- Managing fungal keratitis
- Identifying Acanthamoeba keratitis
- ‘From Targeted Therapy to Targeted Toxicity: Corneal Effects of Novel Cancer Biologics’
- Interstitial keratitis
- ‘Debunking Glaucoma Myths’
Managing fungal keratitis
During a Saturday morning cornea session, Bhupesh Bagga, DO, shared his “fungal keratitis playbook.” Fungal keratitis is the major cause of corneal blindness, especially in tropical countries. Some of the challenges of dealing with this are limited treatment options, poor penetration of antifungals, and increasing antifungal resistance.
So, what do you do if a fungal ulcer comes to your clinic?
Dr. Bagga shared some important things you should assess to determine the severity of infection: size, depth, location, presence of hypopyon, limbal or scleral involvement, and posterior segment involvement.
Old age, late presentation, and poorer visual acuity at presentation have been associated with worse prognosis. Large ulcers, hypopyon, more posterior stromal involvement, and Aspergillus species are associated with worse prognosis. Corneal scraping culture positivity may indicate a worse prognosis as well.
Dr. Bagga also shared the standard/preferred practice pattern of treatment. He noted that you should confirm the microbiology. Then, topical antifungals may be used. He also noted the potential use of topical natamycin 5% or topical voriconazole 1%. In some cases, an addition of oral antifungals might be warranted.
He further discussed what works and what doesn’t for treatment of fungal keratitis. In addition to topical treatment with natamycin (in anterior stromal keratitis of less than 4–6 mm in size) and early intervention with intrastromal injection of antifungals (where the size is 4–6 mm and away from the limbus, and posterior stromal injection is limited), early therapeutic penetrating keratoplasty may be used when the size is less than 8–8.5 mm with minimal involvement of the anterior chamber. Adjuvant photodynamic therapy with rose bengal works on Fusarium keratitis with 250 microns of stromal involvement.
Dr. Bagga added that topical azoles alone do not work for most cases of fungal keratitis. In cases with diffuse involvement or thinning of more than 70%, where the limbus is involved or approached, intrastromal injection will not work. Additionally, he said that photodynamic antimicrobial therapy does not work on Aspergillus flavus keratitis, and the outcome of therapeutic penetrating keratoplasty is poor in cases with advanced keratitis with limbal and scleral involvement. Anterior chamber wash with intracameral antifungals also does not work, he said.
Editors’ note: Dr. Bagga has no relevant financial disclosures.
Identifying Acanthamoeba keratitis
Jeremy Keenan, MD, focused his presentation during the AAO Cornea Day on identifying Acanthamoeba keratitis. In the U.S., the biggest risk factors are contact lens wear and freshwater exposure (but also swimming pools and hot tubs).
When looking for symptoms, Dr. Keenan said to look for pain out of proportion to clinical findings. However, a neurotrophic cornea is also common.
He shared his top 5 early clinical signs of Acanthamoeba:
- Diffuse epitheliopathy
- Pseudodendrites
- Epithelial ridge
- Radial perineuritis
- Multifocal patchy anterior stromal infiltrates
Editors’ note: Dr. Keenan has no relevant financial disclosures.
‘From Targeted Therapy to Targeted Toxicity: Corneal Effects of Novel Cancer Biologics’
Neel Pasricha, MD, spoke about antibody drug conjugates (ADCs), the ocular adverse events that can occur with these, and how to mitigate.
He began by highlighting that traditional chemotherapies are non-specific; as a result, there is no targeting, so they can kill both healthy cells and cancer cells. ADCs, on the other hand, target cancer-specific antigens, and these have been successful in oncology. There are 15 approved and more than 200 in clinical trial in the U.S.
However, ADC keratopathy is a common ocular adverse event (OAE), Dr. Pasricha said, specifically corneal pseudomicrocysts, which can be hard to see.
Of 15 FDA-approved ADCs, three have gotten an FDA black box warning for ocular toxicity, he said. These corneal pseudomicrocysts can develop as soon as a few weeks after treatment. Though they’re reversible, it can sometimes take 2 weeks to 8 months after ADC discontinuation for them to resolve. Patients may also have eye pain and blurry vision.
These pseudomicrocysts, Dr. Pasricha said, don’t just stay in the periphery, though they start there. They also tend to cause a steepening effect. Over time, they migrate toward the center, and patients can get central steepening.
