NUTRITION DISORDERS AND EYE

1. NUTRITION DISORDRS
-VITAMIN DEFICIENCY & EYE
DR. CHRISTINA SAMUEL
M.S OPHTHALMOLOGY,
FELLOW AT SANKARA EYE HOSPITAL
CHENNAI

2. NUTRITIENTS
 Chemical substances that constitute food and
are responsible for the functions of food and
also protect the body from various disorders

3. Types of nutrients
Macronutrients
 Proteins
 carbohydrates
 Fats
Micronutrients
 Vitamins
 Minerals

4. INTRODUCTION- Vitamins
Vitamins may be regarded as organic compounds
required in the diet in small amounts to perform
specific biological functions for normal
maintenance of optimum growth and health of the
organism.

6. WHAT IS VITAMIN A?
• The term “vitamin A” makes it sound like there is one particular nutrient called
“vitamin A”, but this is not true. It is a broad group of related nutrients.
• Vitamin A is a broad term for group of unsaturated nutritional organic
compounds, that includes retinol, retinal, retinoic acid, and several provitamin A
carotenoids, among which beta-carotene is the most important.

7. VITAMIN A is an Essential Fat soluble vitamin occuring in the
following forms:
 Pre formed
 Retinoids (retinal, retinol, retinoic acid)
 Found in animal products
 Pro vitamin A
 Carotenoids
 Must be converted to retinoid form
 Found in plant products

8. HISTORY
 It is recorded in history that HIPPOCRATES cured night
blindness(about 500 B.C)
 He prescribed to the patients Ox liver(in honey)which is now
known to contain high quantity of vitamin A.
 By 1917, Elmer McCollum et al at the University of
Wisconsin–Madison, studied the role of fats in the diet and
discovered few accessory factors. These "accessory factors"
were termed "fat soluble" in 1918 and later "vitamin A" in
1920.

9.  In 1919, Harry Steenbock (University of Wisconsin) proposed
a relationship between yellow plant pigments (beta-
carotene) and vitamin A.
 In 1931, Swiss chemist Paul Karrer described the chemical
structure of vitamin A.
 Vitamin A was first synthesized in 1947 by two Dutch
chemists, David Adriaan van Dorp and Jozef Ferdinand Arens.

10. Structure of vitamin A
NOMENCLATURE
PROVITAMIN A : β-Carotene
VITAMIN A1 : Retinol ( Vitamin A alcohol)
VITAMIN A2 : 3 –Dehydro-retinol
VITAMIN A ALDEHYDE : Retinal
VITAMIN A ACID : Retinoic acid
VITAMIN A ESTER : Retinyl ester
NEO VITAMIN A : Stereo isomer of Vitamin A1, has 70 –
80% of biological activity of Vitamin A1.

11. CHEMISTRY
• Vitamin A is composed of ‘β-IONONE RING’ (CYCLOHEXENYL) to
which ‘POLY ISOPRENOID SIDE CHAIN’ is attached
 Polyisoprenoid chain –all trans configuration, contains 4
double bonds, has 2 methyl groups with terminal carbon
having ‘R’ group
 ‘R’ Group –alcohol/aldehyde/acid
 β-Ionone ring –contains 1 double bond with 3 methyl groups

12. Sources of vitamin A
• Animal : Fish Liver oil, Butter, Milk, Cheese,
Egg Yolk
• Plant : All Yellow –Orange –Red –Dark
Green fruits & vegetables like Tomatoes,
Carrots, Spinach, Papayas, Mangoes, corn,
sweet potatoes.

15. RECOMMENDED DIETARY ALLOWANCE
 Unit of activity is expressed as ‘RETINAL EQUIVALENT’ (R.E.) /
‘INTERNATIONAL UNIT’ (I.U.)
1 Retinal Equivalent = 1μg of Retinol OR 6 μg of β-carotene
1 I.U. = 0.3 μg of Retinol OR 0.34 μg of Retinyl acetate OR 0.6 μg
of β-carotene
Infants & Children : 400 t0 600 μg/day
Adults (Men & Women) : 600 to 800 μg/day
Pregnancy & Lactation : 1000 to 1200 μg/day

16. FUNCTIONS OF VITAMIN A
 VISION
 GENE TRANSCRIPTION
 IMMUNE FUNCTION
 EMBRYONIC DEVELOPMENT AND REPRODUCTION
 BONE METABOLISM
 HAEMATOPOESIS
 SKIN AND CELLULAR HEALTH
 ANTIOXIDANT ACTIVITY
 Recent work suggests that, outside the retina, vitamin A is
chiefly concerned with mucopolysaccharide synthesis and
stability of lysozome membranes. Children aged three
months to four years are most commonly affected.

