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HISTORICAL ASPECTS: HISTORICAL ASPECTS TB : Oldest recognized disease of mankind. India –Rigveda and Atharvaveda (3500-1800 b.c.) - “ Yakshma” Egypt – “ red king” in mummies. Pale-pathological evidence of TB of bones, joints and spine in prehistoric humans.HISTORICAL ASPECTS: HISTORICAL ASPECTS Percival Pott presented the classic description of spinal tuberculosis in 1779.HISTORICAL ASPECTS: HISTORICAL ASPECTS Robert Koch discovered Mycobacterium tuberculosis in 1882.EPIDEMIOLOGY: EPIDEMIOLOGY Tuberculosis (TB) - leading cause of death worldwide from a single infectious disease agent. Indeed up to 1/2 of the world's population is infected with TB. The registered number of new cases of TB worldwide roughly correlates with economic conditions.EPIDEMIOLOGY: EPIDEMIOLOGY The highest incidences : Africa, Asia, and Latin America with the lowest gross national products.EPIDEMIOLOGY: EPIDEMIOLOGY 8 million people get TB every year, of whom 95% live in developing countries . An estimated 2 million people die from TB every year After a century of decline TB is increasing and there are strains emerging which are resistant to antibioticsEPIDEMIOLOGY: EPIDEMIOLOGY This excess of cases is attributable to The changes in the social structure in cities, The human immunodeficiency virus epidemic (AIDS), Failure to improve public health programs, The economic cost of treating.EPIDEMIOLOGY: EPIDEMIOLOGY INDIA 1/5 th of total world population of TB patients. 6 million radiologically proven cases. 1 to 3% of all involve skeletal system.ANATOMY: ANATOMY Thoracic vertebrae-12 2 nd to 8 th are typical and the remaining 5 are atypical Identified by presence of costal facets on the sides of vertebral bodies.ANATOMY: ANATOMY BLOOD SUPPLY: 1 anterior spinal artery 2 posterior spinal arteries Radicular arteries reinforce these. 2 segmental arteries on each side supply each vertebra. Prevertebral venous plexus ( Brescet -Batson) communicates freely with veins of brain, abdomen, pelvis & lower limbsPowerPoint Presentation: CAUSATIVE ORGANISM Mycobacterium tuberculosis. Hematogenous dissemination from primary focus. Bone & joints TB develop generally 2-3 yrs after the primary focus It’s a cell mediated immunity. PATHOLOGYPowerPoint Presentation: 1. TB bacilli phagocytosed by mononuclear cells 2. Epitheloid cell formation 3.Langhans giant cell formed by fusion epitheliod cells. Formed only if caseation necrosis has occurred PATHOLOGYPowerPoint Presentation: 4.Lymphocytes form a ring around the lesion 5.Tubercle formation Epitheloid cells-characteristic of TB. Presence of caseation necrosis almost diagnostic of TB PATHOLOGYPowerPoint Presentation: PATHOGENESIS STEP 1 Bacilli from primary focus through bloodstream reach DISC SPACEPATHOGENESIS: PATHOGENESIS STEP 2 Once infected, soft nucleus centre & fibrous annula wall weaken, decay & collapse. This causes the disc space to close , squeezing down on nerve root causing pain .PATHOGENESIS: PATHOGENESIS STEP 3 The infection spreads to vertebral bodies above & below the disc.PATHOGENESIS: PATHOGENESIS STEP 4 The bones weakened by the infection, crumble under the weight of the human body.PATHOGENESIS: PATHOGENESIS STEP 5 The deformed spinal column compresses spinal cord producing functional impairment .PATHOGENESIS: PATHOGENESIS STEP 6 Over time, the deformed vertebrae heal & fuse. This may further compress nerve roots, causing pain & neurodeficitPATHOGENESIS: PATHOGENESIS 4 types of vertebral affections 1. PARADISCAL (due to arterial spread) 2. CENTRAL (due to venous spread) 3. ANTERIOR (due to subperiosteal spread) 4. APPENDICALPATHOGENESIS: PATHOGENESIS Disease itself Ischemic necrosis due to peri /endarteritis Osteoporosis due to hyperemia DESTRUCTION OF VERTEBRA Progressive deformity CollapsePATHOGENESIS: PATHOGENESIS Cold abscess Formed by collection of products of liquefaction and reactive exudation Composed of mainly serum,leucocytes,caseous material, bone debris and TB bacilli. Tracks away along neighbouring vessels and nerves to reach surface May burst to form sinus.PATHOGENESIS: PATHOGENESIS Caseous exudative type more in children more destruction more exudation abscess formation. Granular type more in adults less destructive insidious onset/course abscess formation rareREGIONAL DISTRIBUTION SPINE TB: REGIONAL DISTRIBUTION SPINE TB Cervical (12%) Cervicodorsal (5%) Dorsal (42%) Dorso-lumbar (12%) Lumbar (26%) Lumbo-sacral (3%)ASSOCIATIONS: ASSOCIATIONSPREDISPOSING FACTORS: PREDISPOSING FACTORS Malnutrition Poor sanitation Living in crowded areas Close contact with TB patients Repeated pregnancies Exanthematous fevers Immuno deficiency statesCLINICAL FEATURES: CLINICAL FEATURES Common in 1 st 3 decades Male=Female Slight pain and stiffness are the earliest complaintsCLINICAL FEATURES: CLINICAL FEATURES Constitutional symptoms : (40% cases) Malaise Loss of appetite/weight Night sweats Evening rise of temperature. Specific features: Pain/night cries Stiffness Deformity Restricted ROM Enlarged Lymph Nodes Abscess Neuro-deficit ACTIVE STAGE:CLINICAL FEATURES: CLINICAL FEATURES Clinical features Percentage 1.Kyphosis 80-85% 2.Neurodeficit 20-30% 3.Palpable cold abscess 15-20% 4.Radiological perivertebral abscess 15-20 % 5.Extra spinal foci 10-15% 6.Skipped lesions 05%CLINICAL FEATURES: CLINICAL FEATURES 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.PowerPoint Presentation: NEUROLOGICAL DEFICIT : Four grades Stage Clinical features I [Negligible] Patient unaware of Neuro -deficit , physician detects extensor planter or ankle clonus II [Mild] Patient aware of deficit but manages to walk with/without support+signs of spasticity. III [ Moderate] Non ambulatory because of paralysis in extension sensory deficit less than 50% IV [Severe] 3+paralysis in flexion sensory deficit more than 50%NEUROLOGICAL INVOLVEMENT: NEUROLOGICAL INVOLVEMENT Classification of causes (Hodgsons) Extrinsic causes Rare causes Intrinsic causes Prolong stretching of cord over deformity Tuberculous meningomyelitis Infective thrombosis/end arteritis Pathological dislocation Syringomylic changes Spinal tumor syndrome Posterior element TBNEUROLOGICAL INVOLVEMENT: NEUROLOGICAL INVOLVEMENT Extrinsic causes In Active disease In Healed disease Inflammatory edema Abscess (fluid/caseous) Granulation sequestrated bone/ disc Pathological subluxation/ dislocation Internal gibbus Dural fibrosis Sequestra from vertebral body Canal Stenosis TB debrisCLASSIFICATION: CLASSIFICATION Griffith classified as Early onset paraplegia (within 2yrs) inflammatory edema, granulation tissue, caseous tissue and rarely ischemic lesion of cord Late onset (more than 2 yrs of onset) recrudescence of disease or mechanical compression of cordINVESTIGATIONS: INVESTIGATIONS CBC- Hb% Lymphocytosis DC:-lymphocyte-monocyte ratio. High lymphocyte & low monocytes count suggest good resistance. if ratio is 5:1,it is favorable ratio. ESR : Raised in active stage of disease Normal ESR over a period of 3 months suggest pt is in stage of repair.INVESTIGATIONS: INVESTIGATIONS Mantoux test 10 mm : everyone 5 mm : HIV infected Evidence of old disease Close contacts of infectious cases in doubtful cases in children a negative Mantoux test rules out TB .INVESTIGATIONS: INVESTIGATIONS Sputum examination : for AFBINVESTIGATIONS: INVESTIGATIONS Aspiration of abscess : smears & culture of pus CULTURE=GOLD STANDARD SOLID MEDIA: 3-8 weeks Lowenstein Jensen (egg Based) Middlebrook 7H11 (agar based) LIQUID BROTH: 1-3 weeksINVESTIGATIONS: INVESTIGATIONS BACTEC media : for faster culture (within 1-2wks) Bactec 460 Bactec9000MB Bactec mgit960bINVESTIGATIONS: INVESTIGATIONS 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 PPDINVESTIGATIONS: INVESTIGATIONS IgM & IgG antibiotics: IgM indicates recent infection. IgG indicates past infection. Disadv: high sensitivity but low specificity PCR: Tissue PCR more specific BIOPSY: CT guided C-Arm guided PercutaneousRADIOLOGY: RADIOLOGY Plain radiography signs : Reduced disc space Blurred paradiscal margins Destruction of bodies Loss of trabecular pattern Increased Prevertebral soft tissue shadow Subluxation/dislocation Decreased Lordosis/ kyphosisRADIOLOGY: RADIOLOGY Posterior element involvement ( 5%) Skip lesions ( 7% )RADIOLOGY: RADIOLOGY Paradiscal lesion: Commonest lesion Spread through arterial supply Reduced disc space (earliest sign) Loss of definitions of vertebral margins. Increased Prevertebral soft tissue shadowRADIOLOGY: RADIOLOGY Reduced disc space in Koch due to Atrophy of disc tissue due to lack of nutrition (due to aseptic necrosis of end plates) Prolapse of nucleus pulposus into soft necrotic vertebral bodiesRADIOLOGY: RADIOLOGY Central type of lesion: (TB of the Centrum) Spread through Batson’s venous plexus/ branches of posterior vertebral artery. Minimal disc space reduction At the end concentric collapse.RADIOLOGY: RADIOLOGY Anterior type lesion : Starts beneath the anterior longitudinal ligament & periosteum Collapse & disc space reduction is usually minimal & occurs late Erosion is primarily mechanical Appendicial type lesion : Rare Isolated infection of pedicles/ lamina/ transverse process/ spinous process Erosions Para vertebral shadows Intact disc spaceRADIOLOGY: RADIOLOGY Lateral shift and scoliosis: Reasons- More destruction of vertebral body on one side Posterior articulation involvement in addition to usual paradiscal lesions (et al Gupta)RADIOLOGY: RADIOLOGY Skipped lesion : More than one TB lesion present in vertebral column with one or more healthy vertebrae in between the 2 lesions. 7% on routine X-rays. More frequently detected on CT/MRIRADIOLOGY: RADIOLOGY Healing is indicated by Decreased soft tissue shadow Disappearance of erosion Return of normal density (mineralization) Bony ankylosisRADIOLOGY: RADIOLOGY Multiple vertebral involvement: 1.Immunocompromized 2. DM 3.HemoglobinopathiesRADIOLOGY: RADIOLOGY MRI :diagnosis of TB of difficult & rare sites, disease of posterior elements vertebral appendages infections of sacroiliac region. USG : to diagnose the presence of tubercular abscesses in Dorso-lumbar vertebral disease.PowerPoint Presentation: Tissue / Fluids T1 T1 T2 T2 Fat in marrow/degenerated areas White Greyish white CSF/clear fluid/water in tissue Black White Granulation tissue Grey Whitish grey Cord contusion/edema Dark grey Whitish Nucleus pulposus hydrated Black/ White Syrinx Black cavity in cord White cavity in cordDIFFERENTIAL DIAGNOSIS : DIFFERENTIAL DIAGNOSIS Pyogenic infections Typhoid spine Brucella spondylitis Mycotic spondylitis Syphilitic infection of spine Tumorous conditions- hemangioma, GCT, aneurysmal bone cyst Primary malignant tumor Multiple myeloma Lymphomas Secondary neoplastic deposits Histiocytosis X Spinal osteochondrosis Traumatic conditions Hydatid cystMANAGEMENT: MANAGEMENT EVOLUTION OF TREATMENT: Undergone tremendous revolutionary changes. Ancient Indians used herbal preparation SIPURDA . Pott & Charcot applied Hot iron to drain