acute and chronic osteomyelitis

1. OSTEOMYELITIS
SPEAKER : DR. SARANG
CHAIRPERSON: DR. S.F. KAMMAR

2. vascular anatomy
Infants :
Metaphysis and diaphyseal vessels penetrate the
physis(growth plate) upto 1 year.
So high incidence of septic arthritis with epiphyseal
involvement in osteomyelitits in infants
Children:
No metaphyseal blood vessels penetrate the physis
and the epiphyseal blood supply is distinct and
seperate.

3. Adults
• Metaphyseal vessels gradually penetrate the
vanishing physis, establish the communication
between metaphysis and subarticular end of the
bone(previously epiphysis)
• thus septic arthritis secondary to osteomyelitis
occurs in adults.

4. • The outer one-third of the cortex is supplied
primarily by the periosteal system, and the
inner two-thirds is supplied by the medullary
arteries.
• The metaphyseal complex primarily supplies
the physis and metaphyseal regions of long
bones. It merges with the medullary and
epiphyseal arterial system following physeal
closure
• The three systems are interconnected such
that if one is injured, another can
compensate to provide revascularisation.

5. Definition
• Osteomyelitis is defined as an inflammation of the
bone caused by an infecting organism.
• it is due to a single organism, but polymicrobial
infections can occur, especially in the diabetic foot.

6. Osteomyelitis is classified based on
Duration
• Acute
• Subacute and
• Chronic osteomyelitis
Mechanism of infection
• Haematogenous- from bacteremia
• Exogenous -open fractures
-contiguous spread from infected local
tissues

7. ACUTE HEMATOGENOUS
OSTEOMYELITIS

8. • Rapidly destructive pyogenic infection
• Hematogenous origin
• Starts in metaphysis of a actively growing
long bone
• Usually in infants and children(M>F)
• May occur in adults due to spread of
infection directly from another site or
through compound fractures,hematogenous
spread is rare but present in
immunocompromised patients.

9. Causative Organisms
• Infants
– Staph. aureus most common
– Streptococcus group B
– Coliform organisms
• 6 months to 4 years
– Staph. Aureus
– H. influenzae
(not common nowadays due to immunization)

10. Causative Organisms
• Older children & adults
– Staph . aureus
• Sickle cell disease
– Salmonella paratyphi
• IV drug abusers - pseudomonas
• Fungal osteomyelitis –in chronically ill patients
on long term intravenous therapy or parenteral
nutrition

11. Etiology
Pre-disposing factors-
1. Disease is common in active bone growth
2. Male > female
3. Poor nutrition
4. Trauma
5. Skin, dental, respiratory, GI, urinary tract infection
6. Burns
7. Iv drug abuse
8. Sickle cell anaemia
9. Immuno compromised state
10.Old age, debilitated state

12. METAPHYSIS is MC site .. Why?
1. Growing end, increased blood supply
2. Hairpin bend of blood vessels
3. Immature cells of metaphysis due to high cell
turnover
4. Defective phagocytosis
5. Dead & dying tissue of cartilage, good nutritive
material for organisms
6. End arteries, arteries open into sinusoids
7. Common site for Trauma – haemorrhage

13. Pathogenesis
• Bacterial seeding
Inflammatory reaction
local ischemic necrosis of bone

14. Abscess formation
as abscess enlarges
intramedullary pressure increases
cortical ischemia

15. • Purulent material escape through cortex into
subperiosteal space
• subperiosteal abscess
• if left untreated
• sequestra formation and finally
chronic osteomyelitis

16. Physical examination
• Fever,
• Pain at the site of infection,
• Limited use of the affected extremity.
• Constitutional symptoms, such as lethargy and
anorexia
• Local signs of inflammation
• Cellulitis
• LNpathy

17. Physical examination
Signs are often age-dependent.
• Neonates
– have a thin periosteum that is easily penetrated
by infection
– will present with swelling at the affected site &
adjacent joint and irritability on movement of the
limb.
• Older children,
– due to thicker metaphyseal cortex and densely
adherent periosteum,
– will have point tenderness

18. • In infants , elderly and immunocompromised
pts clinical findings may be minimal

19. Investigations
• WBC count – often normal
• Erythrocyte sedimentation rate (ESR), usually
raised
• C reactive protein (CRP) usually raised & useful
in monitering the course of treatment.

