PEM ppt based on latest WHO SAM guideline

1. PROTEIN ENERGY
MALNUTRITION
DR. SANDEEP LATHER

2. Malnutrition is globally the most important risk
factor for illness and death.
There were 925 million malnourished people in the
world in 2010(Global Hunger Index)
In India 65% (80 million) under 5 yrs age
malnourished.
The single largest
common denominator in
global child deaths is
malnutrition

3. Malnutrition
Malnutrition (mal-bad,nutrition) is the condition that
results from taking an unbalanced diet in which certain
nutrients are either lacking, or in excess (too high an
intake), or in the wrong proportions
World Health Organization definition:
The term is used to refer to a number of diseases, each
with a specific cause related to one or more nutrients
(for example, protein, iodine or iron) and each
characterized by cellular imbalance between the
supply of nutrients and energy on the one hand, and
the body's demand for them to ensure growth,
maintenance, and specific functions, on the other.
“

4. DEFINATION
HEALTH- Complete Physical , Mental , Social and
Spiritual wellbeing .
PEM- Pathological condition arising from
coincidently lack in varying proportion of Protein
and calories , occuring most frequently in infant and
childern and commenly associated with Infection

5. Under nutrition is a condition in which
there is inadequate consumption, poor
absorption or excessive loss of nutrients.”
O P GHAI

6. Amongst the highest in the world,
 nearly double that of Sub-Saharan Africa.
 22 percent of the country’s burden of
disease.
.
PREVALANCE IN INDIA

7. PEM
A
MULTIFACTORIAL
ENTITY

8. MALNUTRITIONMALNUTRITION
improper and / or inadequate
food intake
inadequate absorption
of food
Deficient supply of food
poor dietary habitsilliteracy
emotional factors metabolic abnormalities
diseases

9. Keith West

10. •1 ) Feeding on artificial milk formulas - reconstituting wrongly.
•2)Feeding on diluted fresh milk
• 3)Breast feeding for a long time
• 4)Delayed weaning
• 5)Feeding via dirty feeding bottles
• 6)working mothers
•1 ) Feeding on artificial milk formulas - reconstituting wrongly.
•2)Feeding on diluted fresh milk
• 3)Breast feeding for a long time
• 4)Delayed weaning
• 5)Feeding via dirty feeding bottles
• 6)working mothers
Malnutrition and Faulty feeding

11. Effect of Maternal nutrition on child heallth
Malnutrition of pregnant women may lead to serious
problems for children.
 More commonly, likely to be small at birth.
Low birth weight is associated with increased risk of
mortality and with a range of health and
developmental problems.
 Cretinism resulting from severe maternal iodine
deficiency

12. Effect of Malnutrition amongst adolescent
girls
Undernutrition in childhood can cause stunting and
influence the size of the child a woman can bear later
in life.
Maternal pelvic size is a strong determinant of
neonatal survival and universally correlated with
height in populations.

13. Protein Energy Malnutrition-
,
Kwashiorkor
mild form to severe form malnutrition
•Severe form malnutritionSevere form malnutrition
•Kwashiorkor: protein deficiencyKwashiorkor: protein deficiency
•Marasmus: energy deficiencyMarasmus: energy deficiency
•Marasmic Kwashiorkor: combination of chronic energy deficiencyMarasmic Kwashiorkor: combination of chronic energy deficiency
and chronic or acute protein deficiencyand chronic or acute protein deficiency
•PreKwashiorker: Poor nutrition +Kwashiorker feature exceptPreKwashiorker: Poor nutrition +Kwashiorker feature except
oedema.oedema.
mild form to severe form malnutrition
•Severe form malnutritionSevere form malnutrition
•Kwashiorkor: protein deficiencyKwashiorkor: protein deficiency
•Marasmus: energy deficiencyMarasmus: energy deficiency
•Marasmic Kwashiorkor: combination of chronic energy deficiencyMarasmic Kwashiorkor: combination of chronic energy deficiency
and chronic or acute protein deficiencyand chronic or acute protein deficiency
•PreKwashiorker: Poor nutrition +Kwashiorker feature exceptPreKwashiorker: Poor nutrition +Kwashiorker feature except
oedema.oedema.

14. Invisible PEM:---- Toddler shows breast addiction,
look entirely normal but small for age, lowered
resistance to infection(6 -24 month age group).
Early lactation Failure syndrome: Abrupt stoppage
of Breastfeeding and early introduction of dilute
starch based liquid diet without any good quality
protine.

15. Classification of PEM
WHO classification
Moderate
Malnutrition
Severe Malnutrition
Symmetrical Oedema No Yes edematous
malnutrition
Weight for Height SD SCORE(Z Score)
b/w-2 to -3
SD SCORE < -3
Severe wasting
Height for age SD SCORE(Z Score)
b/w-2 to -3
SD SCORE < -3
Severe stunting

16. IAP Classification
Grade of malnutrition Weight for age of the
standard
Normal >80%
Grade 1 71-80% Mild malnutrition
Grade 2 61-70% Moderate malnutrition
Grade 3 51-60% Severe malnutrition
Grade 4 <50% Vere severe malnutrition

