CHRONIC NUTRITIONAL DISORDERS

1. CHRONIC NUTRITIONAL DISORDERS

2. Definition • Chronic nutritional disorders (CND) are characterized by delaying or stopping of ponderal growth, stature or both for a period of more than a month with a difference more than 10% of normal values corresponding to the age.

3. There are three forms of CND: • Hypotrophy – slowing or stagnating the ponderal growth. • Hypostature – stagnating uniformly ponderal growth and stature. • Paratrophy – excessive mass.

4. Classification of hypotrophy: According to the origin, hypotrophy can be: • Congenital, prenatal (intrauterine) hypotrophy; • Postnatal hypotrophy (acquired); • Mixed hypotrophy (prenatal – postnatal).

5. I. Congenital hypotrophy: prenatal nutritional disorders • Neuropathic form; • Neurodystrofic form; • Neuroendocrine form; • Encephalopathic form.

6. II. Acquired hypotrophy: Gomes classification (WHO) Degree of severity: • Mild malnutrition – degree I (10 – 20%) • Medium malnutrition – degree II (20 – 30%) • Severe malnutrition – degree III (more than 30%)

7. Clinical forms of acquired hypotrophy: • Severe protein – energy malnutrition (marasmus) • Severe protein malnutrition (kwashiorkor)

8. Modality of evoluation: • Protein deficit; • Global energy deficit; • Protein and energy deficit.

9. Etiology Congenital hypotrophy is a consequence of different factors: • Noxious profession of mother during pregnancy; • Precocious pregnancy; • Placental anomalies; • Deficiency in alimentation; • Hereditary factors – chromosomal mutations (Down’s syndrome, Klinefelter’s, Turner’s syndromes etc. • Genetic disorders: cystic fibrosis, celiac disease, galactosemia etc.

10. Etiology: • Acquired hypotrophy – provoking factors are diverse: they are conventionally divided into two groups: • 1.Exogenic factors • 2.Endogenous factors

11. 1.Exogenic factors: - Alimentary • a) Maternal hypogalactesia; • b)Milk dilution; • c)Chronic vomiting – leading to insufficiency; • d)Anorexic children; • e)Neuropsychic disorders of sucking and deglutition. - Less quality • a)Less proteins in the foods; • b)excessive flour; • c)less lipids in the foods etc. - Infectious • a)Repeated respiratory infections: pneumonia, urinary infections; • b)Chronic gastrointestinal disorders, diarrhea; • c)Long duration and excessive antibioticotherapy. - Negligence, care and education. • a)Negligence of physiological diet regime; • b)Improper weaning foods.

12. 2.Endogenous factors: • - Developmental anomalies of systemic organs; • - Hereditary metabolic disorders; • - Congenital metabolic disorders; • - Malabsorption disorders; • - Endocrine disorders.

13. Pathogenesis • Pathogenesis is very complicated and still not confirmed. It is difficult to explain all the factors and the specific affection according to the age of children. The chronic hypoxia of the maternal organs and the modifications in the feto-placental circulation with oxygen and nutrition transport disturbances to the fetus play a major role in the pathogenesis of intrauterine hypotrophy. Acquired hypotrophy due to insufficient food uptakes the organs of the child start using the storage: carbohydrates, then lipids from the storage. As the storage deplinishes, the protein breakdown starts. It starts from muscle fibres, after that – from parenchyma of the internal organs. In this ways always it manifests with severe disorders involving changes in the systemic organs (digestive, endocrine, CNS, etc.) resulting in decreased immunity.

