The Eye Signs of Vitamin a Deficiency

Total Page:16

File Type:pdf, Size:1020Kb

The Eye Signs of Vitamin a Deficiency XEROPHTHALMIA The eye signs of vitamin A deficiency Clare Gilbert Signs of chronic, long- Co-director: International Centre for Eye Health, Disability Group, London School standing VAD of Hygiene and Tropical Medicine, NOTE: To examine the eye, use a bright London, UK. ICEH torch in natural light. It is vitally important to realise that many Night blindness children who are vitamin A deficient will This can affect children as well as not have the eye signs, known as xeroph- pregnant and lactating women and is one thalmia (dry eye). This means that of the more common manifestations of children with the eye signs are only the deficiency. If VAD is prevalent in the ‘tip of the iceberg’ – there will be many community then there are often local other children in the community who are names for it. It is useful to find out what vitamin A deficient but who have completely these terms are so they can be used when normal eyes and vision. This is why asking about night blindness. It is more community approaches to control are difficult to find out if a child has night so vitally important (page 69–70). blindness, as children do not complain. The different eye signs of vitamin A Mothers need to be asked whether they deficiency (VAD) in children, as graded by have noticed that their child behaves the WHO, are: differently after the sun goes down or • Night blindness (XN) when they are in a dark room. The child • Conjunctival xerosis (X1A) will become less active, and may be • Bitot’s spots (X1B) Picture drawn by a child to illustrate fearful of moving around. Night blindness • Corneal xerosis (X2) night blindness tends to affect women who are pregnant • Corneal ulcer covering less than 1/3 of or lactating, and children aged 2–6 years. three times more likely to die as those the cornea (X3A) from the same community without night Conjunctival xerosis • Corneal ulcer covering at least 1/3 of the blindness, and children with both night This presents as dryness of the cornea, defined as keratomalacia (X3B) blindness and Bitot’s spots were almost conjunctiva (Figure 1) and is another sign • Corneal scarring (XS) nine times more likely to die.1 A study of long-standing deficiency. It can be It is very important to realise that children from Bangladesh showed that almost quite difficult to detect and is therefore do not first develop night blindness, then two-thirds of children with the most not a very reliable sign. Bitot’s spots and then corneal ulcers. severe form of xerophthalmia – known Figure 1. Conjunctival xerosis. Note the Some eye signs reflect long-standing as keratomalacia (a corneal ulcer affecting slight wrinkling of the temporal conjunctiva VAD, whereas other eye signs reflect more than a third of the cornea) – had severe, acute, sudden-onset VAD. A child died within a few months.2 who is vitamin A deficient, but who does Long-standing VAD is most prevalent not have any of the eye signs of long- in children aged 3–6 years (with night standing deficiency, may develop one of blindness, children as young as 2 years the severe eye signs, such as corneal old can be affected). Acute VAD is most ulcers, as a result of infection or diarrhoea. prevalent among children aged 1–4 years Children with any of the eye signs of (see Table 1). To prevent blindness and VAD are at high risk of dying. One of the child mortality from VAD, interventions first studies in Indonesia showed that must therefore be targeted at pre-school- children with night blindness were almost aged children. Clare Gilbert Table 1. World Health Organization (WHO) classification of vitamin A deficiency and the age groups most affected Peak age group Grade of xerophthalmia Type of deficiency Risk of death (years) XN Night blindness 2 – 6; adult women Long standing. Not blinding + X1A Conjunctival xerosis 3 – 6 Long standing. Not blinding + X1B Bitot’s spot 3 – 6 Long standing. Not blinding + X2 Corneal xerosis 1 – 4 Acute deficiency. Can be blinding ++ X3A Corneal ulcer/ <1/3 cornea 1 – 4 Severe acute deficiency. Blinding +++ X3B Corneal ulcer/keratomalacia ≥1/3 1 – 4 Severe acute deficiency. Blinding ++++ XS Corneal scarring (from X3) >2 Consequence of corneal ulceration +/– XF Xerophthalmic fundus Adults Long standing. Not blinding. Rare – 66 COMMUNITY EYE HEALTH JOURNAL | VOLUME 26 ISSUE 84 | 2013 Bitot’s spots Corneal ulcer usually because they were vitamin