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POTT'S SPINE

POTT'S SPINE

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    tuberculosis of spine tuberculosis of spine Presentation Transcript

    • DR HARDIK PAWARTUBERCULOSIS OFSPINE“Yakshma”
    •  common in INDIA 1-3% -osseous involvement >50% affects spinal column- commonest form of skeletal TB. Dorsal spine - most commonly involved Most Common – first 3 decades.
    •  TB :Oldest recognized disease of mankind. India –Rigveda and Atharvaveda (3500-1800 b.c.) -“Yakshma” Greco-ROMAN – PHTHISIS / CONSUMPTION French phsician Laennae Pale-pathological evidence of TB of bones, jointsand spine in prehistoric humans.
    • Percival Pottpresented the classicdescription of spinaltuberculosis in 1779.
    • Robert KochdiscoveredMycobacteriumtuberculosis in 1882.
    • Tuberculosis (TB) - leading cause of deathworldwide from a single infectious diseaseagent.The registered number of new cases of TBworldwide roughly correlates with economicconditions.
    • The highest incidences : Africa, Asia, andLatin America
    • 8 million people get TB every year, of whom95% live in developing countries. An estimated 2 million people having activespinal tb in d worldTB is increasing Day by day and there arestrains emerging which are resistant toantibiotics
    • INDIA1/5thof total worldpopulation of TB patients.6 million radiologicallyproven cases.1 to 3% of all involveskeletal system.
    • Thoracic vertebrae-122ndto 8thare typicaland the remaining 5are atypicalIdentified bypresence of costalfacets on the sidesof vertebral bodies.
    • BLOOD SUPPLY: 1 anterior spinal artery 2 posterior spinal arteries Radicular arteries reinforcethese. 2 segmental arteries oneach side supply eachvertebra. Prevertebral venous plexus( Brescet-Batson)communicates freely withveins of brain, abdomen,pelvis & lower limbs
    • GENERAL1. Malnutrition2. Poor sanitation3. Living in crowded areas4. Close contact with TB patients5. Repeated pregnancies6. Exanthematous fevers7. Immuno deficiency states LOCAL – TRAUMA , MOVEMENTS ,INCREASEDLOADS , DECREASED VASCULARITY
    • CAUSATIVE ORGANISMMycobacteriumtuberculosis.SIZE – 3x0.3 umGram positive AFBHematogenousdissemination fromprimary focusBone & joints TB developgenerally 2-3 yrs afterthe primary focusPATHOLOGYPATHOLOGY
    • 1. TB bacilli phagocytosed1. TB bacilli phagocytosedby mononuclear cellsby mononuclear cells2.2. Epitheloid cell formationEpitheloid cell formation3.Langhans giant cell formed by fusion3.Langhans giant cell formed by fusionepitheliod cells. Formed only if caseationepitheliod cells. Formed only if caseationnecrosis has occurrednecrosis has occurredPATHOLOGYPATHOLOGY
    • 4.Lymphocytes form a4.Lymphocytes form aring around the lesionring around the lesion5.Tubercle formation5.Tubercle formation Epitheloid cells-characteristic of TB. Presence of caseation necrosis almost diagnostic ofTBPATHOLOGYPATHOLOGY
    • PATHOGENESISPATHOGENESISSTEP 1STEP 1Bacilli from primaryfocus throughbloodstream reachDISC SPACE
    • STEP 2STEP 2Once infected, softnucleus centre &fibrous annula wallweaken, decay &collapse.This causes the discspace to close ,squeezing down onnerve root causingpain.
    • STEP 3STEP 3The infection spreadsto vertebral bodiesabove & below thedisc.
    • STEP 4STEP 4The bones weakenedby the infection,crumble under theweight of the humanbody.
    • STEP 5STEP 5The deformedspinal columncompresses spinalcord producingfunctionalimpairment.
    • STEP 6STEP 6Over time, thedeformed vertebraeheal & fuse.This may furthercompress nerveroots, causing pain& neurodeficit
    • Disease itselfIschemic necrosis dueto peri /endarteritisOsteoporosis dueto hyperemiaDESTRUCTION OF VERTEBRAProgressive deformityCollapseKYPHOSISGIBBUS
    • Cold abscessFormed by collection of products ofliquefaction and reactive exudationComposed of mainly serum,leucocytes,caseousmaterial, bone debris and TB bacilli.Tracks away along neighbouring vessels andnerves to reach surfaceMay burst to form sinus.
