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OCULAR
MANIFESTATION OF
VITAMIN A DEFICIENCY.
BY S.PERSIS BENETTA
M.OPTOM 2ND YEAR
Introduction
 Ocular manifestation of Vitamin A deficiency are referred to has..
What is Xerophthalmia?
 The term is used for all the changes in the structures in the eye, including,
 Conjunctiva
 Cornea
 Retina
 Rods
 cones
Etiology
 Dietary deficiency of vitamin A
 Defective absorption from the gut
 Protein energy malnutrition (PEM)
 infections
WHO classification.
Xerophthalmia classification Ocular signs
XN Night blindness
X1A Conjunctival xerosis
X1B Bitot’s spot
X2 Corneal xerosis
X3A Keratomalacia <1/3 corneal surface
X3B Keratomalacia >1/3 corneal surface
XS Corneal scar
XF Xerophthalmic fundus
Clinical features
 Earliest symptom of Xerophthalmia
 One or more patches of dry, lusterless, non wettable conjunctiva
 Patches seen in interpalpebral of the nasal and temporal quadrants
 In advanced cases it involves the whole conjunctiva resulting in
conjunctival thickening, wrinkling.
 Bitot’s spot is raised white, foamy, triangular patch of keratinized
epithelium situated in the bulbar conjunctiva.
 Bilateral
 Temporal
 Punctate keratopathy
 Nasally
 Granular pebby dryness
 Cornea lacks lustre
 Stromal defects
 Due to liquefactive necrosis
 Small ulcers in peripheral
 Large ulcers involve centrally or entire cornea
 These might result in blindness
 Healing of stromal defects results in corneal scar of different densities and
size
 Seed like, raised white lesions scattered uniformly over the fundus
Treatment.
 Local ocular therapy – artificial tears, instilled every 3-4 (hrs)
 Vitamin A therapy – treatment applies to all the stages
 Treatment of underlying conditions
AGE DOSAGE
>1 year 200,000 IU of Vit A oral or 100,000 IU by
intramuscular inj
<1year 50,000 IU of Vit A
Women / pregnant woman
XN 10,000 IU VIT A
X1A 10,000 IU VIT A
X1B 10,000 IU VIT A
Corneal Xerophthalmia 200,000 IU VIT A
CONTROL AND PREVENTION
of VIT A DEFICIENCY.
Short term approach.
Patients Treatment
Infants 6-12 months / weight <8kgs 100,000 IU Vit A, orally every 3-6 months
Children >1 yr / <6yrs 200,000 IU Vit A, orally every 6 months
Lactating mothers 20,000 IU Vit A orally
Infants < 6 months (not being breast fed) 50,000 IU Vit A orally
Vit A supplements – Child Survival and
Safe Motherhood (CSSM)
DOSAGE AGE
First dose (1lakh IU) 9 month along with measles vaccine
Second dose (2lakh IU) 18 month along with DPT/OPV
Third dose (2lakh IU) 2 years
Medium term approach.
 Food fortification with vitamin A
Long term approach.
 Vitamin A rich foods.
 Nutritional health education.
RESEARCH PAPER TALKS
 Cure was associated with certain foods—in early times with topical
application or ingestion of animal and fish liver, and in later years with
ingestion of plant foods containing green and yellow pigments (Wolf,
1996).
 Steenbock (1919) postulated, and later confirmed, that carotenoid from
yellow maize (corn) could support growth and prevent ocular lesions.
 Since Isler et al. (1947) discovered a cost-effective way to synthesize
vitamin A, cure and prevention are also possible through commercially
produced, synthetic vitamin A.
 Breast-fed infants do not usually show clinical deficiency for at least 4 to 6 months after
birth. They may be at a marginally adequate point however, if breast-fed by a
malnourished, vitamin A-depleted mother (Underwood, 1994a).
 At the same time, if breast-fed, even from a malnourished mother whose breast milk
vitamin A has been improved through direct maternal supplementation (200,000 IU of
vitamin A given within 2 months postpartum [WHO/UNICEF/IVACG, in press]), adequate
infant vitamin A status may be prolonged beyond 6 months (Stoltzfus et al., 1993).
 Vitamin A requirements , therefore, are greatest during periods of rapid
growth—infancy and early childhood, adolescence, and pregnancy—and
when the vitamin is lost from the body through normal physiologic
processes, such as lactation, or through nonphysiological losses brought
about by frequent disease, such as malabsorption, diarrhea, and febrile
infections (FAO/WHO, 1988).
 The bioavailability of the provitamin A carotenoids from plants is greatly
influenced by the nature of the embedding matrix (i.e., fibrous, dark green
leafy vegetables [DGLV] or soft-fleshed yellow/orange vegetables and
fruits) and the composition of the accompanying meal.
