Protein and protein energy deficiency. Protein-energy malnutrition in children

What is Protein-energy malnutrition?

With insufficient protein and energy intake, lean body mass and the amount of adipose tissue decrease, and one of these changes may be more pronounced.

Protein deficiency is a pathological condition that develops as a result of a reduction or cessation of protein intake into the body. It can also be caused by increased protein breakdown in the body, for example, in case of burn disease, severe trauma, purulent-septic disease.

In developing countries, protein-energy malnutrition is common; during periods of famine its prevalence can reach 25%.

Primary protein-energy malnutrition occurs in cases where socio-economic factors do not allow for sufficient quantity and quality of food - in particular, if mainly plant proteins with low biological value are consumed. The high prevalence of infections also plays a role.

Protein deficiency is aggravated by insufficient energy intake, since in this case the amino acids in food are not used for protein synthesis, but are oxidized to produce energy.

In developing countries, 2 forms of protein-energy malnutrition occur in children - marasmus and kwashiorkor.

Marasmus is characterized by growth retardation, muscle atrophy (due to protein utilization) and subcutaneous tissue; there is no swelling. The disease is caused by insufficient intake of both proteins and energy.

With kwashiorkor (isolated protein deficiency), growth retardation, edema, hypoalbuminemia, and fatty liver are observed. Subcutaneous tissue is preserved.

Mixed forms can occur in both adults and children; the differences between protein-energy malnutrition and isolated protein malnutrition are of little clinical significance.

In developed countries, secondary protein-energy deficiency is most often observed, developing against the background of acute or chronic diseases. The reasons are decreased appetite, increased basal metabolism, malabsorption, alcoholism and drug addiction; in the elderly - depression, loneliness, poverty. In half of hospitalized elderly, exhaustion is already present at the time of admission to the hospital or develops during hospitalization.

Primary and secondary protein-energy malnutrition can be combined. Thus, with insufficient nutrition, the increase in basal metabolism and decrease in appetite characteristic of infections lead to the appearance of clinical signs of exhaustion more quickly than with normal nutritional status.

Isolated protein-energy malnutrition is rare. It is usually accompanied by a deficiency of other food components - folic acid, vitamin B1, vitamin B2 and vitamin B6, nicotinic acid, vitamin A. With protein-energy deficiency in children, vitamin A deficiency is especially dangerous. With the progression of the disease and the utilization of cellular proteins, a loss of intracellular potassium occurs, phosphorus and magnesium, and this loss is proportional to the excretion of nitrogen. Therefore, against the background of restoration of nutritional status, symptoms of deficiency of these substances may appear.

Pathogenesis (what happens?) during Protein-energy malnutrition

The body's adaptation to energy deficiency, in which the caloric intake does not meet the minimum energy requirement, involves hormonal changes. These changes promote the mobilization of free fatty acids from adipose tissue and amino acids from muscle. Gluconeogenesis and amino acid oxidation provide the energy needed for other organs, especially the brain. As a result, protein synthesis decreases, metabolism slows down, lean body mass decreases, and the amount of adipose tissue decreases. In the first week of fasting, weight loss is 4-5 kg ​​(25% is fat tissue, 35% is extracellular fluid, 40% is proteins). Subsequently, weight loss slows down. Different components of the body are utilized at different rates: skeletal muscles - faster than the heart muscle, gastrointestinal organs and the liver - faster than the kidneys. Skeletal muscle proteins are used to synthesize albumin, so hypoalbuminemia develops later.

When eating mainly plant proteins with low biological value, as well as in cases where only glucose solution is used for parenteral nutrition, protein deficiency may develop. At the same time, insulin secretion increases, which inhibits lipolysis and mobilization of skeletal muscle proteins. The level of amino acids in the blood drops, and the synthesis of albumin and other proteins decreases. As a result, hypoalbuminemia, edema and fatty liver disease, characteristic of kwashiorkor, develop.

Mineral deficiency is due in part to weight loss and loss of extracellular fluid. Losses of potassium and magnesium may be disproportionately high due to the mobilization of intracellular stores of these substances. The deficiency is aggravated by insufficient consumption of minerals (for example, parenteral nutrition using only glucose as an energy source) and an increase in their losses (increased diuresis, diarrhea, fistula).

