LECTURE No. 4. Chronic eating disorders, hypovitaminosis in children

1. Hypotrophy

Hypotrophy is a chronic eating disorder that manifests itself in varying degrees of weight loss.

Etiology, pathogenesis. The disease is polyetiological. There are congenital (prenatal) and acquired (postnatal) malnutrition. Congenital malnutrition is primarily caused by maternal diseases or is associated with intrauterine hypoxia, fetal infection, genomic and chromosomal mutations. Among the causes of acquired malnutrition, exogenous and endogenous are distinguished.

Exogenous causes include nutritional factors (quantitative underfeeding in hypogalactia, pyloric stenosis and pylorospasm or qualitative underfeeding when using age-inappropriate mixtures, late introduction of complementary foods, etc.), infectious factors, intrauterine generalized infections, infections of the gastrointestinal tract, toxic factors, drug poisoning (hypervitaminosis D, etc.), anorexia due to psychogenic and other deprivation, when the child does not receive enough attention, affection, walks, massage, lack of care, regimen, education, etc. Prenatal encephalopathies can be attributed to endogenous causes of malnutrition of various origins, bronchopulmonary dysplasia, hereditary metabolic anomalies and immunodeficiency states, malformations of the gastrointestinal tract and other organs, CNS lesions, endocrine diseases, psychopathy, neurosis, etc.

The pathogenesis of malnutrition is based on a decrease in the utilization of nutrients with a violation of the processes of digestion, absorption and assimilation under the influence of various factors. There are I, II and III degrees of severity of malnutrition.

Clinic. Hypotrophy of the first degree is manifested by a loss of body weight of no more than 20% of that required by age. Paleness of the skin and mucous membranes. The subcutaneous fat layer on the abdomen becomes thinner, tissue turgor and elasticity decrease.

The weight gain curve is flattened. The growth of the child does not lag behind the norm. Other indicators are usually within the normal range or slightly reduced.

With II degree malnutrition, the loss of body weight is 25-30% compared to the age norm. The subcutaneous layer is preserved only on the face, and is especially thin on the abdomen and limbs. The skin is dry, pale, flabby, the skin easily gathers into folds, hangs down in some places, tissue turgor is reduced. Growth retardation is observed, appetite decreases, the child becomes weak, irritable, noisy, whiny, loses previously acquired skills, thermoregulation is disrupted, the child quickly cools down or overheats. The curve of body weight increase is flat.

The Chulitsky body condition index is 1-10. The stool is unstable: “hungry” stool (scanty, dry, discolored, with a sharp and unpleasant odor) is replaced by dyspeptic stool (green with undigested food particles, with mucus).

With malnutrition of the III degree, the loss of body weight is more than 30% of the due to age. There is no increase in body weight, the child is significantly behind in growth. Outwardly - an extreme degree of exhaustion, the child resembles a skeleton covered with skin. The skin is pale gray, dry, the limbs are cold, the subcutaneous fat layer is completely absent. The skin fold does not straighten, there is no elasticity. The mucous membranes are pale, dry, in the mouth - elements of candidal stomatitis (thrush).

Fatness index Chulitsky negative. Breathing is shallow, heart sounds are muffled, blood pressure is reduced.

The body temperature is lowered, there are periodic rises to subfebrile numbers, there is no difference between the axillary and rectal temperatures. Infectious processes are asymptomatic. Often there are signs of subacute rickets.

The abdomen is distended, distended, or bowel loops are contoured. The chair is unstable, often constipation, alternating with soapy-calcareous stools. The child is severely retarded.

Diagnosis malnutrition is usually not difficult. It is much more difficult to find out the causes of malnutrition.

Treatment patients should be comprehensive and include measures aimed at eliminating or correcting causally significant factors, diet therapy, the appointment of restorative procedures, enzymes and symptomatic agents, the elimination of foci of infection, vitamin therapy. In all cases, when prescribing a diet, it is necessary to ascertain food tolerance. During the period of increased food load, scatological control is needed.

With hypotrophy of the I degree, the amount of proteins and carbohydrates is usually calculated per 1 kg of body weight due to age, and fats - per 1 kg of existing body weight.

