Traumatic Hyphema

Key Points at a Glance

Key Points of This Disease

• Traumatic hyphema is a condition in which blood accumulates in the anterior chamber after blunt trauma, mainly caused by ball injuries, traffic accidents, and occupational injuries.
• It is classified into grades 0 (microhyphema) to IV (total hyphema/black ball hyphema) according to the amount of bleeding.
• There is a risk of rebleeding 3 to 7 days after injury (incidence 5–10%), and rebleeding tends to be more severe than the initial episode.
• Basic treatment includes rest, head elevation at 30–45 degrees, atropine pupil dilation, and steroid eye drops.
• Complications affecting visual prognosis such as elevated intraocular pressure, corneal blood staining, and angle recession glaucoma require attention.
• Angle recession can cause glaucoma several years or more after injury, so long-term follow-up is essential.
• Patients with sickle cell disease may develop severe intraocular pressure elevation even with a small amount of bleeding, requiring special management.

1. What is traumatic hyphema?

Traumatic hyphema is a condition in which red blood cells accumulate in the anterior chamber (the space between the cornea and iris) after blunt trauma. A small amount of bleeding that can only be seen with a slit lamp is called microhyphema.

When blunt force is applied to the eye, the intraocular pressure rises sharply and the limbus stretches. The aqueous humor moves posteriorly and toward the angle, damaging the iris and ciliary body, leading to bleeding. The most vulnerable part is the thin attachment of the iris to the ciliary body; a tear here (iridodialysis) displaces the pupil. If a cleft forms in the ciliary body slightly scleral side, angle recession occurs; if the ciliary body detaches from the sclera further scleral side, cyclodialysis results. Both of these are particularly prone to hyphema.

It is classified according to the amount of bleeding as follows.

Grade	Degree of bleeding
0	Microhyphema
I	Less than 1/3 of the anterior chamber
II	1/3 to 1/2 of the anterior chamber
III	1/2 to less than total filling of the anterior chamber
IV	Total hyphema

Among grade IV, when the anterior chamber is completely filled with bright red blood, it is called total hyphema. When filled with dark red to black blood, it is called 8-ball hyphema (black ball hyphema), suggesting impaired aqueous humor circulation and hypoxia.

Q Can hyphema occur without trauma?

A

Besides trauma, hyphema can occur spontaneously after intraocular surgery (iatrogenic), due to iris neovascularization, ocular tumors, blood disorders (e.g., leukemia, hemophilia), or use of anticoagulants. See the section “Causes and Risk Factors” for details.

2. Main Symptoms and Clinical Findings

Traumatic hyphema (Grade II): layered accumulation of red blood cells occupying the lower half of the anterior chamber

Ahuja R (EyeMD). Hyphema - occupying half of anterior chamber of eye. Wikimedia Commons. 2006. Figure 1. Source ID: commons.wikimedia.org/wiki/File:Hyphema_-_occupying_half_of_anterior_chamber_of_eye.jpg. License: CC BY-SA 2.5.

A bright red to dark red blood level is seen filling the lower half of the anterior chamber, clearly showing layered accumulation due to gravitational settling of red blood cells. This corresponds to Grade II in the hyphema grading classification discussed in the section “Main Symptoms and Clinical Findings”.

Subjective Symptoms

Symptoms of traumatic hyphema vary depending on the amount of bleeding.

• Decreased vision: Becomes noticeable when blood covers the pupillary area.
• Eye pain and headache: Occur due to trauma or elevated intraocular pressure.
• Redness: Accompanied by ciliary injection.
• Photophobia (sensitivity to light): Increases when traumatic iritis is present.

Clinical Findings

Hyphema forms a layer inferiorly (layering), and its color changes from red to black over time. Clotted blood appears darker. In the upright position, the height of the blood layer serves as an indicator of the amount of bleeding and is useful for monitoring absorption or rebleeding. It is important to record the height from the inferior corneal limbus in millimeters.

Mild (Grade I–II)

Risk of elevated intraocular pressure: Approximately 13.5%.

Visual impairment: Remains mild if the pupillary area is clear.

Fundus visibility: Usually possible.

Severe (Grade III–IV)

Risk of elevated intraocular pressure: Increases dramatically to 27% in Grade III and 52% in Grade IV.

