To report a young man with a central retinal vein occlusion (CRVO)-like appearance which later evolved to frosted branch angiitis (FBA).As 28-year-old Indian man presented with optic disc swelling, hyperemia, peripapillary hemorrhages, and dilated tortuous veins in the left eye, 6 months after being diagnosed with idiopathic FBA in the right eye. Within 3 days of presentation, the left eye developed FBA, which was promptly and successfully treated with oral steroids.A CRVO-like picture may be the first stage of FBA. Young patients with CRVO and intraocular inflammation should be followed closely for early detection of FBA. Early initiation of oral steroids may preserve visual acuity in such cases.
Refractive small incision lenticule extraction (Relex-SMILE) is now gaining acceptance and popularity as a ''flap-less" refractive surgery which needs only Femto laser and a single machine, unlike the Femto-LASIK which produces a flap as well as needs an excimer laser to complete the refractive surgery. The number of femto-LASIK along with the microkeratome flap LASIK procedures (started at around 1991) (more than 40 million procedures as of 2016) far outnumber the SMILE procedures (started around 2008–2011) (2 million in 2019) worldwide. The incidence of infections and interface complications of LASIK are well documented in the literature. The Food and Drug Administration (FDA, USA) approved LASIK in 1991 and SMILE in 2016. There are few reports of infectious keratitis after SMILE [Table 1].[1234567] This issue of the Indian Journal of Ophthalmology features the successful management of Staphylococcal infection after SMILE with interface wash using antibiotics and photoactivated chromophore for keratitis-corneal collagen crosslinking (PACK-CXL).[7] To the best of our knowledge, there are a total of 10 reported cases of infective keratitis after SMILE procedure; however, this is likely to be under-reported.[1234567] Among these, five cases were presumed bacterial;[12] one patient had bilateral Pneumococcal infection,[3] two patients had Staphylococcal infection,[47] one patient had non-tuberculous Mycobacterial,[5] and another had fungal (Aspergillus)[6] infection [Table 1]. The infection was unilateral in all patients except two[35] patients. All cases presented within 1 week after surgery except one patient (with infection due to Mycobacterium)[5] who presented eight days after surgery. The predisposing factor could not be found in all cases except one, in which the fall of a foreign body was suspected.[7] The infection usually manifested at the interface. Epithelial defect[45] and endothelial plaque[5] were noted in 2 and 1 case respectively. All patients received medical therapy which was modified according to the sensitivity report of the organism. Four cases healed with medical therapy alone.[2] Most cases received one or repeated interface wash with antimicrobials. One patient recovered with PACK-CXL and medical therapy.[4] The current case received both interface wash and PACK-CXL.[7]Table 1: The details of reported SMILE-related corneal infectionsManagement of infections after refractive procedures always brings a heightened sense of urgency and responsibility to the refractive surgeon as the patient population for these surgeries is usually young, economically productive, and undergoing what is essentially a cosmetic procedure with preoperative excellent BCVA which is 20/20. Adding to the woes of the surgeon, the infecting organism which has made its way to the interface is not as easily scraped and it is pharmacologically challenging to deliver the therapeutic drug concentration to the interface. Flap lifting and scraping the bed or as in the case of SMILE, enlarging the incision and using a 26 G needle to scrape under the cap may be done for the microbiological workup.[7] Interface wash with antimicrobials delivers the drug to the site of infection. Scraping of the undersurface of the cap needs to be gentle to avoid perforation. The results of additional procedures such as PACK-CXL in infectious keratitis need further evaluation. In a randomized control trial by Prajna et al.[8] the authors did not find any additional benefit of PACK –CXL in the management of fungal keratitis. The current article,[7] however, presents the successful use of PACK-CXL as an additional procedure to the interface wash with antibiotics. Proposed mechanisms include limited microbial replication due to the intercalation of riboflavin with nucleic acids, damage to the pathogen cell walls by reactive oxygen species, and increased corneal resistance to enzymatic degradation.[4] Also, the inflammatory response may reduce due to CXL-induced apoptosis.[4] The addition of topical corticosteroids after the initial phase of treatment may be appropriate in a case of bacterial infection and may help to counter inflammation after a refractive procedure. As more SMILE procedures are done, further cases may be reported in future.