Starvation usually does not lead to rapid death. The body's adaptation to energy deficiency includes meeting the energy needs of the central nervous system through the oxidation of fatty acids and ketone bodies, and slowing down metabolism, which helps preserve protein reserves. Fasting is more dangerous in acute or chronic diseases. They help increase basal metabolism, accelerate weight loss, as well as the loss of nitrogen and essential food components. Whether this effect is due to the immediate metabolic consequences of inflammation, infection, fever and wound healing or is mediated by the action of inflammatory mediators such as FO alpha, IL-2 and IL-6 is not entirely clear.

Thus, severe protein-energy malnutrition develops with insufficient nutrition against the background of acute or chronic diseases. Thus, it is often observed in AIDS (probably due to decreased appetite, fever and diarrhea).

Symptoms of Protein-Energy Malnutrition

Mild to moderate protein-energy malnutrition. Children do not gain weight or height. In adults, weight loss is observed, although with edema or obesity it may not be as noticeable. The thickness of the skin fold over the triceps brachii muscle and the muscle mass in the shoulder area decrease.

In the absence of kidney disease, the ratio of daily creatinine excretion to height (measured weekly) is a sensitive indicator of protein deficiency. The levels of albumin, transferrin and transthyretin (prealbumin) in the blood decrease. T3 levels decrease and reverse T3 levels increase. Metabolism slows down. Lymphopenia and impaired glucose tolerance are possible. The size of the heart is reduced.

Severe protein-energy malnutrition. Severe protein-energy malnutrition is accompanied by more pronounced changes in clinical and laboratory parameters. Physical examination reveals retraction of the intercostal spaces, atrophy of the temporal muscles and atrophy of the muscles of the limbs. Subcutaneous tissue is atrophied or absent. Characterized by apathy, fatigue, feeling of cold, skin depigmentation and hair depigmentation, sharpened facial features; the skin is dry, covered with cracks. In advanced cases, bedsores form and the skin ulcerates. Blood pressure is reduced, as is body temperature, and the pulse is weakened. The functions of all organs and systems are impaired.

Cardiovascular system, respiratory system and kidneys. The ventilatory response to hypoxia is weakened. Heart and kidney mass decreases in accordance with the decrease in lean body mass and slower metabolism, and therefore cardiac output and GFR, although decreased, are still in line with the body's needs. However, with infection, stress, as well as with rapid restoration of blood volume and nutritional status, heart failure is possible.

Blood. BCC, hematocrit, albumin and transferrin levels, as well as the number of lymphocytes in the blood are reduced. Normocytic normochromic anemia develops, usually due to a decrease in erythropoiesis caused by a decrease in protein synthesis. Anemia is aggravated by a deficiency of iron, folic acid and vitamin B6.

Metabolism. Basal metabolism and body temperature are reduced, apparently due to a drop in T3 levels and the loss of the heat-insulating function of the subcutaneous tissue. In the terminal stage, hypoglycemia develops.

Gastrointestinal tract and pancreas. Atrophy of intestinal villi and increased growth of microflora in the small intestine are observed; the exocrine and endocrine functions of the pancreas are disrupted. Malabsorption and lactose intolerance occur. These symptoms may be caused not by fasting itself, but by atrophy of the gastrointestinal tract from inactivity, since similar changes are observed with total parenteral nutrition.

The immune system. Humoral immunity is usually preserved; laboratory tests reveal a violation of cellular immunity. Pneumonia and other infections, including opportunistic ones, often develop.

Wound healing. The healing of wounds (including surgical wounds) is slowed down. The edges of the wound often separate.

Reproductive system. Egg implantation, growth and development of the fetus are disrupted. Childbirth occurs with complications, lactation decreases. The newborn has growth retardation; Children who survive may experience cognitive impairment in the future.

Treatment of protein-energy malnutrition

In case of mild to moderate protein-energy deficiency, the possible causes of this condition should be eliminated. The daily intake of proteins and energy is increased (in accordance with the ideal weight) to eliminate their deficiency. All patients are prescribed multivitamins. They also treat and prevent mineral deficiency (including microelements) to prevent life-threatening hypokalemia, hypomagnesemia, hypophosphatemia, etc. If the patient is able to eat and swallow, independent nutrition is sufficient. If there is a decrease in appetite or in the absence of teeth, liquid nutritional mixtures are additionally prescribed for self-feeding or tube feeding.

