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What is PEM (Protein energy malnutrition) and its causes

Protein energy malnutrition (PEM) is the commonest health problem in preschool children of developing countries, associated with significant morbidity and mortality. Children are more vulnerable to Protein energy malnutrition due to relatively higher caloric and protein requirements for growth and physical activity. Even subclinical under nutrition in this age group may lead to long-term growth and developmental problems.

WHO defines Protein energy malnutrition as “a range of pathological conditions arising from the coincidental lack in varying proportions of proteins and calories, occurring more frequently in infants and children and commonly associated with infection.” This term includes both – the wasting (predominant weight deficit) as well as the stunting (predominant height deficit).

Prevalence

Although rarely a presenting illness, Protein energy malnutrition is an underlying problem in 50% of childhood morbidity. Reported prevalence of Protein energy malnutrition differs in various nutritional surveys, due to differences in the diagnostic criteria. Recent information indicates that —

• Current prevalence of under nutrition children is 40%, while wasting and stunting is present in 23% and 45%, respectively (NFHS III 2006).

• Prolonged under nutrition i.e. stunting is more common than acute Protein energy malnutrition i.e. wasting.

• While the incidence of severe Protein energy malnutrition has declined in recent years, mild/moderate PEM continues to be widely prevalent.

Ecology: Malnutrition is a result of complex interplay between inadequate dietary intake, due to various dietary, socio-economic and cultural factors and b) increased nutritional requirements, due to infections or illnesses. Common etiological factors, associated with Protein energy malnutrition include —

a) Child-related factors:

• Low birth weight

• Absence or early cessation of breast feeding

• Delayed weaning

• Incorrect dietary habits e.g. food fads.

• Recurrent/persistent infections e.g. diarrhea, respiratory infections, measles, helminthiasis, etc.

b) Maternal Factors:

• Lactation failure

• Maternal malnutrition/illnesses

• Ignorance about child-feeding practices • Inappropriate agricultural practices, production and distribution of food grains.

• Generalized economic depression.

• Inadequate primary health care.

Pathogenesis

Protein energy malnutrition represents a gap between nutritional requirements and dietary intake of the child, though actual pathophysiology is much complex. It is not yet clear, why some malnourished children present differently from others (marasmus vs. kwashiorkor)? Various theories have been suggested to explain different clinical presentations in Protein energy malnutrition, as follows —

a) Dietary theory explains these differences on the basis of relative deficiency of calories and proteins in diet. Accordingly, predominant caloric deprivation leads to marasmus while kwashiorkor indicates primary protein deficiency. However, no significant differences between protein or caloric contents of diets in children with marasmus and kwashiorkor have been consistently found.

b) Duration theory: Duration of nutritional deprivation has significant impact on the clinical spectrum of Protein energy malnutrition, as shown in Viteri‘s triangle. Children with gradual nutritional deprivation e.g. delayed weaning, tend to develop marasmus while those with sudden insult e.g. early cessation of breast feeding or intercurrent infections, are prone for kwashiorkor.

Effect of duration on Protein energy malnutrition (Viterik Triangle)

c) Gopalan theory of adaptation is based on the success of compensatory mechanisms in nutritionally deprived child. During early stages of widening intake- requirement gap, the body tries to adapt by —

i) Curtailing energy expenditure by reduced physical activity and growth,

ii) Efficient utilization of available calories by enhanced glucose uptake by cells, and

iii) Utilizing endogenous stores e.g. muscle proteins and subcutaneous fat via neoglucogenesis.

However, these adaptive mechanisms involve many metabolic and hormonal changes and their success depends on the availability of enough time and endogenous resources for compensation. Children with gradual nutritional deprivation tend to adapt better and develop marasmus-like illness with growth failure, muscle wasting and loss of subcutaneous tissue. Lack of urgency for endogenous catabolism as well as limited muscle mass and hepatic stores in these cases prevent development of edema and hepatomegaly.

In children with sudden nutritional deprivation, less time is available to adjust for lower energy intake, necessitating rapid mobilization of endogenous stores (neoglucogenesis), leading to kwashiorkor-like features with edema (due to protein utilization) and fatty hepatomegaly (due to lipolysis).

d) Role of infections: Infections and nutrition are closely linked to each other and infections e.g. diarrhea, ART or measles, are common preceding events for manifest Protein energy malnutrition in sub clinically undernourished children, due to sudden widening of demand-supply gap. Kwashiorkor is relatively more common in infection-precipitated Protein energy malnutrition than marasmus, due to inadequate adaptation.

e) Golden theory of free radicals attempts to explain edema and other changes in kwashiorkor, due to cell injury and increased cellular permeability following excess accumulation of free-radicals.

• Separation e.g. dead, single or working mother

c) Socio-economic factors: Poverty and unemployment, Large family size, Unhygienic living conditions, Inequitable food distribution in family, with mothers and infants being last priority, Disadvantaged children e.g. girls, orphans, etc.

d) Cultural factors: Wrong beliefs/superstitions e.g. colostrums is harmful, certain hot/cold foods to be avoided in children, milk aggravates diarrhea etc.; Wrong customs e.g. delayed weaning for religious ceremonies (annaprashan).

• Wrong cooking practices e.g. peeling of vegetables before cooking, use of polished food, draining away the water after cooking etc.

e) Community factors:

• Natural/man-made disasters with food shortage e.g. famines, wars, civil unrests.

