Propofol-associated Rhabdomyolysis with Cardiac Involvement in Adults: Chemical and Anatomic Findings Edward B. Stelow, Vandita P. Johari, Stephen A. Smith, John T. Crosson, and Fred S. Apple * Propofol, a central-acting sedative agent, has been im- plicated in the development of rhabdomyolysis in chil- dren. We describe two adults who developed rhabdo- myolysis after receiving high rates of propofol infusion. Rhabdomyolysis of both skeletal and cardiac muscle was suggested in both patients by marked increases of creatine kinase (>170 000 U/L) and cardiac troponin I (11 and 46 g/L in patients one and two, respectively). Creatine kinase and cardiac troponin I values were highly correlated in each patent (r  0.786 and 0.988 in patients one and two, respectively). Autopsy of one patient confirmed the diagnosis of skeletal and cardiac rhabdomyolysis. © 2000 American Association for Clinical Chemistry Rhabdomyolysis is a clinical entity that evolves after skeletal muscle injury. The symptoms and signs are secondary to muscle injury and the effects of the release of toxic intracellular contents. They include muscle weak- ness, myoglobinuria, and renal failure. The causes of the initial injury can range from trauma to venom (1, 2). Drug-induced rhabdomyolysis has been reported as re- sulting from many possible agents, including the use of propofol for sedation of children in the intensive care unit (3–8). We present two cases in which adults developed rhabdomyolysis after receiving high infusion rates of propofol for extended periods of time. We use chemical and anatomic findings to demonstrate rhabdomyolysis secondary to both skeletal and cardiac muscle injury and secondary acute renal failure. Case Reports case 1 The patient was a 47-year-old white woman with a long history of steroid-dependent asthma for which she had been intubated twice previously. She presented after worsening shortness of breath at home that had not been relieved with multiple nebulizer treatments. Her past medical history was significant for obesity, depression, gastroesophageal reflux disorder, herniorrhaphy, chole- cystectomy, and steroid-induced myopathy. She had no known drug allergies. She was medicated at home with theophylline, prednisone, albuterol, and zafirlukast. Upon reaching the emergency department (ED) 1 she had one-word dyspnea that was not relieved with nebulizer therapy. She was hypertensive, tachycardic, and tachy- pneic; however, she was afebrile. Her oxygen saturation while receiving oxygen therapy by face-mask was 87–92% before it rapidly began to worsen. It improved quickly after a difficult intubation that lasted nearly 10 min. The patient received intravenous corticosteroids, midazolam, albuterol, vecuronium, and succinylcholine in the ED. She also received lidocaine for multiple premature ventricular contractions after her hypoxic episode. An electrocardio- gram taken at that time was without signs of infarct or ischemia. Because of a possible infiltrate on her chest x-ray and an increased white blood cell count, the patient received ceftriaxone. She was admitted to the medical intensive care unit (MICU) where she was treated with albuterol, ipratropium, intravenous corticosteroids, ceftri- axone, and theophylline. Propofol was used for sedative purposes and was to be “titrated to desired effect”. She remained afebrile and was stable with good urine output throughout the next day while her propofol was infused at 200 g  kg -1  min -1 . An attempt to wean her ventila- Department of Laboratory Medicine and Pathology, Hennepin County Medical Center, Minneapolis, MN 55415. *Address correspondence to this author at: Hennepin County Medical Center, Clinical Laboratories (812), 701 Park Ave., Minneapolis, MN 55415. Fax 612-904-4229; e-mail fred.apple@co.hennepin.mn.us. Received December 3, 1999; accepted January 28, 2000. 1 Nonstandard abbreviations: ED, emergency department; MICU, medical intensive care unit; CK, creatine kinase; and cTnI, cardiac troponin I. Clinical Chemistry 46:4 577–581 (2000) Case Report 577