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Psychiatric Clinics of North America

Volume 25 • Number 1 • March 2002

Copyright © 2002 W. B. Saunders Company

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Electroconvulsive therapy in the medically ill

Keith G. Rasmussen, MD *

Teresa A. Rummans, MD

Jarrett W. Richardson, MD

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Departments of Psychiatry and Psychology

Mayo Medical School

Rochester, Minnesota USA

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|* Address reprint requests to: Keith G. Rasmussen, MD |

|Department of Psychiatry and Psychology Mayo Clinic 200 First|

|Street SW Rochester, MN 55905 |

|E-mail address:  rasmussen.keith@mayo.edu |

|This work was supported by National Institutes of Health grant no. MH55484-05. |

|PII S0193-953X(03)00057-1 |

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Electroconvulsive therapy (ECT) often is given to depressed patients with a variety of comorbid medical diagnoses. With attention to pretreatment medical and neurological evaluation, ECT can be safe even in highly medically or neurologically complicated patients. This article reviews the most commonly encountered medical and neurological illnesses in ECT patients and provides suggestions for safe and effective use of ECT in such populations.

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Three questions face the practitioner who is treating a patient with combined medical and psychiatric illness for whom electroconvulsive therapy (ECT) is being considered:

1. Is ECT effective in such patients?

2. Does ECT cause deterioration of the underlying medical condition or significant side effects?

3. Is modification of ECT technique indicated to lessen the risk of adverse outcomes?

To answer these questions definitively, prospective trials are needed in which the severity of both the medical and the psychiatric illness are blindly rated in a systematic manner before, during, and after treatment. Such trials are generally lacking. Furthermore, in relying on case reports, one must consider that these publications tend to be biased either in favor of excellent results or unexpectedly poor outcomes; however, a large body of case reports and case series published over several decades do inform the ECT clinician about a reasonable approach to patients with a wide array of medical disorders. This section focuses on medical conditions in which ECT has a direct physiologic effect and therefore places the patient at risk for complications. These include cardiovascular, neurologic, respiratory, and other disorders. In addition, the reader is strongly encouraged to apply the principles contained in the APA Committee on ECT report,[4] which has excellent sections on ECT in medically ill patients.

CARDIOVASCULAR DISEASES

Cardiac complications represent the most common source of significant morbidity and mortality during ECT. Even so, deaths are extremely rare, and the majority of cardiac patients can be given ECT with a low risk of complications.[2] There are several fundamental points in providing safe ECT to such patients. The first is accurate pre-ECT identification, through history, physical examination, and screening laboratory tests, of those patients with cardiovascular disease. The next step is pre-ECT cardiology consultation. The purpose of this is to determine the severity of cardiac disease and may include functional or structural cardiac imaging studies. The cardiology consultant can also recommend any modification of the patient's current treatment regimen to provide further stabilization of the cardiac condition (e.g., an increase in diuretic dosage in a patient with congestive heart failure that is not optimally controlled). Finally, the medical consultant can recommend strategies that may reduce cardiac risk during the ECT treatments, such as the administration of β-blockers to lessen the ECT-induced decrease in cardiac rate-pressure product. A third important strategy for safe administration of ECT to cardiac patients is careful vigilance throughout the ECT course, both at the times of treatment and in the intertreatment period, for any treatment-emergent complications so that prompt intervention can prevent deterioration of a minor complication into a major one.

An elegant demonstration of the importance of these points is provided by two reports from the Payne Whitney Clinic. Gerring and Shields[27] reported on a series of 17 cardiac patients given ECT in 1975–1976. None of the patients had pre-ECT medical consultations, electrolyte studies, or digitalis levels, even though 13 of the patients were on this medication. Most patients did not get continuous ECG monitoring during their treatments, nor were pretreatment antihypertensive medications given. There were four life-threatening cardiac complications and one death in this series. In contrast, Rice et al[75] reported on their experience at the same institution treating 26 cardiac patients with ECT in 1990–1991. All of the technical disadvantages described earlier for the earlier cohort had been reversed, so that routine pre-ECT laboratory and ECG studies were performed, most patients had pre-ECT medical consultations, and ECT technique followed modern standards, including continuous ECG monitoring and the availability of cardiac medications at the time of treatment. No major cardiac complications occurred in this cohort of patients. The following sections consider the aspects of ECT technique in patients with specific types of cardiovascular disorders.

