Kochs spine

kochs spine

1. TUBERCULOSIS OF SPINE DR. PRATIK DHABALIA JUNIOR RESIDENT DEPT. OF ORTHOPEDICS

2. HISTORICAL ASPECTS In India, the Rig Veda and the Atharva Veda (3,500–1,800 BC) mention this disease by the name “ Yakshama ” in all its forms [1, 2] Identification of mycobacterium as the causative organism (1870), use of the Bacilli Calmette Guerin (BCG) vaccination (1945), facilities for radiographic examination, and availability of specific antitubercular drugs (1948–1951) are all important landmarks in the understanding and management of tuberculosis of spine Duraiswami PK, Orth M, Tuli SM. 5000 years of orthopaedics in India.  Clin Orthop Relat Res. 1971;75:269–280. doi : 10.1097/00003086-197103000-00032. Bick KM.  Classics of orthopaedics. Philadelphia: JB Lippincott Co.; 1976.

3. Tuberculous disease of the spine was described by Percivall Pott in 1799 as “That kind of palsy of lower limbs which is frequently found to accompany a curvature of the spine” [3, 4] “ Destruction of disc space and adjacent vertebral bodies, collapse of spinal elements and progressive spinal deformity” 3. Bick KM.  Classics of orthopaedics. Philadelphia: JB Lippincott Co.; 1976.  4. Tuli SM.  Tuberculosis of the skeletal system. 4. New Delhi: Jaypee Brothers Medical Publishers; 2010. 

4. Robert Koch : Discovered Mycobacterium tuberculosis in 1882

5. EPIDEMIOLOGY Tuberculosis : Leading cause of death worldwide from a single infectious disease agent Globally, extrapulmonary tuberculosis (TB) represented 14% of the 6.4 million TB cases reported in 2017 [5] ,of these, skeletal involvement was the third most common, comprising 9.8% of cases, after lymphatic and pleural disease. I nd i a has 1/5 th of total TB Cases out of which 1- 3% of all involve skeletal system. Vertebral tuberculosis is most common form of skeletal tuberculosis and it constitutes about 50% of all skeletal cases. 5. World Health Organization. Chapter 4. Diagnosis and treatment: TB, HIV-associated TB and drug-resistant TB. Global Tuberculosis Report 2018. Geneva: World Health Organization; 2018. 67-102

6. Age Distribution : Can occur at any age but more common in third decade of life . Racial factors : Musculoskeletal tuberculosis affects primarily African Americans, Hispanic Americans, Asian Americans, and foreign-born individuals. Sexual predilection : Pott disease does not have a sexual predilection, the disease is more common in males (male-to-female ratio of 1.5-2:1). Regional Distribution : More prevalent in south African, sub Saharan and Asian countries i.e. developing countries due to major risk factors and lower socio-economic status and over-crowding. Spinal Level : Most commonly Dorsal spine is involved.

7. PREDISPOSING FACTORS Malnutrition Poor Sanitation Over crowding Close contact with TB patient Multiple pregnancy Immunodeficiency state SPINAL LEVEL DISTRIBUTION LEVEL PERCENTAGE CERVICAL 12% CERVICODORSAL 5% DORSAL 42% DORSOLUMBAR 12% LUMBAR 26% LUMBOSACRAL 3%

8. PATHOLOGY AND PATHOGENESIS Main Organism - M. 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 Characteristics Gram positive Acid Fast bacilli Non Motile May have resistance Size 3 x 0.3 Micron

9. Pathological process Modes of Spread – Inhalational Inoculation Ingestion Transplacental

10. Patholog ical Process ctd …

11. Pathological process ctd …

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

13. Pathogenes is ctd ... STEP 1 Bacilli from primary focus through blood stream reach Disc Space

14. Pathogenesis ctd … Step 2 Once infected, soft nucleus center and fibrous annular wall weakens, decays and collapse This caused the disc to close, squeezing down on nerve root causing pain

