12 Bone and Joint Infections.pptx

OSTEOMYELITIS • Definition Osteomyelitis is an inflammation of the bone caused by an infecting organism. It may remain localized, or it may spread through the bone to involve the marrow, cortex, periosteum and soft tissue surrounding the bone. Classification schemes Waldvogel Classification (197...

OSTEOMYELITIS • Definition Osteomyelitis is an inflammation of the bone caused by an infecting organism. It may remain localized, or it may spread through the bone to involve the marrow, cortex, periosteum and soft tissue surrounding the bone. Classification schemes Waldvogel Classification (1970) the most important and widely used system in clinical trials Etiology ⮚Hematogenous seeding from remote source • Most common form in pediatric age • Sluggish metaphyseal capillaries ⮚Contiguous spread from soft-tissue or joint infection • Common in older adults (fe. arthroplasty) • Lower extremity infections related to diabetes or vascular diseases ⮚Direct inoculation from penetrating trauma or surgery • Common in young adults (exposed fractures, arthrocentesis, etc.) Duration of symptoms • Acute: symptoms have been present for less than two weeks; • Subacute: symptoms have been present for more than two weeks, but less than six weeks; • Chronic: symptoms have been present for more than six weeks Classification schemes Cierny and Mader Classification (1984): Subdivides osteomyelitis based on where the infection occurs in the bone and the clinical condition of the patient. Cierny-Mader Classification 12 clinical stages (4 types x 3 host class) ⮚Type: • • • • A: Type I: medullary osteomyelitis. B: Type II: superficial osteomyelitis. C: Type III: localized osteomyelitis. D: Type IV: diffuse osteomyelitis. ⮚Host: • A-Healthy; • B -Compromised locally (BL) or systemically (BS); • C -Requires suppressive or no treatment, Minimal disability, Treatment worse than disease, Not a surgical candidate; Acute Hematogenous Osteomyelitis • Typical in males during childhood and adolescence • The pyogenic organism reaches the bone through the bloodstream from a more or less known focus of infection (tonsillitis, pharyngitis, etc.). • The organism initially localizes in the metaphyseal regions of long bones, which represent highly vascularized areas. • the most commonly affected are the distal femur and proximal tibia. • the growth plate at the epiphysis acts as a natural barrier to the spread of bacteria.. Diagnosis Clinical Presentation ▪ Acute • • • • • Pain Erythema Edema +/-Fever (more common in pediatric) Associated wound or sinus tract if direct/contiguous source ▪ Chronic • • • • • Generalized/systemic signs less common Signs of dystrophy and discoloration of the skin Occasional or persistent localized pulsating gravitational pain Hard swelling Occasional, cyclical, or permanent presence of fistulas with purulent secretion Labs In acute hematogenous osteomyelitis, inflammation indices (ESR, CRP, white blood cells) are often elevated, whereas they are less so in chronic forms. However, these are nonspecific tests, mainly important for disease monitoring. The key is recognizing elevated inflammatory markers and interpreting along with imaging and clinical presentation! Biopsy and culture At least three tissue samples are required to increase the test positivity rate. Microbiology • Organisms vary based on age, type of osteomyelitis and location o Hematogenous commonly monomicrobial o Contiguous or direct inoculation can be monomicrobial or polymicrobial • Children -S. aureus> S. pneumoniae > K. Kingae o Sickle cell predisposes to Salmonella but S. aureusstill more common • Adults -S. aureus, coag-neg o S. aureus overall most common o Incidence of osteomylitis increased with incidence of diabetes in population Imaging • RX: The radiographic picture of osteomyelitis follows the onset of the disease by a few weeks and is quite variable • . In the acute phase, there may be a localized bone resorption pattern. • In chronic cases, overlapping features can include: • lytic lesions with infiltrative or termite-eaten wood patterns, surrounded by well-defined sclerotic rims (Brodie's abscess), sometimes with endosteal scalloping; • periostitis and/or periosteal reaction with Codman's triangles; • deposition of bone, often with a sclerotic appearance surrounding the necrotic bone (sequestrum). The cortex is sometimes interrupted by a fistulous tract. The main differential diagnosis is with neoplastic forms • CT: Computed tomography can be useful preoperatively for further surgical planning Acute Chronic Imaging • MRI: magnetic resonance imaging is considered the primary type of investigation capable of detecting changes from the early days of the disease; • Nuclear medicine: Nuclear medicine is useful not only for diagnosis but also for determining the extent of the septic focus. Treatment Strategies Treatment of acute osteomyelitis is predominantly based on antibiotic therapy. Empiric therapy is based mostly on teicoplanin, daptomicin and 4th generations beta lactams In chronic forms, the indication is surgical and involves sequestrectomy, extensive debridement, and appropriate and Treatment Strategies • In cases with extensive bone involvement (Stage 4 of Cierny-Mader), complete removal of the affected bone segment and the application of reconstructive techniques are necessary: o Masquelet technique: • first surgical step: extensive bone resection and