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OSTEOMYELITIS
Head of Department
Dr. Akshara Gupta M.D.
Professor
Department of Radiodiagnosis
G.R. Medical College, Gwalior
Presented by
DR SANDEEP SINGHAWAL
P.G. STUDENT
Blood supply to a long Bone
1.The nutrient artery:
major source of blood
supply throughout life. It
supplies the marrow and
most of the inner cortex.
2. Periosteal vessels.These
supply the outer cortex.
3. Metaphyseal and
epiphyseal vessels.
NORMAL VASCULAR SUPPLY IN TUBULAR BONES: CHILD, INFANT, AND ADULT.
A. Infant. Note that a small percentage of the metaphyseal blood vessels may
penetrate the cartilaginous growth plate and supply the epiphysis.
B. Child. Observe the vascular supply in the metaphysis; it does not cross the
growth plate.
C. Adult. Note that because the growth plate is no longer present, blood
supplies to the metaphysis and the distal end of the bone are continuous.
 Infant :infections can thus pass to the epiphysis
and then the joint. Acute pyogenic arthritis is
therefore a relatively common sequel of
osteomyelitis in infants.
 Childhood, between 2 and 1 6 years, few
vessels cross the epiphyseal plate though the
periosteum is still relatively loosely attached.
The epiphysis and joint are thus less frequently
infected.
 Adult: metaphyseal and epiphyseal vessels are
again connected so that septic arthritis can
recur.
Osteo – myel- itis
 Infection and inflammation of the bone and/or
bone marrow
 Nelaton coined the term OSTEOMYELITIS in
1844
 Modern chemotherapy – significantly reduced
the deformity & mortality
 Can occur at any age; particularly common
between the ages of 2-12 years of age (M:F of
3:1)
CAUSE
 Staphylococcus aureus: 80-90% of all infections
 Escherichia coli: IVDU (intravenous drug users)
and genitourinary tract infection
 Pseudomonas spp: IVDU and genitourinary
tract infection
 Klebsiella spp: IVDU and genitourinary tract
infection
 Salmonella spp: sickle cell disease
 Haemophilus influenzae: neonates
 group B streptococci: neonates
CLASSIFICATION
 Acute osteomyelitis – within 2 weeks of
onset of symptoms
 Subacute- 2 weeks to 2 months
 Chronic > 2 months
Spread of infection
 Hematogenous spread – MC source
 Contiguous source- adjacent contaminated
site (cutaneous, sinus or dental inf )
 Direct implantation of infection (penetrating
injuries)
 Post Operative infections
Clinical Features
 Young patients present with acute
systemic symptoms – fever, chills , pain &
swelling often with extensive loss of limb
function.
 Adult patients present with symptoms
that vary and tend to be more chronic -
fever, malaise , edema & pain.
Location
 lower limb (most common) lower femur, upper
tibia
 vertebrae: lumbar > thoracic > cervical
The location of osteomyelitis within a bone varies
with age, on account of changing blood supply :
 neonates: metaphysis and/or epiphysis
 children: metaphysis
 adults: epiphyses and subchondral regions
PATHOPHYSIOLOGY
 Implantation of pathogen in medullary tissue
 Vascular and cellular response
 Suppurative edema (increased intramedullary
pressure)
 Mechanical compression of capillaries and sinusoids
 Infarction of marrow tissue and bone with adjacent
hyperemia
 Focal osteolysis and inflammatory exudate.
 Eventually inflammatory process penetrates the
inner cortex & enters the Haversian canal and
lacunar systems to reach the subperiosteal
space
 Involvement of periosteal &
subperiosteal areas causes a loss of
blood supply to cortical bone ->
necrotic
 Cortical and medullary infarcts result
in formation of SEQUESTRUM (dead
bone in situ)
 As the pus lifts the periosteum->
periosteal new born formation occurs
(INVOLUCRUM)
 CLOACA – defect , with continued
discharge ( associated with chronic
osteomyelitis
 Marjolin ulcer(SCC) – malignant
transformation
Advanced osteomyelitis
involving the whole of the
right tibia and lower
end of fibula. Note
sequestrum in tibia
(arrow) and further
sequestrum being
extruded from the fibula
(arrow).
