Tag: OF

  • Astigmatism

    Astigmatism is a common vision condition that causes blurred vision. It occurs when the cornea (the clear front cover of the eye) is irregularly shaped or sometimes because of the curvature of the lens inside the eye.

    An irregularly shaped cornea or lens prevents light from focusing properly on the retina, the light-sensitive surface at the back of the eye. As a result, vision becomes blurred at any distance. This can lead to eye discomfort and headaches.

    Astigmatism frequently occurs with other vision conditions like myopia (nearsightedness) and hyperopia (farsightedness). Together these vision conditions are referred to as refractive errors because they affect how the eyes bend or “refract” light.

    There are many causes to astigmatism. It can be hereditary and is usually present from birth. It can decrease or increase over time.

    comprehensive optometric examination will include testing for astigmatism. If necessary, your optometrist can provide eyeglasses or contact lenses that correct the astigmatism by altering the way light enters the eyes.

    Another option for treating astigmatism is a corneal procedure called orthokeratology (ortho-k). In this painless, noninvasive procedure, the patient wears a series of specially designed rigid contact lenses to gradually reshape the curvature of the cornea.

    Laser surgery can also treat some types of astigmatism. The laser changes the shape of the cornea by removing a small amount of eye tissue.

    Astigmatism

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    What causes astigmatism?

    Possible view through an astigmatic eye -- Image courtesy of Eyemaginations™

    The curvature of the cornea and lens bends the light entering the eye in order to focus it precisely on the retina at the back of the eye. In astigmatism, the surface of the cornea or lens has a somewhat different curvature.

    the surface of the cornea is shaped more like a football instead of round like a basketball, the eye is unable to focus light rays to a single point. Vision becomes out of focus at any distance.

    In addition, the curvature of the lens inside the eye can change, resulting in an increase or decrease in astigmatism. This change frequently occurs in adulthood and can precede the development of naturally occurring cataracts.

    Sometimes astigmatism may develop following an eye injury or eye surgery.

    Astigmatism also occurs due to a relatively rare condition called keratoconus in which the cornea becomes progressively thinner and cone-shaped. This results in a large amount of astigmatism, which causes poor vision that cannot be clearly corrected with eyeglasses. People with keratoconus usually need contact lenses for clear vision and eventually may need a corneal transplant.

    An optometrist can diagnose an astigmatism through a comprehensive eye examination. Testing for astigmatism measures how the eyes focus light and determines the power of any optical lenses needed to improve vision. This examination may include:

    • Visual acuity-When you read letters on a distance chart, you are measuring your visual acuity. Visual acuity is given as a fraction (for example, 20/40). The top number is the standardized testing distance (20 feet) and the bottom number is the smallest letter size read. A person with 20/40 visual acuity would have to get within 20 feet to read a letter that should be seen clearly at 40 feet. Normal distance visual acuity is 20/20.
    • Keratometry/Topography-A keratometer is the primary instrument used to measure the curvature of the cornea. By focusing a circle of light on the cornea and measuring its reflection, it is possible to determine the exact curvature of that area of the cornea’s surface. This measurement is particularly critical in determining the proper fit for contact lenses. A corneal topographer, which is gaining use, generates a contour map of the cornea and provides even more detail of the cornea’s shape.
    • Refraction-Using an instrument called a phoropter, your optometrist places a series of lenses in front of your eyes and measures how they focus light. This is performed using a handheld lighted instrument called a retinoscope or an automated instrument that evaluates the approximate focusing power of the eye. Based on your responses, the power is then refined to determine the lenses that allow the clearest vision. Despite improved technology, patient input remains integral in determining vision needs.

    With the information from these tests, your optometrist can determine if you have astigmatism. Your optometrist will use these findings, combined with those of other tests performed, to determine the power of any lens correction you need to provide clear, comfortable vision. Once testing is complete, your optometrist can discuss treatment options.

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    How is astigmatism treated?

    Eyeglasses are the primary choice for persons with astigmatism.

    People with astigmatism have several options to regain clear vision. They include:

    • Eyeglasses. People with astigmatism primarily choose eyeglasses to improve their vision. The eyeglasses contain a special cylindrical lens prescription that compensates for the astigmatism. This provides additional power in specific parts of the lens.

      Generally, a single-vision lens is prescribed to provide clear vision at all distances. However, patients over age 40 who have presbyopia may need a bifocal or progressive addition lens.

    • Contact lenses. Some people will have better vision with contact lenses rather than eyeglasses. Contact lenses may provide clearer vision and a wider field of view. However, since contact lenses are worn directly on the eyes, they require regular cleaning and care to safeguard eye health.

      Standard soft lenses may not be effective in correcting astigmatism. However, special toric soft contact lenses can correct for many types of astigmatism. Because rigid gas-permeable contact lenses maintain their regular shape while on the cornea, they can compensate for the cornea’s irregular shape and improve vision for people with astigmatism.