A Bitot’s spots (Figure 2) are characteristic If the acute deficiency is not reversed as deficient and the measles infection of VAD and are not caused by any other a matter of urgency, the cornea can resulted in depletion of their vitamin A condition. The slightly elevated, white become ulcerated and melt away. The stores. If you are not sure whether the foamy lesion is usually seen on the bulbar ulcer may have the appearance of a child you are seeing has keratomalacia, conjunctiva near the limbus, at the three small, punched-out area in the cornea ask about recent illness, particularly o’clock or nine o’clock positions. Bitot’s (Figure 4, top image), or the ulcer may measles. spots are more common on the temporal have a more fluffy appearance (Figure 4, Figure 6. Keratomalacia side. The white deposit consists of lower picture). In the absence of keratin, which the conjunctiva starts to secondary infection, the eye can look produce because the deficiency has led surprisingly white, as in both images in to ‘squamous metaplasia’ with the cells Figure 4; however, secondary infection in the conjunctiva becoming more like of the ulcer is common, leading to an skin than a mucous membrane. To a acutely inflamed eye (Figure 5). certain extent the white foamy material Figure 4. Corneal ulceration (X3a) can be wiped away from the surface of without secondary infection the conjunctiva, but does not disappear completely, even after the vitamin A Allen Foster deficiency has been treated. Hence, this sign does not necessarily mean that the The end result of corneal child is currently vitamin A deficient. ulceration Bitot’s spots usually appear in children The end result of corneal ulceration and aged 3–6 years. Bitot’s spots that do not keratomalacia is corneal scarring (Figure 7), respond to vitamin A treatment are more staphylomas (forward bulging of a badly common in school-aged children. damaged cornea) or phthisis bulbi (an eye that has shrivelled up), depending on Figure 2. Bitot's spots at the temporal the extent of the pathology in the cornea. Allen Foster limbus Most of the eye signs of VAD are symmetrical and bilateral, and so can lead to blindness. Figure 7. Corneal scarring Clare Gilbert Clare Gilbert Signs of acute, sudden- onset VAD Alfred Sommer Acute, sudden-onset VAD leads to poten- Figure 5. Corneal ulceration (X3a with tially blinding eye signs and is associated secondary infection with a very high mortality rate in children. Corneal xerosis This is drying of the cornea (Figure 3) and Clare Gilbert is a sign of sudden, acute deficiency. The cornea becomes dry because glands in If a child is found to have the eye signs of the conjunctiva no longer function VAD, spend time talking to his or her normally. This leads to loss of tears and mother or carer. Ask the mother about also loss of mucous, which acts as a the food the child is given, and how ‘wetting agent’. The lack of mucous Allen Foster often he/she is fed. Ask specifically together with lack of tears not only leads about foods which are rich in vitamin A. to the dry appearance but also increases Keratomalacia Ask if the child has been ill recently, or the risk of infection. The most severe form of xerophthalmia is had diarrhoea. Explain that the child is at keratomalacia (Figure 6), in which more Figure 3. Corneal xerosis risk of infection and that they need more than one-third of the cornea is affected. than one dose of vitamin A to treat the The cornea may become oedematous and problem, as is described on page 68. thickened, and then melt away. This Remember that other young children in occurs because the structure of the the family and the community are also collagen in the cornea is affected by a likely to be at risk. process known as necrosis. The cornea can be destroyed in just a few days. References 1 Sommer A, Tarwotjo I, Hussaini G, Susanto D. Children with keratomalacia are often Increased mortality in children with mild vitamin A malnourished, but children who previously deficiency. Lancet. 1983;2(8350):585–8. appeared relatively healthy can also 2 Cohen N, Rahman H, Sprague J, et al.Prevalence and determinants of nutritional blindness in develop keratomalacia following measles Bangladeshi children. World Health Stat Q. Alfred Sommer infection or episodes of diarrhoea; this is 1985;38(3):317–330. © The author/s and Community Eye Health Journal 2013. This is an Open Access article distributed under the Creative Commons Attribution Non-Commercial License..
