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1. Moderator:
Dr. C.R.Buragohain,
Assist. Prof. orthopedics
Presenter:
Dr. S.H.Ranna
P.G.T. Orthopedics
30 -12-2015

2. HISTORY
 HIPPOCRATES 500 BC
removed sequestrum from
osteomyelitic bone.
 PERCIVIAL POTT 1774-
sequestrum forms due to .
Avascularity.
 NELATON 1834coined the
term Osteomyelitis.
 World war I dr.W.BEAR
noticed maggots as
treatment.
Sir NELATON

3. CONT….
 Till 1928 maggots used
in treatment.
Debridement
Disinfection of wound.
Stimulation of healing.
Biofilm inhibition.
• In 1874 W.Howes and
in 1927 Winnet Orr
develops treatment
principle.

4. BLOOD SUPPLY TO LONG
BONES:
the nutrient
blood vessel
 the
metaphyseal
complex and
 the periosteal
capillaries.

5. 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 infantile
osteomyelitits.

6. In Children:
No metaphyseal blood
vessels penetrate the
physis and the
epiphyseal blood
supply is distinct and
seperate.
Blood flow through
metaphysis is turblent
and slow creating a
natural environment
for proliferation of
microbes.

7. In 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.

8. Definition
 an inflammation of the
bone caused by an
infecting organism.
May involve marrow,
cortex, periosteum, and
the surrounding soft
tissue.

9. Classification
Attempts to classify are based
on :
(1)duration and type of
symptoms.
(2)the mechanism of infection.
(3)the type of host response.

10. Based on the duration and type of
symptoms

11. Classified according to mechanism
EXOGENOUS
OSTEOMYELITIS
•OPEN FRACTURE
•SURGERY OR
IOTROGENIC
•SREAD FROM INFECTED
FOCUS
HEMATOGENOUS OM BACTEREMIA
BASED ON HOST RESPONSE
PYOGENIC
OSTEOMYELITIS
NON PYOGENIC
OSTEOMYELITIS

12. ACUTE HEMATOGENOUS
OSTEOMYELITIS
 most common type of bone infection.
Usually in infants and children.
Male: Female ratio 4:1 all age
group.
Hematogenous origin.
Starts in metaphysis of a actively
growing long bone.

13. 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. Less 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.

14. ETIOLOGICAL AGENTS
INFANTS Staphylococcus aureus-
most common.
Group B Streptococcus.
Gram –ve organism.
6 months to 4 years Staphylococcus aureus.
Hemophylous influenza
(not common now a days
due to immunization).
Older children and adults Staphylococcus aureus.
Gram –ve bacteria.
IV drug abusers pseudomonas
Chronic ill patient Fungal osteomyelitis.
Sickle cell disease patient Salmonella.

15. WHY STAPHYLOCOCCUS IS MOST
COMMON?
 S. AUREUS and S. epidermis –
elements of normal skin flora.
 S. aureus – increased affinity
for host proteins(traumatized
bone)
 Enzymes (coagulase, surface
factor A)-host immune
response.
 Inactive L forms –dormant for
years.
 Biofilm (polysaccharide slime
layer)- increases bacterial
adherence to any substances
 Large variety of adhesive
proteins and glycoprotein –
mediate binding of bone
components.

16. PATHOGENESIS
Introduction of bacteria from preexisting
focus/exogenous infection
Pathogenesis depends upon host response, age,
and bacterial virulence.
Formation of glycocalyx surrounding the
infecting organism
Infective embolus enters to nutrient artery
Trapped in a vessel of small caliber (metaphyses)
Blocks the vessels and active hyperemia+PMN
cells exudates

17. Proteolytic enzymes destroy bacteria and
medullary elements
The debris increases and intramedullary pressure
increases
Follows path of least resistance, passes through
Haversian and Volkmann’s canal
Local cortical necrosis and Subperiosteal abscess
formation
Perforation of periosteum/reach joint piercing capsules
Enters soft tissues and may drain out

18. In children younger than 2 years:
Some blood vessels cross the physis
(transphyseal vessels)
Spread of infection from metaphyses
to epiphyses directly
Physis or epiphyses damaged
from infection
Susceptible for Limb shortening or
angular deformity
Septic arthritis