14. These manifestations mainly depend on the degree of hypotrophy and may manifest as the following: • 1. Trophical disturbances syndrome: cellular – adipose layer thinning, flattened growth curve, growth deficiency and constitutional disturbances. Skin turgidity is diminished and presents with symptoms of hypovitaminosis (A, B1, B2, B6, D, PP). • 2. Digestive disorders syndrome: loss of appetite, anorexia, bowel disturbances (constipation or dyspeptic stools), disturbances of the intestinal flora, decrease of food tolerance, signs of maldigestion in coprogram. • 3. Central nervous system disturbances syndrome: emotional disturbances, decreased motor activity, negative emotions, sleep disturbances and thermal disturbances, psychomotor retardation, muscular hypotony and dystony. • 4. Hematopoietic and immunologic disturbances syndrome: anemia, secondary immunodeficiency state, tendency of evolutions without any manifestations, atypical manifestations of acute inflammatory diseases, infections.

15. Clinical picture • Neurologic mechanism is the basis of congenital hypotrophy. It may manifest as severe anorexia and disturbances in the digestive reflexes. The four clinical forms mentioned above depend from 5 indices: weight, height, motor activity, psychic, appetite. • Formula for calculating congenital hypotrophy degree: birth weight/stature(length) at birth. Normal children – more than 60. Degree I – 59-56; degree II – 55-50; degree III – 49 and less.

16. Clinical forms of congenital hypotrophy: • 1. Neuropathic form. Children with this form usually have birth weight and height normal at term. Hypotrophy appears after birth, length in most of the children is normal. The psychomotor and neurological developments are not modified. Compartmental behavioral changes, motor excitations, negative emotions, sleep disturbances, loss of appetite and disturbances of gastric reflexes appear in the first place of clinical picture. • 2. Neurodystrophic form. These children present with changes in the CNS, delayed psychomotor development. The basic symptom is the presence of severe insidious dystrophy in mostly congenital cases. The deviation of the weight in the infant may reach up to 50% and more. Growth retardation is a mild manifestation but weakness, irritability and anorexia are severe. • 3. Neuroendocrine form. These children present with changes in CNS and endocrine function. The psychomotor development is delayed. Body mass deficit and retardation of height are predominant manifestations. Almost all the children with this form or born with signs of hypotrophy and short length. On inspection they have dwarfism, microthoracocephaly, hemiassymetry. Gastric reflexes are modified. Endocrine abnormalities, more likely hypophyseal dwarfism, absence of ossification centers. Thyroid and parathyroid function abnormalities are usually found. • 4. Encephalopathic form. These children present with insignificant retardation in psychomotor development. Height is normal.

17. Acquired hypotrophy • Degree I. It is characterizing by body mass deficit of 10 – 20% or 10 – 24% according to WHO. Ponderal index = 0.90 – 0.76; nutritional index = 0.9 – 0.81. Height remains normal. Subcutaneous fat tissue is thin on abdomen and thorax, skin fold is less than 1,5 cm. Skin turgidity is moderately reduced. Growth curve is stationary or slightly ascending. The child appears weak, otherwise he is healthy. Motor activity is normal or slightly reduced. Appetite is normal or slightly reduced. The children are irritable. The metabolic aspects are low absorption of lipids, increase in the level of free fat acids, hyponatremia and moderate hypokalemia. Immunity is normal or slightly reduced.

18. Acquired hypotrophy • Degree II. Pale or grey colored, dry skin. Body weight deficit – 20-30% or 25-39% according to WHO. Ponderal index = 0.76 – 0.61; nutritional index = 0.8 – 0.71. Height remains normal, subcutaneous fat tissue disappears on abdomen and thorax (the ribs are seen) and slightly reduced on the extremities and face. Hypotonia, loss of appetite, increased incidence of viral infections. Growth curve falls slowly. Skin turgidity is reduced. The gastric, pancreatic and intestinal secretions are reduced. Stools are unstable. SNC manifestations are anxiety and hyperexcitability. Crying without any reason may suggest apathy. The child’s motor development stops: delayed milestones like sitting, crawling. In some cases the child loses the motor activity. Thermoregulation is affected. The first manifestations of less food intake appear. The body easily warms up and cools due to circulatory insufficiency. Low cardiac beats. Liver is enlarged. Immunity is reduced. Hypoproteinemia, decrease of phospholipids in serum, hypoglycemia, hyponatremia, hypocalcemia and hypovitaminosis may be seen.