Recommended publications
  • Topical Serum for Treatment of Keratomalacia
    PROCEDURES PRO > OPHTHALMOLOGY > PEER REVIEWED Topical Serum for Treatment of Keratomalacia Amy Knollinger, DVM, DACVO Eye Care for Animals Salt Lake City, Utah Corneal Anatomy An understanding of corneal anatomy is vital to determine if serum therapy for the treatment of keratomalacia should be initiated. The cornea makes up the anterior por- tion of the globe and provides multiple functions for vision: it is transparent (despite originating from surface ectoderm), thereby allowing for clear vision; it acts as the major refractive (bending of light) surface of the globe; and it provides a protective barrier between the globe and the environment The cornea consists of 4 layers in domestic species, being approximately 0.45–0.55 mm thick in the normal dog. The corneal epithelium is the most external layer overly- What You Will Need ing the stromal layer, which accounts for 90% of the total corneal thickness. The cor- n Sterile gloves neal epithelium in the dog and cat is 5–11 cells thick and has a turnover rate of n approximately 7 days.1 The stroma is made up of collagen fibers, which are precisely Clean #40 clipper blade arranged in parallel sheets running the entire diameter of the cornea, allowing for its n Chlorhexidine scrub and solution transparency. The third layer is an acellular membrane (ie, Descemet’s membrane), n Sterile needle and syringe which forms the basement membrane for the innermost layer, the endothelium. The n corneal endothelium is a single layer of hexagonally shaped cells forming the internal Red top sterile blood collection or barrier between the anterior chamber and the cornea.2 serum separator tube n Centrifuge Corneal Disease n Sterile pipette Corneal ulcers are classified by underlying cause.
    [Show full text]
  • JMSCR Vol||08||Issue||02||Page 208-210||February 2020
    JMSCR Vol||08||Issue||02||Page 208-210||February 2020 http://jmscr.igmpublication.org/home/ ISSN (e)-2347-176x ISSN (p) 2455-0450 DOI: https://dx.doi.org/10.18535/jmscr/v8i2.40 Keratomalacia - A Case Report Authors Deepthi Pullepu1*, Deepthi Janga2, V Murali Krishna3 *Corresponding Author Deepthi Pullepu Department of Ophthalmology, Rangaraya Medical College, Kakinada, Andhra Pradesh, India Abstract Xerophthalmia refers to an ocular condition of destructive dryness of conjunctiva and cornea caused due to severe vitamin A deficiency. Usually affects infants, children and women of reproductive age group. It is estimated to affect about one-third of children under the age of five around the world. Keratomalacia means dry and cloudy cornea which melts and perforates, caused due to severe vitamin A deficiency. Here we describe a case of 21 year old female with neurofibromatosis type 1 presenting with keratomalacia. Keywords: Vitamin A deficiency, Xerophthalmia, Keratomalacia. Introduction blindness is a significant contributor Vitamin A is essential for the functioning of the In India, it is estimated that there are immune system, healthy growth and development approximately 6.8 million people who have vision of body and is usually acquired through diet. less than 6/60 in at least one eye due to corneal Globally, 190 million children under five years of diseases; of these, about a million have bilateral age are affected by vitamin A deficiency involvement. They suffer from an increased risk of visual Corneal blindness resulting due to this disease can impairment, illness and death from childhood be completely prevented by institution of effective infections such as measles and those causing preventive or prophylactic measures at the diarrhoea community level.
    [Show full text]
  • Involvement of the Eye in Protein Malnutrition * -303
    Bull. Org. mond. Sante 1958, 19, 303-314 Bull. Wld Hith Org. INVOLVEMENT OF THE EYE IN PROTEIN MALNUTRITION * D. S. McLAREN, M.D., Ph.D., D.T.M. & H. Medical Research Officer, East African Institute for Medical Research, Mwanza, Tanganyika Formerly at the MRC Human Nutrition Research Unit, National Institute for Medical Research, London SYNOPSIS An extensive review of the literature on protein malnutrition, with special reference to the frequency of involvement of the eyes, has been made by the author. Consideration of accounts from all parts of the world and in many different languages, including early as well as more recent descriptions of the syndrome, indicates that this important complication has not received sufficient attention hitherto. The evidence available suggests that it is nearly always an accompanying deficiency of vitamin A that is responsible. Less commonly reported-and producing less severe effects-is deficiency of the B-complex vitamins, and there is no clear evidence to date that protein deficiency itself damages the eyes in these cases. The ways in which protein lack might interfere with various aspects of vitamin-A metabolism are discussed, but it is pointed out that their actual significance in human disease is not yet known. A low dietary intake of vitamin A is regarded by the author as being the prime factor in the causation of eye complications, and attention is drawn to the necessity to correct this as part of any prophylactic or therapeutic programme aimed primarily at combat- ing protein malnutrition. The syndrome known by such various names as kwashiorkor, nutritional oedema syndrome, sindrome pluricarencial, and many others (Trowell, Davies & Dean, 1954), and characterized chiefly by a dietary deficiency ofprotein, has been reported as occurring amongst most of the malnourished communities of the world.
