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Pott Disease

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Pott Disease

  1. 1. Pott’s sPine Moderator: Dr peeyush sharma Presenter: Dr Pramod mahender
  2. 2. Pott’s disease • This entity was first described by Percivall Pott. He noted this as a painful kyphotic deformity of the spine associated with paraplegia. • Tuberculosis of the spine is one of the oldest diseases afflicting humans. Evidences of spinal tuberculosis have been found in Egyptian mummies dating back to 3400 BC
  3. 3. • One fifth of TB population is in India. • Three percent are suffering from skeletal TB, • 50% of these suffer from spinal lesion and almost 50% are from pediatric group. An estimated 2 million or more patients have active spinal tuberculosis. • Every day 1000 die of tuberculosis in India.
  4. 4. Regional Distribution 1 Cervical 12% 2 cervicodorsal 5% 3 Dorsal 42% 4 Dorsolumbar 12% 5 Lumbar 26% 6 Lumbosacral 3%
  5. 5. Pathophysiology • Pott disease is usually secondary to an extraspinal source of infection. • The basic lesion is a combination of osteomyelitis and arthritis. • The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate. • Tuberculosis may spread from that area to adjacent intervertebral disks. In adults, disk disease is secondary to the spread of infection from the vertebral body. In children, because the disk is vascularized, it can be a primary site.
  6. 6. • Progressive bone destruction leads to vertebral collapse and kyphosis. The spinal canal can be narrowed by abscesses, granulation tissue, or direct dural invasion. This leads to spinal cord compression and neurologic deficits. • Kyphotic deformity occurs as a consequence of collapse in the anterior spine. Lesions in the thoracic spine have a greater tendency for kyphosis than those in the lumbar spine. • The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes. • Healing takes place by gradual fibrosis and calcification of the granulmatous tuberculous tissue. Eventually the fibrous tissue is ossified, with resulting bony ankylosis of the collapsed vertebrae.
  7. 7. • Paravertebral abscess formation occurs in almost every case. With collapse of the vertebral body, tuberculous granulation tissue, caseous matter, and necrotic bone and bone marrow are extruded through the bony cortex and accumulate beneath the anterior longitudinal ligament. • These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion. • In the lumbar region the abscess gravitates along the psoas fascial sheath and usually points into the groin just below the inguinal ligament. • In the thoracic region, the longitudinal ligaments limit the abscess, which is seen in the radiogram as a fusiform radiopaque shadow at or just below the level of the involved vertebra. • Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels.
  8. 8. The lesion could be: • Florid - invasive and destructive lesion. • Non destructive - lesion suspected clinically but identifiable by modern investigations like CT scan or M.R.I. • Encysted disease • Carries sicca • Hypertrophied • Periosteal lesion.
  9. 9. • Recently, two distinct patterns of spinal TB can be identified, the classic form, called spondylodiscitis (SPD) a • atypical form characterized by spondylitis without disk involvement (SPwD). • SPwD seems to be the most common pattern of spinal TB.
  10. 10. Anatomically the lesion could be 1. Paradiscal - destruction of adjacent end plates and diminution of disc space. 2. Appendeceal (Posterior) - involvement of pedicles, laminae, spinous process. 3. Central - Cystic or lytic, concertina collapse. 4. Anterior –longitudinal lig, Aneurysmal phenomenon 5. Synovitis in post facet
  11. 11. History • Presentation depends on the following: – Stage of disease – Site – Presence of complications such as neurologic deficits, abscesses, or sinus tracts • The reported average duration of symptoms at the time of diagnosis is 3-4 months. • Back pain is the earliest and most common symptom. – Patients have usually had back pain for weeks prior to presentation. – Pain can be spinal or radicular. • Constitutional symptoms include fever and weight loss.
  12. 12. • Neurologic abnormalities occur in 50% of cases and can include spinal cord compression with paraplegia, paresis, impaired sensation, nerve root pain, or cauda equina syndrome. • Cervical spine tuberculosis is a less common presentation is characterized by pain and stiffness. Patients with lower cervical spine disease can present with dysphagia or stridor. Symptoms can also include torticollis, hoarseness, and neurologic deficits. • The clinical presentation of spinal tuberculosis in patients infected with the human immunodeficiency virus (HIV) is similar to that of patients who are HIV negative; however, the relative proportion of individuals who are HIV positive seems to be higher.
  13. 13. Natural course of disease • 53% died within 10 yrs of onset • Early stage of healing– focus surrounded by sclerotic bone Ivory vertebra • Early radiological sign of healing– sharpening of fuzzy paradiscal margins & reappearance and minrralization of tuberculae • Several vertebrae destroyed– fibrous tissue • Disc space destroyed bony ankylosis/bone block formation
  14. 14. Lab Studies • Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95% of patients who are non–HIV-positive. • Erythrocyte sedimentation rate (ESR) may be markedly elevated . • The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent • The polymerase chain reaction • A brucella complement fixation test
  15. 15. • IFN- Release Assays (IGRAs) • Recently, two in vitro assays that measure T cell release of IFN- in response to stimulation with the highly tuberculosis- specific antigens ESAT-6 and CFP-10 have become commercially available.
