INTRODUCTION

According to the World Health Organization (WHO), malnutrition is the gravest single threat to global public health. Malnutrition is a broad term which refers to both undernutrition and overnutrition. Individuals are malnourished, or suffer from undernutrition if their diet does not provide them with adequate calories and protein for maintenance and growth, or they cannot fully utilize the food they eat due to illness. People are also malnourished, or suffer from overnutrition if they consume too many calories. Definition Malnutrition can be defined as the insufficient, excessive or imbalanced consumption of nutrients. Several different nutrition disorders may develop, depending on which nutrients are lacking or consumed in excess. Epidemiology The World Bank estimates that India is ranked 2nd in the world of the number of children suffering from malnutrition, after Bangladesh (in 1998), where 47% of the children exhibit a degree of malnutrition. The UN estimates that 2.1 million Indian children die before reaching the age of 5 every year four every minute mostly from preventable illnesses such as diarrhoea, typhoid, malaria, measles and pneumonia. Every day, 1,000 Indian children die because of diarrhoea alone.The 2011 Global Hunger Index Report ranked India 15th, amongst leading countries with hunger situation. At the same time as a large number of population suffers from malnutrition, more than 100 million people (11% of Indian population) in India are overnourished. Etiology Lack of knowledge-People do not understand the nutritional nature of their Childs health problem Poverty- lack of means to obtain and provide food to their child (as in the case of war) Famine and vulnerability-destitution, being orphan (Example HIV taking away parents Lives)

 Infections- there is a reciprocal relationship between malnutrition and infection. During infection, the requirement for nutrients increases, there will be increased loss of nutrients due to diarrhea genesis of fever and other acute phase reactants is at the expense of nutrients. Emotional deprivation- In orphan children and in children whose parents are negligent in giving careto their children, due to different reasons, children will lose appetite for feeding and hence end upin state of malnutrition Cultural factors- Different biases as to who should take the lions share of the family s food (Example, age biasolder children are given more food than the smaller ones, Sex biasmale children are more favored in getting nutritious food than female children in some families, etc.) Mal-distribution of foodstuffs- within the family, it occurs between the different ages and sexes dueto biases, food prejudices and taboos. It also occurs between the different regions of a country because of inappropriate Food and nutrition policy, poor marketing and distribution system due to different reasons like embargo,country under-siege

PEM
Protein Energy Malnutrition (PEM) is a malnutrition resulting from the deficiency of protein and/or energy in diet. PEM is an important nutritional problem among preschool age children. This leads to various degrees of growth retardation. When growth retardation is severe, functional deficiencies, like resistance to infection and poor intellectual development may result. The main cause of PEM is food inadequacy. Epidemiology : PEM characteristically occurs in children less than 5 years of age, whenever the diet is poor in energy and proteins.

Etiology PEM was earlier attributed to the concept of protein gap (deficiency of proteins in diet), which has now given way to the new etiological theory of Food gap, wherein it is not only the deficiency of proteins but inappropriate food (low in energy density, protein and micronutrients - Vitamin A, Iron, Zinc) which is poor both quantitatively and qualitatively, is the chief cause of PEM. Under-nutrition in fetal life, esp. last trimester. Lactation failure. Low energy dense weaning foods. Incorrectly constituted formula. Contaminated water and infections.

Classification of PEM : Even though Marasmus and Kwashiorkor are the two main and polar forms of PEM, clinically it can be broadly classified into five forms.

Classification of PEM (FAO/WHO) Type Percent of Oedema Deficit in standard weight for body weight height Kwashiorkor 80-60 + + MarasmicKwashiorkor Marasmus Dwarfing Underweight <60 <60 <60 80-60 + 0 0 0 ++ ++ Minimal +

Assessment of Nutritional Status

Nutritional Status Assessment

Anthropometry Biochemical & lab methods Clinical assessment Diet survey Ecological studies Functional assessment Vital statistics

Classification of Nutritional Status Based on Anthropometric Parameters Weight for age : There are standard weights laid down for a particular age. Thus a given childs weight (for his particular age), is compared to the standard weight of a normal child.

Gomez classification: The Gomez classification is one of the commonest classifications used to classify malnourishment into various grades

Weight for age (%)=

Weight of child X100 Weight of 'normal child' of same age

Gomez Classification

Malnutrition grade Normal Grade I (Mild) Grade II (Moderate) Grade III (Severe)

Weight/Age (%) of normal >90% 75 89 % 60 74 % < 60 %

The Indian Academy of Paediatrics (IAP) classification on the other hand puts the degree of malnutrition into four grades .This classification is used by the ICDS in India.

