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< Back Crush Syndrome Crush syndrome is a systemic condition caused by prolonged muscle compression, leading to rhabdomyolysis, acute kidney injury, and potential multi-organ failure. Crush Syndrome (traumatic rhabdomyolysis) develops after prolonged compression of muscle tissue, commonly seen in disasters, traffic accidents, or entrapment injuries. ⚠️ Pathophysiology: Muscle breakdown → release of myoglobin, potassium, phosphate Leads to hyperkalaemia , metabolic acidosis , hypovolaemia Myoglobinuria causes renal tubular obstruction → acute kidney injury (AKI) 🚑 Clinical Features: Swollen, tense limbs Dark-coloured urine (myoglobinuria) Hypotension, arrhythmias, AKI 💉 Management: Early and aggressive IV fluid resuscitation (isotonic saline) Avoid potassium-containing fluids Consider mannitol & bicarbonate to prevent AKI Monitor and treat hyperkalaemia Dialysis may be required 🧪 Key Labs: Elevated CK , myoglobin Hyperkalaemia, metabolic acidosis Rising creatinine and urea 🩺 Prevention: Fluid resuscitation even before extrication in disaster settings Fasciotomy only if clear compartment syndrome, not prophylactically crush-syndrome Previous Next

< Back Infection in Reconstruction Surgery infection-reconstruction-surgery Previous Next

< Back Dr. Savas CAMUR Dislocation & Instability Despite advances in implant design, surgical technique, and perioperative protocols, instability continues to challenge both surgeons and patients.Hip dislocation remains one of the most feared complications following total hip arthroplasty (THA), associated with higher morbidity, increased healthcare costs, and up to 25% of all revision procedures. Hip Dislocations and Instability after Arthroplasty Incidence and Timing Reported incidence ranges from 0.2% to 10% globally, with large modern registries showing ~2.3% dislocation rate within 2 years after primary THA. Half of dislocations (≈52%) occur in the first 3 months , and >80% within 2 years postoperatively. Recurrent instability is common — 57% of patients with an initial dislocation experience recurrence, and 11% have ≥5 events , often necessitating revision surgery. Etiopathogenesis and Risk Factors Patient Factors Age <65 years and female sex are independent risk factors. Obesity (BMI >30) and high comorbidity burden (Elixhauser index ≥3) correlate with higher dislocation rates. Neuromuscular disorders, cognitive decline , and inflammatory arthropathy increase postoperative instability risk. Surgical Factors Posterior approach historically carried higher risk, yet modern evidence shows no difference in dislocation rates between posterior, lateral, or anterior approaches when soft tissue repair is adequate. Component positioning remains crucial — excessive cup anteversion, inclination >45°, or combined offset malalignment significantly increase instability. Femoral head size: larger diameters (≥36 mm) reduce dislocation risk by improving impingement-free motion arcs. Implant-Related Factors Cemented fixation and metal-on-poly or metal-on-metal bearings are associated with higher instability compared to ceramic-on-poly. Dual-mobility cups have emerged as effective solutions for high-risk patients. Hip Precautions and Rehabilitation Recent systematic reviews found no statistical difference between restricted vs unrestricted postoperative protocols (2.2% vs 2.0% dislocation rates). ➡️ Early mobilization and functional recovery improve patient satisfaction without increasing risk.Traditional precautions — avoiding >90° flexion, adduction, and internal rotation — have not been shown to reduce dislocation risk following posterior-approach THA. Mechanisms of Instability Soft-tissue insufficiency (capsular laxity, abductor deficiency). Component malalignment (excessive anteversion/retroversion). Impingement (bony or prosthetic). Head–neck ratio mismatch or short offset . Neurologic or proprioceptive deficits. Management Algorithm Initial episode: Closed reduction under sedation → radiographic assessment for component positioning and fracture. Activity modification + physiotherapy. Recurrent dislocation: CT-based evaluation of implant orientation. Consider dual-mobility constructs, constrained liners , or component revision when malposition or soft-tissue insufficiency confirmed. Chronic instability: Multidisciplinary approach — surgical correction of malalignment, soft-tissue reconstruction, or revision arthroplasty. Prevention Principles Accurate component positioning is the strongest modifiable factor. Repair posterior capsule and short external rotators when using posterior approach. Assess combined anteversion intraoperatively. Use larger heads (≥36 mm) to increase jump distance. Consider dual mobility or constrained liners in high-risk or revision cases. 💡 Soft-tissue balance and version alignment matter more than approach choice. Postoperative Protocols Traditional restrictions (avoiding >90° flexion, adduction, or internal rotation) do not significantly reduce dislocation rates . Modern rehabilitation emphasizes: Early mobilization Functional independence Education on safe movement patterns Diagnosis and Evaluation Radiographs: confirm reduction, component orientation, or periprosthetic fracture. CT scan: assess anteversion, inclination, and bone coverage. MRI (metal-artifact reduction): evaluate soft-tissue or abductor insufficiency. Clinical Pearls Most dislocations occur early — meticulous soft-tissue repair and orientation are more impactful than postoperative restrictions. Dual mobility or constrained liners should be considered for revision cases or high-risk primary THAs . Dynamic stability testing intraoperatively (flexion, rotation, extension) predicts postoperative behavior better than static visual assessment. . References Gillinov SM et al. Incidence, Timing, and Predictors of Hip Dislocation After Primary THA for OA. J Am Acad Orthop Surg. 2022;30:1047–1053. Crompton J, Osagie-Clouard L, Patel A. Do Hip Precautions After Posterior-Approach THA Affect Dislocation Rates? Acta Orthop. 2020;91:687–692. Dargel J et al. Surgical approach and risk of dislocation. Clin Orthop Relat Res. 2014. Peters RM et al. Effect of reduced hip precautions on dislocation and function after THA. Bone Joint J. 2019. Previous Next

