emDocs Cases: Evidence-Based Recommendations for Rhabdomyolysis

Author: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX) and Michael Gottlieb, MD, RDMS (EM Attending Physician, Rush Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Welcome back to emDocs Cases! Today we have case-based discussion on a core EM topic, with a look at some controversy and cutting-edge treatments.

A 28-year-old male presents with diffuse myalgias, dark urine, and nausea for 3 days. He recently started drastically increasing his workout regimen, with crossfit and spin classes. Though these symptoms have been occurring for 3 days, he has continued to exercise, but feels his workouts have not been normal. What could be going on?

What is rhabdomyolysis?

Rhabdomyolysis is a disease that exists along a spectrum. It is due to striated muscle damage that causes release of myoglobin, creatine kinase (CK), lactate dehydrogenase, and electrolytes (1-5). The normal myocyte, or muscle cell, is regulated by Na+/K+and Na+/Ca2+pumps on the cell membrane. We’ll try to avoid those medical school flashbacks, but briefly, damage to striated muscle and/or decreased ATP availability results in electrolyte imbalances across the cell membrane and abnormal cell membrane permeability, causing Na+and Ca2+influx (1-3,6-10). This results in increased intracellular water content, destruction of cellular attachments, and cell death. Intracellular contents (K, Ca, Na, Phos, myoglobin, and CK) are released into the serum. Myoglobin is a normal part of muscle, but with excess serum levels, it can precipitate in and damage the kidneys through renal tubule obstruction and production of granular casts, oxidative mechanisms, and vasoconstriction (9-16).

What causes rhabdomyolysis?

There are acquired and inherited etiologies for rhabdomyolysis. In the U.S., the most common causes are overexertion, drug intoxication, and immobility (9-21).  Most cases, about 75%, are due to acquired causes, with many patients have over 2 risk factors for the disease (1,2,15,22,23). Exertional rhabdomyolysis occurs with a variety of sports and exercises, with an incidence approaching 30 cases per 100,000 patient-years (24,25). This form is usually benign, with very low rates of complications (1-5,26). Non-exertional forms are associated with inherited etiologies (genetic disorders/myopathies), elderly patients with immobility, temperature changes, medications, infections, and others. These forms are associated with worse outcomes and increased complication rates (1-5,27). Patients with recurrent episodes, recurrent muscle cramps with exercise, or positive family history of muscular or genetic disorder or rhabdomyolysis may have a genetic cause (27-31).

Statins are associated with rhabdomyolysis, especially in older patients on other predisposing medications. Though close to 10% of patients experience myalgias on a statin, the actual risk of rhabdomyolysis is low (1-2 cases for every 100,000 patients on a statin) (30,31).

What should you look for on history and exam?

Some patients may have no to mild symptoms, while others may experience renal failure, hyperkalemia and other electrolyte abnormalities, dysrhythmias, liver function abnormalities, and even disseminated intravascular coagulation (DIC) (1-5,22,32-40).  For history, focus on risk factors, family history, medication use, urine changes (color and output), and prior episodes of similar symptoms.  The classic triad is acute/subacute myalgias, transient muscle weakness, and dark urine, but like most “classic” triads, these are present concurrently in less than 10% of cases (1-5,22,36). The most common symptoms are muscle pain in > 80%, weakness in > 70%, and muscle swelling in 8%, though these may not occur at the same time (36,41,42). The proximal legs are most often affected. Pediatric patients may have fever or a viral prodrome (21). Urine changes depend on many factors such as the patient’s muscle mass, severity of injury, urine concentration, and renal function (6-8,22,35-37). Less than 5% of patients may have dark colored urine (2,21,36).

The patient has never had this before, and he denies any family history of rhabdomyolysis or genetic/myopathic disease. He states the pain is worse in his proximal legs. He feels his workouts have been worse due to weakness in his legs. He states his urine may be darker.

 What tests should you obtain?

Tests focus on diagnosis and potential complications. CBC, electrolytes (including phosphorus and calcium), renal and liver function tests, CK, uric acid, urinalysis, and ECG are recommended (1,34,39,44-47). Clinicians must evaluate for hyperkalemia with patients with suspected or diagnosed rhabdomyolysis. Abnormalities on testing may include hyponatremia, hyperkalemia, hypo- or hypercalcemia, elevated liver enzymes, elevated serum creatinine, hyperphosphatemia, and metabolic acidosis (1,34,39,44-47). Elevated serum creatinine suggests acute kidney injury (AKI). Hypocalcemia is more common in the initial stages with intracellular influx, followed by hypercalcemia with cell death. Coagulation panel may show findings of DIC (1-5,27-40).

