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Tuberculosis of spine

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Tuberculosis of spine

  1. 1. TUBERCULOSIS OF SPINE MODERATOR: DR. P.S.CHAKRABORTY Assoc.prof.orthopaedics PRESENTER: DR.S.H.RANNA P.G.Student 09-03-2016
  2. 2. INTRODUCTION • Oldest recognition disease of mankind. • In 1779 Percival Pott presented the classical description of spinal tuberculosis. Destruction of disc space Destruction of vertebral bodies. Collapses of spine & kyphosis.
  3. 3. CONT.. • Robert Koch : Discovered Mycobacterium tuberculosis in 1882.
  4. 4. Epidemiology • Leading cause of death worldwide from a single infectious disease agent. • The Number of new cases of tuberculosis worldwide roughly correlates with economic conditions. • 8 million people get TB every year, of whom 95% live in developing countries. • An estimated 2 million people have active Spinal TB worldwide.
  5. 5. IN INDIA • 1/5th of total TB Cases. • 1- 3% of all involve skeletal system. • 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.
  6. 6. Regional distribution of Spine TB Cervical – 12% Cervico-dorsal – 5% Dorsal – 42% Dorso-lumbar – 12% Lumbar – 26% Lumbo-sacral – 3% 8 0 %
  7. 7. Predisposing Factors • Malnutrition. • Poor Sanitation. • Over crowding. • Close contact with TB patient. • Multiple pregnancy. • Immunodeficiency state.
  8. 8. PATHOGENESIS 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
  9. 9. Pathogenesis of TB Spine • STEP 1 • Bacilli from primary focus through blood stream reach Disc Space.
  10. 10. 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.
  11. 11. STEP 3 The infection spreads to vertebral bodies above and below the disc…
  12. 12. STEP 4 The bone weakened by the infection collapses under the weight of human body.
  13. 13. STEP 5 The deformed spinal column compresses spinal cord producing functional impairment.
  14. 14. STEP 6 Over time, the deformed vertebrae heal and fuse This may further compress nerve roots causing pain and neurological deficit.
  15. 15. Types of vertebral lesions • 5 types: 1. Paradiscal- Arterial spread. 2. Central – Venous spread. 3. Anterior- Subperiosteal spread. 4. Appendicular. 5. Articular or synovial.
  16. 16. CLINICAL FEATURE: ACTIVE STAGE CONSTITUTIONAL SYMPTOMS(40%) Malaise Loss of appetite/weight Night sweets. Evening rise of temperature. Specific features: Pain/night caries. Stiffness. Restricted ROM. Enlarged lymph node. Cold abscess. Deformity-Gibbus. Neural deficit-20%
  17. 17. Disease part Location of abscess Cervical or dorsal spine •Paraspinal region of back •Posterior cervical triangle. •Anterior cervical triangle. •Axilla. •Intercostals space. •Chest wall. Dorsolumber and lumbar spine. •Psoas abscess. •Paraspinal region. •Iliac fossa. •Lumber triangle/Petits triangle. •Upper part of thigh. •Below inguinal ligament. •Around the knee. D10 to sacrum Psoas abscess. ABSCESS & LOCATION
  18. 18. CLINICAL FEATURE: HEALED STAGE CONSTITUTIONAL SYMPTOMS(40%) Malaise. Loss of appetite/weight. Night sweets. Evening rise of temperature. Specific features: Pain/night caries. Stiffness. Restricted ROM. Enlarged lymph node. Cold abscess. Deformity-Gibbus. Neural deficit-20%
  19. 19. kyphosis80% Neurodeficit20% cold abscess15% radiological15% extraspinal10% skip lession7% CLINICAL FEATURES- PERCENTAGE
  20. 20. Neurological deficit/Potts paraplegia • 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. • 24% of cervical TB shows neural deficit.
  21. 21. Classification of TB Paraplegia Griffiths, Seddon and Roaf 1956 Early onset paraplegia (group A) <2yrs,active phase Oedema,abscess,caseus& granulation tissue Good prognosis Late onset paraplegia (Group B) >2yrs,mechanical pressure on cord. TB Debris TB Sequestra from body and disc Internal gibbus Canal stenosis / Severe deformity Poor prognosis
  22. 22. 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.
  23. 23. Pathology of TB Paraplegia 1.Inflammatory oedema. Vascular stasis Tubercular toxins. early onset paraplegia Quick recovery 2.Extradural mass: The Commonest mechanism affecting spinal cord function Material compressing may be Fluid pus Granulation tissue Caseous material
  24. 24. 3.Bony Disorders: Sequestra from disc or body. Internal Gibbus. Pathological Dislocation. 4.Meningeal changes Dura is not involved. Cicatrisation of extradural TB granulation tissue (Peridural fibrosis) Poor recovery despite adequate surgical decompression.
