Ophthalmology – Uveitis-Glaucoma-Hyphema Syndrome

What the Syndrome Represents

Uveitis-glaucoma-hyphema (UGH) syndrome is a secondary inflammatory and hemorrhagic glaucoma caused by repetitive mechanical contact between an intraocular lens (IOL) or its haptics and adjacent uveal tissue.

The classic triad is:

• Anterior uveitis
• Elevated intraocular pressure
• Hyphema or microhyphema

The central mechanism is:

IOL-related chafing of the iris or ciliary body → pigment and blood release → inflammation → trabecular obstruction → raised IOP.

Why the Syndrome Has Changed With Modern Cataract Surgery

Historically, UGH was most strongly associated with:

• Iris-supported lenses
• Closed-loop anterior chamber IOLs

These lenses are now rarely used.

Modern UGH more often results from:

• Malpositioned posterior chamber IOLs
• Sulcus placement of an inappropriate IOL
• Subluxated IOL-bag complexes
• Haptic contact with the posterior iris
• Capsular-bag instability

Therefore UGH should not be considered exclusively a complication of old anterior chamber lenses.

Which IOL Situations Carry the Greatest Risk

Important mechanical settings include:

• Posterior chamber IOL haptic in the sulcus
• Single-piece acrylic IOL inadvertently positioned in the ciliary sulcus
• Tilted IOL
• Decentered IOL
• Subluxated capsular bag–IOL complex
• Iris-fixated IOL
• Malpositioned anterior chamber IOL
• Broken or displaced haptic

Why Single-Piece Acrylic IOLs Are Problematic in the Sulcus

Single-piece acrylic lenses generally have:

• Thick haptics
• Square-edged optics
• Relatively bulky design

If placed in the sulcus, they can repeatedly rub against the posterior iris and produce:

• Pigment dispersion
• Iris transillumination
• Chronic inflammation
• Recurrent microhyphema
• Elevated IOP

This is an important modern cause of UGH.

In-the-Bag UGH

UGH can even occur when the IOL is technically:

Inside the capsular bag.

Possible mechanisms include:

• Zonular weakness
• Pseudoexfoliation
• Capsular contraction
• Bag-IOL complex subluxation
• Soemmering ring formation
• Progressive IOL tilt

These changes can bring the lens or haptic into contact with the iris or ciliary body.

Why Pseudoexfoliation Matters

Pseudoexfoliation predisposes to:

• Zonular weakness
• Delayed IOL-bag complex instability
• Lens decentration
• Subluxation

This can create delayed-onset UGH many years after apparently uncomplicated cataract surgery.

When UGH Can Appear

Symptoms may begin:

• Soon after cataract surgery
• Months later
• Years or even decades after implantation

Delayed presentation is particularly common when the cause is:

• Progressive zonular failure
• Capsular contraction
• Late IOL subluxation

What Patients Usually Notice

Symptoms may be intermittent.

Common complaints include:

• Episodes of blurred vision
• Ocular redness
• Ache or discomfort
• Photophobia
• Halos
• Transient reduction in vision

Some patients notice symptoms after:

• Exercise
• Eye rubbing
• Certain head positions

because these may increase IOL-iris contact.

Why Vision May Fluctuate

Transient blur may result from:

• Microhyphema
• Anterior chamber inflammation
• IOP elevation
• Corneal edema
• IOL decentration

Blood may settle rapidly, so the eye can appear relatively quiet between attacks.

The Classic Examination Pattern

Typical findings include:

• Anterior chamber cells
• Pigment
• Elevated IOP
• Microhyphema or frank hyphema
• Iris transillumination defects
• IOL decentration or tilt
• Pigment on the IOL

Not every patient demonstrates the complete triad at every visit.

Microhyphema Can Be Easy to Miss

A patient may have only:

• A few circulating erythrocytes
• Inferior red blood cells
• No visible layered hyphema

Careful slit-lamp examination may therefore be necessary to detect:

Recurrent microbleeding.

Iris Transillumination Defects

Repeated haptic or optic contact can abrade the posterior iris pigment epithelium.

This produces:

• Focal or arcuate iris transillumination defects
• Pigment dispersion
• Pigment on the lens surface

The location of the defect may help identify the site of mechanical contact.

Gonioscopy

Gonioscopy is useful for detecting:

• Blood in the angle
• Heavy trabecular pigmentation
• Peripheral anterior synechiae
• Iris or angle neovascularization
• A malpositioned haptic in selected cases

It is particularly important for excluding:

Neovascular glaucoma.

Why UBM Is So Useful

Ultrasound biomicroscopy (UBM) is one of the most valuable tests when the offending IOL-haptic relationship cannot be seen directly.

It can demonstrate:

• Haptic-iris contact
• Haptic-ciliary body contact
• IOL tilt
• Sulcus malposition
• Capsular bag displacement
• Zonular abnormalities

Anterior Segment OCT

Anterior segment OCT may also help evaluate:

• IOL position
• Iris configuration
• Anterior haptic relationships

However, UBM is often superior for structures located:

Behind the iris.

