For some reason, the college loves rhabdomyolysis. Many questions either ask about it directly, or expect it as one of the differentials. Typically, the candidate is presented with a biochemistry panel strongly suspicious of rhabdomyolysis (eg. raised CK, LDH, potassium) as well as a history suggestive of some sort of crush injury or limb ischaemia. They are then asked to explain the mechanism, list the features, and describe their management.

Previous SAQs on this topic include the following:

• Question 1 from the first paper of 2020
• Question 5 from the first paper of 2017
• Question 6.2 from the second paper of 2012
• Question 12 from the first paper of 2010
• Question 16 from the first paper of 2008
• Question 24 from the first paper of 2007
• Question 4 from the first paper of 2004
• Question 1 from the first paper of 2002

Probably the best resource for something like this would be this UpToDate article. However, one must acknowledge the possibility that the CICM trainee will be unable to pay (or ideologically opposed to paying) a subscription fee to the Wolters Kluwer infohemoth, in which case some excellent freely available resources could be pointed out. One standout example is the 2002 article by Vanholder et al. Another is a 2016 systematic review by Chavez et al, 

Causes of rhabdomyolysis

A nice NEJM article has within it a comprehensive table (Table 1).

It has been rearranged into a familiar framework:

Mechanisms of kidney injury in rhabdomyolysis

In brief summary, these are the cardinal pathophysiological events in rhabdomyolysis:

This has been asked about in Question 30 from the second paper of 2014. The multiple mechanisms which lead to acute kidney injury in rhabdomyolysis are well described in this excellent article. It would probably be counterproductive to digress extensively on this minor topic in this summary.

Manifestations of rhabdomyolysis

This has been examined in Question 16 from the first paper of 2008, and to a lesser extent in Question 1 from the first paper of 2020

• Historical features: Trauma, seizures, immobility, drug exposure
• Symptoms:- muscle pain, decreased mobility, weakness, tea-coloured urine
• Signs: Muscle compartment swelling, tenderness, weakness, fever
• Biochemistry: Elevated CK, AST, LDH, urinary myoglobin; renal dysfunction and electrolyte abnormalities (particularly hyperkalemia, hypocalcemia, hyperphosphataemia, hyperuricemia, lactic acidosis). DIC may also result.
• Imaging: CT or MRI evidence of muscle oedema; ultrasound evidence of decreased compartment perfusion.

Management of rhabdomyolysis

Chavez et al (2016), in theire review of management strategies for rhabdomyolysis, have presented the following conclusions:

• Commence IV fluids within 6 hours - as early as possible
• Aim for a urine output greater than 300ml/hr
• Use of sodium bicarbonate is only indicated to correct systemic acidosis. There is no evidence for any benefit in rhabdomyolysis-induced AKI except for some uncontrolled case series, which does not stop people from recommending it anyway. It appears in the 2010 college answer, which pre-dates this 2013 meta-analysis. The savvy trainee seeking to remain in the good books with examiners who use forced alkaline diuresis will want to mention this therapy in their answer, with the caveat that it is may not be helpful, but is also probably not harmful.
• Free radical scavengers have been recommended historically, without much evidence to support their use (allopurinol, pentoxifylline)
• Avoid replacing calcium: it may exacerbate muscle injury (Chatzizisis et al, in 2008, believed that it would "intensify the accumulation of calcium in the muscular tissue and consequently reinforce the mechanism of rhabdomyolysis")
• Use of mannitol is only indicated if urine output >300ml/hr cannot be maintained 
• Dialysis may be commenced to improve the removal of myoglobin, if a high-permeability membrane filter is available. Even if it is not, standard CVVHDF seems to decrease the risk of renal injury.