It will not be a secret to anyone that proper nutrition is of great importance in the life of every person. The same applies to children. In this article I would like to talk in detail about such a problem as protein-energy malnutrition.

What it is?

At the very beginning, you need to decide on the concepts that will be used in the article. What protein-energy deficiency is is probably clear to everyone. This is a lack of protein in the child's body. It is also worth clarifying that this condition is pathological. More precisely, the human body receives too little or no protein in any form. This can also be caused by too rapid decomposition of the substance. In this case, the cause of this phenomenon may be burns, purulent-septic diseases, or severe injuries.

Main reasons

Why might protein-energy malnutrition occur? It is worth saying that this problem is very common among residents of developing countries. During periods of hunger strike, the percentage of people with this disease reaches 25%. In this case, the cause is insufficient quantity or low quality of food. The problem is aggravated by the lack of energy supply. And all because amino acids from food in this case are not used for food. They are oxidized to produce energy.

Protein-energy malnutrition may occur secondaryly in children for the following reasons:

1. Disruption of digestive processes (decreased absorption of nutrients).
2. Protein loss may occur due to neuroendocrine regulation.

Forms

1. Marasmus. In this case, the child’s growth is delayed and subcutaneous fat is observed.
2. Kwashiorkor. This is precisely isolated protein deficiency. In addition to growth retardation, the child may have swelling and, however, in this case, subcutaneous fat remains.

Severity

If we are talking about a problem such as protein-energy malnutrition, the degree is what also needs to be talked about. There are only three of them:

1. Easy (first, I).
2. Moderate (second, II).
3. Heavy (third, III).

Mild degree

If we are talking about a mild degree of protein deficiency, the child’s body is only weakened. In this case, its resistance to various viruses and infections decreases. The main symptoms that will be present are:

1. Increasing weakness.
2. The child's lethargy and low ability to work.
3. Rapid not only physical, but also psychological fatigue.
4. Chilliness, feeling of cold.
5. Thirst and hunger. There may be increased urination.
6. Dizziness is possible.
7. Numbness of the lower extremities will occur.

The child's growth may also be delayed at this stage.

Moderate degree

We further consider such a problem as protein-energy malnutrition. Stage 2 disease (first) most often occurs in residents of developing countries. In this case, as mentioned above, the growth of children occurs. However, the second degree is also characterized by biochemical changes in the body. Thus, a significant cellular weakening of immunity occurs. And this leads to increased sensitivity to various types of viruses and infections.

Severe form

There is also profound or severe protein-energy malnutrition (i.e. cachexia). However, it is more typical for people with cancer. In this case, the child can lose weight very quickly and diarrhea occurs. The patient’s muscles also suffer; the limbs seem like sticks covered with skin. Hair becomes dull, brittle, and falls out. Water retention in tissues may occur, often leading to swelling. Irreversible changes also occur in the patient’s internal organs. However, all this is individual (the doctor can tell you about this after certain studies). Other symptoms characteristic of such a problem as severe protein-energy malnutrition in children:

1. Apathy, fatigue.
2. Constant feeling of cold.
3. Depigmentation of skin and hair.
4. The skin becomes dry and cracked. The child's face takes on an old look.
5. Blood pressure, pulse, and temperature decrease.

Isolated form

Quite rare, but an isolated form of protein deficiency can still occur. Most often, it is accompanied by a deficiency of such components as vitamins B1, B2, B6, folic and nicotinic acid, vitamin A. If we talk about children, then vitamin A deficiency poses a danger to children. As the disease progresses, intracellular loss of potassium occurs , phosphorus and magnesium.

Treatment

If we talk about such a problem as protein-energy deficiency, treatment is where you also need to focus your attention. So, if a child has one of the first two forms of the disease, the problem can still be dealt with by adjusting the diet. In this case, it is very important to increase your daily protein intake. It will vary for kids of different ages:

1. If the child is between one and seven years old, the daily dose will be approximately 3-4 grams of protein per 1 kg of weight.
2. Schoolchildren's protein needs are slightly lower: 2-3 grams per 1 kg of weight.

The child will be prescribed multivitamin complexes. After all, food alone in this case will not be enough. Regulation of water and electrolyte balance can also be carried out.

If a child has severe protein-energy deficiency, the baby will be sent to the hospital. It is impossible to cope with this problem on your own at home. What will be relevant in this case:

1. Controlled diet.
2. Correction of water-electrolyte balance using infusion therapy.
3. Additional nutrition will also be prescribed with mixtures that are rich in nutrients.
4. If absorption is impaired, the child will be prescribed (infusion of nutrients).
5. Vitamin therapy. However, in this case it will be special. Such people need twice as many vitamins as a healthy person. And this is until the moment of recovery.
6. Patients with anorexia may be prescribed medications that increase appetite. If you need to increase muscle mass, doctors may prescribe anabolic steroids.

Prevention

To avoid protein-energy malnutrition in children, you need to carefully monitor their diet. The following foods will help fill your food with protein:

1. Chicken meat.
2. Fish.
3. Beef.
4. Eggs.
5. Dairy products.

At the same time, it is also important to remember about other useful microelements. Along with protein, the child must receive sufficient amounts of carbohydrates and fats from food.

NUTRITION FOR PROTEIN-ENERGY MALFICIENCY (ICD-10 E44)

In Russia, for many years, the term malnutrition was adopted, which is synonymous with protein-energy malnutrition.

Hypotrophy (impaired nutritional status) is a condition characterized by chronic malnutrition and lack of body weight in relation to height and age.

Depending on the time of occurrence, a distinction is made between prenatal (congenital, intrauterine) malnutrition and postnatal (developed after birth). Prenatal malnutrition is based on a violation of intrauterine development of the fetus due to the constitutional characteristics of the mother, insufficiency of placental circulation, exposure to infectious, hereditary, unfavorable socio-economic, industrial and environmental factors.

In the postnatal period, malnutrition can develop under the influence of endogenous or exogenous factors (Table 24).

Table 24. Factors predisposing to the development of malnutrition in the postnatal period

Endogenous factors	Exogenous factors
Congenital malformations (cardiovascular system, gastrointestinal tract, central nervous system, genitourinary system, liver) Congenital or acquired lesions of the central nervous system (cerebral ischemia, perinatal damage to the nervous system, intracranial hemorrhage) Malabsorption syndromes (with lactase deficiency, celiac disease, cystic fibrosis, etc.) Hereditary immunodeficiencies Endocrine diseases, etc. Hereditary metabolic disorders	Nutritional (quantitative and qualitative underfeeding, early artificial feeding with unadapted milk formulas, incorrect and untimely introduction of complementary foods, feeding irregularities and care defects) Chronic course of nutrition-dependent diseases (anemia, rickets, intestinal dysbiosis, etc.) Severe infectious diseases Severe chronic pathology

Diagnostics

To identify malnutrition in children, clinical and laboratory methods are used (Table 25).

Table 25. Methods for assessing nutritional status

Somatometric methods are a key way to assess the nutritional status of a child. A necessary element of anthropometry is the presence of tables comparing weight-height and age indicators and/or a map of the centile distribution of weight and height indicators. In 2006, the World Health Organization proposed “Standard Growth Charts” for children of all age groups for use in general pediatric practice. These maps contain the distribution of children by weight-age, height-age, weight-height indicators, as well as by body mass index.

Domestic pediatricians classify malnutrition according to the time of occurrence and according to body weight deficiency (Table 26).

Table 26. Classification of malnutrition (according to E.V. Neudakhin, 2001)

A more objective indicator of the state of physical development of a child of a certain age is to take into account not only body weight, but also height. To do this, it is advisable to use centile tables. Combined deficiency of body weight and height develops with long-term malnutrition or with a severe chronic illness of the child.

In epidemiological studies of the prevalence of malnutrition in children, the Z-score indicator is used, which is the deviation of the values ​​of an individual indicator (body weight, height, BMI) from the average value for a given population, divided by the standard deviation of the average value.

In a standard population, the average Z-score is zero with a standard deviation of 1.0. Positive Z-score values ​​indicate an increase in the anthropometric indicator compared to the standard, and negative values ​​indicate a decrease in parameters compared to the standard value. By pronounced negative values, one can judge the lag in physical development. For example, a 3-month-old child has a body weight of 4 kg, while the average body weight of a child of this age is 6 kg.

Z-speed = (4 - 6)/1

In accordance with the formula, his Z-score is -2, which indicates a significant lag in physical development.

Poor nutrition and loss of body weight are manifested not only by protein-calorie deficiency, but also by hypovitaminosis, deficiency of many essential microelements responsible for the implementation of immune functions, optimal growth, and brain development. Therefore, long-term malnutrition is often accompanied by a lag in psychomotor development, delayed speech and cognitive skills and functions, and a high incidence of infectious diseases due to decreased immunity, which in turn aggravates nutritional disorders.

The causes of malnutrition in various diseases in children can be divided into 4 groups:

insufficient and unbalanced nutrition, violation of feeding regime;

malnutrition due to difficulty eating: severe illness, dysphagia, vomiting, cerebral palsy and others;

increased nutritional needs: premature babies, congenital heart defects, chronic lung pathology (bronchopulmonary dysplasia, cystic fibrosis), rehabilitation period after severe infections accompanied by catabolic stress and others.

violation of digestion and absorption of food: malabsorption syndrome, all types of damage to the gastrointestinal tract (after surgery, inflammatory bowel diseases, intestinal protein loss syndrome, etc.)

Dietary correction of malnutrition

Basic rules for organizing therapeutic nutrition for malnutrition:

it is necessary to take into account the age, severity, severity and nature of the underlying disease;

strive to meet the child’s age-related needs for basic nutrients, energy, macro- and micronutrients by gradually increasing the food load, taking into account the child’s food tolerance;

avoid unjustified displacement of human milk or adapted milk formulas with complementary feeding products;

consistently introduce complementary feeding products, taking into account the nutritional status of the child, gradually increasing their volume;

use industrially produced complementary feeding products; the introduction of cereals is recommended as the first complementary feeding.

In case of malnutrition of the first degree, it is necessary to establish a general regime, care for the child, and eliminate feeding defects. When prescribing nutrition, preference should be given to breast milk, and in case of mixed and artificial feeding - to adapted milk formulas enriched with galacto- and fructo-oligosaccharides, which have a beneficial effect on the digestive processes and normalization of the composition of the intestinal microflora; nucleotides, which improve the absorption of nutrients and stimulate the child’s immune system, as well as fermented milk products. In this case, calculations and nutritional correction are carried out based on the proper body weight, which consists of body weight at birth and the sum of its normal increases over the life period. To increase the energy value of the diet and increase the protein quota, it is possible to prescribe meals and complementary foods (porridge, vegetable and meat purees, cottage cheese) 2 weeks earlier than for healthy children.

In case of malnutrition of the second degree, dietary correction is conventionally divided into three periods: the adaptation period (determining food tolerance), the reparation period (intermediate) and the period of enhanced nutrition.

During the adaptation period, which lasts 2-5 days, nutrition is calculated based on actual body weight in accordance with the child’s physiological needs for basic nutrients and energy. The number of feedings is increased by 1-2 per day with a corresponding reduction in the volume of each feeding; additional fluid is administered (5% glucose or saline solutions for oral rehydration). During this period, along with human milk or infant formula enriched with oligosaccharides and nucleotides, it is advisable to use mixtures based on protein hydrolyzate, which are easily digested and absorbed by the child’s body, and adapted fermented milk mixtures.

