What are the causes of acetone syndrome in children?

Pathogenesis

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The easiest way for the body to meet its energy needs is by breaking down glucose. It is always found in small quantities in our blood; its main source is all foods containing carbohydrates. After eating, the level of glucose in the blood quickly rises, and then it is quickly distributed through the bloodstream to all cells of the body.

If a person does not eat on time, the glucose deficiency is covered by glycogen reserves. It is a polysaccharide that is stored in the liver and muscles. Muscle tissue can store up to 400 g of glycogen. This sugar is consumed only locally, at its location, and is not able to enter the blood. There is less glycogen in the liver - about 100 g in adults and 50 g in children of primary school age. It is released into the blood and spread throughout the body. Under normal conditions, this glycogen lasts for about a day; during physical activity, it is used up in less than an hour. In children, glycogen is consumed faster, since their lifestyle is more active than that of adults, and there are fewer polysaccharide reserves.

Causes

Primary acetonemic syndrome is observed in children with a neuro-arthritic body type. Factors causing this type of pathology are:

• presence of severe fear;
• severe physical stress beyond measure;
• emotional instability;
• pain effects;
• stressful situations;
• excess fats and proteins in the child’s diet and lack of carbohydrates.

Secondary acetonemic syndrome occurs against the background of diseases:

• diabetes;
• traumatic brain injury;
• against the background of fasting;
• with a large amount of hormones secreted by the thyroid gland;
• toxicosis resulting from infection;
• the presence of toxins in the liver;
• destruction of red blood cells in the blood.

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If the glycogen storehouse is depleted and sugar does not enter the blood, the body turns on another mechanism - lipolysis. This is the process of breaking down fats into fatty acids and then into coenzyme A. In subsequent reactions, the energy needed by the body is released, cholesterol and ketone bodies are synthesized. Ketones are safe in small amounts and can be found in urine and blood without causing harm. If fat is actively broken down, there is dehydration or kidney problems, acetone does not have time to be eliminated and begins to accumulate. In this case, they talk about acetonemic syndrome. Its signs are an increase in ketones in the blood - acetonemia and their excretion in the urine - acetonuria.

Additionally: Should you be afraid of acetone in the urine and the reasons for its increase, we talked about this here - read more

Differential diagnosis

Mainly differential diagnosis is carried out with diabetic ketoacidosis. The main features of nondiabetic ketoacidosis are the absence of significant hyperglycemia or hypoglycemia, the absence of a classic “diabetic” history, and, as a rule, a significantly better condition of the patient.

It is important to determine the primary or secondary nature of the developed non-diabetic ketoacidosis. When diagnosing secondary acetonemic syndrome, it is necessary to pay some attention to the search for the etiological factor, since this is essential for the choice of further treatment tactics.

Causes of the syndrome

Lack of glucose and acetone syndrome of varying severity can result from:

