Catching a Red Eye

A patient’s red eyes can easily be overlooked, depending on the severity, and although this sign could be truly innocuous, it could also be a key indicator of something far more serious, such as an acute eye disease. Failing to recognize the latter could put your patient’s vision in jeopardy. Consider the following case.

VISIT NO. 1

A 44-year-old White male presented for an annual eye examination. He reported that his last eye examination was 18 months prior at a different clinic. He had showed optic atrophy and decreased vision OD secondary to trauma that had occurred more than 30 years ago.

Cover testing revealed exotropia OD. The patient also presented with an afferent pupillary defect OD. His IOPs were 9 mm Hg OD and 10 mm Hg OS. His VA with his habitual spectacles was -2.50 -2.00 x 110 (20/200) OD and -2.00 -2.50 x 075 (20/20) OS. Autorefraction yielded -1.75 -1.75 x 092 OD and -1.25 -2.50 x 083 OS. Manifest refraction yielded -2.50 -2.00 x 110 (20/100 with eccentric fixation in a trial frame) OD and -1.75 -2.50 x 084 (20/20) OS. Anterior and posterior segment evaluation was unremarkable except for optic atrophy and pallor and scattered chorioretinal atrophy OD. His cup-to-disc ratios were 0.9 OD and 0.4 OS.

The patient was diagnosed with myopic astigmatism OU and optic atrophy OD. He was provided with a new spectacle prescription and was educated on the importance of full-time wear to protect his better-seeing left eye. He was advised to follow up in 1 month for an IOP check.

VISIT NO. 2

The patient returned unexpectedly 8 days later with a chief complaint of a painful right eye with blurred vision, headache, tearing, photophobia, redness, and a feeling of pressure lasting 2 days. This time, his IOPs were 40 mm Hg OD and 12 mm Hg OS. Physical examination of his right eye revealed 2+ injection in his conjunctiva, keratic precipitates in his cornea, and 2+ cell and 1+ flare in his anterior chamber.

Homatropine 5% was instilled, and the patient remained at the clinic until the pressure in his right eye stabilized. He reported that he had been seen for two similar episodes over the past 2 years by a different provider. Notable findings in his right eye included a 3+ afferent pupillary defect, BCVA of 20/100, 3+ anterior chamber reaction, and IOP ranging from 30 mm Hg to 42 mm Hg OD. His cup-to-disc ratios were 0.85/0.85 OD and 0.4/0.4 OS. Management for these episodes typically included prednisolone acetate ophthalmic suspension 1% (Pred Forte, Allergan/AbbVie) and brimonidine tartrate 0.2%/timolol maleate ophthalmic solution 0.5% (Combigan, Allergan/AbbVie), with his symptoms resolving over a period of several days. Visual field and OCT testing had revealed severe retinal nerve fiber layer thinning and significant superior and inferior visual field loss in the right eye (Figures 1 and 2).

IOP-lowering medications proved ineffective at the patient’s second visit with us, with final IOPs reading 50 mm Hg OD and 13 mm Hg OS. He was diagnosed with anterior uveitis and uveitic glaucoma OD and was prescribed prednisolone 1%, cyclopentolate HCl (Cyclogyl, Alcon), dorzolamide/timolol, and 250 mg acetazolamide. He was then referred to ophthalmology to explore surgical treatment options.

UVEITIC GLAUCOMA

Uveitic glaucoma is a complex condition that arises from intraocular inflammation, which affects the consistency of aqueous humor and reduces the permeability of the trabecular meshwork.¹ These inflammatory changes can lead to increased IOP due to trabecular meshwork obstruction or secondary angle-closure mechanisms.¹ The condition may present as either acute or chronic and affects approximately 10% to 20% of patients with uveitis.¹

The mechanisms behind uveitic glaucoma can be categorized as direct or indirect. In cases of open-angle uveitic glaucoma, trabecular meshwork outflow is obstructed by inflammatory cells, proteins, and fibrin.² This obstruction results from the breakdown of the blood-aqueous barrier due to uveitis-induced inflammation, leading to increased protein leakage that further hinders drainage.² Additionally, the inflammatory process increases the viscosity of aqueous humor, making it more difficult to drain. The presence of cytotoxic agents produced by inflammatory cells can cause permanent scarring of the trabecular meshwork and Schlemm canal endothelial cells, further exacerbating the condition. Trabeculitis, or direct inflammation of the trabecular meshwork, can also contribute to outflow resistance.³

In cases of angle-closure uveitic glaucoma, several mechanisms may be at play. Peripheral anterior synechiae or posterior synechiae may restrict aqueous outflow, while swelling of the ciliary body or choroidal effusion can lead to angle obstruction.

