You baby will let you know she is still hungry by wanting more after the feed is finished, or she may start chewing her fists. A baby may also begin to demand feeds more often and if she normally sleeps through the night, she may start waking up early wanting to be fed.

Breast and formula milk give babies all they require for the first six months so you don’t have to worry if your baby seems satisfied with milk alone until this age. By six months of age your baby needs the additional nourishment provided by the solids, and she also needs to learn how to eat.

Starting solid foods for babies, but how?

First solids are really just tasters to get a baby used to different textures and flavors; the main nourishment will still come from the breast or formula milk. The first food should be bland and smooth, like baby rice mixed with either cooled boiled water, or formula or breast milk.

Starting solid foods can be a little tough task. To begin with offer a small amount on the tip of a clean spoon, midway through a feed, once a day. Once your baby has accepted this, you can introduce a small amount of fruit or vegetable puree, for example, banana, potato, or carrot (with no added sugar or salt), mixed with formula or breast milk.

As soon as your baby has got used to taking solids off a spoon, you can begin to introduce new foods and other solids at a second meal. If your baby obviously doesn’t like the taste of something don’t force matters. Try another food and reintroduce the rejected food at a later stage. This is important when starting solid foods for your child. You can simply reintroduce the rejected food in a new form.

A first the baby will simply try to suck anything of the spoon. But it won’t take long to master getting the food off the spoon and into the back of the mouth. Once your baby can do this she will be able to cope with lumpier textures, so you can begin to mash rather than puree food. Your baby will also be able to enjoy a wider variety of tastes and textures.

ADVANCED FEEDING

At around eight months, after about 2 months of starting solid foods, you can introduce food combinations such as baby cereal and fruits, or egg yolk and tomato-remember to remove the seeds from the tomato and to cook the egg thoroughly. Food can be lumpier and more solid so that it encourages your baby to start chewing. Try mincing or mashing the food with fork.

At nine months and over, your baby is likely to be on three meals a day as well as milk, unsweetened diluted fruit juice, or water. Giving your child food at grown-up meal times will encourage her to learn social skills by watching others. As her appetite grows you can gradually increase the amount given at each meal. Offer finger foods such as slices of peeled apple, and banana; this will encourage her to feed herself. Always stay with your child while she is eating in case of choking. This is very crucial when starting solid foods for your baby.

Check out the videos below on the things to remember when starting solid foods for your baby:

Excess production or inadequate elimination of these radicals has been recently identified as an important contributor in cellular aging, disease and death.

Three most important free radicals in human context are – singlet oxygen (0), superoxide & peroxide anions and hydroxyl radicals.

Sources: Free radicals excess is implicated to —

a) Exogenous or environmental sources e.g. smoke, air pollutants, radiation, ultraviolet rays etc.; or

b) Endogenous or metabolic sources e.g. infections, cellular ischemia/ hypoxia, toxic tissue injury.

Anti-oxidants: Important antioxidant substances in body may be broadly divided into three categories —

a) Metabolic enzymes e.g. superoxidase mutase, catalase, glutathione peroxidase etc.

b) Metal ion chelators e.g. plasma proteins, transferring, ceruloplasmin etc.

c) Oxygen scavengers e.g. vitamins (A, E, C) and minerals (selenium, zinc).

Pathology: Free radicals tissue injury is considered as an important cause of altered cellular permeability and metabolism, leading to early cell death in innumerable disease processes, including — a) Hyperoximia-related problems in preterms e.g. retinopathy of prematurity or bronchopulmonary dysplasia, b) Hypoxic-ischemic injuries e.g. neonatal enterocolitis, hypoxic-ischemic encephalopathy, c) Sepsis/septic shock, d) Metabolic disorders e.g. kwashiorkor, Wilson disease, hemochromatosis etc., e) Hemolytic anemia or malignancies, and f) Premature atherosclerosis or aging in adults etc.