17. GOMEZ Classification
Nutritional status Weight for age
Normal >90
First degree malnutrition 75-90
Second degree malnutrition 60-75
Third degree malnutrition <60
ALL CASES WITH OEDEMA TO BE INCLUDED IN GRADE THREE PEM
IRRESPECTIVE FOR AGE
Reference standard WHO growth chart

18. WATERLOW Classification
Nutritional status Height for age(% of expected)
Normal >95
First degree stunting 90-95
Second degree stunting 85-90
Third degree stunting <85

19. Age independent indicesAge independent indices
Name of IndexName of Index CalculationCalculation Normal valueNormal value
Value inValue in
malnutritionmalnutrition
Kanawati andKanawati and
McLaren’s indexMcLaren’s index
Mid armMid arm
circumference /circumference /
head circumferencehead circumference
(cm)(cm)
0.32-0.330.32-0.33
SeverelySeverely
malnourished <0.25malnourished <0.25
Rao and Singh’sRao and Singh’s
indexindex
(weight (in kg) /(weight (in kg) /
heightheight22
(in cm)) x(in cm)) x
100100
0.140.14 0.12-0.140.12-0.14
Dugdale’s indexDugdale’s index
weight (in kg) /weight (in kg) /
heightheight1.61.6
(in cm)(in cm)
0.88-0.970.88-0.97 <0.79<0.79
Quaker armQuaker arm
circumferencecircumference
measuring stickmeasuring stick
(quac stick)(quac stick)
Mid-armMid-arm
circumference thatcircumference that
would be expectedwould be expected
for a given heightfor a given height
75-85%75-85%
malnourishedmalnourished
<75% severely<75% severely
malnourishedmalnourished
Jeliffe’s ratioJeliffe’s ratio
HeadHead
circumference /circumference /
chest circumferencechest circumference
Ratio <1 in a childRatio <1 in a child
>1 year>1 year
malnourishedmalnourished

20. Cont..
Bangle test
Shakir’ tape Mid arm circumfence
MAC/Height <.29-severe malnutrition
0.32-0.33 normal nutrition
Ponderal index-
weight/Height2
>2.5—normal
2-2.5-borderline
<2-svevere malnutrition
BODY MASS INDEX-
weight in kg/height(cm)2
Mid arm muscle
circumference
18.5-25 normal
<13 –severe underweight
<15-moderate malnutrition
MAC-(3.14*SFT)

21. CLASSIFICATION
CLINICAL ( WELLCOME )
 Parameter: weight for age + oedema
 Reference tandard (50th percentile)
 Grades:
 80-60 % without oedema is under weight
 80-60% with oedema is Kwashiorkor
 < 60 % with oedema is Marasmus-Kwash
 < 60 % without oedema is Marasmus

22. KWASHIORKAR
First recognized by prof cicely willams
Pretend not to mind the second one(Krokor)
The disease of first child.
 Red boy. Sugar baby, Disposed child,
Floor dystrophy,
Triad: Growth retardation, pshycomotor
changes,and oedema
 Can affect anyone who suffers from a lack of
protein in the diet, and an excess of
carbohydrates.

23. Kwashiorkor PIC.

24.  Not only dietary in origin. infective, psycho-
social, and cultural factors are also operative.
 Because of lack of physiological adaptation to
unbalanced diet.
 Height and weight are accelerated with treatment
but never equal to those of consistently well-
nourished children.

25. Grading of kwashiorker
1-pedal oedema
2-1+facial oedema
3-2+paraspinal and
chest oedema
4-3+ascites

26. MARASMUS
 Severe form protein-energy malnutrition characterized by energy
deficiency and lack of nutrition in diet.
 Greek word MARASMOS-STARVATION
 characterized by gradual wasting of somatic fat and muscle
stores and preservation of visceral proteins.
In Marasmus the body utilizes all fat
stores before using muscles.
No Subcutaneous fat

27. Grading of Marasmus
1) Wasting in Axilla +Groin.
2)Thigh and Buttock .
3)Chest and Abdomen.
4) Buccal pad of fat.
Wasting of Brown fat occur first because it is more
metabolically active.

28. most commonly in the first year of life due to lack
of breast feeding and the use of dilute animal
milk.
higher risk of developing marasmus.
Ignorance & Poverty / famine
 poor maternal nutrition,
 low socio-economic status,
 children with chronic disease
• and diarrhoea,,

29. Diffefence b/w marasmus and kwashiorkar
KWASHIORKAR MARASMUS
wet form of PEM, sugar baby ,red
boy
Dry form of PEM
Mainly protein deficiency but also
EFA, micronutrients deficiency
Lack of calorie and protien
in diet
Lack of adaption-less cortisol adaptive mechanism involve
Cortisol and anabolic
hormone
Mostly >1 yr of age <1 yr of age
Very thin,
General
appearance
Lethrgic ,moderate malnourished ,
distended abdomen, moon facies
Fretful, irratable ,monkey
facies severe malnourished
edema Present absent
Mental
change
Apatheic, lethrgic, staring look, Alert, roving eye-searchig,
food, irritable
appetite Decrease good
Skin
change
Phrynoderma,thin shiny ,taut
Flanky paint dermatosis, Ulcer
Loose skin fold, lose of fat
pad