With normal tolerance of the prescribed nutrition, the volume of feedings is gradually (over 5 - 7 days) increased to the physiological norm. It is possible to use formulas with a higher protein content, for example, specialized milk formulas for premature babies. With sufficient rates of body weight gain and the absence of dyspeptic symptoms, nutritional calculations can be made based on the proper body weight (body weight at birth + its normal increase over the life period), first the carbohydrate and protein components, and only lastly the fat component of the diet.

During the reparation period, it is possible to introduce complementary foods, starting with industrially produced cereals, followed by the introduction of meat, cottage cheese, and yolk. During this period, enzyme preparations, multivitamin complexes and agents that have a positive effect on metabolic processes should be prescribed.

Throughout the treatment of children with malnutrition, systematic recording of actual nutrition is necessary with calculation of the chemical composition of the daily diet based on the main food nutrients.

With grade III malnutrition, all types of metabolism are sharply disrupted; the child’s condition, as a rule, is very severe, so such children require intensive therapy, and often also the use of not only enteral, but also parenteral nutrition, which requires hospital treatment. III degree hypotrophy caused by nutritional factors is rare, because the main disturbances in the child’s nutrition are detected early and the necessary dietary correction of the diet of these children is carried out even at I - II degrees of malnutrition.

Tactics for managing patients with grade III malnutrition

There are several main tactical steps in the treatment of severe malnutrition in the initial period:

treatment or prevention of hypoglycemia and hypothermia,

treatment or prevention of dehydration and restoration of electrolyte balance,

etiotropic treatment of the infectious process if present,

identifying and overcoming other problems associated with deficiency of vitamins, microelements, anemia, etc.

For children who do not require urgent therapy, optimal nutrition is the basis for adequate nutritional support. To avoid excess load on the gastrointestinal tract, kidneys, and liver, nutrition should be started in small portions with short breaks between meals (2.5-3 hours), if the child eats independently and has maintained his appetite. The energy capacity of the diet should provide at least 80 kcal/kg and no more than 100 kcal/kg/day. With a lower caloric intake, catabolism processes continue, while with a higher caloric intake, severe metabolic disorders may develop. As the child adapts to this calorie content, the amount of food, the protein quota, and the intervals between feedings are gradually increased. The amount of protein in the diet in the first days of feeding should be reduced to 1.0-1.2 g/100 ml of mixture (Table 27).

Nutrients	Amount per kg body weight/day
Electrolytes:	1.0 mmol (23 mg) 4.0 mmol (160 mg) 0.6 mmol (10 mg) 2.0 mmol (60 mg) 2.0 mmol (80 mg)
Microelements:	30 micromoles (2.0 mg) 4.5 µmol (0.3 mg) 60 nanomoles (4.7 µg) 0.1 micromolar (12 µg)
Water-soluble vitamins: Nicothiamide Folic acid Pantothenic acid	70 mcg 0.2 mg 70 mcg 0.1 mg 0.1 mg 10 mcg 0.3 mg 10 mg
Fat-soluble vitamins	0.15 mg 3 mcg 2.2 mg 4 mcg

For children with impaired digestive and absorption function of the intestine (short bowel syndrome, persistent diarrhea, inflammatory bowel disease), enteral nutrition should begin with a very low concentration of the product; it is better to use mixtures containing hydrolyzed protein, starting with a 3% concentration of the product. The use of mixtures containing a protein component split into peptides (Alfare, Nutrilon Pepti TSC, Nutrilak Peptidi SCT, Pregestimil) does not require the active work of proteases and allows for adequate protein supply for repair processes. The concentration of the administered mixture is increased slowly, increasing by 1% per day (Table 28).

Table 28. Concentrations of a mixture based on protein hydrolyzate used in children with severe malnutrition of the third degree

Next, the concentration of the mixture is gradually increased to 13.5%, and if well tolerated - to 15%. Missing calories, electrolytes and nutrients during the period of consumption of a product with a low concentration of nutrients are compensated by parenteral nutrition. For seriously ill children, a slow continuous infusion of nutritional mixtures through a nasogastric tube is indicated, which promotes optimal utilization of nutrients. By varying the rate of infusion, the volume of cavity digestion and intestinal absorption can be gradually increased. This feeding method is effective and logical for children with a reduced absorption surface area, such as intestinal villous atrophy, short bowel syndrome and other conditions.

The transition to fractional enteral nutrition can take from several days to several weeks or even months, depending on the severity of the patient’s condition and the effectiveness of continuous infusion. During the infusion period, sucking and swallowing should be simultaneously stimulated. When switching to split meals, you can first leave a constant infusion at night with simultaneous daytime split meals in small portions 5 - 6 times during the day until the split meals in calorie content do not exceed 75% of the daily intake. From this point on, they switch completely to fractional nutrition, however, oral intake should be increased very slowly, since infusion nutrition is accompanied by a relative decrease in intestinal activity.

An improvement in the child's appetite and the appearance of weight gain indicate an improvement in the child's condition. From this moment, the rehabilitation phase begins, in which a gradual transition to a more high-calorie and protein-rich diet is carried out, as well as the replacement of hydrolyzed mixtures with mixtures containing whole protein. The volume of fractional feeding should be increased slowly by 10 ml at each subsequent feeding (for example, 60 ml, then 70 ml, then 80 ml, etc.) until the volume of nutrition reaches the age norm.

During this period, you should keep a feeding chart for the child, noting the prescribed and actually consumed food. During the rehabilitation period, the energy load gradually increases from 80 - 100 kcal/kg/day to 130 kcal/kg/day with a maximum consumption of up to 150 - 200 kcal/kg/day. If the child cannot digest the 130 kcal/kg/day nutritional intake, revert to smaller volumes, higher frequency, and even continuous infusions of nutritional solutions if necessary. The duration of the rehabilitation period depends on the age, severity of the underlying disease and the speed of adaptation of the child to nutrition. At the same time, increase the protein quota in the diet from 1 to 2.5 - 3.0 g/100 ml. The criteria for the adequacy of nutritional support are: improvement of appetite, general well-being, physical activity and daily weight gain of at least 5 g/kg body weight per day.

Materials for this chapter were also provided by: Bushueva T.V. (Moscow), Rybakova E.P. (Moscow), Stepanova T.N. (Moscow)

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2015

Nutritional marasmus (E41), Protein-energy malnutrition, unspecified (E46), Moderate and mild protein-energy malnutrition (E44), Developmental delay due to protein-energy malnutrition (E45), Kwashiorkor (E40), Marasmic kwashiorkor (E42), Severe protein-energy malnutrition, unspecified (E43)

Pediatric Gastroenterology, Pediatrics

general information

Short description

Recommended
Expert advice
RSE at the RVC "Republican Center"
healthcare development"
Ministry of Health
and social development
Republic of Kazakhstan
dated November 6, 2015
Protocol No. 15

Protocol name: Protein-energy deficiency in children

Protein-energy deficiency- malnutrition of the child, which is characterized by a stop or slowdown in body weight gain, a progressive decrease in the subcutaneous tissue, disturbances in body proportions, nutritional functions, metabolism, weakening of specific, nonspecific defenses and asthenization of the body, a tendency to develop other diseases, delays in physical and neurological development. mental development.

Protocol code:

ICD-10 code(s):
· E40-E 46. Malnutrition (hypotrophy: prenatal, postnatal).
· E40. Kwashiorkor.
· E41. Nutritional insanity.
· E42. Senile kwashiorkor.
· E43. Severe protein-energy malnutrition, unspecified.
· E44. Protein-energy malnutrition, unspecified, moderate and weak.
· E45. Developmental delay caused by protein-energy deficiency.
· E46. Protein-energy malnutrition, unspecified.

Abbreviations used in the protocol:

PEM - protein-energy malnutrition ACTH - adrencorticotropic hormone AMK - amino acid AST - aspartate aminotransferase ALT - alanine aminotransferase AT to TTG - antibodies to tissue transglutaminase IBD - inflammatory bowel diseases VPR - congenital malformation UPS - Congenital heart defect GERD - gastroesophageal reflux disease Gastrointestinal tract - gastrointestinal tract BMI - body mass index CT - CT scan KFK - creatine phosphokinase Exercise therapy - physiotherapy CF - cystic fibrosis NS - nervous system PP - parenteral nutrition SCT - medium chain triglycerides 17-OX - 17-ketosteroids TSH - thyroid-stimulating hormone Ultrasound - ultrasonography FGDS - fibroesophagogastroduodenoscopy alkaline phosphate - alkaline phosphatase CNS - central nervous system ECG - electrocardiogram EchoCG - Echocardiography

Date of development of the protocol: 2015

Protocol users: pediatricians, general practitioners, pediatric neurologists, gastroenterologists, endocrinologists, surgeons, oncologists, hematologists, pulmonologists, resuscitators.

Assessment of the degree of evidence of the recommendations provided.
Level of evidence scale:

A	A high-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias, the results of which can be generalized to an appropriate population.
IN	High-quality (++) systematic review of cohort or case-control studies or High-quality (++) cohort or case-control studies with very low risk of bias or RCTs with low (+) risk of bias, the results of which can be generalized to an appropriate population .
WITH	Cohort or case-control study or controlled trial without randomization with low risk of bias (+). Results that can be generalized to the relevant population or RCTs with very low or low risk of bias (++ or +) whose results cannot be directly generalized to the relevant population.
D	Case series or uncontrolled study or expert opinion.
GPP	Best pharmaceutical practice.

Classification

Clinical classification:

By time of occurrence:
· prenatal;
· postnatal.

By etiology:
· nutritional;
· infectious;
· associated with defects in regimen and diet;
· associated with prenatal damaging factors;
· caused by hereditary pathology and congenital developmental anomalies.

By severity:
· PEM degree I - body weight deficiency 11-20%;
· PEM II degree - body weight deficiency 21-30%;
· PEM III degree - body weight deficiency › 30%.

By periods:
· initial;
· progression;
· stabilization;
· convalescence.

By form:
Acute - manifested by a predominant loss of body weight and its deficiency in relation to the required body weight for height;
· chronic - manifested not only by a lack of body weight, but also by significant growth retardation.

Some special variants of the BEN variety:
· kwashiorkor, nutritional marasmus, marasmic kwashiorkor;
· malnutrition in older children;
· lack of microelements (copper, zinc, selenium).

Clinical picture

Symptoms, course

Diagnostic criteria for diagnosis

:

Complaints and anamnesis:
Complaints: depending on the pathology that led to signs of malnutrition: poor weight and height gain, poor appetite, refusal to eat, vomiting, nausea, choking during feeding, bloating, loose stools, constipation, large volume of stools, abdominal pain, swelling, cramps, cough, shortness of breath, prolonged fever, anxiety, dry skin, hair loss, nail deformation, weakness.

Anamnesis: Determine the disease in the child that led to signs of PEM.

