The Use of Electroconvulsive Therapy in Special Patient Populations

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Oct 30, 2001 - In terms of tera to genic risk, ECT use in preg nancy is con sid - ered rela tively safe. Suc cinyl cho line is not trans ferred to any ex tent across ...
IN REVIEW

The Use of Electroconvulsive Therapy in Special Patient Populations Kiran Rabheru, MD, CCFP, FRCPC1

Background: Despite its well-established efficacy and its increasing use, electroconvulsive therapy (ECT) remains a controversial treatment. Lack of clarity in the issues related to its use in special patient populations (for example, in children, in adolescents, in pregnant women, in the elderly, and in the medically ill) often contributes to the debate about the use of ECT. Method: The literature on ECT use in special patient populations is reviewed, together with the commonly associated high-risk medical conditions in clinical practice. Specific reference is made in each case to the safety, tolerability, and efficacy of the procedure. Results: Much of the literature surveyed consists of case studies, although a few controlled trials are available. In general, ECT use in special populations is relatively safe and extremely effective. In small case series, ECT use in children and adolescents is effective but requires further systematic study. In pregnant women, ECT is very effective, and with proper medical care, it is relatively safe in all trimesters of pregnancy, as well as in the postpartum period. The frail elderly are particularly good candidates for ECT because they are often unresponsive to or intolerant of psychotropic medication. Medical conditions that should receive particular attention during a course of ECT are disorders of the central nervous system (CNS), cardiovascular, and respiratory system. With modern anesthesia techniques and careful medical management of each high-risk patient, most can successfully complete a course of ECT. The process of obtaining informed consent also requires special consideration in this group of patients because their capacity to consent to treatment may be compromised. Conclusions: With careful attention to each patient’s medical and anesthesia needs, ECT is an effective and relatively safe procedure in high-risk special patient populations. (Can J Psychiatry 2001;46:710–719 ) Key Words: electroconvulsive therapy, special patient populations, children, adolescents, pregnancy, postpartum, elderly, frail elderly, medically-ill, brain tumours

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lthough the use of electroconvulsive therapy (ECT) for treatment of severe depression and other mental disorders has been well established (1,2), it continues to create controversy (3,4). It is therefore vitally important for clinicians to be aware of the available evidence for ECT use in special and vulnerable populations. Despite the exponential growth in the understanding of ECT neurobiology (5,6), its mode of action is still unclear. This article critically examines the relevant literature and provides clinical guidelines for the use of ECT in special patient populations. These consist of the child, adolescent, and elderly populations; pregnant and postpartum patients; and those with concurrent medical condi-

tions who require ECT. This paper refers the reader to the American Psychiatric Association (APA) task force report on the practice of ECT (second edition), released in January 2001, for specific indications and contraindications (7). ECT for Adolescents and Children ECT is used infrequently in adolescents and children. There are great concerns regarding possible adverse effects in maturing nervous systems (8–10). As a result, there are few studies available. Some of the clinical conditions responsive to ECT in adolescents and young adults are debilitating and may be life threatening (for example, psychotic depression and catatonic states). For such conditions in adolescents, ECT is considered beneficial and relatively safe (11,12,14,15). There are fewer data on ECT’s effects in younger children, although there is evidence that at least 2% of children suffer from major depression (13). Most reports of children treated with ECT are anecdotal and outdated. They include descriptions that are inadequate or obsolete in terms of diagnostic

Manuscript received and accepted August 2001. 1Associate Professor (part-time), Department of Psychiatry, The University of Western Ontario, London, Ontario. Address for correspondence: Dr K Rabheru, Physician Leader, Geriatric Psychiatry Program, Regional Mental Health Care, London, PO Box 5532, Station B, 850 Highbury Avenue N, London, ON N6A 4H1

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categories, making it difficult to generalize their findings to current patient populations (17,18). Yet young children, like the elderly, do not respond well to alternative treatments, such as antidepressant medications, and thus experience more side effects (16,19). A recent review of studies conducted since 1990 found that the response rate to ECT among adolescents with mood disorders was about 65% (10). Based on this, the Texas Children’s Medication Algorithm Project has developed a treatment algorithm for major depressive disorder (MDD) in this age group (20). These practice parameters delineate indications for ECT in adolescents, including persistent treatmentresistant depres sion that is se vere enough to be lifethreatening by causing suicidality or catatonia. The algorithm may form the basis for developing controlled clinical trials in adolescents and perhaps extend to preadolescent children. The ethical and moral dilemma of treating children with ECT, as well as getting informed consent for such procedures, is not to be underestimated. At present, psychiatrists caring for children with life-threatening and disabling depression face a difficult choice: they may offer ineffective therapy or no treatment, or they may offer ECT—a treatment that many still oppose and for which clinical certainty in children has not been well established. Currently, ECT in children would fall under the category of research that involves greater-thanminimum risk but presents the prospect of direct benefit to the individual subject (19–21). ECT Use in the Elderly ECT is most frequently used in the elderly to treat depression (22,23). Medication resistance is suspected to be age-related (23,24), especially in cases of late-onset depression (25). ECT has been shown to be effective in 70% to 80% of patients who have failed drug therapy (26). Most controlled studies indicate that a history of prior nonresponse to medication trials is associated with a 20% to 30% lower rate of antidepressant response to ECT (27). Overall, approximately 50% of medication-resistant patients subsequently respond to ECT (28). Many elderly patients with severe depression, who are medication-resistant or medication-intolerant respond more reliably and quickly to a course of ECT (29–31). ECT is increasingly used as first-line therapy for severely ill patients who are refusing to eat or drink, are psychotic, or are at high risk for suicide (27). Coexisting medical conditions that frequently occur in the elderly may make ECT the treatment of choice in some patients, due to its speed of action and safety profile. ECT should be considered a first-line treatment for those elderly patients whose hepatic, renal, or cardiac functions prevent the use of pharmacotherapy for depression (27,32). In general, the short-term outcome of ECT treatment in the elderly with depression appears to be more favourable compared with younger adults (33,34). Due to medication

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intolerance, medical complications, or psychotic depression, they often receive ECT earlier in the course of illness than do younger adults. These factors, in essence, probably reduce the duration of the index episode and medication resistance, both of which are positive predictors of response to ECT (34). The elderly, however, may not respond as well to unilateral ECT as do younger patients, more often requiring bilateral ECT (35,36) and a longer treatment course to achieve remission (37). Seizure threshold rises with increasing age—particularly with bilateral ECT—sometimes creating difficulty when it exceeds maximum outputs of available ECT machines (38–40). Reducing or withholding the dosage of sedatives, hypnotics, benzodiazepines, or anticonvulsants prior to ECT, as well as using lower dosages of barbiturate anesthesia and adequate ventilation during ECT, may be helpful (7). Although the use of intravenous caffeine pre-ECT does lengthen seizure duration, it does not appear to reduce seizure threshold (41,42). Since the ECT’s efficacy is not directly related to seizure duration (43,39) and potential cardiac and other complications of caffeine use are known, this augmenting strategy is not generally recommended. Older patients and those with medical illnesses are at greater risk for ECT-related confusion and greater memory deficits (44,45). They tend to have more persistent amnesia for autobiographic information, in addition to anterograde and retrograde amnesia. Baseline pre-ECT cognitive scores and postictal disorientation have been shown to predict the degree of long-term retrograde amnesia in patients who are not neurologically impaired (46). Cognitive impairment associated with depression may actually improve with ECT, even when associated with underlying cerebral vascular disease (47,48). ECT is known to cause hypoprofusion in frontal areas (48); this may contribute to the dementia process in patients with compromised cerebral vascular systems, but there are no controlled studies to help with this clinical question. Therefore, the risk of not treating an older person with severe depression must be weighed against the potential risk of exacerbating cognitive impairment (54). Elderly patients experience stress to their cardiovascular system during ECT and must be evaluated carefully for their ability to tolerate changes such as bradycardia, tachycardia, hypertension, or arrhythmia (32). The specific indications and relative contraindications are well described in the APA task force report (7). Patients who reside in nursing homes have higher rates of depression (55,56), upward of 40% in some studies, with high rates of medical comorbidity and disability over long periods of time (49,50). These patients are at high risk for mortality, especially the “old-old,” who are cognitively impaired, are less functional, and are in poorer health (51). Treating depression in the institutionalized, ill, elderly patient may or may not improve survival (51) but likely improves quality of life and outcomes of other comorbid medical conditions (51–53).

