Bone and Joint Infections PDF

Bone and joint Infections Dr Nishita Patel Infectious Diseases Osteomyelitis Learning objectives Identify etiological agents responsible for osteomyelitis. Describe the presentation of a patient with osteomyelitis. Identify the role of radiographic imaging in the evalua...

Bone and joint Infections Dr Nishita Patel Infectious Diseases Osteomyelitis Learning objectives Identify etiological agents responsible for osteomyelitis. Describe the presentation of a patient with osteomyelitis. Identify the role of radiographic imaging in the evaluation of patients with osteomyelitis. Outline the diagnostic and management approach of a patient with osteomyelitis.  Microbiology- Dr Saviola Staphylococcus aureus: most common cause overall (including pediatric patients) Mycobacterium tuberculosis in cases of vertebral involvement (Pott disease). Mycobacterium tuberculosis, which may spread to the spine from the lungs; Pasteurella multocida in cases caused by cat and dog bites. Pseudomonas and Candida are seen in intravenous drug abuse. Pathogenesis Hematogenous seeding of bone: More common in children compared to adults In children- long bones are usually affected. In adults- the vertebrae are most commonly affected. Usually affect two adjacent vertebral endplates because segmental arteries typically bifurcate to supply two adjacent endplates of contiguous vertebrae Pathogenesis Contiguous spread of infection from adjacent structures (e.g., soft tissues and joints) : From infected joint arthroplasties Diabetic foot infection leading to osteomyelitis because of vascular insufficiency. Pressure-related decubitus ulcerations, especially in the sacrum, buttock, hips, and heel. In setting of open fractures. After placement of orthopedic hardware Clinical Presentation Acute osteomyelitis usually manifests within two weeks. local symptoms such as erythema, swelling, and warmth at the site of infection. Dull pain with or without motion Fever present in 40% of cases Acute vertebral OM New or worsening neck or back pain with fever Recent diagnosis of bacteremia, or endocarditis should raise the suspicion for native vertebral osteomyelitis (NVO). Tenderness to palpation over vertebral bone may be a significant finding in vertebral osteomyelitis. Clinical Presentation In chronic osteomyelitis, symptoms occur over more than two weeks. Presence of swelling, pain, and erythema at the site of infection constitutional symptoms like fever are less common. Suspect Chronic OM if Patients with deep or extensive ulcers that do not heal after several weeks of appropriate therapy, especially with diabetes or debilitated patients. The ability to probe an ulcer to the bone with a blunt sterile instrument is highly suggestive of osteomyelitis. Diagnostic approach Radiographic imaging is an essential for the evaluation of suspected osteomyelitis. Most commonly used imaging are: Plain radiographs Magnetic resonance imaging (MRI) Nuclear imaging A plain radiograph is usually the initial imaging of choice Typically seen are soft tissue swelling, osteopenia, osteolysis, bony destruction, and nonspecific periosteal reaction. Lytic lesions are detectable on plain radiographs after 50% to 75% of the bone matrix has been lost, leading to delay of about 14 days before the appearance of findings suggestive of osteomyelitis and is inadequate to detect early bone disease. Diagnostic approach MRI has the highest combined sensitivity and specificity (78% to 90% and 60 % to 90% respectively) for detecting osteomyelitis. It can detect early bone infection within 3 to 5 days of disease onset except in the setting of surgical hardware. MRI has a high negative predictive value, so a negative result is sufficient for the exclusion of disease after one week of symptoms. Nuclear imaging has a high sensitivity for detecting early bone disease but has very poor specificity. It is especially useful if metal hardware prevents the use of MRI. Three-phase technetium-99 bone scan and tagged white blood cell scans are commonly used. Osteomyelitis Imaging Radiographs Areas of lucency, sclerosis, periosteal reaction, and lysis around hardware if present Diagnostic approach Bone biopsy: Bone biopsy (either open or percutaneously) is essential to establish the diagnosis, to identify the causative pathogen, and provide susceptibility data that helps direct antibiotic therapy. Superficial wound cultures or sinus tracts is not sufficient as they do not correlate well with bone biopsy results. An open bone biopsy is preferred over percutaneous biopsy, if possible. Percutaneous biopsy should be done through intact skin with fluoroscopic or CT guidance. Two samples should be collected, one for histopathology and the other for culture and gram stain. Bone biopsy can be avoided if the patient has positive blood cultures and radiographic evidence of osteomyelitis. Bone biopsy/ histopathology In acute osteomyelitis congested or thrombosed blood vessels, and infiltrates of neutrophils. In Chronic osteomyelitis Presence of necrotic bone. predominance of mononuclear cells replacement of osteoclast by granulation, and fibrous tissue leading to bone loss and the formation of sinus tracts. 