Orthopaedics

1. Infection of Bone & joints
1
PROF. DR. MD. SHAH ALAM
MBBS, FCPS, MS, FRCS
Fellowship Training in Spine Surgery (USA)
Imperial Spine Course (UK)
PROFESSOR
Department of Ortho & Spine Surgery
NITOR, Dhaka, Bangladesh

2. GENERAL ASPECTS OF INFECTION
 Infection is the local & systemic response of living tissue to
the invasion of a pathogenic organism’s, their
multiplication, and the toxin/ enzymes they produce.
 The signs of inflammation are recounted in the classical
mantra: redness, swelling, heat, pain and loss of function.
 In one important respect, bone infection is more
susceptible than soft tissues to vascular damage and cell
death.
2

3. Bone infection
 Micro-organisms may reach the musculoskeletal tissues by
 (a) Direct introduction through the skin (a pinprick, an
injection, a stab wound, a laceration, an open fracture or
an operation),
 (b) Direct spread from a contiguous focus of infection, or
 (c) Indirect spread via the blood stream from a distant site
3

4.  Depending on the type of invader, the site of infection and
the host response, result may be
 A pyogenic osteomyelitis,
 A septic arthritis,
 A chronic granulomatous reaction (classically seen in
tuberculosis of either bone or joint), or an indolent response
to an unusual organism (e.g. a fungal infection).
4

5. Surgeon-dependent factors include
 prophylactic antibiotics,
 skin and wound care,
 operating environment,
 surgical technique, and
 treatment of impending infections, such as in open
fractures.
Simply stated, it is much easier to prevent an infection than
it is to treat it.
5

6. The body’s main defense mechanisms are
 (1) Neutrophil response,
 (2) Humoral immunity,
 (3) Cell-mediated immunity, and
 (4) Reticuloendothelial cells.
6

7. Osteomyelitis
 Nelaton (1834) : coined osteomyelitis
 The root words osteon (bone) and myelo
(marrow) are combined with itis
(inflammation) to define the clinical state in
which bone is infected with
microorganisms.

8. Osteomyelitis
is an acute or chronic inflammatory process of bone,
bone marrow and its structure secondary to infection
with micro organisms.
It may remain localized, or it may spread through the
bone to involve the marrow, cortex, periosteum, and
soft tissue surrounding the bone.
8

9. CLASSIFICATION
Duration
- Acute / Subacute / Chronic
Mechanism
- Heamatogenous (tonsil , lungs , ear/ GIT)
- Exogenous (injection , open fractures)
Host response
- Pyogenic / Granulomatous
9

10. 10
Osteomyelitis
 Based on the duration and type of symptoms
 Acute: <2weeks
Early acute
Late acute(4-5days)
 Subacute: 2weeks—6weeks
Less virulent – more immune
 Chronic: >6 weeks

11.  Age : Infancy and childhood.
 Sex : Males predominate 4:1
 Location : Metaphysis of long bone.
 Poor nutrition, unhygienic surroundings.
 The causal organism in both adults and children
is usually Staphylococcus aureus (found in over
70% of cases).
11
ACUTE
OSTEOMYELITIS

12. Pathophysiology
Infection
◦ Starts in Metaphysis
 Arteriole Loop / Venous Lakes
◦ Spread via Volkman’s canal / Haversian system
◦ Endothelium Leaks
ACUTE
OSTEOMYELITIS

13. –Sharp hairpin turns in
metaphyseal capillaries
– flow becomes
considerably slower and
more turbulent
ACUTE
OSTEOMYELITIS

14. Pathophysiology
 Role of growth plate
 In children < 2 years, more susceptible to limb shortening
or angular deformity. (some vessels may penetrate
through physis & spread infection.)
 In children > 2 years, diaphysis is at greater risk. The
physis effectively acts as a barrier to the spread of a
metaphyseal infection.
ACUTE
OSTEOMYELITIS

15. Acute Osteomyelitis Infants
 Joint involvement is
common
 Nutrient metaphyseal
capillaries perforate the
epiphyseal growth plate,
particularly in the hip,
shoulder, and knee.
15
ACUTE
OSTEOMYELITIS

16. 16
Pathogenesis
why metaphysis is involved
1. Infected embolus is trapped in U-shaped small end
arteries located in metaphyseal region > vascular
stasis > lowered oxygen tension> Bacterial colonization
2. Relative lack of phagocytosis activity in metaphyseal
region
3. Highly vascularised region ---minor trauma—
hemorrhage ----locus minoris resistantae---excellent
culture medium

