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INTRODUCTION — Rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle constituents into the circulation. Creatine kinase (CK) levels are typically markedly elevated, and muscle pain and myoglobinuria may be present. The severity of illness ranges from asymptomatic elevations in serum muscle enzymes to life-threatening disease associated with extreme enzyme elevations, electrolyte imbalances, and acute kidney injury.
The clinical manifestations and diagnosis of rhabdomyolysis will be reviewed here. The causes of rhabdomyolysis; the clinical features and diagnosis of acute kidney injury due to rhabdomyolysis; the management of patients with rhabdomyolysis, including methods to prevent acute kidney injury and related metabolic complications; and the prevention and management of acute compartment syndrome are discussed in detail separately. (See "Causes of rhabdomyolysis" and "Clinical features and diagnosis of heme pigment-induced acute kidney injury" and "Prevention and treatment of heme pigment-induced acute kidney injury" and "Crush-related acute kidney injury (acute renal failure)" and "Acute compartment syndrome of the extremities".)
CLINICAL MANIFESTATIONS — Rhabdomyolysis is characterized clinically by myalgias, red to brown urine due to myoglobinuria, and elevated serum muscle enzymes (including creatine kinase [CK]) . The degree of muscle pain and other symptoms varies widely. Rhabdomyolysis associated with viral infection is discussed in further detail separately. (See "Overview of viral myositis".)
Symptoms — The characteristic triad of complaints in rhabdomyolysis is muscle pain, weakness, and dark urine [2-5]. However, more than half of patients may not report muscular symptoms ; by contrast, occasional others may experience very severe pain. Muscle pain, when present, is typically most prominent in proximal muscle groups, such as the thighs and shoulders, and in the lower back and calves [2,5]. Other muscle symptoms include stiffness and cramping.
Additional symptoms that are more common in severely affected patients include malaise, fever, tachycardia, nausea and vomiting, and abdominal pain . Altered mental status may occur from the underlying etiology (eg, toxins, drugs, trauma, or electrolyte abnormalities).
Physical findings — Muscle tenderness and swelling may be seen, but detectable muscle swelling in the extremities generally develops, when it occurs, with fluid repletion. Such swelling is much less common on hospital admission . Muscle weakness may be present, depending upon the severity of muscle injury. Limb induration is occasionally present. Skin changes of ischemic tissue injury, such as discoloration or blisters, may also be seen but are present in less than 10 percent of patients [5,6].
Laboratory findings — The hallmark of rhabdomyolysis is an elevation in CK and other serum muscle enzymes. The other characteristic finding is the reddish-brown urine of myoglobinuria, but because this may be observed in only half of cases, its absence does not exclude the diagnosis. Routine lab tests, including complete blood count (CBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP), vary greatly depending on the underlying cause of rhabdomyolysis. Infections and crush injuries are associated with marked elevation of the acute phase reactants and peripheral white blood cell (WBC) count, while these markers of inflammation would likely be normal or only minimally raised in patients with other etiologies, such as drug-induced or electrolyte derangements .
Creatine kinase — Serum CK levels at presentation are usually at least five times the upper limit of normal, but range from approximately 1500 to over 100,000 international units/L. The mean peak CK reported for each of a variety of different causes and for patients with both single and multiple causes ranged from approximately 10,000 to 25,000 in the largest series ; exceptions were the three patients with malignant hyperthermia, whose values averaged almost 60,000.
The CK is generally entirely or almost entirely of the MM or skeletal muscle fraction; a small proportion of the total CK may be from the MB or myocardial fraction. The presence of MB reflects the small amount found in skeletal muscle rather than the presence of myocardial disease. Elevations in serum aminotransferases are common and can cause confusion if attributed to liver disease. (See "Muscle enzymes in the evaluation of neuromuscular diseases".)
The serum CK begins to rise within 2 to 12 hours following the onset of muscle injury and reaches its maximum within 24 to 72 hours. A decline is usually seen within three to five days of cessation of muscle injury. CK has a serum half-life of about 1.5 days and declines at a relatively constant rate of about 40 to 50 percent of the previous day's value [5,6,9]. In patients whose CK does not decline as expected, continued muscle injury or the development of a compartment syndrome may be present.
