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Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
Infections of spine
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Infections of spine

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  • 1. POTT’S POTT’S SPINE
  • 2. VERTEBRAL ANATOMY
  • 3.  Centre portion of each intervertebral disc is filled with gel like elastic substance(NUCLEUS PULPOSUS) which along with sturdy elastic collagen fibres(ANNULUS FIBROSUS)transmits stress from vertebra to vertebra  Annulus fibrosus enhances rotational stability of spine and helps to resist compressive forces
  • 4. EMBRYOLOGY OF VERTEBRAL COLUMN  Formed from sclerotome portions of somites(derived from paraxial mesoderm)  Each sclerotome-loosely arranged cells cranially & densely packed cells caudally.  Some of the densely packed cells move cranially opposite the centre of myotome INTERVERTEBRAL DISC
  • 5.  Remainin densely packed cells fuse with loosely arranged cells of immediately caudal sclerotome MESENCHYMAL CENTRUM(primordium of body of vertebra)  Nerves lie in close relation to IVD and intersegmental arteries lie on each side of vertebral bodies.  Notochord persists and enlarges only in the region of IVD…..contributes to formn of NUCLEUS PULPOSUS which later gets surrounded by circular fibres of ANNULUS FIBROSUS
  • 6.  NP+AF INTERVERTEBRAL DISC  Resegmentation of sclerotomes into definitive vertebrae causes myotomes to bridge the IVD…gives them the capacity to move the spine F O R M S
  • 7.  Spinous and transverse processes develop from chondrification centres(which appear at 6th week of embryonic life) in vertebral arch.  Ossification in vertebral arches-8th week  At birth-each vertebra has 3 bony parts connected by cartilageBony halves fuse during 1st 3-5yrs  Five secondary ossificn centres appear in vertebrae after pubrty  All secondary centres unite with rest of vertebrae- 25yrs
  • 8. POTT’S POTT’S SPINE Dr SREEDEVI PK
  • 9. TUBERCULOSIS OF SPINE  Vertebral TB-M.C form of skeletal TB(50% of all cases of TB of bones&joints)  M.C-1st 3 decades  Equal in both sexes  Any one/several vertebrae  M.C-Lowr thoracic & lumbar spine
  • 10. Infectious exudate may spread anteriorly beneath anterior longitudinal ligament~>neighbouring vertebrae Advances&destroys epiphyseal cortex,intervertebral disc&adj vertebrae Infection begins in cancellous area of vertebral body(Central/anterior/epiphyseal in location)
  • 11.  Note:infection of posterior bony arch and tyransverse process is unusual  Granulation tissue develops posteriorly-encircles & compresses spinal cord & nerve roots(more likely in thoracic spine ‘cause of small calibre of spinal canal here)
  • 12. Posterior element involvt of C2(axial CT image showing reactive sclerosis)
  • 13. COURSE……  ANTERIORLY…………… Exudate forms&netrates periosteum,accumulating beneath anterior longit.ligament(ALL) Penetrates the ligament Abscess Migrates in various directions. Abscess tracks along lines of least resistance(along fascial planes,blood vessels & nerves
  • 14. CERVICAL……… Collects behind prevertebral fascia Spreads laterally to sterno mastoid (a point at postr edge)) Protrudes fwd..bulge into pharynx May gravitate to mediastinum Trachea,esophagus ,pleural cavity
  • 15. THORACIC Remains locally confined as a bulbous mass for a long time Back-pressre against spinal cord PARAPLEGIA
  • 16.  Exudate may spread laterally to extrapleural space- induces NON SPECIFIC PLEURAL EFFUSION  If exudate penetrates ALL,  occupies mediastinum OR  gravitates through diaphragm to the LUMBAR ASPECT  Rarely,thoracic cold abscess may track backward b/w transverse processes&follow intercostal nerve-erupts on chest wall.
