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Tuberculosis of spine

1) Tuberculosis of the spine is the most common form of skeletal tuberculosis, frequently affecting the dorsal spine. 2) It is caused by hematogenous spread of Mycobacterium tuberculosis from a primary focus. This can lead to destruction of vertebral bodies and discs, collapse, deformity, and neurological deficits in advanced cases. 3) Treatment has evolved tremendously from ancient herbal preparations and hot iron drainage to modern multi-drug anti-tubercular regimens with aggressive surgical management to prevent deformity and paralysis when needed.

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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
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
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: • 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
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 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
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 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
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
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 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.
Thank you

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Tuberculosis of spine

  • 1.
    Tuberculosis of Spine Dr.Ankit Madharia Junior Resident Lata Mangeshkar Hospital, Nagpur
  • 2.
    Introduction • Skeletal tuberculosisis common in India • Vertebral tuberculosis is the commonest form of skeletal tuberculosis ( > 50%) • Dorsal spine - most commonly involved • Mostly seen in first 3 decades.
  • 3.
    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
  • 4.
    Historical aspects • PercivalPott : Described TB in spinal column in 1779 • ”Destruction of disc space and adjacent vertebral bodies, collapse of spinal elements and progressive spinal deformity”
  • 5.
    Historical aspects • RobertKoch : Discovered Mycobacterium tuberculosis in 1882
  • 6.
    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
  • 7.
  • 8.
    Epidemiology • 8 millionpeople get TB every year, of whom 95% live in developing countries • An estimated 2 million people have active Spinal TB worldwide
  • 9.
    Epidemiology India • 1/5th oftotal TB Cases • 1- 3% of all involve skeletal system.
  • 10.
    Predisposing Factors • Malnutrition •Poor Sanitation • Over crowding • Close contact with TB patient • Multiple pregnancy • Immunodeficiency state
  • 11.
    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
  • 12.
    Pathology • TB bacilliphagocytosed 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
  • 13.
    Pathology • TB bacilliphagocytosed 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
  • 14.
    Pathogenesis of TBSpine STEP 1 Bacilli from primary focus through blood stream reach Disc Space
  • 15.
    Pathogenesis of TBSpine 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
  • 16.
    Pathogenesis of TBSpine • STEP 3 The infection spreads to vertebral bodies above and below the disc
  • 17.
    Pathogenesis of TBSpine STEP 4 The bone weakened by the infection collapses under the weight of human body
  • 18.
    Pathogenesis of TBSpine • STEP 5 The deformed spinal column compresses spinal cord producing functional impairment
  • 19.
    Pathogenesis of TBSpine • STEP 6 Over time, the deformed vertebrae heal and fuse This may further compress nerve roots causing pain and neurological deficit
  • 20.
  • 21.
    Regional distribution ofSpine TB • Cervical – 12% • Cervicodorsal – 5% • Dorsal – 42% • Dorsolumbar – 12% • Lumbar – 26% • Lumbosacral – 3%
  • 22.
    Types of vertebrallesions • 5 types: 1. Paradiscal- Arterial spread 2. Central – Venous spread 3. Anterior- Subperiosteal spread 4. Appendicular 5. Articular
  • 23.
    Types of vertebrallesions • 4 types: 1. Paradiscal- Arterial spread 2. Central – Venous spread 3. Anterior- Subperiosteal spread 4. Appendicular 5. Articular
  • 24.
    Types of vertebrallesions • 4 types: 1. Paradiscal- Arterial spread 2. Central – Venous spread 3. Anterior- Subperiosteal spread 4. Appendicular 5. Articular
  • 25.
    Types of vertebrallesions • 4 types: 1. Paradiscal- Arterial spread 2. Central – Venous spread 3. Anterior- Subperiosteal spread 4. Appendicular 5. Articular
  • 26.
    Types of vertebrallesions • 4 types: 1. Paradiscal- Arterial spread 2. Central – Venous spread 3. Anterior- Subperiosteal spread 4. Appendicular 5. Articular
  • 27.
    Clinical Features • Age:Common in 1st 3 decades • Sex: Male = Female
  • 28.
    Clinical Features Active stage Constitutionalsymptoms: • 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
  • 29.
    Clinical Features Healed stage Constitutionalsymptoms: • 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
  • 30.
    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
  • 31.
    Classification of TBParaplegia 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
  • 32.
    Staging of NeurologicalDeficit 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
  • 33.
    Pathology of TBParaplegia Inflammatory : • Edema of spinal cord – Cause of early cases of Neurodeficit – Vascular stasis – Due to toxins
  • 34.
    Pathology of TBParaplegia Extradural mass: • The Commonest mechanism affecting spinal cord function • Material compressing may be – Fluid pus – Granulation tissue – Caseous material
  • 35.
    Pathology of TBParaplegia Bony Disorders: • Sequestra from disc or body • Internal Gibbus • Pathological Dislocation
  • 36.
    Pathology of TBParaplegia • Meningeal changes – Dura is not involved – Cicatrisation of extradural TB granulation tissue (Peridural fibrosis) – Poor recovery despite adequate surgical decompression
  • 37.
    Pathology of TBParaplegia • 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
  • 38.
    Pathology of TBParaplegia • 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
  • 39.
    Pathology of TBParaplegia • 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
  • 40.
    Clinical features ofPott’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
  • 41.
    Prognosis of recoveryof 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
  • 42.
    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
  • 43.
    Investigations • Mantoux test –Erythema of more than 20 mm at 72 hours – Positive – Negative test, in general, rules out the disease
