**5. Diagnosis**

the presence of iris transillumination corresponding to the rubbing site. The diagnosis is easiest during the attack. A blood cloth or hyphema may be observed. The diagnosis can be confirmed by ultrasound biomicroscopy (UBM) and anterior segment optical coherence to‐ mography (AS-OCT) showing a contact between the optic or haptic and the iris. The compli‐ cations include pseudophakic bullous keratopathy, corneal staining and cystoid macular edema (CME). The differential diagnosis includes amaurosis fugax and vertebrobasilar in‐ sufficiency. Amaurosis fugax occurs more rapidly (within seconds to minutes) and loss of light perception in at least one quadrant. Loss of light perception never occurs in UGH syn‐ drome and there is always a history of cataract extraction and IOL implantation or iris de‐ vice implantation. The differentiation between the two is crucial because patients with amaurosis fugax may be treated with anti-coagulants that may increase the bleeding in UGH syndrome. Patients may respond to topical corticosteroids and anti-glaucoma medica‐

tions. The definite treatment of UGH is replacement or repositioning of the IOL.

topical corticosteroids and anti-glaucoma medications. [32]

Glaucoma has been reported in patients with pars planitis (8%), uveitic from Reiter's syn‐ drome (1%), ankylosing spondylitis, hemorrhagic fever with renal syndrome (nephropathia epidemica) and epidemic dropsy from ingestion of sanguinarine in Argemone mexicana oil. Bilateral acute angle closure glaucoma due to uveal effusion has been described in acquired immunodeficiency syndrome (AIDS) and responded to medical treatment with cycloplegics,

**Figure 4.** Reiter's syndrome. Note the pigment over the crystalline lens after pupil dilation and release of posterior

**4. Other uveitic glaucomas**

366 Glaucoma - Basic and Clinical Aspects

synechiae.

Patients with acute closed-angle glaucoma may present with ocular and brow ace, blurred vision, halos, photophobia and even nausea and vomiting. Patients with open or chronic an‐ gle closure glaucoma are asymptomatic.

All uveitis patients should be routinely evaluated for IOP, which is elevated (>21mmHg) in uveitic glaucoma. In acute closed angle glaucoma, the cornea may be edematous and ciliary and conjunctival congestion may be present. Gonioscopy should be performed to define the type of glaucoma. Topical glycerin 50-100% would clear corneal edema for evaluating the angle and posterior segment. Otherwise, the corneal epithelium may be removed with a blade or 70% alcohol on a cotton-tipped applicator. If the cornea is still cloud, UBM or AS-OCT may replace gonioscopy in evaluating is performed the angle. Optic disc evaluation by slit lamp biomicroscopy and other imaging techniques (OCT, scanning laser polarimetry (GDx) or Heidelberg retinal tomography (HRT)) when the cornea is clear. Visual fields should be obtained in patients with cup/disc ratio of 0.6 or more for baseline and follow-up documentation of the progression of the glaucoma. In patients with cup/disc ratio of less than 0.6, the visual field is usually normal. The visual field may be abnormal due to CME (central relative scotoma) and retinitis or retinal scarring (defects corresponding to these areas). CME and macular atrophy may be confirmed by OCT. Differentiation should be made between steroid responder (the IOP returns to normal upon discontinuation of the corticosteroids) and corticosteroid-induced glaucoma (the IOP remains high). Differentia‐ tion between increased IOP due to increased inflammation and steroid responder may be performed by replacing the corticosteroids with IOP-sparing corticosteroids. The IOP should decrease.