Why the Optic Nerve Must Also Be Evaluated

Repeated or sustained IOP elevation may produce:

Secondary glaucomatous optic neuropathy.

Evaluation should therefore include:

• Optic disc examination
• RNFL OCT
• Macular ganglion cell analysis
• Automated visual fields

Other Retinal Complications

UGH may be associated with:

• Cystoid macular edema
• Vitreous hemorrhage
• Epiretinal membrane in chronic inflammation

The term UGH-plus syndrome is sometimes used when posterior segment complications such as vitreous hemorrhage or CME are present.

OCT of the Macula

Macular OCT is useful when visual loss is greater than expected from:

• IOP
• Hyphema
• IOL position

It can identify:

Cystoid macular edema, a recognized complication of chronic IOL irritation.

Important Diagnostic Alternatives

Recurrent inflammation, hyphema, and elevated IOP in a pseudophakic eye can also result from:

• Neovascular glaucoma
• Uveitic glaucoma
• Retained lens material
• Chronic postoperative endophthalmitis
• Pigment dispersion from another mechanism
• Ghost-cell glaucoma
• Trauma
• Iris or ciliary body tumor
• Carotid-cavernous fistula
• Swan syndrome

Why Neovascular Glaucoma Must Be Excluded

Neovascular glaucoma can produce:

• Elevated IOP
• Hyphema
• Anterior inflammation

Look carefully for:

• Neovascularization of the iris
• Neovascularization of the angle
• Retinal ischemic disease

The underlying management is completely different from UGH.

Swan Syndrome

Swan syndrome refers to recurrent hyphema arising from abnormal vessels at a previous surgical wound.

It may also produce elevated IOP.

Unlike UGH, the bleeding source is typically:

Vascularization at the corneoscleral wound, rather than IOL chafing.

Chronic Postoperative Endophthalmitis

Low-grade infection after cataract surgery may cause:

• Persistent or recurrent anterior uveitis
• Reduced vision
• Sometimes elevated IOP

Clues include:

• Capsular plaque
• Chronic inflammation not clearly related to mechanical contact

This must be considered before attributing recurrent inflammation solely to UGH.

First Management Goal

The initial objectives are:

1. Control inflammation
2. Lower IOP
3. Control hyphema
4. Identify the mechanical cause

Medical therapy is usually:

Temporizing rather than definitive.

Treating the Inflammation

Topical corticosteroids such as:

Prednisolone acetate

can suppress anterior segment inflammation.

The dose depends on:

• Degree of uveitis
• Corneal status
• IOP

Prolonged steroid therapy without correcting the mechanical problem is usually inadequate.

Role of Cycloplegia

Cycloplegic agents may be used when there is:

• Painful anterior uveitis
• Posterior synechiae
• Significant ciliary spasm

Examples include:

• Cyclopentolate
• Atropine in more severe cases

Routine atropine is not necessary in every UGH presentation.

Lowering the IOP

Aqueous suppressants are commonly used first:

• Beta-blocker
• Topical carbonic anhydrase inhibitor
• Alpha-2 agonist

Systemic acetazolamide can be added for:

More substantial pressure elevation.

Prostaglandin Analogues

Prostaglandin analogues may also lower IOP effectively.

During marked active inflammation or CME, many clinicians initially favor other agents, but prostaglandins are:

Not absolutely contraindicated.

They may be useful in chronic pressure management when appropriate.

Hyperosmotic Therapy

For severe acute IOP elevation, hyperosmotic therapy such as:

IV mannitol

may occasionally be required.

This is reserved for significant pressure elevation rather than routine UGH.

Managing the Hyphema

Management may include:

• Activity limitation
• Head elevation
• Control of inflammation
• Control of IOP

Large or persistent hyphema may occasionally require:

Anterior chamber washout.

Anticoagulants and Antiplatelet Drugs

Anticoagulation can increase the severity or persistence of bleeding from mechanically traumatized iris vessels.

However:

Do not discontinue medically necessary anticoagulant or antiplatelet therapy solely because of UGH without coordination with the prescribing physician.

If anticoagulation is excessive, appropriate laboratory assessment may be indicated.

Why Medical Therapy Often Fails Long Term

Steroids and glaucoma drops treat the:

Consequences

of UGH.

They do not eliminate:

Mechanical IOL-uveal contact.

If rubbing continues, inflammation and hemorrhage tend to recur.

Definitive Treatment

The definitive treatment is:

Elimination of the offending IOL-iris or IOL-ciliary body contact.