Indian Academy of Paediatrics (IAP)

Classification Normal I Grade II Grade III Grade IV Grade

Malnutrition grade Weight/Age (%) of normal > 80% 70-80% 60-70% 50-60% <50

Weight for height : The weight for height classification doesnt take age into consideration. Weight is also related to height. Many a times age is not known.

Wasting and Stunting : In the Waterlow classification weight for height and height for age are used to classify children as normal, wasted, stunted and wasted and stunted. Children with low weight for height are considered as wasted and those with low height are stunted.

Wasting and Stunting - Waterlow classification

Weight for height Normal Low Normal Low

Height for age Normal Normal Low Low

Nutritional status Normal Wasted Stunted Wasted and stunted

Interpretation Normal Acute malnutrition Nutritional dwarf Acute or Chronic malnutrition

Marasmus
Marasmus is a form of severe malnutrition characterized by energy deficiency. A child with marasmus looks emaciated. Body weight may be reduced to less than 80% of the average weight that corresponds to the height. Clinical features of Marasmus Diarrhoea is frequent with acid stools. Many infants are hungry but some are anorexic. There is often dehydration. Weight is much below standard for age. Temperature may be subnormal The abdomen may be shrunken or distended with gas Peristalsis may be easily visible because of thinness of abdominal wall The muscles are weak and atrophic. There is loss of subcutaneous fat. The skin and mucus membranes are dry and atrophic Psychological disturbances resulting from a lack of mothers care, can depress the appetite. Growth retardation Wisened old mans look. Hair changes like easily pluckable hair Infection Vitamin deficiency

Kwashiorkor
The term Kwashiorkor was introduced by Cicely Williams into modern medicine. It comes from language of Ga tribe of Ghana, meaning Sickness the older child gets when the next baby is born.while marasmus is seen in an early and abruptly weaned baby in an urban setting, the other pole of PEM, Kwashiorkor is typical in an older child who is breast fed for a rather prolonged period and weaned late in a rural setting. Poverty, insufficient food and land, poor agricultural practice.

Clinical features of Kwashiorkor (i) There are oedema, anorexia, diarrhoea and apathy (ii) Failure of growth is an early sign. Oedema is more marked in the lower limbs. (iii) The characteristic dermatosis consist of areas of both hypo-and hyperpigmentation the first becomes thickened as if varnished lie then peels and appears like "flaky paint" leaving cracks or denuded areas of shallow ulceration In modera te cases the derrnatosis resembles crazy paling; when severe, the desquamated part looks as if there has been a burn. The lower limbs, buttocks and perenium are usually most affected but ulcers can occur over pressure points and deep cracks in skin folds. (iv) The hair is sparse. There maybe changes in pigmentation with diffuse patches or streaks which maybe red or grey in colour. ; (v)Some degree of anemia is always present and may be severe apathy is a characteristic feature and child appears constantly unhappy.Many patients show a mixture of some of as of both marasmus kwashiorkor and die and are said to have marasmic kwashiorkor (vi)Some children adapt to prolonged insuffi cient food by a marked retardation of growth they resemble children a year or more youngermuscles are always wasted so as children may no longer be able to walk or stand.

Biochemical and metabolic disorders

(i) High body water content, loss of the fat and loss of protein from the wasted muscles (ii) Plasma concentrations of essential amino aciids especially branched chain amino acids and with protein, the concentration of amino acids in the plasma rise. (iii) The plasma concentrations of some enzymes such as cholinesterase, alkaline phosphatase, amyease, and lipase are lowered. (iv)The blood urea is usually low and may fall to 6g/100 ml (v)The plasma albumin level is low owing to a failure of synthesis in the liver In severe cases, it is Dually below 20 and sometimes below 10 g/I. ply a IgG is often raised if infections are present but over immunoglobulins are usually normal baa transferrin is lowered, especially in severe cases, and may be a better guide to prognosis than Plasma albumins (vi) I here is fatty liver And the excess of fat in the liver is triglyceride. Plasma triglyceride and cholesterol are low due to it decreased ability of the liver cells to mobilize lipid ,~ the form of lipoproteins (vii) Blood glucose is usually normal. Hypoglycemia may occur and is a complicated matter to be kept in mind. (viii) Plasma potassium level is below normal due to diarrhoea. Plasma magnesium level is also low due to increased losses in the stools (ix) Plasma [H+] may be either raised or lowered (x) The total body water may increase from 60 per cent to 80 per cent. The severity of clinical oedema is not closely associated with the size of the increase in total body water or with the level of plasma albumin. The cause and nature of the oedema still reforms in part a mystery.

