Acute Rhabdomyolysis and Acute Cocaine Intoxication
Gargantilla Madera P1,2*, Martín Cabrejas BM3 and Pintor Holguín E2
1Department of Internal Medicine, Hospital El Escorial, Spain
2European University of Madrid, Spain
3Department of Gynecology and Obstetrics, Hospital Universitario Fundación de Alcorcón, Spain
*Corresponding author: Gargantilla Madera P, Department of Internal Medicine, Hospital El Escorial, European University of Madrid, Madrid, Spain, E-mail: firstname.lastname@example.org
J Fam Med Dis Prev, JFMDP-2-024, (Volume 2, Issue 1), Short Commentary; ISSN: 2469-5793
Received: December 26, 2015 | Accepted: January 18, 2016 | Published: January 21, 2016
Citation: Gargantilla MP, Martín CBM, Pintor HE (2016) Acute Rhabdomyolysis and Acute Cocaine Intoxication. J Fam Med Dis Prev 2:024. 10.23937/2469-5793/1510024
Copyright: © 2016 Gargantilla MP, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Cocaine, Rhabdomyolysis, Creatinin-phosphokinase
Rhabdomyolysis is a condition resulting from the release of large quantities of myocyte breakdown products into the circulation, following injury to striated muscles. It is a clinical and biochemical syndrome, defined as an elevation of serum creatine kinasa activity (sCK) to at least 10 times the normal upper limit followed by a rapid decrease of the sCK level back to normal values . Other muscle enzymes in addition are elevated (aldolase, aminotransferases, lactate dehydrogenase), but it is not necessary to make the diagnosis. When massive amounts of myoglobin are released the binding capacity of the plasma protein is exceeded and it is filtered by the glomeruli, it may cause renal dysfunction.
The clinical presentation can vary widely: the classic triad (myalgia, weakness and pigmenturia) is seen in less than 10% of them. The aetiology is also quite diverse, including excessive muscular stress, direct toxic, physical damage and genetic defects. Many of the common abused drugs have been reported to cause rhabdomyolysis .
We present the case of a 36-year-old male patient, who did not have a previous medical history, and was admitted to the hospital because of myalgia and weakness. He admitted that he had inhaled 6 g of cocaine 12 h before admission denied the intake of any other drugs. The results of physical examination were normal. Blood analysis on admission disclosed a creatinine kinasa (CK) 1,272 U/l, CK isoenzyme BM 54 U/L and myoglobin 1.4 mg/dL. The myoglobinuria was 0.6 mg/dL and his renal function was also normal. The patient improved with intravenous fluid plus sodium bicarbonate and his sCK was decreased to 230 U/l one day later, and then he was discharged.
The interest of this case is based on the fact that in this patient cocaine-induced acute rhabdomyolysis. The first case of rhabdomyolysis associated with acute cocaine intoxication in the medical literature was reported in 1987 . About 24% of the cocaine users develop rhabdomyolysis , because this drug can cause a direct effect on the muscle tissue, inducing vasoconstriction and tissue ischemia. Cocaine-associated rhabdomyolysis may also contribute to hyperthermia and hyperactivity .
The goal of treatment or rhabdomyolysis is to cease muscle destruction (elimination of exposure), hydration and correction of electrolyte abnormalities . An adequate volume of circulating blood is necessary to prevent acute renal kidneys. In the case of drug-induced rhabdomyolysis eliminating the exposure of the toxic may be the only treatment.
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