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Table 1. Risks associated with ECT during pregnancy Risk

Recommendations

Gastric reflux Prolonged gastric emptying

1.

Increased risk of regurgitation, aspira- 2. tion, and pneumonitis, especially after 3. first trimester 4.

Consider pregnant patient as if she has full stomach. Consider intubation after first trimester with caution, due to hypervascularity and edema causing bleeding (78). Consider premedication with nonparticulate antacid (for example sodium citrate) (79), histamine-2 blocker, and gastric motility enhancer. Avoid atropine (increases chance of aspiration); use glycopyrrolate (less likely to cross placenta) (80).

Aortocaval compression 1. Generally later in pregnancy due to compression of venacava and aorta by 2. large, heavy uterus 3. Reduces fetal circulation 4.

Pretreat with intravenous hydration. Avoid glucose solution to prevent diuresis. Ensure adequate oxygenation, but not hyperventilation (78). Place a wedge to elevate patient’s right hip to displace uterus to the left (81).

Medications with ECT during pregnancy a) Muscle Relaxants

b) Anticholinergic agents

c) Barbiturates

1.

Succinylcholine does not cross placenta with normal doses (82).

2.

Check pseudocholinesterase levels if maternal history suggests difficulty metabolizing succinylcholine (83); this can cause respiratory difficulties in newborn.

1.

Not recommended routinely in pregnancy.

2.

Atropine crosses placenta quickly, causing fetal tachycardia and decreased variability in fetal heart rate.

3.

Glycopyrrolate is less likely to cross placenta (79,84).

1.

Short-acting barbiturates typically have no known adverse effects that are special to pregnancy (70).

Treating depression in elderly patients is challenging on all levels. ECT is a very reasonable choice, particularly for the elderly patient who is medically compromised and is either not tolerating or not responding to medications. ECT Use During Pregnancy Treating major mental disorders during pregnancy poses a clinical dilemma, due to potential complications for both the mother and the fetus. The physiological changes of pregnancy, including plasma volume, glomerular filtration rate, intestinal absorption, and protein binding, leave the mother vulnerable to increased medication side effects (57). As well, medications may cause morphologic and behavioural teratogenicity, toxicity, and withdrawal in the fetus (58). These risks, however, must be weighed against the risks of severe untreated mental illness. The consequences (for example, varieties of malnutrition, refusal of prenatal care, inability to follow medical recommendations, attempts at premature self-delivery, substance abuse, suicide, and violence or neonaticide) can be fatal for mother and baby (59). The APA practice guidelines (60,61) suggest ECT as a pri mary treatment for major depression and bipolar disorder during pregnancy. ECT has been reported as a treatment with high efficacy and low risk in the management of these disorders during all 3 trimesters of pregnancy, as well as postpartum (7,62–64). The morbidity from continued illness and the incompletely understood adverse effects of psychotropic drugs have increased ECT’s attractiveness for pregnant patients with severe depression, especially when they have associated high-risk conditions. Medications that pose some teratogenic

risk during the first trimester include benzodiazepines, antipsychotics, lithium and other mood stabilizers (63,65,66), but not tricyclic antidepressants (TCAs) or selective serotonin reuptake inhibitors (SSRIs) (67,68). Later in pregnancy, antipsychotics have been noted to cause neonatal motor abnormalities, and benzodiazepines are associated with neonatal hypotonia, apnea, and temperature dysregulation (65,68). TCA treatment has been reported to cause anticholinergic effects and withdrawal symptoms in neonates (63). Lithium is associated with premature labour, polyhydramnios, neonatal hypothyroidism, or lithium toxicity (63). In terms of teratogenic risk, ECT use in pregnancy is considered relatively safe. Succinylcholine is not transferred to any extent across the placenta, and there is little effect on the fetus (69). The barbiturates used for brief anesthesia have not been fully studied, but the short exposure period is unlikely to cause teratogenicity (70). For the same reasons, neonatal toxicity is relatively low with ECT in the third trimester of pregnancy (71). According to some reports, depression during pregnancy has come to be seen as a specific indication for the first-line use of ECT (73–75). There are, to date, no prospective controlled studies that compare rates of ECT complications during pregnancy with those of other treatments vs no treatment. In the absence of such studies, the available data are case reports that have been reviewed by Miller (62). This recent review of ECT during pregnancy summarizes 300 case reports drawn from period 1942 to 1991. Of the 300 cases, 28 (9.3%) reported complications associated with ECT during pregnancy (62). In many of these cases, there is a lack of detailed information on the use of psychotropic medication, diagnosis,

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number of treatments, trimester of pregnancy, and anesthetic procedures. ECT use in the first trimester was recently reviewed (76). Of 15 cases, 14 were published before 1964; 5 of these (33.3%) reported complications, including premature birth, miscarriages, and vaginal bleeding. The authors recommend caution in prescribing ECT to patients in the first trimester of preg nancy, with the risk of possible spontaneous abortion to be clarified for informed consent. ECT during the third trimester of pregnancy has recently been described in case reports of 2 patients who were treated effectively (77). Potential Risks of ECT Use During Pregnancy There are potential risks related to the physiology of pregnancy that may be increased by ECT. Consequences include spontaneous abortion, preterm labour, uteroplacental insufficiency, or placental abruption. Table 1 outlines the risks associated with ECT during pregnancy. An obstetrician must be consulted prior to ECT to clarify the risks. Preparation for ECT during pregnancy should include a pelvic examination, discontinuation of nonessential anticholinergic medication, uterine tocodynamometry, intravenous hydration, and administration of a nonparticulate antacid. During ECT, elevating the pregnant woman’s right hip, external fetal cardiac monitoring, possible intubation, and avoiding excessive hyperventilation are recommended. With these extra precautions, ECT may be administered with relative safety and effectiveness during pregnancy (62,85). Postpartum Risks Breastfeeding does not need to be interrupted during a course of ECT (7). In contrast to some psychotropic agents, anesthetic agents administered with ECT pose little risk to the nursing infant (86). The exposure to medication administered during ECT is lessened if breastfeeding is delayed by a few hours posttreatment or by collection and storage of breast milk the day prior to ECT. ECT Use in Patients with Medical Conditions Patients being considered for ECT—especially in the elderly where ECT is commonly used—often experience coexisting medical conditions that may cause concern. These are generally related to the central nervous system (CNS), cardiovascu lar, and res pi ra tory sys tems. The pre- ECT medi cal evaluation should identify these conditions, assess their contribution to the overall risk during ECT, and suggest ways to reduce the risk. The treating psychiatrist, in collaboration with the anesthetist, should consider these medical risks to arrive at a final recommendation for ECT, in addition to considering any procedural modification needed to administer the ECT safely. It is important to recognize that medical management is often very difficult in patients with mental disorders. Conversely, effective psychiatric treatment often improves medical outcome and reduces mortality (87).

