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Micronutrient malnutrition

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Micronutrient malnutrition Vanessa Velazquez-Ruiz, MD Emergency Medicine Global Health Fellow St. Luke s-Roosevelt Hospital Map 2008 WHO * Retinol (preformed Vit A ... – PowerPoint PPT presentation

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Title: Micronutrient malnutrition


1
Micronutrient malnutrition
  • Vanessa Velazquez-Ruiz, MD
  • Emergency Medicine
  • Global Health Fellow
  • St. Lukes-Roosevelt Hospital

2
Why talking about micronutrient malnutrition?
3
Micronutrients
  • Affect a variety of health and disease outcomes
  • Child growth and development
  • Maternal health
  • Malnutrition and vulnerability to infectious
    diseases
  • Estimates of micronutrient malnutrition vary from
    20 of the world population (or more than one
    billion persons)
  • Dietary deficiencies represents an enormous
    problem of hidden hunger

4
Agenda
  • Series of lectures
  • Week 1 Vitamin A and D
  • Week 2 Iron, Iodine and Zinc deficiencies
  • Week 3 Obesity and the other spectrum of
    malnutrition

5
Lets begin our journey!!!!
  • Fasten your seatbelts and enjoy the ride

6
Vitamin A
7
Overview
  • Third most common deficiency in the world
  • Affects an estimated
  • 125-130 million preschool age children
  • And 7 million pregnant women in low-income
    countries
  • Prevalent cases of pre school xerophthalmia are
    believed to number about 5 million
  • 10 can be considered potentially blinding

8
  • Leading cause of preventable pediatric blindness
    in developing world
  • Underlying cause of at least 650,000 early
    childhood deaths due to diarrhea, measles,
    malaria and other infectious disease
  • Maternal deficiency may increase risk of maternal
    morbidity and mortality

9
  • NEITHER HUMANS or ANIMALS can synthesize or
    survive without Vitamin A

10
Epidemiology
  • Public Health problem in approx 78 countries
  • Most widespread across South and Southeast Asia
    and Sahelian and Sub-Saharan Africa (where food
    supplies lack preformed vitamin A)
  • Clusters within counties due to common exposures
    to poor diet and inadequate care, malnutrition

11
Epidemiology
  • Age
  • Corneal xerophthalmia- 2-3y/o
  • Acute onset of corneal disease may follow recent
    weaning from breast milk, or s/p illnesses
  • Gender
  • Male gt Girls
  • Socioeconomics
  • Inversely correlates with Vit A deficiency

12
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13
Sources of Vitamin A
  • Retinol (preformed Vit A) animal products, liver
  • Beta-carotenes Provitamin A (converted to Vit A
    in intestines)
  • Plant source of retinol from which mammals make
    2/3 of their Vit A
  • Carotenoids yellow, red fruits/vegetables

14
Vitamin A
  • Essential in regulating numerous key biologic
    processes in the body
  • Morphogenesis
  • Growth
  • Nutrition
  • Vision
  • Reproduction
  • Immunity
  • Cellular differentiation and
  • proliferation

15
Vitamin A deficiency disorders VADDs
16
Main cause of deficiency
  • Insufficient intake
  • Increase requirements during growth, pregnancy
    and lactation, infection
  • Change from breast feeding to inadequate
    complimentary feeding
  • Socio-cultural and economics factors (intra
    household distribution and gender preferences)

17
Clinical features
18
Xerophthalmia
  • Three clinical stages
  • Retinal dysfunction causing night blindness
  • Conjunctiva and corneal xerosis
  • Corneal ulceration and necrosis

19
Night blindness
  • Earliest manifestation
  • Most prevalent stage of xerophthalmia
  • Failure in rod photoreceptors cells in the retina
  • Responsive to Vitamin A supplementation

20
Ask about night blindness
  • A positive history of night blindness is
    associated with low-to-deficient serum retinol
    concentrations in preschool aged children and
    pregnant women
  • Can serve as an indicator of individual and
    community risk of Vitamin A deficiency

21
Conjuctival xerosis with Bitots spots
  • Xerosis of the conjunctiva
  • Appears as dry, non-wettable, rough or granular
    surface (best seen on oblique illumination with
    hand light)
  • Histological transformation of normal columnar
    epithelium with abundant goblet cells to
    stratified, squamous epithelium that lacks goblet
    cells.