Prevention of Free radicals injury depends on avoidance of environmental risk factors, early treatment of primary disease and adequate consumption of natural antioxidant nutrients i.e. vitamins and minerals (as above).

Treatment: Recently, many synthetic antioxidants have been used in selected cases of suspected Free radicals injury e.g. xanthine oxidase inhibitors e.g. allopurinol, N-acetylcysteine, recombinant enzymes e.g. glutathione peroxidase analogues, superoxide dismutase, coenzyme Q derivatives etc. or natural antioxidants (as above), with equivocal results.

Physiology: Vitamin E is an important anti-oxidant (free-radical scavenger) as well as involved in nucleic acid metabolism and stabilization of cellular membranes.

It is widely distributed in vegetable oils,fats and nuts, specially those rich in polyunsaturated fatty acids.

RDA: 3-7 mg of cs-tocoferol equivalent/day (1 mg = 1.5 IU); higher in preterms.

Etiology of Vitamin E deficiency: Vitamin E Deficiency is mainly seen in — a) preterms due to poor stores, b) chronic liver disease, c) Malabsorption syndrome, and d) high iron states e.g. in hemolytic anemia.

Clinically Vitamin B deficiency has been implicated in — a) 1-lemolytic anemia in preterms (at 6-10 weeks)

b) Edema in kwashiorkor

c) Degenerative neuropathy in biliary atresia or chronic liver disease, presenting as ataxia, peripheral neuropathy and posterior-column abnormalities

d) Retinopathy of prematurity

Treatment of Vitamin E deficiency: Though exact role and dose of vitamin B is not established, daily oral supplementation of 5-25 IU in high-risk children e.g. preterms or those with chronic liver disease may prevent/reverse clinical abnormalities.

Physiology of Vitamin C deficiency: Vitamin C or Ascorbic acid is a water-soluble vitamin, essential for synthesis of — a) normal collagen by incorporating proline and hydroxyproline, and b) chondroitin sulphate — a component of intercellular matrix required for epithelial integrity and wound healing. It also facilitates – c) iron absorption, d) folate metabolism (conversion of folic acid into folinic acid) and e) elimination of toxic free radicals (anti-oxidant).

Being a water-soluble vitamin, it is not stored in body and rapidly excreted in urine. Breast feeding is an adequate source of Vitamin C in early infancy. Although widely distributed in many food items (except meat), it is extremely heat-labile, rapidly inactivated on cooking and extrudes in cooking-water.

Etiology of Vitamin C deficiency: Scurvy is usually precipitated by sudden increase in Vitamin C requirements due to infections, acute febrile illnesses, diarrhea etc. in children with subclinical dietary deficiency e.g. in PEM or top-feeding (rare in breast-fed). Wrong cooking practices e.g. overboiling of vegetables in excess water or throwing the excess cooking-water are important causes of dietary Vitamin C deficiency.

Clinical manifestations of Vitamin C deficiency: Scurvy usually presents in late infancy or in toddlers, following an infective episode e.g. diarrhea or viral infection in malnourished children. A typical case present with —

RDA: 30-40 mg/day (Higher in infections e.g. fever, diarrhea)

Sources:

— Richest source: Amla (600 mg)

— Citrus Fruits: Guava (212), orange, lemon, pineapple

— Vegetables: Cabbage (124), tomato, green vegetables.

— Germinated pulses

— Non-veg foods e.g. Liver and kidneys (not in meat)

Functions: Essential for Collagen formation, Wound healing and epithelial integrity, Facilitate iron absorption and folate metabolism, Anti-oxidant effect,

Vitamin C deficiency states:

• Typical: Scurvy

• Others: poor wound healing, anemia, recurrent infections

a) Skeletat signs:

• Pseudoparalysis -severe tenderness and restricted limb movements with pithed-frog posture

• Scorbutic rosary – tender, sharp, nodular beeding at costochondral junctions, due to subluxation.

b) Ski nimucosal signs:

