Marasmus occurs when energy intake, intake of carbohydrates, is insufficient for the body's energy requirements.

The body forced to draw on its own emergency stores. Liver glycogen is exhausted within a few hours, and skeletal muscle protein is then used via gluconeogenesis to maintain adequate amounts of blood glucose in the bloodstream. At the same time, triglycerides in fat depots are broken down into free fatty acids, which provide some energy for most tissues, but not for the nervous system, especially neurons in the brain, who rely on .

Pathophysiology In marasmus, energy intake is insufficient for the body's requirements, and the body draws on its own stores. Liver glycogen is exhausted within a few hours, and skeletal muscle protein is then used via gluconeogenesis to maintain adequate plasma glucose. At the same time, triglycerides in fat depots are broken down into free fatty acids, which provide some energy for most tissues, but not for the nervous system. When near starvation is prolonged, fatty acids are incompletely oxidized to ketone bodies, which can be used by the brain and other organs for energy. Thus, in the severe energy deficiency of marasmus, adaptation is facilitated by high cortisol and growth hormone levels and depression of insulin and thyroid hormone secretion. Because amino acids are mobilized from muscle to provide the liver with substrate for protein synthesis, plasma protein levels decrease less in marasmus than in kwashiorkor. Related Topics: Cortisol - Insulin - Thyroid hormone - Amino acid ~~~~~~~~~~ In kwashiorkor, relatively increased carbohydrate intake with decreased protein intake leads to decreased visceral protein synthesis. The resulting hypoalbuminemia causes dependent edema, and impaired -lipoprotein synthesis causes fatty liver. Insulin secretion is initially stimulated but is reduced later in the disease. Fat mobilization and amino acid release from muscle are reduced, so that less amino acid substrate is available to the liver. In marasmus and kwashiorkor, the insulin response to a glucose load is poor, possibly due to chromium deficiency. Related Topics: ~~~~~~~~~~ Total body protein synthesis is about 300 g/day or 5 (g/kg)/day in the average adult male. The daily obligatory loss is only about 60 to 75 g (9 to 12 g nitrogen), because 75 to 80% is reused. The RDA of protein for an adult is about 0.8 g/kg; infants and children require 1 to 2 (g/kg)/day . Thus, infants require a higher proportion of essential amino acids in their diet than do adults. Related Topics: ~~~~~~~~~~ In protein deficiency, adaptive enzyme changes occur in the liver, amino acid synthetases increase, and urea formation diminishes, thus conserving nitrogen and reducing its loss in urine. Homeostatic mechanisms initially operate to maintain the level of plasma albumin and other transport proteins. The rates of albumin synthesis eventually decrease, and plasma levels fall, leading to reduced oncotic pressure and edema. Growth, immune response, repair, and production of some enzymes and hormones are impaired in severe protein deficiency.

I. Nutritional deficiency Problems a) Malnutrition The primary cause of malnutrition is inadequate and faulty diet. Apart from poverty and other socio economic factors, environmental factors also play an important role in aggravating the dietary deficiency diseases. These precipitating factors are the widespread chronic infections among the poor living under conditions of poor environmental sanitation and personal hygiene. Malnutrition continues to be a major health problem in the world today, particularly in children younger than 5 years of age. Lack of food; however is not always the primary cause for malnutrition. In many developing and underdeveloped nations, diarrhea is a major factor. Additional factors are bottle feeding (in poor sanitary conditions), inadequate knowledge of proper child care practices, parental illiteracy, economic and political factors, and simply the lack of adequate food for children. Levels of Malnutrition India has among the highest levels of child malnutrition in the world, and the persistence of the problem has led to the formulator of the National Nutrition policy by the government of India. UNICEF reports auch programmes through strategies promote BF and to timely introduction of complementary foods, encouraging clean environment with portable water, and tackling diarrhoeal and other infections. Reasons for the problems of Malnutrition in India Food availability and Related Problems Low per capita food availability Low purchasing capacity of the masses Mal distribution of the available food Limited choice of food articles. Poverty and Malnutrition Ramification of poverty Low income of the masses Poverty malnutrition interaction Population Problem and Malnutrition Population explosion Effects on food availability Effects of uncontrolled fertility on nutrition. Social Factors Affecting Nutritional Status