17. Etiological Agents
Older children - Staph aureus
Adults - Staph aureus.
Infants < 6 months Staph aureus
Group B streptococci
6 months – 6 years – Gram -ve H. influenzae is
common pathogen for osteomyelitis but It is replaced by
Kingella kingae.
Staph aureus
Patients with sickle-cell disease - Salmonella
Heroin addicts and immunocompromised patients
Unusual infections (e.g. with Pseudomonas aeruginosa,
Proteus mirabilis or anaerobic Bacteroides species)
17
ACUTE
OSTEOMYELITIS

18. Rare organisms Isolated in Bacterial
Osteomyelitis
Bartonella henselae
Pasteurella multocida or Eikenella corrodens
Aspergillus species, Mycobacterium avium-
intracellulare or Candida
albicans
Mycobacterium tuberculosis
Brucella species, Coxiella burnetii (cause of
chronic Q fever) or other fungi found in
specific geographic areas
Human immunodeficiency virus
infection
Human or animal bites
Immunocompromised patients
Populations in which tuberculosis
is prevalent.
Population in which these
pathogens are endemic

19. Pathogenesis
Introduction of bacteria from :
 Outside through a wound or continuity from a
neighboring soft tissue infection
 Hematogenous spread from a pre existing focus (most
common route of infection)
19
ACUTE
OSTEOMYELITIS

20. Pathogenesis: Host Factors
SYSTEMIC FACTORS LOCAL FACTORS
Malnutrition Chronic lymphedema
Hepatic & renal failure Venous stasis
DM Arteritis
Chronic hypoxia Major vessel compromise
Immune disease Radiation fibrosis
Malignancy Small vessel disease
HIV/AIDS Neuropathy
Ethanol/ Tobacco abuse Extensive scarring
Asplenia
Extremes of age
Immune deficiengy/suppression

21. 21
 Formation of a glycocalyx surrounding the infecting
organisms.
◦ protects the organisms
from the action of phagocytes
prevents access by most antimicrobials.
◦ A surface negative charge of devitalized bone or a
metal implant
promotes organism adherence
 subsequent glycocalyx formation.
Pathogenesis:Bacterial factors:

22. 22
The inflammatory response to osteomyelitis:
 Prostaglandin-E production is five to thirty fold higher in
infected bone.
responsible for bone resorption and
 sequestrum formation.
 Effective phagocytosis is defense in patients with
osteomyelitis.
 Intramedullary oxygen tension is important for phagocytic
function
◦ oxygen tensions of <30 mm Hg impair normal
phagocytic function.

23. Pathogenesis
 Pre-existing focus / Exogenous Infection
 Infective embolus enters nutrient artery
 Trapped in a vessel of small caliber(metaphysis)
 Blocks the vessel
 Active hyperemia + PMN cells exudate
ACUTE
OSTEOMYELITIS

24. Intraosseous pressure increases. intense pain
obstruction to blood flow intravascular thrombosis.
ACUTE
OSTEOMYELITIS
Ischemia and
resorption
pus formation

25.  Follows paths of least resistance.
 Passes through Haversian canal and Volkmann canal.
 Local cortical necrosis.
ACUTE
OSTEOMYELITIS

26.  Enter subperiosteal space.
 Strips periosteum.
 Perforation of periosteum
 Pus in extra periosteal area then submuscular area
 Pus in Intramucular plane then to subfascial plane
 Enters subcuteous tissue and may drain out
ACUTE
OSTEOMYELITIS

27.  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.
27

29. 29

30. Development of Osteomyelitis

31. CLINICAL FEATURES
 There may be a recent history of infection: a septic toe, a
boil, a sore throat or a discharge from the ear
 Fever (High Grade)
 Child refuses to use limb (pseudoparalysis)
 Local redness , swelling , warmth , oedema
 Newborn – failure to thrive , drowsy , irritable.
31
ACUTE
OSTEOMYELITIS

32. CLINICAL FEATURES
 Adults :
 commonest site (haematogenous) thoracolumbar spine.
 History of some urological procedure followed by a mild
fever and backache.
 It is important to remember that all these features may be
attenuated if antibiotics have been administered.
32
ACUTE
OSTEOMYELITIS

