Osteomyelitis is an inflammation of bone caused by an infecting organism. Staphylococcus aureus is the most common cause. Acute hematogenous osteomyelitis usually involves the metaphysis of long bones in children. Diagnosis is based on clinical features like localized tenderness and lab tests showing elevated inflammatory markers. Plain X-rays may initially only show soft tissue swelling and osteopenia before lytic bone changes appear in subacute or chronic cases.

1. OSTEOMYELITIS
DR SAGAR TOMAR
Llrm medical college,meerut,up

2. INTRODUCTION
 Nelaton (1834) : coined osteomyelitis
 The root words are
osteon (bone)
myelo (marrow)
 these are combined with itis (inflammation) to
define the clinical state in which bone is infected
with microorganisms.

3. DEFINATION
Osteomyelitis is an inflammation of bone caused
by an infecting organism.
The infection may be limited to a single portion of
the bone or may involve numerous regions, such as
the marrow, cortex, periosteum, and the
surrounding soft tissue.

4. CLASSIFICATION
 Attempts to classify are based on
(1) the duration and type of symptoms
(2)the mechanism of infection
(3)the type of host response

5. OSTEOMYELITIS
Acute: <2weeks Early acute
Late acute(4-
5days)
Subacute: 2weeks—
6weeks
Less virulent – more
immune
Chronic: >6 weeks
Based on the duration and type of symptoms

6. CLASSIFIED ACCORDING TO MECHANISM
 Osteomyelitis may be (waldvogel
classification)
1. Hematogenous (bacteremia)
2. contiguos (from adjacent root such
as open fracture or seeded implant)
3. chronic

7.  BASED ON HOST RESPONSE
 PYOGENIC
 NON-PYOGENIC

8. ACUTE HEMATOGENOUS
OSTEOMYELITIS
 Acute hematogenous osteomyelitis is the most
common type of bone infection and usually is seen
in children
 It is caused by a bacteremia, which is a common
occurrence in childhood. Bacteriological seeding of
bone generally is associated with other factors such
as localized trauma, chronic illness, malnutrition, or
an inadequate immune system.

9. RISK FACTORS

10.  Single pathogenic organism hematogenous osteomyelitis,
 Multiple organisms direct inoculation or contiguous focus infection.
In infants:
Staphylococcus
aureus
Streptococcus
agalactiae
Escherichia coli
In children over one year
of age:
Staphylococcus
aureus,
Streptococcus
pyogenes
Haemophilus
influenzae1
adults
Staphylococcus aureus is
common organism
isolated.
Etiology

11. Organism
 Staphylococcus aureus
 Coagulase-negative staphylococci or
Propionibacterium species
 Enterobacteriaceae species
orPseudomonas aeruginosa
 Streptococci or anaerobic bacteria
 Salmonella species orStreptococcus
pneumoniae
Comments
Organism most often isolated in all types of
osteomyelitis
Foreign-body–associated infection
Common in nosocomial infections and punchured
wounds
Associated with bites, fist injuries caused by
contact with another person’s mouth, diabetic
foot lesions, decubitus ulcers
Sickle cell disease
Organisms Isolated in Bacterial Osteomyelitis
.

12. WHY STAPHYLOCOCCUS MOST COMMON?
 S.aureus and S.epidermis ----- elements of normal skin flora
 S.aureus -----increased affinity for host proteins (traumatised bone)
 Enzymes (coagulase, surface factor A) ----- hampers hosts immune
response .
 Inactive “L” forms ------dormant for years
 “Biofilm” (polysaccharide “slime” layer) ---- increases bacterial
adherence to any substrate .
 Large variety of adhesive proteins and glycoproteins ----- mediate
binding with bone components.

