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 . here , we report a parturient woman with atonic bleeding who suffered significant blood loss ( hemoglobin 6.0 gdl ) . for surgical curettage , general anesthesia was performed by using short - acting succinylcholine . by the end of the 105-minute procedure , 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 ul ) was below the normal range ( 4.90012.000 ul ) . after red blood cell transfusion , serum potassium was elevated ( 5.7 mmoll ; 4.4 mmoll prior to transfusion ) . 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 . the rapid action of succinylcholine makes this depolarizing muscle relaxant favorable for facilitating tracheal intubation in emergency patients and clinical situations with high aspiration risk . the neuromuscular blocking effects of succinylcholine and mivacurium are terminated by rapid hydroxylation by the butyrylcholinesterase enzyme ( bche ; plasma cholinesterase ) . unfortunately , approximately 25% of individuals in a white population have a hereditary variation of the enzyme , extending the neuromuscular blocking effects of both muscle relaxants up to several hours . apart from genetic variability , acquired diseases such as hepatic failure or physiologic changes during pregnancy are known to reduce the amount of plasma cholinesterase or the efficiency of its enzymatic action . therapeutic alternatives are few ; either the patients are ventilated for 48 hours until the end of prolonged neuromuscular block , or injection of cholinesterase may lead to a shorter duration of action of the neuromuscular blocking agent mivacurium . here , we report a parturient woman with severe atonic bleeding and prolonged succinylcholine block after uterine abrasion under general anesthesia , whose prolonged muscle relaxation was terminated by application of packed red cells . a 31-year - old parturient woman ( 70 kg body weight ) without history of previous anesthesia was admitted to the hospital with atonic bleeding after 25-hour labor preceding successful delivery at home . in order to replace perinatal blood loss , 1 l colloid and 1 l crystalloid solution were given by the emergency team before the patient arrived at the hospital . at admission the patient appeared fully conscious , and heart rate [ hr ] and blood pressure [ bp ] were measured to be 90 beatsmin and 120/60 mmhg , respectively . after rapid sequence induction of general anesthesia with 200 mg propofol , 100 mg succinylcholine ( 1.25 mgkg ) , and 1 mg rapifen , the tubus was successfully placed into the trachea . during general anesthesia maintained with sevoflurane ( 1.5 vol-% ) , blood pressure and heart rate remained stable , obviating the need for immediate blood transfusion with ab0-untested red packed cells . as blood coagulation appeared to be clinically impaired , 4 g fibrinogen and 2 g tranexamic acid were given intravenously . removal of residual placenta was complicated by a retroflected uterus , prolonging the surgical procedure to 105 minutes . after extubation of the trachea at stable cardiovascular conditions , the hr increased to 140 bpm , the tongue was obstructing the airway , and tachydyspnoea could be observed . oxygenation was maintained by applying jaw thrust and supply of 100% oxygen using a face mask . neuromuscular monitoring , manually tested , showed no fading of the  train of four  , thereby excluding dual block . the patient was awake but she could not open her eyes or give hand signs . furthermore , uncoordinated muscle activity was visible . as at this time , automatic bp stopped measuring values in a detectable range , making blood loss the most likely cause . consequently , ab0-compatible red blood cells ( 250 ml ) were transfused at high flow by using a pressure bag and a warming system ( ranger ) . while reinduction of general anesthesia was prepared , the patient immediately regained neuromuscular function , tachydyspnoea stopped , and she was able to open her eyes , give hand signs , and speak . simultaneously , the hr decreased to 90 beatsmin and automatic bp displayed values in the normal range , enabling transfer to the intermediate care unit . the following morning , plasma cholinesterase level was 3.200 ul , which is below the normal range ( 4.90012.000 ul ) , and the patient s blood dna testing revealed that she was a heterozygous carrier of the k variant of plasma cholinesterase . in our patient , signs of physical stress and the inability fof automatic blood pressure measurement ( probably due to shivering ) were misinterpreted to be caused by intravascular volume deficiency , in particular as a hemoglobin level as low as 6.0 gdl . retrospectively , it became clear that she had a prolonged action of succinylcholine due to a genetic variation , namely , the k variant of the butyrylcholinesterase enzyme . the frequency of the k variant of plasma cholinesterase is described to be at 13% , and the enzyme activity is typically decreased by 30% . even in patients carrying the heterozygous k variant , effects of mivacurium or succinylcholine might be prolonged . pregnancy and hemodilution as a result of volume therapy might have further contributed to decreased plasma cholinesterase activity . furthermore , significantly lower levels of plasma cholinesterase are described to occur in up to 10% of parturients . it can be assumed that the immediate improvement of neuromuscular distress was either caused by plasma cholinesterase in the residual serum of packed red cells , or by release from hemolyzed erythrocytes . epstein et al have shown that the activity of serum cholinesterase in stored whole blood was around 87% of initial values after 21 days . it has been demonstrated in patients with k variant that administration of plasma cholinesterase reverses the effect of mivacurium . measured cholinesterase activity in erythrocytes and plasma by hydrolysis of acetyl- , butyryl- , and succinylcholine . determination of activity correlated well among the 3 substrates ( r>0.94 ) , with erythrocyte acetylcholinesterase being 3.7-fold more effective compared to plasma cholinesterase . our patient recovered , most probably due to transfusion of red blood cells , which were hemolyzed in part by high speed transfusion , leading to an increase in serum potassium from 4.4 mmoll to 5.7 mmoll after transfusion . lovely et al reported a patient with compromised plasma cholinesterase activity undergoing first surgery without prolonged succinylcholine blockade , but experiencing it after a second intervention . the authors assumed that packed red blood cells given perioperatively masked atypical plasma cholinesterase the first time succinylcholine was administered . in another study , concentrations of the short - acting opioid remifentanil were lower when incubated with red blood cells compared to plasma incubation , suggesting a role of erythrocyte cholinesterase in remifentanil esterase - dependent metabolism . moreover , in organophosphorus poisoning , erythrocyte cholinesterase might be a bioscavenger when given as whole blood transfusion , as reported by ryniak et al . . in addition to the k variant of plasma cholinesterase , there are other genetic mutations , like the atypical ( a ) and silent ( s ) variant , with different impact on enzyme activity . although the modest reduction of plasma cholinesterase due to the k variant ( 67% of normal enzyme activity ) usually does not cause significant prolongation of succinylcholine effect , the combination with another variant , chronic illness , organophosphorus poisoning , or , as in our case , pregnancy and major blood loss , might lead to clinical appearance . this is in line with the study of levano et al , who genotyped 9 patients with prolonged neuromuscular block after succinylcholine , but 2 of them displayed normal molecular genetic results . application of succinylcholine or mivacurium in these patients must be carefully considered , since rapid - sequence induction can be performed alternatively with rocuronium [ 2022 ] . the routine use of red blood cells to determine prolonged muscle dysfunction is certainly not recommended , but it helped in the case reported .