kochs spine

1. TUBERCULOSIS OF SPINE
DR. PRATIK DHABALIA
JUNIOR RESIDENT
DEPT. OF ORTHOPEDICS

2. HISTORICAL ASPECTS
In India, the Rig Veda and the Atharva Veda (3,500–1,800 BC) mention this
disease by the name “Yakshama” in all its forms[1, 2]
Identification of mycobacterium as the causative organism (1870), use of the
Bacilli Calmette Guerin (BCG) vaccination (1945), facilities for radiographic
examination, and availability of specific antitubercular drugs (1948–1951) are
all important landmarks in the understanding and management of tuberculosis
of spine
1. Duraiswami PK, Orth M, Tuli SM. 5000 years of orthopaedics in India. Clin Orthop Relat
Res. 1971;75:269–280. doi: 10.1097/00003086-197103000-00032.
2. Bick KM. Classics of orthopaedics. Philadelphia: JB Lippincott Co.; 1976.

3. Tuberculous disease of the spine was
described by Percivall Pott in 1799 as
“That kind of palsy of lower limbs which is
frequently found to accompany a curvature
of the spine” [3, 4]
“Destruction of disc space and adjacent
vertebral bodies, collapse of spinal
elements and progressive spinal
deformity”
3. Bick KM. Classics of orthopaedics. Philadelphia: JB Lippincott Co.; 1976.
4. Tuli SM. Tuberculosis of the skeletal system. 4. New Delhi: Jaypee Brothers Medical Publishers; 2010.

4. • Robert Koch : Discovered Mycobacterium
tuberculosis in 1882

5. EPIDEMIOLOGY
• Tuberculosis : Leading cause of death worldwide from a single infectious
disease agent
• Globally, extrapulmonary tuberculosis (TB) represented 14% of the 6.4
million TB cases reported in 2017[5] ,of these, skeletal involvement was
the third most common, comprising 9.8% of cases, after lymphatic and
pleural disease.
• India has 1/5th of total TB Cases out of which 1- 3% of all involve
skeletal system.
• Vertebral tuberculosis is most common form of skeletal tuberculosis and
it constitutes about 50% of all skeletal cases.
5. World Health Organization. Chapter 4. Diagnosis and treatment: TB, HIV-associated TB and drug-resistant TB. Global
Tuberculosis Report 2018. Geneva: World Health Organization; 2018. 67-102

7. Age Distribution: Can occur at any age but more common in third decade of life.
Racial factors: Musculoskeletal tuberculosis affects primarily African Americans,
Hispanic Americans, Asian Americans, and foreign-born individuals.
Sexual predilection: Pott disease does not have a sexual predilection, the disease is
more common in males (male-to-female ratio of 1.5-2:1).
Regional Distribution: More prevalent in south African, sub Saharan and Asian
countries i.e. developing countries due to major risk factors and lower socio-
economic status and over-crowding.
Spinal Level: Most commonly Dorsal spine is involved.

8. PREDISPOSING FACTORS
• Malnutrition
• Poor Sanitation
• Over crowding
• Close contact with TB patient
• Multiple pregnancy
• Immunodeficiency state
SPINAL LEVEL DISTRIBUTION
LEVEL PERCENTAGE
CERVICAL 12%
CERVICODORSAL 5%
DORSAL 42%
DORSOLUMBAR 12%
LUMBAR 26%
LUMBOSACRAL 3%

9. PATHOLOGY AND PATHOGENESIS
Main Organism - M. tuberculosis
• Size 3 x 0.3 Micron
• Gram positive Acid Fast
Bacilli
• Hematogenous dissemination
from primary focus
• Bone and joint TB develop
after 2-3 years after the
primary focus
Characteristics
• Gram positive
• Acid Fast bacilli
• Non Motile
• May have resistance
• Size 3 x 0.3 Micron

10. Pathological process
Modes of Spread –
• Inhalational
• Inoculation
• Ingestion
• Transplacental

11. Pathological Process ctd …

12. Pathological process ctd…

13. Pathogenesis of Potts Spine
Tuberculosis of spine is always
secondary.
Via hematogenous route, bacilli
reach vertebral end plates.
- Segmental Arteries
- Bateson’s Plexus

14. Pathogenesis ctd...
STEP 1
Bacilli from primary
focus through blood
stream reach Disc
Space

15. Pathogenesis ctd…
Step 2
Once infected, soft
nucleus center and
fibrous annular wall
weakens, decays and
collapse
This caused the disc
to close, squeezing
down on nerve root
causing pain