19. Otherwise physis act as a barrier which prevents the spread
of infection from metaphyses.
Metaphyseal cortex is thin
Abscess breaks metaphyseal cortex
Subperiosteal abscess formation occurs
Diaphysis is rarely involved except most severe infection.
Infrequent sequestrum formation

20. In children older than 2 years:
Physis acts as a barrier to the
spread of metaphyseal infection
Metaphyseal cortex in older
children is thicker
Infection spread into diaphysis
Endosteal blood supply may
be jeopardized
With concurrent Subperiosteal abscess
the periosteal blood supply is damaged
Extensive sequestration results

21. CLINICAL FEATURE OF ACUTE
OSTEOMYELITIS
 SIGNS OF INFLAMMATION i.e. rubor, calor,
dolor, tumor.
 Children refuses to use limb i.e. pseudo
paralysis.
 In newborn –failure to thrive,drowsy,irritable
 Fever
 Swelling
 Pain
 Tenderness over metaphyses.

22. INVESTIGATION OF ACUTE OM
 LABORATORY INVESTIGATION:
WBC count is often normal but the
ESR and C-reactive protein level
usually are elevated.
The CRP is the measurement of the
acute phase response and is
especially useful in monitoring the
course of treatment of acute OM
because it normalize much sooner
than ESR.

23. MICROBIOLOGICAL EXAMINATION:
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 30% to 60% cases

24. PLAIN X-RAYS:
 Standard radiograph generally
negative in very early of infection.
 Soft tissue swelling may be seen 1 to 3
days of start of infection.
 Periosteal reaction or bony
destruction becomes visible in X-Rays
after 10 to 12 days.
 Osteolytic changes
 bone mineral loss of at least 30% to 50%
 may take 10 days to 2 weeks

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

26. Bone scan
• can be positive within 24 to 48
• useful in the setting of normal
radiographs and clinical
suspicion of osteomyelitis
hours of the onset of
symptoms.
• Highly sensitive but lacks
specificity
• Gallium scanning
• Indium-111 tagged WBCs

27. Magnetic resonance imaging
sensitivity of 96% to 100% and a
specificity of 95% to 100% in the
detection of osteomyelitis.
It is most useful in spinal and
pelvic infections for planning.
surgical approaches for
debriding subperiosteal or soft-
tissue abscess.

28. Computed tomography
 Identification of sequestra.
 Detection of gas in soft-tissue infections in the
Ultrasonography
 For evaluating the possibility of joint infections in infants,detect a
subperiosteal collection of fluid in early stages.
 But it can not distinguish between a hematoma and pus
Newer methods:
 ELISA
 PCR
For identification of causative organism

29. PELTOLA AND VAHVANEN’S
CRITERIA FOR DIAGNOSIS
 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. Localized classic physical findings
a. bonny tenderness
b. overlying soft tissue edema ,erythema
4 Positive radiological imaging.

30. TREATMENT OF ACUTE OM
1.GENERAL TREATMENT:
 INTRAVENOUS FLUID
Adequate nutritional
supplement.
General supportive treatment
by I taking enough caloric,
protein, vitamins etc

31. Antibiotic therapy :
 In 1983 NADE proposed five principles for
treatment of acute OM.
 An appropriate antibiotic is effective before
abscess formation.
 Antibiotic don’t sterilize avascular tissues or
abscess and such areas require surgical removal.
 If such removal is effective, antibiotic should
prevent their re-formation and primary wound
closure should be safe.
 Surgery should not damage further already
ischemic bone, soft tissue.
 Antibiotic should be continued after surgery.

33. SURGICAL DRAINAGE :
 The two indication for surgical drainage in acute
OM are :
Presence of an abscess which require drainage.
Failure of the patient to improve despite
appropriate IV antibiotic treatment after 24 to 48
hours.
• When a Subperiosteal abscess is found in an
infant, several small holes should be drilled
through the cortex into the medullary canal. If
intramedullary pus is found a small window of
bone is removed.

34. COMPLICATION OF ACUTE OM
Chronic osteomyelitis.
Septic arthritis.
Epiphyseal damage and growth
disturbance.
Septicemia.
Deep vein thrombosis.
Pulmonary embolus.
Pathological fracture.

