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Summary Table

Category	Details
Risk Factors	Young males (peak 10 to 20 years), blunt ocular trauma (sports, paintball, fistfight, airbag deployment), sickle cell disease or trait, bleeding diatheses, anticoagulant use, recent intraocular surgery, neovascularization (proliferative diabetic retinopathy, retinal vein occlusion)
Etiology	Disruption of iris root vessels or ciliary body vessels causing bleeding into the anterior chamber. Most cases are traumatic; spontaneous cases suggest neovascular disease, coagulopathy, or intraocular tumor (juvenile xanthogranuloma in children, melanoma in adults)
Patient Presentation	Eye pain, blurred or decreased vision, photophobia, and somnolence (especially in children) following blunt ocular trauma. May complain of "blood in the eye"
Classic Physical Exam	Visible layering of blood in the anterior chamber when the patient is upright, decreased visual acuity, anisocoria, photophobia. Always check for peaked pupil and Seidel sign to rule out globe rupture
Key Diagnostic Results	Slit-lamp confirmation of red blood cells layered in the anterior chamber, applanation tonometry showing variable intraocular pressure (IOP), B-scan ultrasound if the posterior segment cannot be visualized, CT orbits without contrast if fracture suspected, hemoglobin electrophoresis or Sickledex in at-risk patients
Management	Eye shield (no patch), head of bed elevated to 30 to 45 degrees, bed rest, topical cycloplegic and topical corticosteroid, avoidance of aspirin and NSAIDs, IOP-lowering drops if needed, surgical washout for refractory IOP elevation or corneal blood staining
Keywords	"Layering of blood in the anterior chamber," "eight-ball hyphema," "blackball hyphema," "post-traumatic eye pain after baseball injury," "rebleeding on day 3 to 5," "sickle cell patient with hyphema"

1. Pathophysiology

Hyphema occurs when blunt force is transmitted to the globe, causing rapid anteroposterior compression and equatorial expansion of the eye. This shearing force tears the iris root, the ciliary body, or the major arterial circle of the iris, releasing blood into the anterior chamber. Because the anterior chamber is a closed, gravity-dependent space, red blood cells settle inferiorly, producing the classic visible layering when the patient sits upright.

The clinical danger comes not from the initial bleed but from its consequences. Erythrocytes and fibrin clog the trabecular meshwork, the drainage pathway for aqueous humor. This obstruction raises intraocular pressure (IOP), which can compromise optic nerve perfusion and lead to permanent vision loss if sustained. Prolonged contact between blood and the corneal endothelium produces corneal blood staining, a permanent rust-colored discoloration that mimics a leukoma and is one of the firmest indications for surgical evacuation.

The most feared complication is rebleeding, which classically peaks between days 2 and 5 after the initial injury. Rebleeds tend to be larger than the original hemorrhage and carry a worse visual prognosis. The mechanism involves clot retraction and lysis at the original bleeding site, exposing the damaged vessel before it has time to fully heal.

In sickle cell disease or trait, the pathophysiology takes a dangerous turn. The aqueous humor is hypoxic and acidic, conditions that promote sickling of erythrocytes. Sickled cells are rigid and cannot pass through the trabecular meshwork, so even a small hyphema can produce dramatic IOP elevation. This is the single most tested association in hyphema vignettes, and it changes the entire treatment algorithm.

2. Classification

Grade	Blood in Anterior Chamber	Description
Microhyphema	No layering visible	Circulating red blood cells in the anterior chamber, seen only on slit lamp
Grade I	Less than 1/3	Layered blood in the inferior anterior chamber, less than one-third of the chamber
Grade II	1/3 to 1/2	Layered blood occupies between one-third and one-half of the chamber
Grade III	Greater than 1/2 but not total	Layered blood occupies more than half of the chamber but does not fill it completely
Grade IV (Total)	100% (Eight-Ball / Blackball)	The entire anterior chamber is filled with blood. When clotted and dark, it is called an "eight-ball" or "blackball" hyphema. Carries the highest risk of IOP elevation and corneal staining

Higher grades correlate with worse visual outcomes and higher rates of complications, but even small hyphemas in sickle cell patients can be sight-threatening.