Table 1 - Main causes of malnutrition in children

causes	mechanisms	nosologies and conditions
Insufficient food intake	swallowing disorders (dysphagia), anorexia, disturbances of consciousness, intracranial hemorrhage, chronic cardiac or respiratory failure, underfeeding, malnutrition in adolescents	non-closure of the soft and hard palate, tumors of the oral cavity and pharynx, anatomical disorders of the gastrointestinal tract (gastroesophageal reflux, pylorospasm, pyloric stenosis), congenital heart disease, congenital malformation of the lungs, congenital malformation of the NS, adrenogenital syndrome, psychogenic anorexia
Digestive and nutrient absorption disorders (maldigestion and malabsorption)	disorders of digestion and absorption of proteins, fats, carbohydrates, micro-macronutrients	cystic fibrosis, celiac disease, enteropathic acrodermatitis, allergic enteropathies, impaired transport of glucose - galactose, immunodeficiency states, short bowel syndrome, lymphangiectasia, chloride diarrhea, congenital malformation of the small and large intestine
Loss of nutrients from the body	loss of proteins, vitamins, macro and microelements - through the gastrointestinal tract or kidneys	intestinal fistulas, profuse diarrhea, uncontrollable vomiting, Bartter's syndrome, IBD
Metabolic disorders	catabolic states, organ dysfunctions	severe injuries, sepsis, oncological process, leukemia, liver, kidney failure

Clinical criteria:
· assessment of physical status (compliance with age standards for weight, body length, etc.) using centile tables;
· assessment of somatic and emotional state (aliveness, reaction to the environment, morbidity, etc.);
· assessment of the skin (pallor, dryness, presence of rashes, etc.);
· assessment of the condition of the mucous membranes (presence of aphthae, thrush, etc.);
· assessment of tissue turgor;

The proper (ideal) body weight in children is determined using tables of centile or percentile distributions of body weight depending on the height, age and gender of the child. When studying anthropometric parameters in children, the circumference of the head, chest, abdomen, shoulder, hip, as well as the thickness of the skin and fat folds at standard points is assessed. In young children, great importance is attached to head circumference, number of teeth and size of fontanelles.

Table 2 - Classification of protein-energy malnutrition in young children (according to Waterlow J.C., 1992)

Calculating BMI for young children is not very informative, and it can only be used in children over 12 years of age (Table 3).

Table 3 - Assessment of nutritional status in children over 12 years old by body mass index (Gurova M.M., Khmelevskaya I.G., 2003)

Type of eating disorder	degree	Body mass index
Obesity	I	27,5-29,9
	II	30-40
	III	>40
Increased nutrition		23,0-27,4
Norm		19,5-22,9
Reduced nutrition		18,5-19,4
BEN	I	17-18,4
	II	15-16,9
	III	<15

Assessment of the subcutaneous fat layer (reduction or absence):

· with stage I PEN - reduction on the abdomen;
· with PEN II degree - decrease in the abdomen, limbs;
· with grade III PEN - absence on the face, abdomen, torso and limbs.

Physical and laboratory examination: delayed physical and neuropsychic development.

BEN 1st degree- is not always diagnosed, since the child’s general condition suffers little. Symptoms: moderate motor restlessness, decreased bowel movements, slight pallor of the skin, thinning of subcutaneous fat in the torso and/or abdomen. In the navel area, the subcutaneous fat layer reaches 0.8 - 1.0 cm. Body weight is reduced by 10-20% of its normal value. BMI - 17 - 18.4. Chulitskaya's body condition index reaches 10-15 (normally 20-25). Psychomotor development corresponds to age, immunological reactivity and food tolerance are not changed. In the blood protein spectrum there is hypoalbuminemia. Symptoms of rickets, deficiency anemia.

BENII degree- characterized by pronounced changes in all organs and systems. Decreased appetite, periodic vomiting, sleep disturbance. There is a lag in psychomotor development: the child does not hold his head well, does not sit, does not stand on his feet, and does not walk. Thermoregulation disorders are manifested by significant fluctuations in body temperature during the day. A sharp thinning of subcutaneous fat on the abdomen, torso and limbs. The skin fold in the navel area is 0.4-0.5 cm, the Chulitskaya index decreases to 10.0. The gap in weight is 20-30%, in body length is 2-4 cm. BMI is 15-16.9. Incorrect type of mass growth curve. The skin is pale, pale gray, dryness and flaking of the skin are noted (signs of polyhypovitaminosis). Elasticity, tissue turgor and muscle tone decrease. Hair is dull and brittle. Food tolerance decreases. The nature of bowel movements changes - unstable stools, alternating constipation and diarrhea. Starch, neutral fat, mucus, muscle fibers, and disturbances in intestinal flora can be detected in feces. Urine smells like ammonia. Concomitant somatic pathology (pneumonia, otitis media, pyelonephritis), deficiency conditions.

BENIII degree- anorexia, general lethargy, decreased interest in the environment, lack of active movements. The face is suffering, senile, cheeks are sunken with atrophy of Bisha's lumps, in the terminal period - indifference. Thermoregulation is severely impaired, the child quickly cools down. A fold of skin at the navel level up to 0.2 cm (almost disappears). Chulitskaya's body condition index is negative. The lag in body weight is more than 30%, the lag in body length is more than 4 cm, and delayed psychomotor development. BMI -<15 Дыхание поверхностное, иногда могут отмечаться апноэ. Тоны сердца ослабленные, глухие, может наблюдаться тенденция к брадикардии, артериальной гипотонии. Живот увеличен в объёме вследствие метеоризма, передняя брюшная стенка истончена, контурируются петли кишок, запоры чередуются с мыльно-известковыми испражнениями. Резко нарушена толерантность к пище, нарушены все виды обмена. У большинства больных отмечается рахит, анемия, явления дисбиоза. Терминальный период характеризуется триадой: гипотермией (температура тела 32-33° С), брадикардией (60-49 уд/мин), гипогликемией.

Clinical manifestations of PEM are grouped into syndromes:
· syndrome of trophic disorders: thinning of subcutaneous fatty tissue, decreased tissue turgor, flat growth curve and deficiency of body weight relative to body length, signs of polyhypovitaminosis and hypomicroelementosis;
· syndrome of digestive disorders: anorexia, dyspeptic disorders, decreased food tolerance, signs of maldigestion in the coprogram;
· central nervous system dysfunction syndrome: decreased emotional tone, predominance of negative emotions, periodic anxiety (with stage III PEN - apathy), delayed psychomotor development;
· syndrome of hematopoiesis disorders and decreased immunobiological reactivity: deficiency anemia, secondary immunodeficiency states (the cellular component of immunity is especially affected). An erased, atypical course of pathological processes is noted.

Diagnostics

Diagnostic tests:

Basic (mandatory) diagnostic examinations performed on an outpatient basis:
· general blood analysis;
· general urine analysis;
· coprogram;
· biochemical blood test: total protein, total bilirubin and its fractions, ALT, AST, glucose;
Weighing and measuring the child’s body length

The minimum list of examinations that must be carried out when referred for planned hospitalization: in accordance with the internal regulations of the hospital, taking into account the current order of the authorized body in the field of healthcare.

Basic (mandatory) diagnostic examinations carried out at the inpatient level (during planned hospitalization):
· general blood test (once every 10 days);
· general urine analysis (once every 10 days);
· biochemical blood test: total protein, protein fractions, total bilirubin and its fractions, ALT, AST, glucose, alkaline phosphatase, electrolyte levels (potassium, sodium, magnesium, phosphorus, calcium, chlorine), urea, transferrin, creatinine, cholesterol;
· coprogram;
· ECG;
· EchoCG;
· Ultrasound of the abdominal organs, kidneys, adrenal glands;
· monitoring and analysis of actual nutrition - daily;

Additional diagnostic tests performedat the stationary level:
· determination of sweat chlorides;
· determination of antibodies to tissue transglutaminase (AT to TTG) using the “Biocard celiac” test;
· sowing of biological fluids with colony selection;
· analysis of microbial sensitivity to antibiotics;
· coagulogram;
· immunogram (total number of lymphocytes, CD4 + T-lymphocytes, granulocytes, complement activity, immunoglobulins A, M, G);
· hormones of the thyroid gland (TSH, T3, T4), adrenal glands (cortisol, ACTH, 17 OCS), CPK;
· FGDS with biopsy;
· histological examination of the mucous membrane of the jejunum;
· CT (head, chest, abdominal, pelvic organs);
daily salt excretion;
· genetic research (as prescribed by the geneticist);
· X-ray examination of the chest and abdominal organs;
· consultations with specialists: pulmonologist, gastroenterologist, immunologist,
oncologist, neurologist, hematologist, endocrinologist, medical psychologist, psychiatrist, surgeon, cardiac surgeon, infectious disease specialist, geneticist, nutritionist, resuscitator.

Instrumental studies:
· ECG - for screening diagnostics;
· EchoCG - for diagnostic purposes to identify morphological and functional changes in the heart;
· ultrasound examination of the abdominal cavity, kidneys - for screening diagnostics.
· fibroesophagogastroduodenoscopy with biopsy of the small intestine is performed for diagnostic purposes in children with malabsorption syndrome.
· fibroesophagogastroduodenoscopy is performed for diagnostic purposes in children with regurgitation or vomiting.
· X-ray examination of the esophagus, stomach, biliary tract, intestines, lungs - to exclude congenital malformation.
· CT scan of the head, chest, abdominal, pelvic organs - to exclude a pathological process.

Laboratory research:

· determination of sweat chlorides - if cystic fibrosis is suspected;
· determination of antibodies to tissue transglutaminase (AT to TTG) using the “Biocard celiac” test - in case of malabsorption, to exclude celiac disease;
· sowing of biological fluids with the selection of colonies - during a long-term infectious process;
· analysis of the sensitivity of microbes to antibiotics - for the selection of rational antimicrobial therapy;
· coagulogram - for diagnosing the hemostasis system;
· immunogram (total number of lymphocytes, CD4 + T-lymphocytes, granulocytes, complement activity, immunoglobulins A, M, G) - to exclude an immunodeficiency state;
· hormones of the thyroid gland (TSH, T3, T4), adrenal glands (cortisol, ACTH, 17 OKS), CPK - to exclude pathology of the thyroid gland and adrenal glands;
daily salt excretion - for the diagnosis of metabolic disorders.

Differential diagnosis

Differential diagnosis:
When examining and examining a child with PEM, the cause that led to PEM is determined and a competing pathology is excluded.

In this regard, it is necessary to differentiate the following diseases:
· infectious diseases;
· chronic diseases of the bronchopulmonary system;
· hereditary and congenital enzymopathies;
· endocrine diseases;
organic diseases of the central nervous system;
· surgical diseases;
· genetic diseases;
· diseases occurring with malabsorption syndrome;
· oncological pathology.

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Treatment

Treatment Goals:
· elimination of factors that led to PEM;
· stabilization of the child’s condition;
· optimized diet therapy;
· replacement therapy (enzymes, vitamins, microelements);
· restoration of reduced immune status;
· treatment of concomitant diseases and complications;
· organization of optimal regimen, care, massage, exercise therapy;

Treatment tactics:
· children with stage 1 PEM in the absence of severe concomitant diseases and complications are indicated for outpatient treatment;
· children with PEM II - III degrees, depending on the severity of the condition, are indicated for inpatient examination and treatment;
· in the treatment of children with stage III PEN, with signs of multiple organ failure, in order to correct the ongoing infusion therapy and parenteral nutrition, hospitalization in the intensive care unit;
· treatment of PEM in older children includes the same general principles as in the treatment of PEM in young children. For school-age children, diet therapy used for PEM in adults is acceptable, but taking into account the age-related needs for nutrients, ingredients, calories and the individual characteristics of the sick child.

