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Infection of bone & joint Route of infection: 1- direct through break in the skin, pin prick, stab wound, open # or operation. 2- indirect via the blood.

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Presentation on theme: "Infection of bone & joint Route of infection: 1- direct through break in the skin, pin prick, stab wound, open # or operation. 2- indirect via the blood."— Presentation transcript:

1 Infection of bone & joint Route of infection: 1- direct through break in the skin, pin prick, stab wound, open # or operation. 2- indirect via the blood from distant site as the nose, mouth, respiratory tract or genetourinary tract. Acute haematogenous osteomyelitis: A disease of children. Adult are affected only when immunity is suppressed by debility malnutrition, disease as diabetes or immune deficiency. The causative organisms: The usual organism is staphaureus, less often are other Gr +ve organism. Under 4 years of age H influenzae is fair common. Unusual organisms & opportunistic organisms are more likely to be found in immune deficiency. Patients with sickle cell disease are prone to infection with salmonella. Site of infection: 1- Usually the metaphysis because of the peculiar arrangement of the blood vessels. The non anastomosing terminal branches of the nutrient artery twist back in hair pin loops before entering the large network of sinusoidal veins result in vascular stasis which favor bacterial colonization.

2 2- in young infants there is still free anastomosis between epiphyseal & metaphyseal blood vessels so infection can as easily lodge in the epiphysis. 3- in adult infection more common in the vertebrae than in the long bones. Pathology: 1- inflammation: characterized by acute inflammatory reaction with vascular congestion, exudation of fluid & infiltration by polymorphonuclear leukocyte this will cause increase intra osseous pressure & intense pain, obstruction to blood flow & intra vascular thrombosis so that tissue threatened by impending ischemia 2- suppuration: by the end of 2 nd or 3 rd day pus form within the bone & force it ’ s way along the Volkmann canals to the surface where it produce subperiosteal abscess, in infant infection extend through the physis to the epiphysis & then to the joint. Vertebral infection may spread through the end plate & the intervertebral disc into the adjacent vertebral body. 3- necrosis: causes; 1) increase intra osseous pressure. 2) vascular stasis. 3) infective thrombosis. 4) periosteal stripping. 5) bacterial toxin. 6) leukocyte enzymes. With gradual ingrowth of granulation tissue. The boundary between dead & living bone become defined, pieces of dead bone separate as sequestra. 4- new bone formation: by the end of 2 nd weak new bone form from the deep layers of stripped periosteum with time this new bone thicken to form involucrum enclosing the infected tissue & sequestra. Perforations “ cloacae ” may form in the involucrum though which pus & sequestra discharge & track through the tissue by sinus to the surface of the skin.

3 5- Resolution: if infection is controlled & the intra osseous pressure released at an early stage the progression of OM. Can be aborted, in some cases remodeling may restore the normal contour, in other though healing is sound the bone is left permanently deformed. Clinical picture: Child presents with sever pain, malaise, fever, in neglected cases toxemia. & the child refuse to use his limb, pulse rate > 100 & temperature is raised. Tenderness near one of the big joints & lymph adenopathy common but not specific Diagnosis: 1- plain x-ray normal at 1 st 10 days except for displacement of fat plains which could be also caused by haematoma or soft tissue infection. At the end of the 2 nd weak there is extra cortical fain outline indicate periosteal new bone formation. Later there is periosteal thickening & patchy rarefaction of metaphysis. Later still, there is ragged feature of bone destruction. 2- U/S: detect subperiosteal fluid collection in the early stage of OM. 3- radioscentigraphy: 99mTc-HDP reveal increase activity at both perfusion & bone phase, it is highly sensitive in the very early stage but of low specificity. 3- radioscentigraphy: 99mTc-HDP reveal increase activity at both perfusion & bone phase, it is highly sensitive in the very early stage but of low specificity. 4- MRI.: extremely sensitive even in the early phase of bone infection show reduce signal intensity in T1 weighted image. 4- MRI.: extremely sensitive even in the early phase of bone infection show reduce signal intensity in T1 weighted image. Other investigations: CBP. Aspirate of pus & send for C/S, CRP. Blood culture. Other investigations: CBP. Aspirate of pus & send for C/S, CRP. Blood culture.

