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tuberculosis of the skeletal system

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tuberculosis of the skeletal system, pott's spine, caries sicca, spina ventosa.

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tuberculosis of the skeletal system

  2. 2. Content  General Considerations  Extra-Spinal regional Tuberculosis  Tuberculosis of the spine  Tuberculosis of the Hip joint  Tuberculosis of the Knee joint  Tuberculosis of the Shoulder joint  Miscellaneous bone tuberculosis
  3. 3. General Considerations  1) Epidemiology and Prevalence  2) Pathology and Pathogenesis  3) Diagnosis and Investigations  4) Anti Tubercular Drugs  5) Principals of management of Osteoarticular Tuberculosis.
  4. 4. Tuberculosis: Epidemiology and Prevalence  It is a chronic granulomatous disease caused by bacteria of “Mycobacterium Tuberculosis” complex.  “ YAKSHMA” - described in Rig Veda and Atharva veda (3500 BC)  “ Phthisis” – described by Greeks and Roman’s civilizations.  Tuberculosis lesions have been recorded in Egyptian mummies.  Lichtor and Lichtor (1957) reported the evidence of Tb in Bones, Joints and Spine.  Percival Pott in 1779 described Tb of the Spinal Column.  Laennec discovered the basic microscopic lesion ‘tubercle’ . Also inventor of stethoscope.  Robert Koch in 1882 isolated “ Mycobacterium Tuberculosis”
  5. 5.  Refugees  IV drug abusers  HIV Patients  Alcoholics  Elderly  People with Poor Nutrition  Therapeutically Immunosupressed Patients  Organ transplant receipients  Patients on Cancer chemotherapy. The Risk of Infection
  6. 6. 30 million people are suffering from Tuberculosis (2010 data). 3 million people die every year due to Tuberculosis. Nearly 6 million cases of Tuberculosis in India (2010 data). 1-3% cases are of Skeletal tuberculosis of all Tuberculosis.
  7. 7. Regional Distribution of osteoarticular Tuberculosis  Spine - 44%  Hip - 8.1%  Knee - 8.9%  Sacroiliac Joint - 6.9%  Elbow - 5.1%  Metatarsal and Phalanges – 4.4
  8. 8. Pathology and Pathogenesis  Osteoarticular Tb lesion is a result of hematogenous dissemination from primarily infected visceral focus.  The Primary focus may be active or quiescent. Can be either in the lungs/ lymph nodes of the mediastinum/ Kidney or other viscera.  The infection reaches skeletal system through Batson’s plexus of veins.  Tubercular bacilli reach the joint space via the blood stream through sub-synovial vessels, or indirectly from the lesions in the epiphyseal bone.
  9. 9. Cold Abscess  A cold abscess is formed by a collection of products of liquefaction and the reactive exudates.  Composed of Serum, leucocytes, caseous materials, bone debris, and the tubercle bacilli.  The cold abscess feels warm, though the temperature is not raised as high as in acute pyogenic infections.
  10. 10. Type of the disease Caseous Exudative type  More destruction, more exudation and abscess formation.  Onset is less insidious, constitutional symptoms and local signs of inflammation are marked.  Sinus and abscess formation are common. Granular Type  Less destruction, abscess formation is rare.  Insidious onset.
  11. 11. Diagnosis of skeletal Tuberculosis  X-rays: Localized osteoporosis, articular margins and bony cortices become hazy “ washed out” appearance.  Blood Investigations: Lymphocytosis, low hemoglobin and raised ESR.  Biopsy  PCR : Also useful in differential diagnosis with Brucellosis, Typhoid infection and Syphilitic infection.  Radio-isotope scan  Modern Imaging Techniques: CT Scans, MRI, USG.
  12. 12. Anti Tubercular Drugs Drugs Daily adult dose Main drug toxicity Isoniazid (5-10mg/kg/BW) 300-400mg in single/2 divided dose Peripheral neuropathy convulsions, hepatitis Rifampicin (10mg/kg/BW) 450-600mg in single/2 divided dose Pinkish staining of urine,liver damage, bowel upset. Pyrazinamide (25mg/kg/BW) 750mg in single/2 divided dose Hepatotoxicity, gouty arthritis Ethambutol (15-20mg/kg/BW) 800mg in single / 2 divided dose Retrobulbar neuritis with loss of vision, color blindness Streptomycin inj. (20mg/kg/BW) 1gm injection (In children and elderly twice a week) Vestibular damage, deafness,rashes,nephrotoxicity.