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

16. Pathogenesis ctd … STEP 4 The bone weakened by the infection collapses under the weight of human body

17. Pathogenesis of TB Spine STEP 5 The deformed spinal column compresses spinal cord producing functional impairment

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

19. Regional distribution of Spine TB Cervical – 12% Cervicodorsal – 5% Dorsal – 42% Dorsolumbar – 12% Lumbar – 26% Lumbosacral – 3%

20. Types of vertebral lesions 5 types: Paradiscal- Arterial spread Central – Venous spread Anterior- Subperiosteal spread Appendicular Articular

21. Types of vertebral lesions 4 types: Paradiscal- Arterial spread Central – Venous spread Anterior- Subperiosteal spread Appendicular Articular

22. Types of vertebral lesions 4 types: Paradiscal- Arterial spread Central – Venous spread Anterior- Subperiosteal spread Appendicular Articular

23. Types of vertebral lesions 4 types: Paradiscal- Arterial spread Central – Venous spread Anterior- Subperiosteal spread Appendicular Articular

24. Types of vertebral lesions 4 types: Paradiscal- Arterial spread Central – Venous spread Anterior- Subperiosteal spread Appendicular Articular

25. 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

26. 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

27. Neurological deficit 10-30% cases – Neurological deficit Age: 1 st 3 decades Disease below L1 vertebrae rarely causes Paraplegia Highest Incidence of paraplegia seen in TB of lower thoracic vertebrae

28. 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

29. 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

30. Pathology of TB Paraplegia Inflammatory : Edema of spinal cord – Cause of early cases of Neurodeficit Vascular stasis Due to toxins

31. Pathology of TB Paraplegia Extradural mass: The Commonest mechanism affecting spinal cord function Material compressing may be Fluid pus Granulation tissue Caseous material

32. Pathology of TB Paraplegia Bony Disorders: Sequestra from disc or body Internal Gibbus Pathological Dislocation

33. Pathology of TB Paraplegia Meningeal changes Dura is not involved Cicatrisation of extradural TB granulation tissue (Peridural fibrosis) Poor recovery despite adequate surgical decompression

34. 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

35. 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

36. 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

37. 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

38. Investigations CBC: Hb% ↓ Lymphocytosis ESR: Raised in active stage of disease Normal ESR over period of 3 months suggests patient is in stage of repair CRP: Raised

39. Investigations Mantoux test Erythema of more than 20 mm at 72 hours – Positive Negative test, in general, rules out the disease

40. Investigations Biopsy – In case of doubt, it is mandatory to prove the diagnosis by obtaining the diseased tissue

41. 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

42. Investigation Serological Investigations ELISPOT (Enzyme- linked immunospot) – T-cell based assay from blood IgM & IgG antibodies : High sensitivity, low specificity PCR: Tissue /Pus PCR more sensitive Gene Xpert

43. 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

44. 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

45. 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

46. 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

47. 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

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 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

50. 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

51. 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.

52. 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

53. Radiological Investigations Appendicular type of lesion Rare Isolated infections of pedicles / lamina/ transverse processes/ Spinous process. Intact disc space Para vertebral shadows

54. Radiological Investigations Lateral shift and scoliosis – More destruction of vertebrae on one side Kyphotic deformity Due to collapse of bone Forward angulations

55. Radiological Investigations Healing is indicated by Decreased soft tissue shadow Return of normal density Bony ankylosis

56. Computed tomography (CT) Patterns of bony destruction. Calcifications in abscess (pathognomic for Tb) Regions which are difficult to visualize on plain films, like : Cranio-vertebral junction (CVJ) Cervico-dorsal region, Sacrum Sacro-iliac joints. Posterior spinal tuberculosis because lesions less than 1.5cm are usually missed due to overlapping of shadows on x rays.

57. 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.

