Osteomyelitis is an inflammation of bone and bone marrow caused by an infecting organism. It can be classified based on duration, mechanism of infection, anatomical involvement, and host factors. Acute hematogenous osteomyelitis most commonly affects the metaphysis of long bones in children under 2 years old. It is caused by hematogenous spread from another infection and presents with fever, pain, and swelling as the infection destroys bone and spreads. Proper classification and treatment is important to prevent complications like bone deformity, joint involvement, and chronic infection.

1. OSTEOMYELITIS
Presentation by : Dr.NIKHIL.S.U

2. Points of interest
 Definition, Classification ,pathology, CF,
management based on classification
 Chronic recurrent multifocal osteomyelitis
Mx, Rx
 Acute hematogenous om, differences in
different age group
 Sequestrum

3. ANATOMY
Parts of long bone:
- Diaphysis
- Epiphysis
- Metaphysis

4. Histology of bone
• Basic structural unit of bone: Osteon/haversian
system
Components
a) Haversian canal d) Canaliculi
b) Lamellae e) Volkmann’s canal
c) Lacunae

5. HISTOLOGY OF BONE

6. 1)Haversian canal:
- Present in centre of each haversian system.
- Canal consists of small artery, vein,
lymphatics,thin nerve fiber and supporting
tissues.
2)Lamellae
a) Concentric: thin plates of bony tissue, consists
of ground substance or matrix with collagen
fibers in calcified material.
b) Interstial tissue:
c) Circumferential lamellae: outer and inner
periphery of cortex.

7. 3)Lacunae
-Small space between lamellae, each containing bone
cell osteocyte.
4)Canaliculi
-Fine radiating channels which connect lacunae with
each other and central haversian canal.
5)Volkmann’s canal
-Oblique canals running at right angles.
-Contain neurovascular bundles within
-Connect haversian canal with medullary cavity and
surface of bone.

8. PERIOSTEUM
Made up of
a) Outer layer of fibrous tissue.
b) Inner cambium layer:
- More vascular, cells with osteogenic potential
- Limiting membrane for bone and responsible for
periosteal osteogenesis.
- Attachments
ENDOSTEUM
- Lines walls of bone cavities including marrow spaces
forming inner limiting membrane

10. BLOOD SUPPLY OF LONG BONE
I) Nutrient arteries:
- Largely fed by arterial trunks.
- After entering diaphysis divides.
- Sends lateral branches in cortex, some to sinusoids.
- Anastmose with epiphyseal and metaphyseal
branches.
II) Periosteal vessels:
- Origin-arteries supplying surrounding muscles.
- Supply outer 1/3rd to ½ of cortex.
- Importance: auxiliary source of blood

11. 3)Epiphyseal and metaphyeal arteries:
- Enter bone through small foramina.
- Later branch into arteriolar arcades forming
dense interlocking network.
- Anastomose with nutrient arteries and
contribute 20-40% of total blood supply.
Medullay
vessels
Periosteal vessels
Epiphyseal vessels

12. INTRODUCTION
- Osteomyelitis is defined as inflammation of the bone & bone
marrow caused by infecting organism.
• 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
- Localized or involvement of all layers of bone.
- Difficult and challenging problem confronted by orthopedic
surgeons
- Currently morbidity and mortality has come down
- Key :early diagnosis and treatment.
- Multidisciplinary approach required.

13. Classification
I) Based on duration of symptoms
Acute, Subacute,Chronic
II) Based on mechanism of infection
a) Hematogenous:
from bacteremia
b) Exogenous:
- Open fractures
- Surgery
- Contiguous spread from infected local
tissues

14. III) Kelly’s
Type 1:hematogenous OM
Type 2:OM associated with #union
Type 3:OM without #union
Type 4:post op/post traumatic OM.
IV) Weiland et al
Type 1:soft tissue infection
Type 2:circumferential cortical and endosteal infection.
Type 3:type 2 +segmental defect.

