Journal of ECT • Volume 30, Number 3, September 2014

antidepressant effects when used as an anesthetic agent, 1–3 this vignette recounts a case in which significantly uncomfortable psychiatric complaints followed the use of ketamine during ECT. Although little is known about the psychological effects of ketamine during ECT, one study group recorded several patients experiencing fear and hallucinations upon awakening from ketamine anesthesia compared with none who received propofol.4 Perceptual distortions also have been documented during ketamine infusions.4 Therefore, always screen for such feelings after ECT, whenever ketamine is used as an anesthetic agent. Without concern for such perceptual experiences, some people needing ECT might prematurely drop out of treatment, as noted in this vignette. This patient was on interferon B therapy before starting the partial hospital program, and it was discontinued before ECT administration. She reported that her depressive symptoms were not affected by interferon and also noticed no changes when it was discontinued. Thus, in this one case, it seemed unlikely that interferon or its discontinuation had much impact on her depression. Our patient reported increased distress after ECT number 2, even before she ever had ketamine exposure. Since she was “extremely anxious” before receiving ketamine, it is unclear as to whether ketamine actually did or did not contribute to her perceptual distortions. On 2 occasions, she denied any such distortions before receiving ketamine. Before receiving ECT, she denied perceptual concerns, but ketamine in the ECT procedures might have caused her to be upset by inducing dissociative symptoms. Although a few studies have suggested a potential benefit of ketamine as having antidepressant effects when administered as an anesthetic agent,1–3 it is important to recognize that methohexital has been the standard anesthetic medication during ECT for many decades. Over that prolonged period, it is widely accepted as having been proven to be safe and effective. Therefore, whenever ketamine is considered, note that potentially terrifying adverse effects can follow its use. There should always be a powerful reason for prescribing a newer and possibly more dangerous drug than for administering an agent widely demonstrated for decades to be safe and efficacious. Application of a relatively new pharmaceutical, however, is clearly warranted only when an established medicine is not effective or tolerated and there is evidence to document clinical efficacy with the newer drug. Despite antidepressant actions induced by © 2014 Lippincott Williams & Wilkins

Letters to the Editor

ketamine, methohexital remains the usual drug of choice in pre-ECT applications. Jae Lee, DO Hennepin-Regions Psychiatry Program Minneapolis-St. Paul, MN

Puneet Narang, MD Regions Hospital Minneapolis-St. Paul, MN

Steven Lippmann, MD University of Louisville School of Medicine Louisville, KY 40202 [email protected]

The authors have no conflicts of interest or financial disclosures to report.

REFERENCES 1. Kranaster L, Kammerer-Ciernioch J, Hoyer C, et al. Clinically favourable effects of ketamine as an anesthetic agent for electroconvulsive therapy; a retrospective study. Eur Arch Psychiatry Clin Neurosci. 2011;261:575–582. 2. Okamoto N, Tetsuji N. Rapid antidepressant effect of ketamine anesthesia during electroconvulsive therapy of treatment-resistant depression. J ECT. 2010;26:223–227. 3. Abdallah C, Fascula M, Kelmendi B, et al. The rapid antidepressant effects of ketamine in the electroconvulsive therapy setting. J ECT. 2012;28:157–161. 4. Pomarol-Clotet E, Honey G, Murray G. Psychological effects of ketamine in healthy volunteers; phenomenological study. Br J Psychiatry. 2006;189:173–179.

Remission of Treatment-Resistant Depression With Electroconvulsive Therapy and Ketamine To the Editor: lectroconvulsive therapy (ECT) is a highly efficacious treatment for treatmentresistant depression. However, some patients do not or just poorly respond. As ECT has a high success rate, limited evidence is available for standard practice or augmentation strategies for ECT-resistant patients. We present a case of ECT-resistant depression that responded by using ketamine for anesthesia induction. A 75-yearold woman was hospitalized owing to a severe major depressive episode with psychotic features, already lasting almost a year. The patient experienced low mood, psychomotor retardation, decreased appetite and energy, hopelessness, paranoid and somatic delusions, and suicidal

