Adams Outline Of Fractures Pdf 40 !!BETTER!!
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Osteoporosis is the most common bone disease in humans, representing a major public health problem. It is more common in Caucasians, women, and older people. Osteoporosis is a risk factor for fracture just as hypertension is for stroke. Osteoporosis affects an enormous number of people, of both sexes and all races, and its prevalence will increase as the population ages. It is a silent disease until fractures occur, which causes important secondary health problems and even death (Figure 1) (2).
Bone tissue is continuously lost by resorption and rebuilt by formation; bone loss occurs if the resorption rate is more than the formation rate. The bone mass is modeled (grows and takes its final shape) from birth to adulthood: bone mass reaches its peak (referred to as peak bone mass (PBM)) at puberty; subsequently, the loss of bone mass starts. PBM is largely determined by genetic factors, health during growth, nutrition, endocrine status, gender, and physical activity. Bone remodeling, which involves the removal of older bone to replace with new bone, is used to repair microfractures and prevent them from becoming macrofractures, thereby assisting in maintaining a healthy skeleton. Menopause and advancing age cause an imbalance between resorption and formation rates (resorption becomes higher than absorption), thereby increasing the risk of fracture. Certain factors that increase resorption more than formation also induce bone loss, revealing the microarchitecture. Individual trabecular plates of bone are lost, leaving an architecturally weakened structure with significantly reduced mass; this leads to an increased risk of fracture that is aggravated by other aging-associated declines in functioning. Increasing evidence suggests that rapid bone remodeling (as measured by biochemical markers of bone resorption or formation) increases bone fragility and risk of fracture.
Vertebral fractures might occur during daily chores without any trauma or fall, and they are the predictors of future fracture risk: the probability is fivefold for subsequent vertebral fractures and twofold to threefold for fractures at other sites (14, 15).
Ibandronate is another BP used for the prevention and treatment of postmenopausal osteoporosis, which has proven efficacy in reducing the risk of spinal fractures of postmenopausal women suffering from osteoporosis, but it is not proven in reducing non-vertebral or hip fractures except for higher-risk subgroup. Ibandronate has been studied in trials of up to 3 years and its efficacy and safety beyond 3 years is not known (43).
Raloxifene has been shown to reduce the risk of fractures of the spine in women with postmenopausal osteoporosis, but its efficacy in reducing non-vertebral or hip fractures has not been demonstrated. Increases in hot flushes are contraindicated in fertile women and those who have had venous thromboembolic disease (46).
Denosumab (human monoclonal antibody against RANKL) is used in the treatment of postmenopausal women at a high risk of fracture, patients having a history of osteoporotic fractures, or patients who have failed or are intolerant to other available osteoporosis therapies. It has been shown to reduce the risk of fractures of the spine, hip, and non-vertebral sites. Hypocalcemia must be corrected before the initiation of therapy. Serious infections, dermatitis, rashes, and eczema may occur. ONJ has been reported; drug discontinuation is suggested with severe symptoms. Efficacy and safety beyond 6 years with denosumab have not yet been established (49).
Pathologic fractures occur secondary to altered skeletal physiology and mechanics in the setting of a benign or malignant lesion. Therefore, proper diagnosis, staging, and treatment of pathologic fractures are essential to improve patient outcomes. This activity reviews the evaluation and treatment of pathologic fractures and highlights the role of the interprofessional team in managing patients with this condition.
Objectives:Review the common symptoms and physical exam findings associated with pathologic fractures.Outline the approach to the staging workup for the causative lesion resulting in a pathologic fracture.Summarize the surgical approach to fixation for pathologic fractures based on anatomic location and healing potential.Explain the importance of collaboration and communication amongst the interprofessional team to improve outcomes for patients affected by pathologic fractures.Access free multiple choice questions on this topic.
Pathologic fractures represent a growing concern in the field of musculoskeletal oncology. The incidence of pathologic fractures is rising, primarily due to improved diagnosis and treatment of metastatic disease leading to prolonged survival. Therefore, diagnosis of the causative pathology is of paramount importance in the successful treatment of a pathologic fracture and is a prerequisite for proceeding with surgical intervention. Pathologic fractures occur through areas of weakened bone attributed to either primary malignant lesions, benign lesions, metastasis, or underlying metabolic abnormalities, with the common factor being altered skeletal biomechanics secondary to pathologic bone.
