3.  Centre portion of each
intervertebral disc is filled
with gel like elastic
PULPOSUS) which along
with sturdy elastic collagen
from vertebra to vertebra
 Annulus fibrosus enhances
rotational stability of
spine and helps to resist
4. EMBRYOLOGY OF VERTEBRAL
 Formed from sclerotome portions of somites(derived
from paraxial mesoderm)
 Each sclerotome-loosely arranged cells cranially &
densely packed cells caudally.
 Some of the densely packed cells move cranially
opposite the centre of myotome
5.  Remainin densely packed cells fuse with loosely
arranged cells of immediately caudal sclerotome
MESENCHYMAL CENTRUM(primordium of body of
 Nerves lie in close relation to IVD and intersegmental
arteries lie on each side of vertebral bodies.
 Notochord persists and enlarges only in the region of
IVD…..contributes to formn of NUCLEUS PULPOSUS
which later gets surrounded by circular fibres of
6.  NP+AF
 Resegmentation of sclerotomes into definitive
vertebrae causes myotomes to bridge the
IVD…gives them the capacity to move the spine
7.  Spinous and transverse processes develop from
chondrification centres(which appear at 6th week of
embryonic life) in vertebral arch.
 Ossification in vertebral arches-8th week
 At birth-each vertebra has 3 bony parts connected
by cartilageBony halves fuse during 1st 3-5yrs
 Five secondary ossificn centres appear in vertebrae
 All secondary centres unite with rest of vertebrae-
8. POTT’S POTT’S SPINE
Dr SREEDEVI PK
9. TUBERCULOSIS OF SPINE
 Vertebral TB-M.C form of skeletal TB(50% of all
cases of TB of bones&joints)
 M.C-1st 3 decades
 Equal in both sexes
 Any one/several vertebrae
 M.C-Lowr thoracic & lumbar spine
10. Infectious exudate may spread anteriorly beneath anterior
longitudinal ligament~>neighbouring vertebrae
Advances&destroys epiphyseal cortex,intervertebral
Infection begins in cancellous area of vertebral
body(Central/anterior/epiphyseal in location)
11.  Note:infection of posterior bony arch and
tyransverse process is unusual
 Granulation tissue develops posteriorly-encircles &
compresses spinal cord & nerve roots(more likely in
thoracic spine ‘cause of small calibre of spinal canal
12. Posterior element involvt of C2(axial
CT image showing reactive sclerosis)
Penetrates the ligament
Migrates in various directions.
Abscess tracks along lines of least
resistance(along fascial planes,blood
vessels & nerves
to sterno mastoid
(a point at postr
confined as a
for a long time
16.  Exudate may spread laterally to extrapleural space-
induces NON SPECIFIC PLEURAL EFFUSION
 If exudate penetrates ALL,
 occupies mediastinum
 gravitates through diaphragm to
the LUMBAR ASPECT
 Rarely,thoracic cold abscess may track backward b/w
transverse processes&follow intercostal nerve-erupts on
• Tuberculous exudate enters PSOAS SHEATH
• Appears below inguinal ligament on medial aspect of thigh
• May spread laterally beneath iliac fascia
• Emerges at iliac crest at the anterior superior iliac spine
• Follows great vessels….may erupt alongside femoral vessels in
triangle of Scarpa or in gluteal region
• Or forms an abscess abpve iliac crest posteriorly
19. Route of spread
 TB of spine is always secondary.
 Bacteria reach spine via hematogenous route from
lungs or lymph nodes.
20. TYPES OF VERTEBRAL TB
1) PARADISCAL –
BETWEEN THE TWO
OF TWO ADJACENT
2) CENTRAL- BODY OF
SINGLE VERTEBRA IS
21. 3) ANTERIOR- INFECTION IS LOCALISED TO THE
ANTERIOR PORTION OF THE VERTEBRAE.
