Community medicine ll

Chapter: IChapter: I
Nutrition AndNutrition And
HealthHealth
Community Medicine IICommunity Medicine II
ByBy
Saad Ahmed AbdiwaliSaad Ahmed Abdiwali
BSc, MPHBSc, MPH

Malnutrition
It is a pathological state resulting from
a relative or absolute deficiency
or excess
of one or more essential nutrients.

Conceptual Framework of Malnutrition

Human, Economic, and
Institutional Resources
Potential Resources
Ecological Conditions
Political and Ideological Structure Root
Causes

Household
Food Security
Potential Resources
Causes
Underlying
Causes

Household
Food Security
Potential Resources
Environ. Health,
Hygiene & Sanitation
Causes
Underlying
Causes

Household
Food Security
Potential Resources
Care of Mother
and Child
Environ. Health,
Causes
Underlying
Causes

HealthDiet
Household
Food Security
Potential Resources
Care of Mother
and Child
Environ. Health,
Causes
Immediate
Causes
Underlying
Causes

Nutritional Status
HealthDiet
Household
Food Security
Potential Resources
Care of Mother
and Child
Environ. Health,
Causes
Manifestations
Immediate
Causes
Underlying
Causes

Nutritional Status
HealthDiet
Household
Food Security
Potential Resources
Care of Mother
and Child
Environ. Health,
Causes
Manifestations
Immediate
Causes
Underlying
Causes
Functional Consequences: Mortality,
Morbidity, Lost Productivity, etc.
Consequences

Forms of
Malnutrition
Under-nutrition Over-nutrition
Macronutrient def.
Micronutrient def
Obesity

The main forms of Malnutrition are
Under-nutrition:
a pathological state resulting when nutrient intake
does not meet the requirements. It includes:
 Macronutrient deficiency e.g., protein-energy
malnutrition( marasmus & kwashiorkor).
 Micronutrient deficiency as iron deficiency
anaemia, vitamin A deficiency, vitamin D
deficiency …….etc.
Over-nutrition:
a pathologic state resulting when nutritional intake
exceeds the body needs
 Obesity

Malnutrition
Primary Malnutrition
due to community or
family factors related to
food production, distribution….
etc
Secondary Malnutrition
due to individual factors
affecting intake , absorption
or utilization of food

Primary malnutrition
It is due to reduced intake as in case of the following
1-Insufficient food production
2-Unequal distribution of foods
3-Lack of leisure.
The work of women, the duration of work outside home
and the transportation time all are factors that affect the
likelihood of having proper meals at home. This indicates
the importance of school meals and provision of canteens
at work.
4-Housing and kitchen facilities
5-Lack of transportation
6-Cultural factors

6-Cultural factors
Food attitudes, habits, Values, behaviors,
Religion….
-Celebration food
-Age group or sex linked foods
-Disease linked foods
-Modern foods ( Fast meals)
-Duration of breast feeding
-Food preparation
-Pattern of diet during pregnancy
& lactation

Examples of Negative poor habits :
Unconsumption of satisfactory amounts of protective foods
due to:
•failure to promote the habit during childhood,
•local food customs,
• Religious or ethnic restrictions or economic
restrictions
Examples of Positive poor habits:
a) Excessive use of sweets . This replaces proteins ,
vitamin & and mineral source foods
b) Consumption of highly refined foods especially white
flour and white sugar.

Secondary Malnutrition
Deficient Intake:
due to anorexia, in elderly and mentally ill
Increased food requirements:
during febrile diseases and in hyperthyroidism
Malabsorption:
in patients with diarrhea or patients with gastrectomy
& in elderly patients
Malutilization:
Defects in metabolism as in Liver diseases.
Increased excretion:
Chronic bleeding causes iron deficiency anemia

I-Macronutrient deficiency
Protein Energy malnutrition (PEM)
PEM is a range of pathological
conditions caused by a chronic
deficiency of energy and / or protein,
occurring most frequently in infants
and young children and commonly
associated with infections.

Wellcome classification of PEM
Type of MalnutritionType of Malnutrition BodyBody
(% of standard(% of standard((
EdemaEdema
Under weightUnder weight
(Mild)(Mild)
60- 80%60- 80% NoNo
MarasmusMarasmus
(Mild)(Mild)
< 60%< 60% NoNo
KwashiorkorKwashiorkor
(severe)(severe)
60- 80%60- 80% yesyes
Marasmic-Marasmic-
KwashiorkorKwashiorkor
(severe)(severe)
< 60%< 60% yesyes

Underweight:
A child who does not eat enough to cover
his nutrient needs is “underweight`.
It is characterized
• weight loss 60-80% of the standard,
•low resistant to infection
•associated with nutrient deficiency
( Vitamin A, C, D, B and Minerals as Iron & calcium)
Example: The weight of the child is 8 kgm while the
standard weight for age is 12 kgm
The wt % standard is: 8X 100 = 60.67 %
12

Health consequences of childhood
Malnutrition
1-Growth failure as detected by the growth curve (e.g.
slowly rising, flat or going down).
2-Lack of energy for daily activities & low scholastic
achievement .
3-“apathy” the child is less interested in the world
around him .He does not want to play. He sleeps more
and appears miserable.
3-Lack of immunity against infection.

Relation between Malnutrition
& infectious diseases

(3)
Infection
(1)
Malnutrition
(4)
•Increased need for
•energy& other nutrients
•Decreased appetite so
•less intake of nutrients
•Decreased absorption
•Of nutrients from gut
•Weight loss
•Slower growth
(2)
Ineffective Immune
system
Decreased resistance
of tissue (specially lining
of gut & respiratory
tract

Protein energy malnutrition
Severe acute malnutrition

Outline for nutritional requirement
Feeding during the 1st
6 month of life –
BF
Feeding during the second 6 month of
life
Feeding problems during the 1st
year of
life
Feeding during second year of life
Feeding during later childhood

Objective
At the end of this lecture the students
should be able to
Describe the nutritional requirement of
infants and children
Identify common problems encountered
during feeding of infants

Breast feeding
 Feeding should be initiated as soon after birth
as possible unless contraindicated.
 maintains normal metabolism during transition
 Promotes maternal infant bonding
 The time required for an infant stomach to
empty may vary from 1-4 hrs
 6 – 9 feedings in 24 hrs
 Most infants take 80-90ml per feed
 Satisfactory feeding
 No more wt loss at the end of 1st
week
 Started to gain wt at the end of 2nd
week

Advantage of BF
 Always available at a proper temperature and
requires no preparation time
 Fewer feeding difficulties, low incidence to
allergy
 Contains bacterial and viral antibodies
 High conc. Of secretary IgA
 Substances that inhibit growth of many common
viruses
 Macrophages synthesize complement, lysozyme
and lactoferrin
 Lower incidence of diarrhea as well as otitis media,
pneumonia, bacteremia, and meningitis

Continued…
 Contains bile salt-stimulated lipase, which kills giardia lamblia
and enteameba histolytica
 Supply all necessary nutrients except flouride and
after several months vit. D
 The psychological advantage of BF to the mother and
the infant – well known
 Establishing and maintaining the milk supply
 Empting of the breast – most important stimulus
Suckling – afferent to hypothalamus –pituitary – prolactin and
oxytocin
 Tender or sore nipples- nursing more frequently, manually
expressing milk, nursing in diffirent conditions, and keeping
the breast dry
 Less relaxed anxious mother – express milk feeding

Maternal diet
 Should contain enough calories and other nutrients
 To compensate those secreted in the milk and those required
to produce it
 Role – to maintain wt and generous in fluid, minerals and
vitamin
 Milk is an important component of the diet
 No food need to be withheld from the mother
 Should not take drugs
 Antithyroid medications, lithium, anticancer agent, INH,
chloramphenicol, metronidazole
 Smoking cigarettes and drinking alcohol- discouraged

Feeding during the second 6 month
of life
 By 6 month of age infants capacity to
 Digest and absorb a variety of dietary components
 Metabolize, utilize and excrete the absorbed products of
digestion is near adult capacity
 Teeth are beginning to erupt
 Begin to explore his surrounding
 Addition of other foods is recommended ( weaning)
 Complementary foods – additional foods including
formulas, given to breast fed infants
 Replacement foods – foods other than formula given
to formula fed infants

 Weaning should be stepwise to both breast fed
and formula fed infants
 Cereals, a good source of iron, usually should be
the first food
 Vegetable and fruits are introduced next
 Meats follows shortly and finally eggs
 One new food should be introduced at a time
 Additional new foods should be spaced by 3-4 days
 Adverse reactions (families with food or other allergies)

 Either home prepared or manufactured
complementary foods can be used
 The latter are more convenient and likely to
contain less salt – have supplemental nutrients
( eg Iron)
 Egg containing products should be delayed
 Food should be served 3 -5 time per day
including night
 With this most infants receive adequate
nutrients

Feeding problems during the 1st
year of life
 Underfeeding
 Suggested by restlessness and crying
 Failure to gain wt
 Possible causes
 Check frequency of feeding, mechanics of feeding
 Abnormal mother infant bonding
 Possible systemic disease
 Rx – instructing mother about the art of BF and
psychological support
_ specific management of systemic illnesses

 Overfeeding
 Regurgitation and vomiting
 Reg. –return of small amount of swallowed food
 Vomiting – more complete emptying of stamach
 Too high in fat – delay in gastric emptying, cause
distention and abd. Discomfort,
 Too high in CHT- distention and flatulance
 Loose stools
 Milk stool – loose, greenish yellow containing
mucus with freq. of 6-8 times/24hrs
 All diarrhea - infectious

 Constipation
 Consistency rather than freq. is the basis for
diagnosis
 Perform PR exam
 Aganglionic megacolon, tight or spastic anal
sphincter
 May be caused by an insufficient amount of food or
fluid
 From diets that are too high in fat or protein or
deficient in bulk
 Functional constipation – the most common
 Enemas and suppositories – temporary use

Colic – infantile colic
Common in infants younger than 3 month
The attack usually begins suddenly with a
loud continuous cry
Etiology is not usually apparent
Holding the infant upside helps and burping
Occasionally sedation for prolonged attack

Feeding during the 2nd
year of life
 By the end of 1st
year- 3 meals a day plus 1-2 snacks
 Changes in eating behavior
 Reduced food intake –rate of growth declines
 Lack of interest in food – temporary
 Never force feed
 Self selection of diets – should be respected
 Self feeding by infant
 Basic daily diets
 Grains, fruits, vegetables, meats and dairy products-balanced
diet with
 Snacks between meals- orange or other fruit juice with biscuit
 Vegetarian diet – vitamin B12 and trace mineral deficiency

Feeding during later childhood
After the age of 2 years
The child's diet – the same as family diet
Emphasis on grains, fruits, and vegetables
 Restriction of dietary fat to 30% of total energy
 Saturated fatty acid -< than 10%
 Cholesterol – not more than 100mg/1000kcal
 Poly unsaturated fatty acid -7-8% of energy
 Unsaturated fatty acid – 12-13% of energy
Such diet support normal growth of children

Bread, cereals,rice and pasta group
6-11 servings
Milkand milk product
Meat, poultry, fish
2-3 servings
Vegetable and fruit groups
2-4 servings

These servings usually meat the daily
requirement of 1600kcal(less active
child) and 2800kcal ( more active child)

Severe malnutrition
Objective
At the end of this lecture the students
should be able to describe the def.,
pathogenesis, clinical feature and
management of severe acute malnutrition

Outline
 Introduction
 Epidemiology
 Cause
 Classification
 Pathogenesis
 Clinical feature
 Diagnosis
 Complications
 Principles of management
 Prognosis and mortality

HUMAN NUTRITION
Nutrients are substances that are
crucial for human life, growth & well-
being.
Macronutrients (carbohydrates, lipids,
proteins & water) are needed for
energy and
cell multiplication & repair.
Micronutrients are trace elements &
vitamins,
which are essential for metabolic
processes.

