Therapeutic Pediatric Nutrition Madhu Sharma
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Protein Energy MalnutritionChapter 1

The health and well-being of any individual is based on a combination of various factors. Besides diet and good nutrition, a host of contributory factors go a long way in preventing disease and malnutrition. These may be environmental, sociodemographic, immunization programs, provision of clean water supply and even psychosocial.
Environmental factors include parental education, socioeconomic status, living standards and child rearing practices.
Sociodemographic factors include breastfeeding practices, diet during illness for mother and child, maternal malnutrition, low birth weight babies, recurrent infections, etc.
According to WHO defnition, malnutrition involves a cellular imbalance between supply of nutrients and energy and the body's demand for them to ensure normal growth maintenance and specific tissue functions. Malnutrition accounts for more than 50 percent of all infant mortality in developing countries, especially in the below 5 year's age group.
The most common form of malnutrition in children is protein energy malnutrition (PEM), which earlier was also called protein calorie malnutrition (PCM). It has also been defned as a pathological state characterized by inadequate intake of proteins and calories in varying degrees commonly associated with infections.1 Children between 6–36 months old are generally at high risk of falling prey to this condition, since they are more vulnerable to infections, especially gastrointestinal and measles. Death rates are high among children with untreated PEM, and the risk of dying increase with severity of the condition. Electrolyte imbalance, hypothermia and complicating infections are some of the causes of mortality in these children.
Causes of PEM: PEM occurs primarily due to food deprivation, but other factors play a major role also. These can be discussed as:
  • Low birth weight and infections: Recurrent diarrhea, acute respiratory infections, other preventable infections like measles, tuberculosis, whooping cough and helminthes, can aggravate and complicate a pre-existing condition of low birth weight. Again maternal malnutrition is an important cause of low birth weight.
    2
  • Food deprivation: Poverty is one important cause of food deprivation in small children. Large families contribute to this problem and the priority of food distribution generally is for the male child followed by other male members in the family.
  • Food taboos and myths: Even where resources are not a limiting factor, very often self-imposed restrictions regarding intake of food, can affect provision of adequate nutrients to the child. Food fads and myths related to consumption of specific type of foods at different phases of pregnancy or lactation and subsequently weaning practices can be a sole cause of food deprivation. Very often these fads and myths are interlinked with various cultural beliefs and/or religious beliefs. A common observation made is pertaining to infant feeding practices, where, in most rural classes colostrums is discarded as it is considered poisonous for the baby. The maternal diet is also restricted keeping in mind ‘hot’ or ‘cold’ foods which may be ‘unsuitable for the infant. All such practices can go a long way to adversely affect the availability of essential macro and micronutrients required for adequate growth and development of the child.
  • Ignorance: Many rural and urban mothers are quite ignorant of their infant's need for adequate nutrition. It's a common belief that milk is the ‘best and only’ food for a child, even after he has crossed the first 6 months of his life. They continue to breastfeed exclusively, well up to 12–24 months, making little effort to offer cereal supplements. Alternatively, if breast milk is inadequate, they will continue to feed diluted milk without introducing cereals. Even during illness of the child, solid food is withheld and the baby is kept on undiluted milk or tea with an occasional biscuit or so. Cereal, pulse base foods are considered ‘heavy’ for the child's liver. These factors further contribute to inadequate nutrient intake and subsequently growth failure.
 
