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Protein Energy

Malnutrition
The world health organization (WHO)
defines Malnutrition as –

“The cellular imbalance between the


supply of nutrients and energy and the
body’s demand for them to ensure
growth, maintenance, and specific
functions."
 Malnutrition: A pathological state resulting
from a relative or absolute ‘deficiency’ or
‘excess’ of one or more essential nutrients.

 Comprises four forms:


a) Undernutrition
b) Overnutrition
c) Imbalance
d) Malabsorption
MALNUTRITION

UNDERNUTRITION OVERNUTRITION

DEFICIENCY OF CALORIES DEFICIENCY OF VITAMINS


(energy) AND/OR PROTEINS AND MINERALS

Weight for Age (Underweight) Clinical Examinations


Height for Age (Stunting) Biochemical Estimations
Weight for Height (Wasting)

PROTEIN ENERGY MICRONUTRIENT


MALNUTRITION (PEM) MALNUTRITION (MNM)
(Iron, Vitamin A, Iodine)

UNDERNUTRITION in CHILDREN (PEM and MNM)


EXAMPLES OF ILLNESSES CAUSED BY MALNUTRITION
Global Child Malnutrition Trends 2013:
http://data.unicef.org/resources/2013/webapps/nutrition
Groups of People Typically Suffering from
Most Common Types of Malnutrition
Malnutrition
1. People living in areas where 1. PEM - Protein-Energy Malnutrition.
agricultural production is low, and Protein deficiency: severe Kwashiorkor
transportation and marketing are poor Deficiency of calories and all nutrients:
severe Marasmus
Both: Marasmic Kwashiorkor
2. People who are very poor; seasonal 2. Nutritional anemia
laborers, urban unemployed, landless
agricultural workers
3. Individuals in stages of life at which 3. Vitamin A deficiency, Xeropthalmia
calorie and nutrient needs are
particularly high; pregnant and lactating
women, infants, young children, elderly
4. Individuals in war zones and areas of 4. Iodine deficiency disorders, goiter
civil unrest
5. Vitamin D deficiency, rickets
6. Riboflavin deficiency, B vitamin
7. Niacin deficiency, B vitamin, Pellagra
8. Vitamin C deficiency, scurvy
9. Thiamin deficiency, B vitamin, Beriberi
PROTEIN ENERGY MALNUTRITION (PEM)
“ A range of pathological conditions arising from
simultaneous deficiency of “proteins & energy”
and commonly associated with infections”.

- PEM is the single most important cause of childhood


morbidity and mortality.
- Severe form of PEM is found in about 5% children
below the age of 5 yrs .
- About 50-60% have mild to moderate PEM.

- ..\..\YouTube Video Downloads\Proten Energy


Malnutrition.avi

http://www.targetmap.com/viewer.aspx?reportId=5993
EPIDEMIOLOGY OF PEM
 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 one or
more micronutrient deficiency.
PROTEIN ENERGY MALNUTRITION

 The term marasmus is derived from the Greek word


“marasmos”, which means “withering or wasting away”.
Marasmus involves inadequate intake of protein and calories
and is characterized by emaciation.

 The term kwashiorkor is taken from the Ga language of


Ghana and means "the sickness of the weaning." Williams
first used the term in 1933, and it refers to an inadequate
protein intake with reasonable caloric (energy) intake. Edema
is characteristic of kwashiorkor but is absent in marasmus.

 Children may present with a mixed picture of marasmus and


kwashiorkor, and children may present with milder forms of
malnutrition. For this reason, Jelliffe suggested the term
protein-calorie (energy) malnutrition to include both
manifestations.
DEFINE: PEM
 Underweight: : weight for age < 80% expected
 Marasmus: : weight for age < 60% expected
 Kwashiorkor: : weight for age < 80% + edema
 Marasmic kwashiorkor : wt/age <60% + edema

 Wasting : low weight for height


 Stunting : low height for age
 Underweight : low weight for age

 SAM: severe acute malnutrition


 Weight-for-height of 70% (extreme wasting)
 Presence of bilateral pitting edema of nutritional origin,
“edematous malnutrition”
 Mid-upper-arm circumference of less than 115 mm in
children age 1-5 years old
PROTEIN ENERGY MALNUTRITION
(CLINICAL DIAGNOSIS)
Weight for height below Bipedal edema
60-70% of the median

Visible severe wasting

OK135 S056
WHO Classification for assessing severity of malnutrition by
prevalence ranges among children under 5 years of age

Severity of malnutrition by
Indicator
prevalence ranges (%)

Low Medium High Very high

Stunting <20 20-29 30-39 >=40

Underweight <10 10-19 20-29 >=30

Wasting <5 5-9 10-14 >=15

http://www.who.int/nutgrowthdb/about/introduction/en/index5.html
NUTRITIONAL STATUS IN 100 FOCUS DISTRICTS
AS PER HUNGAMA SURVEY (KEY FINDINGS)
(PARENTHESIS INDICATES NATIONAL FIGURES-NFHS-3)

Moderate
malnutrition

Severe
malnutrition

-4 -3 -2 -1 0

% Severe % of Malnutrition Children


% Moderate
Nutritional Measure (<-3 SD) (< -2SD)
(<-2SD to <-3 SD)

Wasting 3.3 8.0 11.3


(Weight-for-Height) (6.4) (13.4) (19.8)
Underweight 16.4 25.9 42.3
(Weight-for-Age) (15.8) (26.7) (42.5)
Stunting 34 24.8 58.8
(Height-for-Age) (23.7) (24.3) (48)
• Etiology and Epidemiology:
• PEM characteristically occurs in children less than 5 years of
age, whenever the diet is poor in energy and proteins.
• PEM was earlier attributed to the concept of ‘protein gap’
(deficiency of proteins in diet), which has now given way to the
new etiological theory of ‘Food gap’, wherein it is not only the
deficiency of proteins but inappropriate food (low in energy
density, protein and micronutrients - Vitamin A, Iron, Zinc) which
is poor both quantitatively and qualitatively, is the chief cause of
PEM.
• Under-nutrition in fetal life, esp. last trimester, lactation failure,
low energy dense weaning foods, incorrectly constituted formula,
contaminated water and infections (diarrhoea, measles, acute
respiratory infections, intestinal worms etc.) also play important
role in the causation of PEM. The other associated social factors
are poverty, poor environmental conditions, large families, poor
MCH services and poor cooking practices. Ignorance and the
inability to provide adequate food also seem to be important
contributory factors.
ETIOLOGY / CAUSES OF PROTEIN ENERGY
MALNUTRITION

 The most common cause of malnutrition is poverty.