HUMAN NUTRITION/2
Obesity & under-nutrition are the 2
ends of the spectrum of malnutrition.
A healthy diet provides a balanced
nutrients that satisfy the metabolic
needs of the body without excess or
shortage.
Dietary requirements of children vary
according to
age,
 sex &
development.

Assessment of Nutr status
Clinical
Anthropometric
Dietary
Laboratory

Clinical Assessment
Useful in severe forms of PEM
Based on thorough physical
examination for features of PEM &
vitamin deficiencies.
Focuses on skin, eye, hair, mouth &
bones.

Clinical Assessment/2
ADVANTAGES
Fast & Easy to perform
Inexpensive
Non-invasive
LIMITATIONS
Did not detect early cases
Trained staff needed

ANTHROPOMETRY
Objective with high specificity &
sensitivity
Measuring Ht, Wt, MAC, HC, skin fold
thickness, waist & hip ratio & BMI
Reading are numerical & gradable on
standard growth charts
Non-expensive & need minimal training

ANTHROPOMETRY/2
LIMITATIONS
Inter-observers’ errors in
measurement
Limited nutritional diagnosis
Problems with reference standards

Classification
 Wellcome classification
 based on the presence or absence of edema
and a deficit on body weight
 some children with features of kwashiorkor with
wt above 80% are classified
Weight(% of
standard)
Edema present Edema absent
60 - 80 kwashiorkor underweight
< 60 Marasmic
kwashiorkor
marasmus

Continued..
 Advantage
-simplicity
 Disadvantage
 If the age of the
patient is not
known-difficult to
use
 It doesn’t take into
consideration the
chronicity of the
disease process

continued
 Gomez classification
 Grade I – 90 -75 percent –mild malnutrition(1st
)
 Grade II – 75-60 % -moderate malnutrition (2nd
)
 Grade III -< 60 % -severe malnutrition (3rd
)
 Drawbacks –
 combines in one number two different kinds of
deficit: in wt for ht and in ht for age
 90% is too high as well nourished children are
labeled malnourished
 A child can have wasting but not stunting
 A child can have also wasting and stunting
 Doesn’t consider the presence of edema

Waterlow classification: takes Wt & Ht.
Wt/Ht (%)= Wt of subj/ Wt of Nl child of the same Ht Χ
100
HFA= Ht of subj/ Ht of child of same age x 100.
W F H
>90% ≤90%
H
F
>95% normal wasted
A ≤95% stunted Stunted
&wasted

Waterlow classification
% of reference standard
normal mild moderate
severe
Ht for age 95 90-95 85-90 85
(stunting)
Wt for age 90 80-90 70-80 70
(wasting)

Continued…
Indicators Age group Moderate
malnutritio
n
Severe
malnutritio
n
Bilateral
edema
Children
Adolescent
Adults
No Yes
Bilateral
edema
W/H % Children>6
months
Adolescent
70 To 79%
Moderate
wasting
<70 %
Severe
wasting
MUAC 11 to 12cm <11cm

LAB ASSESSMENT
Biochemical
Serum proteins,
creatinine/hydroxyproline
Hematological
CBC, iron, vitamin levels
Microbiology
Parasites/infection

4. Biochemical Examination
Marsmus Kwash
 Serum protein (alb)- Nl/mod ↓
 Hgb/hct- ↓
 Non ess to ess AA ratio- Nl
 Serum FFA- Nl
 Blood glu- Nl/low
 Total body protein- ↓
 Transaminases- Nl/high
 ↓
 ↓ ↓
 ↑
 ↑
 Nl/low
 ↓ ↓
 High

DIETARY ASSESSMENT
Breast & complementary feeding
details
24 hr dietary recall
Home visits
Calculation of protein & Calorie
content of children foods.
Feeding technique & food habits

OVERVIEW OF PEM
The majority of world’s children live
in developing countries
Lack of food & clean water, poor
sanitation, infection & social unrest
lead to LBW & PEM
Malnutrition is implicated in >50% of
deaths of <5 children (5 million/yr)

CHILD MORTALITY
The major contributing factors are:
Diarrhea 20%
ARI 20%
Perinatal causes 18%
Measles 07%
Malaria 05%
55% of the total have malnutrition

EPIDEMIOLOGY
The term protein energy malnutrition
has been adopted by WHO in 1976.
Highly prevalent in developing
countries among <5 children;
 severe forms 1-10% &
 underweight 20-40%.
All children with PEM have
micronutrient deficiency.

PEM
In 2000 WHO estimated that 32% of <5
children in developing countries are
underweight (182 million).
78% of these children live in South-
east Asia &
15% in Sub-Saharan Africa.
The reciprocal interaction between
PEM & infection is the major cause of
death & morbidity in young children.

Cycle
infection
Worsening of malnutrition
malnutrition

PEM in Sub-Saharan Africa
PEM in Africa is related to:
The high birth rate
Subsistence farming
Overused soil, draught & desertification
Pets & diseases destroy crops
Poverty
Low protein diet
Political instability (war & displacement)

PRECIPITATING FACTORS
• LACK OF FOOD (famine, poverty)
• INADEQUATE BREAST FEEDING
• WRONG CONCEPTS ABOUT NUTRITION
• DIARRHOEA & MALABSORPTION
• INFECTIONS (worms, measles, T.B)

Introduction
Malnutrition is defined as chronic
inadequacy in food instances
combined with high levels of illness
Is a long term year round
phenomena
Chronic problem found in majority of
households

More than half of the deaths in
children have stunting and wasting
as the underlying cause
 Occurs more frequently when
infections impose additional
demands, induce greater loss of
nutrients

Most deaths in children have some form
of malnutrition as the background
Stunting is due to chronic malnutrition
Wasting and edema are due to acute
malnutrition
Is both medical and social disorder so
management includes both medical and
social problems identified and managed—
this prevents relapse of the problem

Epidemiology
Most malnourished persons live in
developing countries,
One of every three children under the
age of 5 years in the developing country
 177 million children –are or had been
malnourished
In industrialized countries, malnutrition is
seen mainly among
 young children of low socioeconomic groups,
 the elderly who live alone,
 adults addicted to alcohol and drugs

According to unicef the extent of
malnutrition in Ethiopia is
Stunting ( 24 -59 months) – 43%
Underweight ( 0 -4 yrs) – 38
Wasting (12 -23 months) – 19%

Cause
There are two types
Primary – nutritional insufficiency
Inadequate protein, calorie and nutrient
intake
Secondary – malnutrition following
infections, injury, chronic disease, excessive
nutrient loss as occurs in chronic diarrhea,
HIV, malabsorption syndrome etc…
Social, economic, biologic, and
environmental factors underlying
severe malnutrition

Social and economic –
 Poverty that results in
 low food availability,
 overcrowding and
 unsanitary living condition
ignorance by itself or associated with
poverty leads to poor infant and child
rearing practices
misconception about the use of certain
foods
inadequate feeding conduct during illness
 inadequate BF and weaning practices
-Social problems like child abuse,

Continued…
Biologic factors
 Maternal malnutrition prior or during
pregnancy
Infectious diseases like diarrheal disease,
measles, respiratory and other infections
Diets with low concentration of proteins and
energy like over diluted milk formulas or
bulky vegetable foods that have low nutrient
densities

 Infection
 Anorexic
 Malabsorption
 Intestinal damage
 Increased metabolic rate
 Redistribution of nutrients
 Activation of inflammatory responses
 End result –
 reduced nutrient intake,
 reduced nutrient absorption,
 nutrient loss,
 increased nutrient requirement

Environmental factors
Overcowded or unsanitary living
conditions
Agricultural patterns, drought, floods,
wars and forced migration lead to
cyclic, sudden or prolonged food
scarcities

Pathogenesis
1) Dietary theory –believed in 1960’s
Kwashiorkor-is primary protein malnutrition
accompanied by a relatively excess of
energy
Marasmus is under nutrition with lack of
predominantly energy
Marasmic kwashiorkor is a combination of
chronic energy deficiency and chronic or
acute protein deficit.
Early weaning and prolonged BF without
weaning

2) Maladaptation theory –
• kwashiorkor is essentially failure of
adaptation where the body utilized
proteins and conserve S/C fat
• marasmus is due to the elevated plasma
glucocorticoid concentration which are
associated with an increased rate of muscle
protein catabolism which provided
• energy for the body’s needs and
• released amino acids for the hepatic synthesis
of protein.

Continued…
Aflatoxin theory –
 kwashiorkor results from aflatoxin
poisoning but
 there is no difference in the
amount of aflatoxin in both
marasmus and kwashiorkor

Free radicals theory – Michael Golden
 Imbalance between the
production of toxic free radicals
(superoxide,peroxidase) and their
safe disposal
The factors that increase free
radicals are
infections,
 toxins,
 sunlight,
 trauma, and catalysts such as iron

Formation of free radicals is
decreased by the antioxidant function
of vitamin A, C, and E, by ceruplasmin
and transfferin
The toxic effect of free radicals would
be responsible for cell damage leading
to alteration seen in kwashiorkor, such
as edema, fatty liver, skin changes.
more comprehensive and include all
other theories

Summary
Low nutrient intake
 Dysadapted
 Small bowel
bacterial overgrowth
 Infection
 Aflatoxin
 Fe
kwashiorkor
 Reductive adaptation
marasmus
 Vitamin A, C, E
 Mn, Zn, Se
 Essential fatty acids
 Sulfur containing
amino acids

Birth / breast feeding
 Early abrupt weaning
 Dirty diluted formula
 Repeated infections
e.g GE
 Negative energy
balance
 Marasmus
 Marasmic
kwashiorkor
 Late gradual
weaning
 Starchy family diet
 Acute infections e.g
measles
 Negative nitrogen
balance
 Kwashiorkor
 Marasmic
kwashiorkor

Pathophysiology
Develops gradually allowing the body
to adapt for the low food intake,
enabling survival in a compensated manner.
The adaptive mechanisms:
1. functional limitation & ↓ interaction
with the physical & social environment.

