Chronic om

1. Chronic OSTEOMYELITIS

2. Definition
Osteomyelitis is infection of bone and frequently seeds in trabecular
areas affecting both bone and bone marrow. – APLEY

3. Host Susceptibility( Risk Factor) to Infection
• Local factors ; trauma, scar tissue, poor circulation, diminished
sensibility, chronic bone or joint disease and the presence of foreign
bodies (e.g implants)
• Systemic factors ; malnutrition, general illness, debility, diabetes,
rheumatoid disease, corticosteroid administration and
immunosuppression person.

4. Type of Osteomyelitis
1) Acute Haematogenous Osteomyelitis
2) Sub-acute Haematogenous Osteomyelitis
3) Post- Traumatic Osteomyelitis
4) Chronic Osteomyelitis

5. Acute vs Chronic
Acute:
 Children
 Certain adults (immunocompromised ,
local trauma, drugs addicts((heroin)))
 Common pathogen : Staphylococcus
aureus, H. influenza (in children)
 The infection develops two weeks of an
injury
Chronic:
 Children (chronic may follow on acute)
 Adults (open fracture , operation)
 Common pathogen:
S. aureus ,E. coli, S. pyogenes, Proteus,
Pseudomonas
S. epidermidis (surgical implants)
 The infection starts at least two months of an
injury
SUBACUTE
OSTEOMYLISTIS

6. Pathogenesis
• Inflammation
• Suppuration
• Necrosis
• New bone formation
• Resolution

7. 1. Inflammation
• Earliest change in the metaphysis is acute
inflammatory reaction with vascular congestion,
exudation of fluid and infiltration by
polymorphonuclear leucocyte.
• The intraosseous pressure rises rapidly, causing
intense pain, obstruction to blood flow and
intravascular thrombosis.

8. 2. Suppuration
• By the second or third day, pus forms
within the bone and forces its way along the
Volkmann canals to the surface where it
produces a subperiosteal abscess.
• From the subperiosteal abscess, pus can
spread along the shaft, to re-enter the bone
at another level or burst into the
surrounding soft tissues.

9. 3.Bone necrosis
• By the end of a week there is
usually microscopic evidence of bone
death.
• With the gradual in-growth of
granulation tissue, the boundary
between living and devitalized bone
becomes defined.
• Pieces of dead bone may separate
as sequestra.

10. 4.Reactive new bone formation
• if the pus is not released, new bone
starts forming on viable surfaces in
the bone and from the deep layers of
the stripped periosteum.
• With time, this new bone thickens to
form involucrum, enclosing the
sequestrum and infected tissue.
• If the infection persists, pus and tiny
sequestrated spicules of bone may
discharge through cloacae in the
involucrum and track by sinuses to
the skin surface.

11. 5. Resolution & healing
• If the infection is controlled and intraosseous pressure released at an early
stage, this dire progress can be halted.
• • The bone around the zone of infection becomes increasingly dense; this,
together with the periosteal reaction, results in thickening of the bone
• • If healing does not occur, a nidus of infection may remain locked inside
the bone, causing pus and sometimes bone debris to be discharged
intermittently through a persistent sinus.

12. Chronic OM
• This used to be the dreaded sequel
to acute haematogenous
osteomyelitis; nowadays, it more
frequently follows an open fracture or
an operation.
• The causative organisms:
– Staphylococcus aureus, Escherichia
coli, Streptococcus pyogenes, Proteus
mirabilis and Pseudomonas aeruginosa
– Staphylococcus epidermidis -
presence of foreign implants

13. Predisposing factors
• Untreated acute osteomyelitis
• Dead and dying bone around the focus of infection
• Poor penetration of new blood vessels

14. Clinical features
• Pain
• Fever
• Redness
• Tenderness
• Discharging sinus (seropurulent) with excoriation of surrounding skin
• Tissue become thick and folded inward at the site of scar or sinus
that adhere to underlying bone (long standing case)
• In post-traumatic OM will lead to deformed or ununited bone

16. CHRONIC OSTEOMYELITIS
XRAY
 Bone resorption 
either as a patchy loss
of density or as frank
excavation around an
implant
 Thickening and
sclerosis of the
surrounding bone.
CT and MRI
 Extent of bone
destruction,
reactive oedema,
hidden
abscesses and
sequestra.
IMAGING
 Acute flares  ESR and
WBC levels may be
increased.
 Organisms cultured from
discharging sinuses
should be tested
repeatedly for antibiotic
sensitivity.
LABORATORY
INVESTIGATIONS

18. Subperiosteal
abscess
Sequestrum
Involucrum
Periosteal
reaction

19. TREATMENT
• ANTIBIOTIC
 Chronic infection is seldom eradicated by antibiotics alone.
 Bactericidal drugs  Stop the spread of infection to healthy bone and control acute flares.
 Choice of antibiotic  Capable of penetrating sclerotic bone and non-toxic with long-term
use.
 Example: fusidic acid, clindamycin and cephalosporins.
 MRSA  Vancomycin
 administered for 4–6 weeks (starting from the beginning of treatment or the last
debridement) before considering operative treatment.
 If surgical clearance fails, antibiotics should be continued for another 4 weeks before
considering another attempt at full debridement.

20. • LOCAL TREATMENT
 A sinus may be painless and need dressing simply to protect the clothing.
 An acute abscess may need urgent incision and drainage but this is only a
temporary measure.
TREATMENT

21.  SURGERY
 INDICATION FOR RADICAL SURGERY
 Chronic haematogenous infections
 Intrusive symptoms, failure of adequate antibiotic treatment, clear evidence of a
sequestrum or dead bone.
 Post-traumatic infections
 An intractable wound and/or an infected ununited fracture.
 Postoperative infection
 Presence of a foreign implant
 prompt surgical intervention to remove the implant, whether in case of internal
fixation or substitution.
TREATMENT

22. • Debridement
 All infected and dead soft tissue, devitalized bone or any infected
implant must be excised.
 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.
 Antibiotic cover is continued for at least 4 weeks after the last
debridement.
TREATMENT

23. • Grafting
Porous
antibiotic
Porous gentamicin impregnated beads laid in the cavity and left
for 2 or 3 weeks  replaced with cancellous bone grafts.
Papineau
technique
The entire cavity is packed with small cancellous chips, mixed
with an antibiotic and a fibrin sealant.
Muscle flap
transfer
In suitable large wad of muscle with its blood supply intact can
be mobilized and laid into the cavity  the surface is later
covered with a split-skin graft.
Lautenbach
approach
Radical excision of all avascular and infected tissue  closed
irrigation and suction drainage  appropriate antibiotic
solution in high concentration to allow the ‘dead space’ to be
filled by vascular granulation tissue.
 In refractory cases, it may be possible to excise the infected
or devitalized segment of bone completely then close the gap
by the Ilizarov method.
 This is especially useful if infection is associated with non-
union after fracture

25. • Soft tissue cover
 Small defects  split thickness skin grafts.
 Larger wounds  local musculocutaneous flaps or free vascularized flaps.
 Vacuum-assisted closure (VAC) may help when the deep infection is solved,
not before.
 After care
 Local trauma must be avoided
 Any recurrence of symptoms however slight, should be taken seriously and
investigated.
TREATMENT

26. References
• APLEY and SOLOMON’S 10th EDTION (SYSTEM OF ORTHOPAEDICS
AND TRAUMA )