Thiazides and hypokalaemia in diabetic ketoacidosis

Abstract

Summary In a series of forty-one episodes of diabetic coma or pre-coma, three patients had plasma potassium values of less than 3.0 mEq/l. All three had been taking thiazide diuretics with only one receiving oral potassium supplements. None was previously known to be diabetic, representing 18% of the new diabetics in the series. The mean plasma potassium for the other new diabetics was 4·7 ± 0·2 mEq/l. These findings emphasize that adequate potassium supplements should be given with thiazide diuretics to diabetic subjects and to those with an increased risk of developing the disease.

Diabetes and arterial hypertension

“…Weidmann et al demonstrated a 10% fall in total body sodium, back to normal levels, on diuretics with an improvement in mean blood pressure from 165/93 to 145/82 mmHg [41]. There are, however, a number of disadvantages (Table 3): thiazides have been shown to worsen glucose tolerance in non-insulin-requiring patients, probably because of both hypokalaemia and a further separate action [90,91]. Apart from their considerable side-effects in any subject, recent evidence from the Medical Research Council trial of mild hypertension suggests that they are also associated with a significant incidence of impotence [86], rendering them less than ideal for many male patients.…”

Severe Diabetic Metabolic Decompensation

“…It tends to be associated with severe ketoacidosis and/ or hyperglycaemia and its presence adversely affects the rate at which the metabolic changes can be corrected. (Alberti and Hockaday 1973). Its presence should always be sought for and in the gravely ill, assumed.…”

“…There is evidence to suggest that irrespective of the degree of ketoacidosis, satisfactory response can be obtained by an initial dose of 20 i.u. followed at hourly intervals by a further 5 ‐ 10 units (Alberti et al , 1973). A similar regimen in which the dose of insulin is related to body weight has been used in children (Moseley 1975).…”

“…being largely dependent upon the duration and magnitude of the glycosuria and aggravated by vomiting and previous diuretic therapy. Occasionally, gross deficiencies are present (Pullen et al , 1967; Alberti and Hockaday 1973)and the finding of an initially low serum potassium must alert the clinician to such a possibility (Abramson and Arky 1966). The extracellular potassium level will begin to fall as soon as effective therapy has started.…”