2. INTRODUCTION
•Tuberculosis - oldest disease afflicting humans.
•Seen in Egyptian mummies - back to 3400 BC.
•Among overall cases,
- 10% involve musculoskeletal system
- Among them 50% involves spine.
world’s population
of TB population is
•According to WHO – 1/3rd
affected by tuberculosis
- among them 1/5th
in india.
3. • Every day 1000 dies of tuberculosis in india.
• Neurological involvement- 47%
• Dorso-lumbar spine involved most commonly.
4. TB and HIV
• 10% cases occur in HIV patients
• Disseminated and extrapulmonary disease is
more common with CD4<200
6. WHY MOST COMMONLY OCCURS AT
DL JUNCTION???
• Greater extent of movement
• Degree of weight bearing and microfracture
• Large spongy cancellous bone
• Proximity to kidney and cistern chili
D-L region ---> lumbar ---> upper dorsal --->
cervical ---> sacral.
7. PATHOGENESIS
• secondary infection- lung
- genitourinary system.
• spread - hematogenous route.
• Initially starts with , Inflammatory
reaction. Then there is proliferation of
granulation tissue,
invasion of macrophages,
epitheloid cells, lymphocytes and
tissue necrosis.
8. - Tissue necrosis and breakdown of inflammtory cells
result in paraspinal abscess, which mostly
accumulate in the anterior aspect of vertebral
bodies under anterior longitudinal ligament.
- Skip lesions are also seen ocassionally.
9. CLINICAL PRESENTATION
• Presentation depends on the following:
– Stage of disease
– Site
– Presence of complications such as neurologic deficits,
abscesses, or sinus tracts.
The reported average duration of symptoms at the
time of diagnosis is 3-4 months.
10. CLINICAL FEATURES
• Common in 1st three decades of life.
• Males=females
• Back pain is the earliest
and most common symptom.
– Patients have usually had
back pain for weeks prior
to presentation
11. 1)Constitutional symptoms(40% cases)
• Malaise
• Loss of appetite
• Night sweats
• Evening rise of temperature
2)Specific symptoms
• Night crises
• Stiffness
• Restricted ROM
• Enlarged lymph nodes
• Abscess
• Neurological deficit
12. TYPES OF TB SPINE
1)Caseous exudative :
• More common in children
• More destruction and residual deformity
• More exudation
• Abscess formation
2)Granular type
• More in adults
• Less destructive
• Insiduous onset
• Abscess formation rare
13. INVESTIGATIONS
1) CBC-Decreased Hb, Lymphocytosis
2) ESR-Raised in active stage of the disease
Normal ESR for 3 months suggest patient is in recovery
phase.
3) MONTOUX/TUBERCULIN SKIN TEST- positive test can be
observed 1 to 3 months after infection.
4) ZIEHL-NEELSEN STAINING - Inexpensive method
- Detects acid fast bacilli
- Culture are available only after a few
weeks.(2-3 week)
- Positive only 50% cases.
18. CT SCAN
- Pattern of bony destruction
- calcification in abscess
-detects early lesion before
they appear on xray
MRI
- Detect marrow infiltration
in vertebral bodies.
- changes of discitis
-helps in differentiating
intradural from extradural
lesions
- Skip lesions
- Spinal cord involvement.
19. SPINAL LESION OF TUBERCULOSIS
• Intradural involvement-very rare
• Extradural involvement-
– Paradiscal (due to arterial spread)
– Central(venous spread)
– Anterior(due to subperiosteal spread)
– Appendical
20. Comparision of various types of spine
TB
Paradiscal lesions Central type of lesions
Most common lesion 2nd mostcommon
Arterial supply Spread through venous plexus
Reduced disc space(earliest sign) Minimal disc space reduction
Loss of vertebral margins Concentric collapse
Increased prevertebral soft tissue
Anterior type lesion Appendicial lesion
Starts beneath the anterior longitudinal
ligament
Isolated infection of pedicles
,lamina/transverse process/spinous
process
Collapse and disc space reduction
minimal and late
Intact disc space
Erosion mechanical
21. Clinico radiological classification of spinal tuberculosis
STAGE CLINICO RADIOLOGICAL
FEATURE
DURATION
PRE DESTRUCTIVE •straightening of
curvatures
•spasm of perivertebral
muscles
<2 MONTHS
EARLY DESTRUCTIVE decreased disc space
with paradiscal erosions
2-4 MONTHS
MILD ANGULAR
KYPHOSIS
2-3 vertebrae
involvement
(kyphotic angle 10-30*)
4-9 MONTHS
MODERATE ANGULAR
KYPHOSIS
>3 vertebrae
involvement
(K:30-60*)
6-24 MONTHS
SEVERE KYPHOSIS >3 vertebrae
involvement(K>60*)
>2 YEARS
23. DD: PYOGENIC SPONDYLITIS
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
24. DD-NEOPLASTIC LESIONS
• In early stages of central type of tuberculosis of spine, there is
no involvement of intervertebral disc thereby mimicking
neoplastic lesion.