16. Pathogenesis ctd…
STEP 3
The infection
spreads to
vertebral
bodies above
and below the
disc

17. Pathogenesis ctd…
STEP 4
The bone weakened by
the infection collapses
under the weight of
human body

18. Pathogenesis of TB Spine
STEP 5
The deformed spinal
column compresses spinal
cord producing functional
impairment

19. Pathogenesis ctd…
STEP 6
Over time, the
deformed vertebrae
heal and fuse
This may further
compress nerve roots
causing pain and
neurological deficit

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

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

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

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

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

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

26. 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

27. 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

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

29. 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

30. Staging of Neurological Deficit
Goel 1967, Tuli 1985, Kumar 1988, Jain2002
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

31. Pathology of TB Paraplegia
Inflammatory :
• Edema of spinal cord – Cause of early cases of Neurodeficit
– Vascular stasis
– Due to toxins

32. Pathology of TB Paraplegia
Extradural mass:
• The Commonest mechanism affecting spinal cord
function
• Material compressing may be
– Fluid pus
– Granulation tissue
– Caseous material

33. Pathology of TB Paraplegia
Bony Disorders:
• Sequestra from disc or body
• Internal Gibbus
• Pathological Dislocation

34. Pathology of TB Paraplegia
• Meningeal changes
– Dura is not involved
– Cicatrisation of extradural TB granulation tissue (Peridural fibrosis)
– Poor recovery despite adequate surgical decompression

35. 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

36. Pathology of TB Paraplegia
• Changes in the spinal cord
• Unrelieved compression
• Loss of neurons and white matter
• Lost cells and fibres replaced by gliosis and
neural fibres show loss of myelin
• MRI Shows myelomalacia

37. Clinical features of Pott’s Paraplegia
• Paraplegia itself – Rare
• Spontaneous muscle twitching in lower limbs
• Clumsiness while walking
• Extensor plantar response
• Exagerrated reflexes – Sustained clonus of patella and ankle
• Motor affected first – then Sensory
• Sense of position and vibration – last to disappear

38. 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

39. 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
• CRP: Raised

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

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

42. 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

43. 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
– Gene Xpert

44. Radiological Investigations
• Xray: Plain radiograph signs
– Reduced disc space
– Blurred paradiscal margins
– Destruction of bodies
– Loss of trabecular pattern
– Increased prevertebral soft tissue
shadow
– Subluxation /dislocation
– Decreased lordosis/Kyphosis

45. Radiological Investigations
• Xray: Plain radiograph signs
– Reduced disc space
– Blurred paradiscal margins
– Destruction of bodies
– Loss of trabecular pattern
– Increased prevertebral soft tissue
shadow
– Subluxation /dislocation
– Decreased lordosis/Kyphosis

46. Radiological Investigations
• Xray: Plain radiograph signs
– Reduced disc space
– Blurred paradiscal margins
– Destruction of bodies
– Loss of trabecular pattern
– Increased prevertebral soft tissue
shadow
– Subluxation /dislocation
– Decreased lordosis/Kyphosis

47. Radiological Investigations
• Xray: Plain radiograph signs
– Reduced disc space
– Blurred paradiscal margins
– Destruction of bodies
– Loss of trabecular pattern
– Increased prevertebral soft tissue
shadow
– Subluxation /dislocation
– Decreased lordosis/Kyphosis

48. Radiological Investigations
• Xray: Plain radiograph signs
– Reduced disc space
– Blurred paradiscal margins
– Destruction of bodies
– Loss of trabecular pattern
– Increased prevertebral soft tissue
shadow
– Subluxation /dislocation
– Decreased lordosis/Kyphosis

49. Radiological Investigations
• Xray: Plain radiograph signs
– Reduced disc space
– Blurred paradiscal margins
– Destruction of bodies
– Loss of trabecular pattern
– Increased prevertebral soft tissue
shadow
– Subluxation /dislocation
– Decreased lordosis/Kyphosis

52. Radiological Investigations
• Skipped lesions:
– More than one TB
Lesion in vertebral
column with one or
more healthy vertebrae
in between the 2
lesion.
– 7% on routine xray
– More frequently
detected on CT/MRI

53. Radiological Investigations
• Anterior type of lesion
– Starts beneath the
anterior longitudinal
ligament & periosteum
– Collapse and disc
space reduction is
usually minimal and
occurs late
– Erosion is primary
mechanical

54. Radiological Investigations
• Paradiscal lesions:
– Commonest lesions
– Spreads through arterial
supply
– Reduced disc space –
Earliest sign
– Loss of vertebral margins
– Increased pre-vertebral
soft tissue shadow.