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Medical Conditions of Concern During ECT CNS Space-Occupying Lesions. Patients with space-occupying lesions (SOL) of the brain, with increased intracranial pressure (ICP), have historically been considered to be high-risk during ECT. This view was based primarily on older literature describing neurological deterioration occurring in such patients following ECT (88–91). In these cases, most of the tumours were discovered only after clinical decompensation had occurred. More recently, the APA’s task force on ECT (7,72) concluded that there was no absolute contraindication to ECT, although patients with cerebral SOLs pose a substantially increased risk. Most clinicians continue to view these lesions as contraindications to ECT, especially in cases associated with raised ICP. Much of the ECT risk in patients with SOLs has been attributed to the exacerbation of ICP as a result of ECT’s cerebral hemodynamic effects. Studies of electrically induced seizures are reported to show that cortical blood flow is increased by 300%, and cerebral metabolic rate of glucose and oxygen increases approximately 200% during seizure activity (49). Magnetic resonance imaging (MRI) studies have indicated that ECT induces a temporary functional breakdown of the blood–brain barrier, with increased vascular permeability (91). This marked cerebral hyperperfusion increases cerebral blood volume and puts persons with brain tumours who receive ECT at risk for brain herniation and possible death (92). Small or chronic SOLs pose minimal risk, unless associated with increased ICP or other mass effects (93,94), where risk may be substantial. Most successful prospectively treated SOL cases have involved asymptomatic meningiomas that are unlikely to cause obstruction of cerebrospinal fluid circulation and sudden elevations of ICP or peritumour edema. Although no controlled trials have been done, strategies to reduce the risk have been suggested, such as the use of hyperventilation and medication, including antihypertensives, diuretics, and steroids. Brain Tumours. Several case reports have noted safe and successful ECT in the presence of intracranial tumours, particularly meningiomas (96,97). Recently, there was a firstpublished report of successful ECT administered to a patient with depression who had a brain tumour and increased intracranial pressure (98). In this case, ECT was used to treat se vere, medication- resistant de pres sion. Al though no prospective trials exist, various investigators have successfully administered ECT to patients with brain tumours foll o w i n g p r e t r e a t m e n t w i t h s t e r o i d s , p a r ticu larly dexamethasone, to reduce edema (99). In addition, pretreatment with a beta blocker such as esmolol, a short acting selective beta-1 receptor blocker, has been shown to block seizureinduced increases in heart rate and blood pressure safely and effectively, without significantly effecting seizure duration (100). Along with dexamethasone and esmolol, the authors u s e d f u r o s e m i d e , a s h o r t - a c t i n g d i u r e t i c with

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antihypertensive effects, as well as hyperventilation with 100% oxygen to reduce ICP during ECT with brain tumour (101). Historically, ECT has been associated with poor outcome among patients with brain tumours who had CT or MRI evidence of increased ICP, focal neurological deficits, or a history of headaches (96,102). In the past, few patients with brain tumours had received specific attention to reduce the ECT-associated risk. With increased clinical experience and development of newer pharmacologic agents, ECT may be used cautiously to treat profound depression, even in the presence of ICP. To optimize outcome and minimize post-ECT delirium, combined factors are important. These include unilateral placement of electrodes, lowering the stimulus dose, and spacing the treatments; using little or no anticholinergic medications, particularly those that cross the blood–brain barrier; and obtaining pre-ECT consultations with specialists in neurosurgery and ophthalmology. We require further studies to reevaluate the safety of ECT in such patients. Even though the risk remains high, it must be weighed carefully against the severity and persistence of the psychiatric manifestations in each case. Intracranial Vascular Masses. Patients being considered for ECT who have intracranial vascular masses (IVMs) are at increased risk for serious morbidity and mortality. The concern is for the possibility of rupture, as well as for their mass effect. Cardiovascular side effects during ECT—including arterial hypertension, increased cerebral blood flow, and increased ICP—are of concern for such patients, as evidenced by case reports of catastrophic and fatal events (102). As of June 1995, however, cases of uncomplicated recovery have also been reported (102,103). There have been no reports of ECT-induced rupture of intracranial aneurysm, despite an estimated 4% prevalence in the adult population (104). A recent review of the literature and case reports outlines 8 cases of ECT performed in patients with IVMs, none of whom had adverse outcome (105). While these numbers do not establish unequivocal safety in this population, the individual practitioner must continue to perform risk–benefit analysis on a case-by-case basis. In patients with intracranial aneurysms, the primary anesthetic goal is to try to control the systemic blood pressure. Abrupt changes in transmural pressure from either increases in systemic pressure or decreases in ICP may cause rupture. In contrast to patients with mass lesions (that is, with brain tumours), maneuvers such as hyperventilation to decrease ICP are detrimental. In these patients, safe ECT administration has been reported by avoiding hyperventilation, with close attention to control of blood pressure and heart rate (106). Several publications show that esmolol alone, especially in low doses, may not be sufficient to control hypertension during ECT in patients with intracranial aneurysm (104). These patients have been treated successfully with a combination of

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atenolol, a beta blocker, and intravenous infusion of sodium nitroprusside to prevent tachycardia and hypertension (107). Atenolol use has been associated with severe confusion in 1 case when used in this context (108). Pretreatment does not totally block hypertensive surges but seems to reduce morbidity (109). Stroke. Depression develops in 30% to 60% of patients within 2 years after a stroke (110–112) and impedes recovery and rehabilitation of stroke patients (113). In antidepressantresistant patients with poststroke depression, ECT is effective, but there is no generally accepted recommendation on how long to wait after a stroke before administering ECT (114). Although the risk in patients with stable lesions is thought to be small, fresh lesions— particularly hemorrhagic lesions—may be more likely than ischemic infarctions to rebleed with ECT (115–117). One patient was treated 4 days after a documented cerebral infarction (44). More recently, a well-documented report describes a 79-year-old patient with depression successfully treated with ECT about 7 to 14 days after a cerebellar ischemic stroke (117). Some experts believe that ECT after a fresh stroke may worsen the effects of the original stroke (114) or may be associated with an increased incidence of delirium or cardiac complication (118–120). Because of the potential rebleeding risk with ECT—especially with hemorrhagic lesions (117,119)—careful pharmacologic blunting of the hypertensive surge must be undertaken (107,109). In contrast, patients with ischemic strokes generally do not require aggressive control due to risk of hypotension morbidity (7). ECT is very effective and generally well tolerated in poststroke patients, but they show a high risk of relapse, despite a robust ECT response and maintenance antidepressant therapy (121). It is recommended that caution be used, treatment carefully monitored, and ECT administered in the acute poststroke period only in settings where adequate medical, neurologic, and radiologic consultations are avail able (117). Patients with MRI evidence of subcortical hyperintensities, but without cognitive impairment (silent cerebrovascular disease), generally respond as well as patients who have depression without dementia and do not appear to be at increased long-term cognitive risk with ECT use (122,123). These patients, however, along with others suffering from strokes with dementia, may be at increased risk for confusion or transient cognitive worsening post-ECT (120,125). Table 2 outlines ECT use in other CNS conditions. ECT Use in Patients with Cardiovascular Disorders The most frequent complications during ECT (145) prior to modern anesthetic techniques (146) and effective medical management (147) were cardiovascular. These have reduced dramatically in patients with and without prior cardiac history (148,156). ECT is increasingly being considered for patients with medication- resistant or medication- intolerant

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Table 2. Use of ECT in other CNS conditions Epilepsy ECT: excellent anticonvulsant property (125) Used since 1940s (126) For intractable medication-resistant epilepsy or status epilepticus (127) ECT may cause prolonged or spontaneous seizures (128) May need regular epilepsy medication (129), despite increase in seizure threshold (130) Determine seizure threshold for ECT (131) Dementia Higher risk (21%) of transient post-ECT confusion (132–134), but remits spontaneously (136) Affective benefits comparable to patients without dementia (135) Extensive review found 73% positive response for depressive symptoms (136) Subcortical dementias (for example Parkinson’s) respond better than cortical (for example Alzheimer’s) Cognitive improvement in 29% due to alleviation of depression (136) Parkinson’s disease (PD) For medication-refractory, medication-intolerant patient with severe disability (137) Useful in acute and continuation or maintenance phases (137) Improves motor symptoms, especially the “on-off” phenomenon, independently of psychiatric symptoms (138–140) Benefits persist for days to months and require less dopaminergic medication (141,142) Post-ECT cognitive dysfunction and delirium minimized by levodopa dose reduction and starting with right unilateral ECT proceeding to bilateral if no response by third ECT (143,144).