The majority of neoplastic pathologic fractures are caused secondary to metastatic disease rather than primary bone tumors. In a patient 40 years of age or older, the likelihood that a pathologic fracture through an unknown lesion that is metastatic is 500 times more common than the likelihood of it being a primary bone sarcoma.[1] There are five recognized carcinomas that most frequently metastasize to bone, including lung, breast, thyroid, renal, and prostate. The most common sites for skeletal metastasis include the spine, proximal femur, and pelvis.[2][3] Primary bone sarcomas occur far less frequently, though disregarding the possibility that a pathologic fracture through a solitary bone lesion could be the first evidence of a primary sarcoma could lead to catastrophic consequences, including loss of life or limb.
Osteolytic lesions of bone occur secondary to tumor-induced activation of osteoclasts by upregulation of RANK ligand.[7] Osteoblastic lesions occur secondary to endothelin 1, which is secreted by the tumor.[8] Pathologic fractures occur through these lesions due to altered biomechanics. For example, a lytic lesion or open-section defect might produce a stress concentration that cannot withstand normal or low-demand activity.[9]
Pathologic fractures can be preceded by lesions producing prodromal pain or can be indolent until the time of fracture. Patients may or may not report B symptoms, including unintentional weight loss, fevers, etc. Patients may also report symptoms specific to the particular primary carcinoma, such as urinary abnormalities with renal cell carcinoma or shortness of breath and/or cough with lung carcinoma. Patients may additionally report symptoms of hypercalcemia of malignancy, which could masquerade as mild confusion and gastrointestinal abnormalities to cardiac arrhythmia and renal failure.
Physical exam should include a focused assessment of the extremity or a spinal exam when warranted. Careful attention should be paid to neurovascular examination, though the compromise is uncommon in pathologic fractures of the extremities.
Radiological analysis of pathologic fractures begins with orthogonal radiographs of the fracture site and the involved bone in its entirety. A plain radiograph is the single most important imaging modality and provides the most information about a pathologic lesion. There are a number of aggressive features suggestive of a pathologic lesion that may be identified on X-ray, which include: lesion diameter > 5 cm, cortical interruption, periosteal reaction, and associated pathologic fracture. A chest radiograph should also be obtained. Computed tomography (CT) of the chest, abdomen, and pelvis with oral and intravenous contrast should be obtained for staging purposes. Whole-body bone scintigraphy should also be obtained. Bone scans are particularly useful for identifying osteoblastic activity. If laboratory analysis has confirmed the diagnosis of multiple myeloma, a skeletal survey may be obtained in lieu of a bone scan, which might fail to identify the degree of osteolysis present in other sites. This comprehensive strategy is the gold standard and is successful in identifying the origin of the lesion in 85% of cases.[10]
An impending fracture is a biomechanically weakened area of bone that has a propensity to fracture with far less force than would be required for the normal bone to fracture due to the pathophysiology of the underlying lesion. For instance, normal weight-bearing through a pathologic lesion could tip the scales towards a pathologic fracture due to the biomechanical fragility of the surrounding bony architecture. Impending fractures may require prophylactic fixation, meaning surgical intervention in the form of internal fixation prior to a fracture event as a means of augmenting inherently weak bone and preventing future failure.
Pathologic fractures may occur secondary to benign lesions, metastasis, primary bone lesions, or metabolic bone abnormalities. Treatment of pathologic fractures is dictated by the pathophysiology of the causative lesion and the expected survival.
There are particular considerations for implant choice. Titanium implants are typically used in benign fractures because they are MRI-compatible, allowing for future imaging with less artifact than stainless steel. Biomechanically, titanium is more similar to the normal bone than stainless steel in terms of the modulus of elasticity. In pathologic fractures, however, the surrounding bony architecture is inherently weaker than normal bone and may, in certain cases, require stainless steel implants, which are stronger than titanium but preclude future advanced imaging due to increased artifact. More recently, carbon fiber implants have become an area of interest due to their radiolucency, improved fatigue strength, and modulus of elasticity that is more similar to the normal bone than any metal. A study by Zimel et al. compared carbon-fiber-reinforced polyetheretherketone (CFR-PEEK) with titanium intramedullary nails. There was significantly less implant artifact on MRI associated with carbon fiber implants compared with titanium.[20] 2b1af7f3a8