(xi) Malnourished children are likely to have infections and may have complications requiring drug treatment Some antibiotics and antimalarials act by interfering with nutrition more in the microorganism than in the human host, and they need to be used with care in Protein Energy Malnutrition (PEM). The antibiotics streptomycin, chloramphenicol and the tetracyclines inhibit protein synthesis by interfering with the action of messenger or transfer RNA. All drugs should be used with caution.

Changes in organ system. There is atrophy of cells of pancreas and intestinal mucosa. Plasma concentration of Gh may be raised. Plasma concentration of cortisol is normal, and plasma thyroxine is often low. Lymphoid tissues atrophy. There is atrophy of heart. There is enlarged fatty liver. Case Management Management of a case of PEM focuses on the correction of specific nutrient deficiencies (dietary management), treatment of complications and supper imposed infections. The treatment approach is classified into two phasesThe acute stabilization phase in which the main focus is treatment of infection and other complications like dehydration, hypoglycemia, hypothermia and other electrolyte imbalances. The rehabilitation phase focuses on the restoration of the lost tissue and promotion of catch up growth. Dietary Management 1. Acute Phase Children are most at risk of dying during the acute phase. Dehydration, infection and severe anemia are the main dangers. In PEM, cardiac and renal functions are impaired and in particular malnourished children have a reduced capacity to excrete excess water and a marked inabilityto excrete Sodium. The amount of fluid given and the Sodium load must be carefully controlled to avoid cardiac failure. A cautious approach is

required aiming at administration of about 100kcal/kg/day and 1-1.15g of protein/kg/day. Small frequent feeds (as much as 12 times in 24 hours for the first two days and gradually tapering the number of feeds to be 6 in 24 hours after a week) are ideal as they reduce the risks of diarrhea, vomiting, hypoglycemia and hypothermia. Schedule for Oral Feeding in the First Week Day 1-2 3-5 6-7 Number of Feeds/per day 12 8 6 Volume per feed (Ml/Kg) 11 16 22 Energy Kcal/kg/day 100 Protein Gram/kg/Day 1.0

The maintenance formula can be made as follows: 25 gram of Dried skimmed milk (DSM) 100 gram of Sugar 30 gram of Oil per 1000ml Gives 75 Kcal and 0.9 gram of protein per each 100 ml It is important to give additional Potassium 4mmol/kg/d, Magnesium 2mmol/kg/d, Zinc 2mg/kg/d), Copper 0.2mg/kg/d and a multivitamin preparation and folic acid. Do NOT give iron early before infection is controlled. High dose vitamin A should be given even if there are no eye signs of deficiency. Rehabilitation Phase The aim of this phase is to restore wasted tissues and promote a rapid rate of catch-up growth through administration of high energy and protein. A vigorous approach is required. In this phase there is no danger of recovery syndrome. The synthesis of new tissue requires protein and other nutrients. Synthesis also requires a considerable amountof energy.

Normal rate of growth of children is such that they gain a weight of 1gram/kg/day by taking 105 kcal/kg/d and 0.78gram of protein /kg/d. To increase this rate of growth by 20 times the normal, the energy and protein intakes need to be increased to 200kcal/kg/day and 5kcal/kg/day, respectively. Modification of differentmilks to provide 1 literof high-energy formula Milk (g) Dried skimmed milk Whole dried milk Liquid cow's milk 80 110 900 Sugar (g) 50 50 50 Vegetable oil (g) 60 30 30

The formulas above provide 100kcal and 3g protein/100ml.