Presence of infections may be clinically masked in Protein energy malnutrition due to poor inflammatory responses e.g. fever and leukocytosis. Hypothermia is an important indicator of infection in these children.

Diarrhea in PEM may also result from mal absorption due to intestinal villous atrophy and consequent lactase deficiency, as well as due to hepatic/pancreatic dysfunction.

Diagnosis

Protein energy malnutrition involves assessment of dietary intake, assessment of nutritional status, classification of severity, and identification of complications.

I) Assessment of dietary intake is the first step in screening for Protein energy malnutrition by —

• Dietary recall, the most frequently used method that involves detailed dietary history, including average daily intake in last few days before illness.

• Diary method by asking parents to keep a written record of the exact quantity of food items consumed by the child, for about a week followed by calculation of average daily caloric & protein intake.

• Replicate diet method is the most precise but complex method, mainly used for research purpose. Parents are asked to keep aside exact replica of food items, consumed by the child over a period. Later, investigators weigh these items, calculate dietary value and assess the precise intake.

II) Assessment of nutritional status is based on many anthropometric, morphological and biochemical parameters, discussed as follow —

a) Anthropometric parameters may be broadly divided into — i) age-dependent parameters ii) age-independent parameters and iii) Mass-screening parameters.

Age-dependent parameters are simple and most practical indicators of Protein energy malnutrition, when compared with reference norms for corresponding age. In practice, two parameters are most informative Weight (Wt) – an indicator of the severity of malnutrition as well as of nutritional recovery, and Height (Ht) – an indicator of the duration of malnutrition.

Age-independent parameters are useful when the exact chronological age of child is in doubt. These parameters are derived by comparing the relationship between two age-related parameters — one early indicator e.g. Weight or Mid-arm circumference (MAC) and other late indicator e.g. Height or Head circumference.

Weight for Height and Kanawati index are two commonly used age-independent indicators of Protein energy malnutrition. However, Weight for Height may be misleading in chronic cases due to proportionate fall in Weight as well as Height.

• Screening parameters are simple, inexpensive tools for mass nutritional surveillance of preschool children by paramedical workers. These tools are mainly based on MAC, which is fairly consistent between 1-5 years of age (16-18 cm), due to replacement of body fat with muscle mass. MAC of< 13.5cm and 12.5cm in this age group indicate malnutrition and severe malnutrition respectively (misleading in kwashiorkor due to edema).

Commonly used screening tests in India include —

a) Shakir’s tape is a special plastic tape with three color zones – green, yellow and red, each representing MAC of >13.5 cm, 12.5-

b) Morphological parameters are of limited value for diagnosis of Protein energy malnutrition and include —

• Hair changes e.g. — a) smaller diameter of hair root-bulbs (<11 mm), b) reduced proportion of anagens i.e. growing hair root-bulbs (<50%) and c) reduced anagen: telogen (resting hair root- bulbs) ratio.

• Buccal mucosal changes e.g. – increased proportion of broken or mutilated cells (>50%) in buccal smear, than in well-nourished children (5-10%).

c) Biochemical parameters are mainly useful for early diagnosis of Protein energy malnutrition, before the Weight is affected. These changes are more obvious in kwashiorkor than marasmus, due to poor adaptation (Table 6.3).

Earliest biochemical change in Protein energy malnutrition is a decrease in essential amino acid (EAA) levels – which can’t be synthesized endogenously, leading to altered EAAI non-EAA ratio in plasma.

This ratio (Glycine+Serine÷Glutamine+Taurine/ Valine+Leucine+Isoleucine+Methionine) is <2 in normal children, 2-3.5 in subclinical Protein energy malnutrition and >3.5 in Kwashiorkor.

III) Classification of severity: Various classifications systems for Protein energy malnutrition are in vogue to denote severity and duration of PEM, though some important ones are as follows —

a) Weight-based classifications are simple but do not indicate the duration of malnutrition. Most popular

one in this category is Indian Academy of Pediatrics or lAP classification, Others include Gomez classification (Weight >90% normal; 75-90% grade I, 60-74% grade II, <60% grade III) or Jellife s classification (>90% normal, 81-90% grade I, 71-80% grade II, 61-70% grade III, <60% grade IV).

b) Height-based classifications are rarely used in practice and include Waterlow ‘s classfication (Height >95% normal, 90-95% marginal, 85-90% moderate and <85% severe Protein energy malnutrition) and Mclaren ‘i classfication (Height >93% normal, 80-93% short-stature and <80% nutritional dwarfs).

c) Multi-parameter classifications are most informative and include Welcome trust classification, Waterlow’s classification and WHO classification

d) Clinical classification of marasmus depends on the extent of muscle wasting and subcutaneous fat loss.

Investigations: Although Protein energy malnutrition is a clinical diagnosis, following investigations are required on admission, to exclude or identify complications.

1. Complete hemogram including peripheral smear for anemia and infections (malaria).

2. Urine examination, especially for pus cells (UTI);

3. Stool examination, especially for fat globules (mal absorption), reducing sugars (lactose intolerance) and microscopic ova/cysts;

4. Chest skiagram for tuberculosis, respiratory infections;

5. Tuberculin test, which may be false negative in severe Protein energy malnutrition due to impaired cell mediated immunity.

6. Biochemical tests, specially —

a) S. albumin (hypoproteinemia), b) Blood sugar (hypoglycemia), c) S. Na, K, Ca and Mg (dyseictrolytemia), d) Liver function tests

7) Microbial cultures (blood, urine, others)

8) Other relevant investigations

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