This document provides information on tuberculosis of the skeletal system (Potts disease). It discusses the history, epidemiology, pathogenesis, clinical presentation, investigations including imaging findings, microbiological studies, treatment including medical management and surgical options, as well as outcomes of skeletal tuberculosis. Key points include that India accounts for a large portion of global tuberculosis cases, it most commonly involves the thoracic spine, and treatment involves a combination of anti-tubercular medications and surgery in some cases to address complications or deformities.

2. HISTORY
• Documented in5000-year-old mummies

3. “YAKSHMA”
Yakṣhma (यक्ष्म) in the Rigveda and the Atharvaveda
frequently denotes ‘illness’, in general, perhaps as
rendering the body emaciated

4. IN 1779, PERCIVAL
POT T

5. One fifth of TB
population is in India.
3%suffering from
skeletal TB.
Vertebral TB - form of
skeletal TB(50%).
Almost 50% are from
pediatric group.
2nd greatest killer next
to HIV.

6. In 2017, WHO released a report which revealed as many
as 4.23 lakh deaths from TB in India
19.36 lakh TB cases came into picture in India in 2016.

7. • Early diagnosis.
• Expeditious medical
treatment.
• Aggressive surgical
approach.
• Prevent deformity.
• Best outcome.

9. Cervical (including
atlanto occipital)
12%
Cervicodorsal 5%
Dorsal 42%
Dorsolumbar 12%
Lumbar 26%
Lumbosacral 3%
REGIONAL DISTRIBUTION
(TUBERCULOSIS OF THE SKELETAL SYSTEM BY
S.M.TULI 5TH ED)

10. • Secondary infection.
• Primary site in the lung, viscera or
lymph glands.
• Hematogenous Spread / Batson plexus
of veins.
• Delayed hypersensitivity immune
reaction. Inflammatory reaction with
Langhan’s giant cells, epithelioid cells,
and lymphocytes.
The granulation tissue
proliferates, producing
PATHOLOGY

11. PATHOLOGY
• Granulomatous
• inflammation leads to erosion
of vertebrae.
• Associated disc degeneration due to
end arteritis, finally complete
destruction.
• Weakening of trabeculae
compression collapse. –
Deformity.

13. •Formation of cold abscess
•Collect under ant-long-ligament
•Vertebral collapse
•Expression of collection of tuberculous debris
Diverted forward along
different anatomical sites
Slides along VB and invade
the
vertebral canal through
intervertebral foramen.

14. COLD ABSCESS
•Abscess- collection of liquefied
tissue in the body which is
body’s defense reaction to
foreign material
•NO signs of inflammation
•Collection of dead tubercular
bacilli, serum, leucocytes,
bone debris and caseous
material.
•Can track in to any direction-
along musculo-facial planes or

15. • Paraspinal regions at the back
• Anterior/ posterior cervical triangles
• Brachial plexus in the axilla
• Intercostal spaces on the chest wall
• Abscesses from dorsolumbar and lumbar
spine- track
down the psoas sheath.
• Palpable in the iliac fossa, lumbar triangle,
upper part of the thigh below inguinal ligament
or even track downwards upto the knee or
sometimes upto the great toe

16. • Iliac abscess contained
in the sheath of the iliac
muscle.
• The abscess that has
tracked down the psoas
sheath penetrates
through the iliacus
muscle sheath.
• Becomes palpable as a
mass in the iliac fossa
• Abscess that remains
confined to the psoas
sheath may not be
palpable clinically.

17. TYPES OF VERTEBRAL
INVOLVEMENT
1.PARADISCAL (arterial spread)
2.CENTRAL ( venous spread)
3.ANTERIOR (sub periosteal
tracking of pus)
4.APPENDICIAL

18. • Most common pattern of spinal
tuberculosis.
• Narrowing of the disc space.
• Destruction of subchondral bone.
• Subsequent herniation of the disc.
1. PARADISCAL LESIONS :

20. • Subperiosteal lesion under the ALL.
• The periosteal stripping renders the
vertebrae avascular and susceptible
to infection.
• Both pressure and ischemia combine to
produce anterior scalloping. (multiple
vertebrae)
• Collapse of the VB &diminution of the disc
space is minimal
2. ANTERIOR LESIONS :

22. • Centered on the vertebral body.
• Disc is not involved.
• Infection starts from the center of the
vertebral body.
Batson’s venous
plexus Posterior
vertebral artery
• Concentric collapse producing a
vertebra plana appearance.
3. CENTRAL LESIONS :

24. • Isolated infection involving
pedicles , laminae (neural
arch), transverse processes, &
spinous process.
• Uncommon lesion (< 5%).
• In conjunction with the
typical paradiscal variant
in 30%.
• Rarely present as synovitis of
facet joints.
4. APPENDICIAL LESIONS :

26. • Constitutional symptoms
• Pain in the back ( m/c )
• Swelling
• Stiffness
• Neurological symptoms
• Deformity

27. 1. ATTITUDE AND GAIT
• In upper cervical disease – wry neck
• In upper thoracic disease – Military
attitude
• In lumbosacral – Alderman’s Gait
• In lower lumbar – Pronounced lordosis

28. 2. DEFORMITY OF SPINE:
• Kyphosis
1 vertebrae – Knuckle
gibbus 2-3 vertebrae -
Angular gibbus
>3 vertebrae – Round
kyphosis
• Scoliosis
• Lordosis

29. 3. ABSCESS / SINUS FORMATION :
• Dysphagia and dyspnoea – Retropharyngeal abscess
• Hoarseness of voice due to – Abscess in disease of
upper thoracic region.
• Flexion contracture of hip – Psoas abscess

30. 4. MOVEMENT OF SPINE :
• painful due to protective muscular
spasm
5. Paralysis :
• Association - 10-30%
• Type - Incomplete generally
• More common in thoracic
region.