33. Laboratory Tests
 The most certain way to confirm the clinical diagnosis is
to aspirate pus or fluid from
>the metaphyseal subperiosteal abscess,
>the extraosseous soft tissues or
>an adjacent joint.
 This is done using a 16- or 18-gauge trocar needle.
 Tissue aspiration +ve in more than 60% cases.
 Blood cultures are positive in < 50% cases of proven
infection.
33
ACUTE
OSTEOMYELITIS

34. Laboratory Tests
 The WBC count: unreliable indicator
 The ESR also is unreliable in
 neonates
 patients with sickle cell disease,
 patients taking corticosteroids,
 CRP is a better way to see response of infection to treatment.
 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.
34

35. X-ray findings
 It takes from 10 to 21 days for an osseous lesion to
become visible in x ray, (because a 30–50% reduction
of bone density must occur to become visible)
 By the second week there may be a faint extra-
cortical outline due to periosteal new bone formation;
> classic x-ray sign of early pyogenic osteomyelitis.
ACUTE
OSTEOMYELITIS

36. Radiology
 Plain x-ray
◦ Specificity 75-83%
◦ Sensitivity 43-75%
 Soft tissue swelling 48hrs
 Periosteal reaction 5-7d
 Osteolysis 10d to 3 wks
◦ (need 50% bone loss)

37. X-ray findings: An important late sign : Regional
osteoporosis with a localized segment of increased
density.
ACUTE
OSTEOMYELITIS
 Osteoporosis is a feature of metabolically
active, and thus living bone; the segment that
fails to become osteoporotic is metabolically
inactive and possibly dead

38.  Sequesterum appears dense in comparison with
surrounding decalcified bone due to lack blood
supply.
 When spongy trabeculae are destroyed, it gives
moth eaten appearance.
38

39. ACUTE
OSTEOMYELITIS
Acute osteomyelitis: The 1st x ray is 2 day after symptom
begun, is normal. Metaphyseal mottling and periostel
changes were not obvious until the 2nd film taken after 14
days.

40. RADIONUCLIDE SCANNING
This is a highly sensitive investigation with low
specificity.
> Gives a more physiologic picture,
> reflects inflammatory changes or the reaction
of bone to the infection.
The three most commonly used radioisotopes are
> technetium-99m (99mTc) phosphate,
> gallium-67 (67Ga) citrate, and
> indium-111 (111In)–labeled leukocytes.
40

41. RADIONUCLIDE SCANNING
 The most common is 99mTc phosphate,
 can confirm the diagnosis 24 to 48 hours after
onset in 90% to 95% of patients,
 a negative technetium-99m bone scan effectively
rules out the diagnosis of osteomyelitis.
41

42. ULTRASONOGRAPHY
> may detect a subperiosteal collection of fluid in
the early stages of osteomyelitis
 it cannot distinguish between a haematoma and
pus.
 This modality is highly operator dependent, with
a diagnostic accuracy of only about 60%.

43. MAGNETIC RESONANCE IMAGING
Helpful in cases of doubtful diagnosis.
 It is the best method of demonstrating bone
marrow inflammation.
 It is extremely sensitive, even in the early phase
and
 Assist in differentiating between soft-tissue
infection and osteomyelitis.
43

44.  Determine the extent of medullary involvement.
 Pus can be seen as increased density.
 Adjacent soft-tissue abscesses also are seen
easily.
 CT diagnosis of acute osteomyelitis is based on
detection of intraosseous gas, osteolysis, soft
tissue masses, abscesses, or foreign bodies.
44
CT SCAN

45. Differential
Diagnosis
 Rheumatic fever :
 Onset is more gradual,
 pain and tenderness are less intense.
 Involvement is polyarticular.
 Response to salicylates and ACTH is dramatic.
 Acute suppurative arthritis :
 Pain and tenderness are severe ,
 limted to the joint,
 joint movements is greatly restricted,
 muscle spasm is intense, and
 aspiration reveals purulent synovial fluid.
45

46. Differential Diagnosis
 Cellulitis This is often mistaken for osteomyelitis.
 There is widespread superficial redness and lymphangitis.
 The organism is usually staphylococcus or streptococcus
 Ewing’s tumour
 Fever, leucocytosis, subperiosteal onion peel bone
deposition.
 Destruction is more confined to diaphysis & is more diffuse.
 Sickle-cell crisis In areas where Salmonella is endemic.
 Treat such patients with suitable antibiotics until infection is
definitely excluded.
46

