2. INTRODUCTION
• Oldest recognition disease of
mankind.
• In 1779 Percival Pott presented
the classical description of
spinal tuberculosis.
Destruction of disc space
Destruction of vertebral
bodies.
Collapses of spine & kyphosis.
4. Epidemiology
• Leading cause of death worldwide from a single
infectious disease agent.
• The Number of new cases of tuberculosis
worldwide roughly correlates with economic
conditions.
• 8 million people get TB every year, of whom
95% live in developing countries.
• An estimated 2 million people have active
Spinal TB worldwide.
5. IN INDIA
• 1/5th of total TB Cases.
• 1- 3% of all involve skeletal system.
• Skeletal tuberculosis is common in
India
• Vertebral tuberculosis is the commonest
form of skeletal tuberculosis ( > 50%)
• Dorsal spine - most commonly involved
• Mostly seen in first 3 decades.
7. Predisposing Factors
• Malnutrition.
• Poor Sanitation.
• Over crowding.
• Close contact with
TB patient.
• Multiple pregnancy.
• Immunodeficiency
state.
8. PATHOGENESIS
Causative organism
• Mycobacterium 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
9.
10.
11. Pathogenesis of TB Spine
• STEP 1
• Bacilli from primary focus through blood
stream reach Disc Space.
12. 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.
24. Neurological deficit/Potts paraplegia
• 10-30% cases – Neurological deficit.
• Age: 1st 3 decades.
• Disease below L1 vertebrae rarely
causes Paraplegia.
• Highest Incidence of paraplegia seen
in TB of lower thoracic vertebrae.
• 24% of cervical TB shows neural
deficit.
25. Classification of TB Paraplegia
Griffiths, Seddon and Roaf 1956
Early onset
paraplegia (group A)
<2yrs,active phase
Oedema,abscess,caseus&
granulation tissue
Good
prognosis
Late onset
paraplegia (Group B)
>2yrs,mechanical pressure on cord.
TB Debris
TB Sequestra from body and disc
Internal gibbus
Canal stenosis / Severe deformity
Poor prognosis
26. 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.
27. Pathology of TB Paraplegia
1.Inflammatory oedema.
Vascular stasis
Tubercular toxins.
early onset paraplegia
Quick recovery
2.Extradural mass:
The Commonest
mechanism affecting
spinal cord function
Material compressing
may be
Fluid pus
Granulation tissue
Caseous material
28. 3.Bony Disorders:
Sequestra from disc or
body.
Internal Gibbus.
Pathological Dislocation.
4.Meningeal changes
Dura is not
involved.
Cicatrisation of
extradural TB
granulation tissue
(Peridural fibrosis)
Poor recovery
despite adequate
surgical
decompression.
29. 5.Infarction of
Spinal cord.
Caused by
Endarteritis
Periarteritis
Thrombosis
Paralysis is
irreparable.
Can also happen
postoperatively.
6.Extradural
Granuloma and
tuberculoma.
Rarely a small
tuberculoma of spinal
cord or Diffuse
extradural granuloma
may cause neurodeficit
without any
radiological evidence
TB of vertebrae.
Presents as Spinal
tumor Syndrome
30. Clinical features of Pott’s Paraplegia
• Paraplegia itself – Rare.
• Spontaneous muscle twitching in lower
limbs.
• Clumsiness while walking.
• Extensor plantar response.
• Exaggerated reflexes – Sustained clonus
of patella and ankle.
• Motor affected first – then Sensory.
• Sense of position and vibration – last to
disappear.
32. Mantoux test
Erythema of
more than 20
mm at 72 hours
– Positive
Negative test,
in general, rules
out the disease
Biopsy
In case of
doubt, it is
mandatory to
prove the
diagnosis by
obtaining the
diseased
tissue.
33. 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).
38. Radiological-plan X-rays
• 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
39. Radiological-plan X-rays
• Anterior type of lesion
– beneath the
anterior longitudinal
ligament &
periosteum.
–Collapse and disc
space reduction is
usually minimal and
occurs late.
–Erosion is primary
mechanical.
40. Radiological-plan X-rays
• Paradiscal lesions:
–Commonest lesions.
–Spreads through
arterial supply.
–Reduced disc space –
Earliest sign.
–Loss of vertebral
margins.
–Increased pre-
vertebral soft tissue
shadow.
41. Radiological-plan X-rays
• Central type:
–Spread through
the batson’s
venous plexus/
branches of
posterior
vertebral artery.
–Minimal Disc
space reduction.
–At the end
concentric
collapse.
42. Radiological-plan X-rays
• Lateral shift and
scoliosis.
– More destruction of
vertebrae on one side.
• Kyphosis deformity
– Due to collapse of
bone.