Severe protein-energy malnutrition requires more urgent intervention. Treatment of such patients is difficult for several reasons:

• Diseases that cause protein-energy deficiency are severe and more difficult to treat. Sometimes nitrogen balance can be restored only after the infection has been cured and the fever has resolved.
• Protein-energy malnutrition itself can interfere with the cure of the serious disease that caused it. In such cases, it is necessary to start tube or parenteral nutrition as early as possible.
• The intake of food through the gastrointestinal tract contributes to diarrhea due to atrophy of the mucous membrane and deficiency of intestinal and pancreatic enzymes. In this case, total parenteral nutrition may be indicated.
• The concomitant deficiency of other food components (vitamins, essential minerals, microelements) should be eliminated.

In adults, restoration of nutritional status occurs slowly and not always completely; in children, recovery occurs within 3-4 months. In all cases, educational and rehabilitation programs, as well as psychological and social support measures, are necessary.

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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 conditions, 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 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 enhanced 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

Thiamine

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., Tutelyana 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, 18th 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.

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.

Attached files

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Protein-energy malnutrition(BEN) or nutritional dystrophy, substrate-energy deficiency is a condition characterized by the development of symptoms of protein and energy deficiency, as well as other nutrients (fats, carbohydrates, vitamins, minerals) as a result of their relative or absolute deficiency, which develops as a result of partial or complete fasting.

Protein-energy deficiency can also be caused by insufficient intake of proteins and energy into the human body, as well as increased processes of protein catabolism in the body, for example, in case of burn disease, severe injury, purulent-septic diseases.

With insufficient protein and energy intake, body weight and the amount of adipose tissue decrease, and one of these changes may be more pronounced.

The main manifestations of severe PEM include: swelling, baldness, skin atrophy. The function of all organs and systems is impaired. Patients with PEM are more likely to experience prolonged wound healing, suture failure, increased hospitalization and recovery time, and infectious complications.

The diagnosis is based on medical history, assessment of clinical symptoms, results of anthropometric and laboratory tests.

Treatment consists of correcting water and electrolyte deficiency and prescribing artificial (enteral or parenteral) nutrition.

• Classification of protein-energy malnutrition

• Epidemiology of protein-energy malnutrition

  According to WHO, in 2000, there were 191.9 million malnourished children in developing countries worldwide. In South Asia and East Africa, this problem causes about half of children living there to be stunted.

  According to WHO estimates, by 2015 the incidence of PEM will decrease to 17.6%, which will amount to 113.4 million children under the age of 5 years. Currently, PEM is diagnosed in more than half of children living in North African countries, and in 30% of children from the South African region.

  Each year, approximately 50% of the 10 million deaths in developing countries caused by malnutrition occur in children under 5 years of age.

  In developing countries, primary PEM is most often observed (accounting for 25%), in developed countries - secondary PEM. Kwashiorkor is common in Africa, the Caribbean and the Pacific.

  In the United States, approximately 55% of hospitalized elderly patients have varying degrees of malnutrition. Upon hospitalization, approximately 40% of children show signs of acute PEM, and 27% show symptoms of chronic disease.

  In Russia, during selective studies of population nutrition, it was found 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. More than 50% of patients entering treatment suffer from PEM and severe hypovitaminosis (especially deficiency of folic acid, vitamins B 2 and C).

  According to the clinics of the All-Russian Scientific Research Center of the Russian Academy of Medical Sciences, malnutrition is 30% among inpatient cancer patients. Among patients receiving outpatient treatment for chronic diseases and cancer, about 10% have signs of malnutrition.

• ICD-10 code

  E. 46 - Protein-energy deficiency.

Clinic and complications

With a pronounced deficiency of nutrients, a long phase of compensation is initially observed, 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.

In conditions of predominantly energy deficiency, insanity develops.

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 relation to the preservation of visceral protein. In these cases, kwashiorkor develops. At the same time, decompensation occurs earlier, and patient survival rates decrease.

