Uveitis Glaucoma Hyphema Syndrome

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Continuing Education Activity

Uveitis glaucoma hyphema (UGH) syndrome is a relatively rare clinical condition characterized by chronic postoperative inflammation, high intraocular pressure, and hemorrhage in the anterior chamber in an eye that has undergone cataract surgery with intraocular lens (IOL) implantation. The condition was described in association with the closed-loop anterior chamber intraocular lenses, but the condition has also been described in eyes with modern intraocular lenses. The cause of inflammation is usually the IOL causing irritation to the iris and other intraocular structures. This activity reviews the cause and mechanisms of the development of UGH syndrome, with a detailed review of required medical and surgical management.


  • Describe the pathophysiology of UGH syndrome.
  • Review the clinical features found in the evaluation of UGH syndrome.
  • Summarize the different management options of UGH syndrome.
  • Outline the role of interprofessional collaboration to improve the outcomes in UGH syndrome.


Uveitis glaucoma hyphema (UGH) syndrome or Ellingson syndrome is a complication of intraocular lens implantation where chafing from the implants leads to a spectrum of iris transillumination defects and hyphema with raised intraocular pressure and pigment dispersion.[1] 

F T Ellingson described the UGH syndrome as a late complication of Choyce Mark VII and VIII rigid anterior chamber intraocular lens (ACIOL) implantation in 1978. It can also occur with the posterior chamber intraocular lenses placed in the sulcus causing posterior iris chafing by the loop or the optic. It occurs more commonly with planar loop design than with angulated loops.[2] 

It can develop immediately or over the years, causing a decreased vision in the affected eye. It may present with transient vision loss or the gradual diminution of vision. The eye may appear congested with an increase in intraocular pressure. Blood/clotted blood in the inferior anterior chamber angle and anterior chamber reaction may be present. If untreated, it may lead to glaucomatous optic neuropathy.[1][3]

A careful history and examination, as well as appropriate investigations, can confirm the diagnosis. Ultrasound biomicroscopy is the most reliable investigation to label it as UGH Syndrome. Other evaluation methods include slit-lamp examination, gonioscopy for the visualization of the angles, intraocular pressure measurement, ultrasound brightness (B) scan to visualize the posterior segment in case of vitreous hemorrhage, and optical coherence tomography to visualize both anterior and posterior segments.[4][5][6] Treatment options include intraocular lens explantation or exchange, topical corticosteroids, and cycloplegics.[7]


The UGH syndrome is most commonly caused by rubbing of the iris from the anterior chamber intraocular lenses but can occur from any type of pseudophakic lens.[8] Ellingson noted that Choyce Mark VII and Choyce Mark VIII ACIOLs had warped edges of the footplate which caused injury to the iris root by a rocking motion. This resulted in recurrent ocular inflammation, high intraocular pressure (IOP), and bleeding in the anterior chamber. Removal of the implant usually results in the resolution of the condition.[9] 

The complication was associated with the copies of lenses that had lenses polished on a substandard level with sharp edges at the footplates. Azar 91z model ACIOL (flexible closed-loop ACIOL) implantation was associated with complications because of the problems of design and manufacturing causing sharp edges, vaulting, excess movements, and irritation of ocular tissue.[10][11] 

Iris-supported IOL with metal loops has been reported to cause UGH syndrome. The Kelman multiflex ACIOL (flexible open-loop ACIOL) has an anterior vault to avoid rubbing the iris in the correct configuration. When Kelman multiflex ACIOL is implanted incorrectly ('upside-down lens syndrome), corneal edema increased IOP, cystoid macular edema (CME), and UGH syndrome may occur.[12][13] 

MA50 intraocular lenses placed in the sulcus were associated with complications like UGH syndrome.[14] Other iris-supported intraocular lenses like iris clamp lenses are causative of UGH syndrome.[15]

Lenses with imperfect construction, imperfectly positioned lenses, or improperly sized lenses may cause chafing.[16] A few cases have been seen with the scleral fixated intraocular lenses.[17] Among the scleral fixated lenses, the ab externo approach of hydrophobic acrylic lenses with suture burial technique and even the glued scleral fixated lenses have been shown to cause UGH syndrome as a complication.[18][19] 