Health promotion (a) Good ante-natal care (b) Education on food, hygiene and family planning (c) Education on the importance of colostrum, diet during lactation (d) Various measures under the ICDS initiative, like good nutrition, immunization, education, hygiene and sanitation (e) Promotion of breast feeding (f) Good weaning practices, correct time of weaning,importance of low cost weaning foods (g) Prevention and control of infections during weaning

(h) Improve family diet (j) Correct knowledge on balanced diet (k) Utilization of family planning practices (l) Hygiene & sanitation Specific protection Diet : Protein and energy rich food should be consumed by children. Special attention must be paid to diet during weaning.Adequate quantities of fruits and vegetables must be included in the diet. Immunization : The child must be immunized as per the national schedule. Growth monitoring : Vulnerable children must be identified. Children must be monitored through growth charts.Early diagnosis of growth failure must be done and treated as appropriate Early diagnosis and treatment : Early diagnosis and treatment of infections is also vital. To achieve this, health worker must be alert and mothers should be aware of the signs and symptoms of common infections. Preparation and use ofORS should be known to all mothers. The services availablethrough the IMNCI initiative must be fully utilized. Medical advice : In extreme and serious cases early medical advice and treatment facilities must be available. Hospitalization of the case remains the only choice in complicated cases. Residential Units : Mothers are admitted with their sick children. The mother gets hands on experience in the practical learning of preparation and administration of a therapeutic diet for her child with an expert. This demonstration and involvement of the mother in her childs recovery goes a long way in understanding the problem and mitigating it. Day Care Centre : The mother attends the day care centre along with the child where cooking and feeding is taught to the mother. While the child attends every day, involvement of the mother is partial.

Domicilliary Rehabilitation : The expert comes home and assesses the situation as a whole. The mother is then rendered suitable advice with regards not only to feeding but also about improving various domestic contributory factors to PEM. Responsibilities of Public Health Nurse in Managing PEM The nursing management of PEM consists of providing nutrition rich in the essential nutrients to correct the dietary insufficiency and to promote normal growth and development. The digestivecapacity of malnourished child is initially poor. As a result oral feedings are given in small frequent amounts, limited in proteins and carbohydrates especially fats that are hard to digest. In addition, the nurse is responsible for: 1. Maintaining the childs body temperature within a normal range. 2. Providing periods of rest and appropriate activity. 3. Providing stimulation. 4. Recording intake, output and daily weight. 5. Turning position in bed frequently. 6. Preventing bedsore and infection by keeping the skin clean and dry. 7. Providing appropriate treatment of bedsore and oral thrush if any. 8. Administering iron and folic acid to correct the accompanying anemia. 9. Diluting liquid iron preparations and giving through a straw to prevent staining of tooth enamel.

Water Soluble Vitamins

Infantile thiamine deficiency Thiamine deficiency in infants, which is rarely seen today, is almost invariably an acute disease which mainly affected infants breast-fed by women having deficient thiamine levels

Signs and symptoms Initially the infant is usually of normal appearance with varying degrees of constipation,occasional vomiting, crying and restlessness. The disease usually presents with generalized oedema,dyspnoea, cardiac disturbance, gastrointestinal derangements, and oliguria. Types Pure cardiologic or pernicious form The infant shows signs of cyanosis and an acute cardiac attack can follow with the infant usually dying within 2 to 4 hours. The common age for this form of the deficiency disease is one month up through the third month. It has been reported that this type of deficiency responds very dramatically to thiamine. Aphonic form A milder form of infantile beriberi which causes a typical loss of voice due to paresis or even paralysis of the vocal cords due to neuritis is more frequent in the age group 4 to 6 months.. Pseudo meningitic form Older infants (7 to 9 months), in particular, may manifest symptoms that can be mistaken for bacterial meningitis eg. stiffness of neck and other apparent signs of meningeal irritation accompanied by vomiting, convulsions and sweating.

Treatment Infantile thiamine deficiency: If severe heart failure, convulsions or coma occur, 2550 mg of thiamine should be given very slowly intravenously, followed by a daily intramuscular dose of 10 mg for about a week. This should then be followed by 3-5 mg of thiamine per day orally for at least 6 weeks. Sources Asparagus is an excellent source of vitamin B1. Very good sources of vitamin B1 include mushrooms, spinach, flaxseeds, tuna, green peas, and Brussels sprouts.

RIBOFLAVIN Riboflavin deficiency is rare.Diagnosis of riboflavin deficiency is made clinically and dramatic improvement is seen on supplementation with Vitamin B2.

Deficiency Deficiency of riboflavin leads s glossitis ,cheliosis and ulcers over the cornea with watering of eyes photophobia and blurring of vision. If the pregnant woman is riboflavin deficient, growth and development of the baby is affected. Niacin It is also known as anti pellagra vitamin. Deficiency Deficiency of niacin is more prevalent in maize eating population. Pellagra is characterized by diarrhea, skin rash and mental deterioration with muscle weakness and loss of memory. Skin rash occurs predominantly in sun-exposed areas such as neck and back of hands leading to pigmented, scaly and cracked skin.

