< Back Dr. Natig VELI Multiple Myeloma Multiple Myeloma is a malignant plasma cell disorder that causes bone marrow infiltration, excessive monoclonal protein production, and skeletal destruction through osteoclast activation and osteoblast suppression. It primarily affects older adults and commonly presents with bone pain, anaemia, renal dysfunction, and recurrent infections. Radiographs reveal multiple “punched-out” lytic lesions, while MRI and PET/CT detect marrow and systemic involvement. Diagnosis is based on CRAB criteria and serum or urine monoclonal protein detection. Treatment involves proteasome inhibitors, immunomodulatory agents, corticosteroids, and autologous stem cell transplantation, complemented by bisphosphonates for bone protection and surgery for pathological fractures. Prognosis has improved with modern therapies, yet relapse remains common, requiring multidisciplinary and long-term management. Definition Multiple Myeloma (MM) is a malignant plasma cell neoplasm characterized by clonal proliferation within the bone marrow, excessive production of monoclonal immunoglobulins (M-protein), and widespread skeletal destruction. It accounts for approximately 10% of all haematologic malignancies and is the most common primary malignant bone tumor in adults. Pathophysiology Neoplastic plasma cells stimulate osteoclast activity through cytokines such as RANKL and IL-6, causing osteolytic lesions, hypercalcemia, and bone pain. Osteoblast inhibition results in poor bone repair, while bone marrow infiltration leads to anaemia, thrombocytopenia, and immunodeficiency. Epidemiology Most cases occur between the ages of 60 and 70, with a slight male predominance. Higher incidence is reported in individuals of African descent and in patients with pre-existing monoclonal gammopathy of undetermined significance (MGUS). Clinical Features Patients typically present with bone pain (spine, ribs, pelvis), fatigue, recurrent infections, or anaemia. Advanced cases may show renal dysfunction, hypercalcaemia, and pathological fractures. Spinal involvement can cause cord compression and neurological deficits. Diagnostic Criteria (CRAB Features) C – Hypercalcaemia (>11 mg/dL) R – Renal failure (creatinine >2 mg/dL) A – Anaemia (Hb <10 g/dL) B – Bone lesions (osteolytic defects or pathological fractures) Laboratory Findings Serum protein electrophoresis showing an M-spike, Bence–Jones proteinuria, elevated ESR, β2-microglobulin (prognostic marker), and normocytic anaemia. Bone marrow biopsy confirms clonal plasma cell infiltration (>10%). Imaging X-ray: Multiple “punched-out” lytic lesions, diffuse osteopenia, and vertebral collapse. MRI: Detects early marrow involvement and spinal cord compression. PET/CT: Evaluates disease activity, metastasis, and response to therapy. Differential Diagnosis Metastatic carcinoma (breast, lung, prostate), lymphoma, fibrous dysplasia, and hyperparathyroidism (Brown tumor). Treatment Systemic Therapy: Proteasome inhibitors (bortezomib), immunomodulators (lenalidomide, thalidomide), corticosteroids, and autologous stem cell transplantation in eligible patients. Bone Protection: Bisphosphonates or denosumab to reduce skeletal complications. Radiotherapy: Used for local pain control or impending fractures. Surgery: Indicated for pathological fractures or spinal instability; fixation should consider poor bone quality and systemic disease status. Prognosis Median survival ranges from 5–7 years, improved by novel agents and transplantation. Prognosis depends on cytogenetic abnormalities and treatment response. Relapse is common, emphasizing lifelong follow-up. Orthopaedic Relevance Orthopaedic surgeons often first detect myeloma through evaluation of unexplained fractures or lytic bone lesions. Surgical management should be planned after biopsy confirmation and multidisciplinary discussion, prioritizing pain relief and stabilization. Key Points Most common primary malignant bone tumor in adults. Radiographs show characteristic “punched-out” lytic lesions without periosteal reaction. Multimodal therapy combining systemic and supportive care is essential. Orthopaedic intervention focuses on maintaining function and stability. References Rajkumar SV. Multiple Myeloma: 2024 Update on Diagnosis, Risk-Stratification, and Management. Am J Hematol . 2024;99(5):846–865. Terpos E, et al. Advances in the Diagnosis and Management of Myeloma Bone Disease. Nat Rev Rheumatol . 2023;19(1):36–52. Kyle RA, Rajkumar SV. Multiple Myeloma. N Engl J Med . 2004;351(18):1860–1873. Previous Next

Orthoplastics Approach General Principles Soft Tissue Assessment Reconstructive Ladder Timing of Soft Tissue Coverage Principles of Flap Surgery Microsurgery Basics Soft Tissue Coverage Skin Grafts Local Flaps Regional Flaps Free Tissue Transfer Muscle vs Fasciocutaneous Flaps Bone Reconstruction Bone Loss Management Segmental Defects Masquelet Technique Bone Transport Vascularized Bone Grafts Special Considerations Infected Nonunion Complex Limb Salvage Compartment Syndrome Reconstruction Orthoplastic Approach in Open Fractures Amputation & Prosthetic Considerations