19. Acquired hypotrophy • Degree III. This is the most severe form of malnutrition which may set in usually between 3 and 12 months. In this we have 2 forms of malnutrition: protein – energy and protein.

20. Protein-energy malnutrition (Marasmus): body weight deficit more than 30% or 40% according to WHO. Ponderal index less than 0.60. Nutritional index less than 0.7. Growth stagnation. Pale, grey colored, flaccid skin. Skin folds in medial surfaces of thighs and gluteal region. Ulcers and bed sores, erythema. Triangular face with deep nasolabial grooves, maxillary prominence, sharp chin, thin cheeks and frontal skin wrinkles (“old man face”) may be seen. Absence of buccal fat pad. Atrophy and muscular hypotony. Sudden fall of growth curve, arrhythmic respiration with long expiration and periodic apnoea. Pneumonia with atypical evolution may set in. Low cardiac beats, bradycardia (60 – 80 b/min). Low blood pressure, cold extremities, loss of appetite until anorexia, low digestive tolerance. They may have regurgitation, vomiting, swollen abdomen due to intestinal and abdominal wall atony. There may be constipation, but frequently it is hunger diarrhea. Reduced diuresis. The children are apatic, adynamic, do not react to the surroundings and are hyporeflexic. There are thermoregulatory and hypermetabolic disturbances.

21. Protein malnutrition (kwashiorkor) • edematous dystrophy and loss of the selective proteins. The loss of the selective proteins is due to disequilibrium of the nitrogen balance which is a cause of insufficient protein diet and rarely due to protein loss. It may develop after stopping the breast feeding and transferring to protein less diet (as a rule – vegetarian). The clinical signs set in after 2 – 3 months after stopping the breast feeding. The stagnation of the growth curve may be noted. The generalized edema sometimes masks the loss of weight in the child. The general condition is altered, the child is apathic; fixed vision, grimace, flaccid and dry skin are seen. Thin and grey or red hair. Depigmentated hair. In serum – hypoproteinemia and in blood – anemia.

22. Definitive diagnosis the diagnosis is based on anthropometry, clinical and lab findings. In anthropometry the weight and the height are used. The deviation from the normal weight is calculated using Ponderal Index (PI) and Nutritional Index (NI). • PI (Ponderal Index) = actual weight/ideal weight for that age. • NI (Nutritional Index) = actual weight/weight for the height (but not age).

23. Gomes classification – 3 degrees • Infants with PI of 0.9 – 1.1 and NI of 1.0 – 0.9 are considered eutrophic. Infants with PI and NI less than 0.9 denote malnutrition.

24. Clinical criteria • Clinical criteria include past history and clinical signs. In the history it is necessary to determine prenatal and obstetrical history. The history of infections at mother and child is important. Clinical examination depicts signs of weight loss, loss of adipose tissue, fall of growth curve, change in muscular tone and modifications in the systemic organs. • Metabolic changes: hypothermia, bradycardia, decreased intestinal tolerance, paradoxical reaction to hunger, decreased resistance for infections. Delayed neuropsychic development. • The laboratory findings: decreased serum protein and serum albumin, hyponatremia. The stools pH control and d – xylose test performing if necessary. Immunologic tests and analysis if necessary.

25. Treatment The treatment of hypotrophy is complex and includes: 1. finding the cause and treating the cause of hypotrophy; 2. daily regime, care, education, massage, gymnastics; 3. diet therapy; 4. vitamin therapy, ferment therapy, symptomatic treatment; 5. treating the foci of infection; 6. treating the associated diseases.