Pathologic Features
 Sequestrum formation: necrotic cortical or
medullary bone. represents devascularisation
of a portion of bone with necrosis.
 Involucrum: cortical collar of new bone.
 Cloaca: draining sinus.
 Marjolin’s ulcer: malignant degeneration of
squamous cell lining of cloaca.
Radiologic Features
 Bone scans are the earliest means of diagnosis.
 Positive findings as early as 48 hours of onset of
symptoms
 MC :Technetium – methylene diphosphonate and
Gallium 67 citrate
 Increased uptake (HOT SPOT) of radionuclide as a
response to the inflammation and destruction of
bone
BONE SCAN: EARLY DETECTION OF OSTEOMYELITIS. A. Initial Plain Film. Note that
the initial radiographic examination shows no destructive changes. B. 10-Day
Follow-Up. Note the permeative pattern of bone destruction in the metaphysis
of the distal radius. C. Bone Scan, Initial Presentation. Note that this
examination, performed at the same time as panel A, reveals an area of
increased uptake (a hot spot) (arrow) of technetium.
MRI & CT
 MRI is more sensitive than bone scan in
identification of low grade infections
 T1
 intermediate to low signal central component (fluid)
 surrounding bone marrow of lower signal than normal due
to oedema
 cortical bone destruction
 T2
 bone marrow oedema
 central high signal (fluid)
 CT is superior to both MRI and plain film in depicting
the bony margins and identifying a sequestrum or
involucrum.
Early Signs
 Radiographic Latent period 10 days for extremities
; 21 days for spine
 Represents the time taken for osseous destruction
to be appreciated on radiographs
 Soft tissue swelling and obliterated fat planes
(earliest radiographic sign) 7 to 10 days
 regional osteopaenia
 Moth eaten or permeative cortical and medullary
destruction
 Periosteal reaction – laminated/lamellar 10-14
days
OSTEOMYELITIS: EARLY RADIOGRAPHIC SIGNS. Humerus. Note the
large soft tissue swelling (arrows) representing an early radiographic sign of
osteomyelitis in this pediatric patient. Observe also the lifting of the
periosteum as a result of the infectious process (arrowhead).
 Late signs
Destruction of adjacent cortex 10-14days
Involucrum 3weeks
Sequestrum 4 weeks
Cloaca
Loss of joint space, healing by ankylosis
POSTSURGICAL OSTEOMYELITIS. A. AP Tibia and Fibula. Observe the fracture dislocation
of the fibula. This young adult male suffered a severe injury in a motorcycle
accident. Open reduction and surgical pinning of the complete fracture of the tibia
were performed. B. Lateral Tibia. Just 4 weeks after the surgical intervention, the
patient complained of persistent pain at the area of the fracture site. Note the
typical moth-eaten destructive lesions of osteomyelitis.
OSTEOMYELITIS: PERIOSTEAL RESPONSE. A. Distal Femur. Observe the thick collar of periosteal
new bone (arrows) in the distal femur. Observe also the destructive lesions in the
metaphysis of the distal femur occurring as a result of osteomyelitis. B. Distal Tibia. Note
the extensive laminated periosteal response affecting the diaphysis and metaphysis of the
distal tibia (arrows). The scattered areas of radiolucency throughout the tibia represent
infective destructive lesions. C. Distal Fibula. Note the laminated periosteal response
(arrows) in the distal portion of the fibula in this pediatric patient. There are lytic
destructive lesions noted in the distal portion of the fibula (arrowhead), representing the
infectious focus.
SEQUESTRUM AND INVOLUCRUM
FORMATION. A. AP Tibia and
Fibula. Note the central
necrotic bone (sequestrum)
(arrow), which is surrounded by
an extensive periosteal collar
of new bone (involucrum)
(arrowhead).
Treatment and prognosis
 Treatment is typically with intravenous antibiotics, usually for
extended periods. If a collection, sequestrum or involucrum is
present then drainage and/or surgical debridement is often
necessary. Amputation is performed with failure of medical
therapy or when the infection is life-threatening.