15. Cierny Mader staging system

16. Cierny-Mader classification
ANATOMIC TYPES

18. Physiological cont…..
A Host – With no systemic or local compromising
factor.
B Host - With one or more compromising
factors .(Bl, Bs, Bls)
C Host - So severely compromised that the
radical treatment necessary would have an
unacceptable risk-benefit ratio.

19. V)MAY et al classification
VI)Waldvogel’s classification
- Hematogenous
- Contiguous
- Chronic
VII)Based on host response
- Specific
- non-specific
Importance of these classifications.??

20. ACUTE PYOGENIC OSTEOMYELITIS
- It is rapidly destructive pyogenic infection, usually
hematogenous in origin, diagnosed within 2 weeks of
onset of symptoms.
- MC type of bone infection in children.
- Starts in metaphysis of actively growing long bones in
infants and children
- Runs fulminating course that can terminate fatally
- Can also occur in adults due to spread of infection
directly from another site or from compound
fractures.

21. Etiology
- Disease common in period of active
growth (below 2yrs-8-12yrs).
- Sex: Male:Female 4:1
- Site: Metaphysis, mainly in children(60-70)%
around knee.

22. Risk factors.
-Poor nutrition
-Trauma
-Skin, dental, respiratory, GI, Urinary track infections.
- Associated risk factors: Poor nutrition and unhygienic
surroundings. Bacterial endocarditis
- Burns
- Leukocyte and leucopenia dysfunction
- Iatrogenic intervention, IV drug abuse
- Sickle cell anemia
- Haemodialysis/immunosupressive therapy.

23. Etiologic agents
Bacteria
A)Gram positive:
-Stahylococcus aureus-MC
-streptococcus species-multiple lesions
B) Gram negative:
-Pseudomonas(greenish discharge)
-E-coli,Proteus,Klebsiella
-H influenza-infants
-Salmonella,brucella,nisseria,bacteriods
C)Spirochetes:T.Pallidum
D)Fungal:Actinomycetes,candidiasis,
aspergillosis,mucormycosis
E)Viral:LGV,Smallpox

25. Bacterial associations in specific clinical situations
1)Sickle cell anemia Salmonella
2)Hospital acquired: Gram –ve org.&pseudomonas
3)IV drug abusers: Pseudomonas
4)Diabetes: C.albican
5)Immunosupressive
therapy Fungi,M.avium complex
6)AIDS : Staph.aureus,
atypical mycobacterium

26. Modes of spread of infective foci

27. • Hematogenous spread- Usually involves the
meta physis of long bones in children or the
vertebral bodies in adults
• Direct inoculation of microorganisms into
bone due to penetrating injuries or surgical
contamination
• Contiguous focus of infection in patients with
severe vascular disease .

28. Pathogenesis
- AOM MC affects metaphyseal region of long bones, Femur
27%,tibia 22% & fibula 5%, more than upper extremity.
- Bacteremia common event in childhood, consequence of
other infections such as otitis media, pharyngitis &
sinusitis.
- Its presumed that bacteria gain access to metaphyseal
location via nutrient arteries.
- S.aureus-
i) Surface antigen plays key role in bacterial adherence to
type 1 collagen and endotoxins that suppress local
immune response.
ii) Glycocalyx: may form around bacteria and enhance
adherence to other bacteria and metallic implants.

29. Causes for Metaphyseal osteomyelitis
- Hair pin bend vessels
- Increased vascularity causes pooling of blood, aptly
called ‘lake of blood’.
- Immature cells in metaphysis due to high cell
turnover.
- Relative lack of phagocytosis.
- Presence of degenerating cartilage cells
- End arteries in metaphysis.
- Prone for trauma.
- Single endothelial lining in metaphyseal arteries.

30. Cascade of events
• Infective embolus enters nutrient artery trapped in
vessel of small calibre
• Blocks vessels,area of bone become necrotic
• Active hyperaemia in vicinity with infiltration of PMN
cells which is poured as exudate.
• Increased intraosseous pressure due to exudate and
debris(intense pain)

31. Vessels compressed, further necrosis occurs.(2nd-3rd day)
Exudate follows path of least resistance
Gets accumulated in subperiosteal spaces to form
abscess, damages blood supply.
If perforates spread to soft tissues.