  13. 13. Staging of the tuberculosis of the joints Stages Clinical Radiology Treatment Synovitis ROM >75% Soft tissue swelling, Osteoporosis Chemotherapy Early Arthritis ROM 50-75% Above + moderate diminution of joint space + marginal erosion Chemotherapy + Movements Advanced arthritis Movements restricted >75% Above + marked diminution of J.Space +destruction of J. surface Chemotherapy +surgery (Generally arthrodesis in lower limb) Advanced arthritis + sub/dislocation Ankylosis Joint is disorganized with sub/dislocation Chemotherapy +surgery (Corrective Osteotomy/ Arthrodesis)
  14. 14. Tuberculosis of the Hip Joint  The initial focus of Tuberculous lesion may start in the acetabular roof, epiphysis, metaphyseal region or in greater trochanter region.  As the upper end of the femur is intra-articular the joint gets involved rapidly.  Clinical features : Pain, Limping, deformity, and fullness around the hip.
  15. 15. Stages Clinical findings Radiologic features Synovitis Apparent lengthening, Flexion, Abduction, ER Soft tissue swelling, Osteopenia in sub chondral region Early Arthritis Apparent shortening, Flexion, Adduction , IR Osteopenia, marginal bony erosions on both surface (Acetabular and femoral head) Advanced Arthritis Flexion, Adduction, IR, True shortening Above + Reduction in joint space Advanced arthritis with sub/ dislocation Flexion, Adduction, IR, with gross shortening Gross destruction “ Mortar and pestle appearance”
  16. 16. Management of Tb Hip  Anti Tubercular therapy (ATT).  Traction to be applied ( To relieve Muscle spasm, prevents/corrects deformity, prevents subluxation/dislocation).  Hip mobilization exercises to be done with gradual increase in duration and frequency.  Non weight bearing for 12 weeks followed by partial weight bearing for next 12 weeks.
  17. 17. Surgical Management  In Synovial stage : Arthrotomy and synovectomy  In Early arthritis : Synovectomy + removal of loose bodies, pannus covering articular cartilage.  In advanced arthritis : Debridement along with arthrodesis/ Girdlestone’s Excisional arthroplasty of the joint.
  18. 18. Pott’s Spine
  19. 19. Regional distribution of Spine TB  Cervical – 12%  Cervicodorsal – 5%  Dorsal – 42%  Dorsolumbar – 12%  Lumbar – 26%  Lumbosacral – 3%
  20. 20. Types of vertebral lesions  5 types:  Paradiscal- Arterial spread  Central – Venous spread  Anterior- Subperiosteal spread  Appendicular  Articular
  21. 21. Types of vertebral lesions  5 types: 1. Paradiscal- Arterial spread 2. Central – Venous spread 3. Anterior- Subperiosteal spread 4. Appendicular 5. Articular
  22. 22. Types of vertebral lesions • 5 types: 1. Paradiscal- Arterial spread 2. Central – Venous spread 3. Anterior- Subperiosteal spread 4. Appendicular 5. Articular
  23. 23. Types of vertebral lesions 5 types: 1. Paradiscal- Arterial spread 2. Central – Venous spread 3. Anterior- Subperiosteal spread 4. Appendicular 5. Articular
  24. 24. Types of vertebral lesions 5 types: 1. Paradiscal- Arterial spread 2. Central – Venous spread 3. Anterior- Subperiosteal spread 4. Appendicular 5. Articular
  25. 25. Clinical features of spinal TB  Back Pain/Night cries  Stiffness  Deformity (Gibbus/Knuckle/Kyphosis)  Restricted movements of spine  Malaise  Loss of weight/appetite  Night sweats  Evening rise of temperature  Neurological deficit
  26. 26. Pathogenesis of TB Spine Secondary infection. Primary site in the lung, viscera or lymph glands. Hematogenous Spread / Batson plexus of veins. Delayed hypersensitivity immune reaction. Inflammatory reaction with Langhan’s giant cells, epithelioid cells, and lymphocytes. The granulation tissue proliferates, producing thrombosis of vessels.