20. Bacterial Cultures
From sites of bone infection
• in order to focus antibiotic treatment
• Aspiration performed through thin
metaphyseal bone with an 18-gauge spinal
needle under local infiltration
• Positive in 48% to 85% cases
Blood culture
• Positive in 50% cases

21. Radiography
• Soft tissue swelling will be evident within 48
hours of the onset of infection.
• Periosteal new-bone formation or bony
destruction may be evident by 10 to 12 days.

22. Acute osteomyelitis The first x-ray, 2 days after symptoms began, is
normal .
metaphysealmottling and periosteal changes were not obvious until the
second film, taken 14 days later.
eventually much of the shaft was involved.

23. Bone scan
.
• can confirm diagnosis within 24 to 48 hrs after onset
•Highly sensitive but lacks specificity
•Examples
•Tecnetium99m bone scan
•Gallium scanning
•Indium-111 tagged WBCs

24. Magnetic resonance imaging
• sensitivity of 96% to 100% and a specificity of
75% in the detection of osteomyelitis.
• Can show early inflammatory changes in bone
marrow & soft tissue
• Useful for detecting intraosseous and
subperiosteal abscess

25. Computed tomography
• Identification of sequestra
Newer methods:
FDG-PET
SPECT

26. TREATMENT

27. NADE proposed five principles for the treatment of acute
hematogenous osteomyelitis
(1) an appropriate antibiotic is effective before abscess
formation.
(2) antibiotics do not sterilize avascular tissues or abscesses,
and such areas require surgical removal.
(3) if such removal is effective, antibiotics should prevent their
re-formation, and primary wound closure should be safe.
(4) surgery should not damage further already ischemic bone
and soft tissue.
(5) antibiotics should be continued after surgery.

28. Treatment
• General supportive care
– Intravenous fliuds
– Analgesics
– Comfortable positioning &
immobilization of limb

29. Antibiotic therapy
• If started before significant bone and soft-tissue
necrosis, it is more likely to be successful without
the need for surgical.
• According to culture sensitivity report
• Before culture – according to Gram staining
• If Gram staining –ve then empirical treatment
should cover all possible pathogens
• CRP level monitored to know response to therapy

30. Antibiotic therapy
• Intravenous therapy ranging from 4 to 8 weeks
(Success of treatment correlates most closely with an adequate
serum level of the antibiotic, rather than the route of
administration)
• Transition to oral antibiotics once clinical
improvement was observed
• Treatment continuing until normalization of the
ESR & CRP.

31. Antibiotic therapy
Infants –
recommended that the entire course of
treatment be intravenous as
• more prone to generalized sepsis,
• have less consistent oral antibiotic absorption,
• have a less predictable radiographic and serologic
response to treatment,

32. Surgery
• Indications
– Abscess
– No improvement despite of appropriate antibiotic
therapy
• Principle of surgery is to remove infected
nonviable necrotic bone and soft tissue,
decompression of abscess cavity facilitating
antibiotic delivery.

33. Surgery
• If subperiosteal abscess –
multiple drill holes through cortex
• If intramedullary pus –
cortical window

34. Complications
• Septicemia
• Dehydration & electrolyte imbalance
• Recurrence of infection
• Chronic osteomyelitis
• Growth arrest

35. SUBACUTE OSTEOMYELITIS

36. • Subacute osteomyelitis has a more insidious onset
and lacks the severity of symptom.
• Because of the indolent course of subacute
osteomyelitis, diagnosis typically is delayed for
more than 2 weeks.

37. • Systemic signs and symptoms are minimal.
• Temperature is only mildly elevated
• Mild-to-moderate pain is one of the only consistent
signs suggesting the diagnosis.
• Wbc counts are normal.
• ESR is elevated in only 50% of patients, and blood
cultures are negative.
• Even with an adequate bone aspirate or biopsy
specimen, a pathogen is identified only 60% of the
time.