pusEVOLUTION OF TREATMENT [Preantitubercular Era]: EVOLUTION OF TREATMENT [Preantitubercular Era] Hippocrates advocated traction & other means to correct deformityEVOLUTION OF TREATMENT [Preantitubercular Era]: EVOLUTION OF TREATMENT [Preantitubercular Era] Sanatorium treatmentEVOLUTION OF TREATMENT [Preantitubercular Era]: EVOLUTION OF TREATMENT [Preantitubercular Era] Surgery was not attempted due to fear of secondary infection and death Most of operative procedures were developed for either for treatment or for prevention of paralysis in TB spine Principle was more direct approach to diseased part.EVOLUTION OF TREATMENT [Preantitubercular Era]: EVOLUTION OF TREATMENT [Preantitubercular Era] Surgeries done in Preantitubercular Era : Laminectomy & laminotomy Costotransversectomy Posterior mediastinotomy Calves operation (aspiration without sinus formation) Lateral rhachiotomy Anterolateral decompressionEVOLUTION OF TREATMENT [Preantitubercular Era]: EVOLUTION OF TREATMENT [Preantitubercular Era] Results of Surgeries done in Preantitubercular Era: Serious sinus formation Pseudoarthrosis (4-26%) Recurrence of lesion Neurological deterioration DeathPowerPoint Presentation: Antitubercular drugs (AKT) Black picture has taken a dramatic turn for the better with discovery of Antitubercular drugs (AKT) 1943- PAS 1944- Streptomycin 1951- INH ( MAGIC BULLET ) 1970- RIFAMPIN & SHORT COURSE RX- EVOLUTION OF TREATMENTPowerPoint Presentation: Simultaneously under cover of AKT direct surgical attack was popularized those days Attention was mainly paid on Thoracic spine cases No direct reference was made to the treatment of cervical disease EVOLUTION OF TREATMENTSUPPORTIVE Rx: SUPPORTIVE Rx Rest Braces High protein diet Multivitamins, hematinics Hygiene Bed sore care Chest/ urinary tract care Improve Immune status Treat other comorbid conditions.PRESENT MANAGMENT: PRESENT MANAGMENT Non neurological cases of Spinal TB BROAD TREATMENT REGIMENS Radical surgery Conservative t/t with chemotherapy only Middle path regimen1st line CHEMOTHERAPY: 1 st line CHEMOTHERAPY Bactericidal drugs Dose 1.Isoniazid 5mg/kg 2. Rifampicin 10-15 mg/kg 3. Streptomycin 20mg/kg (max) 4. Pyrazinamide 20-25 mg/kg Bacteriostatic drugs Dose 1 . Ethambutol 25mg/kg (x 2mnths) Then 15mg/kgNewer Drugs: Newer Drugs Amikacin, Kanamycin Ciprofloxacin, Ofloxacin, Levofloxacin Rifabutin Clarithromycin Clofazimine Ethionamide Cycloserine POLICY OF DRUG T/T: POLICY OF DRUG T/T INH +RMP+ETM+ PZN for first 6 months INH + RMP for next 12 months Entire duration of chemotherapy lasts for 16-18 monthsMIDDLE PATH REGIME: MIDDLE PATH REGIME Rationale “All spine TB cases do not require surgery and only those who do not respond to conservative measures should be operated”MIDDLE PATH REGIME: MIDDLE PATH REGIME Treatment is on non-operative lines with AKT, rest & spinal braces 1.Rest: in hard bed or plaster of Paris bed( in children) 2.Drugs : INTENSIVE PHASE- INH (5mg/Kg) + Rifampicin (10mg/Kg) +ETB (15mg/Kg) + PZA(25mg/Kg) for 6 months CONTINUATION PHASE- INH (5mg/Kg) + Rifampicin (10mg/Kg) for next 12 months.MIDDLE PATH REGIME: MIDDLE PATH REGIME supportive therapy- multivitamins, hematinics if necessary & high protein diet. 3.Radiographs & ESR: at 3-6 months interval 4.Gradual mobilisation: with the help of spinal bracesPowerPoint Presentation: Indications of surgery in middle path regime: No progressive recovery after a fair trial of conservative t/t (3-4 wks) Neurological complication develops during conservative treatment Worsening of Neuro -deficit during t/t Recurrence of neurological complications Pressure effects (deglutition/respiratory) Advanced cases of neurological