UGH Syndrome: When Implants Fight Back

Uveitis-glaucoma-hyphema (UGH) syndrome is one of those conditions that reminds us that the treatments we provide sometimes create their own set of problems. First described in 1978, UGH arises when an intraocular implant irritates the adjacent ocular tissues. The resulting triad of inflammation, hyphema, and elevated IOP can jeopardize vision if it goes unrecognized and is not adequately treated.¹

While early cases were often tied to rigid anterior chamber IOLs, today, most cases of UGH originate from late posterior chamber IOL subluxation or malposition. Weak zonules, pseudoexfoliation, and even a Soemmering ring can destabilize an IOL years after cataract surgery, leading to chronic iris-lens contact. Glaucoma drainage devices, malpositioned sulcus lenses, and haptic fixating techniques can also set the stage for mechanical irritation of intraocular structures.¹

DIAGNOSIS AND MANAGEMENT PEARLS

It’s important to recognize that UGH is not always obvious in its presentation (Figure 1). Potential signs include:

• subtle, recurrent, or chronic anterior chamber inflammation
• recurrent microhyphema (ie, red blood cells in the anterior chamber), pigment dispersion, or mild iris transillumination
• unexplained IOP spikes, often occurring years after surgery

Diagnosing UGH requires diligence. Gonioscopy can reveal pigment in the angle, while imaging tools such as ultrasound biomicroscopy (Figure 2) and anterior segment OCT can help confirm IOL-iris contact.¹

Mild cases of UGH can often be managed with topical medications and observation. Antiinflammatory drops, including steroids, and IOP-lowering drops in combination with cycloplegics to mitigate iris movement are a typical starting point.¹ Surgical intervention may be required in persistent, recurrent, or chronic cases, which usually entails IOL repositioning, exchange, or haptic amputation. These often provide definitive relief.¹

REMAIN VIGILANT

Although UGH may be uncommon (with an incidence of 0.4% to 1.6%), it highlights the importance of ongoing surveillance of pseudophakic patients.¹ Many cases of UGH present years after uneventful surgery, and ODs are often the first to spot the subtle signs. Recognizing the signs of this condition allows timely intervention and prevention of irreversible glaucomatous damage or vision loss.

It’s worth noting that UGH syndrome is not the result of a patient failing to adhere to a postoperative care regimen; rather, it is more about the implant wearing out its welcome. As primary eye care providers, our role is to spot these signs of trouble, guide medical management, and coordinate surgical interventions when the implant needs to be re-engineered.