grand round 08.09.11 dr. arif baradia ortho iii. pott’s disease this entity was first described by...

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Grand Round 08.09.11 Dr. Arif Baradia Ortho III

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Page 1: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Grand Round 080911

Dr Arif Baradia Ortho III

Pottrsquos disease

bull This entity was first described by Percivall Pott He noted this as a painful kyphotic deformity of the spine associated with paraplegia

bull 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

bull Three percent are suffering from skeletal TB

bull 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

Regional Distribution 1 Cervical 12

2 cervicodorsal 5

3 Dorsal 42

4 Dorsolumbar 12

5 Lumbar 26

6 Lumbosacral 3

Pathophysiology

bull Pott disease is usually secondary to an extraspinal source of infection

bull The basic lesion is a combination of osteomyelitis and arthritis

bull The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate

bull 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

bull 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

bull 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

bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes

bull 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

bull 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 ALL

bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion

bull 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

bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels

The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion

bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a

bull atypical form characterized by spondylitis without disk involvement (SPwD)

bull SPwD seems to be the most common pattern of spinal TB

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 ndashlongitudinal lig Aneurysmal phenomenon

5 Synovitis in post facet

History

bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits

abscesses or sinus tracts

bull The reported average duration of symptoms at the time of diagnosis is 3-4 months

bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to

presentation ndash Pain can be spinal or radicular

bull Constitutional symptoms include fever and weight loss

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 2: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Pottrsquos disease

bull This entity was first described by Percivall Pott He noted this as a painful kyphotic deformity of the spine associated with paraplegia

bull 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

bull Three percent are suffering from skeletal TB

bull 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

Regional Distribution 1 Cervical 12

2 cervicodorsal 5

3 Dorsal 42

4 Dorsolumbar 12

5 Lumbar 26

6 Lumbosacral 3

Pathophysiology

bull Pott disease is usually secondary to an extraspinal source of infection

bull The basic lesion is a combination of osteomyelitis and arthritis

bull The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate

bull 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

bull 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

bull 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

bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes

bull 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

bull 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 ALL

bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion

bull 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

bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels

The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion

bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a

bull atypical form characterized by spondylitis without disk involvement (SPwD)

bull SPwD seems to be the most common pattern of spinal TB

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 ndashlongitudinal lig Aneurysmal phenomenon

5 Synovitis in post facet

History

bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits

abscesses or sinus tracts

bull The reported average duration of symptoms at the time of diagnosis is 3-4 months

bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to

presentation ndash Pain can be spinal or radicular

bull Constitutional symptoms include fever and weight loss

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 3: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

bull Three percent are suffering from skeletal TB

bull 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

Regional Distribution 1 Cervical 12

2 cervicodorsal 5

3 Dorsal 42

4 Dorsolumbar 12

5 Lumbar 26

6 Lumbosacral 3

Pathophysiology

bull Pott disease is usually secondary to an extraspinal source of infection

bull The basic lesion is a combination of osteomyelitis and arthritis

bull The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate

bull 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

bull 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

bull 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

bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes

bull 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

bull 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 ALL

bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion

bull 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

bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels

The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion

bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a

bull atypical form characterized by spondylitis without disk involvement (SPwD)

bull SPwD seems to be the most common pattern of spinal TB

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 ndashlongitudinal lig Aneurysmal phenomenon

5 Synovitis in post facet

History

bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits

abscesses or sinus tracts

bull The reported average duration of symptoms at the time of diagnosis is 3-4 months

bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to

presentation ndash Pain can be spinal or radicular

bull Constitutional symptoms include fever and weight loss

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 4: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Regional Distribution 1 Cervical 12

2 cervicodorsal 5

3 Dorsal 42

4 Dorsolumbar 12

5 Lumbar 26

6 Lumbosacral 3

Pathophysiology

bull Pott disease is usually secondary to an extraspinal source of infection

bull The basic lesion is a combination of osteomyelitis and arthritis

bull The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate

bull 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

bull 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

bull 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

bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes

bull 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

bull 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 ALL

bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion

bull 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

bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels

The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion

bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a

bull atypical form characterized by spondylitis without disk involvement (SPwD)

bull SPwD seems to be the most common pattern of spinal TB

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 ndashlongitudinal lig Aneurysmal phenomenon

