< Back Spine Surgical Site Infections Previous Next

< Back Shoulder & Elbow Anatomy DCDC shoulder-elbow-anatomy Previous Next

< Back The Femoral Head Edema Zone: A Novel Classification Scheme to Better Predict Osteonecrosis Progression Retrospective single-institution study evaluating whether a new Edema Zone classification (based on extent of femoral head edema on MRI) predicts conversion to total hip arthroplasty (THA) after core decompression for osteonecrosis of the femoral head (ONFH). Compared against the established Japanese Investigation Committee (JIC) classification. 🧠 Key Points Study Population: 94 hips with ONFH treated with core decompression (20 converted to THA within 26 months, 74 did not). Edema Zone vs JIC: Edema Zone classification correlated with THA conversion, while JIC did not (P < 0.001 vs P = 0.83). Predictive accuracy: AUC 0.71 for Edema Zone vs 0.52 for JIC → better prognostic tool . Reliability: Excellent inter-rater reliability for Edema Zone (κ = 0.87), outperforming JIC and other systems. Risk association: Higher Edema Zone grades (≥3) had significantly greater THA conversion rates (e.g., 67% for grade 4). Clinical implication: The Edema Zone classification provides a simple, MRI-based, reliable system to guide surgical decision-making and avoid ineffective core decompressions in high-risk patients. The Journal of Arthroplasty (2025) doi.org/10.1016/j.arth.2025.08.035 Previous Next

< Back Non-Ossifying Fibroma (NOF) Non-ossifying fibroma (NOF) is a benign, non-osteogenic bone lesion composed of fibroblastic cells, typically located in the metaphysis of long bones during childhood and adolescence. It is usually asymptomatic and detected incidentally on radiographs obtained for other reasons. 1.Synonyms Fibrous cortical defect (for smaller lesions) Metaphyseal fibrous defect Fibroxanthoma Nonosteogenic fibroma Fibrous histiocytoma of bone Sometimes confused with “cortical desmoid” (different localization) 2. Associated Conditions / Syndromes NOF can be an isolated finding but may also be associated with certain systemic syndromes: Neurofibromatosis type 1 (NF1) Jaffe-Campanacci syndrome: Multiple NOFs + café-au-lait macules + mental retardation + hypogonadism + cardiac anomalies 3. Epidemiology Age: Common between 5–20 years Sex: Slight male predominance (~1.6:1) Prevalence: Seen radiographically in 30–40% of children Most frequent locations: Distal femur, proximal tibia, distal tibia, proximal fibula 4. Pathogenesis and Genetics Previously thought to be a reactive process; current DNA analyses have revealed KRAS , FGFR1 , and NF1 mutations → suggesting a neoplastic process related to RAS-MAPK pathway activation. Typically eccentric in location, adjacent to the cortex. 5. Clinical Features Usually asymptomatic Large lesions : Mechanical weakness → risk of pathological fracture May cause pain Diagnosis is often facilitated if a pathological fracture is present 6. Imaging Radiograph : Eccentric, metaphyseal, cortically based, well-defined, lobulated radiolucent lesion with internal septations Often 1–3 cm (fibrous cortical defect) or larger (NOF) CT : Demonstrates cortical thinning and intracortical location MRI : Hyperintense on T2; hypointense on T1 if hemosiderin present Periosteal reaction is typically absent 7. Histology Gross : Well-circumscribed, soft, yellow-brown fibrous tissue Cut surface may show small foci of hemorrhage and hemosiderin deposits Microscopic : Well-vascularized fibrous stroma with haphazardly arranged spindle-shaped fibroblasts Interspersed lipid-laden foam cells (xanthomatous histiocytes) Focal multinucleated giant cells Frequent hemosiderin pigment deposition Minimal cellular atypia, rare mitotic figures Occasional ossification or bone trabeculae within fibrous stroma Sclerotic bony rim may be present at the periphery Differential Diagnosis : Aneurysmal bone cyst, fibrous dysplasia, giant cell tumor 8. Treatment and Natural History Small/asymptomatic : Observation (most regress and sclerose spontaneously by late adolescence) Large/high fracture risk : Curettage + bone grafting Prophylactic fixation may be considered Recurrence after surgery is rare NOF at proximal tibia (lateral view) NOF at proximal tibia (AP view) Radiograph and coronal MRI of the proximal tibia show an eccentric, multilobulated cortically based lucent lesion with a thin sclerotic rim and no periosteal reaction. On MRI, the lesion demonstrates low T1 and heterogeneously high T2 signal intensity with a low-signal peripheral rim. Findings are consistent with a non-ossifying fibroma. Previous Next

