Think of rhabdomyolysis and you'll think of an elevated creatine kinase (CK). The condition ranges from an asymptomatic period to a life-threatening condition with a hugely associated rise in CK which can also be accompanied by electrolyte disturbance, renal failure and disseminated intravascular coagulation.

Rhabdomyolysis is caused by a breakdown in skeletal muscle and occurs most commonly following trauma, very often that can be due to a 'long-lie' when a patient is unable to get off a floor until help arrives after a prolonged period. There are other causes including drugs, muscle enzyme deficiencies, electrolyte abnormalities and more.

The presentation itself is pretty vague and suspicion of the disease needs to be pretty high. Patients can experience weakness, myalgia and the dark'coca-cola urine', the diagnosis is then confirmed with a serum elevation in CK.

The big concern with Rhabdomyolysis is the hit the kidneys take. Acute kidney injury is due to the heme pigment that is released from myoglobin and haemoglobin and is nephrotoxic. Early aggressive fluid rehydration aims to minimise ischaemic injury, increase urinary flow rates and thus limit intratubular cast formation. Fluids also help eliminate excess K+ that may be associated. But have a think about the management in your ED, how high does that CK need to be to require i.v. fluids and admission to hospital?

Here's a few facts we need to know:

Normal CK enzyme levels are 45–260 U/l.
CK rises in rhabdomyolysis within 12hours of the onset of muscle injury
CK levels peak at 1–3 days, and declines 3–5 days after muscle injury
The peak CK level may be predictive of the development of renal failure
A CK level of 5000 U/l or greater is related to renal failure
Optimal fluid rate administration is unclear, some papers suggest replacement of isotonic saline at rates of 1-2L per hour. , adjusted to 200-300mL per hour to maintain a diuresis.
Attention needs to be paid to urine output serum markers and fluid status.

A lot of the evidence and knowledge surrounding rhabdomyolysis is from humanitarian disasters; earthquakes, terrorism along with observational cohorts, but at the end of the day we need to work with what we've got.

Have a listen to the podcast and see what you think, the application of the evidence base may change your practice.

Enjoy!

References

Bench-to-bedside review: Rhabdomyolysis -- an overview for clinicians. Huerta-Alardín AL. Crit Care. 2005

Creatine kinase MB isoenzyme in dermatomyositis: a noncardiac source. Larca LJ. Ann Intern Med. 1981

Epidemiologic aspects of the Bam earthquake in Iran: the nephrologic perspective. Hatamizadeh P. Am J Kidney Dis. 2006

Prognostic value, kinetics and effect of CVVHDF on serum of the myoglobin and creatine kinase in critically ill patients with rhabdomyolysis. Mikkelsen TS. Acta Anaesthesiol Scand. 2005

Rhabdomyolysis: an evaluation of 475 hospitalized patients. Melli G. Medicine (Baltimore). 2005

Serum creatine kinase as predictor of clinical course in rhabdomyolysis: a 5-year intensive care survey. de Meijer AR. Intensive Care Med. 2003

Prevention and treatment of heme pigment-induced acute kidney injury (acute renal failure). Paul M Palevsky. UpToDate. 2015

Rhabdomyolysis

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