↓ energy intake
↓Energy expenditure-
↓ activity
Body fat mobilizn
= wt loss
↓ dietary amino acids ↓Protein synt in viscera
& muscles
↑ muscle pro
Catabolism=↑
AA for visceral
Synt of alb, LP

2. hormonal changes in metabolism of
proteins, CHO, &fats.
- Marked recycling of aminoacids (AA),
- ↓ urea synth & excretion,
- t ½ of serum proteins ↑,
- rate of albumin synth ↓ ,  shift of
extracellular alb to intravascular space
(failure of this ↓ serum alb ↓ oncotic
pressure  edema).

Cont…
 Hormonal changes
def food intake
Low plasma
Glu & AA
stress
↓insulin & somatomedin
↑ epinephrine & GH
↑ Glucocorticoids
Reverse T3 ? ↓ T3 & T4
Infection, DHN

Cont…
 Adaptive endocrine changes result in:
- ↑ glycolysis & lipolysis,
- ↑ AA mobilization,
- ↓ storage of glycogen, fats, & proteins,
- ↓ energy expenditure.

Cont…
 3. hematological & Oxygen transport:

Low protein intake
↓ physical act ↓ lean body mass Low availability
Of AA for protein
synth
Lower tissue oxy
demand Reduced Hgb & RBC
synth
Lower Hgb levels as body adapts to Lower needs
for oxy transport (no tissue hypoxia b/c of ↓ demand)

Rx with dietary protein & energy leads to ↑
tissue synth & lean body mass, and ↑
physical activity  greater tissue oxy
demand
 greater needs for hematopoietic
factors.
This leads to:
 ↑ Hgb & RBC synth (when available),
 anemia & tissue hypoxia (if not
available).
► iron should only be given during the
recovery phase.

4. CV & Renal functions
 CV reflexes will be depressed, central circulation
takes precedence over the peripheral
 peripheral circulatory failure which sometimes
mimics hypovolemic shock.
 GFR & renal plasma flow will reduce
5. immune system:
- marked depletion of lymphocytes from the
thymus (atrophy of the gland),
- ↓ complement number & function (↓ opsonin
activity),

Cont…
- phagocytosis, chemotaxis, & IC killing are all
impaired,
- the circulating levels of B-cells & Ig remain
normal, except for IgA- slightly depressed.
6. electrolytes:
- total body K+ ↓(↓ muscle protein & loss of IC
K+,
- IC Na+ ↑ (low insulin action impt for
mobilization of Na+-K+ into & out of the cell
and ↓ in ATP & phosphocreatinine).

7. GI function:
a. atrophy/edema of intestinal epithelium,
b. ↓ brush border enzymes (e.g. disaccharidase)
 mal absorption,
c. gastric, pancreatic, & billiary secretions will all
be depleted,
d. GI mobility ↓  paralytic ileus,
e. def of enzymes, overgrowth of bacteria 
diarrhea,
f. fat accumulation in the liver from def of
lipoprotein.

Cont…
8. CNS & peripheral NS: a long term
complication and includes:
- decreased growth of the brain,
- decreased myelination,
- decreased neurotransmitters,
 decreased velocity of nerve conduction.

Pathophysiologic changes
 Kidney –
 reduced GFR and renal blood flow
 decreased capacity to concentrate or dilute urine or to excrete
an acid urine
 Heart – fragmentation of myofibril and atrophy,
 small flabby heart. Decreased rate and stroke volume.
 Low voltage EKG
 Intestine – thin atrophic wall with a reduction in villous
height.
 marked reduction in the functional capacity of the digestive,
bile salt and transport system for nutrient absorption.
 Liver –
 fatty liver is probably due to reduced release of fats from the
liver to plasma in lipoproteins

Continued…
 Endocrine –
 GH increased with decreased insulin
 cortisol increased,
 T3 and T4 decreased
 Hair – there is atrophy of hair roots of the
scalp.
 Fluid and electrolytes –
 an increased of total body Na
 with a loss of total body K . This loss of K is due to
loss of K rich tissues

 Immune response:
 Disruption of skin integrity and mucus membrane
 Impaired bactericidal action of phagocyte
 Impaired cell mediated immunity
 Low serum transferrin
 low complement level
 low activity of IL-1(poor febrile response),
cachectin, TNF
 Lower mucosal secretory IgA antibody titer
 Nervous system – decreased brain growth,
neurotransmitter prod’n

Clinical features
• PEM can affect all ages but
common among infants and young
children
• Marasmus – before 1 year of age
• Kwashiorkor – after 18 months of
age
• Diagnosis is principally based on
• dietary history and
• clinical features

MARASMUS
The term marasmus is derived from
the Greek marasmos, which means
wasting.
Marasmus involves inadequate intake
of protein and calories and is
characterized by emaciation.
Marasmus represents the end result
of starvation where both proteins and
calories are deficient.

MARASMUS/2
Marasmus represents an adaptive
response to starvation, whereas
kwashiorkor represents a maladaptive
response to starvation
In Marasmus the body utilizes all fat
stores before using muscles.

EPIDEMIOLOGY &
ETIOLOGY
Seen most commonly in the first year
of life due to lack of
 breast feeding and
the use of dilute animal milk.
Poverty or famine and diarrhoea are
the usual precipitating factors
Ignorance & poor maternal nutrition
are also contributory

Clinical Features of Marasmus
Severe wasting of muscle & s/c
fats(60% or less of wt for age)
Severe growth retardation(stunted)
Child looks older than his age
Alert but miserable
Hungry
Diarrhoea & Dehydration
No edema

• The hair sparce, thin, dry, and easily
pluckable
• The skin is dry, thin, and wrinkles –
‘baggy pant ‘

Irritable, ravenously hungry but vomit
easily
Loss of bichat fat pad, last fat tissue to
disappear (monkey’s or little old man’s
face)
Marked weakness
Abdominal distention(due to distended
bowel)

KWASHIORKOR
Cecilly Williams, a British nurse, had
introduced the word Kwashiorkor to
the medical literature in 1933.
The word is taken from the Ga
language in Ghana & used to describe
the sickness of weaning.

ETIOLOGY
Kwashiorkor can occur in infancy but
its maximal incidence is in the 2nd yr
of life following abrupt weaning.
Kwashiorkor is not only dietary in
origin.
Infective, psycho-socical, and cultural
factors are also operative.

ETIOLOGY (2)
Kwashiorkor is an example of lack of
physiological adaptation to unbalanced
deficiency where the body utilized
proteins and conserve S/C fat.
One theory says Kwash is a result of
liver insult with hypoproteinemia and
oedema.
Food toxins like aflatoxins have been
suggested as precipitating factors.

CLINICAL
PRESENTATION
Kwash is characterized by certain
constant features in addition to a variable
spectrum of symptoms and signs.
Clinical presentation is affected by:
• The degree of deficiency
• The duration of deficiency
• The speed of onset
• The age at onset
• Presence of conditioning factors
• Genetic factors

CONSTANT FEATURES OF KWASH
OEDEMA(doesn’t involve serous membrane)
PSYCHOMOTOR CHANGES(Apathetic and irritable,
cry easily, and have an expression of misery and sadness
GROWTH RETARDATION
MUSCLE WASTING

USUALLY PRESENT
SIGNS
MOON FACE
HAIR CHANGES
SKIN DEPIGMENTATION
ANAEMIA

OCCASIONALLY PRESENT
SIGNS
HEPATOMEGALY
FLAKY PAINT DERMATITIS
CARDIOMYOPATHY & FAILURE
DEHYDRATION (Diarrh. & Vomiting)
SIGNS OF VITAMIN DEFICIENCIES
 SIGNS OF INFECTIONS

Continued…
Kwashiorkor –
 soft, pitting, painless edema, usually in
the feet and leg
Subcutaneous fat is preserved
Weight deficit is not as severe as
marasmus
Height may be normal or retarded

Continued…
The hair is dry, brittle, easily
pulled out without pain, pigment
changed to brown, red, or
even yellow white
‘Flag sign’ – due to alternating
period of poor and good protein
intake

Anorexic and diarrhea is common
Hepatomegaly
Protuberant abdomen and peristalsis is
slow
Muscle tone and strength is reduced

Marasmic kwashiorkor
Combines clinical feature of both
kwashiorkor and marasmus
Edema
Muscle wasting and decreased
subcutaneous fat
When edema subsides, the patient
appearance resembles that of
marasmus
Wt less than 60% and edema

Diagnosis
 History – nutritional history
 Physical findings
 Anthropometric measurements
-most children have similar growth potential
regardless of ethnicity
-need for international reference standard
-WHO recommends NCHS as a reference
-wt for ht –index of current nutritional
status
-ht for age –index of past nutritional history
-Harvard status – for under 5th

Assessment of Nutritional Status
1. Nutritional Hx & Dietary measurement:
- hx of breast feeding (frequency, day & night ?),
- total duration of breast feeding,
- any additional food (when was it started? If cow’s milk is
used, is it diluted/not?),
- amount, frequency, & type of additional food. Nutritional
hx should continue until present age.
 Dietary measurement
- measuring the diet/replica of the diet the child is getting,
- referring to the reference diet .

2. Anthropometric Measurement
Wt., ht/length, MUAC, HC, & skin fold thickness (SFT).
Interpretation:
1. NCHS (National Curve for Health Statistics): widely
employed, extends from 5th
to 95th
centile.
Children below the 5th
centile are considered abnormal. In
areas where PEM is prevalent a 3rd
centile is used as a cut
off point.
2. Harvard/Wellcome curve:
- impt for under five children,
- takes the wt & age,
- uses standard wt (expected wt for age, 80%) &
presence/absence of edema. The standard is equivalent
to the 50th
centile of the NCHS curve.