CK is your test of choice for diagnosis, with a threshold of 5X the upper limit of normal (1,000 IU/L) (4,5,46-49). CK will increase 2-12 hours after injury, peak at 24-72 hours, and decline over 5-10 days (41,48,49). Patients with chronic muscle diseases or genetic conditions may have chronically elevated CK levels. For these patients, compare the new CK level with their baseline level (36,50). Uric acid may elevate before serum CK (50).

What about serum myoglobin? It has a half-life of 3 hours and normalizes within 6-8 hours. This results in poor sensitivity, and thus cannot be relied upon for diagnosis (4,47,50,51). Whether myoglobin can predict AKI is inconclusive. Currently, myoglobin is not routinely needed.

Myoglobin is filtered in the urine, which results in moderate to large blood on urinalysis with no to few RBCs on urine microscopy (3,49,52).  A positive dipstick for blood displays sensitivity of 41% for diagnosis (53). Myoglobinuria should also not be relied on, with a wide specificity ranging from 15-91% (51). Thus, do not rely on urine for diagnosis, and do not exclude rhabdomyolysis with a normal urinalysis.

You order ECG, CBC, renal and liver function panels, coagulation panel, uric acid, and urinalysis. His urinalysis shows blood but no RBCs. The CK returns at 52,000 IU/L, and his creatinine is 2.2.  His potassium returns at 5.1 and phosphorus at 5.6, but otherwise his electrolytes and ECG are normal.

What complications can occur? 

Renal injury is common with rhabdomyolysis, with up to 45% of patients demonstrating elevated serum creatinine (1-5,36). Despite this, few patients experience anuric renal failure or require dialysis, especially those with exertional rhabdomyolysis. Severe rhabdomyolysis is associated with renal failure, most commonly due to acute tubular necrosis obstruction of renal tubules (due to myoglobin and granular casts) (1,2,22,27,32-40). As urine pH becomes more acidic, myoglobin has a greater chance of precipitating and obstructing the renal system (4,37).  Hyperkalemia and hyper- or hypocalcemia may cause dysrhythmia. Even the liver can be affected, with close to 25% of patients displaying liver dysfunction (1,34,39,44,45). DIC from coagulation pathway activation is a severe complication (1-5).

Is the peak CK level associated with risk of AKI?

This is a controversial… While AKI is common, the association with the peak CK level and incidence of AKI is controversial (1-5,36,50). A meta-analysis suggests CK levels may be correlated with AKI in crush injuries, but CK levels are not predictive of AKI in other etiologies of rhabdomyolysis (36,50). The real question centers on the patient’s renal function at the time of diagnosis, as creatinine is a predictor of mortality. Patients with AKI may have a risk of mortality reaching over 20% (54).

How do you manage rhabdomyolysis?

Treatment is comprised of two items: 1) addressing the underlying etiology and 2) managing rhabdomyolysis and any complications (1-4,36,47). Underlying etiologies such as hyper- or hypothermia, infection, arterial occlusion, toxicologic, etc. must be treated. IV fluid with goal urine output of 250-300 mL/hour is your treatment of choice for rhabdomyolysis (1-4,36,47). Either balanced solutions (lactated Ringer’s, plasmalyte, etc.) or 0.9% normal saline can be used in the initial stages of rehydration (3,52,55). One study comparing normal saline and lactated Ringer’s found no difference in serum potassium or CK clearance (55). However, after the first several liters of NS, consider switching to a balanced crystalloid due to the risk of hyperchloremic metabolic acidosis with NS, which may reduce urinary clearance of myoglobin (27).

Bicarbonate and Mannitol

Rhabdomyolysis is associated with decreased urinary pH, which further results in myoglobin precipitation and obstruction (4,36,48). Sodium bicarbonate and mannitol have been previously used in rhabdomyolysis. Sodium bicarbonate is thought to improve renal excretion of myoglobin and reduce the acidity of urine, while mannitol is an osmotic diuretic that increases renal blood flow, decreases renal cast formation, and acts as a scavenger of free-radicals (3-6,27,48,56,57). However, there is no randomized controlled trial evidence that demonstrates additional benefit in decreasing acute renal injury, dialysis, or death with sodium bicarbonate or mannitol when compared to aggressive fluid rehydration. Mannitol can actually worsen renal perfusion if it is administered before the patient is resuscitated (3,4,36,58,59).