• Main clinical signs of malnutrition
  • Progressive weight loss syndrome.
  • Asthenovegetative syndrome.
  • Persistent decline in professional performance.
  • Morphofunctional changes in the digestive organs (atrophy of the mucous membrane of the stomach and small intestine, suppression of gastric and intestinal juice secretion, digestion and absorption disorders, dysbacteriosis).
  • Circulatory lability.
  • Immunodeficiencies.
  • Polyhypovitaminosis.
  • Polyglandular endocrine deficiency syndrome.
  • In children with PEM, in addition to a decrease in weight and height indicators, there is increased excitability, attention deficit, anxiety, and impaired social contacts. Adult patients with PEM experience a decrease in body weight, which may be masked by edema. They become apathetic, get tired quickly, have increased sensitivity to cold, and take a long time to heal their wounds.

• Clinical symptoms of insanity
  • Progressive weight loss.
  • Depletion and atrophy of the subcutaneous fat layer and muscles.
  • Growth retardation, retracted abdomen.
  • Apathy and irritability.
  • Dry, pale, cold skin with brown spots of pigmentation.
  • Dry, dull, thin hair.
  • Bone fractures may occur.
  • Achlorhydria and diarrhea.

• Clinical symptoms of kwashiorkor
  • Widespread edema (anasarca), ascites.
  • Patients have a moon-shaped face and a swollen abdomen.
  • Apathy and irritability.
  • Lack of appetite.
  • Patchy areas of skin depigmentation (“enamel or scaly dermatosis”), erythema.
  • Thinning and bleaching of hair. Streaks of discoloration (flag symptom) are found on the hair and nails. The hair becomes lighter and acquires a reddish tint, becomes brittle, and falls out easily.
  • Hepatomegaly.
  • Loss of libido in men, amenorrhea in women.

• Complications of protein-energy malnutrition
  • Infections.

    The main complications of PEM, which determine high mortality and treatment costs, are infectious processes. The frequent development of infections in patients with PEM is associated with a number of factors, among which impaired adaptive response and secondary immunodeficiency are the most important.

  • Immunological disorders.

    Immunological disorders in PEM are characterized primarily by disruption of the T-cell link: the absolute number of T-lymphocytes 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 levels 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-lymphocytes.

  • Signs of multivitamin deficiency. Read more: The importance of vitamins in human nutrition.

    As a rule, PEM is accompanied by a deficiency of vitamins A, B1, B2, B6, folic and nicotinic acids.

    • Signs of hypovitaminosis of vitamins B 2 and B 6 are manifested by changes in the skin, its appendages, tongue and mucous membranes. Dryness and peeling of the skin, cheilitis, glossitis, and stomatitis are detected. Pigment spots may appear on the face, neck, hands, legs and feet. Read more: Deficiency of vitamin B 2 and vitamin B 6.
    • Vitamin B6 deficiency is also characterized by: irritability, insomnia or drowsiness, epileptimorphic convulsions, depression, peripheral polyneuritis, microcytic hypochromic anemia, leukopenia.
    • Lack of vitamins B 1 and E leads to paresthesia and neuropathies. Read more: Vitamin B1 and vitamin E deficiency.
    • Vitamin B12 deficiency leads to megaloblastic anemia. Read more: Vitamin B12 deficiency.
    • Clinical symptoms of folic acid deficiency are: hyperchromic megaloblastic anemia, thrombocytopenia, leukopenia, cheilosis, glossitis, esophagitis, conjunctivitis; atrophic or erosive gastritis, enteritis with achlorhydria and diarrhea, steatorrhea; growth retardation, deterioration of wound healing, exacerbation of chronic infections, low-grade fever. Read more: Folic acid deficiency.
    • With vitamin A deficiency, patients experience twilight vision disorders. Read more: Vitamin A deficiency.
  • Disorders of mineral metabolism.

    With the progression of PEM and the utilization of cellular proteins, a loss of potassium, phosphorus, magnesium, and calcium occurs. Therefore, symptoms of deficiency of these substances may appear.

    • Calcium deficiency can cause paresthesia, cramps, pain in muscles and bones. In severe cases of the disease, calcium deficiency can contribute to the occurrence of osteoporosis of the long bones, spine and pelvis. Read more: Calcium deficiency.
    • In patients with hypocalcemia and hypomagnesemia, Chvostek's and Trousseau's symptoms become positive. Read more: Magnesium deficiency.
    • Due to increased neuromuscular excitability, characteristic of hypokalemia, a “muscle roller” symptom is detected; patients are also concerned about lethargy and muscle weakness. Read more: Potassium deficiency.
    • In patients with zinc, copper and iron deficiency, a skin rash appears, iron deficiency anemia develops, and body temperature rises. Read more: Deficiency of zinc, copper, iron.
  • Violations of adaptive functions.