Coronary Artery Disease

Cardiac complications during ECT are more common in those with coronary artery disease (CAD) than with other cardiac conditions.[102] ECT induces increases in pulse and blood pressure that result in a 200% to 300% increase in myocardial oxygen consumption during and for a few minutes after the seizure[24] ; however, ECT can be safely administered to the majority of patients with CAD. For patients with known CAD, pre-ECT cardiology consultation is recommended to assess the stability of the patient's cardiac status and to assist with risk-reduction strategies.[4] [5] The most important of such strategies is optimal stabilization of cardiac status before treatment.[2] Pretreatment cardiac imaging is commonly requested to assess the stability of the patient's myocardial capacity during stress. Any cardiac medications the patient is taking, with the exception of diuretics or lidocaine-type agents, should be given with a small sip of water the mornings of treatment. A further strategy is the intravenous administration of β-blockers immediately pretreatment to dampen the increase in myocardial oxygen consumption.[8] If pretreatment β-blockade is used, then an anticholinergic agent, such as glycopyrrolate or atropine, should also be given to minimize the risk of vagally mediated prolonged asystole or bradycardia, which sometimes occur early in the seizure or if no seizure is elicited by the electrical stimulus.[43] Depression commonly accompanies the postmyocardial infarction period—hence, the question of how long to wait until ECT is safe. Consideration should be given to the severity of the patient's depression and cardiac stability. A patient a few weeks out of a mild myocardial infarction with stable myocardial function may be safer to treat than a patient many months or years out of myocardial infarction with a very low ejection fraction or with exercise-induced ischemic changes on cardiac imaging. Close communication between psychiatrist and cardiologist is essential in these circumstances.

Dysrhythmias, Pacemakers, and Implantable Defibrillators

Patients with asymptomatic, uncomplicated cardiac conduction delays, such as first degree heart block or bundle branch block, can be safely treated with ECT without special precautions. Patients with atrial fibrillation also usually can be treated safely[59] ; however, pretreatment cardiologic consultation can ensure optimal stabilization and treatment of the dysrhythmia. In particular, ventricular rate should be normalized. Occasionally, conversion to normal sinus rhythm occurs during ECT, so pretreatment anticoagulation would be considered optimal.[59] Patients with any type of malignant ventricular arrhythmia are at higher risk for hemodynamic instability during ECT, so pretreatment cardiology consultation is mandatory for risk assessment and risk-reduction strategies. Lidocaine in antiarrhythmic doses has potent anticonvulsant properties, so it should not be given before an ECT treatment unless truly necessary and no alternative antiarrhythmic is available.

Patients with pacemakers usually do not need any special adjustment or attention aside from ensuring that monitoring and other equipment are well grounded.[2] Consultation with a cardiologist is indicated, and some older types of pacemakers may need to be turned from demand mode to fixed mode before treatment.[2] The use of transesophageal atrial pacing during ECT for patients at significant risk for asystole has been described.[89] Patients with implantable cardiodefibrillators usually can be safely treated with ECT, but pretreatment consultation with a cardiac electrophysiologist is recommended.[4] [61]

Hypertension

Despite the transient, peri-ictal increase in blood pressure, ECT does not result in sustained increases in blood pressure and in fact may result in a decrease in blood pressure.[88] Common sense dictates that optimum blood pressure control be attained in hypertensive patients pre-ECT. Antihypertensive medications (except for diuretics, which could result in a full bladder that may rupture during the seizure) should be given with a small sip of water in the mornings of treatments. If there are significant risks to the patient for even brief periods of hypertension (e.g., vascular aneurysms, cardiac aneurysm, severe left ventricular or valvular compromise), premedication with antihypertensive agents is indicated, selecting the drug that is most appropriate to the patient's clinical situation. Short-acting drugs (e.g., esmolol) administered at the time of anesthesia induction may be preferable to avoid delayed hypotension that can occur with longer-acting drugs (e.g., labetolol). Although β-blockade shortens seizure length during ECT,[92] no direct evidence shows that this interferes with therapeutic efficacy.