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< Back DR. Mutlu COBANOGLU Lumbar Spinal Stenosis Overview Lumbar spinal stenosis is a degenerative disease where the spinal canal in the lower back becomes narrow. This narrowing is usually caused by a mix of bone and soft tissue changes, such as facet joint overgrowth, spondylolisthesis, disc herniation, and thickening or folding of the ligamentum flavum. These changes reduce the space for the spinal nerves, which can compress the cauda equina or nerve roots. The condition most often affects the L4–L5 level and is one of the most common reasons for lumbar spine surgery in patients over 65 years old. Its frequency increases with age, and it is seen slightly more in men than in women. Risk factors include high body mass index, congenital spinal features such as short pedicles, and other degenerative spinal disorders. Diagnosis is mainly made with MRI, which gives detailed information about the central canal, lateral recesses, and neural foramina. Clinical Presentation Patients with lumbar spinal stenosis usually report low back pain that can spread to the buttocks and legs. At first, the pain may be on one side, but it often becomes bilateral as the disease progresses. The key symptom is neurogenic claudication—leg pain, heaviness, or weakness that starts with walking or standing for a long time and improves with sitting or bending forward. This happens because forward flexion opens the spinal canal and foramina. Other typical findings include: ● Pain relief when leaning forward, for example on a shopping cart. ● Negative straight leg raise test in most patients, which helps distinguish it from disc herniation. ● Normal peripheral pulses, which helps separate it from vascular claudication. ● Weakness, numbness, or bladder problems in more advanced cases. ● Symptoms usually disappear while sitting, but return with walking or lumbar extension. Imaging Plain radiographs can show degenerative changes, scoliosis, or spondylolisthesis. Dynamic flexion–extension radiographs provide valuable information in the assessment of spinal instability. CT myelography is only used when MRI is not possible or when MRI results are unclear. MRI is the preferred imaging method for lumbar spinal stenosis. It shows both the severity and the exact location of narrowing. Central canal stenosis is usually defined as a cross-sectional area smaller than 100 mm² or an anteroposterior diameter less than 10 mm. Lateral recess and foraminal stenosis are seen when the perineural fat is lost and the nerve root is directly compressed. Treatment The first approach to lumbar spinal stenosis is nonoperative management. This includes nonsteroidal anti-inflammatory drugs (NSAIDs), structured physical therapy with flexion-based exercises, weight reduction, and lumbosacral bracing. Epidural or transforaminal steroid injections can provide short- to medium-term relief and may delay surgery. Patient education is a key part of treatment. Patients should avoid long standing or walking uphill, pace their daily activities, and use supportive devices when necessary. Regular follow-up is important to detect any progression to neurological problems. Surgical Indications Surgery is considered when symptoms remain severe after 3–6 months of nonoperative treatment, when neurological deficits progress (such as muscle weakness or bladder/bowel problems), or when neurogenic claudication severely limits daily activities. The standard operation is wide pedicle-to-pedicle decompression. This involves removing the thickened ligamentum flavum and part of the medial facet joints to create more space in the spinal canal. If instability is present, for example in degenerative spondylolisthesis, decompression is combined with instrumented fusion. To lower the risk of postoperative instability, more than 50% of each facet joint is preserved whenever possible. Prognosis Surgery usually gives better pain relief and functional improvement than nonoperative treatment, especially in patients with severe neurogenic claudication. Still, recurrence may happen at nearby spinal levels because degenerative changes continue with aging. The long-term outcome depends on the patient’s other health problems, their functional status before surgery, and the amount of decompression performed. Careful patient selection and follow-up are essential to maintain good results. Differential Diagnosis Several conditions can mimic lumbar spinal stenosis and should be considered: ● Vascular claudication – Symptoms get worse with uphill walking or cycling and do not improve with spinal flexion. It is often linked to reduced peripheral pulses. ● Hip osteoarthritis / Hip–spine syndrome – Hip disease can cause pain that overlaps with lumbar stenosis. In cases where both conditions exist, diagnostic hip injections may help identify the main pain source. ● Peripheral neuropathies – Nerve disorders in the legs can produce similar symptoms but are not related to spinal canal narrowing. References 1- Katz JN, Harris MB. Clinical practice. Lumbar spinal stenosis. N Engl J Med. 2008 Feb 21;358(8):818-25. doi: 10.1056/NEJMcp0708097. 2- Zaina F, Tomkins-Lane C, Carragee E, Negrini S. Surgical versus non-surgical treatment for lumbar spinal stenosis. Cochrane Database Syst Rev. 2016 Jan 29;2016(1):CD010264. doi: 10.1002/14651858.CD010264.pub2. 3- Lurie JD, Tosteson TD, Tosteson A, Abdu WA, Zhao W, Morgan TS, Weinstein JN. Long-term outcomes of lumbar spinal stenosis: eight-year results of the Spine Patient Outcomes Research Trial (SPORT). Spine (Phila Pa 1976). 2015 Jan 15;40(2):63-76. doi: 10.1097/BRS.0000000000000731. Previous Next

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