Loop Diuretics

Loop diuretics, like furosemide, have also been used for forced diuresis. However, this has not demonstrated benefit when compared to fluid resuscitation alone, and loop diuretics can worsen urine acidosis (27,36,50). Evidence does not demonstrate improved mortality, need for dialysis, or hospital length of stay with furosemide in patients with acute renal injury and rhabdomyolysis.

Renal Replacement Therapy

Renal replacement therapy (RRT), especially continuous renal replacement therapy (CRRT), may be needed in patients with elevated creatinine and life-threatening electrolyte derangements (1-5,15). The need for RRT ranges from 4-20% in cases of rhabdomyolysis (15,61,62). CRRT removes myoglobin and other inflammatory molecules and is associated with more stable hemodynamics (63,64). Based on a Cochrane review, CRRT does not improve mortality, but it does improve serum Cr, BUN, and potassium (64). If the patient has severe electrolyte changes or evidence of renal failure, consult nephrology to get the ball rolling for RRT (64).

You order 1 L of normal saline for rehydration and encourage him to drink oral fluids as well, but you decide to avoid sodium bicarbonate, mannitol, and furosemide for now. 

What’s the disposition?

Disposition is not always clear cut. Many patients will need admission for rehydration and to evaluate for complications. Despite this, exertional rhabdomyolysis is usually benign, with most patients recovering with no long-term injuries (24-26,65-68). A patient with mild symptoms; clear etiology; normal vital signs, kidney function, and electrolytes; and able to take in oral fluids may be discharged with follow up (24-26,65-68). Patients with an uncertain cause of rhabdomyolysis, renal injury, electrolyte changes, and prior episodes of rhabdomyolysis should be admitted for treatment and further evaluation. Those with prior episodes can benefit from testing for an underlying myopathy or genetic condition.

There are several tools available to help you predict complications and need for RRT. One rule from McMahon et al. utilizes patient characteristics, the etiology, and laboratory findings (62). Patients with a score < 5 had a 2.3% risk of death or RRT, while those with scores > 10 demonstrated a 61.2% risk.

Other scores use laboratory data such as LDH, Cr, and uric acid levels on multiple days, and thus are not useful in the ED (69,70).

You discuss the diagnosis and disposition options with the patient, as well as your findings of acute kidney injury and electrolyte abnormalities. This is his first episode of rhabdomyolysis, and though you feel you have determined the etiology, you plan to admit the patient due to his symptoms, elevated Cr, and electrolyte abnormalities. The patient agrees with the plan.

Key Points

– Rhabdomyolysis is due to striated muscle breakdown and release of intracellular contents: potassium, calcium, phosphate, uric acid, and creatinine kinase.

– There are a wide variety of etiologies that can be classified as acquired or inherited, or exertional and non-exertional forms. Many patients have multiple risk factors.

– Patients often have non-specific symptoms such as myalgias and weakness. Urine changes are not definitive.

– Diagnosis includes elevated CK. Serum and urine myoglobin should not be relied on for diagnosis. Serum Cr at time of diagnosis may be associated with risk of mortality.

– Treatment focuses on managing the underlying cause and fluid resuscitation, targeting a urine output of 250-300 mL/hr.

– Bicarbonate, mannitol, and loop diuretics do not improve outcomes based on the literature.

– RRT may be needed in those with severe renal injury or electrolyte abnormalities.

– Discharge is dependent on the etiology, patient, and electrolyte abnormalities. 

References/Further Reading

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2 thoughts on “emDocs Cases: Evidence-Based Recommendations for Rhabdomyolysis”

  1. Nice review. A few points from the Nephrology side of things:

    – CRRT may clear some myoglobin if convection is used (as opposed to pure dialysis/diffusion). However, this is not clinically significant and therefore does not change outcomes. Renal replacement therapy should be reserved for traditional indications.

    – Loop diuretics does not help clear toxins, but help manage volume overload. Excess volume, especially in AKI, is a associated with mortality. I push a lot of loops to avoid overload.

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