22
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23
Bitots spots gray-yellow patches of keratinized
cells and saprophytic bacilli that aggregate on
temporal limbus (lesions are bubbly, foamy or
cheesy like)
24
Corneal xerosis
  • Corneal xerosis (drying) presents as
    superficial punctuate erosions that lend a hazy,
    non-wettable, irregular appearance to the cornea
  • Usually both eyes
  • Severe xerosis, cornea becomes edematous with dry
    granular appearance (peel of an orange)
  • Vitamin A successfully treats corneal xerosis

25
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26
Corneal Ulceration
  • Appearance Round or oval, shallow or deep,
    sharply demarcated and often peripheral to the
    visual axis
  • Only one eye
  • Vit A will heal lesion leaving a stromal scar or
    leukoma

27
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28
Corneal Necrosis
  • Keratomalacia (corneal melting or softening)
  • Initially opaque localized lesions that can cover
    and blind the cornea
  • Treatment with Vit A leaves a densely scarred
    cornea

29
Conjunctival xerosis and localized corneal
necrosis in a severely malnourished 2-year-old
Indonesian boy.
Same eye 2 months after Vitamin A therapy
30
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31
Poor Growth
  • Experimental Vitamin A depletion in animals
    causes a deceleration in weight gain to a
    plateau as hepatic retinol reserves becomes
    exhausted
  • Corneal xerophthalmia is associated with severe
    linear growth stunting and acute wasting
    malnutrition
  • Recovery from xerophthalmia has been associated
    with gain in weight

32
Infection
  • Predisposes individuals to severe infection
  • Higher mortality rates in children and pregnant
    women
  • Vit A maintains epithelial barrier function and
    regulates cellular and antibody-mediated immunity

33
Treatment
  • Children with any stages of xerophthalmia
  • High potency Vit A at presentation, the next day
    and 1-4 weeks later (WHO recommendations)
  • Children at high risk Vit A deficiency measles,
    diarrhea, respiratory diseases, severe
    malnutrition
  • High dose supplementation single dose if no
    supplement in 1-4 mo

34
Replacement
  • q4-6 months
  • Infants 50K IU PO
  • Infants 6-12mo 100K IU PO
  • Mothers 200K IU PO w/in 8 wks delivery (WHO
    recommendation)
  • Pregnant or women of reproductive age small
    doses 10K IU/d or 25K IU wkly

35
Prevention
  • Dietary diversification
  • Fortification
  • Supplementation

36
Dietary diversification
  • Increase intake from available and accessible
    foods
  • Nutrition education
  • Social marketing
  • Community garden programs
  • Measures to improve food security

37
Fortification
  • Taking advantages of existing consumption
    patterns of fortifiable foods to carry Vitamin A
    into the diets
  • Examples
  • Vitamin A fortification of sugar in Guatemala
  • Vitamin A fortified monosodium glutamate in
    Southeast Asia

38
Supplementation
  • Encompassing community based efforts to provide
    Vit A supplements to high-risk groups
  • Preschool-aged children
  • Mothers within 6-8weeks after childbirth
  • UNICEF procures and distributes over 400 million
    Vit A supplements to nearly 80 countries
  • Integrating vitamin A delivery with immunization
    services during each of three routine contacts in
    the first 6 months of life

39
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40
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41
Nutritional Rickets and Vitamin D deficiency
42
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43
Overview
  • Resurgence in the prevalence of Rickets
  • In developing countries, not only associated with
    effects on bone growth and mineral homeostasis
    but also with infant and child mortality when
    accompanying lower-respiratory tract infections

44
Definition
  • Disease of the growing bones from a failure or
    delay in the calcification of newly formed
    cartilage at the growth plates of long bones and
    failure of mineralization of newly formed osteoid
    (osteomalacia)
  • Bones no longer able to maintain normal shapes

45
Causes of Rickets
  • Calciopenic rickets
  • Phosphopenic rickets
  • Primary defect of mineralization
  • Nutritional Rickets is a form of calciopenic
    rickets and is classically associated with
    Vitamin D deficiency