In case of II degree malnutrition, food tolerance is established within 3-5 days. As a rule, breast milk or acidic mixtures are prescribed (kefir, acidophilic mixture “Malyutka”, biolact, etc.).

The calculation is first carried out on the child’s existing body weight, then on approximately the expected one (existing + 20) and only then on the expected one. After 3-4 days, the protein load is gradually increased, then the carbohydrate load and, lastly, the fat load.

For grade III malnutrition, it is preferable to start diet therapy with the introduction of breast milk every 2 hours, 20-30 ml. Having brought the amount of food to 50 ml, reduce the number of feedings. The order of increasing the load with proteins, carbohydrates and fats is the same as with degree II malnutrition, but more gradual. Food tolerance is determined within 2 weeks.

In case of malnutrition of the II and III degrees, the missing amount of fluid, nutrients and electrolytes is administered intravenously: 5-10% glucose solution, isotonic sodium chloride solution, Ringer's solution, protein hydrolysates, albumin, protein (albumin 3-5 ml/ kg; hemodez up to 15 ml/kg, but not more than 200 ml; rheopolyglucin 3 - 8 ml/kg, etc.). Insulin glucose therapy is indicated (s.c. 1 unit of insulin per 5 g of administered glucose).

Treatment of malnutrition II - III degree must be carried out in a hospital. In the presence of foci of infection, antibiotic therapy is prescribed (avoid nephro-, hepato- and ototoxic drugs), if necessary, surgical intervention is performed. Enzyme therapy, vitamin therapy are widely used.

Stimulants prescribed include apilak, γ-globulin, albumin, plasma, and blood transfusions. In some cases, it is advisable to use anabolic hormones (retabolil-1 mg/kg once every 1 weeks, etc.). Massage and exercise therapy, spending time in the fresh air are recommended. The prognosis depends on the cause that led to malnutrition and the possibilities of eliminating it. With primary malnutrition of the third degree, the prognosis is always serious; mortality rate is up to 2%.

Prevention. If possible, ensure natural feeding, treatment of hypogalactia, rational feeding, early diagnosis of diseases in newborns and infants.

2. Hypovitaminosis

Hypovitaminosis is a group of diseases caused by a deficiency in the body of one or more vitamins.

Vitamins - these are irreplaceable biologically active substances that act as catalysts for various enzyme systems or are part of many enzymes.

Vitamins are necessary for normal metabolism, growth and renewal of tissues, biochemical support of all body functions. Insufficient intake of vitamins leads to disruption of enzymatic reactions, hypo- and beriberi with a corresponding picture of the disease.

Etiology, pathogenesis. Hypovitaminosis is distinguished between primary (exogenous, caused by a deficiency of vitamins in the body with food) and secondary (endogenous, associated with impaired absorption of vitamins in the gastrointestinal tract or their assimilation, with an excessive need for vitamins during treatment with certain antibiotics). Also contributing to the occurrence of vitamin deficiency are excessively low or high ambient temperatures, prolonged physical or mental stress, diseases of the endocrine glands, some occupational hazards and other factors. Of particular importance are limited diet (with insufficient vitamin content in food), helminthiasis (consumption of large amounts of vitamins by helminths), pregnancy and lactation in women (increased need for vitamins for the fetus and infant).

Polyhypovitaminosis was often observed in various countries during social and natural disasters (wars, crop failures), with irrational (unbalanced) nutrition of both groups of people (during long hikes, travels, etc.) and individuals (food canned food, dried products, long monotonous food). In some developing countries, vitamin deficiency diseases are still very common.

Many diseases of the gastrointestinal tract, accompanied by syndromes of insufficiency of digestion and insufficiency of absorption, lead to vitamin deficiency.

3. Vitamin A deficiency

Vitamin A deficiency (retinol deficiency) occurs when there is a lack of vitamin A and carotene in food, a violation of its absorption in the intestine and the synthesis of vitamin A from carotene in the body.

