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Public health importance

nutritional deficiency states

By Addisalem Damtie (MPH)

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Common nutritional problems in Ethiopia

 PEM- Protein Energy Malnutrition

 nutritional anemia

 IDD- Iodine Deficiency Disorder

 VAD- Vitamin A deficiency


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Protein-energy Malnutrition:

• Prevalent in immuno-compromised patients, the


elderly, homeless, etc.
• Most often occurs in developing countries.
• Can occur in people with eating disorders

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PEM is the most important public health problem in under
developed countries in the world today.
Protein –energy malnutrition is broadly defined as a multi
deficiency state which arises from inadequate energy,
protein and micronutrient supply to cells in body to satisfy
physiological requirements.
The two most common forms of PEM:-
Marasmus
kwashiorkor

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According to welcome classification of PEM

WFA%
Oedema
No Yes

60 – 80 Underweight Kwashiorkor

<60 Marasmus Marasmic


kwashiorkor

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Protein-energy Malnutrition…
 Marasmus: A severe deprivation of food over a long time.
- Inadequate energy intake.
– Occurs most commonly in children.
– Muscles and organs weaken due to lack of protein.
– Impairs brain development and learning ability.
– Inability to keep warm; lack of insulation.
– Growth ceases.

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Marasmus …

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SIGN AND SYMPTOMS OF MARASMUS

There is a failure to thrive


Irritability, fretfulness, and
diarrhea are frequent.
Many infants are hungry,
but some anorexic.
There are little or no
subcutaneous fats.
The weight is much below the
standard for age.
Temperature may be subnormal.

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S/sx of marasmus
 A relatively rapid loss of
fat and then slow loss of
lean body tissue.
The muscles are weak
and atrophic and this
makes the limbs appear
as skin and bone

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Cont’d

• Retarded growth
• Wasting of subcutaneous fat and muscles
• Old man‘s face
• Sunken eye balls
• Mild skin and hair changes

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Protein-energy Malnutrition…

Kwashiorkor:
Severe deprivation
of protein.

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Kwashiorkor…
• Kwashiorkor: A sudden, recent deprivation in food
intake.
- Results from protein deficiency.
- Muscle wasting.
- Inadequate fluid-balance: leaking occurs into
the interstitial fluid; edema
- Fatty liver, causes bulging belly.
- Children of the age group of 1-3Yrs

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SIGNS AND SYMPTOMS OF KWASHIORKOR

 Growth failure occurs always


 Wasting of muscle is also typical but may not
be evident because of edema
 There may be mental change
 Hair and skin color change
 Diarrhoea and vomiting
 Hepatomegaly
 Sign of other deficiencies such as vitamins
 Moon face .

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Management of malnutrition

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Recommended criteria for SAM and Admission to TFP

All children who fulfill any of the following


criteria have SAM and they should be admitted
to a
– Therapeutic Feeding Program (In-patient care
(TFU) or
– Out-Patient Treatment Program (OTP):

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Infants less than six months or less than 3 Kg:

• Weight –for- Length (WFL) less than 70% or < -3Z


score
OR
• Presence of pitting Edema of both feet

OR
• Visible Severe Wasting if it is dificult to measure
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Management …
Children 6 months to 5 years:
• Weight –for- Length (WFL) / WFH less than 70 %
or < -3Z score
OR
• Presence of pitting Oedema of both feet

OR
• MUAC <11cm for child length greater than 65 cm

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Management …
• If a child is 6 months to 5 years and has SAM
according to the above criteria, check for the
following:
– serious medical complications that will determine
the choice of treatment modalities
• In-patient (TFU) or
• Out-patient (OTP)

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Management …
• Unable to breast feed, • Shock
drink or feed • Dehydration (watery diarrhea
• Vomiting everything with recent sunken eye balls.)
• Convulsions • Dysentery
• Very Weak, Lethargic or • Persistent diarrhoea
unconscious • Hypoglycaemia
• Hypothermia: axillary • Severe anemia (severe palmar
temp <35 0C or rectal < pallor)
35.5 0C • Jaundice
• Fever ≥ 38.5 0C • Bleeding Tendencies
• Dermatosis +++
• Pneumonia/severe
• Corneal clouding or ulceration
pneumonia  Chest in-
drawing • Measles (now or with eye/mouth
complications
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Management…
• If a child fails the appetite test, it reflects a
severe disturbance of the metabolism and this
child needs to be treated as an in-patient

