Presentation by pg student

1. TUBERCULOSIS OF
SPINE
Moderator- Dr. Sivaprasad
Presenter- Dr. Ravi N.B.

2. INTRODUCTION
• 1-3% osseous involvement
• > 50% effects spinal column
• Dorsal spine - most commonly
involved
• Most common in - first 3 decades

4. HISTORICAL ASPECT
• Percival Pott -presented the classic
description of spinal tuberculosis in 1779.

5. Predisposing factors:
• Malnutrition
• Poor sanitation
• Over crowding
• Close contact with TB patient
• Immunodeficiency state

6. Development of Vertebral
Column

7. Blood supply of spine

8. Venous drainage

9. PATHOLOGY
Causative organism
>Mycobacterium tuberculosis
>Gram positive AFB
> Hematogenous dissemination from the primary focus
> Bone and joint TB develop generally 2-3years after
the primary focus

10. TB bacilli phagocytosed by
mononuclear cells
Epitheloid cell formation
Langhans giant cell formed by fusion
epitheloid cells.

11. Lymphocytes form a ring around the
lesion
Tubercle formation
• Epitheloid cells- characteristic of TB
• Presence of caseation necrosis
almost diagnostic of TB

12. :
Bacilli from primary focus
through bloodstream reach
DISC SPACE
:
Soft nucleus centre & fibrous annula
wall weaken, decay & collapse
This causes the disc space to close,
Squeezing down on nerve root

13. :
Infection spreads to vertebral
bodies above & below the disc
:
Bone weakened by infection,
crumble under the weight of
the human body.

14. :
The deformed spinal column
compresses spinal cord producing
functional impairment
:
Deformed vertebrae heal & fuse
This may further compress nerve
roots causing pain & neurodeficit

15. Types of lesions in spinal TB

17. Pathogenesis
Caseous exudative type Granular type
More in children More in adults
More destruction Less destruction
More exudation Insidious onset/course
Abscess formation common Abscess formation rare

18. Clinical features:
Constitutional symptoms Specific features
Malaise Pain / night cries
Loss of appetite/weight Deformity
Night sweats Enlarged LN
Evening rise of temperature Neurodeficit

19. Clinical features Percentage
Khyposis 80-85%
Neurodeficit 20-30%
Palpable cold abscess 15-20%
Radiological perivertebral 15-20%
abscess
Skipped lesions 05%

20. Kyphotic deformity

22. UMN & LMN

24. Tracts of spinal cord

26. Reflex Arc

27. Ankle clonus & Babinski reflex

29. classified TB
Paraplegia
-> within 2years -> After 2 years
-> inflammatory edema -> compression of cord
Granulation tissue. due to sequestra, internal
Caseous tissue Gibbus, stenosis of canal
-> ACTIVE disease -> HEALED disease
-> Good prognosis. -> Poor prognosis

30. Cold abscess:
1).Formed by collection of
products of liquefaction
& reactive exudation.
2).Compose- serum, leukocytes,
caseous material, bone debris
& TB bacilli.
3).Tracks along neighbouring vessels
& nerve to reach surface.
4).May burst to form sinus.

31. Sites of cold abscess
A). Neck and Axilla
B). Retropharynx
C). Groin
D). Paravertebral

32. Retropharyngeal abscess

34. Psoas abscess
>It can present as lumb in the iliac
fossa.
>It can give rise to Hip flexion deformity
called as Pseudo-hip flexion deformity.
>As a rule associated with TB disease
of vertebral column from dorsal T10th
vertebrae to Sacrum.

36. Complications of Spinal
Tuberculosis
• Paraplegia
• Cold abscess
• Spinal deformity
• Sinuses
• Secondary infection

37. TYPES OF LESIONS
1). -
-> it arises from arterial
spread of infection, begins
in the vertebral metaphysics,
erodes cartilage plate &
destroy disc.

38. 2). :
-> infection begins in
the midsection of
the body.
-> extends centrifugally
to involve whole body

39. 3). :
-> leads to cortical bone
destruction beneath
anterior longitudinal ligament.
-> spread of infection in
subperiosteal & subligamentous
planes, allows extension of
infection to adjacent bodies
without involvement of disc.

40. 4). :
-> the lamina, articular
process or spinous
process is primarily
affected.

41. INVESTIGATIONS
1). CBC- lymphocytosis
lymphocyte-monocyte ratio(5:1)
2). ESR- raised in active stage of disease
3). Mantoux test:( Heaf test )
>As a rule, a positive reaction is present in a patient with
tuberculous disease of some standing (one to 3 months).

42. >A negative test, in general, rules out the
disease.
>False negative : as in severe and disseminated
tuberculosis, during high fever or certain
exanthemata, after virus vaccination, recentviral
infection or steroid therapy, or in immune
incompetent state, or severe under-nutrition or
extremes of age.

