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Case Study

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Electroconvulsive Therapy in a Patient on Chronic Hemodialysis
Phyllis D. Wille

A.B. is a 55-year-old Caucasian male with a history of severe depression, diabetes mellitus, hypertension, seizure disorder, and chronic kidney disease (CKD) necessitating hemodialysis of 4 years duration. He was referred to inpatient psychiatric care for worsening depression associated with suicidal ideation, severe hypokinesia, and inadequate oral intake. His condition had proven resistant to several antidepressant regimens.

A.B. was recently unemployed from his position as a high school physics teacher due to his worsening symptoms. His social history includes a divorce 5 years ago and no contact with his former spouse or children. A.B. is an only child, and both parents are deceased. His social support consisted of professional peers at his former place of employment; however, these supports dwindled as time went on. A.B. agreed to attempt electroconvulsive (ECT) therapy with the hope of regaining his previous level of functioning and returning to his job as a high school physics teacher.

A.B.’s medical history included diet-controlled Type 2 diabetes mellitus, seizure disorder, hypertension, and depression. His hypertension was treated with Norvasc, Clonidine, Irbesartan, and Metoprolol. The seizure disorder was controlled with Keppra, the doses of which varied dependent upon dialysis and nondialysis days.

A complete physical exam was done prior to the inception of ECT therapy. An ECG was unremarkable with normal sinus rhythm, and a chest x-ray revealed no abnormalities. One month prior to ECT, after a fall with a head injury, a CT of the brain revealed prominent ischemic small vessel changes around the ventricles. These changes included several white matter and basal ganglia infarcts that were stable. Spine x-rays done at that time revealed a compression of the T4 vertebral body, with no fractures noted. Blood glucose levels ranged from 88-121 mg/dl. Laboratory values were consistent with a patient with end stage renal disease who was on hemodialysis. Outpatient center hemodialysis records were obtained and indicated stable hemodialysis treatments.

Literature Review
A review of ECT in patients on chronic hemodialysis revealed few recent articles. Although the presence of coexisting medical conditions constitute relative contraindication, no co-morbid medical illness precludes the administration of ECT, provided patients are adequately evaluated and appropriate therapeutic interventions are instituted before, during and after the procedure (Williams & Ostroff, 2005). Cardiovascular disease in patients on hemodialysis and the cardiac effects of ECT therapy, altered pharmacokinetics of anesthetic agents, and fracture risk due to renal osteodystrophy are some of the challenges experienced when performing ECT on this patient population.

The administration of ECT creates autonomic nervous system stimulation while cardiovascular effects are characterized by a catecholamine response that has been associated with arrhythmias (Catelli, et. al., 1995; Weinger, Partridge, Hauger, Mirow, & Brown, 1991). It has been reported that during ECT there is an increase in cardiac output and arterial pressure (Catelli et. al., 1995; Weinger et. al., 1991; Wells & Davis, 1987) . Such acute hyperdynamic states are undesirable because of possible severe cardiovascular complications. Patients on hemodialysis are known to have an increased risk of developing cardiovascular disease and have a 5-25 fold increase in mortality from cardiovascular disease, which further increases the risk of cardiovascular events (Foley, Parfrey, & Sarnak, 1998). Esmolol or labetalol may be used in order to blunt hemodynamic responses. In the setting of ECT, few studies have described the effects of these two antihypertensive drugs (O’Flaherty et al., 1992; Stoudemire, et al., 1990; Weinger, 1991). A study by Catelli et al. (1995), showed comparable peak attenuation of systolic blood pressure with esmolol and labetolol in doses that differed by a factor of 10. The study also indicated that the effects on systolic blood pressure of a large dose of labetolol were still present 10 minutes after seizure and that those of esmolol were not measured at that time. This suggests that if a large dose of a beta-adrenergic blocker is needed for ECT, esmolol might be preferred.

Patients with CKD are at high risk for osteopenia and subsequent bone fractures. Forceful muscle contractions that can occur during ECT therapy increase the risk of bone fracture. It is for this reason that muscle relaxation during ECT is especially important for patients with chronic renal failure. Succinylcholine is typically administered to achieve adequate muscle relaxation during ECT therapy and results in a mild and transient hyperkalemia (Thapa & Brull, 2000). The increase in serum potassium is approximately 0.5-1.0 mEq/L, occurs within 3-5 minutes after the IV administration of succinylcholine, and lasts less than 10-15 minutes (Yentis, 1990). Patients with chronic renal failure have disturbed potassium homeostasis and the use of succinylcholine has raised concerns about an increase in hyperkalemic response with resultant adverse cardiac effects. One study addressed the effect of repeated doses of succinylcholine administration in patients with CKD and did not indicate an excessive increase in serum potassium (Powell & Miller, 1975). This study did demonstrate that 68% of patients who received repeated doses of succinylcholine experienced bradycardia. Pretreatment with glycopyrolate to protect against succinylcholine-induced bradycardia should be considered (Durant & Katz, 1982; Green, Bristow, & Fisher, 1984).

