Nutritional dystrophy, symptoms and treatment. Nutritional dystrophy Nutritional deficiency

Nutritional dystrophy(Latin alimentarius food + Greek dys-+ trophē nutrition; synonym: hunger disease, hunger edema, protein-free edema, epidemic dropsy, military edema, edematous disease) - a disease of prolonged insufficient and malnutrition, manifested by general exhaustion, progressive disorder of all types metabolism, degeneration of tissues and organs with disruption of their functions, a significant decrease in physical and mental activity, edema, cachexia. The term “nutritional dystrophy” began to be steadily used to refer to this disease after its detailed description of the mass incidence of starvation in Leningrad, which was blockaded during the Great Patriotic War. Nutritional dystrophy is not identical to the state of hunger and differs from various forms of partial nutritional deficiency - vitamin deficiency, kwashiorkor, etc., in the totality and severity of metabolic disorders and the functions of all organs and systems of the body.

ETIOLOGY
The leading cause of nutritional dystrophy is the long-term energy and quality deficiency of consumed food, which becomes widespread during periods of social conflicts (war) and natural disasters (crop failure, destruction of food during floods, destructive earthquakes, etc.).
Of aggravating importance are the inevitable consumption of poor-quality food in conditions of hunger with an excess content of table salt, water, poorly digestible fiber, consumed for psychological reasons (“to deceive hunger”), lack of vitamins, heavy physical labor, neuro-emotional stress, cold, increased weakening of the body, infectious diseases (especially gastrointestinal).

In peacetime, in economically developed countries, cases of nutritional dystrophy are extremely rare (in shipwrecked people, in children lost in the forest, etc.).

PATHOGENESIS AND PATHOLOGICAL ANATOMY
Prolonged fasting causes a deficiency in the body of substances necessary to maintain homeostasis and ensure the body's energy expenditure. As a result, energy costs are reduced (a sharp drop in physical and intellectual work capacity), and profound changes occur in metabolism aimed at maintaining the most important parameters of homeostasis through the redistribution of substances, which is of limited and transient significance and is accompanied by a deepening disorder of the trophism and function of various organs. Hormonal regulation is rearranged: the functions of the pituitary gland decrease with the development of hypothalamic-pituitary insufficiency syndrome, the functions of the thyroid gland, adrenal glands, and gonads. Insufficient intake of food proteins into the body leads to hypoproteinemia mainly due to a decrease in albumin content (dysproteinemia), protein-free edema occurs, the enzymatic activity of the digestive glands is disrupted, and the digestion and absorption of foods and their assimilation worsen. Against this background, unprepared intake of large meals, even nutritious ones, becomes unproductive and dangerous.

A direct consequence of fasting is the gradual disappearance of subcutaneous tissue and atrophy of skeletal muscles. In some cases, widespread edema is observed, in others - cachexia with dehydration. Often the edema is represented only by severe ascites. According to pathological data, the heart is atrophic during a protracted course of nutritional dystrophy; in some cases, its weight in an adult decreases to 100 g. Blood clots are often found in the veins of the extremities. In arteries, in some cases, according to K.G. Volkova (1946), - signs of resorption of cholesterol deposits, in others (according to autopsies of those killed in fascist concentration camps) - a sharp development of atherosclerosis with fresh cholesterol deposits. This apparently depends on the fasting conditions. The liver can be reduced by 2-2 1/2 times; atrophy of the spleen, lymph nodes, mucous membrane of the gastrointestinal tract, and endocrine glands is detected; bone marrow is depleted. In those who died from nutritional dystrophy, pneumonia (usually small-focal) is found in more than half of the cases, and just as often - changes in the intestines caused by a protracted course of dysentery or other intestinal infection.

CLINICAL CARD AND COURSE
Based on the severity of manifestations, three degrees (stages) of nutritional dystrophy are conventionally distinguished - mild (I degree), moderate (II degree) and severe (III degree). According to the course, acute, chronic and recurrent nutritional dystrophy is distinguished, occurring without complications and complicated (pneumonia, dysentery, tuberculosis, scurvy). Based on the nature of water metabolism disorders, a distinction is made between the edematous form of nutritional dystrophy (with early or late edema) and the cachectic form.

Nutritional dystrophy of the first degree is characterized by decreased performance, chilliness, and apathy. Fatness is clearly decreased, appetite is increased, thirst, excessive diuresis, and constipation are often noted. Muscle atrophy is not clearly expressed, there may be early swelling (on the legs, feet). There is a tendency towards bradycardia and hypothermia (body temperature is about 36.0° and below).

With nutritional dystrophy of the second degree, performance is sharply reduced, and mental disorders are possible. Urination is sharply increased. Nutrition is significantly reduced, eyes are sunken, the skin of the neck and face is wrinkled; noticeable muscle atrophy is revealed. In the edematous form, pronounced hypostatic edema and ascites are determined. Characterized by bradycardia and hypothermia (body temperature 35.5-35.8°), prolonged constipation (sometimes loose stools). In the blood, leukocytopenia with relative lymphocytosis is determined, erythrocytosis is possible. In many patients, anti-infective immunity sharply decreases and at the same time allergic reactions are suppressed (in people who suffered from bronchial asthma, vasomotor rhinitis, and urticaria, a stable remission of these diseases usually occurs).

With nutritional dystrophy of the third degree, patients completely lose their ability to work and often cannot move independently. Adynamia develops. Speech is slow, monotonous, the face is amicable: when chewing, patients suddenly seem to freeze with food in their mouth. Pain in the muscles and lower back appears, and cramps are often observed. Anorexia and apathy occur, and disgust and shyness weaken in patients; Acute psychoses are not uncommon. At this stage of nutritional dystrophy, the subcutaneous fat layer in patients is absent, the muscles are sharply atrophic. In the edematous form, generalized edema is observed; ascites; in their absence - severe cachexia. The pulse is usually less than 50 beats per minute, body temperature is below 35.5°, blood pressure is reduced. Fainting often occurs. Petechiae are detected on the skin of the legs, thighs, and abdomen, and gingivitis is possible (manifestations of concomitant scurvy). Anemia, thrombocytopenia, and hypocalcemia are determined. Protein and blood sugar levels are reduced; with significant hypoproteinemia and hypoglycemia, ketoacidosis develops, blood pH decreases and a hungry coma occurs.

