Increased acetone in a child - symptoms, treatment and prevention

Anna Soloshchenko, a cardiologist of the highest category at the Alexander Hospital and author of the blog “Your Cardiologist,” told us what to do if a child’s acetone level has risen. And also compiled a list of preventive measures for such conditions.

You can immediately go to the specialist’s information by clicking here, or go deeper into the problem in detail - go to the theoretical and practical part of the article.

High acetone in a child is not a disease; on the contrary, it is a normal physiological process of metabolism, which is incorporated into the body as a backup option for obtaining energy. However, reacting to a situation incorrectly can have very serious consequences. To understand the causes and the correct algorithm for dealing with acetone in a child, read the article to the end. The material presents the theoretical part in an accessible language and gives specific practical recommendations for solving the problem.

All the necessary information about acetone in the body:

What is acetone in children
Reasons for increasing acetone
Symptoms
How to detect acetonemia?
Risk group
Why is acetone dangerous for a child?
How to treat acetone in children: basic principles
How to reduce acetone in a child at home
What should you feed your child?
What should you not eat if you have acetonemia?
Prevention of acetone syndrome
Comprehensive information on acetone in children from Dr. Komarovsky

What is acetone in children

This is a temporary or pathological metabolic disorder in which a characteristic odor appears from the mouth and during urination (acetonemia). Acetone in a child is not limited to an unpleasant odor, its content in the blood sharply increases to toxic levels and leads to poisoning of the body as a whole; due to intoxication, attacks of vomiting and abdominal pain can be observed.

The main danger is dehydration during attacks of severe vomiting, at which time the child loses a huge amount of fluid and it becomes impossible to replenish the required energy and fluid reserves in the usual way. It turns out to be a vicious circle. If a child refuses to drink or a gag reflex immediately occurs, you must immediately call an ambulance and be prepared for hospitalization; in the hospital, the child will be given a drip to replenish the necessary energy and fluid reserves.

You need to understand that hospitalization and IV drips are a last resort; there are simpler ways to restore normal metabolism, which we will discuss below.

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Complications and consequences

Type 1 diabetes mellitus often occurs in childhood and can be complicated by episodes of diabetic ketoacidosis, a severe state of absolute or relative insulin deficiency leading to hyperglycemia, hyperacetonemia, and systemic inflammation. Possible consequences and complications of this condition in children include disruption of acid-base homeostasis: the level of ketones also increases in the urine (which is defined as ketonuria), and along with their excretion during urination, the level of electrolytes (K and Na ions) in the plasma decreases. Cerebral edema (about 1% of cases), acute ischemic or hemorrhagic stroke, pulmonary interstitial edema and coagulopathies (due to impaired clotting factors) are also possible. In addition, as with any increase in blood acidity, the endothelium of blood vessels may suffer: oversaturation of the blood with ketone bodies increases the negative impact of free radicals on cells and leads to oxidative stress. It is believed that ketones, or rather their increased levels, are related to the occurrence of cancer pathologies. In acetonemic syndrome, there is a possibility of liver enlargement and fatty infiltration, and in severe acetonemic crises, the risk of coma and death cannot be excluded. [10], [11], [12]

Reasons for increasing acetone

Doctor Komarovsky about the reasons for the appearance of acetone in children

To understand why acetone in a child’s blood increases, you need to study the theoretical part. Acetone is a common medical jargon for ketone bodies (acetone bodies), a group of metabolic products formed in the liver, but only when there is a lack of glucose.

Glucose is the main source of energy in the body of a child (and an adult). In the event of a sharp depletion of all glucose reserves (fasting of the body, active games, sports, severe stress, high temperature, etc.), the body begins to use the substance stored in this case for energy - glycogen. The supply of glycogen in the body of an adult is sufficient for 1-2 days of normal functioning, approximately 500-700 g, and in the body of a child the supply of glycogen is very low ~ 50-70 g, which is enough for 1-2 hours.

At the very moment when the body has used up all the glucose and glycogen available to it, fat becomes a source of energy. However, when producing energy from fats, a group of substances called ketone bodies is synthesized:

Propanone (acetone).
Acetoacetic acid (acetoacetate).
Beta-hydroxybutyric acid (β-hydroxybutyrate).