psychiatric conditions and significant cardiovascular disease, many of whom are also elderly (149). In healthy patients, post-ECT changes of blood pressure or heart rate and rhythm are transient and safely managed. In the general population, the estimated mortality with ECT is about 1 in 10 000 patients or 3 to 4 in 100 000 treatments (150), mostly due to cardiac complications. Anesthesia effects, muscle relaxants, and hypoxia often contribute to the risk factors for mortality. ECT has a biphasic effect on the cardiovascular system. Initially, coincident with the tonic phase, apnea, and a forced expiration-induced Valsalva effect, there is a marked parasympathetic discharge. The increased vagal tone may cause profound bradycardia, hypotension, and risk for sinus arrest or arrythmias. This vagal effect, including excessive oral secretions, may be attenuated or blocked by atropine or glycopyrrolate pretreatment. Subconvulsive stimuli (missed attempts at inducing seizures) may result in excess vagal outflow, which if not countered by seizure-induced sympathetic activation, may precipitate severe and life-threatening bradyarrythmias and hypotension. Using suprathreshold stimuli and pretreatment with anticholinergic medication to prevent such complications should be considered in high-risk patients (147). This initial phase is followed by sympathetic discharge, causing a 15-fold increase in plasma epinephrine within seconds of the electrical stimulus (151), with the opposite effect. It leads to increase in cardiac output, systemic vascular resistance, hypertension, and tachyarrythmias, thus increasing myocardial oxygen demand. Administering short-acting beta blockers, such as esmolol or labetolol, may attenuate this sympathetic effect. The “rate-pressure product index” (the product of the heart rate and systolic blood pressure) (152)

can be used to predict cardiac ischemia, which may occur when the index is over 20 000 (153). Fortunately, the plasma half-life of norepinephrine is brief, and its effects are transient during ECT, but it can lead to myocardial infarction (MI) or intracerebral hemorrhage in vulnerable, often elderly, patients with known risk factors (154). A controlled study (155) found that preexisting disease predicted the type of cardiac complication. The severe cardiac patients were defined by an ejection fraction less than 50%, a QRS interval of greater than 100 ms, or 10 or more extrasystoles. Patients with preexisting ischemic disease and conduction disorders were at risk for ischemia and arrhythmias, respectively. Despite having 8 major and 14 minor cardiac complications among 40 patients, there were no deaths, and 38 of the 40 were able to complete the ECT course. Authors concluded that with close monitoring, ECT could be given with relative safety to patients with severe cardiovascular disease. A retrospective study of 80 patients who were divided according to their degree of cardiac risk found the cardiac group to be more prone to developing minor but not major complications, compared with case-control subjects, with no deaths or permanent cardiac morbidity during ECT (156). Although these studies suggest a higher cardiac risk associated with ECT in patients with cardiovascular disease, ECT should not be dismissed as an option, because most patients in both trials were able to complete the course of treatment (157). Recent MI is a risk for reinfarction during ECT (158). Although not studied objectively, it is suggested that after an MI, a 3-month interval be allowed to lapse prior to ECT (147). The clinical decision when to administer ECT after an MI, however, is based on its severity and the time lapsed since its

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occurrence, as well as on other effective treatment options available for the psychiatric condition. Other significant cardiovascular risk factors that must be assessed include uncompensated congestive heart failure, severe valvular disease, unstable angina, uncontrolled hypertension, fragile vascular aneurysms, and clinically significant cardiac arrythmias (7).

Clinical Implications

A thorough medical evaluation is critical prior to considering ECT for high-risk cardiac patients (158). In addition to a careful history, physical examination, and appropriate blood work, an ECG and a chest radiograph are useful. Functional cardiac testing may be needed in selected cases where ischemic disease is suspected (159). Optimal medical therapy in preparation for ECT is mandatory to minimize risk during and after treatment. Usual cardiac medication should be continued, unless there are specific contraindications (7). Particular attention must be directed at controlling blood pressure and heart rate by avoiding dehydration and hypotension. Medications to lower cardiovascular risk for anesthesia may be needed, including sympatholytics, other antihypertensives, anticholinergics, and short-acting nitrates (7). Lidocaine should be avoided if possible, due to its potent anticonvulsant effect (7). Anticoagulation with heparin or warfarin may be safely administered during ECT for patients at risk for embolization (160). Cardiac pacemakers generally have a protective effect during ECT, improving the heart’s rate and rhythm. A fixed-rate or demand pacemaker can protect against asystole during excessive vagal tone with ECT (161). Using a magnet, some physicians convert a demand pacemaker to a fixed mode to prevent unnecessary triggering and tachycardia at the time of ECT (162). Implanted defibrillators are also not problematic with ECT (7,163), but a cardiac elec tro physi olo gist should be con sulted prior to treatment. Oxygen administration during ECT protects the myocardium from ischemia (100).

• Although ECT may carry a higher degree of risk in some patients, it

Consent Issues for ECT in Special Patient Populations Obtaining informed consent from patients involves ethical and legal obligations, which have been described in the APA’s conceptual framework (164) and the most recent task force report (7). These include providing adequate information to a patient who is capable of understanding and acting reasonably on such information and providing the opportunity to consent in the absence of coercion. Obtaining informed consent for ECT from special patient populations is often challenging due to their lack of capacity to provide it. Determining capacity to consent is therefore vitally important in these patients, who are often impaired due to their special clinical situation (165). Frequently, they are elderly patients suffering with significant extra burden of medical illness, cognitive dysfunction, and impaired decision-making ability. The difficult question in some cases is the effect of depression on the right to refuse life-saving medical treatment (166). In these situations, conflicts between medical and psychiatric treatment goals are challenging to resolve (167). In the

• Electroconvulsive therapy (ECT) is an effective and relatively safe procedure for treating severe, treatment-refractory mood disorders in special populations, particularly the elderly

• Careful attention should be paid to obtaining informed consent in special patient populations, as well as to the medical and anesthesia procedures before and during the treatment. may prove to be life-saving treatment and and should not be unduly delayed.

Limitations • There are limited controlled data avilable on ECT use in special patient populations, particularly children and adolescents.

• Although cardiovascular and central nervous system disorders pose the greatest risk during ECT, there are limited controlled data to guide clinicians; thus, the risk-benefit ratio must be assessed on a case-by-case basis.

• Obtaining informed consent for ECT from incapable patients is a challenging issue with few concrete guidelines.

special case of pregnancy, the capacity involves the ability to consider the needs of the unborn baby, as well as the mother herself (59). Young children and adolescents also frequently lack the ability to fully understand and appreciate the procedure and its potential consequences. ECT, however, should not be considered different from other medical or surgical procedures with comparable risks and benefits. If the patient is incapable, appropriate substitute consent must be promptly obtained to prevent unnecessary suffering, physical morbidity, and possible fatality (168). Local legal requirements must be met in each case, but judicial and political efforts should be made to correct overregulation (169). Acknowledgements The author thanks B Dishan, S Dunbar, K Berger, and RMHCLondon.

