Baseline studies indicated; see Monitor.
250 mg to 1 Gm/24 hr. May be given as 250-mg doses at 4- to 6-hour intervals. In the treatment of secondary glaucoma and in the preoperative treatment of some cases of acute congestive (closed-angle) glaucoma, the preferred dose is 250 mg every 4 hours. In acute cases, to rapidly lower intraocular pressure, an initial single dose of 500 mg followed by 125 to 250 mg at 4-hour intervals may be given.
Edema of congestive heart failure or drug therapy:
250 to 375 mg or 5 mg/kg of body weight as a single dose daily; when loss of edematous fluid stops, reduce to every other day or give for 2 days followed by a day of rest.
Adults and pediatric patients:
Dose in epilepsy may range from 8 to 30 mg/kg/24 hr in divided doses every 6 to 12 hours (2 to 7.5 mg/kg every 6 hours or 4 to 15 mg/kg every 12 hours). Reduce initial daily dose when given with other anticonvulsants.
Adults and pediatric patients:
5 mg/kg/dose every 8 to 12 hours.
See Maternal/Child.
5 to 10 mg/kg every 6 hours. Do not exceed 1,000 mg/24 hr.
Edema of congestive heart failure or drug therapy:
5 mg/kg as a single dose daily or every other day; see comment under Usual Dose. Do not exceed 1,000 mg/24 hr.
Slowly progressive hydrocephalus in infants 2 weeks to 10 months (unlabeled):
20 mg/kg/24 hr in equally divided doses every 8 hours (8.3 mg/kg every 8 hours). Up to 100 mg/kg/24 hr or a maximum dose of 2 Gm/24 hr has been used.
Reduced dose required when introducing acetazolamide into a treatment regimen with other anticonvulsants.
■ Administer every 12 hours in patients with a CrCl from 10 to 50 mL/min. Avoid use in patients with a CrCl less than 10 mL/min (ineffective).
Each 500 mg should be diluted in 5 mL SWFI. May then be given by IV injection or added to standard IV fluids. IM administration not recommended.
Reconstituted solution stable for 12 hours at RT or 3 days refrigerated.
Compatibility information not available from manufacturer.
Other sources suggest a few specific compatibilities dependent on concentration and manufacturer; consult a pharmacist.
A potent carbonic anhydrase inhibitor and nonbacteriostatic sulfonamide, acetazolamide depresses the tubular reabsorption of sodium, potassium, and bicarbonate. Excreted unchanged in the urine, producing diuresis, alkalinization of the urine, and a mild degree of metabolic acidosis.
Adjunctive treatment of edema due to congestive heart failure, drug-induced edema, centrencephalic epilepsies (petit mal, unlocalized seizures), chronic simple (open-angle) glaucoma, and secondary glaucoma, and preoperatively in acute angle-closure glaucoma when delay of surgery is desired to lower intraocular pressure.
■ Used orally for acute mountain sickness.
Metabolic alkalosis, urine alkalinization, and respiratory stimulant in COPD.
Depressed sodium and potassium levels, hyperchloremic acidosis, marked kidney or liver disease, adrenocortical insufficiency, and hypersensitivity to acetazolamide or any of its components. Long-term use contraindicated in some glaucomas.
Chemically related to sulfonamides; may cause serious reactions in sensitive patients.
■ May be alternated with other diuretics to achieve maximum effect.
■ Greater diuretic action is achieved by skipping a day of treatment rather than increasing dose; failure in therapy may be due to overdose or too-frequent dosage.
■ IM administration not recommended. Administration by IV injection is preferred.
■ Use with caution in impaired respiratory function (e.g., pulmonary disease, edema, infection, obstruction); may cause severe respiratory acidosis.
■ Potassium excretion is proportional to diuresis. Hypokalemia may result from diuresis or with severe cirrhosis.
■ Introduce or withdraw gradually when used as an anticonvulsant.
Obtain baseline CBC and platelet count before use and monitor during therapy.
■ Periodic monitoring of electrolytes is recommended.
Consider birth control options.
Category C: has been shown to be teratogenic in animal studies. Use during pregnancy only if potential benefit justifies potential risks to the fetus.
■ Discontinue breast-feeding or discontinue acetazolamide.
■ Safety for use in pediatric patients not established, but no problems are documented.
Use caution; no documented problems, but age-related renal impairment may be a factor.
May cause hypokalemia with concurrent use of steroids.
■ Hypokalemia may cause toxicity and fatal cardiac arrhythmias with digoxin or interfere with insulin or oral antidiabetic agent response, thus causing hyperglycemia.
■ Alkalinization of urine by acetazolamide potentiates amphetamines, ephedrine, flecainide, methenamine, procainamide, pseudoephedrine, quinidine, and tricyclic antidepressants by decreasing rate of excretion.
■ May decrease response to lithium, methotrexate, some antidepressants, phenobarbital, salicylates, and urinary anti-infectives by increasing rate of excretion.
■ Metabolic acidosis induced by acetazolamide may potentiate salicylate toxicity (anorexia, tachypnea, lethargy, coma, and death can occur with high-dose aspirin).
■ Alkalinity may cause false-positive urinary protein and possibly urinary steroid tests.
■ May depress iodine uptake by the thyroid.
Minimal with short-term therapy. Respond to symptomatic treatment or withdrawal of drug: acidosis, anorexia, bone marrow suppression, confusion, crystalluria, drowsiness, fever, hemolytic anemia, hypokalemia (ECG changes, fatigue, muscle weakness, vomiting), paresthesias, photosensitivity, polyuria, rash, renal calculus, and thrombocytopenic purpura.