Coma with nutritional dystrophy develops relatively suddenly, often as a continuation of the fainting spell that preceded it, sometimes after short-term excitement. In the diagnosis of a hungry coma, the characteristic appearance of patients with nutritional dystrophy (cachexia, edema) is important. The skin is pale, cold, flaky. Body temperature is reduced. The pupils are wide. Muscle tone and tendon reflexes are reduced; Tetanic convulsions are possible. Breathing is harsh, shallow, sometimes arrhythmic. Blood pressure is low, pulse is low. Death occurs from respiratory and cardiac arrest.

The course of nutritional dystrophy is often complicated by intestinal infections (for example, dysentery), pneumonia, tuberculosis, which usually lead to death. In some cases, death occurs suddenly from pulmonary embolism or due to sudden overexertion. With “slow dying,” death often occurs during sleep. According to A. A. Kedrov, by the end of the second month of the siege of Leningrad, the mortality rate among patients with nutritional dystrophy reached 85%.

The diagnosis is established by characteristic clinical symptoms, taking into account a history confirming prolonged fasting. In each case, it is necessary to make sure that the main cause of the patient’s exhaustion is starvation, and not any debilitating disease (in group cases of nutritional dystrophy, infectious diseases are excluded first of all). Bradycardia, body hypothermia, signs of vitamin deficiency, and polyglandular endocrine insufficiency characteristic of alimentary dystrophy have differential diagnostic significance.

TREATMENT
In case of a hungry coma, the patient is warmed with heating pads (subsequently given a warm drink); 40-50 ml of a 40% glucose solution is injected intravenously, then drugs for parenteral nutrition are drip-fed (hydrolysine 1 l or polyamine 400 ml, etc.), 1-2 l of a 5% glucose solution, adding vitamins B6, B12, cocarboxylase ( 200 mg). 30-60 mg of prednisolone is injected into the dropper tube, and for convulsions - 10 ml of a 10% calcium chloride solution.

With a mild degree of nutritional dystrophy, eat fractional meals enriched with proteins and vitamins, limit physical activity, ensure regular sleep, and a hygienic regimen. The total calorie content of food is 3000-3500 kcal, proteins at least 100 g, carbohydrates 500-550 g, fats 70-80 g per day. Dairy products, eggs, meat are preferred. Multivitamin preparations are prescribed. In case of nutritional dystrophy of the II and III degrees, it is necessary to hospitalize the patient for infusion therapy in bed rest, the use of parenteral methods of artificial nutrition, controlled restoration of water and electrolyte balance and the elimination of vitamin deficiency. Enpits are used that contain a set of well-digested essential amino acids and vitamins. If necessary, correction of acid-base imbalance, treatment of infectious complications, dysbacteriosis, and disorders of the immune status are carried out.

In the first hours of medical care, monitoring the mental state of persons with severe or acute manifestations of nutritional dystrophy is of great importance; they must be constantly under medical (or paramedic) supervision. During the period of convalescence, psychological and physical rehabilitation is carried out, which can continue, depending on the severity of the initial condition and the presence of infectious complications, for up to 2-6 months. When the main indicators are normalized and body weight is restored, sanatorium-resort treatment is indicated.

Nutritional dystrophy- This is one of the varieties of such a disease as dystrophy. That is, this is a complete disorder of the body, disruption of the functioning of all organs and tissues. During nutritional dystrophy, a person experiences a disruption in the absorption of proteins, fats and carbohydrates, which should normally enter all cells of our body along with the food consumed.

If we talk about nutritional dystrophy, this means that a person did not eat enough for some long time or severely limited himself in food consumption. This term is not new to medicine and it first appeared during the difficult time of the siege of Leningrad. It was then that death certificates and reports of the dead began to indicate the cause of death - nutritional dystrophy. That is, a person starved for a long time, no food entered his gastrointestinal tract, and all this led to the emergence of nutritional dystrophy. This condition is very serious in nature and leads, in most clinical cases, to death.

Global problem of nutritional dystrophy

Today, the problem of hunger, nutrition and satisfaction of primary needs for the majority of the population of our planet is not fully satisfied. Therefore, the problem of nutritional dystrophy is truly global. Even people with below average income periodically suffer from a deficiency of proteins, fats and carbohydrates from their food intake. As a result, health problems.

Also, it is worth noting that in the 21st century, thinness, one might even say dystrophic, is becoming really extremely popular. Some children, following fashion trends, deliberately tend to lose weight and become malnourished.

If we talk about nutritional dystrophy in children, it leads to the fact that already in adolescence their mental development decreases and their physiological processes slow down.

According to medical statistics, today in the most developed countries there are about 300 million children who are diagnosed with nutritional dystrophy due to constant malnutrition.

In adults, nutritional dystrophy affects 20% of the population in developed countries with normal economic levels.

Dystrophy is the main cause of death in 45% of clinical cases in children under 5 years of age. If we talk about such poor countries as Africa and Asia, then about 3 million children die from malnutrition every year.

Causes of nutritional dystrophy

The main cause of nutritional dystrophy is an acute deficiency of protein, fat and carbohydrates in the human body. The food simply does not receive the most basic nutrients. That is, they may not arrive completely or not at all (a person has been starving for a long time).

Also, there is such a picture when a person eats some foods every day, but they in no way cover the body’s needs for nutrients.

Symptoms of nutritional dystrophy

Symptoms of nutritional dystrophy begin to appear at the stage when the body does not receive any nutrients for a long period of time. That is, the body’s reserves are not replenished and the body, in this case, begins to consume its own resources - burn the fat that has been accumulated, then the muscles disappear, all protein bonds in the body disintegrate. Hormonal levels are completely disrupted, etc. In fact, the body eats itself.

Amino acids in the blood begin to oxidize very quickly due to the fact that insufficient energy enters the body. This means that the proteins, fats and carbohydrates that enter the cells (or do not enter at all) are sorely insufficient to cover all the body’s energy costs.

