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Classification & external resources
ICD-10 M62.8, T79.6
ICD-9 728.88
DiseasesDB 11472
MedlinePlus 000473
eMedicine ped/2003  emerg/508
MeSH D012206

Rhabdomyolysis is the rapid breakdown of skeletal muscle tissue due to traumatic injury, either mechanical, physical, or chemical. The principal result is a large release of the creatine kinase (CK) enzymes and other cell byproducts into the blood system and acute renal failure due to accumulation of muscle breakdown products, several of which are injurious to the kidney. Treatment is with intravenous fluids, and dialysis if necessary.


Signs and symptoms

Major signs and symptoms include:[1]

  • Dark urine due to protein from the destroyed muscle tissue. Alternatively, little or no urine production due to kidney complications.
  • Painful, swollen, or tender muscles. Depending on the cause, this may affect a single area or many parts of the body.
  • Impaired mental status, such as unconsciousness or confusion. This may be due to the effects that rhabdomyolysis has on kidney function, or due to the underlying cause.
  • Some patients have a fever.
  • Most patients have a recent history of muscle strain or injury. This could be caused by a crush injury, or by lying still on a hard surface, such as a floor, for a prolonged time.


Rhabdomyolysis can be either hereditary (for example in disorders of metabolism) or aquired by either mechanical, physical or chemical means:

Any drug that directly or indirectly impairs the production or use of adenosine triphosphate (ATP) by skeletal muscle, or increases energy requirements so as to exceed ATP production, can cause rhabdomyolysis.[3]


Severe cases of rhabdomyolysis often result in myoglobinuria, a condition wherein the myoglobin from muscle breakdown spills into the urine, making it dark, or "tea colored" (myoglobin contains heme, like hemoglobin, giving muscle tissue its characteristic red color). This condition can cause serious kidney damage in severe cases. The injured muscle also leaks potassium, leading to hyperkalemia, which may cause fatal disruptions in heart rhythm. In addition, myoglobin is metabolically degraded into potentially-toxic substances for the kidneys. Massive skeletal muscle necrosis may further aggravate the situation, by reducing plasma volumes and leading to shock and reduced bloodflow to the kidneys.


In general, the diagnosis is made when an abnormal renal function and elevated CPK are observed in a patient. To distinguish the causes, a careful medication history is considered useful. Testing for myoglobin levels in blood and urine is rarely performed due to its cost, but may be useful.

Often the diagnosis is suspected when a urine dipstick test is positive for blood, but no cells are seen on microscopic analysis. This suggests myoglobinuria, and usually prompts a measurement of the serum CPK, which confirms the diagnosis.


The main therapeutic measure is hyperhydration (by administering intravenous fluids), and, if necessary, the use of osmotic diuretics (to prevent fluid overload). Alkalinisation of the urine with bicarbonate reduces the amount of myoglobin accumulating in the kidney.

As the electrolytes are frequently deranged, these may require correction, especially hyperkalemia (elevated potassium levels in the blood). Calcium levels are initially low (hypocalcemia), as circulating calcium precipitates in the damaged muscle tissue, presumably with phosphate released from intracellular stores. When the acute renal failure resolves, vitamin D levels rise rapidly, causing hypercalcemia (elevated calcium). Although this resolves eventually, high calcium levels may require treatment with bisphosphonates (e.g., pamidronate).

If the exacerbating cause includes overdose of skeletal muscle relaxants and/or tricyclic antidepressants, the treatment protocols include gastric decontamination. This procedure is fairly effective because the anticholinergic effects of tricyclics and cyclobenzaprine delay gastric emptying; and, therefore, it becomes possible to obtain tablet residues even after significant time elapse. Ventricular arrhythmias, QRS widening, or intraventricular conduction abnormalities should be treated with sodium bicarbonate 1 meq/kg IV bolus and repeated if arrhythmias persist. This should be followed by IV infusion of sodium bicarbonate to produce an arterial pH of 7.5; the mechanism of sodium bicarbonate's action in this role is unknown.[2] However, sodium bicarbonate's beneficial effect on kidney function is known to be via the effects of alkalinisation both increasing the urinary solubility of myoglobin leading to its increased excretion[4] and stabilizing ferryl myoglobin complex so preventing myoglobin-induced lipid peroxidation.[5][6]


The prognosis depends significantly on the underlying cause.


  1. ^ Clarkson P, Kearns A, Rouzier P, Rubin R, Thompson P (2006). "Serum creatine kinase levels and renal function measures in exertional muscle damage". Med Sci Sports Exerc 38 (4): 623-7. PMID 16679975.
  2. ^ a b Chabria SB (2006). "Rhabdomyolysis: a manifestation of cyclobenzaprine toxicity". Journal of occupational medicine and toxicology (London, England) 1: 16. doi:10.1186/1745-6673-1-16. PMID 16846511.
  3. ^ Larbi EB (1998). "Drug-induced rhabdomyolysis". Annals of Saudi medicine 18 (6): 525–30. PMID 17344731.
  4. ^ Zager RA (1989). "Studies of mechanisms and protective maneuvers in myoglobinuric acute renal injury". Lab. Invest. 60 (5): 619–29. PMID 2716281.
  5. ^ Moore KP, Holt SG, Patel RP, et al (1998). "A causative role for redox cycling of myoglobin and its inhibition by alkalinization in the pathogenesis and treatment of rhabdomyolysis-induced renal failure". J. Biol. Chem. 273 (48): 31731–7. PMID 9822635.
  6. ^ Holt S, Moore K (2000). "Pathogenesis of renal failure in rhabdomyolysis: the role of myoglobin". Exp. Nephrol. 8 (2): 72–6. PMID 10729745.
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Rhabdomyolysis". A list of authors is available in Wikipedia.
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