• Swollen, purple, bleeding gums

• Petechial/ecchymotic hemorrhages over skin (perifollicular) and mucus membranes. Severe GIT or intracranial bleeds are rare.

c) Mental changes in Vitamin C deficiency:

• Apprehensive facial appearance

• Extreme irritability or apathy

d) Signs of subclinical Vitamin C deficiency

• Poor wound healing

• Moderate dimorphic anemia

• Increased susceptibility for infections

Diagnosis of Vitamin C deficiency depends on —

a) Suggestive clinical features with history of precipitating event e.g. fever or diarrhea;

b) Characteristic radiological finding, best seen at the end of long bones at knee joint & include —

i) Ground-glass appearance of the shaft and epiphysis due loss of trabecular pattern,

ii) Thinning or Penciling of cortex with sharply outlined epiphyseal ends,

iii) Wimberger’s ring sign- Ground-glass appearance of epiphyseal centers, surrounded by a white ring of compressed collagen,

iv) White line of Frankel – a thick, irregular, transverse, white line at epiphyseal ends due to thickened provisional zones of calcification.

v) Tummeifeldt’s zone of rarefaction – a narrow zone of metaphyseal raref action proximal to Frankel’s line, due to atrophy of sub-epiphyseal cortex.

vi) Angle sign – a triangular, rarefied, lateral defect proximal to Frankel’s line, representing early stage of the zone of rarefaction.

vii) Corner sign or Pelican spur – a lateral spur-like growth of Frankel’s line, due to compression of soft shaft.

viii) Lifting or separation of periosteum from the cortex due to sub-periosteal hematoma. Actual hematomas are visible only after 1-2 weeks of illness as enveloping-shell appearance, due to calcification.

c) Bwchemwal diagnosis is required only in subclinical cases, based on low ascorbic acid levels in a buffy coat (WBCs) sample of oxalate blood (Normal: 25- 40 mg/dl). A level of zero in this layer indicates scurvy, even without clinical signs. Plasma ascorbic acid levels are unreliable.

DID: Scorbutic bony lesions need to be differentiated from other cases of pseudoparalysis e.g. — a) osteomyelitis/septic arthritis, b) transient synovitis, c) trauma, d) congenital syphilis and e) leukemic bone involvement.

Scorbutic rosary is different from rachitic rosary as — a) it is tender and b) has sharper margins vs. rounded contour of the rachitic beading.

Treatment of Vitamin C deficiency: Vitamin C therapy (P0 500 mg/day for a week) is highly effective with dramatic clinical recovery within 24-48 hours, though radiological improvement may take many weeks. Recurrence must be prevented by adequate diet and therapeutic supplementation (100 mgI day) for many weeks.

Prevention of Vitamin C deficiency includes nutritional counseling, correct cooking practices and Vitamin C supplementation in lactating mothers, top-fed infants & during acute infective illnesses.

Etiology: Folic acid deficiency is rarely dietary due to miniscule daily requirements (< 100 jag/day), usually caused by — a) malabsorption states e.g. fish tape worm infestations, b) increased requirements e.g. in pregnancy and hemolytic anemia, and c) anti-folate drugs e.g. methotrexate, pyrimethamine. Goat and camel milk are poor sources of Folic acid.

Clinically, these cases present with four important manifestations megaloblastic anemia, chronic diarrhea, neurological manifestations e.g. tremors and developmental regression, and skin hyperpigmentation, specially on knuckles & thigh.

Severe deficiency may also be associated with thrombotic episodes and atherosclerosis, due to altered homocysteine metabolism.

Diagnosis depends on peripheral smear findings (megaloblastic anemia), supported by low RBC/serum folate levels (normal: 5-20 ng/ml).

FIGLU test i.e. urinary excretion of formiminoglutamic acid after loading dose of histidine, may detect subclinical deficiency.

Management: Folic acid deficiency is treated with P0 or parenteral folic acid (1-5 mg/day) for 3-4 weeks, along with concomitant vitamin 12 supplementation.