13. BACTERIAL RESISTANCE BY BIOFILM
 If a planktic bacteria (free floating bacteria )
encouters a suitable inert material such as dead or
necrotic tissue ,foreign bodies, or any avascular
body part either by direct contamination,contiguos
spreading or hematogenous apreading
 It attaches itself via vander wall forces (irrevesible
crosslinks)
(devitalised bone devoid of periosteum presents
collagen matrix to which bacteia can attach

14.  Bacteria now begin to produce
mucopolysaccharides layer over themselves
called BIOFILM OR SLIME
 the bacteria begin to COLONISE
 A colonised bacteria can remain viable: when
(a) the inoculum is larger than threshold levels,
(b) host defense mechanisms are impaired,
(c) the tissue on which the bacteria colonize is traumatized (or necrotic),
(d) a foreign body is present, and
(e) the surface (or tissue) is acellular or inanimate (e.g., dead bone, cartilage,
and biomaterials)

15.  After colonisation bacteria begin to develop into
mature colonies.these colonies are resistant to
antibiotics because
---antibiotics are unable to cross mucopolysaccaride layer
(glycocalyx)
---bacteria within slime are dormant or have decreased
metabolic rate and also undergo phenotypic changes active
process such as cell membrane formation which are targeted
by antibiotics would be decreased.
---antibiotic concentration of 1500 times normal is required to
penetrate both biofilm and bacterial cell wall

16. Illustration of the biofilm bacterial colonization process.
First, the bacteria need to find an inert surface (e.g., implant or
dead tissue). Implants or dead tissue that have been integrated by
the host with some type of surface are not inert and will resist
colonization. Then, the colonization process will continue until
mature colonies are formed. Once mature, the colonies can
change based on environmental signals or signals between
colonies.

17. PATHOLOGY:
 the most common site is lower femoral metaphysis
 Other sites- upper tibial
upper femoral
upper humeral metaphyis

18. PATHOGENESIS:
Direct inoculation of
microorganisms into bone
penetrating injuries and
surgical contamination are
most common causes
Hematogenous spread
usually involves the
metaphysis of long
bones in children or the
vertebral bodies in
adults
Osteomyelitis
Microorganisms
in bone
Contiguous focus of infection
seen in patients with severe
vascular disease.

19. PATHOGENESIS
Whatever may be the inciting cause the bacteria reaches the
metaphysis of rapidly growing bone & provokes an inflammatory
response.
why metaphysis is involved
1. Infected embolus is trapped in U-shaped small end arteries located
predominantly in metaphyseal region
2. Relative lack of phagocytosis activity in metaphyseal region
3. Highly vascularised region ---minor trauma—hemorrhage ----locus
minoris resistantae---excellent culture medium

20. PATHOLOGY:
– sharp hairpin turns
– flow becomes considerably slower and
more turbulent
-- relatively fewer phagocytic cells than
physis and metaphysis
Medullary artery
Medullary vein
Hair pin
arrangemaent

21. PATHOLOGY
These are end-artery branches of the nutrient artery
Obstruction
Avascular necrosis of bone
tissue necrosis, breakdown of bone
acute inflammatory response due to infection
Squestra formation
Chronic osteomyelitis

22. THE INFLAMMATORY RESPONSE TO OSTEOMYELITIS:
 Prostaglandin-E production has been shown to be five to thirty fold
higher in infected bone than in normal bone
 postulated to be responsible for bone resorption and sequestrum
formation
 Effective phagocytosis is defense in patients with osteomyelitis
 Intramedullary oxygen tensions important for phagocytic function
 oxygen tensions of <30 mm Hg impair normal phagocytic function

23. PATHOLOGY:
 Pathologic features of chronic osteomyelitis are :
 SEQUESTRUM is a devitalized avascular segment of
bone, surrounded, by pus /infected granulation tissue and is
more dense than surrounding bone .Because of avascularity ,
sequestrum does not decalcify , is more radio opaque and heavy ,
so sinks in waterIts outer surface is usually jagged / irregular due
to erosive process by proteolytic enzymes in granulation tissue
 Features:
 Dead piece of bone
 Pale
 Inner smooth ,outer rough
 Surrounded by infected granulation tissue trying to eat it
 Types-
 ring(external fixator)
 tubular/match-stick(sickle)
 coke and rice grain(TB)
 Feathery(syphilis)
 Colored(fungal)
 Annular(amputation stumps)

24. PATHOLOGY:
Involucrum :
is derived from the word “volvere” i.e. to wrap .It is
the result of reactive new bone formed by periosteal
reaction , in an attempt to wall off the infection by
forming a thick tense wall ,effectively sealing it
off the blood stream just like a wall of abscess.
 It is jagged on its inner surface but
smooth on its outer surface
Cloacae
 are single or multiple openings in involucrum and
are caused by rupture of periosteum due to pus
under tension .Exudates , sequestra are extruded
through the cloacae on the surface