55. Radiological Investigations
• Central type:
– Spread through the
batson’s venous plexus/
branches of posterior
vertebral artery.
– Minimal Disc space
reduction
– At the end concentric
collapse

56. Radiological Investigations
• Appendicular type of
lesion
– Rare
– Isolated infections of
pedicles / lamina/
transverse processes/
Spinous process.
– Intact disc space
– Para vertebral
shadows

57. Radiological Investigations
• Lateral shift and scoliosis
– More destruction of
vertebrae on one side
• Kyphotic deformity
– Due to collapse of bone
– Forward angulations

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

59. Computed tomography (CT)
• Patterns of bony destruction.
• Calcifications in abscess (pathognomic for Tb)
• Regions which are difficult to visualize on plain films, like :
1. Cranio-vertebral junction (CVJ)
2. Cervico-dorsal region,
3. Sacrum
4. Sacro-iliac joints.
5. Posterior spinal tuberculosis because lesions less
than 1.5cm are usually missed due to overlapping of
shadows on x rays.

60. MRI
• Lack of ionizing radiation, highcontrast resolution & 3D
imaging.
• Detect marrow infiltration in vertebral bodies, leading to
early diagnosis.
• Changes of diskitis
• Assessment of extradural abscesses / subligamentous
spread.
• Skip lesions
• Spinal cord involvement.
• Spinal arachanoiditis.

61. USG
- to find out primary in abdomen
- Detect cold abscess
- Guided aspiration
Radionucleotide Scan T 99m
• Increased uptake in up to 60 per cent 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 localise the site of active disease and to detect multilevel
involvement

62. Radiological Investigations
• Spine at risk sign

63. TUBERCULAR
• Chronic back pain -Long standing
history of months to years
• Presence of active pulmonary
tuberculosis -60%
• Most common location thoracic spine
followed by thoraco-lumbar region.
• > 3 contiguous vertebral body
• involvement common
• Vertebral collapse -67%
• Posterior elements involvement
• Skip lesions common
PYOGENIC
• Acute onset-History of days to months.
• Not present.
• Most common location lumbar spine.
• Mostly involves 1 spinal
segment
• 21% only.
• Rare
• Rare

64. Basic Principles Of Management
Early Diagnosis
Expeditious medical
treatment
Aggressive surgical
approach
Prevent Deformity
Expect Good
Outcome

65. Management
• Evolution of treatment:
– Undergone tremendous revolutionary changes
– Ancient Indians used herbal preparation
– Pott & Charcot applied hot iron to drain pus

66. Evolution of treatment
Pre Anti- Tubercular era
• Hippocrates advocated
traction and other means
to correct deformity

67. Evolution of treatment
Pre Anti- Tubercular era
• Sanatorium treatment
– Sanatorium regimes and
rest
– Fresh air, Sunshine
rooftops

68. Evolution of treatment
Pre Anti- Tubercular era
• Surgery was not attempted due to fear of
secondary infection and death
• Operative procedure were developed for
either treatment or prevention of paralysis

69. Evolution of treatment
Pre Anti- Tubercular era
• Results of surgeries done in pre
anti- tubercular era :
– Serious sinus formation
– Pseudoarthrosis
– Recurrence of lesion
– Neurological deterioration
– Death

70. Evolution of treatment
With Anti- Tubercular drugs
• Treatment has taken dramatic turn for better with
discovery of anti tubercular drugs.
– 1943 – PAS
– 1944 – Streptomycin
– 1951 – INH
– 1970 – Rifampicin and short course chemotherapy

71. Evolution of treatment
With Anti- Tubercular drugs
• Supportive treatment
– Rest
– Braces
– High protein diet
– Multivitamins, hematinics
– Hygiene
– Back care
– Chest / urinary tract care
– Improve immune status
– Treat other comorbid conditions.

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

73. Middle path regime
• Rationale
– “ All Spine Tuberculosis cases
do not require surgery and all
those who do not respond to
conservative measures should
be operated”

74. Middle path regime

75. Middle path regime
• Supportive therapy
– Hematinics, Multivitamins, High protein diet
• Rest
– In hard bed
– Cervical TB requires traction in
early stage to put the diseased
part in rest.