In this case, a person suffering from nutritional dystrophy begins to rapidly lose protein - up to 125 grams per day. This leads to:

Complete metabolic disorder;
Imbalance of blood protein and human tissue protein;
The human skeleton changes completely, muscles disappear;
Muscle mass is lost;
There is a sharp decrease in blood sugar, hormones, cholesterol;
The production of glycogen in the liver, as well as in muscle tissue, stops;
Extreme exhaustion syndrome or;
The person completely loses all his strength.

Clinical symptoms of dystrophy

If we talk about the clinical symptoms that are observed in a patient diagnosed with “nutritional dystrophy,” these are:

Very strong painful hunger, a person constantly thinks about food;
Paleness of the skin;
Dry skin;
Wrinkles on the face that appear quite suddenly;
A sharp decrease in body weight;
Weakness in the body;
Muscle numbness, frequent cramps;
Body temperature begins to drop to pathologically low levels;
Blood pressure disorders;
Poor circulation;
Disorders of the gastrointestinal tract (frequent constipation, flatulence);
Tachycardia;
Women lose menstruation;
In men, sexual desire completely disappears - impotence;
Mental disorders – increased irritability, depression;
Constant desire to sleep;
Slow reactions.

Classification of nutritional dystrophy

There is a classification of nutritional dystrophy:

A sharp decrease in body weight – 1st degree or mild stage;
Significant deterioration in a person’s well-being, a state of weakness, loss of interest in life – grade 2 or a clinical condition of moderate severity;
Complete absence of fat layer, muscle dystrophy, skeletal atrophy;
Disruption of the functioning of internal organs, as well as partial or complete cessation of vital systems.

Treatment of nutritional dystrophy

Of course, the first thing that comes into play in the treatment and therapy of nutritional dystrophy is a complete, balanced diet for the patient. Moreover, the total calorie content should be at around 3000 kcal per day.

You need to eat 6 times a day.

It is very important to maintain complete physical and emotional rest for a while.

If the stage is the last in severity, then the patient must undergo treatment in an inpatient medical facility with strict bed rest.

Exhaustion developed as a result of prolonged fasting, or food insufficient in caloric content and poor in protein. The pathogenesis is based on disturbances in protein metabolism, a lack of total protein and blood albumin. The body loses plastic and organ proteins. The amount of fat in tissues and blood and blood sugar levels decrease. Muscle atrophy develops. The function of the endocrine glands weakens. Vitamin deficiency C, complex B, A, P increases. Scurvy and pellagra may develop.

Symptoms, course of nutritional dystrophy

Progressive weight loss, hunger, vomiting, increasing weakness. Hypothermia, muscle pain, polyuria, nocturia. The skin is dry, yellow. Skin turgor is reduced. The muscles are atrophic. The subcutaneous fat is absent. Later, swelling of the entire body and serous cavities increases. Bradycardia, arterial and venous hypotension, slowing of blood flow. Heart sounds are muffled. Tachycardia at the slightest exertion. On the electrocardiogram, the T waves are isoelectric or negative, the P - Q interval is extended. The acidity of gastric juice is reduced. The tongue is lacquered. The mucous membrane of the stomach and intestines is atrophic. Anemia with a tendency to leukopenia and thrombopenia. The total content of serum protein is reduced to 4-5%, albumin to 2-3%. The content of cholesterol, sugar, chlorides and calcium in the blood is reduced. Reduced basal metabolism. The amount of 17-ketosteroids in daily urine is reduced. Patients are lethargic, drowsy. Increasing weakness limits the ability to move. Women experience amenorrhea, men experience impotence.

There are three degrees of dystrophy based on severity. The first is a mild form with moderate atrophy of subcutaneous fat and skeletal muscles with mild general disorders. The second degree is of moderate severity. Significant atrophy of subcutaneous fat, muscles, general metabolic disorder and significant loss of performance. The third degree is a severe form with complete atrophy of subcutaneous fat and muscles, a sharp disturbance of metabolic processes and cardiovascular failure.

On the part of the endocrine system, due to atrophic changes in the glands, individual symptoms of their hypofunction are observed. Patients are apathetic, inhibited, drowsy, and less often excited.

Hemeralopia (“night blindness”) is often observed due to a lack of vitamin A.

Factors that reveal the symptoms of dystrophy and aggravate its course are heavy physical work and cooling.
Complications - often focal confluent pneumonia, exacerbation of tuberculosis, dysentery in a large number of cases, trophic ulcers on the legs, etc.

The diagnosis is facilitated by clarifying the nutritional conditions in the previous period, taking into account calorie and protein content. It seems important, but often difficult, to resolve the question of whether the nutritional factor is the only and main factor in the development of dystrophy. The edematous form is distinguished from renal diseases by the absence of hypertension and changes in the urine, from heart failure by the absence of other signs and objective changes in the heart.

The prognosis depends on the degree of dystrophy. It is unfavorable in grade III and is significantly aggravated by complications of pneumonia, dysentery and other infections.

Severe dystrophy can be complicated by coma, ending in death. With dystrophy of degrees I and II, the prognosis for life and restoration of health is favorable if therapeutic measures are taken in a timely manner.

Recognition is based on anemnesis, clinical data and a thorough examination to exclude tuberculosis, cancer cachexia and other diseases. The edematous form is differentiated from renal diseases, myxedema.

Treatment of nutritional dystrophy

The main principle is to increase energy resources and reduce energy consumption by rationally building a diet with sufficient protein, fat, carbohydrates and vitamins with full calorie content and creating the correct regimen for the patient.

For dystrophy of II and III degrees - complete bed rest in the hospital. In case of I degree - home regime with temporary release from work. A normal room temperature is necessary; for grade III dystrophy, special warming of the patient is required.

The calorie content of food is gradually increased to 50-60 kcal per 1 kg of the patient’s weight with the amount of protein up to 2 g per 1 kg of weight. Food is taken 5-6 times a day.