Besides this, the technique of scleral fixation with friction knots using single-piece lenses showed a risk of UGH syndrome.[20] Other surgical devices, like iris implants, capsular tension rings, and glaucoma filtration devices, have been implicated as a source of mechanical irritation. Among the intraocular lenses, it can occur with scleral fixated lenses, single-piece acrylic intraocular lenses implanted in the sulcus, or sulcus fixated three-piece lenses, and even with the implantation of a single-piece acrylic lens in the bag.[21][22][23] 

Iris transillumination defects may be noted at the area of iris chafing. Single-piece IOL in the capsular bag may be associated with UGH syndrome in pseudoexfoliation syndrome (pseudophacodonesis due to zonular laxity resulting in chafing of the posterior iris surface and focal capsular fibrosis around the haptic causing iris touch), plateau iris syndrome (with anterior rotation of ciliary processes), and intensive facedown position in yoga with pseudophacodonesis secondary to pseudoexfoliation.[24][25] 

Almost all intraocular implants may be associated with UGH syndrome, including retropupillary iris-claw IOL, iris-sutured IOL, placement of single-piece PCIOL (posterior chamber IOL), or multipiece PCIOL in the anterior chamber, express mini glaucoma shunt, and cosmetic iris implants.[26] Systemic anticoagulation may predispose to UGH syndrome.[27] An extensive series comprised of 71 patients with UGH syndrome noted that pseudophacodonesis was a risk factor for UGH syndrome. Their analysis showed that blood thinners did not increase the risk of UGH syndrome.[28] 

There are reports of late-onset UGH syndrome associated with the Soemmering ring cataract, causing an anterior shift of sulcus-fixated leading to iris-haptic touch.[29] Sulcus implantation of single-piece foldable acrylic PCIOL may be associated with UGH syndrome.[30][31] However, Taskapili and colleagues showed that implantation of foldable acrylic PCIOL in the sulcus might have good visual outcomes, an acceptable complication profile, and good centration.[32][30]


The incidence of UGH syndrome has reduced since strict control of the quality of IOLs, refined material for manufacture, and improvement of the manufacturing techniques and lens design.[33] The iris-ciliary touch by the footplates or haptics of IOLs is believed to play a pivotal role in the pathogenesis of the syndrome, including the possible release of inflammatory mediators. The term was originally described in 1977 by Ellingson. The UGH syndrome is most commonly seen in adults but can be seen after pediatric cataract surgery.[34] 

The incidence of UGH syndrome has declined over the years from 2.2 to 3% to 0.4 to 1.2% over one year. The use of first-generation anterior chamber intraocular lenses has been most commonly linked to the development of UGH syndrome, though even single-piece IOL in the capsular bag can cause the syndrome. Though UGH syndrome has been reported usually in adults, it can happen after pediatric cataract surgery also. Lin and colleagues reported a child with anterior migration of the optic of the PCIOL causing UGH syndrome, which subsided after removal of the PCIOL.[35]


The UGH syndrome appears to arise from the repetitive mechanical iris or ciliary body trauma by a malpositioned or subluxated lens.[23] The exact pathology of UGH syndrome is not known, but some hypotheses were made over time. It is believed that there is an activation of innate immunity viz. cytokines, eicosanoids synthesis by mechanical trauma to the iris by the optics or haptics; complement or fibrin activation by the intraocular lens. There is the adherence of bacteria (avirulent bacteria- similar to that found in postoperative endophthalmitis) and leukocytes to the IOL surface.[36] 

The surface of intraocular lenses, especially PMMA (polymethyl methacrylate), activates the plasma-derived enzymes. The contaminants may cause toxicity on the IOL surface during manufacturing. Poorly manufactured edges, iris-claw intraocular lenses, or rigid closed-looped lenses were more prone to cause iris chafing, but the newer generations of lenses have reduced their risk due to their better designs, fabrications, and improved surgical techniques.[37] Unauthorized, poorly manufactured copies of Choyce Mark lenses were the usual culprit rather than the properly manufactured and sized original Choyce Mark lenses.[38] 

