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6 tubular obstruction precipitation of myoglobin casts alterations in glomerular filtration rate myoglobin toxicity treatment is volume expansion mannitol or normal saline maintain urine output at 200 to 300 ml hr hypotension crystal formation alkalinize urine with na bicarbonate protease release from muscle avoid nephrotoxic agents hyperkalemia due to muscle breakdown; renal failure treatment calcium gluconate; diuresis hypocalcemia due to binding by damaged muscle hyperphosphatemia hypercalcemia due to release from muscle; reduced renal excretion treatment diuresis hyperphosphatemia tissue calcification due to release of organic inorganic phosphates from muscle treatment diuresis disseminated intravascular coagulopathy laboratory urine dip stick benzidine positive myoglobin; hemoglobin; hematuria negative porphyria myoglobin urine precedes rise in ck visible pigmentation with level 1 g l testing radioimmunoassay; use urine fresh neutralized urinalysis pattern albumin heme with few rbcs serum normal levels 3 to 80 g l rhabdomyolysis high serum ck very high 20,000; up to hundreds of thousands half life 1 to 3 days serum lactate glycogenoses no rise with exercise mitochondrial disorders rise with minimal exercise serum carnitine low in -oxidation disorders, especially during attack muscle biopsy required for diagnosis in most hereditary disorders pathology scattered muscle fiber necrosis degeneration metabolic analysis perform at least 1 month after episode biopsies performed near time of rhabdomyolysis will give spurious biochemical results mri with gadolinium enhancement increased signal; t 2 t 1 treatment maintain airway circulation prevent acute tubular necrosis normal saline iv 10 to 15 ml kg; continue if adequate urine output isotonic sodium bicarbonate mannitol 0.

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