Vascular Malformations and Anticoagulation

ECT has been safely administered in the presence of known cardiac[14] and aortic aneurysms,[12] although a case of cardiac rupture during ECT has been reported.[3] Pretreatment consultation with a vascular surgeon in cases of known aneurysms or other vascular malformations (e.g., arteriovenous fistula) is important in assessing the risk of rupture during ECT. Risk-reduction strategies may include pretreatment with antihypertensive agents to reduce shear force against the aneurysm.

For patients who are on anticoagulation for deep venous thrombosis, valvular heart disease, atrial fibrillation, or another indication, it is prudent and safe to continue it during ECT with close attention to maintaining the proper PT or PTT.[4]

Congestive Heart Failure and Valvular Heart Disease

As ECT causes a temporary but sharp increase in cardiac rate-pressure product, patients with congestive heart failure are at risk for decompensation during a course of ECT[72] ; however, successful administration of ECT to patients with stable low cardiac output has been described.[86] ECT has been successfully administered to patients with stable valvular heart disease.[32] [68] [72] As with the other cardiac conditions discussed, the most important aspect of management in such cases is careful pre-ECT cardiologic evaluation and risk assessment. In particular, patients with congestive heart failure should have their medical management optimized, with very careful ongoing assessment during the course of ECT looking for signs of congestive decompensation.

NEUROLOGIC DISORDERS

A large body of case reports and case series published over several decades do inform the ECT clinician about a reasonable approach to patients with a wide array of neurologic disorders. This section considers such patients grouped by type of neurologic illness. A thorough consideration of all published papers is beyond the scope of this article, but the interested reader is referred to various reviews published over the years [2] [18] [36] [81] [84] [103] .

Dementia

A vexing problem regarding the literature on ECT in demented patients is the lack of standardized criteria for the establishment of a dementia syndrome independent of depression-related cognitive dysfunction.[87] In fact, in routine clinical circumstances, it is often difficult to determine whether the patient with coexisting severe depression and cognitive dysfunction has a separate dementing illness or depression-related cognitive dysfunction.[87] A further problem with this literature is the lack of long-term cognitive follow-up in most reports. Nevertheless, the extant literature does provide guidance on safe, effective ECT in the depressed, demented patient.

Numerous case reports indicate that ECT can be efficacious in depressed and demented patients for the depressive symptoms without causing undue or long-lasting increases in memory disturbance.[67] Several case series provide more substantial information. In a prospective study, Reynolds et al[74] systematically followed depression ratings in a group of three demented depressives. Two of these patients had an excellent antidepressant response to ECT without cognitive worsening, whereas one had no antidepressant response and a sharp reduction in mini-mental state exam (MMSE) score. Gaspar and Samarasinghe[26] reported data on three patients with a diagnosis of primary dementia and depression. Similarly, two showed a good antidepressant response, and one did not. None of the patients were believed to have sustained a long-lasting (i.e., more than a few days) worsening of their baseline cognitive status, although no systematic cognitive evaluations were done.

In a larger series, Nelson and Rosenberg[55] reported their experience treating 21 depressed and demented patients with ECT. Global antidepressant efficacy ratings based on chart review were similar to those of a depressed but nondemented ECT cohort. Post-ECT confusion was believed to be greater in the depressed and demented group. No efficacy or cognitive follow-up data were presented.