38. • 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.

39. classification
• Radiographic classification of subacute
hematogenous osteomyelitis was described by
Gledhill and was modified by Roberts et al.

40. Type Gledhill Classification Robert et al. Classification
Differential
Diagnosis
I
Solitary localized zone of
radiolucency surrounded by
reactive new bone formation
Ia—Punched-out radiolucency Langerhans' cell
histiocytosis
Ib—Punched-out radiolucent
lesion with sclerotic margin
Brodie abscess
II
Metaphyseal radiolucencies with
cortical erosion
— Eosinophilic
granuloma;
osteogenic sarcoma
III
Cortical hyperostosis in diaphysis;
no onion skinning
Localized cortical and periosteal
reaction
Osteoid osteoma
IV
Subperiosteal new bone and
onion skin layering
Onion skin periosteal reaction Ewing sarcoma
V
— Central radiolucency in epiphysis Chondroblastoma
VI
— Destructive process involving
vertebral body
Tuberculosis;
osteogenic sarcoma

41. type 1,central metaphyseal lesion;type2,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.
Classification of subacute osteomyelitis:

42. • The diagnosis often must be established by an
open biopsy and culture.
• Purulent material is not always obtained on biopsy,
but granulation tissue is a common finding.
• S. aureus and Staphylococcus epidermidis are the
predominant organisms identified in subacute
osteomyelitis.

43. • Biopsy and curettage followed by treatment with
appropriate antibiotics ( IV anibiotics for 48 hrs
followed by 6 weeks of oral antibiotics ) generally
are recommended for all lesions that seem to be
aggressive
For lesions that seem to be a simple abscess in the
epiphysis or metaphysis, biopsy is not
recommended.

44. BRODIE ABSCESS
• localized form of subacute
osteomyelitis that occurs most
often in the long bones of the
lower extremities of young
adults.
• In adults, the metaphyseal-
epiphyseal area is involved.
• Intermittent pain of long
duration is the presenting
complaint, along with local
tenderness over the affected
area.

45. • On plain radiographs, appears as a
lytic lesion with a rim of sclerotic
bone .
• S. aureus is cultured in 50% of
patients; in 20%, the culture is
negative.
• It requires an open biopsy with
curettage to make the diagnosis. The
wound should be closed loosely over
a drain.
• iv antibiotics 2days f/b oral for 6
weeks

46. • More recently, Jones et al. described a based on radiographic
appearance:
Type A - Brodie abscess.
Type B - sequestrum involucrum.
four subtypes:
• B1 localized cortical sequestrum.
• B2 sequestrum with structural involucrum.
• B3 sequestrum with sclerotic involucrum and
• B4 sequestrum without structural involucrum.
Type C -sclerotic
• Physeal damage is indicated by the addition of “P” (proximal)
or “D” (distal) to the classification.

47. CHRONIC OSTEOMYELITIS

48. Introduction
• Chronic osteomyelitis is often defined as
the presence of ongoing bone infection
for longer than 1 month in the presence
of devitalized bone
• Infection mainly involves
- Marrow spaces
-Haversian canals
-Subperiosteal Spaces

49. Hematogenous osteomyelitis of Tubular
bone in child

50. Hairpin Bend vessels flow becomes considerably slower and
more turbulent

51. Factors That Turn Acute Bone Infection
to Chronic Osteomyelitis:
Trauma (orthopaedic surgery or open fracture)
Prosthetic orthopaedic device
Diabetes
Peripheral vascular disease
Alcoholism
Intravenous drug abuse
Chronic steroid use
Immunosuppression
Tuberculosis
HIV and AIDS
Sickle cell disease

52. • The hallmark of chronic osteomyelitis is infected
dead bone within a compromised soft-tissue
envelope
• The infected foci within the bone are
surrounded by sclerotic, relatively avascular
bone covered by a thickened periosteum and
scarred muscle and subcutaneous tissue.
• This avascular envelope of scar tissue leaves
systemic antibiotics essentially ineffective