4)POSTERIOR-POSTERIOR COMPLEX i.e
PEDICLE,LAMIINA,SPINOUS OR TRANSVERSE
PROCESS ARE INVOLVED.
5)APPENDICEAL-RARE, INVOLVES TRANSVERSE
22. COLD ABSCESS
 Collection of pus and tubercular debris from
 Can travel in any direction.
23.  Spread beneath the anterior longitudinal
ligament- pre vertebral abscess.
 Spread posteriorly and cause pressure over the
 Spread through the sides of the vertebra –
para vertebral abscess.
Sometimes penetrates the anterior longitudinal
ligament – lines of least resistance i.e. fascial
24. CLINICAL PICTURE
 Constitutional symptoms antedate local spinal
loss,night sweats,afternoon or evenin rise of temp
 Frequently iniated by an exanthem or trauma.
 Spine- -Stiff and painful on movt.
- Pain is localised to site of involvement/referred
dependin on specific nerve root irritation
- Localised KYPHOTIC deformity.
(Tender to percussion)
27.  If any suspicion of TB spine………..
Palpate spinous processes by sliding finger
from cervical spine to sacrum…….so that even a
small knuckle kyphosis (step/prominence) is not
missed…………..thus making the diagnosis before
gross vertebral destruction has occurred.
 Stiffness,weakness&awkwardness of lower
extremities herald onset of PARAPLEGIA.
28. CHARACTERISTICS OF SPECIFIC
 Pain over cervical vertbrae/referred to
 Pain aggravated by pressure on top of head
 Neck rigidity
 Deformity-normal lordosis is reduced & head is
supported in hands
 Paralysis of arms before legs
 Occasionally death due to dislocation
29.  LOW CERVICAL & UPPER THORACIC
 Pain along brachial plexus or intercostal nerves
 Marked rigidity with angular kyphosis
 Cord symptoms L.C
 Arms affected first
 Horners syndrome
 Neck rigidity-head&neck turn as one
30.  THORACIC&THORACOLUMBAR
 Pain referred to lower extremities(esp lateral
aspect of thighs)
 Girdle pain
 Marked angular kyphosis
 Iliac or psoas abscess
31.  LUMBOSACRAL
 Referred pain to lower extremities
 Deformity slight
 Psoas abscess
 Flexion of hips
32.  ABSCESSES & SINUSES…..
 Cervical&dorsal-Can present away from vertebral
Paraspinal regions,posterior/anterior cervical
triangles,along brachial pkexus in axilla,along
intercostal spaces on chest wall.
 Dorsolumbar&lumbar-Abscess freq tracks down
psoas sheath……palpable in iliac fossa,lumbar
triangle,upper part of thigh below inguinal
33. Psoas abscess-Pseudo-hip flexion deformity(No limitation
of internal & external rotation of hip jt when tested in
position of flexion deformity)
- Can present as a lump in iliac foss
- HEALED STAGE
- -Not ill
- -Regains lost weight
- -No evening rise of temp
- -No spinal pain/tenderness
- -ESR falls
34. -Radiological E/O bone healing in serial Xrays
-But deformity persists
Bony ankylosis of L3-L4 resulting in kyphosis in an old
case of TB spondylitis
Mantoux-helpful in children<2-3yrs….not diagnostic
36. X-RAY APPEARANCES
 Depending on site of lesion TB spine………..
37.  Earliest radiological finding-narrowing of disc
 Loss of definition of paradiscal margins
 Bones look rarefied and osteopenic(40% Ca loss-
 Observed before osseous destructive changes
 Trabecular destruction-atleast 3-5 months from
beginning of infectious process
38.  Late changes-Anterior wedge compression in
anterior vertebral involvement
 Central vertebral body collapse(CONCERTINA
COLLAPSE) in central involvement.