It is because of the above 3 substances and their high concentration in the body that the smell of acetone appears from the child’s mouth and urine. When a critical
concentration
of ketone bodies in the body is reached, intoxication occurs; acetone affects the vomiting center in the brain.

Moreover, as can be understood from the theoretical part, such a reaction of the body is laid down at the genetic level and is the physiological norm for obtaining energy, the so-called plan “B”, during the absence of glucose in the body.

Ketone bodies can also be used (broken down) by the body for energy, but this requires certain enzymes, which are found in sufficient quantities only in children under 1 year of age, so infants do not have acetone. In children over 1 year of age and adults, the necessary enzymes are also produced, but 4-5 days after the appearance of acetone in the blood, and the symptoms of intoxication go away on their own.

In practice, the most common causes of acetone in children are:

respiratory infections;
high temperature (often);
sharp emotional overstrain, stress;
physical exhaustion due to active games or physical activity, but only under unusual and heavy loads;
diabetes
;
unhealthy diet (predominance of fatty foods);
insufficient fluid intake, acetone is excreted from the body through urination; with small doses of fluid, it does not have time to leave in time and the concentration increases.

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Hyperketonemia syndrome in children and adolescents: pathogenesis, causes, diagnosis

Part 2. Read the beginning of the article in No. 6, 2021.

Starvation

Fasting is a state of the body associated with partial or complete disruption of food intake. In a state of starvation, the body's energy sources for the most important structures of the body are sharply reduced. Under conditions of nutrient deficiency in the body, energy production occurs due to the intensification of glucogenesis and the synthesis of ketone bodies. The blood glucose level decreases to the lower limits of normal (3.5 mmol/l) and is maintained at this level during subsequent periods of fasting. In the liver, during fasting, glucose is not able to provide the required amount of oxaloacetate, since it simply is not in the cell. Therefore, during fasting, fatty acids do not “burn” in the TCA cycle, but are converted into ketone bodies.

A decrease in glycogen reserves in the liver is accompanied by an increased supply of free fatty acids from adipocytes. The concentration of fatty acids in the blood increases 3–4 times compared to the post-absorptive state. The level of ketone bodies in the blood increases 10–15 times after a week of fasting. At the same time, carbohydrate deficiency inhibits the oxidation of ketone bodies, slowing down their resynthesis into higher fatty acids [13].

The energy needs of muscles and most other organs are met by fatty acids and ketone bodies. When insulin levels are low, glucose does not penetrate into muscle cells; glucose consumers are insulin-independent cells and, above all, brain cells, but even in this tissue, bioenergetics is partially provided by ketone bodies. At this concentration, acetoacetic acid is actively decarboxylated to form acetone, which is excreted in exhaled air and through the skin. Already on the 3rd–4th day, the smell of acetone emanates from the mouth and skin of the fasting person.

The body includes alternative methods of energy production - gluconeogenesis and the synthesis of keto acids, which are consumed by the central nervous system. During fasting, the release of glucagon increases, which activates lipolysis in adipocytes and oxidation in the liver. The amount of oxaloacetate in mitochondria decreases, since it, having been reduced to malate, enters the cytosol of the cell, where it is again converted into oxaloacetate and used in gluconeogenesis.

Gluconeogenesis continues due to the breakdown of tissue proteins. Amino acids are formed as a result of the breakdown of muscle proteins and are included in gluconeogenesis during prolonged fasting. Pyruvate is formed in the liver from lactate and alanine. Alanine and glutamine are the most important glucogenic amino acids during fasting. Pyruvate and metabolites of the TCA cycle are capable of forming oxaloacetate and being involved in gluconeogenesis.

During fasting, the use of acetyl-CoA in the TCA cycle is suppressed and it is used exclusively for the synthesis of hydroxymethylglutaryl-CoA, which leads to an increase in the formation of ketone bodies. Under these conditions, ketone bodies are an alternative (to glucose) energy material for the brain and other tissues. 75% of the brain's energy needs are met by acetyl-CoA [4].

If fasting continues for days or weeks, other homeostatic mechanisms are activated that ensure the preservation of the protein structure of the body, slowing down gluconeogenesis and switching the brain to utilize ketone molecules. The signal for the use of ketones is an increase in their concentration in arterial blood. With prolonged fasting, extremely low concentrations of insulin in the blood are observed. In this case, intensive ketogenesis is a compensatory adaptive reaction.