involvement (sphincter disturbances, flaccid paralysis, or severe flexor spasms)ALGORITHM FOR MANAGEMENT OF VERTEBRAL TB WITH NEUROLOGICAL COMPLICATIONS: ALGORITHM FOR MANAGEMENT OF VERTEBRAL TB WITH NEUROLOGICAL COMPLICATIONS TUBERCULOUS PARA/QUADRIPLEGIA AKT + REST (3-6 WKS) PROGRESSIVE RECOVERY NO IMPROVEMENT CT AKT SURGERY PROGRESSIVE RECOVERY NO IMPROVEMENT MRI/ MYELOGRAM (REPEAT)PowerPoint Presentation: MRI/ MYELOGRAM NO COMPRESSION COMPRESSION PRESENT INTRISIC DAMAGE TO CORD REPEAT SURGERY Ct AKT + REHABILITATION NO RECOVERY IMPROVEMENT Ct AKTOPERATIVE MANAGEMENT: Surgical options Decompression & global fusion Decompression & anterior interbody fusion Only Decompression Trans-pedicular decompression & global fusion OPERATIVE MANAGEMENTOPERATIVE MANAGEMENT: OPERATIVE MANAGEMENT Surgical approaches for DORSAL SPINE Anterolateral (extrapleural) Anterior (transpleural) Posterolateral (extrapleural) Anterior low cervical incision (for D1-2)POSTOPERATIVE PROTOCOL: POSTOPERATIVE PROTOCOL Removal of Taylor's brace was subject to clinical & radiological follow up ( usually 10-12 wks) If patient neurologically intact Taylor's brace applied after 48 hrs. Patient kept ambulatory If patient is having Neurodeficit Regular neurocharting. Taylor's brace applied after patient could sit up without support Taylor's brace worn for period of 3 months Patient kept ambulatoryFOLLOW UP : FOLLOW UP All patients evaluated at 3 mnths 6 mnths 9 mnths 12 mnths Clinical Radiological Wt gain Pain relief Free ROM Resolution of abscesses Neurological recovery Evaluation Decreased soft tissue shadow Disappearance of erosion Return of mineralization Graft incorporation Bony ankylosis 15mnths 18 mnthsRecovery: Recovery First objective sign can be seen in 24 hrs-12 weeks after decompression. Time taken for near complete recovery varies between 3-6 months No significant neural recovery occurs after 12-18 months.Results: Results 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.Recurrence/ Relapse: Recurrence/ Relapse Extradural granuloma Severe kyphosis Reactivation of lesion Decreased nutrition Resistant organisms Compromised immuno-statusRecurrence/ relapse: Recurrence/ relapse Treatment Necessary surgery Newer anti tubercular drugs Supportive measuresCourse of Kyphosis: Course of Kyphosis Deformity status Percentage of patients Decrease in deformity 2% No change or <10º increase 75% >10º increase 20-25% Natural course of progression is independent of type of treatment given.Course of kyphosis: Course of kyphosis Very few pts- increase to > 30 º seen mostly in Children in growing age. Dorsal spine lesions Involvement of 3 or more vertebral bodies. Can be prevented by Rest/immobilization Braces Necessary surgery Patient Compliance to treatmentPowerPoint Presentation: The future angle (Y) of Kyphotic deformity in TB spine could be reasonably predicted by using formula. Y= a+bx ( Rajshekaran and Shanmugasundaram formula ) x=initial loss of vertebral body a=5.5 (constant) b=30.5 (constant) Course of kyphosisOnly Decompression: Only Decompression Preop Postop KOCH D7-D8Decompression & anterior interbody fusion: Preop Postop Decompression & anterior interbody fusion KOCH D9-D10Decompression & global fusion: Decompression & global fusion Preop Postop KOCH D8-D9Trans-pedicular decompression & global fusion : Trans- pedicular decompression & global fusion Preop Postop KOCH D10-D11MULTIDRUG RESISTANT TUBERCULOSIS: MULTIDRUG RESISTANT TUBERCULOSIS Suspect MDR in patients with No clinical improvement / worsening despite 3 months of treatment No clinical improvement and patient is getting incorrect regimen / inadequate doses History of irregular