1. Insufficient intake of carbohydrates from food, for example, a low-carbohydrate diet for weight loss or for patients with diabetes. Long-term carbohydrate deficiency reduces the liver's ability to store glycogen, so acetone syndrome develops in adherents of such a diet faster than in people who consume sufficient amounts of saccharides. A child's ability to store glycogen develops even before birth. Due to its small amount, infants need more frequent meals containing carbohydrates.
2. Fatty, high-protein foods with a relative lack of carbohydrates.
3. Conditions accompanied by increased energy consumption. For this reason, acetonemic syndrome is typical for children under 8 years of age. Stress, infection, poisoning, and even skipping dinner can lead to the formation of ketones. Some children have a predisposition to acetonuria; they are usually thin, mobile, easily excitable, with poor appetite and a small glycogen reserve. In adults, acetone is released in significant quantities after serious injuries, operations, or recovery from a coma, so at this time the patient is administered glucose intravenously.
4. With toxicosis or gestosis, which is accompanied by vomiting and lack of appetite, the pregnant woman does not receive enough carbohydrates, so the body begins to break down fats and release acetone. As in children, the cause of the syndrome in pregnant women can be any disease or emotional experience.
5. Prolonged, high-intensity exercise on muscles burns up glucose and glycogen reserves, and glucose absorption continues for some time after training or physical activity. To avoid acetone syndrome, it is recommended to consume carbohydrates after exercise - “closing the carbohydrate window.” And vice versa, if the goal of the lesson is to lose weight, it is undesirable to eat for a couple of hours after it, since it is during this time that fat is broken down.
6. Stopping insulin production in type 1 diabetes. In the absence of its own hormone, sugar completely loses the opportunity to enter the cells, so fats are broken down especially quickly. Acetonemic syndrome develops with the onset of diabetes mellitus or an insufficient dose of prescribed insulin and can quickly develop into a ketoacidotic coma.
7. Significant reduction in insulin synthesis in severe stage 2 diabetes. As a rule, at this time the patient is transferred to insulin therapy to prevent hyperglycemia and tissue starvation. If this does not happen, acetone syndrome develops simultaneously with an increase in blood sugar.
8. Severe insulin resistance in patients with type 2 diabetes. In this condition, there is enough sugar and insulin in the blood, but the cell membranes do not allow them to enter. The main reason for resistance is obesity and lack of exercise.
9. Frequent alcohol consumption helps to reduce the amount of glycogen, which accelerates the development of the syndrome.

Clinic, diagnostics

Currently, NAD is considered an enzyme deficiency condition characterized by:

- increased excitability and rapid exhaustion of the nervous system at all levels of reception with the presence of a dominant focus of stagnant excitation in the hypothalamic-diencephalic region;

- deficiency of liver enzymes (glucose-6-phosphatase, hypoxanthine-guanine-phosphoribosylpyrophosphate synthetase);

- low acetylating ability of acetyl coenzyme A due to a deficiency of oxalic acid, necessary for the involvement of acetyl coenzyme A in the Krebs cycle;

— violation of the mechanism of reuse of uric and lactic acids;

- disorders of fat and carbohydrate metabolism;

- disruption of endocrine regulation of metabolism.

Children with NAD immediately after birth are characterized by increased excitability, emotional lability, sleep disturbance, and fearfulness. Aerophagia and pylorospasm are possible. By the age of one year, they usually lag significantly behind their peers in weight. Neuropsychic development, on the contrary, is ahead of age norms. Children quickly master speech, show curiosity, interest in their surroundings, remember well and retell what they hear, but often show stubbornness and negativism in their behavior. Starting from 2–3 years of age, they experience equivalents of gouty attacks and crises in the form of transient night pain in the joints, abdominal pain of a spastic nature, biliary and gastric dyskinesias, odor intolerance, other types of idiosyncrasies, migraines, and acetonemic crises. Sometimes persistent low-grade fever is observed. Possible tics, choreic and tic-like hyperkinesis, affective convulsions, logoneurosis, enuresis. Respiratory and skin allergic manifestations in the form of atopic bronchial asthma, atopic dermatitis, urticaria, Quincke's edema are often observed, and at the age of up to 1 year, allergic skin lesions are extremely rare and usually appear after 2-3 years. In the pathogenesis of skin syndrome, not only allergic but also paraallergic (non-immune) reactions are important, caused by the release of biologically active substances, a decrease in the synthesis of cyclic nucleotides and the powerful inhibitory effect of uric acid on adenyl cyclase. One of the typical manifestations of NAD is saluria with predominant uraturia. Salt excretion is periodically observed simultaneously with dysuria not associated with infection. However, it is possible to develop pyelonephritis, which is often associated with nephrolithiasis. In children of prepubertal and pubertal age, an asthenoneurotic or psychasthenic type of accentuation is often detected. Girls exhibit hysterical character traits. Among neuroses, neurasthenia predominates. Vegetative-vascular dysfunction often occurs in the hyperkinetic type.