Treatment Provision of a high-protein diet and B-complex vitamins is needed for complete restoration of health. Pyridoxine Dietary deficiency of pyridoxine is rare. Deficiency Deficiency of pyridoxine usually occurs due to genetically inherited absence of an enzyme or secondary to some drugs such as prolonged use of Isoniazid Cycloserine Hydralazine D-penicillamine pyrazinamide Symptoms Deficiency of pyridoxine leads to irritability, anemia , Hyperacusia, nausea, vomiting, seizures and wasting or loss of weight. Older children may develop neuritis. Pyridoxine deficiency can lead to persistent convulsions in an infant Treatment Infants respond to intravenous pyridoxine dramatically. Vitamin B12 Vitamin B12 is essential for the formation of red blood cells and deficiency of Vitamin B12 anemia. Deficiency Vitamin B12 deficiency can also lead to anemia, paralysis and weakness of the limbs due to involvement of the nerves in the spinal cord. Dietary deficiency of Vitamin B12 is rare and is usually seen in children on exclusive vegetarian diet with inadequate intake of milk . Also deficiency of Vitamin B12 is seen in patients with due to absence of a factor called as 'Intrinsic Factor' in the stomach

Treatment Cobalamin is available in a solution for injection in doses ranging from 100 to 1000 mcg. Most of the injected doses in excess of 50 mcg are rapidly excreted in the urine. Thus, when therapy is started, repeated doses are recommended in order to replenish body store.Oral pills in dose of 1000-2000mcg Can be given. FOLATE(Vit B9) Helps the body make red blood cells, break down protein, keeps heart healthy. Makes DNA Deficiency Responsible for neural tube defects .anemia, red tongue. Cerebral folate deficiency presents within 46 mo of age with irritability, microcephaly, developmental delay, cerebellar ataxia, pyramidal tract signs, choreoathetosis, ballismus, and seizures. Hereditary folate malabsorption presents within 13 mo of age with recurrent or chronic diarrhea, failure to thrive, oral ulcerations, neurologic deterioration, and megaloblastic anemia and recurrent infections. Treatment Oral folic acid corrects the low CSF folate levels and improves the clinical manifestations. Pregnant women must be given folate supplements. Vitamin C Deficiency of vitamin c causes scurvy. Presentation Infantile scurvy is uncommon before age 7 months. Early clinical manifestations consist of pallor, irritability, and poor weight gain. In advanced infantile scurvy, the major clinical manifestation is extreme pain and tenderness of the arms and, particularly, the

legs. The baby is miserable and tends to remain in a characteristic immobilized posture from subperiosteal pain, with semiflexion of the hips and the knees. Treatment Treatment of Vitamin C deficiency consists of high doses of Vitamin C either through mouth or injection for several weeks. Children should consume a diet rich in Vitamin C to avoid further deficiency.

FAT SOLUBLE VITAMINS

Vitamin A deficiency Vitamin A Deficiency (VAD) is the leading cause of preventable blindness in children. It also increases the risk of disease and death from severe infections Etiological Factors : Vitamin A deficiency is most common in the age group of 1 to 3 years, the preschool children. It results from a very complex web of causation involving ignorance,poverty, infections, lack of food, malnutrition, environmental and social factors. SYMPTOMS Night Blindness Conjunctival Xerosis Bitots spots Corneal xerosis Extra - ocular manifestations : Some extra-ocular manifestations of vitamin A deficiency are also known. Follicular hyperkeratosis, growth retardation and anorexia are some of them.

