AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.

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. 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.

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 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.

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.

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.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

When a patient presents with a hyphema, the most critical first step is obtaining a thorough history of the trauma.

• The mechanism of the injury and the type of assaulting object must be ascertained.
• It is important to determine if the patient was wearing protective eyewear at the time of the trauma.
• The patient's ethnic origin is important. Sickle cell trait/disease is more common in patients of African and Mediterranean descent.
• A good past medical history needs to be obtained, including sickle cell hemoglobinopathy, diabetes, and herpetic infection.
• Past ocular history, including ocular surgery and laser surgery, is important.

Physical

The ocular examination should start with a thorough evaluation of the ocular adnexa, looking for asymmetry.

• The following points should be considered during an ocular examination:
• • In the presence of traumatic hyphema, always consider the possibility of a coexisting ruptured globe, especially if the IOP is normal or low. If a coexisting ruptured globe is suspected, perform exploratory surgery and defer the remainder of the examination until the patient is in the operating room.
  • Hyphema may be associated with other clinical entities, and the following should be suspected in the absence of trauma:
  • • Rubeosis iridis (eg, proliferative diabetic retinopathy, following central or branch retinal vessel occlusion, ocular ischemic syndrome)
    • Surgery (during or after)
    • Iritis (eg, Fuchs heterochromic iridocyclitis, herpes simplex, herpes zoster)
    • Intraocular tumors (eg, juvenile xanthogranuloma, retinoblastoma, malignant melanoma)
    • Iris varix, pupillary microhemangiomas
    • Following laser trabeculoplasty or iridotomy
    • Bleeding disorders
• A full ophthalmic examination includes the following:
• • Visual acuity
  • Begin evaluation of the iris at the pupillary margin and move outward.
  • • The examiner should look closely for sphincter tears.
    • Examine the anterior surface of the iris, which is made of stromal tissue for the presence of abnormal vessels.
    • If the angle is nonoccludable, perform dilation in conjunction with cycloplegia.
    • Carefully examine the vitreous cavity for abnormalities.
    • Study the macula, vessels, and periphery.
    • Note any evidence of neovascularization of the disc or elsewhere. In addition, look for evidence of recent or remote vascular occlusion.
  • Pupillary reaction - Evaluation of pupillary responses is mandatory to rule out afferent pupillary damage.
  • Extraocular eye movement - Carefully perform motility and ocular alignment to look for any signs of entrapment.
  • Signs of corneal staining - Focus corneal examination on the presence or absence of bloodstaining.
  • Any previous corneal scar
  • Red or white blood cells in the anterior chamber
  • Macroscopic hyphema can be documented according to the height of the blood clot (in millimeters) in the anterior chamber. Hyphema can also be graded (I-IV) based on the amount of blood clot spacing in the anterior chamber.
  • • Grade I: Less than one third of the anterior chamber
    • Grade II: One third to one half of the anterior chamber
    • Grade III: One half to nearly total of the anterior chamber
    • Grade IV: Total hyphema (also called 8-ball hyphema)
  • Anterior segment for signs of inflammation (critical)
  • Iris neovascularization, nodules, and heterochromia
  • Measure IOP by applanation tonometry. Glaucoma is more likely to develop with total hyphema or after rebleeding.
  • Perform dilated fundus examination as soon as the corneal clarity and hyphema allow a view of the fundus after dilation.
  • • Note the presence of vitreous and retinal hemorrhage.
    • Document baseline appearance of the optic nerve and color of the neuroretinal rim.
    • If the retina cannot be visualized and if retinal breaks and detachment are suspected, perform ultrasonography earlier.
• Defer gonioscopic examination because it may precipitate rebleeding if hyphema is caused by trauma; otherwise, perform dynamic gonioscopy to look for evidence of abnormal masses or vessels in the filtration angle. Additionally, gonioscopy can help reveal the site of origin of the bleed or a clot in that area. If the patient has an anterior chamber intraocular lens (IOL), gonioscopic examination of the placement of the footplates in the angle should be carefully studied.
• Use an exophthalmometer to look for enophthalmos that is related to the ocular trauma.
• If the patient does not have a history of trauma, examine the carotid arteries for a bruit. This finding may herald ocular ischemic syndrome, as well as neovascularization that leads to hyphema.

Causes

• Trauma is the major cause.
• Other causes include the following:
• • Rubeosis iridis
  • Surgery (during or after)
  • Iritis (eg, Fuchs heterochromic iridocyclitis, herpes simplex, herpes zoster)
  • Intraocular tumors (eg, juvenile xanthogranuloma, retinoblastoma, malignant melanoma)
  • Iris varix, pupillary microhemangiomas
  • Following laser trabeculoplasty or iridotomy
  • Sickle cell disease/trait
  • UGH syndrome

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Hemolytic glaucoma
Ghost cell glaucoma
Hemosiderotic glaucoma

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Sickle cell prep: Screen for sickle cell. (This is mandatory upon presentation for non-white patients.)
• Hemoglobin electrophoresis: Determine if the patient has sickle cell trait or disease.
• If a bleeding disorder is suspected, prothrombin time (PT), partial thromboplastin time (PTT), platelet count, and liver function tests can be useful. 
• Aqueous samples from the anterior chamber are occasionally needed to differentiate rare types of glaucoma.

