Delayed recovery from paralysis associated with plasma cholinesterase deficiency.

INTRODUCTION: This case was to describe a patient presented a 6 h length of apnea associated with low cholinesterase activity.

CASE DESCRIPTION: A 32 years old female patient (body weight 50 kg, height 160 cm) was admitted to the hospital for laparoscopy combined with hysteroscopy exploration. The preoperative interrogation revealed no significant personal or family history of adverse reaction to anesthetics. The patient was healthy, with no chronic or systemic disease. ASA classification is I. We performed a general anesthesia with intubation to the patient. Succinylcholine 100 mg was administered in anesthesia induction. After intubation, cisatracurium 3 mg and 3% sevoflurane were used for anesthesia maintenance. The patient had been mostly unresponsive to external stimuli for 10 min since the end of the operation. Six hours after operation, the patient had totally recovered from paralysis and tracheal tube was extubated. The plasma cholinesterase test showed 291 U/L, significantly below normal (4650-10,440 U/L). Three days after operation, the patient was discharged from hospital with no special discomfort.

DISCUSSION AND EVALUATION: Reduced plasma cholinesterase activity may occur as a result of inherited, acquired defects or iatrogenic causes. If the acquired defects are excluded, low BChE activity is usually considered to be caused by mutations in butyrylcholinesterase gene (BCHE). 80% of the patients experiencing prolonged neuromuscular blockade following mivacurium have butyrylcholinesteraseen enzyme (BChE) deficiency of genetic origin. The novel mutation of BChE gene is usually associated with the ethnic of the patients. There is no specific treatment for butyrylcholinesterase deficiency and the mainstream is to maintain ventilatory support until succinlcholine is metabolized out of the myoneural junction and neuromuscular function recovers. Transfusion of fresh frozen plasma is also viable.

CONCLUSIONS: Plasma cholinesterase deficiency is a genetic or acquired condition. The most obvious feature of this genetic variants is prolonged recovery from paralysis in which administrated with succinylcholine or mivacurium. Once this is suspected, a laboratory test is important. There is no specific treatment for plasma cholinesterase deficiency. The best and safest way is to let the patient recover spontaneously. Mechanical ventilation support is important.