47. Treatment : Nade proposed five principles for the
treatment of acute hematogenous osteomyelitis that
are still applicable today:
(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 removal is effective, antibiotics should prevent
their reformation, and primary wound closure
should be safe; 47

48. Treatment : Nade proposed five principles for the
treatment of acute hematogenous osteomyelitis that
are still applicable today:
(4) Surgery should not damage further to already
ischemic bone and soft tissue; and
(5) Antibiotics should be continued after surgery.
48

49. If osteomyelitis is suspected on
clinical grounds, blood and fluid
samples should be taken for
laboratory investigation and then
treatment started immediately
without waiting for final
confirmation of the diagnosis.
49

50. There are four important aspects to the management
of the patient:
• Supportive treatment for pain and dehydration:
Analgesics/ rehydration (IV Fluid)/ Comfortable
positioning of the limb
• Splintage of the affected part
• Appropriate antimicrobial therapy.
• Surgical drainage.
50

51. Nade’s indications for surgery
1. Abscess formation
ii. Severely ill & moribund child with features of
acute osteomyelitis
iii. Failure to respond to IV antibiotics for >48 hrs.
51

52. Dosage schedule
 Administer IV antibiotics until ……
 the patient’s condition begins to improve and
 the CRP values return to normal levels – which
usually takes 2–4 weeks depending on the
virulence of the infection and the patient’s general
degree of fitness.
52

53. Dosage schedule
 By this time appropriate antibiotic (according to
sensitivity) can be administered orally for another
3–6 weeks. (Can be extended if bone destruction is
more)
 CRP, ESR and WBC values are also checked at
regular intervals and treatment can be discontinued
when these are seen to remain normal.
53

54. Surgical technique
 if pus is aspirated- I/D under general
anaesthesia.
 Periosteum is incised longitudinally over the
point of maximum tenderness & stripped
laterally about half inch on either side.
 If pus is found – and released – no need of
drilling into the medullary cavity.
 If there is no obvious abscess, it is reasonable
to drill a few holes into the bone in various
directions.
54

55. Surgical technique
 If there is an extensive intramedullary abscess,
drainage can be better achieved by cutting a
small window in the cortex.
 The skin is closed loosely over drains, and the
limb is splinted.
 Full weight bearing is usually possible after 3–4
weeks.
 Alternative to this method is Closed irrigation &
suction method
55

56.  Epiphyseal damage and altered bone growth
 Supporative arthritis
 Pathological Fracture
 Overlying soft-tissue cellulitis
 Metastatic infection
 Chronic osteomyelitis
 Epithelioma
56

57. Subacute Osteomyelitis
 It has an insidious onset, mild symptoms, lack of
systemic reaction
 Its relative mildness is due to:
a) Organism being less virulent OR
b) Patient more resistant OR
c) (Both)
 Most common site: Distal femur, Proximal & Distal
Tibia
57

58. Causative Organism
a) Staphyloccocus aureus (30-60%)
b) Others (Streptococcus, Pseudomonas,
Haemophilus influenzae)
c) Pseudomonas aeruginosa (IV drug
user)
d) Salmonella (patient with sickle cell
anaemia)
58

59. 59
Gledhill Classification
1. Central metaphyseal
2. Eccentric metaphyseal
3. Diaphyseal cortical
4. Diaphyseal with periosteal new
bone
5. Ephyseal
6. Metaphyseal and epiphyseal

60. Clinical Features
 Pain (several weeks / months) near one of
larger joint
 Limping
 Swelling & Local tenderness
 Muscle wasting
 Body temperature usually normal (no fever)
 Patient is usually child or adeloscent.
60

61. Investigations
 X-ray (may resemble osteoid osteoma /
malignant bone tumour)
 Biopsy
 Fluid aspiration & culture
 ESR raised
 WBC count may be normal
61

62. BRODIE ABSCESS
 localized form of subacute osteomyelitis
 occurs most often in long bones of lower limb of
young adults.
 Before physeal closure, the metaphysis is most
often affected.
 In adults, the metaphyseal-epiphyseal area is
involved.
 Intermittent pain of long duration
 local tenderness over the affected area.
62

63. Radiological Finding
 A circumscribed, round/oval cavity containing pus and
pieces
of dead bone (sequestra) surrounded by sclerosis.
 Most commonly seen in tibial / femoral metaphysis.
 May occur in epiphysis / cuboidal bone (calcaneum).
 Metaphyseal lesion cause no / little periosteal reaction.
 Diaphyseal lesion may be associated with periosteal new
bone formation and marked cortical thickening.
63

64. A circumscribed, oval cavity
surrounded by a zone of
sclerosis at the proximal
tibia (Brodie’s abscess)
This is a lateral view X-ray of
left tibia and fibula. There is a
marked periosteal reaction at
the diaphysis.

