Classification

Origin	Etiology	Degree of severity	Period of disease
Prenatal Postnatal Pre-postnatal	Exogenous: alimentary, infection, toxical, etc. Endogenous: anomalies of constitution, enzymopathy, endocrinopathy,etc. Mixed	Mild (I degree)10-20% Moderate (II degree) 20-30% Severe (III degree) >30%	Initial Progressing Stabilization Convalescence

Clinical manifestations of protein energy malnutrition Clinical manifestations of malnutrition depend on the severity and duration of nutritional deprivation, the age of the undernourished subject, relative lack of different proximate principles of food, and the presence or absence of associated infections. In India and many other developing countries the major limiting factor in the diet of preschool children is energy. Lack of protein in the diet is more often due to low food intake, rather than a qualitative defect in the diet.

Nutritional marasmus and kwashiorkor are two extreme forms of malnutrition. Patients showing features of both syndromes are said to have marasmic kwashiorkor. Such extreme forms account for a small proportion of cases of malnutrition. A much larger number of subjects suffer mild to moderate nutritional deficit. Patients with mild to severe manifestations of nutritional deficiencies, in whom low protein intake is a common denominator but consumption of carbohydrates and fat as sources of energy varies are described as suffering from protein-energy malnutrition.

Mild to moderate undernutrition. If the dietary intake is deficient for a short period, the body adapts its metabolism to compensate the deficit to some extent. Energy and protein in the diet are expended more efficiently, and nitrogen excretion in the urine and stools is reduced.

If the food deficit persists for a longer period, the malnourished subject conserves his energy by curtailing physical activity. Moderately malnourished children appear slower and less energetic. If the nutrition deficit continues longer, growth of the child is affected. Growth lag is more pronounced in weight than the length. With prolonged deprivation height is also stunted. Head circumference is not reduced significantly. Chest circumference normally exceeds the head circumference by the age of 1 year, but it may not do so till much later in malnourished children. The weight of the child is reduced and appears disproportionate with long body, thin limbs and unduly large head. Buttocks are flattened with wrinkling of skin over the front of thighs. The scapulae look winged. Abdominal wall is thin and therefore abdomen appears distended. As the nutritional deficit exaggerates with the onset of infections, the child may become marasmic or develop kwashiorkor.

Marasmus. A marasmic subject is markedly emaciated. The body weight is less than 70 percent of the expected one for the age. The fat in the adipose tissues is severely depleted because it is used up for providing energy. The contour of atrophic muscles is evident under the thin and wrinkled skin. Loose folds of skin are prominent over the glutei and the inner side of thigh. The buccal pad of fat is preserved till the malnutrition becomes extreme. A higher proportion of saturated fatty acids is stored there and the saturated fat is the last to be depleted. The skin appears dry and inelastic and is prone to be infected. The hair is hypopigmented. The abdomen is distended due to wasting and hypotonia of abdominal wall muscles. Gaseous distension occurs due to bacterial fermentation of unsplit sugars in the colon. The mid-arm circumference is reduced. The bony points appear unduly prominent due to emaciation. The baby appears alert, but is often irritable. Marasmic children may show voracious appetite.

Kwashiorkor. Essential features. Markedly retarded growth, psychomotor changes and edema of dependent parts are three essential clinical features of kwashiorkor. The edema starts in the lower extremities and later involves upper limbs and the face. Muscles of the upper limbs are wasted, but the lower extremities appear swollen. The face appears moon-shaped and puffy. The trunk is affected to a lesser extent. In a previously malnourished child edema is precipitated by debilitating illnesses such as measles or diarrhea. With the onset of kwashiorkor, the previously peevish and irritable undernourished child becomes lethargic, listless and apathetic. He takes little interest in the environment and does not play with his toys.

Other usual clinical features.

The kwashiorkor patient appears miserable and resents examination by the physician. Appetite is impaired and it is difficult to feed him orally. The hair is thin, dry, brittle and devoid of their normal sheen. It becomes straight and hypopigmented. The length of the hair that grows during the period of nutritional deprivation appears reddish brown. During the phases of better nutrition, the growing part of the hair gets appropriately pigmented. This gives appearance of alternate bands of hypopigmented and normally pigmented hair. These children often suffer from recurrent episodes of diarrhea, respiratory and skin infections.

Features which are present but are not essential for the diagnosis.

The liver is enlarged with rounded lower margin and soft consistency in about one-third of cases. Histological examination shows fatty infiltration. The skin changes are not essential for the diagnosis of kwashiorkor. Large areas of skin show erythema, followed by hyperpigmentation. The skin becomes dry and hyperkeratotic. The epidermis peels off in large scales, exposing tender raw area underneath. It gives appearance of old paint flaking off the surface of the wood. The underlying raw skin is easily infected. The skin lesions are marked in areas of the body, most exposed to continuous pressure and irritation. Normally moist areas of skin appear sodden.

Petechiae or ecchymoses appear in severe cases. Dry, inelastic, mosaic skin with follicular keratosis is not pathognomonic of kwashiorkor. This may be due to exposure to dust and inclement weather.