  27. 27.  Granulomatous inflammation leads to erosion of vertebrae.  Associated disc degenaration due to end arteritis, finally complete destruction.  Weakening of trabeculae compression collapse. – Deformity.
  28. 28. •Formation of cold abscess •Collect under ant-long-ligament •Vertebral collapse •Expression of collection of tuberculous debris Slides along VB and invade the vertebral canal through intervertebral foramen. Pathology of Abscess Formation Diverted forward along different anatomical sites
  29. 29. 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
  30. 30. Classification of TB Paraplegia Early onset paraplegia  Appears within 2 years of onset.  Underlying pathology Inflammatory edema TB Granulation tissue Abscess Caseous tissue  Ischaemic lesion of cord (Rare)  Good prognosis Late onset paraplegia  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
  31. 31. Staging of Neurological Deficit 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
  32. 32. Pathology of TB Paraplegia  Extradural mass: • The Commonest mechanism affecting spinal cord function • Material compressing may be  Fluid pus  Granulation tissue  Caseous material Bony Disorders: • Sequestra from disc or body • Internal Gibbus • Pathological Dislocation
  33. 33. Clinical features of Pott’s Paraplegia o Paraplegia itself – Rare o Spontaneous muscle twitching in lower limbs o Clumsiness while walking o Extensor plantar response o Exagerrated reflexes – Sustained clonus of patella and ankle o Motor affected first – then Sensory o Sense of position and vibration – last to disappear
  34. 34. Investigations o CBC: Hb% ↓ Lymphocytosis o ESR: Raised in active stage of disease Normal ESR over period of 3 months suggests patient is in stage of repair. o Biopsy
  35. 35. Radiological Investigations  Xray: o Reduced disc space o Blurred paradiscal margins o Destruction of bodies o Loss of trabecular pattern o Increased prevertebral soft tissue shadow o Subluxation /dislocation o Decreased lordosis/Kyphosis • Skipped lesions: More than one TB Lesion in vertebral column with one or more healthy vertebrae in between the 2 lesion.
  36. 36. BONE SCAN (Technitium (Tc) – 99 m )  Increased uptake (60% 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 localize the site of active disease and to detect multilevel involvement
  37. 37. Biopsy :For definitive diagnosis CT or ultrasound guided or open biopsy during a surgical procedure. Z-N staining: a quick and inexpensive method. Culture :  results are available only after a few weeks  positive only in 60% of cases; most specific. Histology: demonstration of tubercle, 80% cases.
  38. 38. Differential Diagnosis  SPINAL INFECTIONS o pyogenic o brucellosis o fungi / syphilis  NEOPLASTIC o Extradural – Lymphoma / Metastasis etc. o Intradural extramedullary – Meningioma /neurofibroma  DEGENERATIVE / OSTEOPOROTIC  TRAUMA  CONGENITAL DEFECTS  SPINAL OSTEOCHONDROSIS
  39. 39. MIDDLE PATH REGIME  Rest on hard bed  Chemotherapy  X-ray & ESR once in 3 months kyphosis measurement  MRI/CT at 6 months interval for 2 years  Gradual mobilization is encouraged in absence of neural deficits with spinal braces & back extension exercises at 3 – 9 weeks.  Abscesses – aspirate when near surface & instil 1gm Sterptomycin inj.
  40. 40. INDICATIONS- SURGICALTREATMENT  Doubtful diagnosis  Failure to respond to conservative Rx after 3-6 weeks therapy.  Symptomatic abscess.  Neurological indications.  Mechanical instability.  Deformity.  Recurrence of disease.
  41. 41. Surgeries for Pott’s Spine  Anterio-lateral decompression (MC)-Spine is opened from its lateral side & access is made to the front and side of the cord. The cord is laid free from granulation tissue, caseous material, bony spur or sequestrum  Costo-transversectomy-Removal of 2 inches of rib & transverse process and pus comes out.  Radical debridement and arthrodesis(Hongkong operation).  Laminectomy-Indicated in spinal tumor syndrome and paraplegia resulted from post spinal disease.