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ideation. During her life, she already had at least 5 depressive episodes, with the first one at the age of 21 years. Previously, she had been adequately treated with courses of several tricyclic antidepressants, without clinical improvement but with substantially impairing adverse effects. Addition of several antipsychotics (haloperidol, olanzapine, risperidone, flupentixol, and pipamperone) had no effect. Given the serious physical and mental deterioration, ECT was started. Routine examinations before the start of ECT (ie, blood examination, electroencephalogram, and computed tomographic scan of the head) did not reveal any relevant abnormalities. The patient scored 34 on the Hamilton Depression Rating Scale (HDRS), indicating severe depression, and 9 on the Bush-Francis Catatonia Rating Scale (with a score of 3 for mutism, stupor, and withdrawal). Her score on the Mini Mental State Examination (MMSE) was 28/30. At the start of the ECT treatment, the patient took amitriptyline, 25 mg daily; lorazepam, 1 mg daily; and pipamperone, 60 mg daily. After the second ECT, owing to persisting agitation and suicidal ideation, clozapine was started and titrated up to 150 mg. As neither lorazepam nor pipamperone had any positive effect, both were discontinued. During the ECT course, amitriptyline was increased to 50 mg and aripiprazole, 10 mg, was added. From session 17, the medication scheme was unchanged. Initially, bifrontal electrode placement was chosen at a frequency of 2 stimulations per week. A constant-current Thymatron System IV device (Somatics LLC, Lake Bluff, Ill) was used. Induction and modification were achieved with propofol, 80 mg (1.5 mg/kg), and succinylcholine, 25 mg (0.5 mg/kg), before each treatment. Dosing was age based and stimulus parameters were energy, 35%; pulse width, 0.5 milliseconds (ms); frequency, 30 Hz; and stimulus duration, 6.52 seconds. Adequate seizures were obtained ranging from 44 to 55 seconds. As no clinical improvement occurred after 8 sessions, propofol was switched to etomidate (20 mg, 0.4 mg/kg), and bitemporal stimulation was started with stimulus parameters ranging between 35% and 40% energy (pulse width, 0.5 ms; frequency, 30 Hz; and stimulus duration, 6.52–7.45 seconds), without any improvement after 10 sessions. Owing to cognitive adverse effects, bitemporal electrode placement was switched back to bifrontal placement at the 19th session, and racemic ketamine was used for induction (40 mg, 0.7 mg/kg), resulting in adequate seizures. After 4 sessions, a spectacular improvement was observed, with a decrease of HDRS www.ectjournal.com

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Journal of ECT • Volume 30, Number 3, September 2014

Letters to the Editor

score to 8 and a resolution of psychotic symptoms. Afterward, treatment was continued at a rate of one ECT per week, and right unilateral electrode placement was started at session 25, owing to the cognitive adverse effects (MMSE, 21/30). Since then, HDRS scores remained relatively stable, but the MMSE score remained at 21/30. When the patient was stable for several weeks, she was discharged to home, and continuation ECT at tapering frequencies was started. In the current case, we used ketamine as an augmentation option in a patient who was ECT resistant. Recently, more and more studies are published, which compare the use of ketamine with other anesthetic agents during ECT practice. In a double-blind randomized controlled trial,1 ketamine plus thiopentone was compared with placebo plus thiopentone in patients who were referred for ECT. The ECT-ketamine group was modestly superior at week 1 and the 1-week follow-up but not at the end of the treatment course and the 1-month follow-up. This suggests that ketamine speeded up the response to ECT but did not increase efficacy. These results were further substantiated by a double-blind randomized controlled trial by Yoosefi et al, 2 comparing ketamine anesthesia to thiopental anesthesia in 31 patients. Patients in the ketamine group responded faster; but at the end of the study, both treatments were equal. However, 2 studies compared the use of thiopental3 or propofol4 alone with the use of these agents in combination with ketamine or S-ketamine, respectively. Both failed to demonstrate any enhanced antidepressant effects, and increased posttreatment disorientation and restlessness in the propofol–S-ketamine group were found. It can thus be concluded that the available data do not unequivocally support the use of ketamine as augmentation for ECT for the treatment of severe major depressive disorder. Our case is different, as we used ketamine as an augmentation strategy of the ECT treatment scheme because our patient did not react to a change of electrode sites and a change of anesthetic agents. Before the use of ketamine as anesthetic agent, good and adequate seizures were also elicited but without clinical improvement. In contrast, the aforementioned studies included patients without ECT resistance. It may be possible that ketamine may either augment the ECT or be effective on its own in ECT-resistant patients. This last possibility is in line with the results of Ibrahim et al., 2010,5 who found that even in patients with ECT resistance, one dose