35. subacute osteomyelitis
 This has a more insidious in onset and
lacks the severity of symptoms.
 Duration between 2-6 weeks.
 Its relative mildness is due to :
1.Organism being less virulent or
2.Patient being more resistant to
organism or
3.Both of above
4.Administration of inadequate antibiotic
before onset of disease.

36. CLASSIFICATION

38. TREATMENT OF SUB ACUTE OM
 CONSERVATIVE
 If the diagnosis is not in doubt immobilization
and proper antibiotic therapy usually
intravenous followed by oral antibiotic for 6
week to 12 weeks duration cure the disease.
 SURGICAL TREATMENT
 Surgical drainage and curettage indicated if X-
Ray shows no healing after proper conservative
treatment.
 If the diagnosis is in doubt an open biopsy is
needed and the lesion may be currated at the
same time.

39. BRODIE ABSCESS
 It is a localized form of sub
acute osteomyelitis in which
the bone abscess contains pus
or jelly like granulation tissue
surrounded by a zone of
sclerosis.
 In young adults occurs more
often in the long bones of lower
extremities.
 In adult’s metaphyseal –
epiphyseal area is involved.
 Before physeal closure the
metaphysis is more often
affected.

40. CLINICAL SYMPTOMS:
 Deep boring intermittent pain of long
duration which is worse at night, increases
on activity and relieved by rest is the
presenting complain.
 Local tenderness over affected area.
 Organisms of low virulence are believed to
cause the lesion.
 S. aureus is cultured in 50% patient.
 This condition is often requiring an open
biopsy with curettage to make the diagnosis.

41. TREATMENT:
 CONSERVATIVELY
MANAGED IF THERE IS NO
DOUBT: rest and
antibiotic therapy f0r
6week.
 IF NO RESPONSE TO
ANTIBIOTIC TREATMENT:
surgical evacuation and
curettage done with
cancellous bone
grafting if needed.

42. CHRONIC OSTEOMYELITIS
 Duration is > 6 weeks.
 Chronic osteomyelitis mostly occurs :
Sequelae of acute osteomyelitis.
Post operative bone and joint infection.
Untreated or inadequately treated of
open fractures.
Chronic infection from beginning e.g.
tuberculosis, syphilitic, fungal
osteomyelitis etc.

43. Sequestrum: It is a dead piece of
bone separated from normal bone by
a layer of unhealthy granulation
tissue or pus and lying freely in the
cavity.
Involucrum: It is a immature, Subperiosteal,
reactive, living new bone formation around
the dead bone. There is multiple opening in
the involucrum which allows draining of pus
from abscess to the sinus truck.

44. Types of sequestrum :
Tubular or Diaphyseal
sequestrum
Acute Pyogenic OM in children
Ring sequestrum Amputation stump, at
Steinmann pin.
Ivory sequestrum In syphilis
Fine sandy sequestrum Viral osteomyelitis
Coarse sandy sequestrum Central body of vertebrae
Feathery or flake sequestrum Tuberculosis of rib
Kissing sequestrum Peridiscal TB vertebrae
Button hole sequestrum After radiation therapy
Bombay or black sequestrum Calcaneal OM or fungal OM etc.
Coke sequestrum Found in cancellous bone
infection

45. CIERNY AND MADER CLASSIFICATION:

47. JONES at al classification :
Type A:
Brodie
abscess.
Type B:
Sequestrum,
Involucrum.
Type C:
Sclerotic.
B1 :
localized
cortical
sequestrati
on.
B2:
sequestrum
with
structural
involucrum.
B3:
sequestrum
with
sclerotic
involucrum.
B4:
sequestrum
without
structural
involucrum.

48. Clinical features
 h/o pain
,swelling,discharge,trauma
,surgery,
 Discharging bone pieces
 Sinus fixed to bone
 Puckered scar
 Exposed necrotic bone
 Soft tissue contracture
 Bony tenderness
 Thickening of bone

49. LABORATORY INVESTIGATION :
Generally it is
nonspecific and gives
no indication of the
severity of infection.
ESR and CRP are
elevated in most
patients.
WBC count is elevated
in most patients.

50. MICROBIOLOGICAL AND BIOPSY:
Culture and sensitivity and
biopsy of aspirated
material is the gold
standard method for
diagnosis of chronic
osteomyelitis.