Folic acid deficiency in pregnancy is an important cause of neural tube defects in fetus, which can be easily prevented by Routine folic acid supplementation (5 mg OD) to all pregnant mothers from 1 month before to 3 month after conception.

Widely present in animal sources, Vitamin B12 is absent in plant foods, but may be endogenously synthesized by colonic bacteria.

Vitamin B12 absorption requires hydrolysis by gastric acid and combination with a specific protein in stomach - intrinsic fhctor of castle (IFc). This B12-Ifc complex attaches to specific receptor sites in terminal ileum, where B12 component is absorbed, transported in bound form with a plasma protein — Transcobalamin II and stored in tissues, bound to another protein – Transcobalamin I.

Etiology: Vitamin B12 deficiency is rarely dietary due to extremely low requirements (<1-5 jig/day), usually caused by congenital/acquired defects in its absorption e.g. Congenital IFc deficiency or juvenile pernicious anemia, malabsorption disorders, Immerslund syndrome i.e. IFc-B12 receptor deficiency, and congenital transcobalamin deficiency.

Clinically, Vitamin B12 deficiency presents with a triad of — a) Megaloblastic anemia, b) Glossitis, and c) Signs of demyelination e.g. ataxia, parasthesia, hypo/ hyperreflexia (Subacute combined degeneration of cord).

Diagnosis is usually based on —

a) Megaloblastic anemia on smear that does not respond to folic acid therapy, supported by

b) Low serum Vitamin B12 levels (<100 pg/mi)

c) Methylmalonic aciduria (>3.5 mg/day).

Schilling test is used to confirm Vitamin B12 deficiency as well as to differentiate between Ifc deficiency and malabsorption defects.

Management of Vitamin B12 deficiency: Oral Vitamin B12 therapy is generally useless, due to defective absorption. Cases without neurological signs are treated by life-long monthly therapy with IM Vitamin B12 (1 mg), while those with neurological signs need daily therapy during first two weeks, followed by monthly injections.

Etiology: Biotin deficiency is rarely dietary, as it is also synthesized by intestinal bacteria. Important causes include — a) excessive consumption of raw egg-white, which is rich in Avidin — a biotin- binding protein, b) unsupplemented formula or parenteral feeding, and c) genetic biotinidase deficiency an enzyme required to recycle biotin (dependency state).

Clinically, it presents with — a) skin manifestations e.g. exfoliative dermatitis and alopecia, b) GIT manifestations e.g. anorexia and glossitis, and c) neurological manifestations e.g. extreme lassitude and muscle pains. Genetic defects may also present with Rett syndrome.

Diagnosis depends on dietary history, clinical features, organic aciduria and response to biotin therapy.

Treatment includes P0 or TM Biotin deficiency therapy with 0.5-2 mg/day, though higher doses (10 mg/day) are required for dependency states.

Physiology: Vitamin A is a fat-soluble vitamin, existing in two forms —

a) Pre-formed vitamin e.g. retinol, present in animal sources; and

b) Pro-vitamin e.g. /3-carotene, present in plant sources, which is converted to retinol in the gut.

Retinol is actively accumulated in liver (as retinyl palmitate) during last trimester of pregnancy and breastfeeding. Postnatally, retinol is better absorbed than 3-carotene and transported in blood, bound to a retinolbinding protein.

Vitamin A is essential for — a) retinal functions i.e. regeneration of Rhodopsin — a chromoprotein, essential for night vision, b) maintenance of epithelial integrity with cellular regeneration (resistance to infections), and c) removal of toxic free-radicals from body (anti-oxidant).