17. METABOLISM
 LIVER STORES 90% OF VITAMIN A
 ACTIVE METABOLITES
• TRANS RETINOIC ACID
• CIS RETINOIC ACID
 REGULATES EXPRESSION OF KERATIN AND MUCINS
 RHODOPSIN IN VISUAL CYCLE

19. VITAMIN A DEFICIENCY
 Most susceptible populations:
 Preschool children
 Older adults
 Alcoholism
 Liver disease (limits storage)
 Fat malabsorption

20. Vitamin A deficiency may result from :
 -Dietary insufficiency of Vitamin A / Precursors
 -Interference with absorption from intestines
 eg: diarrhoea, malabsorption syndrome, bile salt deficiency
 -Defect in the transport due to protein malnutrition –
‘Kwashiorkar’
 -Defect in the storage due to diseases of liver

21. Tissues chiefly affected –‘Epithelial’ principally which
are not normally keratinised
Includes epithelium of respiratory tract, gastrointestinal
tract, genitourinary tract, eye & paraocular glands,
salivary glands, accessory glands of tongue & buccal
cavity and pancreas
Fundamental change: Metaplasia of normal non-
keratinised living cells into keratinising type of
epithelium

22. OCULAR MANIFESTATIONS OF VITAMIN A
DEFICIENCY
 XEROPHTHALMIA
The term Xerophthalmia was given by a joint WHO and
USAID committee in 1976 to cover all the ocular
manifestations of vitamin A deficiency including the
structural changes affecting the conjunctiva, cornea and
retina and also the biophysical disorders of retinal rods and
cones functions.

23. XEROPHTHALMIA CLASSIFICATION
(modified) (1982)
 WHO CLASSIFICATION
• XN-NIGHT BLINDNESS
• X1A-CONJUNCTIVAL XEROSIS
• X1B-BITOT’S SPOT
• X2-CORNEAL XEROSIS
• X3A-CORNEAL ULCER<1/3RD OF CORNEAL SURFACE
• X3B-CORNEAL ULCER>1/3RD OF CORNEAL SURFACE
• XS-CORNEAL SCAR
• XF-XEROPHTHALMIC FUNDUS

24. XN :NIGHT BLINDNESS(Nyctalopia)
 Earliest symptom of xerophthalmia in children
 Diminished visual acuity in ‘dim light’(Insufficient adaptation
to darkness)
 Defective rhodopsin function.

25.  Night blindness, per se, is not pathognomonic of vitamin
A deficiency, being also a feature of various eye diseases
e.g. retinitis pigmentosa, Oguchi's disease,
choroideremia, gyrate atrophy of the choroid and retina,
onchocerciasis and occasionally congenital.
 If nutritional in origin the symptom will disappear after
consumption of about 30,000 I.U. of vitamin A daily
administered as cod or halibut liver oil

26. X1A CONJUNCTIVAL XEROSIS
Characterised by:
 One or more patches of dry, lustreless,nonwettable conjunctiva.
 Interpalpebral conjunctiva(commonly temporal quadrants)
 Severe cases involves the entire bulbar conjunctiva.
 Desribed as ‘emerging like sand banks at receding tide’when child ceases to cry
 Can lead to conjunctival thickening,wrinkling and pigmentation.

28. X1B BITOT’S SPOTS
 Bilateral
 Bulbar conjunctiva in the interpalpebral area
 Commonly in temporal quadrant.
 Raised triangular greyish/silvery white spots/plaques.
 Firmly adherent to conjunctiva
 Foamy keratinised epithelium(corynebacterium xerosis)

29. X2 CORNEAL XEROSIS
 Dry lustreless appearance of cornea
 Earliest change is punctate keratopathy
 Begins in the lower nasal quadrant
 Bilateral punctate corneal epithelial erosions
 Can progress to epithelial defects
 Reversible on treatment

30. X3A & X3B CORNEAL ULCERATION
/KERATOMALACIA
 Stromal defects occur in late stages due
to colliquative necrosis leading to
corneal ulceration ,softening (melting)
and destruction of
cornea(keratomalacia)
 Corneal ulcers may be small or large
 Stromal defects involving less than 1/3rd
cornea usually heal leaving some useful
vision
 Large stromal defects commonly result
in blindness.

31.  Small ulcers
 1-3mm
 Occur peripherally
 Circular
 Steep margins and sharply
demarcated
 Large ulcers
 More than 3mm
 Occur centrally
 Involve entire cornea

32. KERATOMALACIA
N MALNUTRIRION, DIARRHOEA, MEASLES & PARASITIC INFECTIONS
COMMON IN MALNUTRIRION, DIARRHOEA, MEASLES & PARASITIC INFECTIONS
 GENERALIZED SOFTENING OF STROMA
SLOUGHS
DESCEMETOCELE
PERFORATION

33. XS CORNEAL SCAR
 Healing of stromal defects results in corneal scarring
 Size of the corneal scar depends on the size and density of
corneal defect.