51. Plain X-Rays :
Sequestrum
Involucrum
Ill defined bone
destruction
Local irregular
thickening
Loss of cortico-
medullary
differentiation
PERIOSTEAL NEW BONE
FORMATION
INVOLUCRUM
SEQUESTRUM

52. Sinography:
 Performed if a sinus
track is present.
 Image taken after
injecting of
radiopaque liquid
into sinus.
 It is helpful in
localizing focus of
infection in chronic
osteomyelitis.
 It is helpful in
planning of surgical
treatment.

53. Bone scan:
more useful in acute OM than in
chronic OM.
Technetium 99m bone scan shows
increased uptake in areas of
increased blood flow or increased
osteoblastic activity.
Gallium scan shows increased
uptake in areas where leucocytes or
bacteria accumulates.

54. CT scan:
It gives more information of
x-ray findings and provide
excellent definition of
cortical bone and useful in
identifying in small
sequestra.

55. Magnetic resonance imaging :
More useful for soft tissue
evaluation.
In chronic OM, MRI may reveal a
well defined rim of high signal
intensity surrounding the focus of
active disease called rim sign.
Sinus track and cellulitis appear as
increased signal density on T2
weighted imaging.

56. Principles of treatment:
Identify the organism and its
sensitivity.
Locate and confirm the sequestrum.
To remove dead, devitalized and
infected bone by debridement.
Stabilization of bone.
Dead space management after
debridement.
Proper soft tissue management.
Post operative antibiotic therapy.

57. Bone Debridement:
 The goal of debridement is to leave healthy,
viable tissue. Debridement of bone is done
until punctuate bleeding is noted called the
“PAPRIKA SIGN”
 Copious irrigation with 10 to 14 L of normal
saline is expected.
 The extent of resection during debridement is
important in Type B host patient. Such patient
is treated with marginal resection.
 Repeated debridement may be required.

58. 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

59. SEQUESTROMY AND CURRATAGE:
 EARLY SEQUESTROMY: It
eradicates infection very
early. It gives better
environment for
periosteum to respond.
 DELAYED SEQUESTROMY:
wait till sufficient
involucrum has formed
before doing a
sequestromy to minimize
the risk of fracture or
segmental deformity.

60. POST SEQUESTROMY MEASURMENT:
 No stabilization is necessary when 70% of the
cortex remains intact.
 Greater bone loss- external fixator.
 Focal bone loss- open cancellous bone graft.
 Segmental bone loss- bone graft/bone
transport/other device.
 Radiographically if cortical continuity of the
involucrum is 50% of the overall cortical diameter
on two orthogonal films then the involucrum
structurally adequate.
 Dead space management should be done
adequately.

61. Why dead space management is important?
• It is a predisposing condition for the persistence of
infection because it is poorly vascularized.
 Dead space management is mandatory to arrest
the disease.
 Dead space management maintains the integrity
of the skeletal part.
 Dead space management helps to improve the
local biological environment by bringing in a
blood supply.
 It helps in host defense mechanism.
 It helps to antibiotic delivery to the local tissue
site.
 It improves osseous and soft tissue healing.

62. METHODS OF DEAD SPACE MANAGEMENT:
 Bone grafting with primary or secondary
wound closure.
 Use of antibiotic PMMA beads as
temporary filler before reconstruction.
 Local muscle flaps and skin grafting with
or without bone grafting.
 Micro vascular transfer of muscles,
myocutenous, osseous and osteocuteneous
flaps.
 The use of bone transport.(Ilizarov or
other).

64. OPEN BONE GRAFTING (PAPINEU TECHNIQUE)
 It is a three stage
surgical technique:
Stage 1:
Debridement and
stabilization.
Stage 2: Bone
grafting.
Stage 3: wound
coverage.

65. POLYMETHYL METHACRYLATE ANTIBIOTIC
BEAD CHAIN (PMMA)
 High local level of antibiotic achieved by diffusion
with low systemic toxicity.
 2 key elements :
1. Delivery vehicle –
 Non absorbable – PMMA
 Bio absorbable –cal. Sulfate, synthetic polymers.
2. Antimicrobials – powder form, heat stable, active
against targeted microbes – Aminoglycoside
,Vancomycin, Cefepime, Nafcillin, Imipenem.
 Suction drains are not recommended as the
concentration level of antibiotic is diminished.

