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Veit-Simon Eckle, Eckhard Schmid, Tanja Fehm, Christian Grasshoff
Med Sci Monit 2012; 18(11): CS91-93
Background: The muscle-relaxing effects of succinylcholine are terminated via hydrolysis by plasma cholinesterase. There are multiple genetic variants of this enzyme and clinical circumstances that might influence the activity of plasma cholinesterase and eventually lead to prolonged neuromuscular blockade following succinylcholine application.
Case Report: Here, we report a parturient woman with atonic bleeding who suffered significant blood loss (hemoglobin 6.0 g•dL–¹). For surgical curettage, general anesthesia was performed by using short-acting succinylcholine. By the end of the 105-minute procedure, the patient’s trachea was extubated. After extubation she showed signs of the prolonged neuromuscular blocking action of succinylcholine. At this time, the patient received an AB0-compatible red blood cell transfusion and recovered instantly from neuromuscular blockade. The plasma cholinesterase (3.200 U•L–¹) was below the normal range (4.900–12.000 U•L–¹). Patient’s blood DNA analysis revealed heterozygously the genetic K variant of plasma cholinesterase. After red blood cell transfusion, serum potassium was elevated (5.7 mmol•L–¹; 4.4 mmol•L–¹ prior to transfusion).
Conclusions: Pregnancy, blood loss and genetic variation contributed to impairment of plasma cholinesterase. Due to high-speed red blood cell transfusion, hemolytic release of erythrocyte cholinesterase might have terminated the neuromuscular blocking succinylcholine effect.