  • 17. LUMBAR….. A • Tuberculous exudate enters PSOAS SHEATH • Appears below inguinal ligament on medial aspect of thigh B • May spread laterally beneath iliac fascia • Emerges at iliac crest at the anterior superior iliac spine C • Follows great vessels….may erupt alongside femoral vessels in triangle of Scarpa or in gluteal region • Or forms an abscess abpve iliac crest posteriorly
  • 18. REGIONAL DISTRIBUTION….  DORSAL-42%  LUMBAR-26%  DORSOLUMBAR-12%  CERVICAL-12%  CERVICODORSAL-5%  LUMBOSACRAL-3%
  • 19. Route of spread  TB of spine is always secondary.  Bacteria reach spine via hematogenous route from lungs or lymph nodes.
  • 20. TYPES OF VERTEBRAL TB 1) PARADISCAL – COMMONEST TYPE. BETWEEN THE TWO CONTIGUOUS AREAS OF TWO ADJACENT VERTEBRAE. 2) CENTRAL- BODY OF SINGLE VERTEBRA IS AFFETED.
  • 21. 3) ANTERIOR- INFECTION IS LOCALISED TO THE ANTERIOR PORTION OF THE VERTEBRAE. 4)POSTERIOR-POSTERIOR COMPLEX i.e PEDICLE,LAMIINA,SPINOUS OR TRANSVERSE PROCESS ARE INVOLVED. 5)APPENDICEAL-RARE, INVOLVES TRANSVERSE PROCESS.
  • 22. COLD ABSCESS  Collection of pus and tubercular debris from diseased vertebrae.  Can travel in any direction.
  • 23.  Spread beneath the anterior longitudinal ligament- pre vertebral abscess.  Spread posteriorly and cause pressure over the spinal cord.  Spread through the sides of the vertebra – para vertebral abscess. Sometimes penetrates the anterior longitudinal ligament – lines of least resistance i.e. fascial planes,vessels,nerves
  • 24. CLINICAL PICTURE ACTIVE STAGE  Constitutional symptoms antedate local spinal involvement……anorexia,nausea,weakness,weight loss,night sweats,afternoon or evenin rise of temp  Frequently iniated by an exanthem or trauma.  Spine- -Stiff and painful on movt. - Pain is localised to site of involvement/referred dependin on specific nerve root irritation - Localised KYPHOTIC deformity. (Tender to percussion)
  • 25.  Vertebral muscle spasm+  Night cries…..movt b/w inflamed surfaces.  Cold abscess maybe +  Pressure effects-dysphagia(mediastinal) Dyspnoea Hoarseness(retropharyngeal) Restricted hip extensn(Psoas abscess)
  • 26. GIBBUS DEFORMITY IN TB
  • 27.  If any suspicion of TB spine……….. Palpate spinous processes by sliding finger from cervical spine to sacrum…….so that even a small knuckle kyphosis (step/prominence) is not missed…………..thus making the diagnosis before gross vertebral destruction has occurred.  Stiffness,weakness&awkwardness of lower extremities herald onset of PARAPLEGIA.
