This document summarizes a post graduate seminar on skeletal tuberculosis. It discusses the etiology, pathogenesis, clinical presentation, investigations and management of skeletal tuberculosis. Mycobacterium tuberculosis commonly affects the lungs but can spread to bones and joints. Skeletal tuberculosis is transmitted through airborne droplets and causes chronic granulomatous lesions. Symptoms include low grade fever, pain and swelling. Investigations include x-rays showing bone destruction, biopsy to identify tubercles, and cultures. Treatment involves antitubercular drugs administered under DOTS guidelines for 6-8 months. Surgery may be needed for complications or neurological involvement. Proper treatment can cure tuberculosis in most cases.

1. POST GRADUATE SEMINAR
Topic:- Skeletal Tuberculosis-General Aspect
Date- 02-03-2016
Presenter- Moderator-
Dr. Baharul Islam Choudhury Dr. P.
Tahbildar
PGT, Orthopedics Proff & HOD
Date – 02- 03- 2016

2.  It is a chronic granulomatous disease caused by bacteria of
“Mycobacterium Tuberculosis” complex.
 The disease usually affects the lungs, although other organs like
viscera, spine,bone, joint, CNS, tendon sheath & bursae.
 It is transmitted through the airborne spread of droplet nuclei
produced by patient with infectious Pulmn.TB.
 If properly treated, it is curable in virtually all cases, but if
untreated, the disease may be fatal within 5 yrs in 50-60% of cases.

6. REGIOLNAL DISTRIBUTION

7.  The etiological agent is ‘Mycobacterium Tuberculosis complex’.
 These are aerobic, nonmotile, noncapsulated,
nonsporing.
 These are rod shaped of about 3 by .5 micro m in
size occurring singly, in pairs or in small clumps.
 These are called acid fast baciilli or ‘AFB’.
 These are slow growing , generation time of
about 15-20 hrs.
 Optimum temperature for growth is 37 deg.C
& growth does not occur < 25 deg & > 50 deg C.

8. PATHOLOGY & PATHOGENESIS
 The skeletal TB is result from hematogenous dissemination from a
primarily infected focus.
 Reaches the skeletal system through arteries or in axial skeleton
through ‘Batson’s plexus of veins’.
 Simultaneous involvement of paradiscal part of 2 contiguous
vertebrae lends support to insemination of bacilli through common
blood supply to this region.
 7% of cases of spinal TB had “skipped lesion” & 12% had
involvement of other bone & joints.

9. PATHOLOGY & PATHOGENESIS
 Osteo articular TB

10. TUBERCLE

11. PATHOLOGY & PATHOGENESIS

14.  May resolve completely
 May heal completely with residual deformity.
 The lesion may be completely walled off & caseous tissue may be
calcified.
 A low grade chronic fibromatous granulating lesion may persist with
grumbling activity.
 The lesion may spread locally or systemically in immunocompromised
patient.

15.  Draws the attention to a mild focus.
 May activate a latent tubercular focus.
 Repeated mechanical strain -> minor hematoma or bone marrow
edema -> determine the frequent localization.

16.  Human immune response is very effective for which only 5%
develops clinically evident primary disease & further 5% so develops
post primary disease.
 The helper subset of T-Lymphocytes is central to cell mediated
immunity against tuberculous infection.

17.  Extensive surgery & use of metal implants offered a favorable nidus
for localization of circulating mycobacteria.
 There is some inflammatory changes in the peri-implant tissue due
to immunological & macrophagic reaction offers a favorable nidus for
circulating mycobacteria.

18. TYPES OF THE DISEASE
 A)- Caseous exudative type- Characterized by more
destruction, more exudation & abscess formation.
 B)- Granular type- Less destructive & abscess formation is
rare.
The lesion in children is caseous exudative type, where as in
adult it is a granular type.

19. STAGES OF ARTICULAR TB
I Synovitis Movement > 75%, soft tissue swelling,
osteoporosis.
II Early arthritis Movement 50 – 75%, moderate diminution of joint
space & marginal erosion.
III Advanced
arthritis
Loss of movement > 75%, marked diminution of
joint space & destruction of joint surface.
IV Advanced
arthritis with
subluxation/defor
mity
Loss of movement > 75% , joint is disorganized
with subluxation / dislocation.
V Afterwarth of
gross arthritis
Gross deformity & ankylosis. Degenerative
osteoarthrosis.

20. TYPES OF SPINAL LESION
I)- Central type Skipped lesion in the vertebral column,
associated with tubercular meningitis due to
spread of infection through Batson’s
perivertebral plexus of vein.
II)- Paradiscal type Vertebral lesion associated with tubercular foci in the
extremities due to spread by way of arteries.
Destruction of adjacent bone end plate &
diminution of intervening disc.
III)- Anterior type Involvement of vertebral body due to extension of
abscess beneath the anterior longitudinal ligament &
the periosteum.
IV)- Posterior type Involvement of pedicle , laminae, transverse orocess
or spinous process.