PATHOGENESIS OF PEM
Gopalan in 1968 introduced a new hypothesis, that of ‘adaptation’.2 This was termed as ‘dysadaptation’, stating that kwashiorkor in fact was a failure of adaptation. This was explained on biochemical and hormonal factors. The malnourished child adapts himself to the unfavorable circumstances and to the calorie and protein gap. They reduce their activity, curtail their growth thereby bringing down the basal metabolic rate (BMR) and thus save energy for survival. This reduction in BMR and lack of insulating fat leads to hypothermia which may prove fatal.23
The basic adaptation to explain the mechanism was that the gradual wasting of muscle and subcutaneous fat would also protect certain other metabolic processes. Like, the essential amino acids are made available, which it was assumed, would enable the liver to maintain the synthesis of components essential for homeostasis, like serum albumin and β-lipoprotein. This could explain the absence of edema or fatty liver in marasmus.3
The high level of catabolic hormones including cortisol causes muscle and fat breakdown. The anabolic hormones like insulin and insulin like growth factors maintain near normal anabolism to prevent edema and fatty liver by enabling the synthesis of albumin and β-lipoproteins from the available pool of amino acids.
Another theory postulated in the pathogenesis of PEM is that of free radicals which are assumed to play a role in edema, skin changes and fatty liver. The free oxygen radicals which are toxic to cell membranes are produced during infections. In the malnourished child, defciency of nutrients like vitamins A, C and E and selenium which are antioxidants can result in the accumulation of toxic free oxygen radicals. These further damage the liver cells resulting in kwashiorkor.
 
CLASSIFICATION OF PEM
Various parameters are used to classify PEM like, weight for age, height for age or weight for height. The most widely used accepted criterion is the weight for age. This has been done by various workers of different times. The most widely used are the Gomez classifcation and the Indian Academy of Pediatrics (IAP) classifcation4,5 as given in Tables 1.1 and 1.2.
Other classifcations used are by Jellife in 1965 and Wellcome in 1970 (Tables 1.3 and 1.4)
Jelliffe's Classifcation: Proposed in 1965, it has been categorized into 4 classes as shown in Table 1.3.6
Wellcome Trust or International Classifcation: This is based on clinical assessment as suggested by Wellcome Trust in 1970. Besides weight for age, it also considers presence or absence of edema as seen in Table 1.4.7
 
SPECTRUM OF PEM
There are three forms of PEM recognized, based on the clinical presentations:4
Table 1.1   The Gomez classification
% Expected
Classification
Category of Nutritional Status Wt. for age
>90%
Normal
Normal
76–90
Mild malnutrition
1st degree malnutrition
61–75
Moderate malnutrition
2nd degree malnutrition
< 60
Severe malnutrition
3rd degree malnutrition
Table 1.2   The IAP classification
% of Expected Weight (Wt. for age)
Nutritional Classification*
>80%
Normal
71–80
Grade 1
61–70
Grade 2
51–50
Grade 3 (severe malnutrition)
< 50
Grade 4 (severe malnutrition)
*If coexisting edema of nutritional origin, the letter K is suffixed along with grade of nutrition to denote kwashiorkor
Table 1.3   Jelliffe's classification of PEM
Nutritional Status (PEM)
Wt. for age (Harvard) % of expected
Normal
>90
First degree
80–90
Second degree
70–80
Third degree
60–70
Fourth degree
<60
Table 1.4   Wellcome Trust classification
Weight for age (Boston) % of expected
Edema
Clinical type of PEM
60–80
+
Kwashiorkor
60–80
Underweight
< 60
Marasmus
< 60
+
Marasmic Kwashiorkor
  • Kwashiorkor
  • Marasmus
  • Marasmic Kwashiorkor
A picture of the various features of PEM can be had from Table 1.5
 