  43. 43.  Knee Joint is the largest joint in the body having the largest intra articular space.  It is the 3rd most common site for osteoarticular tuberculosis.  Accounts for nearly 10% of all skeletal tuberculous lesion.
  44. 44. Pathology  The initial focus occurring by hematogenous dissemination may start in the synovium, or in the subchondral bone (Distal femur, proximal Tibia, Patella).  The synovium lesion may for many months remain purely as tubercular synovitis.  The synovial membrane gets congested, edematous and studded with tubercles.  The synovial lining which is normally a single cell layer in thickness becomes hypertrophied and thickened with granulation tissue.
  45. 45.  The joint fluid in the initial stages is increased (Serous, Opaque, turbid, yellowish and may contain fibrinous flakes).  In advanced stage of the disease tuberculous process becomes osteoarticular.  The Tuberculous granulation tissue like the pannus erodes the articular margins, destroys the bone and involves the cruciate ligament, periarticular tissues, capsule and ligaments.
  46. 46.  The Pannus may erode the margins of the articular cartilage, grow between the articular cartilage and the subchondral bone, thus detaching the cartilage from the bone.  Nutrition of the articular cartilage is thus interfered.  It looses its smooth glistening appearance, there may be fibrillation of its surface, it becomes roughened, pitted and erosion of the cartilage exposes the subchondral bone.
  47. 47.  As the disease advances large areas at pressure points show osseous destruction and the whole joint is obliterated with granulation/fibrous tissue, capsular apparatus and ligaments are disrupted and joint gets a triple deformity.  Triple deformity I. Flexion deformity II. Posterior subluxation III. Lateral rotation
  48. 48. Clinical Features • The onset and course is insidious • The knee shows – Swelling • warm • patellar tap is present due to synovial effusion • the thickened synovium – filling up all parapatellar fossa appreciated earliest in medial parapatellar fossa. • When the arthritis has set – movements are grossly restricted, – painful – accompanied by muscle atrophy. • regional lymphadenopathy.
  49. 49. • Quadricep muscle shows gross wasting • In the neglected case – triple deformity • Once the flexion deformity established – tensor fasciae latae further increases the deformity. • In long case – Posterior capsule of the knee joint gets contracted
  50. 50. Differential Diagnosis • Monoarticular affections – rheumatic arthritis (in children) – chronic traumatic synovitis due to chronic internal derangement ofknee (e.g. • meniscal tears • loose bodies • osteochondritis dissecans • chondromalaciapatellae • Rheumatoid arthritis (in adults) • subacute pyogenic arthritis/synovitis
  51. 51. • Hemarthrosis • villonodular synovitis • synovial chondromatosis
  52. 52. Staging of the tuberculosis of the joints Stages Clinical Radiology Treatment Synovitis ROM >75% Soft tissue swelling, Osteoporosis Chemotherapy Early Arthritis ROM 50-75% Above + moderate diminution of joint space + marginal erosion Chemotherapy + Movements Advanced arthritis Movements restricted >75% Above + marked diminution of J.Space +destruction of J. surface Chemotherapy +surgery (Generally arthrodesis in lower limb) Advanced arthritis + sub/dislocation Ankylosis Joint is disorganized with sub/dislocation Chemotherapy +surgery (Corrective Osteotomy/ Arthrodesis)
  53. 53. Treatment • Non operative treatment with antitubercular drugs is employed in – tubercular synovitis • Traction is applied to – prevent (or correct) flexion and subluxation deformity – keep the joint surfaces distracted. • In addition to the systemic drugs, the joint may be aspirated
  54. 54. • With the quiescence of acute local signs, gently active and assisted knee bending should be. • Usually after 12 weeks of treatment the patient may be permitted ambulation with suitable orthosis and crutches. • After 6 to 12 months of treatment, in cases with favorable response, the crutches or orthosis may be discarded. • Unprotected weight bearing is usually permitted 9 to 12 months after the start of treatment.
  55. 55.  Arthrodesis of the grossly destroyed knee in children should be deferred till the completion of growth potential of the distal femur and proximal tibia.
