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.
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.
View Image
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.
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.
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.
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)
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), as shown in the image below
View Image
Total or 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. Increased pigmentation of the angle due after ocular trauma has been associated with an increased risk of developing glaucoma. 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.
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.
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.
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)
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.
Glaucoma can be seen 10 years or after following ocular trauma. Therefore, these patients need to be followed periodically indefinitely. Also see the clinical guideline summary from the US Preventative Services Task Force, Screening for glaucoma: recommendation statement.
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 intraocular pressure (IOP).
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
Inhibits the substance that converts plasminogen to plasmin. Has antiplasmin activity. Aminocaproic acid is the most commonly used antifibrinolytic in the United States.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
Blocks responses of sphincter muscle of iris and muscle of ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).
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).
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
Prostaglandin F2-alpha analog and selective FP prostanoid receptor agonist. Exact mechanism of action unknown but believed to reduce IOP by increasing uveoscleral outflow.
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
Disclosure: Nothing to disclose.
Specialty Editors
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
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
Disclosure: Nothing to disclose.
Chief Editor
Hampton Roy, Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Disclosure: Nothing to disclose.
Additional Contributors
Andrew I Rabinowitz, MD, Director of Glaucoma Service, Barnet Dulaney Perkins Eye Center
){kind=link}
){kind=link}