Kwashiorkor
The word ‘kwashiorkor’ was first described by Dr. Cicely Williams in 1933.5
Table 1.5   Clinical features of PEM
Spectrum
Clinical symptoms
Always present
Sometimes present
Marasmus
Wasting
Hunger, Wizened appearance
Kwashiorkor
Edema
Mental changes: irritability, poor appetite
Skin Changes: flaky paint dermatosis
Hair: sparse, loose, straight
Marasmic Kwashiorkor
Wasting+Edema
Any of the above symptoms and signs
The word originates from the African language- Ga of Ghana, meaning the ‘red boy’ due to the characteristic pigmentation. Other workers from the West Indies described this as ‘sugar baby’ due to the characteristic ‘prominent cheeks’ and edema. This defciency is known to occur with the coming of the second sib, when the child is displaced from the breast by another child. This condition is seen mostly in children in their second year of life, following abrupt weaning. They appear to be apathetic, irritable, weak and inactive, with the presence of edema and fatty liver. The edema is detected by the production of a defnite pit on exerting moderate pressure for 3 seconds with the thumb over the lower end of the tibia and dorsum of the foot.
Initially, parents may miss these features and on the contrary be satisfied by the false image of a ‘fatty child’ But what is not generally realized by the lay person is that this fat appears typically on the belly and is commonly referred to as ‘pot belly’, but from his buttocks would be fat and give a wasted appearance (Figs 1.1A and B).
The typical signs of PEM are described by the following associated abnormalities:
  • Body: All body parts, especially buttocks, arms and legs have decreased subcutaneous fat layer.
  • Skin: The skin appears dry and faky (faky paint dermatosis). Hyper-pigmented plaques may be visible over areas of trauma.
  • Hair: It becomes thin, sparse and brittle. It also turns dull brown or red, giving an appearance of a ‘fag sign’.
  • Nails: There will be fssures or ridges and increased fragility.
  • Abdomen: The presence of edema due to accumulation of ascetic fuid and also hepatomegaly (fatty liver), makes the abdomen appear distended.
  • Mouth: Signs of vitamin B group defciency-cheilosis, angular stomatitis and papillary atrophy are commonly present.
  • Behavior: The child neither appears irritable and avoids social interaction, nor responds socially. They have a poor appetite and refuse to eat.
6
zoom view
Fig. 1.1A: Child with sparse hair
zoom view
Fig. 1.1B: Child with pot belly
  • Defciencies: It is common to observe defciency signs of vitamins, like, vitamin A, D and B group and minerals like iron and iodine.
 
MARASMUS
The term marasmus is derived from the Greek ‘marasmos’ which means wasting. In this condition, there is gross wasting of muscle and sub cutaneous tissues, marked stunting but no edema. This picture can be seen in early infancy unlike in kwashiorkor (Fig. 1.2).
The marasmic condition is typical of sequel to prolonged starvation, chronic or recurrent infections and limited food intake.7
zoom view
Fig. 1.2: Marasmic child
Marasmus represents an adaptive response to starvation, unlike kwashiorkor which represents maladaptive response to starvation. In marasmus, the body utilizes all fat stores before using muscles. It is commonly seen in the first year of life due to lack of breastfeeding and the use of diluted animal milk. Poverty or famine like conditions and presence of diarrhea besides ignorance and poor maternal nutrition, are the precipitating factors. There is severe wasting of the shoulders, arms, buttocks and thighs with no visible rib outlines. The typical appearance of a marasmic child is described as:
  • A ‘thin old’ man.
  • Baggy pants (the loose skin of the buttocks hanging down)
  • Child may be alert despite his condition.
  • Absence of edema on the lower extremities.
  • Prominent ribs.
  • Large head with sunken eyes.
  • A hungry child.
  • Associated diarrhea or dehydration
In marasmus there is a marked defcit of weight but not as much in height. The marasmic infant has a good appetite but may also appear irritable, fretful and apathetic as in cases of kwashiorkor. Though the skin might appear dry, the typical characteristic peeling or patchy hypo-pigmentation may not be there.
It is worth mentioning here that during the past decade or so, the profle of PEM presenting in our hospitals has gradually changed. Frank cases of kwashiorkor are rarely encountered, but the marasmic type of picture is frequently observed. The prevalence of clinical form of 8malnutrition has been reduced to less than 1 percent. Hospital statistics also show that in recent years, admissions due to severe PEM have come down significantly.8
 
MARASMIC KWASHIORKOR
This condition is intermediary between marasmus and kwashiorkor, since such children present with a mixed picture. The body weight is less than 60 percent of the expected along with the presence of edema. The degree of stunting seems greater in marasmic kwashiorkor, indicating that duration of illness in this condition is greater than in kwashiorkor.
 