Urine findings and myoglobinuria — Myoglobin, a heme-containing respiratory protein, is released from damaged muscle in parallel with CK. Myoglobin is a monomer that is not significantly protein-bound and is therefore rapidly excreted in the urine, often resulting in the production of red to brown urine. It appears in the urine when the plasma concentration exceeds 1.5 mg/dL . Visible changes in the urine only occur once urine levels exceed from about 100 to 300 mg/dL, although it can be detected by the urine (orthotolidine) dipstick at concentrations of only 0.5 to 1 mg/dL [3,6]. Myoglobin has a half-life of only two to three hours, much shorter than that of CK. Because of its rapid excretion and metabolism to bilirubin, serum levels may return to normal within six to eight hours.
Thus, it is not unusual for CK levels to remain elevated in the absence of myoglobinuria . In rhabdomyolysis, myoglobin appears in the plasma before CK elevation occurs and disappears while CK is still elevated or rising. Therefore, there is no CK threshold for when myoglobin appears. As above, rhabdomyolysis does not occur unless CK is elevated five times or more above the upper limit of normal (see 'Creatine kinase' above). Routine urine testing for myoglobin by urine dipstick evaluation may be negative in up to half of patients with rhabdomyolysis . Pigmenturia will be missed in rhabdomyolysis if the filtered load of myoglobin is insufficient or has largely resolved before the patient seeks medical attention due to its rapid clearance.
Both hemoglobin and myoglobin can be detected on the urine dipstick as "blood"; microscopic evaluation of the urine generally shows few red blood cells (RBC) (less than five per high-powered field) in patients with rhabdomyolysis whose positive test results from myoglobinuria . Such testing is not a reliable method for rapid detection of myoglobin if RBC are present or in patients with hemolysis due to its lack of specificity for myoglobin. Hemoglobin, the other heme pigment capable of producing pigmented urine, is much larger (a tetramer) than myoglobin and is protein-bound. As a result, much higher plasma concentrations are required before red to brown urine is seen, resulting in a change in plasma color. (See "Etiology and evaluation of hematuria in adults", section on 'Red to brown urine'.)
Other manifestations — Other manifestations of rhabdomyolysis include fluid and electrolyte abnormalities, many of which precede or occur in the absence of kidney failure, and hepatic injury ; additionally, cardiac dysrhythmias and risk of cardiac arrest may result from the severe hyperkalemia that occurs with significant myonecrosis . Later complications include acute kidney injury, compartment syndrome, and, rarely, disseminated intravascular coagulation.
Fluid and electrolyte abnormalities — Hypovolemia and abnormalities in serum electrolytes and uric acid are common in patients with rhabdomyolysis [3,11,12]:
●Hypovolemia results from "third-spacing" due to the influx of extracellular fluid into injured muscles and increases the risk of acute kidney injury .
●Hyperkalemia and hyperphosphatemia result from the release of potassium and phosphorus from damaged muscle cells. Levels of potassium may increase rapidly, but the levels of potassium and phosphate decrease as they are excreted in the urine. Hyperkalemia is more common in patients with oliguric acute kidney injury .
●Hypocalcemia, which can be extreme, occurs in the first few days because of entry into damaged myocytes and both deposition of calcium salts in damaged muscle and decreased bone responsiveness to parathyroid hormone [14,15]. During the recovery phase, serum calcium levels return to normal and may rebound to significantly elevated levels due to the release of calcium from injured muscle, mild secondary hyperparathyroidism from the acute renal failure, and an increase in calcitriol (1,25-dihydroxyvitamin D) [14,15]. (See "Etiology of hypocalcemia in adults", section on 'Extravascular deposition' and "Etiology of hypercalcemia", section on 'Rhabdomyolysis and acute renal failure'.)
●Severe hyperuricemia may develop because of the release of purines from damaged muscle cells and, if acute kidney injury occurs, reduced urinary excretion.
●Metabolic acidosis is common, and an increased anion gap may be present.