Poor finish of the edges (serrated, sharpened, or uneven), warped footplates, imperfect polishing, and finishing of injection-molded intraocular lenses lead to the mechanical excoriation of the iris, which increased the risk of the UGH Syndrome.[39] The recurrent hyphema is thought to occur from recurrent mechanical trauma to the angle of the anterior chamber, the iris, or the ciliary body—disruption of the blood-aqueous barrier results in uveitis. The increased IOP may be caused by various factors, including hyphema, uveitis, pigment dispersion, direct damage to the angle of the anterior chamber, and steroid response from the steroid drops used to treat the syndrome.

The UGH syndrome was originally reported with ACIOLs. Material, edges of the implant, manufacturing process, and quality control are important factors influencing the occurrence of the UGH syndrome. The ACIOL should be properly sized (ACIOL diameter= horizontal white to white diameter in mm + 1 mm).[40]

Smaller ACIOLs are unstable and may rotate or tilt, causing damage to the anterior segment structures. A larger ACIOL causes damage to the angle, and the vault may touch and decompensate the corneal endothelium.

PCIOLs placed in the sulcus may irritate the posterior iris surface and cause UGH syndrome. Specifically, single-piece acrylic PCIOLs with square optic edges and thick square haptics or small uniplanar haptics may rub the posterior pigmented surface of the iris. Multi-piece PCIOL with posterior angulation (causing a posterior shift of the optic), smooth optic surface, and round edges is preferred for placement at the ciliary sulcus.[30] The position and size of the PCIOL are also crucial for the placement of a sulcus IOL.


The optic of the IOL may be covered with a thick membrane composed of inflammatory cells, fibrosis, and red blood corpuscles (RBCs). The optic may get discolored and have brownish color due to the deposition of hemoglobin from RBCs. The inflammatory deposits are usually more severe at the margin of the optic, and the inflammatory debris may cover the whole IOL optic.[38]

The debris may get deposited on the haptic or footplate as well. The inflammatory debris and RBCs may cover the whole IOL optic totally or partially, forming a ‘cocoon membrane.’[41] The junction of the optic and haptic in multipiece IOL forms a nidus for inflammatory deposits.

History and Physical

The UGH syndrome is a complication of cataract surgery. The UGH syndrome may occur after uneventful ocular surgery or after an ocular surgery with intraoperative complications resulting in malposition of the implant. Patients usually present with episodes of blurred vision weeks to months after surgery. The blurring of vision may be accompanied by pain, photophobia, erythropsia (apparent reddish hue of the visible objects), and redness in the eyes. The vision is blurred, but complete vision loss is usually not seen unless accompanied by advanced glaucoma. The patient often presents with intermittent white-out of vision or intermittent decreased vision.[3] Usually, there are multiple acute episodes of blurred vision or pain in cases with UGH syndrome.

There are a few variations of UGH Syndrome, including UGH Plus and IPUGH (Incomplete Posterior UGH) syndrome. UGH Plus includes vitreous hemorrhage with UGH seen with anterior chamber lenses with iris support posterior chamber lenses placed in the sulcus or the capsular bag.[23] There is a communication between the vitreous cavity and the anterior chamber through the anterior hyaloid face, whose integrity is disrupted after surgery, spontaneously or due to degenerative changes. This causes the passage of blood and gives rise to the simultaneous bleed in both the anterior chamber and the vitreous cavity. IPUGH syndrome is bleeding into the posterior chamber (usually in between the IOL and the posterior capsule, similar to endocapsular hematoma or 'in-the-bag hyphema') without uveitis. Some cases of IPUGH syndrome may have glaucoma.[42]

Slit-lamp examination shows conjunctival congestion, anterior chamber cells, and the presence of microscopic hyphema. Sometimes macroscopic hyphema is visible even without a slit lamp. Due to the endothelial touch by an intraocular lens, corneal edema may be noted.[43] 

Keratic precipitates may be seen over the corneal endothelium. Transillumination defect in the iris may be seen at the area of repetitive uveal trauma by the implant. C or J-shaped haptics typically create an arcuate transillumination defect. 'Iris transillumination defect and microhyphema syndrome' has been described with implantation of PCIOLs with 'elliptical polypropylene haptics containing a 10 degrees anterior angulation' in the sulcus.[44] 

