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Year : 2018  |  Volume : 12  |  Issue : 4  |  Page : 651-652

Prolonged neuromuscular blockade in a middle-eastern female patient homozygous for atypical plasma cholinesterase

Department of Anesthesia, Pain Management and Perioperative Medicine, Henry Ford Hospital, Detroit, Michigan, USA

Correspondence Address:
Dr. Jose R Navas-Blanco
Department of Anesthesia, Pain Medicine and Perioperative Medicine, Henry Ford Hospital, 2799 West Grand Boulevard, CFP-341, Detroit, Michigan 48202
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/sja.SJA_181_18

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Date of Web Publication4-Oct-2018

How to cite this article:
Rico-Mora DA, Walton L, Navas-Blanco JR. Prolonged neuromuscular blockade in a middle-eastern female patient homozygous for atypical plasma cholinesterase. Saudi J Anaesth 2018;12:651-2

How to cite this URL:
Rico-Mora DA, Walton L, Navas-Blanco JR. Prolonged neuromuscular blockade in a middle-eastern female patient homozygous for atypical plasma cholinesterase. Saudi J Anaesth [serial online] 2018 [cited 2023 Mar 23];12:651-2. Available from:


Pseudocholinesterase (PchE, also known as “butyrylcholinesterase ”) is a serine enzyme capable to hydrolyze choline esters found in succinylcholine, mivacurium, and ester local anesthetics.[1] There are several genetic variants of PchE deficiency. The most important variants are the atypical or dibucaine-resistant, the fluoride-resistant, the silent variant, and the K-variant.[2] The neuromuscular prolongation after succinylcholine in patients with heterozygous or homozygous atypical PchE is variable. Several confounding factors may play a significant role in this prolongation of effect, such as male gender, concomitant use of metoclopramide or etomidate, liver disease, and pregnancy – this latter has been found to decrease PchE activity as early as the 10th week of gestation.[3]

The authors present the case of a middle-eastern patient undergoing dilation and curettage who developed prolonged muscle paralysis after single administration of succinylcholine and required postoperative mechanical ventilation. She had no documented allergies and denied prior surgeries. Given that the patient was not appropriately fasted, and due to the emergent nature of the procedure, the decision was to proceed with rapid sequence induction and intubation with propofol, fentanyl, and succinylcholine (1 mg/kg) to facilitate endotracheal intubation, which was uneventful. No further neuromuscular blocker was administered. Ten minutes after the procedure finalized (approximately 45 min after induction), the patient had a persistent neuromuscular blockade, evidenced by train-of-four of 0 and the absence of spontaneous respirations. The decision was made to deepen the anesthesia with intravenous propofol and midazolam and to take the patient sedated and intubated to the postanesthesia care unit. The patient was extubated approximately 4 h after induction in the postanesthesia care unit, after the patient showed adequate muscle strength (head lift >10 s), following verbal commands and tidal volume >5 cc/kg (375 cc/breath) with minimal pressure support from the ventilator. The patient was discharged home on the postoperative day one; on further questioning, she had no recall about the episode. Dibucaine inhibition test was performed using preoperative and postoperative blood samples with results of 20% and 19%, respectively (reference range >80%).

This case highlights the importance that besides genetic factors, ethnicity also plays a significant role in the development of this clinical condition, especially in the patient described in our case. Hosseini et al. studied the differences in PchE activity between the Irish population and the Iranian population which corroborated the findings from Szeinberg et al. The differences were based on the dibucaine inhibition test and fluoride test. They concluded that the Iranian population has intrinsically lower levels of PchE activity compared with the Irish population (this latter has higher dibucaine and fluoride numbers). In addition, no difference was observed regarding PchE activity between Iranian Jewish and Muslims.[4],[5] We emphasize the significance of providing the most appropriate management to prevent detrimental outcomes for these patients (e.g., the use of neuromuscular monitoring, mechanical ventilation to avoid respiratory distress, and sedation to avoid awareness) as well as provide adequate education and communication of the diagnosis of PchE deficiency to the patient, family and the medical team in order to prevent exposure to succinylcholine in the future surgical procedures.

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  References Top

Reti IM, Torres J, Morad A, Jayaram G. Pseudocholinesterase activity in an ECT patient: Case report. Psychosom 2011;52:392-3.  Back to cited text no. 1
Darvesh S, Hopkins DA, Geula C. Neurobiology of butyrylcholinesterase. Nat Rev Neurosci 2003;4:131-8.  Back to cited text no. 2
Dell-Kuster S, Levano S, Burkhart CS, Lelais F, Zemp A, Schobinger E, et al. Predictors of the variability in neuromuscular block duration following succinylcholine: A prospective, observational study. Eur J Anaesthesiol 2015;32:687-96.  Back to cited text no. 3
Hosseini J, Firuzian F, Feely J. Ethnic differences in the frequency distribution of serum cholinesterase activity. Ir J Med Sci 1997;166:10-2.  Back to cited text no. 4
Szeinberg A, Pipano S, Assa M, Medalie JH, Neufeld HN. High frequency of atypical pseudocholinesterase gene among Iraqi and Iranian jews. Clin Genet 1972;3:123-7.  Back to cited text no. 5


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