  • 44.
    Investigations • Biopsy – Incase of doubt, it is mandatory to prove the diagnosis by obtaining the diseased tissue
  • 45.
    Investigations • Guinea pigInoculation – Pus/ aspirate is inoculated intraperitoneally . – Positive cases reveal tubercle after 5-8 weeks – One of the most reliable proof of Tuberculous pathology
  • 46.
    Investigations • Smear andculture – 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
  • 47.
    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
  • 48.
    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
  • 49.
    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
  • 50.
    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
  • 51.
    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
  • 52.
    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
  • 53.
    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
  • 54.
    Radiological Investigations • Skippedlesions: – 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
  • 55.
    Radiological Investigations • Anteriortype of lesion – Starts beneath the anterior longitudinal ligament & periosteum – Collapse and disc space reduction is usually minimal and occurs late – Erosion is primary mechanical
  • 56.
    Radiological Investigations • Paradiscallesions: – Commonest lesions – Spreads through arterial supply – Reduced disc space – Earliest sign – Loss of vertebral margins – Increased pre-vertebral soft tissue shadow.
  • 57.
    Radiological Investigations • Centraltype: – Spread through the batson’s venous plexus/ branches of posterior vertebral artery. – Minimal Disc space reduction – At the end concentric collapse
  • 58.
    Radiological Investigations • Appendiculartype of lesion – Rare – Isolated infections of pedicles / lamina/ transverse processes/ Spinous process. – Intact disc space – Para vertebral shadows
  • 59.
    Radiological Investigations • Lateralshift and scoliosis – More destruction of vertebrae on one side • Kyphotic deformity – Due to collapse of bone – Forward angulations
  • 60.
    Radiological Investigations • Healingis indicated by – Decreased soft tissue shadow – Return of normal density – Bony ankylosis
  • 61.
    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.
  • 62.
    MRI • Lack ofionizing 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.
  • 63.
    USG - to findout 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
  • 64.
  • 65.
  • 66.
    Basic Principles OfManagement Early Diagnosis Expeditious medical treatment Aggressive surgical approach Prevent Deformity Expect Good Outcome
  • 67.
    Management • Evolution oftreatment: – Undergone tremendous revolutionary changes – Ancient Indians used herbal preparation Sipurda – Pott & Charcot applied hot iron to drain pus
  • 68.
    Evolution of treatment PreAnti- Tubercular era • Hippocrates advocated traction and other means to correct deformity
  • 69.
    Evolution of treatment PreAnti- Tubercular era • Sanatorium treatment – Sanatorium regimes and rest – Fresh air, Sunshine rooftops
  • 70.
    Evolution of treatment PreAnti- 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
  • 71.
    Evolution of treatment PreAnti- Tubercular era • Results of surgeries done in pre anti- tubercular era : – Serious sinus formation – Pseudoarthrosis – Recurrence of lesion – Neurological deterioration – Death
  • 72.
    Evolution of treatment WithAnti- 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
  • 73.
    Evolution of treatment WithAnti- 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.
  • 74.
    Present management Cases of spinalTB Conservative treatment with chemotherapy only Middle path regime Radical surgery
  • 75.
    1st line chemotherapy Bactericidaldrugs 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
  • 76.
    Newer drugs • Amikacin,Kanamycin, Capriomycin • Ciprofloxacin, Ofloxacin, Levofloxacin • Rifabutin • Clarithromycin • Clofazimine • Ethionamide • Cycloserine
  • 77.
    Policy of drugtreatment- 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
  • 78.
    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”
  • 79.
    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.
  • 80.
    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
  • 81.
    Middle path regime •Monitoring – Radiographs and ESR at 3-6 months interval – MRI at 6 months interval for 2 years
  • 82.
    Middle path regime •Gradual mobilization – Encouraged in absence of neurological deficit with support of spinal braces – As soon as the diseased part permits
  • 83.
    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.
  • 84.
    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
  • 85.
    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)
  • 86.
    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
  • 87.
    Algorithm for managementof pott’s paraplegia
  • 88.
    Algorithm for managementof pott’s paraplegia
  • 89.
    Operative Management Surgery Indications 1Decompression(+/- 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
  • 90.
  • 91.
  • 92.
    Anterior approach tosubaxial Cx spine • Smith and robinson
  • 93.
    Surgical approaches todorsal spine • Anterior transpleural - transthorasic
  • 94.
    Surgical approaches to dorsal spine •Anterolateral extrapleural approach
  • 95.
    Surgical approaches todorsal spine • Posterolateral approach
  • 96.
    Surgical approach tolumbar spine • Anterolateral retroperitoneal approach to lumbar spine
  • 97.
    Surgical approach to lumbarspine • Anterior transperitoneal /retroperitoneal approach to the spine
  • 98.
  • 99.
    Follow up • Patientevaluated 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
  • 100.
    Recovery • Time takenfor near complete recovery varies between 3-6 months • No significant neural recovery occurs after 12-18 months
  • 101.
    Results • Definition offavorable status- – No residual neural impairment – No sinus/ cold abscess – No impairment of physical activity due to spinal disease / lesion – Presence of radiographic quiescent disease
  • 102.
    Recurrence/ Relapse • Extraduralgranuloma • Severe kyphosis • Reactivation of lesion – Poor nutrition – Resistant organism – Immuno compromised status
  • 103.
    Recurrence/ Relapse • Necessarysurgery • Newer anti TB drugs • Supportive measures
  • 104.
    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.
  • 105.