treat it.
  • 6.
    Etiology • Patient dependentfactors: Nutrition immunologic status, alcohol abuse, smoking, infection at a remote site, congestive heart failure, depression, and other comorbidities
  • 7.
    Etiology • Surgeon dependentfactors: prophylactic antibiotics, (golden hours) skin and wound care, (CDC guidelines for skin preparation) operating environment, surgical technique, treatment of impending infections, such as in open fractures. Duration of hospital stay
  • 8.
    Diagnosis • Symptoms andSigns (classical triad) • Laboratory Studies: •CBC WBC
  • 9.
  • 10.
    Diagnosis •CRP • Better • increaseswithin 6 hours of infection, reaches a peak elevation 2 days after infection, and returns to normal within 1 week after adequate treatment has begun. • Can misleading
  • 11.
    Diagnosis •D-dimer • Better thanCRP, ESR • Specificity of 93% and a sensitivity of 89%. • D-dimer can return to normal levels after 2 days postoperatively.
  • 12.
    Diagnosis •Imaging Studies •Plane Radiography •Soft tissue swelling and bone distraction • 30% to 50% of the bone matrix must be lost to show a lytic lesion on radiographs • Initial image less than 5% • After one week around 30% • 2-3 weeks 90%
  • 13.
    Diagnosis •CT • Can showsoft-tissue abscess easly • Acute osteomyelitis (based on detection of intraosseous gas, osteolysis, soft-tissue masses, abscesses, or foreign bodies) • Identifies sequestra in chronic osteomyelitis.
  • 14.
  • 15.
    Diagnosis •Radionuclide scanning • Doesnot detect the presence of infection but, instead, reflects inflammatory changes or the reaction of bone to the infection.
  • 16.
    Diagnosis •MRI • MRI isthe most appropriate tool to rule out cartilaginous epiphyseal infection. • Detect changes much earlier than radiograph
  • 17.
    Diagnosis •Culture studies • Isolatingand identifying the offending organism and determining antibiotic susceptibility. • Antibiotics should be stopped 14 days before culture • 3-5 different site • Cultures of superficial wounds or sinus tracks should not be relied on because they are poor indicators of deep infection and usually are polymicrobial.
  • 18.
    Treatment • Identify theinfecting organism and administer effective antibiotic treatment or chemotherapy. • Provide analgesia and general supportive measures, including rest of the affected part or splintage of the affected joint. • Release pus as soon as it is detected. • Eradicate avascular and necrotic tissue. • Stabilize the bone if it has fractured and restore continuity if there is a gap in the bone. • Maintain or regain soft-tissue and skin cover.
  • 19.
    ACUTE HAEMATOGENOUS OSTEOMYELITIS •Mainly a disease of children • Adults also affected • Incidence of Surgery is decreased • Staphylococcus aureus (found in over 70% of cases) • Group B Strep is most common organism in neonates • Metaphysis of long bone the commonest site in children
  • 20.
  • 21.
  • 22.
  • 23.
  • 24.
    Clinical features •History andexamination • History of recent disease • Symptoms • Signs • Redness, hotness, Edema and Swelling are late signs
  • 25.
    Diagnosis • PLAN X-RAY •First week : no abnormality • Second week: faint extracortical outline due to periosteal new bone formation • Later periosteal thickening becomes more obvious.
  • 26.
    Diagnosis • Ultrasonography: fluidcollection • CT • RADIONUCLIDE SCANNING • MRI: best method of demonstrating bone marrow inflammation. It is extremely sensitive.
  • 27.
    Diagnosis • Laboratory Studies •The most certain way to confirm the clinical diagnosis is to aspirate pus or fluid from the metaphyseal subperiosteal abscess, the extraosseous soft tissues or an adjacent joint. • Aspiration will give a positive result in over 60% of cases • Blood cultures should be obtained if fever above 38 °C is detected • CBC CRP ESR
  • 28.
    Differential diagnosis • Cellulitis •Acute arthritis • Necrotic myositis • Acute rheumatism • Sickle cell crisis
  • 29.
    Treatment Treatment Non-operative Antibiotics Early with noabscess Typically broad-spectrum IV antibiotic for 4-6 weeks Operative Drainage, detriment with antibiotic Abscess or no response to antibiotic
  • 31.
    Complications • Epiphyseal damageand altered bone growth • Suppurative arthritis. • Metastatic infection • Pathological fracture. • Chronic osteomyelitis.
  • 32.
    Chronic Osteomyelitis • Sequelto acute haematogenous osteomyelitis • The usual organisms are Staphylococcus aureus, Escherichia coli, Streptococcus pyogenes, Proteus mirabilis and Pseudomonas aeruginosa • In the presence of foreign implants Staphylococcus , is the commonest of all. • The commonest predisposing factors is local trauma, such as an open fracture or a prolonged bone operation
  • 33.
    Clinical factors • Pain,pyrexia, Redness and tenderness with sinus • X-ray examination will usually show bone resorption with thickening and sclerosis of the surrounding bone. • CT and MRI they will show the extent of bone destruction and reactive oedema, hidden abscesses and sequestra. • CRP, ESR and WBC levels may be increased. • Organisms cultured from discharging sinuses should be tested repeatedly for antibiotic sensitivity. • Superficial swab sample may not reflect the really persistent infection in the deeper tissue
  • 34.
  • 35.
    Treatment • Antibiotic:Chronic infectionis seldom eradicated To suppress the infection and prevent its spread to healthy bone and to control acute flares. • Operation : The presence of a foreign implant may prompt surgical intervention to remove the implant • Depridement: all infected soft tissue and dead or devitalized bone, as well as any infected implant, must be excised
  • 36.
    • Dealing withthe ‘dead space Porous antibiotic- impregnated beads can be laid in the cavity and left for 2 or 3 weeks and then replaced with cancellous bone graft • The local concentrations of antibiotic achieved are 200 times higher than levels achieved with systemic antibiotic administration
  • 37.