The most pronounced manifestation of metabolic disorders in children with NAD, requiring intensive medical care, is an acetonemic crisis. Its development can be facilitated by many factors that, under conditions of increased excitability of the nervous system, have a stressful effect: fear, pain, conflict, hyperinsolation, physical or psycho-emotional stress, changes in the microsocial environment, dietary errors (high content of proteins and fats) and even positive emotions “in excess” " Increased excitability of the autonomic centers of the hypothalamus, which occurs with NAD, under the influence of stress factors causes increased lipolysis and ketogenesis, resulting in the formation of a large number of ketone bodies. In this case, irritation of the vomiting center of the brain stem occurs, which causes vomiting.

Acetonemic crises occur suddenly or after precursors (aura), which include anorexia, lethargy, agitation, migraine-like headache, nausea, abdominal pain mainly in the umbilical region, acholic stool, and the smell of acetone from the mouth.

Clinical picture of acetone crisis:

— repeated or uncontrollable vomiting for 1–5 days (trying to give water or feed the child provokes vomiting);

— dehydration and intoxication (pallor of the skin with a characteristic blush, physical inactivity, muscle hypotension);

- anxiety and excitement at the beginning of the crisis are replaced by lethargy, weakness, drowsiness, in rare cases, symptoms of meningism and convulsions are possible;

- hemodynamic disorders (hypovolemia, weakening of heart sounds, tachycardia, arrhythmia);

- spastic abdominal syndrome (cramping or persistent abdominal pain, nausea, stool retention);

- enlargement of the liver by 1–2 cm, persisting for 5–7 days after the crisis has stopped;

— increase in body temperature to 37.5–38.5 °C;

- the presence of acetone in the urine, vomit, exhaled air, and an increased concentration of ketone bodies in the blood;

- hypochloremia, metabolic acidosis, hypoglycemia, hypercholesterolemia, beta-lipoproteinemia;

- in the peripheral blood there is moderate leukocytosis, neutrophilia, a moderate increase in ESR.

Symptoms of acetonemia

The first symptoms are associated with intoxication of the body with ketones. You may feel lethargic, fatigue, nausea, headache, heaviness or other abdominal discomfort.

As the concentration of ketones increases, the following are observed:

• persistent vomiting. Attacks can last for several hours, during which time the patient loses all the fluid consumed during this period. The vomit smells of acetone. Vomiting of bile and even blood is possible;
• the same smell is felt from the patient’s breath, and sometimes from his skin;
• pain in the peritoneum, often similar to the symptoms of an acute abdomen: sharp, aggravated by pressure. Possible diarrhea;
• rapidly increasing weakness. The child lies down and reacts sluggishly to things that were previously interesting to him;
• photophobia - the patient asks to turn off the lights, draw the curtains, complains of pain in the eyes;
• the temperature may rise;
• dehydration due to frequent vomiting and diarrhea, the patient has dry lips, little saliva, urine is excreted in a small volume, dark in color.

If a child is prone to acetone syndrome, he will experience the same symptoms over and over again. After just a couple of episodes of acetonemia, parents learn to quickly recognize and treat this condition. Treatment at home is possible with the initial manifestations of the syndrome. If the baby drinks little and begins to urinate less often, since all the liquid comes out with vomiting, you need to call a doctor. The younger the child, the faster he develops dehydration.

How to treat?

Therapeutic measures aimed at eliminating the causes and symptoms of acetonemia are divided into 2 stages: relief of the acetonemic crisis (carried out during attacks) and therapy in between attacks .

Stopping the crisis

Excessive vomiting leads to serious consequences associated with metabolic disorders and fluid loss, which negatively affects the condition of all organs and systems of the child. Therefore, attacks of vomiting must be prevented and suppressed.

During attacks, it is necessary to ensure that the child consumes a sufficient amount of fluid, which will restore the normal water balance of the body and remove toxins and waste.

You need to drink frequently, but in small portions, so as not to provoke new attacks of vomiting.

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A patient in a hospital setting is prescribed infusion therapy (administration of solutions using a dropper). Infusion therapy is aimed at:

1. Eliminate fluid deficiency in the body, detoxify, improve metabolic processes and microcirculation.
2. Restoring the normal acid-base balance of the body.
3. Supplying the body with easily digestible carbohydrates to maintain vitality.

