A 22 year old, normally fit and well young man presented to the ED 24 hours following a strenuous exercise class with generalised myalgia and ‘coca-cola’ coloured urine following the consumption of diclofenac. No systemic symptoms. No history of any regular or recreational drug use.
His observations were T 36.5oc, BP 115/84, HR 65, pO2 100% RA, RR 12, and on examination the abdomen was soft with mild tenderness over the lower abdomen and quadriceps which was reproducible on exertion. No other findings on examination.
This refers to the breakdown of striated muscle fibres and the release of potentially toxic muscle enzymes, myoglobin and intracellular constituents such as potassium and calcium into the systemic circulation. Biochemically it is defined as an acute increase of creatinine kinase to more than five times the upper normal limit where the fraction of CK-MB is <5% (thereby excluding an MI). Referred to as the ‘hidden killer’ with a mortality of 5%, the consequences of rhabdomyolysis can be fatal due to hypovolaemia, hyperkalaemia, metabolic acidosis, acute renal failure and disseminated intravascular coagulation (DIC) that ultimately results from the intracellular damage caused by abnormal circulation of intracellular contents and the subsequent activation of calcium dependent proteases and lipases. Unfortunately, its presentation is often very non-specific and its incidence is therefore underestimated. The most common presenting symptoms however are myalgia and coca-cola coloured urine, which is caused by myoglobinuria (myoglobin >250ng/ml, which corresponds with >100mg of muscle breakdown). This presents with a urine positive dipstick for haem (blood) but without red cells on urine microscopy.
In general, the treatment of rhabdomyolysis centres around identification and treatment of the cause and supportive monitoring and treatment of associated complications (acute renal failure/ hyperkalaemia/ DIC) until CK returns to normal levels.
Acute renal failure is the most common complication of rhabdomyolysis and affects 30-40% of patients. Its management forms the mainstay of rhabdomyolsis treatment with intravenous fluids, which support intravascular volume and thereby improve renal function and urinary excretion of creatinine kinase, whilst also diluting myoglobin and other renal toxins. Haemodialysis or filtration may be required in some cases, especially if associated with hyperkalaemia. Hyperkalaemia itself is treated with calcium salts, insulin and dextrose, whilst DIC is treated with FFP, cryoprecipitate and platelets. These complications can lead to arrhythmias and even death and therefore warrant urgent treatment.
In this particular case, the patient is most likely to be suffering from exercise induced rhabdomyolysis, and requires monitoring of renal function, electrolytes and clotting function with administration of intravenous fluids until CK returns to normal. Investigations to rule out other causes of rhabdomyolysis such as metabolic and immunological disorders are often advisable.
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