CLINICAL
ANTERIOR
‘WHAT’S WRONG WITH MY EYES?’
TWO WEEKS OF OCULAR ISSUES UNCOVERS SIGHT-THREATENING INFECTION
JOSH JOHNSTON, O.D., F.A.A.O.
IN JUNE, a 14-year-old Asian female contact lens-wearer presented complaining of red eyes, blurred vision, pain, excessive tearing, swelling of her eyes and photophobia. She said she was diagnosed with a corneal ulcer/infection, had been dealing with these symptoms for two weeks and was looking for a second opinion. Upon questioning, the patient reported sleeping in her ortho-k contact lenses and relatively good contact lens hygiene. She also said she was an avid swimmer.
Her current treatment plan consisted of ganciclovir ophthalmic gel 0.15% (Zirgan, Bausch + Lomb), t.i.d. OU, atropine b.i.d. OU, valacyclovir (Valtrex, Glaxo Smith Klein), 1 gram t.i.d. po, prednisolone ophthalmic suspension (Pred Forte, Allergan) t.i.d. OU, Ofloxacin 0.3% (Ocuflox, Allergan) q2 OU and erythromycin ophthalmic ointment (generic) q.h.s. OU.
Exam revealed severe bilateral corneal ulcers and keratitis — the worst cases I’d ever seen — and uncorrected vision that was light perception OU.
Based on her history and clinical presentation, I suspected the patient had Acanthamoeba keratitis (AK) OU.
Here, I discuss the etiology, symptoms, clinical signs, diagnosis/management options, as well as the ICD-10 codes for AK and what the patient’s diagnosis was.
Corneal ulcer, unspecified | H16.00 |
Ring corneal ulcer | H16.02 |
Perforated corneal ulcer | H16.07 |
Central corneal ulcer | H16.01 |
Hypopyon corneal ulcer | H16.03 |
ETIOLOGY
Acanthamoeba is a ubiquitous free-living protozoa, most commonly found in soil, dust, fresh water, air and swimming pools. It can exist in two forms; the motile trophozoite form (most common form in water) and the dormant cyst form, which is highly resistant to disinfection and can survive in hostile environments. Both types can be found in contact lens wearers.
Although AK can occur in anyone, it primarily affects contact lens wearers, with an estimated 85% of cases in the United States, reports the CDC. Practices that increase the risk of AK: failing to properly disinfect lenses (i.e. topping off lens care solutions or using tap water for lens cleaning), improper lens storage and handling, wearing lenses while swimming, showering or in a hot tub and a history of cornea trauma, according to the CDC.
SYMPTOMS
• Decreased vision
• Excessive tearing
• Pain
• Photophobia
• Severe redness
• Swelling of eyes
CLINICAL SIGNS
Early on, the AK patient reports severe symptoms, yet minimal signs are seen. Signs are usually unilateral and include a slow progression from epithelial to stromal disease. A typical clinical progression of worsening signs include:
• A diffuse superficial punctate keratopathy or epithelitis
• Radial neuritis
• Anterior multifocal infiltrates in the stroma
• Deep stromal keratitis and, uncommonly, a characteristic ring infiltrate later in the presentation
• Scleritis
• Diffuse keratitis
• Keratic precipitates
• Anterior chamber inflammation with cell and flare
Note the large stromal ring infiltrate with an overlying epithelial defect and stromal white blood cell infiltration in this patient.
Keep in mind that AK can be misdiagnosed as epithelial herpes simplex, as its late presentation can appear similar to fungal or other infectious ulcers.
DIAGNOSIS/MANAGEMENT
The fast diagnosis of AK is crucial, as time allows Acanthamoeba to penetrate deep into the stroma, threatening vision. High suspicion of AK should arise when, upon questioning, patients admit to the risk factors outlined. A diagnostic marker for AK is lack of improvement with antiviral and antibiotic treatment.
To make a definitive diagnosis, the following should be employed:
• Slit lamp exam. This aids in the differential diagnosis, as a lack of dendrites suggests the ulcer is not epithelial herpes simplex.
• Corneal scraping with slides sent to pathology.
• Corneal cultures (gold standard) plate culture with Agar.
In my practice, we perform corneal scrapings and cultures to overlap sensitivity, specificity and accuracy: Slides catch some things a culture might miss and vice versa.
• Confocal microscopy. This enables you to view cultures at high magnification (300x) to visualize bacteria and confirm a diagnosis based on morphology.
In terms of management, no single FDA-approved treatment for AK exists. Typically, a combination of agents is used topically, requiring daily follow-up appointments to monitor for improvement.
These topical agents include:
• Polyhexamethylene biguanide 0.02%. This compounded drug kills the amoeba. Specifically, it’s an antiseptic that lyses cells and causes fatal membrane damage.
• Chlorhexidine acetate 0.02%. This compounded drug is also an antiseptic and, therefore, acts as a biocide in killing both forms of the amoeba.
• Brolene 0.1%. This compounded drug is an anti-microbial.
• Neomycin ophthalmic solution. This drug has some efficacy in treating AK and has a synergistic affect with the other drugs mentioned.
• Topical bevacizumab 1% (Avastin, Genentech). This is prescribed for corneal neovascularization.
All are administered every 30 minutes to 1 hour for the first days. Depending on the severity, this could continue seven to 14 days. The treatments are often continued for several months (6 to 12 months in severe cases). (See “Future Treatments” below.)
When you encounter the following, refer the patient to a corneal specialist, who can determine the etiology and develop the best treatment plan.
• Large central ulcer
• Severe anterior chamber reaction with hypopyon
• Inability to culture
• Unsuccessful treatment plan.
From here, the corneal specialist can determine whether surgery (a penetrating keratoplasty, for instance) is warranted.
Potential Future Treatment
Collagen crosslinking was recently FDA approved for the treatment of progressive keratoconus and corneal ectasia post-refractive surgery. It has also been proposed as a new treatment for infectious keratitis. Specifically, UV light kills the bacteria attacking the cornea by blocking cell wall synthesis and blocking digestive enzymes produced by fungi and bacteria that damage the collagen in the cornea. This procedure can be combined with topical anti-infectives to better fight infectious keratitis.
THAT PATIENT
I ordered corneal scrapings and cultures, which revealed AK. I prescribed the aforementioned treatments. I never did determine how the patient developed AK, though I assumed it got into her storage case somehow. OM
DR. JOHNSTON practices at Georgia Eye Partners. He focuses on ocular surface disease and has extensive experience in co-managing cataract and refractive surgery patients. Email him at drj@gaeyepartners.com, or visit tinyurl.com/OMcomment to comment. |