Osteomyelitis is an inflammation of bone caused by a bacterial infection. It can be classified based on duration of symptoms (acute, subacute, chronic), mechanism of infection (hematogenous, contiguous), or host response. Common causative organisms include Staphylococcus aureus and gram-negative rods. Diagnosis involves blood tests, imaging like x-rays, CT, MRI and bone scans, and bone biopsy. Treatment involves antibiotics, surgical debridement of infected bone, and management of any dead space to prevent ongoing infection.

1. Osteomyelitis
Presented By
Dr. Bhaskar
PG Resident 2nd Year

2. 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.

3. Introduction
 Osteomyelitis is an inflammation of bone caused
by an infectingorganism.
 It may remain localized, or it may spread through
the bone to involve the marrow, cortex, periosteum,
and soft tissue surrounding thebone.

4. Classification
 Classification are basedon
(1)the duration and type ofsymptoms
(2)the mechanism of infection
(3)the type of hostresponse

5. Osteomyelitis
Based on the duration and typeof symptoms
The time limits defining these classes are
arbitrary, however.

6. Classified according to mechanism
 Osteomyelitis may be
1. Exogenous(trauma, surgery (iatrogenic),
or a contiguousinfection)
2. Hematogenous (bacteremia)

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

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

9. Host susceptibility to bone infection is increased by
(a) Local factors :
trauma, scar tissue, poor circulation, diminished sensibility,
chronic bone or joint disease and the presence of foreign
bodies including implants
(b)Systemic factors :
malnutrition, general illness, debility, diabetes, rheumatoid
disease, corticosteroid administration and all forms of
immunosuppression, either acquired or induced.

10. 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)

11.  Preexisting focus / Exogenous Infection
 Infective embolus enters nutrient artery
 Trapped in a vessel of small
Caliber(metaphysis)
 Blocks the vessel
 Active hyperemia + PMN cells exudate

12.  Hyperemia and immobilization causes decalcification.
 Proteolytic enzymes destroy bacteria and
medullary elements.
 The debris increase and intramedullary
pressure increases.

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

14.  Enter subperiosteal space.
 Strips periosteum.
 Perforation of periosteum/ reach joint by piercing
capsule.
 Enters soft tissue and may drain out

15. Pathogenesis
.
Metaphysis is involved
1. Infected embolus is trapped in U-
shaped(hairpin loops) small end arteries
located predominantly in metaphyseal region
2.Relative lack of phagocytosis activity in
metaphysealregion
3.Highly vascularised region ---minor
trauma— hemorrhage ---excellent culture
medium

16. Clinical Features
• IN INFANTS
• In children under 1 year old
• The baby simply fails to thrive and is drowsy but irritable.
• Suspicion should be aroused by a history of birth difficulties,
umbilical artery catheterization or a site of infection
(however mild) such as an inflamed intravenous infusion
point or even a heel puncture.
• Metaphyseal tenderness and resistance to joint movement
can signify either osteomyelitis or septic arthritis

17. • IN CHILDREN
• The patient, usually a child over 4 years
• presents with severe pain, malaise and a fever; in neglected
cases, toxemia may be marked.
• There may be a recent history of infection: a boil, a sore
throat or a discharge from the ear.
• Even the gentlest manipulation is painful and joint movement
is restricted (‘pseudoparalysis’).
• Local redness, swelling, warmth and oedema are later signs

18. Laboratory findings
 The white blood cell count may be normal or will show
leucocytosis
• The causative organism can be identified in approximately 50%
of patients through blood cultures.
• Erythrocyte sedimentation rate and C-reactive protein level
usually are elevated.

19. • Bone aspiration usually gives an accurate bacteriological
diagnosis and should be performed with a 16- or 18-gauge
needle in the area of maximal swelling and tenderness,
usually the long bone metaphysis.
 Any material aspirated should be gram stained and cultured
to determine the sensitivity to antibiotics.

20. X-ray findings
 X-ray films are negative within 1-2 weeks
 Careful comparison with the opposite side may show abnormal
soft tissue shadows.
 By the time there is x-ray evidence of bone destruction, the
patient has entered the chronic phase of the disease.