Acute kidney injury — Acute kidney injury (AKI, acute renal failure) is a common complication of rhabdomyolysis. The reported frequency of AKI ranges from 15 to over 50 percent [3,8,16]. The risk of AKI is lower in patients with CK levels at admission less than 15 to 20,000 units/L; risk factors for AKI in patients with lower values include dehydration, sepsis, and acidosis . Volume depletion resulting in renal ischemia, tubular obstruction due to heme pigment casts, and tubular injury from free chelatable iron all contribute to the development of renal dysfunction. Reddish-gold pigmented casts are often observed in the urine sediment. AKI in patients with rhabdomyolysis is discussed separately. (See "Clinical features and diagnosis of heme pigment-induced acute kidney injury".)
Compartment syndrome — A compartment syndrome exists when increased pressure in a closed anatomic space threatens the viability of the muscles and nerves within the compartment . Compartment syndrome is a potential complication of severe rhabdomyolysis that may develop after fluid resuscitation, with worsening edema of the limb and muscle . Lower extremity compartment syndrome can also be a cause of rhabdomyolysis, as may occur after tibial fractures. Compartment syndrome is discussed separately. (See "Acute compartment syndrome of the extremities".)
Disseminated intravascular coagulation — Infrequently, severe rhabdomyolysis may be associated with the development of disseminated intravascular coagulation due to the release of thromboplastin and other prothrombotic substances from the damaged muscle [5,19,20]. (See "Clinical features, diagnosis, and treatment of disseminated intravascular coagulation in adults".)
EVALUATION AND DIAGNOSIS
Indications for diagnostic testing — Diagnostic testing should be performed in individuals with:
●Both myalgias and pigmenturia.
●Either myalgias or pigmenturia, with a history suggesting the presence or recent exposure to a potential cause or event. (See "Causes of rhabdomyolysis", section on 'Causes'.)
●The absence of myalgias or pigmenturia in a clinical setting associated with increased risk for rhabdomyolysis, as symptoms may be vague or absent in up to 50 percent of patients. The diagnosis should be suspected following prolonged immobilization, in any stuporous or comatose patient or in a patient who is otherwise unable to provide a medical history and has one or more of the following:
•Evidence of pressure necrosis of the skin
•Signs of multiple trauma or a crush injury
•Blood chemistry abnormalities suggesting the possibility of increased cell breakdown, such as hyperkalemia, hyperphosphatemia, and /or hypocalcemia
•Evidence of acute kidney injury
Diagnostic evaluation — We obtain the following key diagnostic laboratory studies:
●Creatine kinase – Fractionation of the creatine kinase (CK) is generally not required but may be helpful, in addition to the clinical history and examination, in excluding other potential causes of CK elevation such as acute myocardial infarction, stroke, and other diseases of the heart and brain. (See 'Creatine kinase' above.)
Other muscle enzymes in addition to CK are typically elevated (eg, aldolase, aminotransferases, lactate dehydrogenase), but such testing is not usually necessary to make the diagnosis. However, elevations in aminotransferases or lactate dehydrogenase may suggest the need for CK testing if it has not been performed in a patient in whom such abnormalities may potentially be due to muscle injury rather than hepatic injury or another cause.
●Urinalysis, including dipstick and microscopic evaluation – Evidence of myoglobinuria should be sought by routine urine dipstick evaluation combined with microscopic examination. Testing of the unspun urine or the supernatant of the centrifuged urine will be positive for "heme" on dipstick if myoglobinuria is present, even if red to reddish brown urine is not evident macroscopically. The visual and microscopic examination of the sediment from a fresh urine specimen is required to exclude the presence of red blood cells (RBC) as the cause of positive testing; RBC in an older specimen may hemolyze over time, confounding the results. (See 'Urine findings and myoglobinuria' above.)
In patients with persistent red to reddish-brown urine, myoglobinuria is suggested when the urine tests positive for heme by dipstick after centrifugation, while the plasma has a normal color and tests negative for heme (algorithm 1). (See "Etiology and evaluation of hematuria in adults", section on 'Red to brown urine'.)
