Glaucoma, Hyphema 

  • Author: Inci Irak-Dersu, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Feb 24, 2010
 

Background

Hyphema is the collection of red blood cells in the anterior chamber. A microhyphema occurs when the red blood cells are only detectable microscopically. In a macroscopic hyphema (hyphema), a visible layer of red blood cells in the anterior chamber may be detected even without the aid of slit-lamp magnification. Complications are more frequently related to hyphema than microhyphema.

Next

Pathophysiology

Trauma is the most common cause of hyphema; consequently, hyphema is often seen in younger patients. A blunt, compressive force acting on the globe creates tears in the ciliary body, iris, and other anterior segment structures (see image below). These tears cause shearing of blood vessels, including those that make up the major arterial circle of the anterior segment. Hyphema also may be caused by intraocular tumors, which may be benign or malignant.

Layered hyphema from blunt trauma. Layered hyphema from blunt trauma.

Neovascularization of the iris or ciliary body may result in hyphema. This neovascularization can be caused by posterior segment ischemia, which usually is associated with microvascular disease in diabetes. Retinal ischemia also can occur subsequently to retinal arterial or venous occlusion. Another cause of the neovascularization is carotid stenosis, which can lead to ocular ischemia. Hyphema also may be iatrogenic in origin; it can occur any time after intraocular surgery, especially surgery that involves the filtration angle. Certain types of anterior chamber intraocular lenses used after cataract extraction lend themselves to hyphema, especially rigid lenses, which is called uveitis-glaucoma-hyphema (UGH) syndrome.

Corneal bloodstaining results from blood being forced into corneal endothelial cells, thereby "staining" the otherwise clear cornea. Bloodstaining is an ominous sign and often heralds the need for surgical evacuation of the hyphema.

The acute rise in intraocular pressure (IOP) is related to red blood cells and their byproducts clogging the trabecular meshwork; another cause is direct trauma to the meshwork, which occurs concurrently with the initial trauma.

Chronic glaucoma following hyphema is partly caused by fibrotic changes in the trabecular meshwork induced by inflammation. Inflammation occurs as a reaction to any kind of ocular damage: cyclodialysis, angle recession, and shearing of the iris blood vessels.

The relative risk of developing glaucoma after ocular trauma associated with hyphema has been found to be 6.9. If there is 360º angle recession, the relative risk of developing glaucoma increases to 7.5.[1]

Secondary angle-closure glaucoma that results from pupillary block may also occur. Pupillary block is seen when the clot completely secludes the pupil/lens interface, thereby blocking the flow of aqueous from the posterior to the anterior chamber.

Previous
Next

Epidemiology

Frequency

United States

In North America, the incidence of hyphema is 17-20 cases per 100,000 people per year. The rebleeding rate is 10-20%.

Mortality/Morbidity

Most hyphema cases are due to blunt trauma. Less common causes are systemic diseases and following eye surgery. Spontaneous hyphema is quite rare. Morbidity of disease depends on underlying pathology, associated diseases, and risk factors.

Race

The African American population has a higher risk for sickle cell hemoglobinopathy. This group is more likely to have complications of hyphema, including central retinal artery occlusion.

Sex

The male-to-female ratio is 3:1.

Age

The young population is most affected. Approximately 77% are younger than 30 years. The peak incidence is in people aged 10-20 years.

Previous
 
 
Contributor Information and Disclosures
Author

Inci Irak-Dersu, MD  Associate Professor, Director of Glaucoma Service, Department of Ophthalmology, University of Arkansas College of Medicine, Jones Eye Institute

Inci Irak-Dersu, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, American Society of Cataract and Refractive Surgery, and Arkansas Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Andrew I Rabinowitz, MD  Consulting Staff, Department of Ophthalmology, Barnet Dulaney Perkins Eye Center

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

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

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, and Pan-American Association of Ophthalmology

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. Jul 2008;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. Feb 1999;106(2):375-9. [Medline].

  3. Walton W, Von Hagen S, Grigorian R, Zarbin M. Management of traumatic hyphema. Surv Ophthalmol. Jul-Aug 2002;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). Apr 2009;48(3):331-3. [Medline].

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

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

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

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

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

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

  11. Shingleton BJ, Hersh PS. Traumatic hyphema. In: Eye Trauma. 1991:104-116.

Previous
Next
 
Layered hyphema from blunt trauma.
Total or 8-ball hyphema.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.