30. Cont….
Hair change Red colour,
Flag sign
Sparse
hypopigmented
occurence Less common More common
prognosis Good Better than k
Other feature Hepatomegaly-fatty infiltration of
liver,
absent
Associated micronutrient deficiency Present ,but sign
appear during
recovery phase
Anaemia-dimorphic anaemia
Circulatory insufficiency,
cardiomyopathy,
Dehydration
Renal function also impair
recovery Late to recover early

31. Pathological changes in malnutrition in various organ systemsPathological changes in malnutrition in various organ systems
Upper GITUpper GIT Mucosa shiny and atrophic. Papillae of tongue flattened.Mucosa shiny and atrophic. Papillae of tongue flattened.
Small and largeSmall and large
intestineintestine
Mucosa and villa atrophic; brush border enzymes reduced; hypotonic, rectalMucosa and villa atrophic; brush border enzymes reduced; hypotonic, rectal
prolapseprolapse
LiverLiver Fatty liver, deposition of triglycerides.Fatty liver, deposition of triglycerides.
PancreasPancreas
Exocrine secretion depressed ; glucagon production decreases; insulin levelsExocrine secretion depressed ; glucagon production decreases; insulin levels
low; atrophy and degranulation or hypertrophy of islets seen.low; atrophy and degranulation or hypertrophy of islets seen.
EndocrineEndocrine
systemsystem
Elevated growth hormone; thyroid involution and fibrosis; adrenal glandsElevated growth hormone; thyroid involution and fibrosis; adrenal glands
atrophic and cortex thinned; increased cortisol, catecholamine activity unaltered.atrophic and cortex thinned; increased cortisol, catecholamine activity unaltered.
Immune systemImmune system
Humoral immunity- decreasae level of secretory igA level ,prone to GIT andHumoral immunity- decreasae level of secretory igA level ,prone to GIT and
respiratory infection.respiratory infection.
Cellular immunity-low, Thymus involuted; lymphoenia; paracortical areas ofCellular immunity-low, Thymus involuted; lymphoenia; paracortical areas of
lymph nodes depleted of lymphocytes; germinal centers smaller and fewerlymph nodes depleted of lymphocytes; germinal centers smaller and fewer
CNSCNS
Head circumference and brain growth retarded ; cerebral atrophy on CT / MRI ;Head circumference and brain growth retarded ; cerebral atrophy on CT / MRI ;
abnormalities in auditory brainstem potentials and visual evoked potentials.abnormalities in auditory brainstem potentials and visual evoked potentials.
CVSCVS
Cardiac volume, muscle mass and electrical properties of the myocardiumCardiac volume, muscle mass and electrical properties of the myocardium
changes ; systolic functions affected more .changes ; systolic functions affected more .

32. Biochemical indices in children with malnutritionBiochemical indices in children with malnutrition
TransferrinTransferrin ↓↓ <0.45 mg/ml indicative of severe malnutrition<0.45 mg/ml indicative of severe malnutrition
AlbuminAlbumin
↓↓ Albumin concentration <3g /dl is associated with early illness;Albumin concentration <3g /dl is associated with early illness;
between 2.5 and 2.9 are low and below 2.5 g / dl arebetween 2.5 and 2.9 are low and below 2.5 g / dl are
pathologicalpathological
Pattern of circulatingPattern of circulating
amino acids in bloodamino acids in blood
Essential amino acidsEssential amino acids ↓,↓, non essential amino acids are normalnon essential amino acids are normal
oror ↑↑ therefore their ratio istherefore their ratio is ↑↑ Mean value 1.5; subclinical illnessMean value 1.5; subclinical illness
2-4; frank kwashiorkor >3.52-4; frank kwashiorkor >3.5
24 hr urinary 3-24 hr urinary 3-
methylhistidinemethylhistidine
excretionexcretion
Present exclusively in skeletal muscle and white muscle fibers ;Present exclusively in skeletal muscle and white muscle fibers ;
released when actin and myosin catabolized; excreted in urine;released when actin and myosin catabolized; excreted in urine;
reflects muscle mass 24 hr excretionreflects muscle mass 24 hr excretion ↓↓ in malnutritionin malnutrition
Urinary creatinineUrinary creatinine
height index (CHI)height index (CHI)
Breakdown product of creatinine ; reflects muscle massBreakdown product of creatinine ; reflects muscle mass
Ranges 0.25-0.75 in Kwashiorkor and 0.33-0.85 in marasmus;Ranges 0.25-0.75 in Kwashiorkor and 0.33-0.85 in marasmus;
recovered child -1recovered child -1
height)sameofchild(normalcreatinineurinehour24
creatinineurinehour24
CHI

33. PATHOPHYSIOLOGY
 Adaptive Starvation
 In the face of inadequate intakes, activity and energy expenditure
decrease.
 Despite this adaptive response ,fat stores are mobilized to meet
energy requirements.
 Energy Metabolism during Starvation
 Glycogen levels become depleted.
 Fat is used to make ATP and is used as an energy source.
 Gluconeogenesis occurs by synthesizing glucose from protein
compounds/muscle breakdown_after fat stores are depleted.