25. CLINICAL FEATURES
 calor, rubor, dolor, tumor
 Heat, red, pain or tenderness, swelling
 Initially, the lesion is within the medually cavity, there is
no swelling, soft tissue is also normal.
 The merely sign is deep tenderness.
 Localized finger-tip tenderness is felt over or around the
metaphysis.
 it is necessary to palpate carefully all metaphysic areas
to determine local tenderness,

26. DIAGNOSIS OF ACUTE OSTEOMYELITIS
 PELTOLA AND VAHVANEN’S CRITERIA (if 2/4
are found)
1. Purulent material on aspiration of the affected
bone
2. Positive finding s of bone tissue or blood culture
3. Localised classic physical findings
a. bonny tenderness
b. overlying soft tissue edema ,erythema
4 Positive radiological imaging

27. DIAGNOSIS
LABORATORY DIAGNOSIS
 Include - complete blood count
- erythrocyte sedimentation rate (ESR)
- C- reactive protein (CRP)
 The white blood cell count will show a marked
leucocytosis as high as 20,000 or more
 Peak elevation of the ESR occurs at 3 to 5 days
after infection and returns to normal approximately
3 weeks after treatment is begun.

28. ERYTHROCYTE SEDIMENTATION RATE
 The ESR becomes elevated when infection is
present
 Fractures or other underlying diseases can cause
elevation of the ESR.
 The ESR also is unreliable in neonates, patients
with sickle cell disease, patients taking
corticosteroids, and patients whose symptoms have
been present for less than 48 hours

29. C-REACTIVE PROTEIN
 CRP, synthesized by the liver in response to
infection, is a better way to follow the response of
infection to treatment.
 CRP 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

30. PLAIN RADIOGRAPH
The earliest changes are swelling of the soft tissue,
periosteal thickening and/or elevation, and focal
osteopenia.
The more diagnostic lytic changes are delayed and
are associated with subacute and chronic
osteomyelitis.
Osteoporosis is a feature of metabolically
active living bone; the segment that fails to
become osteoporotic is metablically inactive
and possibly dead.
Soft tissue swelling--- 1-3 days
Periosteal reaction---10-12 days
Osteomyelitis of the tibia of a
young child. Numerous
abscesses in the bone show as
radiolucency.

31. SINOGRAPHY:
Sinography can be performed if a sinus track
is present
Roentgenograms made in two planes after
injection of radiopaque liquid into sinus.
Helpful in locating focus of infection in
chronic osteomyelitis.
A valuable adjunct to surgical planning

32. RADIONUCLEOTIDE SCAN
 The most common is 99mTc phosphate, which can
detect osteomyelitis within 48 hours after clinical
onset of infection.
 The uptake of this compound is related primarily to
osteoblastic activity, although regional blood flow
also plays a role in skeletal uptake.
 The three-phase bone scan consists of images
taken in
(1) the flow phase,
(2) the immediate or equilibrium phase
(3) the delayed phase

33. RADIONUCLEOTIDE SCAN
 Flow phase- shows blood flow
 Immediate or equilibrium - shows relative flow
and distribution of radio isotope into extracellular
matrix
 Delayed phase-shows osteoblastic activity
 Osteomyelitis shows increase uptake in all three
phase

34. MRI
 MRI has very high sensitivity and specificity for the
diagnosis of osteomyelitis.
 three types of images
T1 image- shows fat as a high bright signal
T2 image- shows water as a bright signal
STIR image – produced by suppressing the fat
signal
 The classic findings of osteomyelitis on MRI are a
decrease in the normally high marrow signal on T1
images and a normal or increased signal on T2
images

35. MRI
 The reported abnormal images reflect an increase
in water content, resulting from edema in the
marrow cavity. Marrow fat is replaced by edema
and cellular infiltrates that are lower in signal than
fat on T1 images and higher in signal than fat on T2
and STIR image

36. ULTRASONOGRAPHY
 may detect a subperiosteal collection of fluid in
early stages of osteomyelitis.
 To establish if joint effusion is present
 To localise needle aspiration

37. CT SCAN
 detecting smaller areas of cortical destruction,
 Small foci of gas or foreign bodies,
 sequestra formation (areas of necrotic bone
separated by granulation tissue from living bone)
 involucra (a layer ofliving bone that has formed
along the sequestrum),
 cloacae (an opening in the involucrum through
which the sequestrum and granulation tissue may
be discharged)
 surrounding soft-tissue abscesses and
 the replacement of the normal bone marrow fat with
pus.

