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Rhabdomyolysis after exercise with an electrical muscle stimulator

Estes, Mary Ellen Zator, MSN, FNP-BC, NP-C, FAANP

doi: 10.1097/01.NPR.0000544286.79459.19
Department: Clinical Case Report

Mary Ellen Zator Estes is an NP in internal medicine at PMG Jay C. Tyroler, MD, PC, Fairfax, Va., and a nurse consultant, Vienna, Va.

The author has disclosed no financial relationships related to this article.

Ms. R, a 45-year-old woman, presented to the NP at the local urgent care center with a 3-day history of bilateral arm pain that started soon after she participated in vigorous exercise using an electrical muscle stimulator (EMS) device. The patient finished 25 minutes of exercise wearing an EMS device that delivered an electric current during her workout. Ms. R later lifted weights and noted that her arms were more sore than usual. The following day, Ms. R noted bilateral arm swelling with her left arm more swollen than the right. She said her left arm looked to be twice its normal size (she did not take a photo). In addition, Ms. R complained of intermittent paresthesia in both hands.

Ms. R denied muscle twitching, hand-arm incoordination, uncontrolled movement of her arms, and discolored urine. Ms. R's physical exam demonstrated a left upper arm that was mildly enlarged and bigger than her right upper arm. Her extremities were warm and dry with brisk capillary refill. Bilateral radial pulses were 2/4+, and deep tendon reflexes of her upper extremities were 1-2/4+; upper extremity strength was 5/5. There were no skin changes or lesions on the arms, and the remainder of the exam was within normal limits (WNL). The patient's ECG showed normal sinus rhythm without any T wave changes. Ms. R had a history of seasonal allergies and took loratadine 10 mg as needed. The remainder of her history was noncontributory. Lab tests were done while Ms. R was at the urgent care center. (See Stat lab results.)

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Introduction

Rhabdomyolysis is a serious and potentially life-threatening condition caused by the breakdown of skeletal muscle. Traumatic and nontraumatic etiologies lead to the rapid destruction and cell necrosis of skeletal muscle and the release of the muscle contents into the circulation. Pathology can affect selected body areas or the entire body. An individual can be asymptomatic but still harbor the risk of progressing to clinically significant pathology, including hypovolemia, severe electrolyte imbalance, acute kidney injury (AKI), and acute kidney failure. Rhabdomyolysis is the cause of 10% to 55% of all cases of AKI.1,2

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Causes

Rhabdomyolysis can occur in individuals of any age; however, the majority of cases occur in adults.3 The cause of rhabdomyolysis is broad and diverse. Causative factors of rhabdomyolysis can be divided into two categories: traumatic and nontraumatic (see Traumatic causes of rhabdomyolysis and Nontraumatic causes of rhabdomyolysis).6 Males, Blacks, children under the age of 10, adults older than age 60, and the morbidly obese are at a higher risk of developing rhabdomyolysis.2

The unifying mechanism of traumatic causes is an external insult to the body. Traumatic causes of rhabdomyolysis and the severity of the external insults that can trigger onset can stem from sudden catastrophic events such as a crush injury and lightning strike, to commonplace events such as a bee sting. With the popularity of high-intensity workouts, the risk of rhabdomyolysis increases due to the exertional stress placed on the body.

Conversely, nontraumatic etiologies of rhabdomyolysis can occur due to medical conditions, such as sepsis or viral infections, or the ingestion of substances, such as cocaine or excessive alcohol ingestion, and also from prescription medications such as HMG-CoA reductase inhibitors (statins).1

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Pathophysiology

A traumatic or nontraumatic situation triggers the onset of the cascade of events that cause damage to muscle cells or myocytes. The damaged skeletal myocytes swell, which leads to cell membrane rupture. The myocytes then expel their intracellular contents into the peripheral circulation. Contents from the skeletal muscles that affect the body most acutely in rhabdomyolysis include the protein myoglobin and the creatine kinase (CK) enzyme.

These elements can be detected in the blood, and myoglobin can also be found in the urine. In addition, hypovolemia can result from fluid shifts in the body due to the movement of fluids from the intravascular space into interstitial spaces. The fluid shift can occur at a single location, such as the injured area or systemically.

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Clinical presentation

The triad of severe myalgia, muscle weakness, and dark urine (dark red, brown, or tea colored) are associated with rhabdomyolysis. In addition, muscle stiffness, swelling, and point tenderness may be present. Electrolyte imbalance may lead to malaise, nausea, vomiting, abdominal pain, fever, oliguria, anuria, tachycardia, and altered mental status. Additional signs and symptoms may occur depending on the cause of the rhabdomyolysis.

