1. Malnutrition
Protein / Energy

2. Definitions of Malnutrition
Kwashiorkor: protein deficiency
Marasmus: energy deficiency
Marasmic/ Kwashiorkor: combination of chronic energy deficiency and chronic or acute protein deficiency
Failure to thrive: marasmus in U. S. children under 3.

3. Definitions of Malnutrition
PEM
Primary: inadequate food intake
Secondary: result of disease
FTT
In-organic: inadequate food intake
Organic: result of disease

4. History Marasmus well known for centuries Kwashiorkor: Cicely Williams
Ga tribe in Ghana
“the sickness the older child gets when the next baby is born”
Starch edema, sugar babies
Similar but different diseases

5. How many? 36% of children in the world are underweight 43% stunted
9% wasted
Better nutrition, but more children in high risk areas, yields more children affected.

6. Causes Social and Economic Poverty Ignorance
Inadequate weaning practices
Child abuse
Cultural and social practices
Vegan
Low fat diets

7. Biologic factors Maternal malnutrition, prematurity Infectious disease
Start life with poor stores
Infectious disease
Diarrhea, Aids, TB, measles
Environmental
Unsanitary living, poor quality water
Agricultural/cultural patterns
Droughts, floods, wars, forced migrations

8. Age of child Infants and young children Marasmus < 1 year
High nutritional needs
Early weaning or late weaning
Poor hygiene
Marasmus < 1 year
Kwashiorkor >18 months with starchy weaning foods

9. Pathophysiology Develops slowly, adapts to decreased intake
Marasmus
Less fragile metabolic equilibrium
Less effective adaption or acute problem
Kwashiorkor, mixed

10. Energy Decreased intake yields decreased activity
Decreased play and physical activity
Mobilization of body fat, weight loss,
Subcutaneous fat
Muscle wasting
Maintains visceral protein in marasmus
Nl albumin
Larger protein deficit leads to faster visceral protein falls and edema.

11. Biologic differences Marasmus Kwashiorkor Weight loss
Nl or low protein
Boarderline hgb, hct
NL AA profile
Nl blood glucose
Nl enzymes
Nl transaminase
Kwashiorkor
NO weight loss
High extracellular water
Low hgb, hct
Low protein
Elevated AA profile
Low enzymes
High transaminase

12. Pathophysiology Cardiac Immune system Cytokines (glycoproteins)
Output, heart rate and blood pressure decrease
Postural hypotension
Immune system
T lymphocytes and complement decreased
Susceptible to bacterial infection
Cytokines (glycoproteins)
Poor immune response
TNF inc leading to anorexia, muscle wasting and lipid changes

13. Pathophysiology Decreased total body potassium GI function
Not electrolytes, but problem in rehabilitation
GI function
Poor absorption of lipids, and sugars
Decreased enzyme and bile production
Increase incidence of diarrhea, and bacterial overgrowth

14. Pathophysiology CNS Parental adaptation
Decreased brain growth and myelnation
Electrical changes similar to dylexia
Parental adaptation
Increased breastfeeding
Altered expectations

15. Diagnosis Anthropometry 4 groups Acute: Wasting: low weight for height
Chronic: Stunted: low height for age
4 groups
Normal
Wasted not stunted: acute PEM
Wasted and stunted: acute and chronic PEM
Stunted not wasted: past PEM, nutritional dwarfs

16. Diagnosis Normal: ± 1 SD Mild: -1.1 to -2 SD Moderate -2.1 to -3 SD
Severe greater than -3
Less than 5th percentile in US
BMI in adolescents
Moderate <15 ages 11-13, <16.5 ages 14-17
Severe <13 ages 11-13, <14.5 ages 14-17

17. Diagnosis Mild to moderate Marasmus
Weight loss if acute, decreased growth velocity of chronic
Decreased activity
Marasmus
Skin and bones, thin hair, monkey face
Hypoglycemia, hypothermia

18. Diagnosis Kwashiorkor Soft pitting edema, starting in feet and legs
Skin lesions
Skin dry, with hyperkeratosis and hyperpigmentation
Preserved fat layer, small weight deficit, ht may be normal
Dry brittle hair
Anorexia, with vomiting and diarrhea

19. Diagnosis Mixed Edema, with or without skin lesions
Muscle wasting and loss of subcutaneous fat

20. Treatment Acute/ life threatening Fluid and electrolyte
K and Mg shifts
Oral rehydration, slowly ml/kg
Infections: main cause of death
Aggressive treatment, but disease alters metabolism of drugs
Other deficiencies
Anemia and heart failure, care with transfusions and no diurretics
Vitamin A: immediate treatment

21. Treatment Slow re-feeding Nutritional rehabilitation
Small frequent feeding around the clock
Patient encouragement of food
Nutritional rehabilitation
Play and teaching
controlinfections

22. Recovery? At home Reach weight for height and replete muscle mass
Normal is 25-75% weight for height and continue for one months after
Treat other deficiencies
Family problems
Who does this include here?
Tube feeding.
Disabilities
FTT

23. What does it mean? Poverty Brain development
Correlation of income, wt, ht and hgb in US
What is wealth?
Importance of food choice
Brain development
Iron deficiency: neuro transmitters
Brain waves:

24. What does it mean? Learning: Difference in treatment by parents
Duration of breastfeeding
Expectations
Long term effects
INCAP two villages, one protein and one calorie
At 18 protein supplemented group had higher performance scores irrespective of educational exposure. They had taught themselves.

25. What does it mean? Learning: Difference in treatment by parents
Duration of breastfeeding
Expectations
Slums of Kingston, Jamaica
Educational intervention, early rise plateau
Nutritional intervention, late rise
Additive effect
Education lasts, not nutrition, but high IQ mom’s and nutrition group did as well as education.

26. Implications Children learn by interacting with the environment
Poverty: limited environment
Malnutrition: limited interaction
Additive effect!
Loss to society of human potential
Lead graph