31. RADIOLOGICAL
DIAGNOSIS:
1. X-RAYS
2. CT SCAN
3. MRI SPINE
4. BONE
SCAN

32. 1. X RAY FINDINGS :
• Early changes :-
haziness and local osteoporosis of end
plates of
two adjacent vertebrae
 narrowing of intervertebral disc space.
• Late changes :-
 paravertebral shadow
 ant wedge compression collapse - deformity
 central or concertina collapse
 destruction of post element
X ray changes appear after 3-5 months.

33. PARA VERTEBRAL
SHADOW- X RAY
1. Cervical
region
- Shadow in Retropharyngeal
space
- V-shaped
shadow
2. Upper
thoracic
mediastinu
m
- Change in contour of tracheal
shadow
3. Below 4th
thoracic
- Fusiform or bird nest
shadow
4. Below
D10
5.
Aneurysma
l
phenomen
- Bilateral widening of psoas
shadow
-tense thoracic vertebral abscess
showing scalloping effect

35. 2. CT SCAN

36. 3.
MRI

38. • Increased uptake (60% patients) with active
tuberculosis
• > 5mm lesion size can be detected.
• Avascular segments and abscesses show a cold
spot due to decreased uptake.
• Highly sensitive but nonspecific.
• Aid to localize the site of active disease and to detect
multilevel involvement
4. BONE SCAN (TECHNITIUM
(TC) – 99 M )

41. • Mantoux / Tuberculin skin test
• ESR may be markedly elevated (neither specific nor
reliable).
• ELISA : for antibody to mycobacterial
antigen-6 , sensitivity 94% and specificity
of 100%
• Polymerase chain reaction PCR : sensitivity 40% only.
LABORATORY TESTS

42. Biopsy : For definitive diagnosis
• CT or ultrasound guided or open biopsy during a
surgical procedure.
1. Ziehl-Neelsen staining: a quick and inexpensive
method
2. Culture : - results are available only after a few
weeks
- positive only in 60% of cases; most
specific.
3. Histology: demonstration of tubercle, 80% cases.
MICROBIOLOGY STUDIES:

43. • Most dreaded and crippling
complication.
• Incidence 10-30%.
• age group – first three decades of
life.
• region – thoracic.

44. 1)To eradicate or at least arrest the
disease.
2) To treat major complications
like paraplegia.
3) To prevent or correct deformity.

45. TULI’S MIDDLE PATH REGIME FOR
TREATMENT OF KOCH’S SPINE
1) Bed rest - with or without traction
2) Drugs – ATTany one regime as preferred
3)Radiograph &ESR – radiologically the kyphosis
and disease activity by ESR is measured 3
monthly.
4)Gradual mobilization with exercise
5)Abscess:
* Repeated aspiration.
* Streptomycin and/or INH instillation.

46. 6) Sinuses :
* Usually heal by 6-12 weeks of ATT.
* Excision of the tract with or without debridement.
7) Neurological complication :
5 indications for surgery (mainly decompression
surgery)
(I) Not showing progressive recovery after 3-6 weeks of
Rx.
(ii) Pt. developing neurological complication during Rx.
(iii) Neurological status becoming worse while
undergoing Rx.
(iv) Recurrence of neurological complication.
(v)In advanced cases with motor, sensory or
sphincter involvement or having severe flexor spasm
8) Operative debridement
- in nonresponsive 3-6m of chemotherapy.
- cases with recurrence of disease.

47. 9) Excisional surgery:
- posterior spinal disease associated with
abscess / sinus formation +/- neural
involvement.
10) Posterior SpinalArthrodesis:
- severe kyphotic deformity
(prevention / correction).
- mechanical instability.
- spine at risk signs.
11)Post –operative:
- hard bed for 2-3 weeks/ neurological
recovery.
- brace for 2 years.

48. INDICATIONS- SURGICALTREATMENT
•Doubtful diagnosis.
•Failure to respond to conservative Rx after 3-
6 weeks therapy.
•Symptomatic abscess.
•Neurological indications.
•Mechanical instability.
•Deformity.
•Recurrence of disease.
•Posterior spinal disease.
•Spinal tumor syndrome.

49. TYPES OF SURGERY

50. •Nursed on a hard bed / POP posterior shell
(children) upto 3 months.
•Careful and assisted turning of the patient is
permitted from the first day.
•At the end of 3-6 months / neurological
recovery pt. mobilized with the help of spinal
brace.
•Spinal brace is discarded after 1- 1 ½ years.

51. •CERVICAL SPINE :
Four post cervical
brace
Minerva Jacket
SOMI Brace

52. •UPPER DORSAL SPINE D1-D3:
No simple brace to control the spine
effectively.
Only satisfactory method is to extend the
usual spinal brace upward with the
attachment of a cervical collar.

53. D4-L2
VERTEBRAE
- acceptable to young girl as
it gets accommodated
according to body
contour.
MILWAUKEE BRACE:
- growing age ; mainly used for
correction of scoliosis.

55. • Maintain high suspicion not to overlook diagnosis.
• Earlydiagnosis is essential for good results.
• EarlyMRIis anessential tool for diagnosis of Potts
spine.
• Not all patients can be treated bychemotherapy alone
and neither do all patients requiresurgery.

56. THANK YOU