tuberculosis of spine

Tuberculosis of SpineDr. Ankit MadhariaJunior ResidentLata 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

EpidemiologyIndia

• 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 1Bacilli from primary focus through blood stream reach Disc Space

Pathogenesis of TB SpineStep 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 SpineSTEP 4

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


The deformed spinal column compresses spinal cord producing functional impairment


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

Clinical Features• Age: Common in 1st 3 decades

• Sex: Male = Female

Clinical FeaturesActive 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 FeaturesHealed 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 ParaplegiaGriffiths, 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 DeficitGoel 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 ParaplegiaExtradural mass:

• The Commonest mechanism affecting spinal cord function

• Material compressing may be– Fluid pus

– Granulation tissue

– Caseous material

Pathology of TB ParaplegiaBony 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• 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 DiagnosisExpeditious 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 treatmentPre 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

Evolution of treatmentWith 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 treatmentWith 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 chemotherapyBactericidal 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 + 1H3R3

Z3E3 + 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 surgery1. 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 ManagementSurgery 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 gainPain reliefFree ROM

Resolution of abscessesNeurological recovery

Radiological:Decreased soft tissue shadow

Disappearance of erosionsReturn of mineralization

Graft incorporationBony 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

tuberculosis of spine

Health & Medicine

pathogenesis of tb spine

yakshma tb

joint tb

tuberculosis of spine

active spinal tb

pathology tb bacilli

historical aspects tb

total tb cases