  • 28. CHARACTERISTICS OF SPECIFIC SPINAL INVOLVEMENT  CERVICAL  Pain over cervical vertbrae/referred to occiput/upper extremities  Pain aggravated by pressure on top of head  Neck rigidity  Deformity-normal lordosis is reduced & head is supported in hands  Paralysis of arms before legs  Occasionally death due to dislocation
  • 29.  LOW CERVICAL & UPPER THORACIC  Pain along brachial plexus or intercostal nerves  Marked rigidity with angular kyphosis  Abscess- retropharyngeal,supraclavicular,mediastinal.  Cord symptoms L.C  Arms affected first  Horners syndrome  Neck rigidity-head&neck turn as one
  • 30.  THORACIC&THORACOLUMBAR  Pain referred to lower extremities(esp lateral aspect of thighs)  Girdle pain  Marked angular kyphosis  Iliac or psoas abscess
  • 31.  LUMBOSACRAL  Referred pain to lower extremities  Deformity slight  Psoas abscess  Flexion of hips
  • 32.  ABSCESSES & SINUSES…..  Cervical&dorsal-Can present away from vertebral column:- Paraspinal regions,posterior/anterior cervical triangles,along brachial pkexus in axilla,along intercostal spaces on chest wall.  Dorsolumbar&lumbar-Abscess freq tracks down psoas sheath……palpable in iliac fossa,lumbar triangle,upper part of thigh below inguinal ligmt,knee
  • 33. Psoas abscess-Pseudo-hip flexion deformity(No limitation of internal & external rotation of hip jt when tested in position of flexion deformity) - Can present as a lump in iliac foss - HEALED STAGE - -Not ill - -Regains lost weight - -No evening rise of temp - -No spinal pain/tenderness - -ESR falls
  • 34. -Radiological E/O bone healing in serial Xrays -But deformity persists Bony ankylosis of L3-L4 resulting in kyphosis in an old case of TB spondylitis
  • 35. INVESTIGATIONS………  BLOOD-Hb-anemia TC –lymphocytosis ESR raised S.proteins-Hypoproteinemia Mantoux-helpful in children<2-3yrs….not diagnostic though
  • 36. X-RAY APPEARANCES  Depending on site of lesion TB spine……….. 1) PARADISCAL-M.C 2) CENTRAL 3) ANTERIOR 4) APPENDICEAL
  • 37.  Earliest radiological finding-narrowing of disc space  Loss of definition of paradiscal margins  Bones look rarefied and osteopenic(40% Ca loss- radiolucent signs)  Observed before osseous destructive changes  Trabecular destruction-atleast 3-5 months from beginning of infectious process
  • 38.  Late changes-Anterior wedge compression in anterior vertebral involvement  Central vertebral body collapse(CONCERTINA COLLAPSE) in central involvement.  Destruction of posterior elements in posterior affection.  Soft tissue swelling&calcificn-highly predictive of TB  Healing stages-vertebral body&posterior elements dense(sclerosis)
  • 39. Collapsed vertebral body L1-L3
  • 40.  Cervical-b/w vertebral bodies&pharynx(retropharyngeal)-birdnest shadow  Upper thoracic-V-shapd/bulbous/heart shaped shadow&widened mediastinum  Low thoracic&thoracolumbar-fusiform shadow occupy site of psoas shadow . Increased density and lessening of size of shadow indicates calcification and healing
  • 41. Axial CT-vertebral body destruction,paravertebral abscess ext into spinal canal
  • 42. MODERN IMAGING TECHNIQUES  CT SCAN • Assessmt of destructive lesions of vertebral column • Paravertebral soft tissue swellings • Degree of neural compromise • Specially useful in- 1) posterior spinal disease 2)CraNiovertebral&cervicodorsal TB 3)Sacroiliac joint TB • Suspected areas of disease should be localized before taking CT
  • 43.  ISOTOPE BONE SCAN-Localises diseased area by demonstratin a hot spot even when lesions<5mm  Note:atleaqst 30-40% calcium must be removed from a particlr area for radiolucent changes to become visible
  • 44. Anterior wedging and erosion of T9
  • 45. Axial CT image showing vertebral body destruction&adj soft tissue mass
  • 46.  MRI • Diagnosis of TB in rare sites incl posterior elements,vertebral appendages&sacroiliac jt • Excellent modality to judge health of spinal cord…detects cord compression.  ULTRASOUND ECHOGRAPHS To diagnose presence & size of tuberculous abscess in lumbar vertebral disease.
