Rhabdomyolysis

The protocol for Rhabdomyolysis:

Rhabdomyolysis

 

Let’s break it down!

Let’s face it, Rhabdomyolysis is way overlooked.  Only about 26,000 cases are reported in the US annually, but soldiers are at a particularly high risk of developing it.  Whether it’s because of a crush injury, tourniquet, burn, snake bite, or blunt trauma, there are plenty of reasons why soldiers would develop this dangerous condition 

What does “Rhabdomyolysis” mean? 
When you break down the term, it’s defined like this: Rhabdo (striated) + myo (muscle) + lysis (breakdown).  Anything and everything that can lead to the breakdown of skeletal muscle (crush injuries, burns, exercise, etc.) is fair game for Rhabdomyolysis.  You may hear people refer to it as developing “Rhabdo” 

What exactly is it?
Rhabdomyolysis is really a cascade of events following muscle breakdown that leads to several different electrolyte and protein level abnormalities (creatine kinase, calcium, etc.).  For the sake of simplicity, I’ll focus your attention on just 2 of the important ones:

1. Myoglobin: the breakdown of muscle leads to the release of these oxygen-carrying proteins into the bloodstream (where they don’t belong).  The myoglobin then physically accumulates within the renal tubule system and leads to kidney damage/failure 

2. Potassium: the breakdown of cells within the muscles causes a release of potassium from the cells into the bloodstream, which can lead to a fatal cardiac arrhythmia 

The diagnosis of rhabdomyolysis is confirmed by an elevated creatine kinase (an enzyme released from damaged muscle) greater than 5x the upper limit of normal.  However, access to lab equipment for a solid diagnosis might be unrealistic for most austere medics.  Instead, rhabdomyolysis can be suspected using good clinical judgment.

For example, anybody with a history of crush injuries, excessive exercise, tourniquet application, burns, poisoning, etc. should already be suspected of having it.  The big 2 signs/symptoms that would push you towards a firm diagnosis include:

  • Myalgia (Muscle Pain) or weakness: Occurs in a little less than 50% of all cases, usually in the thighs, calves, and lower back.  This makes sense because typically, these are the most utilized muscles during exercise.

 

  •  Tea-Colored Urine: Also often referred to as “Coca-Cola urine”.  This is a classic sign of myoglobin build-up in the urine.  Although not as common as most people think (only seen in about 10% of cases), it’s considered to be a slam dunk if you’re already suspecting rhabdomyolysis.

 

Some other signs/symptoms, mostly caused by dehydration, include:

  • Fever 
  • Malaise (general feeling of discomfort)
  • Nausea/Vomiting  
  • Oliguria: low urine output (less than 500mL in 24 hours)
  • Anuria: No urine output or less than 100mL in 24 hours

 

If you do happen to have some urine dipsticks around, you can dip one of these bad boys into a cup of the patient’s urine and look for a positive “blood” test.  Although there typically aren’t any actual red blood cells in the urine, the test picks up myoglobin the same way it picks up hemoglobin. For more information on urinalysis dipstick tests, click here

 

 

 

 

 

The cornerstone treatment for rhabdomyolysis is simple: aggressive fluid resuscitation.  This accomplishes two things:

  • Helps “flush out” myoglobin   Generous intravenous fluid boluses will help maintain renal function and prevent myoglobin deposition in the kidneys

  • Rehydrates the patient  In cases of rhabdomyolysis, a substantial amount of fluid in the intravascular space shifts into the damaged muscles, which can be noted by increased muscle swelling  As a result, patients can be profoundly dehydrated and will benefit from intravenous fluid boluses.

Since hyperkalemia is a potential issue for Rhabdo patients, normal saline is preferred over lactated ringers.  If all you have is lactated ringers, it will still work! The potassium content in lactated ringers is only 4 mEq/L, which is still less than a patient with hyperkalemia (5.1 to 7.0mEq/L)

Titrating to urine output is the gold standard because it definitively proves adequate kidney function and rehydration.  The best way to measure it is with a foley catheter.  If you don’t remember how to put one in, these videos will help:

 

From the urinalysis dipstick, you may find that the pH of your patient’s urine is low (ex. 5.5 or 6.0); indicating acidosis.  In general, this is problematic because metabolic acidosis can worsen cast formation in the kidneys.  “Urinary alkalinization” refers to the idea of administering a basic substance, such as Sodium Bicarbonate (pH of 8.4), to make the blood/urine for alkaline.

The problem with urinary alkalinization is that there isn’t a whole lot of evidence backing it up.  No large randomized control trials show that urinary alkalinization is superior to early aggressive hydration.  Also, sodium bicarbonate can drop serum calcium concentrations significantly, causing hypocalcemia

So should you do it? It’s not globally recommended, but it’s worth keeping in your bag of tricks.

This is a video of a gentleman setting up a standard 40mEq ampule of sodium bicarbonate.  For urinary alkalinization, you would just empty this into a 500mL bag and run at 100ML/hr until the patient’s urine pH at least 6.5.

As we discussed earlier, hyperkalemia is a very dangerous complication of rhabdomyolysis.  But would you be able to tell if the patient is hyperkalemic?  If you had blood lab capabilities, then you could very easily quantify the amount of potassium in a patient’s blood (Normal is 3.5 – 5.0 mEq/L and hyperkalemia would typically be from 5.1 – 7.0mEq/L).

Another way to identify hyperkalemia, which is probably more feasible for austere medics, is to utilize a cardiac monitor.  Since high potassium levels affect the electrical conduction of the heart, there are certain EKG changes that we can expect.  Without getting too far in-depth into cardiology, the TWO signs of hyperkalemia that you would look for is peaked T-waves and/or a widened QRS.  The images help show the difference:

 

Normal Sinus Rhythm (no potassium abnormalities)

Image result for normal sinus rhythm

 

Hyperkalemia ECG changes (begins with peaked T waves and progresses into a widened QRS):

Related image

 

A basic 4-lead ECG is all you need to identify the changes.  Once discovered, that’s your green light to treat with Sodium Bicarbonate and Calcium Gluconate.  This is how they both work:

  • Sodium Bicarbonate: Lowers the serum potassium levels by facilitating the shift of potassium from the bloodstream back into the muscle cells, where they belong (evidence of effectiveness, however, is controversial)

 

  • Calcium Gluconate: This doesn’t actually lower potassium levels, but instead normalizes the gradient between threshold potential and resting membrane potential.  In other words, high potassium levels aren’t as big of a shock to the heart when calcium levels are also high 

 

Both of these drugs have a rapid onset.  You’ll notice the EKG normalize within a matter of minutes following administration.  Below is a fascinating video showing how fast these treatments work:

As we discussed earlier, sodium bicarbonate has a tendency to drop serum calcium levels (one of the many reasons urinary alkalinization is generally avoided).  If you see signs of hypocalcemia, just stop the sodium bicarbonate infusions.  The video below shows a patient with classic perioral tingling and muscle tetany symptoms induced by hypocalcemia.

The overall prognosis of rhabdomyolysis is favorable as long as it is recognized and treated promptly.  However, the mortality for these patients is still approximately 5%, so these are not patients we want to hold on to. Our treatment is not necessarily different than what they might provide at an ER, the patient has the potential to go into full renal failure.  This could require dialysis, among other things, which is not something we can provide out in the field or at a Role 1 aid station. Thus, an Urgent evacuation is warranted. Once full treatment is initiated, it can take anywhere between a few weeks to a few months for the patient to fully recover.

 

Good luck out there!

 

References

Brandon Simpson, PA-C
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