Customs, superstitions and taboos. Diet during illness Caste and false social status. Food tastes and faulty cooking methods. Food combinations. Influence of industrialization and urbanization and modernization. Ignorance and lack of education. Alcohol and malnutrition. Protein Energy Malnutrition Protein Energy Malnutrition is defined as a range of pathological conditions arising from coincident lack of varying proportions of protein and calorie, occurring most frequently in infants and young children and often associated with infection. -WHO 1973 PEM has been identified since long as a major nutritional problem in India. Insufficiency of food the so called food gap appears to be the chief cause of PEM, which is a major health problem particularly in the first years of life. Various studies on dietary intake reveal that the gap intake among children on habitual cereal pulse based diet is primarily due to inadequate intake of such diets and not the quality of protein. Severe form of malnutrition (PEM) leads to two clinical forms of disorders. They are as follows: Kwashiorkor Kwashiorkor is the condition of deficiency of protein with an adequate supply of calories. A diet consisting mainly of starch grains or tubers provides adequate calories in the form of carbohydrates but an inadequate amount of high quality proteins. The child with kwashiorkor has thin, wasted extremities and a prominent abdomen from edema (ascites). The edema often masks the severe muscular atrophy, making the child appear less debilitated than he or she actually is. The skin is scaly and dry and has areas of depigmentation. Diarrhoea commonly occurs from lowered resistance to infection and produces electrolyte imbalance. Protein deficiency increases the childs susceptibility to infection, which eventually results in death. Marasmus

Marasmus results from general malnutrition of both calories and protein. It is common occurrence in underdeveloped countries during the times of the drought, especially in cultures where adults eat first, the remaining food is often in sufficient in quality and quantity for the children.

Marasmus is usually a syndrome of physical and emotional deprivation and is not confined to geographic areas where food supplies are inadequate. Marasmus is characterized by gradual wasting and atrophy of body tissues, especially of subcutaneous fat. The child appears to be very old, with flabby and wrinkled skin. The child is fretful, apathetic, withdrawn and so lethargic Causes of Protein Energy Malnutrition a) Nutritional Factors Poor caring practices include

Not feeding the sick children. Not providing the adequate complementary feeding. Not supporting mothers to breast- feed adequately. Non breastfed. Late weaning. Inadequate supplementation. Failure to feed during illness. Failure to increase to caloric intake immediately after the illness. b) Non Nutritional Factors Due to poverty, mother is not able to provide sufficient food to the child resulting in under nutrition.

Non- immunization Improper growth monitoring. Poor weight gain during adolescence Poor environmental and personal hygiene Illiteracy Large family

False beliefs Failure to utilize Health/Hospital care. Low agricultural inputs, marketing, distribution of food and income. Poor and inadequate water and sanitation facilities. Political Problems Inadequate resources include money, material and manpower refers to the poor quality, expensive and non convenience.

Lack of health care services and information regarding maternal and child care practices on basis of inadequate time and resources for taking care of health diet, emotional and psychological needs of women and children. Poor caring practices include

Poor antenatal care. Food taboos during and after pregnancy. Inadequate management of sick and malnourished. Infestation like ascariasis particularly giardiasis may lead to anorexia. Signs and Symptoms of different types of PEM Kwashiorkor

Oedema of the face and lower limbs Failure to thrive Anorexia Diarrhoea Apathy Dermatosis ( hypo and hyper- pigmentation) Sparce Soft and thin hair Angular stomatitis Cheilosis Anemia Marasmus

Failure to thrive Irritability Fretfulness and apathy are common Diarrhoea is frequent Many are hungry but some may be anorexic The child is shrunk and there is little or no subcutaneous fat. There is often dehydration Temperature is subnormal Watery diarrhea and acid stools may be present.

