Chapter 5. Adverse Effects - When Mortality Occurs with ECT

Written by Juli Lawrence

When mortality occurs with ECT, it typically happens immediately following the seizure or during the postictal recovery period. Cardiovascular complications are the leading cause of death and of significant morbidity (Pitts 1982; Burke et al. 1987; Welch and Drop 1989; Zielinski et al. 1993; Rice et al. 1994). Despite the short-lived increases in cerebral blood flow and intracranial pressure, cerebrovascular complications are notably rare (Hsiao et al. 1987). Given the high rate of cardiac arrhythmias in the immediate postictal period, the majority of which are benign and resolve spontaneously, ECG should be monitored during and immediately following the procedure (see Section 11.8) and patients should not be taken to the recovery area until there is resolution of significant arrhythmias. Vital signs (pulse, systolic and diastolic pressure) should be stable prior to the patient's leaving the recovery area (Section 11.10). Patients with pre-existing cardiac illness are at greater risk for post-ECT cardiac complications (Prudic et al. 1987; Zielinski et al. 1993; Rice et al. 1994). Indeed, there is evidence that the type of pre-existing cardiac disease predicts the type of complication that may be encountered following ECT. For example, ventricular arrythmias are more common in patients with pre-existing ventricular abnormalities than in patients with ischemic heart disease (Zielinski et al. 1993). Management of cardiac complications is discussed in Chapter 11.

Two other possible sources of morbidity are prolonged seizures and tardive seizures (Weiner et al. 1980a). Management of prolonged seizures is described in Section 11.9. Failure to terminate seizures within a period of 3 to 5 minutes may increase postictal confusion and amnesia. Inadequate oxygenation during prolonged seizures increases the risk of hypoxia and cerebral dysfunction, as well as cardiovascular complications. In animal studies, seizure activity that is sustained for periods exceeding 30-60 minutes, regardless of steps taken to maintain appropriate levels of blood gases, is associated with an increased risk of structural brain damage and cardiovascular and cardiopulmonary complications (Meldrum et al. 1974; Ingvar 1986; Meldrum 1986; Siesjo et al. 1986; O'Connell et al. 1988; Devanand et al. 1994).

Prolonged seizures and status epilepticus may be more likely in patients receiving medications that lower seizure threshold or interfere with seizure termination (e.g. theophylline, even at therapeutic levels) (Peters et al. 1984; Devanand et al. 1988a; Abrams, 1997a), in patients receiving concomitant lithium therapy (Weiner et al. 1980b), in patients with pre-existing electrolyte imbalance (Finlayson et al. 1989), and with the repeated induction of seizures within the same treatment session (e.g., multiple monitored ECT) (Strain-and Bidder 1971, Maletzky 1981).

There has been concern as to whether the rate of spontaneous seizures is increased following the course of ECT (Assael et al. 1967; Devinsky and Duchowny 1983). The evidence indicates, however, that such events are extremely rare and probably do not differ from population base rates (Blackwood et al. 1980; Small et al. 1981). There are no data concerning rates of tardive seizures, i.e., seizures that occur following termination of the ECT-induced seizure, but experience indicates that these are also rare events. As noted in Section 11.9, prolonged or tardive seizures occurring during the immediate postictal period are often not accompanied by motor manifestations, underscoring the need for EEG seizure monitoring (Rao et al. 1993). Nonconvulsive status epilepticus may also occur in the interictal period, with an abrupt onset of delirium, unresponsiveness, and/or agitation as distinguishing clinical features (Grogan et al. 1995). Cessation of EEG abnormalities and improved cognitive function following short-acting anticonvulsant treatment (e.g. intravenous lorazepam or diazepam) may prove diagnostic (Weiner and Krystal, 1993).

