Rhabdomyolysis

Rhabdomyolysis is the breakdown of skeletal muscledue to injury, either mechanical, physical or chemical. The principal result of this process is acute renal failuredue to accumulation of muscle breakdown products in the bloodstream, several of which are injurous to the kidney. Treatment is with intravenous fluids, and dialysisif necessary.

Causes

The injury that leads to rhabdomyolysis can be due to mechanical, physical and chemical causes:

• mechanical: crush trauma, excessive exertion, intractable convulsions, choreoathetosis, surgery, compression by a tourniquetleft for too long, local muscle compression due to comatosestates, compartment syndrome, rigidity due to neuroleptic malignant syndrome
• physical: high feveror hyperthermia, electric current
• chemical: metabolic disorders, anoxiaof the muscle (e.g. Bywaters' syndrome, toxin- and drug-related; various animal toxins, some antibiotics, methylenedioxymethamphetamine (MDMA) better known as ecstasy, statins, alcohol

Drug-induced rhabdomyolysis appears to be increasing in incidencepossibly due to the introduction of increasingly potent drugs into clinical practice. Any drug which 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 (Larbi 1998).

Pathophysiology

Severe cases of rhabdomyolysis often result in myoglobinuria, a condition where the myoglobinfrom 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 damagein 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 toxicsubstances for the kidneys. Massive skeletal muscle necrosismay further aggravate the situation, by reducing plasmavolumes and leading to shockand reduced bloodflow to the kidneys.

Diagnosis

The diagnosis is typically made when an abnormal renal functionand elevated creatine kinaseand potassiumlevels are observed in a patient. To distinguish the causes, a careful medication history is considered useful. Testing for myoglobinlevels in blood and urine is rarely performed due to its cost.

Clinical sequelae

• Hypovolemia(sequestration of plasma water within injured myocytes)
• Hyperkalemia(release of cellular potassium into circulation)
• Metabolic acidosis(release of cellular phosphate and sulfate)
• Acute renal failure(nephrotoxic effects of liberated myocyte components)
• Disseminated intravascular coagulation(DIC)
• Hypocalcemia(low calcium levels due to precipitation with phosphate), followed by hypercalcemia(as renal function recovers)

Therapy

The main therapeutic measure is hyperhydration (by administering intravenous fluids), and if necessary the use of diuretics(to prevent fluid overload). Alkalinisation of the urine with bicarbonatereduces 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). Calciumlevels are initially low (hypocalcemia), as circulating calcium precipitates in the damaged muscle tissue, presumably with phosphatereleased from intracellular stores. When the acute renal failure resolves, vitamin Dlevels rise rapidly, causing hypercalcemia(elevated calcium). Although this resolves eventually, high calcium levels may require treatment with bisphosphonates(e.g. pamidronate).

References

• Cecil Textbook of Medicine
• The Oxford Textbook of Medicine
• Intensive Care Medicine by Irwin and Rippe
• The ICU Book by Marino
• Procedures and Techniques in Intensive Care Medicine by Irwin and Rippe
• Pathogenesis and treatment of renal dysfunction in rhabdomyolysis, S. Holt, K. Moore, Intensive Care Medicine, Volume 27, Number 5, 803 - 811.
• Pathogenesis and treatment of renal dysfunction in rhabdomyolysis, (reply) Panagiotis Korantzopoulos, Dimitrios Galaris, Dimitrios Papaioannides, Intensive Care Medicine, Volume 28, Number 8, 1185 - 1185.
• The pathophysiology of altered calcium metabolism in rhabdomyolysis-induced acute renal failure. Interactions of parathyroid hormone, 25-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol, Llach F., Felsenfeld A. J., Haussler M. R. ,New Engl J Med 1981; 305:117-123, Jul 16, 1981.
• Serum creatine kinase as predictor of clinical course in rhabdomyolysis: a 5-year intensive care survey, Arthur R. de Meijer, Bernard G. Fikkers, Marinus H. de Keijzer, Baziel G. M. van Engelen, Joost P. H. Drenth, Intensive Care Medicine, Volume 29, Number 7, 1121 - 1125.

External links

• Baggaley, P.: Rhabdomyolysis.
• Rhabdomyolysis. Medline Plus.
• Craig, S.: Rhabdomyolysis. eMedicine.
• Larbi, E.B. Drug-induced rhabdomyolysisda:Rhabdomyolyse

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It uses material from the http://en.wikipedia.org/wiki/Rhabdomyolysis Wikipedia article Rhabdomyolysis.