Treatment between attacks

To normalize the child’s condition and eliminate the causes and consequences of the disease, the child must:

1. Take enzyme preparations that improve the digestion of food and restore normal metabolism.
2. Dieting.
3. Taking antiviral drugs and antibiotics (carried out strictly as prescribed by a doctor).
4. Taking painkillers (if the patient complains of abdominal pain).
5. Cleansing enemas to detoxify the body.

Find out about the symptoms and treatment of arthritis in children from our article.

Danger and possible consequences

Most often, ketone bodies are formed in small quantities, are excreted by the kidneys and lungs and are not associated with health risks. Acetonemic syndrome is dangerous only for children, weakened patients and diabetics.

In babies, due to their low weight, the concentration of ketones quickly rises, vomiting begins and dangerous dehydration develops. In this condition, it is impossible for them to provide carbohydrates in food, so hospitalization and intravenous glucose infusions are required.

For diabetes mellitus, acetone is safe if it is caused by a low-carbohydrate diet or physical work. But if acetone syndrome is accompanied by high blood sugar, the risk increases significantly. In this condition, polyuria is observed - excessive urine production, which causes dehydration. The body reacts to a lack of fluid by retaining urine, and therefore ketones. Diabetic nephropathy, accompanied by renal failure, can also lead to the accumulation of acetone. An increase in ketone concentration increases blood density and acidity. The complex of the above disorders is called diabetic ketoacidosis. If it is not stopped in time, ketoacidosis leads to hyperglycemic coma.

Etiology and pathogenesis

The main factor against which AS occurs is a constitutional abnormality—neuroarthritic diathesis (NAD). However, any stressful, toxic, nutritional, endocrine influences on energy metabolism, even in children without NAD, can cause the development of acetonemic vomiting.

Normally, the catabolic pathways of carbohydrate, protein and fat metabolism intersect in the Krebs cycle, a universal pathway for energy supply to the body.

The triggering factor for the development of ketosis is stress with a relative advantage of counter-insular hormones and nutritional disorders in the form of fasting or excessive consumption of fatty and protein foods (ketogenic amino acids) with a lack of carbohydrates. An absolute or relative lack of carbohydrates causes lipolysis to be stimulated to meet the body's needs.

Ketosis causes a number of adverse effects on the baby's body. Firstly, with a significant increase in the level of ketone bodies, which are anion donors, metabolic acidosis occurs with an increased anion gap - ketoacidosis.

Its compensation is carried out due to hyperventilation, which leads to hypocapnia, causing vasoconstriction, including cerebral vessels. Secondly, excess ketone bodies have a narcotic effect on the central nervous system, up to the development of coma. Thirdly, acetone is a fat solvent and damages the lipid bilayer of cell membranes.

In addition, the utilization of ketone bodies requires additional amounts of oxygen, which can cause a discrepancy between oxygen delivery and oxygen consumption, that is, contributes to the development and maintenance of the pathological condition.

Excess ketone bodies irritate the mucous membrane of the gastrointestinal tract, which is clinically manifested by vomiting and abdominal pain. The listed adverse effects of ketosis in combination with other disorders of water-electrolyte and acid-base balance (hypo-, iso- and hypertonic dehydration, metabolic acidosis due to bicarbonate loss and/or lactate accumulation) contribute to a more severe course of the disease and increase the length of stay in the intensive care unit therapy.

NAD is a polygenically inherited metabolic abnormality, which is based on a violation of purine metabolism with excess production of uric acid and its precursors, instability of other types of metabolism (primarily carbohydrate and lipid) with a tendency to ketosis and mediator functions of the nervous system, which determine the characteristics of its reactions.

Genetic factors causing hyperuricemia include a number of enzyme defects: deficiency of hypoxynthine guanyl phosphoribosyltransferase; glucose-6-phosphatase deficiency; increasing the catalytic activity of the enzyme phosphoribosyl-pyrophosphate synthetase.

