Uveitis Glaucoma Hyphema Syndrome (UGH) is a specific complication that can occur in the eye following the implantation of an artificial lens, often after cataract surgery. This condition is characterized by a distinctive triad of eye problems that, if left untreated, can lead to serious, permanent vision loss. UGH syndrome is considered a rare but significant mechanical failure where the intraocular lens interacts poorly with delicate internal structures.
Defining UGH Syndrome
UGH is an acronym describing the three main components of the syndrome: Uveitis, Glaucoma, and Hyphema. The simultaneous or sequential presentation of these three conditions in an eye with an artificial lens defines the disorder. Although the incidence has decreased with modern surgical techniques, it remains a recognized clinical entity.
Uveitis refers to inflammation of the uvea (the iris, ciliary body, and choroid). This inflammation is a response to irritation or injury within the eye. Glaucoma in this context is secondary, caused by an increase in fluid pressure inside the eye. This elevated pressure can damage the optic nerve over time, leading to vision loss. Hyphema is the pooling of blood in the anterior chamber, the space between the cornea and the iris.
The Underlying Cause
The primary cause of UGH syndrome is mechanical irritation, or “chafing,” of internal eye structures by a malpositioned or poorly designed intraocular lens (IOL). The IOL can rub against the iris, ciliary body, or the angle where the iris meets the cornea. This constant friction initiates the entire syndrome.
Mechanical trauma causes a breakdown of the blood-aqueous barrier, which separates blood vessels from the anterior chamber. The IOL’s contact with the highly vascular uveal tissue leads to micro-bleeding and the release of red blood cells into the anterior chamber, resulting in hyphema. The irritation also causes the release of pigment and inflammatory cells, which contribute to uveitis.
The continuous shedding of pigment, inflammatory debris, and blood cells clogs the eye’s natural drainage system, known as the trabecular meshwork. This obstruction prevents the aqueous humor from flowing out properly, causing the intraocular pressure to rise, which results in glaucoma. UGH syndrome can occur with any type of lens if it is unstable or malpositioned.
Recognizable Symptoms and Clinical Presentation
Patients with UGH syndrome often present with recurrent episodes of blurred vision and eye discomfort weeks or months after the initial eye surgery. The irritation and bleeding are episodic, meaning the symptoms may come and go. A noticeable symptom is light sensitivity (photophobia), which is a common sign of inflammation.
Patients may report ocular pain or a deep ache in the affected eye, frequently associated with spikes in intraocular pressure. A distinct sign is the visible presence of blood in the anterior chamber, sometimes appearing as a layering of red cells or haziness near the iris. In some cases, patients report seeing a reddish hue over objects, called erythropsia, due to the presence of blood.
The mechanical irritation drives persistent inflammation (uveitis), sustaining the cycle of pressure elevation and recurrent bleeding (hyphema). If the condition is not addressed, sustained high pressure can lead to irreversible damage to the optic nerve and permanent vision loss. The ophthalmologist may observe defects in the iris, known as transillumination defects.
Diagnosis and Treatment Options
Diagnosis of UGH syndrome begins with a comprehensive eye examination, including a detailed history of prior eye surgery and current symptoms. A slit-lamp biomicroscopy is performed to examine the anterior chamber, looking for signs like hyphema, inflammatory cells, and the position of the IOL. Eye pressure is measured using tonometry to check for elevated intraocular pressure.
Specialized imaging is often required to confirm the mechanical cause of the syndrome. Ultrasound biomicroscopy (UBM) provides high-resolution images of the front of the eye. This allows the ophthalmologist to visualize contact points between the IOL haptics and the uveal tissue. UBM is crucial for localizing the source of the mechanical friction.
Initial management focuses on controlling acute symptoms using medical therapy. This typically involves topical corticosteroid eye drops to suppress uveitis and reduce inflammation. Pressure-lowering drops are also prescribed to manage glaucoma and prevent optic nerve damage from high intraocular pressure.
While medication controls symptoms, definitive treatment almost always requires surgical intervention to eliminate the source of friction. This involves either repositioning the existing IOL so it no longer chafes the uveal tissue, or exchanging the problematic lens for a more stable type. Surgical resolution of the mechanical issue is necessary for long-term cessation of recurrent inflammation, bleeding, and pressure spikes.