Vitamin A is found in many products of animal origin (butter, egg yolk, liver of some fish and marine animals); Plant foods contain carotene, which is provitamin A, from which this vitamin is synthesized in the human body. Vitamin A is fat soluble. The daily requirement for an adult is 1,5 mg (5000 IU).

Vitamin promotes normal metabolism, growth and development of the body, provides physiological functions of the epithelium of the skin and mucous membranes, sweat, sebaceous and lacrimal glands, the organ of vision.

Clinic. Hemeralopia (night or night blindness due to dystrophic changes in the retina and optic nerves), xerophthalmia (dryness of the conjunctiva, the formation of whitish opaque plaques on it), keratomalacia (ulceration of the cornea), hyperkeratosis (dystrophic changes in the epithelium of the skin, mucous membranes and skin glands) appear - dryness, flaking and pallor of the skin, keratinization of hair follicles, atrophy of the sweat and sebaceous glands, etc.), a tendency to pustular skin diseases, infectious lesions of the respiratory system, urination, digestive tract, general malaise, weakness; in children - delayed growth and development, neurological disorders.

Diagnosis established on the basis of anamnesis, clinical and laboratory data. In a biochemical study of blood serum, the content of retinol in case of vitamin A deficiency is below 100 μg / l, carotene - below 200 μg / l. Ophthalmological examination allows to determine the time of dark adaptation.

Treatment. A nutritious diet including foods rich in retinol and carotene (liver, eggs, cow's milk, fish oil, rose hips, carrots, peas, sea buckthorn, green onions), retinol preparations in a daily dose for adults from 10 to 000 IU/day, depending depending on the severity of vitamin deficiency for 100-000 weeks under close medical supervision (large doses and uncontrolled treatment can cause hypervitaminosis A). For hemeralopia, xerophthalmia and retinitis pigmentosa, riboflavin is prescribed simultaneously.

Prevention. A varied diet with the inclusion of foods rich in retinol and carotene, in conditions of a forced monotonous diet - additional prescription of retinol, 1-2 tablets (3300-6600 IU).

4. Vitamin B deficiency₁ (thiamine)

Vitamin B deficiency₁ (thiamine) occurs when there is a lack of this vitamin in food (primarily eating polished rice in the countries of East and Southeast Asia), a violation of its absorption in the intestines and assimilation (with severe intestinal lesions that occur with malabsorption, persistent vomiting, prolonged diarrhea, etc.). d.).

Predispose to the development of the disease pregnancy and lactation, hard physical labor, febrile illness, thyrotoxicosis, diabetes mellitus. The daily requirement of an adult for vitamin B is about 2 mg. Vitamin B is part of a number of enzymes involved in carbohydrate metabolism, in the body it turns into cocarboxylase, which is a prosthetic group of enzymes involved in carbohydrate metabolism. In the development of a complete clinical picture of avitaminosis B₁ concomitant deficiency of other B vitamins is also important.

Clinic. It manifests itself as widespread damage to peripheral nerves (polyneuritis), the cardiovascular system and edema. Complaints include general weakness, fatigue, headache, shortness of breath and palpitations during physical activity. Then the phenomena of polyneuritis are added: paresthesia and decreased skin sensitivity of the lower extremities, and later other parts of the body, a feeling of heaviness and weakness in the legs, lameness, and fatigue when walking. The calf muscles become hard and painful on palpation. The characteristic gait of beriberi patients is that they step on the heel and then the outer edge of the foot, sparing the toes. Next, tendon reflexes fade and muscle atrophy occurs.

Violation of the activity of the cardiovascular system is manifested by tachycardia, degenerative changes in the heart muscle with circulatory failure, a decrease in blood pressure, mainly diastolic. There are symptoms of dystrophic lesions and dysfunctions of the digestive system, visual disturbances, mental disorders.

According to the prevailing symptoms, there are edematous form (with more pronounced lesions of the cardiovascular system and edema) and dry (with predominant damage to the nervous system), as well as an acute, malignant, fulminant form, often ending in death. It is difficult to recognize beriberi in young children.