34. ETIOLOY OF KWASHIORKAR AND
MARASMUS
Classical theory of protein deficient
Gopalan theory of dysadaptation
 Marasmus occur as a result of adaptation to chronic nutritional
deficiency via cortisol while k is an acute condition body fail to
response to nutrtitional stress resulting in edema poossibly
because of excess carbohydrate
Golden theory of free radical

35.  Clinical signs and symptoms of micronutrient deficiencies
 Iron – fatigue, anemia, developmental delay and mental retardation.
 Vitamin D – Poor growth, rickets, and hypocalcaemia
 Tremor: During t/t,def. vit B,GABA↑,demylination. KWASHI SHAKE.
 Vitamin A – Night blindness, xerophthalmia, poor growth, and hair
changes. phrynoderma
 Folate – Glossitis, anemia (megaloblastic), and neural tube defects (in
fetuses of women without folate supplementation)
 Zinc – Anemia, dwarfism, hepatosplenomegaly, hyper pigmentation and
hypogonadism, acrodermatitis enteropathica, diminished immune
response, poor wound healing.

36. WHY KWASHIORKOR IN SOME AND
MARASMUS IN OTHERS
Variability among infants in nutrient requirements and
in body composition at the time of dietary deficit.
Giving excess carbohydrate to marasmus child reverses
adaptive response to low protein intake lipogenesis and
less apolipoprotein synthesis.
This results in mobilization of protein stores, decreased
albumin synthesis, hypoalbuminemia and edema.

37. Severe Acute Malnutrition
…a silent life threatening emergency
Theme of special issue INDIAN PEDIATRICS(IAP
JOURNAL) Aug,2010.
WHO and UNICEF propose diagnostic criteria as_
Weight/height of <70% and/or
 presence of bilateral pitting edema “and/or
Visible severe wasting, and/or

MUAC of < 11 cm in children , 6-60 months of age.
However, the suggested MUAC cut-offs are not based on
Indian population, and need validation.

38. ASSESSMENT OF NUTRITIONAL
STATUS OF CHILDREN1. History
Should include H/O
(i) Recent intake of food and fluids;
(ii) Usual diet (before the current illness);
(iii) Breastfeeding;
(iv) Duration and frequency of diarrhea and vomiting, type
of diarrhea, Loss of appetite, Fever, H/O contact with
tuberculosis, measles etc.
(v) Family circumstances (to understand the child’s
social background),
2. Anthropometric indicators
Evidence of deviations from average height & weight
Evidence of depletion of fat depots
Evidence of decrease in muscle mass
3. Evidence of specific deficiencies

39. DIET HISTORY
ASSESS DAILY FOOD INTAKE WITH ASSESSMENT OF CALORIE AND PROTEIN

40. Daily Calories Requirement
HOLIDAY AND SEGAR FORMULA:
1-10 kg– 100 kcal/kg
10-20 kg— 1000+50 kcal/kg for each kg above
10 kg.
Above 20 kg– 1500 +20 kcal /kg for each kg above
20 kg.

41. Energy Expenditure in normal Child
BMR: 50%
ACTIVITY: 25%
GROWTH: 12%
FECALLOSS: 8%
SPECIFIC DYNAMIC ACTION:5%

56.
Nutrients Human Cow
(gm)
Lactose 7 4.5
Ca:P >2 <2
Protein 1.1 3
Casein:whey 40:60 80:20
Fat 3.8 3.7
MILK 100 gm

57. (i) Anthropometry-weight, height/length, mid arm
circumference
(ii) Signs of dehydration and shock (cold hands, slow
capillary refill, weak and rapid pulse)
(iii) Lethargy or unconsciousness
(iv) Severe palmar pallor
(v) Localizing signs of infection, including ear and throat
infections, skin infection or pneumonia
(vi) Fever or hypothermia
(vii) Mouth ulcers, skin changes of kwashiorkor
(viii) Eye signs of vitamin A deficiency
(ix) Signs of HIV infection.
Physical examination

58. ANTHROPOMETRIC INDICATORS
OF NUTRITIONAL STATUS
1. Weight: index of acute nutritional status
2. Height or length: unaffected by excess
fat or fluid; assesses growth failure
3.
Weight for height measurement: more
accurately assesses body build
A. Measure child’s height
B. Find age for which measured height is on the 50th
% on the growth curve
C. Child’s actual weight (numerator)
50th% wt based on age of plotted ht
(denominator)

59. What is Anthropometry?
Greek
 Anthro- : man
 -pometry: measurements
 Literal meaning: “measurement of humans”

The study of measurements or proportions of the
human body according to sex, age, etc. for
identification purposes
 Dimensions of bones, muscles, and adipose (fat) tissues

60. Measurement of Height
Without footwear
Heels & back touching the wall
Lower border of the eye socket in the same
horizontal plane as external auditory
meatus
Looking straight ahead
A right angled block slides down until
touches the head
Gentle but firm pressure upwards applied to
the mastoids from underneath
Record to last 0.1 cm

62. 65
Mid-Upper Arm Circumference
(MUAC) for Assessment and
Admission
It increases rapidly in 1st
year of life (11-16 cm)
and remain stable{16-17 cm} in 1 to 5 year.
A value below 11.5 cm indicates severe
malnutrition.
Wasted
13.5 <12.5
12.5 TO 13.5
Normal

63. Use Appropriate Growth Charts
Many growth charts are available
Examples
 IAP (IAP Growth Monitoring guidelines 2007)
 WHO (MGRS Study 2006)
 British 2005
 ICMR
 1989 Affluent Indian (Agarwal et al)
 2009 Affluent Indian (Khadilkar et al)