After a long complete fast, the food regimen is expanded especially carefully, starting with fruit juices in half with alkaline mineral waters, then vegetable and meat soufflés and weak broth are introduced into the diet. The transition to a diet with increased calorie content is carried out by the 5-10th day of treatment. If you have no appetite - table grape wine. Vitamins C and vitamin B complex in therapeutic doses. Intravenous infusion of hypertonic glucose solution. For grade III dystrophy - repeated intravenous infusions of blood, plasma and their substitutes. For better protein absorption, use anabolic steroid preparations: methandrostenolone or methylandrostenediol. In case of violation of the secretory function of the stomach and intestines with diarrhea - gastric juice, acidin-pepsin, pancreatin, abomin. For edema - potassium acetate, small doses of thyroidin. Camphor, caffeine, cordiamin according to indications. In a comatose state, the patient must be warmed with heating pads; repeated intravenous infusion of 20% glucose solution is indicated; subcutaneous or intravenous drip infusion of saline (500 ml) with 5% glucose solution and hydrocortisone (50-100 mg), repeated intravenous infusions of blood, plasma or their substitutes. Cardiac drugs, adrenaline, mesaton, norepinephrine. For respiratory distress, intravenous or intramuscular administration of lobeline (1 ml of 1% solution) or cititon (1 ml).

In the first days, patients are given food in limited quantities. Gradually, its calorie content is increased to 50-60 calories per 1 kg of weight. For third-degree dystrophy, transfusions of plasma and plasma substitutes of 100-200 ml are used daily. Intravenous blood transfusions. Anabolic steroid preparations are used: methylandrostenediol 0.01 g per day 2 times, methandrostenolone 0.005 g 2-3 times a day. For edema, potassium acetate, thyroidin 0.05-0.1 g per day. Heart remedies To improve the function of the stomach and intestines, acidopepsin, lipocaine, pancreatin, gastric juice. In a comatose state, intravenous infusions of 20% glucose solution, 100 ml each, subcutaneous infusions of saline, cardiac drugs and drugs that increase blood pressure (adrenaline, mesaton) For respiratory distress, lobelia, cititon.

Nutrition is one of the main factors determining health, well-being, life expectancy and active human activity.

Currently, according to UN estimates, only 25% of humanity eats normally, and more than half of the world's population is malnourished or poorly nourished. Hunger as a social problem continues to exist in various countries of the world, and in connection with this, diseases associated with malnutrition are widespread.

Starvation(substrate-energy deficiency) is a typical pathological process that occurs with the complete absence or insufficient supply of nutrients, as well as with a sharp violation of their composition or digestibility. During fasting, the body switches to endogenous nutrition, i.e. utilizes its own reserves of nutrients, as well as products formed during tissue destruction and atrophy. In this case, a state of prolonged stress develops, as a result of which the enzyme systems responsible for the biosynthesis of hormones that ensure the development of the general adaptation syndrome are activated and rebuilt. Based on this, a number of pathologists consider fasting as a typical pathological process caused by adaptation to a deficit of calories, food substrates and essential food components.

Fasting can be physiological or pathological.

Physiological (temporary) starvation occurs in some animals as an adaptive reaction developed in the process of evolution, for example, during winter or summer hibernation of gophers, marmots, badgers, hedgehogs, during cold torpor of amphibians, fish, reptiles, insects and is combined with deep inhibition of the central nervous system, decreased vital activity, which allows the animal to maintain its vital functions for a long time during unfavorable periods of the year.

Pathological fasting can be exogenous or endogenous. Exogenous starvation occurs in the absence or deficiency (as well as a violation of the composition) of food. Endogenous starvation is associated with pathological processes in the body itself (decreased or lack of appetite, impaired food intake due to pathology of the oral cavity, esophagus, impaired digestion, absorption, vomiting, regurgitation in children, etc.).

There are the following forms of fasting: absolute fasting– in the complete absence of food and water; complete fasting– in the complete absence of food, but with water intake; incomplete fasting– insufficient nutrition in relation to the total energy consumption (in given conditions).

Partial fasting(inadequate, one-sided nutrition) - insufficient intake of one or more nutrients from food with its normal total calorie content. Partial fasting can be protein, fat, carbohydrate, mineral, water, vitamin. Under natural conditions, the distinction between incomplete and partial fasting is difficult, because malnutrition is usually combined with a violation of the composition of food.

Imbalance– a condition caused by an incorrect ratio of essential nutrients in the diet with or without absolute deficiency of any of them.

The most severe type of fasting is absolute fasting, without taking water, leading to the death of the body within 4-7 days due to symptoms of dehydration and intoxication.

Complete fasting, in the development of which three periods are distinguished.

First period (2-4 days)– the period of initial adaptation (emergency adaptation) to new conditions of existence and wasteful expenditure of energy. Irritability, headache, and weakness appear. Due to the stimulation of the food center, a strong feeling of hunger arises. The basal metabolism increases. During the first day, the body's energy needs are mainly met through the oxidation of reserve carbohydrates; the respiratory coefficient is close to 1.0. Starting from the second day, the body’s energy consumption is mainly covered by fat oxidation, and the level of glucose in the blood is maintained due to the processes of gluconeogenesis. Despite the economical consumption of protein, due to plastic needs, its breakdown occurs and synthesis decreases. A negative nitrogen balance develops.

Second period (40-50 days)- period of maximum adaptation, “stationary” (period of long-term stable adaptation). Energy resources are consumed relatively evenly, energy costs are reduced, and basal metabolism is reduced. The rate of weight loss slows down, the feeling of hunger weakens.

The bulk of energy is generated through the oxidation of fats. The respiratory coefficient decreases to 0.7. Fat is mobilized from the depot, lipemia, hypercholesterolemia, ketonemia, ketonuria, and acidosis develop. There is an accumulation of intermediate metabolic products that have a toxic effect.

A number of adaptive mechanisms are observed to be activated, aimed at maintaining homeokinesis under conditions of nutritional deficiency, characterizing adaptation to starvation and indicating a transition to endogenous nutrition. glycolytic and lipolytic enzyme systems are activated; the activity of transamination enzymes in the liver increases. There is a selective activation of a number of lysosomal enzymes involved in the degradation of such cell components as proteins (cathepsins), nucleic acids (acid RNAase and DNAase), polysaccharides, mucopolysaccharides. This activation is adaptive in nature, aimed at recycling macromolecules and subcellular structures that are less important for the life of the cell. Low molecular weight fragments formed during intralysosomal digestion are included in general metabolism and can be reused for the biosynthesis of macromolecules important for the life of the cell and partially to cover energy needs.