65. Treatment
Conservative :
a) Immobilization
b) IV Antibiotics for 48 hours followed by oral drug
(flucloxacillin + fusidic acid) for 6weeks
Surgical (if the diagnosis is in doubt / failed conservative
treatment) :
a) Open biopsy
b) Perform curettage on the lesion follwed by antibiotic
65

66. Chronic Osteomyelitis
“ A severe, persistent and incapacitating infection of
bone and bone marrow ”
66
Chronic osteomyelitis is still a major cause of musculoskeletal
morbidity in children around the world. The hallmark of chronic
osteomyelitis is infected dead bone within a compromised soft-tissue
envelope.

67. Aetiological Agents
Usual organisms (with time there is always a mixed
infection)
 Staph.aureus(commonest)
 Staph.pyogenes
 E.coli
 Pseudomonas
 Staph.epidermidis (commonest in surgical implant)
 Klebsiella causes most extensive destruction
 Animal bites – pasturella multocida
 Human bites – eikenella corrodens
67

68. Reason for such a situation(4 failures).
 Failure to suspect correct diagnosis within the first 3 – 4
days of onset due to lack of a “high index of suspicion”.
 Failure to perform the simple clinical investigations which
can confirm the suspicion.
 Failure to initiate properly planned therapeutic program.
 Failure to continue treatment till the disease is eliminated.

69. Aetiology
 progression / sequel /Inadequately treated acute
osteomyelitis
 Haematogenous spread
 Iatrogenic- foreign implant (internal fixation)
 Penetrating trauma
 Open fractures
69
CHRONIC OSTEOMYELITIS

70. Clinical
Features
 During the period of inactivity, asymptomatic.
 H/O Recurrent acute flare ups at indefinite interval over
months/years
 Aching Pain / Pyrexia/ Redness/ Tenderness( Acute flare)
 Discharging sinus (seropurulent discharge).
70

71. Clinical
Features
 H/O spontaneous closure of sinus & subsidence of infection
following expulsion of large bony fragment
 Skin- thin/ dusky/ distorted(cicatrix) & easily traumatized/
ulcer.
 Muscles- Scarred & causes contracture of adjacent joints.
 Bone- Misshapen.
71

72.  Incidence of infection increases with increase in
grade of open fractures (Guistilo, Anderson) :
◦ Approx. 2% for type I and type II
◦ Approx. 10% to 50% for type III
 The tibia most common site for infection.
CHRONIC OSTEOMYELITIS

73. Pathogenesis
Inadequate treatment of acute OM /
Foreign implant /
Open fracture
Inflammatory process continues with time
together with persistent infection by Staphylococcus aureus
Persistent infection in the bone leads to increase in
intramedullary pressure due to inflammatory exudates
(pus)
stripping the periosteum
73
CHRONIC OSTEOMYELITIS

74. Vascular thrombosis
Bone necrosis (Sequestrum formation)
New bone formation occur (Involucrum)
Multiple openings appear in this involucrum (Cloaca),
through which exudates & debris from the
sequestrum pass via the sinuses (Sinus formation)
Constant destruction of neighboring soft tissue may lead to cicatrix
formation.
74
CHRONIC OSTEOMYELITIS
Pathogenesis

75. Pathology
 The presence of sclerotic, necrotic piece of bone usually
cortical surrounded by radiolucent inflammatory exudate
and granulation tissue known as sequestrum.
 Types-
 ring(external fixator)
 tubular/match-stick(sickle)
 coke and rice grain(TB)
 Feathery(syphilis)
 Colored(fungal)
 Annular(amputation stumps)
 Features:
 Dead piece of bone
 Pale
 Inner smooth ,outer rough
 Surrounded by infected granulation tissue trying to
eat it
75

76. The involucrum is the sheath of reactive, new,
immature, subperiosteal bone that forms around the
sequestrum.
 The involucrum is irregular and is often
perforated by openings.
The involucrum may gradually increase in density
and thickness to form part or all of a new
diaphysis.
CHRONIC OSTEOMYELITIS