< Back Femoral Shaft Fractures femoral-shaft-fractures-peds Previous Next

< Back Dr. Sefa Giray BATIBAY Osteosarcoma High-grade, malignant, osteoid-producing sarcoma of bone. Most common primary bone sarcoma. Arises predominantly in metaphysis of long bones (esp. around the knee). Epidemiology Bimodal age distribution: Adolescents (10–20y): Most common (~75%) Elderly (>65y): Often secondary to Paget’s, radiation, infarct M:F = 1.5:1 Peak incidence: Distal femur > Proximal tibia > Proximal humerus Epidemiology Bimodal age distribution: Adolescents (10–20y): Most common (~75%) Elderly (>65y): Often secondary to Paget’s, radiation, infarct M:F = 1.5:1 Peak incidence: Distal femur > Proximal tibia > Proximal humerus Aetiology & Genetics Mostly sporadic Associated tumor suppressor mutations: RB gene (Retinoblastoma) TP53 (Li-Fraumeni syndrome) Rare hereditary syndromes: Rothmund-Thomson, Bloom, Werner Histology Malignant mesenchymal spindle cells producing lace-like osteoid High N:C ratio, nuclear atypia, mitoses Diagnostic criteria: Malignant stroma Osteoid production Subtypes INTRAMEDULLARY Conventional (high-grade) Telangiectatic Small-cell Low-grade variants SURFACE Parosteal (low-grade) Periosteal (intermediate-grade) Dedifferentiated surface (high-grade) OTHERS Intracortical (rarest) Extraskeletal (soft tissue OSA, rare, radiosensitive) Clinical Features Progressive pain + swelling , often attributed to trauma Night/rest pain common Mass effect, ↓ROM, neurovascular compromise possible Median delay to diagnosis: ~4 months Imaging X-ray: Mixed lytic–blastic lesion Sunburst , Codman’s triangle , “Hair-on-end” Cortical destruction + soft tissue extension MRI: Assess extent, skip lesions, neurovascular invasion Includes entire bone CT Chest: Mandatory for lung metastasis detection Bone scan / PET-CT: Staging, skip lesions Staging Most are Enneking Stage IIB (high grade, extracompartmental, no mets) Stage III if lung/bone mets Skip lesions → considered metastasis Differential Diagnosis Ewing sarcoma (t(11;22), small round blue cells) Osteomyelitis (sequestrum, Brodie abscess) ABC (vs Telangiectatic OSA) Fibrosarcoma, Lymphoma, EG, Leukemia Labs ↑ ALP & LDH → indicator of high tumor burden Histological response post-chemo: >90% necrosis = good prognosis Biopsy Core biopsy by definitive surgeon Incorrect biopsy track → ↑amputation risk Treatment 1. Neoadjuvant chemotherapy 8–12 weeks: MAP regimen (Methotrexate + Doxorubicin + Cisplatin ± Ifosfamide) 2. Wide resection Limb-salvage preferred Criteria: good chemo response, resectable margins 3. Reconstruction options Endoprosthesis Allograft/autograft Rotationplasty (esp. in children with extensive disease) Amputation (if salvage not possible) 4. Adjuvant chemotherapy Continue for 6–12 months post-op Radiation OSA = radioresistant Reserved for: Extraskeletal OSA Palliative settings Spine/pelvis with close margins Complications Limb salvage: Prosthetic infection (2–10%) Aseptic loosening (esp. tibia) Nonunion/fracture of grafts Local recurrence Rotationplasty: Malrotation Vascular compromise Cosmesis concerns Amputation: Neuroma, phantom pain, wound healing Prognosis 5-yr survival (localized): ~85% (good chemo response) ~65% (general) 5-yr survival (metastatic): ~20% with pulmonary mets Bone mets = poor outcome Prognostic factors: Response to chemo Stage at diagnosis ALP/LDH levels Tumor size/location Surgical margins VEGF or MDR expression Clinical Features Progressive pain + swelling , often attributed to trauma Night/rest pain common Mass effect, ↓ROM, neurovascular compromise possible Median delay to diagnosis: ~4 months References: Whelan JS, Davis LE. Osteosarcoma: Biology, diagnosis, and treatment strategies.Current Oncology Reports. 2018;20(1):2. [DOI: 10.1007/s11912-018-0652-0] Isakoff MS, Bielack SS, Meltzer P, Gorlick R. Osteosarcoma: Current treatment and a collaborative pathway to success. J Clin Oncol. 2015;33(27):3029–3035.[DOI: 10.1200/JCO.2014.59.4895] Orthopaedic Knowledge Update: Musculoskeletal Tumors 4. Eds: Letson GD, Mankin HJ.American Academy of Orthopaedic Surgeons (AAOS), 2016. WHO Classification of Tumours Editorial Board. Soft Tissue and Bone Tumours. WHO Classification of Tumours, 5th Edition, Volume 3. International Agency for Research on Cancer (IARC); 2020. Peabody TD, Attar S, eds.Orthopaedic Oncology: Primary and Metastatic Tumors of the Skeletal System. Cancer Treatment and Research Series. Springer; [Indexed in PubMed/Medline]. Category Subtype Features Intramedullary Conventional Osteosarcoma Heterogeneous histology: may contain cartilaginous, fibrous, giant cell, or small round blue cell components. Telangiectatic Osteosarcoma Resembles aneurysmal bone cyst; blood-filled cavities with scant osteoid lining. Small-cell Overlaps with Ewing sarcoma; small round blue cells producing immature osteoid. Fibrous dysplasia-like High-volume fibrous stroma + immature osteoid. Desmoplastic fibroma-like Low-volume fibrous stroma + immature osteoid. Surface Parosteal Osteosarcoma Low-grade; arises from outer periosteal layer. Periosteal Osteosarcoma Intermediate-grade; from between bone surface and inner periosteum. Dedifferentiated surface High-grade surface variant. Intracortical Intracortical Osteosarcoma Extremely rare; arises within cortical bone. Extraskeletal Extraskeletal Osteosarcoma Soft tissue origin; <5% of all cases; requires wide resection and radiation. Osteosarcoma pathology CT of parosteal osteosarcoma MRI of parosteal osteosarcoma Previous Next