5 Synovitis in post facet

History

bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits

abscesses or sinus tracts

bull The reported average duration of symptoms at the time of diagnosis is 3-4 months

bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to

presentation ndash Pain can be spinal or radicular

bull Constitutional symptoms include fever and weight loss

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 5: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Pathophysiology

bull Pott disease is usually secondary to an extraspinal source of infection

bull The basic lesion is a combination of osteomyelitis and arthritis

bull The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate

bull 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

bull 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

bull 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

bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes

bull 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

bull 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 ALL

bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion

bull 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

bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels

The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion

bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a

bull atypical form characterized by spondylitis without disk involvement (SPwD)

bull SPwD seems to be the most common pattern of spinal TB

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 ndashlongitudinal lig Aneurysmal phenomenon

5 Synovitis in post facet

History

bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits

abscesses or sinus tracts

bull The reported average duration of symptoms at the time of diagnosis is 3-4 months

bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to

presentation ndash Pain can be spinal or radicular

bull Constitutional symptoms include fever and weight loss

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 6: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

bull 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

bull 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

bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes

bull 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

bull 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 ALL

bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion

bull 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

bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels

The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion

bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a

bull atypical form characterized by spondylitis without disk involvement (SPwD)

bull SPwD seems to be the most common pattern of spinal TB

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 ndashlongitudinal lig Aneurysmal phenomenon

5 Synovitis in post facet

History

bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits

abscesses or sinus tracts

bull The reported average duration of symptoms at the time of diagnosis is 3-4 months

bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to

presentation ndash Pain can be spinal or radicular

bull Constitutional symptoms include fever and weight loss

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 7: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

bull 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 ALL

bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion

bull 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

bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels

The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion

bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a

bull atypical form characterized by spondylitis without disk involvement (SPwD)

bull SPwD seems to be the most common pattern of spinal TB

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 ndashlongitudinal lig Aneurysmal phenomenon

5 Synovitis in post facet

History

bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits

abscesses or sinus tracts

bull The reported average duration of symptoms at the time of diagnosis is 3-4 months

bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to

presentation ndash Pain can be spinal or radicular

bull Constitutional symptoms include fever and weight loss

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 8: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion

bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a

bull atypical form characterized by spondylitis without disk involvement (SPwD)

bull SPwD seems to be the most common pattern of spinal TB

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 ndashlongitudinal lig Aneurysmal phenomenon

5 Synovitis in post facet

History

bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits

abscesses or sinus tracts

bull The reported average duration of symptoms at the time of diagnosis is 3-4 months

bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to

presentation ndash Pain can be spinal or radicular

bull Constitutional symptoms include fever and weight loss

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 9: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a

bull atypical form characterized by spondylitis without disk involvement (SPwD)

bull SPwD seems to be the most common pattern of spinal TB

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 ndashlongitudinal lig Aneurysmal phenomenon

5 Synovitis in post facet

History

bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits

abscesses or sinus tracts

bull The reported average duration of symptoms at the time of diagnosis is 3-4 months

bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to

presentation ndash Pain can be spinal or radicular

bull Constitutional symptoms include fever and weight loss

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 10: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

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 ndashlongitudinal lig Aneurysmal phenomenon

5 Synovitis in post facet

History

bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits

abscesses or sinus tracts

bull The reported average duration of symptoms at the time of diagnosis is 3-4 months

bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to

presentation ndash Pain can be spinal or radicular

bull Constitutional symptoms include fever and weight loss

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 11: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

History

bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits

abscesses or sinus tracts

bull The reported average duration of symptoms at the time of diagnosis is 3-4 months

bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to

presentation ndash Pain can be spinal or radicular

bull Constitutional symptoms include fever and weight loss

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 12: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

bull 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

bull 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

bull 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

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 13: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Natural course of disease

bull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic

bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy

paradiscal margins amp reappearance and minrralization of tuberculae

bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block

formation

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 14: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Lab Studies

bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive

bull Erythrocyte sedimentation rate (ESR) may be markedly elevated

bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent

bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 15: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

bull IFN- Release Assays (IGRAs)bull 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

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 16: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 17: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

X Ray appearances

bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess

formation bull Bone lesions may occur at more than one level

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 18: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

X Ray appearances

Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding

osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from

neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle

appears and shows the progress on follow up bull Skipped lesion (10 cases) can be diagnosed on

suspicion and in correct size film

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 19: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 20: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 21: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Clinico-radiological Classification

stage features Usual duration

I Pre-destructive

Straightening spasm hyperemia in scinti

lt3 mo

II Early-destructive

Diminished space paradiscal erosion Knuckle lt10

2-4 mo

III Mild kyphos 2-3 verte k10-30 3-9 mo

IV Moderate kyphos

gt3 verte K30-60 6-24 mo

V Severe kyphos

gt3 verte Kgt60 gt2 years

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 22: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

