Bone & Joint Infections Final 2024 PPT PDF

BONE AND JOINT INFECTIONS Prof. NABIL ABDELMONEAM GHALY Professor of Orthopaedic Surgery Ain Shams University Cairo- Egypt  Definition “…suppurative process in bone caused by a pyogenic organism” Pelligrini, VD, et al, 1996 “…pr...

BONE AND JOINT INFECTIONS Prof. NABIL ABDELMONEAM GHALY Professor of Orthopaedic Surgery Ain Shams University Cairo- Egypt  Definition “…suppurative process in bone caused by a pyogenic organism” Pelligrini, VD, et al, 1996 “…presence of bacteria & an inflammatory response causing progressive destruction of bone.” Fears, RL, et al, 1998 BONE AND JOINT INFECTIONS HAEMATOGENOUS SPECIFIC( TB,…) NON-SPECIFIC EXOGENOUS OPEN FRACTURES POST- OPERATIVE IN BONES → OSTEOMYELITIS (OM) IN JOINTS → SYNOVITIS … ARTHRITIS  ACUTE HEMATOGENOUS OSTEOMYELITIS  ACUTE HEMATOGENOUS OSTEOMYELITIS Age group: Acute hematogenous osteomyelitis is almost a disease of children. When adults are affected it is usually because of defective immunity by debility, disease or drugs, e.g. Diabetes mellitus,AIDS,…. Trauma may determine the site of infection , possibly by causing a fluid collection or a small hematoma ACUTE HEMATOGENOUS OSTEOMYELITIS Causative organisms: 1)Staph aureus…. Most common 2)Strept pyogenes 3)Strept pneumonaie 4)Haemophilus influenzae(5-50% in children under 4 years) 5)Salmonella (common in patients with Sickle cell anaemia) 6)Others ; gram negative and anaerobic organisms)  ACUTE HEMATOGENOUS OSTEOMYELITIS Source and Route of infection: In children: Blood stream may be invaded from a minor skin abrasion, boil, a septic tooth or infected umbilical cord. In adults: Entry could be through an indwelling catheter, arterial line or contaminated syringe. Sites of infection: Usually in the metaphysis, due to its peculiar vascular pattern: the non- ananstmosing terminal branches of the nutrient artery twist back in hair –pin loops causing relative vascular stasis. IN CHILDREN mostly in proximal tibia or distal and proximal ends of femur. In adults, hematogemous infection is more common in vertebrae than in long bones. Pathology : ACUTE 1)Inflammation 2)Suppuration : Intra-osseous abscess Sub-periosteal abscess 3)Resolution(with ttt) or → CHRONIC  In Infants , infection spreads through the physis into the epiphysis and then to the joint. In older children the physis is a barrier to the direct spread except where the metaphysis is partially intracapsular (e.g. hip and shoulder) as pus may discharge through periosteum to the joint  CHRONIC 1)Bone necrosis → Sequestrum 2)New bone formation → Involucrum 3)Cavity,discharging sinus → Cloaca  Diagnosis C/O: - Sudden onset of fever, severe pain and malaise. - Parents may notice that the child refuses to use one limb - History of infection as septic toe, boil, sore throat or discharge from ear.  Diagnosis O/E : - The child looks ill. - Pulse over 100/minute. - Temperature is high. - Tenderness of affected area. - Restricted joint movement. - Slight flexion deformity of near joint due to muscle spasm. Diagnosis Laboratory: - leukocytosis with neutrophilia - ESR elevated - CRP positive - Blood culture may be positive The most certain way is to aspirate pus from the metaphyseal subperiosteal abscess or adjacent joint  Diagnosis Plain X-ray - Shows no abnormality of the bone before the second week - After 2 weeks,there may be a faint extra cortical line due to periosteal new bone formation. - An important late sign is a combination of regional osteoporosis with a localized segment of increased density.  Diagnosis U.S: - May detect subperiosteal collection MRI - Is extremely sensitive even in the early phases of bone infection RADIOACTIVE ISOTOPE SCAN - Sensitive even in the early phases of bone infection → Hot spot Differential diagnosis: 1)Cellulitis. 2) Acute suppurative arthritis. 3) Acute rheumatic arthritis. 4) Sickle cell crisis.  Treatment Once osteomyelitis is suspected, blood and fluid samples should be taken, then treatment is started immediately before confirmation of the diagnosis.  Treatment Patient should be admitted to hospital 1)Supportive treatment: Antipyretics –analgesics 2)Splintage : →Rest – prevent joint contracture 3)Antibiotics : Start with parentral (I.V.) treatment till CRP returns to normal values,then continue oral therapy for 3-6 weeks 4)Drainage : If clinically no improvement within 36 hours of starting treatment or even earlier if are signs of deep pus there Follow-up Once signs of inflammation subside, movements are encouraged. Full weight bearing is possible after 3-4 weeks.  Chronic osteomyelitis Used to be a dreaded sequel to acute hematogenous osteomyelitis, now adays more frequently follows an open fracture or operation. Causative organisms: 1)Staph aureus. 2)E coli. 3)Strept pyogenes. 4)Proteus. 5)Pseudomonas. 