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Electrolyte Imbalances: Electrolyte disturbances may occur during thiazide therapy. Observe for signs of electrolyte imbalance (e.g., dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, confusion, seizures, oliguria, muscle pains, cramps, muscular fatigue, hypotension, tachycardia, nausea, vomiting).
Perform periodic determination of serum electrolyte concentrations (particularly potassium, sodium, chloride, and bicarbonate); institute measures to maintain normal serum concentrations if necessary.
Serum and urinary electrolyte measurements are especially important in patients with diabetes mellitus, vomiting, diarrhea, on parenteral fluid therapy, or expecting to undergo excessive diuresis.
Measure electrolytes weekly or more frequent early in the course of treatment; it may be possible to extend the interval between measurements to ≥3 months once electrolyte response has stabilized.
Hypokalemia: Hypokalemia may develop (with consequent weakness, cramps, cardiac dysrhythmias) during concomitant use corticosteroids, adrenocorticotropic hormone, and especially with brisk diuresis, severe liver disease or cirrhosis, vomiting or diarrhea, or after prolonged therapy.
Hypokalemia may cause cardiac arrhythmias and sensitize or exaggerate the heart's response to toxic effects of digitalis (e.g., increased ventricular irritability).
Avoid or use potassium-sparing diuretics, potassium supplements or foods with high potassium content to treat hypokalemia.
Hypochloremia: Hypochloremic alkalosis may occur with hypokalemia, especially in patients with other losses of potassium and chloride such as those with vomiting, diarrhea, GI drainage, excessive sweating or paracentesis or potassium-losing renal disease. Patients with hepatic cirrhosis who are receiving thiazide are very susceptible to hypokalemic hypochloremic alkalosis.
A chloride deficit is generally mild and usually does not require specific treatment, except under extraordinary circumstances (as in liver or renal disease). Treatment of metabolic or hypochloremic alkalosis may require chloride replacement.
Hyponatremia: Dilutional hyponatremia may occur or be aggravated during thiazide therapy and can occasionally be life-threatening.
Dilutional hyponatremia most commonly occurs in hot weather in patients with chronic congestive heart failure or hepatic disease and is usually present before diuretic therapy and is manifested by signs of edema associated with hyponatremia.
Thiazide-induced hyponatremia has been associated with death and neurologic damage in elderly patients. CNS manifestations include seizures, coma, and extensor-plantar response.
Geriatric patients, especially females who are underweight, have poor oral intake of fluid and electrolytes, and/or excessive intake of low sodium nutritional supplements may be at increased risk of dilutional hyponatremia induced by the drugs.
This is usually treated by restriction of fluid intake to about 500 mL per day and withdrawal of the diuretic. Sodium chloride should not be administered except the hyponatremia is life threatening.
Hyperuricemia: Hyperuricemia is usually asymptomatic and rarely leads to clinical gout except in patients with a history of gout, familial predisposition to gout or chronic renal failure. If therapy is required, may be treated with a uricosuric agent.
Hyperglycemia and glycosuria: Thiazides and related diuretics can produce hyperglycemia and glycosuria in diabetic patients. Insulin or oral antidiabetic agent requirements of diabetics may be altered by the thiazide. Precipitation of diabetes mellitus may occur in prediabetic patients receiving thiazides. However, the risk of developing diabetes mellitus among hypertensive patients receiving thiazides was shown to be no greater than among those receiving no drug therapy.
Abnormal glucose tolerance usually does not develop in patients receiving thiazides who previously exhibited normal glucose tolerance. Hyperglycemia and impairment of glucose tolerance are almost always reversible by discontinuance of the drugs, and correction of hypokalemia may improve glucose tolerance.
Postsympathectomy: Antihypertensive effects may be enhanced in the postsympathectomy patients.
Hypomagnesemia: Thiazide diuretics increase urinary excretion of magnesium, resulting in hypomagnesemia.
Hypercalcemia: Hypercalcemia may occur, infrequently, especially in patients receiving vitamin D or having mild hyperparathyroidism.
Hyperlipidemia: Use with caution in patients with moderate or high cholesterol concentrations and in patients with elevated triglyceride levels. Thiazides may increase concentrations of total serum cholesterol, total triglyceride, and low density lipoproteins in some patients although these appear to return to pretreatment levels with long-term therapy.
Pathologic changes in the Parathyroid gland: With hypercalcemia and hypophosphatemia, have occurred occasionally during prolonged thiazide therapy.
Use in Children: Safety and efficacy have not been established with chlorthalidone.
Use in the Elderly: Elderly patients are more likely to have age-related renal function impairment, which may require caution in patients receiving thiazide diuretics.