    • Orthokeratology. Orthokeratology (ortho-k) involves the fitting of a series of rigid contact lenses to reshape the cornea. The patient wears contact lenses for limited periods, such as overnight, and then removes them. People with moderate astigmatism may be able to temporarily obtain clear vision without lenses for most of their daily activities. Orthokeratology does not permanently improve vision. If patients stop wearing the retainer lenses, their vision may return to its original condition.
    • Laser and other refractive surgery procedures. Astigmatism can also be corrected by reshaping the cornea through LASIK (laser in situ keratomileusis) or PRK (photorefractive keratectomy). PRK removes tissue from the superficial and inner layers of the cornea. LASIK removes tissue only from the inner layer of the cornea.

    If you have an astigmatism, you have a wide range of options to correct your vision problem. In consultation with your optometrist, you can select the treatment that best meets your visual and lifestyle needs

  • BILATERAL RETINITIS FOLLOWING TYPHOID FEVER

    Abstract

    Background

    Post typhoid fever immune related reactions affecting the eye is a rare finding which can have various presentations in which typhoid retinopathy is not a well recognized sequelae.

    Case presentation

    Here we present a case of 59 year old male who presented with right eye sudden painless loss of vision 4 weeks after typhoid fever which was diagnosed and treated successfully. His BCVA was 2/60 in right eye and 6/6 in left eye. Fundus examination showed retinitis along with macular serous detachment in right eye and retinitis in left eye. Significant improvement in BCVA in right eye was observed after treatment with oral steroid with resolving retinitis lesions. Diagnosis of post typhoid immune mediated retinitis was made with good resolution following treatment.

    Conclusions

    Immune mediated retinitis is a rare sequelae to typhoid infection which can be successfully treated with systemic steroids with good resolution of the lesions.

    Keywords: Post typhoid fever, Immune mediated, Typhoid retinopathy, Retinitis

    Background

    Typhoid or enteric fever is a systemic disease which is characterized by fever and abdominal pain caused due to dissemination of Salmonella typhi or paratyphi. It is transmitted by food or water due to fecal contamination by ill or asymptomatic chronic carriers. A high incidence of typhoid fever in developing countries correlates with poor sanitation and lack of access to clean drinking water []. Ocular manifestations of typhoid fever are rare and include lid edema or abscess, dacryoadenitis, conjunctival petechiae or chemosis, corneal ulceration, uveitis, vitreous haemorrhage, retinal haemorrhage and detachment, stellate maculopathy, pigmentary retinopathy, optic neuritis, internal or external ophthalmoplegia, orbital haemorrhage or abscess. These complications are caused either by direct invasion of the organisms into the ocular tissue, or by hypersensitivity reaction such as vitreous haemorrhage after typhoid vaccination []. Here we are presenting a case of retinitis with macular serous detachment developing post typhoid fever.

    Case report

    A 59 year old male presented to our hospital 1 week after experiencing diminution of vision in the right eye. He gave a history of typhoid fever 4 weeks prior to presentation for which Widal test was performed to confirm diagnosis. The test results showed significant titres for ‘O’ antigen (>1:80) and ‘H’ antigen (>1:160) and negative for ‘AH’ and ‘BH’ antigens. He was subsequently started on oral Ofloxacin 400 mg twice daily for 2 weeks following which fever subsided. There was no known history of diabetes mellitus or hypertension. On ocular examination his best corrected visual acuity was 2/60 in the right eye and 6/6 in left eye. Anterior segment findings were unremarkable with IOP being within normal range for both eyes. Fundus examination of right eye showed white fluffy lesions along the superior and inferior arcades with superficial haemorrhages in around the macula with a macular star suggestive of retinitis (Fig. 1a). Left eye fundus showed few dispersed retinitis lesions with superficial haemorrhage along the superior arcade with intact foveal reflex (Fig. 1b). On optical coherence tomography of right eye underlying macular serous retinal detachment was noted (Fig. 2a). Blood tests were done to rule out VDRL and HIV status. X-cyton analysis of the anterior chamber aspirate was negative for organisms like Mycobacterial Tuberculosis, Toxoplasma Gondii, Hepes Simplex Virus, Cytomegalovirus and Varicella Zoster Virus. After analysis of the reports diagnosis of post typhoid retinitis in both eyes was made. Patient was started on oral prednisolone 1 mg/kg body weight which was tapered over 2 months along with monitoring of systemic and ocular health. Patient came for follow up every 2 weeks for 3 months. Every visit fundus photo was documented. After 2 months of initiating treatment there was an improvement in the BCVA in right eye to 6/6 which was maintained on further visits. Fundus examination revealed resolving lesions in both eyes (Fig. 3a, b) and OCT of the right eye showed resolution of the serous detachment (Fig. 2b).