64. Indicators of malnutrition
Indicator Interpretation
Stunting Low height for age Indicator of chronic malnutrition,
the result of prolonged food
deprivation and / or disease or
illness.
Wasting Low weight for
height
Suggests acute malnutrition ,
the result of more recent food
deficit or illness
Under
weight
Low weight for age Combined indicator to reflect
both acute and chronic
malnutrition

65. Investigations for PEM
Full blood counts
Blood glucose profile
Septic screening
Stool & urine for parasites & germs
Electrolytes, Ca, Ph & ALP, serum
proteins
CXR and Mantoux test.
Exclude HIV & malabsorption

66. Additional diagnostic evaluation
 Measures of protein nutritional status include serum
albumin, retinol-binding protein, prealbumin, transferrin,
creatinine, and BUN levels.
 Retinol-binding protein, prealbumin and transferrin
determinations are much better short term indicators of
protein status than albumin.

 a better measure of long-term malnutrition is serum
albumin because of its longer half life.

67. Complications
 *anorexia or no appetite,
 intractable vomiting,
 convulsions,
 lethargy or not alert,
 unconsciousness,
 lower respiratory tract infection (LRTI),
 severe dehydration, severe anaemia,
 hypoglycaemia, or hypothermia

68. Immediate management
of any acute problems
such as those of severe
diarrhea, renal failure,
and shock and,
ultimately, the
replacement of missing
nutrients are essential.
TREATMENTTREATMENT

70. Treatment of mild –moderate malnutrition
mild to moderate malnutrition make up greatest
proportion of malnourished children.
very important to intervene at this stage
at least to give 150 Kcal/kg /day
protein 3 gm/kg /day

71. Ten Steps to Recovery
THE WHO TEN STEPS

72. Treatment of Malnutrition

73. 1. hypoglycemia
All severely malnourished children are at risk of
developing hypoglycaemia (blood glucose< 54 mg dl )
Important cause of death during the first 2 days of
treatment.
Signs of hypoglycaemia –
low body temperature
(< 35.5 Celcius) ,
lethargy,
loss of consciousness.
Reasons –
serious systemic infection or
child - not fed for 4-6 hours

74. Treaatment of hypoglycemia
Asymptomatic
Give 50 ml of 10%
glucose or sucrose
solution orally or by
nasogastric tube followed
by the first feed ,no i.v.
fluid.
Feed with starter F-75
started every 2 hourly day
and night
Symptomatic
Give 10% dextrose i.v. 5
ml / kg
Follow with 50 ml of 10%
dextrose or sucrose
solution by nasogastric
tube
Feed with starter F-75
started every 2 hourly day
and night .

75. 2. Treat/prevent hypothermia
 Rectal temperature less than <35.5ºC or 95.5ºF or
axillary temperature less than 35ºC or 95ºF
 Due to impaired thermoregulatory control,
 low BMR and
 decreased thermal insulation from body fat.
 At risk-
 - Infants under 12 months,
 - large areas of damaged skin or
 - serious infections
 - marasmic children

 Hypoglycemia, hypothermia and Gram negative
sepsis occur as a triad

76. Treatment of hypothermia
• Feed the child immediately
• Cloth the child with warm clothes
• head should be covered well with a scarf or a cap
• Provide heat using radiation (overhead warmer), conduction (skin
contact) or convection (heat convector)
• Give appropriate antibiotics
Prevention
• Feed the child 2 hourly starting immediately after admission
• Place the child’s bed in a draught free area
• Always keep the child well covered.
• The child could also be put in the contact with the mother’s bare chest or
abdomen (skin to skin) as in kangaroo mother care to provide
MONITORING-
• Record the temperature half hourly till it reach 36.5 c
• Measure blood glucose.
.

77. Dehydration
 ASSESSMENT
H/O diarrheoa , vomitting
Thirst , Recent shunken eye
Decrease urine output, tachycardia, feeble pulse
 Unreliable sign
 Mental state
 Mouth ,tongue, tear
 Skin turgor
It is important to recognize the fact that
dehydration can co-exist with edema.

78. Treatment of dehydration
For rehydration in child with SAM use RESOMAL-ORS
orally or through a nasogastric tube
Every 30 minute for the first 2 hrs-5 ml/kg
Alternate hr for up to 10 hrs 5-10 ml/kg
Initiate feeding within two to three hours of startingInitiate feeding within two to three hours of starting
rehydration with F-75 formula on alternate hours withrehydration with F-75 formula on alternate hours with
reduced osmolarity ORSreduced osmolarity ORS
Be alert for signs of overhydrationBe alert for signs of overhydration
(F-imnci)(F-imnci)

79. COMPOSITION OF ORSINGREDIENTS LOW
OSMOLARI
TY
(NEW)
(mmol/l)
WHO –
ORS
(OLD)
(mmol/l)
ReSoMal
( Mg – 3;
Zn – 0.3;
Cu –
0.045
mmol/l)
Sodium 75 90 45
Potassium 20 20 40
Chloride 65 80 70
Citrate 10 10 7
Glucose 75 111 125
Osmolarity 245 311 300

80. Maganese: enzymic cofactor in SOD, oxidative
phosphorylation, bone mineralization.
Deficiency: Growth retadation, wt. loss,
hypocholestremia, increase PT,
Daily requirement: 1-5 mg/ day
 excess: cholestasis, encephalopathy, goiter,
cardiomyopathy.