Etiology Vitamin A deficiency is most common in toddlers and preschool children from low socio-economic status. Common causes of VAD include —

a) Dietary deficiency

b) Mal absorptive states e.g. chronic diarrhea, worm infestations etc.

c) Impaired metabolism e.g. in chronic liver disease

d) Reduced transport proteins e.g. in malnutrition, nephrotic syndrome etc.

e) Higher requirements in infections e.g. measles.

t) Less intrauterine stores e.g. in pre terms

g) Darner disease – a genetic defect (Vitamin A dependency)

Clinical manifestations of Vitamin A deficiency may be divided into two broad groups – ophthalmic (xerophthalmia) and extra-ophthalmic manifestations.

A) Xerophthalmia denotes a spectrum of ocular signs in Vitamin A deficiency including — Night blindness i.e. inability to see clearly in dim- light or slower dark-adaptation.

• Conjunctival Xerosis i.e. dry, wrinkled, lusterless, muddy conjunctiva due to cornified epithelium and Bitot’ spots – chalky gray triangular plaques, generally near the temporal limbus, due to heaped-up dry epithelium.

• Cortical lesions of variable severity Xerosis i.e. dull, dry and cloudy comea, Ulcers, limited to few layers of cornea, or keratomalcia i.e. liquefaction and rupture of full-depth cornea, leading to loss of vision. Even milder cases may lead to comeal scarring on recovery.

• Fundal changes e.g. retinal xerosis and detachment.

B) Extra-ocular manifestations include —

• Phrynoderma (Follicular hyperkeratosis), presenting as dry and scaly skin with toad-like texture, especially over extensor aspects of extremities e.g., dorsum of tibia, knees and elbows. Phrynoderma is also associated with essential fatty acid deficiency.

• Recurrent respiratory infections, due to squamous metaplasia of respiratory mucosa,

• Recurrent urinary tract infections, pancreatitis or parotitis due to epithelial metaplasia of urinary or exocrine tracts.

• Rarely, atrophy of genital epithelium may lead to reproductive dysfunction in adults.

Diagnosis of Vitamin A deficiency is largely clinical, though subclinical deficiency may be identified by —

a) Conjuctival impression cytology (dC), to detect loss of mucus-secreting goblet cells and epithelial metaplasia on special staining,

b) Dark-adaptation test, and

c) Low plasma carotene levels (<20 j.tgIL).

Treatment: As per WHO recommendation, Standard treatment of Vitamin A deficiency includes 3 doses of concentrated Vitamin A (1 lac lU/nil), given orally, on day 1, 2 and 14. In cases with mal absorption/persistent vomiting, IM therapy (strength: 50,000/mi) may be used, given as half of the oral dose with same schedule.

All cases treated for Vitamin A deficiency should receive dietary counseling and Vitamin A prophylaxis till 6-8 years of age (2 lac TU every 6 month) to prevent the recurrence.

Local ophthalmic treatment of corneal lesions, with antibiotics, mydriatics and eye-padding is equally important.

Prevention of Vitamin A deficiency includes nutritional counseling, Vitamin A supplements and prevention of precipitating illnesses e.g. measles.

National program for prevention of nutritional blindness due to it.

This program was launched in 1971 as a separate health program but later incorporated in child survival and safe motherhood or CSSM program (1992) and subsequently, in Reproduction & child health or RCH program (1997).

Objectives: To decrease the incidence of Vitamin A deficiency and subsequent blindness.

Beneficiary: Children from 6 months to 5 years. Components of this program include —

a) Regular prophylaxis with 6-monthly administration of Oral Vitamin A 1,00,000 IU (< 1 year) and 2,00,000 IU in older children; from 6 months to 5 years of age. This protocol was first developed by National institute of nutrition, Hyderabad and later adopted by WHO as global strategy.

Under RCH program, routine Vitamin A supplementation is limited to two doses, first with measles vaccine at 9 months and second with first DPT/OPV boosters at 15-18 months.

b) Additional doses of Vitamin A, after illnesses e.g. measles, severe PEM, chronic diarrhea and long febrile illnesses.

c) Dietary counseling, to encourage consumption of cheap and locally available Vitamin A rich foods

d) Prevention of precipitating illnesses e.g. measles by vaccination coverage and breast feeding promotion.

e) Periodic monitoring and evaluation

Note: In national program, Oral Vitamin A is supplied as multi-dose liquid preparation (1 lac lU/mi), with a special 2 ml spoon. Only this spoon should he used and not the regular 5 ml spoons, to avoid over dosage.

