TB SPINE.pptx

tuberculosis spine surgery xray finding treatment

1. TUBERCULOSIS OF SPINE PRESENTER DR. SHUBHANSHU

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 Identification of mycobacterium as the causative organism (1870) U se of the Bacilli Calmette Guerin (BCG) vaccination (1945) F acilities for radiographic examination, and availability of specific antitubercular drugs (1948–1951) are all important landmarks in the understanding and management of tuberculosis of spine

3. T uberc u lous dis e a s e 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 bodies, collapse of a n d p ro g r e ss i v e s p i n a l s p i na l vertebral elements de f or m ity”

4. R o bert K o ch : D i s c ov ere d Mycoba c teri u m tuberculosis in 1882

5. EPIDEMI O L OGY Tuberculosis : Leading cause of death worldwide from disease agent a single infectious Globally, extrapulmonary tuberculosis (TB) represented 14% of the 6.4 million TB cases reported in 2017 ,of these, skeletal involvement was the third most common, comprising 9.8% of cases, after lymphatic and pleural disease. India 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.

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 conta c t with T B pat i ent Multiple pregnancy Immunodeficiency state SPINAL LEVEL DISTRIBUTION LEVEL PERCENTAGE CERVICAL 12% CERVICODORSAL 5% DORSAL 42% DORSOLUMBAR 12% LUMBAR 26% LUMBOSACRAL 3%

8. P A THOLO G Y AND P A THOGE N ESIS Main Organism - M. tuberculosis Size 3 x 0.3 Micron Gram pos i t i v e A c i d 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. Pathological 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 Batson’s Plexus

13. Pathogenesis ctd... STEP 1 Bacilli from primary focus through blood stream reach Disc Space tuberculous granulation doesnt form proteolytic enzyme in joint 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… STE P 3 The inf e ct i on spreads to vertebral bodies ab o ve 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. Pannus - at periphery granulation tissue form ring of articular cartilage Rice Bodies - loose sheet or flakes of necrosed articular cartilage and acumulation of articular cartilage in synovial joint Kissing lesion- Necrosis of subcondral bone on each side of joint

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

21. Types of vertebral lesions 5 types: Paradis c a l - Arterial s p read Central – V enous sp r ea d An t er io r - Subperio s t e al s p re a d Appendicular Articular

22. Types of vertebral lesions 5 types: Paradis c a l - Arterial s p read Central – V enous sp r ea d An t er io r - Subperio s t e al s p re a d Appendicular Articular

23. Types of vertebral lesions 5 types: Paradis c a l - Arterial s p read Central – V enous sp r ea d An t er io r - Subperio s t e al s p re a d Appendicular Articular

24. Types of vertebral lesions 5 types: Paradis c a l - Arterial s p read Central – V enous sp r ea d An t er io r - Subperio s t e al s p re a d Appendicular Articular

25. Types of vertebral lesions 4 types: Paradis c a l - Arterial s p read Central – V enous sp r ea d An t er io r - Subperio s t e al s p re a d Appendicular Articular

26. 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

27. Clinical Features Healed sta g e 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

28. Neurological deficit 10-3 % ca s es – Neu r olo g i cal defic i t A g e: First 3 decad e s Disea s e below L1 verteb r ae ra r e l y causes Parap l e g i a Highest Incidence of paraplegia seen in TB of lower thoracic vertebrae

29. Classification of TB Paraplegia Griffiths, Seddon and Roaf 1956 (Pre anti-tubercular era) Early onset paraplegia (group A) • Late onset paraplegia (Group B) Appears w ithin 2 y ea r s of on s et – during the Active phase Underlying pathology Inflammatory edema TB Granulation tissue Abscess Caseous tissue Ischaemis lesion of cord (Rare) Good prognosis Appears more than 2 y ea r s of disease in vertebral column Underlying pathology –due to mec hani c al pre s s u r e on c o rd TB Debris TB Sequestra from body and disc Internal gibbus Canal stenosis / Severe deformity Poor prognosis

30. Staging of Neurological Deficit Goel 1967, Tuli 1985, Kumar 1988, Jain 2002 Stage Severity Clinical Features I Negligible Pa t ient una w are of neu r odeficit, physici a n detec ts plantar extensors or ankle clonus II Mild Pa t ient aware of deficit but wa lks with s u pp o r t 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

31. Pathology of TB Paraplegia Inflamm a t ory : Edema of spinal cord – Cause of early cases of Neurodeficit Vascular stasis Due to toxins

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

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

34. Pathology of TB Paraplegia Meningeal changes Dura is not involved Cicatrisation of extradural TB granulation tissue (Peridural fibrosis) Poor rec o very de s pite ade q uate s u rg ica l de c ompres s ion

35. 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

36. 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

37. 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

38. 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

39. 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

40. Investigations Mantoux test Ery t hema of more than 20 mm at 72 hou r s – Positi v e Negati v e tes t , in genera l, rules out the disease 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 Fa s t ba c illi Culture of pus in Lo w en s tein jen s en media Aspirate of pa r averteb ra l ab s c e ss or s p inal diseased tissue seldom demonstrates mycobacterium (Moon 2002) Bactec For faster c u lture of Mycobacterium tuberculosis

