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Lindee Abe, ARNP
We just did a post about DOMS, so let’s explore muscle breakdown a little bit further. Next up….let’s talk rhabdomyolysis. Most of us don’t see rhabdomyolysis. The military is one environment that comes to mind that sees increased numbers of rhabdomyolysis, specifically exertional rhabdomyolysis. We also read about the elderly being at higher risk due to medication, decreased kidney function, and inability to tolerate hot environments. Let’s take a look at what this condition is, how to spot it, how to treat it, and how to prevent it.
What is Rhabdomyolysis?
To try and make it as simple as possible, it is the breakdown of muscle fibers from skeletal muscle. This break down of muscle causes a cascade of several substances into the blood stream, such as potassium, myoglobin, phosphate, and creatinine kinase. The problem this creates is the release of myoglobin into the blood stream that can then precipitate in the kidney during filtration and cause an obstruction. Myoglobin is nephrotoxic and the combination of that with hypovolemia causes a hypoperfusion of the kidneys. There are many underlying conditions that can cause this destruction of skeletal muscle, including exertional activity, heat-related illness, electrical shock, trauma, infection, inflammation, endocrine conditions, and genetic metabolic conditions. As you can see, this is a pretty extensive list. The key principle is that if a condition can cause ischemia to muscle or damage to muscle, then it has the potential to cause rhabdomyolysis.
Blunt trauma and crush injuries cause rhabdomyolysis. Trauma can also necessitate a fasciotomy for relief of symptoms. Less common conditions that have the potential to cause rhabdomyolysis include neuroleptic malignant syndrome and malignant hypothermia. The most commonly thought of bacteria related to causing rhabdomyolysis is Legionella. There are several viruses that can cause rhabdomyolysis that include HSV, west nile virus, HIV, CMV, EBV, and influenza A & B.
There are also several medications that would increase a patient’s risk of developing rhabdomyolysis through direct myotoxicity, including corticosteroids, HMG-CoA reductase inhibitors, colchicine, zidovudine, erythromycin, colchicine, itraconazole, and cyclosporine. Statins are most commonly associated with muscle toxicity. The actual risk of developing rhabdomyolysis from statins alone is low. Patients who take both statins and cytochrome P450 inhibitors are at increased risk.
What does it look like clinically?
It can present in numerous ways. The textbook patient presentation everyone learns in school includes muscle weakness, muscle aches, and tea-colored urine. In reality this occurs in about 10% of patients. The muscle weakness and pain is not always present, with the dark urine being a more common reason patients will present for evaluation. Additional symptoms that can occur with rhabdomyolysis include fever, nausea/vomiting, tachycardia, and fatigue. The complication that every provider should be thinking of with a patient they suspect as having rhabdomyolysis is acute renal failure, as this will occur in one third of the patients.
Additional complications include disseminated intravascular coagulation (DIC) and multi-organ failure. It is important to consider this diagnosis in patients who have elevated phosphate or aspartate transaminase on their lab work. Rhabdomyolysis can cause both of these markers can be elevated. Patients can present with nonspecific symptoms.
The gold standard test used for diagnosis of rhabdomyolysis is a serum CK level. The diagnostic criteria for rhabdomyolysis is a CK five times the upper limit of normal. This level is also based on gender, activity level, and race. In general, any CK level above 1,000 IU/L is suggestive of rhabdomyolysis. Kidney damage can be seen with CK levels above 5,000 IU/L. Myoglobin levels can also detect rhabdomyolysis. After injury, myoglobin (6-8 hours) has a shorter half life when compared to CK (approximately 36 hours). Additional lab abnormalities that can occur include elevated potassium, coagulopathies, decreased calcium (elevated calcium later on in the disease process).
Treating Rhabdomyolysis
The primary treatment for rhabdomyolysis is fluid resuscitation. Rhabdomyolysis causes a hypovolemic state in the patient that requires correction with aggressive fluid resuscitation. The most common method of fluid resuscitation is normal saline at a rate of 1.5 L/hr. Another treatment protocol includes alternating 500 mL of saline with 500 mL of 5% glucose solution with 50 mmol sodium bicarbonate every 2-3 L of solution. Regardless of the method of resuscitation, the goal is a urine output of 200 mL per hour. This goes along with the goal of a urine pH greater than 6.5 and plasma pH less than 7.5. Aggressive fluid resuscitation should continue until myoglobinuria has stopped or the patient develops oliguria. If the patient develops oliguria, then hemodialysis is an additional treatment modality. Quick fluid resuscitation is more likely to be effective in preventing oliguria.
There has been some discussion about the use of mannitol, but there is no definitive evidence that is effective and may have additional complications. Diuretics are generally discouraged. Don’t correct hypocalcemia unless the patient is symptomatic. Calcium levels will naturally increase later in the disease course with fluid resuscitation and recovery, so treating it too early can cause hypercalcemia later in the recovery.
Can rhabdomyolysis be prevented?
In certain cases, there are modifiable factors that patients can use if they have a history of rhabdomyolysis. Obviously, if rhabdomyolysis is due to trauma, infection, or electrical injuries it would be hard to prevent those etiologies. Some risks (medications, heat-related illness, or exercise-induced causes) can be prevented. Some suggestions for preventing exertional rhabdomyolysis include gradual acclimatization with activity and gradually increasing the intensity of the activity, drinking sufficient fluids during activity, resting as needed during exercise, and consuming adequate calories for activity level.
The risk for developing rhabdomyolysis from hot environments can be mitigated by limiting exposure. These patients should be monitored for signs and symptoms of heat related illness. They should also avoid hot environments when ill, have an area to cool off during breaks, and increase fluid intake. Discontinue medications that cause rhabdomyolysis. Consider alternate therapy that may provide similar results without the side effect of rhabdomyolysis. Take caution in patients with a history of muscular dystrophy. This Is especially true when using certain anesthetic agents, specifically succinylcholine.
There’s a lot to know about rhabdomyolysis and this was just a quick review. If you are working in the summer months with patients who exert themselves, this should be a diagnosis in your list of differentials. Consider rhabdomyolysis as a cause of muscle breakdown.
References:
Sauret, J., Marinides, G., & Wang, G. (2002). Rhabdomyolysis. Am Fam
Physician. ;65(5):907-913.
Torres, P. A., Helmstetter, J. A., Kaye, A. M., & Kaye, A. D. (2015). Rhabdomyolysis:
pathogenesis, diagnosis, and treatment. The Ochsner journal, 15(1), 58–69.
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