77. 77

78. SEQUESTRUM
PERIOSTEAL NEW BONE
FORMATION
INVOLUCRUM
CHRONIC OSTEOMYELITIS

80. Staging Of Osteomyelitis:
 The Cierny-Mader staging system.
 It is determined by the status of the disease
process.
 It takes into account the state of the bone, the
patient's overall condition and factors affecting the
development of osteomyelitis.
80
CHRONIC OSTEOMYELITIS

81. The Cierny-Mader Classification
 Medullary Osteomyelitis -
confined to medullary
cavity.
 Superficial Osteomyelitis
Contiguous type of
infection. Confined to
surface of bone.
 Localized Osteomyelitis –
Full-thickness cortical
sequestration which can
easily be removed
surgically.
 Diffuse Osteomyelitis -Loss 81
CHRONIC OSTEOMYELITIS

82. 82

83. DIAGNOSIS
 The diagnosis 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.

84. CLINICAL
 Physical examination should be focused on integrity of skin
and soft tissue .
 Determination of area of tenderness.
 Assessing bone stability.
 And evaluation of neurovascular status of the limb

85. LABORATORY
 Lab studies generally are nonspecific and give no
indication for severity of the infection.
 ESR and C- Reactive protein are elevated in most
patients.
 But WBC’S elevated in only 35%.

86.  Signs of cortical destruction and periosteal
reaction strongly suggest the diagnosis of
osteomyelitis.
X-ray examination
- Usually show bone resorption (patchy loss of
density / osteolytic lesion)
- Thickening & sclerosis around the bone
(involucrum)
- Presence of sequestra
86
Multiple imaging technique are available to
evaluate chronic osteomyelitis ,however no
technique can absolutely confirm or exclude
presence of osteomyelitis.

88. MR
I
 Has very high sensitivity and specificity.
 Advantage:
◦ Useful for differentiating between bone and soft-
tissue infection.
◦ Helpful in surgical planning.
 Disadvantage:
◦ A metallic implant in the region of interest may
produce focal artifacts.
◦ False positives in tumors and healing fractures.

89. Sinograph
y
• 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

91. 91
• 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
Principles of Treatment

92. Treatment according to type (Cierny)
Type I Medullary cortical de-roofing and medullary debridement
Type II Superficial shallow decortication back to bleeding bone
Type III Localised saucerisation and debridement
Type IV Diffuse infected area excised en-bloc and stabilised
with ex-fix
92
CHRONIC OSTEOMYELITIS

93. Treatment -
Antibiotics
- Seldom eradicated by antibiotics alone.
- Bactericidal drugs are important to:
a) Stop the spread of infection to healthy bone
b) Control acute flares
- Antibiotics used in treating chronic osteomyelitis
(Fusidic acid, Clindamycin, Vancomycin,
Cefazolin)
93
CHRONIC OSTEOMYELITIS

94. Antibiotic
choice
 Guided by microbiology department
 Clindamycin (98% serum level) and
vancomycin(14% serum level) have good bone
penetration
 Minimum length 6 weeks with 3 months being the
standard treatment course
 May need to treat for 6-12 months
94
CHRONIC OSTEOMYELITIS

95. - Antibiotic (IV route) is given for 10 days prior to
surgery.
- After the major debridement surgery, antibiotic is
continued for another 6 weeks (min) but usually
>3months.
[treat until inflammatory parameters (ESR) are
normal]
95
CHRONIC OSTEOMYELITIS

96. Surgical
Treatment
- After 10 days of antibiotic administration,
debridement is done to remove:
a) All the infected tissue
b) Dead / devitalised bone (Sequestrectomy)
c) Sinus tract
96
CHRONIC OSTEOMYELITIS

97. 97
Operative procedures
1-Sequestrectomy.
2-Saucerization.
3-Curettage.
4-Excision of an infected bone.
5-Amputation.