Gomez classification:
WFA(% of ref)= Wt of subj/ Wt of Nl child of the same
age
WFA (% of ref) Interpretation
90-100 normal
75-89 Grade I/ mild
malnutrition
60-74 G II/ moderate
malnutrition
<60 G III/ severe
malnutrition

Cont…
Wellcome’s Classification:
Wt for Age
(WFA)
edema no edema
60-80% Kwashiorkor Underweight
<60% Marasmic
kwash
Marasmus

Investigation
 Hct and Hgb
 WBC count and differential
 RBS
 Urinalysis and urine culture
 Chest X-ray
 Blood culture
 Total serum protein
 Ratio of non essential to essential a.a-
 Reduced urinary creatinine clearance

Poor prognostic signs
 Age less than 6 months
 Deficit in Wt for Ht > 30%
 Stupor, coma, or other alteration in mental status
 Infections, particularly pneumonia or measles
 Petechiae or hemorrhagic tendencies
 Dehydration and electrolyte disturbances, particularly
hypokalemia, and severe acidosis
 Heart failure, hypothermia, hypoglycemia
 Total serum protein below 3 gm/dl
 Severe anemia with clinical signs of hypoxia
 Clinical jaundice or elevated serum bilirubin
 Extensive exudative or exfoliative cutanous lesions

Complications
Hypoglycemia
Hypothermia
Dehydration
Infection especially pneumonia, sepsis,
UTI, gastroenteritis
Fluid and electrolyte imbalance
Anemia
Developmental delay

Hypoglycemia
Life threatening comp’n
At risk because of alteration in glucose
metabolism
Signs –low body temperature, lethargy,
eye lid retraction, twitching or convulsion
RBS <54 mg/dl
Immediately give glucose containing
solution po or iv

Hypoglycemia: a common cause of
death in the 1st
2 days.
Can be due to a systemic infec or not
being fed for 4-6 hr.
- often have hypothermia, limpness,
drowsiness, lethargy.

- rx should be immediate (before lab
confirmation): 5ml/kg of 10% glucose,
this can also be given orally.
- also consider broad spectrum
antibiotics.

Dehydration
Useful signs –
thirst,
dry tongue and mouth,
 low urinary output,
weak and rapid pulse,
 low blood pressure,
 cool and moist extremities, and
declining state of consciousness.
Unreliable signs – sunken eyeball,
decreased skin turgor, irritability and
apathy

Rehydration should be preferably orally
or through NG tube
Solution should contain less Na and
more K – ORS ( not ideal) Resomal
(best)
Indication for iv fluid – shock and coma

156
Types of ORS
Solution Glu
g/dl
Na
mEq/L
K
meq/L
Cl
meq/L
WHO 2.0 90 20 80
Rehydralyt
e
2.5 75 20 65
Pedialyte 2.5 45 20 35
Infalyte 2.0 50 20 40

particular renal problem that makes the
children sensitive to sodium overload.
Dehydration:
- ‘narrow therapeutic window”
inappropriate rehydration can lead to
fluid overload & cardiac failure

- rx when possible should be orally, even
for severe DHN, unless there is shock,
loss of consciousness, or confirmed
severe DHN.
- fluids: half strength Darrow’s solution,
RL with 5% dextr, half strength saline
with 5% dextrose,

- oral rehydration: 5ml/kg of ReSoMal q 30min
for the 1st
2 hr, orally/ NG tube, then adjust
according to wt,
i.e. if continued wt loss, ↑ the rate by
10ml/kg/hr;
if no wt gain, ↑ rate by 5ml/kg/hr;
if wt gained but still signs of DHN, continue
same rx;
wt gained & no signs of DHN, stop rehydration.
NB: continuous reassessment vital!!

- in kwash, increased total body water &
Na+,
- frequently hypovolemic due to dilatation
of the blood vessels with a low cardiac
output,
-

definite watery diarrhea, clinical
deterioration DHN.
- a fast weak pulse, cold peripheries,
disturbed consciousness, absence of
signs of heart failure shock
(hypovolemic/ septic).

- mx uses the same fluids as in marasmus,
amount 10ml/kg/hr for 2 hr.
- watch for signs of over-hydration: ↑ RR,
grunting, ↑ liver size, vein engorgement,
- as soon as the patient improves, stop
all IV intake.
- also treat hypoglycemia, hypothermia,
infection.

If pts is in shock
give 15ml/kg over the 1st
hr & reassess,
dose can be repeated if wt loss/ wt is
stable.
- as soon as consciousness improves/
PR drops, stop the drip &
Give NG tube with 10ml/kg/hr
ReSoMal.

SIGN OF OVERHYDRATION
.Engorged neck vein
RR increment by more than 10
PR increment by 15
RUQ tenderness
Liver size increased by 1cm
Peripheral edema
Any sign of respiratory distress like
grunting and cyanosis

Hypothermia
Body temperature <35.5 degree
Due to impaired thermoregulatory
mechanism, reduced fuel substrate or
severe infection
Use kangaroo technique, put a hat
and the room should be kept warm
(b/n 28 -32 degree)
The should always sleep with the mother

Anemia
Usually due to Fe and/or folic acid
deficiency
Clinically pale , low HGB/ HCT
Fe treatment in phase II
Indication for transfusion –HGB
<4gm/dl , HCT <12% or heart failure
10ml/kg of packed RBC/ whole blood
slowly over 3hr.

Infection
Clinical manifestations may be
mild
Classical signs ( fever,
tachycardia and leukocytosis)
may be absent
Assume that children with
severe malnutrition have a
bacterial infection

Gram positive and gram negative
Safer to treat all with broad spectrum
antibiotics
Po route is preferred unless the patient
is in septic shock (a fast and weak pulse,
cold extremities, low BP and disturbed
consciousness)

Management
 Ten essential steps in the routine care of severely
malnourished children
 Treat / prevent hypoglycemia
 Treat / prevent hypothermia
 Treat / prevent dehydration
 Correct electrolyte imbalance
 Treat infection
 Correct micronutrient deficiencies
 Initiate feeding
 Replete wasted tissue (catch-up growth)
 Provide sensory stimulation and emotional support
 Prepare for follow up after recovery

Admission criteria
Age 6mo to 18 yrs - W/H or W/L <70% or
- MUAC <11cm with L
>65cm or
- Bilateral pitting edema
Adults -MUAC <170mm or
- BMI <16 or
-Presence of bilateral
pitting edema (exclude
other causes)

Nutritional therapy
Routine medicines
• Vitamin A – one capsule on the day of
admission and discharge
• Folic acid – a single dose of 5mg folic
acid
• Other nutrients – no need b/c F75 and
F100
• Antibiotics – should be given to all
• 1st
line treatment – oral amoxacillin
(ampicillin)
• 2nd
line teatment – Add chloramphenicol or
gentamycin

Routine medicines
1. Vitamin A

Continued…
 Duration of antibiotic –
 every day during phase I and 4 more days –in
patient
 7 days total in out patient care
 Malaria
 Measles vaccine on the 4th
week of treatment
 Deworming – at the start of phase II
 worm medicine is only given children who can walk
 Albendazole 400mg PO STAT
 mebendazole 100mg TWICE DAILY FOR 3 DAYS

Cont…
2. Folic acid: on the day of admission, one dose of folic
acid (5mg) to children with anemia.
3. Antibiotics: should be given to every severely
malnourished patient, even if no clinical signs of
systemic infection (nearly all are infected).
- small bowel bacterial overgrowth occurs in all these
children: systemic infection, malabsorption, & chronic d.
- in children with kwash, bacteria that are normally not
invasive, such as S. epidermidis can cause systemic
infection/ septicemia.
- recommended also in those who go to phase II directly.

Antibiotic regimen:
 Oral amoxicillin (oral ampicillin, if unavailable): 1st
line,
 2nd
line rx: add chloroamphenicol, or
- add gentamicin, or
- change to amoxicillin/clavulinic acid.
4. Iron: given in phase II.

Phase I:
- pts with inadequate appetite and/or a
major medical cxn,
- formula used in this phase is F-75,
- promotes recovery of normal metabolic
fn & nutrition-ele balance,
- rapid wt gain is dangerous (F-75
ensures that).

Phase I
Diet – F75 (one sachet mixed
with 2 liters of water)
provides 75 kcal per 100 ml
8 feeds per day –larger volume
feeding can result in osmotic
diarrhea

 Naso-gastric feeding is used if
 the child takes less than 75% of the prescribed
diet
 pneumonia with fast breathing
 painful lesions of the mouth
 cleft palate or other physical deformity
 disturbance of consciousness
Surveillance using multichart

Transition phase
 Criteria to progress from phase I
 Return of appetite
 Beginning of loss of edema and
 No iv line, no NG tube
 Diet – F100 (100kcal in 100ml)
 The no. of feeds, their timing, and volume is the
same as phase I this leads to a 30% increase in
energy intake & thus the wt gain should be
~6g/kg/day,
 Transition phase should last 1-5 days

- criteria to move back to phase I include:
1. Increasing edema, new onset edema,
2. Rapid increase in liver size,
3. Significant refeeding diarrhea (& wt
loss),
4. Medical cxn, if NG tube needed,
5. Intake <75% of feeds in transition
phase,
6. Wt gain >10g/kg/d (excess fluid
retention).

Phase II
 Criteria to progress
 Good appetite (taking >90% of F-100)
 Loss of edema entirely
 designed for rapid wt gain (>8g/kg/day).
 Diet – F100
 Have unlimited intake
 5 feeds of F100 are given
 One porridge may be given
 Always offer plenty of clean water while eating
 Children must never be forced fed
 Provide additional quantity of diet after feeding

Phase II: amount increased to ~180-
225ml/kg/day of F-100,
 iron is added here

 .
- criteria to move back to phase I:
Development of edema,
refeeding diarrhea with wt loss,
Wt loss of >5% of body wt at any visit
Wt loss for 2 consecutive weighing,
Static wt for 3 consecutive weighing.

Criteria for failure to respond
 Primary failure to respond (phase I)
 Failure to regain appetite (Day 4)
 Failure to start to loss edema (Day 4)
 Edema still present (Day 10)
 Failure to enter phase II and gain 5g/kg/d (Day 10)
 Secondary failure to respond
 Failure to gain more than 5g/kg/d for three
consecutive days (during phase II)
 Measure to take
 Extensive history and examination or lab. Test
 Look for hidden infection

Cont…
Discharge criteria:
Age
6mo-18
yr
• W/L (W/H) ≥85% on
more than one occasion,&
No edema for 10 days.
• target wt gain reached &
no edema for 10 days.