< Back Dupuytren's Disease dupuytrens-disease Previous Next

< Back Achilles Tendon Disorders achilles-tendon-disorders Previous Next

< Back Dr. Alpe DUNKI Pathologic Fracture Management Pathological fractures occur in structurally weakened bone, most commonly due to metastatic disease, but also from primary tumors or metabolic bone disorders. Management begins with accurate diagnosis, staging, and biopsy planning before any surgical fixation. The femur, pelvis, and spine are typical sites, with lung, breast, thyroid, renal, and prostate cancers being leading causes. Predictive tools such as Harrington criteria, Mirel’s score, and CT-based structural rigidity analysis guide the need for prophylactic fixation. 1. Definition and Overview A pathologic fracture is a break in bone caused by abnormal weakening of bone structure , usually due to benign or malignant lesions . The core principle of management: accurate diagnosis and staging of the underlying pathology before surgical fixation . These fractures reflect compromised skeletal biomechanics , most frequently secondary to metastatic disease , though they may arise from primary sarcomas , benign lesions , or metabolic bone disorders. 2. Etiology and Epidemiology Metastatic bone disease accounts for the majority of pathologic fractures in adults. The five cancers most likely to metastasize to bone: lung, breast, thyroid, renal, and prostate . Spine, pelvis, and proximal femur are the most common sites. In patients >40 years, a metastatic fracture is ~500 times more common than a primary sarcoma-related one. Approximately 8% of patients with bone metastases will experience a pathologic fracture during the disease course 3. Pathophysiology Osteolytic lesions: Tumor-induced activation of osteoclasts via RANKL signaling → bone resorption. Osteoblastic lesions: Mediated by endothelin-1 , stimulating abnormal bone formation. Biomechanical weakness arises from cortical destruction or cavitary defects that reduce the bone’s load-bearing capacity. Result: fractures occur during normal or minimal stress 4. Clinical Presentation and Evaluation Symptoms: Chronic or progressive pain, swelling, reduced function, or a sudden increase in pain after minimal trauma. May present with systemic signs of malignancy (weight loss, fatigue, hypercalcemia). Imaging protocol: Plain radiographs of the entire affected bone. CT of chest/abdomen/pelvis for staging. Bone scintigraphy for osteoblastic lesions or skeletal survey for myeloma. MRI for soft tissue or neurovascular involvement. PET/CT for systemic evaluation. Laboratory workup: CBC, metabolic panel, calcium, alkaline phosphatase, ESR, urinalysis, PSA, CEA, and serum/urine electrophoresis to identify possible myeloma or metastasis. Biopsy should be performed only after staging , adhering to strict oncologic principles to avoid contamination 5. Classification and Prediction of Impending Fractures Impending fracture : Bone so weakened that fracture is likely with normal activity. Harrington Criteria (1980): 50% cortical destruction Lesion >2.5 cm Persistent pain after radiotherapy Lesser trochanter fracture → Indicates need for prophylactic fixation Mirel’s Classification (1989): Considers site, pain, lesion type, and size. Score ≥8 → Prophylactic fixation recommended . CT-based Structural Rigidity Analysis (CTRA): A modern quantitative alternative; superior predictive value for femoral fractures 6. General Treatment Principles Management goals: Stabilize the fracture Restore function and mobility Control pain Prevent further complications Address underlying malignancy Treatment strategy depends on: Primary pathology (benign vs. malignant) Expected survival Healing potential of the lesion Patient activity level and comorbidities 7. Surgical Management – Core Principles Surgical fixation must follow comprehensive oncologic workup and biopsy . Implant choice principles: Favor load-sharing constructs over purely load-bearing. Implant should outlast expected survival . Bypass lesion by at least two cortical diameters . Allow immediate postoperative stability and early mobilization . Cement augmentation enhances fixation in poor-quality bone. Material considerations: Titanium: MRI-compatible, lower modulus of elasticity, suited for benign lesions. Stainless steel: Stronger, preferred in metastatic lesions but produces imaging artifacts. Carbon-fiber (CFR-PEEK): Radiolucent, MRI-compatible, high fatigue strength – emerging as optimal for oncologic fixation 8. Lesion-Specific Management