98. 98
• Means removal of sequestrum.
• If it lies within the medullary cavity, a window is made
in the overlying involucrum and sequestrum removed
Sequestrectomy

99. 99
• 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
Saucerization

100. Closure of dead space: methods
 Bone grafting with primary or secondary closure;
 Use of antibiotic PMMA beads as a temporary filler
of the dead space before reconstruction;
 Local muscle flaps and skin grafting with or without
bone grafting;
 Microvascular transfer of muscle, myocutaneous,
osseous, and osteocutaneous flaps; and
 The use of bone transport (Ilizarov technique).
100

101. 101

102. Open cancellous grafting – Papineau technique
 Useful when free flaps or soft-tissue transfer options
are limited because of anatomic location
 or in patients who smoke
 or are medically compromised.
3 stages 1. Debridement
2. Grafting
3. Wound coverage
 Useful for bone deficiencies of less than 4cm
 (preferably autogenous) mixed with an antibiotic and
fibrin sealant
102

103. Vascularised bone graft
 Heals as a segmental fracture
 Indicated when defect is > 6cm
 Iliac crest for defects > 8cm
 Fibula 6-35cm can be bridged
Bypass graft
 Involves the establishment of a cross union between
the fibula and tibia proximally and distally to the
defect which has been debrided and bone grafted
103

104. Polymethylmethacrlate antibiotic bead
chain
**The principal of treatment is to deliver 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.
104

105. 105

106. INTRAMEDULLARY ANTIBIOTIC CEMENT
NAIL
106

107. 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.
107

108. 108
-local muscle flap
-Vascularised pedicle
-free tissue transfer
Tibia – proximal 1/3 – gastronemius flap
middle 1/3 - soleal flap
lower 1/3 – free muscle transfer
Soft tissue transfer

109. Biodegradable antibiotic delivery system
 Advantage-
1-Removal of implant not required.
2- May contain osteoconductive and
osteoinductive material, which can be used to
promote new bone formation.
3-Reabsorb within 8 weeks
 Disadvantages
purulent discharge
109

110. Closed suction drain
• Success rates of approximately
85%. (modified Lautenbach
drainage systems)
• A more recent wound closure
technique is negative pressure
wound therapy (NPWT)
110

111. Ilizarov technique
**Useful in chronic osteomyelitis with infected
nonunions
**Allows radical resection of infected bone by
corticotomy through normal bone
***proximal and distal to the area of diseased bone
is transported until union is achieved.
111

112. Hyperbaric oxygen
• Used only as an adjuvant to
other traditional method of
treatment.
112
CHAMBER USED FOR HYPERBARIC
OXYGEN THERAPY

113. Amputation
• Very rarely performed ,preferred in a case with
long –standing discharging sinus if the sinus
undergo malignant change.
113

114. Complications
1) Pathological Fracture
This occurs in the bone weakened by chronic
osteomyelitis
2) Deformity
In children the focus of osteomyelitis destroys part of
the epiphysis growth plate.
3) Shortening/ lengthening
Destruction of growth plate arrest growth.
Stimulation of growth plate due to hyperemia
4) Epithelioma
5) Amyloidosis
114
CHRONIC OSTEOMYELITIS

115. REFERENCES
 1)Tachdjian’s pediatric orthopaedics
 2)Cambell’s text book of orthopaedics 13th
 3) Turek’s 4th edition
 4) Apleys system of orthopaedics 9th edition
 5) Netter’s orthopaedics
 6)Rockwood and Green’s orthopaedics
 7) Internet
115

116. 116

117. 117
CHRONIC OSTEOMYELITIS

118. Jone’s classification for children (based on radiographic
appearance) : Most recent
 type A, Brodie abscess;
 type B, sequestrum involucrum;
B1, localized cortical sequestrum;
B2, sequestrum with structural involucrum;
B3, sequestrum with sclerotic involucrum;
B4, sequestrum without structural involucrum.
 type C, sclerotic.
 Physeal damage is indicated by the addition of “P”
(proximal) or “D” (distal) to the classification.
118

119. In either case it is critical to preserve the
involucrum
preferable to wait at least 3-6 months before
performing a sequestrectomy
Early sequestrectomy
- Eradicate infection
-Better environment for
periosteum to respond
Delayed sequestrectomy
Wait till sufficient
involucrum has formed
before doing a
sequestrectomy to
mimimize the risk of
fracture, deformity &
segmental loss
When to do sequestrectomy?
CHRONIC OSTEOMYELITIS

120. Post sequestrectomy
 NO STABLISATION IS NECESSARY WHEN 70% OF THE ORIGINAL
CORTEX REMAINS INTACT- only protect by cast
 Greater bone loss-Ext fix
 Focal bone loss-open cancellous BG/conventional BG
 Seg. bone loss—BG/Bone transport/other devices
ADEQUACY OF INVOLUCRUM
Radiologically if cortical continuity of the involucrum is 50% of
the over all cortical diameter on 2 orthogonal views , then it is
adequate.
CHRONIC OSTEOMYELITIS