    Violations of adaptive systems are a limiting factor in the treatment of patients.

    • In patients with PEM, the lability of the cardiac conduction system is reduced.
    • The ability of the kidneys to concentrate urine is reduced.
    • Reduced gastrointestinal peristalsis.
    • Patients experience disorders of respiratory and thermoregulatory functions.
    • Skin lesions are mildly painful and occur without swelling or hyperemia.
    • The rate of wound healing is slowed down, and the incidence of postoperative complications increases.
    • Pyuria is not observed in urinary tract infections.

Protein-energy malnutrition, or protein-calorie malnutrition, is a deficiency of energy due to chronic deficiency of all macronutrients. It usually includes deficiencies of many micronutrients. Protein-energy deficiency can be sudden and total (starvation) or gradual. Severity ranges from subclinical manifestations to overt cachexia (with edema, hair loss and skin atrophy), and multiorgan and multisystem failure is observed. Laboratory tests, including serum albumin, are commonly used for diagnosis. Treatment involves correcting fluid and electrolyte deficiencies with intravenous fluids, followed by gradual oral replacement of nutrients if possible.

In developed countries, protein-energy malnutrition is a common condition among nursing home residents (although often unaware of it) and among patients with disorders that reduce appetite or impair the digestion, absorption and metabolism of nutrients. In developing countries, protein-energy malnutrition occurs in children who do not consume enough calories or protein.

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ICD-10 code

E46 Protein-energy malnutrition, unspecified

E64.0 Consequences of protein-energy malnutrition

E45 Developmental delay due to protein-energy malnutrition

Classification and causes of protein-energy malnutrition

Protein-energy malnutrition can be mild, moderate or severe. The stage is determined by determining the difference in percentage of the patient’s real and calculated (ideal) weight corresponding to his height, using international standards (normal, 90-110%; mild protein-energy malnutrition, 85-90%; moderate, 75-85%; severe , less than 75%).

Protein-energy malnutrition can be primary or secondary. Primary protein-energy malnutrition is caused by inadequate intake of nutrients, while secondary protein-energy malnutrition results from various disorders or medications that interfere with the utilization of nutrients.

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Symptoms of protein-energy malnutrition

Symptoms of moderate protein-energy malnutrition can be general (systemic) or affect specific organs and systems. Characterized by apathy and irritability. The patient is weakened and performance is reduced. Cognitive abilities and sometimes consciousness are impaired. Temporary lactose deficiency and achlorhydria develop. Diarrhea is frequent, and it is aggravated by a deficiency of intestinal disaccharidases, especially lactase. Gonadal tissues are atrophic. PEM can cause amenorrhea in women and loss of libido in both men and women.

Loss of fat and muscle mass is a common feature of all forms of PEM. In adult volunteers who fasted for 30-40 days, weight loss was obvious (25% of initial weight). If the fast is longer, weight loss can reach 50% in adults and possibly more in children.

Cachexia in adults is most obvious in areas where there would normally be visible fat deposits. The muscles decrease in volume, and the bones protrude noticeably. The skin becomes thin, dry, inelastic, pale and cold. Hair is dry and falls out easily, becoming thin. Wound healing is impaired. In elderly patients, the risk of hip fractures, bedsores, and trophic ulcers increases.

In acute or chronic severe protein-energy malnutrition, heart size and cardiac output are reduced; The pulse slows down and blood pressure decreases. Breathing intensity and vital capacity of the lungs decrease. Body temperature drops, sometimes leading to death. Edema, anemia, jaundice and petechiae may develop. Liver, kidney or heart failure may occur.

Cellular immunity is weakened, and susceptibility to infections increases. Bacterial infections (eg, pneumonia, gastroenteritis, otitis media, urogenital tract infections, sepsis) are characteristic of all forms of protein-energy malnutrition. Infections lead to the activation of cytokine production that worsens anorexia, leading to further loss of muscle mass and a significant decrease in serum albumin levels.

