newwww Vitamin A Deficiency 1 - Copy.pptx Vitamin A Deficiency

Vitamin A deficiency
Presented by
1.Genet Teklay
2.Eldom Efrem
3.Abenezer Lemma
4.Tsadiku Tekle
5.Mohamedamin
6.Abrahim Adem
7.Zemenu
8.Msganaw
9. Samual Markos

Outline
• Introduction
• Source and metabolism of vitamin A
• Function 0f vitamin A
• Epidemiology of vitamin A deficiency
• Causes and risk factors of vitamin A deficiency
• Clinical features “
• Diagnosis “
• Treatment”
• Prevention”

Introduction
• Vitamin A is one of the four fat-soluble vitamins that is
found in diet as
– Pre formed vitamin A (retinol, Retinyl esters) found in animal
products
– Pro vitamin A (α-carotene, β-carotene) found in plant based
products
• The bioavailability of preformed Retinyl esters is more than
80%, while that of carotenes (plant source) are lower

Common sources of Vit. A
animal foods
IU/100mg or ml Plant foods IU/100ml or mg
Fish liver oil 100,000 Red palm oil 50-100,000
Animal liver 10,000 Carrot 10,000
Butter 3,000 Spinach 10,000
Cheese 1,500 Sweet potatoes 5,000
Kidney 1,000 Apricots, mangoes 2,000
Eggs 1,000 Tomatoes 1,000
Fish 200 Green beans 1,000
Fresh milk 150 Yellow maize 350
meat 20 Rise, white maize negligible

Metabolism of Vit. A
Pro vitamin A cleaved to retinol and preformed vit. A hydrolyzed into retinol
↓
Lipids and fat soluble vitamins are emulsified
↓
Uptake at the brush border
↓
Retinols are re esterified to long-chain fatty acids
↓
Released as a component of chylomicrons into the lymphatic system
↓
apolipoproteins B and E are taken up by hepatocytes through receptor mediated
endocytosis
↓
Retinyl esters in the apolipoprotein are released, and stored as lipid globules within the
hepatic stellate cells
↓
Retinol is released from the liver and transported by RBP

Function of Vit. A
• Vision
– retinal is essential component of rod and cones
that is used in phototransduction
– Retinoic acid is important in preventing
xerophthalmia
• Reproduction
– retinol and retinal are essential for
• supporting spermatogenesis in the males
• preventing fetal resorption in the female

• Regulation of gene expression- retinoic acid
– Growth and differentiation of cells
– Maintenance of epithelial integrity
• Essential for normal differentiation and mucus secretion of epithelial
tissues
– Embryology
• differentiation and maturation of different organ systems in the fetus
– Immune function
• Antioxidant function

Epidemology
• VAD is the leading cause of preventable childhood
blindness
• It is associated with high risk of mortality and
blindness, especially among pre-school-age children
• According to WHO, a one third of the world’s
preschool-age population has VAD
• In Africa and South East Asia the prevalence is as high
as 50%
• VAD causes around 250,000 - 500,000 cases of
childhood blindness each year

Who are at risk
• Infants and Preschool children
– poor stores at birth
– milk and supplementary food (low vit. A)
– Infection (measles, diarrheal disease)
• Pregnant and breast feeding women
• Low socioeconomic status
• Liver disease (limited storage)
• Alcoholics
• Fat malabsorption patients

Causes of Vit. A Deficiency
• Inadequate consumption of vitamin A rich
food
• Repeated infections like measles or diarrhea
• Protein energy malnutrition (↓ synthesis of
RBP)
• Problems of absorption
• Excess alcohol consumption (reduces liver
vitamin A storage)
• Zinc and iron deficiency

• VAD can be defined clinically or sub clinically
 Sub clinical VAD- in both children and adults
– A plasma or serum retinol concentration <0.70
μmol/L
 severe vitamin A deficiency -A concentration
of <0.35 µmol/L indicates.

Clinical Manifestation
• Night blindness
• Xerophthalmia
• Follicular hyperkeratosis (phrynoderma)
• Dry skin, pruritis
• Poor bone growth
• Excessive deposition of periosteal bone secondary to reduced
osteoclastic activity
• Anemia
• Keratinization of mucous membranes
• Impairment of the humoral and cell-mediated immune system
• Infertility

Ocular manifestations of VAD
1) Xerophthalmia: “is the clinical spectrum of
ocular manifestations of VAD ranging from the
mild night blindness to potentially blinding
stages’’ (WHO)

 There are primary and secondary signs:
 Primary signs: specific for xerophthalmia
1) X1A Conjunctival xerosis
2) X1B Bitot’s spot with conjunctival xerosis
3) X2 Corneal xerosis
4) X3A Corneal ulceration involving < 1/3
5) X3B Corneal ulceration/keratomalacia involving 1/3
≥
 Secondary signs: non specific but are high likely
indicative of xerophthalmia
1) XN Night blindness
2) XF Xerophthalmic fundus
3) XS Xerophtalmic scar

WHO-classification
• The WHO has a grading system for vitamin A
deficiancy

XN-Night Blindness
• Night blindness (nyctalopia) is the earliest
manifestation of vision loss in VAD
• It is the difficulty of seeing in a relatively low
light (impaired adaptation to the dark)
• It is one of the most common manifestations
of VAD
– especially in children age 2-6 or pregnant or
lactating women.