66. CLOSED SUCTION DRAIN
 Success rates of approx. 85% have been
reported for the modified Lautenbach
method.
 A more recent wound closure technique is
negative pressure wound therapy (NPWT.
 The advantage of this technique are:
It allows a change in antibiotic delivery based
on culture results obtained from surgical
biopsy.
Gradual decrease in the size of the soft tissue
dead space.

67. disadvantage
Frequent
occlusion of the
delivery
catheter.
Risk of
contamination
with secondary
infection.

68. SOFT TISSUE TRANSFER:
Three methods commonly used:
Primary closure- if no infection.
Let tissue heal by secondary
intention.
Local muscle flaps and free
vascularized muscle flaps in the
presence of a large soft-tissue
defect or an inadequate soft-tissue
envelope.

69. Limb reconstruction
 Ilizarov external fixation:
 Is used for
reconstruction of
segmental defects.
 Used for difficult cases of
osteomyelitis when
stabilization and bone-
lengthening are
necessary.
 May also be used to
compress nonunion and
to correct Malunions.

70. Amputation
 Is reserved only for those extreme cases of chronic
osteomyelitis where:
 1. Persistence of severe pus pouring infection of
very long duration, not responding to multiple
operative interventions.
 2. Systemic complication like amyloidosis / CRF
 3. Infection associated with extensive deformation
of neighboring joints and low socioeconomic
status of the patient / high risk patients who
cannot afford / tolerate multiple surgeries.
 4. Chronic osteomyelitis associated with vascular
complications.
 5. Chronic osteomyelitis with epithelioma.

71. GARRÉ’S SCLEROSING OSTEOMYELITIS
 Chronic form of nonsuppurative osteomyelitis.
 Affects children and adults.
 Cause is unknown.
 Characterized by marked sclerosis and cortical
thickening.
 Abscesses and sequestra are absent
 C/o intermittent pain of moderate intensity for a
longer duration.
 Swelling and tenderness present over affected bone.
 Biopsy specimens show only chronic, low grade,
nonspecific osteomyelitis.
 No specific treatment but fenestration of sclerotic
bone and antibiotics are advisable.
 D/D: osteoid Osteoma and Paget disease.

72. INFECTED IMPLANTS
 lifelong risk for bacterial seeding on the
implant.
 Infections associated with prosthetic
joints occur less frequently than aseptic
failures.
 THR-1st 2yr <1%, TKR <2%
 revision surgery > 40%.
 5% in int. fixation device- 2% in close
fracture,30% in open fracture.

73. pathogenesis of implant-associated
infection race for the
surface
IMPLANTS
HOST
MICRO-ORGANISM
adaptation
and
integration
adhesion and
colonization.

74. CLASSIFICATION OF PERIPROSTHETIC INFECTIONS:
1. Positive
Intra-operative
Cultures
Two or more
positive
cultures from
the surgical
site.
Treatment -
appropriate
parental
antibiotics for 6
weeks
2.Early
Postoperativ
e Infection
Infection occurs
within first month.
Clinically apparent
wound infections or
infections of
hematomas that
have progressed to
deep infections
Treatment -
debridement,
exchange of the
polyethylene liners,
retention of the
components, and
intravenous
administration of
antibiotics for 4
weeks.

75. 3.Late Chronic
Infection
Infection is
apparent more
than 1 month
after the
operation and
has an insidious
clinical onset.
Typically, patients
have never had a
pain-free interval
after the
operation
Treatment -
debridement,
removal of the
components, and
appropriate
antibiotics for 4
to 6 weeks. This
may be followed
by implantation
of a new
prosthesis after
the patient has
been free of
infection.

76. 4. Acute
Hematogeno
us Infection
The acute
infection is
characterized
by the
precipitous
onset of
clinical
symptoms in a
previously well-
functioning hip
Treatment - If the
prosthesis is well
fixed, treat the
infection in the
same manner as
for an early
postoperative
infection; if the
prosthesis is
loose, treatment
should be the
same as for a late
chronic infection.

77. Infections in internal fixation
devices
 increasing or new onset of pain that
may be located at the implant insertion
site or at the fracture site.
 Local signs may include cellulitis,
abscess formation, and wound drainage.
 Constitutional symptoms include fever,
chills, night sweats, tachycardia, and
anemia.
 Obtain radiographs as soon as the
diagnosis is suspected.

80. THANK YOU ALL..