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Diagnostic testing

The hallmark lab feature of rhabdomyolysis is an increased CK level. The normal CK value is less than 200 U/L and the CK level increases to five times that of the normal upper limit in rhabdomyolysis.2,21 CK values can run in the thousands, and in extreme trauma, even over 100,000 U/L. Higher values indicate more muscle damage. The CK level rises 2 to 12 hours after the injury, peaks in 3 to 5 days, and decreases in 3 to 10 days.2,21,22 Skeletal muscle or CK-MM subtype (isoenzyme found in muscle tissue) comprises 95% of the total CK value in rhabdomyolysis. The cardiac CK-MB subtype (isoenzyme found in cardiac tissue) rises in rhabdomyolysis but comprises less than 5% of the total CK value.23

The comprehensive metabolic panel (CMP) may reveal hyperkalemia. It is important to remember that there is an expulsion of intracellular muscle contents, including potassium, in rhabdomyolysis. If left undiagnosed and untreated, this hyperkalemia can lead to cardiac arrest. Hyperphosphatemia may be caused by the release of phosphorus from the injured skeletal muscle. With hyperphosphatemia, hypocalcemia may occur as calcium enters damaged muscle cells. In severe cases, hypocalcemia can lead to cardiac rhythm disturbances.

Hyperuricemia, caused by purine release from the skeletal muscle injury, can lead to urate crystal formation in renal tubules leading to obstruction and AKI. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase can also be elevated even though they are more specific for liver damage. In addition, the erythrocyte sedimentation rate and C-reactive protein can be increased in some patients with rhabdomyolysis, especially traumatic causes. The white blood cell count in the complete blood cell (CBC) count may be elevated in infectious etiologies of rhabdomyolysis. Metabolic acidosis must be suspected if there is an elevated serum anion gap.

Table

Table

The urinalysis may show myoglobinuria. Myoglobin is a small molecule in both weight and size. Under normal conditions, the healthy kidney can filter the myoglobin without difficulty. In rhabdomyolysis, the excessive quantity of excreted myoglobin released from skeletal muscles is filtered through the kidneys and leads to renal tubular obstruction. Myoglobin precipitates and forms casts that further clog the glomerular filtration. This cascade of events progresses into AKI if not treated promptly.

Myoglobin is visibly seen as the reddish- to brown-colored urine. The reddish color of the urine should not be confused with hematuria, as there are no red blood cells (RBCs) in the urine. On microscopic analysis, no RBCs are seen in the urine. Myoglobinuria will decrease and return to its preinjury level within 1 to 6 hours.23 Hematuria may be present if the kidneys directly suffered an assault. Proteinuria may also be present with rhabdomyolysis due to the expulsion of proteins such as myoglobin from the damaged skeletal muscles.

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Complications

Complications of rhabdomyolysis seen predominantly in the early phase of the condition include fluid and electrolyte imbalances, cardiac dysrhythmias, cardiac arrest, compartment syndrome, hypovolemia, and metabolic acidosis. Severe cases of rhabdomyolysis can lead to acute tubular necrosis that can progress to kidney failure, requiring dialysis or hemofiltration. Disseminated intravascular coagulation is a rare complication of rhabdomyolysis.

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Treatment

There are currently no consensus guidelines that define the treatment of rhabdomyolysis.24 The treatment for rhabdomyolysis is dictated by its etiology and the severity of the condition with the goal of preserving kidney function and preventing severe adverse conditions. Mild cases of rhabdomyolysis can often be treated on an outpatient basis. Removal of the cause of the rhabdomyolysis, such as discontinuing a medication or halting strenuous exercise, coupled with rehydration (such as with a commercial sports drink or electrolyte replacement product) may be sufficient.

In cases of more severe rhabdomyolysis, treatment may be needed at an intermediate care center or ED. An I.V. infusion of 0.9% sodium chloride is sufficient to sustain a desired urine output of 200 to 300 mL/hr.2,21,23 Serum lab values and the ECG should be monitored. I.V. or oral sodium bicarbonate may be given to alkalinize the urine to prevent cast formation in the renal tubules. Sodium bicarbonate can also be given to treat metabolic acidosis. I.V. mannitol and furosemide are often used to increase urine output and prevent AKI despite the lack of evidence-based research that demonstrates improved morbidity and mortality with their use.2,21,22

The most severe cases of rhabdomyolysis require expert medical care and monitoring, necessitating hospitalization. ICU monitoring for severely injured patients or those with preexisting cardiac or renal conditions may be necessary. Active fluid resuscitation may also be necessary to stabilize the patient. Monitoring of kidney function is paramount in preventing kidney failure. Limbs must be monitored for compartment syndrome and a fasciotomy should be performed if indicated before limb necrosis occurs.

