Find information on thousands of medical conditions and prescription drugs.


Rhabdomyolysis is the breakdown of skeletal muscle due to injury, either mechanical, physical or chemical. The principal result of this process is acute renal failure due to accumulation of muscle breakdown products in the bloodstream, several of which are injurous to the kidney. more...

Gastroesophageal reflux...
Rasmussen's encephalitis
Raynaud's phenomenon
Reactive arthritis
Reactive hypoglycemia
Reflex sympathetic...
Regional enteritis
Reiter's Syndrome
Renal agenesis
Renal artery stenosis
Renal calculi
Renal cell carcinoma
Renal cell carcinoma
Renal cell carcinoma
Renal failure
Renal osteodystrophy
Renal tubular acidosis
Repetitive strain injury
Respiratory acidosis
Restless legs syndrome
Retinitis pigmentosa
Retrolental fibroplasia
Retroperitoneal fibrosis
Rett syndrome
Reye's syndrome
Rh disease
Rheumatic fever
Rheumatoid arthritis
Rift Valley fever
Rocky Mountain spotted fever
Romano-Ward syndrome
Roseola infantum
Rubinstein-Taybi syndrome
Rumination disorder

Treatment is with intravenous fluids, and dialysis if necessary.


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 tourniquet left for too long, local muscle compression due to comatose states, compartment syndrome, rigidity due to neuroleptic malignant syndrome
  • physical: high fever or hyperthermia, electric current
  • chemical: metabolic disorders, anoxia of 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).


Severe cases of rhabdomyolysis often result in myoglobinuria, a condition where 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.


The diagnosis is typically made when an abnormal renal function and elevated creatine kinase and potassium levels 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.

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)


[List your site here Free!]

A case of hypokalemia and rhabdomyolysis in a patient with short bowel syndrome
From JPEN: Journal of Parenteral and Enteral Nutrition, 7/1/03 by Guardino, Jason M

Rhabdomyolysis caused by the metabolic disturbances seen in chronic short bowel syndrome has not been reported in the English literature to our knowledge. Presented is a case of hypokalemic-induced rhabdomyolysis associated with short bowel syndrome.

A 48-year-old man was presented to the emergency department with complaints of severe generalized weakness and pain. He had a history of acute aortic dissection with resultant ischemic bowel, necessitating partial resection of the small bowel, ileostomy, and colostomy. He developed chronic diarrhea because of the short bowel syndrome and required parenteral nutrition. This was complicated by multiple episodes of central venous catheter bloodstream infections. For 2 years he demonstrated poor tolerance of oral nutrition; 7 weeks before presentation, he underwent surgical ileocolic anastomosis, with discontinuation of parenteral nutrition. Subsequently, he reported pain and weakness of the extremities, poor appetite, and a weight loss of 14 kg. He denied any fevers, chills, seizures, trauma, vomiting, nausea, contacts with ill individuals, and recent travel, and also denied abuse of diuretics, laxatives, alcohol, or illicit drugs. His medications included metoprolol and codeine, with no recent change in his doses.

Physical examination was remarkable for temperature 35.8, pulse 111, respiration 22, and blood pressure 159/86; the patient was a cachectic appearing male. Mucosal membranes were dry, and there was no jugular venous distention. Neuromuscular examination revealed tenderness to palpation at the proximal muscle groups of upper and lower extremities. There was demonstrable weakness of the same muscle groups. Sensation, reflex, and cranial nerve test results were normal.

Laboratory data are summarized in Table I.

An electrocardiogram (EKG) revealed sinus rhythm and left ventricular hypertrophy with new ST segment changes and U waves.

The patient was diagnosed with rhabdomyolysis secondary to hypokalemia. He received IV hydration and potassium replacement totaling 710 mmol. The patient did well and on the day of discharge reported resolution of his symptoms. Follow-up laboratory results are shown in Table I. A repeated EKG result was normal.

Nontraumatic rhabdomyolysis associated with hypokalemia may be a relatively common occurrence1 and has been documented in several settings.2-4 The mechanism of hypokalemic-induced rhabdomyolysis may relate to the impairment of the physiologic vasodilatory effects mediated by the local release of potassium by skeletal muscle cells.5

No other obvious cause for rhabdomyolysis in this patient was identified. The presence of short bowel syndrome in this case was a predisposing factor to the development of severe hypokalemia and subsequent rhabdomyolysis.


1. Singhal PC, Abramovici M, Venkatesan J, et al: Hypokalemia and rhabdomyolysis. Mineral Electrolyte Metab 17:335-339, 1991

2. Lucatello A, Sturani A, Di Nardo A, et al: Acute renal failure in rhabdomyolysis associated with hypokalemia. Nephron 67:115-116, 1994

3. Prat G, Petrognani R, Diatta B, et al: Hypokalemia causing rhabdomyolysis and precordialgia. Intensive Care Med 27:1096, 2001

4. Cervello A, Alfaro A, Chumillas MJ: Hypokalemic myopathy induced by Giardia lamblia. N Engl J Med 329:210-211, 1993

5. Rose, BD, ed. Hypokalemia. IN Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed. McGraw-Hill, New York, NY, 2001, pp 859-860

Jason M. Guardino, DO, MS; John K. Hix, MD; and Douglas Seidner, MD

From the Cleveland Clinic Foundation, Cleveland, Ohio

Received for publication, February 28, 2003.

Accepted for publication, March 26, 2003.

Correspondence: Dr. Jason M. Guardino, Desk E13, Internal Medicine, 9500 Euclid Avenue, Cleveland, OH 44195. Electronic mail may be sent to

Copyright American Society for Parenteral and Enteral Nutrition Jul/Aug 2003
Provided by ProQuest Information and Learning Company. All rights Reserved

Return to Rhabdomyolysis
Home Contact Resources Exchange Links ebay