Hyper-vitaminosis A:

Being fat-soluble, excess Vitamin A is not readily excreted in urine and accumulates in tissues with following presentations —

a) Acute hypervitaminosis, due to acute preventive or therapeutic overdose (>3, 00,000 IU), presents as Pseudotumor cerebri i.e. transient, self-limiting, benign intracranial hypertension with headache, vomiting, drowsiness, bulging fontanels and/or papilledema. Exact mechanism is unknown, probably relates to massive rupture of lysosomal membranes.

b) Chronic hypervitaminosis due to prolonged Vitamin A deficiency therapy e.g. for acne, presents with – anorexia, weight loss, dry pruritic skin, alopecia, tender extremities (hyperostosis on X-ray), hepatosplenomegaly and pseudotumor cerebri.

c) Hypercarotenemia – asymptomatic, transient yellowish discoloration of skin/body fluids, due to excess consumption of (3-carotene containing fruits.

Massive Vitamin A deficiency administration in first trimester may also have severe teratogenic effects on fetus.

Salient features of some general nutritional programs are discussed here, while those against specific nutritional deficiencies have been discussed in relevant chapters.

Applied nutrition program in India (ANP) was also started in 1962, primarily to create self-reliance at community and family level.

Objectives of ANP are —

a) To promote local food production e.g. poultry, horticulture, kitchen garden etc.

b) To provide nutritional education

c) To provide supplementary nutrition to preschool children (3-6 years) and pregnant/lactating mothers.

Organization: Program is sponsored and implemented by state governments, with local Balsevika under supervision of block development officer as implementer in the field.

Activities: Applied Nutrition program in India is a community awareness program rather than supplementary nutrition program, with emphasis on promotion of agricultural/non-agricultural food production, increased consumption of low-cost, locally grown foods and create awareness about their nutritive values.

Although one of the best conceived nutritional program, it could not achieve desire results and currently continues to be a low-priority program.

Baiwadi nutrition program in India (1970-71) are implemented by voluntary organizations, with grant-in aid from social welfare ministry.

It aims to provide supplementary nutrition to rural pre-school children (3-6 years) along with pre-primary education, through Baiwadis – most peripheral center at village/community level.

Special nutrition program in India (1970-7 1), a state-sponsored program at present, is being gradually merged with ICDS. Primary objective of this program is provide supplementary nutrition and Vitamin A prophylaxis to pre-school children and supplementary nutrition and iron/folic acid supplementation to pregnant/lactating mothers, though a net work of Baiwadis.

Wheat-based supplementary nutrition program in India (1986), a jointly funded scheme by center & state with same objectives and beneficiary group as for special nutrition program, was initially started to cover nonICDS areas with one difference — use of subsidized wheat from public distribution system for supplementary nutrition. However, it is also being gradually incorporated under ICDS.

a) Infections

Common : ARI, Diarrhea, TB, helminthiasis

Severe Gram —ye sepsis, septic shock, DIC

Opportunistic Candidiasis

b) Hypothermia

c) Metabolic

Hypoglycemia

Hypocalcaemia

Hypomagnesemia

d) Fluid & electrolyte imbalance

Dehydration

Hypokalemia

Hypernatremia

e) Lactose intolerance

f) Severe anemia & other nutrient deficiencies

g) Congestive cardiac failure

Late (Recovery) complications:

a) Diarrhea (lactose intolerance)

b) CCF (high protein & solute diet)

c) Unmasking of subclinical vit/mineral deficiencies

d) Recovery syndromes (see text)

Long-term effects:

a) Growth retardation

b) Cognitive & learning disabilities

Hypomagnesemia, if present, should be treated with TM 50% magnesium sulfate (0.2 mllkg 12 hourly for 2-3 days).