    • Caseous exudativetype• more in children• more destruction• more exudation• abscess formation.Granular type• more in adults• less destructive• insidious onset/course• abscess formation rare
    • Cervical (12%)Cervicodorsal (5%)Dorsal (42%)Dorso-lumbar (12%)Lumbar (26%)Lumbo-sacral (3%)
    • 1. PARADISCAL (due to arterial spread)2. CENTRAL (due to venous spread)3. ANTERIOR (due to subperiosteal spread)4. APPENDICAL5. ARTICULAR TYPE
    • 7%12%20%Skip lesionsOther bone TBVisceral TB
    •  Common in 1st3 decades Male=Female Slight BACK pain and stiffness are theearliest complaints PRSSURE SYMPTOMS – due to clod abscess
    • Constitutional symptoms:(40% cases) Malaise Loss of appetite/weight Night sweats Evening rise oftemperature.Specific features: Pain/night cries Stiffness Deformity - Gibbus Restricted ROM Enlarged Lymph Nodes Abscess Neuro-deficit 20%ACTIVE STAGE:
    • Clinical featuresClinical features PercentagePercentage1.Kyphosis 80-85%80-85%2.Neurodeficit 20-30%20-30%3.Palpable cold abscess 15-20%15-20%4.Radiologicalperivertebral abscess15-20 %15-20 %5.Extra spinal foci 10-15%10-15%6.Skipped lesions 05%05%
    • NEUROLOGICAL Deficit:20-40% cases: NeurodeficitMainly seen in adults due to• Inelasticity of Prevertebral fascia.• Loss of flexibility of spine.• Degenerative changes like OA.
    • NEUROLOGICAL DEFICIT (tuli 1985, kumar 1988)• Four gradesStageStage Clinical featuresClinical featuresI [Negligible] Patient unaware of Neuro-deficit,physician detects extensorplanter or ankle clonusII[Mild]Patient aware of deficit but managesto walk with/without support+signs ofspasticity.III[ Moderate]Non ambulatory because ofparalysis in extension sensory deficitless than 50%IV[Severe]3+paralysis in flexion sensory deficitmore than 50%
    •  Classification of causes (Hodgsons)Extrinsic causesExtrinsic causes Rare causesRare causesIntrinsic causesIntrinsic causes•Prolong stretching ofcord over deformity•Tuberculousmeningomyelitis•Infectivethrombosis/end arteritis•Pathological dislocation• Syringomylic changes•Spinal tumor syndrome•Posterior element TB
    • Extrinsic causesExtrinsic causesIn Active disease In Healed disease• Inflammatory edema•Abscess (fluid/caseous)• Granulation sequestratedbone/ disc• Pathological subluxation/• Internal gibbus• Dural fibrosis• Sequestra fromvertebral body• Canal Stenosis•TB debris
    •  Griffith seddon classified TB PARAPLEGIA Early onsetparaplegia (within2yrs)inflammatory edema,granulation tissue,caseous tissue andrarely ischemic lesionof cordACTIVE diseaseGood prognosis Late onset (morethan 2 yrs of onset)recrudescence ofdisease ormechanicalcompression of cord- Caseous tissue,debris,sequestra,internal gibbus,stenosis of canal,deformityHEALED DISEASEPOOR PROGNOSIS
    •  CBC-• Hb%• Lymphocytosis• DC:-lymphocyte-monocyte ratio.High lymphocyte & low monocytes countsuggest good resistance. if ratio is 5:1,it isfavorable ratio. ESR :• Raised in active stage of disease• Normal ESR over a period of 3 months suggest ptis in stage of repair.
    • Mantoux test 10 mm: everyone 5 mm: HIV infected Evidence of old disease Close contacts of infectiouscases in doubtful cases inchildren a negativeMantoux test rules out TB.