We read with interest the article by Ullman et al.1 reporting a patient who developed an anaphylactic reaction in response to topical moxifloxacin. We would like to share the details of our patient who developed Stevens-Johnson syndrome after the use of topical moxifloxacin eyedrops (Vigamox). The preparation also contained inactive ingredients, including boric acid, sodium chloride, and purified water and could have contained hydrochloric acid and sodium hydroxide to adjust the pH. A 48-year-old woman presented to us with numerous reddish lesions all over her body that had been present for the preceding 4 days. She had visited a general medical practitioner (7 days before visiting us) for ocular redness, for which she was prescribed topical moxifloxacin. She developed reddish elevated lesions around her eyes 36 hours after starting the eyedrops. Gradually, the lesions increased in number and involved the trunk and upper and lower extremities. Cutaneous examination showed numerous tender erythematous to purpuric macules coalescing to form patches, distributed over the periocular region, face, neck, trunk, abdomen, and extremities (Figure 1). Mucosal involvement (ocular, oral, and genital) was severe, characterized by erythema and painful erosions. There was no history of intake or application of any other drug except topical moxifloxacin over the previous 3 weeks. Causality assessment was done using WHO Uppsala Monitoring Center criteria and the Naranjo scale. Both the algorithms labeled the reaction as having a "probable" (Naranjo score = 5) relationship between the drug and development of Stevens-Johnson syndrome. Severity assessment by the Hartwig scale showed the reaction as severe (level 5). Topical moxifloxacin was withdrawn, and the patient was given supportive management. She responded well and recovered within 8 days.Figure 1: Numerous purpuric macules, patches, and erosions over the trunk and extremities suggestive of Stevens-Johnson syndrome.Stevens-Johnson syndrome and toxic epidermal necrolysis are severe mucocutaneous reactions that occur usually as a result of drugs and rarely to infections. The reactions are characterized by blistering and epithelial sloughing. Management of the condition involves determination and stoppage of the implicated drug and symptomatic management/supportive treatment. Topical moxifloxacin 0.5% is used commonly in ophthalmology in view of its broad-spectrum bactericidal efficacy against most common ocular pathogens. Although topical antibiotics are commonly used in cases of acute conjunctivitis by many clinicians, their exact role in such disease (which is most commonly viral in origin) without epithelial defect or corneal infiltrate needs further research. Benzalkonium chloride in some antibiotic drops can cause a conjunctivitis medicamentosa. Topical steroids might mitigate the inflammation and associated symptoms in adenoviral conjunctivitis but has the risk of prolonging the natural history of disease, dry eye,2 enhanced viral replication, and increased duration of viral shedding, making the patient contagious for a longer duration.3 Antivirals are ineffective, and the standard therapy is ocular hygiene and symptomatic management with frequent lubricating drops.4 Our case was unique because the patient developed Stevens-Johnson syndrome caused by the topical moxifloxacin eyedrop, itself. The most common side effects with topical moxifloxacin are dry eyes, redness, itching, irritation, and tearing. A severe form of corneal toxicity in both eyes with circumcorneal congestion and corneal edema has been reported after use of topical moxifloxacin in bilateral bacterial conjunctivitis; the corneal changes resolved after therapy was stopped.5 Two cases were reported that showed sterile corneal ulcers that persisted as long as the topical moxifloxacin was continued; the ulcers resolved after a change of antibiotic eyedrop.6 A 12-year-old girl was reported to develop Stevens-Johnson syndrome after using topical ofloxacin.7 Thus, rare instances of such adverse reactions should be kept in mind when prescribing topical moxifloxacin.