 PEM is primarily due to two factors:
 1. An inadequate intake of food both in quantity and
quality
 2. Infections like -
 Diarrhoea
 Respiratory Infections
 Measles
 Intestinal worm infestation
 These infections increase requirements for calories,
proteins and other nutrients, while decreasing their
absorption and utilization.
 The other main factors causing PEM are:
 Poor hygiene and poor environmental conditions
 Large family size
 Poor maternal health and nutritional status
 Poor maternal nutrition during Pregnancy
 Failure of Lactation
 Premature termination of breast feeding
 Delayed weaning
 Social and cultural feeding practices
 Low birth weight
 Mal-absorption states like-
 Short bowel syndrome (small intestine insufficiency)
 Small bowel bacterial overgrowth
 Celiac disease
 Enzyme defects
Death

Figure from WHO, 2000


WHAT IS AT THE ROOT OF THE PROBLEM?

Image: 1000 days.org infographic What causes maternal and child malnutrition
http://www.thousanddays.org/resource/infographic-what-causes-maternal-and-child-malnutrition/
MALNUTRITION & INFECTION CYCLE

INADEQUATE DIETARY
INTAKE

APPETITE LOSS WEIGHT LOSS


NUTRIENT LOSS GROWTH FALTERING
MALABSORPTION IMMUNITY LOWERED
ALTERED METABOLISM MUCOSAL DAMAGE

DISEASE: INCIDENCE , DURATION,


SEVERITY
UNICEF Conceptual framework of the
determinants of child under-nutrition
Protein energy malnutrition (PEM) manifests in two
different forms:

A. Nutritional marasmus
B. Kwashiorkor

A. Nutritional Marasmus
 Protein and calorie deficiency
 Common in infants and children below 3 years of age.
Onset is more between 6-18 months of age.

B. Kwashiorkor
 Protein deficiency only
 Common in children below 3yrs
 Onset is more between 18months to 24 months
The clinical presentation depends upon the type ,
severity and duration of the dietary deficiencies. The
five forms of PEM are :

1. Kwashiorkor
2. Marasmic-kwashiorkor
3. Marasmus
4. Nutritional dwarfing
5. Underweight child

St.A
nn's
Degr
ee
Coll
ege
for
Wo
CLASSIFICATION OF PEM
(FAO/WHO)
Body weight Oedema Deficit in
as percentage weight for
of standard height
Kwashiorkor 60 – 80 + +

Marasmic < 60 + ++
kwashiorkor
Marasmus < 60 0 ++

Nutritional < 60 0 Minimal


dwarfing
St.A
Underweight 60 – 80 0 + nn's
Degr
child ee
Coll
Source: FAO / WHO 1971 Expertege
Committee on Nutrition 8th Report.
for
WHO Technical Report Series 477
Wo
Patho-
physiology
of PEM

Hoffer L J CMAJ
2001;165:1345-1349

©2001 by Canadian Medical Association. Photo by: Lianne Friesen and Nicholas Woolridge.
PATHO-PHYSIOLOGY
 In general, marasmus is an insufficient energy intake to match the
body's requirements. As a result, the body draws on its own stores,
resulting in emaciation.
 In kwashiorkor, adequate carbohydrate consumption and decreased
protein intake lead to decreased synthesis of visceral proteins. The
resulting hypo-albuminemia contributes to extra-vascular fluid
accumulation. Impaired synthesis of lipoproteins produces a fatty
liver.
 Protein-energy malnutrition also involves an inadequate intake of
many essential nutrients. Low serum levels of zinc have been
implicated as the cause of skin ulceration in many patients.
 Serum levels of zinc are also correlated closely with the presence of
edema, stunting of growth, and severe wasting.
 The classic "mosaic skin" and "flaky paint" dermatosis of
kwashiorkor bears considerable resemblance to the skin changes /
dermatosis of zinc deficiency.
http://www.sciencedirect.com/science/article/pii/S1357303906000983
MARASMUS
 The term marasmus is derived from the Greek
marasmos, which means wasting.
 Marasmus involves inadequate intake of protein and
calories. As a result, the body draws on its own stores,
resulting in emaciation
 Marasmus represents the end result of starvation
where both proteins and calories are deficient.
 Marasmus represents an adaptive 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
http://www.desnutricao.org.
br/ingles/3_2/principal_alter
acoes.htm#0
CLINICAL FEATURES OF MARASMUS
 Growth retardation and failure to thrive: With reduced energy intake, a
decrease in physical activity occurs along with a slower and ultimately,
lack of growth
 Low weight for height: Weight loss occurs by a decrease in fat mass, then
a decrease in muscle mass, as clinically measured by changes in arm
circumference.
 Wasting of muscle and subcutaneous fat: The most perceptible and
frequent clinical feature in marasmus is the loss of muscle mass and
subcutaneous fat mass. Some muscle groups, such as buttocks and upper
limb muscles, are more frequently affected than others. Facial muscles
are usually spared longer. Facial fat mass is the last to be lost, resulting in
severe cases, in the characteristic elderly appearance of children with
marasmus.
 All skin and bones – monkey face or little old man face appearance. This
is secondary to a loss of buccal fat pads.
 Muscle mass loss results in a decrease of energy expenditure. Reduced
energy metabolism can impair the response of children with marasmus to
changes in environmental temperature, resulting in an increased risk of
hypothermia.
CLINICAL FEATURES OF MARASMUS
 Abdomen is usually shrunk, very thin abdominal wall. There is no
oedema in Marasmus.
 Entire digestive tract from mouth to rectum is affected. The mucosal
surface is smooth and thin, and secretory functions are impaired. The
decrease in gastric hydrochloric acid secretion results in bacterial
overgrowth in the duodenum. The peristalsis is slow.
 Increased susceptibility to infections and intestinal infestations:
condition can rapidly worsen with the onset of complications such as
diarrhea, respiratory infection, or measles.
 The child is usually very hungry and has a good appetite
 Apathy is a sign of serious forms of marasmus; children are
increasingly motionless and seem to “let themselves die”.
 The brain normally grows to almost its full adult size within the first
two years of life. Marasmus impairs brain development and learning
ability.
Old man’s
face
Severe
wasting