81. Copper: Connective tissue cross linkage,
Hemopoiesis, lipid metabolism.
Def: neutropenia, Hypochromic anemia,
hypopigmented hair, impaired myelination,
subperiosteal hematoma.
Excess: ICC, Hemolytic anemia, zinc deficiency.

82. ZINC:
Protein and nucleic acid synthesis.
Def: Growth retardation,Hypogonadism, skin
changes, diarrhoea.
Daily requirement: 5-15 mg/ day,
In Def: 1-2 mg/kg elemental zinc.
Excess can cause Iron and Copper def. hence can be
used in Wilsons disease.
Epithelial repair, T Cell immunity, intestinal perm.,
Human milk-0.53 mg/100ml.

83. Septic Shock
•Start RL with 5% D or
•½ NS and 5% Dextrose @ 15 ml /kg/hr for 1
hour and monitor PR, RR, CRT AND URINE
OUTPUT.

84. •A)If at the end of 1 hr there is improvement
(pulse slows, CRT improves), it is severe
dehydration with shock, Repeat RL 15 ml/kg
over 1 hour. If accept orally –start ORS,if not
give RL 10 ml/kg/hr till accept orally.
B)If at the end of 1 hr there is no improvement,
consider septic shock and manage accordingly

85. Electrolyte disturbance
DO N’T treat edema with diuretic
sodium-total body sodium increase but plasma sodium maytotal body sodium increase but plasma sodium may
be low,be low, Prepare food without adding saltPrepare food without adding salt
serum K-serum K-
 <2 mEq/l or <3.5 mEq/l with ECG CHANGES give Kcl<2 mEq/l or <3.5 mEq/l with ECG CHANGES give Kcl
@0.3to0.5 mEq/kg/hr.@0.3to0.5 mEq/kg/hr.
 Give supplemental potassium at 3-4 mEq/kg/day for atGive supplemental potassium at 3-4 mEq/kg/day for at
least 2 weeks. Syp POTCLOR 15 ml=20mEq.least 2 weeks. Syp POTCLOR 15 ml=20mEq.
 MgMg-G-Give 50% magnesium sulphate (equivalent to 4 mEq/ml.) I.M. (0.1-ive 50% magnesium sulphate (equivalent to 4 mEq/ml.) I.M. (0.1-
0.2 ml/kg/dose) in 2 diveded dose is given for 1-3 days.0.2 ml/kg/dose) in 2 diveded dose is given for 1-3 days.

86. Anemia
Blood transfusion redquired: If Hb. <4 g/dl, or if
respiratory distress and Hb. 4-6 g/dl.
Then give 10 ml/kg slowly over 3 hour.
Furosemide 1 mg/kg/ i.v. at the start of transfusion.
If CARDIAC FAILURE present, transfused packed
cell(5-7 ml/kg).
Give iron for 2 month at least , to replanish iron
store.

87.  infectionsinfections
 System-System-Skin,Respiratory,GIT Infection and UTI most common
 Cause- multiple infection mainly
gram negative bacteria,gram negative bacteria, HIV, TB and malaria
 Screen all systems for infection
Fever may and may not be present
 Hypoglycemia and hypothermia are considered markers ofHypoglycemia and hypothermia are considered markers of
severe infectionsevere infection
Unbound iron in gut lead to over growth of E. COLI.Unbound iron in gut lead to over growth of E. COLI.
TREAT INFECTION

88. TREATMENT
 Give antibiotic to all severly malnourished child
 A broad spectrum antibiotic
 if child has No complications - Oral cotrimoxazole 5mg/kg 12 hourly orif child has No complications - Oral cotrimoxazole 5mg/kg 12 hourly or
trimethoprim) or Ampicllin+gentamycin for 5 days.trimethoprim) or Ampicllin+gentamycin for 5 days.
 Infected child or complications present- IV ampicillin 50 mg/kg /dose 6 hourlyInfected child or complications present- IV ampicillin 50 mg/kg /dose 6 hourly
and IV gentamicin 2.5 mg/kg/dose 8 hourlYand IV gentamicin 2.5 mg/kg/dose 8 hourlY
 if staphylococcal infection is suspected -Add IV cloxacillin 100 mg /kg/day 6if staphylococcal infection is suspected -Add IV cloxacillin 100 mg /kg/day 6
hourly.hourly.
 For septic shock or no improvement or worsening in initial 48 hours, andFor septic shock or no improvement or worsening in initial 48 hours, and
meningitis- Add third generation cephalosporin i.e. IV cefotaxime 100 mg/kgmeningitis- Add third generation cephalosporin i.e. IV cefotaxime 100 mg/kg
/day 8 hourly +i.v. amikacin 15mg/kg/day 8 hourly./day 8 hourly +i.v. amikacin 15mg/kg/day 8 hourly.
 Dysentery - Ciprofloxacin 30 mg/kg /day in 2 divided doses.Dysentery - Ciprofloxacin 30 mg/kg /day in 2 divided doses.
IV ceftriaxzone 50 mg /kg / day in 24 or 12 hourly if child is sick or hasIV ceftriaxzone 50 mg /kg / day in 24 or 12 hourly if child is sick or has
already received nalidixic acidalready received nalidixic acid
• source -who guidelinesource -who guideline

89. Parasitic Worm: Mebendazole 100 mg orally, Twice
a day for3 days.
T.B. : Contact with adult T.B. patient, Poor growth
Despite good intake, Chronic cough, Chest infection
not respond to Antibiotics.

