RİSK ALTINDAKİ BÖBREK: EZİLME SENDROMUNA BAĞLI AKUT BÖBREK HASARI

Abstract

Ezilme sendromu, depremler veya diğer yıkıcı afetlerde ölümün ikinci en yaygın nedenidir. Ezilmeyle ilişkili akut böbrek hasarı (ABH), ezilme sendromunun en önemli bileşenidir. Bu nedenle, sağlık profesyonellerinin patofizyoloji, klinik ve laboratuvar özellikleri, komplikasyonlar ve tedavi hakkında bilgi sahibi olmaları büyük öneme haizdir. Ezilme yaralanmalarına ikincil gelişen ABH'nin patogenezi çok yönlüdür. Kompartman sendromuna bağlı hipovolemi ve renal hipoperfüzyon, iskemik akut tübüler nekroza yol açabilen başlıca mekanizmadır. Ayrıca, miyoglobinüri miyoglobin tıkaçlarının ve doğrudan tübüler toksisitenin oluşumuna neden olabilir. Oksidatif hasar, artmış sitokin düzeyleri ve diğer faktörler de patogeneze katkıda bulunabilir. Ezilme sendromu, ciddi elektrolit dengesizlikleri, sepsis ve kanama gibi durumları tetikleyebilir ve bu durum ABH'yi daha da kötüleştirebilir. Erken tanı ve uygun tedavi, agresif hidrasyon ve elektrolit dengesinin yönetimi gibi faktörler, renal hasarı önlemeye veya en aza indirmeye yardımcı olabilir. Bu derleme, ezilme sendromu bağlamında ABH'nin patofizyolojisi, komplikasyonları ve tedavisi hakkında bir genel bakış sunmaktadır.

Keywords

• Ezilme sendromu
• akut böbrek hasarı
• rabdomiyoliz

THE KIDNEY AT RISK: UNDERSTANDING CRUSH SYNDROMERELATED ACUTE KIDNEY INJURY

Abstract

Crush syndrome (systemic manifestations of traumatic rhabdomyolysis) is the second leading cause of death after earthquakes or other destructive disasters. Crush-related acute kidney injury (AKI) is the most important component of crush syndrome, and medical professionals living in disaster-prone regions should know about its pathophysiology, clinical and laboratory features, complications, and treatment. Pathogenesis of AKI on the basis of crush injuries is multifaceted. The most important mechanism is compartment syndrome-related hypovolemia, and consequent renal hypoperfusion, which may result in ischemic acute tubular necrosis. Also, rhabdomyolysis-related myoglobinuria may result in the formation of kidney-damaging myoglobin casts and direct tubular toxicity. Formation of uric acid plugs, oxidant injury, increased serum levels of cytokines, and still many other factors may take a role in the pathogenesis as well. Crush syndrome can cause serious electrolyte imbalances, sepsis, and bleeding, which can further exacerbate AKI. Early recognition and appropriate management, which includes aggressive hydration and management of electrolyte imbalances can help to prevent or minimize kidney damage. This review provides an overview of the pathophysiology, complications, and treatment of AKI in the context of crush syndrome.

Keywords

• Crush syndrome
• acute Kidney injury
• rhabdomyolysis

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