V.C - L - Gross Pathologies of the Vertebral Column - Spinal Tuberculosis, Scheurmann's disease, Ankylosing Spndylitis Flashcards
When was spinal tubercolosis first discovered? What is it also known as? What was the relationship between for the discovery of spinal TB?
Spinal TB - aka as Pott’s disease after being discovered by Sir Percival Pott - was discovered in 1779 He first discovered the relationship between tubercolosis spondylitis, kyphosis and paraplegia
What bacteria is spinal tuberculosis caused by?
Spinal tubercolosis (STB) is the extrapulmonary manifestation of tuberculosis caused by mycobacterium tuberculosis - initially asymptomatic
What percentage of cases of tuberculosis does STB account for?
STB accounts for 2% of all tubercolosis cases 15% of tuberculosis cases are extrapulmonary TB
What types of inflammation is spinal TB said to be a combination of?
A combination of osteomyeltitis and arthritis involving multiple vertebrae
What is the most commonly affected area of the spine by spinal tuberculosis? (try and rank the vertebral column in order of prevalence) What age groups is spinal TB more common in?
The lower thoracic spine is the most common area of involvement * Thoracic spine - 65% * Lumbar - 20% * Cervical - 10% * Thoracolumbar - 5% Spinal TB is more common in children and young adults
What is the estimated increase in risk of developing spinal TB in patients with HIV?
Estimated 20-37 times greater risk of developing spinal TB in patients with HIV
TB is estimated to affect 1.7 billion worldwide Despite this number, what percentage of the population contain the latent bacterium?
90-95% of the population contain the latent bacterium for tuberculosis - a debilitated immune system eg HIV, makes the occurrence of TB more likely
What is the transmission of tuberculosis?
TB is spread through aerosol (airborne) transmission into the lungs
Usually, any pathogen is stopped by the mucus membrane surrounding the airway. TB avoids this mucus lining. What cells then engulf the TB?
TB is engulfed by alveolar macrophages due to TB expressing foreign proteins on their surface and it is therefore phagocytosed
What does the TB release which is necessary for to inhibit phagolysosomal formation? What does this allow for?
TB releases SapM (secreted acid phosphatase of M.Tubercolosis) and PknG (protein kinase G) which inhibits phagolysosomal formation which would normally break down the foreign bacteria and this allows MTB to survive and proliferate forming a localised infection
What symptoms occur once a localised infection forms?
Once a localised infection forms, mainly asystemic and flu like symptoms appear
What happens to the localised infection after 3 weeks? talk up until a ghon focus is formed
After 3 weeks, cell mediated immunity initiates immune cell coverage of the mycobacterium with lymphocytes which forms a granuloma to prevent spread The tissue within the immune cells then dies via aprocess called caseous necrosis (caseation) and now a ghon focus is formed
TB can spread to nearby lymph nodes via immune cells from the Ghon focus or from direct extensions, resulting in the same process occurring. When the the immune cells from the ghon focus cause spread of the TB, what is this now known as? Where does it usually occur?
The Ghon focus + spreading immune cells to nearby lymph nodes is known as a Ghon complex and it usually forms in the subpleural area. Ghon’s complex is a lesion seen in the lung that is caused by tuberculosis. The lesions consist of a calcified focus of infection and an associated lymph node.
What is the evolution of the ghon complex known as?
The ghon complex often undergoes fibrosis followed by calcification leading to what is known as a Ranke complex - which will form scars in the lung
At this point in certain cases, where the ranke complex is formed, the immune system rids of the tb infection. However, in other cases, the tb remains latent in the “immune cell capsule”. With a compromised immune system, the reactivation can cause spread into the upper part of the lungs where it is believed that oxygenation is greater. What will now happen when the TB moves to the upper part of the lung?
With fibrous necrosis this time, cavities will form in the lung allowing the bacteria to disseminate, either through airways, haemategnously or lymphatically - leading to systemic military TB
DESCRIBE THE PATHOGENESIS OF SYSTEMIC MILITARY TB?
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What is the common spread of TB from the lungs to the vertebral column and how?
Haematogenous spread of MBTB commonly occurs through Batson’s venous plexus - valveless network connecting the deep pelvic veins and the thoracic veins to the internal vertebral venous plexuses However, lymphatic drainage to the para-aortic lymph nodes or arterial routes through arterial arcade, in the subchondral region of each vertebra can occur.
Where does STB initially affect?
