Electroconvulsive therapy (ECT) has been a safe and effective treatment for severe depression and other psychiatric illnesses since its introduction into clinical practice in 1938.
In a previous column (“Anesthesia Advances Add to the Safety of ECT”1), we described how modern anesthesia techniques make ECT safe. Here we discuss how advancements in anesthesia techniques and ECT procedures make ECT more comfortable and tolerable for patients.
Over the past 75 years, a large number of patients have been treated successfully with ECT, but until recently, many who received ECT could expect post-treatment nausea or headache.2 Although these unpleasant effects are generally mild, for some the nausea and headache can be severe enough to cause them to avoid needed treatment. Now, even these previously common aftereffects can be prevented with medications originally developed to prevent postoperative pain and nausea. In addition to these specific anesthesia interventions, other periprocedural advancements, including liberalization of concomitant and pre-treatment medications, add to the comfort and tolerability of ECT.
Headache is the most commonly reported complaint after ECT; it may occur in about half of patients. It is typically mild and transient and usually responds to simple, over-the-counter analgesics, such as acetaminophen and ibuprofen. In some patients, however, it may be more severe, making prophylactic intervention with an intravenous agent, such as ketorolac, appropriate.
Post-ECT headache develops immediately or shortly after the patient regains consciousness following ECT.3 The headache may be associated occasionally with nausea and rarely with photophobia. It is usually bilateral and constant but may be unilateral or pulsatile.
The NSAID ketorolac can be given intravenously.4 Ketorolac is indicated for the short-term management of moderately severe acute pain that requires analgesia at the opioid lev-el, and it is frequently given to patients after they have had surgery. Although the pain-relieving properties of ketorolac are similar to those of morphine, the drug does not cause respiratory depression or cloud the sensorium.
Because ketorolac is an NSAID, it is contraindicated in anyone with sensitivity to this class of drugs or with a bleeding tendency. Because it can be administered intravenously, ketorolac can be given immediately before treatment and is very effective in significantly reducing the incidence of post-ECT headache. Generally, no prophylactic analgesic is given before the first treatment; rather, if the patient awakens with headache, he or she is offered ibuprofen or acetaminophen by mouth. If the headache turns out to be of moder-ate or severe intensity, the patient is offered prophylaxis with intravenous ketorolac at subsequent ECT sessions.
For patients with a history of migraine or other, more severe headache, the likelihood that they will experience a post-treatment headache is higher than in patients who do not have this history. For those patients, treatment of post-ECT headache may require antimigraine medications.5
Nausea following ECT is less common than headache but still occurs in up to 25% of patients. Nausea may be related to the anesthetic, to the ECT treatment itself, or to air in the stomach from assisted ventilation. It may occur in conjunction with, or independently from, headache. Post-ECT nausea can prevent otherwise well patients from leaving the treatment recovery area in a timely manner and going about the rest of their day.
When nausea occurs without headache, the primary treatment is with the serotonin 5-HT3 receptor antagonist ondansetron. Since the untoward effects of prophylaxis with this medication are few, most patients at increased risk for post-ECT nausea are given ondansetron intravenously before treatment. Older antinausea medications such as the dopamine-blocking agents, including phenothiazine derivatives (eg, prochlorperazine), butyrophenones (haloperidol, droperidol), trimethabenzamide, and metoclopramide, are associated with more adverse effects (eg, sedation). These older antinausea medications are reserved for the extremely rare case in which ondansetron is not effective.
1. Kellner CH, Bryson EO. Anesthesia advances add to safety of ECT. Psychiatr Times. 2012;29(1):12-15.
2. American Psychiatric Association Task Force on Electroconvulsive Therapy. The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. Washington, DC: American Psychiatric Association; 2001.
3. Dinwiddie SH, Huo D, Gottlieb O. The course of myalgia and headache after electroconvulsive therapy. J ECT. 2010;26:116-120.
4. Gillis JC, Brogden RN. Ketorolac. A reappraisal of its pharmacodynamic and pharmacokinetic properties and therapeutic use in pain management. Drugs. 1997;53:139-188.
5. Markowitz JS, Kellner CH, DeVane CL, et al. Intranasal sumatriptan in post-ECT headache: results of an open-label trial. J ECT. 2001;17:280-283.
6. Rasmussen KG, Petersen KN, Sticka JL, et al. Correlates of myalgia in electroconvulsive therapy. J ECT. 2008;24:84-87.
7. Boylan LS, Haskett RF, Mulsant BH, et al. Determinants of seizure threshold in ECT: benzodiazepine use, anesthetic dosage, and other factors. J ECT. 2000;16:3-18.
8. Sackeim HA, Dillingham EM, Prudic J, et al. Effect of concomitant pharmacotherapy on electroconvulsive therapy outcomes: short-term efficacy and adverse effects. Arch Gen Psychiatry. 2009;66:729-737.
9. Plath S. The Bell Jar. New York: Harper & Row; 1971.