Transillumination defects may also be seen in multiple other disorders causing iris atrophy and may not be a specific sign of the UGH syndrome.[28] About 5-15% of patients with PCIOL in the sulcus have iris-transillumination defects at the peripheral 1/2 or 2/3rds of iris due to rubbing by the IOL optic. Around 1% of the patients may have an IOL-induced hemorrhage.[44]

Sometimes neovascularization of the iris can be seen. A poorly positioned optic or haptic of IOL or other implant causing visible mechanical trauma to the uveal tissue is usually observed. Other slit-lamp findings include pigments on the corneal endothelium, posterior synechia, inflammatory deposits over the optic or haptic of the IOL, and pseudophacodonesis. Blood in the angle or within the trabecular meshwork can be visualized with the help of gonioscopy. Gonioscopy can also aid in finding the haptic that may have caused the anterior chamber angle structure erosion and may also help visualize blood in the trabecular meshwork between the attacks. Gonioscopy in dilated pupils may be used to locate the exact location of the haptics of an IOL and to identify areas of uveal touch by the implant.[45]

A slit-lamp examination may also help visualize and quantify anterior chamber cells, flare, vitreous cells, or any deposits over the intraocular lens. PCIOL placed in the sulcus may cause reverse pupillary block characterized by posterior bowing of the iris, transillumination defects of the iris, pigment dispersion syndrome, increased pigmentation of the anterior chamber angle, increased IOP, and uveitis. This is especially seen in axial myopia and vitrectomized eyes.[46] In addition, fundus examination should be done using a 90D lens. Indirect ophthalmoscopy using a 20D lens should be used to examine the peripheral retina. The optic nerve examination is of paramount importance to identify the retinal nerve fiber layer defects and other evidence of glaucomatous damage.


Anterior segment photograph helps document the disease, monitor the response to therapy, and counsel the patient. Ultrasound biomicroscopy (UBM) is helpful in the diagnosis of UGH Syndrome as it may be used to confirm the position of haptics and optics and their relationship with surrounding ocular structures.[47] 

It may also be used to visualize the malpositioned intraocular lenses and their proximity to uveal tissue. Anterior segment optical coherence tomography can also be used to visualize the anterior chamber angle structures as it is non-invasive. If the structures are not seen with (AS-OCT), then UBM can be done.

Cosmetic iris implants may lead to uveitis hyphema glaucoma syndrome, and corneal decompensation, so specular microscopy helps evaluate the corneal endothelial status by providing the endothelial counts and morphology of the cells.[21] Central corneal thickness also helps to quantitate corneal edema, which is often associated with the UGH syndrome. Ultrasound brightness Scan (B Scan) is helpful in the diagnosis of atypical UGH syndrome cases which present with vitreous hemorrhage.[47] 

Glaucoma evaluation can be performed by gonioscopy, central corneal thickness, perimetry, and optical coherence tomography of the optic nerve. All the other causes of uveitis need to be ruled out. An individualized approach should be used to investigate such cases. It may include complete blood count, erythrocyte sedimentation rate, serology for human immunodeficiency virus (HIV), Mantoux test, chest X-ray, X-ray of the spine, and lumbosacral joint both anterior-posterior and lateral views, and autoimmune antibody assays.[48] 

Optical coherence tomography of the macula can be used to detect cystoid macular edema in UGH cases. Fundus fluorescein angiography helps to rule out the other causes of vitreous hemorrhage or iris new vessels.[49] A coagulation profile and a history of anticoagulant medications should be sought in cases with recurrent hyphema in UGH syndrome.

Treatment / Management

In patients with UGH Syndrome, intraocular pressure needs to be reduced using topical and systemic medications. Antiglaucoma medications and corticosteroids are used to lower intraocular pressure and control the anterior segment inflammation.[50] 

Inflammation needs to be controlled with the use of topical steroids. The dosage and the type of steroid preparation are selected based upon the diffusion across the cornea and potency of the preparation.[51] Adjuvant therapy in the form of non-steroidal anti-inflammatory drugs and cycloplegics is also helpful in relieving ciliary spasm and inflammation. These medications bring symptomatic relief to the patient. Cycloplegics need to be added for relieving ciliary spasms and iris sphincter spasms.