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In-patient care (TFU):
All children with SAM need to be treated in an in-patient
care facility if they fulfill any one of the following:
1. Infants below six months of age with SAM OR
2. Children 6 months to 5 years with SAM who have any
one of the medical complications or failed appetite test
OR
3. Children with SAM and referred from OTP for in-
patient care OR
4. When OTP is not available where the care taker lives
or if the care taker’s choice is inpatient care
• A child who fulfills any of the first three criteria is
classified as severe complicated acute malnutrition
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1. Stabilization phase
• children with complicated SAM are initially
admitted to an in-patient facility for
stabilization.
• F-75 is the "starter" formula to use during
phase 1, beginning as soon as possible and
continuing for 2-7 days until the child is
stabilized .
– F-75 contains 75 kcal and 0.9 g protein per 100 ml

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Stabilization phase…
During this phase:
– Life-threatening medical complications are treated
– Routine drugs are given to correct specific
deficiencies
– Feeding with F-75 milk (low caloric and sodium) is
begun
• F-75 is specially made to meet the child’s needs
without overwhelming the body’s systems in
the initial stage of treatment. Use of F-75
prevents deaths.
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2. Transition phase
• Once the child appetite recovers and the main medical
complications are under control and edema start to
reduce,
– Transition phase is started where F-100 or RUTF (Ready-to-
Use Therapeutic Food) is introduced.
• This phase is important for slow transition as the
introduction of large amounts of RUTF or F100 could
lead to
– Imbalance of body fluids and severe medical complications.
• In this phase:
– Routine drugs are continued
– Feeding with RUTF or F100 is started

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Transition phase…
• F-100 is used as a "catch-up" formula to
rebuild wasted tissues.
• F-100 contains more calories and protein:
– 100 kcal and 2.9 g protein per 100 ml.

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3. Rehabilitation Phase
• Children that progress through phase 1 and transition
phase enter this phase when they have
– Good appetite and no major medical complication.
• During this phase :
– Routine drugs, deworming tablets and iron, are started
– Feeding with RUTF or F100 is increased in amount
– Child starts gaining weight
• Whenever possible, it is implemented as OTP with
RUTF.
• Otherwise, it can be implemented in in-patient
centres with RUTF or F100.
• RUTF is high-energy, nutrient-dense food used for
nutrition rehabilitation during this phase
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Rehabilitation Phase…
• It is similar in composition to F100 (except
RUTF contains iron).
• The RUTF Plumpy’nut has a caloric value of
500 kilocalories (kcal) and 12.5 gm of protein
per one sachet of product (92 gms).

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Recognize Dehydration and the need for
ReSoMal
• Consider the diagnosis of dehydration in non-
edematous child and give ReSoMal if there are:
– Definite history of significant recent fluid loss
(diarrhea looking like water, appearing with sudden
onset in the last hours or days)
– Clear history of a recent change in the child's
appearance
– If the eyes are sunken then the mother must say
that the eyes have changed to become sunken
since the diarrhea or vomiting started

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Signs of Dehydration to follow
• Lethargic A lethargic child is not awake and alert when
he should be. He is drowsy and does not show interest
in what is happening around him.
• Restless, irritable The child is restless and irritable all
the time, or whenever he is touched or handled.
• Sunken eyes The eyes of a severely malnourished child
may always appear sunken, regardless of the child’s
hydration status.
– Ask the mother if the child’s eyes appear unusual.
• Thirsty See if the child reaches out for the cup when
you offer ReSoMal.
– When it is taken away, see if the child wants more.

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• ReSoMal is a rehydration solution for children with SAM.
• It is a modification of the standard Oral Rehydration
Solution (ORS) recommended by WHO.
• ReSoMal contains
– Less sodium,
– more sugar,
– more potassium than standard ORS and is intended for
severely malnourished children with diarrhea
• Do not give standard ORS to severely malnourished
children.

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Nutritional anemia

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Iron deficiency
Iron deficiency is the world's most common nutritional
disorder. It affects around 2 billion people.

In developing countries, 51% of children under the


age of four years, 40% of all women and 51% of
pregnant women are affected.

Iron deficiency anemia reduces the ability of the blood


to carry oxygen from the lungs to the brain muscles and
other organs.
Reduced capacity to work and to learn,
Fatigue, shortness of breath even after slight
exertion, dizziness, headache, and loss of
appetite are also common with anemia.

It diminishes the ability to fight infection and


thus increases vulnerability to transmissible
diseases.
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Anemic expectant mothers face the risk of death
resulting either from spontaneous abortion, the stress
of labor or other delivery complications.