Prognosis
 Upon treatment the acute signs of the disease
are corrected
 Catch-up growth in height may take long or
might never be achieved
 Mortality rate can be as high as 40%
 Immediate cause of death are comp’n
particularly infections, hypoglycemia, and
dehydration
 Mortality rates can be reduced to < 10% by
prevention and treatment of comp’n

Prevention of
Malnutrition
Primary prevention
1-Increas food production
2-Establishment of an efficient food
distribution system
3-Proper environmental sanitation and
raising the standard of living
4-Prevention and control of infectious
diseases (vaccination)
5- Adequate services for vulnerable groups

Secondary prevention:
Early detection and treatment of
malnutrition . This can be done through
periodic nutritional surveillance .i.e.
systematic collection , dissemination
and analysis of data related to
malnutrition in order to plan a program
for prevention & control of this
condition

Tertiary prevention
Rehabilitation services to offer health
education for mothers to care and feed for
the malnourished children to allow them to
live normal life.

II-Micronutrient deficiencies
Micronutrients are the nutrients that enable the
body to produce enzymes, hormones and other
substances essential for proper growth & development.
As tiny as the amounts are, the consequences of their
deficiencies are severe.
Vitamin A & D, iodine and iron are the most important in
global public health terms; their lack represents major
threats to the health and development of populations all
over the world, particularly low income countries. It
affects more under five children and pregnant women

Vitamin A deficiency (VAD)
Functions of Vitamin A
a-Integrity of epithelial tissues in skin and mucous membrane
which are barriers against external infections especially
respiratory tract infections
b-Integrity of epithelial tissues lining of urinary and biliary
tracts ,conjunctiva and lacrimal glands (preventing xerosis)
c- Synthesis of the visual purple (rhodopsin) from protein
(opsin) and vit. A itself
d- Promoting the proper growth.

Important sources of vitamin A
I – Animal: Milk including human milk (colostrums),
liver, poultry , kidney; eggs, butter & Cod liver oil
are the richest source for the vitamin
II- Plant:orange / yellow fruits and vegetables
(mangoes, apricots, carrots) and dark green leaves.

Clinical features
I - For children, VAD causes:
1-Severe visual impairment and
Bitots spots, Conjunctival &
corneal xerosis, keratomalacia & night
blindness (the most severe total blindness).
2-Xerosis &follicular hyperkeratosis of skin
3-Increased the severity &mortality of
illness (diarrheal diseases & measles)

Prevalence of VAD
Mild subclinical

II- For pregnant women
in high-risk areas, VAD occurs specially during
the last trimester when the demand by both the
fetus and the mother is highest.
It is demonstrated by high prevalence of night
blindness during this period.
These women will secrete later breast milk, which
is deficient in vitamin A.

Prevention of VAD
Short term Long term

I - Short-term intervention:
• Breast-feeding: Promoting
breast-feeding
• Vitamin A supplementation

II- Long term approach
a) Food fortification (with sugar) maintains
vitamin A status especially for high-risk
groups .
b) Home gardens. For vulnerable rural
families, growing vegetables in home gardens
complements fortification

Iodine deficiency disorders
(IDD)
IDD remains a major threat to the
health of populations all over the world,
particularly among preschool children and
pregnant women in developing countries.
It is not only easy to control but it can be
eliminated.

The main causes of IDD are:
1-Lack of iodine in food usually in places
far from the sea.
2- Goitrogens, which are chemical
substances in water or food leading to the
development of goiter by reducing the
amount of iodine that the thyroid gland
takes up from the blood.

Prevalence of I DD:
Mild : sporadic

Health consequences of IDD
• Hypothyroidism
• Retarded physical development
• Mental dysfunction
• Spontaneous abortion & still
birth
• Cretinism

What are the Measures for
prevention of iodine deficiency
disorders?
A-Primary prevention (Elimination
of IDD):
The primary intervention strategy for elimination of
IDD is “Universal Salt Iodization” (USI).
Salt was chosen because it is :
•widely available and
•consumed in regular amounts
•low costs of iodizing.

“Universal Salt Iodization” (USI).
(For Elimination of IDD):

B- Secondary prevention (Screening
for Neonatal Hypothyroidism)
Neonatal hypothyroidism is the most common
disorder that should be screened.
Congenital hypothyroidism leads to mental
retardation , which can be prevented if medical
treatment is given within the first 1-2 months of life.
All the neonates are routinely screened for estimation
of the level of the thyroid hormones by taking blood
sample from the heel of the neonate within the first
week of life.

B- Secondary prevention (Screening
for Neonatal Hypothyroidism)

Vitamin D deficiency
( Rickets and osteomalacia)
Rickets is a systemic disease of the
growing skeleton characterized by
defective calcification of the bones
during growth.
The term osteomalacia is applied to the
same pathological condition when it
affects a skeleton that has completed its
growth

Function of vitamin D
Vitamin D is needed at times of rapid growth
that is, in infants and young children,
adolescents, and pregnant women.
It has the following functions:
a) Promotion of absorption of calcium and
phosphorous from the intestine.
b) Calcification of bone matrix

Clinical signs
Active rickets
in young children:
Epiphyseal
enlargement-
Beading of ribs-
Persistently open
anterior fontanelles
 (after 18 months of age)
Muscular hypotnia

Healed rickets
in older children
•Frontal or parietal
bossing,
•knock knees or bow
knees
•Deformities of the
thorax

Osteomalacia (in adults women):
Local or generalized
skeletal deformities
of the pelvis with
tender bones
.

Sources of vitamin D
a-The ultraviolet rays (UVRs)
activate the provitamin (7-
dehydrocholesterol) in the
deep layers of the skin , but it
can be filtered by air pollution
and glass.
b- Food sources are only of
animal origin e.g., milk, butter,
cheese, fatty fish (salmon and
sardines), eggs, liver and cod-
liver oil.
c- Fortified milk.

Ecological factors for Vitamin D
deficiency:
- Biological
Dietary
Social
- Environmental

I- Biological factors
a- Order of the child: The later the
child of an undernourished mother,
the higher the probability of
developing Vit. D deficiency.
b- Twins
c- Low birth weight
d- High parity will lead to
osteomalacia

II-Dietary factors
a-Deficient intake of Vitamin D or
calcium
b- Presence of phytic acid and
oxalates in diet preventing calcium
absorption.
c- Artificially fed babies.

III- Social Factors
a-Poverty
b-Ignorance of mothers about proper
feeding and rearing of children
c-Cultural factors as wrapping
infants and preventing exposure to
sunshine, and early marriages of
girls who are still in need of dietary
calcium.
d-Living in squatter areas.

III- Environmental factors
a-Amount of sunshine and
ultraviolet rays (UVRs).
In cloudy and dusty atmosphere
the UVRs are absorbed .
b- High prevalence in Rural
areas due to ignorance, poverty
and unhealthful social habits

Prevention of vitamin
D deficiency
Health &
nutrition education
Socioeconomic development
Prevention and control
of air pollution.
Enrichment of milk or baby formula
with vitamin D.
Vitamin D supplements for the high-
risk groups.

Iron deficiency anemia (IDA)
Iron deficiency is the most wide
spread nutritional disorder, affecting
both developed & developing
countries. The main clinical
manifestations are:
• pale conjunctivae,
•spoon shaped nails and
•atrophic lingual papillae.
•Easy fatigability
Hematological tests will confirm the
diagnosis.

Target groups and level of
anemia
Hblevel
(g/100 ml)
Children 6 months to 5 year
Children 6 years to 14 years:
Men
Women (not pregnant)
Women (pregnant)
<11
<12
<13
<12
<11
Mild, moderate, and severe
anemia
Mild
Moderate
Severe
Below the values given
above, but more than
10
7 – 10
Below 7
Hemoglobin levels in anemia

High Risk For Iron Deficiency Anemia
•Pregnant women those with :
•repeated pregnancy and delivery
within a short intervals
• having parasitic diseases
•Growing children, low birth weight
school age children
•The elderly,
•Any one suffering from parasitic
diseases

Iron Stores in the blood
Two main components
Functional component:
It is in the circulating hemoglobin (with a smaller
quantity in body tissue, myoglobin and enzymes).
A deficiency of iron in the functional component
does not ordinarily occur until iron stores are
completely exhausted.
The storage component
Found in the liver, spleen and bone marrow in the
form of ferritin and haemosiderin in.
It serves as reserve source for the functional
component.

Etiology:
The diminishing of iron stores results from
Low iron intake
Increased demand which occurs in :
women due to pregnancy, blood loss with menstruation,
high parity, Short interbirth interval and parasitic
infestation.
children due to rapid growth, and low birth weight,
artificially-fed babies, recurrent infections and parasitic
infestation.
Inadequate absorption:
Tanic acid , phytates, oxalates, carbonates, phosphates
and some forms of dietary fiber inhibit absorption. These
are found mainly in tea, coffee, some vegetables.

Factors known to affect absorption of iron :
1- Tanic acid , phytates, oxalates,
carbonates, phosphates and some forms of
dietary fiber inhibit absorption. These are
found mainly in tea, coffee, some
vegetables.
2-Absorption increases when iron stores
decreases as during growth
and pregnancy.

Iron sources
1- Haem-iron is
found in animal
foods (liver, kidney,
spleen, meat,).

2- Non-Haem iron
is found in
vegetables ,
fruits, cereals,
pulses,.
It comprises
the major source
of dietary iron
in poor
Communities

Health consequences of iron deficiency
anaemia
Pregnant
females:
increased risks
of maternal
morbidity & mortality.
Fetus and neonates
of anemic mother:
intrauterine growth
retardation.
increased perinatal
mortality
Adults
Impaired work
Capacity
easy
fatigability,
which
affects
Children
infectious
diseases.
vulnerable to
lead poisoning,
Impaired physical
activity & scholastic
achievement

Prevention & control of iron def.anaemia
Iron Supplements
Nutritional
Education
Prevention &control of infectious diseases
Adequate MCH services
Food fortification

I- Iron Supplementation
short-term strategy
for countries with a significant
problem of iron deficiency anaemia.
Providing iron tablets to a target population
The target groups for supplementation programs are :
• Pregnant and lactating women, Women in the
child-bearing period, and adolescent girls both
iron &folic acid tablets are recommended
• Infants and preschool age children (6-30
months) Oral iron preparation is given

II- Nutritional education
•to ensure that people eat
more iron rich food
•to promoting the intake of iron absorption
enhancers, & reducing the ingestion of
absorption inhibitors

III- Prevention and control of of
infectious and parasitic diseases
Immunization &effective, timely
curative care can diminish the adverse
nutritional consequences of viral and
bacterial diseases, as well as parasitic
infestations.

IV- Adequate MCH services
Routine laboratory investigations
during antenatal care to estimate HB
level, nutritional education, health
care for under five

V- Food fortification
The fortification of widely consumed
such as sugar and salts with iron is one of
the most effective ways of preventing
iron deficiency.