32. 2nd route of spread of infection
Exudate into medullary cavity destroying
marrow elements,blood supply.
In advanced stages cortex may be surrounded
by pus, depriving blood supply
Diaphyseal sequestration.(1 week)
3rd route of spread-
Through the physis into joints.

35. -Metaphysis is intra capsular in
1) Upper and lower ends of humerus
2) Upper end of radius
3) Lower end of ulna
4) Upper and lower ends of femur.

39. Neonatal OM
-Occurs in 2 distinct varieties
1) Seen in 2-8 weeks of age, typically discharged
with their mothers from hospital
- S.aureus: MC
- Manifests by lack of movement, visible swelling of
extremity.
- Fever and irritability not present., inflammatory
response not mounted, Diagnosis difficult.
- High index of suspicion, aspiration done and
antibiotics to be started.
2) Second form encountered in NICU units
- Typically seen in LBW infants, neonates requiring
endotracheal intubation,IV lines.

40. Features in neonatal OM
- In children < 2 years, transphyseal blood vessels
cross the physis, allow the spread of infection into
the epiphysis.
- Cortex is porous, pus collects in subperiosteal
space.
- Less phagocytic cells in metaphysis
- Resulting abscess breaks through thin
metaphyseal cortex forming subperiosteal absess.
- Susceptible to shortening and angular deformity.
- Even joint is also involved, hip joint being
common.
-

41. - Pelvis of 1yr old girl who had osteomyelitis of proximal femur and septic arthritis
of hip.
-These infections resulted in destruction of physis and epiphysis

42. Infantile and childhood
- Within 3 yrs, with decrease in maternally acquired
antibodies predispose to infections.
- Important to keep vigilance with respect to different
infections.
- physis effectively acts as barrier.
- Metaphyseal cortex is thicker, hence diaphysis is at
greater risk.
- Endosteal blood supply jeopardized.
- With concurrent subperiosteal absecess, blood
supply is damaged, can result in extensive
sequestration &chronic OM.
- With closure of physis, acute OM is rare.
- Seen only in immunocompromised

43. -In age group 3-12yrs,
- MC organism is S.aureus, next common being
S.pyogenes(Grp. A beta hemolytic streptococci)
Adoloscent
- MC by S.aureus.
- Also susceptible for infection with
N.gonnorhoeae involving skin, Joints.
- Vertebral bodies commonly involved, abscess spread
slowly and large sequestra may form.
- Destruction of cortical bone, which leads to
pathological fracture.

44. Clinical features
- Antecedent infection present.
- Symptoms of acute illness: Immobility of involved limb,
Irritability,restlessness,headache,vomiting,convulsions,
chills,high grade fever
- Pain, definite interval present between trauma & signs of
osteomyelitis.
- Initially swelling absent, soft tissues becomes
edematous(red) indicating subperiosteal abscess.
- limb in position of ease

46. 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

47. Evaluation
- History and physical examination.
- Lab tests:
a) Hb %-
b) ESR- Raised(60mm in 1hr)
c) TLC: Polymorphonuclear Leucocytosis
d) CRP: Elevated, acute phase reactant,
normalizes much sooner then ESR.
e) Aspiration of pus: from subperiosteal
space/cortex to obtain marrow aspirate.
Gram stain, culture and sensitivity

48. -Radiological investigations:
A)X-Ray:
i) Negative
but may show soft
tissue swelling
ii) Skeletal changes such
as periosteal elevation after
10 days, lytic changes after
2-6 weeks
iii) Useful to look for anatomic
abnormalities
.

49. 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

50. I) Three phase bone scan
99mTc-MDP
i) Increased uptake in all 3
phases of scan
ii) Highly sensitive(95%) in
acute infection.
iii) Poor in presence of
neuropathic arthropathy,
fractures,
tumour.
II) Gallium scan and indium
111labelled leukocyte scan used
in conjugation with technetium
scanning

51. MRI Scan
i) As sensitive as bone scan
ii) Detects changes in water
content of marrow before
disruption of cortical bone.
iii) IOC for vertebral OM.