Muscles are weak and atrophic Limbs appear as skin and bones Marasmic Kwashiorkor These children exhibit a mixture of some of the features of both marasmus and kwashiorkor. Management of PEM Therapeutic Management

Adequate nutritious diet either by breastfeeding or a proper weaning diet. Five grams of protein/ kg body weight/day should be given for the existing weight. Rehydration with an oral rehydration solution that also replaces electrolytes. Treatment of infections. Medications such as antibiotics and antidiarrheals. Health education Fats: Forty percent of total calories can be from fat which can be tolerated by children. Saturated fats such as butter, milk and coconut oil are preferred because unsaturated fatty acids worsen diarrhea. Energy: It is important that there should be enough calories in the diet; otherwise proteins will be utilized for energy purposes and not for building the tissues. Vitamin A should be supplied immediately. Anemia: Folic acid should be given

Nursing Care Management Provision of essential physiologic needs, such as protection from infection, adequate hydration, skin care and restoration of physiologic integrity because children usually weak and withdrawn, they depend on others for feeding. Oral rehydration with an approved oral rehydration solution is commonly used in cases of PEM where diarrhea and infection are not immediately life threatening. Health education concerning the importance of proper nutrition, whether breastfeeding or bottle feeding, when being weaned to semisolid foods. Children with marasmus may suffer from emotional starvation as well; care should be consistent with care of the child with failure to thrive )Vitamin Deficiency Vitamin A deficiency Vitamin A deficiency is a major nutritional problem affecting young children leading to blindness. In India about 5 7 percent children suffer annually from eye damage caused by vitamin A Deficiency, Recent evidence suggests that mild vitamin A deficiency probably increases morbidity and mortality in children, highlighting the public health importance of this disorder. Surveys show, that 1-5 percent of children have clinical signs of vitamin A deficiency. The prevalence rates are higher in school age children than in younger age groups, but severe forms of the deficiency resulting in blindness are confined to children below 3 years.

The causes of severe form of vitamin A deficiency like Xerophthalmia arises when the diet contains practically no whole milk and butter and very limited amounts of fresh vegetables and fruit so lacks both retinol and carotenes.Xerophthalmia and keratomalacia both occur in the first year of life amongst artificially fed infants but rare amongst the breast fed. If the mothers diet during pregnancy is low in vitamin A, the child is born with low stores of vitamin A. Protein energy Malnutrition further aggravates the partial deficiency because absorption and plasma transport of vitamin A are impaired.Diarrhoea is known to be a precipitating factor in keratomalacia. The major factors contributing to low availability of vitamin A are lack of awareness of the importance of consuming vitamin A rich food and poverty leading to limited accessibility to vitamin A rich food. The Clinical Forms of the Deficiency will include:Vitamin A Deficiency: - Vitamin A deficiency is seen more commonly in younger children i.e. between 6 months and 3 years. Vitamin A is indispensable for normal functioning of the eyes. It helps in the production of retinal pigments which are required for vision in dim light. Conjunctival Xerosis:-.The conjunctiva becomes dry, appears muddy and wrinkled due to failure to shed the epithelial cells and consequent keratinisation. The pigmentation gives the conjunctiva a peculiar smoky appearance. This symptom in children under 5 years is more likely to be due to dietary deficiency. Night blindness:- This is the first sign of Xerophthalmia. The child is not able to see in darkness in a dark room or when it gets dark in the late evening. This is due to lack of retinal pigments. Bitots spots:- Although Bitots spots differ somewhat in size, location and shape, they have similar appearance. They are accumulations of fomy cheesy material on the conjunctiva on either side of the cornea, often in association with other signs of Xerophthalmia, such as blindness. In children under 5 years of age they are usually due to vitamin A deficiency. Corneal Xerosis/ ulceration: - The cornea becomes dry (xerosis). If the disease is not treated, the xerosis can progress within hours to an ulcer of the cornea. Corneal Xerosis may progress suddenly and rapidly to keratomalacia. Keratomalacia:- In this softening and dissolution of the cornea occurs. If the process is not stopped by treatment, perforation of the corneal leads to prolapsed of the iris, extrusion of the lens and infection of the whole eyeball which almost invariably occurs. The chance of saving any useful vision are slight. Heating results in scarring of the whole eye and frequently in total blindness. Xerophthalmia fundus:-In school children or young adults with prolonged vitamin A deficiency ophthalmoscopic examination may show lesions appearing as spots, either white or yellow scattered along the sides of the blood vessels. The spots may fuse and the lesions are most numerous on the periphery of the fundus ( boral portion) and never appear on the macula (the yellow spot on the retina. Corneal scars:- These are white, opaque patches on the cornea as a result of healing of an older ulcer. Vision may be affected seriously, depending on the size of