Diagnosis established on the basis of anamnesis (nature of nutrition, the presence of diseases that contribute to the manifestation of thiamine deficiency), characteristic changes in the cardiovascular and nervous systems, laboratory data from a biochemical blood test: when the thiamine content in daily urine decreases below 100 mcg, hourly (on an empty stomach) - below 10 mcg, cocarboxylase content in erythrocytes below 20-40 mcg/l. Characterized by an increase in the content of pyruvic acid in plasma (above 0,01 g/l) and increased excretion in the urine (more than 25 mg per day). Recently, a number of more complex modern methods have also been used for this purpose.

Differential diagnosis with infectious (poliomyelitis, diphtheria, etc.) and toxic polyneuritis (poisoning with mercury, methyl alcohol, etc.) is based on taking into account the epidemic situation, the history of the disease, as well as on the results of biochemical studies of thiamine metabolism. The differential diagnosis of the edematous form of beriberi with myocarditis, myocardial dystrophies is facilitated by the presence of symptoms of polyneuritis.

Treatment. Complete food rich in vitamin B (cereals, dried brewer's yeast, cookies, egg yolk, nuts, legumes, pork, black bread). In severe and moderate cases, treatment in a hospital. Bed rest. Vitamin B is prescribed₁ 30-50 mg IM or SC followed by switching to oral administration; simultaneously prescribed nicotinic acid (25 mg), riboflavin (10-20 mg), vitamin B₆.

Symptomatic therapy: cardiovascular drugs, diuretics, to increase the tone of the nervous system - injections of strychnine (1: 1000, 1-1,5 mg each). With endogenous vitamin B deficiency₁ caused by chronic bowel diseases - their treatment.

Prevention. Eat a varied diet including foods rich in thiamine.

5. Vitamin B deficiency₂ (riboflavin)

Vitamin B deficiency₂ (riboflavin) occurs when there is a lack of vitamin B₂ in food, disruption of its absorption in the intestines, assimilation, or with increased destruction in the body. Riboflavin is found in many foods of animal and plant origin. The daily requirement of an adult is 2-3 mg.

In the body, riboflavin, interacting with ATP, forms flavin mono- and flavin dinucleotides, which are involved in the regulation of redox processes. With aribof lavinosis, cellular hypoxia occurs. Riboflavin is involved in the implementation of the visual function of the eye and the synthesis of hemoglobin. In the pathogenesis of ariboflavinosis, the lack of other B vitamins is also important.

Clinic. Manifested by decreased appetite, weight loss, headache, weakness, impaired twilight vision, dystrophic changes in the skin and mucous membranes, burning sensation of the skin, pain in the eyes, the appearance of conjunctivitis, angular and aphthous stomatitis (cracks and maceration of the epithelium and crusts in the corners of the mouth), seborrheic dermatitis, especially pronounced in the area of ​​the nasolabial folds, on the wings of the nose, ears, dry itchy dermatitis on the hands.

With a long course, disorders of the nervous system are observed: paresthesia, increased tendon reflexes, ataxia and others, as well as hypochromic anemia. The course is chronic, with exacerbations in the spring and summer months.

Diagnosis is established on the basis of anamnesis (nature of nutrition, presence of diseases), clinical and laboratory data in a biochemical study: with a decrease in the content of riboflavin in daily urine below 100 mcg, in hourly urine - below 10 mcg, in blood serum - below 3 mcg / l, erythrocytes - below 100 µg/l). Decrease in dark adaptation matters.

Differential diagnosis carried out with pellagra, beriberi A, multiple sclerosis. In doubtful cases, the results of studies of the content of vitamins in the blood and urine are the most conclusive.

Treatment. A complete diet (yeast, liver, kidneys, egg yolk, peanuts, mackerel, cod, cheese, cottage cheese, meat, leafy vegetables), taking riboflavin 10-30 mg orally for 2-4 weeks. At the same time, other B vitamins are prescribed. In case of endogenous deficiency, treatment of intestinal diseases accompanied by malabsorption.