MANAGEMENT OF PEM
Treatment of severe malnutrition is a challenging task and involves mul-tipronged approach. Most of the cases of severe malnutrition are not without complications on presentation. Severe infection is one major complication to be tackled. Management of these children involves hospitalization in majority of the cases. Noncomplicated cases can be managed on outpatient basis in a hospital or any primary health care center. But children presenting with complications can be managed in a hospital setting alone. Initial approach involves treating the complications first which may be:
 
Resuscitation
This involves tackling the life threatening medical emergencies on priority, which may include:
  1. Hypothermia/Hypoglycemia: These are generally found together.
    The child is managed by keeping him warm and ‘bedding in’ with the mother is encouraged. Feeding if possible may be initiated. For hypoglycemia, the child is put on IV glucose10 percent, if immediate feeding is not possible. Child is treated for sepsis.
  2. Infections: Infections are a major cause of mortality in PEM. Appropriate antibiotic therapy is initiated.
  3. Anemia: If not managed appropriately, severe anemia may lead to heart failure. If required blood transfusion is resorted to.
 
Dehydration/Electrolyte Imbalance
Most often such children present with diarrhea. Depending upon the severity of stooling, ORS should be initiated. In moderate dehydration 70–100 ml/Kg ORS in 4 hours is given by sips. In severe dehydration, 100 ml/Kg normal saline or ringer lactate is given over 3–6 hours. 9Mostly hypokalemia is present which can be managed by potassium supplement.
 
Congestive Heart Failure
In case of presence of heart failure, fuid intake is restricted and kept on maintenance dose. Diuretics may be given to prevent fuid overload.
 
Vitamin Deficiencies
Defciency of vitamins is a common feature among children with PEM. Vitamin A can be supplemented in all cases. Vitamin K also is given to those with forid PEM and accompanied by diarrhea. All B complex vitamins, vitamin C, E and D too are administered along with calcium and zinc. Magnesium also needs to be supplemented if seizures, tetany or apathy are present.
 
Dietary Management
Different workers have laid down special formulae for achieving high energy intakes and to fulfill protein requirements for maximum catch-up growth rates.
The general pattern followed by them was of providing first class protein, in the form of milk protein powder, oil for energy along with sugar for favor as well as extra energy. Oil is used to increase the density of the feed without increasing the bulk. Medium chain triglycerides are more desirable to enhance absorption and metabolism.
Almost all workers advocated regimens providing calories of around 150–200 per kg/d for maximum catch up growth. The protein requirements have been suggested around 3–4 g/Kg/d. But certain workers preferred to maintain calories at around 100 cal/kg/d initially and gradually increased over a week till the full volume is tolerated. This is specially so in children with kwashiorkor until the edema disappeared.
WHO in 1999,9 laid down guidelines for routine treatment of severe malnutrition where the nutrition component was also stressed as follows:
 
Stabilization Phase—Initiate Refeeding
Feeding should be initiated gradually as soon as possible after admission. It should be formulated to provide just suffcient calories and proteins to maintain basic physiological functions. The main features include:
  • Small frequent feeds of low osmalarity (<350) mOsm/L and low lactose (<2–3g/Kg/d)
  • Oral or nasogastric feeds
    10
  • 100 cal./Kg/d-(not to exceed in initial phase)
  • 1.0–1.5 gprot./Kg/d
  • 130 ml/Kg/d of liquid (may begin with 100 ml/Kg/d if edema present)
  • Feed should be of low viscosity, easy to prepare and socially acceptable.
  • Continue breastfeeding if already doing so.
The above regimen is achieved using the F75 formula which is designed to provide 75 cals./100 ml and 0.9 g protein per 100 ml of the feed (Table 1.6). These should be fed by cup and spoon. The recommended schedule suggested is as shown in Table 1.7.
For children with good appetite, without edema, the schedule can be completed in 2–3 days. Careful monitoring should be done for:
  • Amounts offered and left over
  • Vomiting
  • Stool frequency and consistency
  • Daily body weight.
There may be accompanying diarrhea in some children, in which case milk based feeds can be replaced with soya based or any lactose free feeds till such time the stools settle down. Gradually low lactose feeds like curd may be initiated, and if tolerated, the amounts increased, and even milk based cereal feeds can be initiated.
In both types of PEM, basal energy expenditure increases gradually during refeeding. As the child loses weight, total body water as percentage of body weight increases and the child becomes relatively over hydrated. In children with edema, initiation of nutritional recovery is characterized by a progressive loss of extracellular fuid resulting in an initial loss of weight, followed by stabilization for 10–12 days and again followed by weight gain10
Methods of feeding should be ideally from a cup and spoon along with continuation of breastfeeds. Even when breastfeeds are inadequate, non nutritive sucking should be encouraged which itself can enhance lactation. In case oral feeds are difficult to achieve, tubefeeding can be resorted to for a few days till such time oral feeding is restored adequately.
A weight gain of 0.5 Kg/week in children and 70 gms/week in infants is the goal. With recurrent infections this goal may be difficult; therefore control of infections is very important.
 
