76: Electroconvulsive Therapy

Published on 06/02/2015 by admin

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CHAPTER 76 Electroconvulsive Therapy

9 Describe the technique of electroconvulsive therapy, including appropriate monitors and medications

Commonly a psychiatrist, anesthesiologist, and nurse attend the patient. An intravenous line is established, and routine monitors, including electrocardiogram, intermittent blood pressure, and pulse oximetry are placed. On rare occasions, predicated on the patient’s comorbidities, arterial cannulation and continuous monitoring may be required. The psychiatrist places EEG leads to measure the cortical seizure. An additional blood pressure cuff is placed on a leg. This cuff will be inflated before administering muscle relaxants so the muscles are isolated from the circulation and after the ECT stimulus the duration of the motor seizure can be measured. Before inducing anesthesia, the patient is preoxygenated for a number of minutes with 100% oxygen.

Anticholinergic medications may be administered to lessen the effects of the initial parasympathetic discharge. In addition, they have antisialagogue properties. The medication most commonly used is glycopyrrolate, 0.2 to 0.4 mg intravenously.

Methohexital is the most common anesthetic induction agent used because it has a rapid, short duration of action, low cardiac toxicity, and, most important, minimal anticonvulsant properties. Side effects include hypotension, myoclonus, and pain on injection. A typical dose of methohexital is 0.75 to 1 mg/kg. In patients with left ventricular dysfunction, etomidate is an effective induction agent since it has minimal effects on myocardial contractility and cardiac output. Etomidate may also enhance seizure duration in patients who had prior ECT but whose seizure durations were thought inadequate to achieve a therapeutic effect. Side effects include pain on injection, nausea and vomiting, and delays in return of cognitive function. A typical dose of etomidate is 0.15 to 0.3 mg/kg.

Propofol has a rapid onset and a short duration of action and allows cognitive function to return soon. Although propofol use is associated with shorter seizure durations, recent investigations suggest that there is no difference in outcome when compared to methohexital. A typical dose of propofol is 0.75 to 1 mg/kg.

Although ketamine has also been used in ECT, compared with methohexital the EEG seizure duration is decreased; ketamine has the additional effects of increasing ICP and myocardial oxygen consumption. It does not seem to be an agent of choice.

The short-acting opioid remifentanil has been used for its anesthetic-sparing effects, providing a stable anesthetic when swings in heart rate and blood pressure are undesirable while having no effect on seizure duration. Potent volatile anesthetic agents offer no advantage over intravenous agents, with the possible exception of late in pregnancy, during which time ECT has been noted on occasion to produce titanic uterine contractions.

After anesthetic induction, the blood pressure cuff on the leg is inflated and acts as a tourniquet. The patient is hyperventilated by Ambu bag to lower seizure threshold. Typically the short-acting muscle relaxant succinylcholine (0.5 to 1.5 mg/kg) is administered. Before administering the electroconvulsive stimulus, a compressible mouth oral guard protector is inserted to protect the patient’s teeth, lips, and tongue from injury during the associated severe masseter contraction. Only rarely, based on patient circumstances, is the patient intubated. During the seizure itself the patient receives positive-pressure ventilation with 100% oxygen until spontaneous ventilation returns and the patient awakens. When stable, monitoring continues in the postanesthetic care unit until the patient is oriented and meets discharge criteria. Often the patient is confused or complains of a headache; benzodiazepines or opioids are appropriate treatments for these problems. However, benzodiazepines should be avoided before ECT because they increase seizure threshold.

Finally, it is common over a course of therapy that anesthetic medications require modification in their dosing; usually more medication is required. These adjustments must be made based on review of prior records and whether the patient experienced a seizure of therapeutic duration.

14 What are some of the adverse effects of electroconvulsive therapy?

An induced seizure lasting longer than 2 or 3 minutes is considered prolonged and can result in increased cognitive deficits. Prolonged apnea is said to occur if it takes longer than 5 minutes to regain spontaneous ventilations after ECT treatment and may be caused by a pseudocholinesterase deficiency, resulting in prolonged succinylcholine activity. Emergence delirium is characterized by restless agitation, aimless repetitive movements, grasping objects in view, or restless attempts to remove the monitors and intravenous line. It usually lasts from 10 to 45 minutes or more after the seizure and responds to benzodiazepines. Anterograde amnesia may occur immediately after an ECT treatment but tends to resolve usually within an hour. Retrograde amnesia is the most common persistent adverse effect of ECT. It is more commonly seen in elderly patients and those with preexisting cognitive impairment. Memory loss of events several months or years in the past can occur. Usually retrograde amnesia improves during the first few months after ECT, although many patients have incomplete recovery. Other adverse effects include headache, muscle aches, nausea, and fatigue.