Non-drug treatment:
· optimal sleep schedule, in accordance with age, stay in a regularly ventilated, bright room, wet cleaning is carried out twice a day. The air temperature should be maintained in the room (ward) in the range of 25-26° C.
· diet therapy: mixtures based on deep hydrolysis of milk protein, with MCT, without lactose, high calorie content (Nutrilon Petit Gastro, Alfare, Humana HN MCT; for children over one year old: Nutricomp Energy, Nutricomp Energy Fiber, Nutrien Elemental, Fresubin Energy, Diben, Reconvan , Nutrien Immun, Supportan, Pedia Shur. Mixtures for premature infants based on partial protein hydrolysis, with MCT, high calorie content: Humana O-NA, Pre Nutrilon, Pre Nan, Similac Special care;

Drug treatment:
Essential medicines (Table 8):
Enzyme preparations - medicines that help improve the digestion process and include digestive enzymes (enzymes). The most optimal are microspherical and microencapsulated forms of pancreatin. Enzyme preparations are prescribed long-term at the rate of 1000 units/kg per day at main meals.
Vitamins fat-soluble, water-soluble- for the correction of deficiency conditions (ascorbic acid, B vitamins, vitamin A, E, D, K), for parenteral administration - Addamel, Vitalipid.
Antibiotics - Various groups of antibiotics are used to prevent and treat infections .
Probiotics - living microorganisms that are normal flora of the human intestinal tract. In children with PEM, dysbiotic processes are observed. Probiotic preparations are prescribed - containing lacto and bifido bacteria (Bifiform, Lacidofil, Normobakt).
Iron supplements - used for PEM to correct iron deficiency (Totema, Aktiferrin, Ranferon).
Drugs that replenish thyroid hormone deficiency recommended for hypothyroid conditions of various etiologies.
Glucocorticoids have a pronounced anti-inflammatory, antiallergic, antishock, antitoxic effect.
Immunological drugs, used for replacement and immunomodulatory therapy. They reduce the risk of developing infections in primary and secondary immunodeficiency, while the antibodies have all the properties that are characteristic of a healthy person, and are used as replacement therapy in children - Octagam 10%.
Plasma replacement drugs intended for the correction of severe disorders of protein metabolism (hypoproteinemia), restoration of colloid-oncotic pressure, impaired hemodynamics - albumin solution 5%, 10%, 20%).
Amino acid solutions - special nutritional solutions for parenteral nutrition of children, for patients with acute and chronic renal failure, patients with various liver diseases and for the treatment of hepatic encephalopathy. Infusion solutions consisting of electrolytes and amino acids, which are metabolic analogues or physiological substances for the formation of proteins. Balanced in the content of essential and non-essential amino acids - Infezol 40, Infezol 100, Aminoplasmal E 5%, 10%, Aminoven infant 10%.
Fat emulsions- the use of fat emulsions provides the body with polyunsaturated fatty acids and helps protect the vein wall from irritation by hyperosmolar solutions. An energy source that includes an easily utilized lipid component (medium chain triglycerides) - providing the body with essential fatty acids as part of parenteral nutrition - Lipofundin MCT\LCT, Intralipid 20%, SMOFlipid 20%.
Glucose solution- glucose is involved in various metabolic processes in the body, 5%, 10%, 20%.
Combined drugs - include combined containers for parenteral administration: two-component “two-in-one” (AMK solution and glucose solution), three-component “three-in-one” (AMK solution, glucose solution and fat emulsion), also (AMK solution, glucose solution, fat emulsion with inclusion omega 3 fatty acids) - Oliclinomel, SmofKabiven central, SMOF Kabiven peripheral.

Drug treatment provided on an outpatient basis:
For PEM of 1 - 2 degrees, traditional diet therapy is carried out with a gradual change in diet, highlighting:
· stage of adaptation, careful, tolerant nutrition;
· stage of reparative (intermediate) nutrition;
· stage of optimal or enhanced nutrition.
During the period of determining food tolerance, the child adapts to its required volume and corrects water-mineral and protein metabolism. During the reparation period, protein, fat and carbohydrate metabolism are corrected, and during the period of increased nutrition, the energy load is increased.
For PEM, in the initial periods of treatment, reduce the volume and increase the frequency of feeding. The required daily amount of food for a child with malnutrition is 200 ml/kg, or 1/5 of his actual body weight. The volume of fluid is limited to 130 ml/kg per day, and in case of severe edema - to 100 ml/kg per day.
With stage I PEN, the adaptation period usually lasts 2-3 days. On the first day, 2/3 of the required daily amount of food is prescribed. During the period of determining food tolerance, its volume is gradually increased. Upon reaching the required daily amount of food, enhanced nutrition is prescribed. In this case, the amount of proteins, fats and carbohydrates is calculated for the proper body weight (let’s say the amount of fat is calculated for the average body weight between the actual and the expected).

Table 4 - Dietary treatment of stage 1 PEM

number of feedings	calorie content, kcal/kg/day	proteins, g\kg\day	fats, g\kg\day	carbohydrates\g\kg\day
according to the age n = 5-6 (10)	calculations according to age and proper weight Proper body weight = body weight at birth + the sum of its normal increases over the life period
	0-3 months 115	2,2	6,5	13
	4-6 months 115	2,6	6,0	13
	7-12 months 110	2,9	5,5	13

In case of stage II PEN, 1/2-2/3 of the required daily amount of food is prescribed on the first day. The missing amount of food is replenished by ingesting rehydration solutions. The adaptation period ends when the required daily amount of food is reached.

Table 5 - Calculation of nutrition for PEM II degree during the adaptation period

With normal tolerance, a reparation period begins, when the volume of nutrition gradually (over 5-7 days) increases, while the calculation of nutrients is carried out based on the proper body weight. First, the carbohydrate and protein components of the diet are increased, then the fat component. This becomes possible with the introduction of complementary foods: dairy-free cereals, meat and vegetable purees.

Table 6 - Calculation of nutrition for stage II PEN during the repair period

During the period of enhanced nutrition, the content of proteins and carbohydrates is gradually increased, their amount begins to be calculated on the proper weight, the amount of fat - on the average weight between the actual and the expected. At the same time, the energy and protein load on actual body weight exceeds the load in healthy children. This is due to a significant increase in energy consumption in children during the period of convalescence with PEM.

Table 7 - Calculation of nutrition for stage II PEN during the period of enhanced nutrition

In the future, the child’s diet is brought closer to normal parameters by expanding the range of products, increasing the daily volume of food consumed and reducing the number of feedings. A period of enhanced nutrition, during which the child receives high-calorie nutrition (130-145 kcal/kg/day) in combination with medications that improve the digestion and absorption of food. The volume of feeding should be increased gradually under strict monitoring of the child’s condition (pulse and respiratory rate). If tolerated well, at the stage of enhanced nutrition, high-calorie nutrition is provided (150 kcal/kg per day) with an increased content of nutrients, but the amount of proteins does not exceed 5 g/kg per day, fats - 6.5 g/kg per day, carbohydrates - 14-16 g/kg per day. The average duration of the enhanced nutrition stage is 1.5-2 months.
To correct micronutrient deficiency characteristic of any form of PEM, dosage forms of vitamins and microelements are used. This requires an extremely balanced approach. Despite the fairly high incidence of anemia in PEM, iron supplements are not used in the early stages of nursing. Correction of sideropenia is carried out only after stabilization of the condition, in the absence of signs of an infectious process, after restoration of the basic functions of the gastrointestinal tract, appetite and persistent weight gain, that is, no earlier than 2 weeks from the start of therapy. Otherwise, this therapy can significantly increase the severity of the condition and worsen the prognosis if the infection develops.
To correct micronutrient deficiency, it is necessary to provide iron at a dose of 3 mg/kg per day, zinc 2 mg/kg per day, copper - 0.3 mg/kg per day, folic acid (on the first day - 5 mg, and then - 1 mg/kg per day). mg/day) followed by the prescription of multivitamin preparations, taking into account individual tolerance.

Table 8 - Essential medications:

Name	Therapeutic range	A course of treatment
Mixture “Nutrilon Pepti Gastro”, “Alfare”, “Nutrilak Peptidi TSC”, mixtures for premature infants, mixtures for children over 1 year old “Nutrien Elemental”, “Nutrien Immun” (UD - A)	calculation depending on the adaptation period	individual correction, 2-3 months Depending on the clinical manifestations, for CF - for life (see CF treatment protocol) long-term, at least 6 months Long-term, 3-6 months Course duration 2-3 months Duration 1 month Duration 2 months Duration 2 months Duration 1 month
Pancreatin (UD - B)	1000 U\kg per day of lipase, with CF 6000-10000 IU\kg\day for lipase
Colecalciferol (UD - B)	500-3000 U/day, 1-4 drops 1 time per day
Ferrous sulfate (UD - A)	4 mg\kg 3 times a day, orally
Retinol	daily requirement for vitamin A for children: under the age of 1 year - 1650 IU (0.5 mg), from 1 year to 6 years - 3300 IU (1 mg), from 7 years and older - 5000 IU (1.5 mg ).
Tocopherol (UD - A)	for children over 10 years of age, the daily dose of vitamin is 8-10 mg; for children under 3 years of age, the daily dose is from 3 to 6 mg; for children under 10 years of age, no more than 7 mg.
Folic acid (UD - A)	maintenance dose for newborns - 0.1 mg/day; for children under 4 years old - 0.3 mg/day; for children over 4 years of age and adults - 0.4 mg/day. For hypo- and vitamin deficiency (depending on the severity of vitamin deficiency): age 12 years - up to 5 mg/day; children - in smaller doses depending on age
Zinc sulfate (UD - B)	2-5 mg/day
Preparations containing antidiarrheal microorganisms (Lactobacillus, Bifidobacterium, Bacillus clausii spores) (UD - C)	in age dosage

Drug treatment provided at the inpatient level:
depending on the cause that led to PEM. In case of PEN II - III degrees, comprehensive nutritional support is provided using enteral and parenteral nutrition.
A justified type of enteral nutrition in severe forms of PEM is long-term enteral tube feeding, which consists of a continuous slow supply of nutrients into the gastrointestinal tract (stomach, duodenum, jejunum - drip, optimally - using an infusion pump).

Table 9 - Calculation of nutrition for stage III PEN during the adaptation period

Table 10 - Calculation of nutrition for stage III PEN during the repair period

High-calorie complementary foods are gradually introduced into the child's diet, and it is possible to introduce adapted fermented milk formulas.
With good tolerance of the prescribed diet at the stage of enhanced nutrition, the calorie content increases to 130-145 kcal/kg/day per proper body weight, with an increased content of nutrients, but no more: proteins - 5 g/kg/day, fats - 6.5 g /kg/day, carbohydrates - 14-16 g/kg/day. The average duration of the enhanced nutrition stage is 1.5-2 months (see Table 7).