In infants, marasmus causes hunger, weight loss, growth retardation, and loss of subcutaneous fat and muscle mass. The ribs and facial bones protrude. Flabby, thin, “dangling” skin hangs in folds.

Kwashiorkor is characterized by peripheral edema. The abdomen protrudes, but there is no ascites. The skin is dry, thin and wrinkled; it becomes hyperpigmented, cracks, and then develops hypopigmentation, friability and atrophy. The skin of different areas of the body may be affected at different times. Hair becomes thin, brown or gray. Hair on the scalp falls out easily, eventually becoming sparse, but eyelash hair can even grow excessively. Alternating between undernutrition and adequate nutrition results in hair that has a “striped flag” appearance. Sick children may be apathetic, but become irritable if they are tried to rouse them.

Complete fasting is fatal if it lasts more than 8-12 weeks. Thus, the symptoms characteristic of protein-energy malnutrition do not have time to develop.

Primary protein-energy malnutrition

Throughout the world, primary protein-energy malnutrition occurs mainly in children and the elderly, i.e. those with limited access to food, although the most common cause in old age is depression. This may also be a consequence of fasting, therapeutic fasting or anorexia. The cause may also be poor (cruel) treatment of children or the elderly.

In children, chronic primary protein-energy malnutrition has three forms: marasmus, kwashiorkor, and a form that has characteristic features of both (marasmic kwashiorkor). The form of protein-energy malnutrition depends on the ratio of non-protein and protein energy sources in the diet. Fasting is an acute severe form of primary protein-energy malnutrition.

Marasmus (also called dry protein energy malnutrition) causes weight loss and wasting of muscle and fat stores. In developing countries, marasmus is the most common form of protein-energy malnutrition in children.

Kwashiorkor (also called the wet, puffy or edematous form) is associated with premature weaning of an older child, which usually occurs when a younger child is born, “pushing” the older child off the breast. Thus, children with kwashiorkor are usually older than those with marasmus. Kwashiorkor may also result from acute illness, often gastroenteritis or other infection (likely secondary to cytokine production) in children who are already protein-energy malnourished. A diet that is more deficient in protein than energy may be more likely to cause kwashiorkor than marasmus. Less common than marasmus, kwashiorkor tends to be limited to certain regions of the world, such as rural Africa, the Caribbean and the Pacific Islands. In these areas, staple foods (eg cassava, sweet potatoes, green bananas) are poor in proteins and rich in carbohydrates. In kwashiorkor, the permeability of cell membranes increases, causing extravasation of intravascular fluid and protein, leading to peripheral edema.

Marasmic kwashiorkor is characterized by the combined features of marasmus and kwashiorkor. Children affected by it are edematous and have more body fat than with marasmus.

Starvation is a complete lack of nutrients. Sometimes fasting is voluntary (as during a period of religious fasting or during anorexia nervosa), but usually it is caused by external factors (for example, natural circumstances, being in the desert).

Secondary protein-energy malnutrition

This type usually results from disorders that affect GI function, cachectic disorders, and conditions that increase metabolic demands (eg, infections, hyperthyroidism, Addison's disease, pheochromocytoma, other endocrine disorders, burns, trauma, surgery). In cachectic disorders (eg, AIDS, cancer) and renal failure, catabolic processes lead to the production of excess cytokines, which in turn leads to malnutrition. End-stage heart failure can cause cardiac cachexia, a severe form of malnutrition with a particularly high mortality rate. Cachectic disorders may reduce appetite or impair nutrient metabolism. Disorders that affect GI function may impair digestion (eg, pancreatic insufficiency), absorption (eg, enteritis, enteropathies), or lymphatic transport of nutrients (eg, retroperitoneal fibrosis, Milroy's disease).

Pathophysiology

The initial metabolic reaction is a decrease in metabolic rate. To provide energy, the body first “breaks down” fat tissue. However, then the internal organs and muscles also begin to deteriorate, and their mass decreases. The liver and intestines “lose” the most weight, the heart and kidneys occupy an intermediate position, and the nervous system loses the least weight.

Diagnosis of protein-energy malnutrition

The diagnosis is based on the medical history, when clearly inadequate food intake is established. The cause of inadequate nutrition, especially in children, must be identified. In children and adolescents, the possibility of abuse and anorexia nervosa must be kept in mind.

