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Failed Reversal of Neuromuscular Blockade Despite Sugammadex: a Case of Undiagnosed Pseudocholinesterase Deficiency

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Failed Reversal of Neuromuscular Blockade Despite Sugammadex: a Case of Undiagnosed Pseudocholinesterase Deficiency CASE REPORT Failed reversal of neuromuscular blockade despite sugammadex: A case of undiagnosed pseudocholinesterase deficiency Gozde Inan, MD*, Elif Yayla, MD** and Berrin Gunaydin, MD*** *Consultant; **Resident; ***Professor Department of Anesthesiology and Reanimation, Gazi University, School of Medicine, Besevler, Ankara (Turkey) Correspondence: Gozde Inan, MD, Gazi University School of Medicine, Department of Anaesthesiology and Reanimation, Besevler, Ankara (Turkey); Tel: +90 312 202 4166; Fax: +90 312 202 4166; E-mail address: [email protected] ABSTRACT The management of an undetected pseudocholinesterase deficiency in a parturient who underwent urgent cesarean section has been presented. After rapid sequence induction with succinylcholine, rocuronium was used for maintenance of neuromuscular block. At the end of the operation neostigmine was given to antagonize the residual block. Upon persistent prolonged neuromuscular blockade sugammadex was administered. Probable reasons, drug interactions, the importance of suspecting pseudocholinesterase deficiency and the need of neuromuscular monitoring have been argued in this case report. Key words: Pseudocholinesterase deficiency; Cesarean section; Sugammadex Citation: Inan G, Yayla E, Gunaydin B. Failed reversal of neuromuscular blockade despite sugammadex: A case of undiagnosed pseudocholinesterase deficiency. Anaesth Pain & Intensive Care 2015;19(2):184- 186 INTRODUCTION induction of neuromuscular block was provided by succinylcholine and maintained with rocuronium, Prolonged neuromuscular blockade is a common neostigmine and sugammadex were administered complication that every anesthesiologist has to antagonize the blockade. We aimed to discuss the experienced sometime in his clinical practice. management of prolonged neuromuscular block Pseudocholinesterase (PChE) deficiency should probably due to an undetected PChE deficiency in be suspected in case of prolonged neuromuscular a parturient who underwent emergency cesarean blockade.1 PChE is an enzyme synthesized in the liver, section (C/S). which hydrolyses esters such as in muscle relaxants (succinylcholine, mivacurium) and ester type local CASE REPORT anesthetics. Mostly, in clinic practice PChE deficiency presents challenge to the anesthesiologist causing Thirty-six year-old, G2P1 parturient at 38.3 weeks prolonged paralysis following succinylcholine or of gestation admitted for an emergency cesarean mivacrium administration. There is no treatment delivery. Her prior surgeries included a C/S and for PChE deficiency and diagnosis is confirmed by a hysteroscopy due to secondary infertility. She laboratory findings. The suspicion and awareness described a prolonged emergence after her previous of this condition can help management of such C/S but we were unable to reach any anesthetic cases. When suspected, supportive care should be records. Her pregnancy remained uneventful till obtained with possible postoperative ventilation delivery of the new born. need. On arrival to the operating room, the patient This situation can complicate anesthetic presented with deceleration and emergent C/S management, especially if it is undetected. A case of was planned. Night shift team from anesthesia unrecognized PChE deficiency is reported, in which department decided to perform spinal anesthesia but after 3 failed attempts, anesthesia plan was 184 ANAESTH, PAIN & INTENSIVE CARE; VOL 19(2) APR-JUN 2015 case report converted to general anesthesia. PChE deficiency can be inherited, acquired or 2 Anesthesia was induced with propofol 2 mg/kg and iatrogenic and results in impairment of esters. succinylcholine 1 mg/kg IV after preoxygenation Non-genetic factors include; physiologic causes like for 3 min and maintained with 0.75 MAC of advanced age and pregnancy, diseases like renal sevoflurane in 50% air-oxygen mixture. After the disease, malnutrition, liver disease, malignancy, delivery of the newborn, remifentanil infusion (0.1- collagen vascular disease, burns, hypothyroidism, 0.2 µg/kg/min) and bolus dose of rocuronium (20 and some medications (oral contraceptives, 3-6 mg) were administered. The surgical procedure clindamycine, insecticides, metoclopramide). continued for approximately 50 min. Five minutes A literature search revealed reports of PChE after discontinuation of anesthetics, neostigmine deficiency mostly from obstetrical literature. Two (2 mg) with atropine (1 mg) were administered to main reasons could explain this finding; initially antagonize the residual neuromuscular blockade. pregnancy, itself leads to PChE deficiency. Blitt Since the patient failed to provide