Concern remains among many that electroconvulsive therapy (ECT) causes "brain damage." This ambiguous term presumably refers to lesions that could, in principle, be observed either grossly or microscopically in postmortem studies, and the assertion that it occurs appears to be based largely on old reports with dubious relevance to modern practice. Fortunately, using modern technique, ECT is so safe that mortality around the time of treatment is extraordinarily rare and as a result there has been little opportunity for postmortem examination of individuals who had recently had ECT. We report a case in which postmortem brain examination was performed roughly a month after the patient's last treatment.
1433urinary excretion rose to 2 17 1/24 h, with chloride 249 mmol/24 h and potassium 178 mmol/24 h. Mean fall in body weight was 0-29 kg/day. The patient became oedema free over two weeks.Case 4-A 40-year-old man with severe ischaemic heart disease presented with congestive cardiac failure.
CommentAdding relatively small doses of metolazone to high-dose "loop" diuretics significantly increased urine volume and excretion of sodium chloride and potassium, enabling body weight to fall and oedema to clear. The response was immediate and sustained. An initial dose of 2-5 mg metolazone is recommended. Profound natriuresis with associated kaliuresis may lead to hypovolaemia and hypokalaemia respectively. These complications should be anticipated by gradual dose titration according to urine volume and changes in body weight and adequate potassium supplementation. Ideally the patient should be treated with caution in hospital, as dangerous, uncontrolled losses of fluid and electrolytes may occur.4We are grateful to Sisters M Morris and G Alcock for metabolic nursing, and to Miss J E Davies for secretarial work.
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