    [Show full text]
  • Clinical Case Revista Colombiana De Ciencias Pecuarias
    Estrada RD et al Melting ulcer in a colt 31 Clinical case Revista Colombiana de Ciencias Pecuarias Melting ulcer in a colt: clinical management and evolution ¤ Úlcera fundente en un potro: manejo clínico y evolución Úlcera colagenolítica em um potro: manejo clínico e evolução Rubén D Estrada 1, MV; Susana Penagos 2, est MV; Elizabeth Viera 2, est MV; Paula A Angulo 2, est MV; Maria P Arias 2*, MV, MS, PhD. 1MV Actividad independiente 2Facultad de Medicina Veterinaria y Zootecnia, Universidad CES, AA 054591, Medellín, Colombia (Received: June 1, 2012; accepted: November 19, 2012) Summary Anamnesis : a colt showing a whitish coloration accompanied by abundant secretion on the left eye was examined. Clinical and laboratory findings: at ophthalmological examination, signs of melting ulcer were observed. Culture isolation revealed positive growing of Flavobacterium sp. and Gram-negative rods. Treatment approach : several keratectomies and tarsorrhaphies, as well as exhaustive antiproteinases, anti- inflammatory, and antibiotic treatments, were conducted. Treatment focused on reducing inflammatory response, eliminating infective organisms, and promoting epithelial healing. Colt showed complete recovery of vision after 3 months. Conclusions: clinical management of melting ulcer implies exhaustive, though unexpensive, treatment. Key words: cornea, keratectomy, keratomalacia, ophthalmology, tarsorrhaphy Resumen Anamnesis : se examinó un potro que presentó una coloración blanquecina acompañada de abundante secreción en el ojo izquierdo. Hallazgos clínicos y de laboratorio : al examen oftalmológico se observaron signos de ulcera fundente. El aislamiento por cultivo mostró crecimiento de Flavobacterium sp. y cocos Gram negativos. Abordaje terapéutico : se realizaron varias queratectomías y tarsorrafias, además de un tratamiento exhaustivo con antiproteinasas, antiinflamatorios y antibióticos enfocado a reducir la respuesta inflamatoria, eliminar los microorganismos infecciosos y promover la cicatrización epitelial.
    [Show full text]
  • Bilateral Keratomalacia Secondary to Diet Induced Vitamin a Deficiency in an Ethiopian Young Woman: a Case Report
    Bilateral Keratomalacia… Kumale T. et al. 295 CASE REPORT Bilateral Keratomalacia Secondary to Diet Induced Vitamin A Deficiency in an Ethiopian Young woman: A Case Report Kumale Tolesa Daba1*, Dagmawit Kifle1, Jafer Kedir Ababora1 ABSTRACT OPEN ACCESS BACKGROUND: Diet induced vitamin A deficiency is less Citation: Kumale Tolesa Daba, Dagmawit commonly seen in otherwise healthy adults, due to large store of Kifle, Jafer Kedir Ababora. Bilateral vitamin A in the body. Night blindness is the commonest Keratomalacia Secondary to Diet Induced Vitamin A Deficiency in an Ethiopian manifestation of vitamin A deficiency in adults, whereas Young woman: A Case Report. Ethiop J Keratomalacia is a rare manifestation. Health Sci. 2018;29(2):295 doi:http://dx.doi.org/10.4314/ ejhs. v29i2.18 CASE REPORT: A 27 years old Ethiopian woman came to Jimma Received: June 22, 2018 University Department of Ohthalmology with a compliant of Accepted: October 27, 2018 protrusion of the globe content of both eyes within a week, after Published: March 1, 2019 Copyright: © 2019 Kumale Tolosa Daba, having redness and fear of light of both eyes for 2 months. She was et al. This is an open access article a mother of twins and had low socioeconomic status. On general distributed under the terms of the Creative examination, she was cachectic with enlarged parotid glands. On Commons Attribution License, which permits unrestricted use, distribution, and ocular examination, she was bilaterally blind and had dry ocular reproduction in any medium, provided the surface. There was bilaterally melted cornea with prolapsed uveal original author and source are credited.