Obesity is a disease in which excess body
fat has accumulated to such an extent that
health may be seriously affected
(WHO,2000). It is a complex condition
one with serious social and psychological
dimensions that affects virtually all age
and socioeconomic groups

Over weight (preobese) means a
weight in excess of the average
for a given height and age. It is
usually due to obesity, but can
arise from other causes such as
abnormal muscle development.
Generally, men have higher
rates of overweight, while
women have higher rates of
obesity

Assessment of obesity
1-Body weight: 10% increase over the weight
standards. It is considered a rough measure.
2-Body mass index (BMI): It is a simple index of
weight for height that is commonly used for
adults. However, it does not take into account
factors such as gender and age. Also it does
not distinguish between weight associated
with muscle and that associated with fat.

3-Waist measurement: It is a simple method
of identifying and recording central fat
distribution. People who are over-wight and
have central fat are at a greater risk of
developing heart disease and diabetes.
4-Broca’s index : Height (cm) – 100

5-Skin fold thickness:
assessing body fat at triceps, sub-scapular or suprailiac regions.

BMI= Weight in KG
Height 2
( meter )

Classification BMI
Underweight
Normal weight
Pre-obese
Obese
Below 18.5
18.5- 24.9
25.0- 29.9
more than 30
WHO Classification of obesity

Life
changes
Endocrine
Familial
Emotional
Social
condition
Eating
habits
Physical
activity
Genetic
factors
Sex
Age
Risk
factors
of obesity

1- Age:
Obesity can occur
in any age , and
generally increases
with age .
Infants with
excessive weight
gain have an
increased
incidence of obesity
in later life

2-Sex:
women gain most between 45 and
49 of age.

3-Genetic factors:
A close correlation is recorded
between the weights of identical
twins even when they are reared in
dissimilar environments

4-Physical inactivity:
Physical inactivity may cause
obesity which in turn restricts
activity

5-Eating habits:
Eating between meals ,preference to sweets and
fats are established early in life of obese
subjects.

6-Socioeconomic status
There is an inverse relationship
between socioeconomic status and
obesity.

7- Psychological factors
emotional disturbance is deeply
involved in the etiology of obesity
. Overeating is a symptoms of
depression, anxiety,frustration
and loneliness in childhood and
adult life.

8-Familial tendency :
obesity runs in families but this is
not it is not necessarily explained
by the influence of genes

9- Endocrine Factors
Endocrinal disorders (as
hypothyroidism, Cushing's
syndrome and hypothalamic
tumors) result in weight gain.

10-Life changes:
Aging: due to decline in activity
without a compensating decrease in
food intake
Critical events : after marriage-
pregnancy and retirement
Smoking cessation

Prevention of
Obesity
Primary
prevention
Secondary
Prevention

Prevention of obesity
Primary prevention
1- Promoting healthy
eating & inducing
dietary
changes
2-Proper feeding
& rearing of children
3-Increased physical
activity

Secondary prevention:
1. Screening and assessment of the condition
2. Managing obesity by:
• Behavior modification
• Dietary changes
• Physical activity
3. Managing health consequences of obesity.

Screening TechniquesScreening Techniques

I.MUAC MeasurementI.MUAC Measurement
 Steps in MUAC measurementSteps in MUAC measurement
 Ask the mother to remove clothing that may cover theAsk the mother to remove clothing that may cover the
child’s left arm. If possible, the child should stand erectchild’s left arm. If possible, the child should stand erect
and sideways to the measurer.and sideways to the measurer.
 Estimate the midpoint of the left upper armEstimate the midpoint of the left upper arm
 Straighten the child’s arm and wrap the tape around theStraighten the child’s arm and wrap the tape around the
arm at the midpoint. Make sure the numbers are rightarm at the midpoint. Make sure the numbers are right
side up. Make sure the tape is flat around the skinside up. Make sure the tape is flat around the skin
 Inspect the tension of the tape on the child’s arm. MakeInspect the tension of the tape on the child’s arm. Make
sure the tape has the proper tension and is not too tightsure the tape has the proper tension and is not too tight
or too looseor too loose
 When the tape is in the correct position on the arm withWhen the tape is in the correct position on the arm with
correct tension, read and call out the measurement tocorrect tension, read and call out the measurement to

MUAC MeasurementMUAC Measurement

MUAC MeasurementMUAC Measurement
 Interpretation of MUAC measurement for age group 6Interpretation of MUAC measurement for age group 6
month-18 yearsmonth-18 years

MUAC Measurement
 Interpretation of MUAC measurement
in adult
 MUAC < 17 cm= SAM
 MUAC< 18 cm with recent history of
weight loss
 MUAC 17-21 cm=MAM
 MUAC >=21 cm Normal

II. Weight MeasurementII. Weight Measurement
 Steps in Weight measurementSteps in Weight measurement
1. Explain the procedure to the child’s mother or
caregiver before starting
2. Install a 25kg hanging spring scale (graduated by
100g). If mobile weighing is needed, the scale
can be hooked on a tree or a stick held by two
people
3. Attach the washing basin / pants and recalibrate
to zero
4. Remove the child’s clothes and place him or her
into the basin
5. Ensure nothing is touching the child and the
basin/pant

Read the scale at eye level (if the childRead the scale at eye level (if the child
is moving about and the needle doesis moving about and the needle does
not stabilize, estimate weight bynot stabilize, estimate weight by
using the value situated at theusing the value situated at the
midpoint of the range of oscillations)midpoint of the range of oscillations)
7.7. When the child is steady record theWhen the child is steady record the
measurement to the nearest 100gmmeasurement to the nearest 100gm
8. Calibrate the scale with a material8. Calibrate the scale with a material
with known weight every week.with known weight every week.

Weight MeasurementWeight Measurement

Weight measurementWeight measurement

III. Height MeasurementIII. Height Measurement
 For children less than 85 cm, the measuring board is
placed on the ground.
 The child is placed, lying along the middle of the board. The
assistant holds the sides of the child’s head and positions
the head until it firmly touches the fixed headboard with
the hair compressed.
 The measurer places her/his hands on the child’s legs,
gently stretches the child and then keeps one hand on the
thighs to prevent flexion. While positioning the child’s legs,
the sliding foot-plate is pushed firmly against the
bottom of the child’s feet.
 To read the measure, the foot-plate must be perpendicular
to the axis of the board and vertical.
 The height is read to the nearest 0.1 centimeter.

W/H %W/H %
W/H % =W/H % = Actual WeightActual Weight x 100%x 100%
Median WeightMedian Weight
 W/H % < 70% =Marasmic (SAM)W/H % < 70% =Marasmic (SAM)
 W/H % between 70% and 80%=MAMW/H % between 70% and 80%=MAM

BMI
 Body Mass Index (BMI) for adult
BMI=Weight in Kg
(Height in meter)2
BMI < 16 Kg m2
= SAM

IV.Checking for Bilateral PittingIV.Checking for Bilateral Pitting
OedemaOedema

V. Checking for Severe VisibleV. Checking for Severe Visible
WastingWasting
Ask the mother toAsk the mother to
remove all the clothremove all the cloth
and look the arms, thighsand look the arms, thighs
and buttocks for loss ofand buttocks for loss of
muscle bulk andmuscle bulk and
sagging of skinsagging of skin

Pathphysiology and basis for
treatment of SAM

Endocrine System
EndocrineEndocrine
SystemSystem
Insulin is reducedInsulin is reduced
and there isand there is
glucoseglucose
intolerance. IGF-Iintolerance. IGF-I
is very low,is very low,
although growthalthough growth
hormone is high.hormone is high.
Cortisol is usuallyCortisol is usually
high.high.
The endocrineThe endocrine
system may not besystem may not be
able to respondable to respond
appropriately to largeappropriately to large
meals. Give smallmeals. Give small
frequent meals. Dofrequent meals. Do
not give steroids.not give steroids.

Metabolism and temperature regulation

Malnourished infants
•Do not cry -they are thus
neglected
•Have no strength -do not
stimulate milk
•Have a very high mortality
•Are often infected

I. INFANTS WITH FEMALE
CARE TAKER

Infant with Visible Severe Wasting

Registration and measurements
1) Precision of the
scale: 10 to 20g
for the babies
below 8kg
2) The table weight
for height stops at
49cm length ,
therefore it is
quite difficult to
calculate the WLP
for these infants.

Product used
Diluted F- 100
Why Should be diluted?
•Because babies of that age need
more water and they are wasted,
they need 100kcal/kg

Phase 1
♥Breastfeed every 3 hours, at least for 20 minutes,
more often if the child ask for more.
♥One hour after breast-feeding, complete with F100
diluted using the supplementary suckling technique:
complete
F-100 diluted: 130ml/kg/day
(100kcal/kg/day),divided in 8 meals
 To prepare F-100 diluted : dilute F100 one sachet
in to 2.7 liters of water
 In order to prepare small amount use already
prepared 100ml of F100 and add 35 ml of water to
make it diluted and you will get 135 ml diluted F100

Amount of F 100 Diluted for infants

The Suckling Technique
-The mother holds the tube at the breast with one hand
and uses the other for holding the beaker.
-It may take one or two days for the infant to get used
of the tube but it is important to persevere.
-The supplementation is given via an NGT n°8 (n°5 is too
small)
-The tip is cut back beyond the side ports approximately
1cm and the cap at the end of the tube is removed
-F-100 diluted is put in a beaker. The mother holds it.
-The end of the tube is put in a cup.
-The tip of the tube is put on the breast at the nipple
and the infant is offered the breast.
-When the infant sucks on the breast with the tube in is
mouth, the milk from the cup is sucked up through the
tube and taken by the infant.
-The beaker is placed at least 10cm below the level of
the breast so the milk does not flow too quickly and
distress the infant.

Routine medicine
*Vitamin A:50.000 IU at admission only
* Folic acid:2.5mg (1/2tab)
* Ferrous sulphate: when the child sucks well and
starts to grow. Take the quantity of F100
enriched with ferrous you need in phase II. Add
1/3 of water to obtain the correct dilution.
* Antibiotics:- Amoxicillin (from 2kg):
30mg/kg 2 times a day (60mg/day)
with
- Gentamicin(5mg/kg/d IM)
- Don’t use Chloramphenicol

Surveillance
•Weigh infant daily and see if his
weight is increasing.
•The scale should have a 10 to 20g
precision.
•If the infant is taking the same
quantity of F100D and is increasing, it
means that the breast-milk quantity is
increasing.