  25. 25. 5.Infarction of Spinal cord. Caused by Endarteritis Periarteritis Thrombosis Paralysis is irreparable. Can also happen postoperatively. 6.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
  26. 26. Clinical features of Pott’s Paraplegia • Paraplegia itself – Rare. • Spontaneous muscle twitching in lower limbs. • Clumsiness while walking. • Extensor plantar response. • Exaggerated reflexes – Sustained clonus of patella and ankle. • Motor affected first – then Sensory. • Sense of position and vibration – last to disappear.
  27. 27. 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.
  28. 28. 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.
  29. 29. 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).
  30. 30. Radiological-plan X-rays • Plain radiograph signs – Reduced disc space. – Blurred Paradiscal margins. – Destruction of bodies. – Loss of trabecullar pattern. – Increased prevertebral soft tissue shadow. – Subluxation /dislocation. – Decreased lordosis/Kyphosis.
  31. 31. Radiological-plan X-rays • Plain radiograph signs – Reduced disc space. – Blurred Paradiscal margins. – Destruction of bodies. – Loss of trabecullar pattern. – Increased prevertebral soft tissue shadow. – Subluxation /dislocation. – Decreased lordosis/Kyphosis
  32. 32. Radiological-plan X-rays • Plain radiograph signs – Reduced disc space. – Blurred Paradiscal margins. – Destruction of bodies. – Loss of trabecullar pattern. – Increased prevertebral soft tissue shadow. – Subluxation /dislocation. – Decreased lordosis/Kyphosis
  33. 33. Radiological-plan X-rays • Plain radiograph signs – Reduced disc space. – Blurred Paradiscal margins. – Destruction of bodies. – Loss of trabecullar pattern. – Increased prevertebral soft tissue shadow. – Subluxation /dislocation. – Decreased lordosis/Kyphosis
  34. 34. Radiological-plan X-rays • 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
  35. 35. Radiological-plan X-rays • Anterior type of lesion – beneath the anterior longitudinal ligament & periosteum. –Collapse and disc space reduction is usually minimal and occurs late. –Erosion is primary mechanical.
  36. 36. Radiological-plan X-rays • Paradiscal lesions: –Commonest lesions. –Spreads through arterial supply. –Reduced disc space – Earliest sign. –Loss of vertebral margins. –Increased pre- vertebral soft tissue shadow.
  37. 37. Radiological-plan X-rays • Central type: –Spread through the batson’s venous plexus/ branches of posterior vertebral artery. –Minimal Disc space reduction. –At the end concentric collapse.
  38. 38. Radiological-plan X-rays • Lateral shift and scoliosis. – More destruction of vertebrae on one side. • Kyphosis deformity – Due to collapse of bone. – Forward angulations- -1-2-knuckle -3-gibbus ->3 round kyphosis.
  39. 39. Spine at risk sign
  40. 40. Radiological-CT Scan • 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.
  41. 41. Radiological-MRI • Lack of ionizing radiation, high contrast resolution & 3D imaging. • Detect marrow infiltration in vertebral bodies, leading to early diagnosis. • Changes of discitis. • Assessment of extradural abscesses / subligamentous spread. • Skip lesions. • Spinal cord involvement. • Spinal arachanoiditis.
  42. 42. 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.
  43. 43. Basic Principles Of Management Early Diagnosis Expeditious medical treatment Aggressive surgical approach Prevent Deformity Expect Good Outcome
  44. 44. Evolution Of Treatment: – Undergone tremendous revolutionary changes. – Ancient Indians used herbal preparation Sipurda. –Pott & Charcot applied hot iron to drain pus. –Hippocrates advocated traction and other means to correct deformity
  45. 45. Sanatorium treatment –Sanatorium regimes and rest –Fresh air, Sunshine rooftops
  46. 46. Surgeries At Pre Antitubercular Era • Laminectomy & laminotomy :Chipault 1896. • Costo-transversectomy :Menard in 1894. • Posterior mediastinotomy : By Obalinsky for drainage of abscess. • Calves operation :1957 to aspirate abscess. • Lateral rhachiotomy of Capener: Capener in 1933. • Anterolateral decompression of Dott and Alexander: • Posterior decompression with posterior spinal Arthrodesis: 1911 onwards.