Dr. Pasricha share three lessons learned so far pertaining to this issue. First, toxicity is off target. Additionally, if you look at linker technology linking the antibody to toxic drug, there are various technologies used. He also said there are various toxic payloads involved in this; the problem is not easy to pinpoint.
Dr. Pasricha highlighted grading systems, specifically the Common Terminology Criteria for Adverse Events (CTCAE), but he said this has several limitations: it mixes visual acuity with clinical findings, there are no photos, and ambiguous terms.
A multicenter interspecialty consensus is seeking a better grading system, and Dr. Pasricha shared some improvements to cornea grading specifically, noting a scale for visual acuity and symptoms and the presence of photos.
A delay in patients being able to obtain eye exam screening is another concern, and there are expanding options to do portable eye exam screenings at infusion centers and oncology clinics.
Wrapping up with his key takeaway points, Dr. Pasricha summarized the ways to mitigate OAEs from ADCs, noting again the importance of the consensus OAE grading scales and portable eye exam screenings. He added that there is a pending ICD-10 addition of “corneal pseudomicrocysts,” and he said it’s important to try to inhibit off-target ADC internalization (macropinocytosis).
Editors’ note: Dr. Pasricha has financial interests with 2A Biosciences, AbbVie, Alcon, Amgen, ArriVent BioPharma, AstraZeneca, Denali, Diatiro, Glaukos, GlaxoSmithKline, Globe Biomedical, Hexagon Bio, Iksuda Therapeutics, LigaChem Biosciences, Sanofi, and Vanda Pharmaceuticals.
Interstitial keratitis
Olivia Lee, MD, highlighted interstitial keratitis (IK) in her presentation, discussing the essentials and what’s new. This is an immune-mediated, non-suppurative stromal inflammation with vascularization. Signs include stromal haze, infiltrates/scarring, and vascularization/ghost vessels. She added that HSV, not syphilis, is now the leading cause of active IK. The key point is the treatment is focused on identifying the cause and treating underlying etiology, but it’s also about treating inflammation.
Dr. Lee went on to discuss some of the new things in the last 5 years relating to IK.
Microsporidia is a new recognized cause, she said, adding that 13% of proven microsporidial keratitis presents as immune stromal keratitis. It mimics herpetic IK, with disciform keratitis, immune rings, and intact epithelium. Diagnosis involves scraping smear and pan-microsporidial PCR.
In terms of syphilitic interstitial keratitis, Dr. Lee said an update is a change from the CDC that lumbar puncture is no longer required before treating isolated ocular syphilis.
There have also been advances in genetic/genomic host-pathogen characterization for IK associated with leprosy. There is correlation of ocular findings with bacillary load, and it’s also curable with multidrug therapy (she noted that the WHO multidrug therapy for multibacillary disease is rifampicin plus dapsone plus clofazimine for 12 months).
Dr. Lee also shared some advances in the imaging of IK. She said that AS-OCT and in vivo confocal microscopy are now central to early diagnosis and monitoring.
Editors’ note: Dr. Lee has no relevant financial disclosures.
‘Debunking Glaucoma Myths’
During a Friday afternoon glaucoma session, Bryan Ang, MD, addressed the myth that normal-tension glaucoma (NTG) is simply missed elevated IOP.
He initially conceded that sometimes it can be missed elevated IOP. First, he said that IOP peaks do occur outside clinic hours, and IOPs may underestimate with thinner corneas. There can also be prior intermittent/resolved episodes of IOP elevation.
However, very often this is not the case. Many NTG eyes don’t have elevated IOPs—even with 24-hour measurements. Dr. Ang also said that thin corneas are unlikely to fully explain apparently normal IOPs in NTG. Glaucomatous optic neuropathy is not just about stress but also susceptibility.
Even without “elevated” IOPs, NTG eyes are more susceptible to optic nerve injury. NTG should be seen as part of the open-angle glaucoma spectrum. Dr. Ang cautioned not to forget that IOP in this group of patients remains a key modifiable risk factor.
Editors’ note: Dr. Ang has financial interests with AbbVie, Alcon, Bausch + Lomb, Glaukos, Johnson & Johnson Vision, Leica, Santen, and Zeiss.
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