    [Show full text]
  • Therapy-Resistant Dry Itchy Eyes Rima Wardeh* , Volker Besgen and Walter Sekundo
    Wardeh et al. Journal of Ophthalmic Inflammation and Infection (2019) 9:13 Journal of Ophthalmic https://doi.org/10.1186/s12348-019-0178-7 Inflammation and Infection BRIEFREPORT Open Access Therapy-resistant dry itchy eyes Rima Wardeh* , Volker Besgen and Walter Sekundo Abstract An 8 years old male presented to our clinic with dry eye symptomes. Different therapiy attemps were made in the last few months and did not lead to any improvement. Examining this patient revealed multiple signs of vitamin A deficiency, which could confirmed by laboratory examination. The initial substitution of vitamin A led to a fast rehabilitation and a following nutrition consulting kept the patient symptom-free over 6 month follow up. Vitamin A deficiency -although rare in the developed countries- is an importent differential diagnosis of the dry eye especially in children. Vitamin A deficiency not only causes ocular manifistaion, but also general symptoms. Dietary change and initial subtitution is the key element for a fast and sustaining improvement. Medical history follow-up examination showed no improvement in the An 8-year-old male child was referred to our pediatric visual acuity nor in the corneal surface. In addition, the ophthalmology department because of burning sensation conjunctiva had developed triangular-shaped superficial and itching in both eyes during the last 4 months. His spots with keratinization in the bulbar conjunctiva nas- mother reported that the child was always pinching his ally, inferiorly, and temporally near the limbus of both eyes while reading or focusing. Topical therapy with eyes. With these findings, the diagnosis of conjunctival dexamethasone eye drops, antihistamine eye drops and corneal xerosis due to vitamin A deficiency was sus- (ketotifen), antibiotic eye drops (ofloxacine) and im- pected.
    [Show full text]
  • The Definition and Classification of Dry Eye Disease
    DEWS Definition and Classification The Definition and Classification of Dry Eye Disease: Report of the Definition and Classification Subcommittee of the International Dry E y e W ork Shop (2 0 0 7 ) ABSTRACT The aim of the DEWS Definition and Classifica- I. INTRODUCTION tion Subcommittee was to provide a contemporary definition he Definition and Classification Subcommittee of dry eye disease, supported within a comprehensive clas- reviewed previous definitions and classification sification framework. A new definition of dry eye was devel- T schemes for dry eye, as well as the current clinical oped to reflect current understanding of the disease, and the and basic science literature that has increased and clarified committee recommended a three-part classification system. knowledge of the factors that characteriz e and contribute to The first part is etiopathogenic and illustrates the multiple dry eye. Based on its findings, the Subcommittee presents causes of dry eye. The second is mechanistic and shows how herein an updated definition of dry eye and classifications each cause of dry eye may act through a common pathway. based on etiology, mechanisms, and severity of disease. It is stressed that any form of dry eye can interact with and exacerbate other forms of dry eye, as part of a vicious circle. II. GOALS OF THE DEFINITION AND Finally, a scheme is presented, based on the severity of the CLASSIFICATION SUBCOMMITTEE dry eye disease, which is expected to provide a rational basis The goals of the DEWS Definition and Classification for therapy. These guidelines are not intended to override the Subcommittee were to develop a contemporary definition of clinical assessment and judgment of an expert clinician in dry eye disease and to develop a three-part classification of individual cases, but they should prove helpful in the conduct dry eye, based on etiology, mechanisms, and disease stage.