The metabolic rate is generally reduced: after a week of fasting, oxygen consumption decreases by approximately 40%, oxidative processes in mitochondria are inhibited and oxidative phosphorylation is inhibited with the formation of ATP, i.e., a hypoenergetic state develops.

Accumulating in the blood, ketone bodies suppress the secretion and activity of glucocorticoids, thereby preventing the destruction of structural proteins of the body and inhibiting the secretion of glucagon [2]. If alanine or other glycogenic amino acids are administered to a fasting person at this time, the level of glucose in the blood increases and the concentration of ketone bodies decreases.

During fasting, ketosis does not pose a danger, since it does not reach the level of ketoacidosis. The latter develops with accompanying factors - dehydration, alcohol intoxication and other conditions.

Alcohol intoxication

Overproduction of ketoacids and ketoacidosis after excessive drinking are common observed conditions. Ethyl alcohol catabolism occurs mainly in liver mitochondria. Here, from 75% to 98% of the ethanol introduced into the body is oxidized. Alcohol oxidation is a complex biochemical process. Nicotinamide adenine dinucleotide (NAD) plays a major role in ethanol metabolism. This enzyme converts ethanol into the toxic metabolite acetaldehyde and reduced NADH, and the latter corresponds to the synthesis of acetoacetate and β-hydroxybutyrate.

Alcohol dehydrogenase catalyzes a reversible reaction, the direction of which depends on the concentration of acetaldehyde and the NADH/NAD+ ratio in the cell. An increase in the concentration of acetaldehyde in the cell causes the induction of the enzyme aldehyde oxidase. During the reaction, acetic acid is formed.

The acetic acid obtained during the reaction is activated by the enzyme acetyl-CoA synthetase. The reaction takes place using coenzyme A and the ATP molecule. The resulting acetyl-CoA, depending on the ATP/ADP ratio and the concentration of oxaloacetate in the mitochondria of hepatocytes, can be “burned” in the TCA cycle or used for the synthesis of fatty acids or ketone bodies.

In the initial stages of alcoholism, acetyl-CoA in the TCA cycle is the main source of energy for the cell. Excess acetyl-CoA in citrate leaves the mitochondria, and fatty acid synthesis begins in the cytoplasm.

During the period of acute alcohol intoxication, despite the presence of a large amount of acetyl-CoA, the lack of oxaloacetate reduces the rate of citrate formation. Under these conditions, excess acetyl-CoA is used for the synthesis of ketone bodies. An increase in the concentration of NADH compared to NAD+ slows down the lactate oxidation reaction, and the lactate/pyruvate ratio increases. The concentration of lactate in the blood increases, which leads to hyperlactic acidemia and lactic acidosis. An increase in the blood levels of lactate, acetoacetic acid and β-hydroxybutyrate causes metabolic acidosis during alcohol intoxication [14].

Promotes enhanced ketogenesis during alcohol intoxication and hypoglycemic conditions associated with vomiting and fasting. It is also known that in such patients the level of insulin in the blood is reduced, while the levels of cortisol, growth hormone, glucagon and adrenaline are increased. Ethanol inhibits gluconeogenesis. Dehydration in these cases promotes ketogenesis.

Ketosis due to hormonal imbalance

Blood glucose levels are influenced by a wide range of hormones, with only insulin causing the hypoglycemic effect. All hormones have a contrinsular effect with an increase in blood glucose levels: glucagon, adrenaline, glucocorticoids, adrenocorticotropic (ACTH), somatotropic (STG), thyroid-stimulating (TSH), thyroid.

The effects of insulin and counter-insular hormones normally regulate stable blood glucose levels. When insulin concentrations are low, the hyperglycemic effects of other hormones, such as glucagon, adrenaline, glucocorticoids and growth hormone, are enhanced. This happens even if the concentration of these hormones in the blood does not increase.

The pathogenesis of ketosis with an excess of thyroxine, glucocorticoids, somatotropin and/or other hormones is essentially similar to the already discussed mechanisms of hyperproduction of ketoacids due to an excess of contrainsular hormones [6]. It is known that during periods of increased growth, as well as during hyperthyroidism, significant weight loss occurs.