3. Diagnostic Workup

Test	Purpose	Findings
Visual acuity	Baseline assessment	Decreased acuity proportional to grade
Slit-lamp examination	Best initial test	Layering of red blood cells in the anterior chamber, cells and flare
Applanation tonometry (IOP measurement)	Detect ocular hypertension	Often elevated; guides urgency of treatment
Gonioscopy	Confirmatory for angle recession (delayed, after clearing)	Performed weeks later to assess angle damage
Dilated fundoscopy	Evaluate posterior segment	Check for retinal detachment, vitreous hemorrhage, commotio retinae
B-scan ocular ultrasound	Used when fundus is not visible due to dense hyphema	Detects posterior segment pathology
CT orbits without contrast	Suspected globe rupture or orbital fracture	Identifies fracture, intraocular foreign body
Sickledex / Hemoglobin electrophoresis	Mandatory in African-descent patients and those of unknown status	Identifies sickle cell trait or disease before initiating IOP therapy
Coagulation studies (PT, PTT, INR, CBC)	Spontaneous or recurrent hyphema	Identifies bleeding diathesis

The workup begins at the bedside. Before anything else, the examiner must rule out globe rupture, because applying pressure or instilling drops in a ruptured globe causes catastrophic extrusion of intraocular contents. Red flags include a peaked or teardrop pupil, a positive Seidel sign (fluorescein streaming away from a corneal defect under cobalt blue light), severe chemosis, and deep or shallow anterior chamber asymmetry. If globe rupture is suspected, place a rigid shield, obtain a CT, and consult ophthalmology immediately.

The best initial test for hyphema itself is the slit-lamp examination, which confirms layered red blood cells in the anterior chamber and quantifies the grade. Visual acuity and IOP measurement follow immediately. Tonometry is the most important physiologic measurement because IOP determines the urgency of treatment and the threshold for surgery.

In any patient of African, Mediterranean, Middle Eastern, or Indian descent, or in any patient with unknown sickle status, sickle screening is mandatory before treatment is finalized. This single step is one of the most tested decision points in hyphema cases.

When the hyphema is dense enough to obscure the fundus, B-scan ultrasonography evaluates the posterior segment for retinal detachment, vitreous hemorrhage, or a ruptured posterior globe. CT is reserved for suspected fracture, intraocular foreign body, or globe rupture.

4. Management & Treatment

Intervention	Indication	Notes
Rigid eye shield	All cases	Never use a pressure patch (risk of globe rupture)
Head of bed at 30 to 45 degrees	All cases	Allows blood to settle inferiorly and clear from the visual axis
Activity restriction	All cases	Bed rest with bathroom privileges; avoid bending and Valsalva
Topical cycloplegic	Comfort, prevent synechiae	Atropine 1% one drop two to three times daily, or cyclopentolate 1% three times daily
Topical corticosteroid	Reduce inflammation, reduce rebleed risk	Prednisolone acetate 1% four to eight times daily
Topical IOP-lowering agents	IOP greater than 24 mmHg	Timolol 0.5% twice daily, brimonidine, or dorzolamide
Oral acetazolamide	Refractory IOP elevation	250 mg four times daily. CONTRAINDICATED in sickle cell
Mannitol IV	Severe IOP elevation refractory to topical therapy	Caution in sickle cell (causes hemoconcentration and worsens sickling)
Antifibrinolytics (aminocaproic acid or tranexamic acid)	Reduce rebleeding risk	Oral aminocaproic acid 50 mg/kg every 4 hours, maximum 30 g/day, for 5 days. Use is selective and institution-dependent
Avoid aspirin and NSAIDs	All cases	Increase rebleeding risk
Surgical anterior chamber washout	See indications below	Definitive when medical therapy fails

The first move in management is protection and stabilization. Place a rigid eye shield (never a pressure patch), elevate the head of the bed to 30 to 45 degrees, and restrict activity. Elevation lets blood settle inferiorly so the visual axis clears and the trabecular meshwork superiorly is partially spared. Patients are typically managed as outpatients with daily follow-up, but admission is reasonable for non-compliant patients, children, sickle cell patients, total hyphema, and high IOP.

Topical therapy has three components:

A cycloplegic agent (atropine 1% two to three times daily, or cyclopentolate 1% three times daily) relieves ciliary spasm, reduces photophobia, and prevents posterior synechiae by keeping the iris mobile.
A topical corticosteroid (prednisolone acetate 1% four to eight times daily) reduces inflammation and may reduce rebleeding rates.
If the IOP is elevated above 24 mmHg, start a beta blocker (timolol 0.5% twice daily) and add an alpha agonist (brimonidine) or topical carbonic anhydrase inhibitor (dorzolamide) as needed.

Aspirin and NSAIDs are contraindicated because they inhibit platelet aggregation and increase rebleeding risk. This is a frequent test point.

Sickle cell patients require a modified algorithm. Acetazolamide is avoided because it lowers aqueous pH and promotes intraocular sickling, paradoxically raising IOP. Mannitol is also problematic because it causes hemoconcentration and dehydration, worsening sickling. The threshold for surgical intervention is much lower in these patients: IOP greater than 24 mmHg for more than 24 hours is generally accepted as an indication for washout in sickle patients, compared to the much higher thresholds used in non-sickle patients.