    •  Sputum examination :for AFB
    • Aspiration of abscess :smears & culture of pusCULTURE=GOLD STANDARDSOLID MEDIA: 3-8 weeksLowenstein Jensen (egg Based)Middlebrook 7H11(agar based)LIQUID BROTH:1-3 weeks
    •  BACTEC media: for faster culture (within 1-2wks)Bactec 460 Bactec9000MB Bactec mgit960b
    • ELISPOT (Enzyme-linked immunospot) T-cell based assay from blood 1 tube of blood needed Useful in outbreaks for contact investigations showed greater sensitivity than PPD
    • IgM & IgG antibodies:IgM indicates recent infection.IgG indicates past infection.Disadv: high sensitivity but low specificityPCR:Tissue PCR more specificBIOPSY:CT guidedC-Arm guidedPercutaneous
    • Plain radiography signs : Reduced disc space Blurred paradiscalmargins Destruction of bodies Loss of trabecularpattern Increased Prevertebralsoft tissue shadow Subluxation/dislocation Decreased Lordosis/kyphosis
    •  Posterior elementinvolvement(5%) Skip lesions(7%)
    • Paradiscal lesion:Commonest lesionSpread through arterialsupplyReduced disc space(earliest sign)Loss of vertebralmargins.Increased Prevertebralsoft tissue shadow
    • Reduced disc space inKoch due to Atrophy of disc tissuedue to lack of nutrition(due to aseptic necrosisof end plates) Prolapse of nucleuspulposus into softnecrotic vertebral bodies
    • Central type of lesion: (TBof the Centrum)Spread through Batson’svenous plexus/ branchesof posterior vertebralartery.Minimal disc spacereductionAt the end concentriccollapse.
    • Anterior type lesion:Starts beneath theanterior longitudinalligament & periosteumCollapse & disc spacereduction is usuallyminimal & occurs lateErosion is primarilymechanicalAppendicial typelesion :lesion : Rare Isolated infection ofpedicles/ lamina/transverse process/spinous process Erosions Para vertebral shadows Intact disc space
    • Skipped lesion :More than one TBlesion present invertebral columnwith one or morehealthy vertebrae inbetween the 2lesions.7% on routine X-rays.More frequentlydetected on CT/MRI
    • Lateral shift and scoliosis:Reasons-More destruction of vertebral body on onesideKyphotic deformity :Due to collapse of boneForward angulation – 1-2 knuckle3 – gibbuslarge no round kyphosis
    • Healing is indicated by1. Decreased soft tissueshadow2. Disappearance oferosion3. Return of normaldensity(mineralization)4. Bony ankylosis
    • Figure a – Separation of the facet joint. The facetjoint dislocates at the apex of the curveFigure b – Posterior retropulsion.Figure c – Lateral translation.Figure d – Toppling sign.
    • Multiple vertebralinvolvement:1.Immunocompromized2. DM3.Hemoglobinopathies
    • CT SCAN• Patterns of bony destruction.• Calcifications in abscess(pathognomic for Tb)• Regions which are difficult tovisualize on plain films, like :1. Cranio-vertebral junction (CVJ)2. Cervico-dorsal region,3. Sacrum4. Sacro-iliac joints.5. Posterior spinal tuberculosisbecause lesions less than 1.5cmare usually missed due tooverlapping of shadows on x rays.MRI• Lack of ionizing radiation, highcontrast resolution & 3D imaging.• Detect marrow infiltration invertebral bodies, leading to earlydiagnosis.• Changes of discitis• Assessment of extraduralabscesses / subligamentousspread.• Skip lesions• Spinal cord involvement.• Spinal arachanoiditis.
    • • MRI :diagnosis of TB ofDfficult & rare sites,Disease of posterior elementsVertebral appendagesEpidural exiensionInfections of sacroiliac region.Follow upUSG : to diagnose thepresence of tubercularabscesses in Dorso-lumbarvertebral disease.
    • LOCATION OF PARAVERTEBRAL ABSCESS
    • Angle of Kyphosis
    • BONE SCAN (Technitium (Tc) - 99 m )• Increased uptake in up to 60 per cent patients with activetuberculosis.• >= 5mm lesion size can be detected.• Avascular segments and abscesses show a cold spot due todecreased uptake.• Highly sensitive but nonspecific.• Aid to localise the site of active disease and to detectmultilevel involvement.
    • 1. Pyogenic infections2. Typhoid spine3. Brucella spondylitis4. Mycotic spondylitis5. Syphilitic infection ofspine6. Tumorous conditions-hemangioma, GCT,aneurysmal bone cyst7. Primary malignanttumor8. Multiple myeloma9. Lymphomas10. Secondary neoplasticdeposits11. Histiocytosis X12. Spinal osteochondrosis13. Traumatic conditions14. Hydatid cyst
    • EVOLUTION OF TREATMENT:Undergone tremendous revolutionarychanges.Ancient Indians used herbal preparationSIPURDA.Pott & Charcot applied Hot iron to drain pus
    • Hippocrates advocatedtraction & other meansto correct deformity
    • BASIC PRINCIPLES OFMANAGEMENT• Early diagnosis• Expeditious medical treatment• Aggressive surgical approach• Prevent deformity• Expect good outcome
    • Sanatorium treatment
    • Surgery was not attempted due to fear ofsecondary infection and deathMost of operative procedures weredeveloped for either for treatment or forprevention of paralysis in TB spinePrinciple was more direct approach todiseased part.