Stress

Under stress, the sympathetic nervous system is activated and counter-insular hormones are released, the body's carbohydrate reserves are depleted, and the liver's ability to synthesize and store glycogen is impaired. There is an excessive intake of non-esterified fatty acids into the liver. As a result of increased production of glucocorticoids, protein breakdown and increased formation of ketone bodies from ketogenic amino acids occurs.

Hypercortisolism

Acetonemic syndrome may be the first clinical manifestation of hypercortisolism, when the characteristic signs of the disease have not yet formed.

Glucocorticoids enhance the mobilization of neutral fats from adipose tissue and inhibit lipogenesis. But this effect in the body can be overlapped by other effects of these hormones: the ability to cause hyperglycemia and stimulate insulin secretion, accumulation of glycogen in the liver, which leads to inhibition of fat mobilization and its deposition in adipose tissue; the ability in large doses to delay fat-mobilizing and stimulating fat oxidation by somatotropin.

This may explain the accumulation of fat in fat depots during hypercortisolism (Cushing's disease and syndrome). In addition, in this condition, the formation of dihydrocortisone is increased, which stimulates the pentose cycle and the conversion of carbohydrates into fats. Corticotropin, by stimulating the secretion of glucocorticoids, can influence fat metabolism in the same direction, but, in addition, it also has an extra-adrenal fat-mobilizing effect [6].

Thyrotoxicosis

An excess of thyroid hormones in the blood can be a consequence of diseases manifested by hyperfunction of the thyroid gland. A severe complication of the underlying disease, accompanied by hyperfunction of the thyroid gland, is thyrotoxic crisis, which is a sharp exacerbation of all symptoms of thyrotoxicosis. Excessive intake of thyroid hormones into the blood causes severe toxic damage to the cardiovascular system, liver, nervous system and adrenal glands. The clinical picture is characterized by severe agitation (up to psychosis with delusions and hallucinations), which is then replaced by weakness, drowsiness, muscle weakness, and apathy. Dyspeptic disorders intensify: thirst, nausea, vomiting, loose stools. Possible liver enlargement. Against this background, the processes of ketogenesis sharply intensify, which can provoke symptoms of acetonemia.

Thyroxine has a fat-mobilizing effect. With hyperthyroidism, carbohydrate metabolism is increased. Increased utilization of glucose by tissues. Phosphorylase of the liver and muscles is activated, resulting in increased glycogenolysis and depletion of these tissues in glycogen. Hexokinase activity and glucose absorption in the intestine increase, which may be accompanied by nutritional hyperglycemia. Liver insulinase is activated, which, together with hyperglycemia, causes intense functioning of the insular apparatus and, in case of its functional inferiority, can lead to the development of diabetes mellitus. Strengthening the pentose pathway of carbohydrate metabolism promotes the formation of NADP-H2. In the adrenal glands, this causes increased steroidogenesis and greater production of corticosteroids [4].

Hormone deficiency

Hypoglycemia always occurs with panhypopituitarism, a disease characterized by a decrease and loss of function of the anterior pituitary gland (secretion of adrenocorticotropin, prolactin, somatotropin, follitropin, lutropin, thyrotropin). As a result, the function of the peripheral endocrine glands sharply decreases. However, hypoglycemia also occurs with primary damage to the endocrine organs (congenital dysfunction of the adrenal cortex, Addison's disease, hypothyroidism, hypofunction of the adrenal medulla, glucagon deficiency). With a deficiency of contrainsular hormones, the rate of gluconeogenesis in the liver decreases (impacting the synthesis of key enzymes), glucose utilization in the periphery increases, and the formation of amino acids in the muscles, the substrate for gluconeogenesis, decreases.

Glucocorticoid deficiency

Primary adrenal insufficiency is a consequence of decreased secretion of hormones from the adrenal cortex. This term refers to variants of hypocortisolism that differ in etiology and pathogenesis. Symptoms of adrenal insufficiency develop only after 90% of the adrenal tissue volume has been destroyed.

The causes of hypoglycemia in adrenal insufficiency are similar to the causes of hypoglycemia in hypopituitarism. The difference is the level of occurrence of the block - with hypopituitarism, the secretion of cortisol is reduced due to ACTH deficiency, and with adrenal insufficiency due to the destruction of the tissue of the adrenal glands themselves.

