This document discusses spinal tuberculosis, including: 1. It affects the dorsal spine in 42% of cases and describes 4 types of vertebral lesions. 2. Symptoms include back pain, stiffness, and potential neurological deficit in advanced cases. 3. Investigations include blood tests, imaging like xray, CT and MRI to determine lesion type and severity. 4. Management involves chemotherapy initially but may require surgical intervention for abscesses, severe deformity or neurological deficit.

1. SPINAL TUBERCULOSIS
DIAGNOSIS &
MANAGEMENT

3. Regional distribution of Spine TB
• Cervical – 12%
• Cervicodorsal – 5%
• Dorsal – 42%
• Dorsolumbar – 12%
• Lumbar – 26%
• Lumbosacral – 3%

4. Types of vertebral lesions
• 5 types:
1. Paradiscal- Arterial spread
2. Central – Venous spread
3. Anterior- Subperiosteal spread
4. Appendicular
5. Articular

5. Types of vertebral lesions
• 4 types:
1. Paradiscal- Arterial spread
2. Central – Venous spread
3. Anterior- Subperiosteal spread
4. Appendicular
5. Articular

6. Types of vertebral lesions
• 4 types:
1. Paradiscal- Arterial spread
2. Central – Venous spread
3. Anterior- Subperiosteal spread
4. Appendicular
5. Articular

7. Types of vertebral lesions
• 4 types:
1. Paradiscal- Arterial spread
2. Central – Venous spread
3. Anterior- Subperiosteal spread
4. Appendicular
5. Articular

8. Types of vertebral lesions
• 4 types:
1. Paradiscal- Arterial spread
2. Central – Venous spread
3. Anterior- Subperiosteal spread
4. Appendicular
5. Articular

9. Clinical Features
Active stage
Constitutional symptoms:
• Malaise
• Loss of weight/appetite
• Night sweats
• Evening rise of temperature
Specific Symptoms:
• Pain/Night cries
• Stiffness
• Deformity
• Restricted ROM
• Enlarged lymph nodes
• Abscess
• Neurodeficit

10. Clinical Features
Healed stage
Constitutional symptoms:
• Malaise
• Loss of weight/appetite
• Night sweats
• Evening rise of temperature
Specific Symptoms:
• Pain/Night cries
• Stiffness
• Deformity
• Restricted ROM
• Enlarged lymph nodes
• Abscess
• Neurodeficit

11. Neurological deficit
• 10-30% cases – Neurological deficit
• Age: 1 3 decadesst
• Disease below L1 vertebrae rarely causes Paraplegia
• Highest Incidence of paraplegia seen in TB of lower thoracic vertebrae

12. Classification of TB Paraplegia
Griffiths, Seddon and Roaf 1956 (Pre anti-tubercular era)
Early onset paraplegia (group A)
• Appears within 2 years of onset –
during the Active phase
• Underlying pathology
– Inflammatory edema
– TB Granulation tissue
– Abscess
– Caseous tissue
– Ischaemis lesion of cord (Rare)
• Good prognosis
Late onset paraplegia (Group B)
• Appears more than 2 years of
disease in vertebral column
• Underlying pathology –due to
mechanical pressure on cord
– TB Debris
– TB Sequestra from body and disc
– Internal gibbus
– Canal stenosis / Severe deformity
• Poor prognosis

13. Pathology of TB Paraplegia
• Infarction of Spinal cord
• Caused by
– Endarteritis
– Periarteritis
– Thrombosis
• Paralysis is irreparable
• Ischaemic necrosis seen as an area of High intensity in T2 MRI
• Can also happen postoperatively

14. Staging of Neurological Deficit
Goel 1967, Tuli 1985, Kumar 1988, Jain 2002
Stage Severity Clinical Features
I Negligible Patient unaware of neurodeficit, physician detects plantar
extensors or ankle clonus
II Mild Patient aware of deficit but walks with support
III Moderate Non ambulatory due to spastic paralysis (in extension),
sensory deficit less than 50 %
IV Severe III + Flexor spasm / Paralysis in flexion / Flaccid/ Sensory
deficit more than 50 % / Sphincter Involved

15. Prognosis of recovery of cord functions
Cord involvement Better prognosis Poor prognosis
Degree Partial (Stage I & II) Complete (Stage IV)
Duration Shorter Longer(>12 months)
Type Early onset Late onset
Speed of onset Slow Rapid
Age Younger Older
General condition Good Poor
Vertebral disease Active Healed
Kyphotic deformity <60 degree >60 degree
Cord on MRI Normal Myelomalacia

16. Investigations
• CBC:
– Hb% ↓
– Lymphocytosis
• ESR:
– Raised in active stage of disease
– Normal ESR over period of 3 months suggests patient is in stage of repair
• HIV
• CXR

17. Investigations
• Mantoux test
– Erythema of more than 20 mm at 72 hours – Positive
– Negative test, in general, rules out the disease

18. Investigations
• Biopsy
– In case of doubt, it is mandatory to prove the diagnosis by obtai
diseased tissue

19. Investigations
• Smear and culture
– Pus: Zeill- Neilson stain → Acid Fast bacilli
– Culture of pus in Lowenstein jensen media
– Aspirate of paravertebral abscess or spinal
diseased tissue seldom demonstrates
mycobacterium (Moon 2002)
– Bactec For faster culture of Mycobacterium
tuberculosis

20. Investigation
• Serological Investigations
– ELISPOT (Enzyme- linked immunospot)
– T-cell based assay from blood
– IgM & IgG antibodies : High sensitivity, low specificity
– PCR: Tissue /Pus PCR more sensitive

21. Plain radiograph
 Focal areas of erosion and
osseous destruction in the
anterior corners of the
vertebral body are typical
plain film findings.