Miotics (including pilocarpine) should be avoided as they increase the mechanical chaffing of the iris. In sulcus placed PCIOLs causing reverse pupillary block leading to UGH Syndrome, laser peripheral iridotomy may help.[46] Depending upon the cause of the UGH Syndrome, the treatment modality changes from patient to patient.[52]

Specific treatment may be offered in patients where the cause is localized. In patients with Express shunts, localized iris chaffing might be managed with laser iridoplasty. Rarely, if an iris blood vessel is found to be the source of bleeding, an argon/ neodymium-doped yttrium aluminum garnet (Nd YAG) laser can be used to stop the bleed. Special concern is necessary for myopic, vitrectomised patients presenting with the signs and symptoms of UGH syndrome. Those with raised intraocular pressure due to the concavity of iris or reverse pupillary block may be treated with peripheral laser iridotomy only.[53][54]

Intraocular lens exchange, explant, repositioning, or amputation of IOL haptic should be performed if the inflammation is not controlled medically and the vision is reduced. Intraocular lens exchange is the definitive treatment of UGH Syndrome where there is no other pathology responsible for the signs and symptoms of the patient. Also, inflammation is not controlled with medical management only.[28] Explanation of the IOL may not be needed in cases with IPUGH syndrome.[42] The UGH syndrome is one of the most common indications (around 12%) of IOL exchange.[55]

Suturing the haptics of in-the-bag IOL to the iris in an eye with pseudophacodonesis may successfully resolve the associated UGH syndrome.[56] Intracameral injection of an anti-vascular endothelial growth factor (anti-VEGF) agent bevacizumab has been shown to reduce the frequency of acute attacks of UGH syndrome. Intracameral bevacizumab may also cause regression of iris neovascularization and reduce the inflammatory macular edema.

Differential Diagnosis

 The differential diagnoses include:

  • Trauma - The UGH syndrome might be confused with blunt trauma to the eye in patients with hyphema and anterior segment inflammation. History is important to distinguish between the two.[57] Also, traumatic cases have other signs of ocular trauma.
  • Inflammatory glaucomas- Rubeosis iridis may be present. A history of surgery may or may not be there.[7] Other signs of uveitis are present.
  • Hyphematous conditions - Vascular abnormalities, iris tufts, varices causing bleed may be confused with UGH syndrome. Herpes zoster and herpes simplex uveitis may be associated with hyphema.
  • Retinal vascular occlusions (especially central retinal venous occlusion) should be ruled out in cases with iris new vessels and neovascular glaucoma.
  • Coagulation disorders and sickle cell disease should be excluded in cases with UGH syndrome.[58]
  • Uveitis - Usually, uveitis can be controlled well by using corticosteroids and cycloplegics. In inflammation due to UGH syndrome, patients' signs and symptoms persist even after using topical corticosteroids and cycloplegics.[59][60]
  • Retinoblastoma - Few cases may present as hyphema in the late stages. 
  • Chronic postoperative endophthalmitis - It needs to be differentiated as the patient presents with similar complaints. Initially, there is relief in the symptoms using topical or systemic corticosteroids.[61][62] The presence of hyphema and uveal touch by the implant with transillumination defects in the iris favors the diagnosis of UGH syndrome.


Though UGH syndrome may be managed conservatively, surgery with explantation of the implants is usually curative. Surgery, however, may not guarantee the resolution of UGH syndrome. Rigid anterior chamber intraocular lenses were used around in the 1950s. Bullous keratopathy, cystoid macular edema, and inflammation were very common at that time. Today, the use of polymethyl methacrylate lenses, acrylic, and silicone lenses with better designs and quality have reduced the complications. In a large series of 71 patients with UGH syndrome, the patients treated surgically achieved better final visual acuity and lower IOP, while the conservatively treated patients did not experience improved visual acuity or reduced IOP.[28]