Table 11 - Indicators of the adequacy of diet therapy

Table 12 - Essential medications at the hospital level
To correct leading syndromes, it is recommended:

INN	Therapeutic range			A course of treatment
Correction of protein metabolism disorders: 1) Presence of hypoproteinemic edema, restoration of oncotic pressure
Albumin solution 10%	3-10ml/kg/day IV, drip			until the effect is achieved under the control of a proteinogram and hemodynamic parameters
2) Parenteral nutrition
Amino acid solutions	2-5 years - 15 ml/kg/day, 6-14 years -10 ml/kg/day IV, drip			until the effect is achieved under the control of water balance and electrolyte levels in the blood serum
Fat emulsions	0.5 - 2.0 g\kg/day, intravenously, drip			until the effect is achieved under the control of plasma triglyceride concentrations
Correction of metabolic processes carried out against the background of restored protein levels in the blood:
Potassium orotate	10-20 mg/kg/day orally			3-4 weeks
Levocarnitine	>12 years 2-3 g/day 6-12 years - 75 mg/kg/day, 2-6 years - 100 mg/kg/day, up to 2 years - 150 mg/kg/day orally			3-4 weeks
Correction of water and electrolyte disorders: Combination therapy is recommended (the ratio of solutions is determined by the type of dehydration)
Sodium chloride solution 0.9%	20 -100 ml/kg/day (depending on age and total body weight) IV, drip			Until the effect is achieved, under the control of water balance and the level of electrolytes in the blood serum.
Glucose solutions 5%, 10%	the rate of administration should not exceed 0.75 g/kg/h IV, drip
Potassium chloride solution 4%, 7.5% diluted with 10% glucose solution + insulin depending on the volume of glucose solution	the dose is determined by potassium deficiency in the blood, IV, drip
Correction of micronutrient deficiency:
Combined calcium preparations				3-4 weeks
Combination magnesium preparations
Correction of hypovitaminosis: a combination of drugs is possible
Pyridoxine (B1)		0.02-0.05 g/day IM	7-10 days
Thiamine (B6)		12.5 mg/day IM
Cyanocobalamin (B12)		30 -100 mcg/day s.c.
Ascorbic acid 5%		1-2 ml per day IM
Retinol		children over 7 years old 5000 IU orally	within 2-3 weeks
Rickets:(see protocol for treatment of rickets)
Iron-deficiency anemia:(see protocol for the treatment of IDA in children)
Correction of impaired digestion:
Microcapsular pancreatic enzymes	1000-2000 U/kg/day, orally			7-21 days
Correction of dysbiotic disorders:
Probiotics containing bifidobacteria, lactobacilli	according to age dosage			within 2-4 weeks

To carry out total parenteral nutrition, the dose of amino acids should be 2-2.5 g/kg, fat - 2-4 g/kg, glucose - 12-15 g/kg. In this case, the energy supply will be 80-110 kcal/kg. The indicated dosages must be approached gradually, increasing the amount of administered drugs in accordance with their tolerability, while maintaining the necessary proportion between plastic and energy substrates (see algorithm for creating PP programs).
The approximate daily energy requirement is from 2 weeks to 1 year - 110-120 kcal/kg.
Parenteral nutrition is carried out mainly intravenously. Through the central veins it is carried out in cases where PN is intended to be carried out for longer than 1 week, and when the peripheral veins are poorly defined. The use of the central venous route is especially indicated in patients who, along with PN, need other intensive care measures. In order to exclude phlebitis and thrombophlebitis, concentrated glucose solutions (› 5%) are infused only through the central veins. When PN lasts no more than 1 week, peripheral veins are prominent and isotonic solutions are used, preference is given to the peripheral route of drug infusion. An important factor in the absorption of nitrogen-calorie sources of PP is the simultaneous use (through two parallel droppers) of amino acid mixtures and fat emulsions (or glucose solutions). Otherwise, amino acids can also be used for energy purposes. Fat emulsions should not be mixed with electrolyte solutions and medications (due to the risk of fat particles sticking together). Considering cases of adverse reactions as a result of transfusion of fat emulsions (chills, fever, chest pain, lower back pain, nausea, vomiting, etc.), the procedure should be carried out during the daytime, in the presence of medical personnel. In some cases, if there is an individual intolerance to the drug, its infusion is started under the cover of intramuscular administration of an antihistamine (suprastin, diphenhydramine). Electrolyte, trace element components and ascorbic acid can be added to 5; 10; 20% glucose solutions. B vitamins are administered separately, intramuscularly.

Parenteral nutrition through the central veins is carried out after preliminary catheterization of one of the large-caliber veins, most often the jugular.

All drugs should be administered at a minimum speed (within 22-24 hours), which ensures maximum absorption of the administered substances and significantly reduces the possibility of complications. Protein preparations can be mixed with concentrated solutions of glucose, electrolytes, vitamins, and microelements. Mixing these substances in the same container with fat emulsions is not allowed.

Algorithm for compiling PP programs:

Calculation of the total volume of fluid a child needs per day.
Resolving the issue of using drugs for special-purpose infusion therapy (blood products, plasma, immunoglobulin) and their volume.
Calculation of the amount of concentrated electrolyte solutions needed by the child, based on the physiological daily requirement and the magnitude of the identified deficiency. When calculating the need for sodium, it is necessary to take into account its content in blood substitutes and solutions used for jet intravenous injections.
Determination of the volume of amino acid solution:
Based on the following approximate calculation (Table 13):

Table 13 - Volume of amino acid solution

Determination of the volume of fat emulsion.
At the beginning of use, its dose is 0.5 g/kg, then increases to 2.0 g/kg.

Determination of the volume of glucose solution.
The daily dose of glucose (except for newborns) should not exceed 6-7 g/kg, but to ensure sufficient effectiveness of carbohydrate, its dosage should not be less than 2-3 g/kg per day. The rate of glucose utilization in the normal state is 3 g/kg/h, and in pathology it can decrease to 1.8-2 g/kg/h. These values ​​determine the rate of glucose administration - no more than 0.5 g/kg/h. To increase glucose utilization, using insulin at a dose of 1 unit per 4-5 grams of dry matter glucose is indicated in cases where blood sugar rises to 10 mmol/l.
On the first day of PN, a 10% glucose solution is prescribed, on the second - 15%, from the third day - a 20% solution (under blood glucose control).
Checking and, if necessary, correcting the relationships between plastic and energy substrates. If there is insufficient energy supply per 1 g of amino acids, the dose of glucose and/or fat should be increased, or the dose of amino acids should be reduced.
Distribute the resulting volumes of drugs for infusion, based on the fact that the fat emulsion does not mix with other drugs and is administered either continuously throughout the day through a tee, or as part of a general infusion program in two or three doses at a rate not exceeding 5-7 ml/ hour. Amino acid solutions are mixed with glucose and electrolyte solutions. The rate of their administration is calculated so that the total infusion time is 24 hours a day.
When carrying out partial PN, the calculation is carried out according to the above algorithm, but taking into account the volume of food, its energy value and protein content in milk.

Drug treatment provided at the emergency stage: depending on the cause that led to PEM.
· Correction of hypoglycemia;

Table 14 - Prevention/treatment of hypoglycemia in protein-energy malnutrition

Child's condition	First stage of treatment	Subsequent treatment
If consciousness is not impaired, but the serum glucose level is below 3 mmol/l	A bolus injection of 50 ml of 10% glucose or sucrose solution (1 tsp sugar per 3.5 tbsp water) through the mouth or nasogastric tube is indicated	Then such children are fed frequently - every 30 minutes for 2 hours in a volume of 25% of the volume of the usual single feeding, followed by transfer to feeding every 2 hours without a night break
If the child is unconscious, lethargic, or has hypoglycemic seizures	It is necessary to administer a 10% glucose solution intravenously at a rate of 5 ml/kg.	Then, glycemia is corrected by administering a glucose solution (50 ml of a 10% solution) or sucrose through a nasogastric tube and switching to frequent feedings every 30 minutes for 2 hours, and then every 2 hours without a night break.

Antibacterial therapy with broad-spectrum drugs is indicated for all children with impaired serum glucose levels.
· Correction of hyper/hypothermia;

Table 15 - Prevention / treatment of hypothermia in protein-energy malnutrition (Koletsko B., 2009)

· Correction of dehydration;
Table 16 - Conducting rehydration therapy for protein-energy deficiency (Bauer K., Jochum F., 1999)

rehydration therapy		feeding	condition monitoring
first 2 hours	subsequent 4-10 hours	after 10 hours of rehydration therapy	first 2 hours	subsequent 12 hours
if there are signs of dehydration or watery diarrhea, rehydration therapy is carried out through the mouth or nasogastric tube with a solution for rehydration of children with PEM (ReSoMal) at the rate of 5 ml/kg every 30 minutes for 2 hours; administer the same solution at 5-10 ml/kg per hour, replacing the administration of the rehydration solution with feeding with formula or breast milk at 4, 6, 8 and 10 hours		every 2 hours without an overnight break	every 30 min	each hour
			- pulse rate, - breathing rate, - frequency and volume of urination, - stool frequency, - frequency of vomiting

· Correction of electrolyte balance:
It is necessary to ensure regular intake of essential minerals in sufficient quantities into the child’s body. It is recommended to use potassium at a dose of 3-4 mmol/kg per day, magnesium at a dose of 0.4-0.6 mmol/kg per day. Food for children with PEM should be prepared without salt; only ReSoMal solution is used for rehydration. To correct electrolyte disturbances, use a special electrolyte-mineral solution containing (in 2.5 l) 224 g of potassium chloride, 81 g of potassium citrate, 76 g of magnesium chloride, 8.2 g of zinc acetate, 1.4 g of copper sulfate, 0.028 g sodium selenate, 0.012 g of potassium iodide, at the rate of 20 ml of this solution per 1 liter of food.

Other types of treatment: depending on the pathology that led to PEM.

Surgery: for pathology requiring surgical correction (congenital malformation of the gastrointestinal tract, congenital heart disease).

Indicators of treatment effectiveness:
· adequate increase in weight and height indicators;
· elimination of the cause of PEM;
· favorable prognosis of the underlying disease that led to PEM.

Drugs (active ingredients) used in treatment

Albumin human

Ascorbic acid

Bifidobacterium bifidum

Dextrose

Ferric sulfate

Fat emulsions for parenteral nutrition

Potassium chloride (Potassium chloride)

Kolekaltsiferol

Complex of amino acids for parenteral nutrition

Lactobacilli

Levocarnitine

Sodium chloride

Orotic acid

Pancreatin

Pyridoxine

Retinol

Enteral nutrition mixtures

Bacillus clausii spores, multiresistant to various chemotherapeutic drugs and antibiotics

Thiamin

Tocopherol

Folic acid

Cyanocobalamin

Zinc sulfate

Groups of drugs according to ATC used in treatment

Hospitalization

Indications for hospitalization indicating the type of hospitalization: (planned, emergency):

Indications for emergency and planned hospitalization:
· life-threatening conditions due to PEM II-III degrees;

Indications for planned hospitalization:
· clarification of the etiology of PEM II-III degrees (primary or secondary);
· treatment of PEM II-III degrees, which is impossible in an outpatient setting (correction of water and electrolyte imbalances, treatment of infections, parenteral nutrition, multiple organ failure);
· hospitalization in a specialized hospital for cognitive disorders.

