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INTRODUCTION: Allergic Ocular Diseases (AODs) like Atopic Keratoconjunctivitis (AKC) and Vernal Keratoconjunctivitis (VKC) are chronic forms of ocular allergy that can cause severe visual complications. Pathogenesis of AODs is uncertain and treatment has been a challenge for ophthalmologists. Tacrolimus, a 23-member cyclic macrolide lactone derived from [streptomyces tsukubaensis] now in ointment form has been successfully used in AODs. AIM: To study the therapeutic effect of 0.1% Tacrolimus eye ointment in patients with Allergic Ocular Diseases (AODs). MATERIALS AND METHODS: This prospective observational study was conducted on 36 patients with severe AOD and moderate cases not responding to conventional treatment. They were treated with 0.1% tacrolimus eye ointment twice daily for minimum three months in addition to conventional treatment and observed for a period of 6 months. Symptoms and signs after treatment were evaluated. Grades of clinical signs were assessed based on slit lamp clinical photographs; development of possible complications was assessed and analysed by Wilcoxon signed rank test. RESULTS: Mean age of patients was 9.3±4.3 years and mean duration of AODs was 3.1±1.8 years. The scores on both the four point scales for signs and symptoms decreased significantly (p<0.0001) after 1 month of 0.1% Tacrolimus eye ointment treatment. Itching was the first symptom to show dramatic relief and conjunctival hyperaemia was the first sign to show improvement. 88.88% of patients were successfully weaned off topical steroids in 6 months into Tacrolimus treatment. Even in patients unresponsive to 0.1% topical Cyclosporine, symptoms and signs scores decreased significantly (p<0.0001). The most common adverse reaction was a transient burning sensation (36.11%). CONCLUSION: Topical 0.1% Tacrolimus eye ointment was found to be a safe and effective treatment in cases of AODs and also worked as steroid sparing and replacing agent. It was also found effective in patient's refractory to topical Cyclosporine.
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Chronic Myeloid Leukaemia (CML) causes retinopathy manifesting as venous dilation and tortuosity, perivascular sheathing, retinal haemorrhages, microaneurysms, cotton-wool spots and optic nerve infiltration. Retina is the most commonly involved intraocular structure in CML. However, retinal involvement is a rare form of presentation of CML and few cases have been reported. We report a case of CML presenting as unilateral sudden visual loss. Fundus showed multiple white centered retinal haemorrhages in both eyes with unilateral macular oedema. Blood work-up showed raised WBC count, high platelet count and low Haemoglobin. Cytological analysis of bone marrow biopsy confirmed Philadelphia chromosome. After a course of Imatinib, visual acuity improved and haemorrhages resolved with normalization of macular thickness. In our case, patient presented early, leading to early detection producing better visual prognosis. This highlights the importance of detailed hematological work up in patients with retinal involvement to rule out leukaemic retinopathy.
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Ocular injury secondary to foreign body remains an important cause of ocular morbidity with or without blindness in working population. Intraocular foreign body may have varied clinical presentation. Initially it may look an apparently normal eye followed by obvious ocular symptoms depending upon its location and degree of inflammation. It can result in partial or full thickness penetration of sclera with or without involvement of posterior segment. We hereby present two cases of metallic intrascleral foreign body entry through upper lid in young carpenters following hammer and chisel injury. In case 1, Intrascleral location of foreign body was confirmed with X ray orbit and B scan ultrasonography while in case 2 the diagnosis of intrascleral foreign body was missed at the first visit to ophthalmology clinic Both the patients underwent exploratory surgeries where intrascleral metallic foreign bodies were found without ocular penetration. An intrascleral foreign body may be missed due to small penetrating scleral wound covered by a large subconjunctival haemorrhage accompanied by minimal or no signs of inflammation and failure on part of treating ophthalmologist to suspect an intrascleral foreign body. To establish a diagnosis of intraocular particularly intrascleral foreign body, careful history taking and clinical examination along with use of imaging studies are mandatory steps which help in successful management and good visual outcome. These cases highlight the importance of considering a presumptive diagnosis of retained intrascleral foreign body in every patient with a history of penetrating ocular trauma through lid or a visible wound/scar on the lid.
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Lamellar laceration of the cornea may occur following ocular trauma. The management of lamellar laceration will depend on whether the lacerated corneal flaps are displaced or undisplaced. We hereby report an unusual case of large traumatic lamellar corneal laceration in right eye in a 14-year-old girl presenting with diminution of vision. Slit lamp biomicroscopic examination showed partial thickness corneal flap of 11.5mm X 7mm from 11o'clock to 6 o'clock position with 3 mm superonasal displacement associated with stromal folds and shifting of inferior limbus and conjunctiva. Surgery was the appropriate option which included visualization of inferior limbus by incising conjunctiva, repositioning of displaced corneal flap and securing it with sutures. Immediate examination and proper surgical management of lamellar corneal injuries results in good visual outcome and prevention of complications like fibrous ingrowth and infection.