< Back Distal Humerus Fractures distal-humerus-fractures Previous Next

< Back Dr. Hakan ESKARA Bone Tumor Classification Overview of bone tumour classification systems and key characteristics that distinguish benign from malignant lesions. Accurate classification of bone tumors is a critical step in determining an effective treatment plan. The WHO introduced the classification of soft tissue and bone tumors (fifth edition) in 2020. The new WHO classification of soft tissue and bone tumors, introduced in 2020 (fifth edition), has made significant improvements in classification and introduced many new diagnoses. The basis for the classification of bone tumors is histopathological. Bone Tumor Classification Group Benign Intermediate (Local Agressive) Malignant Chondrogenic Subungual exostosis, Periosteal chondroma, Enchondroma, Osteochondroma, Chondroblastoma vb. Chondromatosis NOS, Atypical cartilaginous tumor Chondrosarcoma (G1-3), Periosteal, Clear cell, Mesenchymal, Dedifferentiated Osteogenic Osteoma NOS, Osteoid osteoma NOS Osteoblastoma NOS Low-grade central osteosarcoma, Osteosarcoma NOS, Parosteal, Periosteal, High-grade surface, Secondary Fibrogenic — Desmoplastic fibroma Fibrosarcoma NOS Vascular (Bone) Hemangioma NOS Epithelioid hemangioma Epithelioid hemangioendothelioma NOS, Angiosarcoma Osteoclastic Giant Cell-Rich Aneurysmal bone cyst, Non-ossifying fibroma Giant cell tumor of bone NOS Malignant giant cell tumor of bone Notochordal Benign notochordal cell tumor — Chordoma NOS (chondroid dahil), Dedifferentiated, Poorly differentiated Other Mesenchymal (Bone) Chondromesenchymal hamartoma, Simple bone cyst, Fibrous dysplasia, Osteofibrous dysplasia, Lipoma, Hibernoma Osteofibrous dysplasia-like adamantinoma, Mesenchymoma NOS Adamantinoma (dediff.), Leiomyosarcoma NOS, Pleomorphic sarcoma undiff., Bone metastases Hematopoietic — — Plasmacytoma, Hodgkin, Non-Hodgkin lenfomalar, Langerhans histiocytosis, Erdheim-Chester, Rosai-Dorfman Undifferentiated Small Round Cell — — Ewing sarcoma, CIC-rearranged, BCOR altered sarcoma Previous Next

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Knee & Sports Topics General Principles Knee Joint Anatomy & Biomechanics Physical Examination of the Knee Knee Imaging Osgood Schlatter's Disease Extensor Mechanism Problems General Problems ACL Rupture PCL Rupture Patellofemoral Pain Syndrome Patellar Instability Femoroacetabular Impingement (FAI) Meniscal Tears Posterolateral Corner Injury General Principles High Tibial Osteotomy (HTO) Distal Femoral Osteotomy (DFO) Tibial Tubercle Osteotomy Osteochondral Allografts Meniscal Allograft Transplantation Cartilage Repair Techniques (ACI, MACI) General Principles Hip Arthroscopy Snapping Hip (Coxa Saltans) Hamstring Injuries Iliotibial Band Friction Syndrome

< Back Free Tissue Transfer free-tissue-transfer Previous Next