•When the infant is gaining weight at 20g per
day (what ever his weight), decrease the
quantity of F100 diluted to one half of the
maintenance intake,
-If the weight gain is maintained (10g per day
what ever his weight) then stop “ss” feeding
completely,
-If weight gain is not maintained then
increase the amount by 75% of the
maintenance amount.
-Keep the child in the centre for a further 5
days on breast milk alone to make sure that
he continues to gain weight.
Surveillance cont…

Care for the mother (1)
-Explain the mother what you do and why; do not
make the mother feel guilty, reassure her.
-Be attentive to her.
-Screen the mother for malnutrition( with MUAC and
check for presence of bilateral pitting Oedema)
-She should drink at least 2 litters per day: WHO-
ORS or sugared water or normal water.

She must eat enough: 2500kcal/day
–1 porridge in the morning
–1 family meal
–1 porridge in the afternoon
which means that at the 2100kcal for
the care takers an additional porridge
has to be given to the mother (~
400kcal)

The mother who is admitted in the centre
with her child has to receive:
• Vitamin A:
–If the child is below 2 months: 200.000UI
(there should be no risk of pregnancy)
–If the child is above 2 months: 25.000UI
once a week
• Micronutrients’ supplementation

Discharge Criteria for Infant
With Female Care taker

II. INFANTS WITH OUT ANY
PROSPECT OF BEING BREAST-FED
• Admission criteria

Transition Phase
• During transition phase ,only F 100 diluted
should be used.
• Full strength F 100 should never be used
• In transition phase the volume
of F 100 diluted is increased by
one-third

Phase II
• Amount of F 100 diluted to be given for infants not breast
fed in phase II

Discharge Criteria for Infants with out
any prospect of breast- fed

Follow-up in SFC/MCH
for 6 months

Recording and Reporting
• OTP/TFP Register
• Multi chart
• OTP card
• Referral slips
• OTP ration/follow up card
• Discharge certificate
• Supply register
• Monthly Reporting Format

Adress Birth Date Age SexSerial # Registration # First name Name
Date Weight Height W/H Oedema MUAC Diagnosis Date Weight Height W/H Oedema MUAC
Admission Discharge
Outcome
Registration book

Out comes
• Cured
• Death
• Defaulter
• Unknown
• Transfer out
• Medical referral
• Non responder

Acceptable Alarming
Recovery rate >75% <50%
Death rate <10% >15%
Defaulter rate <15% >25%
Weight gain(g/kg/d) >=8g <8g
Length of stay(weeks) <4 >6
Coverage >50-70% <40%
Standards Sphere project
Minimum Humanitarian Standard

Complications
How to diagnose and treat?

351
Dehydration
• Malnourished children are SENSITIVE to excess
sodium intake!
• All the signs of dehydration in a normal child
occur in a severely malnourished child who is
NOT dehydrated – only a HISTORY of fluid loss
and very recent change in appearance can be
used
• Giving a malnourished child who is not really
dehydrated treatment for dehydration is very
dangerous
• Misdiagnosis of dehydration and giving
inappropriate treatment is the commonest cause
of death in severe malnutrition.

352
Dehydration
• The treatment of dehydration is different in the
severely malnourished child from the normally
nourished child
• Infusions are almost never used and are
particularly dangerous
• ReSoMal must not be freely available in the unit
– but only taken when prescribed
• The management is based mainly on accurately
monitoring changes in weight

353
Dehydration
• The next two slides show that severely
wasted patients cannot excrete excess
sodium and retain it in their body.
• This leads to volume overload and
compromise of the cardiovascular system
• The resulting heart failure can be very
acute (sudden death) or be misdiagnosed as
pneumonia

354
Dehydration - Diagnosis
• History of recent change in appearance of eyes
• History of recent fluid loss
• NO OEDEMA - Oedematous patients are over-
hydrated and not dehydrated (although they are
often hypovolaemic from septic shock)
• Check the eyes lids to see if there is lid-
retraction – a sign of sympathetic over-activity
• Check if the patient is unconscious or not

355
Conscious Unconscious
Sleeping Awake
Eyes not closed Eyes closed
Dehydration or
Hypoglycaemia
Mild/Mod
Eye-lid
retracted
Eye-lid
normal
Dehydration or
Hypoglycaemia
Mild/Mod
Eyes not closed Eyes closed
Dehydration or
hypoglycaemia
Mild/moderate
Eyes Sunken
Not recent Recent onset
Not dehydrated
How to diagnose dehydration in severe malnutrition

356
Monitoring Rehydration
FLUID BALANCE is measured at intervals by WEIGHTING the child – the
change in weight gives a very accurate estimate of fluid balance. Do not
attempt to measure the volume of fluid lost this is much less
accurate and very time-consuming – it is quick and accurate
to weigh the child.
THERE MUST BE AN ACCURATE SCALE IN PHASE ONE,
that is easy to use and safe for acutely ill children
 Monitor every hour
• the liver edge marked on the skin before any rehydration
treatment starts
• the weight, the respiration and pulse rate
• the heart sounds

357
Conscious
Unconscious
Resomal
ONLY Rehydrate until the weight
deficit (measured or estimated) is
corrected and then STOP – DO
not give extra fluid to “prevent
recurrence”
IV fluid
Darrow’s solution
or 1/2 saline & 5% glucose
or Ringer lactate & 5% dextrose
at 15ml/kg the first hr & reassess
- 5ml/kg /30min first 2hrs
- 5 to 10ml/kg/hr 12 hrs
- If improving, 15ml/kg 2nd hr;
- If conscious, NGT: ReSoMal
- If not improving =>Septic shock
Treatment of dehydration

358
• If there is continued weight loss, then:
– Increase the rate of administration of
ReSoMal by 10ml/kg/hour
– Formally reassess in one hour
• If there is no weight gain, then:
– Increase the rate of administration of Resomal
by 5ml/kg/hour
– Formally reassess every hour
• If there is clinical improvement but there are still
signs of dehydration
– continue with the treatment until the
appropriate weight gain has been achieved.

359
• If there is weight gain and deterioration of the
child’s condition with the rehydration therapy
– Then the diagnosis of dehydration was definitely
wrong.
– Stop and start the child on F75 diet.
• If there is no improvement in the mood and look
of the child or reversal of the clinical signs
– Then the diagnosis of dehydration was probably
wrong:
– either change to F75 or alternate F75 and Resomal.

360
Weight
Gain
Clinically
Improved
Clinical Not
improved
Stable Loss
- Increase
ReSoMal by
10ml/kg/hr
- Reassess
every hr
- Increase
ReSoMal:
5ml/kg/hr
- Reassess
every hr
F75
- STOP ALL
rehydration fluid
- Give F75
- Re-diagnose &
assess
Target
weight
continue

Diagnosis of Dehydration in
Kwashiorkor patients
• ALL CHILDREN WITH OEDEMA HAVE AN INCREASE
BODY WATER AND SODIUM
• OEDEMATOUS PATIENTS CAN NOT BE
DEHYDRATED,BUT CAN BE HYPOVOLUMIC
• IN KWASHIORKOR PATIENTS WITH FREQUENT
WATERY DIARRHOEA ,CLINCAL DETERIORATION
AND EXCESSIVE WEIGHT LOSS( Weight loss >2%
per day ) :THE FLUID LOSS CAN BE REPLACED WITH
30 ML/LOSS STOOL
• TREATMENT OF HYPOVOLAMEIA IN KWASIORKOR
IS SMILAR TO MANAGEMENT OF SEPTIC SHOCK

362
Eye-lid drooping/normal or closed
when asleep/unconscious
Septic shock Septic shock with
Hypoglycaemia
•No History of recent eyes sinking
•No history of major fluid loss
Eye-lid retracted or slightly open when
asleep/ unconscious
Signs of Septic shock present
Fast weak pulse, cold peripheries, pallor,
drowsiness
Note: Lid retraction without shock
– treat immediately for hypoglycaemia
How to diagnose septic shock

363
How to diagnose and treat Septic Shock?
• Diagnosis = Septic shock to be present
a fast weak pulse with
cold peripheries
Pallor
Disturbed consciousness
• Treatment of incipient septic shock
- Give second line and first line antibiotics together
- Kept warm to prevent or treat hypothermia,
- Give sugar-water by mouth or NGT as soon as the
diagnosis is made (to prevent hypoglycaemia).
- Physically disturb as little as possible

364
Septic shock
Conscious
Unconscious
Loosing conscious
F 75 by mouth or
NGT
- Darrow’s solution,
or 1/2 saline & 5% glucose,
or Ringer Lactate & 5% glucose
at 10 ml/kg the first hr
- Reassess every 10min(see p.37)
- If possible, Blood transfusion: 10ml/kg in
3 hours, without anything else.
- If improving, F-75;
- If conscious, NGT: F75

365
What is the diagnose of this child?

366
All rehydration (oral or intravenous) therapies should
be stopped immediately if
– The target weight-increase has been achieved
– The visible veins become full (go to F75)
– The development of oedema (overhydration – go to F75)
– The development of prominent neck or superficial veins*
– An increase in the liver size by more than one
centimetre.*
– The development of tenderness over the liver.*
– An increase in the respiration rate by 5 breaths per
minute or more*
– The development of a “grunting” respiration.*
– The development of crepitations in the lungs*
– The development of a triple rhythm*

367
Diagnosis
• Physical deterioration with a gain in weight
• An increase in liver size.
• Tenderness over the liver
• An increase Resp Rate (>50/min for 5 to 11mo &
>40/min for 1-5 years, or an acute increase in
respiration rate of more than 5 breaths/min).
• ”Grunting respiration” during each expiration –
sign of “stiff lungs”.
• Crepitations in the lungs
• Prominent superficial and neck veins
• Heart sounds - Development of triple rhythm
• Increasing or reappearance of oedema during treatment
• A fall in Hb concentration (needs laboratory) – falling Hb is
usually a sign of fluid overload and NOT of loss of red cells
How to diagnose Heart Failure

368
Weight Increase Weight decrease
Pneumonia
Aspiration
Fluid overload
Heart failure
Weight stable
Examine daily weights
Respiratory distress

369
• Stop all intake of fluids or feeds (oral or IV)
• No fluid or food should be given until the heart
failure has improved or resolved (even 24-48 hours.)
• Small amounts of sugar-water can be given
orally if worried about hypoglycaemia
• Give frusemide (1mg/kg) – usually not very effective.
• Digoxin can be given in small single dose
(5 mcg/kg – note that this is lower than the normal dose of digoxin).
• Even if very anaemic do not transfuse –
Heart Failure treatment takes precedence
Treatment of heart failure

370
- Weight
- Respiration rate & sound
- Liver size
- Pulse rate
- Jugular vein or visible veins engorgement
- Heart sounds
Monitoring during treatment of heart failure

371
How to diagnose and treat Anaemia
Check Hb at admission if any
clinical suspicion of anaemia
- Hb >= 40g/l or
-Packed cell vol>=12%
-or between 2 and 14
days after admission
- Hb < 40g/l or
- Packed cell vol<12%
No acute treatment
Iron during phase 2
ONLY during the first 48
hours after admission:
Give 10ml/kg whole or
packed cells 3hours - No
food for 3 to 5 hrs

