Anesthetic Management of a Patient With a History of Rhabdomyolysis for Dental Treatment

Rhabdomyolysis refers to the breakdown of skeletal muscle causing the release of intracellular muscle constituents, such as creatinine kinase, myoglobin, and potassium, into the bloodstream.¹ In patients at high risk of rhabdomyolysis, the use of suitable anesthetics, with attention to intravenous fluid management, electrolyte balance, respiration, and metabolism, should be addressed. Here, we report the general anesthetic management of an outpatient with a history of rhabdomyolysis.

A 23-year-old man weighing 72 kg with a body mass index of 32.4 kg/m² was scheduled to undergo general anesthesia for dental treatment and biopsy for fibrous hyperplasia of the buccal mucosa. He had presented with symptoms of rhabdomyolysis at the age of 22 and had recovered after receiving fluid infusion and the administration of antibiotics for 3 days. He had trisomy 21, tetralogy of Fallot with atrioventricular septal defect repaired at 2 years of age, epilepsy, and intellectual impairment (difficulty communicating) as additional complications.

General anesthesia was induced using thiamylal sodium (425 mg), fentanyl (200 μg), and rocuronium bromide (30 mg) intravenously, followed by the continuous administration of midazolam (0.1 mg/kg/h) and remifentanil (0.2 μg/kg/min). Anesthesia was maintained with nitrous oxide (2–2.5 L/min) in oxygen (1 L/min), midazolam (0.06–0.1 mg/kg/h), and remifentanil (0.1–0.25 μg/kg/min). The total infusion volume of Ringer's acetate solution with 1% glucose was 700 mL. The durations of surgery and anesthesia were 75 and 156 minutes, respectively. No problems were encountered, and no symptoms of rhabdomyolysis occurred during the perioperative period.

Drugs with suitable safety profile are needed in the management of anesthesia in patients at risk of rhabdomyolysis. Volatile anesthetics, propofol, and succinylcholine were not used for this case. Volatile anesthetics are well-known triggers of malignant hyperthermia. It has been suggested that propofol causes rhabdomyolysis as one symptom of propofol infusion syndrome. There is a strong association between propofol infusion syndrome and propofol infusions at doses greater than 4 mg/kg/h of longer than 48 hours' duration.² However, the possibility of metabolic acidosis increases with infusion of propofol at doses over 4.5 mg/kg/h (75 mcg/kg/min) for 2–3 hours or more.³ Furthermore, it has been reported that administration of propofol during status epilepticus is involved in the genesis of rhabdomyolysis.⁴ For these reasons, we thought it appropriate to avoid using propofol for this case. Succinylcholine was not used to avoid excessive and unwanted fasciculation.

In this case, Ringer's acetate solution was used as the infusion fluid. The preferred intravenous fluid in order to prevent the development of rhabdomyolysis is not clear. When malignant hyperthermia develops, the infusion of cooled physiological saline is effective in lowering body temperature without increasing potassium concentration. The infusion of Ringer's lactate solution is not recommended under conditions of metabolic acidosis. However, there is no clear evidence for selecting intravenous fluids in a malignant hyperthermia crisis.⁵

We performed anesthetic management of a patient with a history of rhabdomyolysis using thiamylal sodium, midazolam, rocuronium bromide, nitrous oxide, fentanyl, and remifentanil, without evidence of rhabdomyolysis.

This research was originally published in the Journal of the Japanese Dental Society of Anesthesiology. 2015;43(2):259–261.