Protein consumption is reduced to a minimum, but ultimately this leads to an increase in negative nitrogen balance. Since all enzymes are protein compounds, prolonged protein deficiency leads to disruption and weakening of their function, and changes in metabolism. There is a sharp decrease in the secretion of enzymes of the digestive tract: suppression of the activity of pepsin, trypsin, amylase, lipase, etc., associated with a complete shutdown of the digestive function. Hypoproteinemia develops (weakening of the protein-forming function of the liver), and the oncotic pressure of the blood decreases. The exchange of water between blood and tissues, the ratio between intracellular and extracellular water is disrupted, and edema may appear.

The main vital functions of the body during the first and second periods are maintained within limits close to the physiological norm. Body temperature fluctuates at the lower limits of normal, blood pressure may initially rise, then drop slightly or fluctuate within normal limits. Myocardial contractility decreases, and the risk of collaptoid conditions increases. A slight initial tachycardia gives way to bradycardia. The mass of circulating blood decreases in proportion to the loss of total weight. The motor activity of the stomach and intestines initially increases sharply (hungry contractions, sometimes of a spastic nature), and later decreases. The amount of urine excreted decreases, the water balance becomes positive due to the accumulation of water in the body. Adynamia and apathy increase, sometimes clouding of consciousness, mental disorders occur, and anemia develops. Due to nutritional deficiency and under the influence of stress caused by hunger, secondary immunodeficiency occurs. The degree of atrophy and weight loss of different organs and tissues is uneven. The weight of the heart (3.6%) and brain (3.9%) decreases the least, and adipose tissue decreases the most (97%).

Third period (3-5 days)– terminal (period of decompensation), ending in coma and death. It begins after fat reserves are exhausted. It is characterized by a rapidly growing disorder of basic functions and metabolism due to disruption of the processes of energy supply to cells and the activity of enzyme systems. There is deep depression of the central nervous system, weakness, apathy, offered food is rejected. The breakdown of protein, including vital organs, and the excretion of nitrogen in the urine increases. Protein is also used for energy purposes. The respiratory coefficient is 0.8. Ketonemia, acidosis and intoxication of the body with products of impaired metabolism increase. Body temperature decreases, edema progresses (chloride retention and increased osmotic concentration in tissues, hypoproteinemia), weight loss increases. Death during complete starvation occurs with a loss of 40-50% of body weight. People who die from starvation usually exhibit atrophic changes in organs and tissues. Life expectancy during complete fasting depends on body weight, age, gender, state of nutrition before fasting, individual metabolic characteristics, and on average is 60-75 days.

Conditions that increase metabolism, increase energy costs, shorten the life of a starving organism (the predominance of excitation processes in the nervous system, increased activity of a number of endocrine glands, muscle activity, overheating, dehydration, etc. Children suffer from starvation more severely than adults and die earlier; Old people can fast longer than young people; women tolerate fasting more easily than men.

Even at the very beginning of the terminal period of fasting, properly carried out fattening can restore body functions. Initially, liquid food is introduced in limited quantities (in the absence of appetite, by force). After restoring the excitability of the food center, the volume of food is gradually increased, but without overload. Long-term consequences of suffering from starvation can be: fear of starvation, the desire to create food reserves, asthenic or apathetic states.

Incomplete fasting characterized by the possibility of long-term existence of the body with insufficient food supply and ongoing digestion processes. In this case, the main role is played by the lack of protein, and the body dies in the same way as with complete starvation, when 40-45% of the body’s own proteins are consumed. With prolonged incomplete fasting, a complex of disorders characteristic of nutritional dystrophy develops.

Nutritional dystrophy(from Latin alimentarius - related to nutrition, synonyms: hunger disease, edema disease, hunger edema, military edema). Nutritional dystrophy occurs as a result of prolonged malnutrition (lack of all food components).

The disease was widespread during the Great Patriotic War, during the siege of Leningrad (1941-1943). Its duration ranged from 2-3 weeks with death to 2 years with gradual recovery. Contributing factors are neuro-emotional stress, cold, heavy physical labor, infection, etc. It manifests itself as general exhaustion, progressive disorder of all types of metabolism, degeneration of tissues and organs with disruption of their functions. The main symptoms are general depression, anorexia, cachexia, diarrhea, splenomegaly, ascites, edema. Edema is a consequence of inhibition of the protein-forming function of the liver, leading to a decrease in the oncotic pressure of the blood plasma. The death of the body is associated with extreme depletion of the neuroendocrine system, mainly the diencephalic-pituitary parts, and overstrain of nerve cells.

Protein-calorie (protein-energy) deficiency. The development of protein-calorie (protein-energy) malnutrition (PCM) is associated with the consumption of low-calorie foods containing insufficient amounts of protein.

MCI is one of the leading causes of child mortality in developing countries. It occurs mainly in children under 5 years of age, sometimes in older children, and less often in adults. Aggravating factors are: neuropsychic shocks, concomitant infections, unfavorable climatic conditions (strong insolation, high humidity and air temperature), heavy physical labor, etc. CSD in children is always accompanied by a slowdown in growth and development. Its influence has the most detrimental effect on the growth and development of nervous tissue - cortical and subcortical structures of the brain (especially at the age of 6 months to 3 years), which leads to disruption of the mental and intellectual development of the child. Under some circumstances, CDI leads to nutritional dwarfism. In this case, children have reduced weight and height while maintaining normal body proportions. Severe forms of CND include nutritional insanity.

