Etomidate enabled electroconvulsive therapy without suppressing adrenocortical function in a case with difficulties in inducing seizures by conventional methods.
Electroconvulsive therapy (ECT) is the most effective treatment for severe depression and is often the last resort in patients with medically treatment-resistant depression.1 The clinical effect of ECT relies upon the quality of the seizures elicited.2 In a patient not responding to ECT due to poor seizure quality, eliciting an adequate seizure may be the initial challenge. Anesthesia influences seizure quality.3 Etomidate is an ultrashort-acting, non-barbiturate hypnotic intravenous anesthetic agent with minimal cardiovascular effects, making it suitable for ECT. Etomidate lacks the strong anticonvulsant properties of standard ECT anesthetics (i.e., thiopental and propofol4) and leads to higher-quality and longer seizures.5 However, etomidate inhibits 11β-hydroxylase and steroid biosynthesis, including corticosteroids.6 A major concern is the potential for adrenocortical suppression in rapid-sequence induction of anesthesia in critically ill patients. We present a patient who had null seizures at the maximal stimulus dosage until a change in anesthesia to etomidate, and review the literature on the effect of anesthesia on ECT seizure quality. A 61-year-old man with recurrent major depressive disorder was hospitalized due to moderate depression with suicidal ideation (17-item Hamilton Depression Rating Scale [HAM-D] score = 21). Several treatment regimens with combinations of antidepressants failed, and he consented to ECT. ECT was administered thrice weekly (Table 1). The initial three ECT sessions with rising stimulation doses to the maximal 1021 mC with 3.5-mg/kg thiopental as standard anesthesia completely failed to elicit a seizure. Even 0.5-mg alfentanil augmentation and 50 mg chlorprothixene the evening before ECT to lower the seizure threshold had no effect. Anesthesia was changed to 0.2 mg/kg etomidate and elicited high-quality seizures of >60 s with clinical effect (HAM-D score = 16 after seven seizures), which allowed a down-titration of stimulus, potentially reducing the associated cognitive side-effects of ECT. The patient received 11 high-quality and clinically effective ECT treatments as an inpatient. He was discharged shortly after with fewer depressive symptoms (HAM-D score = 9) and was followed up in outpatient care with once-weekly maintenance ECT. The morning before his 25th maintenance ECT, his serum cortisol was 179 nM and the following morning 212 nM, which is higher than the minimum expected morning plasma cortisol concentration of 133 nM. Similarly, 24-h measurement of total urine cortisol production after the 25th ECT was 101 nmol (reference interval 10–124 nmol), indicating no adrenal suppression. At one of the ECT sessions, after etomidate administration, he had limb contractions before a muscle relaxant was administered. The contractions were confused with a seizure and lasted for ~30 s before termination with 5 mg diazepam and ECT was aborted. Follow-up MRI, electroencephalography (EEG), and neurological assessment concluded that the contractions were myoclonus due to late injection of the muscle relaxant. The patient received 26 successful ECT treatments with etomidate and gave written consent to publishing this case report. We present how etomidate enabled high-quality seizures in a patient unresponsive to ECT during standard thiopental anesthesia. Although >35 treatments using etomidate were given, the patient showed no signs of corticoadrenal suppression in terms of lower circulating levels of cortisol. This is in line with evidence that, although three ECT sessions weekly constitutes repeated use of etomidate in a relatively short time interval, serum levels of cortisol and adrenocorticotropin do not reach abnormally low levels during or after a sequence of ECT with etomidate in this patient population.7 Myoclonus is a very common side-effect during induction with etomidate and can be misinterpreted as a seizure. Unlike thiopental and propofol, which have strong anticonvulsant properties; etomidate has a disinhibitory effect on extrapyramidal motor activity responsible for the majority of myoclonus observed. A more specific and potent etomidate analogue was abandoned during phase II studies due to involuntary muscle movements.8 While involuntary muscle movements are undesirable in a non-ECT setting, they may be desirable for ECT as the cortical disinhibitory effect may be what enables etomidate to provide higher-quality seizures. Etomidate leads to higher-quality seizures and longer motor seizures in ECT.5, 9 In the most recent review of anesthesia for ECT, etomidate and ketamine yielded the longest seizures.3 The same review found that etomidate and a 1:1 (racemic)-ketamine and propofol mixture yielded the highest-quality seizures. The only comparison between etomidate and s-ketamine suggests that s-ketamine showed no difference in seizure duration but may provide higher-quality seizures based on higher postictal suppression, EEG coherence, ictal amplitude, and peak heart rate.10 Given the limited study size and adverse side-effects of s-ketamine (i.e., dissociative symptoms, vomiting, and hypertension), etomidate appears favorable. Our case highlights the impact of anesthesia on seizure generation during ECT, and how etomidate, largely abandoned in intensive care settings, may be considered the anesthetic of choice when patients fail to achieve high-quality seizures and clinical effect during ECT. All authors declare that they have no financial interests or any other conflict of interest with other people or organizations that could inappropriately influence this work.
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