Hypoglycemic conditions in patients with chronic adrenal insufficiency can occur both on an empty stomach and 2-3 hours after eating a meal rich in carbohydrates. Attacks are accompanied by weakness, hunger, and sweating. Hypoglycemia develops as a result of decreased cortisol secretion, decreased gluconeogenesis, and glycogen stores in the liver.

Catecholamine deficiency

This condition can occur with adrenal insufficiency with damage to the adrenal medulla. Catecholamines, entering the blood, regulate the release and metabolism of insulin, reducing it, and also increase the release of glucagon. With a decrease in the secretion of catecholamines, hypoglycemic conditions are observed, caused by excess insulin production and reduced glycogenolysis activity.

Glucagon deficiency

Glucagon is a hormone that is a physiological antagonist of insulin. It is involved in the regulation of carbohydrate metabolism and affects fat metabolism, activating enzymes that break down fats. The main amount of glucagon is synthesized by the alpha cells of the pancreatic islets. However, it has been established that special cells of the duodenal mucosa and gastric mucosa also synthesize glucagon. When glucagon enters the bloodstream, it causes an increase in the concentration of glucose in the blood, up to the development of hyperglycemia. Normally, glucagon prevents an excessive decrease in glucose concentration. Thanks to the existence of glucagon, which prevents the hypoglycemic effect of insulin, fine regulation of glucose metabolism in the body is achieved.

With a deficiency of the above hormones, the insulin content is reduced, and the excretion of ketone bodies in the urine is increased [4].

The role of the liver in energy metabolism disorders

The liver is involved in maintaining normal serum glucose levels through glycogenogenesis, glycogenolysis, and gluconeogenesis. The basis of carbohydrate metabolism disorders in liver diseases is damage to mitochondria, which leads to a decrease in oxidative phosphorylation. Liver functions are secondarily affected. In severe acute hepatitis, hypoglycemia is usually observed, and in liver cirrhosis this occurs in the final stage - with liver failure [15]. Hypoglycemia is explained by a decrease in the ability of the liver (due to extensive damage to its parenchyma) to synthesize glycogen and a decrease in the production of insulinase (an enzyme that destroys insulin).

Carbohydrate deficiency also leads to increased anaerobic glycolysis, as a result of which acidic metabolites accumulate in cells, causing a decrease in pH. In liver cirrhosis, the level of lactate in the blood serum may also increase due to the reduced ability of the liver to utilize it for gluconeogenesis.

In liver diseases, the role of fats as an energy source increases. In the liver, fatty acids are synthesized and broken down to acetyl-CoA, as well as the formation of ketone bodies, saturation of unsaturated fatty acids and their inclusion in the resynthesis of neutral fats and phospholipids. Catabolism of fatty acids is carried out by β-oxidation, the main reaction of which is the activation of fatty acids with the participation of the coenzyme acetyl-CoA and ATP. The released acetyl-CoA undergoes complete oxidation in the mitochondria, as a result of which the cells are provided with energy.

In a number of liver diseases, the synthesis of lipoproteins is also reduced, which leads to the accumulation of triacylglycerides with subsequent infiltration and fatty degeneration of the liver. The causes of this condition, in particular, are the lack of lipotropic substances in food (choline - a component of lecithin, methionine). The formation of ketone bodies increases [4].

So, the clinical picture of secondary acetonemic syndrome directly includes the phenomena of ketosis, signs of the underlying disease against which ketosis developed, as well as manifestations of the condition that triggered the pathological process (stress, excessive physical activity, infection, etc.).

Acetonemic cyclic vomiting

In practice, one has to deal with idiopathic acetonemic vomiting, which occurs with ketoacidosis (acetonemic vomiting, non-diabetic ketoacidosis). In the English-language literature, it is included in the syndrome of idiopathic cyclic vomiting [16, 17].

The pathogenesis of acetonemic vomiting is not fully understood. It is assumed that in children after infectious diseases, skull injuries, organic diseases of the central nervous system, a dominant focus of stagnant excitation remains for a long time in the hypothalamic-diencephalic region, inducing disorders of fat metabolism (increased ketogenesis, disruption of the normal use of ketone bodies due to depletion carbohydrate reserves in the body). In the pathogenesis of acetonemic vomiting, constitutional anomalies, relative incompetence of liver enzyme systems, and disturbances in endocrine regulation of metabolism may play a role.