    [Show full text]
  • GOBLET CELL RESPONSE to VITAMIN a TREATMENT for CORNEAL Xerophthiklmia ALFRED SOMMER, M.D., and WILLIAM R
    GOBLET CELL RESPONSE TO VITAMIN A TREATMENT FOR CORNEAL XEROPHTHikLMIA ALFRED SOMMER, M.D., AND WILLIAM R. GREEN, M.D. Baltimore, M1 yland In 11 patients with active corneal xerophthalmia, conjunctival bi­ opsies were obtained at various intervals after m&sslve-dose system­ ic vitamin A therapy. Goblet cells began tb repopulate the infero­ nasal quadrant of the conjunctivas after two weeks, and they reached normal concentrations after one month. Corneal healing proceeded much more rapidly than that, suggesting that a full complement of mucus-secreting conjunctival goblet -,Uls is not essential for ,stora­ tion and maintenance of normal corneal appearance. By its effect on tear filir dynamics, loss guardian, we obtained 3 X 4 mm biopsy of mucus-secreting goblet cells is thought specimens of temporal (and usually l'er­ to contribute to the corneal changes ob- onasal) bulbar conjunz'tiva before therapy 14 ther­ served in vitamin A deficiei-y. In a or at a predetermined interval aftei, recent study ofpatients with mild vitamin apy began, or both. Posttreatment con­ A-responsive conjunctival xerosis, how- junctival specimens were always obtained Spei­ ever,' it often took longer for goblet cells from a previously unbiopsied eye. to return than it reportedly takes for mens were fixed and processed In routine stain and corneal xerophthalmia to heal." We fashion and stained with Dane's report the goblet cell response to with PAS to Identify goblet cells.' herein vitamin defi­ vitamin A therapy in patients with vita- All subjects had severe A min A-responsive vorneal xerosis and ul- ciency' and all responded to standard7 systemic vitamin A therapy.
    [Show full text]
  • Corneal Ulceration Diagnosis Andtreatmentof Promote Healing
    Veterinary NURSING EDUCATION Diagnosis and Treatment of Corneal Ulceration Sara Grabiel-Duncan, BS, LVT, VTS (Ophthalmology) Anatomy gland, which contributes 35-50% of LEARNING OBJECTIVE: The cornea is composed of 5 distinct layers: tears and the gland of the nictitating Readers should gain a basic membrane which contributes 35-65% understanding of the anatomy 1. Pre-corneal tear film—the most of the aqueous component of tears. and physiology of the cornea superficial (outermost) layer of the cornea This layer is responsible for providing and diagnosing corneal ulcers. is a fluid layer which functions to hydrate, nutrition and oxygen to the cornea and They will also be able to identify protect and lubricate the cornea, provide conjunctiva and also functions to keep potential management options nutrition to corneal cells and tissues the epithelium hydrated. available. of the avascular cornea, and maintain optical clarity. The pre-corneal tear film is • Mucoid layer—the innermost Diagnosis and Treatment composed of at least three distinct layers: layer of the pre-corneal tear film is lceration of the cornea is one of the composed of mucin and is produced Umost prevalent clinical abnormalities • Oil layer—the superficial (outermost) primarily by conjunctival goblet cells. affecting the canine cornea. Diagnosis layer consists of oils produced by the This layer increases the surface area and treatment of corneal ulceration is not meibomian glands located within and binds the middle aqueous layer to identical for all types of corneal ulcers. the eyelids. The oil layer permits the the corneal surface. (Blinking partially An inaccurate diagnosis and improper eyelids to move in a gliding action inter-mixes the three component treatment of corneal ulcers may have and prevents evaporation of the second layers of the tear film) profound effects on corneal sepsis, healing, (aqueous) layer of the tear film.
    [Show full text]
  • Keratomalacia in a Patient with Psychogenic Vitamin a Deficiency
    CASE REPORT Keratomalacia in a Patient With Psychogenic Vitamin A Deficiency Sidney M. Gospe III, MD, PhD,* Bozho Todorich, MD, PhD,*† Yevgeniya G. Foster, MD,‡ Gary Legault, MD,*§ Suzanne K. Woods, MD,‡¶ Alan D. Proia, MD, PhD,*k and Melissa Daluvoy, MD* corrected promptly. We report a rare example of a patient Purpose: fi To report the clinical and histopathological ndings of with subacute painful bilateral vision loss arising from a patient with bilateral keratomalacia arising from severe vitamin A keratomalacia from severe VAD secondary to malnutrition deficiency from panic disorder-related malnutrition. related to a psychiatric disorder. Methods: Case report. Results: A 47-year-old male with panic disorder presented with 1 CASE REPORT month of painful vision loss sequentially affecting the right and left A 47-year-old white man presented to the emergency eyes. He exhibited bilateral conjunctival xerosis with complete department complaining of 1 month of pain, redness, photophobia, corneal melt in the right eye and a large corneal epithelial defect with and decreased vision in the right eye (OD), with similar symptoms underlying anterior chamber inflammation in the left eye. Laboratory starting in the left eye (OS) 1 week later. Over-the-counter vasoconstrictor eyedrops did not relieve his symptoms, and his investigation revealed undetectable serum vitamin A levels attributed vision had progressively deteriorated bilaterally with worsening eye to self-induced vomiting and starvation. He was treated with high- pain. He denied ocular trauma or contact lens use. dose vitamin A, but the right eye required enucleation. The The patient had a medical history of gastroesophageal reflux histological findings are reported.