In the largest series to date of depressed and demented patients given ECT, Rao and Lyketsos[67] described 31 patients, 16 diagnosed with vascular dementia, 4 with Alzheimer's dementia, and 11 with dementia of uncertain cause. Half the patients were believed to suffer delirium (criteria not specified) with ECT. Two thirds were believed to have a “good response” in terms of depression. MMSE score actually increased an average of 1.62 points by treatment end. This indicates the beneficial effect of ECT on attention and concentration after clearing of the acute post-treatment confusion, even in demented patients. Of note, one patient had tardive seizures in the recovery room after ECT. No efficacy or cognitive data were presented separately for the different demented groups.

To summarize, several dozen depressed ECT patients believed to have a separate dementing illness have been described in the literature. Approximately two thirds obtained noticeable antidepressant benefit, with approximately half showing greater than usual confusional states. Sorely needed is a trial with systematic cognitive evaluations in patients diagnosed with dementia by standardized criteria, and subclassified by dementia type, compared with nondemented ECT controls and with depressed and demented patients treated with medications. Finally, in an effort to spare excess memory disturbance, consideration should be given to treating depressed and demented patients with right unilateral or bifrontal electrode placement and twice-weekly treatment frequency.

Parkinson's Disease

A variety of case reports, small series, and one sham-ECT-controlled trial document that ECT is highly effective for depression in Parkinson's disease and may improve motor function as well[52] [69] ; however, delirium is common during ECT,[22] as is treatment-emergent dyskinesia,[15] but post-treatment cognitive function may be improved.[63] The duration of ECT-related antiparkinsonian effects has been variable, but long-term follow-up data have been presented. For example, Fall et al[19] systematically followed up 16 nondemented, nondepressed patients with advanced Parkinson's disease before, immediately after, and for up to 1.5 years after courses of mostly unilateral ECT. Fifteen subjects experienced some improvement in the motor symptoms of PD, which was dramatic in some cases. Half of the patients had sustained improvement for 3 to 18 months after ECT, without maintenance ECT. Approximately one third developed severe confusional states during ECT, the duration of which was a few days to 2 weeks. Interestingly, 4 of these 5 patients went on to have long-lasting (i.e., at least several months) motor improvement. Baseline increases in cerebrospinal fluid (CSF)-to-serum albumin ratios, which were thought to reflect violation of the blood-CSF barrier, accurately predicted the 5 subjects who developed interictal delirium. None of the 11 subjects who did not develop interictal delirium had pre-ECT increases in this ratio, indicating that violation of the blood-CSF barrier before ECT predisposes to ECT-induced confusion.

In another series, Pridmore et al[65] treated seven advanced, nondepressed PD patients with only four unilateral ECT treatments. Immediate post-ECT and 2-week post-ECT ratings in all spheres of motor function indicated improvements. Four patients developed severe, although temporary, confusion. One patient developed a dyskinesia responding to lowering of the levodopa dose. In a follow-up report on these and several other such patients given index (but not maintenance) ECT, three of nine initial ECT responders had improvements lasting 2 to 10 weeks, whereas the other six responders had improvements lasting 10 to 35 months.[64]

Attempts have been made to prolong the acute ECT-induced improvement in motor symptoms of Parkinson's disease using maintenance ECT, in which treatments are given every few weeks for variable lengths of time.[1] [20] [34] [83] [98] [101] In these reports, a total of 13 patients with Parkinson's disease given maintenance ECT are described. Several of the patients had had several courses of index ECT with good, although relatively short-lived, motoric improvement. In each case, maintenance ECT seemed to extend this period of improvement, in some cases for up to 1 year. The frequency of such treatments was highly variable, depending on the length of each patient's improvement, and was balanced against cognitive impairment.

Several summary points can be made regarding the use of ECT in Parkinson's disease patients:

• It is highly effective for the severe depression so often seen in such patients.

• In a substantial proportion of patients, a variety of extrapyramidal signs (EPS) phenomena also may improve, often faster than the depression.

• The duration of this antiparkinsonian benefit may be from a few days to years.

• Maintenance ECT may extend the period of improvement in patients who can tolerate it from a cognitive standpoint.

• Treatment emergent dyskinesias and delirium are relatively common[15] [22] and may be helped by careful reduction of dopaminergic doses.