14 Treatment / Management Hematogenous osteomyelitis is primarily monomicrobial Osteomyelitis due to contiguous spread or direct inoculation is usually polymicrobial or monomicrobial. Combined medical and surgical approach to management is recommended. Surgical management Surgical debridement of all diseased bone to increase antibiotics penetration and removal of necrotic bone. NVO rarely requires surgical debridement except if there are associated neurological complications necessitating relief of spinal cord compression or to drain epidural or paravertebral abscesses. Debridement is needed in cases of osteomyelitis associated with spinal implants. Revascularization In the presence of significant peripheral vascular disease, revascularization of the affected limb before surgical intervention is important. Control diabetes mellitus to improve wound healing. Prolonged antibiotic therapy is the cornerstone of treatment for osteomyelitis. Results of culture and sensitivity should guide antibiotic treatment. Pathogen-Specific Antibiotic Therapy for Osteomyelitis in Adults Staphylococcus aureus penicillin-resistant (MSSA) Treatment of choice(TOC) is IV nafcillin Alternative therapies are cefazolin, clindamycin, or vancomycin. Staphylococcus aureus methicillin-resistant (MRSA) TOC is IV vancomycin Alternative regimen is linezolid. Streptococci (group A, B, Beta hemolytic, Streptococcus pneumoniae) TOC is penicillin G Alternative regimens include ceftriaxone, clindamycin, vancomycin, or cefazolin. Pathogen-Specific Antibiotic Therapy for Osteomyelitis in Adults Enterobacteriaceae quinolone sensitive TOC is ciprofloxacin Alternative regimens include ceftriaxone, cefepime or ceftazidime Enterobacteriaceae, quinolone-resistant (Escherichia coli) TOC is piperacillin/tazobactam or Ticarcillin/clavulanate An alternative regimen is ceftriaxone Pseudomonas aeruginosa TOC is cefepime or ceftazidime Alternative regimens include meropenem, Imipenem, or ciprofloxacin Enterococci TOC is penicillin G Alternatively, vancomycin, daptomycin or linezolid Anaerobes TOC is clindamycin or ticarcillin/clavulanate Alternatively, metronidazole (for gram-negative anaerobes) Treatment/management The recommended duration in adults is 4 to 6 weeks of parenteral antibiotic therapy. In fully debrided(where the clean disease-free margins documented) or in case of amputated bone, a 2-week course of antibiotics postoperatively is sufficient to allow for wound healing of the surgical site. Vacuum-assisted wound closure devices are used where large or deep wounds are left after extensive debridement. Hyperbaric oxygen therapy is not routinely recommended.  Charcot arthropathy especially in people with Differential diabetes Diagnosis SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis) Arthritis including rheumatoid arthritis Metastatic bone disease Fracture, including pathological and stress fractures. Gout Avascular necrosis of the bone Bursitis Sickle cell vaso-occlusive pain crises Septic Arthritis  Identify the common bacterial organisms in the etiology of septic arthritis. Learning Summarize clinical presentation of septic arthritis. Outline the laboratory and imaging studies used in the Objectives evaluation of septic arthritis. Outline the management for patients affected by septic arthritis.  Location: The knee is the most commonly affected joint followed by the hip. Etiology in Pathogens : Staphylococcus aureus is the most common in adults. Adults Special circumstances are : Salmonella sp. in patients with sickle cell Pseudomonas sp. in trauma/puncture wounds In young sexually active patients think of Neisseria gonorrheae  2 main manifestations of disseminated gonococcal infections: 1) A triad of tenosynovitis, dermatitis, and polyarthralgias without purulent arthritis in which the synovial fluid is not usually positive for the organism. The tenosynovitis and Gonococcal polyarthralgias are thought to be immune mediated (a response to the disseminated infection). Septic Arthritis 2) purulent arthritis without associated skin lesions with recovery of organisms from joint fluid.  After trauma: suspect polymicrobial joint infection In IV drug user: suspect the sternoclavicular and sacroiliac joint infection and common pathogens involved are Etiology in Serratia marcescens and Pseudomonas aeruginosa. Adults In individuals with leukemia: suspect Aeromonas sp. infections.  Hematogenous seeding from systemic infection: Due to high vascularization of the joint synovium and lack of basement membrane systemic infection reach joint space. Pathophysiology- Direct inoculation native joint From injury, puncture wounds, and intra-articular injections. Contiguous spread from adjacent osteomyelitis. The hip and shoulder are vulnerable to contiguous spread.  First bacterial invasion of the synovium and joint space occurs Microbial surface adhesins promote the binding of the Pathophysiology bacteria to intra-articular proteins. of native joint Subsequent inflammation and release of inflammatory cytokines and proteases into the joint space mediate joint destruction.  