Crush syndrome ( CS ) is a medical condition that can occur when muscle tissue is severely damaged and releases myoglobin into the bloodstream. Recent studies have advanced our understanding of its pathophysiology and management, which can result in renal failure, cardiac arrhythmias, and even death if not rapidly and adequately managed. The condition can be caused by traumatic injuries, natural disasters, and industrial accidents, and its incidence varies depending on the underlying cause of the injury. Rapid and controlled release of the compressive force, aggressive fluid resuscitation, and electrolyte monitoring are the mainstays of management, but new therapies such as remote ischemic preconditioning and mesenchymal stem cell therapy are emerging. Prognostic factors that can inform clinical decision-making and improve patient outcomes include the extent of muscle damage, the timing and effectiveness of treatment, and the presence of associated injuries or comorbidities. The pathophysiology of crush syndrome is complex and multifactorial, involving a combination of direct tissue damage, toxic effects of cellular components released into the bloodstream, dysregulated immune responses, and activation of various physiological systems such as the renin-angiotensin-aldosterone system (RAAS). Early recognition and rapid, effective management of crush syndrome are essential to prevent its devastating complications.
Dear Readers, We have completed our book thanks to our friends who do valuable studies in the light of science. The concept of health, which continues to be important in every age, has once again revealed its importance with the covid-19 epidemic that has affected the world for the last few years and the earthquake disaster that our country has experienced deeply. We, the healthcare professionals who believe in the continuity of education, think that societies equipped with knowledge and using intelligence and evidence-based knowledge will pass the health exams with much less injury and loss. For this reason, the aim of the book for us is to shed some light on future studies and to illuminate the darkness by warning its readers through the known information and unknowns in it. We hope that our presented book will be easy to understand and will open new horizons for all humanity as well as supporting scientists from faculties of medicine, dentistry, pharmacy and veterinary medicine. I would like to thank the scientists working in the health sciences and our team of authors who supported our book. Dr. Enes Karaman
Mineral bone disease (MBD) is a common complication of chronic kidney disease (CKD) and is characterized by abnormalities in bone and mineral metabolism. Chronic kidney disease- Mineral bone disease (CKD-MBD) encompasses a spectrum of disorders ranging from bone abnormalities such as osteoporosis and osteomalacia to soft tissue calcification, which can lead to cardiovascular disease. The underlying mechanisms of CKD-MBD are primarily linked to deviations in the serum levels of multiple biomarkers, including Fibroblast Growth Factor 23 (FGF-23), klotho, phosphate, calcium, vitamin D, and parathyroid hormone (PTH). Osteoporosis is a particularly significant concern for individuals with CKD as they are at an increased risk of fractures due to alterations in calcium and phosphate metabolism. These changes can lead to bone loss, bone pain, and fractures. Osteoporosis is often asymptomatic until a fracture occurs, which is why screening for bone mineral density is critical. Treatment options for CKD-MBD and osteoporosis may include dietary modifications, medications, and dialysis. Maintaining adequate levels of calcium, phosphate, and vitamin D is crucial to preventing CKD-MBD. Medications such as bisphosphonates, calcimimetics, and vitamin D analogs may be used to prevent bone loss and reduce the risk of fractures. In patients with advanced CKD, dialysis may be necessary to control hyperphosphatemia and secondary hyperparathyroidism. Prevention is key to managing mineral bone disease and osteoporosis in CKD. Patients with CKD should undergo regular monitoring of their bone mineral density and bone metabolism markers. Lifestyle modifications such as weight-bearing exercise, smoking cessation, and limiting alcohol intake may also help to reduce the risk of developing osteoporosis. Overall, early recognition and intervention are essential in managing mineral bone disease and osteoporosis in individuals with CKD.
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