Rhabdomyolysis - Exercise Induced

2/05/2003

Question: What are causative factors in exercise-induced rhabdomyolysis?

 

 

Link Directly to Fulltext article in Ovid

<1>

Unique Identifier:12394880

Authors: Sandhu RS. Como JJ. Scalea TS. Betts JM.

Institution: R Adams Cowley Shock Trauma Center, University of Maryland Medical System, Baltimore 21201, USA.

Title: Renal failure and exercise-induced rhabdomyolysis in patients taking performance-enhancing compounds.

 

Source: Journal of Trauma-Injury Infection & Critical Care. 53(4):761-3; discussion 763-4, 2002 Oct.


 

 

 

Link Directly to Fulltext Article at Publisher

<2>

Unique Identifier:11898964

Authors: Sauret JM. Marinides G. Wang GK.

Institution: Department of Family Medicine, State University of New York at Buffalo School of Medicine and Biomedical Sciences, 14215, USA. sauret@acsu.buffalo.edu

Title: Rhabdomyolysis. [Review] [29 refs]

 

Source: American Family Physician. 65(5):907-12, 2002 Mar 1.

Abstract: Rhabdomyolysis is a potentially life-threatening syndrome resulting from the breakdown of skeletal muscle fibers with leakage of muscle contents into the circulation. The most common causes are crush injury, overexertion, alcohol abuse and certain medicines and toxic substances. Several inherited genetic disorders, such as McArdle's disease and Duchenne's muscular dystrophy, are predisposing factors for the syndrome. Clinical features are often nonspecific, and tea-colored urine is usually the first clue to the presence of rhabdomyolysis. Screening may be performed with a urine dipstick in combination with urine microscopy. A positive urine myoglobin test provides supportive evidence. Multiple complications can occur and are classified as early or late. Early complications include severe hyperkalemia that causes cardiac arrhythmia and arrest. The most serious late complication is acute renal failure, which occurs in approximately 15 percent of patients with the syndrome. Early recognition of rhabdomyolysis and prompt management of complications are crucial to a successful outcome. [References: 29]


 

  

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Unique Identifier:9148081

Authors: Le Gallais D. Bile A. Mercier J. Paschel M. Tonellot JL. Dauverchain J.

Institution: Laboratoire de Physiologie des Interactions, Hopital Arnaud de Villeneuve, Montpellier, France.

Title: Exercise-induced death in sickle cell trait: role of aging, training, and deconditioning.

 

Source: Medicine & Science in Sports & Exercise. 28(5):541-4, 1996 May.

Abstract: The pathophysiological process of exercise-induced death in subjects with sickle cell trait (SCT) remains unclear. Concerning the cause of death, authors have suggested stressful environmental conditions such as altitude, heat and humidity, or abnormal patient conditions such as deconditioning, fatigue, and disease. These conditions are thought to lead to hypoxemia, hyperlactatemia, acidosis, dehydration, hyperthermia, or exercise-induced rhabdomyolysis, all of which may initiate sickle cell crisis, disseminated intravascular coagulation, myoglobinuria, and renal failure. We report the case of a 41-yr-old, healthy, and apparently well-conditioned subject with SCT who died during a cross-country race under normal environmental conditions in good weather (in terms of temperature and humidity). The medical and athletic history of the subject were unremarkable. We refer to an epidemiological study that reported a relation between age and exercise-induced sudden death in subjects with SCT. We then review the pathophysiological effects of aging in association with deconditioning and high-level training reported in the literature, particularly the decrease in aerobic metabolism in deconditioned subjects, and the exercise-induced hypoxemia in highly trained subjects. We discuss the consequences of deconditioning and high-level training in subjects with SCT during exercise, and conclude that these factors may be involved in the age-dependent risk of exercise-related sudden death in subjects with SCT.


 

 

<20>

Unique Identifier:7973777

Authors: Kark JA. Ward FT.

Institution: Department of Clinical Physiology, Walter Reed Army Institute of Research, Washington, DC 20307-5100.

Title: Exercise and hemoglobin S. [Review] [256 refs]

 

Source: Seminars in Hematology. 31(3):181-225, 1994 Jul.


 

 

<22>

Unique Identifier:8198305

Authors: Sinert R. Kohl L. Rainone T. Scalea T.

Institution: Department of Emergency Medicine, State University of New York Health Science Center, Brooklyn/Kings County Hospital Center.

Title: Exercise-induced rhabdomyolysis. [Review] [28 refs]

 

Source: Annals of Emergency Medicine. 23(6):1301-6, 1994 Jun.

Abstract: STUDY OBJECTIVE: To describe the syndrome of exercise-induced rhabdomyolysis and to investigate the relation between exercise-induced rhabdomyolysis and the development of acute renal failure. DESIGN: Retrospective chart analysis on all patients with a discharge diagnosis of rhabdomyolysis from January 1988 to January 1993. SETTING: An urban tertiary care center with 225,000 annual emergency department visits. TYPE OF PARTICIPANTS: Thirty-five patients met the inclusion criteria for exercise-induced rhabdomyolysis: a history of strenuous exercise, creatine phosphokinase level more than 500, and urine dipstick positive for blood without hematuria. We excluded patients with a history of trauma, myocardial infarction, stroke, or documented sepsis. Charts also were examined for the presence of nephrotoxic cofactors (ie, hypovolemia and/or acidosis). RESULTS: All 35 patients were men without significant past medical history and were an average age of 24.4 years. The average admission creatine phosphokinase was 40,471 U/L. No patient presented with or developed nephrotoxic cofactors during hospitalization. None of our study patients experienced acute renal failure. CONCLUSION: Previous literature has described a 17% to 40% incidence of acute renal failure in rhabdomyolysis. None of our patients developed acute renal failure, signifying a much lower incidence of acute renal failure in exercise-induced rhabdomyolysis without nephrotoxic cofactors than in other forms of rhabdomyolysis. [References: 28] CAS Registry/EC Number EC 2-7-3-2 (Creatine Kinase).


 

 

 

 

 

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