38. CULTURAL STUDIES
 Key to the successful management of osteomyelitis
is the isolation of the involved pathogens before the
initiation of antibiotics in order to tailor optimal
antimicrobial therapy
 Cultures of superficial wounds or sinus tracks
should not be relied on because they have been
shown to be poor indicators of deep infection and
usually are polymicrobial.
 The preferred specimen in most bacterial and yeast
infections is aspirated fluid (joint or purulent fluid). A
deep wound biopsy or a curetted specimen after
cleaning the wound is acceptable.

39. TREATMENT
1. General treatment: nutritional therapy or
general supportive treatment by intaking
enough caloric, protein, vitamin etc.
2. Antibiotic therapy
3. Surgical treatment
4. Immobilization

40. TREATMENT
NADE’S PRINCIPLES
1. an appropriate antibiotic will b effective before pus formation
2. Antibiotics will not sterilize avascular tissues or abscess and
such areas require surgical removal
3. If such removal is effective, antibiotics should prevent there
reformation and therefore primary wound closure should be
safe.
4. Surgery should not further damage already ischeamic bone
and soft tissue.
5. Antibiotics should be continued after surgery.

41. ANTIBIOTICS THERAPY
PATHOGEN FIRST LINE DRUG SECOND OPTIONS

42.  OPERATIVE INDICATIONS
1. The presence of an abscess requiring drainage
2. Failure of the patient to improve despite
appropriate intravenous antibiotic treatment

43. COMPLICATIONS
 Chronic osteomyelitis- 2% in >3wks, 19% in < 3wks
 Septic arthritis
 Growth disturbance
 Septicemia
 DVT
 Pulmonary embolism

44. SUBACUTE OSTEOMYELITIS
 This has a more incidious in onset and lacks the
severity of symptoms
 Duration between 2-6 weeks
 The indolent course of subacute osteomyelitis is
thought to be the result of increased host
resistance, decreased bacterial virulence, or the
administration of antibiotics before the onset of
symptoms

45. SUB ACUTE OSTEOMYELITIS CLASSIFICATION
Type Gledhill Classification Robert et al. Classification
I Solitary localized zone of
radiolucency surrounded by
reactive new bone formation
Ia—Punched-out radiolucency
Ib—Punched-out radiolucent
lesion with sclerotic margin
II Metaphyseal radiolucencies with
cortical erosion
—
III Cortical hyperostosis in diaphysis;
no onion skinning
Localized cortical and periosteal
reaction
IV Subperiosteal new bone and onion
skin layering
Onion skin periosteal reaction
V — Central radiolucency in epiphysis
VI — Destructive process involving
vertebral body

46.  Anatomical
 type 1, central metaphyseal
lesion;
 type 2, eccentric metaphyseal
lesion with cortical erosion;
 type 3, diaphyseal cortical
lesion;
 type 4, diaphyseal lesion with
periosteal new bone formation,
but without definite bony lesion;
 type 5, primary subacute
epiphyseal osteomyelitis; and
 type 6, subacute osteomyelitis
crossing physis to involve
metaphysis and epiphysis

47. TREATMENT
 biopsy and curettage folllowed by treatment with
appropriate antibiotics

48. BRODIE’S ABSCESS
 A Brodie abscess is a localized form of subacute
osteomyelitis that occurs most often in the long
bones of the lower extremities of young adult
 Organisms of low virulence are believed to cause
the lesion. S. aureus is cultured in 50% of patients;
in 20%, the culture is negative.
 The WBC count and blood culture usually shows no
abnormality but the ESR is sometimes elevated.

49. BRODIE’S ABSCESS
 Bone abscess containing pus or jelly like granulation tissue
surrounded by a zone of sclerosis
 Age 11-20 yrs, metaphyseal area, usually upper tibia or lower
femur
 Deep boring pain, worse at night, relieved by rest
On xray-Circular or oval luscency surrounded
by zone of sclerosis
 Treatment:
 Conservative if no doubt - rest + antibiotic for 6 wks.
 if no response – surgical evacuation & curettage,
 if large cavity - packed with cancellous bone graft

50. BRODIE’S ABSCESS
Brodie abscess. (A) AP radiograph of the femur
showing a lucent area (arrow) with cortical thickening
and sclerosis. (B) Axial CT image showing a central
sequestrum (arrowhead) and sinus tract (cloaca)
(arrows) leading through the thickened cortex.