Myoglobinuria lacks sensitivity as a test for rhabdomyolysis; it may be absent in 25 to 50 percent of patients with rhabdomyolysis due to the more rapid clearance of myoglobin, compared with CK, following muscle injury. Myoglobin also decreases rapidly in a similar fashion in patients with renal failure, suggesting a role for extrarenal metabolism and clearance in such patients [21,22].
We also obtain the following tests, which may help in prompt recognition of other potentially dangerous manifestations, in differential diagnosis, and in identifying the cause (see 'Management' below):
●Complete blood count, including differential and platelet count
●Blood urea nitrogen, creatinine, and routine electrolytes including potassium
●Calcium, phosphate, albumin, and uric acid
Additional testing, such as evaluation of suspected metabolic myopathy or toxicology screening for drugs of abuse, depends upon the clinical context. (See 'When to suspect metabolic myopathy' below and "Clinical assessment of substance use disorders" and "Screening for unhealthy use of alcohol and other drugs in primary care".)
Diagnosis — We make the diagnosis of rhabdomyolysis in a patient with either an acute neuromuscular illness or dark urine without other symptoms, plus a marked acute elevation in serum creatine kinase (CK). The CK is typically at least five times the upper limit of normal, and is usually greater than 5000 international units/L. No absolute cut-off value for CK elevation can be defined, and the CK should be considered in the clinical context of the history and examination findings. (See 'Creatine kinase' above.)
Additional testing, such as electromyography (EMG), magnetic resonance imaging (MRI), and muscle biopsy, is not required for the diagnosis of rhabdomyolysis. These studies are generally reserved for patients in whom an underlying inflammatory myopathy is suspected. (See 'Differential diagnosis' below.)
When to suspect metabolic myopathy — There are subtle differences in the clinical manifestations of the various metabolic myopathies, but one of these conditions should be suspected when the following clinical circumstances are present:
●There are recurrent episodes of rhabdomyolysis after exertion or in association with fasting or a viral illness. The last two associations occur most commonly with carnitine palmitoyltransferase deficiency and the other disorders of lipid metabolism.
●There is a history of exercise intolerance, recurrent cramps, and fatigue beginning in childhood, and episodes of pigmenturia occurring in adolescence.
●There is a family history of rhabdomyolysis or exercise intolerance, particularly in siblings, thereby suggestive of an autosomal recessive inheritance pattern.
●The individual has normal strength and muscle enzymes during interictal periods. One exception is muscle phosphorylase deficiency, a disorder in which chronic muscle weakness may develop after repeated episodes and CK levels do not return to normal between attacks. (See "Myophosphorylase deficiency (glycogen storage disease V, McArdle disease)".)
The diagnostic approach to a suspected metabolic myopathy is discussed separately. Histochemical analysis of a muscle biopsy specimen will demonstrate the deficient enzyme. (See "Approach to the metabolic myopathies", section on 'Evaluation and diagnosis' and "Approach to the patient with muscle weakness".)
DIFFERENTIAL DIAGNOSIS — The differential diagnoses of myalgia, elevated creatine kinase (CK) and other muscle enzymes, and dark urine are fairly extensive. However, when present together, and if the CK elevation is acute and myoglobinuria is present, the diagnosis of rhabdomyolysis can generally be made with confidence. The following conditions may be considered, depending upon the combination of findings that are present, but distinctions can usually be made with readily available information from the medical history as well as the physical and laboratory examinations:
●Myocardial infarction – Although serum CK also rises acutely with myocardial infarction, patients with rhabdomyolysis alone do not have ischemic chest pain or electrocardiogram (ECG) signs of myocardial infarction. Additionally, the CK-MM fraction is elevated, while little or no CK-MB is present. Assays for cardiac troponins (both the I and T isoforms) are highly sensitive and specific for cardiac muscle injury, although both isoforms can sometimes be elevated in patients with rhabdomyolysis [23-25].
The basis for this elevation is not clear but may relate to nonischemic cardiac events that may occur in patients with rhabdomyolysis, including seizures, sepsis, and renal failure , or, in the case of troponin T, to cross-reaction with diseased skeletal muscle [24,27]. (See "Troponin testing: Clinical use" and 'Creatine kinase' above and "Criteria for the diagnosis of acute myocardial infarction" and "Troponin testing: Analytical aspects", section on 'What is troponin'.)