  47. 47. Surgeries At Pre Antitubercular Era • Surgery was not attempted due to fear of secondary infection and death. • Operative procedure were developed for either treatment or prevention of paralysis. • Principle was more direct approach to diseased part.
  48. 48. Results of surgeries done in pre anti- tubercular era : –Serious sinus formation. –Pseudo-arthrosis. –Recurrence of lesion. –Neurological deterioration. –Death.
  49. 49. • Treatment has taken dramatic turn for better with discovery of anti tubercular drugs. –1943 – PAS –1944 – Streptomycin –1951 – INH(magic bullet) –1970 – Rifampicin and short course chemotherapy. Evolution of treatment With Anti- Tubercular drugs
  50. 50. Supportive treatment –Rest. –Braces. –High protein diet. –Multivitamins, hematinics. –Hygiene. –Back care. –Chest / urinary tract care. –Improve immune status. –Treat other co-morbid conditions.
  51. 51. Present management Cases of spinal TB Conservative treatment with chemotherapy only Middle path regime Radical surgery
  52. 52. 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
  53. 53. 2nd Line drugs • Amikacin, Kanamycin, Capriomycin • Ciprofloxacin, Ofloxacin, Levofloxacin • Rifabutin • Clarithromycin • Clofazimine • Ethionamide • Cycloserine
  54. 54. Drugs for MDR TB. Group 1 Rifabutin,ethambutol,pyrazina mide. Group 2 Kanamycin,amikacin,capreomyc in,streptomycin Group 3 Levofloxacin,moxifloxacin,ofloxacin. Group 4 Paraaminosalicycyclic acid,cycloserine,thionamide. Group 5 Clofazimine,amoxycillin,clarithromy cin
  55. 55. Adverse effect of ATT Streptomycin Eight nerve damage, aplastic anaemia,neutropenia. PAS Gastrointestinal irritation. Isoniazid. Peripheral neuritis,psychological disturbance. Thioacetazone Liver damage,skin rash. Ethambutol Optic neurutis,retrobulbar neuritis. Rifampicin Increased SGPT,sr bilirubin,influenzae like syndrome Pyrazinamide Hepatotoxicity,arthralgia
  56. 56. 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”
  57. 57. 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.
  58. 58. Middle path regime • Drugs –INH+ RMP+ ETB DOTS –INH + PZA –INH+ RMP –INH • Supportive therapy –Hematinics, Multivitamins, High protein diet
  59. 59. Middle path regime • Monitoring –Radiographs and ESR at 3-6 months interval –MRI at 6 months interval for 2 years.
  60. 60. Middle path regime • Gradual mobilization –Encouraged in absence of neurological deficit with support of spinal braces –As soon as the diseased part permits.
  61. 61. 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.
  62. 62. 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.
  63. 63. Middle path regime • Absolute Indications of surgery 1. No progressive recovery after fair trial of conservative treatment(3-4wks). 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).
  64. 64. Middle path regime Surgery Indications Decompression(+/- fusion) Too advanced disease, Failure to respond to conservative therapy Debridement +/- decompression +/- fusion Recurrence of disease or of neural complications Anterior transposition of cord (Extra pleural anterolateral approach) Sever Kyphosis (>60 degree) + / neural deficit Laminectomy Extradural granuloma/ Old healed disease presenting as secondary canal stenosis/ Posterior spinal disease
  65. 65. APPROACH FOR ABSCESS DRAINAGE Ilio-psoas abscess Anterior approach. Anterolateral approach. Medial site of thigh Ludloffs approach Cervical spine abscess Longitudinal incision anterior or posterior to sterno-cleidomastoid.
  66. 66. Antero-lateral approach Ludloff approach
  67. 67. Atlanto-axial region Transoral approach. Transthyroid approach. Retropharyngeal approach. Cervical spine Anterior approach Cervico- dorsal region Trans-thoracic trans-pleural approach. Anterior sternum splitting extra pleural approach. Some surgical approaches
  68. 68. Some surgical approaches Dorsal spine Anterior transpleural approach. Anterolateral extra pleural approach. Posterolateral approach. Thoraco- lumber region Antero-lateral extra pleural approach. Extra pleural extra peritoneal approach through bed of 11th rib. Lumber spine Retroperitoneal approach.
  69. 69. Transoral approach.C1-C2
  70. 70. ANTERIOR APPROACH FOR CERVICAL SPINE
  71. 71. Anterior transpleural - transthorasic
  72. 72. 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
  73. 73. Middle path regime
  74. 74. Middle path regime
  75. 75. FOLLOW UP • Patient evaluated every 3 months interval for 2yrs. 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.

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