42. I n v e s ti g a tion 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 Inc r ea s ed preverteb r al s o ft 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 Inc r ea s ed preverteb r al s o ft 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 Inc r ea s ed preverteb r al s o ft 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 Inc r ea s ed preverteb r al s o ft 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 Inc r ea s ed preverteb r al s o ft 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 Inc r ea s ed preverteb r al s o ft 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 v ertebrae 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 u s ually 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 bats o n ’ 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/ tran s verse pro c e s ses/ 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 c o llap s e of bone Forward angulations

55. Radiological Investigations Healing is indicated by Dec r ea s ed s o ft tiss u e shadow Re turn of no r mal den s ity 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 % on l y . 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. Mana g eme n t 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 tracti o n a n d ot h er m e a n s 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 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 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 ch e motherapy only Middle pa t h 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 D o se 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 str e ptom y cin and INH s o luti o n inje c ted at the cavity Cervical prevertebral abscess drained if causing difficulty in respiration / swallowing. Drainage of perispinal abscess considered when its ra diologi c al si z e incre a s e s m ar k e d ly 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 Patient mobilized 3-5 months afte r surgery with spinal brace – Spin a l brace s can b e gr a du a ll y discard after 1-2 years after surgery

81. WHO INDEX-TB Guidelines - for extrapulmonary TB in India 2RHZE/10RHE All patients require close monitoring for development or progression of neurological deficit in the first 4 weeks of treatment. Some patients require surgical intervention. Total treatment duration: 12 months (extendable to 18 months on a case-bycase basis) Optimum management of spinal TB requires the involvement of multiple specialists including a spinal orthopaedic surgeon, microbiologist/infectious diseases specialist and spinal radiologist, as well as physiotherapists and orthotists. All presumptive spinal TB cases should be referred and managed in specialist centres.

82. Patients without neurological deficit should be advised to return to the clinic immediately if new symptoms develop, and all ambulant patients should be assessed weekly for neurological signs. Patients with neurological deficit require staging and grading of their deficit. These patients should be assessed weekly with neural charting to detect neural recovery or deterioration. Repeat X-rays of the spine are suggested every 3 months following initiation of treatment to assess for radiological healing. Repeat MRI scans are suggested at 6, 9, 12 and 18 months following initiation of treatment to assess healing. At the end of treatment, all patients require follow up every 6 months for at least 2 years, and should be told to return to the clinic promptly if they develop new symptoms in the interim. While some require early surgical intervention, most patients can be managed with ATT alone in the initial phase of treatment. Surgery may be required for two principal purposes in spinal TB-to establish diagnosis, or to treat spinal deformity, instability and neurological deficit.

83. Where available, percutaneous biopsy under CT guidance reduces the need for open biopsy, but this may still be required in some cases, particularly where imaging results are atypical for spinal TB and the diagnosis is uncertain. Patients with large, fluctuant cold abscesses may require therapeutic aspiration to relieve symptoms and promote healing.

84. Indications for surgery in TB spine with neurological deficit: Neural complications developing or getting worse or remaining stationary during the course of non-operative treatment (3–4 weeks) Paraplegia of rapid onset Spinal tumour syndrome Neural arch disease Severe paraplegia – flaccid paraplegia, paraplegia in flexion, complete sensory loss and complete loss of motor power for more than 6 months Painful paraplegia in elderly patients.

85. Indications for surgery in spinal TB without neurological deficit: When diagnosis is uncertain and open biopsy is indicated Mechanical instability – panvertebral disease, where bony involvement of both the vertebral body and posterior complex is seen on imaging, or disease affects facet joints bilaterally Suspected drug resistance – where patients show inadequate clinical improvement or deterioration on ATT Spinal deformity – severe kyphotic deformity at presentation, or in children at high risk of progression of kyphosis with growth after healing of disease.

86. Indications for instrumented stabilization: ● Panvertebral disease ● Long segment disease where a > 4–5 cm long graft is required to bridge the gap after surgical decompression in dorsal spine ● In lumbar and cervical spine ● When kyphosis correction surgery is contemplated ● Lesion in a junctional area Preparation for surgery ● Multidrug therapy at least 3 to 6 weeks before surgery to suppress the infection ● Medical treatment for comorbidities ● Nutritional support ● Correct hypoproteinemia ● Obtain relevant imaging studies

87. 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

88. 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

89. Algorithm for management of pott’s paraplegia

90. Algorithm for management of pott’s paraplegia

91. 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

92. Surgical a pproaches

93. A n t e r i o r app r o a ch to the C1-C2 Transoral approach

94. A nt erio r app r o a c h t o sub a xia l C x spine Smith and robinson

95. Surgical approaches to dorsal spine Anterior transpleural - transthorasic

96. Surgical approaches to dorsal spine A n ter o l a t eral extrapleural approach

97. Surgical approaches to dorsal spine Posterolateral approach

98. Surgical approach to lumbar spine Anterolateral ret r op e ritoneal ap p roach to lumbar spine

99. Surgical approach to lumbar spine Anterior transperitoneal / r etr op e ritoneal ap p roach to the spine

100. Post operative care

101. 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

102. R e c o v e r y Time taken for near complete recovery varies between 3-6 months No significant neural recovery occurs after 12-18 months

103. R esu l t s Definition of favorable status- No residual neural impairment No sinus/ cold abscess No impairme n t of physical a c ti v ity due to s p inal dise a se / les ion Presence of radiographic quiescent disease

104. Recurrence/ Relapse Extradural granuloma Severe kyphosis Reactivation of lesion Poor nutrition Resistant organism I m muno c o mpromi s ed status

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

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