Treatment of Xerophthalmia: An established case of xerophthalmia responds well to treatment with vitamin A. The following regime can be followed : 2,00,000 IU (110mg) of Retinol palmitate (oil miscible vitamin A) is administered orally for 2 days. In cases of persistent vomiting/diarrhoea, water miscible vitamin A 1,00.000 IU is administered as IM Injection, followed by 2,00,000 IU, 1 to 4 weeks later. For infants less than 1 year old or less than 8 Kg weight, half the dose is used. Prevention Dietary modifications should be achieved through promotion of growth, production and consumption of vitamin A / beta-carotene rich foods Nutrition education: Educate the community on the importance of vitamin rich diet, its regular intake and the harmful effects of its deficiency. Fortification of ghee, hydrogenated vegetable oil and butter are being done as a government policy to augment the vitamin A status of the community. Technology for the fortification of sugar, mono sodium glutamate, bread and milk also exists. Periodic massive dosage: Vitamin A administration is now integrated with immunization program. The first dose of 100,000 IU is given at 9 months of age along with measles vaccines. Thereafter, the second and subsequent doses of 200,000 IU are given at 6 monthly intervals till 3 years of age. In all, a total dose of 9,00,000 IU is administered.

Vitamin D Essential for formation of bones and teeth. Helps the body absorbs and use calcium. Symptoms In infancy and childhood deficiency of Vitamin D causes deformed bones characteristic of rickets

Treatment Rickets and osteomalacia are almost always treated with oral supplements of vitamin D, with the recommendation to acquire daily exposure to direct sunlight. An alternative to sunlight is the use of an ultraviolet (UV) lamp. Rickets heals promptly with 4,000 IU of oral vita-min D per day administered for approximately one month. Vitamin E deficiency Definition Vitamin E deficiency is a very rare problem that results in damage to nerves Epidemiology Premature, very low birth infants (birth weight less 1500 gms or 3 pounds 4 ounce) are risk of vitamin E deficiency SYMPTOMS Vitamin E Deficiency Symptoms in Infants include: Retrolental fibroplasia (an eye disease) in premature infants Loss of weight and delayed growth Poor feeding habits Developmental problems that include physical and mental problems

Vitamin E Deficiency Symptoms in Children: Chronic cholestatic hepatobiliary disease (liver disease) causing neurological deficits Spinocerebellar ataxia (gross lack of coordination of muscle movements) with loss of deep tendon reflexes Loss of vibration and position senses

 Ophthalmoplegia (paralysis of extra-ocular muscles responsible for eye movements) Muscle weakness Ptosis (drooping upper eyelid) Dysarthria (motor speech disorder) Slow growth in children

Vitamin E deficiency that occurs with cholestatic liver disease, or other malabsorption syndromes, can betreated with weekly injections of 100 mg alpha-tocopherol that may continue for few weeks. VITAMIN K Causes Newborns are especially prone to vitamin K deficiency. A nursing-mothers milk is low in the vitamin breast milk can supply only about 20% of the infantsrequirement. Infants are born with low levels of vitamin K in their body; they do not have any vitamin Kproducing bacteria in their intestines. SYMPTOMS As a result, a form of vitamin K deficiency, called hemorrhagic disease of the newborn, may develop. This disease involves spontaneous bleeding beneath the skin or muscle hematoma and hematuria , and occurs in about 1% of all infants. In rare cases, it causes death due bleeding in the brain.

TREATMENT Vitamin K deficiency in newborn infants is treated and prevented with a single injection of phylloquinone (5mg).

MINERALS
CALCIUM Deficiency of calcium causes Rickets and tetany . Rickets The characteristic signs of rickets are a protruding abdomen, beaded ribs (rachitic rosary), bowed legs, knock knees, cranial bossing , pigeon chest and an enlargement of the epiphyses. Tetany Muscle tone decreases and become flabby.It affects hand feet and the face. Sources of calcium Richest source: Milk and cheese Good source: Figs asparagus nuts figs beans cauliflower cabbage and asparagus Daily requirement: Infants under one year: 360-540mg Children 1-18 yrs: 0.8-1.2 mg IRON Iron deficiency is one of the most common vitamin or mineral deficiencies in the world, affecting 20% or more of women and children especially in developing countries. Adolescent women who have started menses or who are pregnant are particularly at risk for developing iron deficiency.