Eight-ball hyphema: High risk of pupillary block and secondary angle closure.

Fundus visibility: Often impossible; ultrasound examination is required.

The main complications are as follows.

• Elevated intraocular pressure: Caused by trabecular meshwork obstruction by red blood cells.
• Iridodialysis: Pupil displacement due to tearing of the iris root (see iridodialysis).
• Angle recession: May lead to secondary glaucoma in the long term.
• Corneal blood staining: Occurs when high intraocular pressure persists with severe hyphema.
• Vitreous hemorrhage: Depends on the severity of trauma.
• Lens subluxation/dislocation: When associated with damage to the zonules.

The following complications are important in children:

• Deprivation amblyopia: In infants, if severe hemorrhage persists for more than 2 weeks, light stimulation is blocked, leading to amblyopia.
• Permanent visual impairment due to corneal blood staining: Occurs when severe hemorrhage and high intraocular pressure persist for several weeks.
• Late-onset secondary glaucoma: May develop after absorption of hemorrhage from angle recession.

3. Causes and Risk Factors

Traumatic

Blunt trauma is the most common cause. Typical examples include balls, fists, traffic accidents, and occupational injuries. Compression force to the eye causes rupture of blood vessels in the iris, ciliary body, and trabecular meshwork, leading to accumulation of red blood cells in the anterior chamber.

Iatrogenic

• After intraocular surgery: Can occur after any ophthalmic surgery, including cataract surgery. In cataract surgery patients taking warfarin, bleeding events increase about threefold compared to non-users (overall incidence 9–10%), but most are self-limited hyphema or subconjunctival hemorrhage⁵⁾.
• UGH syndrome (uveitis-glaucoma-hyphema syndrome): A malpositioned intraocular lens chronically irritates the iris, causing inflammation, neovascularization, and recurrent hyphema.
• After Nd:YAG laser iridotomy: Usually mild and self-limited.
• After trabeculotomy: Hyphema due to Schlemm’s canal rupture is almost inevitable but typically resolves spontaneously within 2–3 days.

Spontaneous

In hyphema without trauma history, consider the following causes.

• Neovascularization: Iris and angle neovascularization secondary to diabetic retinopathy, retinal vein occlusion, ocular ischemic syndrome, etc.
• Ocular tumors: Iris melanoma, retinoblastoma, etc.
• Blood disorders: Leukemia, hemophilia, von Willebrand disease.
• Vascular abnormalities: Juvenile xanthogranuloma (JXG), iris microhemangiomas (Cobb’s tufts).
• Drug-induced: In addition to anticoagulants and antiplatelet drugs, spontaneous hyphema has been reported with ibrutinib (BTK inhibitor)¹⁾.
• Inflammatory: Herpetic uveitis, Fuchs heterochromic iridocyclitis.
• After ICL (implantable collamer lens) surgery: The haptics of the ICL may form an iridociliary cyst, whose rupture can cause hyphema or posterior chamber hemorrhage⁶⁾. It can occur even without trauma or eye rubbing. UBM identification of the cyst is useful for diagnosis; it often resolves with conservative treatment, and urgent ICL removal is not always necessary.

Sickle cell disease

Sickle cell disease is a particularly important risk factor. In the hypoxic environment of the anterior chamber, red blood cells sickle and become rigid, making them difficult to pass through the trabecular meshwork. As a result, even a small amount of bleeding can cause severe intraocular pressure elevation. Furthermore, sickled red blood cells within vessels can cause central retinal artery occlusion or ischemic optic neuropathy. Sickle cell trait also poses a risk.

Prevention and Daily Care

• Sports injuries, such as being hit in the eye by a ball, are an important cause of hyphema. Wear appropriate protective eyewear during sports.
• If you are taking anticoagulants or antiplatelet drugs, consult your primary care physician before eye surgery.
• If diagnosed with hyphema, follow the prescribed rest and sleep with your head elevated.

Q Can cataract surgery be performed while taking anticoagulants?

A

Cataract surgery while continuing warfarin increases bleeding events, but most are self-limited hyphema or subconjunctival hemorrhage, with no adverse effects on postoperative visual acuity⁵⁾. However, collaboration between the primary care physician and ophthalmologist is important for individual risk assessment.

