Probable Succinylcholine-Induced Rhabdomyolysis in a Male Athlete

Athletes often use anabolic steroids and protein building amino acids in an effort to increase muscle mass and improve performance. We report a case of rhabdomyolysis after elective knee surgery in a young athlete who regularly included a protein-rich supplement in his diet. Case Report A 16-yr-old male football player had elective repair of a right posterior cruciate and lateral collateral ligaments under general anesthesia. He was 183 cm tall, weighed 90.9 kg, and denied any previous medical or surgical history, allergies, smoking, alcohol, steroids, or other drug use. As part of his regular diet, he had been drinking Amino Fuel Registered Trademark (Twin Labs, Ronkonkoma, NY), an anabolic liquid containing L-carnitine, L-leucine, L-isoleucine, and L-valine with no other additives known to produce rhabdomyolysis. Anesthesia was induced with 2 mg midazolam, 20 micro gram sufentanil, and 170 mg propofol intravenously (IV). Succinylcholine (SCh) 100 mg IV was used for endotracheal intubation. Fasciculations were intense and occurred over the entire body. Anesthesia was maintained with propofol, a sufentanil infusion, and isoflurane; neuromuscular block was maintained with vecuronium, 18 mg total dose. A Foley catheter was inserted prior to surgical incision. A tourniquet was applied for only 80 min. Total anesthesia time was 405 min. The anesthetic course was extremely stable intraoperatively (blood pressure 110/60 mm Hg, heart rate 70 bpm, temperature 36.1 degrees C, end tidal CO2 28-33 mm Hg, O2 saturation 99%-100%), except for the patient's urine output. He was given 4700 mL of lactate Ringer's solution, but the urine output was only 300 mL and it was dark yellow. Due to low urine output, he received 500 mL of lactated Ringer's solution upon his arrival in the postanesthesia care unit. One hour later, tea-colored urine in the Foley catheter and peaked T waves on the electrocardiogram were noted. At this time, urine output was about 100 mL/h. Myoglobinuria was suspected. A stat Chem 6, urinalysis, and serial creatinine phosphokinase (CPK) levels were ordered. The K+ concentration was 6.5 mEq/L; the result of a repeat analysis was 6.9 mEq/L. Other electrolytes were normal, as were blood urea nitrogen and creatinine. Arterial blood pressure, heart rate, and temperature remained unchanged. The patient was immediately treated with a 1-mL ampule of dextrose 50% and 10 units of regular insulin IV. He also received a 1-mL ampule of 10% calcium gluconate IV, 44 mEq of NaHCO3-1 in 1 L of 5% dextrose at 150 mL/h to alkalinize the urine, and two 15-g doses of sodium polystyrene sulfonate per os. His urine output remained greater than 100 mL/h, and his vital signs were stable and unchanged. The surgeon ruled out compartment syndrome. Urine myoglobin was ordered as well as a Sequential Multiple Analysis 12. Repeat K+ level was 6.2 mEq/L, which proceeded to normal values (4.6 mEq/L) within a few hours. The first postoperative CPK value was 31,180 U/L, and the CPK value went to a maximum of 74,950 U/L at 1 day postoperatively (normal values, 20-190 U/L). It slowly decreased and after 1 wk was 5717 U/L. Serum glutamic oxaloacetic transaminase increased to 2560 U/L postoperatively and then decreased to 580 U/L 1 wk postoperatively (normal values, 7-47 U/L). Serum glutamic pyruvic transaminase rose to 269 U/L postoperatively (normal values, 10-50 U/L), and lactic dehydrogenase increased to 1728 U/L 1 day postoperatively (normal values, 100-240 U/L). Urine myoglobin was >250,000 ng/mL (normal values, <15 ng/mL). Blood urea nitrogen/creatinine, gamma-glutamyl transpeptidase, and CPK-isozyme-myocardial band results were normal. The patient's urine was tested for steroids on the second postoperative day and the result was negative. (Due to the short plasma half-life of steroids, the negative result does not eliminate steroid use.) The patient remained in the intensive care unit for 2 days. Vital signs remained stable, and he was discharged 9 days postoperatively. A loss of muscle mass had occurred over his entire body, and at the time of his discharge he weighed only 72.7 kg (a 18.2-kg loss in 1 wk). The patient returned to the operating room 8 wks later for irrigation and debridement of a right tibial wound infection and the removal of two screws from the tibia. He was extremely depressed because he could not play football due to his infection and muscle loss. He still weighed 72.7 kg and did not gain any weight or muscle mass despite weight lifting and dietary supplementation. The preoperative laboratory test values were normal, including a CPK value of 78 U/L. The procedures proceeded uneventfully under epidural anesthesia. Discussion There are numerous reports of rhabdomyolysis after general anesthesia with halothane or enflurane with or without SCh [1-6]. Most of the patients in these cases were subsequently found to have malignant hyperthermia or muscular dystrophy, either Duchenne's [1-3] or Becker [4,5]. There are a few dystrophies presenting after age 20 yr, but these seemed unlikely in our patient. Rhabdomyolysis, or muscle necrosis, is the syndrome resulting from skeletal muscle injury with the release of cell contents (e.g., K+, phosphorous, creatine, myoglobin) into the plasma. It results from conditions in which the demand for oxygen exceeds the supply or in which there is an inability to use the available supply and can occur from increased muscle energy production or disturbances in muscle blood flow or metabolism [7]. Complications arise from local muscle injury as well as renal failure, life-threatening ventricular dysrhythmias, increased K+, disseminated intravascular coagulation, hypocalcemia, and hyperphosphatemia [8,9]. After childhood, SCh-induced rhabdomyolysis is rare without an underlying cause [10]. Since at least 200 g of muscle must be injured to see myoglobin in the urine [8], the cause seemed unlikely to be surgery on one knee. In a case report, a 20-yr-old body builder developed rhabdomyolysis after a 20-wk course of anabolic steroids [11]. Anabolic drugs cause a decrease in protein catabolism [12]. Although our patient claimed not to be taking anabolic drugs, he was taking supplemental dietary amino acids. This would affect his metabolism in a similar manner (by changing the ratio of anabolic to catabolic metabolism), and this alteration in muscle metabolism may be the risk factor in this case. Treatment is aimed initially at prevention of acute renal failure. Maintaining adequate plasma volume is most important. The glomerular tubules excrete myoglobin, which dissociates into ferrihemate at pH < 5.6. Ferrihemate is toxic to the proximal tubular cells. Urine alkalinization prevents dissociation, and the use of loop or osmotic diuretics is beneficial [9]. The life-threatening hyperkalemia must also be treated (e.g., with insulin, glucose, CaCl2, NaHCO3-). SCh-induced fasciculations produce muscle damage and myoglobinuria [13], the degree of which is usually small and insignificant. Rhabdomyolysis is an adverse reaction to SCh with possible myoglobinuric acute renal failure. Pretreatment with a nondepolarizing muscle relaxant may be tried to prevent fasciculations but is of questionable value [13]. With the advent of puberty, the incidence of myoglobinemia decreases [10]. It is hard to explain the late onset of this patient's myoglobinuria. Most studies show the onset to be within 1-3 h, but it can occur as early as 15 min after SCh administration [1,5,10,14]. We believe that myoglobinuria occurred earlier in this patient but was not detected due to the low urine output. Grossly visible myoglobinuria is a function of glomerular filtration rate and urine flow rate. Therefore, visible myoglobinuria does not correlate with the extent of muscle injury [9]. Anesthesiologists must frequently anesthetize young, muscular athletes for multiple orthopedic procedures. We advise avoidance of SCh in patients, regardless of their drug history.