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of ketamine induced a fast but transient decrease in depressive symptoms, although less so than in patients who were not ECT resistant. Another possibility is that the administration of ketamine led to the previously described rapid-acting although short-lasting antidepressant effect, but that ECT consolidated this improvement in mood symptoms. However, we did not see an immediate response after the first administration of ketamine but only an improvement after session 3. Despite high remission rates of ECT, a significant minority of patients are ECT resistant. For this population, evidence-based guidelines are lacking. Ketamine may be useful either as primary treatment or as an augmentation strategy that can be safely combined with ECT to enhance its efficacy or provide more rapid relief. Peter Niemegeers, MD Collaborative Antwerp Psychiatric Research Institute (CAPRI) Faculty of Medicine and Health Sciences University of Antwerp Antwerp, Belgium [email protected]

Didier Schrijvers, MD, PhD Collaborative Antwerp Psychiatric Research Institute (CAPRI) Faculty of Medicine and Health Sciences University of Antwerp Antwerp, Belgium Psychiatric Hospital Duffel Duffel, Belgium

Yamina Madani, MD Psychiatric Hospital Duffel Duffel, Belgium

Bernard GC. Sabbe, MD, PhD Collaborative Antwerp Psychiatric Research Institute (CAPRI) Faculty of Medicine and Health Sciences University of Antwerp Antwerp, Belgium Psychiatric Hospital Duffel Duffel, Belgium

Peter Niemegeers has received support from Johnson & Johnson, which was not involved in the preparation of this manuscript. Didier Schrijvers and Yamina Madani have no conflicts of interest or financial disclosures to report. Bernard G.C. Sabbe has received grants from and was a consultant for BristolMyers Squibb, Janssen Pharmaceuticals, and Lundbeck, none of which was involved in the preparation of this manuscript. REFERENCES 1. Loo CK, Katalinic N, Garfield JB, et al. Neuropsychological and mood effects of ketamine in electroconvulsive therapy: a randomised controlled trial. J Affect Disord. 2012;142:233–240.

2. Yoosefi A, Sepehri AS, Kargar M, et al. Comparing effects of ketamine and thiopental administration during electroconvulsive therapy in patients with major depressive disorder: a randomized, double-blind study. J ECT. 2013. 3. Abdallah CG, Fasula M, Kelmendi B, et al. Rapid antidepressant effect of ketamine in the electroconvulsive therapy setting. J ECT. 2012;28:157–161. 4. Järventausta K, Chrapek W, Kampman O, et al. Effects of s-ketamine as an anesthetic adjuvant to propofol on treatment response to electroconvulsive therapy in treatment-resistant depression: a randomized pilot study. J ECT. 2013;29:158–161. 5. Ibrahim L, Diazgranados N, Luckenbaugh DA, et al. Rapid decrease in depressive symptoms with an N-methyl-D-aspartate antagonist in ECT-resistant major depression. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35:1155–1159.

Electroconvulsive Therapy After Division and Repair of Strap Muscle and Anterior Jugular Vein To the Editor: uicidal attempt involving neck injury is rare, but it can be fatal.1,2 It requires emergency surgical and psychiatric intervention. Electroconvulsive therapy (ECT) is an emergency intervention for patients with depressive disorders who made nearfatal suicidal attempts. However, convulsive muscle movements during ECT may disrupt repaired wounds. This risk can be eliminated or at least mitigated by adequate muscle relaxation using neuromuscular blocking agents.However, because of their short duration of action, repeated administration may be required during the dose titration session. This, along with the need for optimal dose of muscle relaxants, implies a great challenge during ECT. Increased dose of succinylcholine may lead to prolonged apnea. There are reports of ECT a week after mitral valve replacement surgery and 4 days after vertebroplasty.3,4 Electroconvulsive therapy was given 2 weeks after cardiac bypass graft surgery.5 In these situations, injury or repair of the skeletal muscles was hardly encountered. Suicidal wounds involving neck muscles may completely dissect skeletal muscles and the surrounding major blood vessels. The repaired wound and the ligature of blood vessels need to be dealt with extra caution during ECT because of the convulsive movements of skeletal muscles surrounding the blood vessels. We report an ECT that

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© 2014 Lippincott Williams & Wilkins

Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Remission of treatment-resistant depression with electroconvulsive therapy and ketamine.

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