  • 47.  GALLIUM SCAN-For disseminated TB  BIOPSY-By percutaneous technique with CT guidance………biopsy mateial subjected to culture BIOPSY & CULTURE-MOST DEFINITIVE DIAGNOSTIC TEST
  • 48.  Radiological & MRI e/o healing lags behind biological healing processes in spinal TB.  X-rays,MRI-Upto 5months of starting multidrugtherapy may actually show deterioration in most pts.  If images don’t show improvement whwn repeated>6 months after onset of Rx….consider alternate diagnosis/therapeutically refractory disease.  Rarely-healing accomp by fat replacemt of healed area
  • 49. COMPLICATIONS 1) PARAPLEGIA 2) COLD ABSCESS 3) SINUSES 4) SECONDARY INFECTION 5) FATALITY
  • 50. DIFFERENTIAL DIAGNOSIS  Pyogenic infections  Typhoid spine  Brucella spondylitis  Mycotic spondylituis  Syphilitic infection  Tumorous conditions  Primary malignant tumors  Multiple myeloma
  • 51.  Lymphomas  Secondary neoplastic deposits  HistiocytosisX  Local developmental abnormalities of spine  Spinal osteochondrosis  Traumatic conditions  Osteoporotic conditions  Spondylolisthesis
  • 52. MANAGEMENT  AIMS OF Rx  Halt progression of destruction and deformity  Prevent and overcome paraplegia. Treatment should be prolonged ….and a cautious attitude maintained for many years…as recrudescence of disease can occur even years later!!
  • 53. GENERAL SUPPORTIVE CHEMOTHERAPY SURGERY
  • 54. CHEMOTHERAPY  Isoniazid(INH)-most effective anti-TB drug  INH-5mg/kg/day……300mg usually(adults) 10-15mg/kg/day……………...children.  S/E-peripheral neuropathy,anemia,hepatitis  Pyridoxine 50mg to be supplemented daily MONITOR LFT
  • 55.  Ethambutol-25mg/kg/day X 60days 15mg/kg single dose thereafter. S/E-Visual disturbances……avoid in children PERIODIC OPHTHALMIC CHECK UPS
  • 56.  Streptomycin  Adults 0.75-1g/day X 60days 1g/day 2-3times weekly thereafter Children 15-25mg/kg/day  INTRAMUSCULAR S/E-Ototoxicity,nephrotoxicity AVOID IN RENAL INSUFFICIENCY
  • 57.  RIFAMPICIN  Adult-600mg  Children-10mg/kg/day  Oral single daily dose given ½ hr before breakfast  Relatively mild toxic effects  Colors urine&othr body fluids bright orange
  • 58.  ***COMBINATION CHEMOTHERAPY***  Delays emergence of drug resistant strains of bacilli.  Rx regimen- HRE X 6MONTH…. If at the end of 6months,clinical & radiological response satisfactory, IE X 12-18MONTHS
  • 59.  Failure to respond to first line drugs……(due to bacterial resistance/allergic intolerance/toxic effects)…..use SECOND LINE DRUGS  Cycloserine,Ethionamide,Kanamycin,Amikacin,Thiocetazo ne  Failure to respond despite adq chemotherapy with radiological e/o progression of disease or neurological involvement emerges. SURGICAL INTERVENTION 
  • 60. SURGICAL TREATMENT  INDICATIONS 1) Failure to respond to ATT 2) Radiological e/o progression(enlargmt of paraspinal abscess shadow) 3) Imminent vertebral collapse 4) Instability of spine 5) Progressive neurological deficit
  • 61.  SURGICAL OBJECTIVES 1) Excise infected tissue as completely as possible 2) Decompress intraspinal neural elements 3) Reduce spinal deformity 4) Provide stability by spinal fusion
  • 62.  PRINCIPLES 1) Removal of all diseased tissue by thorough debridement 2) Correction of deformity 3) Interbody bone grafting & stabilization. 4) Relief of pressure on intraspinal contents.