Indirect mechanisms such as steroid-induced glaucoma can also play a significant role. An IOP increase in response to steroid therapy is implicated in approximately 42% of uveitic glaucoma cases.⁴ IOP elevation is most pronounced between weeks 4 and 6 of steroid use but can appear as early as week 1.⁵

Clinically, uveitic glaucoma can present with a combination of inflammatory, glaucomatous, and nongranulomatous features. Typical granulomatous findings include mutton fat keratic precipitates and iris nodules.⁶ Anterior and posterior synechiae are also common findings of uveitic glaucoma, and IOP elevation often occurs alongside chronic inflammation.

Identifying the underlying systemic cause of uveitic glaucoma is crucial for choosing an effective treatment. Granulomatous uveitis may indicate conditions such as sarcoidosis, syphilis, or tuberculosis, while fine or stellate keratic precipitates suggest diagnoses such as Fuchs heterochromic iridocyclitis or herpetic uveitis.^5,7,8 A unilateral rise in IOP with uveitis may point to conditions such as Posner-Schlossman syndrome, herpes-related uveitis, or Fuchs heterochromic iridocyclitis.^5,7,8

Treatment

The primary goal of treating uveitic glaucoma is to control inflammation while preventing permanent structural alterations that affect aqueous outflow.⁶ This requires a delicate balance between controlling inflammation and reducing IOP. Antiinflammatory therapy remains a cornerstone of treatment, with corticosteroids administered topically, periocularly, intravenously, or orally, depending on disease severity and location.⁹ Prednisolone 1% and difluprednate ophthalmic emulsion 0.05% (Durezol, Novartis) are effective topical options, with difluprednate requiring less frequent dosing and helping with medication compliance.⁶ Soft steroids are less likely to induce a steroid response but are less effective in treating intraocular inflammation.⁶

Mydriatics and cycloplegics can be used with steroids to help with pain management by paralyzing the ciliary muscle to reduce iris spasms.⁶ Cycloplegics can also help stabilize the blood-aqueous barrier and prevent or break posterior and peripheral anterior synechiae, although they should be avoided in cases of angle closure.

IOP-lowering medications should be administered in conjunction with antiinflammatory therapy to help IOP return to a normal range.⁹ Beta-blockers, carbonic anhydrase inhibitors, and alpha-adrenergic agonists are considered first-line agents in the treatment of uveitic glaucoma.⁹ The role of prostaglandin analogs remains controversial due to their potential to disrupt the blood-aqueous barrier, worsen uveitis, and induce cystoid macular edema.⁸ Pilocarpine should be avoided in patients with uveitis, as it can break down the blood-aqueous barrier, prolong inflammation, and cause formation of posterior synechiae. Alpha-adrenergic agonists may be employed as second-line agents for acute IOP spikes.⁹ Clinical trials of the Rho kinase inhibitor ripasudil have shown effectiveness in 50% of glaucoma patients.^9,10 Ripasudil appears to be more effective in those with ocular inflammation receiving topical steroids, suggesting potential antiinflammatory properties in addition to IOP reduction.^9,10

Surgical interventions (eg, selective laser trabeculoplasty, laser peripheral iridotomy, iridectomy, and trabeculotomy) are necessary in approximately 30% of uveitic glaucoma cases, particularly when medical therapy proves inadequate or in instances of acute angle closure.^11,12 Iridectomy is especially useful for cases involving pupillary block or iris bombe, as it establishes aqueous outflow between the anterior and posterior chambers.⁹ For patients with refractory glaucoma, trabeculectomy has shown greater efficacy in uveitic glaucoma compared with primary open-angle glaucoma.¹³

TAKE-HOME POINT

This patient was misdiagnosed by his previous eye care provider and required surgical intervention after two visits with us. His case is a prime example of why red eyes are best treated by primary eye care providers versus an ER or urgent care center, where misdiagnosis of acute eye diseases often occurs and can lead to severe visual consequences.¹⁴