21. X-ray findings
 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

22. USG
 Ultrasound cannot directly access bone marrow
abnormalities present in osteomyelitis but can
document osteomyelitis indirectly by identifying
periosseous soft tissueabnormalities
 The very first sonographic sign, seen even before any
periosteal reaction, is edematous swelling of the deep
soft tissues

23. Bone scan
 Radioisotopic bone scanning is valuable in early localization
(within 24 to 48 hrs) of bone infection.
 Technitium-99m bone scan is very sensitive , it is the choice
for acute hematogenous osteomyelitis, the overall accuracy
being 92%.
Bone scan revealing
hot spot in right
tibia in delayed
phase

24. Gallium scans and indium-111-labeled leukocyte scans also can
aid in diagnosis when used in conjunction with technetium
scanning.

25. Magnetic Resonance Imaging:
 Magnetic resonance imaging
has very high sensitivity and
specificity.
 Advantage:
 Useful for differentiating
between bone and soft-
tissue infection.
 Helpful in surgical
planning.
A case of chronic osteomylitis of fibula

26. Differential diagnosis :
oma
 Tuberculosis –
 Thin wateryd/s
 Undermining ,bluishdiscoloration
 Diaphyseal involv. Morecommon
 H/o pulm. T.B.
 Often multifocal
 Soft tissue infection(Cellulitis)
 absence of bonychanges
 Ewing sarcoma
 radiological d/d
 acute presentation
 Bx isdiagnostic.
 Foreign body
 Osteoid osteoma
 Histiocytic eosinophilicgranul
 Garre’sosteomyelitis

27. SUBACUTE HEMATOGENOUS OSTEOMYELITIS
 More insidious onset and lacks the severity of symptoms
 Diagnosis typically is delayed for more than 2 weeks.
 a pathogen is identified only 60% of the time
• 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.
• S. aureus and Staphylococcus epidermidis are the predominant
organisms
• Biopsy and curettage followed by treatment with appropriate
antibiotics generally are recommended for all lesions
that seem to be aggressive.

29. Brodie’s abcess
• Localized form of subacute osteomyelitis that
occurs most often in the long bones of the lower
extremities of young adults.
 Deep boring pain, worse at night, relieved by rest
 Circular or oval lucency surrounded by zone of
sclerosis
 Treatment:
 Conservative if no doubt - rest + antibiotic for
6 wks.
 if no response – surgical evacuation &
curettage, if large cavity - packed with
cancellous bone graft

30. Garre’ s osteomyelitis
• Chronic form of disease in
which the bone is thickened and
distended but abscesses and
sequestra are absent
 Corticalthickening
 Acute local pain, pyrexia
subside- fusiform swelling
 Acute stage-rest, antibiotics
 Sx: Gutter holing,
excision+curettage

31. Chronic osteomyelitis
If any of sequestrum, abscess cavity, sinus tract or cloaca is
present.
• Hematogenous infection with an organismof low virulence
may be present by chroniconset.
• It is due to the fact that the causative organism can lie dormant
in avascular necrotic areas occasionally becoming reactive
from a flare up.

32. Pathology:
 Pathologic features of chronic osteomyelitis are :
 The presence of sclerotic, necrotic piece of
bone usually cortical surrounded by
inflammatory exudate and granulation tissue
known as sequestrum.
 Features:
 Types-
 ring(external fixator)
 tubular/match-stick(sickle)
 coke and rice grain(TB)
 Feathery(syphilis)
 Colored(fungal)
 Annular(amputation stumps)

33. Pathology:
 The involucrum
the sheath of reactive, new, immature,
subperiosteal bone that forms around the
sequestrum, effectively sealing it off the blood
stream just like a wall ofabscess.

34. Classification

36. Clinical features
 During the period of inactivity, no symptoms are present.
 Only Skin-thin, dark, scarred, poor nourished, past sinus, an
ulceration that is not easily toheal
 Muscles-wasting contracture, atrophy
 Joint-stiffness
 Bone-thick, sclerotic,
 often contain abscesscavity

37. Clinical features
 At intervals, a flare-upoccurs,
 The relapse is often the result of poor body condition and
lower resistance.
 A lighting up of infection is manifested by aching pain that is
worse at night.
 Locally there will be some heat, swelling, redness, tenderness,
edema, because pus may build up in cavity, then a sinus may
open and start to exudates purulent materials and smallsequestra.
 The sinus closed and the infection subsided.

