Infective inflammation of the bone

1. Chronic Osteomyelitis
Dr Arvind Kumar (M. S. Ortho)
Assistant Professor and consultant

2. Definition
• Osteomyelitis is the infection of the bone or BM which leads to a
subsequent Inflammatory process.
• Micro-Organisms may reach bones via the Bloodstream or by Direct
Invasion. (e.g : skin puncture, operation, open fracture)
• Factors which affects it’s development
– Virulence of the organism involved
– Host Factors (Age, Immunity, Diseases)
– Local factors (site of Involvement, damaged muscle presence of
foreign material , vascularity)

3. • It is nearly always a sequel to acute osteomyelitis, generally secondary to
open fractures, bacteremia and contiguous soft tissue infection. It is
difficult to treat and is characterized with frequent relapses
• Occasionally infection is subacute or chronic from the beginning.
• Cause. As with acute osteomyelitis, the Staphylococcus is the usual
causative organism, but streptococci, pneumococci, typhoid bacilli, or other
bacteria may be responsible.
• Chronic osteomyelitis from contiguous soft tissue infection is becoming
more common due to increasing prevalence of diabetic foot infection and
peripheral vascular disease

5. Pathology
1. Inflammation.
• Earliest Change
• Increase interaosseous pressure leads to Pain.
2. Suppuration
• Pus at medulla >> Volkmann canals>>Surface >> Subperiosteal Abscess>>
spread along the shaft>> burst into the soft tissue
• May extend to Epiphysis in Neonates and Children.
• May extend to Interverteberal Discs in Adults.
3. Necrosis/Sequestrum
• Begin in a week.
• causes : increase in intraosseous pressure, vascular stasis, infected
thrombosis, periosteal stripping which increasingly compromise blood
supply

6. 4. New-bone formation
• New bone formation from the stripped surface of periosteum
• Bone thickens to form an involucrum enclosing the infected tissue.
5. Resolution
bone will heal if infection is controlled and intraosseous pressure is
released, though it may remain thickened. or progress to complications

7. Pathology
• It is commonest in the long bones. It is often confined to one end of
the bone, but it may affect the whole length. The bone is thickened
and generally denser than normal, though often honeycombed with
granulation tissue, fibrous tissue, or pus. Sequestra (Fragment of dead
bone) are commonly present within cavities in the bone. Often a sinus
tract leads to the skin surface: the sinus tends to heal and break down
recurrently, but if a sequestrum is present it never heals permanently.

10. Investigations
1. Lab studies
• CBC: leucocytosis
• Elevated CRP & ESR (nonspecific).
• Blood Culture
• Culture & sensitivity test; by aspiration from the subperiosteal abscess,
+ve in only 50% of patients with hematogenous osteomyelitis.
2. Radiological studies
• X-ray
• MRI
• Radionuclide bone scanning
• CT scan
• US

11. X-Ray
• 1st 10 days Show No Abnormality .
Only after two or three weeks do visible changes appear, and they may never do
so if efficient treatment is started very early.
• By the end of the 2nd Week signs of rarefaction of Metaphysis and
New Bone Formation. Then sigs of healing
• Soft-tissue edema at 3-5 days after infection.
• Bony changes are not evident for 14-21 days:
– Early radiographic signs of rarefraction (thining of bony tissue
sufficient to cause decreased density of bone) of the
metaphysis and new bone formation outlining the raised
periosteum
– Sclerosis and thickening of the bone cortex at healing
• Approximately 40-50% focal bone loss is necessary to cause
detectable lucency on plain films; a negative X-Ray does not
exclude osteomyelitis

13. Clinical Features
• a purulent discharge (the main symptom is usually a purulent
discharge from a sinus over the affected bone. Discharge of pus
may be continuous or intermittent)
• Pain may be the predominant feature
• ‘flare-up’, or ‘flare’, of infection (Reappearance of a sinus that
has been healed for some time and it is heralded by local pain,
pyrexia, and the formation of an abscess)
• On examination the bone is palpably thickened, and there are
nearly always a number of overlying scars or sinuses.

