How is hyphema glaucoma treated?

Updated: Jul 29, 2020
  • Author: Inci Irak Dersu, MD, MPH; Chief Editor: Hampton Roy, Sr, MD  more...
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Treatment of microhyphemas in which the intraocular pressure (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) are used to treat associated iritis.

Topical steroids (eg, prednisolone acetate) can be used 4 times a day to treat concurrent traumatic iritis.

The use of oral steroids is controversial. Despite their direct antifibrinolytic properties, no clear benefit in resolution of hemorrhage or preventing rebleeding has been noted.

Aminocaproic acid (Amicar), an antifibrinolytic agent, reduces recurrent hyphemas. Intravenous and oral forms are available.

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. Additionally, 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, particularly gastrointestinal discomfort, than aminocaproic acid, but the oral form is not available in the United States. [2] Similar to aminocaproic acid, it does not affect final visual acuity or have associated risks of rebleeding; therefore, it was suggested that antifibrinolytics may be saved for high-risk patients such as sickle cell trait patients. [3]

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 intravenous mannitol or acetazolamide for further control.

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