The hereditary factor of disorders of purine metabolism is confirmed by the results of family genetic studies of children with NAD: the frequency of detection of neuropsychiatric diseases in the pedigree of such children is up to 18%, gout is registered in 22% of cases. In first-degree relatives, urolithiasis, uric acid diathesis, and metabolic arthritis are 20 times more common than in the control group. Diseases of the circulatory system (coronary heart disease, hypertension) and diabetes mellitus are 2 times more common.

Free purines and the compounds that form them are of particular importance in the life of the body; the synthesis of purine bases is the central link in the biosynthesis of nucleotides, which take part in almost all intracellular biochemical processes:

- they are activated precursors of DNA and RNA;

- nucleotide derivatives - activated intermediate products of many synthetic reactions;

- adenine nucleotide of adenosine triphosphoric acid - a universal energy “currency” in biological systems;

- adenine nucleotides - components of three main coenzymes: NAD, FAD and SOA;

- purine nucleotides play a general regulatory role in the biological activity of cells, turning into cyclic nucleotides - cyclic adenosine monophosphate and cyclic guanosine monophosphate.

In humans, the main sources of purine synthesis are phosphoribosyl monophosphate and glutamine, from which inosinic acid is formed - the main precursor of purine nucleotides, containing a fully prepared purine ring system.

From year to year, interest in the study of purine metabolism and its final product, uric acid, is growing, which is associated with a steady increase in the frequency of both asymptomatic and clinically manifest hyperuricemia, a biological abnormality unique to humans.

There are three main ways in which uric acid is formed in the body:

- from purines, which are released during tissue breakdown;

- from purines contained in food;

- from synthetically created purines.

Hyperuricemia can be detected in almost 38% of people, and the level of uric acid in the blood depends on age, gender, nationality, geographical area, level of urbanization, and type of diet.

Hyperuricemia can be primary or secondary. There are two ways of developing primary hyperuricemia - metabolic and excretory. The first is associated with a significant intake of purines into the body and their enhanced formation. Increased synthesis of uric acid, characteristic of NAD, can be caused by various enzyme defects, the main of which are:

- lack of glutaminase, which transforms glutamine into glutamic acid and ammonia;

— deficiency of hypoxynthine guanyl phosphoribosyltransferase, which ensures the synthesis of purine bases (hypoxanthine and guanine) and nucleotides (inosine monophosphate and guanosine monophosphate);

- hypoproduction of uricase, which converts uric acid into a more diluted allantoin;

- excess phosphoribosylpyrophosphate synthetase, which catalyzes the synthesis of phosphoribosylpyrophosphate from ATP and ribose-5-phosphate;

- hyperactivity of xanthine oxidase, which oxidizes hypoxanthine into xanthine and uric acid.

Diagnostics

Determining the cause of poor health in a diabetic patient is usually not difficult if he regularly uses a glucometer and monitors his health. Diagnosing the first appearance of acetone syndrome in a child can be more difficult; usually children with characteristic symptoms are hospitalized in the infectious diseases department, and after the correct diagnosis is established, they are transferred for treatment to the gastroenterological department. In the future, parents can purchase tools for determining acetone at home, and diagnose and treat the syndrome in a timely manner without the help of doctors.

Laboratory methods

In the hospital, blood and urine are drawn to detect ketones. Acetone in urine is determined by a semi-quantitative method, the result of such an analysis is from 1 to 4 plus signs. The higher the concentration, the more benefits.

Analysis transcript:

Blood ketones are determined in mmol/l, the norm is from 0.4 to 1.7, depending on the method used in the analysis. An increase to 100-170 mmol/l is observed in ketoacidotic coma.

Express methods

At home, acetone in urine is easily detected with special test strips that operate on the principle of litmus paper. The most common are Ketoglyuk (50 pieces for 240 rubles), Uriket (150 rubles), Ketofan (200 rubles). The concentration of ketones is determined by the degree of coloration of the test strip after immersion in urine.

Rules of use:

1. Collect urine in a container. For analysis, urine must be fresh; it cannot be stored for more than 2 hours.
2. Take out the test strip. Close the container immediately, as the remaining strips will deteriorate from contact with air.
3. Dip part of the indicator strip into the urine for 5 seconds.
4. Remove the strip. Touch the napkin with its edge to absorb excess urine.
5. After 2 minutes, compare the color of the indicator with the scale on the package and determine the level of ketones. The more saturated the color, the higher the acetone.