  16. 16. • Microbiology studies to confirm diagnosis: Obtain bone tissue or abscess samples to stain for acid-fast bacilli (AFB), and isolate organisms for culture and susceptibility. CT-guided procedures can be used to guide percutaneous sampling of affected bone or soft tissue structures. These study findings may be positive in only about 50% of the cases.
  17. 17. X Ray appearances • Lytic destruction of anterior portion of vertebral body • Increased anterior wedging • Collapse of vertebral body • Reactive sclerosis on a progressive lytic process • Enlarged psoas shadow with or without calcification • Vertebral end plates are osteoporotic. • Intervertebral disks may be shrunk or destroyed. • Vertebral bodies show variable degrees of destruction. • Fusiform paravertebral shadows suggest abscess formation. • Bone lesions may occur at more than one level.
  18. 18. X Ray appearances Discovertebral lesions, detected in 93% of patients, • Localized fluffy osseous destruction with surrounding osteoporosis is the earliest signs. • concentric collapse and may look like A.V.N. • Local lytic lesion may cause problem of diagnosis from neoplasic lesion. • destruction of adjacent vertebrae, Konstram (K) angle appears and shows the progress on follow up. • Skipped lesion (10% cases) can be diagnosed on suspicion and in correct size film.
  19. 19. X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies.
  20. 20. X-ray of the spine in a child showing complete destruction of D12 and L1 vertebral bodies leaving only the pedicles.
  21. 21. Kumar’s clinico-radiological Classification stage features Usual duration I Pre- Straightening, spasm, <3 mo destructive hyperemia in scinti II Early- Diminished space 2-4 mo destructive paradiscal erosion Knuckle <10 III Mild kyphos 2-3 verte k:10-30 3-9 mo IV Moderate >3 verte K:30-60 6-24 mo kyphos V Severe kyphos >3 verte K:>60 >2 years
  22. 22. CT scanning • CT scanning provides much better bony detail of irregular lytic lesions, sclerosis, disk collapse, and disruption of bone circumference. • Low-contrast resolution provides a better assessment of soft tissue, particularly in epidural and paraspinal areas. • It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses. • In contrast to pyogenic disease, calcification is common in tuberculous lesions.
  23. 23. MRI • MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine • MRI findings useful to differentiate tuberculous spondylitis from pyogenic spondylitis include thin and smooth enhancement of the abscess wall and well-defined paraspinal abnormal signal, whereas thick and irregular enhancement of abscess wall and ill-defined paraspinal abnormal signal are suggestive of pyogenic spondylitis. • contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis. • most effective for demonstrating neural compression.
  24. 24. Myelography • Spinal tumor syndrome • Multiple vertebral lesions • Patients not recovered after decompression 4. Block present : second decompression 5. Block not present : intrinsic damage 1.Ischemic infarction 2.Interstitial gliosis 3.atrophy 4. tuberculous myelitis 5.Myelomalacia
  25. 25. Differentials 1. Pyogenic infections 2. Typhoid spine 3. Brucella Spondylitis 4. Mycotic Spondylitis 5. Syphilitic 6. Tumorous condition 7. Primary malignant tumor 8. Multiple Myeloma 9. Lymphomas 10.Secondary 11.Histocytosis-X 12.Spinal Osteochondrosis 13.Spondylolisthesis 14.Hydatid disease
  26. 26. Complications of tuberculosis 1. Paraplegia 2. Cold abscess 3. Sinuses 4. Secondary infection 5. Amyloid disease 6. Fatality
  27. 27. Tb spine with PARAPLEGIA • INCIDENCE 10-30% • Dorsal spine (MC) • Motor functions affected before /greater than sensory • Sense of position & vibration last to disappear
  28. 28. Patho of Tuberculoses Paraplegia 1. Inflammatory Edema –vascular stasis,toxin 2. Extradural Mass – Tuberculous ostetis+ abscess 3. Bony Disorder – Sequestra, Internal Gibbus 4. Meningeal changes – ‘dura as rule not involved’ Extradural grnulation -- contract, cicatrization peridural fibrosis  paraplegia
  29. 29. 5. Infarction of spinal cord - Ant spinal artery Endarteritis,Periarteritis,Thrombosis 6. Changes in Spinal cord- Myelomalacic,Syringomyelic change,Atrophy –upto 50%dec in dia-good functions
  30. 30. 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.
