Hyphema Glaucoma 

Updated: Jul 29, 2020
Author: Inci Irak Dersu, MD, MPH; Chief Editor: Hampton Roy, Sr, MD 



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.

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.



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%.


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.


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.


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


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.

Patient Education

Promote public awareness about wearing goggles in high-risk sports or work environments.

For excellent patient education resources, visit eMedicineHealth's Eye and Vision Center. Also, see eMedicineHealth's patient education articles Hyphema (Bleeding in Eye), Glaucoma Overview, Glaucoma FAQs, and Glaucoma Medications.




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. Hyphema may be accompanied by a foreign object in the eye.

Sports injuries, motor vehicle accidents, and work-related injuries are common causes of hyphema.

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.

Asking about the use of blood thinners in addition to alternative medicine, such as ginkgo biloba, is important.


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)

    • Intraocular surgery (during or after): Increased use of angle-based microinvasive glaucoma surgeries such as goniotomy or trabeculotomy procedures has been associated with higher incidence of postoperative hyphemas.

    • 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), as shown in the image below

      Total or 8-ball hyphema. 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.


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

  • Spontaneous hyphema associated with anticoagulant treatment, hemophilia, and other blood disorders


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.





Laboratory 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.

Other Tests

Ultrasound biomicroscopy is a useful tool to identify angle recession or cyclodialysis cleft occurs following hyphema/ocular trauma.



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.

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)


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


No special diet is required for patients with hyphema.


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.

Long-Term Monitoring

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.

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 intraocular pressure (IOP).

Inpatient & Outpatient Medications

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.



Medication Summary

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

Topical beta-blockers

Class Summary

Decrease aqueous production and IOP.

Timolol maleate (Betimol, Timoptic, Timoptic XE, Istalol)

Nonselective beta-adrenergic receptor blocker. May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor or by outflow.

Osmotic diuretics

Class Summary

Decrease the IOP by reducing vitreous volume. They increase blood viscosity. Avoidance in patients with sickle cell disease is recommended.

Mannitol (Osmitrol)

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.

Isosorbide dinitrate (Isordil, Dilatrate-SR)

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.

Glycerin (Osmoglyn)

Commercially unavailable; available from compounding pharmacies; 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.


Class Summary

Prevent recurrent hyphema.

Aminocaproic acid (Amicar)

Inhibits the substance that converts plasminogen to plasmin. Has antiplasmin activity. Aminocaproic acid is the most commonly used antifibrinolytic in the United States.

Tranexamic acid (Cyklokapron)

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.


Class Summary

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).

Atropine ophthalmic (Isopto Atropine)

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.

Homatropine (Homatropaire)

Blocks responses of sphincter muscle of iris and muscle of ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).

Cyclopentolate (Cyclogyl)

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.

Carbonic anhydrase inhibitors

Class Summary

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


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.


Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.

Dorzolamide (Trusopt)

Topical carbonic anhydrase inhibitors are less effective than oral agents but have less systemic side effects.

Brinzolamide (Azopt)

Brinzolamide catalyzes a reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. It may be used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one topical ophthalmic drug is being used, administer them at least 10 minutes apart.

Prostaglandin analogs

Class Summary

These selective agonists act on prostaglandin receptors in the eye to lower IOP by increasing uveoscleral outflow. In hyphema, possible increased inflammation associated with this class of medicines should be kept in mind. In addition, the IOP lowering effect may take longer than with other classes of antiglaucoma medications.

Bimatoprost ophthalmic solution (Lumigan, Latisse, Durysta)

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.

Travoprost ophthalmic solution (Travatan Z)

Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.

Latanoprost (Xalatan, Xelpros)

Latanoprost may decrease IOP by increasing the outflow of aqueous humor. Patients should be informed about possible cosmetic effects to the eye/eyelashes, especially if uniocular therapy is to be initiated.

Latanoprostene bunod ophthalmic (Vyzulta)

Metabolized into latanoprost acid in the eye. Enhances conventional trabecular uveoscleral outflow of aqueous humor.

Antiglaucoma, Alpha2 Agonists

Class Summary

Within this class, the alpha2 selective agonist brimonidine is the most commonly used for the treatment of ocular hypertension. Alpha2 adrenergic agonists work by decreasing aqueous production.

Brimonidine (Alphagan P)

Brimonidine is a relatively selective alpha2 adrenergic-receptor agonist that decreases IOP by dual mechanisms, reducing aqueous humor production and increasing uveoscleral outflow. Brimonidine has minimal effect on cardiovascular and pulmonary parameters. A moderate risk of allergic response to this drug exists. Caution should be used in individuals who have developed an allergy to Iopidine. IOP lowering of up to 27% reported.


Questions & Answers


What is hyphema glaucoma?

What is the pathophysiology of hyphema glaucoma?

What is the prevalence of hyphema glaucoma?

What is the mortality and morbidity associated with hyphema glaucoma?

What are the racial predilections for hyphema glaucoma?

What are the sexual predilections for hyphema glaucoma?

Which age groups have the highest prevalence of hyphema glaucoma?

What is the prognosis for hyphema glaucoma?

What is included in patient education about hyphema glaucoma prevention?


Which clinical history findings are characteristic of hyphema glaucoma?

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What causes hyphema glaucoma?

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What are the differential diagnoses for Hyphema Glaucoma?


What is the role of lab tests in the workup for hyphema glaucoma?

What is the role of imaging studies in the workup for hyphema glaucoma?

What is the role of ultrasound biomicroscopy in the workup for hyphema glaucoma?


How is hyphema glaucoma treated?

What are the supportive measures used in the treatment of hyphema glaucoma?

What is the role of surgery in the treatment of hyphema glaucoma?

Which specialist consultations are beneficial to patients with hyphema glaucoma?

Which dietary modifications are used in the treatment of hyphema glaucoma?

Which activity modifications are used in the treatment of hyphema glaucoma?

How is hyphema glaucoma prevented?

What is included in the long-term monitoring of hyphema glaucoma?

When is inpatient care indicated for the treatment of hyphema glaucoma?

Which medications are used in the treatment of hyphema glaucoma?


What is the role of medications in the treatment of hyphema glaucoma?

Which medications in the drug class Antiglaucoma, Alpha2 Agonists are used in the treatment of Hyphema Glaucoma?

Which medications in the drug class Prostaglandin analogs are used in the treatment of Hyphema Glaucoma?

Which medications in the drug class Carbonic anhydrase inhibitors are used in the treatment of Hyphema Glaucoma?

Which medications in the drug class Cycloplegics are used in the treatment of Hyphema Glaucoma?

Which medications in the drug class Antifibrinolytics are used in the treatment of Hyphema Glaucoma?

Which medications in the drug class Osmotic diuretics are used in the treatment of Hyphema Glaucoma?

Which medications in the drug class Topical beta-blockers are used in the treatment of Hyphema Glaucoma?