    [Show full text]
  • A Review of Topical and Systemic Vitamin Supplementation in Ocular Surface Diseases
    nutrients Review A Review of Topical and Systemic Vitamin Supplementation in Ocular Surface Diseases Paolo Fogagnolo 1,*, Stefano De Cilla’ 2, Micol Alkabes 2, Pierfilippo Sabella 1 and Luca Rossetti 1 1 Ophthalmology Unit, Department of Health Sciences, San Paolo Hospital, Università degli Studi di Milano, 20142 Milan, Italy; pierfi[email protected] (P.S.); [email protected] (L.R.) 2 Ophthalmology Unit, Ospedale Maggiore della Carita, 28100 Novara, Italy; [email protected] (S.D.C.); [email protected] (M.A.) * Correspondence: [email protected] Abstract: In the homeostasis of the ocular surface, vitamins play a critical role in regulating inflam- matory responses and promoting cell differentiation, development and correct function. Systemic vitamin supplementation has been available for many decades; in recent years, thanks to pharma- cological advancements, topical vitamin delivery has also become available in an attempt to better treat ocular surface disease (OSD) and dry eye disease (DED). In this paper, we reviewed the current evidence on the role of vitamin supplementation in OSD and DED. We originally searched the PubMed archive, inspected the references and restricted the search to pertinent papers. The body of evidence was evaluated using the amelioration of both signs and symptoms as the outcome, when available. We found that in patients with vitamin deficiency, systemic supplementation of Vitamin A is effective in treating OSD, reducing both DED signs and symptoms. Additionally, systemic supplementation of vitamin D is useful in reducing DED symptoms and increasing tear volume. Citation: Fogagnolo, P.; De Cilla’, S.; Vitamin A is also effective in reducing DED signs and symptoms when administered locally.
    [Show full text]
  • Ocular Surface Disease
    Ocular Surface Disease Authors: Alex Lange Maciej Jesse Vista Klinik Binningen Table of Contents • Dry-Eye Syndrome • Nutritional Disorders • Rosacea • Exposure Keratopathy • Seborrhoic blepharitis • Floppy Eyelid Syndrome • Chalazion • Superior Limbic Keratokonjunctivitis • Sarcoidosis • Recurrent Corneal Erosion • Ichthyosis • Persistant Corneal Epithelial Defect • Ectodermal Dysplasia • Neurotrophic Keratopathy • Xeroderma pigmentosum • Trichiasis and Distichiasis • Noninflammantory Vascular Anomalies of • Mucus-fishing Syndrome the Conjunctiva • Dellen • Herediatary Hemorrhagic Teleangiectasia • Contact lens-related Problems • Lymphangiectasia • Limbal Stem Cell Deficiency Dry—Eye Syndrome • Definition: «Multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance, and tear-film instability with potential damage to the ocular surface. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface» (DEWS, 2007) • Dry eye represents a disturbance of the lacrimal functionl unit (LFU), consisting of the lacrimal glands, ocular surface (cornea, conjunctiva, and meibomian glands), eyelids and the sensory nerves that connect them • LFU regulates the components of the tear film and responds to environmental, endocrinologic, and cortical influences Quelle: https://openi.nlm.nih.gov/detailedresult.php?img=PMC3587314_IRI-32-19-g001&req=4 Dry – Eye Syndrome • Function of the LFU: - Tear-film integrity (lubricating, antimicriobial, and nutritional roles) - Ocular surface health (maintaining corneal transparency and surface stem cell population) - Quality of image projected onto the retina Mechanism of Dry Eye Core mechanisms • Tear-film hyperosmolarity • inflammatory events leading to cell death by apoptosis • loss of goblet cells • disturbance of mucin expression • tear-film instability • Tear-film instability exacerbates ocular surface hyperosmolarity -> vicious circle Dry Eye Syndrome - vicious circle Figure from AAO, Basic and Clinical Science Course, Section 8 , 2013-2014.
    [Show full text]