Thin, flaccid (wt for ht <


skin hanging -3SD or
in folds <70% of
median)

Source: Talc
CATCH-UP GROWTH
IN MARASMUS
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.
 Kwashiorkor can occur in
infancy but its maximal
incidence is in the 2nd yr of life
following abrupt weaning.
 ETIOLOGY
 Kwashiorkor is not only dietary in origin. Infective,
psycho-socical, and cultural factors are also operative.
 Kwashiorkor is an example of lack of physiological
adaptation to unbalanced deficiency where the body
utilizes proteins and conserves S/C fat. So, kwashiorkor
represents a maladaptive response to starvation.
 One theory says Kwashiorkor is a result of liver insult
with hypoproteinemia and oedema.
 In kwashiorkor, adequate carbohydrate consumption
and decreased protein intake lead to decreased
synthesis of visceral proteins.
 The resulting hypoalbuminemia contributes to
extravascular fluid accumulation. Impaired synthesis
of B-lipoprotein produces a fatty liver.
KWASHIORKOR
These children exhibit thin limbs and swollen bellies,
classic symptoms of kwashiorkor, severe protein
deficiency. This child (left) although looking like an
infant is probably 3-4 years old.

Kwashiorkor is an African word meaning "red boy"


referring to the thin, light-colored, reddish
hair. Although superficially looking fat, these kids are
malnourished. Overall health and mental development
will be impaired.
CLINICAL FEATURES OF KWASHIORKOR
 Growth retardation and Gross muscle wasting
 Oedema is present – slight or gross (moon face
appearance): Proteins and hormones that previously
maintained fluid balance diminish, and fluid leaks into the
interstitial spaces. The child's limbs and abdomen
become swollen with edema, a distinguishing feature of
kwashiorkor.
 No subcutaneous fat wasting but fat is not firm
 “Pot Belly”: Liver may be enlarged due to the
accumulation of fat. A fatty liver develops due to a lack of
the protein carriers (β lipoprotein) that transport fat out
of the liver.
 Child is irritable and apathetic.
 Diarrhoea and other infections are very common.
 Appetite is poor.
 Skin changes seen – ‘flaky paint dermatosis’: an
inadequate protein synthesis leaves the skin patchy and
scaly, often with sores that fail to heal.
 Hair becomes sparse and easily pulled out
 Straw coloured / reddish brown hair: Without sufficient
tyrosine to make melanin, the child's hair loses its color
 Flag Sign in hair: Bands of discoloured hair are reported
as a sign of kwashiorkor. These reddish-brown stripes have
been termed the "flag sign" or "signa bandera“ (periods of
poor nutrition are interspersed with good nutrition).
 Proteins play important roles in fluid balance, lipoprotein
transport, immune function, and production of tissues,
such as skin, cells lining the GI tract, and hair.
 Many symptoms of kwashiorkor can be explained based on
this. So, children with insufficient protein intake will not
grow and mature normally, and they don’t.
Hair - thinner
and lighter

Moon face
No appetite

Oedema
(symmetrical
oedema
involving at
Skin least the feet)
lesions

Source: Talc
This infant presented with symptoms indicative of a dietary protein
deficiency, including edema and ridging of the toenails. Image
courtesy of the Centers for Disease Control and Prevention
EARLY V/S LATE PRESENTATION
Flag sign

The flag sign in the hair of a child recovering from Kwashiorkor. The
picture was made at INCAP in Guatemala and used as a clinical
standard for examiners in international nutrition surveys.

Reproduced from: Interdepartmental Committee on Nutrition for National


Defense (1963). Manual for Nutrition Surveys 2nd ed. Department of
Health, Education and Welfare, Public Health Service, NIH, US
Government Printing Office, Washington DC 1963.
Comparison of features of Kwashiorkor and Marasmus

Feature Kwashiorkor Marasmus


Risk Group Older infant/young Infants 6-24 months
child1-3yrs
Condition / Acute PEM (rapid Chronic PEM (slowly
Onset onset) develops)
Growth failure 60-80% wt. for age <60% wt. for age
/ Wt. Loss
Muscle wasting Present, masked by Present, severe
odema
Oedema Present (sometimes Absent
mild)
Hair changes Sparse, brittle, lose Sometimes: sparse
colour and weak
Mental changes Irritable, moaning, Sometimes quiet and
apathetic apathetic
Feature Kwashiorkor Marasmus
Dermatosis, flaky- Common Does not occur
paint
Appetite Poor Usually good
Anaemia Severe (sometimes) Present, less severe
Subcutaneous fat Often retained but Severe loss of
not firm subcutaneous fat
Face May be oedematous. Old man face. Skin
Moon face and bones
Fatty infiltration Enlarged fatty liver. Absent
of liver Pot belly.
Infections like Very common Very common
Diarrhoea
Serum albumin Low (<3g/dl); (severe Normal or slightly
<2.5g/dl) decreased
Urinary urea/g Low Normal or decreased
creatinine
MEASURING / DETECTING MALNUTRITION
DETECTION OF PEM

