TB SPINE.pptx

TUBERCULOSIS OF SPINE
PRESENTER
DR. SHUBHANSHU

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
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

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
bodies, collapse of
and progressive
spinal
spinal
vertebral
elements
deformity”

• Robert Koch : Discovered Mycobacterium
tuberculosis in 1882

EPIDEMIOLOGY
• Tuberculosis : Leading cause of death worldwide from
disease agent
a single infectious
• Globally, extrapulmonary tuberculosis (TB) represented 14% of the 6.4
million TB cases reported in 2017 ,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.

Age Distribution: Can occur at any age but more common in third decade of life.
Racial factors: Musculoskeletal tuberculosis affects primarilyAfricanAmericans,
HispanicAmericans,AsianAmericans, 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 southAfrican, sub Saharan andAsian
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.

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%

PATHOLOGYAND PATHOGENESIS
Main Organism - M. tuberculosis
• Size 3 x 0.3 Micron
• Gram positiveAcid 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

Pathological process
Modes of Spread
• Inhalational
• Inoculation
• Ingestion
• Transplacental

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

Pathogenesis ctd...
STEP 1
Bacilli from primary
focus through blood
stream reach Disc Space
tuberculous granulation
doesnt form proteolytic
enzyme in joint space

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

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

Pathogenesis ctd…
STEP4
The bone weakened by
the infection collapses
under the weight of
human body

Pathogenesis of TB Spine
STEP5
The deformed spinal
column compresses spinal
cord producing functional
impairment

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

Pannus - at periphery granulation tissue form
ring of articular cartilage
Rice Bodies - loose sheet or flakes of
necrosed articular cartilage and acumulation of articular
cartilage in synovial joint
Kissing lesion-Necrosis of subcondral
bone on each side of joint

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
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: First 3decades
• 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) • Late onset paraplegia (Group B)
• 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
• 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, 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

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

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
• CRP: Raised

Investigations
• 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

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
– Gene Xpert

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

• 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

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

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
– 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
antitubercular era :
– Serious sinus formation
– Pseudoarthrosis
– Recurrence of lesion
– Neurological deterioration
– Death

• 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

• 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

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
• 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.

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

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

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

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 discard after 1-2 years after
surgery

WHO INDEX-TB Guidelines -
for extrapulmonary TB in India
2RHZE/10RHE
All patients require close monitoring for development or progression of
neurological deficit in the first 4 weeks of treatment.
Some patients require surgical intervention.
Total treatment duration: 12 months (extendable to 18 months on a case-bycase
basis)
Optimum management of spinal TB requires the involvement of multiple
specialists including a spinal orthopaedic surgeon, microbiologist/infectious
diseases specialist and spinal radiologist, as well as physiotherapists and
orthotists.
All presumptive spinal TB cases should be referred and managed in
specialist centres.

Patients without neurological deficit should be advised to return to the clinic
immediately if new symptoms develop, and all ambulant patients should be
assessed weekly for neurological signs. Patients with neurological deficit require
staging and grading of their deficit.
These patients should be assessed weekly with neural charting to detect neural
recovery or deterioration. Repeat X-rays of the spine are suggested every 3
months following initiation of treatment to assess for radiological healing.
Repeat MRI scans are suggested at 6, 9, 12 and 18 months following initiation of
treatment to assess healing.
At the end of treatment, all patients require follow up every 6 months for at least 2 years, and should be
told to return to the clinic promptly if they develop new symptoms in the interim.
While some require early surgical intervention, most patients can be managed with ATT alone in the
initial phase of treatment.
Surgery may be required for two principal purposes in spinal TB-to establish diagnosis, or to treat
spinal deformity, instability and neurological deficit.

Where available, percutaneous biopsy under CT guidance reduces the need for open
biopsy, but this may still be required in some cases, particularly where imaging results are
atypical for spinal TB and the diagnosis is uncertain.
Patients with large, fluctuant cold abscesses may require therapeutic aspiration to relieve
symptoms and promote healing.

Indications for surgery in TB spine with
neurological deficit:
• Neural complications developing or getting worse or remaining stationary during the
course of non-operative treatment (3–4 weeks)
• Paraplegia of rapid onset
• Spinal tumour syndrome
• Neural arch disease
• Severe paraplegia – flaccid paraplegia, paraplegia in flexion, complete sensory loss and
complete loss of motor power for more than 6 months
• Painful paraplegia in elderly patients.

Indications for surgery in spinal TB
without neurological deficit:
• When diagnosis is uncertain and open biopsy is indicated
• Mechanical instability – panvertebral disease, where bony involvement of both the
vertebral body and posterior complex is seen on imaging, or disease affects facet joints
bilaterally
• Suspected drug resistance – where patients show inadequate clinical improvement or
deterioration on ATT
• Spinal deformity – severe kyphotic deformity at presentation, or in children at high risk
of progression of kyphosis with growth after healing of disease.

Indications for instrumented stabilization:
● Panvertebral disease
● Long segment disease where a > 4–5 cm long graft is required to bridge the
gap after surgical decompression in dorsal spine
● In lumbar and cervical spine
● When kyphosis correction surgery is contemplated
● Lesion in a junctional area
Preparation for surgery
● Multidrug therapy at least 3 to 6 weeks before surgery to suppress the infection
● Medical treatment for comorbidities
● Nutritional support
● Correct hypoproteinemia
● Obtain relevant imaging studies

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

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

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

• Anterolateral extrapleural approach

• 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

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