• Twice-weekly treatment frequency and right unilateral or bifrontal electrode placement should be considered as methods to reduce memory impairment.

Neuroleptic-Induced Movement Disorders

Variable results have been reported with the use of ECT in patients with tardive dyskinesia. For example, Yassa et al[100] found ECT helpful in reducing dyskinetic movements in only one of nine such patients treated. Furthermore, Holcomb et al[35] reported increased signs of tardive dyskinesia in a parkinsonian patient who had good resolution of his parkinsonism with ECT. DeQuardo et al[10] even found temporary spontaneous dyskinesias after ECT in a patient with Wilson's disease. These results, combined with the known increase in levodopa-related dyskinesias occurring commonly in patients with Parkinson's disease treated with ECT,[15] indicate that ECT is unlikely to help dyskinetic movements in patients with tardive dyskinesia and may even aggravate them. Interestingly, several cases of improvement in tardive dystonia with ECT have been reported,[39] [44] [62] which is not surprising given the similarity of this syndrome to parkinsonian extrapyramidal signs, although one negative outcome has been reported.[30]

Neuroleptic malignant syndrome, one form of malignant catatonia,[60] often is treated, after withdrawal of the neuroleptic, by administering dopamine agonists, such as bromocriptine, and muscle relaxants, such as dantrolene or lorazepam. ECT may represent a lifesaving option for patients who do not respond to these measures.[56] [60] It may be the most effective treatment for neuroleptic malignant syndrome, particularly when it occurs in a patient who was already catatonic.

Cerebrovascular Disease

Several isolated case reports[11] [96] of safe use of ECT in poststroke patients have been published. Murray et al[53] and Currier et al,[9] describing experience at Massachusetts General Hospital from 1969 to 1991 giving ECT to poststroke patients, indicated that, of 34 such patients, 32 improved significantly with ECT. Neither location of stroke, whether right-left or cortical-subcortical, nor time since stroke (< l month to 12 years) was associated with clinical response. Five of six patients showed improvement in their preexisting cognitive impairment with ECT without neurologic worsening.

Martin et al[47] compared 14 poststroke ECT patients with 14 nonstroke ECT patients and found a similar incidence of 4 of 14 in each group developing interictal delirium. Interestingly, all 4 of the poststroke patients developing such delirium had caudate strokes, buttressing the investigators' contention that basal ganglia lesions predispose to ECT-related delirium. The poststroke ECT patients had a good clinical response without neurologic worsening. Of note, the more ECT treatments given after the delirium became apparent, the longer the delirium lasted.

In addition to patients with a history of cerebrovascular accident (CVA), those with known intracerebral aneurysms or vascular malformations would be expected to have a high risk with ECT. At least two cases of patients safely administered ECT after cerebral aneurysm repair have been reported,[21] [38] and numerous cases of patients with known aneurysms that have not been surgically corrected pre-ECT have been reported; in none of those has a bleed occurred.* To the authors' knowledge, however, two cases of ECT-associated intracerebral hemorrhages have been reported,[76] [97] both in patients without known pre-ECT cerebrovascular disease. Most investigators reporting on ECT in patients with known aneurysms used antihypertensive treatments to dampen the ECT-related increase in blood pressure. Drop et al[17] consider intracerebral aneurysms at high risk for rupture during ECT and recommend that appropriate antihypertensive measures (e.g., β-blockade and sodium nitroprusside) and monitoring should be undertaken during ECT in such patients.

To summarize the literature on ECT in patients with histories of stroke or intracerebral aneurysm, numerous reports of safe ECT administration exist to provide some confidence to the clinician; however, caution must be exercised, and measures to control excessive blood pressure increases should be considered.[17]

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     * References [6] [16] [25] [37] [42] [54] [79] [93] .