CLINICAL FORMS OF PEM

 Marasmus:
 Severe wasting
 Marasmic kwashiorkor
 Severe wasting in the presence of edema
 Kwashiorkor
 Malnutrition with edema

NUTRITIONAL GRADING / CLASSIFICATIONS


GOMEZ CLASSIFICATION OF MALNUTRITION
% of reference weight for age= ((subject weight)/(weight of normal child of same age)) * 100

Weight for age(%) = __weight of the child ___ x 100


weight of a normal child
of same age
WEIGHT FOR AGE
(% of NCHS Standards) NUTRITIONAL GRADE

90 - 110 Normal

75 – 89 Grade I (Mild Undernutrition)

60 – 74 Grade II (Moderate Undernutrition)

< 60 Grade III (Severe Undernutrition)


IAP CLASSIFICATION
(INDIAN ACADEMY OF PAEDIATRICS)

WEIGHT FOR AGE


(% of Harvard NUTRITIONAL GRADE
Standard)

 80 Normal

Grade I (Mild Undernutrition)


70 – 89.9

Grade II (Moderate Undernutrition)


60 – 69.9

Grade III (Severe Undernutrition)


50 – 59.9

Grade IV (Severe Undernutrition)


< 50
WELLCOME CLASSIFICATION OF MALNUTRITION
Indicator: Weight-for-age and edema

% expected OEDEMA
Weight for Age
Present Absent
80 - 60 Kwashiorkor Underweight
< 60 Marasmic- Marasmus
Kwashiorkor

Advantage: Useful for classifying more severe forms of malnutrition


Limitations: Does not take account of height differences.
Age of the child must be known.
WATERLOW’S CLASSIFICATION OF MALNUTRITION

% Weight for height = ((weight of patient) / (weight of a normal child of the


same height)) * 100

% Height for age = ((height of patient) / height of a normal child of the same
age)) * 100

Weight for Height Height for age


( wasting) (stunting)

Normal >90 >95


Mild 80-90 90-95
Moderate 70-80 85-90
Severe <70 <85

J. C. WATERLOW, MAD., F.R.C.P., Professor


Department of Human Nutrition, London School of Hygiene and Tropical Medicine
WATERLOW’S CLASSIFICATION

WT./HT > M – 2SD < M –2 SD

HT. FOR AGE

> M – 2SD NORMAL WASTED


(Acute)

< M – 2SD STUNTED WASTED & STUNTED


(Chronic) (Acute & Chronic)
WASTING AND STUNTING
When a population is short this points to nutritional deprivation or disease in
childhood.

Image:http://www.bing.com/images/search?q=Forms+Of+Malnutrition&Form=IQFRDR#view=detail&id=8D2A19491AEE9E080EF2302
D4FD4004D2EA0FB5&selectedIndex=2; http://download.thelancet.com/flatcontentassets/pdfs/nutrition_2.pdf
STANDARD DEVIATION (SD) CLASSIFICATION
BASED ON WHO CHILD GROWTH STANDARDS
CUT OFF VALUES

NUTRITIONAL GRADE
CUT-OFF LEVEL WEIGHT FOR HEIGHT FOR WEIGHT FOR
AGE AGE HEIGHT

Median ± 2SD Normal Normal Normal

Median – 3 SD to Moderate Moderate Moderate


Median – 2 SD Underweight Stunting Wasting

Severe Severe Severe


< Median – 3 SD
Underweight Stunting Wasting
Mid upper arm circumference :

- MUAC tape

 >13.5cms : Normal
 12.5 to 13.5cms : Mild malnutrition or “at risk”
 11.5 to 12.5cms : Moderate Acute Malnutrition
 < 11.5cms : Severe Acute Malnutrition

- SHAKIR’S tape

 Green : normal or well nourished


 Yellow : mildly malnourished or at risk
 Orange : moderately malnourished
 Red : severely malnourished
 Mid-upper arm circumference in adults (MUAC):
This method as well as used in children, can be used to
grade the degree of body wasting in adults.
 Given below are the appropriate cut-off points for
classification of adult-malnutrition by mid-upper arm
circumference.
Circumference(cm) Classification
male > or =23 normal
<23 malnourished
female > or =22 normal
<22 malnourished
 There is a separate color coded MUAC tape to be used for
adults.
 Red: 0 – 21 cm
 Yellow: 21 cm - 23 cm
 Green: from 23 cm
UNICEF Technical Bulletin No.13
MID UPPER ARM MUSCLE AREA IN ADULTS
 The mid upper arm muscle area estimates lean body mass. This area is
derived from the triceps skin-fold thickness (TSF) and mid upper arm
circumference. Both are measured at the same site, with the patient's
right arm in a relaxed position.
 The average mid upper arm circumference is about 32 ± 5 cm for men
and 28 ± 6 cm for women. The formula for calculating the mid upper
arm muscle area in cm2 is shown below.

 This formula corrects the upper arm area for fat and bone. Average
values for the mid upper arm muscle area are 54 ± 11 cm2 for men and
30 ± 7 cm2 for women. A value < 75% of this standard (depending on
age) indicates depletion of lean body mass. This measurement may be
affected by physical activity, genetic factors, and age-related muscle
loss.
Mid Upper Arm Muscle Area in Adults
Percentage of Men (cm2) Women (cm2) Muscle Mass
Standard (%)

100 ± 20* 54 ± 11 30 ± 7 Adequate

75 40 22 Marginal

60 32 18 Depleted

50 27 15 Wasted

*Mean mid upper arm muscle mass ± 1 standard deviation. From National
Health and Nutrition Examination Surveys I and II.
BODY MASS INDEX:
Indicator used is weight for height. Mostly used
to assess overnutrition in adults.