CT scanning

bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference

bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas

bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses

bull In contrast to pyogenic disease calcification is common in tuberculous lesions

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 23: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

MRI

bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine

bull 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

bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis

bull most effective for demonstrating neural compression

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 24: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after

decompression 1 Block present second decompression2 Block not present intrinsic damage

1Ischemic infarction 2Interstitial gliosis

3atrophy 4 tuberculous myelitis

5Myelomalacia

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 25: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 26: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Complications of tuberculosis

1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 27: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Tb spine with PARAPLEGIA

bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than

sensorybull Sense of position amp vibration last to disappear

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 28: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+

abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not

involvedrsquoExtradural grnulation --

contract cicatrization peridural fibrosis paraplegia

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 29: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

5 Infarction of spinal cord - Ant spinal artery

EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-

MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 30: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Seddonrsquos Classificationbull

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 ndash 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

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 31: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896

)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp

Alexander1947

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 32: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

BASIC PRINCIPLES OFMANAGEMENT

10487291048729

bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 33: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

bull 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

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 34: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp

sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4

timesbull Spinal brace--- 18 months-2 years

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 35: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -

surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest

after 3-6 months- spinal arthrodesis (recommended)

bull Post op--Spinal brace--- 18 months-2 years

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 36: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Drugs in middle path

phase duration drug

Intensive 5-6 months

INH 300-400mg

Rifampicin ofloxacin400-600mg streptomycin

Continuation

7-8 months

-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin

Prophylactic

4-5 months

-do Ethambutol 1200mg

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 37: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Surgical indications1 No sign of Neurological recovery after trial of 3-4

weeks therapy2 Neurological complication during treatment3 Neuro deficit becoming worse4 Recurrence of neuro complication5 Prevertebral cervical abscessesneurological

signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement

flaccid paralysisSevere flexor spasms

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 38: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post

elements of vertbbull Spinal tumor syndrome resulting in cord

compressionbull Rapid onset paraplegia due to thrombosistrauma

etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 39: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

1 Decompression +- fusion

Failed responseToo advanced

2 Debridement+- fusion

Failed response after 3-6 monthsDoubtful diagnosisInstability

3 Debridement +-DECOMP+- fusion

Recrudescence of disease

4 Debridement+- fusion

Prevent severe Kyphosis

5 Anterior transpostion

Severe Kyphosis +neural deficit

6 Laminectomy secondary stenosis posterior disease

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 40: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

APPROACH1 Cervical spine ndash Anterior retropharyngeal

(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial

border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash

1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash

L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 41: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

DYNAMIC CAGE GovenderampPrabhoo

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER
Page 42: Grand Round 08.09.11 Dr. Arif Baradia Ortho III. Pott’s disease This entity was first described by Percivall Pott. He noted this as a painful kyphotic

SYNTHES PLATE WITHSPACER

  • Grand Round 080911
  • Pottrsquos disease
  • Slide 3
  • Regional Distribution
  • Pathophysiology
  • Slide 6
  • Slide 7
  • Slide 8
  • Slide 9
  • Anatomically the lesion could be
  • History
  • Slide 12
  • Slide 13
  • Natural course of disease
  • Lab Studies
  • Slide 16
  • Slide 17
  • X Ray appearances
  • X Ray appearances (2)
  • Slide 20
  • X-ray of the thoracolumbar spine (Lateral view) showing wedge c
  • X-ray of the spine in a child showing complete destruction of T
  • Clinico-radiological Classification
  • CT scanning
  • MRI
  • Slide 26
  • Myelography
  • Slide 28
  • Differentials
  • Complications of tuberculosis
  • Tb spine with PARAPLEGIA
  • Patho of Tuberculoses Paraplegia
  • Slide 33
  • Seddonrsquos Classification
  • Evolution of treatment
  • BASIC PRINCIPLES OF MANAGEMENT 10487291048729
  • Slide 37
  • What is Middle path regime
  • Slide 39
  • Drugs in middle path
  • Slide 42
  • Surgical indications
  • Other indications
  • Slide 45
  • APPROACH
  • DYNAMIC CAGE GovenderampPrabhoo
  • SYNTHES PLATE WITH SPACER