Nutritional insanity(exhaustion, atrexia, cachexia, mummified or dry form of nutritional dystrophy) is a chronic disease that occurs under conditions of prolonged incomplete fasting, consumption of food low in protein and carbohydrates. Distributed mainly in Africa. It usually occurs in children who develop CUD in the first year of life, often as a result of artificial feeding with highly diluted milk. It is characterized by general emaciation, metabolic disorders, and dysfunction of most organs and systems. In the development of the disease, there may be a long period of balanced fasting, during which the body maintains homeostasis by reducing energy consumption and reducing metabolism by 15-30%. However, more often the body is not able to fully ensure the energy balance, and its own reserves - lipids from fat depots, tissue proteins - begin to be spent on energy needs. The content of glucose, cholesterol and neutral fat in the blood decreases, the concentration of lactic acid increases; Acetonuria appears and acidosis develops. The most serious changes occur in protein metabolism - protein synthesis decreases, hypoproteinemia develops. The secretory and endocrine activity of the glands, primarily the gastrointestinal tract, is disrupted; dystrophy of all organs and tissues develops, hunger edema appears. From the cardiovascular system - bradycardia, hypotension, slowing of blood flow. Disorders of the functions of the endocrine organs (pituitary gland, adrenal glands, thyroid and gonads), and diencephalic-thalamic parts of the central nervous system are noted. There is a decrease in memory, lethargy, delayed physical development, depletion of muscles and subcutaneous fat layer (“monkey face”, the face of a “little old man”), hair changes may appear (thinning, lightening), vitamin deficiency, the body’s resistance decreases, and susceptibility to infections increases . If the diet does not change, the body dies, often from an associated infection.

Kwashiorkor(Proctor-Williams disease, “red child”, “red Kvashi”) is a disease that occurs mainly in young children as a result of a deficiency in the diet of proteins, especially animals, with sufficient or excess caloric content of food. A concomitant factor is a lack of vitamins, mainly group B. A monotonous carbohydrate diet, typical of the poor population of tropical countries, plays a role in the occurrence of the disease. The disease is widespread mainly in tropical Africa, Central and South America, India, and Indochina. Kwashiorkor usually develops after the baby is weaned, especially with a sharp transition (without prior complementary feeding) to feeding with adult food. It is characterized by a distortion of metabolic processes and disruption of the functions of most organs and systems. In the pathogenesis of the disease, the main role is played by a deficiency of essential amino acids, which leads to disruption of the synthesis of vital proteins and, thereby, to retardation of growth and development of organs and tissues. Forced (due to a lack of protein) excess consumption of carbohydrates leads to hyperproduction of insulin and aggravates the pathology of protein metabolism. There is a delay in physical development, mental disorders, decreased body resistance, heart failure, dysproteinemia, widespread edema, anemia, diarrhea, damage to the gastrointestinal tract, liver, pancreas, kidneys, skin (diffuse depigmentation of the skin, layered pigmented dermatosis - snake skin), hair (dyspigmentation , redness, thinning, “flag” symptom - multi-colored hair on the head), etc. Death occurs from acute renal failure or associated infection.

Vitamin deficiency. Vitamin metabolism disorders - avitaminosis and hypovitaminosis - are usually combined with BKN, aggravating the course of any form of nutritional deficiency. They can be primary (exogenous) and secondary (endogenous). Primary ones develop in the absence or deficiency of a vitamin in food; they are an independent form of partial nutritional deficiency; secondary ones arise due to pathological changes in the body (impaired absorption or assimilation of vitamins).

The main manifestations of hypovitaminosis are presented in table. 8.

Disorders of mineral metabolism and microelements metabolism may be associated with a decrease, absence, or excessive content in food and water; increased loss, retention in the body due to impaired excretion of these substances; the body's inability to absorb them. Data on the causes and consequences of disorders of mineral metabolism and microelements metabolism are given in table. 9.

Fasting treatment

The method of dosed fasting (fasting-dietary therapy) consists of voluntary abstinence from eating with unlimited (in case of complete fasting) water consumption and a series of detoxification hygienic procedures, followed by restorative dietary nutrition according to a special scheme. Modern science recognizes fasting treatment for obesity, atherosclerosis, bronchial asthma, chronic gastritis, chronic non-calculous cholecystitis, pancreatitis, diseases of the musculoskeletal system, neurodermatitis, psoriasis, eczema. Absolute contraindications to its implementation are: pregnancy, malignant tumors, active tuberculosis, thyrotoxicosis, chronic hepatitis, liver cirrhosis, renal failure, IDDM, diseases of the blood system, decompensation of heart failure, etc.

Table 8

Hypovitaminosis and its manifestations in humans

Vitamin name	Main manifestations of deficiency
A (retinol)	Impaired twilight vision (night blindness) - hemeralopia Xerophthalmia - drying of the conjunctiva and cornea Keratomalacia - softening of the cornea Keratinization (keratinization) of the epithelium of the conjunctiva, ducts of the lacrimal glands, cessation of secretion
B 1 (thiamine)	Polyneuritis, Beriberi disease (disturbances in the nervous, digestive and cardiovascular systems)
AT 2	Dystrophic phenomena with angular stomatitis, dermatitis, photophobia. Cataract
B 6 (pyridoxine)	Increased excitability of the nervous system, pellagroid skin changes, depression
B 12 (cyanocobalamin)	Addison-Beermer disease (B 12 deficiency anemia)
C (ascorbic acid)	Scurvy, hemorrhagic diathesis, nephropathy of pregnancy, gingivitis, soreness and swelling of the gums
D	Rickets in children, osteomalacia (softening of bones) in adults. Decreased calcium and phosphorus in the blood
E (tocopherol)	Infertility, muscle weakness, peripheral circulatory disorders, trophic ulcers, hemolytic anemia, collagenosis
R (rutin)	Fragility of blood capillaries, increased permeability of their walls, petechiae
Pantothenic acid	Disorders of the nervous, endocrine systems, metabolism, dystrophic phenomena
PP (nicotinic acid)	Pellagra: dermatitis, diarrhea, dementia

Dosed fasting enhances the processes of dissimilation, promotes the removal of “toxins” from the body - pathological deposits of fat, salts, and metabolic products. By switching to endogenous nutrition, the body consumes its own fats, carbohydrates, and proteins, while the least active components of cells and tissue are the first to decompose, as a result of which, through fasting, the body manages to get rid of unnecessary, already obsolete elements.