 Complications :
 sinus track formation with occasional superimposed squamous
cell carcinoma (Marjolin ulcer)
 secondary sarcoma (e.g. osteosarcoma): rare
 pathological fracture
 secondary amyloidosis
Thank You

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Osteomyelitis

  • 1. OSTEOMYELITIS Head of Department Dr. Akshara Gupta M.D. Professor Department of Radiodiagnosis G.R. Medical College, Gwalior Presented by DR SANDEEP SINGHAWAL P.G. STUDENT
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  • 3. Blood supply to a long Bone 1.The nutrient artery: major source of blood supply throughout life. It supplies the marrow and most of the inner cortex. 2. Periosteal vessels.These supply the outer cortex. 3. Metaphyseal and epiphyseal vessels.
  • 4. NORMAL VASCULAR SUPPLY IN TUBULAR BONES: CHILD, INFANT, AND ADULT. A. Infant. Note that a small percentage of the metaphyseal blood vessels may penetrate the cartilaginous growth plate and supply the epiphysis. B. Child. Observe the vascular supply in the metaphysis; it does not cross the growth plate. C. Adult. Note that because the growth plate is no longer present, blood supplies to the metaphysis and the distal end of the bone are continuous.
  • 5.  Infant :infections can thus pass to the epiphysis and then the joint. Acute pyogenic arthritis is therefore a relatively common sequel of osteomyelitis in infants.  Childhood, between 2 and 1 6 years, few vessels cross the epiphyseal plate though the periosteum is still relatively loosely attached. The epiphysis and joint are thus less frequently infected.  Adult: metaphyseal and epiphyseal vessels are again connected so that septic arthritis can recur.
  • 6. Osteo – myel- itis  Infection and inflammation of the bone and/or bone marrow  Nelaton coined the term OSTEOMYELITIS in 1844  Modern chemotherapy – significantly reduced the deformity & mortality  Can occur at any age; particularly common between the ages of 2-12 years of age (M:F of 3:1)
  • 7. CAUSE  Staphylococcus aureus: 80-90% of all infections  Escherichia coli: IVDU (intravenous drug users) and genitourinary tract infection  Pseudomonas spp: IVDU and genitourinary tract infection  Klebsiella spp: IVDU and genitourinary tract infection  Salmonella spp: sickle cell disease  Haemophilus influenzae: neonates  group B streptococci: neonates
  • 8. CLASSIFICATION  Acute osteomyelitis – within 2 weeks of onset of symptoms  Subacute- 2 weeks to 2 months  Chronic > 2 months
  • 9. Spread of infection  Hematogenous spread – MC source  Contiguous source- adjacent contaminated site (cutaneous, sinus or dental inf )  Direct implantation of infection (penetrating injuries)  Post Operative infections
  • 10. Clinical Features  Young patients present with acute systemic symptoms – fever, chills , pain & swelling often with extensive loss of limb function.  Adult patients present with symptoms that vary and tend to be more chronic - fever, malaise , edema & pain.
  • 11. Location  lower limb (most common) lower femur, upper tibia  vertebrae: lumbar > thoracic > cervical The location of osteomyelitis within a bone varies with age, on account of changing blood supply :  neonates: metaphysis and/or epiphysis  children: metaphysis  adults: epiphyses and subchondral regions
  • 12. PATHOPHYSIOLOGY  Implantation of pathogen in medullary tissue  Vascular and cellular response  Suppurative edema (increased intramedullary pressure)  Mechanical compression of capillaries and sinusoids  Infarction of marrow tissue and bone with adjacent hyperemia
  • 13.  Focal osteolysis and inflammatory exudate.  Eventually inflammatory process penetrates the inner cortex & enters the Haversian canal and lacunar systems to reach the subperiosteal space
  • 14.  Involvement of periosteal & subperiosteal areas causes a loss of blood supply to cortical bone -> necrotic  Cortical and medullary infarcts result in formation of SEQUESTRUM (dead bone in situ)  As the pus lifts the periosteum-> periosteal new born formation occurs (INVOLUCRUM)  CLOACA – defect , with continued discharge ( associated with chronic osteomyelitis  Marjolin ulcer(SCC) – malignant transformation
  • 15. Advanced osteomyelitis involving the whole of the right tibia and lower end of fibula. Note sequestrum in tibia (arrow) and further sequestrum being extruded from the fibula (arrow).