58. 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

59. Radiological Investigations Spine at risk sign

60. TUBERCULAR Chronic back pain -Long standing history of months to years Presence of active pulmonary tuberculosis -60% Most common location thoracic spine followed by thoraco-lumbar region. > 3 contiguous vertebral body involvement common Vertebral collapse -67% Posterior elements involvement Skip lesions common PYOGENIC Acute onset-History of days to months. Not present. Most common location lumbar spine. Mostly involves 1 spinal segment 21% only. Ra r e R a r e

61. Basic Principles Of Management Early Diagnosis Expeditious medical treatment Aggressive surgical approach Prevent Deformity Expect Good Outcome

62. Management Evolution of treatment: Undergone tremendous revolutionary changes Ancient Indians used herbal preparation Pott & Charcot applied hot iron to drain pus

63. Evolution of treatment Pre Anti- Tubercular era Hippocrates advocated traction and other means to correct deformity

64. Evolution of treatment Pre Anti- Tubercular era Sanatorium treatment Sanatorium regimes and rest Fresh air, Sunshine rooftops

65. 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

66. 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

67. Evolution of treatment W ith 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

68. Evolution of treatment W ith 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.

69. Present management Cases of spinal TB Conservative treatment with chemotherapy only Middle path regime Radical surgery

70. 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”

71. Middle path regime

72. Middle path regime Supportive therapy – Hematinics , Multivitamins, High protein diet Rest In hard bed Cervical TB requires traction in early stage to put the diseased part in rest.

73. Middle path regime Monitoring Radiographs and ESR at 3-6 months interval MRI at 6 months interval for 2 years

74. Middle path regime Gradual mobilization Encouraged in absence of neurological deficit with support of spinal braces As soon as the diseased part permits

75. 1 st 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

76. 2 nd line Drugs Aminoglycosides – Kanamycin, Amikacin, Capreomycin Fluoroquinolones – Ofloxacine , Ciprofloxacine , levofloxacine Ethionamide Cycloserine PAS Clofazimine Rifabutin

77. 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.

78. 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

79. Middle path regime Absolute Indications of surgery No progressive recovery after fair trial of conservative treatment Neurological complications develops during conservative treatment Worsening of neurological deficit during t/t Recurrence of neurological complications Pressure effects (deglutition/respiration) Advanced cases of neurological involvement(Sphincter disturbances, flaccid paralysis or severe flexor spasm)

80. Middle path regime Post Operatively Patient nursed in hard bed Pat i ent m o b i l i zed 3 - 5 m onths aft e r surgery with spinal brace Spinal braces can be gradually discarded 1- 2 years after surgery

81. Newer Drugs BEDAQUILINE Brand name – Sirturo Diaryl Quinoline class Mycobacterial Atp inhibitor For MDR Nausea, chest pain, QT prolongation Dose monitoring when given with rifampicin Black box warning DOSE - 400mg daily for 2 weeks then 200mg 3 times a week for 22 weeks

82. DELAMANID Brand name – deltyba Nitroimidazole class Inhibits formation of mycolic acid Nausea, arrhythmias, headache, dizziness Dose – 100mg twice a day x 24 weeks in divided doses

83. Algorithm for management of pott’s paraplegia

84. Algorithm for management of pott’s paraplegia

85. 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

86. Surgical spproaches

87. Anterior approach to the C1-C2 Transoral approach

88. Anterior approach to subaxial Cx spine Smith and robinson

89. Surgical approaches to dorsal spine Anterior transpleural - transthorasic

90. Surgical approaches to dorsal spine Anterola t eral extrapleural approach

91. Surgical approaches to dorsal spine Posterolateral approach

92. Surgical approach to lumbar spine Anterolateral retroperitoneal approach to lumbar spine

93. Surgical approach to lumbar spine Anterior transperitoneal /retroperitoneal approach to the spine

94. Post operative care

95. Follow up Patient evaluated at 3 months interval upto 2 years. Evaluation Clinical: Radiological: Decreased soft tissue shadow Disappearance of erosions Return of mineralization Graft incorporation Bony ankylosis Weight gain Pain relief Free ROM Resolution of abscesses Neurological recovery

96. Recove r y Time taken for near complete recovery varies between 3-6 months No significant neural recovery occurs after 12-18 months

97. Resul t s 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

98. Recurrence/ Relapse Extradural granuloma Severe kyphosis Reactivation of lesion Poor nutrition Resistant organism Immuno compromised status

99. Recurrence/ Relapse Necessary surgery Newer anti TB drugs Supportive measures

100. Thank you