Multiple nutritional deficiencies. As the nutritional deficiencies are generally multiple, anemia due to iron, protein, vitamin B₁₂ or folate deficiency is often associated. Deficiencies of vitamin B complex factors, especially ariboflavinosis, are common. Keratomalacia due to vitamin A deficiency is reported in 10 to 20 percent of patients with kwashiorkor. Associated scorbutic changes manifest as bleeding gums, subperiosteal hemorrhage or even ecchymotic spots. Subclinical ascorbic acid deficiency is frequent in malnutrition. The clinical evidence of florid rickets may not be so evident in a case of protein-energy malnutrition when growth has stopped, since rickets is a disease of growing bones.

As long as the child is not growing, skeletal changes of rickets may not be clinically overt. The latter become evident after the child is put on adequate calories and proteins, but without vitamin D supplementation. Cases of atrophic rickets may, however, be seen even with severe malnutrition.

Mild to moderate undernutrition

1. Reduced physical activity.

2. Slow gain in weight, arrested growth, underweight.

3. Thin buttocks, wrinkling of skin over front of thighs.

4. Chest circumference lags behind head circumference after the age of 1 year.

Marasmus

1. Emaciated. Muscles markedly wasted, loose folds of skin wrapped over the bones.

2. Body weight less than 70 percent of expected weight for age.

3. Mid-arm circumference less than 12,5 cm.

4. Dry inelastic skin, more prone to develop pyoderma.

5. Distended abdomen.

6. Irritable.

7. Voracious appetite.

Kwashiorkor

Essential

1. Retarded growth.

2. Edema of dependent parts.

3. Mental changes (apathy, listlessness, lethargy).

Usual

4. Impaired appetite.

5. Hair thin, dry, brittle, straight, hypopigmented (reddish brown) "flag sign" with alternating bands of black and brown hair.

6. Diarrhea.

7. Recurrent infections.

8. Distended abdomen.

May be

8. Skin changes. Flaky paint dermatosis.

10. Enlarged liver with rounded lower margin. Fatty infiltration of liver.

Nutrition and resistance to infection. The resistance of the human organism to infections is adversely affected in malnutrition.

1. The skin and mucosa do not offer effective physical barriers against infection.

2. Impaired chemotaxis, normal phagocytosis, defective candidacidal and bactericidal capacity were observed in in-vitro studies of polymorphonuclear leukocytes.

3. Cell mediated immunity. The bacterial infections, which require cell mediated immune responses for protection against them, tend to be unusually severe in malnourished subjects. The thymus gland and thymus dependent lymphoid tissues are atrophied and cases of PEM cannot be sensitized easily by several antigens. Delayed hypersensitivity reactions, which recall previous sensitization, are also reduced.

4) Humoral antibodies. Circulating immunoglobulin levels are usually normal or elevated in malnourished subjects. Malnourished subjects without associated infections do not show elevation of immunoglobulin level. Elevation of IgA is attributed to frequent association of gastrointestinal and respiratory infections.

The number and proportion of B-lymphocytes are not altered. Humoral antibody response to a variety of immunizing antigens such as tetanus and diphtheria toxoids, polio and measles vaccine is adequate.

As the secretory IgA is generally reduced, recovery from infections is delayed and infections tend to be severe in malnourished subjects. The period of infectivity is prolonged because of the increased duration of replication and shedding of pathogens. Systemic spread is also more likely.

Diagnosis and differential diagnosis. The thickness of adipose layer is the main diagnostic criterion of hypotrophy and its degree. In hypotrophy of the I degree adipose layer disappears from abdomen, sometimes from chest, but is seen on extremities; in the II degree it is thin all over the body surface except face; in the III degree it disappears completely. In differential diagnostics it is necessary to take into account all diseases mentioned above (Etiology). In patients with hypostature (even lag in height and weight) it is necessary to exclude different kinds of nanism both disproportional (chondrodystrophy, congenital osteopsathyrosis, vitamin D-resistent forms of rickets, grave vitamin D-dependent rickets) and proportional (hypophisial, hypothyroid, mitral, cerebral etc). It is necessary to remember about constitutional hyposomia. In some families tendency to delayed rate of growth exists because of different hereditary peculiarities of endocrine system. It’s considered that height of a healthy child may fluctuate within the limits ±1,5σ of healthy children height arithmetical mean. If their height oversteps these limits hyper- or hyposomia are spoken about. Hyposomia in the limits 1,5-2,5σ may be both normal variant and consequence of pathologic condition. When a child’s height is less than mean minus 3σ, nanism is diagnosed.

Therapy of hypotrophy (three-phase feeding)

1. Period of finding out (ascertaining) food tolerance

2. Intermediate period

3. Period of high-caloric diet

Diary book of the observation for the child with hypotrophy must has:

1.Quantity of the food, that child eats during 1 intake and daily.

2.Quantity of the fluid (entered orally and parenteral).

3.Volume of vomiting.

4.Volume of urination.

5.Frequency and characteristic of stool.

6.Data about body weight, daily raise or loss of body weight.

7.Calculation quantity of proteins, fats, carbohydrates, calories per kg and daily, and its correction if necessary.

Period of finding out (ascertaining) food tolerance: