Status epilepticus following electroconvulsive therapy.

Electro convulsive therapy (ECT) induced status epilepticus is known to occur in patients undergoing ECT. Its recognition and management under general anesthesia are of paramount importance; otherwise it may endanger the life of the individual.

INTRODUCTION

In the field of psychiatric medicine one of the physical methods of treatment is electroconvulsive therapy which is widely used for a variety of conditions and is life-saving in many situations. The procedure, though appearing to be short and easy to administer, it is not devoid of complications. Certain untoward incidents may occur during the procedure such as aspiration, apnoea, bronchospasm, laryngeal spasm, cardiac asystole, retrograde amnesia, post-ictal confusion, orthostatic hypotension, status asthmaticus, and rarely status epilepticus. The problems can be both anesthetic induced or ECT provoked which needs to be discussed for further evaluation.

Status epilepticus is a rare complication of electro convulsive therapy (ECT). Prolonged seizures are more common after multiple monitored ECT (MMECT), where several seizures are induced at one session. Status epilepticus may be difficult to detect because motor activity may be slight and localized and monitoring ECT by electroencephalogram (EEG) might reveal a higher incidence of prolonged seizures.

CASE REPORT

A young male aged 26 years, weighing 50 kg with ASA grade I, earlier subjected to ECT many times with no complications on previous occasions of ECT. Investigated for normal routine tests like CBP, ESR, blood sugar (fasting and post-prandial), blood urea, Sr. creatinine, ECG, X-ray chest etc. Direct opthalmoscopic examination of both eyes was normal and there was no suspicion of raised ICT. After observing NBM for 6 h written informed consent was obtained for ECT and anesthesia.

Twenty-three G cannula was fixed on the dorsum of the hand and injection thiopentone 2.5% solution 250 mg was administered. Succinylcholine 35 mg was given and after the cessation of fasciculations, a rubber mouth gag was placed in the mouth to prevent tongue-bite and buccal mucosal injury. Bitemporal stimulus was given and at 180 millicoulombs patient developed a prolonged convulsion for 2 ½ minutes. After cessation of GTCS patient developed severe masseter spasm causing opening of the mouth difficult and stridor continued. Air entry into the lungs was minimal causing lowering of SpO2 and tachycardia upto 180 beats/min.

Despite physical methods like forward thrusting of the jaw to release the laryngeal spasm, it worsened. Then the whole body developed stiffness and board-like rigidity, pupils were dilated and not reacting to light. Pulse was 160 beats/min and SpO2 decreased. Injection succinylcholine 25 mg was repeated to relieve laryngeal spasm and thiopentone sodium 125 mg was given for sedation and neuroprotection. After the relief of the spasm the patient again developed a seizure of less intensity and plantar flexion of the lower limb with tonic clonic movements was observed. Pupillary dilation with no reaction to light was seen in both eyes. There was no EEG recording available at the time to record the changes.

Blood glucose levels at the time were 140 mg/dL. A 200 mg bolus of phenytoin was given intravenously and 4 mg intravenous lorazepam was administered. Pulse and BP recording at this time were normal and the patient did not regain consciousness for 40 min after the seizure.

Eventually, patient regained full consciousness and was coherent but rigor like movements were present. The patient was asked to remain under observation for 24 h in the hospital and did not develop any further seizures.

DISCUSSION

Prolonged seizures after ECT may be associated with hyperoxygenation, cerebral hyperexcitability, and the use of MMECT. Antidepressant and neuroleptic drugs may also reduce the seizure threshold. Abnormal seizure activity has also been reported when ECT is combined with lithium carbonate, and theophylline. In this patient the anesthetic procedure was standard, and the patient was on olanzapine and lorazepam, neither drug being known to significantly reduce seizure threshold. Although this was his first ECT during the current episode, he had received ECTs on multiple occasions in the past with no complications. Although past ECTs without complications is a relative indicator of safety, it needs to be viewed with caution as exemplified by Rao et al. who reported a case of nonconvulsive status epilepticus after the ninth ECT. There was a past history of seizure disorder and later questioning revealed that the patient had stopped taking his anti-epileptic medications for the last 10 days. The history of drug default was missed as the patient came on an outpatient basis for ECT and reported to be continuing his antiepileptic medications. The accompanying person was unaware of the patient's drug history and the history of drug default was obtained later, only after his parents arrived at the hospital. This highlights the need for a thorough history of drug compliance in those with a history of epilepsy, and this may have been the cause for the development of status epilepticus in this patient.

Convulsive status epilepticus is best terminated without delay, as it has a risk of locomotor injury. Intra venous benzodiazepine administration is usually effective. Status epilepticus after ECT is not a contra indication to further ECT, although MMECT is best avoided and further ECT may be given under the cover of antiepileptic drugs. In this patient simultaneous EEG recording was not available and the chances of the condition being missed or recognized late were possible. Thus, anesthetists and psychiatrists administering ECT need to keep a high index of suspicion for this rare complication.

FOR FURTHER READING

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Peters SG, Wocuos DN, Peterson GC. Status epilepticus as a complication of concurrent electroconvulsive and theophylline therapy. Mayo Clin Proc 1984;59:568-70

Prakash R, Leavell SR. Status epilepticus with unilateral ECT: A case report. J Clin Psychiatry 1984;45:403-4

Rao KM, Gangadhar BN, Janakiramaiah N. Nonconvulsive Status Epilepticus after the Ninth Electroconvulsive Therapy. Convuls Ther 1993;9:128-9

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Weiner RD. ECT-induced status epilepticus and further ECT: A case report. Am J Psychiatry 1981;138:1237-8

Weiner RD, Whanger AD, Erwin CW, Wilson WP. Prolonged confusional state and EEG seizure activity following concurrent ECT and lithium use. Am J Psychiatry 1980;137:1452-3