Metabolic acidosis in rhabdomyolysis: Pathophysiological mechanisms

Rhabdomyolysis is defined as a syndrome which occurs after damage/breakdown (lysis) of skeletal muscle cells. The causes of rhabdomyolysis can be divided into natural and unnatural. Large quantities of breakdown products of damaged muscle cells, including proteins, especially myoglobin (Mb), phosphorus, potassium, uric acid, etc., are released into the bloodstream. These products may be harmful and are responsible for a number of clinical symptoms and disturbances in laboratory tests observed in rhabdomyolysis. Metabolic acidosis (MO), with an increased anion gap, is one of the main complications of rhabdomyolysis. The causes of MO are an increase in endogenous acid, hyperkalemia and acute renal failure (ARF). The latter is perhaps the most serious clinical consequence of rhabdomyolysis, the severity of which depends on the severity of the rhabdomyolysis. The main pathophysiological mechanisms responsible for ARF are renal vasoconstriction, tubular obstruction, the toxicity of Mb and lipid oxidation.