• However, in chronic tubercular lesion intervertebral disc is
involved making it easy to differentiate from neoplastic lesion
(disc not involved -“good disk, bad news; bad disk,
good news”)
28. SEDDON’S CLASSIFICATION OF
TUBERCULOUS PARAPLEGIA:
• GROUP A (EARLY ONSET PARAPLEGIA) a/k/aParaplegia
associated with active disease :
- During the active phase of the disease within first 2 years of onset
- Pathology can be inflammatory edema, granulation tissue,
abscess, caseous material or ischemia of cord.
GROUP B (LATE ONSET PARAPLEGIA) a/k/a Paraplegia associated
with healed disease:
- Usually after 2 years of onset of disease.
- Can be due to recrudescence of the disease or due tomechanical
pressure on the cord.
- Pathology can be sequestra, debris, internal gibbus or
stenosis of the canal.
29. KUMAR’S CLASSIFICATION OF TUBERCULOUS
PARA/TETRAPLEGIA (Predominantly based on motor
weakness)
Stage Clinical features
I Negligible Patient unaware of neural deficit,
Plantar extensor and / or ankle clonus
II Mild Patient aware of deficit but manages to walkwith
support (Spastic paresis)
III Moderate Nonambulatory because of paralysis (in extension),
sensory deficit less than 50%
IV Severe III + Flexor spasms / paralysis in flexion/sensory deficit
more than 50% / sphincters involved
30. BASIC PRINCIPLES OF MANAGEMENT
• Early diagnosis
• Medical Treatment – AKT and brace
• Surgical Approach to drain abscess,
debridement and fusion
• Stabilization to Prevent Deformity
32. RNTCP GUIDELINES
Category Type Regimen
I All “new” pulmonary,
extrapulmonary and other TB
patients
2(HRZE)3 + 4(HR)
II All relapses, treatmentafter
defaults, failures andothers.
2(HRZES)+ 1(HRZE)+
5(HRE)
•ENTIRE DUARTION OF CHEMOTHERAPY LASTS FOR 16-18 MONTHS
•10 MG PYRIDOXINE FOR PREVENTION OF PERIPERAL NEUROPATHY
33.
34. SMYPTOMS COMMONLY SEEN AFTER
TAKING AKT
• Hepatits(isoniazide)
• Peripheral neuritis(isoniazide)
• Color changes in urine(rifampicine)
• Optic neutitis(ethambutol)
• Deafness(steptomycin)
35. SURGICAL INDICATIONS
• failure of conservative management
• Abscess formation
• Progressive neurological deficiet
• Advanced cases- Sphincter involvement, flaccid paralysis or severe
flexor spasms
• Residual kyphotic deformity
36. Various surgical Approaches
Cervical Dorsal Lumbar
Anterior Anterior trans thoracic Antero lateral approach
to lumbar spine
Anterior trans
abdominal approach
Posterior midline spinal
Approach-MC used in all
posterior method of spine
TB
37. SURGICAL STEPS (ALL POSTERIOR)
posterior midline approach
lamina, facet joints, and transverse processes were exposed
posterior pedicle screws installed
Decompression
(Partial or total laminectomy If necessary, a facetectomy or pediculectomy)
Debridement(Drainage of abscess)
Fusion
38. FOLLOW UP AND EVALUATION
• Followup at every three months interval upto 1.5 year.
• Clinical: Investigation
1. Weight gain - CBC
2. Pain relief - ESR
3. Free ROM - CRP
4. Resolution of Abscess
•
1.
Radiological
Decreased soft tissue shadow
2. Disappearance of erosion
3. Return of mineralisation
4. Bony Ankylosis