Vetdrugs 2.0Acetazolamide is a systemic carbonic anhydrase inhibitor that changes bicarbonate transport in the kidney and decreases aqueous-humor production in the eye. Its veterinary uses include selected glaucoma cases and recurrent hyperkalemic periodic paralysis in horses. Although it increases urine production, its diuretic effect is relatively weak and becomes self-limiting as body bicarbonate is depleted.
Its value depends on the specific ocular or acid-base disorder rather than on diuresis alone. It has been used historically for canine hydrocephalus, but clinical effectiveness for that indication has not been established.
Group
Carbonic anhydrase inhibitor; systemic ocular hypotensive; bicarbonaturic diuretic
Mechanism of Action
Carbonic anhydrase catalyzes the reversible conversion of carbon dioxide and water to carbonic acid, which supplies hydrogen and bicarbonate ions. In proximal renal tubules, enzyme inhibition reduces hydrogen-ion availability and bicarbonate reclamation. More bicarbonate, sodium and water remain in the tubular fluid and are excreted, producing alkaline urine and a tendency toward metabolic acidosis.
Increased distal sodium delivery can increase potassium loss. Changes in potassium balance and systemic acid-base status provide the rationale for reducing episodes of equine hyperkalemic periodic paralysis, a disorder of skeletal-muscle sodium channels. Acetazolamide does not repair the inherited channel defect.
In the ciliary processes of the eye, inhibition reduces bicarbonate-dependent ion and fluid transport into aqueous humor. Lower aqueous production can reduce intraocular pressure. With continued renal bicarbonate loss, the diuretic and urine-alkalinizing effects diminish as the available bicarbonate pool falls.
Dose Rates
Dogs
| Use / stage | Dose | Route | Schedule | Instructions |
|---|---|---|---|---|
| Glaucoma | 5–8 mg/kg | PO | Every 8–12 h | Do not use in: Acidemia, Marked sodium or potassium depletion, Severe renal or hepatic dysfunction; Systemic treatment; monitor intraocular pressure, acid-base status and potassium. |
| Diuresis | 4–8 mg/kg | PO | Every 8–12 h | Do not use in: Acidemia, Marked sodium or potassium depletion, Severe renal or hepatic dysfunction |
| Glaucoma — Initial | 50 mg/kg | IV | A separately described one-time IV regimen, followed by a distinct oral course; do not substitute it for routine oral dosing. | |
| Glaucoma — Maintenance | 7 mg/kg | PO | Every 8 h | Oral follow-up described after a separate one-time IV regimen. |
| Glaucoma | 50–75 mg/kg | PO | Every 8–12 h | Distinct high-dose historical alternative; the source documents systemic adverse-effect limitations. This is retained for comparison rather than presented as interchangeable with lower regimens. |
Cats
| Use / stage | Dose | Route | Schedule | Instructions |
|---|---|---|---|---|
| Glaucoma | 7 mg/kg | PO | Every 8 h | Do not use in: Acidemia, Marked sodium or potassium depletion, Severe renal or hepatic dysfunction; Historical regimen; systemic carbonic anhydrase inhibitors are generally not recommended in cats because of adverse effects. |
| Glaucoma — Initial | 50 mg/kg | IV | Historical one-time IV regimen; systemic carbonic anhydrase inhibitors have substantial feline adverse-effect concerns. Retained as a qualified alternative. |
Horses
| Use / stage | Dose | Route | Schedule | Instructions |
|---|---|---|---|---|
| Hyperkalemic periodic paralysis | 2–4 mg/kg | PO | Every 8–12 h | Do not use in: Acidemia, Marked sodium or potassium depletion, Severe renal or hepatic dysfunction; For recurrent episodes despite dietary management; monitor electrolytes. |
| Hyperkalemic periodic paralysis | 4 mg/kg | IV | Do not use in: Acidemia, Marked sodium or potassium depletion, Severe renal or hepatic dysfunction; Reported parenteral regimen; repeat interval and infusion instructions are not established here. | |
| Hyperkalemic periodic paralysis | 2.2–4.4 mg/kg | PO | Every 12 h | Alternative twice-daily regimen for recurrent episodes; combine with dietary management and monitor potassium. |
| Hyperkalemic periodic paralysis | 0.5–2.2 mg/kg | PO | Every 12 h | Lower-dose alternative reported for maintenance; titrate to clinical and electrolyte response. |
| Hyperkalemic periodic paralysis | 2–3 mg/kg | PO | Every 8–12 h | Alternative schedule when dietary adjustment does not control episodes. |
Indications
- Systemic reduction of aqueous-humor production and intraocular pressure in selected glaucoma cases.
- Prevention or reduction of recurrent hyperkalemic periodic paralysis episodes in susceptible horses.
