Core process
Skeletal-muscle breakdown releases creatine kinase, myoglobin, potassium, phosphate and other intracellular contents. Complications may include acute kidney injury, electrolyte emergencies, dysrhythmia and compartment syndrome.
Interactive diagnostic, risk-stratification, treatment and monitoring guidance for emergency clinicians.
Skeletal-muscle breakdown releases creatine kinase, myoglobin, potassium, phosphate and other intracellular contents. Complications may include acute kidney injury, electrolyte emergencies, dysrhythmia and compartment syndrome.
| Finding | Interpretation | Caveat |
|---|---|---|
| CK ≥5× upper limit of normal | Common working definition | Absolute threshold depends on laboratory ULN and clinical context |
| Urine dipstick positive for blood with few/no RBCs | Suggests pigment/myoglobin | Absence does not exclude rhabdomyolysis |
| Hyperkalemia | Potentially immediate lethal complication | Repeat unexpected values and obtain ECG without delaying treatment when unstable |
| Rising creatinine | Renal injury/evolving AKI | Risk depends on multiple variables, not CK alone |
Predicts risk of the composite outcome of renal replacement therapy or in-hospital mortality using admission values. It supports—but does not replace—clinical judgment.
Use the score with renal function, electrolytes, hemodynamics, urine output and overall trajectory.
Published risk bands: scores below 5 were associated with low risk, while scores of 10 or more were associated with substantially higher risk. The original outcome was renal replacement therapy or death—not AKI alone.
Balanced crystalloid or normal saline may be selected based on the patient and local protocol. Reassess frequently. Urine-output goals are individualized; commonly used adult targets are approximately 1–3 mL/kg/hour, capped near 300 mL/hour in trauma guidance.
Routine bicarbonate or mannitol to prevent AKI is not supported by strong evidence. Consider bicarbonate for another clear indication, such as selected severe metabolic acidosis or hyperkalemia.
Early hypocalcemia is often observed without replacement unless symptomatic or needed for cardioprotection in life-threatening hyperkalemia. Rebound hypercalcemia may occur during recovery.
Base dialysis on standard clinical indications—refractory hyperkalemia, severe acidosis, volume overload, uremic complications or progressive renal failure—not CK or myoglobin level alone.
Disposition and therapy should integrate kidney function, potassium, acid-base status, volume status, urine output, cause, comorbidities and follow-up reliability.
Discharge is not defined by one universal CK cutoff. Consider clinical stability, normal or improving renal function/electrolytes, controlled etiology, oral hydration, functional status, reliable follow-up and the likelihood of rebound or delayed toxicity.
Reference links are provided for professional education. Follow current local protocols, specialist guidance and patient-specific clinical judgment.
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