This material was presented in the 25th European Congress of Psychiatry which was organised by the European Psychiatry Association in Florence, Italy from 1-4th April 2017. I had access to the material as I attended the full Congress. Please note that this material remains the intellectual property of the European Psychiatry Association and its authors and any citation should include a full reference to it. For more information on the EPA and how to become a member, please visit: http://www.europsy.net/

1. The authors have no conflict of interests or financial disclosures to report.
e-mail correspondence: erenyildizhan@hotmail.com
ErenYıldızhan1, Nesrin BuketTomruk1, Miray Dereli1,Armağan Özdemir1, HakanYıldırım2, Özge Canbek1
From the departments of Psychiatry1 and Anesthesiology2 of
Bakırköy Research and Training Hospital for Psychiatric and Neurological Diseases
INTRODUCTION
Pseudocholinesterase (PCE) deficiency is a condition in which
butyrlycholinesterase - the enzyme responsible for the breakdown of
butyrylcholine - is deficient. Agents such as succinylcholine,
mivacurium and ester linked local anesthetic compounds are also
subject for breakdown with this enzyme. There may be no sign of the
deficiency if there is no contact with the suspected drugs or some
poisons. 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
for acquired PCE deficiency.
Types of genetic deficiency are dibucaine resistant (0.03% -0.01%),
fluoride resistant (0,0007%), silent (0.01-0.008%) variants (frequencies
are given respectively in parenthesis). There is also the Kalow (K)
variant with 1.5% frequency that causes minimal clinical significance
in which there is only 30% reduction in enzyme activity.
Prolonged apnea after succinylcholine administration is also a
problematic phenomenon after the ECT procedure.
In our hospital, ECT has been applied with anesthesia since 2006 and
Succinylcholine is muscle relaxant of choice in the ECT sessions, like
most of the similar clinics in Turkey. Detection of the serum
pseudocholinesterase level of the patient is part of our routine
preoperative laboratory workup.
CASE REPORT
H.D. is a 29 year-old, single white woman with a history of
schizophrenia. Her weight was 80 kg. She had primary school
education of 5 years and she has no history of occupation. She was
admitted to our inpatient clinic because of hostility, irritability. She was
believing that there were defamatory comments about her on the
television.
Her first psychotic episode was when she was 13 years old, and she
was diagnosed early onset schizophrenia in the child psychiatry
department. During a period of 15 years, she had been 30 psychiatric
hospitalizations, approximately 2 times a year, warranting a diagnosis
of treatment resistant schizophrenia.
In the psychiatric ward, she was very reluctant to talk with the medical
staff. Psychiatric examination revealed lack of self-care, increased
psychomotor activity, auditory hallucinations, delusions of reference
and persecution. She was fully oriented. Physical and neurological
examinations were normal.
Modified Electroconvulsive Therapy in
Pseudocholinesterase Deficiency: A Case Report
Her psychiatric symptom severity was recorded with positive and
Negative Syndrome Scale (PANSS), with an initial total score of 148
(PANSS positive: 41; PANSS negative: 38; PANSS general: 69).
Blood work was normal except for vitamin B12 deficiency anemia and
she was given cyanocobalamin 1000 mg intramuscularly twice a day
for 5 days. She was given haloperidol 20 mg/day, biperiden 10 mg/day
intramuscularly and quetiapine 400 mg/day orally. Since she did not
respond to the initial treatment, quetiapine was stopped;
chlorpromazine 50 mg/day intramuscularly and lorazepam 7,5 mg/day
orally was added to her treatment.
Because of homicidal risk and paranoid thought content,
electroconvulsive therapy was recommended, and consent was
obtained from the family member of the patient. When we checked for
the PCE level as part of the pre-ECT workup, we detected severe PCE
deficiency (PCE level: 126 IU/L, normal values of PCE are between
3,200-6,600 IU/L). Lorazepam was stopped 3 days before the first
ECT session, since it had propensity to increase the seizure threshold.
Modified ECT with anesthetic and muscle relaxant was administered
for three sessions a week. Since the patient had severe PCE
deficiency, rocuronium 25 mg was used intravenously as muscle
relaxant, instead of succinylcholine. Propophol 60 mg intravenously
was used as anesthetic compound. Ventilation was applied through a
face mask. Suggamadex 100 mg was given intravenously to shorten
the waking period after the convulsion had stopped. Dramatic
improvement was observed in the hostility of the patient after the 4th
ECT session as recorded with a 30-point decline in total PANSS scale.
9 ECT sessions were conducted successfully without complication.
PANSS total score was 67 (PANSS positive: 12; PANSS negative:
22; PANSS general: 33) five days after the last ECT. When the
improvement of the delusions of persecution and reference was
observed, we discharged the patient to the outpatient clinic.
ECT session Number of ECTs Anesthetic
(propophol)
Muscle Relaxant
(rocuronium)
Energy %
Thymatron System IV
(Somatics, LCC, Lake Buff, III)
Seizure duration
1 1 60 mg 25 mg 20 59 sec
2 1 60 mg 25 mg 20 47 sec
3 1 60 mg 25 mg 20 53 sec
4 1 60 mg 25 mg 20 57 sec
5 1 60 mg 25 mg 20 50 sec
6 1 60 mg 25 mg 20 49 sec
7 1 60 mg 25 mg 20 50 sec
8 1 60 mg 20 mg 20 44 sec
9 1 70 mg 20 mg 20 46 sec
DISCUSSION
Although there is a low prevalence of clinically significant genetic PCE
deficiency, there are also acquired cases of PCE deficiency. Chronic
psychotic patients are in increased risk for malnutrition, the use of
polypharmacy is increasing the risk of hepatic and renal diseases and
cardiovascular events are also seen with increased prevalence in these
patients so we can expect the incidence of the acquired cases of PCE
deficiency to be also increased than the general population.That’s why
we suggest the detection of the PCE levels to be a part
of routine pre-ECT laboratory assessments.