  • 16. Pathologic Features  Sequestrum formation: necrotic cortical or medullary bone. represents devascularisation of a portion of bone with necrosis.  Involucrum: cortical collar of new bone.  Cloaca: draining sinus.  Marjolin’s ulcer: malignant degeneration of squamous cell lining of cloaca.
  • 17. Radiologic Features  Bone scans are the earliest means of diagnosis.  Positive findings as early as 48 hours of onset of symptoms  MC :Technetium – methylene diphosphonate and Gallium 67 citrate  Increased uptake (HOT SPOT) of radionuclide as a response to the inflammation and destruction of bone
  • 18. BONE SCAN: EARLY DETECTION OF OSTEOMYELITIS. A. Initial Plain Film. Note that the initial radiographic examination shows no destructive changes. B. 10-Day Follow-Up. Note the permeative pattern of bone destruction in the metaphysis of the distal radius. C. Bone Scan, Initial Presentation. Note that this examination, performed at the same time as panel A, reveals an area of increased uptake (a hot spot) (arrow) of technetium.
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  • 20. MRI & CT  MRI is more sensitive than bone scan in identification of low grade infections  T1  intermediate to low signal central component (fluid)  surrounding bone marrow of lower signal than normal due to oedema  cortical bone destruction  T2  bone marrow oedema  central high signal (fluid)  CT is superior to both MRI and plain film in depicting the bony margins and identifying a sequestrum or involucrum.
  • 21. Early Signs  Radiographic Latent period 10 days for extremities ; 21 days for spine  Represents the time taken for osseous destruction to be appreciated on radiographs  Soft tissue swelling and obliterated fat planes (earliest radiographic sign) 7 to 10 days  regional osteopaenia  Moth eaten or permeative cortical and medullary destruction  Periosteal reaction – laminated/lamellar 10-14 days
  • 22. OSTEOMYELITIS: EARLY RADIOGRAPHIC SIGNS. Humerus. Note the large soft tissue swelling (arrows) representing an early radiographic sign of osteomyelitis in this pediatric patient. Observe also the lifting of the periosteum as a result of the infectious process (arrowhead).
  • 23.  Late signs Destruction of adjacent cortex 10-14days Involucrum 3weeks Sequestrum 4 weeks Cloaca Loss of joint space, healing by ankylosis
  • 24. POSTSURGICAL OSTEOMYELITIS. A. AP Tibia and Fibula. Observe the fracture dislocation of the fibula. This young adult male suffered a severe injury in a motorcycle accident. Open reduction and surgical pinning of the complete fracture of the tibia were performed. B. Lateral Tibia. Just 4 weeks after the surgical intervention, the patient complained of persistent pain at the area of the fracture site. Note the typical moth-eaten destructive lesions of osteomyelitis.
  • 25. OSTEOMYELITIS: PERIOSTEAL RESPONSE. A. Distal Femur. Observe the thick collar of periosteal new bone (arrows) in the distal femur. Observe also the destructive lesions in the metaphysis of the distal femur occurring as a result of osteomyelitis. B. Distal Tibia. Note the extensive laminated periosteal response affecting the diaphysis and metaphysis of the distal tibia (arrows). The scattered areas of radiolucency throughout the tibia represent infective destructive lesions. C. Distal Fibula. Note the laminated periosteal response (arrows) in the distal portion of the fibula in this pediatric patient. There are lytic destructive lesions noted in the distal portion of the fibula (arrowhead), representing the infectious focus.
  • 26. SEQUESTRUM AND INVOLUCRUM FORMATION. A. AP Tibia and Fibula. Note the central necrotic bone (sequestrum) (arrow), which is surrounded by an extensive periosteal collar of new bone (involucrum) (arrowhead).
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  • 29. Treatment and prognosis  Treatment is typically with intravenous antibiotics, usually for extended periods. If a collection, sequestrum or involucrum is present then drainage and/or surgical debridement is often necessary. Amputation is performed with failure of medical therapy or when the infection is life-threatening.  Complications :  sinus track formation with occasional superimposed squamous cell carcinoma (Marjolin ulcer)  secondary sarcoma (e.g. osteosarcoma): rare  pathological fracture  secondary amyloidosis