53. • Bacteria settle down in metaphysis
• Primary focus in metaphysis (form abscess in
metaphysis)
• Subperiosteal abscess
• Sequestrum formation (dead bone )
• Involucrum formation (new bone formed by
cambium layer of periosteum)
• Pus eventually perforates periosteum and forms
abscess in soft tissues.
• Ultimately abscess burst on surface and forms
discharging sinus

54. Chronic osteomylitis involving metaphysis of
tibia

55. SEQUESTRUM
• Dead piece of bone separated from living bone
by a layer of unhealthy granulation tissue and
lying freely in the cavity
• Types
1) Tubular – in pyogenic infections below 2 yrs
2) Feathery – pyogenic infections
3) Course sandy – tuberculosis
4) Dense ivory – syphilis

56. 5) Coloured ( Black) – in ulna & tibia
osteomyelitis
6) Ring – Amputation stump & pin track
infections
7) Bombay – Calcaneal OM
8) Corolliform – Pyogenic infections
9) Buttonhole – Pott’ puffy tumour,
Tuberculosis of skull bones

57. INVOLUCRUM:
it is a immature,subperiosteal,reactive,living new
bone formation around dead bone

59. CLASSIFICATION OF CHRONIC
OSTEOMYELITIS
• Cierny and Mader classification system is
based on physiological and anatomical
criteria, to determine the stage of
infection
• The physiological criteria are divided into
three classes based on three types of
hosts

60. • Class A hosts have a normal response to
infection and surgery
• Class B hosts are compromised and have
deficient wound healing capabilities
• When the results of treatment are
potentially more damaging than the
presenting condition, the patient is
considered a class C host

61. • Anatomical criteria consist of four types
• Type I, a medullary lesion, is characterized
by endosteal disease
• In type II, superficial osteomyelitis is
limited to the surface of the bone

62. • Type III is a localized infection characterized by
full-thickness cortical sequestration and
cavitation (in this type, complete débridement
of the area would not lead to instability)
• Type IV is a diffuse osteomyelitic lesion that
creates mechanical instability, either at
presentation or after appropriate treatment

63. Stage Characteristic Features
I Medullary Endosteal disease
II Superficial Cortical surface infected because of coverage
defect
III Localised Cortical sequestrum that can be excised without
compromising stability
IV Diffuse I, II and III plus mechanical instability before or
after debridement.
Anatomical Type
Cierney and Mader staging system of
Chronic Osteomyelitis

64. Class Host’s immune
system
Features
A host Normal Immunocompetent with good local vascularity
B host Compromised Local or systemic factors that compromise
immunity or healing
C host Prohibitive Minimal disability, prohibitive morbidity
anticipated, poor prognosis for cure, treatment
worse than disease
Physiological classification

65. Clinical Staging
(Cierny-Mader, 1985)
Anatomic Type
+ CLINICAL STAGE
Physiologic Class
Example: IV B tibial osteomyelitis = diffuse tibial lesion in a systemically
compromised host

66. • USE OF THIS CLASSIFICATION
• - To decide whether treatment should be
• 1) Simple or Complex
• 2) Curative or Palliative
• 3) Limb sparing or Ablative

67. CLINICAL FEATURES
• DURING THE PERIOD OF INACTIVITY
- Usually no symptoms
- Skin over the focus is dusky, thin,
scarred
- Break in the skin causes ulceration that
heals slowly
- Muscles are scarred & leads to
contractures of the adjacent joints

68. • DURING ACUTE EXACERBATION
- Aching pain worsening at night, overlying
soft tissue becomes edematous, warm
redddened & tender
- patient is febrile
- As infection progresses, sinus may open
up & drain extruding small sequestrum at
intervals

69. - Intervals between flare ups may be
months or years
- Flare ups may be due to poor general
condition & lowered resistance
- Recurrent toxemia will eventually cause
debilitary & sometimes fatal amyloidosis