An article in the current issue of the Indian Journal of Ophthalmology (IJO) focuses on the identification of bugs that cause microbial keratitis using clinical photographs, with focus being on Pythium and fungi.[1] In this study, consultants and fellows were equally able or unable to identify the causative organisms as fungi or Pythium.[1] Diagnosis of the causative organism of microbial keratitis clinically helps in the early start of the correct medical management and thereby expedites healing. Clinical features may, to a certain extent, aid in the identification of the bacteria, fungus, parasite, or oomycete. Wreathe patterns or pin head–shaped infiltrates are usually seen in Nocardia keratitis. Cracked windshield appearance is seen in cases of atypical mycobacteria. Satellite lesions, endothelial exudates, and hyphate edges are noted in cases of fungal keratitis. Serpiginous keratitis is seen in patients with pneumococcal infections.[2] However, typical appearance may not always be seen due to multiple causes including mixed infections, alteration in appearance due to medical management, and drug toxicity. Pythium keratitis is now being recognized as a distinct entity. The clinical appearance may be like fungal keratitis, but it does not respond to antifungal drugs. Many cases of nonhealing fungal keratitis were later identified as being caused by Pythium.[3] Broad septate or sparsely septate hyphae growing on blood or chocolate agar, responding to linezolid and azithromycin rather than to antifungal agents and in advanced cases needing therapeutic keratoplasty with recurrence being common after corneal grafting distinguishes this organism.[3] Clinical features of Pythium keratitis are now being described more and more in literature.[4–6] Thick central infiltrate, reticular dot-like lesions, tentacular projections, peripheral furrowing, thinning and guttering, and multifocal lesions are all variably described in the literature.[3] Early spread to the limbus is also a feature. Many of the clinical characteristics may be confused with fungal keratitis such as hyphate edges and multifocal lesions. It is important to distinguish the two as medical management is entirely different. Pythium differs from fungi by not having ergosterol in its cell membrane and this renders most antifungal agents ineffective as they act primarily by inhibiting ergosterol synthesis.[6] A study from eastern India showed 100% positivity in the identification of Pythium in samples stained with iodine-potassium iodide-sulfuric acid and 93.8% positivity in samples with with the Gomori methenamine silver stain.[6] Both of these methods are not routinely used in microbiology labs. Ten percent potassium hydroxide with or without calcofluor white and Gram stain can also identify these aseptate or sparsely septate, broad, ribbon-like filaments. Colonies of Pythium on blood and chocolate agar show flat, feathery, colorless carpet-like growth which are difficult to scrape.[3,6] The distinction between fungal and Pythium keratitis according to this study was not only clinical but aided by smear, culture, and histopathology.[6] Initially, out of the 18 patients (1.4% of the 1251 patients with microbial keratitis) who were finally found to have Pythium keratitis, 13 (72.22%) were diagnosed as fungal keratitis, 4 as Pythium, and 1 as Acanthamoeba keratitis.[6] The initial smear examination was inconclusive in five patients; in three patients, the smear showed no organisms, three patients were suspected of having Pythium keratitis, and seven patients were suspected of fungal keratitis.[6] Reports of Pythium keratitis are more from the southern part of India, not merely due to increased prevalence but also due to lack of awareness.[3,6,7] The study from eastern India[6] found male agricultural workers to be affected, but the study from south India found females and software professionals also to have Pythium keratitis.[5] Distinguishing features of Pythium keratitis which are agreed upon by various authors include the following: The reticular dot-like pattern of the stromal infiltrates at the ulcer border Tentacle-like extensions Subepithelial ring infiltration Peripheral thinning Hypopyon Plaque-like lesions. A combination of these features along with an agricultural background and exposure to contaminated water may trigger suspicion. However, contact lens wearers and software professionals with no exposure to contaminated water have also been diagnosed with Pythium keratitis.[5] In conclusion, a high index of suspicion combined with clinical assessment and supported by microbiologists with awareness of the pathogen and expertise in diagnostic tools needed to identify this organism may lead to early diagnosis and proper management of this so-called "new bug" on the block.
A 50-year-old man had bilateral inferior atrophic patches on the iris with visible iris fibrils (shredded-wheat appearance) some of which were floating in the anterior chamber ([figure 1][1]).[1][2] There was no previous history of pain, redness, trauma or any ocular procedure. Corneal sensation was
Sir, I read with interest the case report on the closure of a macular hole over a serous retinal pigment epithelial detachment (PED) with intravitreal bevacizumab.[1] I want to humbly discuss a few facts. The role of anti-vascular endothelial growth factor (anti-VEGF) agents in serous PED without subretinal or intraretinal fluid or active choroidal neovascular membrane/idiopathic polypoidal choroidal vasculopathy may require further research. In the present case,[1] the shallow subretinal fluid at one margin of the macular hole could have been related to the macular hole itself or the mechanical effect of the high PED. In such a scenario, fundus fluorescein angiogram and indocyanine green angiogram would add significant scientific value and justification for the use of bevacizumab in this case, if they are available. Furthermore, we need to consider the fact that intravitreal anti-VEGF agents can cause retinal pigment epithelial tears[2] in cases of high serous PEDs. The rare but potentially blinding complications of intravitreal anti-VEGF agents such as endophthalmitis[3] and retinal detachment should be kept in mind. The goal of management with intravitreal bevacizumab in the presented case[1] may need elucidation. A history of systemic or local steroid use is also relevant in the presented case, as central serous chorioretinopathy, though unlikely in a 73 year old, needs to be ruled out. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
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