Epilepsy

Giving ECT to epileptics is cause for concern; however, ECT potently increases the seizure threshold during the course of treatments, and seizure lengths progressively shorten, indicating that ECT has an anticonvulsant action.[78] Early ECT clinicians knew about this effect and put it to use in treating epileptics with intractable seizure disorders. For example, Taylor[91] reported on 19 epileptics given ECT at a state hospital. One patient had no change in spontaneous seizure frequency, one had a modest reduction, and 17 of 19 had a complete resolution of such seizures while they were being treated with weekly ECT sessions. Caplan,[7] in a similar population and using the same ECT method (i.e., thrice-weekly ECT for a few weeks, followed by weekly maintenance treatments), also found a reduction in the patients' spontaneous seizure frequency. Both investigators found good psychopathologic improvement in psychosis, mood disorders, and aggression. In Caplan's report,[7] when ECT was stopped, spontaneous seizure frequency returned within 1 month to the pre-ECT levels, indicating that the anticonvulsant action of ECT is temporary. Wolff[99] and, more recently, Sackeim et al,[78] Griesemer et al,[28] Regenold et al,[73] Schnur et al,[82] and Viparelli and Viparelli[94] have all described cases of patients with well-defined epilepsy using modern diagnostic criteria who had highly refractory seizures in whom substantial, although usually temporary, reductions in seizure frequency were accomplished with ECT. In addition, occasional reports document that status epilepticus can occur, fortunately rarely, after ECT, even in nonepileptics.[29] [31] [66]

In the modern era, with highly sophisticated and extensive antiepileptic treatments available, it would be extremely rare that an epileptic patient would be given ECT for the purpose of reducing seizure frequency. More commonly, such patients are given ECT for a mood, psychotic, or behavioral dyscontrol disorder. Surprisingly, no large series of such patients describing outcome, both therapeutic and cognitive, vis-a-ag-vis nonepileptic ECT patients exists. Such a series would be a welcome addition to the ECT literature. At present, it can be confidently stated that epilepsy itself does not present a contraindication to ECT, and no evidence shows that spontaneous seizure frequency increases with ECT. It would be prudent to maintain antiepileptic medication at therapeutic levels during ECT to avoid withdrawal-associated status epilepticus.[33] If seizure induction becomes impossible during the course of treatment because of the anticonvulsant action of ECT, however, then careful, temporary downward adjustment of the patient's anticonvulsant medication may be warranted, in consultation with a neurologist, taking into account the nature and severity of the patient's seizure disorder.

Intracranial Tumors

The original report of Shapiro and Goldberg[84] describing neurologic deterioration after ECT in six patients subsequently found to have brain tumors led to the belief that brain tumors constituted an absolute contraindication to ECT. This viewpoint was supported in the review by Maltbie et al,[46] in which 35 patients who had brain tumors found after ECT were described. In that series, the rates of neurologic morbidity and mortality were quite high. Mattingly et al,[49] however, reviewed 10 cases in which presence of the tumor was known in advance of ECT. None of the patients had focal neurologic findings, increased intracranial pressure (ICP), or papilledema before treatment. Neurologic deterioration was not noted with ECT, and none of the patients died within 1 month after treatment. In 8 cases, the tumors were meningiomas, and in 2 cases, they were metastatic breast cancers. The investigators concluded that, in the absence of complicating factors, such as increased ICP or focal neurologic findings, ECT may be safe if the psychopathology warrants this treatment. Several other cases of successful and neurologically uncomplicated administration of ECT to patients with meningiomas have been described.[40] [41] [50] [85] Recently, the first case of an ECT patient with increased ICP associated with a brain tumor, known in advance, was reported.[57] The investigators used dexamethasone, furosemide, and β-blockade before treatment to decrease both brain edema and the increase in ICP associated with ECT. The patient enjoyed a good therapeutic response without neurologic deterioration.

A prudent summary of the brain tumor and ECT literature is that presence of any tumor probably presents an increased risk for neurologic complications caused by ECT. In the absence of focal neurologic findings, brain edema, mass effect, or papilledema, the risks probably are relatively small. In the presence of such findings, however, the increased risk is probably quite high, and ECT should be considered only in the context of profoundly urgent psychopathology. In any case of known intracranial tumor in which ECT is being considered, consultation with a neurosurgeon or neurologist to advise on risk assessment and risk-reduction strategies (e.g., dexamethasone and furosemide) is indicated.