References 1. Potter WZ, Rudorfer MW. Electroconvulsive therapy—a modern medical procedure. N Engl J Med 1993;328:882–3. 2. Fink M. Indications for use of ECT. Psychopharmacol Bull 1994;30:269–75. 3. Cloud J. New sparks over electroshock. Time Magazine 2001 Feb:46–8. 4. Smith, Daniel. Shock and disbelief. Atlantic Monthly 2001 Feb:79–90. 5. Lerer B, editor.Neurobiology of ECT, Part 1. Neurochemistry and neurogenetics [special issue]. The Journal of ECT 1998;14:149–219. 6. Lerer B, editor. Neurobiology of ECT, Part 2. Neurophysiology and neuropeptides [special issue].The Journal of ECT 1999;15:1–101. 7. American Psychiatric Association. A task force report on the practice of electroconvulsive therapy: recommendations for treatment, training, and privileging. 2nd ed. American Psychiatric Association; 2001. 8. Fink M, Coffey CE. ECT in pediatric neuropsychiatry. In: Coffey CE, Brumback R, editors. Textbook of Pediatric Neuropsychiatry. Washington (DC): American Psychiatric Press; 1998. p 1389– 408. 9. Kellner CH, Beale MD, Bernstein HJ. Electroconvulsive Therapy In: Noshpitz JD, editor. The Handbook of Child and Adolescent Psychiatry. Volume 6. New York (NY): Wiley. 1998. p 269–72. 10. Rey JM, Walter G. Half a century of ECT use in young people. Am J Psychiatry 1997;154:595–602. 11. Walter G, Rey JM, Mitchell PB. Practitioner review: electroconvulsive therapy in adolescence. J Child Psychol Psychiatry 1999;40:325–34. 12. Taiebo O, Cohen D, Mazet P, Flament M. Adolescent experiences with ECT. J Am Acad Child Adolesc Psychiatry 2000;39:943–4.

October 2001

The Use of Electroconvulsive Therapy in Special Patient Populations

13. American Academy of Child and Adolescent Psychiatry. Summary of the practice parameters for the assessment and treatment of children and adolescents with depressive disorders. J Am Acad Child Adolesc Psychiatry 1998;37:1234–8. 14. Bertagnoli MW, Borchardt, CM. A review of ECT for children and adolescents. J Am Acad Child Adolesc Psychiatry 1990;29:302–7. 15. Walter G, Rey JM. An epidemiological study of the use of ECT in adolescents. J Am Acad Child Adolesc Psychiatry 1997;36:809–15. 16. Walter G, Koster K, Rey JM. Electroconvulsive therapy in adolescents: experience, knowledge, and attitudes of recipients. J Am Acad Child Adolesc Psychiatry 1999;38:594–9. 17. Cizadlo C, Wheaton A. Case study: ECT treatment of a young girl with catatonia. J Am Acad Child Adolesc Psychiatry 1995;34:332–5. 18. Bender L. One hundred cases of childhood schizophrenia treated with ECT. Trans Am Neurol Assoc 1947;72:165–69. 19. Findling RL, Reed MD, Blumer JL. Pharmacological treatment of depression in children and adolescence. Pediatric Drugs 1999;1:161–82. 20. Hughes CW, Emslie GJ, Crismon ML, Wagner KD, Birmaher B, Geller B, and others. The Texas childhood medication algorithm project: report of the Texas consensus conference panel on medication treatment of childhood major depressive disorder. J Am Acad Child Adolesc Psychiatry. Forthcoming. 21. Rudnick A, Knapp P. Ethics of ECT for Children. J Am Acad Child Adolesc Psychiatry 2001;40:387–8. 22. Thompson JW, Blaine JD. Use of ECT in the United States in 1975 and 1980. Am J Psychiatry 1987;144:557–62. 23. Gerson SC, Plotkin DA, Jarvik LF. Antidepressant drug studies, 1964 to 1986: empirical evidence for aging patients. J Clin Psychopharmacol 1988;8:311–22. 24. Prudic J, Sackeim HA, Devanand DP. Medication resistance and clinical response to electroconvulsive therapy. Psychiatry Res 1990;31:287–96. 25. Alexopoulos GS, Myers BS, Young RC, Kakuma T, Feder M, Einhorn A, and others. Recovery in geriatric depression. Arch Gen Psychiatry 1996;53:305–12. 26. Stewart RB. Advances in pharmacotherapy: depression in the elderly issues and advances in treatment. J Clin Pharm Ther 1993;18:243–53. 27. Prudic JM, Sackeim HA, Rifas S. Medication resistance, response to ECT, and prevention of relapse. Psychiatr Ann 1994;24:228–31. 28. Kamholz BA, Mellow AM. Management of treatment resistance in the depressed geriatric patient. Psych Clin N Am 1996;19:269–86. 29. Janicak PG, Davis JM, Gibbons RD, Ericksen S, Chang S, Gallagher P, and others. Efficacy of ECT: a meta-analysis. Am J Psychiatry 1985;142:297–302. 30. Sackheim HA. The efficacy of electroconvulsive therapy in the treatment of major depressive disorder. In: Fisher S, Greenberg RP, editors. The limits of biological treatments for psychological distress: comparisons with psychotherapy and pla cebo. Hillsdale (NJ): Erlbaum; 1989. p 275–307. 31. Segman RH, Shapira B, Gorfine M, Lerer B. Onset and time course of antidepressant action: psychopharmacological implications of a controlled trial of electroconvulsive therapy. Psychopharmacology (Berl) 1995;119:440–8. 32. Greenberg L, Fink M. The use of electroconvulsive therapy in geriatric patients. The Clinics in Geriatric Medicine 1992;8:349–54. 33. Tew JD Jr, Mulsant BH, Haskett RF, Prudic J, Thase ME, Crowe RR, and others. Acute efficacy of ECT in the treatment of major depression in the old-old. Am J Psychiatry 1999;156:1865–70. 34. Black DW, Winokur G, Nasrallah A. A multivariate analysis of the experience of 423 depressed inpatients treated with electroconvulsive therapy. Convuls Ther 1993;9:112–20. 35. Heshe J, Roder E, Theilgaard A. Unilateral and bilateral ECT: a psychiatric and psychological study of therapeutic effect and side effects. Acta Psychiatr Scand Suppl 1978;275:1–180. 36. Pettinati HM, Mathisen KS, Rosenberg J, Lynch JF. Meta-analytical approach to reconciling discrepancies in efficacy between bilateral and unilateral electroconvulsive therapy. Convuls Ther 1986;2:7–17. 37. Rich CL, Spiker DG, Jewell SW, Neil JF, Black NA. The efficacy of ECT. 1: response rate in depressive episodes. Psychiatry Res 1984;11:167–76. 38. Krystal AD, Dean MD, Weiner RD, Tramontozzi LA 3rd, Connor KM, Lindahl VH, and others. ECT stimulus intensity: are present ECT devices too limited? Am J Psychiatry 2000;157:963–7. 39. Sackheim HA, Devanand DP, Prudic J. Stimulus intensity, seizure threshold, and seizure duration: impact on the efficacy and safety of electroconvulsive therapy. Psychiatr Clin North Am 1991;4:803–43. 40. Lisanby SH, Devanand DP, Nobler MS, Prudic J, Mullen L, Sackeim HA, and others. Exceptionally high seizure threshold: ECT device limitations. Convuls Ther 1996;12:156–64. 41. Fochtmann LJ. Animal studies of electroconvulsive therapy: foundations for future research. Psychopharmacol Bull 1994;30:321–444. 42. McCall WV, Reid S, Rosenquist P, Foreman A, Kiesow-Webb N. A reappraisal of the role of caffeine in ECT. Am J Psychiatry 1993;150:1543–5. 43. Nobler MS, Sackheim HA, Solomou M, Luber B, Devanand DP, Prudic J. EEG manifestations during ECT: effects of electrode placement and stimulus intensity. Biol Psychiatry 1993;34:321–30. 44. Alexopoulos GS, Shamoian CJ, Lucas J, Weiser N, Berger H. Medical problems of geriatric psychiatric patients and younger controls during electroconvulsive therapy. J Am Geriatr Soc 1984;32:651–4.