22. Plain radiograph
 Contiguous
vertebral body
involvement
 Destruction of the
intervertebral disk
 Progerssive vertebral
collapse

23. Plain Radiograph
 Compression
fracture and
secondary
osteosclerosis

24. Plain radiograph
 Paraspinal abcess
formation may be detected
as areas of fusiform soft
tissue swelling around the
spine

25. Plain radiograph
 Central lucency with
surrounding sclerosis
suggestive of chronic
infection.

26. Radiological Investigations
• Healing is indicated by
– Decreased soft tissue
shadow
– Return of normal density
– Bony ankylosis

27. Scintigraphy
 Initially bone scans and gallium studies can be negative despite
active disease.
 Later on increased bony metabolism manifests as increased
radionuclide uptake.
 Useful in determining the number of active sites of the disease.
 Helpful in determining the involvement of posterior elements of the
spine.
 Also useful in chronic infection in monitor the response to
therapy.

28. scintigraphy
 Posterior view from whole
body bone scan showing
increased radionuclide
uptake in middle and
lower thoracic spine

29.  SPECT scans showing
involvement of vertebral
bodies and extension into
posterior elements

30.  As tubercular lesions
demonstrate high 18F-
FDG uptake, 18F-FDG
PET/CT is a promising
technique for the diagnosis
of spinal infection

31. CT findings
 Anterior vertebral body
destruction

32. CT findings
 Vertebral body
collapse
 Disk space
narrowing
 Large paraspinal soft
tissue masses
representing abcess
formation

33. CT findings
 Cloaca formation may be
visualised resulting from
spontaneous
decomprssion of the
vertebral body abcess

34. CT findings
 Large abcess in left psoas
muscle attributable to
spontaneous
decompression of the T12
intraosseous abcess

35. CT findings
 CT scan through lower
part of the chest showing
large left pleural effusion
with atelectasis due to
cephalic extension of the
paraspinal abcess and
rupture into left pleural
cavity.

36. CT findings
 In chronic stages there
is marked bone
destruction with
sequestrum formation

37. MR findings
 Highly sensitive and specific for spinal tuberculosis
 Provides early detection
 Best to know extent of soft tissue and spinal involvement
 CT is superior to MRI in the evaluation of the degree of
bony destruction, deformity and calcification.

38. MR findings
 T1 images typically show
decreased signal within
the affected vertebral
bodies, loss of disk
height and paraspinal
soft tissue masses

39. MR findings
 T2 images show non
specific increased
signal intensity within
areas of osseous and
soft tissue changes.
 Extent of paraspinal
abcess formation
anteriorly is better
visualised.

40. MR findings
 Contrast enhanced
sequences are helpful in
distinguishing tuberculous
lesions from other
granulomatous diseases.
 The presence of thick rim of
enhancement around the
paraspinal and intraosseous
abcesses is found to be
diagnostic of spinal
tuberculosis.

41.  T2-weighted magnetic
resonance image of the
thoracic spinal cord of a
patient with 2 hyperintense
intramedullary
tuberculomas.

42.  T1-weighted gadolinium-
enhanced magnetic resonance
image of the thoracic spinal
cord in a patient with acquired
immunodeficiency syndrome
(AIDS) and leptomeningeal
tuberculosis. Note the
numerous granulomas on the
dorsal surface of the cord and
the dural enhancement

51. Syringomyelia can occur as a complication of arachnoiditis .
• Early syrinx formation is due to spinal cord ischemia
• Late onset syrinx in chronic arachanoiditis is due to focal scarring of the
subarachnoid space by adhesions which impedes free circulation of CSF thus forcing
CSF into the central canal of the spinal cord via VR spaces
• The differential diagnosis of nodular or diffuse thickening in spinal canal onMRI :
1. meningeal carcinomatosis.
2. lymphoma.

52. Present management
Cases of
spinal TB
Conservative
treatment with
chemotherapy
only
Middle path
regime Radical surgery

53. 1 line chemotherapyst
Bactericidal drugs Dose
Isoniazid 5 mg/kg
Rifampicin 10-15 mg/kg
Streptomycin 20 mg/kg
Pyrazinamide 20 -25 mg/kg
Bacteriostatic drugs Dose
Ethambutol 25 mg/kg

57. • Sinus heals 6-12 weeks after treatment.
• Neural complications if showing progressive recovery on ATT b/w 3-4 weeks :-
surgery unnecessary
• Excisional surgery for posterior spinal disease associated with abscess / sinus
formation +/- neural involvement.
• Operative debridement–if no arrest after 3-6 months of ATT / with recurrence of
disease .
• Post op spinal brace→18 months-2 years

60. Algorithm for management of pott’s
paraplegia

61. Algorithm for management of pott’s
paraplegia

63. Post operative care

64. Take home message
• Conservative and operative management
have their distinct advantages and
disadvantages
• Judicious choice of treatment for pott’s
spine usually gives good results.