76. Middle path regime
• Monitoring
– Radiographs and ESR at 3-6 months
interval
– MRI at 6 months interval for 2 years

77. Middle path regime
• Gradual mobilization
– Encouraged in absence of
neurological deficit with support of
spinal braces
– As soon as the diseased part permits

78. 1st line chemotherapy
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

79. 2nd line Drugs
• Aminoglycosides – Kanamycin, Amikacin,
Capreomycin
• Fluoroquinolones – Ofloxacine, Ciprofloxacine,
levofloxacine
• Ethionamide
• Cycloserine
• PAS
• Clofazimine
• Rifabutin

80. Middle path regime
• Abscess drainage
– Superficial abscess drained and
streptomycin and INH solution injected at
the cavity
– Cervical prevertebral abscess drained if
causing difficulty in respiration /
swallowing.
– Drainage of perispinal abscess considered
when its radiological size increases markedly
despite treatment.

81. Middle path regime
• Sinuses
– Usually heal within 6-12
weeks of starting the t/t
– Small number of cases
require longer treatment
and excision of sinus

82. Middle path regime
• Absolute Indications of surgery
1. No progressive recovery after fair trial of conservative
treatment
2. Neurological complications develops during
conservative treatment
3. Worsening of neurological deficit during t/t
4. Recurrence of neurological complications
5. Pressure effects (deglutition/respiration)
6. Advanced cases of neurological involvement(Sphincter
disturbances, flaccid paralysis or severe flexor spasm)

83. Middle path regime
• Post Operatively
– Patient nursed in hard bed
– Patient mobilized 3-5 months after surgery
with spinal brace
– Spinal braces can be gradually discarded 1-
2 years after surgery

84. Newer Drugs
BEDAQUILINE
• Brand name – Sirturo
• Diaryl Quinoline class
• Mycobacterial Atp inhibitor
• For MDR
• Nausea, chest pain, QT prolongation
• Dose monitoring when given with rifampicin
• Black box warning
• DOSE - 400mg daily for 2 weeks then 200mg 3 times a week for 22 weeks

85. DELAMANID
• Brand name – deltyba
• Nitroimidazole class
• Inhibits formation of mycolic acid
• Nausea, arrhythmias, headache, dizziness
• Dose – 100mg twice a day x 24 weeks in divided doses

86. Algorithm for management of pott’s
paraplegia

87. Algorithm for management of pott’s
paraplegia

88. Operative Management
Surgery Indications
1 Decompression(+/- fusion) Too advanced disease, Failure to
respond to conservative therapy
2 Debridement +/-
decompression +/- fusion
Recurrence of disease or of neural
complications
3 Anterior transposition of
cord (Extrapleural
anterolateral approach)
Sever Kyphosis (>60 degree) + /
neural deficit
4 Laminectomy Extradural granuloma/ Old healed
disease presenting as secondary
canal stenosis/ Posterior spinal
disease

89. Surgical spproaches

90. Anterior approach
to the C1-C2
• Transoral approach

91. Anterior approach to subaxial Cx spine
• Smith and robinson

92. Surgical approaches to dorsal spine
• Anterior transpleural - transthorasic

93. Surgical
approaches to
dorsal spine
• Anterolateral
extrapleural
approach

94. Surgical approaches to dorsal spine
• Posterolateral approach

95. Surgical approach to lumbar spine
• Anterolateral
retroperitoneal approach to
lumbar spine

96. Surgical approach
to lumbar spine
• Anterior transperitoneal
/retroperitoneal approach to
the spine

97. Post operative care

98. Follow up
• Patient evaluated at 3 months interval upto 2 years.
Evaluation
Clinical:
Radiological:
Decreased soft tissue shadow
Disappearance of erosions
Return of mineralization
Graft incorporation
Bony ankylosis
Weight gain
Pain relief
Free ROM
Resolution of abscesses
Neurological recovery

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

100. Results
• Definition of favorable status-
– No residual neural impairment
– No sinus/ cold abscess
– No impairment of physical activity due to spinal disease / lesion
– Presence of radiographic quiescent disease

101. Recurrence/ Relapse
• Extradural granuloma
• Severe kyphosis
• Reactivation of lesion
– Poor nutrition
– Resistant organism
– Immuno compromised status

102. Recurrence/ Relapse
• Necessary surgery
• Newer anti TB drugs
• Supportive measures

103. Thank you