BMI = _Weight (kgs)_


(Ht)2 mtrs

BMI = 18.5 – 25 Kg / m2 :Normal nutritional status

 BMI for Age: New WHO child growth reference


standards for children between 2-5yrs and 5-19yrs
The International Classification of adult underweight, overweight and obesity
according to BMI (Source: Adapted from WHO, 1995, WHO, 2000 and WHO 2004)

Classification BMI(kg/mt.sq.)
Principal cut-off points Additional cut-off points
Underweight <18.50 <18.50
Severe thinness <16.00 <16.00

Moderate thinness 16.00 - 16.99 16.00 - 16.99

Mild thinness 17.00 - 18.49 17.00 - 18.49


18.50 - 22.99
Normal range 18.50 - 24.99
23.00 - 24.99
Overweight ≥25.00 ≥25.00
25.00 - 27.49
Pre-obese 25.00 - 29.99
27.50 - 29.99
Obese ≥30.00 ≥30.00
30.00 - 32.49
Obese class I 30.00 - 34-99
32.50 - 34.99
35.00 - 37.49
Obese class II 35.00 - 39.99
37.50 - 39.99

Obese class III ≥40.00 ≥40.00


Growth chart / road to health card:

- Indicator used : weight for age

- Best method for early detection and grading


of ‘PEM’, long before clinical signs and
symptoms appear.

- Helps to take corrective measures in pre-


clinical stage and prevent severe
malnutrition.
Biochemical Markers of PEM

Index Mild Moderate Severe


Albumin (g/dL) 2.8-3.5 2.1-2.7 < 2.1
Transferrin 151-200 100-150 < 100
(mg/dL)

Total 1200-1500 800-1199 < 800


lymphocyte
count (per
mm3)

Pre-albumin 15-30 10-15 0-10


mg/dL
Values Commonly Used to Grade Severity of Protein-Energy
Under-nutrition in Adults
Measurement Normal Mild Moderate Severe Under-
Undernutrition Undernutrition nutrition

Normal weight 90–110 85–90 75–85 < 75


(%)

Body mass 19–24* 18–18.9 16–17.9 < 16


index
Serum albumin 3.5–5.0 3.1–3.4 2.4–3.0 < 2.4
(g/dL)

Serum 220–400 201–219 150–200 < 150


transferrin
(mg/dL)

Total 2000–3500 1501–1999 800–1500 < 800


lymphocyte
count (per
mm3)
*In the elderly, BMI < 21 may increase mortality risk.
BIOCHEMICAL
PARAMETERS
 “Prevention of PEM is the fight against
poverty and ignorance”.
 It must be appreciated that there is no single
shot solution to the treatment or prevention
of PEM.
 It is a complex problem involving each of the
social, economic, educational, political,
administrative, medical and health
dimensions.
 An integrated effort involving all these and
also awareness and a positive attitude
towards the condition might help to limit it.
A. HEALTH PROMOTION:
 Good ante-natal, natal and postnatal care of mothers
 Education on food, hygiene and family planning
 Education on the importance of colostrum, diet during
lactation
 Various measures under the ICDS initiative, like good
nutrition, immunization, education, hygiene and
sanitation, etc.
 Promotion of breast feeding and other IYCF practices
 Appropriate and timely complementary feeding,
importance of low cost complementary foods
 Prevention and control of infections infant feeding
 Improve overall family diet
 Correct knowledge on balanced diet
 Utilization of family planning practices

UNICEF and MCN_understanding-


malnutrition booklet.pdf
LOW COST WEANING FOODS DEVELOPED
BY ICMR USING LOCAL INGREDIENTS
NUTRITIONAL PROGRAMMES IN INDIA
 Ministry of Social Welfare
 ICDS programme
 Balwadi nutrition programme
 Special Nutrition programme (merged with ICDS)
 Ministry of Health and Family Welfare

 Prophylaxis against Nutritional Anaemia


 Vitamin A prophylaxis programme
 Iodine Deficiency Disorders Control programme
 Ministry of Education

 Mid Day Meal programme


MID DAY MEAL PROGRAM
 It was Madras Presidency in the year 1923 that started the concept of
providing cooked meals to children studying in corporation schools of
Madras city.
 It was expanded to a larger scale in 1961, thus India became one of the
first countries to have started the Midday Meal Programme, then called
as the School Lunch Programme.
 Other states also joined in and programmes run by Gujarat and Kerala
are also widely acclaimed.
 In 2001, a landmark decision was given by the honourable Supreme Court
of India, which made it mandatory for all government primary schools to
provide cooked meals.
 The primary aim of the programme was to provide at least one
nourishing meal to the school going children per day. This meal
provides one third the total daily energy requirement and half
the need of proteins (300Kcal and 8-12 g of proteins).
 The objectives were :
 ●● It served as an incentive for the children to attend school.
 ●● To reduce dropouts from school.
 ●● To improve the nutritional status of the child
B. SPECIFIC HEALTH PROTECTION
 Immunization: The child must be immunized as per the
national schedule. Food hygiene and personal hygiene.
 Food fortification

 Diet: Protein and energy rich food should be consumed by


children. Special attention must be paid to diet during
complementary feeding. Adequate quantities of fruits and
vegetables must be included in the diet.
 Usually, in Kwashiorkor, 120kcal and 3g of protein
per kilogram of body weight per day are sufficient for
long-term treatment. Thus a 10kg child should
receive about 1200kcal and 30g of protein daily.
 But, a marasmic child during the early part of
recovery may be capable of consuming and utilizing
150 to 200kcal and 4 to 5g of protein per kilogram of
body weight per day.
 Principle of Diet in PEM:
 1.The protein intake can range from 1.5 to 4.0 grams per kg body
weight per day or at-least 20% of the total energy. High biological
value (HBV) protein should be emphasized in the diet.
 2.Calories should be supplied in sufficient amount for maximum
protein utilization. Children with chronic malnutrition may require
caloric intakes more than 120-150 kcal/kg/d to achieve appropriate
weight gain.
 The formula for determining adequate caloric intake is:
kcal/kg = (RDA for age x Ideal Body weight)/actual weight

Foods that can be included to increase Protein Density


Preferred sources of Macro nutrient to be
included in the diet for PEM
Food combinations that can be used in the diets for PEM
C. EARLY DIAGNOSIS & TREATMENT:
 Growth monitoring: Vulnerable children must be identified.
Children must be monitored through growth charts. Periodic
surveillance of risk groups
 Early diagnosis of lag in growth /growth failure must be done and
treated as appropriate.
 Early diagnosis and treatment of infections and diarrhoea is
also vital. To achieve this, health worker must be alert and mothers
should be aware of the signs and symptoms of common infections.
 Preparation and use of ORS should be known to all mothers.