    • Surgeries done in Preantitubercular Era:• Laminectomy & laminotomy : Chipault (1896 )• Costotransversectomy Menard (1896)• Posterior mediastinotomy• Calves operation (aspiration without sinusformation) (1917)• Lateral rhachiotomy Capener (1933 )• Anterolateral decompression Dott &Alexander(1947)
    • Results of Surgeries done inPreantitubercular Era:Serious sinus formationPseudoarthrosis (4-26%)Recurrence of lesionNeurological deteriorationDeath
    • Antitubercular drugs (AKT) Black picture has taken a dramatic turn forthe better with discovery of Antituberculardrugs (AKT)1943- PAS1944- Streptomycin1951- INH (MAGIC BULLET)1970- RIFAMPIN & SHORT COURSE RX-EVOLUTION OF TREATMENTEVOLUTION OF TREATMENT
    • Simultaneously under cover of AKTdirect surgical attack was popularizedthose daysAttention was mainly paid on Thoracicspine casesNo direct reference was made to thetreatment of cervical diseaseEVOLUTION OF TREATMENTEVOLUTION OF TREATMENT
    • RestBracesHigh protein dietMultivitamins, hematinicsHygieneBed sore careChest/ urinary tract careImprove Immune statusTreat other comorbid conditions.
    • Non neurological cases ofSpinal TBBROAD TREATMENT REGIMENSRadical surgeryConservative t/t withchemotherapy onlyMiddle pathregimen
    • Bactericidal drugs DoseDose1.Isoniazid 5mg/kg5mg/kg2. Rifampicin 10-15 mg/kg10-15 mg/kg3. Streptomycin 20mg/kg20mg/kg4. Pyrazinamide 20-25 mg/kg20-25 mg/kgBacteriostatic drugs DoseDose11. Ethambutol 25mg/kg (x 2mnths)25mg/kg (x 2mnths)Then 15mg/kgThen 15mg/kg
    • • Amikacin, Kanamycin,capriomycin• Ciprofloxacin, Ofloxacin, Levofloxacin• Rifabutin• Clarithromycin• Clofazimine• Ethionamide• Cycloserine
    •  INH +RMP+ETM+ PZN for first 3 months INH + RMP +PZN for 9 months INH + RMP for next 6 monthsEntire duration of chemotherapy lasts for 16-18months10 mg pyridoxine for prevention of peripheralneuropathy
    •  Rationale“All spine TB cases do not require surgery andonly those who do not respond to conservativemeasures should be operated”
    • Treatment is on non-operative lines withAKT, rest & spinal braces1.Rest: in hard bed or plaster of Paris bed( inchildren)2.Drugs :INH +Rifampicin +ETB FOR 4 monthsINH + PZA FOR 4 MONTHSINH + RMP FOR 4 MONTHSINH FOR LAST 4 MONTHSTOTAL DURATION 16 months.
    • supportive therapy- multivitamins, hematinics if necessary & high protein diet.3.Radiographs & ESR: at 3-6 months interval4.Gradual mobilisation:with the help of spinal braces5. Abscess are aspirated6. Sinus excision7. decompression
    • Indications of surgery in middle path regime:1. No progressive recovery after a fair trial ofconservative t/t (3-4 wks)2. Neurological complication develops duringconservative treatment3. Worsening of Neuro-deficit during t/t4. Recurrence of neurological complications5. Pressure effects (deglutition/respiratory)6. Advanced cases of neurological involvement(sphincter disturbances, flaccid paralysis, or severeflexor spasms)
    • TUBERCULOUS PARA/QUADRIPLEGIATUBERCULOUS PARA/QUADRIPLEGIAAKT + REST (3-6 WKS)AKT + REST (3-6 WKS)PROGRESSIVE RECOVERY NO IMPROVEMENTPROGRESSIVE RECOVERY NO IMPROVEMENTCT AKT SURGERYCT AKT SURGERYPROGRESSIVE RECOVERY NO IMPROVEMENTPROGRESSIVE RECOVERY NO IMPROVEMENTMRI/ MYELOGRAMMRI/ MYELOGRAM(REPEAT)(REPEAT)
    • MRI/ MYELOGRAMMRI/ MYELOGRAMNO COMPRESSION COMPRESSION PRESENTNO COMPRESSION COMPRESSION PRESENTINTRISIC DAMAGE TO CORD REPEAT SURGERYINTRISIC DAMAGE TO CORD REPEAT SURGERYCt AKT + REHABILITATIONCt AKT + REHABILITATIONNO RECOVERY IMPROVEMENTNO RECOVERY IMPROVEMENTCt AKTCt AKT
    •  In patients without neurological deficit IN in TB paraplegia