Physical examination data can usually confirm the diagnosis. Laboratory studies are necessary to identify the cause of secondary protein-energy malnutrition. Measurement of plasma albumin, total lymphocyte count, CD4+ T lymphocytes, and response to skin antigens helps determine the severity of protein-energy malnutrition or confirm the diagnosis in borderline conditions. Measuring C-reactive protein or soluble interleukin-2 receptor levels can help determine the cause of malnutrition when the cause is unclear and confirm abnormal cytokine production. Many additional indicators may differ from normal values: for example, decreased levels of hormones, vitamins, lipids, cholesterol, prealbumin, insulin-like growth factor-1, fibronectin and retinol-binding protein are characteristic. Urinary creatinine and methyl-histidine levels can be used to assess the extent of muscle mass loss. As protein catabolism slows, urinary urea levels also decrease. These data are rarely taken into account when choosing treatment tactics.

Other laboratory tests can also identify associated abnormalities that require treatment. Serum electrolyte levels, BUN and creatinine, BUN, glucose, possibly Ca, Mg, phosphate and Na should be determined. Blood glucose and electrolyte levels (especially K, Ca, Mg, phosphate, and sometimes Na) are usually low. Indicators of urea and creatinine, BUN in most cases remain at low values ​​until renal failure develops. Metabolic acidosis may be detected. A general blood test is performed; normocytic anemia (primarily due to protein deficiency) or microcytic anemia (due to concurrent iron deficiency) is usually present.

Indicators used to assess the severity of protein-energy malnutrition

In the elderly BMI

The Delayed Type Hypersensitivity Index indicates the amount of induration detected by skin testing using a common antigen derived from Candida sp. or Trichophyton sp. The degree of induration is 0 - 1.0 cm.

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Prevention and treatment of protein-energy malnutrition

Globally, the most important strategy for preventing protein-energy malnutrition is to reduce poverty and improve nutrition knowledge and health care.

Mild to moderate protein-energy malnutrition, including short-term fasting, is treated by eating a balanced diet, preferably orally. Liquid oral nutritional supplements (usually lactose-free) may be used if solid foods cannot be adequately digested. Diarrhea often complicates oral feeding because fasting increases gastrointestinal sensitivity and introduces bacteria into Peyer's patches, contributing to infectious diarrhea. If diarrhea persists (presumably due to lactose intolerance), yogurt-based formulas are given rather than milk-based formulas because people with lactose intolerance can tolerate yogurt and other fermented milk products. Patients also need to be prescribed multivitamin supplements.

Severe protein-energy malnutrition or prolonged fasting requires treatment in a hospital setting with a controlled diet. The main priorities are the correction of fluid and electrolyte imbalances and the treatment of infections. The next step is to supplement macronutrients orally or, if necessary, through a tube: nasogastric (usually) or gastric. Parenteral nutrition is prescribed if severe malabsorption is present.

Other treatments may be needed to correct specific nutritional deficiencies that may occur with weight gain. To avoid micronutrient deficiency, patients should continue to take micronutrients at doses approximately 2 times the recommended daily allowance (RDA) until recovery occurs.

It is necessary to treat the disorders underlying the developed pathological condition. In children with diarrhea, feeding may be delayed for 24 to 48 hours to avoid worsening the diarrhea. Feeding is carried out frequently (6-12 times/day), but in order to avoid damage to the already limited absorption capacity of the intestine, it should be carried out in small quantities (

The energy distribution of macronutrients should be approximately: 16% protein, 50% fat and 34% carbohydrates. As an example, we give a combination of skim cow's milk powder (110 g), sucrose (100 g), vegetable oil (70 g) and water (900 ml). Many other milk formulas can be used (for example, whole fat fresh milk plus corn oil and maltodextrin). Powdered milk used in infant formula is diluted with water.

Usually additives are added to milk formulas: MD 0.4 mEq/kg/day intramuscularly for 7 days; B vitamins in double RDA, given parenterally for the first 3 days, usually with vitamin A, phosphorus, zinc, manganese, copper, iodine, fluoride, molybdenum and selenium. Since the absorption of dietary iron in children with protein-energy deficiency is difficult, it is prescribed in supplements orally or intramuscularly. Parents are instructed about nutritional requirements.

