Osteomyelitis may be a very dreadful condition for both the suffering patient & the treating orthopaedic surgeon.Here is the brief presentation on it deeply focused on its standard management.

2. MANAGEMENT
OF
OSTEOMYELITIS
MAJ (DR) JANE ALAM MAMUN
DEPT OF ORTHOPAEDIC SURGERY
COMBINED MILITARY HOSPITAL
DHAKA , BANGLADESH

3. INTRODUCTION
 Osteomyelitis is the infection bone (osteon)
and bone marrow (myelo ).
 Auguste Nelaton coined the
term osteomyelitis in 1834.

4. CLASSIFICATIONOFOSTEOMYELITIS
 According to Duration & Clinical course:
 Acute Osteomyelitis (< 2 weeks)
 Sub acute Osteomyelitis(2-6 weeks)
 Chronic Osteomyelitis ( >6 weeks)
 According to aetiology:
 Bacterial/viral/ Fungal/ Parasitic osteomyelitis
 According to route of entry:
 Haematogenous/ Post-traumatic/ Contagious

5.  Chronic Osteomyelitis:
 Chronic pyogenic osteomyelitis— Sequel of acute
pyogenic osteomyelitis
 Chronic post operative or post traumatic
osteomyelitis
 Chronic osteomyelitis of insidious onset:
 Tubercular osteomyelitis.
 Chronic non-suppurative osteomyelitis
CLASSIFICATIONOFOSTEOMYELITIS

6. OSTEOMYELITIS
 The causative organisms in both adults and children is usually:
 Staphylococcus aureus (found in over 70% of cases)
 Streptococcus pyogenes which is found in chronic skin
infections,
 Group B streptococcus (S. agalactaie) especially in
newborn
 S. pneumoniae.
 Gm negative : E.Coli, Pseudomonas, Proteus, anaerobes
Bacteroids
• In children between 1 and 4 years of age
 Haemophilus influenzae
• Sickle cell disease : SalmonellaTyphi
• Drug users: Pseudomonas

7. OSTEOMYELITIS
 Microorganism
spread by:
 indirect spread via
the bloodstream
 direct spread from a
contiguous focus of
infection
 direct introduction
through the skin

8. ACUTEHAEMATOGENOUSOSTEOMYELITIS
Age:
 Can occur at any age
 Infants and children are
most commonly affected.
Sex:
 Male:Female= 4:1.
Site:
 Most common site is the
metaphyseal area of long
bones (Distal femur,
proximal tibia, proximal
humerus)

9.  Stages:
1. Stage of Inflammation
2. Satge of Suppuration
3. Stage of Necrosis
4. Stage of New bone formation
5. Stage of Resolution or Intractable chronicity
PATHOLOGY

10. PATHOLOGY
Bacteremia>Organisms once
localized in bone> proliferate>
induce inflammatory reaction
and cause cell death.
Bone necrosis & Pus is formed
within bone by 2nd or 3rd day
Pus can spread throughout the
Volkman’s cannal and reach the
periosteum
Subperiosteal abscess
-Along the shaft
-Re enter into bones
-Rupture of periosteum and the
formation of draining sinus.

11. PATHOLOGY
Bacteremia>Organisms once
localized in bone> proliferate>
induce inflammatory reaction
and cause cell death.
Bone necrosis & Pus is formed
within bone by 2nd or 3rd day
Pus can spread throughout the
Volkman’s cannal and reach the
periosteum
Subperiosteal abscess
-Along the shaft
-Re enter into bones
-Rupture of periosteum and the
formation of draining sinus.

12. Segmental bone necrosis sequestrum (dead
piece of bone)
After first week of infection chronic inflammatory
cells become more numerous
Cytokines from leukocytes stimulates osteoclastic
bone resorption ingrowth of fibrous tissue
deposition of reactive bone in the periphery
Reactive woven or lamellar bone which forms
sleeve of living tissue surrounding dead bone is
called as involucrum.(New bone formation)
Pus & sequestrum discharge through Cloacae to
skin giving rise to chronic discharging sinus

14. CLINICALFEATURES
Infants:
 Drowsy
 Fail to thrive
 Irritable
 Infection foci
(umblical
cord )
 O/E:
 Metaphyseal
tenderness
 Resistance
to
movement
 Features of
septic
arthritis
Chindren >4yr:
 Pain
 Fever
 Refusal to bear
weight
 O/E :
 Tachycardia
 Raised temp
 Localized
tenderness and
restricted
movement
Adults :
Haematogenous
spread common
in Thoraco-
lumber spine
associated with
fever, local
tenderness and
backache.
C
a
r
d
i
n
a
l