4 Deferential diagnosis: 1- cellulitis: there is wide spread superficial redness & lymphangitis. 1- cellulitis: there is wide spread superficial redness & lymphangitis. 2- streptococcal necrotizing myositis: caused by group A, beta haemolytic streptococci cause acute myositis although rare should be kept in mind because it may rapidly go out of control toward muscle necrosis, septicaemia & death. 2- streptococcal necrotizing myositis: caused by group A, beta haemolytic streptococci cause acute myositis although rare should be kept in mind because it may rapidly go out of control toward muscle necrosis, septicaemia & death. 3- acute supurative arthritis: progressive rise in CRP. value over 24-48 hour is suggestive of septic arthritis. 3- acute supurative arthritis: progressive rise in CRP. value over 24-48 hour is suggestive of septic arthritis. 4- acute rheumatism: pain less sever & flit from one joint to another. 4- acute rheumatism: pain less sever & flit from one joint to another. 5- sickle cell crises: some times indistinguishable from Ac. OM. 5- sickle cell crises: some times indistinguishable from Ac. OM. 6- Gaucher ’ s disease: pseudo arthritis may closely resemble OM. 6- Gaucher ’ s disease: pseudo arthritis may closely resemble OM. Treatment: Treatment: 1- General supportive measures: analgesic given for pain & i.v fluid given to treat dehydration caused by fever. 1- General supportive measures: analgesic given for pain & i.v fluid given to treat dehydration caused by fever. 2- splinting: for comfort & to prevent joint contracture. 3- AB. Blood & aspirated material sent for examination & C/S. mean while initial choice depend on finding from direct examination of pus smear & best guess of the most likely pathogen until the organism is identified & it ’ s AB. sensitivity is known. 4- drainage: if AB. given early drainage is unnecessary but if improvement dose not occur after 36 hours & there are features of deep pus “ swelling, oedema, fluctuation “ & if pus aspirated abscess should be drained by operation. 2- splinting: for comfort & to prevent joint contracture. 3- AB. Blood & aspirated material sent for examination & C/S. mean while initial choice depend on finding from direct examination of pus smear & best guess of the most likely pathogen until the organism is identified & it ’ s AB. sensitivity is known. 4- drainage: if AB. given early drainage is unnecessary but if improvement dose not occur after 36 hours & there are features of deep pus “ swelling, oedema, fluctuation “ & if pus aspirated abscess should be drained by operation.

5 Chronic OM.: Either follow Ac. OM. but more frequently follow open fracture or operation. The usual organism is staph aureus, E. coli S. pyogenes, proteus & pseudomonas, but in the presence of foreign implant staph epidermidis which is normally non pathogenic is the commonest of all. Pathology: Bone destroyed at the focus of infection, cavities containing pus & pieces of dead bone “ sequestra ” are surrounded by vascular tissue & beyond that by areas of sclerosis the result of chronic reactive new bone formation, the sequestra act as substrate for bacterial adhesion in the same way as foreign implant. Clinical feature: Patient presented with; pain, pyrexia, redness & tenderness have recurred or with discharging sinus. In post traumatic OM. the bone may be deformed or non united.

6 Imaging: 1- x-ray: show bone resorption either as patchy or Franck excavation with thickening & sclerosis of the surrounding bone, sequestra show up as unnaturally dense fragment in contrast to the surrounding vascularised bone. 2- radioisotope: sensitive but not specific Tc-HDP show increase activity in both perfusion & bone phase. 3- CT & MRI: together will show the extent of bone destruction & reactive edema, hidden abscess & sequestra. Treatment::Tr. 1- AB. bactericidal drugs are important to stop the spread of infection to healthy bone & to control acute flair. 2- local Tr. For sinus need dressing, colostomy paste can be used to stop excoriation of skin. 3- operation: indicated when there are significant symptoms combined with clear evidence of sequestrum under AB. cover all infected soft tissue & dead bone must be excised, double lumen tube laid down in the resulting cavity & tissues are closed then AB. solution instilled 4 hourly & cleared shortly before the next instillation until the effluent is sterile, usually 3-6 Wk. Acute suppurative arthritis: Infection reach the joint 1- by direct invasion 2- penetrating wound 3- direct spread from adjacent bone abscess 4- by blood spread from distant site.