drug intakeMULTIDRUG RESISTANT TUBERCULOSIS: MULTIDRUG RESISTANT TUBERCULOSIS Suspect MDR TB and send specimen for AFB culture. Suspect MDR in patients with Known contact with an MDR case HIV infection, alcoholics, drug addicts Appearance of new lesions while on R XMULTIDRUG RESISTANT TUBERCULOSIS: MULTIDRUG RESISTANT TUBERCULOSIS Primary Resistance “In a patient who has never received anti -TB drugs before”. infection with primary drug resistant organisms infection from a patient with acquired resistance Secondary resistance “In this, the organism is initially sensitive & resistance arises during course of treatment”. due to non-adherence incorrect regimen inadequate dosageMULTIDRUG RESISTANT TUBERCULOSIS: MULTIDRUG RESISTANT TUBERCULOSIS Multi-drug resistance (MDR): Resistance to both INH and RMP Monoresistance: Resistance to any 1 of first-line TB drugs Poly-drug Resistance: Resistance to 2 or more first-line anti-TB drugs other than to both INH and RMP Extensively drug resistant TB (XDR): MDR with resistance to 3 or more of second line drugsDrug resistance in India:: Drug resistance in India: INH 16% in previously untreated pts 46% in previously treated pts RMP: Recent data: 23 - 34% Increase from 2.8% in 1980 to 31% in 1984 amongst hospitalized patients 95% of these were also INH resistant. Prevalence of MDR TB in newly diagnosed pts is 3.4%Management of MDR-TB: Management of MDR-TB CONSULT PULMONOLOGIST Start on at least 3 new anti-TB drugs (drugs never taken before, one of these should be injectable & wait for culture report). The first line drugs thought to be sensitive should be continued. Do not limit the regimen to 3 agents. If resistant to other first line drugs in addition to H and R, regimens with 4 to 6 drugs have better results.MANAGEMENT OF MDR-TB: MANAGEMENT OF MDR-TB Hospital-based treatment or home DOT. No Intermittent treatment. Once the results are available, the drugs that pt is resistant to should be withdrawn and the patient continued on the final regimen of at least 5 sensitive drugs .MANAGEMENT OF MDR-TB: MANAGEMENT OF MDR-TB Drugs should be continued for at least 18-24 months. Monitor closely for bacteriological and clinical response and adverse reactions . (with help of Pulmonologist) Adverse reactions occur more frequently with regimens used for MDR-TBSecond-line drugs: Second-line drugs Inj Kanamycin, Capreomycin, Viomycin, Amikacin – 15 mg/kg Quinolones : Ofloxacin - 600-800 mg Ciprofloxacin - 1000-1500 mg Levofloxacin - 500-1000 m Gati/Moxi - 400 mg Ethionamide / Prothionamide – 15 mg/kg Cycloserine - 15 mg/kgSecond-line drugs: Second-line drugs PAS – 200-300 mg/kg (10-12 gm/day) Clofazimine - 100-300 mg/day Thiacetazone – 150 mg/day Linezolid - 600 mg / day Others – Co-amoxy-clav, ClarithromycinEXAMPLES: EXAMPLES Resistance to H and R: KM + PZA + ETH + Levofloxacin + Ethionamide / PAS Resistance to H, R, PZA: KM + ETH + Levofloxacin + Ethionamide + PASEXAMPLES: EXAMPLES Resistance to H, R, PZA, ETB, SM: KM + Levofloxacin + Ethionamide + PAS + Cycloserine Resistance to SM, H, E, R, Ethionamide , PAS, KM, Ofloxacin : Capreomycin + PZA + Cycloserine + Levofloxacin + Clofazimine + LinizolidTAKE HOME MESSAGE: TAKE HOME MESSAGE Tuberculosis of dorsal spine is not uncommon . Children and adults present differently. Cord compression is rather rare in children. Conservative treatment preferred in children while operative treatment preferred in adults.TAKE HOME MESSAGE: TAKE HOME MESSAGE 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 Posterior decompression for anterior cord compression is not only useless but also hazardous. You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.