6. Deficiency of nicotinic acid (vitamins PP, B₃ and etc.)

Deficiency of nicotinic acid (vitamins PP, B₃ etc.) is due to insufficient intake of this vitamin with food, insufficient absorption in the intestines (with various diseases of the stomach and small intestine, accompanied by absorption deficiency syndrome) or an increased need for it (during pregnancy, heavy physical work, etc.).

Clinic. It manifests itself as damage to the digestive, nervous systems and skin. Loss of appetite, dryness and burning in the mouth, vomiting, diarrhea alternating with constipation, and general progressive weakness appear. The tongue is bright red, swollen, with painful ulcerations. Atrophic and erosive changes are also found in other parts of the digestive tract. Damage to the nervous system is manifested by general irritability, symptoms of polyneuritis, and sometimes signs of damage to the spinal cord (usually the posterolateral columns). Skin lesions are manifested by pellagritic erythema, accompanied by skin itching, hyperpigmentation (mainly on open areas of the body and extremities), peeling of the skin, and the appearance of follicular papules. The functions of the endocrine system are disrupted, and hypoproteinemia develops. In severe cases, all the symptoms of pellagra appear, which occurs in some countries in Africa and Asia.

Nicotinic acid and its amide are effective antipellagrimic agents and are involved in cellular respiration. With their deficiency in the body, significant metabolic disorders and functions of many organs, dystrophic and degenerative changes in organs and tissues, most pronounced in the skin, nervous and digestive systems, occur. Typically, with pellagra, there are signs of deficiency of other B vitamins, as well as the amino acid tryptophan, contained in complete proteins. The daily requirement of adults for nicotinic acid and its amide is 20-25 mg.

Diagnosis is established on the basis of anamnesis, clinical and laboratory data in biochemical studies: the content of N1-methylnicotinamide in daily urine is below 4 mg, in hourly urine - below 0,3 mg, the content of nicotinic acid is below 0,2 mg. The content of other B vitamins in the blood and urine decreases.

Treatment in moderate and severe cases, inpatient: full-fledged fractional meals with a gradual increase in calorie content, nicotinic acid or nicotinamide orally 25-100 mg per day for 2-3 weeks in combination with other B vitamins. In endogenous forms - parenteral administration of nicotinic acid and its amide.

Prevention. A varied, balanced diet with sufficient content in the diet of foods rich in nicotinic acid (chicken, meat, legumes, liver, green vegetables, fish). In the endogenous form - timely diagnosis and treatment of intestinal diseases, prophylactic administration of nicotinic acid and its amide, additional administration of vitamin PP to persons with an increased need for it.

7. Vitamin B deficiency₆ (pyridoxine)

Only the endogenous form is observed when the bacterial flora of the intestine, which synthesizes pyridoxine in sufficient quantity for the body, is suppressed by long-term use of antibiotics, sulfanilamide and anti-tuberculosis drugs, especially with a simultaneous increased need for this vitamin (with significant physical exertion, pregnancy, etc.). Vitamin B₆ found in sufficient quantities in many products of plant and animal origin, especially in yeast. In the body, it is converted into pyridoxal-5-phosphate and is part of enzymes involved in the deoxylation and transamination of amino acids, histamine metabolism, and fat metabolism. The daily requirement for pyridoxine in adults is 2-2,5 mg.

Clinic. Manifested by irritability or lethargy, insomnia, polyneuritis of the upper and lower extremities, paresthesia, dyspeptic disorders, anorexia, stomatitis, seborrheic and desquamative dermatitis of the face, scalp, neck, hypochromic anemia, dystrophic changes occur in the cells of various organs, especially the digestive and nervous systems , skin; young children experience growth retardation.

Diagnosis is established on the basis of anamnesis, clinical and laboratory data in a biochemical study (the content of N-pyridoxic acid in daily urine is below 0,5 mg, hourly - below 30 μg, pyridoxine content in whole blood is below 50 μg / l). After taking 10 g of tryptophan, the release of xanthurenic acid exceeds 50 mg.

Treatment. Complete nutrition (liver, yeast, grains and legumes, rice, peanuts). Pyridoxine preparations 10-50-100 mg per day for 2-3 weeks orally, for chronic diseases of the gastrointestinal tract - parenterally, elimination of etiological factors.