debridement, antibioticloaded cement spacer • After two months, the spacer is replaced with a graft of crushed bone. o Bone transport with circular external fixator. o Microsurgical reconstruction with free bone flaps. Masquelet Circular External Fixator (Ilizarov) Prosthetic Joint Infections Introduction: the “Burden” of PJI ▪Prosthetic joint infection (PJI) is a serious complication of prosthetic joint implantation which brings a large burden to both the individual and society 1. ~2% of total procedures (~150.000/year in Italy), with this number expected to rise 2. Treatment of PJI often requires repeated surgical intervention and prolonged iv antibiotic therapy 3. PJI can present at any time after index arthroplasty ± signs of infection 4. Cultures are negative in up to 15% of cases Risk Factors Surgical Factors ▪Knee >>> hip arthroplasty ▪Intraoperative time ▪Primary <<< revision surgery Patient Factors ▪Presence of comorbidities (RA, DM, cancer, CKD, …) ▪History of immunosuppression ▪Increasing ASA score ▪Smoking ▪History of recent infection It is unclear whether the surgical approach or use of cemented or non-cemented arthroplasty plays a role! Classification and Etiology ▪PJIs are often categorized using the timing of infection into Pathogenesis: The “Issue” of Biofilms ▪Presence of orthopedic hardware enhances susceptibility to infection due to formation of a biofilm ▪The process of biofilm formation consists of bacterial adherence to hardware, followed by multiplication. ▪In the presence of biofilm, antibiotic administration may be associated with an initial clinical response, followed by relapse within days or months unless the hardware is removed. Clinical Presentation ▪Clinical presentation depends on the timing of infection Clinical Presentation – Early ▪Patients may present with hematoma formation or superficial necrosis of the incision ▪One or more of the following findings may be observed 1. joint pain 2. warmth 3. erythema 4. wound drainage or dehiscence 5. joint effusion and fever Clinical Presentation – Delayed and Late ▪Chronic infections show pain and more subtle symptoms 🡪 function deteriorates over time 🡪 pain worsens over time ▪Fever is present in less than half of cases. Sinus tract associated with intermittent drainage may be observed; in the absence of a sinus tract, physical exam findings are often minimal. Diagnosis • The diagnosis of PJI rests in general on a combination of factors including history and physical examination, synovial fluid analysis, serum inflammatory markers, culture data, and intraoperative findings Diagnosis - Imaging ▪Radiographic imaging may be of value but usually does not provide a definitive diagnosis of PJI. Typical findings include periosteal reaction, scattered patches of osteolysis, transcortical sinus tracts, and implant loosening. ▪FDG-PET is not useful within the first year of arthroplasty due to false-positive results associated with postoperative inflammation ▪Use of CT scan is limited by imaging artifacts caused by metallic implants Diagnosis – Intraoperative Evaluation ▪Intraoperative specimens should consist of at least 3 periprosthetic tissue samples obtained with different instruments and put into separate sterile containers ▪Removed implants should always undergo sonication Diagnosis – Synovial Fluid Analysis ▪For cases in which a definitive diagnosis of PJI cannot be made, synovial fluid analysis may be used in conjunction with serum inflammatory markers ▪Synovial fluid should be sent for cell count with differential, Gram stain, aerobic and anaerobic culture ▪While in the setting of early-onset PJI, the synovial fluid cell count is often >10,000 cells/microL (>90% neutrophils), in the setting of delayed- and late-onset PJI, the synovial fluid cell count is often >3000 cells/microL (80% neutrophils). Treatment ▪In general, management of PJI consists of surgery and antimicrobial therapy. ▪The approach depends mainly on the timing and microbiology of infection, and individual patient circumstances. ▪Surgical options for PJI include debridement and retention of prosthesis, resection arthroplasty with reimplantation (in one or two stages), resection arthroplasty with no reimplantation, or amputation ▪Whenever possible, initiation of antibiotic therapy should be delayed until specimens for culture are obtained. Treatment Treatment ▪In acute PJI (<4 weeks) or acute hematogenous infections with duration of symptoms <3 weeks, debridement, antibiotics, and implant retention (DAIR) is the treatment of choice. The original implant may be kept in place, but all mobile parts should be exchanged. ▪In cases with longer duration of symptoms (>30 days) and/or sinus tract formation, a complete removal of the prosthesis is necessary. Available options include 1. One-stage exchange arthroplasty – prosthesis resection with debridement of the soft tissue and bone followed by implantation of a new prosthesis during the same surgery 2. Two-stage exchange arthroplasty – as above, but this time the implantation of the new prosthesis is preceded by the placement of a joint spacer Treatment - Surgery Treatment - Antibiotics ▪The approach to antibiotic therapy depends on the surgical approach and the microbiology of the infection ▪Patients should undergo serial examinations in the outpatient setting to monitor for refractory or recurrent infection ▪Serum inflammatory markers may be helpful to detect clinical failure. Treatment - Antibiotics