 Development of programmes for early rehydration of children


with diarrhoea.
 Development of supplementary feeding programmes

 Deworming of heavily infested children

 Home to home Ambulatory treatment

 Medical treatment in the vicinity: In extreme and serious cases


early medical advice and treatment facilities must be available.
Hospitalization of the case remains the only choice in complicated
cases.
D. REHABILITATION:
 Hospital treatment

 Nutritional rehabilitation services

 Residential Units: Mothers are admitted with their sick


children. The mother gets hands on experience in the
practical learning of preparation and administration of a
therapeutic diet for her child with an expert. This
demonstration and involvement of the mother in her child’s
recovery goes a long way in understanding the problem and
mitigating it.
 Day Care Centre: The mother attends the day care centre
along with the child where cooking and feeding is taught to
the mother.
 Domiciliary Rehabilitation: The expert comes home and
assesses the situation as a whole. The mother is then
rendered suitable advice with regards not only to feeding but
also about improving various domestic contributory factors to
PEM.
Severe Acute Malnutrition
Status
 Malnutrition is an underlying cause in >55% of
under-5 deaths
 Prevalence of Sever Acute Malnutrition – 6.4% (NFHS
– 3, 05-06)

States are urged to address the issue of Malnutrition by


planning establishment of NRC: MoHFW
Strategy
 Nutrition Rehabilitation Center established for
management of Severe Acute Malnutrition
 Madhya Pradesh (121) and Maharashtra (438) : Have
Functioning NRCs
 Bihar, Rajasthan, Chhattisgarh, UP, NCR and most of the
other states have also initiated the process
SEVERE ACUTE MALNUTRITION (SAM)
 Definition: Severe acute malnutrition is defined by a
very low weight for height (below -3z scores of the
median WHO growth standards), by visible severe
wasting, or by the presence of nutritional oedema
(WHO).
 The median under-five case-fatality rate for severe
acute malnutrition typically ranges from 30% to 50%, it
can be reduced substantially when physiological and
metabolic changes are taken into account.
 Management of severe acute malnutrition according to
WHO guidelines reduced the case-fatality rate by 55%
in hospital settings and recent studies suggest that
commodities such as ready-to-use therapeutic foods
(RUTF), can be used to manage severe acute
malnutrition in community settings.
 http://www.who.int/nutrition/topics/malnutrition/en/index.html
Facility Based Management of Children with
Severe Acute Malnutrition - Operational
Guidelines by NRHM, MoHFW, GOI
BILATERAL PITTING EDEMA
 Bilateral pitting oedema usually
starts in the feet and ankles.
 It can be verified when thumb
pressure applied on top of both feet
for three seconds leaves a pit
(indentation) in the foot after the
thumb is lifted. The pit will remain
in both feet for several seconds.
 It is important to test both feet; if
the pitting is not bilateral, the
oedema is not of nutritional origin.
 The presence of bilateral pitting
oedema should be confirmed by a
second person who repeats the test
 A child with oedema of both feet is
automatically considered severely
underweight, regardless of what
the scale shows.
BILATERAL PITTING EDEMA
• If moderate oedema is
diagnosed, check for
oedema around the eyes
(periorbital oedema).
• Do not press on the eyes to
look for pitting. If there is
oedema around the eyes
this is classified as severe
(+3) oedema.
• Children with +3 oedema
are at high risk of mortality
and are always treated in
inpatient care.
SEVERE WASTING (<60% WT. FOR HT.)
WHAT CHANGES OCCUR IN THE BODY
WITH SEVERE MALNUTRITION?

Heart, lungs and  Risk of: heart failure


circulation impaired - dehydration
- hypothermia
 Reduced ability to:
Liver function impaired - digest protein and
energy
- metabolize iron
 Risk of hypoglycaemia
Digestive system impaired  Reduced ability to absorb
food
Immunity and micro-  Risk of infection
nutrient status lowered
 Risk of septic shock
DIFFERENTIATING BETWEEN COMPLICATED /
UNCOMPLICATED FORMS OF SAM
INDIAN PEDIATRICS. VOLUME 50__APRIL 16, 2013
MANAGEMENT AND TREATMENT OF SAM

 Severe acute malnutrition is a life threatening


condition requiring urgent treatment.
 Until recently, the recommendation was to refer
these children to hospital to receive therapeutic
diets along with medical care.
 The situation changed recently with the advent
of ready to use therapeutic foods (RUTF) which
allows the management in the community of
large numbers of children who are severely
malnourished above the age of 6 months
without medical complications.
TREATING IN HOSPITAL, ONLY CHILDREN WITH
COMPLICATIONS / INFECTIONS AND DISCHARGING
THEM AS SOON AS THESE ARE CONTROLLED

http://motherchildnutrition.org/malnutrition-
management/management-severe-acute-
malnutrition/introduction.html
MANAGEMENT OF SEVERE MALNUTRITION
10 STEP MANAGEMENT OF MALNUTRITION

1. Treat/prevent hypoglycaemia
2. Treat/prevent hypothermia
3. Treat/prevent dehydration
4. Correct electrolyte imbalance
5. Treat/prevent infection
6. Correct micronutrient deficiencies
7. Start cautious feeding
8. Achieve catch-up growth
9. Provide sensory stimulation and emotional
support
10. Prepare for follow-up after recovery
Timeframe for management of severe malnutrition
REHABILITATION PHASE (2ND WEEK ONWARDS)

 The return of appetite signals the rehabilitation


phase and usually occurs a week after treatment
is started.
 The goal is to achieve weight gain >10g/kg/day
until the patient is fully recovered.
 Increase in energy & protein intake should be
gradual to avoid cardiac failure.
 A child is considered to have recovered on
reaching a weight for height that is 90% of the
Median.
 Prepare for discharge with emphasis on follow-up
FEEDING FORMULAS: WHAT ARE F-75 AND F-100?