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Even in developed countries, 18% of pregnant women
suffer from iron deficiency anemia.

Maternal anemia almost always leads to infant anemia.

The babies of severely anemic mothers suffer from low


birth weight and confront a greater than average risk of early
death.

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Cont’d

Mental and motor development is impaired in anemic


infants and children, and apathy, inactivity and
significant loss of cognitive abilities can occur.

The effects on a child's development can be


irreversible.

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Causes of iron deficiency
Diminished stores
• Preterm and small for date babies.
• Twins
• Early cord clamping
• APH
• Feto-fetal or feto- maternal transafusion
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Causes …
 Diminished intake
 Increased demand
– Mal-absorption
– Rapid catch up growth in
– Low level of enhancers
preterm and SFD
– High level of inhibitors – Infancy and puberty
– Not breast feeding – Preg and lact.
– Cows milk feeding
 Errors of Iron
– Iron poor diet
metabolism
 Excessive loses
– Congenital transferrin
– Bleeding
deficiency
– Recurrent diarrhea
– hookworm

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ASSESSMENT OF IRON DEFICIENCY AND
ANEMIA
• Clinical (pallor of conjunctiva, tongue and nail
bed and palm)
• Laboratory
– serum ferritin,
– transferrin concentration and saturation,
transferrin receptor,
– erythrocyte protoporphyrin,
– hemoglobin, hematocrit, and erythrocyte
morphology and color (Table 22.2)).
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Public Health Significance of anaemia

The prevalence of anemia as a public health


significance is categorized as follows:
• < 5%, no public health problem;
• 5 – 19%, mild public health problem;
• 20–39%, moderate public health problem
• ≥40%, severe public health problem.

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Treatment
• Treat the underlying cause
• Oral iron therapy
• Parentral iron therapy
• Blood transfusion

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Preventions
 Food fortification
 Food enrichment
 Supplementation
 Dietary improvement
 Public health measures

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Dietary Improvement

 A large variety of iron-rich foods and to increase dietary


iron absorption.

 liver, and eggs are good sources of iron in a form that


the body can readily use.

Grains, legumes, and vegetables, but in a form less


easily absorbed unless taken at the same time with meat
or food rich in vitamin C, or processed in a way to
enhance the absorption of iron.
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Public health measures
Birth spacing, the control of parasitic infections, immunization to
prevent infections, and improved water supply and sanitation.

Changing of dietary habits and food preparation practices


through nutrition education, Control of malaria infection & Control
of febrile and chronic diseases

Pregnant women require much higher amount of iron than is met


by most diets.

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Cont’d
In places where anemia prevalence is high, supplementation
should continue in to the postpartum period, to enable them
acquire adequate stores of iron.

•Many infants beyond 6 months of age need more iron than is


available in breast milk and common weaning foods.

•Infants with low birth weight have less iron stores, and are thus
at a higher risk for deficiency after two months of age.

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Reading assignment
• Folate deficiency
• Vit B12 deficiency

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Iodine
•It is essential for the synthesis of the thyroid
hormones (thyroxin & triodothroxine) –
• Physical growth and neural development.
• Failure to have adequate level of iodine in the
blood:
Insufficient production of these hormones, which
affect many different parts of the body
- muscle, liver, kidney, and the developing
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Where is iodine found in our body?
Every cell in the body contains & utilizes iodine.
WBC cannot effectively safeguard against
infection without adequate amount of iodine.
Concentrated in the glandular system.
Thyroid gland contains the largest amount of
iodine.

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Breasts, salivary glands, pancrease, CSF ,Brain,

stomach, skin, lacrimal glands etc.

The absence of iodine is a promotor of cancer.

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Iodine deficiency, or insufficiency, in any of
these tissues will lead to dysfunction of that tissue.
 For example, iodine deficiency in:
Salivary glands = inability to produce saliva,
producing dry mouth

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Skin = dry skin, and lack of sweating. Three to
four weeks of iodine supplementation will
typically reverse this symptom, allowing your
body to sweat normally again
Brain = reduced alertness, and lowered IQ
Muscles = nodules, scar tissue, pain,
fibrosis, fibromyalgia

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Iodine Deficiency Disorder (IDD).
•Include spectrum of disabilities caused by environmental
iodine deficiency
•The major public health problems worldwide.
•The problem more affects pregnant women and young
children.
•It is a threat to the social and economic development of
countries.
•It is highly prevalent among populations living in high
land areas where the soil has
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low iodine content.
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Iodine Deficiency disorders….
• The most devastating outcomes of IDD are increased perinatal
mortality and mental retardation.
• The greatest cause of preventable brain damage in childhood.
Cause:
• Low level of iodine in soil therefore in local crops & water supplies
• Poor consumption of seafood like fish

