Glaucoma, Hyphema Medication

The goal of pharmacotherapy is to reduce morbidity and to prevent complications.

Class Summary

Decrease aqueous production and IOP.

Timolol maleate 0.25%, 0.5% (Betimol, Timoptic, Timoptic XE)

May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor or by outflow.

Class Summary

Decrease the IOP by reducing vitreous volume.

Mannitol (Osmitrol)

When IOP cannot be controlled with topical drops and IOP is high enough to cause optic nerve damage in a short period of time, osmotic diuretics are indicated.

Isosorbide dinitrate (Ismotic)

May be used to abort an acute attack of glaucoma. In the eyes, may create an osmotic gradient between plasma and ocular fluids and induce diuresis by elevating osmolarity of the glomerular filtrate. These effects may, in turn, inhibit tubular reabsorption of water. Treatment is preferred when less risk of nausea and vomiting than that posed by other oral hyperosmotic agents is desired. May be preferred, if the patient tolerates PO intake.

Glycerin (Ophthalgan)

Oral osmotic agent for reducing IOP. Able to increase tonicity of blood until finally metabolized and eliminated by the kidneys. Maximum reduction of IOP usually occurs 1 h after glycerin administration. Effect usually lasts approximately 5 h.

Class Summary

Prevent recurrent hyphema.

Aminocaproic acid (Amicar)

Inhibits the substance that converts plasminogen to plasmin. Has antiplasmin activity. Aminocaproic acid is the most commonly used antifibrinolytic in the United States.

Tranexamic acid (Cyklokapron)

Alternative to aminocaproic acid. Inhibits fibrinolysis by displacing plasminogen from fibrin. Hyphema is not a labeled indication for tranexamic acid use. More commonly is used in Scandinavian countries.

Class Summary

Anticholinergic agents block the responses of the iris sphincter muscle and ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).

Atropine ophthalmic (Isopto Atropine, Atropine sulfate, Atropine-1)

Acts at parasympathetic sites in smooth muscle to block response of sphincter muscle of iris and muscle of ciliary body to acetylcholine, causing mydriasis and cycloplegia.

Cyclopentolate HCl 1% (Cyclogyl)

Blocks muscle of ciliary body and sphincter muscle of iris from responding to cholinergic stimulation, thus causing mydriasis and cycloplegia.

Induces mydriasis in 30-60 min and cycloplegia in 25-75 min. These effects last up to 24 h.

Homatropine (Isopto Homatropine)

Blocks responses of sphincter muscle of iris and muscle of ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).

Class Summary

Decrease aqueous production and IOP. These drugs are sulfonamide compounds that decrease the IOP by inhibiting aqueous production.

Acetazolamide (Diamox)

Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP. Used for adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and preoperatively in acute angle-closure glaucoma when delay of surgery desired to lower IOP.

Methazolamide (Neptazane, GlaucTabs)

Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.

Class Summary

These selective agonists act on prostaglandin receptors in the eye to lower IOP by increasing uveoscleral outflow.

Bimatoprost ophthalmic solution (Lumigan)

A prostamide analogue with ocular hypotensive activity. Mimics the IOP-lowering activity of prostamides via the prostamide pathway. Used to reduce IOP in open-angle glaucoma or ocular hypertension.

Travoprost ophthalmic solution (Travatan)

Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.

Unoprostone ophthalmic (Rescula)

Prostaglandin F2-alpha analog and selective FP prostanoid receptor agonist. Exact mechanism of action unknown but believed to reduce IOP by increasing uveoscleral outflow.