• F-75 is the "starter" formula used during initial management of


malnutrition, beginning as soon as possible and continuing for 2-7 days
until the child is stabilized.
• Severely malnourished children cannot tolerate normal amounts of
protein and sodium or high amounts of fat. They may die if given too
much protein or sodium. They also need glucose, so they must be
given a diet that is low in protein and sodium and high in carbohydrate.
• F-75 has is specially mixed to meet the child's needs without
overwhelming the body's systems in the initial stage of treatment.
• Use of F-75 prevents deaths. F-75 contains 75 kcal and 0.9 g protein
per 100 ml.
• As soon as the child is stabilized on F-75, F-100 is used as a "catch-
up" formula to rebuild wasted tissues.
• F-100 contains more calories and protein: 100 kcal and 2.9g protein
per 100 ml

http://motherchildnutrition.org/malnutrition-management/info/feeding-
formulas-f75-f100.html
FORMULA DIETS FOR SEVERELY MALNOURISHED
CHILDREN
 Impaired liver & intestinal function + infection
 Food must be given in small amounts, frequently (PO/NG)
 Unable to tolerate usual amounts of dietary protein,
fat, Na
 Diet low in above, high in carbohydrates
 F-75
 75kcal /100ml
 Initial phase treatment, 130ml/kg/d
 Feed @ 2-3hr (8 meals/d)
 F-100
 100kcal /100ml
 Feed @ 4-5 h (5-6 meals/d)
 Rehabilitation phase (appetite returned)
No cooking is
If there is no cereal flour, or there are no cooking
required
facilities, one of the following recipes for F-75 can be used:
for F-100:
Alternatives Ingredient Amount for F-75 Amount for F-100
Dried skimmed milk 25 g 80 g
Sugar 100 g 50 g
If you have
Vegetable oil 30 g 60 g
dried
skimmed milk Mineral mix* 20 ml 20 ml
Water to make 1000 ml 1000 ml** 1000 ml**
Dried whole milk 35 g 110 g
Sugar 100 g 50 g
If you have
Vegetable oil 20 g 30 g
dried
whole milk Mineral mix* 20 ml 20 ml
Water to make 1000 ml 1000 ml** 1000 ml**
Fresh cow's milk, or full-
cream 300 ml 880 ml
If you have
(whole) long life milk
fresh
cow's milk, or Sugar 100 g 75 g
full- Vegetable oil 20 g 20 g
cream (whole) Mineral mix* 20ml 20ml
long life milk
Water to make 1000 ml 1000 ml** 1000 ml**
COMMUNITY-BASED MANAGEMENT OF
ACUTE MALNUTRITION (CMAM)

111
 Commercial Pre-packed Plumpy'Nut
 Plumpy'Nut is a ready-to-use therapeutic spread produced by Nutriset and
presented in individual sachets. It is a paste of groundnut composed of
vegetable fat, peanut butter, skimmed milk powder, lactoserum,
maltodextrin, sugar, mineral and vitamin complex.
 Plumpy'Nut is specifically designed to treat acute malnutrition without
complications and has the following characteristics:
 It is nutritionally equivalent to F-100 (therapeutic milk used for in-patient
care in Phase 2)
 One sachet has an energy value of 500Kcal
 One sachet has a weight of 92 g
Nutrients and Energy Composition of Plumpy'Nut

Nutrient Per sachet of 92 g Nutrient Per sachet of 92 g


Energy 500 kcal Vitamin A 840 mcg
Proteins 12.5 g Vitamin D 15 mcg
Lipids 32.86 g Vitamin E 18.4 mg
Calcium 276 mg Vitamin C 49 mg
Phosphorus 276 mg Vitamin B1 0.55 mg
Potassium 1 022 mg Vitamin B2 1.66 mg
Magnesium 84.6 mg Vitamin B6 0.55 mg
Zinc 12.9 mg Vitamin B12 1.7 mcg

Copper 1.6 mg Vitamin K 19.3 mcg


Iron 10.6 mg Biotin 60 mcg
Iodine 92 mcg Folic acid 193 mcg
Selenium 27.6 mcg Pantothenic acid 2.85 mg
Sodium < 267 mg Niacin 4.88 mg
What should be the dosing for Plumpy'Nut ?
The number of packets per day to be given to a child/adolescent
depends on the weight of the child. The table below provides the
accurate dosing based on the weight range of the child/adolescent:

Weight (kg) Packets / day Packets / w

3.5 - 3.9 1.5 11


4.0 - 5.4 2 14
5.5 - 6.9 2.5 18
7.0 - 8.4 3 21
8.5 - 9.4 3.5 25
9.5 - 10.4 4 28
10.5 - 11.9 4.5 32
12.0-13.5 5 35
>13.5 200kcal/kg/day 200kcal/kg/day
The RUTF can be made / produced locally by mixing
together ground roasted peanut powder, milk powder, and
sugar in a ratio of 30:28:25 (grams), along with 15 grams
of gingili oil.