A. Impending Fractures Prophylactic fixation before fracture reduces morbidity, surgical complexity, and blood loss. Indicated when Mirel ≥8 or biomechanical analysis supports instability. Elective stabilization allows easier postoperative rehabilitation B. Completed Pathologic Fractures Fracture healing potential varies by tumor type: Multiple myeloma – 67% Renal carcinoma – 44% Breast carcinoma – 37% Lung carcinoma – 0% Thus, implant strategy is tailored to tumor biology: Myeloma: plates/screws or intramedullary devices. Lung carcinoma: wide resection or endoprosthesis. Renal cell carcinoma metastases → wide excision when feasible; improves 5-year survival (4.8 vs. 1.3 years). Preoperative embolization is crucial for highly vascular lesions (renal, thyroid) to minimize intraoperative blood loss 9. Surgical Site–Specific Strategies Upper Extremity Proximal humerus: arthroplasty (hemi, total, or reverse) or endoprosthesis Diaphysis: locked intramedullary nail or plate fixation Distal humerus: dual plating or total elbow replacement Lower Extremity Femoral head/neck: hemiarthroplasty, total hip replacement, or endoprosthesis. Subtrochanteric/diaphyseal: cephalomedullary nailing Distal femur: locking plate or retrograde nail (avoid tumor spread) Proximal tibia: locking plate or modular endoprosthesis Pelvis Small lesions: radiation or radiofrequency ablation. Load-bearing fractures: fixation with screws ± cement. Peri-acetabular lesions: Managed per Harrington classification , from curettage + cement (Type I) to acetabular reconstruction (Type IV). Spine Most common metastatic site. Surgery aims for stabilization, decompression, and palliation . Tokuhashi score guides decision-making: 9 → operative ≤5 → palliative care 10. Adjuvant and Systemic Therapy Radiation Therapy Adjuvant or postoperative use to prevent local progression. Radiosensitive: myeloma, lymphoma, prostate, breast. Radioresistant: renal, thyroid, sarcoma, melanoma. Single-fraction 8 Gy provides similar pain control to multiple fractions. Complications: delayed wound healing, infection, radiation-induced fractures Chemotherapy Used for chemosensitive tumors (e.g., sarcomas, myeloma). Administered neoadjuvantly or adjuvantly . Decision based on ECOG performance status and overall prognosis 11. Postoperative and Rehabilitation Care Goals: early mobilization, pain control, and return to function. Anticoagulation: recommended postoperatively, especially for lower limb surgery. Physical therapy: begins immediately to maximize function. Bisphosphonates or denosumab: reduce risk of skeletal-related events (SREs) — including fractures, spinal cord compression, and hypercalcemia. Without therapy, SREs occur in >50% of metastatic breast or prostate cancer patients. Benefits must be balanced against risks: hypocalcemia, osteonecrosis of the jaw, and atypical fractures 12. Complications and Prognosis Mechanical: fixation failure, implant loosening, periprosthetic fracture. Infectious: wound infection, sepsis, prosthetic infection. Systemic: venous thromboembolism, pulmonary cement embolism (BCIS). BCIS: hypoxia and hypotension due to cement pressurization—reported in up to 75% of oncologic arthroplasty patients . Prognosis depends primarily on primary tumor biology and extent of metastasis . Example: 6-month survival — prostate (98%), breast (89%), renal (51%), lung (50%) 13. Interprofessional Collaboration and Patient Education Multidisciplinary management is essential — orthopedic oncology, radiology, pathology, medical and radiation oncology, and palliative care. Preoperative coordination ensures accurate diagnosis, staging, and risk optimization. Patient education should emphasize early reporting of bone pain and the benefit of prophylactic stabilization. The overarching aim is early stabilization, mobilization, and durable reconstruction that outlasts patient survival References 1. Rizzo SE, Kenan S. Pathologic Fractures. [Updated 2023 May 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. 2. Fields RC, Beauchamp CP, Srinivasan S, et al. Management of pathological fractures: current consensus. Knee Surg Sports Traumatol Arthrosc. 2024;32(3):1125-1135. 3. Boussouar S, Pasche C, Bluemke DA, et al. A tailored approach for appendicular impending and pathologic fractures from metastatic bone disease. Cancers (Basel). 2022;14(4):893. 4. Conti A, Bertolo F, Boffano M, et al. Pathological hip fracture in the elderly: review and proposal of an algorithm. Lo Scalpello J. 2020;34:128-136. Previous Next