43. 4). Sputum examination for AFB
5). Aspiration of abscess- smear & culture
of pus

44. Culture of pus
Solid media Liquid broth
3-8 weeks 1-3 weeks
Lowenstein jensen
Middlebrook

45. 6). BACTEC media- faster culture (1-2 weeks).
7). ELISPOT(Enzyme-linked immunospot)-
8). IgM & IgG antibodies-
IgM-recent infection, IgG-past infection
9). PCR- Tissue PCR more specific

46. 10). Biopsy:
>Whenever there is doubt (particularly in early stages) it is
mandatory to prove the diagnosis by obtaining the diseased
tissue (granulations and/or bone and/or lymph nodes).
>Microscopic exam- reveal typical tubercles in untreated cases
of shorter duration of disease.
>Epitheliod cells surrounded by lymphocytes in the configuration
of a tubercle

47. RADIOLOGY
A). Plain radiograph: localized osteoporosis is the 1st radiological
sign of active disease.
> Antero-posterior, lateral view and chest X-ray are mandatory
>Reduced disc space
>blurred paradiscal margins
>destruction of bodies
> increased Prevertebral shadow
> subluxation/ dislocation
>decreased lordosis/kyphosis

49. Kyphosis deformity:

50. is indicated by
> decreased soft tissue shadow
>disappearance of erosion
> Return of normal
density(mineralization)
>bony ankylosis

52. B). Computed tomography:
>Pattern of bony destruction
>Calcification in abscess(pathognomic)
>Regions which are difficult to
visualise in plain films like-
a). Cranio-vertebral junction
b). Cervical-dorsal region
c). Sacrum & sacro-iliac joints
d). Posterior spinal TB

53. C). MRI-
>Detects marrow infiltration in vertebral bodies, leading
to early diagnosis
>Changes of discities
>Assessment of extradural abscess & subligamentous
spread
>Skip lesions
> Spinal cord involvement

55. D). USG-
> to find out primary in abdomen
> to detect cold abscess
> guided aspiration
E). Radionucleotide scan T99m-
>increased uptake in active tuberculosis
>5mm lesion can be detected
>localise site of active disease & to detect multilevel
involvement

56. MANAGEMENT
Evolution of treatment
Preantitubercular era
-> In ancient India, skeletal tuberculosis treated with
‘SIPUDRU’, a herbal preparation
->Pott & Charcot applied hot iron to drain pus
->Hippocrates and Galen tried to correct kyphotic deformity
due to tuberculosis of the spine, by manual pressure,
traction and mechanical appliances but failed

57. Sanatorium treatment
>Sanatorium regimes and rest
>Fresh air, sunshine and rooftops

58. Natural Course of Skeletal Tuberculosis
without Chemotherapy
A). Stage of onset: 1month to 1year
warm tender swelling with marked localized osteoporosis and
minimal destruction
B). Stage of destruction: 1year to 3years
gross destruction with deformity, subluxation,contractures and
abscess formation. The abscesses finally ruptured and drained
as sinuses with frequent secondary pyogenic infection.
C). stage of repair and ankylosis:
improvement in the patient’s general condition.The abscesses
resorbed, sinuses underwent healing, and the destroyed bones
were remineralized.

60. CHEMOTHERAPY
1st line chemotherapy

61. 2nd line drugs

62. Policy of drug treatment
-> INH+RMP+ETM+PZN for 1st
6months
->INH+ RMP for next 12months

70. Middle path regime
Treatment is non-operative lines with
AKT, rest and spinal brace.
1).Rest- in hard bed or POP(in children)
2).Drugs-
->INH+RMP+ETM+PZN for 1st 6months
->INH+ RMP for next 12months

71. 3).Supportive treatment-
Multivitamins and high protein diet
4).Radiograph and ESR at 3-6 month
interval
5). Gradual mobilization with help of
spinal brace

72. Indications of surgery in
middle path regime
• No progressive recovery after a fair trail of
conservative treatment(3-4weeks).
• Neurological complications develop during
conservative treatment.
• Worsening of Neurodeficit during treatment.
• Recurrence of neurological complications.
• Pressure effects(deglutation / respiratory).
• Sphincter disturbance.

73. Algorithm for management of spine
TB with neurological complications

75. Operative management
Surgical options
1). Only decompression
2). Decompression with anterior interbody
fusion
3). Transpedicular decompression & global
fusion
4). Decompression & global fusion

76. Anterior approach to C1 &
C2
Transoral approach

77. Anterior approach to subaxial
cervical spine
Smith and Robinson approach

78. Anterior transpleural-transthoracic
approach to dorsal spine

79. Posterolateral approch for
dorsal spine

80. Anterolateral retroperitoneal
approch to lumbar spine

81. Anterior transperitoneal /retroperitoneal
approach to lumbar spine

84. Post-operative care
If neurologically intact If neurodeficit present
>Taylor’s brace applied >Regular neurocharting
after 48hours. >Taylor’s brace applied
>Patient kept ambulatory. after patient could sit up
Without support
>Taylor brace worn for 3months

85. Follow up
Patient evaluated at 3months interval for 2years
Evaluation
Clinical Radiological
Weight gain Decreased soft tissue shadow
Pain relief Disappearance of erosion
Free ROM. Return of mineralization
Resolution of abscess.
Neurological recovery

86. Recovery
• Time taken for near complete
recovery varies between 3-
6months.
• No significant neural recovery
occurs after 12-18months.

87. Results
Definition of favourable status-
>no residual neural impairment
>no sinus/cold abscess
>no impairment of physical activity due to
spinal disease
>presence of radiographic quiescent disease

88. Recurrence/Relapse
> Extradural granuloma
> Reactivation of lesion
Poor nutrition
Resistant organism
Immune compromised status

89. Reference
• SM TULI-Tuberculosis of the
skeletal system ( 5th edition )
• Campbell operative
orthopaedics(14th edition )

90. Thank you