Tuberculosis By Saad Hmemat

We will talk about… Epidemiology… Pathology… Clinical features… X-ray… Investigations… Diagnosis… Treatment…

Epidemiology Decline in its prevalence in developed countries due to effectiveness of public health programmes, improvement of nutritional status & advanced chemotherapy. Extra-pulmonary TB has risen again in the last 20 years due to increase in proportion of elderly people & spread of IV drug abuse.

Skeletal manifestations of the disease chiefly seen in spine & large joints, but also may appear in any bone or any synovial or bursal sheath. Predisposing conditions include: Debilitating disorders like AIDs & other disorders result in reduced defence mechanism. Diabetes Drug abuse Prolonged corticosteroid use as medication

Pathology Mycobacterium tuberculosis enters human via lung (droplet infection) or gut (swallowing infected milk products) or rarely through skin, that will cause granulomatous reaction which is associated with tissue necrosis & caseation. Initial lesion in lung, pharynx or gut is a small one with lymphatic spread to regional lymph nodes, a combination called primary complex. This bacilli usually fixed in nodes with no clinical illness results but occasionally the response is excessive with enlargement of glands in neck or abdomen, even though there is no clinical illness.

Initial infection has two important sequels: Bacilli within nodes which are apparently healed may survive for many years so that a reservoir exists. Body has been sensitised to the toxin and reinfection should occur, the response is quite different & the lesion being a destructive one which spread by contiguity Note: a positive heaf test being index of sensitisation (which is a diagnostic skin test performed to determine whether or not someone exposed to TB infection).

If resistance to original infection is low, widespread dissemination via blood stream months or years later during period of lowered immunity & bacilli deposited in extra pulmonary tissues giving rise to miliary TB or multiple TB lesion, Secondary spread. When foci develop into destructive lesions tertiary term applied. Bones or joints affected in about 5% of patient with TB with predilection for the vertebral bodies & large synovial joints. Multiple lesions occur in about one third of patient.

It’s difficult to tell whether infection started in joint and then spread to adjacent bone or vice versa.. ex: synovial membrane & subchondral bone have common blood supply and infected simultaneously. Once bacilli gain a foothold they elicit chronic inflammatory reaction, characterised histologically by tuberculous granuloma or tubercle which is a collection of epithelia & multi-nucleated giant cells surrounding area of necrosis with round cells mainly lymphocytes around periphery. Within affected area small patches of caseous necrosis appear, that may coalesce into larger yellowish mass or centre may break down to form an abscess containing pus & fragment of necrotic bone.

Bone lesion spread quite rapidly & epiphyseal plate is no barrier to invasion & soon infection will reach joint. Only in vertebral bodies & more rarely in greater trochanter of femur or metatarsal and metacarpal infection persist as a pure chronic osteomyelitis. If the synovium is involved it become thick & oedematous giving rise to a marked effusion. A pannus of granulation tissue may extend from synovial reflection across the joint, articular cartilage slowly destroyed. At the edges of the joint along the synovial reflection there maybe active bone erosion. In addition, increased vascularity causes local osteoporosis.

If unchecked, caseation & infection extend into surrounding soft tissue to produce abscess that may burst through skin forming sinus or TB ulcer or it may track along tissue planes to point at some distant site. If the disease arrested at an early stage healing maybe by resolution to apparent normality. If articular cartilage has been severely damaged, healing is by fibrosis & incomplete ankylosis with progressive joint deformity. Within the fibrocaseous mass mycobacterium remain imprisoned retaining potential to flare up into active disease many years later.

Clinical features The patient usually a child or young adult complains of pain & swelling in joint. In advanced cases there maybe attacks of fever, night sweats, lassitude (lack of energy) and loss of weight. The joint splinted (secured) by muscle spasm during waking hours, relaxes with sleep & the inflamed or damaged tissues are stretched or compressed causing sudden episodes of intense pain, term called Night cries.

Muscle wasting, tender, enlarged regional lymph nodes & movement are limited in all directions. As articular erosion progresses the joint becomes stiff & deformed. TB of spine. Patient may not be present until there is visible abscess usually in the groin or the lumbar region to one side of midline, or until collapse causes a localised kyphosis with slight pain. Occasionally the presenting feature is weakness or instability in the lower limb. In people with lowered resistance we may see multiple foci of infection with bone & joint lesions at different stages of development.

X-Ray Soft tissue swelling & peri-articular osteoporosis are characteristic. Bone ends take on a “washed out” appearance & the articular space is narrowed. In children the epiphyses maybe enlarged probably the result of long continued hyperaemia. Later on there is erosion of subarticular bone seen on both sides of the joint, indicating an inflammatory process starting in the synovium.

Cystic lesion may appear in the adjacent bone ends but there is no or little periosteal reaction. In the spine the characteristic appearance is one of bone erosion & collapse around a diminished intervertebral disc space, soft tissue shadows may define a paravertebral abscess

Investigations ESR usually increased & there may be a relative lymphocytosis. Mantoux (tuberculin sensitivity test) or heaf test will be positive (a sensitive but not specific tests). Cloudy, increased protein concentration, elevated white cell count & acid-fast bacilli are identified in 10-20% of cases in aspirated synovial fluid. Synovial biopsy for histological examination is more reliable, sections will show the characteristic histologic features & acid- fast bacilli maybe identified. Cultures are positive in about 80% of patient who have not received antimicrobial treatment.

Diagnosis Diagnosis is often delayed simply because the diseases is not suspected, except in areas where tuberculosis is common. Features that should trigger more active investigation are: Long history of pain & swelling Involvement of only one joint Marked synovial thickening Severe muscle wasting Enlarged regional lymph nodes Peri-articular osteoporosis on X-ray Positive Mantoux test (tuberculin sensitivity test)

Joint TB must be differentiated from the following: Transient synovitis, at first it seems no different from any other low-grade inflammatory arthritis & always settles down after a few weeks rest in bed. (common in children) Mono-articular rheumatoid arthritis, starts in a single large joint (indistinguishable from tuberculosis) & diagnosis have to wait the results of synovial biopsy. Subacute arthritis Hemorrhagic arthritis, the physical signs of blood in a joint may resemble tuberculous arthritis. Pyogenic arthritis

Treatment Rest Chemotherapy Operation

Long ago TB should be treated by rest through splintage of the joint and traction to overcome muscle spasm & prevent collapse of the articular surface. Those who are diagnosed & treated early are kept in bed only until pain and systemic symptoms subsides, thereafter are allowed restricted activity until joint changes resolve (usually 6 months to a year). Those with progressive joint destruction need longer period of rest & splintage to prevent ankylosis in bed position.

The most effective treatment is a combination of anti-tuberculous drugs that should always include rifampicin & isoniazid. During the last decade drug resistance has increased & this has led to addition of potentiating drugs.

Operative drainage or clearance of tuberculous focus is necessary nowadays. Once the condition is controlled & arthritis has completely subsided, normal activity can be resumed & the patient must report any renewed symptoms. If joint is painful & articular surface is destroyed, arthrodesis or replacement arthroplasty may be considered. It’s essential to give chemotherapy for 3 months before & after the operation.

If there is any question feel free to contact Alan Graham Apley but unfortunately he’s dead !!! Instead, you can ask our awesome doctor !

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