51. CHRONIC OSTEOMYELITIS
 Duration > 6 weeks
 The hallmark of chronic osteomyelitis is infected
dead bone within a compromised soft tissue
envelope.(sequestrum)
 The infected foci within the bone are surrounded by
sclerotic, relatively avascular bone covered by a
thickened periosteum (involcrum) and scarred
muscle and subcutaneous tissue.
 This avascular envelope of scar tissue leaves
systemic antibiotics essentially ineffective

52. CIERNY AND MADER CLASSIFICATION
 Cierny and Mader developed a classification system for
chronic osteomyelitis, based on physiological and
anatomical criteria, to determine the stage of infection.
 Based on host
class A- NORMAL
class B- COMPROMISED
class C-PROHIBITIVE
 Based on anatomy
type 1-MEDULLARY
type 2-SUPERFICIAL
type 3-LOCALISED
type 4-DIFFUSE
 pairing of these forms 12 clinical stages
 Clinical Stage
(Type+ Class = Clinical Stage)

53. CLASSIFICATION
 Cierny et al -
 Includes four anatomic stages
 Stage-1, or medullary,
osteomyelitis is confined to the
medullary cavity of the bone.
 Stage-2, or superficial,
osteomyelitis involves only the
cortical bone.
 Stage-3, or localized,
osteomyelitis usually involves
both cortical and medullary bone
but does not involve the entire
diameter of the bone.
 Stage-4, or diffuse, osteomyelitis
involves the entire thickness of
the bone, with loss of stability.

54. CLASSIFICATION
 With this system, a patient with osteomyelitis is classified as an A, B,
or C host.
 An “A” host has no systemic or local compromising factors. They
have a normal response to infection and surgery.
 A “B” host is affected by one or more compromising factors.
 Bs-systemic compromise
 Bl-local compromise
 Bls-both sys and local compromise
 are compromised and have deficient wound healing capabilities.
 A “C” host is so severely compromised that the radical treatment
necessary would have an unacceptable risk-benefit ratio

55. DIAGNOSIS
 The diagnosis of chronic osteomyelitis is based on
clinical, laboratory, and imaging studies.
 The “gold standard” is to obtain a biopsy specimen
for histological and microbiological evaluation of the
infected bone.
 Investigations
x ray
ct scan
sinogram
usg
mri
radionucleotide scan

56. TREATMENT
 Involves
 Antibiotic suppression
 Surgical debridement
 Reconstruction
 Correct host morbidity
-control blood sugar level in diabetic
-smoking cessation
-treatment of liver or renal malfunction
-optimising nutrition
-treatment of chronic disease

57. SURGICAL INTERVENTION
 Debridement-
- it includes sequestrectomy and curettage
- Removal of all sequestra ,purulent material,and scarred and necrotic tissue until the
PAPRIKA SIGN ( active punctate bleeding bone)
-
- It results in the formation of DEAD SPACE
- methods described to eliminate this dead space are
- (1) bone grafting with primary or secondary closure;
- (2) use of antibiotic PMMA beads as a temporary filler of the dead space before
reconstruction;
- (3) local muscle flaps and skin grafting with or without bone grafting;
- (4) microvascular transfer of muscle, myocutaneous, osseous, and osteocutaneous
flaps; and
- (5) the use of bone transport (Ilizarov technique).

58. SEQUETRECTOMY AND CURRETTAGE
Sequestrectomy and curettage.
A, Affected bone is exposed, and sequestrum is removed.
B, All infected matter is removed.
C, Wound is either packed open or closed loosely over
drains.