 Destruction of posterior elements in posterior
 Soft tissue swelling&calcificn-highly predictive of TB
 Healing stages-vertebral body&posterior elements
39. Collapsed vertebral body L1-L3
40.  Cervical-b/w vertebral
 Upper thoracic-V-shapd/bulbous/heart shaped
 Low thoracic&thoracolumbar-fusiform shadow
occupy site of psoas shadow
. Increased density and lessening of
size of shadow indicates calcification and healing
41. Axial CT-vertebral body
destruction,paravertebral abscess ext
into spinal canal
42. MODERN IMAGING TECHNIQUES
 CT SCAN
• Assessmt of destructive lesions of vertebral column
• Paravertebral soft tissue swellings
• Degree of neural compromise
• Specially useful in-
1) posterior spinal disease
3)Sacroiliac joint TB
• Suspected areas of disease should be localized before
43.  ISOTOPE BONE SCAN-Localises diseased area by
demonstratin a hot spot even when lesions<5mm
 Note:atleaqst 30-40% calcium must be removed
from a particlr area for radiolucent changes to
44. Anterior wedging and erosion of T9
45. Axial CT image showing vertebral
body destruction&adj soft tissue mass
46.  MRI
• Diagnosis of TB in rare sites incl posterior
elements,vertebral appendages&sacroiliac jt
• Excellent modality to judge health of spinal
cord…detects cord compression.
 ULTRASOUND ECHOGRAPHS
To diagnose presence & size of tuberculous abscess in
lumbar vertebral disease.
47.  GALLIUM SCAN-For disseminated TB
 BIOPSY-By percutaneous technique with CT
guidance………biopsy mateial subjected to culture
BIOPSY & CULTURE-MOST DEFINITIVE
48.  Radiological & MRI e/o healing lags behind biological
healing processes in spinal TB.
 X-rays,MRI-Upto 5months of starting multidrugtherapy
may actually show deterioration in most pts.
 If images don’t show improvement whwn repeated>6
months after onset of Rx….consider alternate
diagnosis/therapeutically refractory disease.
 Rarely-healing accomp by fat replacemt of healed
 AIMS OF Rx
 Halt progression of destruction and deformity
 Prevent and overcome paraplegia.
Treatment should be
prolonged ….and a cautious
attitude maintained for many
years…as recrudescence of
disease can occur even years
 Isoniazid(INH)-most effective anti-TB drug
 INH-5mg/kg/day……300mg usually(adults)
 S/E-peripheral neuropathy,anemia,hepatitis
 Pyridoxine 50mg to be supplemented daily
55.  Ethambutol-25mg/kg/day X 60days
15mg/kg single dose thereafter.
S/E-Visual disturbances……avoid in children
56.  Streptomycin
0.75-1g/day X 60days
1g/day 2-3times weekly thereafter
AVOID IN RENAL
57.  RIFAMPICIN
 Oral single daily dose given ½ hr before
 Relatively mild toxic effects
 Colors urine&othr body fluids bright orange
58.  ***COMBINATION CHEMOTHERAPY***
 Delays emergence of drug resistant strains of
 Rx regimen-
HRE X 6MONTH….
If at the end of 6months,clinical & radiological
IE X 12-18MONTHS
59.  Failure to respond to first line drugs……(due to
bacterial resistance/allergic intolerance/toxic
effects)…..use SECOND LINE DRUGS
 Failure to respond despite adq chemotherapy with
radiological e/o progression of disease or neurological
60. SURGICAL TREATMENT
1) Failure to respond to ATT
2) Radiological e/o progression(enlargmt of
paraspinal abscess shadow)
3) Imminent vertebral collapse
4) Instability of spine
5) Progressive neurological deficit
61.  SURGICAL OBJECTIVES
1) Excise infected tissue as completely as possible
2) Decompress intraspinal neural elements
3) Reduce spinal deformity
4) Provide stability by spinal fusion
62.  PRINCIPLES
1) Removal of all diseased tissue by thorough
2) Correction of deformity
3) Interbody bone grafting & stabilization.
4) Relief of pressure on intraspinal contents.