52. “Any local swelling,or inflammation,painfulness and
restricted movement accompanied by fever should
elicit the tentative diagnosis of acute OM.”
Differential diagnosis
1) Rheumatic fever- gradual, joint swelling-poly
2) Ewing’s sarcoma- radiological signs
3) Acute suppurative arthritis- muscle spasm more
marked, limited mvts,effusion
4) Cellulitis- no intense pain
5) Erysipelas- raised red margins

53. Criteria for diagnosis in special instances
1) Bone aspiration yields pus;
2) Bacterial culture of bone or blood is positive;
3) Presence of the classical signs and symptoms
of acute osteomyelitis exists; and
4) Radiographic changes typical for osteomyelitis
occur.

54. MANAGEMENT
Treatment
-Appropriate treatment shortly after onset lowers
morbidity.
-In order to treat any sepsis, identify triggering
organism
-In some patients antibiotic treatment is doomed to
failure without surgical treatment.
-Bacterial screening starts with 3 blood cultures taken
at interval of 30 mins which gives 65% of isolating
organism
-Choice of antibiotic is based on highest bactericidal
activity, least toxicity and lower cost.

55. Nade’s principles of treatment of acute OM.
1)An appropriate antibiotic is effective before pus
formation.
2)Antibiotics do not sterilise avascular tissues or
abscesses,such areas require surgical removal.
3)If such removal is effective antibiotics should
prevent their reformation and primary wound
closure should be safe.
4)Surgery should not damage further already
ischaemic bone and soft tissues
5)Antibiotics to be cotinued after surgery.

56. Conservative management
- Analgesics and appropriate positioning(splinting).
- Supportive measures like IV fluids, blood
transfusion, high protein diet.
- Prerequisites for Antibiotics;
- Antibiotic selection: Drug which penetrates
infected tissues and attains sufficient levels in bone
and pus.
- Dosage should be 2-3 times the standard dose to
ensure peak serum bactericidal titre of 1:8 or
greater.
- If abscess not found, IV antibiotics to be started
based on gram stain.
- If gram negative, empirical antibiotic coverage for
most likely organism to be started.

57. - Under most circumstances most appropriate antibiotic is
semi synthetic penicillin(oxacillin/naficilllin) or 1st
gen.cephalosporins
- If allergic, clindamycin because of good intra osseous
penetration
- In children <3yrs,with anatomical/functional asplenia, in
whom pneumococcal infection is of concern, 3rd
generation cephalosporin is started
- In non-immunized Hib child, Cefuroxime or combination
of semi-synthetic penicillin/3rd gen cephalosporin would
be appropriate.
- In neonates addition of Aminoglycoside is necessary.
- Parenteral antibiotic continued till appropriate
clinical/lab response has occurred.

58. Switch to oral therapy
1)Clinical &lab improvement towards resolution.
2)Availability of oral agent tolerated by child
3)Likely compliance with antibiotic regime.
-Once oral therapy is initiated serum bactericidal
titres/serum antibiotic levels can be determined to
ensure effective dosing.
- Peak titre of 1:8 constitutes effective dosing.
-Serum bactericidal titres are assessed by drawing
blood 60-90 mins after 2nd or 3rd dose of antibiotic.
- When oral therapy not possible, out-patient
antibiotic therapy is initiated.

60. -End point of treatment: Recommended duration ranges from
4-8 weeks, but success has been reported with 23 days of
treatment.
-Tachdjian’s: Combined oral and IV for 6 weeks—
CRP level checked at about 4-5 weeks
If CRP normal CRP on higher levels
Antibiotics continued for continue antibiotics, lab inv
again
6weeks only at 2-3 weeks
If it exceeds >12weeks,MRI to
R/O any surgically treatable cause

61. SURGICAL TREATMENT
Indications
a) Presence of an abscess requiring drainage
b) Failure of the patient to improve despite
appropriate antibiotic therapy in 24-48 hrs
- Objective of surgery is to drain any abscess cavity, all
non viable or necrotic tissue.
- When subperiosteal abscess found in infant,
several small holes drilled through cortex into
medullary cavity creating a small window.
- -Skin is closed loosely over drains and limb is
splinted.
- -Limb is protected for weeks to prevent
pathological fracture.
- -IV antibiotics to be continued.

62. Technique for drainage of acute osteomyelitis
TIBIA
- Tourniquet applied whenever possible, don’t
EXSANGUINATE if infection present.
- Make anteromedial incision 5-7.5cms over
affected part of tibia.
- Periosteum elevated,any compressed pus will
escape.
- Drill several holes 4mm through cortex into
medullary canal,if pus escapes drill to outline
cortical window and cortex removed with
osteotome.

64. - Evacuate any intra medullary pus and necrotic
tissue.
- Irrigate cavity with 3L saline with pulsatile
lavage system with antibiotics.
- Skin closed loosely over drains,do not close
wound if it produces excessive tension on skin.

65. After treatment
- Long leg posterior slab is applied with foot in
neutral position, ankle at 90 degrees, knee at
20 d flexion.
- Antibiotics continued based on culture
sensitivities
- Generally 6 week course of iv antibiotics given
- Orthopedic and infectious disease follow up
done for one year.

66. COMPLICATIONS
Early:
1) Septic arthritis.
2) Tenosynovitis.
3) Thromophlebitis, deep vein thrombosis
Antibiotics, surgical drainage, anticoagulation and assisted
ventilation.
4) Multiple pyogenic abscess.
5) Adverse reactions antibiotics.
Late
1) Chronic osteomyelitis
2) Pathological fracture
3) Local growth disturbances over growth-due to prolonged hyperaemia
4) Premature closure of epiphysis
5) Deformity

67. SUBACUTE OM
• Insidious onset, indolent course
• Mild pain , temp
• ESR - 50% ;
• Blood culture –Negative
• Aspiration , biopsy – Positive in 60% cases

68. Gledhill Classification
Central metaphyseal
Eccentric metaphyseal
Diaphyseal cortical
Diaphyseal with
periosteal new bone
Ephyseal Metaphyseal and
epiphyseal

69. Cause of indolent course
• Low virulence bacteria
• Strong host response
• Antibiotics before symptoms
Purulent material is not always obtained
on biopsy.
Granulation tissue is common finding
S. Aureus and S. epidermidis are commonly isolated

70. Brodie Abscess
• Localised subacute osteomyelitis
• Long bones lower limb
• Young adult before physeal closure metaphysis
• In Adults Metaphyseal-epiphyseal area
• Intermittent pain, local tenderness.
• X ray- lytic lesion ,sclerotic rim.
• S.aureus in 50% , negative culture in 20%
• Treatment – open biopsy + curettage
wound closed over a drain.

71. Chronic osteomyelitis
Pathology
• Pathologic features of chronic osteomyelitis are
the presence of necrotic bone the formation of
new bone, and the exudation of
polymorphonuclear leukocytes joined by large
numbers of lymphocytes, histiocytes, and
occasionally plasma cells
• New bone forms from the surviving fragments of
periosteum and endosteum in the region of the
infection. It forms an encasing sheath of live
bone, known as an involucrum, surrounding the
dead bone under the periosteum

72. • The involucrum may gradually increase in
density and thickness to form part or all of a
new diaphysis
• Prostaglandin-E production has been shown to
be five to thirtyfold higher in infected bone
than in normal bone. The production of large
amounts of prostaglandin was postulated to
be responsible for bone resorption and
sequestrum formation

73. Sequestrum
• **It is a piece of dead bone, surrounded by
infected granulation tissue, it appears pale
and has smooth inner and rough outer surface
**Formation of sequestrum take 6 weeks
**On x-ray sequestrum appears denser than
the surrounding bone because the
decalcification which occurs in normal bone
does not occur in dead bone.

74. Types of Sequestrum
1-Ring sequestrum-at the end of stump of amputation.
2-Tubular sequestrum-long segment of cortex
3-Black or Bombay sequestrum- calcaneal om
4-Ivory sequestrum - syphilis
5-Feathery sequestrum- pyogenic infection
6- Course sandy-tb
7- Kissing-tb spine
8- Button hole- potts puffy tumor.
colored, corolliform

75. Involucrum and cloacae
• Involucrum is the dence sclerotic bone
overlying a sequestrum, there may be some
holes in the involucrum for pus to drain out
called cloacae.

76. C/F
• (A)-Presenting complaints-
1-chronic discharging sinuses.
2-pain-usually minimal only only during acute
exacerbation .
3-Fever-only during acute exacerbation.

77. • Examination-
1-chronic discharging sinuses-these sinuses
are fixed to bone. Sequestrum may be visible
at the mouth of sinuses.
2-Thickened irregular bone.
3-Tenderness on deep palpation of bone
4-Adjacent joint may be stiff either due to
excessive soft tissue scarring around the joint
or arthritis of joint.

78. Management
• Laboratory Studies
• Leukocyte count
May be elevated in cases of acute osteomyelitis, but it
is often normal in chronic cases .
• Erythrocyte sedimentation rate
Is usually elevated in both acute and chronic
osteomyelitis, and it decreases after successful treatment.
An erythrocyte sedimentation rate that returns to
normal during the course of therapy is a favorable
prognostic sign.
In a compromised host, the erythrocyte
sedimentation rate may be altered for reasons other than
osteomyelitis.

79. • CRP – A measure of acute phase response
- Useful in monitoring the course of treatment.
- Falls within three days of antibiotic treatment
• Culture- Blood culture for haematogenous
osteomyelitis
- Cultures of specimens from the sinus tract
are not reliable for predicting which organisms will
be isolated from infected bone.
Antibiotic treatment of osteomyelitis should be
based on sensitivity studies in meticulously
performed cultures of bone taken at the time of
débridement or deep bone biopsies.
A lysis-centrifugation technique has been described
to improve the sensitivity of cultures of
osteomyelitis samples.

80. Radiological features
1-Most common initial radiographic finding
is soft tissue swelling or subtle lucencies with
in metaphysis.
2-By the end of 2nd week there may be faint
extra cortical outline due to periosteal new
bone formation
3-Thickening and irregularity of cortices.
4-Latter periosteal thickening ,patchy
calcification at metaphysis

81. 5-patchy sclerosis giving rise to a honey-
combed appearance.
6-sequestrum-appear denser than the
surrounding.
7-bone cavity is seen as an areas of rarefaction
surrounded by sclerosis

82. C.T scan
• C.T provides excellent definition of cortical
bone and a fair evaluation of the surrounding
soft tissue and useful in identifying sequestra

83. M.R.I
• **In chronic osteomyelitis,M.R.I may reveal a
well-defiened rim of high signal intensity
surrounding the focus of active disease(rim
sign)
**sinus tracks and cellulitis appear as areas of
increase intensity on T2 –weighted M.R.I

84. Complication
• 1-Acute exacerbation
2-Growth abnormality
3-pathological fracture.
4-Joint stiffness.
5-sinus tract malignancy
6-Amyloidosis

85. Principles of Treatment
• 1-Adequet drainage.
2-Through debridement.
3-obliteration of dead space.
4-Wound protection.
5-specific antimicrobial coverage.
6-Correct host defect.
7-Removal of infected granulation tissue and
sinuses

86. Operative procedures
• 1-Sequestrectomy.
2-Saucerization.
3-Curettage.
3-Excision of an infected bone.
4-Amputation.

87. Sequestrectomy
• Means removal of sequestrum.
If it lies within the medullary cavity, a window
is made in the overlying involucrum and
sequestrum removed

88. Saucerization
• Means conversion of broad base, narrow
mouth bone cavity into narrow base, broad
mouth bone cavity so that this allows free
drainage of the infected material.
• -Paprika sign – punctate bleeding
-excision of sinus tract

89. Management of Dead Space
Open bone grafting
Papineau technique – 3 stages
1Debridement
2 Grafting
3 Wound coverage

91. • Soft tissue transfer
-local muscle flap
-vascularised pedicle
-free tissue transfer
• Tibia – prox 1/3 – gastronemius flap
mid 1/3 - soleal flap
lower 1/3 – free muscle
transfer

92. Polymethylmethacrlate antibiotic bead
chain
• **The principal of treatment is to deliver
levels of antibiotics locally in concentrations
that exceed the minimal inhibitory
concentration. **short-term(for 10
day),long-term(80 day)
or permanent implantation possible.
**Generally removed after 6 weeks.
**Aminoglycosides ( most common penicillins,
cephalosporins and clindamycin,vancomycin.

