eMedicine Specialties > Ophthalmology > Intraocular Pressure

Glaucoma, Hyphema: Treatment & Medication

Author: Inci Irak-Dersu, MD, Assistant Professor, Director of Glaucoma Service, Department of Ophthalmology, University of Arkansas College of Medicine, Jones Eye Institute
Contributor Information and Disclosures

Updated: Dec 28, 2007

Treatment

Medical Care

Treatment of microhyphemas in which the IOP is not elevated usually involves limiting activities that cause rapid movements of the globe during the first 72 hours.

Patients who have concurrent elevation of IOP may require topical and oral ocular hypotensive medications to lower the IOP. These patients also require cycloplegia and topical steroids. Non-white patients should all be screened for sickle cell trait or disease because sickling can lead to obstruction of the central retinal artery and profound irreversible visual loss.

• Cycloplegics (eg, cyclopentolate tid, atropine qd) and topical steroids (eg, prednisolone acetate qid) are used to treat associated iritis.
• The use of oral steroids is controversial. Despite their direct antifibrinolytic properties, no clear benefit in preventing rebleeding has been noted.
• Topical steroids can be used 4 times a day to treat concurrent traumatic iritis.
• Aminocaproic acid (Amicar), an antifibrinolytic agent, reduces recurrent hyphemas. Intravenous and oral forms are available; approval for the topical gel form is pending with the US Food and Drug Administration (FDA).
• If treatment is started within the first 3 days of the occurrence of a hyphema, aminocaproic acid (50 mg/kg PO q4h for 5 d) has been found to be useful in decreasing rebleeding. However, adverse effects, such as hypotension, nausea, and renal and hepatic toxicity, limit its use. Also, in total hyphemas, this drug may delay resorption of blood. In addition, no obvious benefit to improve the final visual outcome has been noted. Although commercially unavailable, topical aminocaproic acid may limit systemic adverse effects.
• Another antifibrinolytic agent, tranexamic acid (Cyklokapron), reportedly has fewer adverse effects than aminocaproic acid but is not available in the United States.
• IOP reduction is usually necessary if it is higher than 24 mm Hg in patients with sickle cell or higher than 30 mm Hg in other patients.
• The threshold for treating glaucoma has been reduced in patients with sickle cell because of their susceptibility to glaucomatous optic nerve damage and central retinal artery occlusion at even slightly increased pressure. Glaucoma can be treated with topical medications (eg, beta-blockers [Timoptic bid and new generation drops]).
• Avoid oral carbonic anhydrase inhibitors, especially acetazolamide (eg, Diamox), in patients with sickle cell trait or disease. These drugs tend to increase sickling of erythrocytes. Methazolamide may be a better choice in this situation (Neptazane 50 mg PO q8h).
• Use hyperosmotic agents like IV mannitol for further control.
• Supportive treatment
• Wearing a metal or hard plastic shield at all times (during the day and at night) is recommended. Patching is recommended when a risk of corneal staining exists; however, measurements should be taken for occlusion amblyopia.
• Strict bed rest has not been shown to be beneficial in comparison to mild activity.
• Head elevation (up to 30°) helps level the blood inferiorly and keeps the central cornea and pupil aperture clean.
• Aspirin should be avoided to prevent rebleeding.

Surgical Care

Corneal bloodstaining is an ominous sign, and these cases are often best treated with surgical evacuation of the blood. A vitrectomy instrument or an irrigation/aspiration cannula may be used for this purpose. Two clear corneal paracentesis incisions can be used to evacuate the clot. If the IOP has caused some optic nerve damage and the pressure is unlikely to be stabilized with only surgical wash-out, a trabeculectomy can be performed at the same session.

All attempts at treating the elevated IOP with medications should be made prior to surgical wash-out of the hyphema. It is reasonable and helpful to not wash-out the eye until at least 72 hours have transpired to allow for clot formation. The maximum blood clot formation is achieved 4-7 days after trauma. If clot formation has not occurred, opening the eye may simply lead to persistent hemorrhage.

• Indications for anterior chamber wash-out are as follows:
  • Total hyphema does not resolve in 5 days.
  • IOP remains elevated despite the maximum medical treatment. A normal optic nerve can tolerate an IOP as high as 50 mm Hg for 5 days. If the patient had previous optic nerve compromise or a history of sickle cell trait or disease, consider surgical intervention for elevated IOP above 24 mm Hg that lasts beyond 1-2 days.
  • Decreasing visual acuity
  • Signs of corneal bloodstaining
  • Increased risk of synechia formation (ie, hyphema filling more than 50% of the anterior chamber and lasting longer than 8 d)

Consultations

When the results of sickle cell prep or hemoglobin electrophoresis are positive, consultation with a pediatrician or internist is indicated.

Diet

No special diet is required for patients with hyphema.

Activity

• Instruct patients to keep activity to a minimum during the first 5 days of hyphema to reduce the chances of a rebleed. Although no evidence exists regarding ambulation versus bed rest and whether one is superior to the other in the prevention of rebleeding, limiting activity is wise to avoid new injuries.
• Hyphemas in infants and children are difficult to treat because preventing a rebleed is paramount.
  • The importance of limiting a child's activity over the first 72 hours cannot be overemphasized to the caregivers.
  • Watching television from a distance of greater than 10 feet is acceptable because of the minimal eye movement that occurs with viewing a fixed screen at this distance.

Medication

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

Topical beta-blockers

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.

Osmotic diuretics

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 (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/glycerol (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.

Antifibrinolytics

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.

Cycloplegics

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 sulfate 0.5%, 1%, 2% (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 2% and 5% (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).

Carbonic anhydrase inhibitors

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.

Prostaglandin analogs

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.

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