Patient experiences cloudy vision after removing soft contact lens

Conjunctival injection, an epithelial defect, disciform infiltrate, fibrin in the anterior chamber and a hypopyon were seen in the left eye.

Mark E. Patron

Andre J. Witkin

A 62-year-old man presented with a chief complaint of cloudy vision in his left eye. He described 3 weeks of foreign body sensation following removal of his soft contact lens, accompanied by intermittent episodes of severe pain. He had previously seen two other eye care providers who had treated him with topical steroids and antibiotics without resolution of his symptoms. He reported more recent symptoms of excessive tearing, swollen lid, redness and now significantly decreased vision in the left eye. He was subsequently referred to the New England Eye Center for further evaluation.

The patient’s medical history was significant for hypertension and non-insulin-dependent diabetes mellitus type 2 with good glycemic control. His ocular history included silicone hydrogel soft contact lens wear with no overnight use, as well as left eye irritation after being hit by a tree branch 2 months prior. He worked as a grants manager, enjoyed mowing the lawn at home and had recently been on a Caribbean cruise.

Examination

On examination, the patient’s best corrected visual acuity was 20/20 in the right eye and hand motions in the left eye. Pupillary exam was normal in the right eye, and there was no view to the pupil in the left eye. Extraocular movements were full in both eyes. IOPs were 18 mm Hg in the right eye and 26 mm Hg in the left eye. On slit lamp exam, the left eye showed 2+ conjunctival injection, a 4 mm × 6 mm epithelial defect bordered by a raised disciform infiltrate penetrating to 80% of the stroma, fibrin in the anterior chamber and a 1-mm hypopyon (Figure 1).

Figure 1. Slit lamp photo of the left eye showing a disciform infiltrate penetrating to 80% of the stroma and bordering a 4 mm × 6 mm epithelial defect. Conjunctival injection, fibrin in the anterior chamber and a 1-mm hypopyon are also present. Image: Cox C, Wu HK

What is your diagnosis?

Disciform keratitis

The differential diagnosis for a patient with disciform keratitis includes bacterial, viral, parasitic and fungal infections, as well as topical anesthetic abuse. This patient had multiple risk factors for infection, including diabetes, hydrogel soft contact lens wear, prior trauma by a tree branch, gardening and a recent history of swimming in the Caribbean Sea.

Disciform keratitis is most commonly associated with either herpes simplex virus (HSV) or the parasite Acanthamoeba castellanii. Herpetic keratitis is a common entity often mistaken for adenoviral conjunctivitis because a classic primary symptom is foreign body sensation secondary to HSV-induced blepharoconjunctivitis. It is important to remember that HSV keratitis can resemble nearly any other infection, although its hallmark symptom in recurrent episodes is corneal hypoesthesia. Acanthamoeba keratitis is significantly less common, but should be high on the differential in a soft contact lens wearer with disciform keratitis exhibiting raised epithelial ridges, particularly with corneal evidence of radial perineuritis. Fungal etiologies are considered if a patient is in any way immunocompromised or if there is a history of trauma to the eye by vegetable matter. Bacteria causing disciform keratitis include multiple gram-negative rods, one of which can be the potentially devastating organism Pseudomonas aeruginosa. Pseudomonas is fairly common in contact lens wearers and may present as a ring infiltrate progressing rapidly over the course of a few hours, often accompanied by a thick, purulent discharge. Interestingly, topical anesthetic abuse can present with disciform keratitis associated with an overlying epithelial defect. This possibility should be considered in patients who have access to such eye drops, such as health care workers.

Corneal cultures showed that our patient was positive for Acanthamoeba infection, and confocal microscopy was performed to establish a treatment baseline. Confocal microscopy showed double-walled cysts penetrating 28 µm to 300 µm into the corneal stroma, consistent with chronic, long-standing Acanthamoeba keratitis.

Acanthamoeba

Acanthamoeba is a parasite found in freshwater environments and its accompanying soil, such as in ponds, lakes, swimming pools, hot tubs and gardens. It can also be found in residential water, particularly if homes use well water as their primary source of tap water. This is significant for patients who clean their contact lens cases with tap water or shower with their lenses on. It is frequently seen in patients who come from areas in the northeast region of the United States where residences are not situated along a city water line and therefore depend on well water. In the greater United States, Acanthamoeba keratitis is strongly associated with contact lens wear and exposure to contaminated water, with reports ranging from 40% to 93% of associated cases.

With daily handling and poor hygiene, hydrogel lenses can become co-infected with bacteria, thus increasing the risk for adherence of Acanthamoeba and allowing for subsequent penetration of intact corneal epithelium. As mentioned above, Acanthamoeba infection can present with disciform keratitis exhibiting a raised epithelial ridge, as well as perineuritis that may manifest as pain out of proportion to clinical signs. Importantly, pseudodendrites are also possible early manifestations of Acanthamoeba, which may be mistaken for HSV keratitis. More serious presenting signs of Acanthamoeba keratitis can include uveitis, cataract, elevated IOP, hypopyon and/or scleritis.

Diagnosis

Diagnosis of Acanthamoeba infection is made by obtaining corneal epithelial scrapings and sending these for culture in Page’s saline. The scraping sample is inoculated onto a lawn of Escherichia coli over non-nutrient agar, upon which Acanthamoeba will leave identifiable tracks by eating through the lawn of E. coli. Some argue that confocal microscopy may be useful in establishing the diagnosis because this technique provides direct visualization of the cysts and trophozoites associated with the parasite. This evaluation is technician-dependent, however, which can result in highly variable readings and is therefore somewhat unreliable for initial diagnosis. Confocal microscopy may be more useful for establishing an initial baseline and then measuring a patient’s response to treatment over time. Routine culture remains the gold standard for making a primary diagnosis.

Follow-up

The patient was started on once-an-hour polyhexamethylene biguanide (a cationic antiseptic that inhibits trophozoite membrane functions) and hexamidine diisethionate (an aromatic deaminase that inhibits DNA synthesis of both trophozoites and cysts). Additionally, topical antibiotic eye drops were given to protect against likely co-infection.

On subsequent visits, the patient still had significant stromal scarring 3 to 4 months into his treatment course. This was expected given the deep stromal penetration of Acanthamoeba organisms as seen with confocal microscopy, as well as by his extensive ring infiltrate. Future options include an optical vs. therapeutic penetrating keratoplasty, which may help to improve his vision over the long term. His risk of graft failure is high, however, given the significant extent of his disease. Acanthamoeba can persist for years in its dormant cyst state, then reactivate or cause significant inflammation once treatment has been discontinued.

References:

• Carvalho FR, Foronda AS, Mannis MJ, Höfling-Lima AL, et al. Twenty years of Acanthamoeba keratitis. Cornea. 2009;28(5):516-519.
• Erie JC, McLaren JW, Patel SV. Confocal microscopy in ophthalmology. Am J Ophthalmol. 2009;148(5):639-46.
• Hammersmith KM. Diagnosis and management of Acanthamoeba keratitis. Curr Opin Ophthalmology. 2006;17(4):327-331.
• Kitzmann AS, Goins KM, Sutphin JE, Wagoner MD. Keratoplasty for treatment of Acanthamoeba keratitis. Ophthalmology. 2009;116(5):864-869.
• Yanoff M, Duker JS. Ophthalmology. Elsevier; 2009:262-284.

• Catherine Cox, MD, and Helen K. Wu, MD, can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; Web site: www.neec.com.

• Edited by Mark E. Patron, MD, and Andre J. Witkin, MD. Drs. Patron and Witkin can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; Web site: www.neec.com.