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Hyphema Glaucoma Treatment & Management

  • Author: Inci Irak Dersu, MD, MPH; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Mar 24, 2016
 

Medical Care

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.

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.

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Surgical Care

Corneal bloodstaining is an ominous sign, and these cases are often best treated with surgical evacuation of the blood.[3] 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)
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Consultations

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

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Diet

No special diet is required for patients with hyphema.

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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.

A single or binocular patch does not affect the outcome regarding visual acuity or time of rebleed.

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.

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Contributor Information and Disclosures
Author

Inci Irak Dersu, MD, MPH Associate Professor of Clinical Ophthalmology, State University of New York Downstate College of Medicine; Attending Physician, SUNY Downstate Medical Center, Kings County Hospital, and VA Harbor Health Care System

Inci Irak Dersu, MD, MPH is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Martin B Wax, MD Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Research and Development, Head, Ophthalmology Discovery Research and Preclinical Sciences, Alcon Laboratories, Inc

Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Society for Neuroscience

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Andrew I Rabinowitz, MD Director of Glaucoma Service, Barnet Dulaney Perkins Eye Center

Andrew I Rabinowitz, MD is a member of the following medical societies: Aerospace Medical Association, American Academy of Ophthalmology, American Society for Laser Medicine and Surgery, American Academy of Ophthalmology, American Medical Association

Disclosure: Nothing to disclose.

References
  1. Sihota R, Kumar S, Gupta V, et al. Early predictors of traumatic glaucoma after closed globe injury: trabecular pigmentation, widened angle recess, and higher baseline intraocular pressure. Arch Ophthalmol. 2008 Jul. 126(7):921-6. [Medline].

  2. Rahmani B, Jahadi HR. Comparison of tranexamic acid and prednisolone in the treatment of traumatic hyphema. A randomized clinical trial. Ophthalmology. 1999 Feb. 106(2):375-9. [Medline].

  3. Walton W, Von Hagen S, Grigorian R, Zarbin M. Management of traumatic hyphema. Surv Ophthalmol. 2002 Jul-Aug. 47(4):297-334. [Medline].

  4. Hack KM, Pedersen R. Mental status changes and bradycardia: don't forget the eye! Traumatic hyphema can mimic increased intracranial pressure. Clin Pediatr (Phila). 2009 Apr. 48(3):331-3. [Medline].

  5. Campbell D, Shields MB, Liebmann JM. Ghost cell glaucoma. Ritch R, Shields B, Krupin T, eds. The Glaucomas. 1989. Vol 2: 1239-1247.

  6. Culom RD Jr, Chang B, eds. Hyphema and microhyphema. The Wills Eye Manual. 1994. 32-6.

  7. Drug Facts and Comparisons Staff. Drug Facts and Comparisons. 1999.

  8. Gharaibeh A, Savage HI, Scherer RW, Goldberg MF, Lindsley K. Medical interventions for traumatic hyphema. Cochrane Database Syst Rev. 2013 Dec 3. 12:CD005431. [Medline].

  9. Herschler J, Cobo M. Trauma and elevated intraocular pressure. Ritch R, Shields B, Krupin T, eds. The Glaucomas. 1989. Vol 2: 1225-1237.

  10. Hersh P, Zagelbaum B, Shingleton B, Kenyon K. Anterior segment trauma. Albert D, Jakobiec F, Azar D, Gragoudas E, eds. Principles and Practice of Ophthalmology. 2nd ed. Philadelphia: WB Saunders; 2000. 5201-5221.

  11. Shields MB. Glaucomas associated with intraocular hemorrhage and glaucomas associated with ocular trauma. Textbook of Glaucoma. 1992. 381-399.

  12. Shingleton BJ, Hersh PS. Traumatic hyphema. Eye Trauma. 1991. 104-116.

 
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Layered hyphema from blunt trauma.
Total or 8-ball hyphema.
 
 
 
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