7 Pathology: Haematogenous infection settle in the synovial membrane cause acute inflammatory reaction with serous or seropurulent exudate& increase in synovial fluid. As pus appear in the joint articular cartilage is eroded & destroyed partly by bacterial enzyme & partly by enzyme released from synoveum, inflammatory cell & pus. If infection goes untreated it will spread to the underlying bone or burst out of the joint to form abscess & sinuses. With healing there may be 1- complete resolution & a return to normal. 2- partial loss of articular cartilage & fibrosis of the joint. 3- loss of articular cartilage & bony ankylosis. 4- bone destruction & permanent deformity of the joint. Clinical feature: Infant present with feature of septicemia, failure to thrive, fever, increase pulse & baby is irritable. In children & adult present with rapid pulse, fever, joint swelling, reluctance to move the limb, local warmth & marked tenderness Ix. x-ray early normal but U/S show joint effusion, increase joint space because of fluid in the joint, late sign is narrowing or irregularity of joint space. Tr.: The 1 st priority is to aspirate the joint & examine the fluid 1- general supportive care: analgesia for pain & iv. Fluid for dehydration. 2- splinting: the joint must be rested on splint or widely spilt plaster, for hip should be held abducted & 30 degree flexed on traction to prevent dislocation. 3- AB. Initially given on judgment of the most likely pathogen until substituted after full bacteriological Ix.

8 4- drainage: under anesthesia the joint opened through small incision drained & washed with physiological Saline. catheter left in place & suction irrigation done for another 2-3 days. Complication: 1- bone destruction & at the hip joint dislocation are serious threat. 2- cartilage destruction may lead to either fibrous or bony ankylosis 3- growth disturbance present either as localized deformity or as shortening of the bone Tuberculosis: The skeletal manifestation of the disease are seen chiefly in the large joint & the spine but the infection may appear in any bone. Pathology: Mycobacterium tuberculosis enter the body via the lung “ droplet infection “ or via the gut “ swallowing infected milk product “ or rarely through the skin the initial lesion in lung, pharynx or gut is a small one with lymphatic spread to regional LN. this combination is the primary complex. This initial infection has 2 sequels; 1) bacilli may survive many years within the LN. which are apparently healed or even calcified. 2) the body has been sensitized to the toxin “ +ve Heaf test ” & if reinfection occur the response is quite different. If resistance to the original infection is low wide spread dissemination via blood stream may occur giving rise to miliary TB. Some of these foci develop into destructive lesion to which the term tertiary may be applied.

9 Of these foci bone & joint are affected in about 5% of patient with TB. There is predilection to vertebral body & large joints. Once the bacilli gain a foot hold they elicit chronic inflammatory reaction characterized by a collection of epithelloid cell with multi nucleated giant cell surrounding an area of central necrosis with round cell at the periphery this lesion called TB. granuloma. Bone lesion tend to spread quite rapidly, epiphyseal cartilage is no barrier to invasion & soon the infection reach the joint. If the synovium is involved it become thick & edematous giving rise to marked effusion, pannus of granulation tissue may extend across the joint & articular cartilage slowly destroyed. If unchecked caseation & infection extended into the surrounding soft tissue to produce cold abscess this may burst through the skin produce sinus or track along tissue planes to point at distant site. If disease is arrested at an early stage healing may be by resolution to apparent normality, if articular cartilage has been damaged, healing is by fibrosis & incomplete ankylosis with progressive joint deformity. Clinical feature: There may be a history of previous infection or recent contact with TB. Patient usually child or young adult complain of pain & joint swelling, in advance cases there may be attack of fever or lassitude & loss of weight, muscle wasting is characteristic & synovial thickening is marked. Movements are limited in all directions. TB. of spine may deceptively cause slight pain, occasionally patient present with feature of weakness or loss of sensibility in the lower limbs.

10 X-ray: show soft tissue swelling & periarticular osteo porosis, the bone end take on washed out appearance & the articular space is narrowed, in children the epiphysis may be enlarged probably the result of long continued hyperemia. In the spine there is bone erosion & collapse. Ix.: ESR. increased, relative lymphocytosis, Mantou test +ve., synovial fluid aspirate appear cloudy, the protein concentration increase & WBC. increase, acid fast bacilli identified in synovial fluid in 10- 20% & culture +ve. in 50%. Culture from synovium +ve. in 80% Tr.: 1- rest ; with modern chemotherapy this no longer mandatory, rest & splintage varied according to the individual patient. 2- chemotherapy : a recommended regimen is refampcin, INH. & ethambutol “ or pyrazinamide ” for 8 Wks. & there after refampcin & INH. for 6-12 months. Syreptomycin & ethambutol are toxic & should not be used for long term. 3- operation: 1) cold abscess may need immediate drainage. 2) if the joint is painful & articular cartilage surface is destroyed; arthrodesis or replacement arethroplasty may be considered. 3- operation: 1) cold abscess may need immediate drainage. 2) if the joint is painful & articular cartilage surface is destroyed; arthrodesis or replacement arethroplasty may be considered.


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