Patients with diabetes can use models of glucometers that can detect both sugar and blood ketones. To detect acetone, you will have to purchase separate strips.

Diagnosis of the disease

An important diagnostic method is to assess the clinical picture of the disease. Thus, we can talk about the presence of acetonemia when:

• bouts of vomiting are repeated many times;
• attacks last longer;
• repeated at least 2 times a week;
• alternate with periods of remission when the patient feels normal;
• attacks have the same course (individual for each patient);
• arise and fade spontaneously.

To make an accurate diagnosis, it is necessary to conduct a number of laboratory tests:

1. Blood test (quantitative indicators of glucose, leukocytes, neutrophils, and ESR are assessed).
2. A urine test to determine the level of ketone bodies (the amount is indicated by a + sign, values ​​can range from + to ++++).
3. Electrolyte study to determine the degree of dehydration of the body, identifying what kind of water (salted or unsalted) it predominantly loses.

Relief of acetone syndrome

The general rule for treating acetone syndrome is to eliminate dehydration. The patient needs to be given liquids often, but little by little. If repeated vomiting is observed, you will have to literally drink a spoon every 5 minutes until the symptoms of dehydration disappear and urine begins to be released in normal quantities. At the same time, it is necessary to eliminate the cause of acetonemia.

In patients with diabetes

If acetone appears in diabetes mellitus, the first step is to measure blood glucose. If it is significantly elevated (> 13 mmol/l), the risk of ketoacidosis is high. To reduce glucose, you need to take Metformin, eliminate carbohydrates from the diet, or take corrective insulin injections.

Acetone will begin to decrease only after normal urination is restored. To do this, you need to drink plenty of unsweetened water, preferably regular non-carbonated water at room temperature. For prolonged vomiting, special rehydration solutions are used - Regidron, Trisol, Gidrovit. Food and drinks with carbohydrates are allowed only after glycemia has normalized.

If a patient with diabetes experiences lethargy and unusual breathing, you should call an ambulance. Such symptoms are characteristic of a precomatose state; it will not be possible to cope with it at home.

In the hospital, the patient’s blood sugar will be reduced using insulin therapy, and the volume of fluid in the body will be restored with droppers. If you contact a doctor in a timely manner, acetonemic syndrome does not cause significant harm to the body.

In children

Acetonemic syndrome is a common phenomenon in children, most often it can be quickly stopped. Some kids “give out” acetone for every ailment, for example, a cold or a single vomiting, and even for situations that are new to them or too active games. There is no need to be afraid of this; by adolescence, glycogen reserves will increase, and the syndrome will no longer bother you.

Additionally : Breath smells like acetone - what does this mean and what is the danger?

As soon as an unusual condition is noticed in a child - tearfulness, lethargy, drowsiness - you should immediately measure the acetone in the urine. To do this, you should always have test strips at home. If there is even a slight increase, it means there is a lack of carbohydrates. The fastest way to replenish it is with a sweet drink: compote, juice, tea. After this treatment, the formation of ketones stops, and there will be no vomiting.

Often acetone syndrome cannot be prevented at the very beginning. It happens that a child’s vomiting begins early in the morning, after a night’s sleep. In this case, the tactics are the same - feed the baby. It is better to use dried fruit compote, glucose solution or lemon with honey. The drink must be warm. Carbonated drinks are not advisable as they can increase abdominal pain. If vomiting recurs, give liquid very often, a teaspoon at a time. If a child has diabetes, but there is no hyperglycemia, sweet drinks should be accompanied by insulin.

During treatment, you need to monitor the presence of urination. With sufficient fluid intake, the child should go to the toilet at least once every 3 hours, and the urine should be light-colored.

You need to call an ambulance for acetone syndrome in children in the following cases:

• the baby is less than 4 months old;
• vomiting, despite treatment, becomes more severe, all the liquid drunk is lost;
• no urine for more than 6 hours;
• vomit contains small dark brown particles;
• confusion or inappropriate behavior is observed;
• there is unusual breathing;
• Abdominal pain does not go away after a bout of vomiting.