22. STAGES OF NEUROLOGICAL DEFFICIENCY

23. PREDISPOSING FACTOR
 Poor socio-economic status.
 Corticosteroid therapy.
 Alcoholism.
 Prolonged illness.
 Diabetic state.
 Anticancer chemotherapy.
 Immunosupressive therapy.
 Old age.

24. GENERAL CLINICAL PICTURE
 Low grade fever.
 Lassitude.
 Anorexia.
 Loss of weight.
 Night sweats.
 Pain ( night cries).
 Swelling.
 Sinus formation.
 Muscle wasting.
 Tachycardia.
 Anemia.
 Regional lymph node enlargement.
 Painful limitation of movement.

25.  X-RAY-
> Localized osteoporosis.
> Washed out appearance of articular cartilage.
> Bony destruction & osteolysis.
> Soft tissue swelling.
> Diminution of joint space.
> Collapse, subluxation, dislocation, deformity of joint.
> Irregular growth or premature fusion.
> Coke like sequestrum.
> Subperiosteal new bone formation.
> Dystrophic calcification

27. BLOOD-
> Relative lymphocytosis.
> Low Hb%.
> Raised ESR.

28.  MANTOUX TEST-
The test is of limited value in the diagnosis of active TB
because of its relatively low sensitivity & its specificity & its
inability to discriminate between latent infection & active disease.
Tuberculin test may be negative although active TB is
present in various conditions.

29.  BIOPSY-
Whenever there is doubt it is mandatory to prove the diagnosis
by obtaining the diseased tissue ( granulation/ synovium/ bone/
lymph node).
Microscoping examination of aspiration cytology, core biopsy,
needle biopsy, open biopsy would reveal typical “tubercle”.

30. SYNOVIAL FLUID ANALYSIS-
Leucocytosis, (10 to 20 thousands per ml) in which
polymorphs predominates.
Glucose content is reduced, & protein is elevated with poor
mucin clot.

31. SMEAR & CULTURE-
Direct smear examination of the pathological material of cases
who were not on ATT may reveal AFB-
In the synovial fluid aspirate in 10%.
In the synovial tissue in 20%.
In regional lymph node in 30%.
Culture may be positive in 30 to 60% of such material. But it generally
takes 8 weeks.

32.  ISOTOPE SCINTIGRAPHY-
99mTc, 67Ga, & 111In are the currently utilized isotopes.
Sensitivity is very high but lack of specificity.
A positive scan localize the suspicious region for future
observation & identifying an easily accessible site for tissue
diagnosis.

33.  SEROLOGICAL IVVESTIGATION-
ELISA for antibody to mycobacterial antigen -6 has
sensitivity of 94% & specificity of 100% in the serological diagnosis
of bone & joint TB.
PCR method gives 40% sensitivity & 100 % specificity. It
may be positive even if mycobacterium is dead , formalin preserved
Or test material contain fragment of bacterium.

34. INVESTIGATION
 CT- SCAN-
>Demonstrate small destroyed areas, marginal erosion much
before than X-ray.
> Demonstrate the soft tissue swelling.
> Good choice for detecting disease in difficult areas.
> CT guided needle biopsy is very effective for obtaining tissues
for pathological & microbiological diagnosis.

35. INVESTIGATION
 MRI-
Shows the predestructive lesions,
Encroachment of vertebral canal, displacement of the dural sheath,
localized tuberculoma, generalized granuloma, shrinkage of the cord
substance. Myelitis can be appreciated by the study of T1 & Ta-
weighted images.
Suggest the nature
of soft tissue mass.

36. INVESTIGATION
 USG-
Estimate the presence of soft tissue abscess & its
behavior under treatment.
May be an ideal first line investigation for tubercular
tenosynovitis.

37. NATURAL COURSE OF SKELETAL TB WITHOUT
CHEMOTHERAPY
Before the availability of ATT osteoarticular TB passed
through three stages spanned over a period of 3 to 5 yrs.
> Stage of onset- with localized swelling, localized
osteoporosis but minimal destruction.
> Stage of destruction- Gross destruction of joint
with deformity, subluxation, cotractures & abscess
formation. There may be dissemination of disease which
leads to death of nearly 1/3rd of patient.
> Stage of repair & ankylosis- The abscess resorbed,
sinus underwent healing, remineralization of bone &
fusion & deformity of joint.

38. EVOLUTION OF TREATMENT OF SKELETAL TB
The availability of ATT (1948-51) , divides the treatment of TB into 2
eras.
(i) Pre-antitubercular era- Patient were treated either by orthodox
conservative regime or by various operative procedure.
(ii) Post-antitubercular era- Two different lines of treatment-
> Operative in all cases in conjunction with ATT.
> ATT in all cases with operation for failure or complications.

39. (A)- Rest
(B)- Supportive
> Anti- anemic
> Multivitamines
> High protein diet
> Blood transfusion.

