# Hyphema and Traumatic Glaucoma

## Introduction

Hyphema is defined as blood in the anterior chamber, most commonly resulting from blunt ocular trauma. Traumatic glaucoma can occur acutely due to hyphema, or develop as a late sequela from angle recession, trabecular meshwork damage, or lens-related mechanisms. Proper management requires understanding the natural history of hyphema, risk factors for rebleeding, and the mechanisms underlying both acute and chronic post-traumatic glaucoma.

## Anatomy and Pathophysiology

### Mechanism of Hyphema

Blunt trauma causes **equatorial expansion** of the globe with compression in the anteroposterior axis. Sudden stretching of the iris root and ciliary body tears blood vessels. The **major arterial circle of the iris** and branches of the anterior ciliary arteries are the usual sources. Blood accumulates in the anterior chamber, layering inferiorly with gravity.

### Mechanisms of Acute IOP Elevation

Obstruction of the trabecular meshwork by red blood cells, fibrin, and inflammatory debris. Pupillary block from organized clot. **Eight-ball (total) hyphema**: complete filling of the anterior chamber with dark clotted blood; very high risk of IOP elevation.

### Mechanisms of Chronic Traumatic Glaucoma

**Angle recession**: separation of the longitudinal and circular fibers of the ciliary muscle. Trabecular meshwork scarring and dysfunction. Peripheral anterior synechiae (PAS) from prolonged inflammation. Lens subluxation causing pupillary block or phacolytic mechanism. Ghost cell glaucoma from old vitreous hemorrhage.

## Classification of Hyphema

### Grading System

| Grade | AC Blood Fill | Rebleed Risk | IOP Elevation Risk |
|-------|--------------|--------------|-------------------|
| Microhyphema | Circulating RBCs only (no layering) | Low | Low |
| I | < 1/3 | ~4% | Low-moderate |
| II | 1/3 to 1/2 | ~4% | Moderate |
| III | > 1/2 (not total) | ~4% | High |
| IV (Eight-ball) | Total fill; dark clot | High | Very high (corneal blood staining risk) |

## Clinical Evaluation

### History

Mechanism and timing of trauma. Anticoagulant or antiplatelet medication use. **Sickle cell disease or trait** screening: critically important due to increased risk of complications. Bleeding disorders.

### Examination

Visual acuity. IOP measurement (avoid applanation if corneal laceration suspected; use Tono-Pen or pneumotonometry) Slit-lamp examination: grade hyphema, assess for corneal blood staining, iridodialysis, lens subluxation, sphincter tears. Gonioscopy: defer in acute phase; perform after resolution to assess for angle recession. Dilated fundus exam: rule out commotio retinae, retinal tears, vitreous hemorrhage, globe rupture. B-scan ultrasonography if fundus view is obscured.

![Slit-lamp photograph demonstrating a Grade II hyphema layering in the anterior chamber](images/hyphema-grade2.jpg)

## Management

### Medical Treatment

**Activity restriction**: bed rest with head of bed elevated 30-45 degrees; limited ambulation. **Eye shield** (rigid): prevent further trauma; no pressure patch. **Cycloplegic agent**: atropine 1% to stabilize the blood-aqueous barrier and provide comfort. **Topical corticosteroids**: prednisolone acetate 1% to reduce inflammation (taper over 2-3 weeks) **Avoid aspirin and NSAIDs**: increase bleeding risk. **Aminocaproic acid (ACA)**: oral antifibrinolytic agent.

Dose: 50 mg/kg every 4 hours (maximum 30 g/day) for 5 days. Stabilizes the clot and reduces rebleeding rate from approximately 20-30% to 3-5%. Side effects: nausea, vomiting, hypotension; contraindicated in pregnancy and renal disease. **Tranexamic acid (TXA)**: alternative antifibrinolytic; 25 mg/kg TID for 5 days. IOP management: **timolol**, brimonidine, dorzolamide; oral acetazolamide if needed. **Avoid carbonic anhydrase inhibitors in sickle cell patients** (acetazolamide lowers aqueous pH, promoting sickling in the anterior chamber)

Avoid pilocarpine (increases inflammation) and prostaglandin analogues (may promote inflammation)

### Rebleed

Occurs in 20-30% of cases without antifibrinolytics, typically on **days 2-5** after initial injury. Risk factors: large initial hyphema, aspirin/NSAID use, sickle cell disease/trait, poor compliance with activity restriction. Rebleeds are often larger than the initial hyphema and carry higher risk of complications.