Prevention

Preventive actions:
· optimal care;
· regular medical examinations;
· nutrition sufficient in frequency and volume, adequate in calorie content and content of essential nutrients;
· vitamin and mineral correction;

Further management (after hospitalization):
· expansion of diet;
· ensuring weight gain and growth;
· sensory stimulation and emotional support;
· further rehabilitation;

Information

Sources and literature

1. Minutes of meetings of the Expert Council of the RCHR of the Ministry of Health of the Republic of Kazakhstan, 2015
   1. List of used literature: 1. Parenteral and enteral nutrition: national manual / edited by M.Sh. Khubutia, T.S. Popova.-M.: GEOTAR-Media, 2014.- 162-198 p. 2. Guide to Clinical Nutrition. Ed. Lufta V.M., Bagnenko S.F., Shcherbuka Yu.A. St. Petersburg, 2010. 428 p. 3. National program for optimizing the feeding of children in the first year of life in the Russian Federation. Ed. Baranova A. A., Tutelyan V. A. M., 2010. 68 p. 4. Clinical dietetics of childhood. A guide for doctors. Ed. T. E. Borovik, K. S. Ladodo. M.: Medicine, 2008. 606 p. 5. Uglitskikh A.K. Comprehensive assessment of nutritional status in children in the hospital // Anesthesiol. and resuscitator. 2005. No. 2, p. 52–57. 6. Calder P. C. ω-3 fatty acid, inflammation and immunity-relevance to postsurgical and critically ill patients // Lipids. 2004; 39:1147–1161. 7. Mazurin A.V., Vorontsov I.M. Propaedeutics of childhood diseases. St. Petersburg, “Foliant”, 2000. - pp. 827-923. 8. National program for optimizing the feeding of children in the first year of life in the Russian Federation, Moscow, 2008. 9. Nutrition of a healthy and sick child. /Manual for doctors. Edited by Tutelyan V.A., Konya I.Ya., Kaganov B.S. M., 2007.- P 51-52, 60-62. 10. Pediatric gastroenterology: a guide for doctors / edited by N.P. Shabalov. 2nd ed., revised - M.: MEDpress-inform, 2013.-187-427 11. Kleiman: Nelson Textbook of Pediatrics, 18 th ed., 2007, Chapter 43. 12. Sermet-Gauelus I., Poisson- Salomon A. S., Colomb V. et al. Simple pediatric nutritional risk score to identify children at risk of malnutrition // AJCN. 2000. V. 72. R. 64–70. 13. Sawaya A. L., Martins P. A., Martins V. J. B. et al. Malnutrition, long term health and the effect of nutritional recovery // Nestle Nutrition Institute. 2009, 63, p. 95–108. 14. Practical skills of a pediatrician./Manual for doctors. Edited by Usov I.N. and others. Mn.: Higher school, 1990.- P. 28-39 15. Pediatrics: national manual / edited by A.A. Baranov. – M., 2009.-165-167p. 16. Collins S, Dent N, Binns P et al., Management of severe acute malnutrition in children. www.thelancet.com 2010 17. Chronic eating disorders in young children / edited by R. A. Avdeev, N. L. - Krasnoyarsk: KrasSMA Publishing House, 2008. 18. B. Koletzko, C. Agostoni, P. Ball, V. Carnielli, C. Chaloner, J. Clayton, V. Colomb, M. Dijsselhof, C. Fusch, P. Gandullia et al. ESPEN/ESPGHAN Guidelines on pediatric parenteral nutrition. J Pediatr Gastroenterol Nutr, Vol. 41, Suppl. 2, November 2005 19. Biesalski HK, Bischoff SC, Boehles HJ, Muehlhoefer A, Working group for developing the guidelines for parenteral nutrition of The German Association for Nutritional Medicine. Water, electrolytes, vitamins and trace elements – Guidelines on Parenteral Nutrition, Chapter 7. GMS Ger Med Sci. 2009;7: Doc21. 4. 20. Fusch C, Bauer K, Böhles HJ, Jochum F, Koletzko B, Krawinkel M, Krohn K, Mühlebach S, Working group for developing the guidelines for parenteral nutrition of The German Society for Nutritional Medicine. Neonatology/Paediatrics – Guidelines on Parenteral Nutrition, Chapter 13. GMS Ger Med Sci. 2009;7: 21. Fundamentals of clinical nutrition: Lecture materials for courses of the European Association of Parenteral and Enteral Nutrition: Trans. from English / Ch. ed. L. Sobotka. - 2nd ed. - Petrozavodsk: IntelTek, 2003. - 416 p. 22. Popova T.S., Shestopalov A.E., et al. Nutritional support for patients in critical conditions. -M.: LLC "Publishing House" M-Vesti", 2002. - 320 pp. 23. Parenteral nutrition of newborns: clinical manual\edited by Volodin N.N. - Moscow, 2015 P.27 24.WHO. Management of severe malnutrition: a manual for physicians and other senior health workers. Geneva: WHO 2003 25. Ann Ashworth, Sultana Khanum et al. Guidelines for the inpatient treatment of severely malnourished children. Geneva: WHO 2003

Information

Developers:
1) Nazarova A.Z. - Candidate of Medical Sciences, Head of the Clinical and Diagnostic Department of the Scientific Center of Pediatrics and Pediatric Surgery.
2) Sharipova M.N. - Doctor of Medical Sciences, Deputy Director for Scientific Work of the Scientific Center of Pediatrics and Pediatric Surgery.
3) Adamova G.S. - Candidate of Medical Sciences, doctor of the complex somatics department of the Scientific Center of Pediatrics and Pediatric Surgery.
4) Litvinova L.R. - clinical pharmacologist of JSC National Scientific Cardiac Surgery Center.

There is no conflict of interest.

Reviewer:
1) Khabizhanov B.Kh. - Doctor of Medical Sciences, Professor of the Department of Internship and Residency in Pediatrics No. 2 of KazNMU named after S. Asfendiyarov;
2) Dzhaksylykova K.K. - Doctor of Medical Sciences, Professor of the Department of Internship in Pediatrics and Pediatric Surgery of Semey State Medical University.

Conditions for reviewing the protocol: review of the protocol 3 years after its publication and from the date of its entry into force or if new methods with a level of evidence are available.

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Insufficient supply of nutrients and energy from food (partial or complete starvation) leads to the development of a pathological condition of the body, which is indicated in International Classification of Diseases and Causes of Death, 10th revision (ICD-10) How protein-energy malnutrition (PEM).

In the medical literature, there are other terms in relation to this disease: nutritional dystrophy, malnutrition, substrate-energy deficiency, cachexia.

The term PEM does not accurately reflect the essence of the problem, since along with protein and energy deficiency, as a rule, there is a deficiency of other nutrients (vitamins, minerals, fats, carbohydrates).

Causes of protein-energy malnutrition

Both historically and currently, undernutrition in most cases has social causes. These include extreme conditions (a striking example is the blockade of Leningrad), protest forms of starvation, and poverty. A number of diseases also contribute to the development of PEM.

Main reasonsprotein-energy malnutrition:

1. Insufficient supply of nutrients:

A) socio-economic, religious and other reasons;
b) iatrogenic causes (hospitalization, fasting due to examinations, hospital diets, dietary restrictions for various diseases, irrational artificial nutrition);

C) psychoneuroendocrine disorders with appetite suppression and perversion of eating behavior (neurogenic anorexia, psychosis);
d) mechanical disorders of oral food intake: gastrointestinal obstruction, dental disorders, dysphagia;

2. Disorders of digestion and/or absorption of nutrients: maldigestion and malabsorption syndromes.

3. Hypercatabolic states:

A) conditions in which cytokines are released that accelerate catabolism, cancer, fever, infections;
b) endocrine diseases with impaired anabolism and accelerated catabolism (hyperthyroidism, diabetes mellitus).

5. Increased loss of nutrients (disorders associated with the loss of protein and other nutrients) nephrotic syndrome, chronic obstructive pulmonary diseases, intestinal fistulas, exudative enteropathy, plasmorrhea in burn disease, desquamative dermatitis.

6. Increased need for nutrients:

A) physiological conditions (pregnancy, lactation, childhood and adolescence);
b) pathological conditions (the period of convalescence after injuries and acute infectious diseases, the postoperative period).

7. Intake of nutrient antagonists into the body: alcoholism, poisoning with vitamin antagonists and medications.

Prevalence of protein-energy malnutrition

According to FAO/WHO estimates, at the end of the 20th century, at least 400 million children and 0.5 billion adults were hungry on the planet. Their number has increased by a quarter in 15 years, and the proportion of undernourished children in the world has increased in the late 90s.

Fish consumption in Russia during the period from 1987 to 1998 decreased by 2/3; meat, poultry and sugar - by 1/2; sausages, margarine and butter - by 1/3. Selective studies of the nutrition of the Russian population showed that about 25% of those surveyed are malnourished, and 80% have a deficiency of vitamins and microelements.

PEM is one of the main problems of patients in medical and surgical hospitals. Numerous studies have shown that more than 50% of patients entering treatment suffer from protein-energy deficiency and severe hypovitaminosis (especially deficiency of folic acid, vitamins B2 and C).

In 1994, McWriter and Pennington assessed the nutritional status of 500 patients in various UK hospital departments and identified PEM in 200 patients (40%).

Rice. 35.1. The nutritional status of patients in 5 types of departments, determined in 100 hospitals in the UK (McWriter, Pennington, 1994): 1 - surgical departments; 2 - therapeutic departments; 3 - pulmonology departments; 4 - trauma departments; 5 - geriatric departments.

According to the clinics of the All-Russian Scientific Research Center of the USSR Academy of Medical Sciences, hospital fasting among cancer patients occurs in 30% of cases. Among people receiving outpatient treatment for chronic diseases and cancer, about 10% also have signs of malnutrition.

The cost of hospitalization for a patient with normal nutritional status is approximately 1.5-5 times less than for a patient with malnutrition.

Patients with protein-energy malnutrition are much more likely to experience delayed wound healing, suture failure, increased mortality, increased length of hospitalization and recovery, and infectious complications.

Pathogenesis of protein-energy malnutrition

Reduced nutrient intake, regardless of etiology, causes similar changes. This is a loss of not only fat and muscle tissue, but also bone and visceral tissue.

Fasting requires the body to generally save energy and plastic material. But, as with insulin-dependent diabetes mellitus, complete fasting creates a metabolic situation of redistribution of resources in favor of insulin-independent organs and tissues. Insulin-dependent structures are in the most disadvantaged position. Glycogen reserves last for about a day.

With minor fasting, the liver provides up to 75% of glucose due to the breakdown of glycogen. Increasing the duration of fasting leads to an increase in the level of gluconeogenesis, lipolysis and ketogenesis. Insulin production decreases, and the hormonal-metabolic picture of fasting is sharply dominated by the action of a complex of contrainsular regulators.

In this case, the energy resources of the somatic component of the body - skeletal muscles and adipose tissue - are mobilized. Muscle protein has an energy value of about 40,000 kcal. A negative nitrogen balance of 10-12 g/day occurs, which indicates catabolism of 75-100 g/day of protein. The level of short-chain amino acids (valine, leucine, isoleucine) increases in the blood. In this case, the loss of more than 30% of the protein is incompatible with life.

Another potential source of energy is fat (130,000 kcal). Amino acids and lipolysis products are used by the liver for resynthesis of glucose and for the formation of ketone bodies in order to save protein in visceral organs and meet the energy needs of the brain.

The daily energy requirements of a man at rest after 3-5 days of fasting require the use of 160 g of triglycerides, 180 g of carbohydrates (synthesized by gluconeogenesis) and 75 g of muscle protein. Thus, fats provide most of the energy during fasting. A person with normal nutritional indicators with complete fasting has enough of his own reserves for 9-10 weeks.