Table 9

Basic information about the causes and consequences of disturbances in mineral metabolism and microelements metabolism (according to V.A. Frolov)

Mineral substance (trace element)	Form and metabolic disorders and its etiology	Manifestations of metabolic disorders
Sodium	Hyponatremia
Reducing sodium content in food products. Increased sweating, chronic diarrhea, prolonged vomiting. Decreased sodium reabsorption in the renal tubules. Excessive intake of water into the body or its retention in the body (relative hyponatremia - hyponatremia from dilution)	Decrease in osmotic pressure of blood and intercellular fluid. The entry of water into cells. Excessive release of potassium from the protoplasm of cells. Falling blood pressure (up to collapse), cardiac dysfunction, muscle adynamia, weakness
Hypernatremia
Excess sodium intake from food. Sodium retention in the body in case of increased reabsorption in the kidney tubules (as a result of increased aldosterone production, protein metabolism disorders, fasting)	Increased osmotic pressure of blood and intercellular fluid. The release of water from cells, their degeneration. Water retention in the body, development of edema. Increased blood pressure (as a result of the potentiating effect of sodium on coronary arteries)
Potassium	Hypokalemia
Reduced potassium content in foods. Loss of potassium in the body as a result of chronic diarrhea and prolonged vomiting. Excessive excretion of potassium in the urine, due to a decrease in its reabsorption and renal tubules under the influence of excess aldosterone	Reduced excitability of nerve and muscle cells. Decrease in vascular tone, disturbance of excitability, conductivity and contractility of the heart muscle
Hyperkalemia
Decreased excretion of potassium by the kidneys; release of intracellular potassium as a result of increased tissue breakdown	The occurrence of potassium intoxication. A sharp decrease in the functions of the heart muscle. Arrhythmia, bradycardia, collapse. Death from sudden cardiac arrest

Continuation of table 9

Magnesium	Excess magnesium in the body
Long-term excess intake of magnesium from food. Displacement of calcium by magnesium from organic and mineral compounds. Excessive deposition of magnesium in muscles and bone tissue	Decreased tactile sensitivity, drowsiness, paresis and paralysis.
Iron	Lack of iron in the body
Insufficient iron content in foods. Pathology of iron absorption in the intestine. (Inflammatory processes, lack of hydrochloric acid in gastric juice, hypovitaminosis C)	Development of hypochromic iron deficiency anemia
Excess iron in the body
Increased systemic or local destruction of red blood cells. Occupational hazards associated with inhalation of ferrous dust or iron vapors	Iron deposits in the form of hemosiderin in tissues. Development of pulmonary siderosis
Cobalt	Cobalt deficiency in the body
Insufficient cobalt content in food products. Pathology of cobalt absorption in the small intestine	Slowing the maturation of normoblasts, slowing the release of mature red blood cells into the peripheral blood
Fluorine	Fluoride deficiency in the body
Insufficient fluoride content in drinking water	Caries. Violation of bone formation processes
Excess fluoride in the body
Excess fluoride in drinking water	Development of fluorosis (destruction of tooth enamel). Osteoporosis
Iodine	Iodine deficiency in the body
Insufficient content in drinking water	Development of hypothyroidism. Endemic goiter

At the same time, restoration processes are enhanced. After fasting, cell regeneration occurs and their functions increase. In addition, the therapeutic effect of fasting is associated with adaptation to metabolic acidosis. In this regard, short periods of fasting can benefit the body. However, the use of this method does not always give a lasting positive effect and requires medical supervision. Treatment and subsequent restoration of normal nutrition requires great care, careful monitoring of the patient to avoid complications and is carried out only in a hospital setting, self-medication is excluded. At the end of treatment, an achloride diet (fruit juices, kefir) with a sufficient content of vitamins and mineral salts is used. Care should be taken with increasing the volume of food, given the hypofunction and atrophy of the gastrointestinal tract during the period of therapeutic fasting. Repeated therapeutic fasting is possible only after complete recovery from the previous fast. The recommended duration, including the initial fasting and recovery periods, is 15 days to avoid the transformation of therapeutic fasting into a stressful one.

Or losing weight. If the body receives insufficient energy value, one of the forms of nutritional dystrophy may develop. The most important reason for the development of this disease is the lack of protein in the diet and low calorie content of food. This disease is sometimes called protein-energy malnutrition (PEM). An additional effect on the body during dystrophy is caused by a lack (deficiency) of other important substances in the diet. For example, deficiency can gradually layer on top of the current disease and further influence its severity.

With nutritional dystrophy, neuropsychic and physical fatigue develops. Men are affected by PEM more often than women, because they have a higher basal metabolic rate and lower fat reserves (there are exceptions). Sometimes pregnant and nursing mothers suffer from protein-energy deficiency.
In contrast to PEM, endogenous wasting develops in various diseases, and not due to primary nutritional characteristics. It is clinically similar to protein-energy deficiency and can arise from diseases of the digestive system and poor digestion of food (enterocolitis, diseases of the endocrine glands, tuberculosis). The nature of nutrition in such diseases is also of no small importance.

Clinical picture of nutritional dystrophy

This disease is characterized by a variety of clinical symptoms (subjective, objective), which mainly depend on the severity of the disease.
Protein-energy malnutrition is divided into three degrees: 1 – mild, 2 – moderate, 3 – severe (nutritional insanity). The disease is also divided into acute, subacute, and chronic forms.
The course of the disease is long-term, chronic and lifelong. The latter depends on concomitant diseases and eating disorders. Therefore, sometimes a complicated form of the disease is isolated.

Symptoms of the disease

Important initial symptoms when nutritional dystrophy are:

growing weakness
severe fatigue
chilliness
feeling of thirst
feeling hungry
I want something salty
constipation
frequent urination
decreased ability to work
severe weakness of the muscles of the lower extremities

Sometimes dizziness, numbness of the limbs or decreased sensitivity in the fingers occur. In a prolonged form, aversion to food and loss of appetite may occur. In the first and second degrees of the disease, diarrhea may appear (layering of intestinal infection).

The most characteristic sign of nutritional dystrophy is weight loss, first the face begins to lose weight, wrinkles form, giving the face an senile appearance. Then weight loss begins to spread to the hips, buttocks, and also the abdominal wall.