The concept of cyclic vomiting syndrome as a mitochondrial pathology is promising [18, 19]. Since mitochondria are, figuratively speaking, the energy stations of the cell, energy metabolism is disrupted in this disease. Under conditions of stress and hypoxia, energy metabolism is disrupted with a predominance of faster anaerobic glycolysis, but only 2 ATP molecules are formed, whereas under aerobic glycolysis - 38 [5]. There is an energy deficit.

Such disorders are closely related to disorders of purine metabolism, since energy in the body is stored in the form of nucleotides, among which adenine and guanine are purines, and they are metabolized to uric acid, and thymine, cytosine and uracil are pyrimidines and are metabolized to form ketone bodies, ammonia and β-isobutyric acid. These ideas pathogenetically bring together the syndrome of cyclic vomiting and the syndrome of acetonemic vomiting, and also explain the need and possible ways of metabolic correction.

Others believe that the reason for the sharp increase in ketone bodies may be insufficient consumption of carbohydrates in children with an excess of fats and ketogenic amino acids.

Crises can occur suddenly at intervals of several weeks or months. Provoking factors may be: poor diet (fried and baked foods), fever, refusal to eat, physical and mental stress.

Harbingers of cyclic vomiting syndrome are anorexia, lethargy or increased excitability, nausea, headaches, abdominal pain, and the smell of acetone from the mouth.

Then repeated or uncontrollable vomiting appears, which can last from one to five days. Cramping pain in the abdomen intensifies. During a crisis, the patient becomes drowsy. As a result of vomiting, hemodynamic disturbances may develop: tachycardia, soft pulse, muffled heart sounds, hypotension.

The liver is moderately enlarged. In some cases, the temperature rises. The smell of rotten apples is felt in the exhaled air and vomit. There is a high concentration of ketone bodies in the urine. Seizures can resolve spontaneously without treatment.

An excess of ketone bodies has a narcotic effect on the central nervous system, which is clinically manifested by lethargy and lethargy.

A biochemical blood test reveals a disorder of lipid metabolism (hypercholesterolemia), a tendency to hypoglycemia, and hyperketonemia. General blood test: moderate leukocytosis, neutrophilia, accelerated ESR.

Acetone is found in urine and exhaled air, and an increased concentration of ketone bodies is found in the blood. The electroencephalogram reveals various abnormalities that do not disappear completely after the attack stops.

This syndrome is more common in preschool age and is accompanied by attacks of repeated vomiting and ketonemia. Such patients are often diagnosed with increased excitability, uric acid nephropathy, diabetes mellitus, and obesity.

Ketosis during prolonged vomiting, malnutrition or fasting represents a classic compensatory process designed to compensate for the energy deficit, more precisely, the lack of carbohydrates, through alternative energy substrates of keto acids.

The diagnosis of acetonemic vomiting syndrome can be confirmed only after excluding other diseases accompanied by vomiting: appendicitis and peritonitis, encephalitis, meningitis, the onset of cerebral edema, poisoning, toxicosis and infectious diseases, etc. But primarily diabetic ketoacidosis.

Acetonemic crises in most children stop after 10–12 years, but there remains a high probability of developing pathological conditions such as gouty crises, vegetative-vascular dystonia of the hypertensive type, and arterial hypertension.

Transient ketosis in children and adolescents can be detected during fever, stress, infectious diseases, fasting (during illness), eating foods rich in fat, and strenuous physical activity. In these cases, the content of ketone bodies in the urine is no more than 2+.

Treatment

Treatment and prevention of hyperketonemia depend on the cause of its occurrence, but in all cases are aimed at improving liver function and normalizing energy metabolism. This is achieved by limiting the fat content in the diet, prescribing lipotropic agents (methionine, etc.), B vitamins, and, if necessary, insulin and cocarboxylase.

During an attack of cyclic acetonemic vomiting syndrome, severe dehydration, hypovolemia, metabolic acidosis and electrolyte disturbances are the main factors that determine the severity of the condition. It is necessary first of all to eliminate acidosis: prescribe gastric and intestinal lavage with 1–2% sodium bicarbonate solution. A 5–10% glucose solution with the addition of the required amount of insulin, as well as Ringer’s solution, have antiketogenic properties [20].