26. Treatment • In degree I of prenatal hypotrophy the children at birth have satisfactory general condition and the weight gain is normal if the child is under medical supervision. The children with II – III degree of congenital hypotrophy and prematures require care in special centers. The diet in children with hypotrophy is fixed taking into consideration the etiology and the metabolic disorders. In the case of celiac disease the gluten containing diet is restricted like wheat flour. The children with lactase insufficiency should be restricted from the milk containing diet. These are fed with lactic acid products (mixture containing acidophilic bacteria) or soya formulas. In cystic fibrosis limited lipids and rich protein diet is indicated. The necessary lipid is got from vegetable oils.

27. The diet therapy is carried on in 3 levels: • Level I - rest and minimum diet; • Level II – increase in the caloric input (intermediary); • Level III – returning to normal regime.

28. Diet therapy • The diet therapy is given according to the degrees of hypotrophy. Before starting the diet therapy the daily required diet is calculated 170 – 200 ml/kg body weight or 1/5 of the body mass, but not more than 1 litre/day. At the level I at the severity of hypotrophy by I degree is 2/3, II degree – 1/2, and III degree – 1/3 from 1/5 of the body weight. • In the following days if the appetite is good then the digestive tract tolerance is considered as satisfactory and the volume of the food is raised from 1/3 to ½ or 2/3. If the tolerance is good in the time of 3 – 5 days, then the volume of the food is raised to 2/3 from 1/5 of the real body mass. In the loss of appetite and less tolerance the volume previously consumed is indicated.

29. I level • In the I level of diet therapy the required liquid can be given in the form of carrot soup, 5% glucose solution, rice porridge, tea, fruit juice and vegetable soup. In children with II – III degree hypotrophy i/v 5-10% glucose solution, Ringer’s solution can be administered. In the stage of minimum diet the food for 1 kg of body weight should contain: • Protein - 0.7 – 1.5 – 2.0 g; • Lipids - 2.0 – 4.0 g; • Carbohydrates - 8.0 – 11.0 g; • Calories - 60 – 70 – 100. The protein is slowly raised daily until it reaches 3 – 4 g/kg/day.

30. Level II • Increased calories intake. The child receives the necessary food per day (2/3 or ½ of the basic mixture). In this level the following may be consumed: mother’s milk, milk from the donator, industrial milk formulas. From the seventh month – yoghurt, curds, biolact, rich carbohydrates and lipids foods can be used. • The correction mixture is distributed in small portion, 10-20-30-50-60 ml, before each alimentation with the basic mixture. • In the intermediary stage the lipid quantity in the natural alimentation is raised up to 3 g/kg, in the mixed alimentation – 3,5 g/kg, and in artificial alimentation – up to 4 g/kg. • The fat quantity remains low - 4 - 4,5 g/kg and the carbohydrates touch the lower limits of normal quantity. • In the adaptation stage in 5th and 7th day of II level, pure mixture (without fat or decreased fat) is mixed step by step with mixture rich in protein and fat, curds, biolact and Enpit lipid. In this level the lipids are increased up to 5 – 6 g/kg body mass. • Carbohydrates up to 13 – 15 g/kg in the intermediary stage are done ultimately by introducing lactate mixture, juices, fruit mash in the food in the first months of life. After 6 months mashed vegetables and gruel are added.

31. Level III Returning to the optimum diet regime corresponding to the biologic age. Egg yolk, vegetable oil, butter, cheese of cow’s milk and meat are added accordingly to the age limits. In this period optimum diet for 1 kg of real mass should contain: • Protein - 4 – 4,5 g; • Lipids - 6 – 6,5 g; • Carbohydrates - 15 – 16 g; • Calories - 130 – 150/kg In the case of destruction of the intestinal flora biologically active substances are added like: Bifidum-bacterin and bificol. In severe malnutrition there is hypovitaminosis. To regulate this parenteralhydrosoluble vitamins are administered in the early stage of the treatment like: vitamin B1, B2, C and cocarboxylase. In the intermediary stage vitamin B5, B6, B12, B15, nicotinic acid and liposoluble vitamins A and E are administered. Pepsin with hydrochloric acid, pepsin, gastric juice, pancreatic ferments may be administered to help digestion. The ferments are prescribed at the end of the period of the minimal diet when the volume of the diet corresponds with 1/5 of the real weight in the duration of 3 – 4 weeks.