70. DIAGNOSIS
• The diagnosis of chronic osteomyelitis is
based on CLINICAL, LABORATORY &
IMAGING studies

71. • POSSIBLE CLINICAL FINDINGS
- Asymptomatic
- Pain
- Fever
- Tenderness
--Erythema
- Swelling
- Sinus Tract
- Limp
- Drainage

72. • LAB. INVESTIGATIONS
- Nonspecific
- Gives no indication of severity of infection
 Raised ESR & CRP
 Raised WBC ( Raised Lymphocytes) in 35%
patients
 Biopsy with Culture & Sensitivity (Gold
Standard)

73. IMAGING

74.  It takes from 10 to 21 days for an osseous lesion to
become visible on conventional radiography, because a
30–50% reduction of bone density must occur before
radiographic change is apparent
- earliest radiographic changes appears after 8 to 10 days
- In early stages, bone appears moth eaten &
osteoporotic due to CORTICAL DESTRUCTION with
sclerotic areas
- PERIOSTEUM IS ELEVATED by subperiostel laminations
of new bone
-grdually each necrotic dense area becomes surrounded
by white ring representing new bone formation, the
INVOLCRUM

75. Ssequestrum with normal structural involucrum of a
proximal humerus.

76. SEQUESTRUM
PERIOSTEAL NEW BONE
FORMATION
INVOLUCRUM

77. SINOGRAPHY
 Helpful if the sinus is present in locating
focus of the infection in chronic
osteomyelitis

78. Sinogram

79. Scintigraphy
They are more useful in acute om than
chronic
• TC 99m Poly Phosphate scan
• Gallium citrate scan
• Indium
• Sensitivity (84 to 100 percent) and specific
(70 to 96 percent)

80. 1)99M Tc Scan
- Shows increased uptake in the areas
of increased blood flow or oseoblastic
activity

81. 2) 67Ga Scan
- shows increased uptake in areas where
leucocytes or bacteria accumulate
- normal Ga scan excludes presence of
osteomyelitis
- useful as follow up examination after
surgery

82. These leukocytelabeled
images suggest multiple areas
of bilateral pedal osteomyelitis.

83. CT SCAN
- Provides excellent definition of cortical
bone
- especially useful in identification of
Sequestra

84. CT Scan

85. MRI SCAN
- for evaluation of soft tissue involvement
- reveals a well defined rim of high signal
intensity surrounding the focus of active
disease ( RIM SIGN)

86. A case of chronic osteomylitis of fibula

87. MR images chronic osteomyelitis of right
distal femur.

88. TREATMENT
.

89. • Chronic OM generally cannot be
eradicated without surgical treatment
• Surgery for Chronic OM consists of
sequestrectomy & resection of scarred &
infected bone & soft tissue

90. • THE GOALS OF SURGERY
- Eradication of infection by achieving a
viable & vascular environment
-Radical debridement
-Prevent recurrences

91. SEQUESTRECTOMY & CURETTAGE
 All sinus tracts are excised completely
along with sequestra, purulent material &
scarred and necrotic tissue
 if sclerosis bone seals off a cavity within
the medullary canal, it is opened into the
canal in both directions to allow blood
vessels to grow into the cavity

92. • When medullary canal is infected
intramedullary reaming has shown
favourable results in the treatment of
medullary osteomyelitis.

93. • AFTER TREATMENT
- Limb is splinted until the wound is healed &
then it is protected to prevent pahological
fracture
- prolonged antibiotic therapy is given usually for
6 weeks
- bony & soft tissue defects must be filled to
reduce chances of continued infection & loss of
function

94. • METHODS TO ELIMINATE THIS DEAD SPACE
1) Bone grafting with primary or secondary
closure
2) use of PMMA beads
3) local muscle flaps & skin grafting with or
without bone grafting
4) microvascular transfer of muscle,
myocutaneos, osseous & osteocutaneous flaps
5) use of bone transport( Ilizarov’s technique)

95. • OPEN BONE GRAFTING( PAPINEAU TECHNIQUE)
This procedure is based on the following principles:
- granulation tissue markedly resists infection
- autogenous cancellous bone grafts are rapidly
revascularized and are resistant to infection

96. • DONE IN 3 STAGES
1)Excision of infected tissue without or
with stabilization using an external fixator
or an intramedullary rod
2) Cancellous autografting
3) skin closure

97. PMMA BEAD CHAINS
• -The rationale is to deliver levels of antibiotics locally in
concentrations that exceed the minimal inhibitory
concentrations
• Primary wound closure is done
• Suction drains are not recommanded
• Aminoglycosides are mc used
-most commercially available bone cements have a
prepackaged form available with GENTAMICIN (500mg
/40g)
- In short-term implantation, the beads are removed
within 10 days and in long-term implantation, they may
be left for 80 days

98. Preparation of antibiotic beads

99. Polymethylmethacrylate (PMMA) beads connected
together in a chain are the most widely used drug
delivery system.

101. BIODEGRADABLE ANTIBIOTIC
DELIVERY SYSTEMS
• -Biodegradable substrates contain
osteoconductive and osteoinductive materials,
which can be used to promote new bone
formation
- Bioabsorbable substrates (calcium sulfate or
calcium phosphate) that can be mixed with
antibiotics ( Vancomycin or Tobramycin)
-These beads typically resorb by about 8 weeks
after surgery

102. • Advantages
- 2nd procedure is not required to remove the
implant
- Calcium in the substrate can be used in new
bone formation

103. CLOSED SUCTION DRAINS
• -For resistant focal infections, topical instillation
of solution containing mild detergent ( eg.
Alevaire) & one or more antibiotic seems to be
effective

104. -Closed suction antibiotic ingress and egress high-
volume irrigation systems(Lautenbach
continuous irrigation method) can be used over
3 to 21 days
- the material collected through suction tube is
cultured every day when 3 successive negative
cultures are obtained, the antibiotic detergent
solution is discontinued

106. SOFT TISSUE TRANSFER
• - Soft-tissue transfer is done to fill dead space
left behind after extensive debridement
- transfer of vascularized muscle tissue improves
the local biological environment by bringing in a
blood supply for antibiotic delivery and osseous
and soft-tissue healing.

107.  Most commonly, a local muscle flap is used in
the treatment of chronic osteomyelitis of the
tibia
 The gastrocnemius muscle is used for defects
around the proximal third of the tibia
 the soleus muscle is used for defects around the
middle third
 A microvascular free muscle transfer is required
for defects around the distal third of the tibia

108. - When a microvascular free muscle flap is used,
and segmental bone loss has occurred,
autogenous cancellous bone grafting can be
done about 6 weeks after the initial free flap
transfer
- free fibular graft can be used for segmental
bone loss of the tibia
- If chronic osteomyelitis involves segmental bone
loss of the tibia and the fibula, the results of a
free fibular graft are not good, and amputation
or reconstruction by the Ilizarov technique is
advised

109. ILIZAROV’S TECHNIQUE
 The Ilizarov technique has been helpful in the treatment
of chronic osteomyelitis and infected nonunion
-

110. • BELFAST TECHNIQUE
2 Stage Technique
- in 1st stage, all necrotic & infected tissues
are debrided & is covered with soft tissue
transfer
- in 2nd stage , at later time autogenous
cancellous grfating is done after infection
has been completely subsided

111. Adjunctive techniques
• Silver iontophoresis
• hyperbaric oxygen therapy
• Pulsed electromagnetic fields and
ultrasound

112. AMPUTATION FOR CHRONIC
OSTEOMYELITIS
• - Malignant change of sinus tract
- Madura Mycosis
- Joint contractures & stiffness

113. COMPLICATIONS
• Growth disturbances
• Pathological fractures
• Muscle contractures
• Secondary septicemia
• Epithelioma
• Malignant changes( Squamous cell ca,Reticulum
cell ca, Fibrosarcoma)
• Joint stiffness
• Amyloidosis

114. MISCELLANEOUS CONDITIONS

115. SCLEROSING OM OF GARRE
• - Idiopathic cortical sclerosis
- mc site Tibia
-chronic form of disease in which the bone is
thickened and distended, but abscesses and
sequestra are absent
-affects children and young adults
-cause is unknown, but it is thought to be an
infection caused by a low-grade, possibly
anaerobic bacterium

117. • CLINICAL FEATURES
- Intermittent pain
- Swelling & Tenderness over affected bone

118. • INVESTIGATIONS
- ESR : slightly raised
- C/S : usually negative
- X Ray : expanded bone with generalised
sclerosis
- Biopsy : chronic low grade non specific
OM

119. • DIFFERTIAL DIAGNOSIS
- Paget’s disease
- Osteoid osteoma

120. • TREATMENT
- Fenestration of sclerotic bone
- Antibiotics

121. RESIDUAL STAGE OF OSTEOMYELITIS
- characterized by a complete absence of the signs and
symptoms of infection, including drainage
-The bone is sclerotic, and its blood supply and strength
are normal

122. • TREATMENT
-correcting leg-length inequality or angular
and joint deformities
-contracted scars must be released
-adherent scars must be replaced by
myocutaneous flaps

123. PATHOLOGICAL FRACTURE IN
OSTEOMYELITIS
-Because the involucrum is sometimes insufficient, the
shaft of a long bone may fracture during the acute or
subacute stage of osteomyelitis before immobilization
has been started
-all operations necessary to combat the infection should
be carried out thoroughly, and bone fragments are then
realigned and immobilized as with any other fracture
-External fixation or cast immobilization usually is
preferred
-If bone loss is significant, the defect can be filled with
autogenous bone graft, a vascularized osseous graft, or
bone transport using the Ilizarov technique

124. CHRONIC RECURRENT MULTIFOCAL
OSTEOMYELITIS
• It is characterized by an insidious onset of
mild-to-moderate pain with signs of
inflammation over the affected parts,
which tend to recur
• often affects the metaphysis of long
bones

125. • ETIOLOGICAL FACTORS
- Infectious disease : Propiobacterium acne
- Autoimmune Diseases : Psoriasis & IBD
- Genetic Predisposition : LPIN2 gene

126. • CLINICAL FEATURES
- Nonspecific : pain, swelling, restricted
mobility
- Duration : from days to several years

127. • INVETIGATIONS
- raised ESR & CRP with normal WBC count
- Cultures : negative
- Biopsy : may be useful

128. TREATMENT
• No effective treatment for CRMO available
• Cases of disease remission after treatment with
IFN gamma have been reported
• Resolution of symptoms followed by recurrence
months later is characteristic of this disease
• Generally, the symptoms continue to recur over
2 years, and the disease generally is self-limiting
• The long-term prognosis seems to be good

129. Spine OM
• Commonly affects lumbar spine < thoracic
spine < cervical spine
• Usual site : vertebral bodies
• Simultaneous involvement of the 2
adjacent vertebral end plates with
intervening discs

131. • ETIOLOGY
- richly vascular metaphyseal bone near
anterior longitudinal ligament
- avascular disc
- end arterial supply of interosseous artery
in adults

132. • X Ray Findings
- disc space narrowing with end plate
erosion with vertebral body destruction
- vertebral end plate sclerosis with
increased density in subchondral bone
- spinal fusion

133. • TREATMENT
- IV Antibiotics
- Rest
- Spinal immobilisation
- Surgery

134. TUBERCULOUS OM
• - chronic granulomatous infection caused
by AFB
- usually secondary to primary elsewhere
- commonly involving metaphysis in
children & epiphysis in adults

135. • CLINICAL FEATURES
-swelling
- local tenderness
- muscle spasm
- cold abscess with chronic discharging
sinus

136. • INVESTIGATIONS
- Tubeculin test
- Biopsy :typical tubercles
- Blood : lymphocytosis
- X Ray: osteoporosis, loss of outline of
articular cortex, granular foci

137. • TREATMENT
- Sinuses with sequestra : curretage &
excision
- AKT

138. Thank you