  31. 31. Kumar’s classification of tuberculous paraplegia stage Clinical features 1 Negligible Unaware of neural deficit, Plantar extensor/ 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
  32. 32. Evolution of treatment Pre-antitubercular era • Artificial abscess- Pott in 1779 • Laminectomy & laminotomy : chipault(1896 ) • Costo-transversectomy: Menard in 1896 • Posterior mediastinotomy • Calves operation 1917 • Lateral rhachiotomy of carpener 1933 • Anterlateral decompression of Dott& Alexander:1947
  33. 33. BASIC PRINCIPLES OF MANAGEMENT • Early diagnosis • Expeditious medical treatment • Aggressive surgical approach • Prevent deformity • Expect good outcome
  34. 34. • Studies performed by the British Medical Research Council indicate that tuberculous spondylitis of the thoracolumbar spine should be treated with combination chemotherapy for 6-9 months. According to a 1994 recommendation by the US Centers for Disease Control and Prevention, this is the treatment of choice.
  35. 35. What is Middle path regime? • Admission rest in bed • Chemotherapy • X-ray & ESR once in 3 months • MRI/ CT at 6 months interval for 2 years • Craniovertebral ,cervicodorsal, lumbosacral& sacroiliac joints • Gradual mobilization • 3-9 weeks- back extention exercise 5-10 min 3-4 times • Spinal brace--- 18 months-2 years
  36. 36. • Abcesses – aspirate near surface • Instille 1gm Streptomycin +/- INH in sol • Sinus heals 6-12 weeks • Neural complications if responds 3-4 weeks :- surgery unnecssary • Excisional surgery for posterior spinal disease • Operative debridement for patients –if no arrest after 3-6 months- spinal arthrodesis (recommended) • Post op--Spinal brace--- 18 months-2 years
  37. 37. Drugs in middle path phase duration drug Intensive 5-6 INH Rifampicin months 300- ofloxacin400-600mg / 400mg streptomycin Continua 7-8 -do 3-4mth Pyrazinamide tion months 1500mg 4-5mth Rifampicin Prophyla 4-5 -do Ethambutol 1200mg ctic months
  38. 38. 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
  39. 39. Other indications • Recurrent paraplegia • Painful paraplegia– d/t root compression,etc • Posterior spinal disease--involving the post elements of vertb • Spinal tumor syndrome resulting in cord compression • Rapid onset paraplegia due to thrombosis,trauma etc • Severe paraplegia • Secondary to cervical disease and • cauda equina paralysis
  40. 40. 1 Decompression Failed response,Too advanced +/- fusion 2 Debridement+/- Failed response after 3-6 fusion months,Doubtful diagnosis,Instability 3 Debridement +/- Recrudescence of disease DECOMP+/- fusion 4 Debridement+/- Prevent severe Kyphosis fusion 5 Anterior Severe Kyphosis +neural deficit transpostion 6 Laminectomy STS,secondary stenosis, posterior disease
  41. 41. APPROACH 1. Cervical spine – Anterior retropharyngeal (smith-Robinson’s) Anterior approach – Anterior/Medial border of sternocleidomastoid 2. Dorsal spine (D1 to L1) – 1 Transthoraccic transpleural 2 Anterolateral decompression(D2 – L1) 3. Lumbar spine – Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant. approach
  42. 42. Tuli’s recommended approch • Cervical spine –T1  Anterior approch • Dorsal spine –DL junction  Antrolateral approch • Lumbar spine &Lumboscral junction  Extraperitoneal Transverse Vertebrotomy
  43. 43. Surgical technique • Costotransversectomy– in tense paravertebral abscess remove– transverse process rib – 2 inchs
  44. 44. Anterolateral decompression • Posterior part of rib • Transverse process • Pedicle • Part of the vertebral body • Griffith Seddon Roaf -- prone position • Tuli --- right lateral position • Advantage:- 1 avoid venous congestion 2 avoid excessive bleeding 3 permits freer respiration 4 better look at site
  45. 45. Posterior Spinal Arthrodesis • By– Albee & Hibbs • Albee– tibial graft inserted longitudinally in to the split spinous vertebral process • Hibbs– overlapping numerous small osseous flap from contiguous laminae spinous process & articular facets • Indications– 1 mechanical instability 2 to stabilise craniovertebral region 3 as part of panvertebral operation
  46. 46. DYNAMIC CAGE :Govender&Prabhoo
  48. 48. Yilmaz C, Selek HY, et al. Anterior instrumentation for the Treatment of Spinal Tuberculosis. J Bone and Joint Surg 1999; 81-A : 1261-67 • “we feel that every attempt should be made to minimize this deformity with some form of instrumentation wherever indicated, and preferably anteriorly.’”
  49. 49. Th ank you Th a nk you