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Electrical muscle stimulators

The FDA is responsible for protecting the health of the general public by assuring the safety and efficacy of drugs, biological products, and medical devices such as an EMS device.25 An EMS device is used frequently in physical therapy and rehabilitation, primarily in patients who experience a stroke, serious injury, or major surgery.

In EMS therapy, an electrode is placed on the body part to be stimulated, and an electric impulse is delivered to that area. The muscle contracts when receiving the stimulation. Repeated stimulation can lead to improvement in range of motion and muscle tone. EMS treatments are also used to prevent muscle atrophy, relax muscle spasms, and build strength in injured areas.26

In addition, an EMS device is used as an adjunct in physical exercise regimens. These devices can be used at home or during the course of commercial exercise programs at designated facilities. Some EMS devices target a specific body area such as the abdominal muscles.27-30 According to the FDA, “no EMS device [has] been cleared at this time for weight loss, girth reduction, or for obtaining ‘rock hard’ abs... without the addition of diet and regular exercise,” despite the claims of many EMS companies.26

Adverse reactions such as shocks, burns, bruising, skin irritation, and pain have been reported with EMS devices. Thus, EMS devices should be avoided by patients who are pregnant, those with pacemakers and implantable defibrillators, and those with skin diseases or patches of abnormal skin. Caution needs to be exercised in patients with diabetes mellitus and avoided in areas with peripheral vascular disease and peripheral neuropathy.26

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Discussion

Ms. R engaged in a workout regimen despite not exercising on a regular basis prior to using an EMS device. The overexertion coupled with using the EMS device led to traumatic rhabdomyolysis. Considering that Ms. R did not seek medical attention for 3 days, it is almost certain that her CK values would have been higher if her serum level had been drawn 24 to 48 hours earlier. In addition, it is possible that she may have experienced some early stages of compartment syndrome due to the size of her limbs and paresthesia of her hands.

When the extremely elevated CK level was reported to the NP, Ms. R was contacted and directed to the local ED where she received a 2 L 0.9% sodium chloride I.V. infusion. She was instructed to take a teaspoon of sodium bicarbonate daily and to refrain from all exercise. An office visit 2 days later showed Ms. R's CK level decreased to 9,876 U/L, AST to 153 U/L, and ALT to 77 U/L. A follow-up appointment was scheduled for Ms. R 3 days later, but she canceled it and did not return to the office.

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Implications for practice

NPs possess expert history-taking and advanced physical exam skills. These skills are essential when dealing with patients with rhabdomyolysis. It is difficult to establish specific health history questions because the etiologies of rhabdomyolysis vary so greatly. For example, the direction of the history and physical exam employed in the burn victim experiencing rhabdomyolysis is vastly different from the patient with rhabdomyolysis due to statin use. The key is to recognize the rhabdomyolysis triad when present and conduct a focused patient history and focused physical exam with the goal of preventing AKI, acute kidney failure, and other complications.

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Conclusion

Information regarding the risk of rhabdomyolysis should be shared with any patient who chooses to use an EMS device and those who engage in an EMS exercise program. EMS should be avoided in high-risk individuals. Rhabdomyolysis needs to be considered as a differential diagnosis in cases of extreme physical exertion when muscle pain is present, whether or not an EMS device is used. Rapid identification and treatment of rhabdomyolysis lead to a more favorable prognosis.

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Traumatic causes of rhabdomyolysis4-12

  • Extreme muscle strain, overexertion, or excessive physical activity
  • Muscle compression necrosis from prolonged immobilization or coma
  • Third-degree burns, including lightning and electrical shock
  • Crush injury
  • Physical abuse
  • Ischemic limb injury
  • Snake venom, insect bites, and bee stings
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Nontraumatic causes of rhabdomyolysis13-20

  • Medications (such as statins, fibrates, levofloxacin, antipsychotics, Parkinson medications, isoniazid, colchicine, retrovir, cyclosporine, itraconazole, erythromycin, sitagliptin, lamotrigine)
  • Substance use (excessive alcohol use, amphetamines, barbiturates, benzodiazepines, heroin, cocaine, lysergic acid diethylamide, phencyclidine, synthetic cannabinoid)
  • Hyperthermia and heat stroke
  • Hypothermia
  • Malignant hyperthermia triggered by inhaled volatile general anesthetics and succinylcholine
  • Status epilepticus
  • Metabolic disorders
  • Muscle disorders such as Duchenne muscular dystrophy and McArdle disease
  • Inflammatory myopathies such as polymyositis and dermatomyositis
  • Severe infections/sepsis
  • Severe hypothyroidism
  • Severe dehydration
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