4. Diagnosis and Examination Methods

The diagnosis of hyphema involves the following stepwise examinations. Basic assessments include history taking, visual acuity testing, pupillary light reflex testing, intraocular pressure measurement, and slit-lamp microscopy. In cases of massive hyphema, the consensual light reflex of the fellow eye should also be checked.

• Slit-lamp microscopy: Confirms blood accumulation in the anterior chamber and records the height, color, and grade of the hemorrhage. Large hyphemas can also be detected with a penlight.
• Visual acuity testing: Evaluates the degree of vision loss.
• Pupillary light reflex testing: In cases of massive hemorrhage, also check the consensual reflex of the fellow eye.
• Intraocular pressure measurement: Assesses the presence of elevated intraocular pressure.
• Seidel test: Uses fluorescein staining to check for corneal perforation.
• Gonioscopy: Essential for evaluating angle recession and peripheral anterior synechiae. However, it carries a high risk of rebleeding and should be avoided for 1–2 weeks after injury⁴⁾.
• Ultrasound biomicroscopy (UBM) and anterior segment OCT: Useful for observing angle recession, cyclodialysis, and ciliary body edema. However, UBM is contraindicated in penetrating ocular trauma due to the risk of infection and globe compression.
• Ultrasound (B-mode): Used to evaluate retinal detachment or vitreous hemorrhage when the fundus is not visible.
• Imaging (CT/MRI): Performed when severe conjunctival edema, hypotony, and subconjunctival hemorrhage suggest a ruptured globe. MRI is contraindicated if a metallic foreign body is suspected.
• Sickle cell screening: Consider screening in all patients of African descent.

Test	Main Purpose
Slit-lamp microscopy	Grade classification and follow-up
Gonioscopy (1–2 weeks after injury)	Angle recession, peripheral anterior synechiae
UBM / anterior segment OCT (UBM contraindicated in penetrating ocular trauma)	Structural evaluation of ciliary body and angle
Ultrasound (B-mode)	Posterior segment evaluation when fundus is not visible
CT / MRI (MRI contraindicated for metallic foreign bodies)	Evaluation of globe rupture and intraocular foreign bodies

5. Standard Treatment

Conservative Treatment (Medical Therapy)

The basic principle of treatment is to wait for spontaneous absorption with rest. Strenuous exercise is prohibited, supine position is avoided, and the patient is kept at rest with the head of the bed elevated 30–45 degrees in a sitting or semi-recumbent position. Hospitalization is recommended for children, cases where the hyphema level exceeds 1/3 to 1/2 of the anterior chamber, patients who cannot follow instructions, and those with sickle cell disease accompanied by elevated intraocular pressure.

Pharmacotherapy

• Atropine ophthalmic solution (1%): Once daily (at bedtime). Mydriasis and cycloplegia reduce inflammation and stress on the angle.
• Rinderon ophthalmic solution (0.1%): Four times daily (morning, noon, evening, bedtime). Anti-inflammatory.
• Adona tablets (30 mg): 3 tablets, divided into 3 doses after each meal. Hemostatic agent.

For elevated intraocular pressure, add the following (4 alone, or 5+6, or a combination of 4–6):

• Timoptol ophthalmic solution (0.5%): Twice daily (morning and evening). Beta-blocker to suppress aqueous humor production.
• Diamox tablets (250 mg): 2 tablets, divided into 2 doses (after breakfast and dinner). Carbonic anhydrase inhibitor.
• Aspara potassium tablets (300 mg): 2 tablets, divided into 2 doses (to prevent hypokalemia when used with Diamox).

Antifibrinolytic agents (tranexamic acid) are useful for reducing the risk of rebleeding ⁴⁾. However, their effect on visual prognosis is unclear ⁴⁾.

Precautions in Treatment

• Pilocarpine hydrochloride is absolutely contraindicated. It exacerbates inflammation and widens the angle, increasing bleeding and inducing rebleeding.
• In patients with sickle cell disease, avoid carbonic anhydrase inhibitors (e.g., Diamox). Increased acidity of the aqueous humor promotes sickling in the anterior chamber ⁴⁾. Similarly, hyperosmotic agents (e.g., mannitol) may trigger sickle cell crisis due to dehydration.
• Aspirin and NSAIDs are not used for pain management because they increase the risk of bleeding.
• If intraocular pressure cannot be controlled with medication, surgical intervention should be considered.