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    a Fundus photo of right eye with white fluffy lesions suggestive of retinitis in the superior and inferior temporal arcades with macular star. b Fundus photo of left eye with white fluffy retinitis lesions in the superior temporal arcade

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    a Pre treatment OCT of right eye suggestive of macular edema. b A normal OCT photo of right eye post treatment

    An external file that holds a picture, illustration, etc. Object name is 40942_2017_65_Fig3_HTML.jpg

    a Post treatment fundus photo of right eye showing resolved retinitis lesions with few dispersed hard exudates. b Post treatment fundus photo of left eye with resolved retinitis lesions

    Retinitis is characterized by confluent areas of retinal whitening which progresses along the retinal blood vessels, often associated with intraretinal hemorrhages and hard exudates. A significant number of retinitis cases are thought to be idiopathic in etiology but a small proportion of cases are infectious in etiology such as Toxoplasma gondii (toxoplasmosis), Leptospira spp. (leptospirosis), Mycobacterium tuberculosis (tuberculosis) and other viral and fungal etiologies []. Non infectious causes of retinitis include sarcoidosis, Behcet’s disease. Infectious causes are usually unilateral and may be associated with mild vitritis. Patients can present with Neuroretinitis like picture with optic disc edema and macular hard exudates []. The macular star becomes prominent over first 3 weeks with neuroretinitis resolving over 6–8 weeks []. Leakage from the optic nerve head can lead to retinal swelling, exudation and edema, whereas retinal venous occlusion due to vasculitis results in intraretinal haemorrhage, cotton wool spots and retinal and optic nerve head edema []. It was postulated that microbial pathogens may be responsible for immune mediated ocular and systemic pathology through postinfectious immunological effects. These may be due to molecular mimicry eliciting an immune response that cross react with self antigens. Even though active infection is an unusual cause of retinal vasculitis, it is possible that many idiopathic and systemic disease associated cases are precipitated by previous encounters with microbes bearing DNA sequence homologous to retinal and vascular autoantigens. Similarity between S-antigen and peptides derived from yeast, E. coli, and Hepatitis B virus was found and there was an ability of these microbial peptides to elicit an immune response post infection []. Immune mediated retinitis is a clinical diagnosis most often when there is past history of infection few weeks or days prior to the onset of ocular manifestations. In this case, treatment with oral steroids was initiated due to inflammation of the retina, especially the macula which caused decrease in vision. By taking into consideration the time of onset of ocular presentation, previous history of typhoid fever and the response to oral steroids; the most likely diagnosis was post typhoid fever immune mediated retinitis with macular neurosensory detachment in the right eye and retinitis in left eye. In our case as the disc edema was not prominent, neuroretinitis was not considered as the diagnosis. Similar case reports by Relhan et al. [] and Laul et al. [] showed immune mediated response post typhoid fever presenting with neuroretinitis, vasculitis and macular detachment. Successful treatment with steroids was seen in them. Fusco et al. [] reported a case of bilateral chorioretinitis and stellate maculopathy post typhoid fever. However, in our case Xcyton analysis was done to rule out possible infectious retinitis before initiating steroid therapy, as it could exacerbate non immune mediated retinitis. Xcyton multiplex PCR analysis even though has the advantage of increasing the diagnostic yield it has certain disadvantages like false positive and negative results due to cross reactivity and preferential amplification, negative internal control if there is high amount of a particular target causing exhaustion of reagents and high cost.

    Conclusion

    Immune mediated retinitis can occur following systemic infection and can be managed with steroids followed by good resolution of the lesions. PCR analysis of the aqueous is a rapid diagnostic tool wherein multiple organisms can be detected and sight threatening bacterial and viral infections can be ruled out before initiation of steroid therapy.

    Authors’ contributions

    PM carried out AC tap for Xcyton analysis, did the manuscript editing and review, TT did the data acquisition, literature search and manuscript preparation, GG did the data acquisition and analysis and manuscript review, SA did the data acquisition and analysis. All authors read and approved the final manuscript.

    Acknowledgements

    None.

    Competing interests

    The authors declare that they have no competing interests.

    Contributor Information

    M. Prabhushanker, moc.liamg@reknahsuhbarprd.

    Tasneem T. Topiwalla, moc.liamg@spotsat.

    Geetha Ganesan, moc.liamg@nasenageeg.

    Sripal Appandaraj, moc.liamg@rd.lapirs.

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    7. Laul R, Atif Ali MIR, Shafi S. Typhoid aftermath: presenting as vasculitis, neuroretinitis and macular neurosensory detachment. Int J Med Res Health Sci. 2015;4:737–739. doi: 10.5958/2319-5886.2015.00143.5. [CrossRef[]
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