• Increased consumption of goitrogens like cassava, cabagge (These are


factors in the food that interfere with iodine uptake by the thyroid
gland.)etc

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The major consequences of iodine deficiency

Mental retardation
Defects in the development of nervous
system
Goiter
Physical sluggishness
Reduced work capacity

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Impaired work performance
Decreased average intelligence by 10-15 IQ
points
Loss of memory
Inability to produce enough milk for offspring

Cretinism- (severely stunted physical and


mental growth and deafness due to untreated
congenital hypothyroidism)
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Iodine Status Assessment
• Goiter classification ( 0-2)
• Urinary iodine concentration
• TSH (thyroid stimulating hormone)
concentration
• Other common clinical measures:
– Ultrasonoagraphy of thyroid volume
– Serum concentrations: thyroxin,

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Iodine Interventions
1. Universal Iodization of Salt
2. Iodization of irrigation water
3. Iodized Oil Supplementation
Iodization of Salt
• Iodized salt
– Universally and regularly consumed
– Costs ~$0.04/yr/person
– Simple technology
• At a level that assures 150 µg/day is safe for all populations
(WHO, UNICEF, FAO, ICCIDD, IAEA)
Iodization of irrigation water
– Effected in Xinjiang, China
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– Maternal urinary iodine increased from <10 to 55 µg/L69
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Iodine Interventions …
• Iodized Oil Supplementation
– Effective in high risk groups (Children,
pregnant and post partal women)
– Administered every 6 to 12 months
– IDD moderate-severe

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Vitamin A deficiency

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Causes of VAD
• Decrease in take of Vit A rich sources
• Inadequate intestinal absorption, with chronic
intestinal disorders or fat malabsorption
• Low intake of fat
• Increased Vitamin A excretion ( cancer, urinary
tract disease and chronic infectious disease)
• Low protein intake or PEM
• Increased need
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WHAT ARE THE CONSEQUENCES OF VITAMIN A DEFICIENNCY?

• Vitamin A deficiency has long been associated


with blindness. But more importantly, recent
research reveals that vitamin A deficiency is
associated with increased morbidity and
mortality among young children.
• Vitamin A deficiency leads to a cessation of
growth, deterioration of epithelium and
eventually death.
• Vitamin A deficiency is one of the most serious
nutritional diseases in developing countries
because:
– It causes blindness
– It affects young children below 15 years

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THE COMMON SYMPTOMS OF VITAMIN A
DEFICIENCY?
1. Night blindness:
• The child cannot see in the dusk or half
darkness.
• He/she has to go in to the house early
in the evening

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2. Conjuctival xerosis:
• The conjuctival covering the white
surface of the eyeballs become dry and
rough instead of being moist, smooth
and shining.
• The child cannot open and close his/her
eyes because it is painful.

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3. Bitot’s spots:
• A foamy, or cheesy accumulation, which forms
in the inner quadrant of the cornea in the
eyes.
• The cornea, the central transparent part of the
eye becomes cloudy.
• It reflects more advanced vitamin A deficiency,
but tends to be reversible with treatment.

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4. Corneal ulceration:
• an ulcer on the cornea may leave scar,
which can affect vision.
5. Keratomalacia:
• The eyeballs become opaque and soft,
jelly like substance.
• Hereafter there will be a rapid
destruction of the eyeball and no hope
of recovery after the condition
reached the stage of keratomalacia.
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Diagnostic criteria for vitamin A
deficiency at the community level
 WHO identifies vitamin A deficiency
as a major public health problem if:
 prevalence of any one of the following
in children below six years of age
exceeds the prescribed levels

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Identifications of vitamin A deficiency at
the community level
Vitamin A deficiency sign/symptoms Who cut - off level for
identifying a public
health problem

Night blindness >1%


Bitot’s Spot >0.5%
Corneal scar
>0.05%

Conjuctival >0.01%
Xerosis/ulceration/kratomalacia

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Prevention and Control of Vitamin A
deficiency
• The elimination of VAD can best be achieved
through a comprehensive approach that
combines strategies.
• There are five main types of intervention for
VAD as suggested by WHO:
A. Promoting breast milk
B. Supplementation C. Food fortification
D. Dietary modification E. Infection control
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Thank you

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