Miscellaneous

More than 12 cases of patients with multiple sclerosis receiving full courses of ECT for psychopathologic states have been reported, with the suggestion that gadolinium-enhancing lesions before ECT may presage a particularly high risk for neurologic deterioration during treatment.[48] [80] Isolated case reports and small series also describe safe and effective use of ECT in a diversity of other neurologic conditions, such as cerebral palsy,[71] hydrocephalus with shunt,[45] and spinocerebellar ataxia.[23]

PULMONARY DISORDERS

The two most common pulmonary disorders encountered in ECT practice are asthma and chronic obstructive pulmonary disease. A paucity of data exist about the relative efficacy and safety of ECT in patients with these conditions. Although there seems to be no a priori reason to believe that ECT would be less effective in such patients, some considerations regarding safety should be discussed. The first is the risk for bronchospasm. Taylor[90] described a psychotically depressed, asthmatic man who developed two episodes of short-lived bronchospasm during his otherwise effective and uncomplicated course of ECT. The American Psychiatric Association (APA) Committee on ECT[4] recommends that patients with asthma and chronic obstructive pulmonary disease receive prescribed bronchodilators before each treatment and that special attention be given to oxygenation of such patients. A second safety concern is the risk for prolonged seizures or status epilepticus in patients taking theophylline during ECT. Peters et al[58] and Devanand et al[13] each described a patient who went into status epilepticus with ECT while taking theophylline, and Abrams[2] has described three more. Rasmussen and Zorumski[70] described a series of seven patients given theophylline during ECT with nontoxic, therapeutic blood levels, none of whom developed status epilepticus. It is recommended that theophylline be discontinued before ECT. If that is medically contraindicated, then careful attention should be given to maintaining the lowest therapeutic blood level, concomitant caffeine augmentation should not be given, and ready access to rapidly acting anticonvulsant medication (e.g., intravenous diazepam) should be ensured.

MISCELLANEOUS MEDICAL DISORDERS

A variety of other medical considerations occur in ECT practice. In pregnancy, the most common adverse events are premature labor, uterine contractions, and vaginal bleeding.[4] [51] [95] During the third trimester, raising gastric pH before the procedure with a nonparticulate antacid can minimize the risk for aspiration pneumonitis. Adequately oxygenating but not hyperventilating the patient before, during, and immediately after the procedure can minimize the risk for fetal hypoxia.[4] [51] [95] The reader is especially referred to the APA Committee on ECT report,[4] which has thorough recommendations regarding the use of ECT in pregnant women.

Patients with diabetes mellitus should have their blood glucose levels monitored closely during their ECT course. Glucose levels just before ECT may demonstrate significant hypoglycemia in diabetics who are fasting and not taking insulin. If this occurs, glucose can be given intravenously during the procedure. Electrolyte abnormalities, such as hyperkalemia and hyponatremia, can lead to severe complications, including cardiac dysrhythmias and seizures, respectively. Significant reflux in those patients with hiatal hernias, gastroparesis, obesity, and pregnancy may require measures to prevent aspiration pneumonia. Histamine-2 antagonists or antacids may decrease gastric acid, but for patients at severe risk for aspiration, intubation may be necessary. Urinary retention from anticholinergic agents given during ECT can predispose to urinary tract infections and even bladder rupture if not monitored. With the use of skeletal muscle paralysis, the risk for bone fractures is minimal with modern ECT; however, patients with severe osteoporosis or recent fractures may need higher than usual muscle relaxant dosing.[4] Testing the adequacy of paralysis with a peripheral nerve stimulator is recommended in these circumstances. For the patient with unstable cervical spine disease, pretreatment consultation with an orthopedic or neurologic surgeon is recommended to assess the risk for injury, with the neck manipulation needed to ventilate the patient during the treatment. With the increase in intraocular pressure associated with ECT, precipitating glaucoma is concerning; however, no published cases of this complication exist. Administering antiglaucoma medications, except anticholinesterases, before ECT is recommended for individuals with documented glaucoma requiring treatment.[4] [77]

SUMMARY

ECT is often a necessary treatment for severe psychiatric disorders in patients with medical or neurologic comorbidity. Although the available data consist largely of cases and case series, ECT is effective in treating psychopathology despite the comorbidity. With appropriate precautions and monitoring during and after ECT, complications can be minimized.