STB initially affects anterior structures of the vertebral column - anterior longitudinal ligament and the antero-inferior part of the vertebral body
How does STB first appear in the vertebral column?
STB first appears antero-inferiorly then spreads to the centre of the vertebral body or disc It usually affects the (lower) thoracic region of the vertebral column
What is the clinical presentation of STB?
* Weight loss * Local pain with stiff movement, swelling & effusion * Fever * Fatige * Night sweats * Paraparesis * Gibbus * Cold abscesses are present
What can the reduction in body weight lead to? What is a cold abscess?
- Reduction in body weight can lead to muscle wasting A cold abscess refers to an absence that lacks intense inflammation usually associated with infection - found in deep tissue of the infection site
Antero-inferior destruction reduces the intervertebral disk space and adjacent vertebral bodies, leading to collapse of the spinal elements. What does the anterior wedging of the vertebrae form?
The anterior wedging of the vertebrae can form a gibbus (localised kyphotic deformity >20 degrees saggital index) which has a characteristic angulation
What does the inadequate size of the IV disc due to the antero-inferior destruction of the body/disc?
This can result in an increased risk of compression fractures due to the absence of the disc
How is suspected STB diagnosed? (state how the two tests are carried out)
Mantoux test - tuberculin injection into the skin intradermally - previous exposure to TB allows the immune system to create a small localised reaction around 48-72 hours after creating a large induration and redness Interferon gamma (Ifn-y) release assay (IGRA) - usues blood samples to identify the bacterium - more specific to MBTB than other types of mycobacterium (mycobacterium bovis and leprae)
Visual identification would include either Xray, MRI or CT When is each used?
Xray - mainly performed initially to patients with suspected TB - bone mineral density must be >70% for any lesions to be visible MRI - predominant test used in diagnosis - helps identify numerous presentations CT - more effective in identifying the shape and calcification of soft tissue abscesses
What is looked for in an MRI and CT in someone with STB? (mnemonic - SADDER)
- Sclerosis - mainly visible using a CT
- Abscess - refers to cold abscesses or calcifications
- Disc space reduction - usually visible using a CT
- Destruction of the vertebral body
- Erosion of the vertebral body or osteoporosis
- Rarefaction - reduction of bone density (also reduction of nervous tissue)
The treatment plan of STB depends on the presence of neurological complications If no neurological complications, what is the treatment?
If no neurological complications, a course of Anti-TB drugs consisting of rifampicin, isioniazid, pyraziname, ethambutol for 2 months, and then rifampicin and isioniazid for 6-18 months Different sites agree on 2 months of initial cocktail and then vary depending on how long for the final two drugs - between 6 and 12 months is most common
If there are neurological complications, what is the treatment?
4 options * Posterior decompression and fusion with bone autografts * Anterior debridement/decompression and fusion with autografts * Anterior debridement/decompression and fusion, followed by simultaneous or sequential posterior fusion with instrumentation * Posterior fusion with instrumentation, followed by simultaneous or sequential anterior debridement/decompression and fusion
What is the most common of the 4 methods of treating STB with neurological complications? * Posterior decompression and fusion with bone autografts * Anterior debridement/decompression and fusion with autografts * Anterior debridement/decompression and fusion, followed by simultaneous or sequential posterior fusion with instrumentation * Posterior fusion with instrumentation, followed by simultaneous or sequential anterior debridement/decompression and fusion
Anterior debridement/decompression and fusion with autografts
A classification system was introduced in 2008 to allow choosing the option for treating STB to become easier What was this classifciation system?
Gulhane Askeri Tip Akademisi (GATA) classification
This classification was introduced in 2008 as a practical guide for STB treatment based on clinical and radiological criteria; What is the clinicial and radiological criteria via which it is based on? What is the classification system known as again?
Kyphosis Saggital index Instability Neurological problems Abscess formation Disc degeneration Vertebral collapse Gulhane Askeri Tip Akademisi - GATA classification
* Which vertebral level is more commonly associated with STB? * What do the SapM and PknG proteins released by MBTB inhibit? * MBTB spread to the vertebral column is mainly hematogenous. - True or false * Where is vertebral destruction commonly first identified?
* Which vertebral level is more commonly associated with STB? - THORACIC REGION * What do the SapM and PknG proteins released by MBTB inhibit? - PAHGOLYSOSOMAL FORMATION * MBTB spread to the vertebral column is mainly hematogenous. - True or false = TRUE via Batson’s * Where is vertebral destruction commonly first identified? - ANTERO-INFERIOR VERTEBRAL BODY