●Hematuria and hemoglobinuria – Both hematuria and hemoglobinuria (due to hemolysis) may result in red to reddish-brown urine and may be confused with myoglobinuria. Careful examination of the urine for red blood cells (present in hematuria, by definition), of serum for evidence of hemolysis, and of the CK (which is not elevated in hemolysis, or most patients with hematuria) will help distinguish these conditions. Other causes of red to brown urine include various foods and drugs, but such patients lack evidence of skeletal muscle injury, including CK elevation. (See 'Urine findings and myoglobinuria' above and 'Evaluation and diagnosis' above and "Etiology and evaluation of hematuria in adults", section on 'Red to brown urine'.)
●Inflammatory myopathy – Patients with inflammatory myopathy can also exhibit myalgias and elevated CK and may exhibit myoglobinuria . These patients can be differentiated from patients with rhabdomyolysis by the chronicity of disease, usually symmetric proximal muscle weakness developing over weeks to months, relative stability of the laboratory abnormalities compared with patients with rhabdomyolysis, and the systemic features associated with the inflammatory myopathies, such as dermatomyositis.
Patients with rhabdomyolysis generally do not exhibit electromyographic or histologic changes suggestive of myositis except in rare patients in whom both are present [29-31]; concurrent statin therapy may be a risk factor . (See 'Evaluation and diagnosis' above and "Clinical manifestations of dermatomyositis and polymyositis in adults" and "Diagnosis and differential diagnosis of dermatomyositis and polymyositis in adults".)
●Immune-mediated necrotizing myopathy – Patients on statin medications may develop an immune-mediated necrotizing myopathy with markedly elevated levels of CK and weakness that does not improve with discontinuation of statins but that does respond to aggressive immunosuppressive therapy [33-36]. These patients can be distinguished from patients with rhabdomyolysis by the persistence of symptoms and findings, including the elevation in CK, in the absence of treatment with immunosuppressives and by their histopathologic changes. (See "Diagnosis and differential diagnosis of dermatomyositis and polymyositis in adults", section on 'Differential diagnosis'.)
●Renal colic – In patients presenting with back pain, rhabdomyolysis may be confused with renal colic. Additionally, urine dipstick testing may be positive for blood. However, urolithiasis is not associated with marked elevations of the CK, and myoglobinuria is not present. (See "Diagnosis and acute management of suspected nephrolithiasis in adults".)
MANAGEMENT — The major issues in the treatment of patients with rhabdomyolysis, which are discussed in detail separately, include:
●Recognition and management of fluid and electrolyte abnormalities, which should be initiated regardless of renal function and which may prevent severe metabolic disturbances and acute kidney injury (see "Clinical features and diagnosis of heme pigment-induced acute kidney injury" and "Prevention and treatment of heme pigment-induced acute kidney injury")
●Identification of the specific causes and the use of appropriate countermeasures directed at the triggering events, including discontinuation of drugs or other toxins that may be etiologic factors (see "Causes of rhabdomyolysis", section on 'Causes')
●Prompt recognition, evaluation, and treatment of compartment syndrome in patients in whom it is present (see "Crush-related acute kidney injury (acute renal failure)" and "Acute compartment syndrome of the extremities")
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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Rhabdomyolysis (The Basics)")
SUMMARY AND RECOMMENDATIONS
●The clinical manifestations of rhabdomyolysis include myalgias, weakness, red to brown urine due to myoglobinuria, and elevated serum muscle enzymes (including creatine kinase [CK]). The degree of myalgias and other symptoms varies widely, and some patients are asymptomatic. Fever, malaise, tachycardia, and gastrointestinal symptoms may be present. Muscle swelling may occur with rehydration. (See 'Clinical manifestations' above and 'Symptoms' above and 'Physical findings' above.)