• It is considered to be both a sensitive and
specific indicator for serum retinol level
– Appears when the serum retinol level falls below
0.7 µmol/L
• It generally responds rapidly to vitamin A
therapy, within 1–2 days

X1A- Conjunctival Xerosis
• is characterized by a dull and dry appearance
of the conjunctiva with slight wrinkling
• It is caused by the loss of goblet cells and
insufficient mucin secretion
• This change occurs ,especially, in the exposed
part of the bulbar conjunctiva
• It is fully reversible with vit. A
supplementation

X1B- Bitot spot
• Superficial foamy, gray, triangular lesion on the bulbar
conjunctiva that appears in the palpebral aperture
• more commonly temporally
• consists of desquamated, keratinized epithelium,
inflammatory cells, debris, and Corynebacterium
xerosis
• Corynebacterium xerosis metabolizes the debris,
producing the foamy appearance of Bitot spot
• Reversible with vitamin A supplementation

X2- Corneal Xerosis
• It is characterized by a dull and hazy appearance
of the cornea
• It is caused by drying of the cornea secondary to
conjunctival gland dysfunction
• It can quickly progress to the stage of corneal
ulceration
• Up to this stage, high-dose Vitamin A
supplementation can result in the full
preservation of vision

Corneal and conjunctival xerosis

X3A-Corneal Ulceration
• If the acute deficiency is not reversed as a matter
of urgency, the cornea can become ulcerated
and melt away
• The ulcer may have the appearance of a small,
punched-out area or fluffy appearance
• In the absence of secondary infection, the eye
can look surprisingly white
• However, secondary infection of the ulcer is
common, leading to an acutely inflamed eye

Punched-out area Fluffy appearance
Corneal ulcer without secondary inflammation
Corneal ulcer with secondary
inflammation

X3B-Keratomalacia
• It is the most severe form of xerophthalmia in
which > 1/3 of the cornea is affected
• It is the melting away of the cornea by
liquefactive necrosis
• It can perforate and destroy the cornea in just
a matter of days
• Nearly 2/3 of children with keratomalacia die
within months

XS- Corneal Scarring
• A consequence of corneal ulceration and
keratomalacia
– Staphylomas - forward bulging of a badly damaged
cornea

– Phthisis bulbi – the eye shrivels up
• Corneal scarring due to VAD is often symmetric and
bilateral

XF- Xerophthalmic fundus
• Small white spots near the retinal vessels and
the retinal periphery that occur as a result of
prolonged VAD

Diagnosis
• History
– Dietary Hx
– Hx. Of frequent GI and respiratory tract infections
– Medical and vaccination Hx.
– current pregnancy or lactation, ANC follow-up
– Known malabsorptive disorders
– Surgical history
– History of alcohol consumption

Physical examination
– Ocular examination
– Body weight/ anthropometry
– Jaundice
– Abdominal exam for hepatomegaly

• Laboratory tests
– Serum vitamin A/retinol (reference range: 20-60 mcg/dL)
– Serum retinol binding protein (reference range: 30-75
ug/ml)
– Serum zinc (reference range: 75-120 mcg/dL)
– Liver biopsy: considered the gold standard for evaluating
total body vitamin A
– Impression cytology: conjunctival specimens can be
viewed for the presence of goblet cells.
– Dark adatopmetry and night vision threshold tests

Management
• Correct the underlying nutritional deficit with
both vitamin and protein-calorie supplements
• High-dose vitamin A is the treatment for all
patients (oral or IM)

• Maintenance of adequate corneal lubrication
• Prevention of secondary infection and corneal
melting
• If there is corneal ulceration or clouding add
antibiotic eye drops( ttc or chloramphenicol)
• Concomitant zinc supplementation if there is zinc
deficiency
• Patient education

Prevention
• . Distribution of massive dose capsules
– Children under one year…..100,000IU every 4-6 months
– Children over one year……..200,000IU every 4-6 months
– Children at birth …………..50,000IU
– Mothers after giving birth…300,000IU
– Pregnant & lactating mother…10,000IU daily for 2
weeks
• 2. Fortification
• 3. Nutrition and health education
• 4. Immunization

Reference
- nelson text book of pediatrics21th edition
- Who pediatrics guidelines
- national library of medicine

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