Surgical Treatment

Approximately 5% of traumatic hyphema cases require surgery.

• Anterior chamber washout: Perform anterior chamber irrigation using an irrigation cannula (Simcoe cannula) through a corneal side port. If the blood clot is large or hardened, remove it with forceps or use a vitreous cutter to cut and aspirate it.
• Timing of surgery: Around day 4 after injury is suitable for anterior chamber washout. At this time, the risk of rebleeding is reduced, and the blood clot has partially separated from the ocular tissues.

Indications for surgery are as follows:

Patient Group	Surgical Indication Criteria
Healthy individuals	IOP ≥50 mmHg for 5 days, or ≥35 mmHg for 7 days
Patients with sickle cell disease	IOP ≥25 mmHg for more than 24 hours
Signs of corneal blood staining	Indicated without waiting for the above criteria
Total hyphema in children	Early intervention is indicated considering the risk of amblyopia due to visual deprivation

Glaucoma surgery (e.g., filtering surgery) is indicated when high intraocular pressure persists after anterior chamber washout. Lens extraction is necessary if lens dislocation or damage is present. Laser iridotomy should be considered for pupillary block.

Q Is hospitalization necessary for hyphema?

A

In many cases, outpatient management is possible with close follow-up. However, hospitalization is recommended for children, cases with large amounts of bleeding (exceeding 1/3 to 1/2 of the anterior chamber), sickle cell disease with elevated intraocular pressure, or when the patient cannot comply with activity restrictions.

6. Pathophysiology and Detailed Mechanisms

Mechanism of Traumatic Hyphema

When blunt force is applied to the eye, intraocular pressure rises sharply. The corneal limbus stretches, and aqueous humor moves posteriorly and into the angle. This mechanical change damages the blood vessels of the iris and ciliary body, causing bleeding into the anterior chamber.

Depending on the severity of the injury, the following stepwise structural damage occurs:

• Iridodialysis: A tear occurs at the thinnest part where the iris attaches to the ciliary body, causing pupil displacement (traumatic mydriasis, iridodialysis).
• Angle recession: A cleft forms within the ciliary body slightly on the scleral side. Hyphema is particularly likely in these two conditions.
• Cyclodialysis: The ciliary body detaches from the sclera further on the scleral side. This may cause hypotony.

Rebleeding

Rebleeding occurs 3 to 7 days after injury due to contraction and lysis of the initial clot ⁴⁾. The incidence is reported to be 5–10% ⁴⁾. Rebleeding is often more severe and copious than the initial bleed. Elevated intraocular pressure is observed in more than 50% of rebleeding cases.

Risk factors for rebleeding include the following:

• Low intraocular pressure or elevated intraocular pressure
• Hemorrhage occupying more than 50% of the anterior chamber
• Systemic hypertension
• Aspirin use

Mechanism of intraocular pressure elevation

Intraocular pressure elevation associated with hyphema occurs through multiple mechanisms.

• Trabecular meshwork obstruction by red blood cells: A large number of normal red blood cells physically obstruct the trabecular meshwork.
• Hemolytic glaucoma: Macrophages containing hemoglobin obstruct the trabecular meshwork. It is characterized by a reddish-brown discoloration of the trabecular meshwork⁴⁾.
• Ghost cell glaucoma: Degenerated red blood cells (ghost cells) appear 1 to 4 weeks after vitreous hemorrhage⁴⁾. Red blood cells with Heinz bodies and loss of deformability obstruct the trabecular meshwork. Khaki-colored vesicles are seen in the anterior chamber. Ghost cell glaucoma rarely occurs from hyphema alone.

Corneal blood staining

When severe hyphema is accompanied by sustained high intraocular pressure, the posterior surface of the cornea becomes stained with blood. This may leave visual impairment even after the hyphema resolves, and early anterior chamber washout is necessary.