14. Clinical features
Non-specific and difficult to recognize. Raise suspicion :
• Persistent sinus tract
• Exposed bone
• Tissue necrosis overlying bone
• Chronic wound overlying surgical hardware
• Chronic wound overlying fracture
• May also present as recurrent condition with periods
of quiescence, with exacerbation, patient complaining
increasing pain at affected site

16. DIAGNOSIS : CLINICAL
DURING PERIOD OF
INACTIVITY NO SYMPTIMS ARE
PRESENT
SKIN
THIN,DARK,SCARRED,POOR
NOURISHED, PAST DINUD.OR
ULCERATION MAY BE VISIBLE
MUSCLE WAISTING
CONTRACTURE,ATROPHY
JOINT STIFFNESS BONE THICK SCLEROTIC
ABSCESS CAVITY MAY BE
PRESENT

17. Imaging
• Radiographic examination
– The bone is often thickened and shows irregular and patchy sclerosis which
may give a honeycombed appearance. If a sequestrum is present it is seen
as a dense loose fragment, with irregular but sharply demarcated edges,
lying within a cavity in the bone
• Radioisotope scanning
– increased uptake in the vicinity of the lesion
• MRI and CT scanning
– localisation of abscess cavities and sequestra in diffuse disease, thus
allowing accurate planning of operative treatment.

19. DIAGNOSIS :
BONE SCANS

20. SURGICAL
TREATMENT

21. BONE
DEBRIDMENT

22. SAUCERIZATION

23. SEQUESTEREECTOMY

24. SEQUESTERECTOMY …WHEN?????
EARLY : IF PATIENT
PRESENTS EARLY
SEQUESTERECTOMY
ERADICATES INFECTION
AND LEAVES ABETTER
ENVIORNMENT FOR
PERIOSTEUM TO
RESPOND
LATE : IN CASES OF LATE
PRESENTATION THE
PROCEDURE IS DELAYED
TILL FORMATION OF
INVOLUCRUM TO
MINIMIZE RISK OF
FRACTURE AND
SEGMENTAL LOSS
IN EITHER CASES IT IS
CRITICAL TO PRESERVE
NVOLUCRUM
3-6 MONTHS IS
CONSIDERED AS A
PREFFERABLE TIME TO
WAIT

25. POST
SEQUESTERECTOMY
NO STABILISATION NEEDED IF 70% OF THE
ORIGINAL CORTEX REMAINS INTACT
IF MORE THEN 70% LOSS IS SEEN MANY
SPLINTAG OPTIONS AS:
A) CASTING
B) EXTERNAL FIXATORS
C) IF FOCAL BONE LOSS : OPEN CANCELLOUS/
CONVENTIONAL BONE GRAFTS
D) IF SEGMENTAL BONE LOSS: BONE
TRANSPORT AS ILLIZAROV DEVICES MAY BE
USED

26. MANAGEMENT OF THE DEAD
SPACE

27. THE OPTIONS
TO FILL THE
SPACE?

28. PAPINEAU
TECHNIQUE

29. PMMA
ANTIBIOTI
C BEADS

30. DURATION OF
BEADS
IMPLANTATION??

31. INTRAMEDULLARY
ANTIBIOTIC NAIL

32. CLOSED
SUCTION
DRAINS

33. VACCUM ASSISTED
PRESSURE
SYSTEMS

34. BONE
STABILIZATION

35. SOFT
TISSUE
COVERAGE
THREE METHODS ARE COMMONLY USED
PRIMARY CLOSURE- IF NO INFECTION
HEALING BY SEACONDRY INTENTION
SPLIT SKIN GRAFTING FOR SMALL SOFT TISSUE
DEFECTS
LOCAL MUSCLE FLAPS /FREE VASCULARIZED
MUSCLE FLAPS FOR LARGER DEFECTS
HEALING BY SEACONDRY INTENTION THOUGH
NOT PREFFERED AS SCAR TISSUE FORMED MAY
BE AVASCULAR

36. LIMB
RECONSTRUCTIO
N

37. AMPUTATION

38. ADJUNCT
THERAPIES

39. COMPLICATIONS
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40. Thank You
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