Succinylcholine-Induced Masseter Spasm

Masseter spasm (masseter muscle rigidity) is increased jaw tone after succinylcholine, with a tightly clenched jaw that prevents mouth opening while limb muscles relax. It can occur as a variant of normal response or as an early feature of malignant hyperthermia.

Epidemiology. Incidence is about 1% in children given succinylcholine with halothane, and lower with newer volatile agents, and about 0.3% in adults. Its link with malignant hyperthermia is clinically important, since a substantial minority of those with marked rigidity prove susceptible on testing. Estimates vary between series.

Types. Mild increase in jaw tone (common, benign) versus severe rigidity (jaw cannot be opened with 5 to 10 kg force, or persistent beyond 2 minutes). Generalised muscle rigidity is a much stronger marker of malignant hyperthermia.

Risk factors. Children, young age, family history of malignant hyperthermia, muscle disease (myotonia, central core disease, King-Denborough syndrome), strabismus surgery and volatile anaesthetic exposure.

Pathophysiology.

Succinylcholine causes sustained contracture of masseter muscle fibres. In malignant hyperthermia, uncontrolled calcium release from the sarcoplasmic reticulum (ryanodine receptor defect) produces hypermetabolism.

Jaw tightness with inability to open the mouth, rigid jaw, difficult laryngoscopy, rise in end tidal carbon dioxide, tachycardia, arrhythmia, masseter tenderness later, myoglobinuria and dark urine.

Red flags.

• Rising end tidal carbon dioxide despite constant ventilation.
• Generalised rigidity.
• Unexplained tachycardia, arrhythmia or hyperkalaemia.
• Temperature rise (a late sign).
• Dark urine.

Assess jaw tone and presence of rigidity in other muscles. Monitor end tidal carbon dioxide, heart rate, temperature, ECG and potassium. Send blood gas, potassium, creatine kinase, lactate and urine myoglobin. Creatine kinase peaks at 12 to 24 hours, and values over 10,000 units/L support a pathological reaction.

Differential diagnosis.

• Normal increase in jaw tone.
• Inadequate dose or early laryngoscopy.
• Temporomandibular joint problem.
• Trismus from infection or trauma.
• Myotonia.
• Malignant hyperthermia.

Mild increase in tone with normal vital signs. Continue anaesthesia cautiously with a non-triggering technique (stop volatile agent, use total intravenous anaesthesia), monitor end tidal carbon dioxide, temperature and creatine kinase, and postpone elective surgery if rigidity persists.

Severe rigidity or any sign of hypermetabolism. Start the malignant hyperthermia response. Stop volatile anaesthetic and succinylcholine, hyperventilate with 100% oxygen at 10 L/min or more, change to total intravenous anaesthesia, call for help, and give dantrolene.

• Dantrolene: 2.5 mg/kg IV rapidly, repeated at 1 mg/kg to 2.5 mg/kg until end tidal carbon dioxide and heart rate normalise; reconsider diagnosis if cumulative dose reaches 10 mg/kg; maximum 10 mg/kg in most cases; monitor temperature, end tidal carbon dioxide, potassium and creatine kinase; caution in hepatic impairment.

Airway. If the jaw cannot be opened, ventilate by facemask or supraglottic airway where possible, and use a non-depolarising agent such as rocuronium 0.6 to 1.2 mg/kg IV to relax muscle. A difficult airway plan applies.

Follow up. Check creatine kinase at 6 to 12 hours and daily until falling, and monitor urine colour and renal function. Admit for at least 12 to 24 hours with ECG and temperature monitoring. Refer to a malignant hyperthermia testing service, advise relatives, and issue an alert.

Monitoring. Continuous end tidal carbon dioxide, ECG, temperature, urine output, potassium and creatine kinase.

Referral and escalation. Critical care for hypermetabolism. Anaesthetic malignant hyperthermia service for testing and counselling.