●The laboratory findings that characterize rhabdomyolysis include an acute elevation in the CK and other muscle enzymes and a decline in these values within three to five days of cessation of muscle injury. The other characteristic finding is the reddish-brown urine of myoglobinuria, but this finding is often absent because of the relative rapidity with which myoglobin is cleared. The serum CK is generally entirely or almost entirely of the MM or skeletal muscle fraction, although small amounts of the MB fraction may be present. (See 'Laboratory findings' above and 'Creatine kinase' above and 'Urine findings and myoglobinuria' above.)
●Other manifestations include fluid and electrolyte abnormalities, many of which precede or occur in the absence of acute kidney injury, and hepatic injury. Hypovolemia, hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, and metabolic acidoses may be seen. Hyperkalemia may result in cardiac dysrhythmias. Later complications include acute kidney injury (AKI), hypercalcemia, compartment syndrome, and, rarely, disseminated intravascular coagulation. (See 'Other manifestations' above and 'Fluid and electrolyte abnormalities' above and 'Acute kidney injury' above and 'Compartment syndrome' above and 'Disseminated intravascular coagulation' above.)
●We diagnose rhabdomyolysis in a patient with an acute muscular illness or injury based upon a marked acute elevation in serum CK; the CK is typically at least five times the upper limit of normal and is frequently greater than 5000 international units/L. Key diagnostic laboratory studies include the creatine kinase and urinalysis, including dipstick and microscopic evaluation. Myoglobinuria (present in 50 to 75 percent of patients at the time of initial evaluation) results in a positive test for blood on the urine dipstick but without red blood cells on the microscopic examination of the urine. (See 'Evaluation and diagnosis' above.)
●The differential diagnosis depends upon the combination of findings present. It includes myocardial infarction, other causes of red or brown urine, inflammatory myopathy, and local causes of pain, such as deep vein thrombosis or renal colic. (See 'Differential diagnosis' above.)
- Knochel JP. Rhabdomyolysis and myoglobinuria. Annu Rev Med 1982; 33:435.
- Giannoglou GD, Chatzizisis YS, Misirli G. The syndrome of rhabdomyolysis: Pathophysiology and diagnosis. Eur J Intern Med 2007; 18:90.
- Gabow PA, Kaehny WD, Kelleher SP. The spectrum of rhabdomyolysis. Medicine (Baltimore) 1982; 61:141.
- Warren JD, Blumbergs PC, Thompson PD. Rhabdomyolysis: a review. Muscle Nerve 2002; 25:332.
- Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review: Rhabdomyolysis -- an overview for clinicians. Crit Care 2005; 9:158.
- Khan FY. Rhabdomyolysis: a review of the literature. Neth J Med 2009; 67:272.
- Dimitriu A, Lupescu O, Ciurea N, et al. Markers of inflammation in crushing trauma of the lower limbs. Therapeutics, Pharmacology and Clinical Toxicology 2016; 20:20.
- Melli G, Chaudhry V, Cornblath DR. Rhabdomyolysis: an evaluation of 475 hospitalized patients. Medicine (Baltimore) 2005; 84:377.
- Mikkelsen TS, Toft P. Prognostic value, kinetics and effect of CVVHDF on serum of the myoglobin and creatine kinase in critically ill patients with rhabdomyolysis. Acta Anaesthesiol Scand 2005; 49:859.
- Akmal M, Massry SG. Reversible hepatic dysfunction associated with rhabdomyolysis. Am J Nephrol 1990; 10:49.
- Grossman RA, Hamilton RW, Morse BM, et al. Nontraumatic rhabdomyolysis and acute renal failure. N Engl J Med 1974; 291:807.
- Koffler A, Friedler RM, Massry SG. Acute renal failure due to nontraumatic rhabdomyolysis. Ann Intern Med 1976; 85:23.
- Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009; 361:62.
- Llach F, Felsenfeld AJ, Haussler MR. The pathophysiology of altered calcium metabolism in rhabdomyolysis-induced acute renal failure. Interactions of parathyroid hormone, 25-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol. N Engl J Med 1981; 305:117.
- Akmal M, Bishop JE, Telfer N, et al. Hypocalcemia and hypercalcemia in patients with rhabdomyolysis with and without acute renal failure. J Clin Endocrinol Metab 1986; 63:137.