– Forward angulations-
-1-2-knuckle
-3-gibbus
->3 round kyphosis.
44. Radiological-CT Scan
• 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.
45. Radiological-MRI
• Lack of ionizing radiation, high contrast
resolution & 3D imaging.
• Detect marrow infiltration in vertebral bodies,
leading to early diagnosis.
• Changes of discitis.
• Assessment of extradural abscesses /
subligamentous spread.
• Skip lesions.
• Spinal cord involvement.
• Spinal arachanoiditis.
46. 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.
47. Basic Principles Of Management
Early Diagnosis
Expeditious medical
treatment
Aggressive surgical
approach
Prevent Deformity
Expect Good
Outcome
48. Evolution Of Treatment:
– Undergone tremendous
revolutionary changes.
– Ancient Indians used
herbal preparation
Sipurda.
–Pott & Charcot
applied hot iron to
drain pus.
–Hippocrates
advocated traction
and other means to
correct deformity
50. Surgeries At Pre Antitubercular Era
• Laminectomy & laminotomy :Chipault 1896.
• Costo-transversectomy :Menard in 1894.
• Posterior mediastinotomy : By Obalinsky for
drainage of abscess.
• Calves operation :1957 to aspirate abscess.
• Lateral rhachiotomy of Capener: Capener in 1933.
• Anterolateral decompression of Dott and
Alexander:
• Posterior decompression with posterior spinal
Arthrodesis: 1911 onwards.
51. Surgeries At Pre Antitubercular Era
• Surgery was not attempted due to
fear of secondary infection and
death.
• Operative procedure were developed
for either treatment or prevention of
paralysis.
• Principle was more direct approach to
diseased part.
52. Results of surgeries done in pre
anti- tubercular era :
–Serious sinus
formation.
–Pseudo-arthrosis.
–Recurrence of
lesion.
–Neurological
deterioration.
–Death.
53. • Treatment has taken dramatic turn for
better with discovery of anti tubercular
drugs.
–1943 – PAS
–1944 – Streptomycin
–1951 – INH(magic bullet)
–1970 – Rifampicin and short course
chemotherapy.
Evolution of treatment
With Anti- Tubercular drugs
58. Drugs for MDR TB.
Group 1 Rifabutin,ethambutol,pyrazina
mide.
Group 2 Kanamycin,amikacin,capreomyc
in,streptomycin
Group 3 Levofloxacin,moxifloxacin,ofloxacin.
Group 4 Paraaminosalicycyclic
acid,cycloserine,thionamide.
Group 5 Clofazimine,amoxycillin,clarithromy
cin
59. Adverse effect of ATT
Streptomycin Eight nerve damage, aplastic
anaemia,neutropenia.
PAS Gastrointestinal irritation.
Isoniazid. Peripheral neuritis,psychological disturbance.
Thioacetazone Liver damage,skin rash.
Ethambutol Optic neurutis,retrobulbar neuritis.
Rifampicin Increased SGPT,sr bilirubin,influenzae like syndrome
Pyrazinamide Hepatotoxicity,arthralgia
60. 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”
61. Middle path regime
•Rest
–In hard bed
–Or POP bed for children
–Cervical TB requires traction in
early stage to put the diseased
part in rest.
63. Middle path regime
• Monitoring
–Radiographs and ESR at 3-6
months interval
–MRI at 6 months interval
for 2 years.
64. Middle path regime
• Gradual mobilization
–Encouraged in absence of
neurological deficit with
support of spinal braces
–As soon as the diseased part
permits.
65. 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.
66. 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.
67. Middle path regime
• Absolute Indications of surgery
1. No progressive recovery after fair trial of
conservative treatment(3-4wks).
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).
68. Middle path regime
Surgery Indications
Decompression(+/- fusion) Too advanced disease, Failure
to respond to conservative
therapy
Debridement +/-
decompression +/- fusion
Recurrence of disease or of
neural complications
Anterior transposition of cord
(Extra pleural anterolateral
approach)
Sever Kyphosis (>60 degree) +
/ neural deficit
Laminectomy Extradural granuloma/ Old
healed disease presenting as
secondary canal stenosis/
Posterior spinal disease
69. APPROACH FOR ABSCESS DRAINAGE
Ilio-psoas
abscess
Anterior approach.
Anterolateral
approach.
Medial site
of thigh
Ludloffs approach
Cervical
spine abscess
Longitudinal incision
anterior or posterior to
sterno-cleidomastoid.
72. Some surgical approaches
Dorsal spine Anterior transpleural approach.
Anterolateral extra pleural
approach.
Posterolateral approach.
Thoraco-
lumber
region
Antero-lateral extra pleural
approach.
Extra pleural extra peritoneal
approach through bed of 11th rib.
Lumber spine Retroperitoneal approach.
76. 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