    •  1. Abscess drainage by anatomical levelcervical spine - retropharyngeal- post triangle of neck- supraclivicular regiondorsal spine – costotransversectomyMENARDLUMBAR spine – paravertebral
    •  2. HONG KONG PROCEDURERADICAL DEBRIDEMENT AND ARTHRODESIS 3. ANTEROLATERAL DECOMPRESSION 4. POSTERIOR SPINAL ARTHRODESISALBESS PROCEDUREHIBB’S PROCEDURE
    • SURGERY INDICATIONS1 Decompression (+/- fusion) Too advanced ds, failure to respond toconservative therapy2 Debridement + /- decompression +/- Recurrence of disease or of neuralfusion complication3 Anterior transposition of cord Severe kyphosis (>60⁰) + neural deficits(Extrapleural anterolateral approach)4 Laminectomy Extradural granuloma / tuberculoma (STS), Oldhealed disease presenting as secondary canalstenosis / posterior spinal disease
    • SURGICAL APPROACHES :WORKERS C1-C2 CERVICAL C7-D1 DORSAL DORSO- LUMBAR L5-S1LUMBARKirkaldy-Willis - Anterior Transpleural Anterolateral or Anterolateral Retroperitoneal Transperitoneal,(1965) through bed of transpleural sympathectomy paramedian3rd rib or ureter incision inapproach TrendelenburgpositionHodgson Transoral / Through Transpleural via Anterior Bed of 11th rib Renal approach Transperitoneal in(1969) transthyroi anterior or bed of 3rd rib transpleural extrapleural Trendelenburgd posterior∆ /split sternal for decompression extraperitone position. Lowerextensive lesion al / left midline incisiontranspleuralvia bed of 9thribKemp et al - Anterior Anterior cervical Trans-sternal for Bed of 12th rib Retroperitoneal Retroperitoneal(1973) D3-D4.Anterior approach through obliquetranspleural for renal incisionD5-D12Smith & AnteriorRobinson(1985)Mc Afee et al Retrophary(1987) ngeal extra-mucosalAnterior -- -- -- -- -- -Tuli et al Transoral Anterior Low anterior Anterolateral or Anterolateral Retroperitoneal Retroperitoneal or(1988) for cervical transpleural approach Retropsoasdrainage transversevertebrotomy
    • Tuli’s recommended approach• Cervical spine -T1Anterior approach• Dorsal spine -DL junctionAnterolateral approach• Lumbar spine &Lumbosacral junctionExtraperitoneal Transverse Vertebrotomy
    • ANTERIOR APPROACH TO THECERVICAL SPINE (C2 to D1)Smith & Robinson• Oblique / transverse incision.• Plane b/w SCM & carotid sheath laterally & T-O medially.• Longitudinal incision in ALL open a perivertebral abscess, orthe diseased vertebrae may be exposed by reflecting the ALL& the longus colli muscles.Hodgson approach via posterior triangle by retracting SCM,Carotid sheath, T & O anteriorly & to the opposite side.
    • SURGICAL APPROACHES TODORSAL SPINE• Anterior transpleural transthoracic approach (Hodgson &Stock, 1956)• Anterolateral extrapleural approach (Griffiths, Seddon & Roaf,1956)• Posterolateral approach (Martin,1970){Dura is exposed by hemilaminectomy first &thenextended laterally to remove the posterior ends of2 - 4ribs, corresponding transverse processes & the pedicles}.
    • TRANSTHORACIC TRANSPLEURAL• Left sided incision preferable• Incision is made along the rib which in the mid-axillary line, liesopposite the centre of the lesion (i.e. usually 2 ribs higher than thecentre of the vertebral lesion).• For severe kyphosis, a rib along the incision line should be removed.• AJ-shapedparascapularincisionforC7-D8lesions,scapulauplift& rib resection.• After cutting the muscles & periosteum, rib is resectedsubperiosteally.
    • • Semicircular incision• For severe kyphosis, additional 3-4 transverse processes andribs have to be removed.• Intercostal nerves serve as guide to the intervertebralforamina & the pedicles.