After the first appearance of the syndrome, you need to contact your pediatrician to determine its cause. To rule out problems with carbohydrate absorption, he will prescribe general blood and urine tests and a sugar test.

Diagnostics[edit | edit code]

Based on medical history, analysis of complaints, clinical symptoms and the results of additional instrumental and laboratory tests.

Diagnostic criteria:

• repeated severe, persistent episodes of vomiting;
• interictal period of varying duration between episodes of vomiting;
• duration of episodes of vomiting from several hours to days;
• negative examination results that could link the etiology of vomiting with manifestations of pathology in the gastrointestinal tract;
• attacks of vomiting are characterized by stereotypy - each episode is similar to the previous one in time, intensity and duration;
• in some cases, attacks of vomiting may end spontaneously and without treatment;
• associated symptoms include nausea, abdominal pain, headache, adynamia, photophobia, lethargy;
• vomiting is accompanied by fever, pallor, diarrhea, dehydration, excessive salivation and social maladjustment;
• vomitus often contains bile (76%), mucus (72%) and blood (32%) as a result of retrograde prolapse of the cardiac part of the stomach through the gastroesophageal sphincter (propulsive gastropathy).

In cases where acetonemic vomiting develops against the background of known provoking factors (infection, perioperative fasting, central nervous system tumors, etc.), secondary nondiabetic ketoacidosis is diagnosed.

Laboratory diagnostics[edit | edit code]

There are no specific changes in the clinical blood test - the picture primarily reflects the pathology against which the episode of ketosis developed.

The most typical sign in a clinical urine test is the presence of ketonuria from “one plus” (+) to “four pluses” (++++) by the semi-quantitative method with nitroprusside. Glucosuria (the presence of glucose in the urine) is not a mandatory symptom, but almost always appears against the background of infusion (intravenous drip infusion) of glucose solutions.

The results of a biochemical blood test are diagnostically significant: the longer the episode of acetonemic vomiting lasts, the more pronounced the dehydration, the higher the hematocrit (the ratio of blood cells to plasma) and the total protein. with significant dehydration, an increase in urea in the blood is determined above 8.8 mmol/l (a consequence of prerenal oliguria and hemoconcentration). Isotonic dehydration is more common (a consequence of “balanced” losses of sodium and water). In severe acidosis, serum potassium is normal or elevated. In cases of prolonged vomiting and mild acidosis, hypokalemia is observed.

When studying indicators of the acid-base state, compensated (full or partial compensation of acidosis is carried out due to hyperventilation) or decompensated metabolic acidosis with an increased anion gap is more often determined.

Functional diagnostics[edit | edit code]

An important component of the examination is echocardioscopy with determination of central hemodynamic parameters - more often a decrease in the end-diastolic volume of the left ventricle, a decrease in central venous pressure, a moderate decrease in the ejection fraction and, due to this, a decrease in the stroke volume of the left ventricle are determined. Despite these changes, the cardiac index may be increased due to significant tachycardia.

Literature

1. Kurilo L.V. Primary acetonemic syndrome in children. // Medicus Amicus. - 2002. - No. 5 - P. 4-7.
2. Kazak S., Beketova G. Diagnosis and diet therapy of acetone syndrome in children. // Lilies of Ukraine. - 2005. - No. 1 - P. 83-86. (Ukrainian)
3. Zaichik A. Sh., Churilov L. P. Fundamentals of pathochemistry. - St. Petersburg: Elbi-SPb - 2000. - 687 p.
4. Lukyanchikov V.S. Ketosis and ketoacidosis. Pathobiochemical and clinical aspect. // RMJ.— 2004.— Volume 12.— No. 23.
5. Gumenyuk N. I., Kirkilevsky S. I. Infusion therapy. Theory and practice. - K.: Book Plus - 2004. - 208 p.
6. Korpachev V.V. Sugars and sweeteners. - K.: Book Plus - 2004. - 320 p.