Prolonged postictal apnea is a rare event that occurs primarily in patients with a pseudocholinesterase deficiency resulting in slow metabolism of succinylcholine (Packman et al. 1978). Maintaining adequate oxygenation is critical in instances of prolonged apnea, which will usually resolve spontaneously within 30 to 60 minutes. When prolonged apnea is encountered, it is helpful to obtain a dibuciane number assay or a pseudocholinesterase level prior to the next treatment in order to establish etiology. At subsequent treatments, either a very low dose of succinylcholine may be used or a non-depolarizing muscle relaxant, such as atracurium, may be substituted (Hickey et al. 1987; Hicks, 1987; Stack et al. 1988; Kramer and Afrasiabi 1991; Lui et al. 1993).

To some extent, medical adverse events can be anticipated. Whenever possible, the risks of such events should be minimized by optimization of the patient's medical condition prior to ECT and/or modifications in ECT procedures. Patients with preexisting cardiac illness, compromised pulmonary status, a history of CNS insult, or medical complications following prior courses of anesthesia or ECT are especially likely to be at increased risk (Weiner and Coffey 1988; Zieliniski et al. 1993). ECT psychiatrists should review the medical work-up and history of prospective ECT patients (see Chapter 6). Specialist consultations or additional laboratory studies may be called for, as well as changes in medication regimens. In spite of careful pre-ECT evaluation, medical complications may arise which have not been anticipated. ECT facilities should be staffed with personnel prepared to manage potential clinical emergencies and should be equipped accordingly (see Chapters 9 and 10). Examples of these events include cardiovascular complications (such as cardiac arrest, arrythmias, ischemia, hyper- and hypotension), prolonged apnea, and prolonged or tardive seizures and status epilepticus.

Major adverse events that occur during or soon after the ECT course should be documented in the patient's medical record. The steps taken to manage the event, including specialist consultation, use of additional procedures, and administration of medications, should likewise be documented. As cardiovascular complications are the most likely source of significant adverse events and are seen most frequently in the immediate post-ECT period, the treatment team should be capable of managing the major classes of cardiovascular complications. A set of predetermined procedures for dealing with instances of prolonged or tardive seizures and status epilepticus are helpful.

5.2. Systemic Side Effects

Headache is a common side effect of ECT and is observed in as many as 45% of patients during and shortly following the postictal recovery period (Devanand et al. 1995; Freeman and Kendell 1980; Gomez 1975; Sackeim et al. 1987d: Tubi et al. 1993; Weiner et al. 1994). However, the precise incidence of postECT headache is difficult to determine due to methodological issues such as the high baseline (preECT) occurrence of headache in patients with depression, the potential effects of concurrent medication or medication withdrawal, and differences between studies in the assessment of headache. PostECT headache appears to be particularly common in younger patients (Devanand et al. 1995) and especially in children and adolescents (Rey and Walter 1997; Walter and Rey 1997) It is not known whether pre-existing headache syndromes (e.g., migraine) increase the risk of postECT headache, but ECT may exacerbate a previous headache condition (Weiner et al. 1994). The occurrence of postECT headache does not appear to be related to stimulus electrode placement (at least bifrontotemporal vs. right unilateral) (Fleminger et al. 1970; Sackeim et al. 1987d; Tubi et al. 1993; Devanand et al. 1995), stimulus dosage (Devanand et al. 1995), or therapeutic response to ECT (Sackeim et al. 1987d; Devanand et al. 1995).

In most patients the postECT headache is mild (Freeman and Kendell 1980; Sackeim et al. 1987d), although a sizable minority will report severe pain associated with nausea and vomiting. Typically the headache is frontal in location and has a throbbing character.

The etiology of postECT headache is not known. Its throbbing character suggests a similarity with vascular headache, and ECT may be associated with a temporary change in quality of headache from muscle-contraction type to vascular type (Weiner et al. 1994; Weinstein 1993). Indeed, ECT upregulates 5-HT2 receptors and 5-HT2 receptor sensitization has been associated with development of vascular headache (Weiner et al. 1994). Other suggested mechanisms include electrically induced temporalis muscle spasm or acute increase in blood pressure and cerebral blood flow (Abrams 1997a; Weiner et al. 1994).