the scars. Management of Vitamin A Deficiency Immediately on diagnosis, water soluble 1, 00,000 IU of vitamin A intramuscularly can be given for corneal xerosis, ulcer, keratomalcia, xerophthalmia, severe infection and malnutrition. Immediately on diagnosis for less severe forms like night blindness, conjunctival xerosis, Bitots spot, oil solutions as palmitate 2, 00,000 IU can be given orally. On second day oil solution of 2, 00, 000 IU orally should be given prior to the discharge from the hospital. Preventive Measures Nutrition and health education should be given to the mothers. Pregnant and lactating mothers should be encouraged to consume dark green leafy vegetables and yellow or orange fruits so that there is sufficient storage in vitamin A in the liver of new born. Mothers should be motivated to feed their children as vitamin A present in the milk is adequate for 3 to 6 months of infants life. The weaning diet should be consist of dark green leafy vegetables, yellow or orange fruits, whole milk, butter, fish and egg. National Vitamin A supplementation programme is a more effective alternate approach. Other measures:Medical paramedical personnel should be trained to detect and treat xerophthalmia They should know the importance of giving vitamin A oily solution once in 6 months at the door steps of the beneficiaries as community approach but not at hospital as clinical approach. They should monitor periodically National Vitamin A prophylaxis programme. Medical and paramedical personnel should be given nutrition education. To prevent vitamin A deficiency intake of green leafy vegetables, yellow fruits its and vegetables like papaya, mango, pumpkin and carrots should be promoted for long term measures kitchen garden should be encouraged. Vitamin D Deficiency Deficiency of vitamin D causes rickets in young children in the age group of 6 months to 2 years. It reduces calcifications of bones which affects growth of bones and cause deformity of bones such as curved legs, pigeon chest, rickety rosary, deformed pelvis. There is delayed teething, standing and walking. It is no more a serious problem because of improvement in child health care services, socio-cultural practices, plenty of available sunshine. Rickets is preventable by simple methods like exposure of children to sunshine regularly and administration of vitamin D as prophylaxis periodically. It requires education of mothers and family members about the importance of exposure of children to sunshine regularly and to give food rich in vitamin D such as butter, cheese, egg yolk, liver, fortified food such as milk, vanaspati oil etc. Fish liver oil is very good source of vitamin D and is available in the form of capsule which can be given under the direction of medical officer. Excessive intake of vitamin D is harmful. It may cause loss of appetite, nausea, vomiting, excessive thirst and drowsiness. There may be renal failure, cardiac arrythemias and unconsciousness. All this is due to increased level of calcium in the blood due to increased absorption of calcium. It is very important to recognize the signs of rickets and refer the child to PHC/ Hospital etc. for therapeutic treatment as early as possible. The mothers and family

members need to be educated about the observations of signs and reporting in the health center to treat and vitamin d deficiency in children. c) Iron Deficiency The iron deficiency causes nutritional anaemia in children. About 50 percent of children have anaemia. It is due to malnutrition. It usually leads to various others problems such as general weakness affecting work performance, reduced immunity and resistance to infections resulting in increased morbidity and mortality. It affects physical and psychological behaviour of the children. There is decrease in the concentration of hemoglobin and it is lower than the normal cut off point set up by WHO, which is 11 g/dl in children 6 months to 6 years. Anaemia is aggravated by worm infestation and malarial parasites. It may also be caused because of these infections. Another factor which causes anaemia is folic acid (folate) deficiency. Anaemia in children can be prevented by preventing and controlling of anaemia in pregnant and nursing mothers by improvement in diet and prophylactic treatment by iron folic acid, and nursing mothers by improvement of diet of children emphasizing on breast feeding, proper weaning and supplementation etc, iron folic acid drops/ tablets as prophylaxis, prevention and treatment of worm infestation and malaria. Fortified salt with iron has been tried out by National Institute of Nutrition to control anemia in regions with high prevalence of anaemia and is accepted by the government as a public health approach to prevent anaemia. Commercially Iron fortified salt is available in the market. The mothers and family members and community people need to be educated by health workers about all these preventive measures. Monitoring of growth and development and anaemia is very important to make an assessment of malnutrition and anaemia and accordingly take corrective measures.