DIAGNOSIS Anemia ,low hemoglobin or red cell volume may lead to reduced school and work performance and may affect cognitive function, as well as leading to cardiovascular and growth problems. Diagnosis is made most simply by hemoglobin level or hematocrit and red cell morphology. ETIOLOGY A variety of etiologies exist for anemia, including dietary deficiencies of folate or vitamin B12, infections and inflammatory states , and conditions that result in insufficient production of red blood cells or excessive destruction of red blood cells. In INFANTS The iron content of a newborn infant is approximately 75 mg/kg body weight, and much of this iron is found in hemoglobin. The body iron of the new-born is derived from maternalfetal iron transfer,80% of which occurs during the third trimester of pregnancy. Preterm infants, with less opportunity to establish iron stores, have a substantially reduced endowment of body iron at birth than term infants. Adolescence Adolescents have very high iron requirements, and the iron demand of individual children during periods of rapid growth is highly variable and may exceed mean estimated requirements. Boys going through puberty experience a large increase in erythrocyte mass and hemoglobin concentration. The addition of menstrual iron loss to the iron demand for growth leads to particularly high iron requirements for pre and postmenarchal adolescent girls. Causes of Anaemia Inadequate intake of iron Poor diet Poverty Ignorance Inadequate folate/vitamin C intake

Poor absorption and bioavailability Absorption Only 5% Poor absorption-Non haeme iron Inhibitors: Phosphates, phytates,oxalates,fibre Tea (tannin), Eggs (Phosphate), Milk (Calcium) Excessive loss of iron Normal man (1mg/day) Menstruation (2mg/day) IUDs Intestinal worms Malaria Repeated / frequent pregnancies Increased demand of iron Pregnancy Growth

Prevention and Control of Anaemia 1. 2. 3. 4. 5. 6. 7. 8. 9. Breastfeeding and appropriate weaning Dietary modification Deworming Control of infection Supplementation Iron Fortification Nutrition education Home gardening Care of pregnant and lactating women

Daily requirements of iron: Infants 10-15 mg 1-3yrs 15mg 4-10yrs 10mg 11-18yrs 18mg

Management Premature neonates: 2 to 4 mg elemental iron/kg/day divided every 12 to 24 hours maximum daily dose = 15 mg Infants and children less than 12 years: Prophylaxis: 1 to 2 mg elemental iron/kg/day maximum 15 mg in 1 to 2 divided doses. Mild to moderate iron deficiency anemia: 3 mg elemental iron/kg/day in 1 to 2 divided doses. Severe iron deficiency anemia: 4 to 6 mg elemental iron/kg/day in 3 divided doses.

FLUORINE
Fluorine Excess (Fluorosis) : Ingestion of large amounts of fluorine occurs when the drinking water contains fluorine in excess of 3-5 ppm. SYMPTOMS Fluorosis presents as dental or skeletal fluorosis, depending on the water content of fluorine, duration and level of exposure.

Dental fluorosis If exposure takes place during calcification of teeth (first 7 years of life), the teeth are more likely to get affected by fluorosis. The mottling of teeth is common. The enamel loses its lustre and the texture becomes rough. There could be brown bands alternating with white chalky patches. Mottling may progress to small pits. Upper incisors are affected the most, even though all the teeth are vulnerable. Skeletal Fluorosis and Fluoride Poisoning : When the concentration of fluorine exceeds 10 ppm, a crippling skeletal fluorosis may ensue There may be sclerosis of spine, pelvis and limbs. The ligaments of spine may be calcified, producing a poker back.The tendinous insertion of muscles may be ossified, producing the characteristic rose thorn shadow in the X-Ray. Fluorine Deficiency It causes dental daries Prevention Reduction of sugar intake Dental hygiene Fluoridation of water

COPPER
Deficiency Causes: Myelopathy- Sufferers typically present difficulty walking aused by sensory ataxia Neutropenia-Causing defective immune systems Skeletal changes Fractures Anemia

Daily requirements: Infants and children:0.05mg/kg Sources: Liver Kidney other meats shellfish nuts and dried legumes

ZINC
Deficiency of zinc causes hypogonadism and dwarfism There is loss of taste acuity Hypogeusia Anorexia Hepatosplenomegaly Delayed closure of epiphyses Anemia

Daily requirement Breast fed new born: 0.7-5mg Infants: 3-5mg Children 10mg Adolescents 13mg Sources of Zinc Rich sources: Oysters and herrings Good sources: Meat eggs liver and milk Fair sources :Cereals pulses nuts vegetables and fruits

IODINE
Deficiency of iodine causes cretinism in children. Abortions, stillbirths and congenital anomalies and mental/physical underdevelopment. If iodine deficiency occurs during the most critical period of brain development from the fetal stage up to the third month after birth, the resulting thyroid failure will lead to irreversible alterations in brain function. Food Rich in Iodine Marine vegetation,sea foods, fruits grown on the seaboard. Prevention 1. Use of Iodized salt or oil 2. Iodine monitoring 3. Manpower training 4. Mass communication