41. First line Drugs Second line Drugs
Isoniazid
Rifampicin
Pyrazinamide
Ethambutol
Streptomycin
Thiacetazone
Paraaminosalicylicacid
Ethionamide
Cycloserine
Kanamycin
Amikacin
Capreomycin
Fluroquinolones
Macrolides
Rifabutin

42. Catagory Definition & examples
Cat I Sputum positive new cases
Sputum negative seriously ill
Seriously ill extrapulmonary
PulmTB, TB meningitis,AbdominalTB, Bone & jointTB
spinalTB.
Cat II Treatment defalter
Treatment failure
Relapse
Cat III Smear negative new pulm.TB with limited parenchymal
involvement.
Tubercular lymphadenitis, skinTB.
Cat IV Chronic or MDR cases

43. Drug Mechanism of
action
WHO
recommended
doses
Side effects
Isoniazid Bacteriocidal, Inhibits
the synthesis of
mycolic acid
5 mg/kg daily dose.
10 mg/kg 3 per wk
dose.
Peri. neuropathy,
behavior disorder,
hepatitis, convulsion
Rifampicin Bacteriocidal, Inhibit
DNA depended RNA
synthesis
10 mg/kg both daily
& 3 per wk dose
Hepatitis, pinkish
staining of urine,saliva,
flu like syndrome,
rashes
Pyrazinamid
e
Bacteriocidal, Inhibit
mycolic acid
synthesis
30-40 mg/kg Gouty arthritis,
hepatotoxicity
Ethambutol Bacteriostatic 15-20 mg/kg Retrobulbar neuritis,
loss of vision, colour
blindness.
Streptomycin Bacteriocidal &
bacteriostatic. Inhibits
the protein synthesis
15-20 mg/kg Vestibular damage,
deafness,
nephrotoxicity, contact
dermatitis.

45.  DOTS- Directly observed treatment short course, means
administering potent antimycobacterial regimens in an intermittent
manner under direct supervision.
 RNTCP- Revised national tuberculosis control programme
based on the DOTS strategy in 1993 & gradually expanded &
covered entire country under DOTS by 24th Mar 2006.

46. Catagory Initial phase Continuation
phase
Duration
I 2 (HRZE)3 4 (HR)3 6 Months
II 2 ( HRZES)3 +
1 (HRZE)3
5 (HRE)3 8 Months
III 2 (HRZ)3 4 (HR)3 6 Months

47.  Multi-drug Resistance (MDR) TB- Defined as resistance
to Isoniazide & Rifampicin.
Treatment of MDR –TB :-
6 months of initial phase with Streptomycin +
Quinolone + Pyrazinamide + Ethambutol.
18 months of continuation phase with
Ethionamide + Quinolone + Pyrazinamide +
Ethambutol.

48.  Corticosteroid :-
Cortisone may help keep alive a moribund patient till the ATT
can take effect.
Steroid is useful in patient with severe hypersensitivity reaction.
A short course anabolic steroid may help a debilitated patient to
be prepared for surgery.
NSAID:-
Used for relief of pain in early painful stage of disease.

49.  Aspiration of joint.
 Drainage of abscess.
 Excision of sinus

50. SURGERY IN TUBERCULOSIS OF BONE &
JOINT
 INDICATION-
> If response to conservative treatment is not favorable or
outcome is unacceptable.
> No sign of neurological recovery after trial of 3-4 wks therapy.
> Neurological complication develop during conservative
treatment.
> Neuro deficit become worse on drugs & rest.
> Recurrence of neurological complication.
> Cervical abscess hampers in deglutition& respiration.
> Advanced cases sphincter involvement, flaccid paralysis,
severe flexor spasm.

51. Surgery in osteoarticular TB
Surgery Indication
Synvectomy & joint
debridement
Synovitis & Early arthitis
Osteotomy Sound or unsound ankylosis
in bad position
Arthrodesis
Ischiofemoral & Iliofemoral
Adult with unsound ankylosis
with active or healed disease
Excisional Arthroplasty
( Girdlestone’s)
Sound or unsound ankylosis.

57. Sign of Healing
 Disappearance of all systemic & local features
 Return of painless motion.
 Repeated ESR is normal & no progression.
 Remineralization & restoration of bony outline.
 Resolution of edema & soft tissue swelling.
 Bony alkylosis.

58. Prophylaxis
Immuno-prophylaxis-
0.1 ml intradermal injection of live attenuated BCG vaccine proximal
to the insertion of deltoid after birth.
Give protection upto 80% & immunity lasts for 10-15 yrs.
Chemoprophylaxis:-
Combination of Isoniazid & Ethambutol once daily dose for 4-6 months.
Indications-
> Close contacts
> Person with +ive tuberculin test .
>TB infected person without active disease but develop high
risk condition.
> Patient with old inactive disease who are assessed to have
received inadequate therapy.

60. THANKS ALL OF YOU