15. INVESTIGATION
 LAB Inv :
 CBC : Leucocytosis, Hb may be decreased
 ESR : raised within 24-48 hrs
 CRP : raised within 12-24 hrs
 Blood Culture
 Pus or Fluid C/S

16. INVESTIGATION
 X-ray:
1st wk :
• No bony abnormality
• Sometime soft tisue swelling
2nd wk onward:
• Faint extra cortical outline
due to periosteal new bone
formation
Late:
 Periosteal thickening
more
 Patchy rarefaction of
metaphysis

17. INVESTIGATION
 USG:
 Sub periosteal collection
• CT SCAN :
 Planar bone definition
 MRI :
 More useful in axial
skeleton
 Bone marrow
inflammation
 Early diagnosis
 Radionuclide scanning

18. TREATMENT
 If osteomyelitis is suspected on clinical grounds
treatment started immediately without waiting
for final confirmation of the diagnosis.
 There are 04 important aspects to the
management :e patient:
1. Appropriate antimicrobial therapy (first emperical,
then specific)(IV for 2-3 wks then orally for 4-6 wks)
2. Surgical drainage if required
3. Splintage and rest of the affected part
4. Supportive treatment for pain and dehydration

19. AntimicrobialTherapy
Upto 6 month
3rd generation
Cephalosporin
,Cefotaxime
+
Flucloxacillin
or
Flucloxacillin +
Benzylpen(Gm
positive
Streptococcus)+
Gentamicin (Gram
negative cover)
6months to
6years
Cefotaxime/
Cefuroxime
+
Flucloxacillin
Older child &
Adult:
Flucloxacillin,
Fusidic acid/
Benzylpenicillin

20. AntimicrobialTherapy
Elderly &
previously unfit
patient
3rd generation
Cephalosporin
+
Flucloxacillin
+
Gm negative
cover
With Sickle cell
disease
Added
Salmonella cover
by
Fluoroquinolone
(Ciprofloxacin)
MRSA infection:
(ward/hospital
induced)
I/VVancomycin
orTiecoplanin
with 3rd
generation
Cephalosporin

21. Drainage
 Not required if antibiotic
can be started within
48hrs
 If antibiotic doesn’t
response within 36hrs
and
 sign of persistent deep
pus collection, drainage
is mandatory
Splintage
 Hip: Simple skin traction
 Other limbs : Slab/ half
cylindrical cast
Supportive Rx
 Rest
 Analgesics
 Antipyretics
 Fluid
TREATMENT

22. SUBACUTEHAEMATOGENOUS
OSTEOMYELITIS
 Usually a child or adolescent who
has had pain near one of the larger
joints for several weeks or even
months
 distal femur and the proximal and
distal tibia are the frequent sites
 Usually insidious onset with mild
to moderate S/S
 The typical radiographic lesion is a
circumscribed, round or oval
radiolucent ‘cavity’ surrounded
by a halo of sclerosis (the classic
Brodie’s abscess)

23. SUBACUTEHAEMATOGENOUS
OSTEOMYELITIS
 Treatment may be conservative if the diagnosis is not in
doubt.
 Immobilization and antibiotics (flucloxacillin and fusidic acid)
intravenously for 4 or 5 days follwed by orally for another 6
weeks usually result in healing, though this may take up to 12
months.
 Open biopsy
 Curettage

24. POST-TRAUMATICOSTEOMYELITIS
 Most common cause of
osteomyelitis in adults usually in
open fractures
 Anaerobic organisms also
appears in contaminated wounds.
 Prophylactic antibiotic
(Flucloxacillin+ Benzylpenicillin or
Fusidic acid),
 Thorough cleansing and
 Debridement,
 Drainage by leaving the wound
open,
 Immobilization of the fracture and
further antibiotics.

