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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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< Back Dr. Özcan KAYA He was born in 1983. Following his pre-undergraduate studies, he began his medical education at Istanbul University's Istanbul Faculty of Medicine in 2001 and earned his MD in 2007. He completed his residency at Istanbul University's Istanbul Faculty of Medicine and became an Orthopedics and Traumatology Specialist in 2013. During his residency, he served as a spine surgery observer at Thomas Jefferson University & Rothmann Institute, one of the leading spine clinics in the United States, examining patients and participating in surgeries. He continues to practise at Istanbul Biruni Hospital. For more info, visit https://drozcankaya.com.tr/ Spine ozcankaya.md@gmail.com Previous Next

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< Back Alper DUNKI Musculoskeletal Infections and Microbiology Spot Knowledge Staphylococcus aureus is the leading cause of MSK infections. MRSA strains (community vs hospital) differ in virulence. Children 6 mo–4 yrs: Kingella kingae is most common. Sickle cell disease: Salmonella is typical pathogen. Implant infections: Biofilm formation → requires debridement. MRI is nearly 100% sensitive in early osteomyelitis. Epidemiology & Microbiology Main pathogens: S. aureus , S. epidermidis, coagulase-negative staphylococci. Gram-negative: E. coli, Proteus, Klebsiella, Enterobacter . IV drug users: Pseudomonas, Serratia, fungi . Gonococcal arthritis: Neisseria gonorrhoeae in young adults. Post-shoulder surgery: Propionibacterium acnes . Pathogenesis Synovium lacks basement membrane → easy microbial entry. S. aureus virulence factors: Protein A, polysaccharide capsule, biofilm, PVL toxin. Biofilms protect bacteria in prosthetic joint infection → need surgery + antibiotics . Clinical Findings Septic arthritis: monoarticular, knee most common. Kocher criteria (peds): fever, non-weight bearing, ESR >40, WBC >12,000. Osteomyelitis (peds, MRSA risk): fever >38°C, Hct <34%, WBC >12,000, CRP >13. Diagnosis Radiology: joint space narrowing, periosteal reaction, Codman’s triangle. MRI: gold standard, early detection. Lab: CRP, ESR monitoring. Synovial fluid: WBC >50,000, >90% PMN highly suggestive. Treatment Osteomyelitis: 4–6 wks (≥6 for MRSA). Septic arthritis: 3–4 wks. Adults empiric: Vancomycin + Ceftriaxone. Children (MRSA): IV Vancomycin (15 mg/kg q6h). Implant infection: add Rifampin (synergy vs biofilm). C. difficile must be considered in prolonged antibiotic use . Antibiotic Prophylaxis in Orthopaedics Not routine in elective surgery without implants. Give ≤1 h before incision (Vanco: 2 h prior). 1st line: cephalosporins. Clinda/Vanco for β-lactam allergy. Duration: ≤24 h. Prevention of Surgical Site Infection Risk factors: DM, obesity, malnutrition, smoking, RA, MRSA colonization. Measures: chlorhexidine prep, double gloving, monofilament sutures, drains <24h, normothermia, glycemic control. Periprosthetic Joint Infection Knee arthroplasty: Synovial WBC >2,500/mm³ or >90% PMN → chronic infection. Gram stain not useful. Atypical & Rare Infections Necrotizing fasciitis: S. pyogenes, CA-MRSA; urgent surgery. Gas gangrene: Clostridium spp., surgery + high-dose PCN/Clinda. TB: spine most common, 4-drug ≥6 months. NTM: M. marinum (hand infections post-water exposure). Vibrio vulnificus: severe necrotic infection after seawater. Candida albicans: rare prosthetic infection. Lyme (Borrelia): late monoarthritis. HIV/AIDS: optimize immunity pre-surgery . References Masters EA, et al. Nat Rev Microbiol . 2022. Touaitia R, et al. Antibiotics . 2025. Sanpera I, et al. Current Concepts in Septic Arthritis . 2024 . Previous Next

< Back Open Fracture Management Open fractures require urgent assessment, debridement, and staged fixation to minimise infection and optimise outcomes. Galeazzi fracture is a distal radial shaft fracture with dislocation of the distal radioulnar joint (DRUJ). Internal fixation of the radius and assessment of DRUJ stability are essential. open-fracture Previous Next