717

45. Tomac TA, Rummans TA, Pileggi TS, Li H. Safety and efficacy of electroconvulsive therapy in patients over age 85. Am J Geriatr Psychiatry 1997;5:126–30. 46. Sobin C, Sackeim HA, Prudic J, Devanand DP, Moody BJ, McElhiney MC. Predictors of retrograde amnesia following ECT. Am J Psychiatry 1995;152:995–1001. 47. Baldwin RC, Benbow SM, Marriott A, Tomenson B. Depression in old age: a reconsideration of cerebral disease in relation to outcome. Br J Psychiatry 1993;163:82–90. 48. Blackburn TA, Decalmer P. Case report: is ECT safe in patients with cerebral vascular disease? Int J Geriatr Psychiatry 1994;9:757–61. 49. Gurland BJ, Cross PS. Epidemiology of psychopathology in old age. Psychiatr Cli North Am 1982;5:11–25. 50. Abrams RC, Teresi JA, Butin DN. Depression in nursing home residents. Clin Geriatr Med 1992;8:309–22. 51. Kroessler D, Fogel BS. Electroconvulsive therapy for major depression in the oldest old: Effects of medical comorbidity on post treatment survival Am J Psychiatry 1993;1:30–7. 52. Devanand DP, Verma AK, Tirumalastti F, Sackeim HA. Absence of cognitive impair ment af ter one hun dred life- time treat ments. Am J Psy chia try 1991;148:929–32. 53. Stoudemire A, Hill CD, Morris R, Martino-Saltzman D, Markwalter H, Lewison B. Cognitive outcome following tricyclic and electroconvulsive treatment of major depression in the elderly. Am J Psychiatry 1991;148:1316–40. 54. Squire LR. Memory functions as affected by ECT. Ann N Y Acad Sci 1986;462:302–14. 55. Katz IR, Lesher E, Kleban M, Jethanandani V, Parmelee P. Clinical features of depression in the nursing home. Int Psychogeriatr 1989;1:5–15. 56. Katz IR. Association of antidepressants and other medications with mortality in the residential care elderly. J Geriatr Psychiatry Neurol 1994;7:221–6. 57. Elrad H, Gleicher N. Physiologic changes in normal pregnancy. In: Gleicher N, editor. Principals of medical therapy in pregnancy. New York (NY): Plenum Press; 1985. 58. Miller LJ. Clinical strategies for the use of psychotropic drugs during pregnancy. Int J Psychiatry Med 1991;9:275–98. 59. Miller LJ. Psychiatric disorders during pregnancy. In: Stewart DE, Stotland N L, editors. Psychological aspects of women’s health care: the interface between psychiatry and obstetrics and gynecology. Washington (DC): American Psychiatric Press; 1993. 60. American Psychiatric Association. Practice guidelines for major depressive disorder in adults. Am J Psychiatry 1993;150 (Suppl):1–26. 61. American Psychiatric Association: Practice guidelines for the treatment of patients with bipolar disorder. Am J Psychiatry 1994;151 (Suppl):1–26. 62. Miller LJ. Use of electroconvulsive therapy during pregnancy. Hosp Comm Psychiatry May 1994;45:444–50. 63. Altshuler LL, Cohen L, Szuba MP, Burt VK, Gitlin M, Mintz J. Pharmacological management of psychiatric illness during pregnancy: dilemmas and guidelines. Am J Psychiatry 1996;153:592–606. 64. Walker R, Swartz CM. Electroconvulsive therapy during high risk pregnancy. Gen Hosp Psychiatry 1994;16:348–53. 65. Miller LJ. Pharmacotherapy during the perinatal period. Directions in Psychiatry 1998;18:49–64. 66. Delgado-Escueta AV, Janz D. Consensus guidelines: preconception counseling, man age ment and care of the preg nant woman with epi lepsy. Neu rol ogy 1992;42:149–60. 67. Chambers CD, Johnson KA, Dick LM, Felix RJ, Jones KL. Birth outcomes in pregnant women taking fluoxetine. N Eng J Med 1996;335:1010–5. 68. Cohen LS, Rosenbaum JF. Psychotropic drug use during pregnancy: weighing the risks. J Clin Psychiatry 1998;59:18–28. 69. Guay J, Grenier Y, Varin F. Clinical pharmacokinetics of neuromuscular relaxants in pregnancy. Clin Pharmacokinet 1998;34:483–96. 70. Shnider SM, Levinson G. Anesthesia for Obstetrics, 3rd ed Baltimore (MD): Williams and Wilkins; 1993. 71. Ferrill MJ, Kehoe WA, Jacisin JJ. ECT during pregnancy: physiologic and pharmacologic considerations. Convuls Ther 1992;8:186–200. 72. The American Psychiatric Association. Task Force on ECT. The practice of ECT: rec om men da tions for treat ment, train ing and privi leg ing. Con vuls Ther 1990;6:85–120. 73. Fink M. Convulsive and drug therapy of depression. Annu Rev Medicine 1981;32:405–12. 74. Kalinowsky LB, Hippius H, Klein HE. The convulsive therapies: biological treatment in psychiatry. New York (NY): Grune and Stratton; 1982. 75. Consensus Conference: electroconvulsive therapy. JAMA 1985;254:2103–8. 76. Moreno ME, Munoz JM, Valderrabanos JS, Gutierrez TV. Electroconvulsive therapy in first trimester of pregnancy. The Journal of ECT 1998;4:251–4. 77. Bhatia SC, Baldwin SA, Bhati SK. Electroconvulsive therapy during the third trimester of pregnancy. The Journal of ECT 1999;15:270–4. 78. Diaz JH. The physiologic changes of pregnancy have anaesthetic implications for both mother and fetus. In: Diaz JH, editor. Prenatal anesthesia and critical care. Philadelphia: Saunders; 1991. 79. Abboud T, Raya J, Sadri S. Fetal and maternal cardiovascular effects of atropine and glycopyrrolate. Anesth Analg 1983;62:426–30.

