osteoarticular tuberculosis -general consideration and principles of management

1. Tuberculosis of bones and
joints

2. General consideration
1. Tuberculosis is still endemic disease in developing country
2. It is estimated that India alone has got one fifth global burden of
tuberculosis.
3. India Rank 1 in world total tuberculosis case load
4. After Lung and lymph node, bone and joints is the next most
common site of tuberculosis in the body.

3. Bone and joints tuberculosis
• Spine most commonly affected, 50% of all cases of osteoarticular
tuberculosis.
• Next in order of frequency Hip, Knee, elbow, foot, hand, shoulder, bursal
sheath and others
• Tubercular osteomyelitis affect end of long bone, (unlike pyogenic OM
metaphysis) this is the reason behind early involvement of joints in TB
osteomyelitis.

4. • Spine/ Pott’s spine
• Joints - Tubercular arthritis (MC Hip)
• Long and flat bones - Tubercular osteomyelitis (MC tibia)
• Short bones – Tubercular dactylitis / spina ventosa
• Tendon sheath ( MC flexor and wrist) & bursae

6. Etiology
• Common causative organism is Mycobacterium tuberculosis.
• Osteoarticular tuberculosis is always secondary to some primary
focus in lung, lymphnode etc
• Mode of spread from primary focus either haematogenous or by
direct extension from adjacent viscera.

7. Pathology
• Tubercular infection leads to chronic granulomatous inflammation with caseation
necrosis.
• The response to tubercular infection may be proliferative, exudative or both
• Proliferative response:- commoner leads to chronic granulomatous
inflammation, heal with fibrosis.
• Exudative response:- in some cases, malnourished, immunodeficient etc
extensive caseation necrosis without much cellular reaction.

8. Pathogenesis cont..
• Sequestration & peri-osteitis are not very common (unlike pyogenic
infections)
• Ischemic necrosis and end arteritis may result in a very small
sequestrum which is usually not visible radiologically (unless calcified)
• Granulation tissue spreads onto the free surface of cartilage eroding it
in patches, later causing loosening and separation of the cartilaginous
tissue as it proceeds causing necrosis of cartilage with erosion of
exposed bone.

9. Osteolytic lesion with a small sequestrum

10. • Marginal erosions are common in TB of weight bearing joints (hip,
knee, ankle)
• Necrosed cartilage and fibrinous material form ‘rice bodies’ in
synovial joints, tendon sheaths and bursae.
• Abscesses that form may track along the fascia planes and form
sinuses

12. • Can be divided into 4 pathological stages –
1. Inflammatory edema & exudates (pre-destructive stage)
2. Necrosis & cavitation
3. Destruction & deformation
4. Healing & repair

13. • Insidious onset
• Low grade fever
Weight loss
Night sweat
• Movement restriction, muscle wasting, regional
lymph node involvement and neurologic symptoms
Clinical features

14. Principles of management

15. • Relative lymphocytosis, a low level of hemoglobin and
a raised ESR are found in active tubercular disease
• The Mantoux test is non-diagnostic in an endemic
region and may be negative in an immuno-deficient
individuals
• The sensitivity of AFB staining may vary from 25 to 75
%
Laboratory investigations

16. • Synovial fluid aspiration – routine, microscopy, culture
• Biopsy (needle/open) – culture and histopathology
• Culture of AFB requires a long incubation period of 4 to 6 weeks,
although Bactec radiometric culture takes < 2 weeks

17. Serological tests
• Non-diagnostic in lesions with a low level of bacilli
• IgG and IgM titres show significant differences between
the initiation of treatment and at three months later (can
be used for follow up)
• PCR -
efficient and rapid method of diagnosis
can differentiate between typical and atypical mycobacteria
However, a positive result is not a substitute for culture
NOT indicative of the activity of the disease
does not differentiate live from dead microorganisms

18. • Radiography
• USG
• CT
• MRI
• Nuclear imaging
Imaging modalities

19. AP and lateral views of the involved region
radiograph of the chest
Radiological stages –
1. Stage of synovitis
2. Stage of arthritis
3. Stage of advanced arthritis
4. Stage of healing
Radiography

20. 1. Stage of synovitis:
• Soft tissue swelling and joint widening due to effusion and
synovial hypertrophy
• The first radiological sign may be juxta-articular
osteoporosis.
• If there is secondary superadded infection, subperiosteal
reaction may result.
• As a result of localized hyperemia growth plate may show
overgrowth, especially in childhood.

21. 2. Stage of arthritis:
• Articular margin and bony cortices become hazy (blurring and
fuzzy) giving rise to "washed out appearance“
• Narrowing of joint space (involvement of articular cartilage)
• “Phemister Triad”
juxta-articular osteopenia,
peripherally located osseous lesions and
gradual narrowing of joint space
are considered pathognomonic of tubercular osteoarthritis
Early loss of articular joint space is more typically seen in
rheumatoid arthritis and thus helps in differentiating from
tuberculosis.