38. X-ray examination
• Usually show bone resorption (patchy loss of density /
osteolytic lesion)
• Thickening & sclerosis around the bone
• Presence of sequestrum
• Occasionaly it may present as a Brodie’s abscess
surrounded by vascular tissue and area of sclerosis

39. SEQUESTRUM
PERIOSTEAL NEW BONE
FORMATION INVOLUCRUM

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

41. 18FDG PETScan
Fluorodeoxyglucose positron emission tomography has the
highest accuracy for confirming or excluding the diagnosis
of Chronic Osteomyelitis.

42. •The “gold standard” is to obtain a biopsy specimen
for histological and microbiological evaluation of
the infected bone.

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

44. Nade’s proposed five principles for the
treatment
(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 and
(5) antibiotics should be continued after surgery.

45. The two main indications for surgery in acute hematogenous
osteomyelitis are
(1) the presence of an abscess requiring drainage and
(2) failure of the patient to improve despite appropriate
intravenous antibiotic treatment.

46. ANTIBIOTICS
• If possible, antimicrobials should be withheld until
percutaneous or surgical deep cultures have been obtained
• Once cultures are obtained, a parenteral antimicrobial
regimen is initiated to cover suspected pathogens(Empirical
Treatment)
• Antibiotic therapy should be pathogen-directed, based on the
results of bone biopsy or blood cultures.

47. Surgical treatment

48. Bone Debridement:
 The goal of debridement is to leave healthy, viable tissue
and removed all dead and devitalized tisue.
 Debridement of bone is done until punctate bleeding is
noted, giving rise to the term the paprikasign.
 Copious irrigation with pulsatile lavage using fluid
 Repeated debridements may be required.

49. 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 doinga
sequestrectomy to minimize the risk
of fracture, deformity & segmental
loss
Sequestrectomy
And Curettage

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

51. Prerequisites for
Sequestrectomy
Radiological
 Well formed involucrum
surrounding the
discretely visible
sequestrum adequately at
least 2/3rd diameter of
bone (3 intact walls on
two views ensure 3/4th
intact walls)
Clinical
 Symptomatic patient
with pus discharge or
chronic unrelieved
disabling pain due to
osteomyelitis per se and
type A/B host.

52. Post sequestrectomy
 NO STABLISATION IS NECESSARY WHEN 70% OF
THE ORIGINAL CORTEX REMAINS INTACT
 If >70% cortical volume has been retained—protect by
splintage
 Greater bone loss-External fixator
 Focal bone loss-opencancellous BG/conventional BG
 Seg. bone loss—BG/Bone transport

53. Saucerization
 Extension of surgical debridement
 Debrided wounds left open widely through excision
of overhanging soft tissue andbone
 Wounds drain freely
 Abscesses do notform
 Limited to areas where it causes acceptable loss of
function e.g. Tibia and femur
 May require stabilization

54. Dead Space
 Adequate debridement may leave a large bone defect, termed a
dead space.
 It is a predisposing condition for the persistence of infection
because it is poorly vascularized.
 Appropriate management of any dead space created by
debridement is mandatory
 to arrest thedisease
 to maintain the integrity of the skeletal part.

55. Management of Dead Space:
The methods described to eliminate this dead space are
(1) bone grafting with primary or secondary closure;
(2) use of antibiotic PMMA beads as a temporary filler of the dead
space before reconstruction;

56. (3) local muscle flaps and skin grafting with or without bone
grafting;
(4) microvascular transfer of muscle, myocutaneous, osseous,
and osteocutaneous flaps; and
(5) the use of bone transport (Ilizarov technique).