Discussion
After reviewing the literature, completing a thorough examination, and obtaining informed consent, ECT therapy was initiated for A.B. He underwent ECT therapy in the morning and had hemodialysis in the afternoon on Mondays, Wednesdays, and Fridays. He was treated with right unilateral electrode placement, and seizure threshold was determined by dose titration. General anesthesia was induced during each treatment with sodium brevital 60 mg and muscle paralysis produced by succinylcholine 60 mg. Glycopyrolate 0.2 mg was also given to control bradycardia. A.B’s pulse during ECT treatment and throughout hospitalization was 66-88. His intratreatment blood pressure readings were systolic 132 - 211 mmHg and diastolic 72 - 118 mmHg. A.B. did develop sustained hypertension during ECT despite the use of labetolol in the initial 2 treatments. Therefore, esmolol was added to subsequent treatments and hypertension control was achieved. He required labetolol 15 mg initially with repeated doses of labetolol 15 mg, in addition to esmolol 50 mg, during each treatment to obtain control of sustained increased blood pressure. Serial electrolyte levels were done prior to initiation of ECT and prior to hemodialysis and were essentially unchanged (see Table 1). He received 7 treatments in the acute phase of treatment before the ECT was stopped secondary to a change in patient condition requiring transfer to a medical unit. A.B had become dramatically less responsive and more somnolent. It was determined that this was the result of overdosing of Keppra on his dialysis days. Once the Keppa was redosed, A.B. regained the earlier improvements brought about by the ECT. ECT was not resumed at the patient’s request.

Inpatient hemodialysis treatments were consistent with those in the outpatient setting. A.B. remained stable on dialysis throughout his hospitalization and his dry weight increased due to an improved appetite. His mood was better and he was participating in physical and group therapies.

A.B. was discharged to an extended care facility with an in-house dialysis unit for further rehabilitative services secondary to his prolonged hospitalization and inability to live independently. He did not regain all cognitive abilities prior to ECT at the time of discharge. Due to his cognitive deficits, it was uncertain that he would be able to return to his teaching position. Despite multiple doses of succinylcholine, A.B. did not demonstrate hyperkalemia during ECT therapy. He also did not experience any episodes of bradycardia due to premedication with glycopyrolate.

Summary
CECT is an effective treatment for patients with the diagnosis of major depression unresponsive to an antidepressant drug regimen, refusal of oral intake, hypokinesia, and suicidal ideation with the need for urgent intervention. A.B. benefited from ECT with an improvement of mood and appetite. Unfortunately, he experienced cognitive deficits, which prevented him from returning to his career as a high school physics teacher, and to this day he continues to live in an extended care facility.

References
Catelli, I., Steiner, L.A., Kaufman, M.A., Alfille, P.H., Schouten, R., Welch, C.A. et al. (1995). Comparative effects of esmolol and labetolol to attenuate hyperdynamic states after electroconvulsive therapy. Anesthesia and Analgesia, 80, 557-561.

Durant, N.N., & Katz, R.L (1982). Suxamethonium. British Journal of Anaesthesia, 54, 195-208.

Foley, R.N., Parfrey, P.S., & Sarnak, M.J. (1998). Epidemiology of cardiovascular disease in chronic renal disease. Journal of American Society of Nephrology, 9, S16-S23.
 
Green, D.W., Bristow, A.S., & Fisher, M. (1984). Comparison of IV glycopyrrolate and atropine in the prevention of bradycardia and arrythmias following repeated doses of suxamethonium in children. British Journal of Anaesthesia, 56, 981-985.

O’Flaherty, D., Hussain, M.M., Moore, M., Wolff, T.R., Sills, S., & Giesecke, A.H.(1992). Circulatory responses during electroconvulsive therapy. The comparative effects of placebo, esmolol and nitroglycerin. Anesthesia, 47, 563-567.

Powell, D.R., & Miller, R., (1975). The effect of repeated doses of succinylcholine on serum potassium in patients with renal failure. Anesthesia and Analgesia, 54, 746-748.

Stoudemire, A., Knos, G., Gladson, M., Markwalter, H., Sung, Y., Morris, R., et al.(1990). Labetolol in the control of cardiovascular responses to electroconvulsive therapy in high risk depressed medical patients. Journal of Clinical Psychiatry, 51, 508-512.

Thapa, S., & Brull, S. (2000). Succinylcholine-induced hyperkalemia in patients with renal failure: An old question revisited. Anesthesia and Analgesia, 91, 237-241.

Weinger, M.B., Partridge, B.L., Hauger R, Mirow, A., & Brown, M.(1991). Prevention of the cardiovascular and neuroendocrine response of electroconvulsive therapy. Effects of pretreatment regimens on catecholamines, ACTH, vasopressin and cortisol. Anesthesia and Analgesia, 73, 563-567.

Wells, D.G., & Davis, G.G. (1987). Hemodynamic changes associated with electroconvulsive therapy. Anesthesia and Analgesia, 66, 1193-1195.

Williams, S., & Ostroff, R. (2005). Chronic renal failure, hemodialysis and electroconvulsive therapy. The Journal of ECT, 1, 41-42.

Yentis, S.M. (1990). Suxamethonium and hyperkalaemia. Anesthesia Intensive Care, 18, 92-101.



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