In adults

It is necessary to eliminate disorders associated with protein-energy malnutrition. For example, if AIDS or cancer leads to excess cytokine production, then megestrol acetate or hydroxyprogesterone may improve food intake. However, since these drugs dramatically reduce testosterone production in men (possibly causing muscle loss), testosterone should also be used at the same time. Because these drugs may cause decreased adrenal function, they should only be used short-term (

Medicines that stimulate appetite (hashish extract - dronabinol) should be given to patients with anorexia when none of the causes of their disease are clear, or to patients in their declining years when anorexia worsens their quality of life. Anabolic steroids have some beneficial effects (eg, increased lean body mass, possibly functional improvements) in patients with cachexia due to renal failure and possibly in elderly patients.

The principles for correcting protein-energy deficiency in adults are generally similar to those in children. For most adults, feeding should not be delayed; Small amounts of food with frequent intake are recommended. It is possible to use commercial formula for oral feeding. Nutrients are given at the rate of 60 kcal/kg and 1.2-2 g protein/kg. If liquid oral supplements are used with solid food, they should be taken at least 1 hour before the meal so that the amount of solid food eaten is not reduced.

Treatment of patients with protein-energy malnutrition in a nursing home requires a variety of conditions, including changes to the environment (eg, making the dining area more attractive); feeding assistance; changes in diet (eg, increased nutrition and calorie supplements between meals); treatment of depression and other underlying disorders; use of appetite stimulants, anabolic steroids or a combination thereof. For patients with severe dysphagia, long-term use of a gastrostomy tube for feeding is indispensable; although its use in patients with dementia is controversial. There are also tangible benefits from avoiding unpalatable medical diets (for example, low-salt, diabetic, low-cholesterol), since these diets reduce food intake and can cause severe protein-energy malnutrition.

Complications of treatment of protein-energy malnutrition

Treatment of protein-energy malnutrition may cause complications (refeeding syndrome), including fluid overload, electrolyte deficiencies, hyperglycemia, cardiac arrhythmias, and diarrhea. Diarrhea is usually mild and goes away on its own; however, diarrhea in patients with severe PEM sometimes causes severe dehydration or death. Causes of diarrhea such as sorbitol used in tube feedings, or Clostridiumdifficile if the patient received antibiotic therapy, they can be eliminated with special interventions. Osmotic diarrhea due to excess calorie intake is rarely seen in adults and can be considered as a cause only when other causes of protein-energy malnutrition have been excluded.

Because protein-energy malnutrition can impair cardiac and renal function, hydration may cause an increase in intravascular fluid volume. Treatment also reduces the concentration of extracellular K and Mg. A decrease in K or Mg can cause arrhythmias. Activation of carbohydrate metabolism during treatment stimulates the release of insulin, which leads to the entry of phosphate into the cells. Hypophosphatemia can cause muscle weakness, paresthesia, paralysis, arrhythmias, and coma. Blood phosphate levels during parenteral nutrition should be measured regularly.

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Prognosis of protein-energy malnutrition

In children, mortality varies from 5 to 40%. Mortality rates are lower in children with mild protein-energy malnutrition and in those who receive intensive care. Death within the first days of treatment usually occurs due to electrolyte deficiency, sepsis, hypothermia, or heart failure. Impaired consciousness, jaundice, petechiae, hyponatremia and persistent diarrhea are ominous prognostic symptoms. The cessation of apathy, edema and anorexia are favorable symptoms. Faster recovery is observed with kwashiorkor than with marasmus.

To date, it has not been fully established what long-term protein-energy malnutrition leads to in children. Some children develop chronic malabsorption syndrome and pancreatic insufficiency. Young children may develop moderate mental retardation, which may persist until school age. Persistent cognitive impairment may occur, depending on the duration, severity, and age at onset of protein-energy malnutrition.

In adults, protein-energy malnutrition can lead to complications and mortality (for example, progressive weight loss increases mortality by 10% in elderly people in nursing homes). Except in cases where organ or system failure develops, treatment of protein-energy malnutrition is almost always successful. In older patients, protein-energy malnutrition increases the risk of complications and mortality from surgery, infection, or other disorders.

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 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!