90. •GIVE TO ALL CHILDREN Up to twice the RDA of
various vitamins.
•Multivitamins –Formulation including vitamins A, C, D,
E, and B12 , Thiamin, Riboflavin and Nicotinic acid.
• Vitamin A orally on day 1 unless there is definite evidence
that a dose has been given in the last month
(< 6 mo- 50,000 IU, 6- 12 m -100,000 IU, >1 yr-200,000 IU)
The reversible stages of keratomalacia, before liquefaction or
perforation of the cornea, were effectively treated by a single
I.M. injection of water-miscible vitamin A.10,000U/Kg
A daily oral supplement ( Vit A 3,000mcg/day) given after the
first week to build up the liver stores
6. CORRECT MICRONUTRIENT DEFICIENCIES6. CORRECT MICRONUTRIENT DEFICIENCIES

91. Folic acid: 1 mg/d (give 5 mg on day 1).
• Zinc: 2 mg/kg/d.
• Vitamin K 2.5 mg im/iv for 2-3 days.
AnemiaAnemia: Iron 2-6 mg/kg /d, once child starts gaining: Iron 2-6 mg/kg /d, once child starts gaining
weight started after 1 week cont. in stabilization phaseweight started after 1 week cont. in stabilization phase
for 3 monthfor 3 month
Copper:Copper: 0.2-0.3 mg/kg/d0.2-0.3 mg/kg/d
Treatment of anaemiaTreatment of anaemia

92. Treatment of Associated condition

93. Vitamin A deficiency classification

94. Diarrhoea
1)Continuing Diarrhoea:
Mucosal Damage and Giardiasis
Stool Microscopy
Metronidazole(7.5 mg/kg 8hourly for 7 days)
Lactose intolerance: Start Starter F 75 Low lactose
feed, Substitute milk.
2)Osmotic Diarrhoea: when diarrhoea worsen with
Starter F -75, Sugar reduced, Osmolarity is <300
mosmol/l.

95. Feeding should be started as soon as possible with a diet, which
has
• Osmolarity less than <350 mosm/L.[F75 333]
• Lactose not more than 2-3 g/kg/day.[1.3]
• Initial percentage of calories from protein of 5%,Fat 33%.
• Adequate bioavailability of micronutrients.
• Low viscosity, easy to prepare and socially acceptable.
Recommended daily energy and protein intake from initial
feeds - 75 kcal/kg and 1 g/kg respectively.
7.CAUTIOUS FEEDING

97. After rehydration
,Start oral or NG feeding with
_F-75.(75 kcal and 1.0g
protein/100 ml at ~130/ml/kg/24 hr)
with nutrient supplementation.
If diarrhea starts or fails to resolve
and lactose intolerance is
suspected_ use non lactose
formula.
If milk protein intolerance is
suspected,a soy protein
hydrolysate formula can be used.
FIRST WEEKFIRST WEEK

98. F_75 STARTER DIETS
Diet contents
(per 100 ml)
F-75 Starter
F-75 Starter
(Cereal based)
Example 1
F-75 Starter
(Cereal based)
Example 2
Cow’s milk or
equivalent (ml)
30 30 25
Sugar (g) 9 6 3
Cereal : Powdered
puffed rice* (g)
- 2.5 6
Vegetable oil (g) 2 2.5 3
Water : make up
to (ml)
100 100 100
Energy (kcal) 75 75 75
Protein (g) 0.9 1.1 1.2
Lactose (g) 1.2 1.2 1.0

99. Feeding patterns in the initial days of rehabilitation
Days Frequency
Volume /
kg/feed
Volume /
kg/day
1-2 2 hourly 11 ml 130 ml
3-5 3 hourly 16 ml 130 ml
6 4 hourly 22 ml 130 ml
Source : WHO guidelines

100. Catch up
growth
• Once appetite returns in 2-3 days, encourage higher intakes
• Increase volume offered at each feed and decrease the
frequency of feeds to 6 feeds per day
• Continue breast feeding ad – lib
• Make a gradual transition from F-75 to F-100 diet
• F-100 contains 100 kcal / 100 ml with 2.5-3.0 g protein / 100 ml
• Increase calories to 150-200 kcal / kg / day, and the proteins to
4-6 g/kg/day

101. F_100F_100
Catch up dietsCatch up diets
Diet contentsDiet contents
(per 100 ml)(per 100 ml)
F-100 Catch upF-100 Catch up
F-100 Catch upF-100 Catch up
(cereal based)(cereal based)
ExampleExample
Cows mild / tonedCows mild / toned
dairy milk (ml)dairy milk (ml)
9595 7575
Sugar (g)Sugar (g) 55 2.52.5
Cereal : Puffed riceCereal : Puffed rice
(g)(g)
-- 77
Vegetable oil (g)Vegetable oil (g) 22 22
Water to make (ml)Water to make (ml) 100100 100100
Energy (kcal)Energy (kcal) 101101 100100
Protein (g)Protein (g) 2.92.9 2.92.9