Catch-up Growth
This is the rehabilitation phase, when the appetite of the child is restored within 8–10 days, return of social smile and the child begins to take interest in the surroundings.11
Table 1.6   Recipes and composition of starter formulae and catch-up formula
Ingredients
Starer formula(F75)
Starer formula with cereal (F75)
Catch-up formula (F100)
Dried skim milk (g)
25
25
80
Sugar (g)
100
70
50
Cereal flour (g)
35
Vegetable oil (ml)
27
27
60
Electrolyte mineral solution (ml)
20
20
20
Water: to make up to final soln. (ml)
1000
1000
1000
Contents per 100 ml
Calories (kcal)
75
75
100
Protein (g)
0.9
1.1
2.9
Lactose (g)
1.3
1.3
4.2
Potassium (mmol)
4.0
4.2
6.3
Sodium (mmol)
0.6
0.6
1.9
Magnesium (mmol)
0.43
0.46
0.73
Zinc (mg)
2.0
2.0
2.3
Copper (mg)
0.25
0.25
0.25
Percent energy from protein
5
6
12
Percent energy from fat
32
32
53
Osmolality (mOsm/l)
413
334
419
(WHO, 2000).
Table 1.7   Feeding schedule for children with severe malnutrition
Days
Frequency (hrly)
Vol./Kg/feed (ml)
Vol./Kg/d (ml)
1–2
2
11
130
3–5
3
16
130
6–7+
4
22
130
These are the first signs of recovery in a child with PEM. The increase in the feeds should be done gradually at this point to avoid risk of heart failure. To achieve the catch up growth the transition made is as follows:
  • Replace F75 by F100 which contains 100 cal. and 2.9 g protein per 100 ml. This can be achieved by incorporating oil and sugar with milk or using milk cereal based preparations.
  • Subsequently, the feeds are increased by 10–20 ml and finally 25–30 ml/Kg/feed. This can provide up till 200 cal./Kg/d.
    12
  • Monitoring for respiration and pulse rates are done regularly. The volume of feeds needs to be decreased as also the frequency (4 hourly) in case increase in respiration is observed. Once stabilized:
  • Increased amounts of F100 formula at least 3–4 hourly can be started
  • Calories given—150–200 kg/d
  • Proteins increased—4–6 g/kg/d
  • Continue breastfeeding
  • Ensure administration of 6 monthly vitamin A dose.
The Indian Academy of Pediatrics in 2006 formed a working committee to bring out a revised consensus on the management of severely malnourished children in the Indian context,11 which were adapted from the WHO guidelines of 2000 mentioned earlier. These guidelines are based on the hospital management of such children.
The modified formulae recommended for F75 and the catch-up formula F100 are as given in Tables 1.8 and 1.9 respectively.
Table 1.8   Starter diets F75
Diet contents (per 100 ml)
F75 starter
F75 cereal based-(1)
F75 Cereal based-(2)
Cow's milk (ml)
30
30
25
Sugar (g)
9
6
3
Cereal puffed rice (g)
2.5
6
Veget. Oil (ml)
2
2.5
3
Water- to make up to 100 ml
100
100
100
Calories (Kcal)
75
75
75
Proteins (g)
0.9
1.1
1.2
Lactose (g)
1.2
1.2
1.2
• Egg white can be replaced by 3 g of chicken or commercially available casein.
• Powdered puffed rice can be replaced by commercial rice or precooked rice amounts)
Table 1.9   Catch-up diets F100
Diets contents (per 100 mL)
F100 catch-up
F-100 catch-up (cereal based) Example 1
Cow's milk/toned dairy milk (ml)
95
75
Sugar (g)
5
2.5
Cereal: Puffed rice (g)
7
Vegetable oil (g)
2
2
Water to make (mL)
101
100
Energy (kcal)
100
100
Protein (g)
2.9
2.9
