Rhabdomyolysis

Introduction

If you break down the word, rhabdomyolysis, its means rod like, muscle and splitting.
The rod like muscle refers to striated skeletal muscle which kind of looks like long rods on microscopy.
So really when you put it all together it literally means the breakdown of skeletal muscles.
This makes perfect sense because rhabdomyolysis is a syndrome characterized by muscle necrosis causing the release of intracellular constituents into the circulation.

Accordingly, the aetiology of rhabdo is really intuitive. Anything that causes injury to muscles can result in this syndrome.

You should consider things like drugs like amphetamines and salicylates , over-exertional states like seizures and Neuroleptic Malignant Syndrome, and trauma, which is usually from falls or long lies.

I always add on statins because it’s a really common drug that is often associated with rhabdo. This actually makes a cute little acronym, “dots”.

Now to understand why you get the clinical features of rhabdomyolysis, you need to understand what’s inside a myocyte and what these components do to the body if you release them suddenly. Myocytes, like other cells, have high levels of certain electrolytes like potassium and phosphate compared to the blood. However, they’re unique in that they utilise myoglobin for oxygen delivery. Moreover, they have high concentrations of creatine kinase which is essential for cellular energy metabolism

Let’s focus on myoglobin for a second. This protein is a close cousin of haemoglobin and has protein or “globin component” and a haeme component. Most the issues of rhabdo come from this second pigmented constituent. In the kidneys, myoglobin is filtered by the glomerulus into the urinary space where the heme pigment is released. This causes an acute kidney injury in three ways:

Firstly, haeme can build up and cause tubular outflow obstruction.
Secondly, it’s cytotoxic which can directly induce tubular epithelial cell injury
Finally, it induces vasoconstriction, which results in renal hypoperfusion.

Bedside:

The first bedside test to think about is an ECG. This should highlight features of hyperkalaemia like tented t waves.

Perform a urine dipstick. Remember there shouldn’t be haemoglobin and red blood cells in the urine but myoglobin. Sometimes this can cause some misleading results depending on the type of dipstick you do. Since you’ve got a urine sample, send it off for a formal MCS.

Bloods:

The first blood test to consider in the emergency department is a VBG so you can quickly see their pH and electrolytes.

Consider other typicals bloods like FBC, EUC, LFTs but don’t forget a CMP!

Think about doing blood cultures if there are any septic features

The most specific test for diagnosis of rhabdomyolysis is a creatinine kinase level. Levels have been shown to correlate with severity. You should expect a CK level of more than 5x higher than the upper limit of normal.

Imaging:

Imaging is probably not necessary unless there is a good indication.

For example, imagine an older person has had a fall, consider doing a CT brain.

For the management of rhabdo, just think about it like a AKI with some extra considerations. There is a great mnemonic for the management of AKIs which is STOPPED

S is for sepsis because you should always think about sepsis as a contributing cause.

T is for toxins because you want to cease any drugs that are going to make the AKI worse like NSAIDs.

O is for outputs and inputs. You want to monitor urine output and also give fluids. Really, the mainstay of therapy for rhabdo is aggressive rehydration to promote renal clearance of released intracellular muscular toxins. One of my clinical supervisors always said that the solution to pollution is dilution. Now this isn’t always true, but probably is for rhabdo.

Both Ps stands for potassium. Hyperkalaemia is extremely important to manage as a priority which is why it gets two letters. There are three steps to managing hyperkalaemia. Firstly, cardiac membrane stabilisation using calcium gluconate. Secondly, shift potassium into cells using insulin and dextrose. Finally, eliminate the potassium definitively by using K+ binders like resonium or diuretics.

E stands for other electrolytes. In the context of rhabo, consider using phosphate binders and calcium replacement.

Finally, D stands for dialysis if necessary.

Common general symptoms include malaise, myalgia, and weakness.

As mentioned before, the patient might have hyperkalaemia from the muscle lysis but also from the AKI. This should make you think about cardiac manifestations like conduction abnormalities causing bradyarrhythmia’s and features like ascending muscle weakness.

Now one thing to remember is that hyperphosphataermia can cause hypocalcaemia. This is because phosphate loves to bind to calcium which can be a problem when there’s lots of it.

Hypocalcaemia should make you consider “SPASM” features like:

Spasms which can be seen when looking for Chvostek’s sign and Trousseau’s sign
Paraesthesias, especially perioral ones
Anxiety
Seizures
Muscle hypertonia

Because of the toxic myoglobin, the patient probably has an acute kidney injury so you would expect low urine output that is concentrated. Importantly, myoglobinuria classically looks like brown dark urine and is sometimes described as being “tea coloured”.

Lets summary everything by putting our mnemonics together.

Rhabdo is caused by DOTS

Present with S5CK SPASM.

And must be STOPPED.

DOTS is our acronym for the causes of rhabdo including drugs, over exertion, trauma and statins

SUCK means serum 5 times higher Creatinine kinase than normal) and spasm are features of hypocalcaemia. Finally, stopped tells us to manage any sepsis first, stopping toxic meds, output and input monitoring, potassium management, electrolyte management and considering dialysis if necessary.