59. POST SEQUESTRECTOMY
 NO STABLISATION IS
NECESSARY WHEN 70% OF
THE ORIGINAL CORTEX
REMAINS INTACT
 If >70% cortical volume has
been retained—protect by cast
 Greater bone loss-Ext fix
 Focal bone loss-open
cancellous BG/conventional
BG
 Seg. bone loss—BG/Bone
transport/other devices
Radiologically if cortical
continuity of the involucrum is
50% of the over all cortical
diameter on 2 orthogonal views
then the involucrum is
structurally adequate

60. SAUCERIZATION
 Extension of surgical
debridement
 Debrided wounds left open
widely through excision of
overhanging soft tissue and
bone
 Wounds drain freely
 Abscesses do not form
 Limited to areas where it causes
acceptable loss of function e.g.
Tibia and femur
 May require stabilization
saucerisation

61. BASIC METODS TO COVER DEAD SPACE

62. OPEN BONE GRAFTING
 The Papineau technique involves local debridement
followed by a period of open management until a
healthy granulation tissue covers the wound base,
after which fresh autogenous cancellous graft is
packed into the defect, followed by frequent
dressing changes until the graft becomes
incorporated
 THREE STAGE OPERATION
Stage I: Débridement and Stabilization
Stage II: Grafting
Stage III: Wound Coverage

63. POLYMETHYLMETHACRYLATE ANTIBIOTIC BEAD
CHAINS
 The antibiotic concentrationare 200 times higher
than levels achieved by systemic (I v)
administration
 Advantage of achieving high local concentration
and while low serum concentration and low toxicity.
 Short term implantation of 10 days to long term
implantation of 80 days as required
 Aminoglycosides most commonly used , others are
penicillin, cephalosporins and clindamycin
Antibiotic
beads

64. BIODEGRADABLE ANTIBIOTIC DELIVERY
SYSTEM
 Advantage over PMMA beads is that a secondary
procedure is not required to remove the implant.
 Antibiotics are mixed with biodegradable substance
such as calcium sulfate or calcium phosphate to
produce reabsorbable beads or injectable filler
 Reasobed in 8 weeks

65. CLOSED SUCTION DRAIN
 Success rates of approximately
85% have been reported for the
modified Lautenbach method of
closed suction antibiotic ingress
and egress irrigation systems
 A more recent wound closure
technique is negative pressure
wound therapy (NPWT), which
consists of a pump that
generates a vacuum and is
capable of creating a negative
pressure environment within a
sealed wound, dressing material
used to pack and seal the
wound, tubing for fluid removal
from the wound area, and a
container to collect waste
materials removed from the
wound

66. SOFT TISSUE TRANSFER
 Soft tissue transfers to fill dead space left behind
after extensive débridement may range from a
localized muscle flap on a vascular pedicle to
microvascular free tissue transfer
 The transfer of vascularized muscle tissue
improves the local biological environment by
bringing in a blood supply that is important in the
host's defense mechanisms and for antibiotic
delivery and osseous and soft tissue healing

67.  ILIZAROV METHOD-
This technique allows radical resection of the
infected bone. A corticotomy is performed through
normal bone proximal and distal to the area of
disease. The bone is transported until union is
achieved.

68. ILIZAROV TECHNIQUE
A case of infected non-union of both bone leg managed by
ilizarov fixator application ,after bone transport the bone union is
acheived

69.  HYPERBARIC OXYGEN THERAPY-HBO
- enhances oxygen-dependent leukocyte killing
through the production of hydrogen peroxide and
superoxide
- optimal tissue oxygen tension enhances
osteogenesis and neovascularization
 Most wound healing patients receive one treatment
per day (20 MIN /DAY) for 20 – 30 days.

70. HYPERBARIC OXYGEN THERAPY

71. CHAMBER USED FOR HYPERBARIC OXYGEN
THERAPY

72. Culture Blood ± bone
Initial antibiotic
selection
Change or confirm d/o culture results
Poor
response
Operative treatment
unroofing ,abscess
drainage, IM reaming
4 wks
antibiotics
Failure
Retreat
as
above
Arrest
Good
response
Continue 2 wks
parenteral & 4 wks
Oral antibiotics
Treatment algorithm of
Cierny-Mader Stage-1, or
hematogenous, long-
bone osteomyelitis.