32. Concomitantly or after the correction of anemia are done by administering iron preparations. Rickets is treated by vitamin D administration. • In the level II the treatment includes manage and gymnastics. • Antibiotics are indicated if there exist a foci of infection or associated infection diseases. • The treatment for hypotrophy is complicated and for a long duration.

33. Prognosis and prophylaxis Prognosis • The prognosis of mild and moderate forms is satisfactory. In the severe form the prognosis is reserved. Prophylaxis • 1. Early diagnosis and correction of the diet. • 2. Maintaining of natural diet. • 3. Calculated mixed or artificial diets with corrected mixtures. • 4. Diversification of the corrected diet. • 5. Early diagnosis and correct treatment of infections.

34. Hypostature • Hypostature is proportional retardation of the ponderal growth and the height. This is characteristic for children with congenital heart defects, with developmental anomalies of the brain, children with encephalopathy and endocrine disorders. These children have trophic changes and nonevident signs of polyhypovitaminosis, hypoproteinemia, intestinal lipid absorption disturbances. Low levels of phospholipids and alfa-lipoproteins and aminoaciduria are observed. • The hypostature children who are hypoplastic (constitutional height retardation) does not show trophic changes. Skin is red, absence of signs of hypovitaminosis. Normal muscular tone and skin turgidity and normal neuropsychic development which corresponds to the age. Digestive tolerance is normal and resistance to infections is adequate. Hypostature is found in children older than 6 months.

35. Paratrophy • Paratrophy is a chronic disorder of nutrition with excessive body mass.

36. Etiology • Incorrect diet with wrong proportions of the principal ingredients of alimentation and high carbohydrate (surplus of sweet tea, juices, gruel, biscuits), high protein (condensed cow milk, cheese, Enpit). Lymphatico – hypoplastic disorders, allergic disorders, and anemia contribute for paratrophy. Surplus of breast milk never leads to paratrophy.

37. Pathogenesis • The excessive carbohydrate and protein intake leads to intestinal dysfunction, digestive disturbances, disturbances in the intestinal flora, anemia, endogenous intoxication, acidosis and hypovitaminosis. Excessive carbohydrates contribute to vitamin B1 deficiency (marble skin, decreased muscle tone). Hypovitaminosis A manifests as dry skin, purulent eruptions over skin, repeated infections, anorexia, hypertension. The children with paratrophy have a predisposition to rickets and anemia.

38. Clinical manifestations • Basic symptoms of paratrophy are neuropsychic disturbances. Children are adynamic, emotionally labile, apathic, insomnolent and have selective appetite for diet. Skin is pale, soft, dry and sometimes the skin is cream colored (due to excessive protein intake). Excessive adipose tissue and decreased muscular tonus are present. In the serum the level of phospholipids is low and cholesterol is high. Due to decreased immunity the children are prone to viral infections, otitis and urinary tract infections. Various intestinal disturbances are met in children with paratrophy. • The stools are pasty. In the case of excessive carbohydrates the stools are loose, with acidic pH, yellow color, with mucus and positive iodine test (blue in the case of starch presence). Microscopic the starch is in high quantity; cells, fatty acids and leukocytes are present.

39. Diagnosis and treatment Diagnosis • The diagnosis in paratrophy is based on the clinical manifestations. In the peripheral blood – iron deficient anemia, folic acid deficiency anemia and vitamin B6 and B12 deficiency is found. Treatment • Regulation of diet. Introducing of vegetable components in the diet. Feeding in the intervals between the meals is strictly prohibited. Acidic diet mixture with less lipids is preferable. In general physical exercise, massage, walking and cold water baths are indicated.