  56. 56. Operative Treatment • In the synovial stage – arthrotomy and synovectomy should be carried out. • In early arthritis, – synovectomy, – removal of loose bodies, debris, pannus, loose articular cartilage and – careful curettage of osseous juxta-articular foci • Postoperatively antitubercular drug therapy, – traction, – intermittent active and assisted exercises, – suitable brace ambulation should be continued
  57. 57. • In adults with advanced arthritis or in cases which resulted in painful fibrous ankylosis during the process of healing, the knee joint may be treated by arthrodesis. • This option provides  painless stable knee  prevents recrudescence  corrects deformity  patients can do long hours of standing and walking.  However it imposes a lot of restrictions in sitting,using public transport and many other social activities.
  58. 58. Arthroplasty
  60. 60.  The incidence of tuberculosis of shoulder joint is rare and accounts for only 1–2.8% of cases of skeletal Tb  Tuberculous disease of the shoulder is rare constituting nearly 1-2% of skeletal tuberculosis.  The disease originates in the head of the humerus, glenoid of the scapula or rarely from the synovium.
  61. 61.  It is extremely uncommon for the disease to present at the stage of synovitis.  Painful limitations of abduction and external rotation occurs early and there is marked wasting of the deltoid, supraspinatus and other muscles.  As the disease progresses there is marked destruction and atrophy of upper end of the humerus and glenoid and the shoulder undergoes fibrous ankylosis.
  62. 62.  The common variety is a dry atrophic form (Caries sicca)  Very rarely there may be swelling and cold abscess or sinus formation presenting in the deltoid region along with biceps tendon, in the axilla or in the supraspinatous fossa.  In the unattended cases the scapula-humeral muscles contract. Pull the humeral head against the glenoid and fix the shoulder in adduction.
  63. 63. Three types of Tb shoulder Type I: “caries sicca” Marked wasting of the shoulder. Painful restriction of all movements. Type II: “caries exudata” Swelling of the joint, cold abscess. Sometimes a sinus. Type III: “caries mobile” Restriction of active movements of the shoulder. Nearly full passive abduction.
  64. 64. Differential Diagnosis  Adhesive capsulitis / frozen shoulder/ periarthritis  Rheumatoid arthritis of the shoulder joint.
  65. 65. Radiological findings  Generalized rarefaction of bones is present with varying degree of erosion of articular margins or actual destruction of upper end of humerus or the glenoid.  In the absence of sinus formation little periosteal reaction is seen.  In advanced cases inferior subluxation of the humeral head.
  66. 66. Management  ATT  Shoulder spica in 70-90 degrees of abduction, 30 degrees forward flexion and 30 degrees of internal rotation to encourage ankylosis of gleno-humeral joint in functioning position.  Following 3 months of spica is replaced by abduction brace.  Scapulo-thoracic and elbow joint movements are encouraged after spica removal.
  67. 67. Arthrodesis of Shoulder-Extra articular arthrodesis  Before the availability of effective antitubercular drugs bony fusion of the joint was obtained by an extra articular operation carried out by inserting an autologous tibial strut graft (12-15cm) between the scapula and humerus through a posterior approach.
  68. 68. Intra articular arthrodesis With the availability of effective anti tubercular drugs intra-articular arthrodesis is preferred. Synovectomy, joint debridement, removal of loose sequestra , destroyed tissue, freshening of the joint surfaces and insertion of bone grafts at the site of desired fusion.
  69. 69. Tuberculosis of the short tubular bones  Tuberculosis of the metacarpal, metatarsal and phalanges is uncommon after the age of 5 years.  In children the disease may occur in more than one short tubular bone at a time.  Tuberculous infection of metacarpals, metatarsals and phalanges is known as tuberculous dactylitis.
  70. 70.  The hand is more frequently involved than the feet.  During childhood these short tubular bones have a lavish blood supply through a large nutrient artery.  The interior of the short tubular bone is converted virtually into a tuberculous granuloma.  This leads to a spindle shaped expansion of the bone aka “ Spina Ventosa"
  71. 71.  With the occlusion of the nutrient artery of the involved bone and the destruction of internal lamellae, there is endosteal destruction and concomitant subperiosteal new bone formation.  Abscess and sinus formation is quite common.  Differential diagnosis : 1) chronic pyogenic Osteomyelitis  Management : ATT, bracing excisional arthroplasty, corrective osteotomy or amputation.