372
Hypoglycaemia
• The good results of day-care show that
significant hypoglycaemia is very uncommon
• Best prevented by regular feeding
• Often there are no clinical signs at all
• Treatment has no adverse effects
• Always treat children with septic shock as if
they also have hypoglycaemia

373
 Give the patient:
- If Conscious: about 50 ml of 10% sugar water (~10gm
or two tea spoon of sugar in 100ml) or F-75 by mouth
- If Loosing consciousness: 50 ml of 10%sugar water
by NGT.
- If Unconscious: Give sugar water by NGT AND
glucose as a single IV injection (~ 5ml/kg of 10% solution
– stronger solutions of glucose clot and obliterate the vein).
 Start second-line and first line antibiotics together
 Reassess after 15 minutes; If rapid improvement
does not occur then revise your diagnose.
•Check for eye-lid retraction (sign of active sympathetic
nervous system activity)
•Check if the patient is loosing consciousness
How to diagnose and treat Hypoglycaemia

374
Hypothermia – effect of the environmentb
• Thermo neutral temperature range is
28o
C to 32o
C
• Nearly all hypothermia is due to a
low environmental temperature, lack
of cover or washing – The figure
shows the effect of lowering room
temperature to 25o
C

375
Warm the patient using the “kangaroo
technique” for children with a caretaker
Put a hat on the child and wrap mother an child
together
Give hot drinks to the mother (hot water is sufficient)
to warm her skin.
Monitor body temperature during re-warming.
Treat for hypoglycaemia and give second-line
antibiotic treatment.
•Check the T of the patient:T rectal<35° - T axi. <35.5° C
•Check the temperature (T) of the room (28 - 32°C)
•Check that the child sleeps with his/her mother
•Do not wash severely ill children!
How to diagnose and treat Hypothermia

376
Fever
• Has malaria treatment been given?
• Is the child on routine antibiotics?
• Most fever is due to a high environmental
temperature.
• Treat with sponging with room-temperature
water. (never use alcohol)
• Give EXTRA WATER to drink
• Do NOT give aspirin or paracetamol – it does not work in the
severely malnourished and they have defective liver function.
• Children on admission may have aspirin poisoning if the
mother has noted the fever

377
A marasmic child had a weight of 5.5kg at 1 year of
age;
He had 6 loosed stools yesterday and his weight the
next day decreased to 5.2kg.
His liver size was drawn on the skin and the
respiratory rate recorded.
 What will be your advice?

378
• He lost 300g which is 6% of his body weight. He
has no oedema.
• The nurse ordered 25ml (5ml/kg) of ReSoMal
every 30 min for the 2 first hours and then the
same amount in the next 2 hours. He had
improved and he then was given F75 with the
other children in Phase 1.
• When they took his weight, after 4 hours, he was
5.45kg, the liver size was the same and the
respiratory rate was around 40/min’.

11/21/15 379
Food security
Saad Ahmed Abdiwali, (MPH)

11/21/15 380
Outline
 What is food security?
 Dimensions
 Realities and myths around hunger

11/21/15 381
What is food security?
 Food security describes a situation in
which people do not live in hunger or fear of
starvation.

11/21/15 382
food security
 Food security exists when all people, at all
times, have access to sufficient, safe and
nutritious food to meet their dietary
needs and food preferences for an active
and healthy life (FAO)
 Food security for a household means
access by all members at all times to
enough food for an active, healthy life.

11/21/15 383
Dimensions
Food security includes at a minimum
• the ready availability of nutritionally adequate
and safe foods, and
• an assured ability to acquire acceptable foods in
socially acceptable ways (that is, without
resorting to emergency food supplies,
scavenging, stealing, or other coping strategies).

11/21/15 384
Food sovereignty
is the right of peoples
 to define their own food preferences and agriculture/food
production system;
 to protect and regulate both domestic agricultural production
and trade in order to achieve sustainable development
objectives;
 to determine the extent to which they want to be self-reliant; to
restrict the dumping of products in their markets; and

11/21/15 385
 Rosset (2003) argues that "Food sovereignty goes beyond the
concept of food security… [Food security] means that…
[everyone] must have the certainty of having enough to eat each
day[,] … but says nothing about where that food comes from or
how it is produced."
 Food sovereignty includes support for smallholders and for
collectively owned farms, fisheries, etc., rather than
industrializing these sectors in a minimally regulated global
economy

11/21/15 386
 Food sovereignty” “right of peoples to define their
own food, agriculture, livestock and fisheries systems”,
in contrast to having food largely subject to
international market forces.
 Food sovereignty is the right of peoples to healthy and
culturally appropriate food produced through
ecologically sound and sustainable methods, and their
right to define their own food and agriculture systems.

11/21/15 387
Viewpoint: Hunger is not a myth, but myths
keep us from ending hunger
 World Hunger: 12 Myths, 2nd Edition,
by Frances Moore Lappé, Joseph Collins
and Peter Rosset, with Luis Esparza. )
 Source:
http://www.food first.org /pubs/ backgrdrs/ 1998/ s98v5n3.htm
)

11/21/15 388
Myth 1: Not Enough Food to Go Around
 Reality
 Enough food is available to provide at least
2.15 kg of food per person a day worldwide.
 The problem is that many people are too poor
to buy readily available food.

11/21/15 389
Myth 2: Nature's to Blame for Famine
 Reality
 It's easy to blame nature.
 Food is always available for those who can afford it.
 Human-made forces are making people increasingly
vulnerable to nature's vagaries
 The real culprits are an economy that fails to offer
everyone opportunities, and a society that places
economic efficiency over compassion.

11/21/15 390
Myth 3: Too Many People
 Reality
 Although rapid population growth remains a
serious concern in many countries, nowhere does
population density explain hunger.
 For every Bangladesh, a densely populated and
hungry country, we find a Nigeria, Brazil or Bolivia,
where abundant food resources coexist with hunger

11/21/15 391
Myth 4: The Environment vs. More Food?
Reality
 Efforts to feed the hungry are not causing the
environmental crisis.
 Large corporations are mainly responsible for deforestation-
creating and profiting from developed-country consumer
demand for tropical hardwoods and exotic or out-of-season
food items.
 Most pesticides used in the Third World are applied to
export crops, playing little role in feeding the hungry.

11/21/15 392
Myth 5: The Green Revolution is the Answer
 Reality
 production advances of the Green Revolution
are no myth
 Great production increases were achieved
through the green revolution but hunger has
persisted
 Increasing production alone cannot alleviate
hunger.
 Fails to alter the distribution of economic
power that determines who can buy the
additional food.

11/21/15 393
Myth 6: We Need Large Farms
 Reality
 Small farmers typically achieve at least four to
five times greater output per acre than large-
scale farmers, in part because they work their
land more intensively and use integrated, and
often more sustainable, production systems.
 Secure land tenure is needed, to give farmers
incentives to invest in land improvements, to
rotate crops, or to leave land fallow for the
sake of long-term soil fertility.

11/21/15 394
Myth 7 The Free Market Can End Hunger
 Reality
 The trade promotion formula has proven an
abject failure at alleviating hunger
 Export crop production squeezes out basic
food production

11/21/15 395
Myth 9
Too Hungry to Fight for Their Rights
 Reality
 Bombarded with images of poor people as
weak and hungry, we lose sight of the
obvious: for those with few resources, mere
survival requires tremendous effort
 If the poor were truly passive, few of them
could even survive.

11/21/15 396
Myth 10 More U.S. Aid Will Help the Hungry
 Reality
 Foreign aid can only reinforce, not change, the
status quo.
 Our aid is used to impose free trade and free
market policies, to promote exports at the
expense of food production

11/21/15 397
Myth 11 -We Benefit From Their Poverty
 Reality
 Low wages-both abroad and in inner cities at
home-may mean cheaper bananas, shirts,
computers and fast food for most Americans
 Enforced poverty in the Third World
jeopardizes U.S. jobs, wages and working
conditions as corporations seek cheaper labor
abroad.

11/21/15 398
Myth 12: Curtail Freedom to End Hunger?
 Reality
 we see no correlation between hunger and
civil liberty ??
 freedom taken as the right to unlimited
accumulation of wealth-producing property
and the right to use that property however
one sees fit-is in fundamental conflict with
ending hunger

11/21/15 399
Steps proved to be most effective at achieving
food security? seven pro-poor action areas
1. Investing in Human Resources
2. Improving Access to Productive Resources and
Remunerative Employment
3. Improving Markets, Infrastructure, and Institutions
4. Expanding Appropriate Research, Knowledge, and
Technology
5. Improving Natural Resource Management
6. Good Governance
7. Pro-poor National and International Trade and
Macroeconomic Policies

Infant and young child feeding
in emergencies situation
By
SAAD AHMED ABDIWALI
400

“Breast feeding is the most precious gift
a mother can give her infant. When there
is illness or malnutrition, it may be life
saving gift; when there is poverty, it may
be the only gift.” Ruth Lawrence, MD
401

PRACTICAL STEPS
on how to ensure appropriate infant and
young child feeding in emergencies.
1. Endorse or Develop Policies
• Each agency should, at central level, endorse or develop a
policy
• Policies should be widely disseminated and procedures at all
levels adapted accordingly.
2. Train Staff.
• ensure basic orientation for all relevant staff (at national and
international level) to support appropriate IYCF
• health and nutrition program staff and
• Specific expertise on breastfeeding counseling and support will
require technical training
402

Cont…
3. Co-ordinate Operations
an agency or group of agencies should responsible for:
• Policy co-ordination:
• Intersect oral co-ordination:
• Development of an action plan for the emergency operation
• Dissemination of the policy and action plan to operational
and non-operational agencies including donors
4. Assess and Monitor
 determine the priorities for action and response
 Obtain key information through RA & by informed observation
and discussion includes :
• Demographic profile: women, infants and young children,
pregnant women, un accompanied children
• predominant feeding practices
403

Cont…
5. Protect, Promote and Support Optimal IYCF with
Integrated Multi-Sectoral Interventions
• Ensure demographic breakdown at registration of children under five
with specific age categories:
0-<12months, 12-<24 months, 24-59 months to identify the size of
potential beneficiary groups
• Establish registration of new-borns within two weeks of delivery to
ensure timely access to additional household ration entitlement
6. Minimizes the Risks of Artificial Feeding as much as
possible.
• Procurement, management, distribution, targeting and use of breast
milk substitutes, other milks, bottles and teats should be strictly
controlled and comply with the International Code.
404

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