Prosthetic joint infections are classified into: Early within 3 months of implantation Delayed within 3-24 months of surgery Late: occurring after 24 months Pathogens: Pathophysiology- Most early prosthetic joint infections are caused by prosthetic joint Staphylococci due to direct inoculation Delayed cases are due to gram negatives and coagulase-negative Staphylococcus epidermidis Late cases are usually secondary to hematogenous spread from various foci.  Biofilm formation is very common on man made materials. These bacteria first attach and then begin to elaborate a polysaccharide matrix and results in a complex aggregation of microorganisms, polysaccharide, and DNA that may contain one or more species of bacteria. Biofilms Bacteria can communicate with one another via diffusible products. This process is known as quorum sensing. on prosthetic These products induce changes is the cells receiving the joints signals causing them to be very resistant to immune cells and antibiotics. To improve isolation of bacteria in these biofilms, investigators have sonicated prosthetic joints, then can culture of perform PCR. Can cause implant to fail.  Septic arthritis classically presents with acute onset monoarticular joint pain, fever, swelling, and limited movement of the affected joint. Lower extremities joints (hips, knees, and ankles) especially History and knee is affected in most cases of septic arthritis. Involvement of less common joints such as the sacroiliac or Physical sternoclavicular joint occurs in injection drug users. In a young, healthy and sexually active person Examine for presence of dermatitis, tenosynovitis, and migratory polyarthralgia.  Effusions are common on examination. Physical The range of motion is limited and palpation may be associated with pain. Exam Most staphylococcal infections are associated with monoarticular involvement but Neisseria often involves multiple joints. Most prosthetic joint infections will have a draining sinus.  The most useful diagnostic test is an evaluation of the synovial fluid from the affected joint : Synovial fluid should be sent for gram stain, culture, crystals analysis, and white blood cell count with differential. In native joint synovial fluid, a white blood cell (WBC) count greater than Laboratory 50,000 and 90% neutrophil predominance suggests a bacterial infection. In prosthetic joint infections, synovial fluid WBC count of 1000 with a Studies neutrophil predominance (>60%) suggests septic arthritis. Culture growth of bacteria from the synovial fluid confirms the diagnosis. Other tests include An elevated erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) support the diagnosis but are not definitive. Two sets of blood cultures should be obtained to rule out bacteremia. If Neisseria is suspected, one should obtain cultures from the oropharynx, vagina, cervix, urethra or anus.  Plain radiographs may reveal widened joint spaces, bulging of the soft tissues, or subchondral bony changes (late finding). A normal plain radiograph does not rule out septic arthritis. Imaging Ultrasonography is useful in identifying and Studies quantifying the joint effusion as well as in needle aspiration of the joint. MRI is sensitive for early detection of joint fluid and may reveal abnormalities in surrounding soft tissue and bone, and the extent of cartilaginous involvement.  Combination of antimicrobial therapy and joint fluid drainage (arthrotomy, arthroscopy, or daily needle aspiration). Empiric intravenous antimicrobial therapy should be Treatment / initiated promptly after joint aspiration is complete and cultures is obtained. Management Empiric antibiotic coverage includes antistaphylococcal coverage (nafcillin, oxacillin, or vancomycin) for all. If the patient is immunocompromised, then a third- generation cephalosporin like ceftriaxone, ceftazidime or cefotaxime should be added to antistaphylococcal coverage.  In nongonococcal septic arthritis Give intravenous antibiotics for 2 weeks followed by another 1 to 2 weeks of oral antibiotic therapy for a total duration of three to four weeks. Longer antibiotic therapy for 4 to 6 weeks may be Treatment/ reasonable in cases of Pseudomonas aeruginosa. In Gonococcal arthritis Management Give intravenous ceftriaxone for 24 to 48 hours then transitioned to oral therapy for the remainder of the treatment. If no improvement is seen within 5-6 days, the joint should be re-aspirated, recultured for fungi, mycobacteria and Lyme disease.  Early involvement by an orthopedic surgeon is essential to drain joint fluid. Prosthetic joint infection often requires aggressive debridement and/or removal of the prosthesis. The new joint is then replaced with cement which is impregnated with antibiotics. In osteomyelitis associated with prosthetic joints, removal of the hardware is indicated Treatment/ When the prosthesis is removed, a two-stage exchange Management arthroplasty is more commonly used. If surgical debridement is not feasible based on the location of the infection, then extended antibiotic therapy for months may be used. Immobilization of the joint is not needed after 2-3 days. Aggressive physical therapy is necessary to restore joint function and prevent muscle atrophy.