    • ANTEROLATERAL DECOMPRESSION• Griffith et al -- prone position• Tuli --- Right lateral position• Advantage:-1. avoid venous congestion2. avoid excessive bleeding3. permits free respiration4. Lung & mediastinal contents fall anteriorly• Parts to remove :• Posterior part of rib (~8cm from the TP)• Transverse process (TP)• Pedicle• Part of the vertebral body
    • • Semicircular incision• For severe kyphosis, additional 3-4 transverse processes andribs have to be removed.• Intercostal nerves serve as guide to the intervertebralforamina & the pedicles.
    • ANTERO-LATERAL APPROACH TOLUMBAR SPINE ( LUMBO-VERTEBROTOMY)• Left side approach• Semicircular incision• Expose and remove transverse processsubperiosteally.• Preserve lumbar nerves
    • EXTRA PERITONEAL ANTERIORAPPROACH TO LUMBAR SPINE• 45 ⁰ right lateral position with a bridge centered over the area to beexposed.• Similar incision as nephroureterectomy or sympathectomy• Strip peritoneum off posterior abdominal wall and kidney,preserving ureter.• Longitudinal incision along psoas fibers for abscess drainage• Retract the sympathetic chain• Double ligation of lumbar vessels.
    • EXTRA PERITONEAL APPROACH TOLUMBO-SACRAL REGION• Left side preferred ( left Common iliac vessels longer& retracted easily).• Lazy "S" incision• Strip & reflect the parietal peritoneum along withureter & spermatic vessels towards right side.
    • TRANS PERITONEAL HYPOGASTRIC/SUPRAPUBIC ANTERIOR APPROACH TOLUMBO-SACRAL REGION• Supine position• Midline incision from umbilicus to pubis.• Lumbo-sacral region identified distal to aortic bifurcation and leftcommon iliac vein.• Longitudinal incision on parietal peritoneum over lumbo-sacralregion in midline.• Avoid injury to sacral nerve & artery and sympathetic ganglion.
    • POSTERIOR SPINALARTHRODESIS• By- Albee & Hibbs• Albee- Tibial graft inserted longitudinally in to the splitspinous processes across the diseased site.• Hibbs- overlapping numerous small osseous flaps fromcontiguous laminae , spinous processes & articular facets• Indications-1. Mechanical instability of spine in otherwise healed disease.2. To stabilize the craniovertebral region (in certain cases of T.B.)3. As a part of panvertebral operation
    • TREATMENT OF PARAPLEGIA INSEVERE KHYPHOSIS• Griffiths et al (1956) :anterior transposition of cord throughlaminectomy• Rajasekaran (2002): posterior stabilization f/b anteriordebridement and bone grafting ( titanium cages) in activestage of disease and vice versa for healed disease.• Antero-lateral (Preferred approach) .
    • SURGICAL CORRECTION OF SEVEREKYPHOTIC DEFORMITY• Fundamentals of correction:1. to perform an osteotomy on the concave side of the curveand wedge it open ( secured with strong autogenous iliacgrafts) .2. to remove a wedge on the convex side and close this wedge( Harrington compression rods and hooks)
    •  Removal of Taylors brace was subject to clinical &radiological follow up ( usually 10-12 wks)If patient neurologicallyintact Taylors brace appliedafter 48 hrs. Patient kept ambulatoryIf patient is havingNeurodeficit Regular neurocharting. Taylors brace applied afterpatient could sit up withoutsupport Taylors brace worn for periodof 3 months Patient kept ambulatory
    •  All patients evaluated at3 mnths6 mnths9 mnths12 mnthsClinical Radiological•Wt gain•Pain relief•Free ROM•Resolution of abscesses•Neurological recoveryEvaluationEvaluation• Decreased soft tissueshadow• Disappearance oferosion• Return of mineralization• Graft incorporation• Bony ankylosis15mnths18 mnths
    •  First objective sign can be seen in 24 hrs-12weeks after decompression. Time taken for near complete recoveryvaries between 3-6 months No significant neural recovery occurs after12-18 months.
    • Definition of favorable status- No residual neural impairment No sinus/ cold abscess. No impairment of physical activity due tospinal disease/lesion. Presence of radiographic quiescent disease.
    •  Extradural granuloma Severe kyphosis Reactivation of lesionDecreased nutritionResistant organismsCompromised immuno-status
    • TreatmentNecessary surgeryNewer anti tubercular drugsSupportive measures
    • Surgery has its distinct advantages.necrotic biowaste is removed completely &abscesses are drained• Early relief from pain• Early bony fusion• Prevention & correction of deformity• Confirmation of diagnosis by histopathology