34. XF XEROPHTHALMIC FUNDUS
 Uncommon in occurence
 Typical seed like lesions
 Whitish/yellow in colour
 Raised lesisions
 Scattered uniformly over fundus
 At the level of optic disc.
 FFA reveals these dots to be focal retinal pigment epithelial
defects
 Rarely these patients can present with scotomas corresponding
to the area of retinal involvement
 Respond to vitamin A therapy with scotoma disappearing in 1-2
weeks and retinal lesions fading in 1-4 months

36. 2. Parenteral therapy: IN CASES OF
-severe disease
-unable to take oral feeds
-Repeated vomiting and diarrhoea
-malabsorption
 Intramuscular injections of water miscible vit A
preparation
 Dose – 1,00,000 IU(Half the oral dose)

37.  Local ocular therapy-
 Intense lubrication-instilled every 3-4 hours
 Topical retinoic acid
 Treatment of keratomalacia and corneal ulcer
 Treatment of corneal perforation

38. PROPHYLAXIS AGAINST XEROPHTHALMIA
 1.Short term approach
-Periodic administration of vitamin A supplements
-WHO recommended ,universal distribution schedule of vit A for prevention
is as follows:
i) Infants <6months (not being breastfed)—50,000 IU
ii)Infants 6-12 months and any child <8kg – 1,00,000 IU
every 3-6months
iii)Children over 1 year and under 6 years --- 2,00,000 IU orally every 6 months
iv)Lactating mothers – 2,00,000 IU orally once at delivery or during next 2
months to maintain level of vitamin A in breast milk

39. PROPHYLAXIS

40.  Under vitamin A supplementation program through
Reproductive and child health program(RCH) and now
National Rural Health Mission(NRHM)
-- Children between 9 and 36 months of age are to be
provided with vitamin A solution every 6 months starting
with 1,00,000 IU at 9 months of age along with measles
vaccination and subsequently 2,00,000 IU every 6
months till 36 months of age.

41.  2.Medium term approach-
- fortification of food with Vit A
 3. Long term approach-
- Promotion of adequate intake of Vit A rich foods in high
risk groups particularly preschool aged children on a
periodic basis and to mothers within 6-8 weeks after
childbirth
- Other measures like nutritional education,social
marketing, home or community garden programs and
measures to improve food security.

42. HYPERVITAMINOSIS A
 Ingestion of large amounts of preformed vitamin A from the
diet, supplement intake or medications
 Acute:
 Single doses of >3,00,000 IU
 Headache ,Blurred vision,nausea ,vomiting,
drowsiness,irritability i.e signs of raised ICP(Benign
intracranial hypertension)
 Serum Vit A values-200-1000 IU/dl

43.  Chronic – long-term megadose; possible permanent
damage ( >50,000 IU/day for several wks)
 Bone and muscle pain
 Loss of appetite
 Skin disorders
 Headache
 Dry skin
 Hair loss
 Increased liver size
-Manifestations reversible when vitamin A discontinued

44. DEFICIENCY OF VITAMIN B1{THIAMINE}
 Can result in Corneal anaesthesia
 Conjunctival dystrophy
 Corneal Dystrophy
 Acute Retrobulbar neuritis

45. DEFICIENCY OF VITAMIN B2{RIBOFLAVIN}
 FUNCTIONS- plays an important role in cellular growth
 It acts as a co – factor for a number of enzymes involved in
energy metabolism.
 SOURCES
 Eggs , liver, green leafy vegetables
 Milk

46. DEFICIENCY MAY CAUSE
Keratitis
Susceptibility of cataract
Photophobia
Burning Sensation
Conjunctival irritation
Vascularization of Cornea

47. DEFICIENCY OF VITAMIN C
 It may be associated with haemorrhages in the conjunctiva, lids,
anterior chamber, retina and orbit.
 It delays wound healing
 it causes bleeding of gum
 Effective anti-oxidant
 Protects eyes against u.v rays
 Delays cataract formation < more than 300 mg>

48.  SOURCES
 Citrus
 guava
 mango
 Amla
 Pineapple

49. DEFICIENCY OF VITAMIN D
 It may be associated with Zonular Cataract
 Papilledema
 Increased lacrimation

50. VITAMIN E
FUNCTIONS
 Potent anti-oxidant
 Prevents ARMD
SOURCES
 Broccoli
 Carrot
 Spinach
 Fish

51. OMEGA -3- FATTY ACID
Functions
 Essential fatty acid –used to produce new cells , muscle, nerves and organs
 Protects against ARMD, dry eye syndrome
SOURCES
 Fish
 walnut
 flax seeds

52. ZINC
 This trace mineral has a protective effect on early ARMD
 Acutely concentrated in the eye and hence very important
SOURCES
 Almonds
 Wheat germs
 Dairy

53. SELENIUM
Helps in treating :
 Retro-bulbar pain
 Oedema
 Grave’s disease
SOURCES
 Turkey
 Brazelnuts
 Tuna

54. LEUTIN AND ZEAXANTHIN
 THEY ARE XANTHOPHILS- CAROTENOIDS
 THEY ABSORB EXCESSIVE LIGHT ENERGY TO PREVENT DAMAGE
 MESO ZEA XANTHINE IS PRESENT IN THE RETINA FROM INGESTED LEUTINS.
FUNCTIONS
 Anti-oxidants
 Prevents ARMD