< Back Alper DUNKI Imaging Principles Plain radiography remains the first-line and often diagnostic in most bone tumors, while CT provides detailed cortical and 3D anatomical evaluation. MRI offers superior soft-tissue and marrow contrast, essential for assessing intramedullary extension and surgical margins. PET/CT assist in detecting metastases and evaluating treatment response. 1. Introduction Imaging plays a central role in the diagnosis, staging, and surgical planning of musculoskeletal (MSK) tumors. Plain radiography , CT , MRI , nuclear medicine scans , and PET/CT remain the core modalities, often complemented by angiography and ultrasound for specific indications. Selection of modality depends on tumor type, location, aggressiveness, and tissue composition 2. Plain Radiography (X-ray) Serves as the first-line imaging tool and remains diagnostic in >80% of bone tumor cases Reveals: Tumor location within the bone (epiphyseal, metaphyseal, diaphyseal). Cortical destruction or thickening , periosteal reactions (e.g., Codman triangle , sunburst pattern ). Matrix type — osteoid, chondroid, or fibrous. Soft-tissue calcification patterns suggesting tumor type. Limitation: early detection in pelvic and spinal lesions is poor due to overlapping structures. 3. Computed Tomography (CT) Preferred modality for assessing extent of cortical destruction and 3D anatomy . Helical CT with ≤1 mm slice thickness allows high-resolution multiplanar and 3D reconstructions Contrast-enhanced CT delineates: Relationship of tumor to vessels and neurovascular bundles . Vascular invasion or distortion aiding surgical planning. 3D reconstruction helps estimate need for en bloc vessel resection or approach modification. 4. Magnetic Resonance Imaging (MRI) Superior to CT for evaluating intramedullary spread and extraosseous soft-tissue extension Advantages: Multiplanar imaging (axial, sagittal, coronal). Excellent contrast resolution for tumor–muscle–fat differentiation. Contrast-enhanced MRI defines vascular involvement , cystic components , and nerve proximity . MRI is essential for surgical margin planning and defining safe resection limits . Characteristic tumor appearances: Lipomas, liposarcomas, PVNS, hemangiomas, and fibromatoses show distinctive patterns. Pitfalls: Hemorrhagic high-grade sarcomas may mimic hematomas — clinical follow-up is vital. 5. Bone Scintigraphy (Bone Scan) Used to detect metastatic spread or multifocal disease Bone tumors imaging Three-phase bone scan reflects tumor biologic activity : “Tumor blush ” pattern — increased uptake during late flow phase in malignant lesions. Also used to monitor chemotherapy response by comparing uptake pre- and post-treatment. 6. Angiography and Venography Angiography: Demonstrates arterial displacement, occlusion, or encasement by tumors CT angiography is increasingly replacing conventional techniques. Preoperative embolization reduces intraoperative bleeding in hypervascular metastases (e.g., renal carcinoma). Venography: Shows venous obstruction or compression by tumor mass. Indirectly suggests neural invasion when adjacent vein occlusion is present. 7. Positron Emission Tomography / CT (PET/CT) Functional imaging using FDG uptake proportional to tumor glucose metabolism Applications: Initial staging, monitoring therapy response, and recurrence detection. PET-CT fusion combines functional and structural data — useful in detecting small metastatic lesions . Standardized Uptake Value (SUV) quantifies uptake, helping to distinguish malignancy from infection or inflammation . 