718

The Canadian Journal of Psychiatry

80. Ali-Melkkila T, Kaila T, Kanto J, Lisalo E. Pharmacokinetics of glycopyrronium in parturients. Anesthesia 1990;45:634–7. 81. Eckstein KL, Marx GF. Aortocaval compression and uterine displacement. Anesthesiology 1974;40:92–6. 82. Moya F, Kvisselgaard N. The placenta transmission of succinylcholine. J Am Soc Anaesthes 1961;22:1–6. 83. Weis OF, Muller FO, Lyell H, Badenhorst CH, van Niekerk P. Materno-fetal cholinesterase inhibitor poisoning. Anesthesia and Analgesic 1983; 62:233–5. 84. Abboud TK, Read J, Miller F, Chen T, Valle R, Henriksen EH. Use of glycopyrrolate in the parturient: effect on the maternal and fetal heart rate and uterine activity. Obstet Gynecol 1981;57:224–7. 85. Walker R, Swartz CM. Electroconvulsive therapy during high risk pregnancy. Gen Hosp Psychiatry 1994;16:348–53. 86. Lee JJ, Rubin AP. Breast feeding and anesthesia. Anesthesia 1993;48:616–25. 87. Thompson D, Hylan TR, McMullen W, Romeis ME, Buesching D, Oster G. Predictors of a medical-offset effect among patients receiving antidepressant therapy. Am J Psychiatry 1998;144:557–62. 88. Gralinick AA. A fatality incident to electroshock treatment. J Nerv Ment Dis 1945;102:483–95. 89. Shapiro MF, Goldberg HH. Electroconvulsive therapy in patients with structural disease of the nervous system. Am J Medical Signs 1957;233:186–95. 90. Rond PC. Pontine tumor uncovered with electroshock treatment. Am J Psychiatry 1956;113:118–118–9. 91. Nobler MS, Sackeim HA. Mechanisms of action of electroconvulsive therapy: functional brain imaging studies. Psychiatric Annals 1998;28:23–9. 92. Mander AJ, Whitfield A, Kean DM, Smith MA, Douglas RH, Kendell RE. Cerebral and brain stem changes after ECT revealed by nuclear magnetic resonance imaging. Br J Psychiatry 1987;151:69–71. 93. Kellner CH, Pritchett JT, Beale MD, Coffey CE. The handbook of ECT. Washington (DC): American Psychiatric Press; 1997. 94. Malek-Ahmadi P, Sedler RR. Electroconvulsive therapy and asymptomatic meningioma. Convuls Ther 1989;5:168–70. 95. Malek-Ahmadi P, Beceiro JR, McNeil BW, Weddige RL. Electroconvulsive therapy and chronic subdural hematoma. Convuls Ther 1990;6:38–41. 96. Fried D, Mann J. Electroconvulsive treatment of a patient with known intracranial tumor. Biol Psychiatry 1988;23:176–80. 97. Starkstein SE, Migliorelli R. ECT in a patient with a frontal craniotomy and residual meningioma. J Neuropsychiatry Clin Neurosci 1993;5:428–30. 98. Patkar AA, Hill KP, Weinstein SP, Shwartz SL. ECT in the presence of brain tumor and increased intracranial pressure: evaluation and reduction of risk. Journal of ECT 2000;16:2:189–97. 99. Kellner CH, Rames L. Dexamethasone pretreatment for ECT in a patient with meningioma. Clin Gerontology 1990;10:67–72. 100. Gaines GY, Rees, DI. Anaesthetic considerations for electroconvulsive therapy. Southern Medical Journal 1992; 85:469–82. 101. Howie MB, Black HA, Zvara D, McSweeney TD, Martin DJ, Coffman JA. Esmolol reduced autonomic hyperactivity and length of seizures induced by electroconvulsive therapy. Anesth Analog 1990;71:384–8. 102. Maltbie AA, Wingfield MS, Volow MR, Weiner RD, Sullivan JL, Cavenar JO Jr. Electroconvulsive therapy in the presence of brain tumor: case reports and an evaluation of risk. J Nerv Men Dis 1980;168:400–5. 103. Gardner MW, Kellner CH. Safe use of ECT with an intracranial aneurysm. Journal of ECT 1998;14:290–1. 104. Bader GM, Silk KR, Dequardo JR, Tandon R. Electroconvulsive therapy in intercranial aneurysm. Convuls Ther 1995;11:139–43. 105. Salaris S, Szuba MP, Traber K. ECT and intracranial vascular masses. Journal of ECT 2000 16:198–203. 106. Hunt SA, Caplen, E. ECT in the presence of cerebral aneurysm. Journal of ECT 1998;14:124–5. 107. Viguera A, Rordorf G, Schouten R, Welch C, Drop LJ. Intracranial hemodynamics during attenuated responses to electroconvulsive therapy in the presence of an intracerebral aneurysm. J Neurol Neurosurg Psychiatry 1998;64:802–5. 108. Kramer BA. Severe confusion in a patient receiving electroconvulsive therapy and atenolol. J Nerv Ment Dis 1986;174:562–3. 109. Najjar F, Guttmacher LB. ECT in presence of intracranial aneurysm. Journal of ECT 2000;16:71–2. 110. Robinson RG, Bolduc PL, Price TR. Two year longitudinal study of post-stroke mood dis or der: di ag no sis and out come at one and two years. Stroke 1987;18:837–43. 111. Folstein MF, Maiberger R, McHugh PR. Mood disorder as a specific complication of stroke. J Neurol Neurosurg Psychiatry 1977;40:1018–20. 112. Finkelestein S, Benowitz LI, Baldessarini RJ, Arana GW, Levine D, Woo E, and others. Mood, vegetative disturbance, and dexamethasone suppression test after stroke. Ann Neurol 1982;12:463–8. 113. Parikh RM, Robinson RG, Lipsey JR, Starkstein SE, Fedoroff JP, Price TR. The impact of post-stroke depression on recovery in activities of daily living over a 2year follow-up. Arch Neurol 1990;47:786–9. 114. Pritchett JT, Kellner CH, Coffey CE. Electroconvulsive therapy in geriatric neuropsychiatry. In: Coffey CE, Cummings JS, editors. Textbook of geriatric neuropsychiatry. Washington (DC): American Psychiatric Press; 1994. p 650–1.

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115. Farah A, McCall WV, Amundson RH. ECT after cerebral aneurysm repair. Convuls Ther 1996;12:165–70. 116. Weisberg LA, Elliott D, Mielke D. Intracerebral hemorrhage following electroconvulsive therapy. Neurology 1991;41:1849. 117. Weintraub D, Lippmann SB. Electroconvulsive therapy in the acute poststroke period. Journal of ECT 2000;16:415–8. 118. Murray GB, Shea V, Conn DK. Electroconvulsive therapy post-stroke depression. J Clin Psychiatry 1986;47:58–60. 119. Hsiao JK, Messenheimer A, Evans DL. ECT and neurological disorders. Convuls Ther 1987;3:121–36. 120. Martin M, Figiel G, Mattingly G, Zorumski CF, Jarvis MR. ECT induced interictal delirium in patients with a history of a CVA. J Geriatr Psychiatry Neurol 1992;5:149–55. 121. Currier MB, Murray GB, Welch CC. Electroconvulsive therapy for post-stroke depressed patients. J Neuropsychiatry Clin Neurosci 1992;4:140–4. 122. Coffey CE, Hinkle PE, Weiner RD, Nemeroff CB, Krishnan KR, Varia I, and others. Electroconvulsive therapy of depression in patients with white matter hyperintensity. Biol Psychiatry 1987;22:629–36. 123. Coffey CE. Brain morphology in primary mood disorders: implications for electroconvulsive therapy. Psychiatric Annals 1996;26:713–6. 124. Fiegel GS, Hassen MA, Zorumski C, Krishnan KR, Doraiswamy PM, Jarvis MR, and others. ECT-induced delirium in depressed patients with Parkinson’s disease. J Neuropsychiatry Clin Neurosci 1991;3:405–11. 125. Sackeim HA, Decina P, Prohovnik S, Malitz S, Resor SR. Anticonvulsant and antidepressant properties of electroconvulsive therapy: A proposed mechanism of action. Biol Psychiatry 1983;18:1301–10. 126. Kalinowsky LB, Kennedy F. Observations in electric shock therapy applied to problems of epilepsy. J Ner Ment Dis 1943;98:56–67. 127. Krystal AD, Coffey CE. Neuropsychiatric considerations in the use of electroconvulsive therapy. J Neuropsychiatry Clin Neurosci 1997;9:283–92. 128. Devinsky O, Duchowny MS. Seizures after convulsive therapy: a retrospective case survey. Neurology 1983;33:921–5. 129. Weiner RD. ECT-induced status epilepticus and further ECT: a case report. Am J Psychiatry 1981;138:1237–8. 130. Cantor C. Carbamazepine and ECT: A paradoxical combination. J Clin Psychiatry 1986;47:276–7. 131. Sackeim HA, Decina P, Kanzler M, Kerr B, Malitz S. Effects of electrode placement on the ef fi cacy of ti trated, low dos age ECT. Am J Psy chia try 1987;144:1449–55. 132. Summers WK, Robins E, Reich T. The natural history of acute organic mental syndrome after bilateral electroconvulsive therapy. Biol Psychiatry 1979;14:905–12. 133. Mulsant BH, Rosen J, Thornton JE, Zubendo GS. A prospective naturalistic study of electroconvulsive therapy in late-life depression. J Geriatr Psychiatry Neurol 1991;4:3–13. 134. Zwil AS, McAllister TW, Price TRP. Safety and efficacy of ECT in depressed patients with organic brain disease: review of a clinical experience. Convuls Ther 1992;8:103–9. 135. Nelson JP, Rosenberg DR. ECT treatment of demented elderly patients with major de pres sion: a ret ro spec tive study of ef fi cacy and safety. Con vuls Ther 1991;7:157–65. 136. Price TRP, McAllister TW. Safety and efficacy of ECT in depressed patients with dementia. A review of clinical experience. Convuls Ther 1989;5:61–74. 137. Rasmussen K, Abrams R. Treatment of Parkinson’s disease with electroconvulsive therapy in electroconvulsive therapy. In: Kellner CH, editor. The Psychiatric Clinics of North America 1991;14:925–33. 138. Balldin J, Eden S, Granerus AK, Modigh A, Svanborg A, Walinder J, and others. Electroconvulsive therapy in Parkinson’s syndrome with “on-off” phenomenon. Acta Neurol Scand 1987;76:191–9. 139. Balldin J, Granerus AK, Linstedt G, Modigh A, Walinder J, and others. Predictors for improvement after electroconvulsive therapy in parkinsonian patients with onoff symptoms. J Neural Transm 1981;52:199–211. 140. Anderson K, Balldin J, Gottfries CG, Granerus AK, Modigh K, Svennerholm L, and others. A double- blind evaluation of electroconvulsive therapy in Parkinson’s disease with “on-off” phenomena. Acta Neurol Scand 1987;76:191–9. 141. Nymeyer L, Grossberg GT. Delirium in a 75-year-old woman receiving ECT and levodopa. Convuls Ther 1997;13:114–6. 142. Zervas IM, Fink M. ECT and delirium in Parkinson’s disease. Am J Psychiatry 1992;149:1758. 143. Fiegel GS, Hassen MA, Zorumski C, Krishnan KR, Doraiswamy PM, Jarvis MR, and others. ECT-induced delirium in depressed patients with Parkinson’s disease. J Neuropsychiatry Clin Neurosci 1991;3:405–11. 144. Kellner CH, Beale MD, Pritchett JT, Bernstein HJ, Burns CM. Electroconvulsive therapy and Parkinson’s disease: the case for further study. Psychopharmacol Bull 1994;30:495–500. 145. Maclay WS. Death due to treatment. Proceedings of the Royal Society of Medicine 1953;46:13–20. 146. Folk WF, Kellner CH, Beale MD, Conroy JM, Duc TA. Anesthesia for electroconvulsive therapy: a review. Journal of ECT 2000;16:157–70. 147. Perrin GM. Cardiovascular aspects of electric shock therapy. Acta Psytchiatrica et Neurologica Scandanavica 1961;36:1–45.