103. Rebuild Tissues
Advance to 200 ml/kg/day div q 3 to 4 hours.
Complementary foods should be added as soon as
possible to prepare the child for home foods at
discharge.
Khichri, dalia, banana, curd-rice and other culturally
acceptable and locally available diets can be offered.
Step 8

104. Complementing Proteins
Plant proteins are
deficient in different
essential amino acids
Cereals
 Low in lysine
Beans
 Low in methionine
Must eat both cereal and
beans together to get
balanced amino acids
 Complementing proteins
Rice and Beans

105. Balanced Protein
Protein are made of
amino acids
Essential amino acids
 Body cannot make
 Required in diet
Animal proteins have
perfect balance of amino
acids
 Meat
 Milk
 Eggs

106. STEP
9
tender, loving care
structured play and physical
activity as soon as the child is well
enough
a cheerful, stimulating
environment.
Encourage mother’s involvement
Stimulation, Play and Loving Care

107. STEP
10
Preparation for
Discharge
Nutritional education
Immunization
Home care sensitization
Follow Up

108. Before treatment and At discharge

109. DISCHARGE
Ready for discharge when reach 90% weight for
height
No oedema
Absence of infection
eating at least 120-130 Cal/kg/day and receiving
micronutrient
Cosistent weight gain(at least 5g/kg/day for 3
consecutive days) on exclusive oral feeding
Complete immunization appropriate for age
Caretaker sensitized to home care
Return to social smile (elizabeth)

110. Children discharge early : what to do?
Child >1 yr,appetite good, weight gain,no edema
,compelete antibiotic, Vit. K every 2 weeks.
Mother : available, motivated and trained to look
after have resource reside near hospital
Local health care ; can provide ,trained

111. •Hospital management of all children with SAMN-
not operationally feasible
•Home-based management is an unavoidable alternative for a large
number of children
•DIET CHART USING --> Besan panjiri, khichdi, parantha and enrichingDIET CHART USING --> Besan panjiri, khichdi, parantha and enriching
them with jaggery and oil.them with jaggery and oil.
•Should provide 150kcal /kg/d and 4 gm / kg of proteinsShould provide 150kcal /kg/d and 4 gm / kg of proteins
•Nutritional and hygiene education to motherNutritional and hygiene education to mother
•Multivitamin for 16 wks.Multivitamin for 16 wks.
HOME BASED REHABILITATIONHOME BASED REHABILITATION
INDIAN PEDIATRICS AUG 10

112. Primary failure Secondary failure
Failure to regain
appetite by day 4
Failure to start losing
edema by day 4
Presence of edema on
day 10
Failure to gain at least
5 g/kg /day by day 10
Failure to gain at least
5 g/kg /day for 3
consecutive days
during the rehabilitation
phase
Inadequate feeding
Infection,T.B.,HIV.
Psycological
Nutritional Deficiency.
TREATMENT FAILURE

113. REFEEDING SYNDROMES
•Pseudotumor cerebri– over energetic nutritional correction may cause
raised ICP.
•Nutritional recovery syndrome— abdominal distension, Ascites, HSM,
Parotid swelling, Gynaecomastia, Eosinophilia---related to endocrinal
disturbances--- A/W using high quantity of proteins for Rx.
•Encephalitis Like Syndromes—20% cases of kwashiorkor become drowsy
within 3-4 day of starting therapy d/t high protein in Rx. There may be
coarse tremors, rigidity, bradykinesia and myoclonus several days later.
•Development of severe hypophosphatemia after cellular uptake of
phosphate during 1st
wk. Serum P <0.5 can cause weakness,
rhabdomyolysis, neutrophil dysfunction, cardiorespiratory failure, arrythmia
,seizures or sudden death. MONITOR SERUM PHOSPHATE .

114. Direct causes of death
 Hypoglycemia
 Hypothermia
 Dehydration
 Infection
 S.Anaemia
 Dyselectrolytemia

115. Mortality rate of diarrhea
patients with malnutrition
is fourfold of the diarrhea
patients without
malnutrition.

116. Severe Malnutrition: Consequences
 Mental developmen
 Malnutrition affect brain development,
intelligence and school work performance.
 Behaviors of recovered severely malnourished
children
 shy, isolated, withdrawn
 decreased attention span
 immature, emotionally unstable
 fewer peer relationships/reduced social skills
 played less/stayed nearer to mothers

117. PROGNOSIS
Kwashiorkor & Marasmus-Kwashorkor
have greater risk of morbidity & mortality
compared to Marasmus and under weight
Early detection & adequate treatment are
associated with good outcome
Late ill-effects on IQ, behavior & cognitive
functions occur which may be reversible to
some extent if rehabilitation achived.

118. Nutritional programme in india
1. Vitamin A prophylaxis programme
2. Prophylaxis against nutritional anaemia
3. Iodine deficiency disorder control programme
4. Special nutrition programme
5. Balwadi nutritional programme
6. ICDS programme
7. Mid day meal programme

119. THANKS
RELAXRELAX
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