References

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2. Abrams R. Electroconvulsive therapy in the high-risk patient. New York: Oxford University Press; 1997. p. 97-111.

3. Ali PB, Tidmarsh MD. Cardiac rupture during electroconvulsive therapy. Anaesthesia 1997;52:884-6.   Abstract

4. American Psychiatric Association, Committee on Electroconvulsive Therapy. ed 2 Washington, DC: APA Press; 2001. The Practice of Electroconvulsive Therapy.

5. Applegate RJ. Diagnosis and management of ischemic heart disease in the patient scheduledto undergo electroconvulsive therapy. Convulsive Therapy 1997;13:128-44.  

6. Bader GM, Silk KR, Dequardo JR, et al. Electroconvulsive therapy and intracranial aneurysm. Convulsive Therapy 1995;11:139-43.  

7. Caplan G. Electrical convulsion therapy in the treatment of epilepsy. Journal of Mental Science 1946;92:784-93.  

8. Castelli I, Steiner LA, Kaufman MA, et al. Comparative effects of esmolol and labetolol to attenuate hyperdynamic statesafter electroconvulsive therapy. Anesth Analg 1995;80:557-61.   Abstract

9. Currier MB, Murray GB, Welch CC. Electroconvulsive therapy for post-stroke depressed geriatric patients. J Neuropsychiatry Clin Neurosci 1992;4:140-4.   Abstract

10. Dequardo JR, Liberzon I, Tandon R. Recurrent post-ECT dyskinesias [letter]. Convulsive Therapy 1992;8:42-3.  

11. Dequardo JR, Tandon R. ECT in post-stroke major depression. Convulsive Therapy 1988;4:221-4.  

12. Devanand DP, Malitz S, Sackeim HA. ECT in a patient with aortic aneurysm. J Clin Psychiatry 1990;51:255-6.   Abstract

13. Devanand DP, Sackeim HA, Decina P, et al. Status epilepticus following ECT in a patient taking theophylline. J Clin Psychopharmacol 1988;8:153.   Citation

14. Dolinski SY, Zvara DA. Anesthetic considerations of cardiovascular risk during electroconvulsivetherapy. [published erratum appears in Convulsive Therapy 13:284, 1997] Convulsive Therapy 1997;13:157-64.  

15. Douyon R, Serby M, Klutchko B, et al. ECT and Parkinson's disease revisited: A “naturalistic” study. Am J Psychiatry 1989;146:1451-5.   Abstract

16. Drop LJ, Bouckoms AJ, Welch CA. Arterial hypertension and multiple cerebral aneurysms in a patient treatedwith electroconvulsive therapy. J Clin Psychiatry 1988;49:280-2.   Abstract

17. Drop LJ, Viguera A, Welch CA. ECT in patients with intracranial aneurysm [letter]. Journal of ECT 2000;16:71-2.  

18. Dubovsky SL. Using electroconvulsive therapy for patients with neurological disease. Hospital and Community Psychiatry 1986;37:819-25.  

19. Fall PA, Ekman R, Granerus AK, et al. ECT in Parkinson's disease: Changes in motor symptoms, monoamine metabolitesand neuropeptides. J Neural Transm 1995;10:129-40.  

20. Fall PA, Granerus AK. Maintenance ECT in Parkinson's disease. J Neural Transm 1999;106:737-41.   Abstract

21. Farah A, McCall WV, Amundson RH. ECT after cerebral aneurysm repair. Convulsive Therapy 1996;12:165-70.  

22. Figiel GS. ECT and delirium in Parkinson's disease [letter]. Am J Psychiatry 1992;149:1759.   Citation

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