Prevention. For long-term treatment with antibiotics, sulfonamides and anti-tuberculosis drugs, as well as for conditions accompanied by an increased need for pyridoxine (during pregnancy, sharply increased physical activity, etc.), prophylactic administration of vitamin B₆.

8. Vitamin C (ascorbic acid) deficiency

Vitamin C plays an important role in redox processes, carbohydrate metabolism, collagen and procollagen synthesis, and normalization of vascular permeability.

Clinic. It manifests itself as general weakness, increased fragility of capillaries with the formation of petechiae, bleeding from the gums, hemorrhagic effusions into the joints and pleura, dystrophic changes in the mucous membranes, anemization, and disorders of the nervous system.

Treatment. Good nutrition (fresh green vegetables, fruits, rose hips, citrus berries, black currants, cranberries) and prescription of medications containing vitamin C.

Prevention. A complete, balanced diet, preventive intake of ascorbic acid in conditions of possible deficiency (during long hikes with a predominant diet of canned and dried foods, women during pregnancy and lactation, etc.), proper preparation of food, preventing significant losses of ascorbic acid during culinary processing of products.

9. Vitamin D deficiency

Vitamin D deficiency is the most important₂ (ergocalciferol) and D₃ (cholecalciferol). The main amount of vitamin D is formed in the skin when it is exposed to light (ultraviolet rays); a smaller part comes from food. Vitamin D is fat-soluble, found in small quantities in butter, milk, egg yolk, especially high levels are found in the liver and adipose tissue of cod, some other fish and marine animals. In the body, it participates in the regulation of calcium and phosphorus metabolism. If there is a lack of foods containing vitamin D in food, as well as insufficient exposure to sunlight on the skin, a clinical picture of deficiency of this vitamin occurs in the form of rickets (see lecture below on Rickets in children). An adult's daily requirement for vitamin D is 100 IU, a child's is 500-1000 IU.

For the diagnosis in adults, data from biochemical laboratory studies are of primary importance (a decrease in the content of inorganic phosphorus in the blood below 30 mg / l, an increase in the activity of alkaline phosphatase).

Treatment. Vitamin D preparations₂ and D₃ in combination with calcium preparations and ultraviolet irradiation. In the future - dispensary observation and repeated courses of treatment (an overdose of vitamin D can cause intoxication). In case of vitamin D deficiency in adults caused by diseases of the digestive tract and impaired bile secretion, in addition to prescribing vitamin D preparations, the underlying disease is treated.

10. Vitamin K deficiency

Vitamin K deficiency is rare in adults. It is caused by the cessation of the flow of bile into the intestine, which is necessary for the absorption of phylloquinones (with obstruction and compression of the biliary tract), as well as chronic intestinal diseases, accompanied by a syndrome of insufficiency of absorption. It is also observed with an overdose of dicoumarin. Vitamin K enters the body with food and is partly formed by the intestinal microflora.

Clinic. Hemorrhagic syndrome (bleeding from the nose, gums, gastrointestinal, intradermal and subcutaneous hemorrhages).

Diagnosis is confirmed by clinical observation data (the presence of diseases that contribute to vitamin K deficiency), as well as laboratory biochemical studies: hypoprothrombinemia below 30-35%, proconvertin deficiency, as well as factors IX and x are characteristic.

Treatment carried out in a hospital with vitamin K (vikasol) under the control of the level of prothrombin and coagulogram.

Hypopolivitaminoses, polyavitaminosis are more common than isolated relative or complete insufficiency of one of the vitamins. In the pathogenesis of hypovitaminosis and polyavitaminosis, one should take into account the mutual influence of certain vitamins, their synergism and antagonism.

The underlying disease leading to the syndrome of malabsorption is treated, vitamin preparations are prescribed, parenteral administration of the vitamin. Prevention: timely diagnosis and treatment of diseases of the gastrointestinal tract, in which the absorption of nutrients and vitamins is disturbed, the inclusion of vitamin therapy in the course of treatment of chronic diseases of the digestive tract.

Author: Gavrilova N.V.

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