57. Four basic methods of immediate, biological management of dead space using living
tissue or cancellous bone grafts.

58. Dead space management
PAPINEAU TECHNIQUE
 3 stages
STAGE I: DÉBRIDEMENT AND STABILIZATION
STAGE II: GRAFTING
STAGE III: WOUND COVERAGE
LIMITATIONS-cannot be usedwhen:
 Segmental defect >4 cm.
 Poor quality softtissue
 Poor vascularsupply

59. Muscle flaps
 Increases the blood supply to that area.
 Superior to skin flaps.
 Obliterates dead space in irregularlycontoured
osseous cavity.
 Resistance to recurrentsepsis.
 Gastocnemius mostcommon -covers proximal 1/3
of tibia , knee, distal 1/5 of femur.

60. Indications :
 Adjacent soft tissue cannot cover the area.
 Area should anatomically permit transportation of a
local muscle flap without compromising its
neurovascular bundle.
 Debridement procedure hasn’t compromised the
mechanical integrity of osseous structures.
 Gross purulence has beeneliminated.

61. Vascularized muscular &
musculocutaneous flaps
 Pedicle flap,
 freeflap

62. Vascularize bone segment
transfer
 Indications :
 restoration of bone mass with soft
tissue coverage
 >6 cm. in length
 Fibula, iliac crest, ribs, lat. Scapula,
metatarsal,lat. portion of radius.

63. Management of Dead Space:
Antibiotic Beads
 May be used to sterilize and temporarily
maintain a dead space.
 Beads are made withPMMA+antibiotics
 Cement -40 gm.
 Genta- 1-2 gm. or vanco 1-2gm.
 The gentamycin concentration remain for 30 days
after implantation.
 Usually removed within two to four weeks
and are replaced with a cancellous bone
graft.

64. Management of Dead Space:
 Use of vacuum-assisted
closure system,
 a device that applies
localized negative pressure
over the surface of wounds
and aids in the removal of
fluids.
 useful as an adjunct therapy
for high-energy soft-tissue
injuries.

65. Closed suction drains
• Modified Lautenbach method of
closed suction antibiotic ingress and
egress irrigation systems.
• An advantage of this technique is that
it allows a change in local antibiotic
delivery based on culture results
obtained from surgical biopsies.
• The technique also aids in the gradual
decrease in the size of the soft tissue
dead space

66. Soft-Tissue Coverage:
 Three methods commonlyused:
 Primary closure- if no infection
 Let tissue heal by secondary intention
 Small soft-tissue defects may be covered with a split-
thickness skin graft.
 Local muscle flaps and free vascularized muscle flaps in
the presence of a large soft-tissue defect or an inadequate
soft-tissue envelope.
 Healingby so-called secondary intention should be
discouraged, since the scar tissue that fills the defect may later
become avascular.

67. Bone Stabilization:
 If skeletal instability is present at the site of an infection,
measures must be taken to achieve stability
 External fixation is preferred over internal fixation because
of the tendency of the sites of medullary rods to become
secondarily infected and to spread the extent of the infection.
 Rigid fixation helpful in union of fracture sites.

68. Limb reconstruction:
 Ilizarov external fixation
 Is used for reconstruction of segmental defects and difficult
infected nonunions.
 Based on the technique of distraction osteogenesis
 Used for difficult cases of osteomyelitis when stabilization and
bone-lengthening are necessary.
 May also be used to compress nonunions and to correct
malunions.

69. AMPUTATION:
 Infrequently performed
 INDICATIONS
1. Malignancy
2. Arterial insufficiency
3. Nerve paralysis
4. Joint Contracture & stiffness making limb
nonfunctional

70. Complementary therapies:
 Hyperbaric oxygen:
 Augment host immunesystem
 Allow formation of peroxides
 Promote wound healing
 Electrical stimulation : For non unions with acceptable
alignment
 Types:
 direct current
 Inductivecoupling
 Capacitivecoupling
 Ultrasound: low intensity

71. Complications :
 Acute exacerbations- mostcommon
 Growth abnormalities
 Deformities
 Pathological fracture
 Joint Stiffness
 Amylodosis
 Malignancy(0.25%) –sq. cell carcinoma most
common, reticulam cell
carcinoma,fibrosarcoma
 Septic arthritis- hip, ankle, shoulder ,elbow

72. •References
1. Campbell 12th edition
2. Apleys 10th edition

73. Thank You !!!!!