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heme pigment casts and lipid peroxidation from hydroxyl radicals generated
by heme and free iron.
Clinical assessment. Laboratory results reflect the release of myocyte
contents into the blood stream and include elevated serum CK as well as
potential
electrolyte
derangements
such
as
hyperkalemia,
hyperphosphatemia, and hypocalcemia which may occur independently
from AKI but be further exacerbated if renal dysfunction is present. The
severity of rhabdomyolysis ranges from asymptomatic elevations in serum
muscle enzymes to oliguric AKI associated with life-threatening electrolyte
abnormalities. AKI is generally associated with serum CK levels >5,000
units/L although identifying patients at risk for developing renal
complications may be difficult using the initial measurement as the value
may continue to rise if there is ongoing muscle injury. Clinical factors
increasing the risk for AKI at lower concentrations of serum CK include
dehydration, metabolic acidosis, and sepsis.
In the setting of myoglobinuria a urine dipstick will test positive for
heme, but microscopic evaluation will be negative for red blood cells. The
urine sediment may reveal pigmented granular casts and a red to brown
discoloration of the urine supernatant.
Management. The mainstay of therapy for rhabdomyolysis includes early
vigorous hydration to ensure adequate intravascular volume and promote
urine flow. The benefit of high urine flow is the removal of obstructing
pigmented casts, which initiate the cytotoxic insults. Children should be
given IV isotonic saline to ensure adequate renal perfusion. Urine output
should be monitored closely. The IV fluid rate will depend on the urine
flow rate and should be reevaluated regularly to avoid volume excess. A