We often worry about patients developing rhabdomyolysis and consequently developing AKI. However, there is much debate and little consistency in the published data, over how to diagnose and who needs admission to treat. So its important to consider both clinical context along with laboratory values

Causes of Rhabdomyolysis

  • Muscle ischaemia (e.g.)
    • Crush injuries/Direct trauma
    • Falls with or without immobilisation (most frequent cause in elderly)
    • Immobilisation
    • Seizures
    • Exersize
    • Limb Ischaemia
  • Medication induced (e.g. statins, amphetamine, cocaine, neuroleptics, alcohol)
  • Temperature extremes (most commonly hyperthermia)
  • Sepsis
  • Electrolyte disturbance (hypernatraemia, hypokalaemia, hypophosphataemia)
  • Genetic (generally muscular dystrophies, or those causing electrolyte problems)

Clinical Triad

Although often quoted, it is often hard to establish esp. in elderly patients, that have been on the floor for some time after a fall, and is not always present.

  • Myalgia
  • Muscle weekness
  • Dark Urine

What the evidence shows

  • Age is the biggest risk in developing AKI – a CK of 5000U/l in an elderly patient holds the same risk as 25000U/l in a young adult [1]
  • Myoglobinuria (can be seen as blood on urine dip) is pathognomonic – it is not predictive enough to be used as a rule out (too many false negatives)[2]
  • No universally agreed Cut-off for Creatinine Kinase (CK) level [2]
  • Peak CK seems to be related to risk of AKI (but poorly except crush injury)[2]
  • Peak CK on average happens at about 17hrs – but can take upto 53hrs from the time of muscle damage [1,2]

Creatinine Kinase (CK)

The most commonly used definition in the literature for rhabdomyolysis is CK of 5x upper limit of normal OR 1000U/l. However, this may be used as part of the diagnostic criteria it doesn’t predict who is at risk of developing serious consequences such as AKI. [2]

There seems to be some consensus that ‘peak CK’ values of over 5000U/l, indicate an elevated risk of developing AKI. However, in children and older patients that there is evidence we should be using 3000U/l. [1,3]

Requires treatment

  • Under 16 or 50 yrs and over: CK over 3000U/l require admission for treatment
  • 16 to 49 yrs: CK over 5000U/l require admission for treatment

However ‘peak CK’ occurs 17-53 hrs after injury!


CK below threshold in ED

Most of the available data state that initial CK is of little prognostic value, there is some evidence that if your CK is <1000U/l at presentation it is unlikely to reach a significant level [3]. However there is no great data and senior input is advised.

If you feel the patient requires further monitoring, fluid replacement would be recommended

  • Need speciality admission for other reasons – can be monitored by admitting team
  • No requirement for admission – could have a repeat CK done at 17hrs post injury on CDU (Older patients will likely need a frailty assessment, younger patients will likely have a significant mechanism of injury we would like to observe)

Useful investigations

Look for the cause of rhabdomyolysis to treat plus:

  • FBC
  • U&E & Blod gas – Hyperkalaemia & help monitor renal function
  • Calcium & Phosphate – both of these have been shown to be predictors of mortality. Hypocalcaemia (esp <2.1mmol/l) indicates poor prognosis, as does elevated phosphate levels (>1.2mmol/l however, this is within the reference range)[4]
  • Urine Dip – myoglobin in urine, shows up as erythrocytes on dipstick (neither sensitive nor specific)
  • ECG – risk of arrhythmia
  • ISS (injury severity scale) – guess what the worse the injury the higher the risk!

Treatment in ED

Treat the cause of rhabdomyolysis and stop any precipitants e.g. statins

The following is aimed at promoting excretion of myoglobin to prevent accumulation and AKI.

  • 0.9% sodium chloride @ 10-15ml/kg/hr to achieve high urinary flow rates >100ml/hr
  • Sodium bicarbonate 1.26% to maintain urinary pH> 6.5 (under specialist input)

The patient’s volume status must be carefully evaluated and once the patient has been adequately fluid resuscitated care must be taken not to precipitate pulmonary oedema.



  1. Byerly S, et al. Peak creatinine kinase level is a key adjunct in the evaluation of critically ill trauma patients. The American Journal of Surgery 214 (2017) 201e206
  2. Stahl K, et al. A systematic review on the definition of rhabdomyolysis, Journal of Neurology. 2019 Jan
  3. Talving P, et al. Relationship of creatine kinase elevation and acute kidney injury in pediatric trauma patients. J Trauma Acute Care Surg. 2013;74:912e916.
  4. Baeza-Trinidad R, et al. Creatinine as predictor value of mortality and acute kidney injury in rhabdomyolysis, Internal Medicine J. 2015;45(11):1173-8.

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