Nutrient deficiencies: Iron-deficiency anemia due to poor dietary intake and/or co-parasitic infestations is common, which should be treated with oral iron therapy (1 mg/kg/d of elemental iron) along with deworming agents (P0 albendazole 400 mg, single dose). Blood transfusions, though necessary in severe cases, should be avoided in PEM due to risk of CCF and should not exceed 10 mI/kg of packed cells at one time.

Other necessary nutrient supplements in PEM include – single doses of Vitamin A (P0 50,000- 2,00,000 IU), Vitamin K (2.5 mg TM) and Mg SO4 (2 ml 50% sol TM) on admission and daily oral supplementation with folic acid (1 mg) and zinc (2 mg/kg), from first day onwards.

g) Congestive cardiac failure is not uncommon in kwashiorkor, due to impaired cardiac function, fluid overload, and sudden shift of edema fluid in intravascular compartment after blood/plasma transfusions. Diagnosis of CCF in an edematous child may be difficult, but absence of Weight loss despite reducing edema or presence of basal crepitations suggests this possibility. Digitalis therapy carries high risk of toxicity in PEM and hence in these cases, CCF should preferably managed with diuretics and supportive therapy, unless refractory.

Step II – Dietary management: Intensive and supervised dietary therapy needs to be started, soon after the control of complications.

For the sake of simplicity, dietary management may be divided into three steps calculation of nutritional requirements; selection of appropriate type, frequency and method of supplementation, and monitoring of nutritional intake.

a) Calculation of nutritional requirements: Dietary requirements in PEM are relatively higher than in well-nourished children due to additional needs for catch-up growth and replenishment of stores. However, most of them are anorexic or cannot tolerate higher intake due to mal absorption e.g. lactose intolerance. Cases with kwashiorkor also carry risk of CCF if treated with high protein diet since beginning. Hence, it is advisable to begin the dietary therapy with minimum essential intake i.e. 100 cal/kg and 2 gm/kg of proteins according to actual weight and increase by 10-20% every alternate day, till the final aim is achieved (Table 6.11).

b) Selection of appropriate feeds, frequency & mode of administration: Diet plan in PEM cannot be generalized and needs to be tailored in each case. Depending on the age, severity, acceptance and economic feasibility, early dietary therapy may be provided with — i) regular home-made diet in higher quantity and better quality (in mild to moderate PEM), ii) regular home diet, supplemented by high- energy feeds, or iii) therapeutic diets in initial phase, followed by gradual shift to home diet.

Some noteworthy principles of early dietary therapy are as follows —

• Diet should be age-appropriate, acceptable and closely resemble the home diet

• It should be energy-dense i.e. high caloric value with low-bulk. Caloric content and palatability may be improved by adding edible oil or animal- fats e.g. ghee, butter etc. Coconut oil is excellent source of extra calories and being a medium-chain triglyceride, absorbed directly without emulsification. Upto 10-15% of total calories may be given as visible fat in PEM.

• It is preferable to use high biological value proteins e.g. eggs. Protein content in vegetarian diet may be increased by using Soya-bean or ground-nut preparations.

• High-carbohydrate diet should be avoided in early stages, due to frequent lactose-intolerance in severe PEM.

• In anorexic patients, nasogastric feeding with relatively liquid diets e.g. enriched milk may be used initially followed by gradually thickening.

• Feeds should be given more frequently and in smaller aliquots, to improve acceptability. Breast feeding should be continued, if possible, even in older children as a source of additional energy.

• Feeds must be prepared hygienically, involving parents in the selection/preparation of therapeutic diets to improve their nutritional awareness.

• Dietary practices and cultural beliefs e.g. regarding consumption of eggs or non-vegetarian diet should be respected to improve acceptability.