During fasting, there is an uneven loss of mass in individual organs, which was noted by the classics of nutrition science. Mesoderm derivatives, as well as organs and tissues that store carbohydrates and lipids, lose a lot of weight. With an average weight deficit at the time of death of 50-55%, the greatest losses are observed in adipose tissue, reduced by almost 99% in those who died by starvation. There is even a disappearance of fat in lipomas and a reverse development of lipid deposits in large arteries.

The omentum and mesentery become thin connective tissue films. The epicardium and yellow bone marrow are deprived of fat, giving them a gelatinous or slimy appearance. Skeletal muscles, which are also insulin-dependent, reduce their mass by 70%. Atrophic changes in the lymphoid organs are very large: the weight of the spleen decreases by 72%.

Lipochrome deposition is noted in all atrophied organs, and hemosiderosis is observed in the spleen. The liver loses 50-60% of its mass, the salivary glands - 65%, other digestive organs - from 30 to 70%. The most pronounced atrophy of the mucous membrane of the stomach and the glandular apparatus of the pancreas. In the bones, dystrophic osteopathy with osteoporosis and subperiosteal fractures is observed.

The loss of weight between blood and skin roughly corresponds to the relative total loss of body weight, with atrophy of the skin glands, thinning of the epidermis, and loss of skin papillae.

At the same time, atrophy of vital insulin-independent organs is expressed to a much lesser extent. The brain, adrenal glands (especially their medulla), and eyes do not lose mass at all. In this case, the spinal cord loses more mass than the brain and shows more signs of degenerative changes.

Mass kidney loss is 6-25%, which is 2-9 times less than average. According to V.D. Zinzerling (1943), atrophic processes do not spread at all to the kidneys of those who died of starvation. The lungs lose 18-20% of their mass.

Among the endocrine glands, the thyroid atrophies especially strongly. In some experiments, gonads almost do not lose their weight, and the sexual ability of starving animals, especially males, persists for a long time.

Fortunately, there is evidence that fasting does not have an irreversibly sterilizing effect. Thus, the Israeli doctor M. Dvoretsky (1957) reported extremely high fertility in families formed by persons who suffered nutritional dystrophy during their imprisonment in Nazi concentration camps.

During fasting, the fetus is in a privileged position in relation to the mother's body. Although malnutrition in pregnant women leads to the birth of children with intrauterine malnutrition, the weight loss of the maternal body is much more significant than that of the fetus. Insufficient nutrition of lactating women leads to a reduction and cessation of lactation and a decrease in the protein and fat content in breast milk.

Forms of protein-energy malnutrition

With a pronounced deficiency of nutrients, there is most often a long phase of compensation, when endocrine-metabolic mechanisms protect the visceral protein pool and mobilize fats and proteins from the somatic pool (adipose tissue and skeletal muscles) for energy needs. This manifests itself in the form of an edematous or marantic form of starvation (alimentary marasmus).

With nutritional marasmus (mummified or dry form of nutritional dystrophy), atrophy of muscles and fatty tissue (“skin and bones”) reaches a significant degree, but the skin and hair usually remain normal, there are no changes in the function of the liver and other internal organs, swelling occurs. In marasmus, there is a significant excess of glucocorticoid levels.

If protein deficiency develops at an accelerated pace against the background of providing the energy value of malnutrition with the help of carbohydrates, then compensation may from the very beginning be insufficient in terms of sparing visceral protein. Then the edematous form of fasting (kwashiorkor) develops. Decompensation occurs earlier, and patients have lower survival rates.

The word kwashiorkor comes from the language of the West African people living in what is now Ghana. It means “illness of the firstborn after the birth of the youngest.” Kwashiorkor was first described by Williams in 1935 in West African children fed exclusively on maize. After weaning, the firstborn is deprived of a source of complete protein and his nutrition becomes insufficient.

Kwashiorkor, which is an expression of visceral protein deficiency, is characterized by edema, skin desquamation, hair loss, often liver enlargement or decreased liver function, and anorexia. In this case, there is secondary hyperaldosteronism, and the systemic effects of cytokines are pronounced.

Some cases of starvation (malnutrition) may occur in an intermediate way: at first more reminiscent of the arrowroot form, and with decompensation - the kwashiorkor form.

There is no clear opinion why a person is exhausted according to one type or another. According to the traditional point of view, marasmus develops under conditions of predominantly energy deficiency, and kwashiorkor develops under conditions of protein deficiency.

Distinctive features of BEN forms are presented in Table. 35.1. Both forms have common symptoms, for example, polydeficiency anemia and hypovitaminosis.

Table 35.1. Forms of protein-energy malnutrition

Distinctive features	BEN forms
	Kwashiorkor	Marasmus
Shortage	Mainly protein	Energy and protein
Appearance	Moon face, swollen belly	Atrophy of the facial muscles, sunken cheeks and temporal fossae. Stem-shaped limbs, atrophy of subcutaneous fat and skeletal muscles. Stunted growth. The stomach is pulled in
Leather and its derivatives	Spots of abnormal pigmentation and hyperkeratosis, “enamel or scaly dermatosis”, erythema. Streaks of discoloration on hair (flag symptom) and nails. Hair becomes lighter and takes on a reddish tint, becomes brittle and falls out easily	Dry, wrinkled, with signs of polyhypovitaminosis, decreased turgor. Hair is dry, dull, thin
Eating behavior	Apathy, lack of appetite	Active. Appetite present
Liver	Enlarged, painful, steatosis or steatohepatitis, occasionally cirrhosis possible	Moderate atrophy
Gastrointestinal tract		Atrophic changes are less pronounced
Water-salt metabolism	Edema, ascites, sodium retention, hypokalemia, hypophosphatemia, hypomagnesemia	No swelling. In the final stage of hyperkalemia
Blood proteins	Severe hypoalbuminemia, decreased transferrin, transthyretin and retinol-binding protein. Increased acute phase globulins Decreased VLDL and LDL	At the lower limit of the norm, VLDL may increase
The immune system	Severe T- and B-cell immunodeficiency	T-cell functions are predominantly impaired
Hormonal background	Hyperaldosteronism, high levels of cachectic cytokines, relatively less glucocorticoids. Insulin is reduced. Gyrotropin is normal. Cortisol is normal. Somatomedin is reduced	Extremely high levels of glucocorticoids, glucagon and somatostatin. Insulin is normal. Thyrotropin is reduced. Triiodothyronine is reduced. Thyroxine is normal or elevated
Creatinine excretion	Moderately increased	Sharply increased
Forecast	Pessimistic. High risk of infectious complications. Treatment (nutrition) is difficult	Better than kwashiorkor

According to the International Classification, forms of protein-energy deficiency are distinguished only in severe cases. With a moderate degree of PEM with a clear predominance of loss of the visceral or somatic protein pool, it is advisable to make a diagnosis as follows: “Moderate protein-energy deficiency with a tendency to develop kwashiorkor (marasmus).”

Complications of protein-energy malnutrition

The main complications of PEM, which determine high mortality and treatment costs, are infectious processes.

The frequent development of infections in patients with protein-energy deficiency is associated with a number of factors, among which the most important are disorders of the adaptive response and secondary immunodeficiency.

Immunological disorders in PEM are characterized primarily by disruption of the T-cell component. The absolute number of T cells decreases, their function and differentiation are impaired.

The function of immunoglobulins changes. The IgG content often increases, but can also be decreased. There is a decrease in IgA and, accordingly, a weakening of the induction of the immune response of the mucous membranes to the presence of the antigen. This is due to a decrease in the number of IgA-producing cells, disruption of the synthesis of secreted components and the function of T cells.

Many components play a role in the formation of immunodeficiency in PEM (Table 35.2).

Table 35.2. The relationship between nutritional disorders, immune function and susceptibility to infection (according to S. Dreizen., 1979 and R. K. Chandra, 1988)

Immunity and resistance disorders	Nutrient deficiencies
Cellular immunity	Protein, energy, vitamins B6, B12, folate
Humoral immunity	Protein, vitamins A, C, PP, B 2, B 6, folate, pantothene, biotin
Phagocytic-macrophage system, interferon, complement	Protein, energy, iron, folate
Protective barriers of tissues and mucous membranes	Protein, vitamins A, B2, B6, B12, C, folate, iron
Epithelial regeneration	Protein, vitamins C, zinc
Collagen synthesis and maturation	vitamins A, PP, C, B 2, iron
Normoblastic hematopoiesis	Protein, iron, zinc, copper, vitamins B 12, folate
Blood clotting	Protein, calcium, vitamin K

Isolated deficiency of certain types of nutrients can also lead to immune system disorders. Thus, zinc deficiency causes lymphoid atrophy, which can be detected by a decrease in the delayed-type hypersensitivity reaction (skin test with antigen). Individuals with iron or magnesium deficiency may experience an increased incidence of infectious diseases and abnormal immune tests.

Lack of pyridoxine, folic acid, vitamins A and E leads to damage to the cellular immune system and disruption of antibody synthesis. With vitamin C deficiency, the phagocytic activity of leukocytes decreases and the function of T-lymphocytes decreases.

Decreased adaptation in protein-energy deficiency

Disorders of adaptive systems are a limiting factor in the treatment of patients, since they are associated with changes in the capabilities of various physiological systems and, when nutrition is restored, can lead to dysequilibric states and altered nutrient needs.

An important point in reducing adaptation can be a decrease in the activity of the sodium pump, which is responsible for 30% of the body’s energy expenditure at complete rest. A decrease in its activity leads to changes in tissue energy expenditure and disruption of intracellular electrolyte ratios. In this case, there is a decrease in the lability of the conduction system of the heart, the ability of the kidneys to concentrate urine, and peristalsis decreases. gastrointestinal tract (GIT).

Another reason for basal energy expenditure is related to protein catabolism. In PEM, the content of intracellular ribonucleic acid (RNA), peptides, enzymes. Amino acid and ion losses are associated with protein kinetics, which are used as an energy source.

The next disrupted adaptive function is related to the inflammatory response and immune response. Skin lesions are not painful, do not swell and do not turn red. In case of pneumonia, X-ray examination does not reveal massive infiltration. Urinary tract infections occur without pyuria. Signs of fever, tachycardia and leukocytosis can be smoothed out. When exhausted, thermoregulatory function is impaired.

Clinical problems arising from PEM: muscle atrophy, decreased respiratory and thermoregulatory function, fractures, bedsores, decreased wound healing rate, impaired immune and hormonal function, increased incidence of postoperative complications, decreased resistance to infections, depression and many others.

Previously, the main indicators that are used in clinical practice to assess the degree and form of protein-energy malnutrition are given. A predominant decrease in anthropometric parameters characterizes marasmus-type exhaustion; a pronounced decrease in laboratory markers of the visceral protein pool (albumin, transferrin) characterizes kwashiorkor. Immunological parameters worsen in both forms of the disease.

Particular attention should be paid to visceral protein markers, since their level (primarily albumin) correlates with mortality and the development of complications.

When working with debilitated patients, it is necessary to treat all laboratory and instrumental examination data with caution. There is practically no area of ​​the body’s activity that is not affected by PEN.

Often, inexperienced clinicians find it difficult to interpret test results and their dynamics in such patients. It must be remembered that they can vary greatly depending on the degree of hydration and can be very high before the start of treatment (infusions). To assess the dynamics, in parallel with any analyzes it is necessary to evaluate the hematocrit.