Angle recession glaucoma

This is an important chronic complication after blunt trauma. A tear occurs between the circular and longitudinal muscles of the ciliary body, causing recession of the angle. In cases with angle recession of 180 degrees or more, glaucoma develops at a high rate of 6–20% over 10 years. Since onset often occurs several years or more after injury, long-term intraocular pressure follow-up is essential.

Q How often does rebleeding occur?

A

The overall incidence of rebleeding is 5–10%, and it often occurs 3 to 7 days after injury⁴⁾. Since rebleeding tends to be more severe than the initial hemorrhage, it is important to maintain rest and undergo close observation during this period.

Q What should be monitored long-term as a related complication?

A

The most important long-term complication is angle-recession glaucoma. In cases with angle recession of 180 degrees or more, glaucoma develops in 6–20% within 10 years. Since it often occurs several years or more after injury, regular follow-up of intraocular pressure, visual field, and optic nerve is essential after trauma.

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7. Latest Research and Future Perspectives (Investigational Reports)

For patients: Please read carefully

The following content is currently under research or in clinical trials and is not standard treatment available at general hospitals. It is reference information for professionals regarding future medical developments.

Reports of Drug-Related Hyphema

With the widespread use of molecular targeted drugs, drug-related spontaneous hyphema has been reported.

Aldecoa et al. (2023) reported spontaneous hyphema in a 60-year-old woman taking ibrutinib (BTK inhibitor) 420 mg/day for 4 months for chronic lymphocytic leukemia ¹⁾. The hyphema completely resolved within 2 weeks after discontinuation of ibrutinib and topical steroid eye drops. Ibrutinib is suggested to reduce platelet adhesion to von Willebrand factor and inhibit collagen-induced platelet aggregation.

Chiang et al. (2022) reported spontaneous hyphema in a 37-year-old man with acute myeloid leukemia and severe COVID-19 pneumonia ²⁾. In addition to severe thrombocytopenia (6×10⁹/L), prolonged prone positioning was presumed to contribute to increased episcleral venous pressure.

Iris Microhemangiomas and Congenital Heart Disease

Ison et al. (2022) reported spontaneous hyphema from iris microhemangiomas (Cobb’s tufts) in a 56-year-old woman with Eisenmenger syndrome ³⁾. Chronic hypoxemia (resting SpO₂ 78%) and secondary erythrocytosis (Hb 22.5 g/dL) were thought to induce dilation of iris stromal vessels and contribute to microhemangioma formation. Bleeding resolved with topical atropine and dexamethasone.

Hyphema After ICL Surgery

Zhang et al. (Pictures & Perspectives) reported spontaneous hyphema and posterior chamber hemorrhage after ICL (implantable collamer lens) surgery ⁶⁾. A 23-year-old woman presented with sudden vision loss without trauma, eye rubbing, or anticoagulant use. UBM examination revealed rupture of an iris-ciliary body cyst associated with the ICL haptics and surrounding hemorrhage. Bleeding resolved with conservative treatment using tobramycin-dexamethasone eye drops (4 times daily) and 1% atropine sulfate gel (twice daily) for 17 days. Emergency ICL removal was not necessarily required.

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8. References

1. Aldecoa KAT, Macaraeg CSL, Dadlani A, Yadlapalli S. Spontaneous hyphema during ibrutinib treatment in a CLL patient. Case Rep Hematol. 2023;2023:1691996.
2. Chiang J, Chan L, Stallworth JY, Chan MF. Spontaneous hyphema in the setting of COVID-19 pneumonia. Am J Ophthalmol Case Rep. 2022;26:101447.
3. Ison M, Dorman A, Imrie F. Spontaneous hyphema from iris microhemangioma in Eisenmenger syndrome. Am J Ophthalmol Case Rep. 2022;26:101536.
4. European Glaucoma Society. European Glaucoma Society Terminology and Guidelines for Glaucoma, 5th Edition. Br J Ophthalmol. 2021;105(Suppl 1):1-169.
5. American Academy of Ophthalmology Preferred Practice Pattern Cataract and Anterior Segment Committee. Cataract in the Adult Eye Preferred Practice Pattern. Ophthalmology. 2022;129(1):P52-P110.
6. Zhang W, Li F, Zhou J. Anterior segment hemorrhage after implantable collamer lens surgery. Ophthalmology. (Pictures & Perspectives).