adequate tidal et al.7, found significantly lower cholinesterase volume following 10 min, sugammadex 2 mg/kg activity in pregnant patients than in nonpregnant was given IV. After the patient was able to open her patients. In a case series of patients with PChE eyes on command and her spontaneous breathing deficiency, PChE level of a 31-year old gravid in improved, she was extubated. However, 1 hour whom prolonged paralysis developed following later she developed dyspnea and tachycardia in the mivacurium administration to facilitate tracheal ward. The patient was sedated with intermittent intubation in C/S, increased to normal range boluses of midazolam (1 mg) and her ventilation after the following 2 months (initially; 1017 IU/L, was supported using continuous positive airway later; 3124 IU/L, normal; 2000-11000 IU/L).8 It pressure (CPAP) 5 cmH2O with pressure support was estimated that in parturients, PChE deficiency 9 (PS) 10 cmH2O. She gradually regained muscle incidence is nearly 1:3200. Screening the enzyme strength and provided adequate tidal volume levels during pregnancy before birth giving in such 3.5 hours after the induction of succinylcholine a risky population might be beneficial. The enzyme dose. Oxygen was administered by nasal cannula levels should be repeated after several months to afterwards. Blood gas analysis revealed normal show as if this situation is due to pregnancy. In the oxygenation, ventilation and acid–base status (pH: presented case report, serum pseudocholinesterase 7.47, PaCO2: 29 mmHg, PaO2: 113 mmHg, HCO3: activity which was studied on the next day of the 23.7 meq/L, SaO2: 97 %, BE: 1.1). operation found 64 U/L (normal 4000-12000 On the following day laboratory analysis U/L), and after 3 months control level of serum demonstrated a serum PChE activity of 64 U/L pseudocholinesterase increased to 214 U/L but still (normal 4000-12000 U/L). The patient was was lower than the normal clinical range. discharged home 2 days later. Three months after Succinylcholine is the most preferred neuromuscular her C/S serum PChE level was repeated and found blocker especially in emergency procedures. By a out to be 214 U/L. questionnaire, 170 anesthetists were surveyed to assess their usage of succinylcholine in adult elective DISCUSSION and emergency anesthesia practice.10 Ninety-seven Our case presents a parturient suffering from percent of the respondents told that they prefer postoperative respiratory insufficiency after C/S succinylcholine in emergency mainly in anticipated under general anesthesia. Night shift team failed difficult intubation (74%), C/S (54%) and obesity to diagnose the possible PChE deficiency and (49%). Prolonged blockade was reported as an 10 subsequently administered anticholinesterase for incidence of 39% in that questionnaire. reversal of neuromuscular blockade. In patients undergoing C/S, succinylcholine has Once prolonged neuromuscular blockade been the mainstay of rapid sequence intubation occurs, to determine the possible reason all process with its favourable features like quick onset causes like electrolyte imbalances (hypokalemia, and short duration of action. However, since the hypocalcemia, hypermagnesemia), hypothermia, development and introduction of sugammadex several drugs, renal and hepatic diseases should be into clinic practice, a new approach for reversal of reviewed. In case of succinylcholine or mivacurium neuromuscular blockade, the on-going usage of 11 administration as neuromuscular blocker agent, a succinylcholine has been questioned. Recently, deficiency in PChE should be suspected as these replacement of succinylcholine with rocuronium drugs are metabolized by plasma cholinesterase.1 and sugammadex combination has been suggested ANAESTH, PAIN & INTENSIVE CARE; VOL 19(2) APR-JUN 2015 185 sugammadex and pseudocholinesterase deficiency for rapid sequence intubation.12 In a patient with II block induced with neostigmine following catatonic schizophrenia and pseudocholinesterase succinylcholine administration was reported.14 deficiency, rocuronium was selectively antagonized This report also underlines the importance of using by sugammadex, safely and efficiently for intubation neuromuscular monitoring. If a neuromuscular 13 during electroconvulsive therapy. stimulator have been used it would help to confirm Succinylcholine should not have been chosen for succinylcholine-induced paralysis with train of four the present case because of the patient’s previous stimulation. The patient might be kept sedated prolonged recovery history should maintain a and mechanically ventilated till she regained her suspicion of PChE deficiency. Even it was used muscular strength. neostigmine should not be the choice of drug It is also very important to identify these patients for reversal of neuromuscular blockade. But to ensure their future healthcare by informing the situation was thought to be a residual
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