22. 3. Stage of advanced arthritis:
• Collapse
• subluxation or dislocation
• migration of bone
• deformity of joint

23. 4. Healing –
• Re-mineralization
• Cortical and articular margins become distinct
• Fibrous ankylosis may occur during healing phase
(pyogenic arthritis – bony ankylosis)
• In contrast to pyogenic arthritis, the development of bone
ankylosis is uncommon in tubercular arthritis

24. • Helpful in the evaluation of large joints
• Demonstrates joint effusion, synovitis and capsular
thickening
• Soft tissue abscess like psoas abscess
• Cortical disruption & irregularity of articular margins
• Guided joint fluid aspiration or synovial biopsy is
possible
USG

25. • Lytic areas and marginal erosions seen much before
plain radiographs
• Swelling in soft tissues, granulation, exudations,
abscess and early calcification can also be
demonstrated much earlier
• Joint space better evaluated by CT
• Computed tomography guided aspirations and needle
biopsy for difficult areas like sacroiliac joints
CT

26. • MRI may be helpful in characterizing the lesion as
tubercular when the radiographs are normal
• MRI helpful in detecting
bone marrow inflammation,
Skip lesion in potts spine
intra-osseous abscess,
sequestrum,
cortical destruction,
cloaca and sinus tract formation
MRI

27. • Chondral lesions and subchondral bone erosions may
be visible at a stage when the joint space is still well
preserved.
• Penumbra sign - A thin intermediate signal intensity
rim along the periphery of a bone or soft tissue
abscess on unenhanced T1 -weighted images, due to
layer of granulation tissue along its wall. It is useful in
identifying soft tissue abscesses.

28. • Tenosynovitis may be seen
• Bursitis may be seen as distended bursa or multiple
small abscesses.
• Repeat imaging can be helpful in follow-up and if there
is deterioration, then a representative biopsy is
mandatory from the area.

29. • Fluid loculations
• Enhancing synovium
• erosions

30. • The pre-destructive stage can be visualized by MRI and also
probably by bone scans.
• Isotope bone scan or MRI may reveal subclinical active lesion in
40 % of patients in addition to the presenting lesion.
• Out of technetium-99m, gallium-67 and indium-111 isotopes
used in skeletal scintigraphy, technetium-99m is the most
sensitive, though not specific.
• Positive scan helps in localizing and for follow-up.
• 18Fluorine fluorodeoxyglucose-positron emission tomography
(18F-FDG- PET) has also been found useful in localizing
tubercular disease and in differentiating soft tissue infection
from osseous infection
Nuclear imaging

31. Treatment
• Aim is to control infection and care of disease part.
• Most case respond with conservative therapy few needs surgical
intervention

32. Conservative treatment
• Rest
• Traction/ proper positioning of affected part
• Antitubercular drugs
• Building up the patient resistance
Later- mobilization, physiotherapy, protected weight bearing.

33. Treatment: Rest
• Thomas urged that TB should
be treated by rest – which
had to be ‘prolonged,
uninterrupted, rigid and
enforced’.
HughOwenThomas

34. Treatment; Rest
• Traction
• Provides rest of the joint
• Relieves muscle spasm
• Prevents and corrects deformity
• Maintains joint space
• Minimises chance of developing deformity

35. Anti- tubercular drugs
• First Line Anti-Tubercular Drugs
• Isoniazide (H) 5mg/kg
• Rifampicin (R) 10mg/kg
• Pyrazinamide (Z) 30mg/kg
• Ethambutol (E) 15-20 mg/kg
• Streptomycin (S) 15mg/kg

36. Second-Line Anti-Tubercular Drugs
Parenteral agent
• Kanamycin (Km) 15mg/kg 15mg/kg1515mg/kg15mg/kg 15mg/kg
• Amikacin (Amk) 15mg/kg
• Capreomycin (Cm) 15mg/kg
Fluoroquinolones
• Levofloxacin (Lfx) 15mg/kg
• Moxiflxacin (Mfx) 7.5-10mg/kg
• Gatiflxacin (Gfx) 15mg/kg
• Oflxacin (Ofx) 15mg/kg
Oral Bacteriostatic Drugs
• Ethionamide (Eto) /Prothionamide (Pto) 15mg/kg
• Cycloserine (Cs) Terizidone (Trd) 15mg/kg
• p-aminosalicylic acid (PAS) 300mg/kg

37. • Group 5 Drugs
• Clofazimine (Cfz)
• Linezolid (Lzd)
• Amoxicillin/clavulanate (Amx/Clv)
• Thioacetazone (Th)
• Clarithromycin (Clr)
• Imipenem (Ipm)

38. •TMC207 (Bedaquiline) &
•OPC-67683 (Delamanid) : Phase III
research

39. TB disease category Intensive
phase
Continuation
phase
All forms of PTB and EPTB except TB
meningitis and osteoarticular TB
2RHZE 4RH
TB meningitis,
osteoarticular TB
2RHZE 10RH
New WHO Recommended regimen

40. Surgical treatment
• Aim –
• To establish diagnosis
• To prevent joint destruction
• To decrease bacterial loads (remove necrotic/ infected material )
• To correct deformity
• To achieve stability
• To achieve mobility

41. Surgical treatment
• Biopsy
• Curretage of lesion
• Joint debridement
• Synovectomy
• Osteotomy
• Decompression and spinal fusion
• Arthrodesis
• Arthroplasty

42. Any question???????