TB Spine Diagnosis

Tuberculosis of Spine
Dr. Ankit Madharia
Junior Resident
Lata Mangeshkar Hospital, Nagpur

Introduction
• 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.

Historical aspects
• TB: Oldest recognized disease of mankind
• India – Rigveda and Atharvaveda (3500-1800 BC) and Samhita’s
of Charaka and Shushruta (1000 and 600 BC) : “YAKSHMA”
• TB also recognized in Egyptian mummies

Historical aspects
• Percival Pott : Described TB in
spinal column in 1779
• ”Destruction of disc
space and adjacent
vertebral bodies, collapse of
spinal elements and
progressive spinal deformity”

Historical aspects
• Robert Koch : Discovered
Mycobacterium tuberculosis in
1882

Epidemiology
• Tuberculosis : Leading cause of death worldwide from
a single infectious disease agent
• The Number of new cases of tuberculosis worldwide
roughly correlates with economic conditions

Epidemiology
• 8 million people get TB every year, of whom 95% live in
developing countries
• An estimated 2 million people have active Spinal TB
worldwide

Epidemiology
India
• 1/5th of total TB Cases
• 1- 3% of all involve skeletal system.

Predisposing Factors
• Malnutrition
• Poor Sanitation
• Over crowding
• Close contact with TB
patient
• Multiple pregnancy
• Immunodeficiency state

Pathology
• 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

Pathology
• TB bacilli phagocytosed by the
mononuclear cells
• Epitheloid cell formation
• Langhans giant cell formation by fusion
of epitheliod cells
• Lymphocytes form a ring around the
lesion
• Tubercle formation

Pathogenesis of TB Spine
STEP 1
Bacilli from
primary focus
through blood
stream reach
Disc Space

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

• STEP 3
The infection
spreads to
vertebral
bodies above
and below the
disc

STEP 4
The bone weakened by
the infection collapses
under the weight of
human body

• STEP 5
The deformed spinal
column compresses spinal
cord producing functional
impairment

• STEP 6
Over time, the
deformed vertebrae
heal and fuse
This may further
compress nerve roots
causing pain and
neurological deficit

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

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

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

Clinical Features
• Age: Common in 1st 3 decades
• Sex: Male = Female

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

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

Neurological deficit
• 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

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

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

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

Extradural mass:
• The Commonest mechanism affecting spinal cord
function
• Material compressing may be
– Fluid pus
– Granulation tissue
– Caseous material

Bony Disorders:
• Sequestra from disc or body
• Internal Gibbus
• Pathological Dislocation

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

• 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

• 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

• 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

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

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

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

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

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

Investigations
• Guinea pig Inoculation
– Pus/ aspirate is inoculated intraperitoneally .
– Positive cases reveal tubercle after 5-8 weeks
– One of the most reliable proof of Tuberculous pathology

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

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

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

• 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

• 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

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

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

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

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

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

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.

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.

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

• Spine at risk sign

Clinico-radiological classification of
Typical TB Spondylitis

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

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

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

• Sanatorium treatment
– Sanatorium regimes and
rest
– Fresh air, Sunshine
rooftops

• Surgery was not attempted due to fear of
secondary infection and death
• Operative procedure were developed for
either treatment or prevention of paralysis

• Results of surgeries done in pre
anti- tubercular era :
– Serious sinus formation
– Pseudoarthrosis
– Recurrence of lesion
– Neurological deterioration
– Death

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

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.

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

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

Newer drugs
• Amikacin, Kanamycin, Capriomycin
• Ciprofloxacin, Ofloxacin, Levofloxacin
• Rifabutin
• Clarithromycin
• Clofazimine
• Ethionamide
• Cycloserine

Policy of drug treatment- DOTS
• H: Isoniazid (300 mg) R: Rifampicin (450 mg),
Z: Pyrazinamide(1500 mg) E: Ethambutol (1200 mg),
S: Streptomycin (750 mg)
New* (Category I) Previously treated**(Category II)
New sputum smear-positive,
New sputum smear-negative,
New extrapulmonary tuberculosis,
Sputum smear-positive relapse,
Sputum smear-positive failure,
Sputum smear-positive treatment
after default,
2H3R3Z3E3 + 4H3R3
2H3R3Z3E3S3 + 1H3R3Z3E3
+ 5H3R3E3

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”

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.

Middle path regime
• Drugs
– INH+ RMP+ ETB 4 months
– INH + PZA 4 months
– INH+ RMP 4 months
– INH 4 months
• Supportive therapy
– Hematinics, Multivitamins,
High protein diet

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

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

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.

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

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)

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

Algorithm for management of pott’s
paraplegia

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

Anterior
approach to the
C1-C2
• Transoral approach

Anterior approach to subaxial Cx
spine
• Smith and robinson

Surgical approaches to dorsal spine
• Anterior transpleural - transthorasic

Surgical
approaches to
dorsal spine
• Anterolateral
extrapleural
approach

Surgical approaches to dorsal spine
• Posterolateral approach

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

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

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

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

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

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

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

Take home message
• Conservative and operative management
have their distinct advantages and
disadvantages
• Judicious choice of treatment for pott’s
spine usually gives good results.

TB Spine Diagnosis

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