Forms of weight loss: 1 - loss of 19% of weight, 2 - loss of 29%, 3 - 39%, 4 - 40% or more. The third and especially the fourth form are characteristic of nutritional insanity.
The second and third forms of weight loss - atrophy of smooth, skeletal muscles is formed. Muscle weakness reaches a high degree, which leads to loss of movement, the patient is unable to move. Muscle weakening and atrophy can give the patient’s face a mask-like appearance. In the absence of swelling, facial features become pointed and the skin tightly fits its oval. The legs lose a lot of weight and look like “sticks”. The skin on the face is usually pale or has a grayish-yellow tint. Due to the loss of the fat layer, the skin becomes wrinkled, dry and flabby, and peeling appears. Hair becomes dull, lifeless, brittle, and falls out on the pubis or armpits. Insufficient intake of vitamins increases changes in hair and skin.

PEM can be accompanied by edema (there is an expression “swollen from hunger”). Sometimes, in the absence of visible edema, increased fluid retention occurs in the body. Therefore, there is no edematous or non-edematous form. For example, enough cooling, salt, excess water and swelling begins to form. Consequently, the disease can pass from an edematous form to a non-edema form and vice versa. The initial period of the disease is not complete without the appearance of swelling of the face and limbs, which can disappear after bed rest. Sometimes swelling is combined with polyuria or excessive urination. Sometimes (late stages of the disease) cavitary edema of the abdomen develops (ascites), i.e. A large belly develops in an extremely emaciated person. The decrease in basal metabolism depends on the severity of the disease. Severe chilliness appears, the temperature drops to 34 degrees, which does not increase even with the accumulation of infection in the body.

The general condition depends on the degree of PEM: from satisfied to extremely severe. When moving into a serious condition, muscle weakness, general weakness, slowness of movements gradually intensify, apathy, indifference to the environment, and immobility increases.

Changes in organ activity during nutritional dystrophy

The cardiovascular system There is a decrease in heart rate (bradycardia) to 50, sometimes up to 30 per minute without any unpleasant sensations. In the later stages of the disease, heartbeats become more frequent. There is a natural decrease in blood pressure, muffled heart sounds, and ECG changes that indicate dystrophic damage to the heart muscles.

Respiratory system Slowing down the breathing rate. Due to muscle weakness and shallow breathing, the respiratory movements of the ribs and diaphragm are reduced. The vital capacity of the lungs decreases. Bronchitis and pneumonia often develop.

Digestive system More significant are the changes in the digestive system, which often bother the patient. Characterized by increased appetite, which disappears in severe and protracted forms of dystrophy. Changes in taste are possible - distortion or dulling of the perception of sour, sweet, salty. The tongue changes mainly due to a deficiency of B vitamins. Heaviness in the pancreas, belching, bloating, especially after eating, and vomiting in severe patients are noted. Gastric secretion is inhibited until the absence of pepsin (Achilia) and hydrochloric acid. Due to impaired motor function of the stomach, food quickly passes into the intestines, which contributes to intestinal upset. Gas formation (flatulence) increases.

Atrophy of the intestinal muscles leads to intestinal atony and persistent constipation. In mild cases, stool is absent for 3 days, in severe cases – for weeks. Laxatives and enemas are sometimes not effective and feces are removed mechanically. In severe PEM, diarrhea occurs due to dysfunction of the digestive organs. The stool is copious, liquid, light-colored, without mucus and blood, and often contains remnants of undigested food. Diarrhea can be of any degree as a result of intestinal infection. Hypovitaminosis plays a role in the origin of diarrhea, particularly in the later stages of the disease. Thus, diarrhea during PEM is often caused by a complex of factors. Such diarrhea is persistent, protracted and dramatically aggravates the patient’s condition. With PEN, liver atrophy is detected without significant impairment of its function, in contrast to pure protein deficiency.

urinary system Frequent and excessive urination are characteristic clinical signs of PEM. Up to 6 liters of urine are excreted per day, a significant part at night. The frequency of urination at night reaches up to 8 times. Urine tests do not indicate kidney damage.
Many clinical manifestations of the disease are, to one degree or another, explained by changes in the regulatory function of the nervous and endocrine systems, in particular, changes in appetite, polyuria, bradycardia, hypotension, chilliness, and decreased temperature.

Nervous and endocrine system For example, dysfunction of the autonomic nervous system can lead to a slower heartbeat and lower blood pressure. Hypofunction of the thyroid gland also contributes to this. With PEM, the functions of the pituitary gland, adrenal glands, and the thyroid and gonads are disrupted. In its severe form, atrophy of the gonads is detected, which leads to the cessation of menstruation and the development of early menopause in young women and impotence in men. In the development of these phenomena, protein deficiency and, subsequently, vitamin deficiency in the body are of particular importance. The same reasons underlie polyneuritis from damage to the peripheral nerves, which is manifested mainly by changes in tactile, pain, and temperature sensitivity of the fingers, hands, and feet. Tendon reflexes weaken. Polyneuritis occurs gradually, gradually and, unlike polyneuritis of other origins, almost always occurs without pain.

Mental changes Peculiar changes in the psyche. At first, there is increased excitability, easy entry into conflicts, tearfulness, some narrowing of the range of interests in the direction of primarily food needs, decreased attention and weakened memorization. With stage 3 disease, indifference to surrounding people and surroundings may occur, and sometimes there may be a loss of feelings of shame, disgust, and self-preservation. Patients become unkempt.

Blood There is moderate hypochromic anemia, a decrease in the content of leukocytes and platelets in the blood. The protein content in the blood decreases due to albumin.

Treatment of nutritional dystrophy

It should be aimed at normalizing metabolic processes, as well as ensuring the predominance of the absorption of nutrients over their consumption. To do this, treatment includes good nutrition, physical and mental rest, and staying warm. In the third degree, bed rest is required, as well as in the initial treatment of the second degree of dystrophy. In the first degree of the disease, bed rest is not needed; it can only increase weakness, lethargy, and reduce muscle tone. , also rest during the day. The main thing in treatment is nutrition, which should have increased energy value and contain complete proteins and carbohydrates. The fat content is within physiological norms or lower, in case of possible digestive disorders. Fats are mainly milk or vegetable oils. The amount of vitamins in the diet is doubled. These nutritional principles are prescribed individually according to the treatment regimen, depending on the course of the disease. For nutritional dystrophy of 1-2 degrees, a total table of 3700 kcal is usually prescribed. Fatty fish and meats and cooking fats should be excluded. At 2-3 tbsp. a more gentle diet is prescribed with a gradual transition to enhanced nutrition.