Side effects
Common adverse effects of acetazolamide include the following: paraesthesia, fatigue, drowsiness, depression, decreased libido, bitter or metallic taste, nausea, vomiting, abdominal cramps, diarrhea, black stool, polyuria, kidney stones, metabolic acidosis and electrolyte changes (hypokalemia, hyponatremia). Whereas less common adverse effects include Stevens–Johnson syndrome, anaphylaxis and blood dyscrasias. Contraindications
Contraindications include:
Hyperchloremic acidosis
Hypokalemia (low blood potassium)
Hyponatremia (low blood sodium)
Adrenal insufficiency
Impaired kidney function
Hypersensitivity to acetazolamide or other sulphonamides. Marked liver disease or impairment of liver function, including cirrhosis because of the risk of development of hepatic encephalopathy. Acetazolamide decreases ammonia clearance. Interactions
It is possible that it might interact with:
Amphetamines, because it increases the pH of the renal tubular urine, hence reducing the clearance of amphetamines. Other carbonic anhydrase inhibitors — potential for additive inhibitory effects on carbonic anhydrase and hence potential for toxicity. Ciclosporin, may increase plasma levels of ciclosporin. Antifolates such as trimethoprim, methotrexate, pemetrexed and raltitrexed. Hypoglycemics, acetazolamide can both increase or decrease blood glucose levels. Lithium, increases excretion, hence reducing therapeutic effect. Methenamine compounds, reduces the urinary excretion of methenamines. Phenytoin, reduces phenytoin excretion, hence increasing the potential for toxicity. Primidone, reduces plasma levels of primidone. Hence reducing anticonvulsant effect. Quinidine, reduces urinary excretion of quinidine, hence increasing the potential for toxicity. Salicylates, potential for severe toxicity. Sodium bicarbonate, potential for kidney stone formation. Anticoagulants, cardiac glycosides, may have their effects potentiated by acetazolamide. Mechanism of action
Acetazolamide is a carbonic anhydrase inhibitor, hence causing the accumulation of carbonic acid.
Indocyanine green angiography can be used to predict how the patient will respond to PDT.Laser photocoagulation, which effectively burns the leak area shut, may be considered in cases where there is little improvement in a 3- to 4-month duration, and the leakage is confined to a single or a few sources of leakage at a safe distance from the fovea. Laser photocoagulation is not indicated for cases where the leak is very near the central macula or for cases where the leakage is widespread and its source is difficult to identify. Laser photocoagulation can permanently damage vision where applied. Carefully tuned lasers can limit this damage. Even so, laser photocoagulation is not a preferred treatment for leaks in the central vision and is considered an outdated treatment by some doctors. Foveal attenuation has been associated with more than 4 months duration of symptoms, however a better long-term outcome has not been demonstrated with laser photocoagulation than without photocoagulation.In chronic cases, transpupillary thermotherapy has been suggested as an alternative to laser photocoagulation where the leak is in the central macula.Yellow micropulse laser has shown promise in very limited retrospective trials. Oral medications
Spironolactone is a mineralocorticoid receptor antagonist that may help reduce the fluid associated with CSR. In a retrospective study noted by Acta Ophthalmologica, spironolactone improved visual acuity in CSR patients over the course of 8 weeks.Eplerenone is another mineralocorticoid receptor antagonist that has been thought to reduce the subretinal fluid that is present with CSR.