Amylase rich foods (ARF) are easily digestible and enriched sources of proteins and vitamins, prepared by soaking common cereals or pulses in water for 12 hours > sprouting by wrapping in a moist cloth for 48 hours, > drying > roasting> grueling to make porridge. On soaking, the amylase breaks down grain-starch into easily-digestible maltodextrins, reducing the viscosity and bulk of diet. Germination also enhances vitamin content.

c) Monitoring: During dietary therapy, all cases should be closely monitored for dietary intake, signs of recovery, and recovery phase complications.

Common complications in recovery phase are —

a) Diarrhea due to relative lactase deficiency and other mal absorptive states, precipitated by increased nutritional intake,

b) Congestive cardiac failure due to shift of edema fluid in intravascular compartment, following high solute & protein diet,

c) Un-masking of subclinical vitamin & mineral deficiencies e.g. scurvy, zinc deficiency, due to disturbed adaptation.

Two well-defined clinical syndromes seen during the recovery phase are Kahn ‘.c and Gomez recovery syndromes, probably caused by unmasking of subclinical nutrient deficiencies.

Kahn’s recovery syndrome is characterized by sudden onset of tremors and encephalopathy, probably due to unmasked deficiency of gamma aminobutyic acid (GABA) – a major neuro-inhibitor.

Gomez recovery syndrome is characterized by progressive abdominal distension, ascites, hepatomegaly and diarrhea, due to secondary malabsurption and dyselectrolytemia e.g. hypokalemia.

Step III – Consolidation phase begins after 1-2 weeks of intensive dietary therapy and aims to maintain nutritional gains and prepare for discharge. Important steps in this phase include —

a) Gradual shift from therapeutic to home-diet,

b) Continued vitamin/mineral supplementation,

c) Completion of age-appropriate immunization,

d) Nutritional counseling to parents,

e) Evaluation of home environment,

f) Continuous growth monitoring.

Ideally, all PEMs need close supervision till complete recovery, defined as achievement of ideal Weight for Height, which nzay take 6-8 weeks. However, as to wait fill complete recovery in overcrowded hospitals is neither possible nor desirable, fulfillment of a discharge criteria should be adhered, to prevent the recurrence.

Prevention: Malnutrition is more of a socio-economic problem, rather than medical disease. A comprehensive approach is required, especially in developing countries to overcome it. Important preventive steps against PEM include —

I. Promotion of general health and nutrition

A) Actions at family level to promote:

• Correct Breast feeding & weaning practices

• Consumption of cheap, local, nutritive foods

• Correct cooking practices

• Avoidance of wrong food taboos & habits

• Equitable food distribution in the family

• Setting of kitchen gardens/poultry keeping

• Correct feeding practices during illnesses

• Nutrition in pregnant/lactating mothers

• General child health/hygiene,

Family planning practices

B) Action at community level:

• Nutritional surveillance

• Nutritional education

• Development of local low-cost foods

• General measures to improve child health e.g.

- Improved water supply and sanitation

— Widespread immunization services

— Preventive/curative health-care facilities

• Creation of local-job opportunities

C) Action at national level to promote:

• Agricultural production

• Food-storage facilities & public distribution

• General rural/urban-slum development

• Poverty-alleviation measures,

• Food-subsidies to high-risk population

• Targeted health and nutritional programs

D) Action at International level:

• International aid to stimulate socioeconomic development in developing countries.

• World food program (1963), to meet food requirements in needy countries.

• International cooperation during emergencies e.g. natural disasters and wars

U) Specific protection to high-risk children:

• Nutritional surveillance in pre-school children

• Nutritional supplementation/food fortification

• Periodic deworming & iron supplements etc.

• Immunization to control infections

III) Early diagnosis and management:

• Growth monitoring of under-5 children

• Nutritional assessment at all contact points

• Early diagnosis & management of PEM

• Early diagnosis & treatment of infections

IV) Follow-up and rehabilitation:

• Nutritional rehabilitation centers/services

• Follow-up of recovered cases