 Populations with subclinical deficiency—tissue concentrations of vitamin A
low enough to have adverse health consequences, even in the absence of
xerophthalmia, WHO's current definition of VAD (WHO, 1996a).
Approaches To The Prevention Or
Correction Of Vad.
 Vitamin A intervention approaches are commonly grouped into two main
control strategies: (1) direct increase in vitamin A intake through dietary
modification with natural or fortified foods and supplements and (2)
indirect public health measures to control disease frequency. Information,
education, and communication (IEC), including social marketing and
specific vitamin A-oriented nutrition education, may or may not
accompany each of the above interventions.
 VAD-endemic areas require special attention to micronutrient
supplementation.
 Vitamin A plays a central role in the body’s ability to fight off infectious
diseases, deficiency can have far-reaching health consequences. People
with a Vitamin A deficiency are more susceptible to measles, diarrhoea,
respiratory infections and HIV/AIDS.
 Improving the vitamin A status of deficient children aged 6 months to 6 years
dramatically increases their chances of survival.
 Good vitamin A status is associated with reduction in the rate of hospital
admissions and reduced need for out-patient services at clinics and therefore
lowers overall cost of health services.
 Recent studies suggest that preventing vitamin A deficiency of women during
and before pregnancy greatly reduces their risk of mortality and morbidity
around the time of childbirth, probably through increasing resistance to
infection and lowering levels of anaemia
 Many International organizations like UNICEF and WHO have made the
strategies for the prevention and elimination of vitamin A deficiency
disease and they provide these strategies to the affected countries in the
form of action plan, literature
 It isthe responsibility of the governments and the health departments of
the affected countries to implement these strategies for the betterment of
the future of common people and children.
References
 Prevention of Vitamin A Deficiency
Barbara A. Underwood, Ph.D.
National Eye Institute https://www.ncbi.nlm.nih.gov/books/NBK230106/
 Strategies for the prevention and elimination Of Vitamin A Deficiency.
Submitted as a part of a SUMMATIVE ESSAY OF INTERNATIONAL
NUTRITION IN MSC IN PUBLIC HEALTH
https://www.researchgate.net/publication/324719932_Strategies_for_the_prev
ention_and_elimination_Of_Vitamin_A_Deficiency_Module_Title_INTERNATION
AL_NUTRITION
Thank You!

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Vitamin A deficiency and prevention

  • 1. OCULAR MANIFESTATION OF VITAMIN A DEFICIENCY. BY S.PERSIS BENETTA M.OPTOM 2ND YEAR
  • 2. Introduction  Ocular manifestation of Vitamin A deficiency are referred to has..
  • 3. What is Xerophthalmia?  The term is used for all the changes in the structures in the eye, including,  Conjunctiva  Cornea  Retina  Rods  cones
  • 4. Etiology  Dietary deficiency of vitamin A  Defective absorption from the gut  Protein energy malnutrition (PEM)  infections
  • 5. WHO classification. Xerophthalmia classification Ocular signs XN Night blindness X1A Conjunctival xerosis X1B Bitot’s spot X2 Corneal xerosis X3A Keratomalacia <1/3 corneal surface X3B Keratomalacia >1/3 corneal surface XS Corneal scar XF Xerophthalmic fundus
  • 6. Clinical features  Earliest symptom of Xerophthalmia
  • 7.  One or more patches of dry, lusterless, non wettable conjunctiva  Patches seen in interpalpebral of the nasal and temporal quadrants  In advanced cases it involves the whole conjunctiva resulting in conjunctival thickening, wrinkling.
  • 8.  Bitot’s spot is raised white, foamy, triangular patch of keratinized epithelium situated in the bulbar conjunctiva.  Bilateral  Temporal
  • 9.  Punctate keratopathy  Nasally  Granular pebby dryness  Cornea lacks lustre
  • 10.  Stromal defects  Due to liquefactive necrosis  Small ulcers in peripheral  Large ulcers involve centrally or entire cornea  These might result in blindness
  • 11.  Healing of stromal defects results in corneal scar of different densities and size
  • 12.  Seed like, raised white lesions scattered uniformly over the fundus
  • 13. Treatment.  Local ocular therapy – artificial tears, instilled every 3-4 (hrs)  Vitamin A therapy – treatment applies to all the stages  Treatment of underlying conditions AGE DOSAGE >1 year 200,000 IU of Vit A oral or 100,000 IU by intramuscular inj <1year 50,000 IU of Vit A Women / pregnant woman XN 10,000 IU VIT A X1A 10,000 IU VIT A X1B 10,000 IU VIT A Corneal Xerophthalmia 200,000 IU VIT A
  • 14. CONTROL AND PREVENTION of VIT A DEFICIENCY.