6)Strept epidermidis (esp. with implants) Pathology: Affected bone is destroyed or devitalized with cavities containing pus and pieces of dead bone (sequestrum), surrounded by vascular tissue, and beyond that by areas of sclerosis. Sequestra causing persistence of the infection until removed or discharged through draining sinuses. Sinuses may close spontaneously then reopen when tissue tension rises. Pathological fracture may develop. Chronic osteomyelitis New bone formation → Involucrum Bone necrosis → Sequestrum Cavity,disch- arging sinus →Cloaca Clinical picture: - Pain, pyrexia, redness and tenderness. - A discharging sinus. - In long standing cases, tissues are thickened and even folded in, where a scar or sinus is attached to the underlying bone. - Seropurulent discharge and excoriation of the surrounding skin. - Patient may present with pathological fracture. Imaging : X-ray shows bone resorption with thickening and sclerosis of the surrounding Involucrum bone. Sequestra seen as Sequestrum unnaturally dense fragments in contrast with the surrounding vascularized bone. Sometimes the bone is crudely thickened and misshapen resembling a bone tumour,involucrum. Imaging : CT and MRI are valuable in planning operative treatment, showing extent of bone destruction, reactive edema, hidden abscesses, and sequestra. Bone scan is sensitive but not specific. Investigations : ESR , CRP and WBC count are elevated in acute flares. Organisms cultured from the discharging sinuses should be tested repeatedly for antibiotic sensitivity..Treatment : Antibiotics :seldom eradicate infection alone, yet given to prevent local spread of the infection and to control acute flares(C&S to be done). Operative treatment: saucerization & sequestrectomy. External fixator may be appliied to avoid fracture In refractory cases it may possible to excise the infected segment and perform segment transfer using Ilizarov technique. JOINT INFECTION Septic Arthritis Aetiology: Organisms: S.aureus, streptococcus or E.coli in adults and H. influenza in infants. Route of infection: -haematogenous spread or -direct spread from penetrating wound, injection or after surgery or from adjacent osteomyelitis. P.F.: septic focus, trauma, R.A. and immuno- compromised patient.  Pathology of Septic Arthritis Synovitis; serous, then seropurulent, then purulent exudates. Progressive damage of articular cartilage. Joint subluxation and/or dislocation. Destruction of bony ends with reactive new bone formation later. Fibrous or bony ankylosis. Diagnosis Clinical picture ❑ Fever ❑ Painful passive mobilization ❑ Local signs of inflammation ✓ Swelling ✓ Redness ✓ Hotness ✓ Puffiness  Diagnosis Laboratory tests * C.B.C * E.S.R * C.R.P. * Blood culture * Aspiration : - presence of pus - gram stained film - culture and sensitivity  Diagnosis Diagnostic imaging -X-ray : - Widened joint space - Lost soft tissue planes - Distended capsule - Ultrasonography : - Effusion. - Edema - Femoral epiphysis ASPIRATION Treatment 1. Antibiotic therapy. 2. Surgical Drainage. 3. Immobilization Treatment Rest and immobilization Supportive treatment. Antibiotics for 4 weeks starting with I.V. antibiotics for 5-7 days. Surgical drainage must be done early to save the articular cartilage. Arthrodesis may be required to achieve fusion in the position of function.  Treatment Principles of antibiotic therapy 1. A specific bacteriologic diagnosis, using cultures from blood, bone, tissue or synovial fluid. 2. The narrowest spectrum drug specific to the infection. 3. Monitor the patient for secondary foci of infection. 4. Be aware of complications related to particular antibiotic e.g. renal or hepatic toxicity. 5. Convert from in hospital I. V. antibiotics to out- patient I.V. or oral administration when appropriate Treatment Drainage : * Early surgical drainage is the clue to a good outcome. * Repeated aspiration is improper. * Thorough washing of the joint. * Suction drain for 1-2 days. CHRONIC SPECIFIC INFECTIONS  Tuberculosis of The Hip Joint The hip joint is the most commonly affected joint by tubercle bacilli. Children are more frequently affected than young adults. Aetiology: Always secondary T.B. Organism: mycobacterium T.B. Predisposing factor: poor nutrition and health conditions, D.M., and immuno-compromise.  TUBERCULOSIS OF THE HIP JOINT Diagnosis: 1) General tuberculous toxemia 2) Gradual increasing pain, limping and stiffness of the hip. 3) All movements are limited. 4) Later on an abscess may be felt 5) Muscle wasting is noticeable.  TUBERCULOSIS OF THE HIP JOINT Treatment: a) General: Improve general nutritional state, proper house sanitation and antituberculous drugs for the proper time. b) Local: Aim of treatment: To get a mobile hip if possible To achieve sound bony ankylosis of hip Early cases (synovial type):- Bed rest, immobilization by traction and synovectomy Late cases (bone destruction):- Arthrodesis of the hip in the sound position POTT'S DISEASE OF THE THORACO-LUMBAR SPINE T.B. of the Spine (Pott’s Disease) Pathology: starts in the vertebral body. Vertebral body is destroyed and replaced by necrotic caseous material.  Early involvement of the disc and adjacent vertebra leading to kyphosis and cold abscess formation. Paraplegia may develop due to cord compression. Diagnosis Tuberculous toxaemia and weakness. Pain local or reffered. Tenderness. Angular kyphus deformity Limited movements of te spine. Cold abscess formation (psoas abscess). Varying degrees of neurological deficit. POTT'S DISEASE Treatment: a) General: proper nutrition, sanitation, and antituberculous drugs b) Local: Conservative treatment: In the active stage bed rest is essential with spinal immobilization using the plaster. In the quiescent stage gradual ambulation is allowed with spinal support. Surgical treatment : Excision of the granulation tissue to allow proper healing with bone grafting of the defects left in the spine. Pott’s Paraplegia Occurs in about 10% of cases. It may result from compression of the thoracic spine due to: -Cold abscess formation. -Granulation tissue. -Inflammatory oedema. -Progressive kyphus deformity, - Thrombosis of vessels of the cord. It is usually spastic and it may progress to be flaccid at the end.