### Sickle Cell Considerations

Even sickle cell **trait** (HbAS) increases risk of complications. Red blood cells sickle in the low-oxygen, low-pH environment of the anterior chamber. Sickled cells obstruct trabecular meshwork more severely than normal RBCs. IOP elevation occurs at lower thresholds and causes optic nerve damage earlier. **Do not use acetazolamide** (lowers pH, promotes sickling) **Do not use epinephrine** or phenylephrine with vasoconstrictive risk.

Lower threshold for surgical intervention (IOP > 24 mmHg for > 24 hours in sickle cell patients vs. > 50 mmHg for > 5 days in normal patients)

![Clinical photograph of a total (eight-ball) hyphema with dark clotted blood filling the anterior chamber](images/eight-ball-hyphema.jpg)

## Surgical Intervention

### Indications

IOP > 50 mmHg for > 5 days (risk of optic atrophy) in non-sickle cell patients. IOP > 35 mmHg for > 7 days (risk of corneal blood staining) IOP > 24 mmHg for > 24 hours in **sickle cell** patients. Total hyphema (eight-ball) with IOP elevation. Corneal blood staining (or impending) Non-resolving Grade IV hyphema after 4-5 days.

### Surgical Techniques

**Anterior chamber washout**: paracentesis with irrigation/aspiration of blood and clot. Clot removal with viscoelastic-assisted technique or automated vitrector. Trabeculectomy or tube shunt placement if IOP remains uncontrolled despite washout. Peripheral iridectomy if pupillary block is present.

## Angle Recession Glaucoma

### Pathophysiology

Angle recession is present in up to 80% of eyes with hyphema. Tear between longitudinal and circular fibers of ciliary muscle. Late development of glaucoma occurs in 5-10% of eyes with angle recession. Risk increases with extent of recession (> 180 degrees) **Can develop years to decades** after initial trauma.

### Gonioscopic Findings

Widened ciliary body band. Irregular and deepened angle compared to fellow eye. Torn iris processes. Compare with the fellow eye.

### Management

Lifelong monitoring with annual gonioscopy and IOP checks. Medical therapy: aqueous suppressants preferred (timolol, brimonidine) Surgical: trabeculectomy or tube shunt for medically uncontrolled glaucoma. Laser trabeculoplasty generally ineffective for angle recession glaucoma.

![Gonioscopic comparison of a normal angle (left) and angle recession with widened ciliary body band (right)](images/angle-recession-gonioscopy.jpg)

## Other Forms of Traumatic Glaucoma

### Ghost Cell Glaucoma

Occurs weeks to months after vitreous hemorrhage. Degenerated, rigid, khaki-colored RBCs obstruct the trabecular meshwork. Anterior chamber has characteristic **"khaki-colored" cells**. Treatment: anterior chamber washout; vitrectomy if persistent.

### Lens-Related Glaucoma

Phacolytic: lens protein leaking through intact capsule of a mature cataract. Phacomorphic: swollen lens causing pupillary block angle closure. Lens particle: retained cortical material after trauma or surgery.

## Key Clinical Pearls

Screen all hyphema patients for sickle cell disease or trait; management differs significantly due to the risk of sickling in the anterior chamber. Aminocaproic acid or tranexamic acid reduces the rebleed rate from approximately 25% to less than 5%. Avoid carbonic anhydrase inhibitors in sickle cell patients as they lower aqueous humor pH and promote sickling. Angle recession glaucoma may develop years to decades after trauma; lifelong monitoring is essential for any patient with a history of hyphema.

## References

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2. Crouch ER, Crouch ER Jr. Management of traumatic hyphema: therapeutic options. *J Pediatr Ophthalmol Strabismus*. 1999;36(5):238-250.
3. Ng DS, Ching RH, Chan CW. Angle-recession glaucoma: long-term clinical outcomes over a 10-year period. *Int Ophthalmol*. 2015;35(3):361-369.
4. Gharaibeh A, Savage HI, Scherer RW, et al. Medical interventions for traumatic hyphema. *Cochrane Database Syst Rev*. 2019;1(1):CD005431.