95. Disadvantages
• 1-PMMA antibiotic beads has been shown to
inhibit local immune response by impairing
various phagocytic immune cell.
2-local bactericidal antibiotic levels last only 2
to 4 weeks after placement, and all the
antibiotic has leached out of the bead, a
foreign body remains that may be colonized
by glycocalyx-forming bacteria.

96. Biodegradable antibiotic delivery
system
• Advantage-
1-Removal of implant not required.
2-Some of these biodegradable substrates
contain osteoconductive and osteoinductive
material, which can be used to promote new
bone formation.
3-Reabsorbe within 8 weeks
• Disadvantages
purulent discharge

97. Ilizarov technique
• **Useful in chronic osteomyelitis with infected nonunions.
**This technique allows radical resection of infected bone by
corticotomy which is performed through normal bone
proximal and distal to the area of disease,bone is transported
until union is achieved.

98. Hyperbaric oxygen
• Used only as an adjuvant to other traditional
method of treatment.
CHAMBER USED FOR HYPERBARIC OXYGEN
THERAPY

99. 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

100. Amputation
• Very rarely performed ,preferred in a case
with long –standing discharging sinus if the
sinus undergo malignant change.

101. Culture Initial antibiotic selection
Change or Confirm
Stage 1 ( Based on culture results)
Cierny-Mader
classification
Poor response Good response ( After 48 hrs
Adequate treatment)
Operative Treatment
* Abscess drainage Continue 2 weeks parenteral
* Unroofing 4 weeks oral antibiotics
* I M Reaming
4 Weeks antibiotics
Failure Arrest
Retreat as above

102. Superficial Biopsy and Initial antibiotic +/- Local or
debridement Culture Selection microvascular
coverage
Stage 2
Cierny - Mader
Classification Change or confirm antibiotic
based on culture
Treatment with antibiotic
for 2 Weeks

103. Debridement Biopsy and Culture Initial antibiotic
treatment
Implant removal Change or confirm
( Based on culture results )
Stage 3 & 4
Cierny - Mader
Classification
Dead space management 6 Weeks of antiobiotic
-Beads ( After major operative debridement )
-Bone grafting
-Muscle flap
Failure Arrest
Stabilisation
-External fixation Retreat as above
-Ilizarov technique
Soft tissue coverage

104. 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.

105. • 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

106. Treatment
• Effective Rx is still impossible
• Antibiotics are of no use
• NSAIDS- affected bones responds well- effective Rx.
Azithromycin- due to anti inflammatory & immuno
modulatory effects
• Physiotherapy – very effective- helps in keeping the
joint supple.
• Steroids – they damp down the inflammation and
allow bone to heal, oral steroids, bisphosphonates,
sulphasalazine have been used in specific cases.
• Outcomes- unpredictable, most undergo spontaneous
resolution

107. Sclerosing osteomyelitis of Garré
• A rare type of osteomyelitis occurring in
children and young adults presenting with
insidious onset of pain, pyrexia and swelling.
• Symptoms recur at intervals for several years
and subside gradually . .
• Radiological appearance is of intense sclerosis
resulting in thickened bone.
• There is predilection for involvement of
mandible and shaft of long bones.

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

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

110. Tuberculous osteomyelitis
• Tuberculous bone infection occurs secondarily
as a result 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

111. • 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.

112. THANK YOU

113. • REFERENCES
1)Tachdjian’s pediatric orthopaedics
2)Cambell’s text book of orthopaedics
3)Hefti’s text book of orthopaedics
4) Harrison’s principles of internal medicine.
5) Netter’s orthopaedics
6)Rockwood and Green’s orthopaedics
7) Internet