SPINAL INFECTION

MOHAMMAD SYARIF
 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

• 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
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
• 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
 PATHOGENESIS OF TB SPINE

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 OF TB SPINE

STEP 3
The infection spreads to vertebral
bodies above and below the disc
PATHOGENESIS OF TB SPINE

STEP 4
The bone weakened by the
infection collapses under the
weight of human body
PATHOGENESIS OF TB SPINE

STEP 5
The deformed spinal column
compresses spinal cord producing
functional impairment
PATHOGENESIS OF TB SPINE

STEP 6
Over time, the deformed
vertebrae heal and fuse
This may further compress nerve
roots causing pain and
neurological deficit
PATHOGENESIS OF TB SPINE
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
TYPES OF VERTEBRAL LESIONS
• 4 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
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: Specific Symptoms:

• Malaise • Pain/Night cries
• Loss of weight/appetite • Stiffness
• Night sweats • Deformity
• Evening rise of temperature • Restricted ROM
• Enlarged lymph nodes
• Abscess
• Neurodeficit
 CLINICAL FEATURES
Healed stage

Constitutional symptoms: Specific Symptoms:

• Malaise • Pain/Night cries
• Loss of weight/appetite • Stiffness
• Night sweats • Deformity
• Evening rise of temperature • 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)

•LATE ONSET PARAPLEGIA (GROUP B) •EARLY ONSET PARAPLEGIA (GROUP A)

• APPEARS MORE THAN 2 YEARS OF DISEASE IN • APPEARS WITHIN 2 YEARS OF ONSET –

VERTEBRAL COLUMN DURING THE ACTIVE PHASE

• UNDERLYING PATHOLOGY –DUE TO • UNDERLYING PATHOLOGY

• MECHANICAL PRESSURE ON CORD – INFLAMMATORY EDEMA

– TB DEBRIS – TB GRANULATION TISSUE

– TB SEQUESTRA FROM BODY AND DISC – ABSCESS

– INTERNAL GIBBUS – CASEOUS TISSUE

– CANAL STENOSIS / SEVERE DEFORMITY – ISCHAEMIS LESION OF CORD (RARE)

• POOR PROGNOSIS • GOOD 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
PATHOLOGY OF TB PARAPLEGIA
Extradural mass:
• The Commonest mechanism affecting spinal cord function
• Material compressing may be
– Fluid pus
– Granulation tissue
– Caseous material
PATHOLOGY OF TB PARAPLEGIA
Bony Disorders:
• Sequestra from disc or body
• Internal Gibbus
• Pathological Dislocation
PATHOLOGY OF TB PARAPLEGIA
• Meningeal changes
– Dura is not involved
– Cicatrisation of extradural TB granulation tissue (Peridural fibrosis)
– Poor recovery despite adequate surgical decompression
PATHOLOGY OF TB PARAPLEGIA
• 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
PATHOLOGY OF TB PARAPLEGIA
• 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

PATHOLOGY OF TB PARAPLEGIA
• 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
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
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
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
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
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
RADIOLOGICAL INVESTIGATIONS
• 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
RADIOLOGICAL INVESTIGATIONS
• 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
RADIOLOGICAL INVESTIGATIONS
• Paradiscal lesions:
– Commonest lesions
– Spreads through arterial
supply
– Reduced disc space –
Earliest sign
– Loss of vertebral margins
– Increased pre-vertebral soft
tissue shadow.
RADIOLOGICAL INVESTIGATIONS
• Central type:
– Spread through the batson’s
venous plexus/ branches of
posterior vertebral artery.
– Minimal Disc space
reduction
– At the end concentric
collapse
RADIOLOGICAL INVESTIGATIONS
• Appendicular type of
lesion
– Rare
– Isolated infections of
pedicles / lamina/
transverse processes/
Spinous process.
– Intact disc space
– Para vertebral
shadows
RADIOLOGICAL INVESTIGATIONS
• Lateral shift and scoliosis
– More destruction of
vertebrae on one side

• Kyphotic deformity
– Due to collapse of bone
– Forward angulations
RADIOLOGICAL INVESTIGATIONS
• 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
RADIOLOGICAL INVESTIGATIONS
• Spine at risk sign
CLINICO-RADIOLOGICAL CLASSIFICATION OF
TYPICAL TB SPONDYLITIS
BASIC PRINCIPLES OF MANAGEMENT

Expeditious medical
Early Diagnosis
treatment

Expect Good
Outcome

Aggressive surgical
Prevent Deformity
approach
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
EVOLUTION OF
TREATMENT
PRE ANTI- TUBERCULAR
ERA
• Sanatorium treatment
– Sanatorium regimes and rest
– Fresh air, Sunshine
rooftops
EVOLUTION OF
TREATMENT
PRE ANTI- TUBERCULAR
ERA
• Surgery was not attempted due to fear of
secondary infection and death
• Operative procedure were developed for either
treatment or prevention of paralysis
EVOLUTION OF
TREATMENT
PRE ANTI- TUBERCULAR
ERA
• Results of surgeries done in pre
anti- tubercular era :
– Serious sinus formation
– Pseudoarthrosis
– Recurrence of lesion
– Neurological deterioration
– Death
EVOLUTION OF
TREATMENT 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
EVOLUTION OF
TREATMENT 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 Middle path
Radical surgery
chemotherapy regime
only
 LINE
1ST
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
New* (Category I) Previously treated**(Category II)
Sputum smear-positive relapse,
New sputum smear-positive, New
Sputum smear-positive failure, Sputum
sputum smear-negative,
smear-positive treatment after default,
New extrapulmonary tuberculosis,

2H3R3Z3E3S3 +
2H3R3Z3E3 + 4H3R3
1H3R3Z3E3
+ 5H3R3E3
• H: Isoniazid (300 mg) R: Rifampicin (450 mg), E:
Z: Pyrazinamide(1500 mg) S: Ethambutol (1200 mg),
Streptomycin (750 mg)
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+ 4 months
ETB 4 months
– INH + PZA 4 months
– INH+ RMP 4 months
– INH
• 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
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 +/- Recurrence of disease or of neural
decompression +/- fusion complications
3 Anterior transposition of Sever Kyphosis (>60 degree) + /
cord (Extrapleural neural deficit
anterolateral approach)
4 Laminectomy Extradural granuloma/ Old healed
disease presenting as secondary canal
stenosis/ Posterior spinal disease
SURGICAL SPPROACHES
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
POST OPERATIVE CARE
FOLLOW UP
• Patient evaluated at 3 months interval upto 2 years.
Evaluation

Radiological:
Clinical:
Decreased soft tissue shadow
Weight gain
Disappearance of erosions
Pain relief
Return of mineralization
Free ROM
Graft incorporation
Resolution of abscesses
Bony ankylosis
Neurological recovery
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.