312 Dusunen Adam The Journal of Psychiatry and Neurological Sciences, Volume 31, Number 3, September 2018 Dusunen Adam The Journal of Psychiatry and Neurological Sciences 2018;31:312-315 Case Report / Olgu Sunumu DOI: 10.5350/DAJPN2018310311 Severe Pseudocholinesterase Deficiency and ECT: a Case Report Eren Yildizhan 1 , Nesrin Buket Tomruk 1 , Hafize Miray Aytac 1 , Hakan Yildirim 2 , Ozge Canbek 1 1 Bakirkoy Research and Training Hospital for Psychiatric and Neurological Diseases, Department of Psychiatry, Istanbul - Turkey 2 Bakirkoy Research and Training Hospital for Psychiatric and Neurological Diseases, Department of Anesthesiology, Istanbul - Turkey ABSTRACT Severe pseudocholinesterase deficiency and ECT: a case report Pseudocholinesterase (PCE) deficiency is an inherited condition in which recovery from anesthetic agents like succinylcholine and mivacurium is slow and complicated by prolonged paralysis of respiratory muscles in susceptible patients. We present a very rare case of a 29-year-old woman with a 15-year history of schizophrenia with pseudocholinesterase deficiency that we encountered in our practice. Since the measurement of PCE levels of all patients eligible for ECT is part of our pre-ECT assessment procedure, we could detect the deficiency before the ECT procedure. We performed modified ECT with propofol and rocuronium instead of succinylcholine as usual. Sugammadex was used for speeding up the recovery. Response to treatment as measured by the Positive and Negative Symptom Scale was good and we completed 9 ECT sessions without complication. We suggest further investigation of this topic because screening for PCE levels in pre-ECT assessment may reduce complications of modified ECT with anesthesia. Keywords: Electroconvulsive therapy, mivacurium, pseudocholinesterase deficiency, schizophrenia, succinylcholine, sugammadex ÖZ Şiddetli pseudokolinesteraz eksikliği ve EKT: Bir olgu sunumu Pseudokolinesteraz eksikliği, eksikliğin görüldüğü hastalarda, suksinilkolin ve mivakuryum gibi anestezi ajanlardan uyanmanın yavaş olduğu ve solunum kaslarının paralizinde uzamaya neden olabilen kalıtımsal bir durumdur. Klinik uygulamamız sırasında karşılaştığımız nadir bir olgu sunmaktayız: 15 yıllık şizofreni öyküsü bulunan ve pseudokolinesteraz eksikliği olduğunu saptadığımız 29 yaşında bir kadın hasta. PCE seviyelerinin tespiti EKT adayı bütün hastalarımızda yaptığımız rutin bir işlem olduğundan, eksikliği EKT uygulamasına başlamadan tespit edebildik. Modifiye EKT’yi suksinik kolin yerine propofol ve rokuronyum ile uyguladık. Uyanmayı hızlandırmak için sugammadex kulanıldı. Pozitif ve Negatif Belirti Ölçeği ile kaydedilen tedaviye yanıt olumluydu ve 9 EKT seansını komplikasyonsuz olarak tamamladık. EKT öncesi tetkiklerin içine pseudokolinesteraz düzeyinin konulmasının, araştırılması gereken bir konu olduğunu ileri sürmekteyiz çünkü bu yöntem anestezili modifiye EKT komplikasyonlarını azaltabilir. Anahtar kelimeler: Elektrokonvulziv tedavi, mivakuryum, pseudokolinesteraz eksikliği, şizofreni, suksinilkolin, sugamadeks How to cite this article: Yildizhan E, Tomruk NB, Aytac HM, Yildirim H, Canbek O. Severe pseudocholinesterase deficiency and ECT: a case report. Dusunen Adam The Journal of Psychiatry and Neurological Sciences 2018;31:312-315. https://doi.org/10.5350/DAJPN2018310311 Address reprint requests to / Yazışma adresi: Eren Yildizhan, Bakirkoy Research and Training Hospital for Psychiatric and Neurological Diseases, Department of Psychiatry, Zuhuratbaba, 34147, Bakirkoy/Istanbul, Turkey Phone / Telefon: +90-212-40-91515 E-mail address / Elektronik posta adresi: erenyildizhan@hotmail.com Date of receipt / Geliş tarihi: November 27, 2017 / 27 Kasım 2017 Date of the first revision letter / İlk düzeltme öneri tarihi: December 6, 2017 / 6 Aralık 2017 Date of acceptance / Kabul tarihi: January 4, 2018 / 4 Ocak 2018 INTRODUCTION P seudocholinesterase (PCE) deficiency is a condition in which butyrylcholinesterase – the enzyme responsible for the breakdown of butyrylcholine – is deficient. Agents such as succinylcholine, mivacurium, and ester-linked local anesthetic compounds are also subject to breakdown by this enzyme (1). Main outcome of the condition is prolonged paralysis and apnea after anesthetic procedures. The deficiency can be acquired or genetic. Liver disease, renal disease, malnutrition, pregnancy, hepatic or gastrointestinal malignancies, and burns are some of the conditions responsible for acquired PCE deficiency (2). Types of genetic deficiency are dibucaine-resistant (0.01-0.03%), fluoride-resistant (0.0007%), and silent (0.008-0.01%)