- Veenstra J, Smit WM, Krediet RT, Arisz L. Relationship between elevated creatine phosphokinase and the clinical spectrum of rhabdomyolysis. Nephrol Dial Transplant 1994; 9:637.
- Olson SA, Glasgow RR. Acute compartment syndrome in lower extremity musculoskeletal trauma. J Am Acad Orthop Surg 2005; 13:436.
- Paletta CE, Lynch R, Knutsen AP. Rhabdomyolysis and lower extremity compartment syndrome due to influenza B virus. Ann Plast Surg 1993; 30:272.
- Criddle LM. Rhabdomyolysis. Pathophysiology, recognition, and management. Crit Care Nurse 2003; 23:14.
- Chatzizisis YS, Misirli G, Hatzitolios AI, Giannoglou GD. The syndrome of rhabdomyolysis: complications and treatment. Eur J Intern Med 2008; 19:568.
- Wakabayashi Y, Kikuno T, Ohwada T, Kikawada R. Rapid fall in blood myoglobin in massive rhabdomyolysis and acute renal failure. Intensive Care Med 1994; 20:109.
- Wakabayashi Y, Nakano T, Kikuno T, et al. Massive rhabdomyolysis associated with influenza A infection. Intern Med 1994; 33:450.
- Korff S, Katus HA, Giannitsis E. Differential diagnosis of elevated troponins. Heart 2006; 92:987.
- Jaffe AS, Vasile VC, Milone M, et al. Diseased skeletal muscle: a noncardiac source of increased circulating concentrations of cardiac troponin T. J Am Coll Cardiol 2011; 58:1819.
- Punukollu G, Gowda RM, Khan IA, et al. Elevated serum cardiac troponin I in rhabdomyolysis. Int J Cardiol 2004; 96:35.
- Inbar R, Shoenfeld Y. Elevated cardiac troponins: the ultimate marker for myocardial necrosis, but not without a differential diagnosis. Isr Med Assoc J 2009; 11:50.
- Rittoo D, Jones A, Lecky B, Neithercut D. Elevation of cardiac troponin T, but not cardiac troponin I, in patients with neuromuscular diseases: implications for the diagnosis of myocardial infarction. J Am Coll Cardiol 2014; 63:2411.
- Rider LG, Miller FW. Laboratory evaluation of the inflammatory myopathies. Clin Diagn Lab Immunol 1995; 2:1.
- Caccamo DV, Keene CY, Durham J, Peven D. Fulminant rhabdomyolysis in a patient with dermatomyositis. Neurology 1993; 43:844.
- Pirovino M, Neff MS, Sharon E. Myoglobinuria and acute renal failure with acute polymyositis. N Y State J Med 1979; 79:764.
- Kim HW, Choi JR, Jang SJ, et al. Recurrent rhabdomyolysis and myoglobinuric acute renal failure in a patient with polymyositis. Nephrol Dial Transplant 2005; 20:2255.
- Gupta S, Blaivas M, Ike RW, Crofford LJ. Polymyositis evolving after rhabdomyolysis associated with HMG-CoA reductase inhibitors: a report of two cases. J Clin Rheumatol 2001; 7:332.
- Christopher-Stine L, Casciola-Rosen LA, Hong G, et al. A novel autoantibody recognizing 200-kd and 100-kd proteins is associated with an immune-mediated necrotizing myopathy. Arthritis Rheum 2010; 62:2757.
- Mammen AL, Chung T, Christopher-Stine L, et al. Autoantibodies against 3-hydroxy-3-methylglutaryl-coenzyme A reductase in patients with statin-associated autoimmune myopathy. Arthritis Rheum 2011; 63:713.
- Needham M, Fabian V, Knezevic W, et al. Progressive myopathy with up-regulation of MHC-I associated with statin therapy. Neuromuscul Disord 2007; 17:194.
- Grable-Esposito P, Katzberg HD, Greenberg SA, et al. Immune-mediated necrotizing myopathy associated with statins. Muscle Nerve 2010; 41:185.