25.  Soft tissue management and repeat
debridement is required if there is evidence
of inadequate debridement or infection.
 Stable implants should be left in place until
the fracture had united
 External Fixation is a very good option
remaining access of wound debridement &
dressing
POST-TRAUMATICOSTEOMYELITIS

26. CHRONICOSTEOMYELITIS
 It is the dreaded sequel to acute haematogenous
osteomyelitis or following open fracture or any bony
operation.
 The usual organisms (usually polymicrobial)
 Staphylococcus aureus
 Streptococcus pyogenes
 Escherichia coli
 Proteus mirabilis
 Pseudomonas aeruginosa
 In the presence of foreign implants, Staphylococcus epidermidis

27.  Clinical features:
 Chronic discharging
sinus
 If flare/recurred
 Pain, pyrexia, redness,
tenderness
 PostTraumatic
 Deformity of bone or
shortening
 Malunion/Non union
 Pathological fracture
 Systemic manifestation
of primary disease like
TB
CHRONICOSTEOMYELITIS

28. STANGINGOFCHRONICOM
(Cierny&Madar)
 Stage 1 or 2,TypeA most
likely to be benefited
 Type B & Stage 1–3 have
a reasonable chance of
recovery patients
 Type C patients have
poor outcomes
 Stage 4 operative
treatment may be
contraindicated

29.  Local X-ray:
 Involved bone becomes thicker and
irregular
 Cortex and medulla may not be
differentiated
 Bone resorption---Patchy loss of
density with thickening and sclerosis
of surrounding bone
 Sequestrum can be seen as an
isolated, more radio-opaque piece of
bone
CHRONICOSTEOMYELITIS (INV)

30.  Other Inv:
 Sinogram : localize the site
of infection
 Radioisotope scintigraphy
 CT or MRI – more helpful
for planning of operative
treatment
 CBC, ESR, CRP may raise in
flare
 Wound swab C/S from
deeper tissue is helpful for
antibiotic choice
 Though 20% C/S shows
negative result PCR can be
done there
CHRONICOSTEOMYELITIS (INV)

31. TREATMENT OF CHRONIC OM
Combination of
Medical & Surgical treatment:
A. ANTIBIOTICTHERAPY
B. LOCALTREATMENT
C. SURGERY
TREATMENTOFCHRONIC
OSTEOMYELITIS

32. A. ANTIBIOTIC
 Used to suppress the infection, prevent spread &
control flare
 Fusidic acid, clindamycin and the cephalosporins are
good choice
 Vancomycin and teicoplanin are effective in (MRSA)
 Antibiotics should given for 4–6 weeks before
considering operative treatment
 Continuous collaboration with a specialist in
microbiology is important.
TREATMENTOFCHRONIC
OSTEOMYELITIS

33. B. LOCALTREATMENT
 Regular dressing of discharging sinus.
 Use of Colostomy paste.
 An acute abscess may need urgent incision and
drainage as a temporary measure.
TREATMENTOFCHRONIC
OSTEOMYELITIS

34. C. SURGERY
Indications :
 chronic haematogenous
infections : intrusive symptoms,
failure of adequate antibiotic
treatment, and/ or clear
evidence of a sequestrum or
dead bone (Sequestrectomy &
Saucerization> cancellous bone
graft)
 for post-traumatic infections:
an intractable wound and/or an
infected nonunited fracture;
 For postoperative infection:
similar criteria and evidence of
bone erosion.
TREATMENTOFCHRONIC
OSTEOMYELITIS

35. 1. Debridement
2. Dealing with dead space
3. Soft tissue cover
4. Aftercare
TREATMENTOFCHRONIC
OSTEOMYELITIS

36. 1. Debridement:
 The wound is inspected after 3 or 4 days and, if there are renewed
signs of tissue death, the debridement may have to be repeated
TREATMENTOFCHRONIC
OSTEOMYELITIS

37. 2. Dealing with the dead space:
 Porous antibiotic- impregnated
beads can be laid in the cavity
and left for 2 or 3 weeks and
then replaced with cancellous
bone grafts.(practically
Vancomycin+Meropenem
impregnated cancellous bone
graft
 Papineau technique
 Lautenbach approach
 Refractory infection associated
with non-union after fracture,
Ilizarov method
TREATMENTOFCHRONIC
OSTEOMYELITIS

38. TREATMENTOFCHRONIC
OSTEOMYELITIS
3. Soft-tissue cover
 by STSG or local
musculocutaneous flaps, or
free vascularized flaps,
 Vacuum-assisted closure
(VAC) may help when the
deep infection is solved
4. Aftercare
 local trauma must be
avoided
 any recurrence of
symptoms, however
slight, should be taken
seriously and investigated

39. CONCLUSION
Osteomyelitis has long been one of the most
difficult and challenging problems confronted by
orthopaedic surgeons. The key to successful
management is early diagnosis and appropriate
surgical and antimicrobial treatment. A
multidisciplinary approach is required, involving
an orthopaedic surgeon, an infectious disease
specialist, and a plastic surgeon in complex cases
with significant soft-tissue loss.