  • 15. Short term approach. Patients Treatment Infants 6-12 months / weight <8kgs 100,000 IU Vit A, orally every 3-6 months Children >1 yr / <6yrs 200,000 IU Vit A, orally every 6 months Lactating mothers 20,000 IU Vit A orally Infants < 6 months (not being breast fed) 50,000 IU Vit A orally
  • 16. Vit A supplements – Child Survival and Safe Motherhood (CSSM) DOSAGE AGE First dose (1lakh IU) 9 month along with measles vaccine Second dose (2lakh IU) 18 month along with DPT/OPV Third dose (2lakh IU) 2 years
  • 17. Medium term approach.  Food fortification with vitamin A
  • 18. Long term approach.  Vitamin A rich foods.  Nutritional health education.
  • 19. RESEARCH PAPER TALKS  Cure was associated with certain foods—in early times with topical application or ingestion of animal and fish liver, and in later years with ingestion of plant foods containing green and yellow pigments (Wolf, 1996).  Steenbock (1919) postulated, and later confirmed, that carotenoid from yellow maize (corn) could support growth and prevent ocular lesions.  Since Isler et al. (1947) discovered a cost-effective way to synthesize vitamin A, cure and prevention are also possible through commercially produced, synthetic vitamin A.
  • 20.
  • 21.  Breast-fed infants do not usually show clinical deficiency for at least 4 to 6 months after birth. They may be at a marginally adequate point however, if breast-fed by a malnourished, vitamin A-depleted mother (Underwood, 1994a).  At the same time, if breast-fed, even from a malnourished mother whose breast milk vitamin A has been improved through direct maternal supplementation (200,000 IU of vitamin A given within 2 months postpartum [WHO/UNICEF/IVACG, in press]), adequate infant vitamin A status may be prolonged beyond 6 months (Stoltzfus et al., 1993).
  • 22.  Vitamin A requirements , therefore, are greatest during periods of rapid growth—infancy and early childhood, adolescence, and pregnancy—and when the vitamin is lost from the body through normal physiologic processes, such as lactation, or through nonphysiological losses brought about by frequent disease, such as malabsorption, diarrhea, and febrile infections (FAO/WHO, 1988).
  • 23.  The bioavailability of the provitamin A carotenoids from plants is greatly influenced by the nature of the embedding matrix (i.e., fibrous, dark green leafy vegetables [DGLV] or soft-fleshed yellow/orange vegetables and fruits) and the composition of the accompanying meal.
  • 24.  Populations with subclinical deficiency—tissue concentrations of vitamin A low enough to have adverse health consequences, even in the absence of xerophthalmia, WHO's current definition of VAD (WHO, 1996a).
  • 25. Approaches To The Prevention Or Correction Of Vad.  Vitamin A intervention approaches are commonly grouped into two main control strategies: (1) direct increase in vitamin A intake through dietary modification with natural or fortified foods and supplements and (2) indirect public health measures to control disease frequency. Information, education, and communication (IEC), including social marketing and specific vitamin A-oriented nutrition education, may or may not accompany each of the above interventions.
  • 26.  VAD-endemic areas require special attention to micronutrient supplementation.  Vitamin A plays a central role in the body’s ability to fight off infectious diseases, deficiency can have far-reaching health consequences. People with a Vitamin A deficiency are more susceptible to measles, diarrhoea, respiratory infections and HIV/AIDS.
  • 27.  Improving the vitamin A status of deficient children aged 6 months to 6 years dramatically increases their chances of survival.  Good vitamin A status is associated with reduction in the rate of hospital admissions and reduced need for out-patient services at clinics and therefore lowers overall cost of health services.  Recent studies suggest that preventing vitamin A deficiency of women during and before pregnancy greatly reduces their risk of mortality and morbidity around the time of childbirth, probably through increasing resistance to infection and lowering levels of anaemia
  • 28.  Many International organizations like UNICEF and WHO have made the strategies for the prevention and elimination of vitamin A deficiency disease and they provide these strategies to the affected countries in the form of action plan, literature  It isthe responsibility of the governments and the health departments of the affected countries to implement these strategies for the betterment of the future of common people and children.
  • 29. References  Prevention of Vitamin A Deficiency Barbara A. Underwood, Ph.D. National Eye Institute https://www.ncbi.nlm.nih.gov/books/NBK230106/  Strategies for the prevention and elimination Of Vitamin A Deficiency. Submitted as a part of a SUMMATIVE ESSAY OF INTERNATIONAL NUTRITION IN MSC IN PUBLIC HEALTH https://www.researchgate.net/publication/324719932_Strategies_for_the_prev ention_and_elimination_Of_Vitamin_A_Deficiency_Module_Title_INTERNATION AL_NUTRITION