73. Hardware removal
Bone stable
DEBRIDEMENT
INTRAMEDULLARY
REAMING
Antibiotics
Continue 2 wks
parenteral & 4 wks Oral
Failure
Retreat as
above
Arrest
Bone
unstable
Suppressive
antibiotic treatment
until stabilisation
Treatment algorithm of
Cierny-Mader Stage-1
long-bone
osteomyelitis
associated with
infection at the site of
hardware

74. Superficial
debridement
Biopsy &
culture
Initial antibiotic
selection
Change or confirm based on culture
results
Continue antibiotics for 2
wks
± Local MUSCLE
coverage
Treatment
algorithm of
Cierny-Mader
Stage-2 long-bone
osteomyelitis

75. Biopsy &
Culture
Initial antibiotic
selection
Change or confirm d/o
culture results
6wks antibiotics
after major
operative
debridement
Failure
Retreat
as above
Arrest
Debridement
Hardware
removal
Dead space
management, beads,
bone grafts, & muscle
flaps
Stabilisation
external fixation
Ilizarov
technique
Soft tissue coverage
Treatment
algorithm of
Cierny-Mader
Stages-3 and 4
long-bone
osteomyelitis.

76. OSTEOMYELITIS RELATED TO IMPLANT
FIRST CASE
HARDWARE REMOVAL
retain hardware
continue antibiotics until healed
HARDWARE STABLE
BONE NOT HEALED
IMPLANT RELATED OSTEOMYELITIS

77. SECOND CASE
remove hardware, antibiotics,
temporary stabilization, spacer,
and reconstruction when clean
Hardware unstable + bone not
healed =

78. THIRD CASE
remove hardware, debride with
effort not to destabilize, control
dead space, and antibiotics
Hardware stable + bone healed

79. FOURTH CASE
remove hardware, temporary
stabilization, spacer, antibi-otics, and
reconstruction when able.
Hardware stable + bone not healed +
systemic effects
Consider amputation if unsuitable hostConsider amputation if unsuitable host

80. CHRONIC MULTIFOCAL OSTEOMYELITIS
 In the 1970s it was noted that a number of children
presented with a low-grade form of bone disease that
behaved clinically like an acute osteomyelitis.
 Typically it affected the long bones and went on to a
sclerotic reaction. The first episode would settle and
some months or even a few years later there would
be recurrence at another site.
 No organisms are grown and the course of the
disease becomes chronic and relapsing.

81.  The clinical importance is to avoid repeated
biopsy once the relapsing nature of the
condition has been recognized.
 Plain radiographs are essential to recognize the
bone infection.
 Skeletal scintigraphy is a good method of
screening for other lesions
 whilst MRI is the best means of judging extent
and activity

82. SCLEROSING OSTEOMYELITIS OF GARRÉ
 A rare type of osteomyelitis occuring in children and
young adults presenting with insidious onset of
pain, pyrexia and swelling.
 Symptoms recur at intervals for several years and
subside graudlly . .
 Radiological appearance is of intense sclerosis
resulting in thickned bone.
 There is predilection for involvement of mandible
and shaft of long bones.

83. SALMONELLA OSTEOMYELITIS
 Subacute form
 More commonly in children with sickle cell anaemia
 Occurs during the convalescent phase after an
attack of typhoid fever
 Mutiple bones are affected ,bilaterally symmetrical
 Radiologically- diaphyseal sclerosis

84. Salmonella osteomyelitis
Bone destruction of radial shaft and dense sequestrum (arrow)

85. TUBERCULOUS OSTEOMYELITIS
 Tuberculous bone infection occurs secondarily
as a resolt of hematogenous spread from a
primary source such as lung or genitourinary
tract.
 Bone infection is most typically slow growing
and indolent. Tuberculous ‘caries’ is seen where
the margin of the bone is scalloped and eaten
away. Large ‘cold’ abscesses occur. This means
that the patient is surprisingly well given the
size of the collection

86.  Little or no surrounding reactive bone with presence of
osteopenia
 Affects epiphysis, metaphysis and diaphysis.
 Eccentric area of osteolysis is seen in metaphysic
 Transepiphyseal spread of lytic lesion
 No sequestrum formation is seen.
 Occasionally, destruction in the mid diaphysis of a short
tubular bone of the hand or foot(tuberculous dactylitis)
may produce a fusiform enlargement of the entire
diaphysis is called as spina vetosa.

87. M. tuberculosis. Sagittal T1-weighted (A) and T2-weighted (B) MR
images showing bone erosions and a large inhomogeneous
posterior soft tissue abscess

88. THANK YOU