Antifibrinolytic therapy with oral aminocaproic acid (50 mg/kg every 4 hours, maximum 30 g/day, for 5 days) or tranexamic acid stabilizes the clot at the bleeding site and reduces rebleeding. Its use varies by institution and is not universal.

Surgical anterior chamber washout is the next best step when medical management fails. Indications include:

IOP greater than 50 mmHg for 5 days, or greater than 35 mmHg for 7 days (non-sickle patients)
IOP greater than 24 mmHg for more than 24 hours in sickle cell patients
Total ("eight-ball") hyphema persisting beyond 5 days
Early corneal blood staining (any duration)
Failure of the hyphema to clear within 9 days, raising concern for peripheral anterior synechiae

The "next best step" logic on a vignette typically follows this hierarchy: rule out globe rupture first, then shield and elevate, then start topical cycloplegic and steroid, then add IOP control, then escalate to washout if criteria are met.

Long-term follow-up includes gonioscopy at 4 to 6 weeks to evaluate for angle recession, which can cause delayed-onset glaucoma even years later. All patients should be counseled on lifelong eye protection, especially during sports.

5. Differential Diagnosis & Distractors

Differential Diagnosis	Why It's Similar	Key Discriminator
Subconjunctival hemorrhage	Red blood visible in the eye after trauma	Blood is under the conjunctiva (on the surface, sclera), not inside the anterior chamber. Vision is normal, no pain
Hypopyon	Layered material in the anterior chamber	The layered material is white or yellow (pus), not red. Suggests endophthalmitis, severe iritis, or Behcet disease
Globe rupture	Trauma, eye pain, decreased vision	Peaked or teardrop pupil, positive Seidel sign, prolapsed uveal tissue, low IOP, 360-degree subconjunctival hemorrhage. Surgical emergency
Traumatic iritis (anterior uveitis)	Post-traumatic eye pain, photophobia, ciliary flush	Slit lamp shows cells and flare without frank layered blood. May coexist with hyphema
Retrobulbar hematoma	Post-traumatic vision loss	Proptosis, restricted extraocular movement, elevated IOP, no anterior chamber blood. Requires emergent lateral canthotomy
Orbital floor (blowout) fracture	Trauma history, eye involvement	Enophthalmos, restricted upgaze (entrapment of inferior rectus), infraorbital numbness, no AC blood unless concurrent hyphema
Vitreous hemorrhage	Decreased vision, trauma or diabetes	Blood is in the posterior segment. Loss of red reflex on fundoscopy, no AC layering
Corneal abrasion	Trauma, pain, photophobia, tearing	Fluorescein staining of the cornea, no AC blood, normal vision
Endophthalmitis with hypopyon	Layering in anterior chamber, post-surgical or post-trauma	Yellow-white layering (pus), severe pain, conjunctival injection, often days after surgery

6. Traps & High-Yield Pearls

The single biggest trap in hyphema vignettes is failing to screen for sickle cell disease or trait before choosing treatment. A vignette describing a young Black male with a basketball injury and a small hyphema is rarely about the hyphema itself; it is testing whether you will recognize the need for sickle screening and the contraindication to acetazolamide and mannitol. Choosing acetazolamide in a sickle patient is one of the fastest ways to lose a question.

The second classic trap is timing of rebleeding. Vignettes describing a patient who returns on day 3 to 5 with worsening vision and a larger hyphema are testing recognition of the rebleed window. This is also why aspirin and NSAIDs are forbidden, and why activity restriction matters even in mild cases.

A third trap is mistaking hypopyon for hyphema. Both layer in the anterior chamber, but hypopyon is white or yellow (pus) and signals infection or inflammation, while hyphema is red (blood) and signals trauma or vascular disease. Read the color descriptor in the vignette carefully.

A fourth trap is applying a pressure patch to a possible globe rupture. Any vignette with a peaked pupil, positive Seidel sign, or 360-degree subconjunctival hemorrhage demands a rigid shield and emergent surgical referral, not eye drops.

Finally, do not forget delayed angle-recession glaucoma. A patient with a remote history of blunt eye trauma who now presents with gradual unilateral vision loss and elevated IOP years later is being tested on the long-term sequela of hyphema.

The core competency being tested is recognizing hyphema as a stratified emergency: identify the grade, rule out globe rupture, screen for sickle cell, control IOP, prevent rebleeding, and know the surgical thresholds. Mastering the sickle cell modification and the rebleeding window will resolve the majority of hyphema questions you will encounter.

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