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CASE REPORT
Year : 2017  |  Volume : 12  |  Issue : 3  |  Page : 223-225

A case report of prolonged apnea during electroconvulsive therapy in a patient with suicidal attempt by organophosphorus poison


Department of Anesthesiology, JNMC, Sawangi (M), Wardha, Maharashtra, India

Date of Web Publication2-Feb-2018

Correspondence Address:
Dr. Karuna Taksande
Department of Anesthesiology, JNMC, Sawangi (M), Wardha, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jdmimsu.jdmimsu_103_17

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  Abstract 


Electroconvulsive therapy (ECT) is a standard practice for psychiatric patients with suicidal behavior. Modified ECT with general anesthesia has evolved over inducing ECT without an anesthetic. The objective of anesthesia is to provide a rapid onset and offset of both unconsciousness and muscle relaxation for the duration of the electrical stimulus and subsequent seizure. Succinylcholine (0.5 mg/kg), due to its short period neuromuscular-blocking agent, is used to reduce muscular convulsion and decrease the risk of serious injury. Organophosphorus poisoning is an important cause for prolonged apnea following succinylcholine. We report a case of prolonged apnea after administration of succinylcholine for the ECT in a patient with a history of organophosphorus poisoning. A case of a 43-year-old male patient, residing at Nalavade, Wardha, previously hospitalized at Sevagram for organophosphorus poisoning which he had taken 11 days before. He was admitted and planned for intermittent modified ECT treatment. The patient was diagnosed with the major depressive disorder, and he was on medication for the same olanzapine. ECT was given. After the procedure, the patient was ventilated for 45 min. Since the patient did not regain spontaneous respiration, he underwent orotracheal intubation. The patient was then shifted to neuro-Intensive Care Unit for 4 h, and after the restoration of respiration depth and rate, and a normal arterial blood gas, the patient was extubated. The case of depression with suicidal tendencies was given modified ECT using low-dose suxamethonium. Apnea following suxamethonium was prolonged due to the recent intake of organophosphate poisoning. It is imperative to take detailed history including drug history to avoid such recurrences. It is mandatory in all cases with a recent history of organophosphate poisoning to estimate the plasma cholinesterase level before any anesthetic procedure.

Keywords: Electroconvulsive therapy, major depressive disorder, organophosphorous poisoning


How to cite this article:
Taksande K, Chatterjee M, Jain V. A case report of prolonged apnea during electroconvulsive therapy in a patient with suicidal attempt by organophosphorus poison. J Datta Meghe Inst Med Sci Univ 2017;12:223-5

How to cite this URL:
Taksande K, Chatterjee M, Jain V. A case report of prolonged apnea during electroconvulsive therapy in a patient with suicidal attempt by organophosphorus poison. J Datta Meghe Inst Med Sci Univ [serial online] 2017 [cited 2019 Jul 19];12:223-5. Available from: http://www.journaldmims.com/text.asp?2017/12/3/223/224701




  Introduction Top


Electroconvulsive therapy (ECT) is a standard practice for psychiatric patients with suicidal behavior. Modified ECT with general anesthesia has evolved over inducing ECT without an anesthetic.

The objective of anesthesia is to provide a rapid onset and offset of both unconsciousness and muscle relaxation for the duration of the electrical stimulus and subsequent seizure. Succinylcholine (0.5 mg/kg), owing to its short period neuromuscular blocking agent, is used to reduce muscular convulsion and decrease the risk of serious injury.

Prolonged apnea following Succinylcholine can occur in patients with qualitative and quantitative abnormalition of the enzyme. Quantitative abnormalities are seen in patients with liver disease, anemia, and antimetabolites.

Organophosphorus poisoning is an important cause of prolonged apnea following succinylcholine. We report a case of prolonged apnea after administration of succinylcholine for the ECT in a patient with a history of organophosphorus poisoning.


  Case Report Top


A 43-year-old male patient, residing at Nalavade, Wardha, an illiterate laborer and married. He was previously hospitalized at Sevagram for organophosphorus poisoning which he had taken 11 days before. He had no history of suicide attempts. Symptoms had been intensified since August 19, 2015, and he had taken the matter up with his family before self-poisoning with agricultural toxin 11 days before, and then, he was admitted in Sevagram where the documents could not be retrieved. Electrolytes, as well as blood tests, were normal at discharge time. The patient then came to psychiatry ward, AVBRH, Sawangi, where he was admitted and planned for intermittent modified ECT treatment.

The patient was diagnosed with the major depressive disorder and he was on medication for the same olanzapine. Previously, he was on oral lithium for 3 months and then, he was diagnosed with lithium-induced hypothyroidism, and treatment was stopped. He was started on 25 μg oral thyroxine. At the time of the ECT, his thyroid profile was normal. In the first session of ECT taken at 11:00 am, NBM and consent were checked, monitors: Electrocardiogram, SpO2, noninvasive blood pressure attached, intravenous line secured, R. L started. Preoxygenation done with 100% of oxygen and premedication was given with injection glycopyrrolate 0.2 mg and induced with injection propofol 100 mg, and injection succinylcholine 40 mg. The patient ventilated for 30 s, then mouth gag was inserted, and ECT was given. After the completion of procedure, the patient was ventilated for 45 min. Since the patient did not regain spontaneous respiration he underwent orotracheal intubation with 8.0 Cuffed ET Tube, air entry was checked and tube fixed and treated with volume control ventilatory support; meanwhile, vitals were stable, and he was catheterized and injection Lasix 10 mg given. The patient was then shifted to neuro-Intensive Care Unit for 4 h and after the restoration of respiration depth and rate, and a normal arterial blood gas (ABG), the patient was extubated. ABG was ordered an hour later which was normal. The patient was then shifted to Psychiatry ward.


  Discussion Top


The prolonged paralysis after succinylcholine can result in two conditions. First, the patient may have a genetically determined plasma cholinesterase functional abnormality, or deficiency in some regions in India. Second, there may be acquired decrease in the plasma cholinesterase activity. Acquired abnormalities can be seen with hepatic dysfunction, pregnancy, or medication with ecothiopate eye drops and some antimetabolite drugs. The plasma cholinesterase is mainly synthesized in the liver, circulates in the plasma, and it facilitates the metabolism of intermediate ester products formed during fatty acid metabolism. Organophosphate poisoning can produce irreversible inhibition of the activity of circulating plasma cholinesterase and result in prolonged respiratory paralysis.[1]

Anticholinesterase agents may be used as therapeutic agents in certain disease states, such as ecothiopate in glaucoma, neostigmine in myasthenia gravis, and cyclophosphamide in cancer treatment.

Organophosphate compounds are used predominantly as pesticides and chemical warfare agents. Due to its easy availability, many of them use it as oral poison to commit suicide or to draw the attention of others. The cholinergic crisis that ensures depends on the severity of organophosphate poisoning. The decision about the use of neuromuscular relaxants needs careful consideration by an anesthesiologist.

Various esters are inhibited by organophosphate poisoning including pseudocholinesterase and particularly acetylcholinesterase. The inhibition of acetylcholinesterase allows acetylcholine to accumulate at peripheral and central nervous cholinergic sites. Initial signs and symptoms are, therefore, attributable to the accumulation and generally are classified as muscarinic, nicotinic, and central.[2]

The possible sequelae of organophosphate poisoning include the well-known cholinergic crisis, an intermediate syndrome, and a delayed neuropathy.[2],[3]

Within minutes to hours of exposure, cholinergic crisis occurs. Muscarinic and central nervous system symptoms should be treated with atropine and Diazepam.

  • Within 24–48 h, and enzyme reactivator, such as pralidoxime (also called 2-PAM) chloride, should be administered
  • An intermediate syndrome may develop 1–4 days after exposure and initial cholinergic crisis. The intermediate syndrome is characterized by sudden weakness of the proximal limb muscles, neck flexors, and respiratory muscles and by cranial nerve palsies.[3] It may be attributed that a delay in administration of PAM or inadequate treatment may contribute to the development of the syndrome [3],[4]
  • Treatment of intermediate syndrome is symptomatic and often requires mechanical ventilation. Recovery occurs predictably; cranial nerve palsies is resolve first, followed by improvement in the respiratory function and renewed strength in proximal limb muscles, and finally, neck flexion is strengthened. The period for recovery is variable from 1 to 2 weeks
  • Late effects of organophosphate poisoning may occur within 1–3 weeks of exposure. Organophosphate-induced delayed neuropathy (OPIDN) is characterized by polyneuropathy affecting primarily the lower limbs. Some patients may exhibit spasticity and ataxia. In contrast with the intermediate syndrome, the respiratory muscles are spared in OPIDN.[2]


Dillard and Webb of Joplin, Missouri, have used low doses of succinylcholine for ECT even after succinylcholine apnea.[5]

However, we have deferred the administration of modified ECT in the next sessions, as it again causes succinylcholine apnea. Direct ECT without muscle relaxant adequately restraining the joint movements facilitated well in subsequent procedures without any untoward incidents.


  Conclusion Top


A case of depression with suicidal tendencies was given modified ECT using low-dose suxamethonium. Apnea following suxamethonium was prolonged due to the recent intake of organophosphate poisoning, which was concealed by attenders. It is imperative to take detailed history including drug history to avoid such recurrences. It is mandatory in all cases with a recent history of organophosphate poisoning to estimate the plasma cholinesterase level before any anesthetic procedure.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Hall AH, Rumack BH. Incidence, presentation and therapeutic attitudes to ant cholinesterase poisoning in the USA. In: Ballantyne B, Marrs TC, editors. Clinical and Experimental Toxicology of Organophosphates and Garbamates. Oxford, England: Butterworth-Heinemann; 1992.  Back to cited text no. 1
    
2.
Marrs TC. Organophosphate poisoning. Pharmacol Ther 1993;58:51-66.  Back to cited text no. 2
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3.
Senanayake N, Karalliedde L. Neurotoxic effects of organophosphorus insecticides. An intermediate syndrome. N Engl J Med 1987;316:761-3.  Back to cited text no. 3
[PUBMED]    
4.
Gadoth N, Fisher A. Late onset of neuromuscular block in organophosphate poisoning. Ann Intern Med 1978;88:654.  Back to cited text no. 4
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5.
Dillard M, Webb J. Administration of succinylcholine for electroconvulsive therapy after organophosphate poisoning: A case study. AANA J 1999;67:513-7.  Back to cited text no. 5
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