Imaging Studies

• In selected cases, obtain a CT scan of the orbit to exclude associated orbital fracture or foreign body.
• Perform ultrasonography to rule out vitreous hemorrhage or retinal detachment.
• CT and ultrasonography may also help in the diagnosis of other associated eye injuries.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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

Drug Category: Topical beta-blockers

Decrease aqueous production and IOP.

Drug Category: Osmotic diuretics

Decrease the IOP by reducing vitreous volume.

Drug Category: Antifibrinolytics

Prevent recurrent hyphema.

Drug Category: 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).

Drug Category: Carbonic anhydrase inhibitors

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

Drug Category: Prostaglandin analogs

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

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• The clot is least adherent to the surrounding tissues on the fourth day following the injury; this is the preferred time for surgery, when it is needed.
• Hyphema may be washed out or removed with a vitrectomy instrument.
• In some cases, a trabeculectomy may be necessary to control IOP.

Further Outpatient Care

• Despite clearing the hyphema, IOP may remain high.
• • In these cases, perform serial gonioscopic examinations to detect angle recession, synechia, and sustained blood clot.
  • Treat the appearance of the optic nerve and visual field.
  • Vitreous hemorrhage and retinal breaks might complicate a case even if the hyphema clears.

In/Out Patient Meds

• If the patient tolerates antiglaucoma medications for controlling IOP, keep these medications.
• As the hyphema clears and IOP decreases, discontinue medications in a stepwise fashion, starting with the one that has the most systemic adverse effects.

Complications

• Corneal bloodstaining is one complication of long-standing hyphema in association with glaucoma.
• • Both hemosiderin and hemoglobin collect in the stroma and give the cornea a yellowish appearance.
  • It usually spontaneously resolves in years. When there is suspicion of corneal bloodstaining in the early stages, the hyphema should be cleared surgically. Washing out the anterior chamber long after the incident has been found to be useful to clear bloodstaining.
  • Anterior segment structures can become difficult to visualize.
• Glaucoma may lead to optic atrophy; this is especially true in patients with sickle cell. Always consider early surgical intervention in resistant cases. A long period of high IOP (ie, 50 mm Hg lasting longer than 5 d) is dangerous.
• The most severe complication of hyphema is not the initial bleed but rather a rebleed, which is usually seen within 72 hours following the initial trauma. The rebleeding rate is 10-20%.
• • Hyphema resulting from a rebleed usually is more extensive than that seen with the initial trauma.
  • Rebleeding may present as total hyphema with blood filling the entire anterior chamber, often called 8-ball hyphema. Such significant hemorrhages often lead to elevated IOPs and corneal bloodstaining. They also are more likely to require surgical care.
  • Peripheral anterior synechia is another complication and is associated with larger hyphemas and longer durations.

Prognosis

• Prognosis depends on the size of the hyphema. Patients with a small-sized hyphema have a good prognosis with simple management and treatment. Patients whose eyes undergo rebleeding have a poor prognosis because they have a larger sized hyphema and are also more likely to have higher IOP.
• Patients who undergo surgery for anterior chamber wash-out or for ocular injury repair following initial trauma also have a poorer prognosis.
• Total hyphema is difficult to treat, and the visual outcome is usually poor.
• In some studies, final vision was found better than 20/50 in almost 75% of all hyphema cases.

Patient Education

• Promote public awareness about wearing goggles in high-risk sports or work environments.
• For excellent patient education resources, visit eMedicine's Eye and Vision Center and Glaucoma Center. Also, see eMedicine's patient education articles Hyphema (Bleeding in Eye), Glaucoma Overview, Glaucoma FAQs, and Understanding Glaucoma Medications.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to identify patients with sickle cell
• Failure to order sickle cell preps in all cases of spontaneous or traumatic hyphema in high-risk ethnic groups

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Layered hyphema from blunt trauma.
	View Full Size Image
Media type:  Photo

Media file 2:  Total or 8-ball hyphema.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Campbell D, Shields MB, Liebmann JM. Ghost cell glaucoma. In: Ritch R, Shields B, Krupin T, eds. The Glaucomas. Vol 2. 1989:1239-1247.
• Culom RD Jr, Chang B, eds. Hyphema and microhyphema. In: The Wills Eye Manual. 1994:32-6.
• Drug Facts and Comparisons Staff. Drug Facts and Comparisons. 1999.
• Herschler J, Cobo M. Trauma and elevated intraocular pressure. In: Ritch R, Shields B, Krupin T, eds. The Glaucomas. Vol 2. 1989:1225-1237.
• 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].
• Shields MB. Glaucomas associated with intraocular hemorrhage and glaucomas associated with ocular trauma. In: Textbook of Glaucoma. 1992:381-399.
• Shingleton BJ, Hersh PS. Traumatic hyphema. In: Eye Trauma. 1991:104-116.
• Walton W, Von Hagen S, Grigorian R, Zarbin M. Management of traumatic hyphema. Surv Ophthalmol. Jul-Aug 2002;47(4):297-334. [Medline].
• 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. 2^nd ed. Philadelphia: WB Saunders; 2000:5201-5221.

Article Last Updated: Dec 28, 2007