8. Ultrasonography (USG) Recommended initial test for superficial soft-tissue masses (per ACR Appropriateness Criteria ) Benefits: No radiation, real-time vascular evaluation, dynamic movement analysis, cost-effective. Evaluates echogenicity, margins, vascularity, and cystic vs. solid composition . Diagnostic accuracy: 77–93% , though specificity for malignancy is limited. Pitfall: differentiation between lipoma and liposarcoma remains challenging. Suspicious features (pain, rapid growth) → further MRI required. 9. MRI Next-line imaging if diagnosis remains uncertain after USG or radiographs Provides superior soft-tissue contrast and local staging . Diagnostic parameters: Size (>5 cm), deep location, heterogeneous T2 signal, ill-defined margins, perilesional edema. Necrosis, bone or neurovascular invasion → suggest malignancy. Post-contrast MRI enhances diagnostic accuracy: Differentiates cystic vs. solid lesions. Identifies necrotic areas and optimal biopsy sites . Reported sensitivity and specificity for differentiating benign vs. malignant: 64–93% and 82–85% , respectively. 10. CT and PET/CT in Soft-Tissue Tumors CT acts as a second-line modality when MRI is nondiagnostic or contraindicated (e.g., pacemaker, claustrophobia). Contrast-enhanced CT evaluates bone involvement and surgical planning . PET/CT : Not routine for primary diagnosis but valuable for metastatic work-up and treatment response evaluation . Studies suggest PET/CT may help differentiate benign and malignant tumors , but ACR discourages routine use. Key Findings Optimal MSK tumor imaging requires multimodal integration . Radiography and MRI form the diagnostic backbone, with CT and PET/CT for staging and surgical planning. Ultrasound remains useful for superficial masses, while angiography assists in vascular evaluation. Advances in functional imaging (PET/MRI) and 3D reconstruction continue to enhance preoperative accuracy and individualized treatment planning. References 1. Rajakulasingam R, Stediuk K, Teh JJ, et al. Current progress and future trends in imaging of bone tumours. Eur Radiol Exp. 2021;5(1):27. 2. Shu H, Ma Q, Li A, et al. Diagnostic performance of US and MRI in predicting malignancy of soft tissue masses: using a scoring system. Front Oncol. 2022;12:853232. 3. Gitto S, Ippolito D, Bandiera E, et al. CT and MRI radiomics of bone and soft-tissue sarcomas. Insights Imaging. 2024;15(1):16. Modality Main Role Advantages Limitations X-ray Initial screening Identifies matrix, periosteal reaction Poor soft-tissue detail CT Cortical detail, 3D mapping High resolution Radiation exposure MRI Soft-tissue and marrow evaluation Multiplanar, no radiation Costly, motion artifacts Bone Scan Detects metastases High sensitivity Low specificity Angiography Vascular mapping Guides embolization Invasive USG Superficial mass evaluation Real-time, no radiation Operator-dependent PET/CT Functional staging Detects active disease Limited initial utility Summary Table of Modalities Previous Next

< Back Chopart Injuries chopart-injuries Previous Next

< Back Skin Grafts skin-grafts Previous Next

< Back High Tibial Osteotomy (HTO) high-tibial-osteotomy Previous Next