46
Effects of Vitamin D deficiency
  • Active Rickets
  • Impaired Calcium homeostasis
  • Consequent to impaired dietary calcium absorption
    or inadequate intake
  • Vit D (or more specifically 1,25-(OH)2D) controls
    the absorption of Calcium
  • ?serum Ca ? induce ? PTH secretion ? osteoclasts
    ? resorb bone ? demineralization of bone
    cartilage at sites of rapid growth remodeling

47
Effects of Vitamin D deficiency
  • Predisposition to lower respiratory tract
    infections by
  • Effects on immune system
  • Muscle weakness and hypotonia
  • Effects of rickets and osteomalacia on rigidity
    and support provided by the ribs during
    respiration

48
Effects of Vitamin D deficiency
  • During pregnancy and early infancy
  • Poor maternal weight gain
  • Higher incidence of maternal hypocalcaemia, poor
    neonatal bone mineralization and fractures, and
    reduced longitudinal growth
  • Increase risk of DM type 1, multiple sclerosis
    and bipolar disorder

49
Sources of Vitamin D
  • Diet
  • Fortified food products
  • Fish oils, egg yolks, mushrooms
  • Animal products (fatty parts, liver)
  • Vit D in diet cholecalciferol or ergocalficerol

50
  • Via skin synthesis under the influence of UV-B
    radiation

51
Factors influencing Vitamin D deficiency
  • Decrease amount of UV-B reaching the earth
  • Season of the year
  • time of the day
  • pollution, clouds
  • distance form equator

52
Factors influencing Vitamin D deficiency
  • Human factors
  • Amount of skin exposure (cloth coverage, social
    and religious customs)
  • Duration of exposure
  • Sunscreens
  • Degree of melanin concentration

53
Factors influencing Vit D deficiency
  • In young children
  • Before children start to walk- decrease sun
    exposure
  • Breast-fed very little Vit D in breast milk
  • Low dietary Calcium intake (ex. Consumption of
    polish rice)
  • Genetic causes
  • Malabsorption (repeated GI infections)
  • Chronic renal, liver disease

54
Clinical Features
  • Results of the widening and splaying of the
    growth plates and resultant deformities of the
    metaphyses of the long bones
  • Widening of wrist, knees and ankles
  • Palpable and enlarged costochondral junctions
    (rickety rosary)
  • Deformities of the long bones

55
Age dependant
  • Early
  • Craniotabes, head asymmetry,
  • frontal bossing, delayed closing
  • anterior fontanelle
  • Delayed tooth eruption, abnormal formation
    enamel, cavities
  • Rachitic rosary

56
  • Late
  • Pigeon chest irregularity, Harrison groove
  • Classic limb abnormalities
  • Genu varum, genu valgum
  • Fraying, widening, cupping metaphysis long bones,
    fxs
  • Lordosis, kyphosis, scoliosis
  • Narrow pelvis obstructed labor

57
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59
Other clinical manifestations
  • Hypotonia and myopathies resulting in delayed
    motor milestones (muscle weakness)
  • Hypocalcemia manifestations like apneic attacks
    and convulsions in infants

60
Diagnosis
  • Clinically presence of bony deformities
  • Radiological examination of growth plates
  • Biochemically
  • hypocalcemia
  • hypophosphatemia
  • elevated alkaline phosphatase
  • elevated PTH
  • Confirmation of low 25(OH)D concentrations

61
Treatment
  • Vitamin D supplements (Oral Vitamin D2 or D3)
  • 5,000 to 15,000 IU/day for 4-8 weeks
  • Single large dose when compliance problematic??
  • Adequate UV radiation
  • Vitamin D Calcium supplementation (50mg/kg for
    several months)
  • Calcium supplementation alone

62
Prevention
  • In US and Canada- fortification of all dairy milk
    formulas with Vit D (400 IU/quart)
  • American Academy of Pediatrics recommends
    supplementation with 200 IU/day to all breast-fed
    and children not drinking at least 500ml of cows
    milk

63
Prevention
  • Large doses of Vitamin D supplementation every 3
    months???
  • Add ground fish bones to pourish????
  • Education about sunlight and animal food
    ingestion

64
To be Continued
  • Stay tuned for more on micronutrient deficiencies
    next week same channel, same time

65
References
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