Lactose (g)
3.8
3
Source: IAP, 2006.11
13
Table 1.10   Starter lactose free diet
Egg white *(g)
5
Glucose (g)
3.5
Cereal flour: Powdered puffed rice** (g)
7
Vegetable oil (g)
4
Water to make (mL)
100
Energy (kcal)
75
Protein (g)
1
Lactose
*Egg white may be replaced by 3 g of chicken or commercially available pure protein like casein.
**Powdered puffed rice may be replaced by commercial precooked rice preparations (in same amounts).
(Source: IAP, 2006).
Table 1.11   Catch-up lactose free diet
Egg white *(g)
20
Glucose or sugar (g)
4
Cereal Flour: Puffed rice** (g)
12
Vegetable oil (g)
4
Water to make (mL)
100
Energy (kcal)
100
Protein (g)
3
Lactose (g)
*Egg white may be replaced by 3 g of chicken or commercially available pure protein like casein.
**Powdered puffed rice may be replaced by commercial precooked rice preparations (in same amounts).
(Source: IAP, 2006).
The cereal-based low lactose (lower osmolarity) diets are recommended as starter diets for those with persistent diarrhea.12 Lactose free diets are rarely needed for persistent diarrhea as most children do well on the above-mentioned, low lactose F75 diets. Children with persistent diarrhea, who continue to have diarrhea on the low lactose diets, should be given lactose (milk) free starter diets, as shown in Table 1.10.13. They can be followed on to lactose free catch-up diets as shown in Table 1.11
The low lactose catch up diets F100, can be started at the rehabilitation phase as shown in Table 1.12.
Complementary foods should be added as soon as possible to prepare the child for home foods at discharge. They should have comparable energy and protein concentrations once the catch-up diets are well tolerated. Khichri, dalia, banana, curd-rice and other culturally acceptable and locally available diets can also be offered liberally.14
Table 1.12   Low lactose catch-up diets (F100)
Catch-up low lactose diets
Example 1
Example 2
Milk (cow's milk or toned dairy milk)
25 ml
25ml
Egg white *(g)
12
Roasted powdered groundnut
5 g
Vegetable oil (g)
4
Cereal flour: Powdered puffed rice** (g)
12
12
Energy (kcal]
100
100
Protein (g]
2.9
2.9
Lactose (g)
1
1
*Egg white may be replaced by 3 g of chicken or commercially available pure protein like casein.
**Powdered puffed rice may be replaced by commercial precooked rice preparations (in same amounts). Jaggery could be used instead of glucose/sugar.
(Source: IAP, 2006).
Nutrition recovery syndrome is a condition encountered generally during the rehabilitation phase of a child with severe PEM. It is marked by heptomegaly, gynacomastia, abdominal distension, ascites, splenomegaly, etc. This is attributed to sudden increase in energy and protein intake by these children. It is mostly self-limiting and might also be associated with tremors (kwashi shake) during treatment. Protein restriction during this period was generally advocated. But recently it has also been thought to result of excess hormones secreted during recovery phase.14
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  1. 15 Fernando E. Viteri. Protein Energy Malnutrition; In: Textbook of Pediatric Nutrition, (Ed). Suskind RM, Raven Press  New York,  1981;189–213.
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