63. WHAT IS DONE??????
 Major focus of disease is removed
 Spinal deformity reduced
 Intraspinal neural elements decompressed
 Bone defect obliterated
 Spinal stability provided by autogenous bone grafts
64.  PREOPERATIVELY, an ATT regimen is
 Severe destruction-external skeletal fixation with a
 Following removal of diseased focus,distraction aids
in overcoming kyphosis.
 Later…bone grafting
65. OPERATIVE AAPROACHES
 Lesions of C4-C6-lateral approach or anterior
 Lesions of C7-T4-posterior thoracoplasty approach
by removing third rib on left side
 Lesions below T40Spine is approached from left
Incision- Along a rib that’s 2ribs
higher than the rib that arises at apex of kyphosis.
66. Surgical procedures
 Lateral rhachotomy
 Albee procedure-aims to unite the spinous processes
by a single cortical graft(s/c aspect of
tibia)….fixed by sewing muscles over it.
 Hibbs procedure-only local bone is used
 Combined procedure
 Circumduction fusion
67. POTT’S PARAPLEGIA
68. POTT’S PARAPLEGIA
Pott’s paraplegia can be due to –
- inflammatory causes- oedema,abscess
- mechanical causes-tubercular debris
- intrinsic causes-pathological dislocation
- spinal tumour d/s- extradural granuloma
Most commonly occurs in TB of dorsal spine because
spinal canal is narrowest in this part
69. Seddon’s Classification:
GROUP A_-Early onset - This comes up in active stage of the disease
within first 2 years.
Compressive Agents are inflammatory edema, granulation, abscess,
casseous material, sequestra and rarely ischaemic lesion.
GROUP B -Late onset- Usually after 2 years of onset of the disease.
 due to recurrence or by mechanical pressure. This can be better divided into
paraplegia with active disease and with healed disease.
Active disease - Caseous material, debris, sequestrated disc or
bone, internal gibbus, stenosis and deformity can cause
Healed disease - Usually internal gibbus and acute kyphotic
deformity can also give late onset paraplegia. Usually there is a
continuous traction, compression leading to paraplegia.
70. Kumar’s classification of
stage Clinical features
1 Negligible Unaware of neural deficit,
Upgoing Plantar / Ankle clonus
2 Mild Walk with support
3 Moderate Nonambulatory,
Paralysis in extention,sensory loss
4 Severe 3+ paralysis in flexion/sensory
loss>50%/ Sphinters involved
71. CLINICAL FEATURES OF PARAPLEGIA-
- increased reflexes
- positive Babinski’s sign
72.  In Pott’s paraplegia , motor functions are affected
 The paralysis follows the following stages-
muscle weakness, spasticity , incoordination,
paraplegia in extension , flexor spasms,paraplegia
in flexion and flaccid paraplegia lastly.
73.  TREATMENT OF POTT’S PARAPLEGIA
2)SPINE PUT TO ABSOLUTE REST
3)PARALYSED LIMBS SHOULD BE TAKEN CARE OF.
4)REPEATED NEUROLOGICAL EXAMINATION TO
CHECK FOR WORSENING.
74. Surgical indications
1. No sign of Neurological recovery after trial of 3-4
2. Neurological complication during treatment
3. Neuro deficit becoming worse
4. Recurrence of neuro complication
5. Prevertebral cervical abscesses,neurological signs&
difficulty in deglutition& respiration
6. Advanced cases- Sphincter involvement,
Severe flexor spasms
75. MIDDLE PATH REGIMEN
Widely accepted regimen for tb spine
 Admission,rest in bed or pop cast.
 X-ray and ESR once in 3 months
 Gradual mobilisation in the absence of neurological
 Spinal braces-18 months to 2 years.
76.  Abscesses are aspirated out drained.
 Sinuses heal within 6-12 weeks
 If no neurological complications develop and patient
is responding to the 3-drug therapy , surgery is
 Excisional surgery for posterior spinal disease.
 Operational debridement for patients who do not
show arrest of disease after 3-6 months of