  • 63. WHAT IS DONE??????  Major focus of disease is removed  Spinal deformity reduced  Intraspinal neural elements decompressed  Bone defect obliterated  Spinal stability provided by autogenous bone grafts
  • 64.  PREOPERATIVELY, an ATT regimen is maintained(atleast 3months)…….  Severe destruction-external skeletal fixation with a HALO-PELVIC DEVICE.  Following removal of diseased focus,distraction aids in overcoming kyphosis.  Later…bone grafting
  • 65. OPERATIVE AAPROACHES  Lesions of C4-C6-lateral approach or anterior approach  Lesions of C7-T4-posterior thoracoplasty approach by removing third rib on left side  Lesions below T40Spine is approached from left Aorta –landmark Incision- Along a rib that’s 2ribs higher than the rib that arises at apex of kyphosis.
  • 66. Surgical procedures  Lateral rhachotomy  Costotrasversectomy  Albee procedure-aims to unite the spinous processes by a single cortical graft(s/c aspect of tibia)….fixed by sewing muscles over it.  Hibbs procedure-only local bone is used  Combined procedure  Circumduction fusion
  • 67. POTT’S PARAPLEGIA
  • 68. POTT’S PARAPLEGIA Pott’s paraplegia can be due to – - inflammatory causes- oedema,abscess - mechanical causes-tubercular debris - intrinsic causes-pathological dislocation - spinal tumour d/s- extradural granuloma Most commonly occurs in TB of dorsal spine because spinal canal is narrowest in this part
  • 69. Seddon’s Classification:  GROUP A_-Early onset - This comes up in active stage of the disease within first 2 years. Compressive Agents are inflammatory edema, granulation, abscess, casseous material, sequestra and rarely ischaemic lesion. GROUP B -Late onset- Usually after 2 years of onset of the disease.  due to recurrence or by mechanical pressure. This can be better divided into paraplegia with active disease and with healed disease. Active disease - Caseous material, debris, sequestrated disc or bone, internal gibbus, stenosis and deformity can cause compression. Healed disease - Usually internal gibbus and acute kyphotic deformity can also give late onset paraplegia. Usually there is a continuous traction, compression leading to paraplegia.
  • 70. Kumar’s classification of tuberculous paraplegia stage Clinical features 1 Negligible Unaware of neural deficit, Upgoing Plantar / Ankle clonus 2 Mild Walk with support 3 Moderate Nonambulatory, Paralysis in extention,sensory loss <50% 4 Severe 3+ paralysis in flexion/sensory loss>50%/ Sphinters involved
  • 71. CLINICAL FEATURES OF PARAPLEGIA- - clumsiness - twitching - increased reflexes - clonus - positive Babinski’s sign
  • 72.  In Pott’s paraplegia , motor functions are affected first.  The paralysis follows the following stages- muscle weakness, spasticity , incoordination, paraplegia in extension , flexor spasms,paraplegia in flexion and flaccid paraplegia lastly.
  • 73.  TREATMENT OF POTT’S PARAPLEGIA 1) ATT 2)SPINE PUT TO ABSOLUTE REST 3)PARALYSED LIMBS SHOULD BE TAKEN CARE OF. 4)REPEATED NEUROLOGICAL EXAMINATION TO CHECK FOR WORSENING.
  • 74. Surgical indications 1. No sign of Neurological recovery after trial of 3-4 weeks therapy 2. Neurological complication during treatment 3. Neuro deficit becoming worse 4. Recurrence of neuro complication 5. Prevertebral cervical abscesses,neurological signs& difficulty in deglutition& respiration 6. Advanced cases- Sphincter involvement, flaccid paralysis, Severe flexor spasms
  • 75. MIDDLE PATH REGIMEN Widely accepted regimen for tb spine  Admission,rest in bed or pop cast.  Chemotherapy  X-ray and ESR once in 3 months  Gradual mobilisation in the absence of neurological involvement.  Spinal braces-18 months to 2 years.
  • 76.  Abscesses are aspirated out drained.  Sinuses heal within 6-12 weeks  If no neurological complications develop and patient is responding to the 3-drug therapy , surgery is unnecessary.  Excisional surgery for posterior spinal disease.  Operational debridement for patients who do not show arrest of disease after 3-6 months of chemotheray.
  • 77. Thank you Thank you

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