This may require:

• IOL repositioning
• Haptic repositioning
• IOL exchange
• Removal of the IOL
• Capsular bag stabilization in selected cases

IOL Repositioning

Repositioning may be appropriate when:

• The existing IOL is suitable
• Malposition can be reliably corrected
• Capsular or zonular support is adequate

Possible strategies include:

• Repositioning into the capsular bag
• Scleral fixation
• Iris fixation in selected anatomy

IOL Exchange

Exchange is favored when:

• The IOL design is inappropriate for its location
• A single-piece acrylic lens is in the sulcus
• Haptic damage is present
• Repositioning cannot reliably eliminate contact

Replacement options depend on remaining support.

What Can Replace the Offending Lens

Depending on anatomy, options may include:

• Posterior chamber IOL in the bag
• Three-piece sulcus IOL
• Scleral-fixated posterior chamber IOL
• Iris-fixated lens
• Selected modern anterior chamber IOL

Choice is individualized.

Role of Anterior Chamber Washout

Washout may be indicated for:

• Persistent significant hyphema
• Uncontrolled IOP from blood
• Corneal blood staining risk
• Simultaneous IOL revision

It does not provide definitive treatment if the mechanical source remains.

Is Laser Ablation Still Important?

Older reports described argon laser ablation of isolated bleeding vessels.

This is now:

An uncommon and highly selected treatment.

Modern management usually focuses on correcting the underlying mechanical IOL problem rather than repeatedly treating secondary bleeding vessels.

What If Glaucoma Persists After IOL Correction?

Some eyes develop permanent trabecular damage from:

• Chronic pigment deposition
• Repeated hemorrhage
• Longstanding inflammation

IOP may therefore remain elevated even after mechanical correction.

These patients may need:

• Glaucoma medications
• Laser in selected anatomy
• Trabeculectomy
• Glaucoma drainage device
• Other glaucoma procedures

Why the Mechanical Cause Should Usually Be Corrected First

When feasible, correcting the IOL problem before glaucoma surgery is logical because:

Continued iris chafing can perpetuate inflammation, bleeding, and surgical failure.

Glaucoma surgery is then reserved for persistent pressure elevation.

Follow-Up During Active Disease

Initial follow-up depends on:

• IOP
• Amount of hyphema
• Severity of inflammation
• Corneal edema
• Optic nerve status

Significant pressure elevation may require:

Review within hours to days.

Long-Term Monitoring

After treatment, monitor:

• IOP
• Anterior chamber inflammation
• Recurrent hyphema
• IOL position
• Optic nerve
• Visual fields
• Macular OCT when indicated

Recurrence suggests persistent:

Mechanical contact or renewed IOL instability.

Expected Outcome

Prognosis is generally good when UGH is:

• Recognized early
• Correctly attributed to IOL contact
• Definitively treated before substantial optic nerve damage occurs

Visual outcome is worse when there is:

• Advanced glaucoma
• Chronic CME
• Corneal damage
• Recurrent vitreous hemorrhage
• Delayed diagnosis

Major Complications

Potential complications include:

• Secondary glaucoma
• Permanent glaucomatous visual-field loss
• Recurrent hyphema
• Chronic anterior uveitis
• Cystoid macular edema
• Vitreous hemorrhage
• Corneal edema
• Progressive visual impairment

High-Yield Takeaways

• UGH syndrome is caused by mechanical chafing of the iris or ciliary body by an IOL or its haptics, producing uveitis, hyphema, and elevated IOP.
• The entire triad does not need to be present simultaneously; recurrent microhyphema or pigment dispersion may be the only clue at a particular visit.
• Historically associated with old anterior chamber lenses, modern UGH more often occurs with malpositioned, subluxated, or incorrectly positioned posterior chamber IOLs.
• A single-piece acrylic IOL in the ciliary sulcus is a particularly important modern cause because its thick haptics and square optic edge can chronically abrade the posterior iris.
• UGH can occur even with an in-the-bag IOL, especially when pseudoexfoliation, zonular weakness, capsular contraction, or late bag-IOL subluxation develops.
• Examination may reveal microhyphema, anterior chamber cells, pigment, iris transillumination defects, and elevated IOP.
• Gonioscopy helps identify angle blood, pigmentation, haptic abnormalities, and—critically—exclude iris or angle neovascularization.
• Ultrasound biomicroscopy is especially valuable for demonstrating hidden haptic-iris or haptic-ciliary body contact.
• Macular OCT should be considered because chronic UGH may produce cystoid macular edema.
• Initial treatment consists of topical corticosteroids, appropriate cycloplegia, and IOP-lowering therapy, but this is usually temporary.
• Anticoagulants can worsen bleeding but should not be stopped automatically without considering the systemic indication.
• The definitive treatment is removal of the mechanical cause, usually by IOL repositioning or exchange.
• Argon laser treatment of bleeding vessels is now a rarely used selected intervention, not the usual definitive strategy.
• If glaucoma persists after IOL correction, chronic trabecular damage may require long-term medications or glaucoma surgery.
• In any pseudophakic patient with recurrent unexplained iritis, hyphema, pigment dispersion, or unilateral elevated IOP, carefully reassess the IOL position and its relationship to the iris and ciliary body.