October 2001

The Use of Electroconvulsive Therapy in Special Patient Populations

148. Gerring JP, Sheilds HM. The identification and management of patients with a high risk for cardiac arrythmias during modified ECT. J Clin Psychiatry 1982;43:140–3. 149. Olfson M, Marcus S, Sackeim HA, Thompson J, Pincus HA. Use of ECT for the inpatient treatment of recurrent major depression. Am J Psychiatry 1998;15:522–9. 150. Abrams R. Electroconvulsive therapy. 2nd ed. New York (NY): Oxford University Press; 1992. 151. Jones RM, Knight PR. Cardiovascular and hormonal responses to electroconvulsive therapy. Anaesthesia 1981;36:795–9. 152. Jones RM, Knight PR, Hill AB. Rate pres sure prod uct. An aes the sia 1980;35:1010–1. 153. Robinson BF. Relation of heart rate and systolic blood pressure to the onset of pain in angina pectoris. Circulation 1967;35:1073–83. 154. Cattan RA, Barry PP, Mead G, Reefe WE, Gay A, Silverman M. Electroconvulsive therapy in octogenarians. J Am Geriatr Soc 1990;38:753–8. 155. Zielinski RJ, Roose SP, Devanand DP, Woodring S, Sackeim HA. Cardiovascular complications of ECT in depressed patients with cardiac disease. Am J Psychiatry 1993;150:904–9. 156. Rice EH, Sombrotto LB, Markowitz JC, Leon AC. Cardiovascular morbidity in high-risk patients during ECT. Am J Psychiatry 1994;151:1637–41. 157. Seiner SJ, Mallya G. Treating depression in patients with cardiovascular disease: Harv Rev Psychiatry 1999;7:85–93. 158. Applegate RJ. Diagnosis and management of ischemic heart disease in the patient scheduled to undergo electroconvulsive therapy. Convuls Ther 1997;13:128–44. 159. Eagle KA, Brundage BH, Chaitman BR, Ewy GA, Fleisher LA, Hertzer NR, and others. Guidelines for perioperative cardiovascular evaluation for noncardiac sur-

719

gery: report of the American College of Cardiology/American Heart Association task force on practice guidelines. Committee on perioperative cardiovascular evaluation for noncardiac surgery. Circulation 1996;93:1278–317. 160. Loo H, Kuche H, Benkelfat C. Electroconvulsive therapy during anticoagulant therapy. Convuls Ther 1985;1:258–62. 161. Weiner RD, Coffey CE. Electroconvulsive therapy in the medical and neurological patient. In: Stoudemire A, Fogel BS, editors. Psychiatric Care of the Medical Patient. New York (NY): Oxford University Press; 1993. 162. Elliot DL, Linz DH, Kane JA. Electroconvulsive therapy, pretreatment medical evaluation. Arch Intern Med 1982;142:979–81. 163. Tchou PJ, Piasecki E, Gutmann M, Jazayeri M, Axtell K, Akhtar M. Psychological support and psychiatric management of patients with automatic implantable cardioverter defibrillators. Int J Psychiatry Med 1989;19:393–407. 164. American Psychiatric Association Task Force on ECT. Electroconvulsive therapy (task force report # 14). Washington, (DC): American Psychiatric Association; 1978. 165. Appelbaum PS, Grisso T. Assessing patients’ capacity to consent to treatment. N Engl J Med 1988;319:1635–8. 166. Lee MA. Depression and refusal of life support in older people. J Am Geriatr Soc 1990;38:710–4. 167. Sullivan MD, Ward NG, Laxton A. The woman who wanted electroconvulsive therapy and do-not-resuscitate status. Gen Hosp Psychiatry 1992;14:204–9. 168. Miller ME, Siris SG, Gabriel AN. Treatment delays in the course of electroconvulsive therapy. Hosp Comm Psychiatry 1986;37:825–7. 169. Johnson SY. Regulatory pressures hamper the effectiveness of electroconvulsive therapy. Law and Psychology Review 1993;17:155–70.

Résumé : L’utilisation des électrochocs chez les populations de patients spéciaux Contexte : Malgré leur efficacité bien établie et leur utilisation croissante, les électrochocs demeurent un traitement controversé. L’absence de transparence des questions liées à leur usage chez les populations de patients spéciaux (par exemple, les enfants, les adolescents, les femmes enceintes, les personnes âgées et les personnes ayant une maladie somatique) nourrit souvent le débat sur l’utilisation des électrochocs.. Méthode : La documentation sur l’utilisation des électrochocs chez les populations de patients spéciaux est examinée de même que les affections médicales à risque élevé souvent associées dans la pratique clinique. Dans chaque cas, on précise l’innocuité, la tolérabilité et l’efficacité de la procédure. Résultats : Une grande partie de la documentation examinée consiste en des études de cas, bien que quelques essais contrôlés soient disponibles. En général, l’utilisation des électrochocs chez les populations spéciales est relativement sûre et extrêmement efficace. Dans une petite série de cas, l’utilisation des électrochocs chez les enfants et les adolescents est efficace mais nécessite d’autres études systématiques. Chez les femmes enceintes, les électrochocs sont très efficaces et avec les soins médicaux appropriés, ils sont relativement sûrs à tous les trimestres de la grossesse de même que dans la période du postpartum. Les personnes âgées de santé fragile sont de particulièrement bons candidats aux électrochocs, parce que souvent ils ne répondent pas aux psychotropes ou ils ne les tolèrent pas. Les affections médicales auxquelles il faut porter une attention particulière durant un traitement d’électrochocs sont les troubles du système nerveux central (SNC), du système cardiovasculaire et du système respiratoire. Grâce aux techniques modernes d’anesthésie et au traitement médical prudent de chaque patient à risque élevé, la plupart peuvent compléter une série d’électrochocs avec succès. Le processus d’obtention d’un consentement éclairé nécessite aussi une attention spéciale chez ce groupe de patients, car leur capacité à consentir au traitement peut être compromise. Conclusions : Si l’on porte une attention particulière aux besoins médicaux et anesthésiques de chaque patient, les électrochocs constituent une procédure efficace et relativement sûre chez les populations de patients spéciaux à risque élevé.