Acute Kidney Injury in Electrical Trauma

Introduction. Electrical burns are a major cause of high mortality and morbidity rates worldwide. The leading cause of death in such cases is usually refractory myoglobinuric acute kidney injury (AKI). Evidence collection. A retrospective informative search was conducted using a spatial–vector descriptive model supplemented by a manual search for relevant articles. Matherials and methods. The scientific literature was found using the search engines Scopus, CrossRef, Google Scholar and PubMed. Evidence synthesis. Victims of electrical trauma frequently develop significant hypovolemia as a result of massive tissue damage caused by extravascular fluid leakage (sequestration), which leads to a further reduction of intravascular volume. Hypovolemia due to extravascular fluid loss may result in prerenal azotemia and acute tubular necrosis, typically aggravated by untimely or insufficient fluid resuscitation. Progressive ischemia in electrical injury, together with edema and tissue necrosis, induces metabolic acidosis, perpetuating a vicious cycle. The renal form of AKI is caused by acute tubular necrosis resulting from renal hypoperfusion, hemolysis, rhabdomyolysis, and inter-fascial compartment syndrome. Three major mechanisms are involved in the pathogenesis of AKI: intrarenal vasoconstriction, formation of hemoglobin or myoglobin casts in distal renal tubules, and the direct cytotoxic effect of myoglobin on nephron endothelium. Rhabdomyolysis occurs in 14–42 % of electrical burn cases. Because the definitions of rhabdomyolysis vary widely, the exact incidence of AKI in rhabdomyolysis is difficult to establish but is estimated to range from 13 % to 48 %. Free myoglobin enters the systemic circulation because of massive skeletal muscle necrosis (rhabdomyolysis) and may lead to pigment-induced acute kidney injury. A blood pH below 7.2 is an indication for bicarbonate infusion until normalization (but not beyond). The only effective treatment for AKI patients with elevated creatinine and potassium levels is renal replacement therapy. Conclusions. The main etiological factor of AKI in electrical injury is the presence of free hemoglobin or myoglobin in the bloodstream. Timely and adequate fluid resuscitation prevents and limits AKI in electrical trauma. The combined use of intermittent and prolonged veno-venous hemodiafiltration represents the optimal methods of extracorporeal detoxification in myoglobinemia.