- Selected short-term urinary alkalinization or diuresis when increased bicarbonate excretion is a desired therapeutic effect.
- Adjunctive treatment of selected metabolic alkalosis cases after correction of associated fluid and electrolyte deficits.
Contraindications
- Acidemia or pre-existing significant metabolic acidosis.
- Marked sodium or potassium depletion and severe renal or hepatic dysfunction.
- Use cautiously in animals with sulfonamide hypersensitivity.
- Systemic carbonic anhydrase inhibitors are generally not recommended in cats because of adverse-effect sensitivity.
- Adrenocortical insufficiency.
- Severe pulmonary obstruction with inadequate ability to increase alveolar ventilation; respiratory acidosis can worsen.
- Prolonged treatment of chronic noncongestive angle-closure glaucoma can mask progressive angle closure.
- Use cautiously with pre-existing hematologic abnormalities. Pregnancy safety is not established; fetal abnormalities have occurred in laboratory animals.
Interactions
- Urinary alkalinization can change renal elimination of other drugs.
- Other potassium-depleting diuretics can increase electrolyte loss.
- Sodium bicarbonate increases urinary calculus risk; high-dose salicylates can cause serious acid-base toxicity.
- Hypokalemia can increase digoxin toxicity.
- Urinary alkalinization can reduce methenamine activity.
- Quinidine, procainamide and tricyclic antidepressants may be excreted more slowly; salicylates and phenobarbital may be excreted faster.
- Corticosteroids, amphotericin B and other potassium-depleting drugs can intensify electrolyte losses.
- Primidone concentrations may fall; altered insulin responses have been reported.
Adverse effects
- Metabolic acidosis, panting and reduced appetite.
- Hypokalemia and bicarbonate depletion.
- Vomiting, diarrhea and weakness.
- Sulfonamide-associated hypersensitivity reactions.
- Rare hematologic suppression, crystalluria, dysuria, dermatologic reactions or other sulfonamide-associated effects.
Toxicity
Excess exposure may produce severe acid-base and electrolyte abnormalities. Monitor bicarbonate, potassium, renal function and hydration; monitor intraocular pressure when treating glaucoma.
Preparations
| Preparation | Form | Strength | Route |
|---|---|---|---|
| Diamox 125 mg Tablets Store at room temperature in a tightly closed container. | Tablet | 125 mg / tablet | PO |
| Diamox 250 mg Tablets Store at room temperature in a tightly closed container. | Tablet | 250 mg / tablet | PO |
| Acetazolamide for Injection USP 500 mg (Gland) Gland Pharma Limited Lyophilized acetazolamide sodium, with strength expressed as acetazolamide. The encoded concentration applies after reconstitution with 5 mL sterile water; larger diluent volumes produce a lower concentration. IV preparation only; use reconstituted solution within 24 hours and inspect for particles or discoloration. Use within 24 hours after reconstitution under the supplied formulation instructions; discard the remainder. Additional diluent changes concentration. | Injection | 500 mg / 5 mL | IV |
| Acetazolamide Tablets BP 250 mg | Tablet | 250 mg / tablet | PO |
Monitoring and Administration
Systemic adverse effects limit its ophthalmic use.
Monitor electrolytes and acid-base status during repeated or high-dose treatment; obtain a baseline CBC and repeat it during prolonged therapy. Use tonometry for glaucoma and blood gases when treating alkalosis.
Alkaline urine can interfere with some urine-protein methods. Reduced thyroid iodine uptake is another reported laboratory effect.
Oral doses may be given with food when gastrointestinal intolerance occurs. Notify the treating clinician about bruising, abnormal bleeding, tremors or rash.
General parenteral dosing of 6-8 mg/kg IV, IM or SC has been reported for ruminants and pigs, but the indication and repeat schedule are not specified. This information alone does not define an indication-specific treatment course.
For metabolic alkalosis, a regimen of 10 mg/kg four times daily is described without an explicit route in that source entry. Volume contraction and hypokalemia can worsen; the missing route prevents a standalone calculator record.
Another glaucoma entry gives 10–25 mg/kg divided into two or three administrations daily, without an explicit route or unambiguous daily-total basis. A separate entry gives 50–75 mg/kg PO two or three times daily. These differ substantially from the lower regimens and must not be merged into one dose range.
A historical pediatric hydrocephalus regimen is 0.1 mg/kg PO every eight hours, while the other supplied monograph states that this use has been ineffective. Preserve this disagreement; do not present the regimen as established effective treatment.
The injectable 500 mg vial is described as requiring at least 5 mL sterile water, with use within 24 hours after reconstitution. Apply the exact product instructions; extra diluent changes the final concentration.