INDIAN PEDIATRICS. VOLUME 50__APRIL 16, 2013


DIARRHOEAL DISEASES
 Major public health problem in India in children below 5
yrs.
 1/3rd of pediatric admissions are due to diarrhoeal diseases.
 Diarrhoea remains the second leading cause of death
among children under five globally. Nearly one in five child
deaths – about 1.5 million each year – is due to diarrhoea
 17% of all deaths in indoor pediatric patients are diarrhoea
related.
 Causes:
 Almost universally infectious in origin
 A wide assortment of organisms cause acute diarroea viz.
viruses, bacteria and parasites like e.histolytica, giardia,
intestinal worms, etc.
 Rotavirus is the most important cause of diarrhoea
mortality in children; it is associated with 28% of deaths
COMMON CAUSES OF ACUTE DIARROEA
 More than 20 viruses, bacteria and parasites have been associated with acute
diarhoea
 Worldwide, rotavirus is the commonest cause of severe dehydrating diarrhoea
causing 0.6 million deaths annually, 90% of which occur in developing
countries
 The incidence of specific pathogens varies between developed and developing
countries
 In developed countries, about 40% of AD cases are due to rotavirus and only
10-20% are of bacterial origin while in developing countries, 50-60% are
caused by bacteria while 15-25% are due to rotavirus
Other viral agents Bacteria Parasites
• Enteric • E. coli (EAEC, EPEC, • Entamoeba
adenoviruses EIEC) histolitica
• Shigella spp
• Astrovirus • Girdia lamblia
• Staphylococcus spp
• Human • Cryptosporidium
• Salmonella spp
calciviruses • Trichuris trichuria
• Yersinia enterocolitica
(norovirus and • Strongyloides
sapovirus) • Campylobacter jejuni
• Vibrio cholera stercoralis
Host Factors:
 Children between 6 months – 2years

 Highest in age group 6 -11 months (weaning time).

 People suffering from PEM.

 Poverty, lack of personal + domestic hygiene, immuno -


deficiency
Mode of transmission:
 Faecal – oral route : transmission may be water borne; food
borne ; via fingers or dirt.
Diarrhoea may be acute(watery), persistent, dysentery:
 Acute diarrhoea : usually lasts for 3-7 days but not more than
14 days
 Persistent diarrhoea : begins acutely but lasts for more than
14 days.
 Dysentery : diarrhoea with visible blood and/or mucus in
stools.
CLINICAL TYPES OF ACUTE DIARRHOEA
Clinical Description Common
type pathogens
Acute This is the most common. It is of Rotavirus, E.
watery recent onset, commencing usually coli, Vibrio
diarrhoea within 48 hours of presentation. cholera
It is usually self limiting and
most episodes subside within 7
days. The main complication is
dehydration.
Acute Also referred to as dysentery. Shigella spp,
bloody This is the passage of bloody Entamoeba
diarrhoea stools. It is as a result of damage histolytica
to the intestinal mucosa by an
invasive organism. The
complications here are sepsis,
malnutrition and dehydration.
WHO GUIDELINE FOR THE
CLASSIFICATION OF DEHYDRATION
Parameters No Some Severe
dehydration dehydration dehydration
Appearance Well, alert Restless, Lethargic,or
irritable unconscious;
floppy
Eyes Normal Sunken Very sunken

Thirst Drinks Thirsty, drinks Drinks poorly or


nomally, not eagerly not able to drink
thirsty
Skin pinch Goes back Goes back Goes back very
quickly (<1 slowly slowly (≥2
second) (1 second) seconds)
Management of Diarrhoea
Rehydration therapy

Oral Intravenous

Mild / moderate Severe dehydration


dehydration
Treatment of Diarrhea
 ORS and supplemental zinc, combined with continued feeding,
are the recommended and effective interventions for the clinical
management of acute diarrhoea:
 use of low concentration oral rehydration salts (ORS)
 routine use of zinc supplementation, at a dosage of 20
milligrams per day for children older than six months
or 10 mg per day in those younger than six months, for
10–14 days
 Only 0.3% children suffering from diarrhea receive Zinc
supplements
 16% receive antibiotics, which are not normally recommended for
treating childhood diarrhea
 Under-five mortality attributable to diarrheal disorders – 15%
 Percentage of children with diarrhea taken to a health facility or
provider – 60%
• According to Lancet- “ORS is potentially the most important
medical advance of this century"
• World Health Organization estimates that 90% of diarrheal deaths
worldwide could be prevented with appropriate treatment with ORS
Composition of ORS recommended by W.H.O

Composition of ORS – bicarbonate


Ingredient Quantity
Sodium chloride 3.5 gms
Sodium bi-carbonate 2.5 gms
Potassium chloride 1.5 gms
Glucose (Dextrose) 20 gms
Potable H2O 1 litre

Composition of ORS – citrate


Ingredient Quantity
Sodium chloride 3.5 gms
Trisodium citrate dehydrate 2.5 gms
Potassium chloride 1.5 gms
Glucose (dextrose) 20 gms
Potable H2O 1 litre
ZINC AND DIARRHOEA
 Zinc deficiency is common in developing
countries and zinc is lost during diarrhoea
 Zinc deficiency is associated with impaired
electrolyte and water absorption, decreased
brush border enzyme activity and impaired
cellular and humoral immunity
 Treatment with zinc reduces the duration
and severity of AD and also reduces the
frequency of further episodes during the
subsequent 2-3 months
 WHO recommends that children from
developing countries with diarrhoea be given
zinc for 10-14 days
 10mg daily for children <6 months
 20 mg daily for children >6 months
Composition of home – made ORS:
Ingredient Quantity
Common salt 3.5 gms
Table sugar 20 gms
Safe water 1 litre
PREVENTION AND
CONTROL OF
DIARRHOEA
REFERENCES
 Normal and Therapeutic Nutrition. Corrine H Robinson and
Marilyn R Lawler.
 Textbook of Preventive and Social Medicine. JE Park and Park
 WHO and AFMC Public Health Textbook
 Child Nutrition: Challenges and Opportunities: Dr Prema
Ramachandran: Nutrition Foundation of India
 Community-based Management of Severe Acute Malnutrition: A
Joint Statement by the World Health Organization, the World Food
Programme, the United Nations System Standing Committee on
Nutrition and the United Nations Children’s Fund: May2007
 Management of SAM: UNICEF
 State of the World’s Children: 2009 to 2012: UNICEF
 Management of Severe Malnutrition: A Manual for Physicians and
other Senior Health Workers: WHO
 Child Health Program: Ministry of Health and Family Welfare:
Govt. of India

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