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Sacad Ahmed abdiwaliDean of Health Sciences, Gollis University at Gollis University
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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
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Human, Economic, and Institutional Resources Potential Resources Ecological Conditions Political and Ideological Structure Root Causes Conceptual Framework of Malnutrition
Human, Economic, and Institutional Resources Household Food Security Potential Resources Ecological Conditions Political and Ideological Structure Root Causes Underlying Causes Conceptual Framework of Malnutrition
Human, Economic, and Institutional Resources Household Food Security Potential Resources Ecological Conditions Environ. Health, Hygiene & Sanitation Political and Ideological Structure Root Causes Underlying Causes Conceptual Framework of Malnutrition
Human, Economic, and Institutional Resources Household Food Security Potential Resources Ecological Conditions Care of Mother and Child Environ. Health, Hygiene & Sanitation Political and Ideological Structure Root Causes Underlying Causes Conceptual Framework of Malnutrition
Human, Economic, and Institutional Resources HealthDiet Household Food Security Potential Resources Ecological Conditions Care of Mother and Child Environ. Health, Hygiene & Sanitation Political and Ideological Structure Root Causes Immediate Causes Underlying Causes Conceptual Framework of Malnutrition
Human, Economic, and Institutional Resources Nutritional Status HealthDiet Household Food Security Potential Resources Ecological Conditions Care of Mother and Child Environ. Health, Hygiene & Sanitation Political and Ideological Structure Root Causes Manifestations Immediate Causes Underlying Causes Conceptual Framework of Malnutrition
Human, Economic, and Institutional Resources Nutritional Status HealthDiet Household Food Security Potential Resources Ecological Conditions Care of Mother and Child Environ. Health, Hygiene & Sanitation Political and Ideological Structure Root 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
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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
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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
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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.
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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
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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.
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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)
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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
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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
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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
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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
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
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
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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
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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).
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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
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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
1st stage of VAD
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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
Health consequences of IDD
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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
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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.
Atrophic Lingual papillae
spoon shaped nails
Pale skin
Easy fatigability
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.
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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
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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
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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
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Prevention of Obesity Primary prevention Secondary Prevention
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Prevention of obesity Primary prevention 1- Promoting healthy eating & inducing dietary changes 2-Proper feeding & rearing of children 3-Increased physical activity
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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
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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.
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Weight MeasurementWeight Measurement
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Weight MeasurementWeight Measurement
Weight measurementWeight measurement
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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.
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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
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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
Liver
GU system
GI system
Immune system
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
Cellular function
Skin, muscles and glands
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
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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.
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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.
Care for the mother (2) 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)
Care for the mother (3) 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
Phase I
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
N.B -Composition of Resomal
Composition of F 75 and F 100
RECORDING AND REPORTING
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
Standard Monthly report
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
Thank You
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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