RENAL PROBLEMS AND CRITICAL CARE Solution 7

The diagnosis is acute rhabdomyolysis following reperfusion. The ischemic-reperfusion injury causes swelling and destruction of muscle cells, leading to the release of cellular contents into the circulation. The mechanism of injury appears to be calcium influx, free radical generation, disruption of the microcirculation and release of cytotoxic materials and proteases into the local environment. The result is acidosis, hyperkalemia, hyperphosphatemia and a massive increase in circulating myoglobin levels. Ususally myoglobin is reabsorbed by the proximal tubule, and metabolized releasing free iron which is soaked up by glutathione, but in rhabdomyolysis this mechanism is overwhelmed. Free iron generates free radicals, which are nephrotoxic. In addition, in the presence of an acidic urine, myoglobin binds with a renal excretory protein (Tamm-Horsfall) to form a cast which obstructs the tubules and causes acute tubular necrosis.

The diagnosis can be made by measuring serum creatine kinase levels and checking urinary myoglobin (the urine is usually tea coloured).

How do you treat rhabdomyolysis?

The most effective way to treat this problem is to recognize it early: the patient requires aggressive fluid loading. The urinary output is maintained at greater than 100ml/hour until myoglobin negative. Adjunct therapies include using a sodium bicarbonate drip to alkalinize the urine and mannitol to promote a diuresis. Loop diuretics acidify the urine and may worsen the outcome.