Therapeutic nutrition for protein-energy deficiency

Treatment of PEM should be carried out in a certain sequence. The first task is to compensate for specific nutritional deficiencies and treat complications such as infection, disorders of the intestinal microflora, and restoration of adaptive functions. In the future, a diet should be developed to restore tissue loss. The ultimate goal is to normalize body composition.

Choosing the preferred treatment methodProtein-energy malnutrition is determined by two main factors:

1) degree and form of BEN;
2) etiology of PEM.

Many experts believe that administering nutrients by intravenous infusion is dangerous because it can easily cross the threshold when the ability to homeostasis is impaired. Complete or predominant parenteral nutrition is indicated mainly in cases where the initial cause of protein-energy deficiency was diseases associated with malabsorption or hypercatabolism. It is also used in the development of complications of PEM.

When using parenteral nutrition during the initial phase of treatment for PEN, it is important not to administer excess protein, calories, fluids, and electrolytes. Administration of nutrients through the gastrointestinal tract allows the intestines to be used as a barrier between the physician and the patient's metabolism, so treatment of protein-energy malnutrition requires maximum use of the digestive system whenever possible.

In the alimentary genesis of PEM, parenteral nutrition is prescribed to patients with severe disease in the form of kwashiorkor with pronounced dystrophic changes in the gastrointestinal tract in parallel with the initiation of enteral nutrition. In case of exhaustion in the form of marasmus, as well as moderate degrees of PEM, enteral mixtures are prescribed. Depending on the situation, probe access or oral administration of the drug (slow drinking through a straw) is used.

In case of severe protein-energy deficiency, it is advisable to use balanced half-element mixtures; in case of moderate degree, standardized polymer media or hypercaloric hypernitrogenic mixtures can be prescribed.

A mild form of PEM is usually compensated for by a gentle diet with a high protein and energy content (in conditions medical and preventive institutions (HCI)- high protein diet).

Specific vitamin and mineral deficiencies should be corrected with active treatment. Usually, the prescription of iron, magnesium, calcium, phosphorus, zinc, folic acid, and vitamin A is required. According to our observations, quite often there is a need to use nicotinic acid to relieve pellagra.

It is considered prudent to administer protein and calories in amounts close to requirements to those patients whose specific deficiencies have been corrected and whose infections have been cured. To achieve the positive nitrogen and energy balance necessary for tissue repair, you need to increase the amount of nutrients.

In most patients, this is possible due to the return of appetite and an increase in oral food intake. However, in some patients it is necessary to increase parenteral nutrition.

In our opinion, one should adhere to the lower limits of the recommended norms, since high protein intake (up to 2.0 g/kg) often does not correspond to damaged metabolic abilities for its absorption.

The criteria for the effectiveness of treatment are a positive nitrogen balance and an increase in nutritional indicators, primarily body weight. However, in patients with kwashiorkor, in the first days of treatment, body weight, as a rule, decreases due to the elimination of hypoalbuminemic edema, and then begins to increase by approximately 100-150 g/day.

Rehabilitation of patients is often associated with a disproportionate increase in body weight (not due to protein, but due to adipose tissue), which requires further correction of body composition.

A special problem is PEM, which developed as a result of anorexia nervosa. In this case, therapeutic nutrition is ineffective without psychotherapeutic influence. Patients, and these are usually young girls, agree with the doctor’s dietary recommendations, but secretly induce vomiting after eating, take laxatives, and imitate poor tolerance to parenteral nutrition solutions. This behavior is caused by fear of obesity or excess (from the patient’s point of view) body weight.

At the initial stage, psychotherapeutic intervention should be aimed at:

Overcoming anosognosic attitude towards the disease, obvious or hidden resistance to treatment;
- correction of the patient’s ideas about ideal body weight;
- correction of the patient’s ideas about ways to control and maintain body weight.

Many patients with protein-energy deficiency underestimate the severity of their condition and refuse hospitalization. Unfortunately, sometimes outpatient doctors do not adequately assess the situation even with severe PEM and do not insist on urgent hospitalization. Moderate and severe PEN, especially with a decrease in the visceral protein pool, should be treated in a hospital setting!

The patient's attention must be drawn to the life-threatening nature of somatoendocrine disorders associated with weight loss. The patient must understand that the main indicator of recovery is the restoration of body weight.

At the initial stages of treatment, the diet should be strictly regulated. The nutritional behavior of patients is monitored by nursing staff. Patients keep a self-observation diary in which they record their daily food intake, time and situation of eating.

In a special column, the psycho-emotional state (feelings, emotions, thoughts, behavior) during meals is noted. It is important that medical staff and relatives condemn pathological eating behavior and, conversely, praise and encouragement for the successes achieved in treatment.

A.Yu. Baranovsky

Proper and nutritious nutrition - necessary condition for normal growth and development of the baby.

However, there are situations when there is a deficiency of macro- or microelements in the baby’s body. This leads to various kinds negative consequences, delays in physical and intellectual development.

We will talk about the causes and treatment of protein-energy malnutrition in children in the article.

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Concept and characteristics

Protein-energy malnutrition is a pathological condition caused by lack of macroelements of the protein group.

This condition can develop rapidly, for example, during periods of fasting, when the baby does not receive adequate nutrition rich in protein.

PEM can also occur gradually, if there are problems in the functioning of the gastrointestinal tract, accompanied by impaired protein absorption.

Causes

We can talk about a pathological process in the case when the child’s body weight rapidly decreases, the baby has lost weight over the last 6-12 months. lost more than 5-10% of my weight.

Various negative factors can lead to this phenomenon, such as:

1. Poor nutrition, caused by a number of reasons, such as, for example, unfavorable economic conditions of the family, the need to follow a strict diet for therapeutic purposes, religious factors, injuries of the jaw apparatus, which lead to the inability to eat food naturally. Various types of psychological abnormalities, in particular anorexia, can also lead to eating disorders.
2. Diseases, disrupting the process of digestion and absorption of protein. These diseases include cancer, diabetes mellitus, and disorders of the gastrointestinal tract.
3. Risk of developing PEM increases during adolescence When a child’s hormonal levels change, rapid growth and development of the body is observed. In this situation, the teenager requires more nutrients, and if they are not supplied in sufficient quantities, pathology develops.

Who is at risk?

Most often, PEM occurs in children living in unfavorable conditions, when the child there is no opportunity to eat fully and properly. PEM often develops in children and adolescents.

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Pathogenesis

Macronutrient deficiency is a condition that the body must adapt. During the adaptation process, various kinds of changes are noted in it. These changes primarily relate to hormonal levels and the activity of the endocrine system.

Other internal organs also suffer because they do not receive sufficient nutrition for their normal functioning.

To normalize the situation, the body redistributes amino acids from muscle and fat tissue to other organs that need it.

As a result, the primary symptom of PEM develops – loss of fat and muscle mass. There is a slowdown in metabolic processes and a sharp loss of body weight.

At the initial stage weight loss is very significant(4-5 kg ​​per week), then these figures decrease slightly, but body weight continues to decrease, although not so rapidly.

Classification and stages

There are 2 main forms of BEN:

• marasmus. There is growth retardation, atrophy of subcutaneous fat and muscle tissue;
• kwashiorkor. The clinical picture in this case is complemented by problems in the functioning of the liver (fatty elements accumulate in its cells, which should not normally be present), and the child experiences swelling. The condition of subcutaneous fat remains unchanged.

Depending on the severity of the course, several forms of pathology are distinguished:

1. Mild 1st degree. It is characterized by a weakening of the body, decreased immunity, and increased fatigue. The child gets tired quickly, feels drowsy, and often refuses outdoor games.
2. Moderate 2nd degree. There is a lag in height and weight. The child is most susceptible to various types of viruses and infections and often gets sick, since the immune system changes at the cellular level.
3. Severe degree. There is a pronounced lag in height, weight, and weakness of muscle tissue, which is especially noticeable in the extremities. There are disturbances in the functioning of the gastrointestinal tract. This manifests itself in the form of diarrhea and abdominal pain after eating. The child’s hair gradually begins to fall out, the quality of the skin and nails deteriorates. Fluid metabolism in the tissues of the body is disrupted, which leads to the development of edema.

The functioning of internal organs is disrupted, which, without receiving enough nutrients, cannot perform their functions normally.

4. Isolated form. In this case, we are talking about insufficient levels of numerous essential micro and macroelements in the body.

Possible complications and consequences

Protein-calorie deficiency – dangerous condition for the child's health, which can lead to various adverse consequences.

These include:

• persistent decrease in immunity, the formation of an inadequate immune response to irritants. This leads to frequent infectious diseases, many of which can cause significant harm to health and development;
• (children most often have a deficiency of vitamins B and A). This can lead to dry skin, the appearance of age spots, changes in the mucous membranes of the body, and the development of inflammatory processes. Nervous disorders such as apathy, depression, and sleep disorders develop. In addition, vitamin deficiency leads to the occurrence of various types of diseases(conjunctivitis, glossitis, leukopenia and many others);
• with PEM it is possible mineral metabolism disorder, which leads to problems with the musculoskeletal system (for example, osteoporosis);
• heart function is disrupted, other internal organs.

Symptoms and clinical picture

Manifestations of pathology can be different. First of all, this depends on the severity of the disease. Thus, with mild protein-energy deficiency, the clinical picture is poorly expressed, the child mainly complains of malaise and weakness.

If PEM is more severe, the clinical picture is more varied. Here main features that characterize PEN:

Diagnostics

Diagnosis of the disease is carried out in stages. First of all, doctor assesses the patient's physical condition in accordance with such criteria as:

• height and weight indicators;
• assessment of physical and emotional indicators (attention, reaction speed, frequency of infectious diseases, etc.);
• assessment of skin condition;
• muscle tone (with PEM it is reduced);
• assessment of the development of the subcutaneous fat layer;
• assessment of the child’s diet (conducted every week).

Mandatory laboratory tests:

Additional Research:

• immunogram;
• genetic testing;
• hardware examinations.

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Treatment

The main therapeutic goal for PEM is the normalization of metabolic processes in the body, when the supply of nutrients is higher than their consumption. In addition to a nutritious diet, the child is prescribed rest (for severe pathology - bed rest), as well as staying warm.

The child's diet should consist mainly of foods rich in easily digestible elements.

Meals should be fractional, that is, the number of meals is 5-6 times a day, the serving size is small. You need to eat these foods How:

It is important to remember that the diet should be as gentle as possible, but no less complete. Large meals are not recommended the amount of food consumed must correspond to the norms for the child’s age and weight. The main condition is a varied diet, rich in micro and macroelements.

Forecast

Protein-energy deficiency is a condition that can lead to death (according to statistics, the mortality rate among children suffering from the pathology is 5-40%).

It all depends on the severity of the disease, its clinical manifestations, and also on How competent was the prescribed treatment?.

Prevention

The development of PEM can be prevented if you follow the following rules:

1. Correct behavior(good nutrition, absence of bad habits, sufficient rest) for the expectant mother during the period of bearing a child.
2. Breast-feeding for as long a period as possible, timely introduction of complementary foods.
3. If the child is bottle-fed, more Monitor height and weight gains carefully.
4. Strengthening the immune system, organizing a proper daily routine and diet.

PEM in a child can lead not only to physical, but also to mental retardation in development. Moreover, this condition is life-threatening for the baby, since the internal organs and systems of his body are not able to normally perform their functions in the absence of normal nutrition.

We kindly ask you not to self-medicate. Make an appointment with a doctor!