The complications of UGH syndrome include:

  • Corneal Staining- Long-standing hyphema causes corneal staining. It usually occurs with hyphema and raised intraocular pressure. It starts from the periphery of the cornea and grows centripetally.[12]
  • Chronic inflammation may be noted and lead to posterior synechia or peripheral anterior synechia.
  • Pseudophakic bullous keratopathy- Endothelial damage due to constantly raised intraocular pressure, damage by the implant itself, and inflammation can result in endothelial pump failure leading to pseudophakic bullous keratopathy that might ultimately need penetrating or endothelial keratoplasty.
  • Vitreous hemorrhage may be noted in a few cases of UGH syndrome where there is a communication between the anterior and posterior segments (posterior capsular rent or defect with rupture of the anterior hyaloid face).[8]
  • Glaucomatous nerve damage- Raised intraocular pressure may result in optic nerve damage, ultimately resulting in blindness.
  • Cystoid macular edema may occur in a few cases.[63]

Deterrence and Patient Education

Patients with UGH syndrome should be educated on their conditions, including their ocular manifestations, treatment, and complications. Complicated cataract surgery and complications afterward cause a significant impairment both in terms of vision and mental well-being. The patient should be well motivated and educated about the nature of the condition and the benefits of timely intervention.

Careful counseling is needed for such persons because the management depends upon the cause of the prevailing condition. The management options include explantation of the intraocular lens or the implant or other procedures to reduce the damage. All the conditions should be assessed beforehand, like the patients' ability to lay supine and any other coexisting medical conditions that may further add to the complications.

Pearls and Other Issues

To prevent the UGH syndrome, the single-piece foldable acrylic PCIOL or other PCIOLs should be implanted within the capsular bag. When this is impossible due to posterior capsular rent or extension of anterior capsulorhexis, multipiece PCIOL should be implanted in the sulcus in the correct orientation (as it has a vault) and preferably with reverse optic capture (haptics in sulcus and optic behind the anterior capsulorrhexis margin).[30]

When capsular support is inadequate, available surgical options include scleral-fixated IOL (glued or without glue, sutured or without suture), iris-fixated IOL (retropupillary iris-claw lens or iris-claw lens in the anterior chamber), iris-sutured PCIOL, and ACIOL. ACIOL should be appropriately sized, and the total ACIOL diameter should be close to horizontal white to white diameter (in mm) plus 1 mm.[40] 

The ACIOLs have a vault, and incorrect orientation causes upside-down lens syndrome associated with complications including corneal decompensation, pupillary capture, chronic anterior uveitis, iris adhesions, and CME.

Enhancing Healthcare Team Outcomes

The UGH syndrome is a late complication of cataract surgery. It has to be managed by an interprofessional team. The key to management is the patient's compliance and knowledge of the patient regarding the outcomes. The optometrist plays a vital role in refraction and documenting the patient's visual acuity. The anterior segment surgeon should discuss all the management options, and the patient should have realistic expectations.

A retina specialist should be consulted if neovascularization of the iris, vitreous hemorrhage, or CME is present. The pharmacist should explain the dosage of the eye drops to be used. Ophthalmic technicians play an important role in glaucoma or retinal investigations. In patients with systemic disorders and patients taking anti-coagulants, physicians and/or cardiologists must be consulted. Excellent interprofessional coordination may ensure the best outcomes for patients with UGH syndrome.

(Click Image to Enlarge)
Uveitis Hyphema Glaucoma Syndrome
Anterior Chamber Intraocular Lens
Uveitis Hyphema Glaucoma Syndrome Anterior Chamber Intraocular Lens Iridectomy
"Contributed by Dr. Koushik Tripathy, MD"

(Click Image to Enlarge)
UGH (Uveitis Glaucoma Hyphema) syndrome after scleral fixated intraocular lens (SFIOL) and iris repair
UGH (Uveitis Glaucoma Hyphema) syndrome after scleral fixated intraocular lens (SFIOL) and iris repair
Contributed by Koushik Tripathy, MD
Article Details

Article Author

Srishty Sen

Article Editor:

Koushik Tripathy


3/1/2022 10:24:11 PM



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