If drinking does not provoke vomiting, sweetened tea, Regidron, Oralit are recommended - in frequent and small volumes. After the condition improves and it becomes possible to take fluids, feeding the child is prescribed. The diet should contain easily digestible carbohydrates and a limited amount of fat (semolina, oatmeal, buckwheat porridge; mashed potatoes, baked apples, crackers, dry cookies).

So, elucidating the mechanisms of development of ketonemic syndrome and identifying the most likely causes of the formation of ketosis make it possible to establish the genesis of the disease, and thereby normalize the patient’s condition and prevent relapses of ketonemia.

Literature

Berezov T. T., Korovkin B. F. Biological chemistry. Textbook. 3rd ed. M.: Medicine, 2004. 704 p.
Stryer, Lubert. Biochemistry (Fourth ed.). New York: W. H. Freeman and Company, 1995. pp. 510–515, 581–613, 775–778.
Murray R., Grenner D., Mayes P., Rodwell V. Human biochemistry. Per. from English M.: Mir, 1993. T. I. 381 p.
Zaichik A. Sh., Churilov L. P. Fundamentals of pathochemistry. St. Petersburg: Elbi-SPb, 2000. 687 p.
Endocrinology and metabolism. In 2 volumes / Ed. Felinga F. et al. Per. from English Kandrora V.I., Starkova N.T.M.: Medicine, 1985. T. 2. 416 p.
Endocrinology: national guide / Ed. Dedova I. I., Melnichenko G. A. M.: GEOTAR-Media, 2008.
Treatment of diabetic coma in children. Guidelines. M., 2006. 14 p.
Brown LM, Corrado MM, van der Ende RM et al. Evaluation of glycogen storage disease as a cause of ketotic hypoglycemia in children // J Inherit Metab Dis. 2015, May; 38(3):489–493.
Chibiras P. P. Hypoglycemic ketonemia as a cause of neurotoxicosis in children // Issues of maternal and childhood protection. 1982. No. 2. P. 30–33.
Genes S.G. Hypoglycemia. Hypoglycemic symptom complex. M.: Medicine, 1970. 236 p.
Kronenberg G. M. et al. Obesity and lipid metabolism disorders. Per. from English edited by I. I. Dedova, G. A. Melnichenko. M.: Read Elsiver LLC, 2010. 264 p.
Lukyanchikov V.S. Ketosis and ketoacidosis. Pathochemical and clinical aspect // RMJ, 2004, v. 12, no. 23, p. 1301.
Maslovskaya A. A. The mechanism of development of ketosis in diabetes mellitus and fasting // Journal of the Grodno State Medical University. 2012, no. 3 (39), 8–10.
Emergency medical care. Per. from English / Ed. J. E. Tintinally, R. L. Crome, E. Ruiz. M.: Medicine, 2001. 1000 p.
Ryabchuk F.N., Pirogova Z.I. Coenzyme acetylation and the level of free fatty acids in the blood in children with acetonemia and biliary insufficiency // Treating Doctor. 2012, no. 8, p. 42–46.
Li BUK: Cyclic vomiting: new understanding of an old disorder // Contemporary Ped. 1996, 13(7): 48–62.
Krakowczyk H., Machura E., Rusek-Zychma M., Chrobak E., Ziora K. Assessment of the natural history and clinical presentation of acetonemic vomiting. 2014, 71 (6): 323–327.
Boles R. et al. Cyclic vomiting syndrome and mitochondrial DNA mutations // Lancet. 1997, 350: 1299–1300.
Salpietro CD, Briuglia S, Merlino MV et al. A mitochondrial DNA mutation (A3243 G mtDNA) in a family with cyclic vomiting // Am. J. Pediatr. 2003. 162. 727–728.
Marushko Yu. V., Shev G. G., Polkovnichenko L. N., Moshkina T. V. Therapeutic approaches for acetone syndrome in children // Child’s Health. 2012, No. 1, p. 61–65.

V. V. Smirnov1, Doctor of Medical Sciences, Professor A. V. Simakov

Federal State Budgetary Educational Institution of Russian National Research University named after. N. I. Pirogova Ministry of Health of the Russian Federation, Moscow

1 Contact information

Symptoms

Symptoms of high concentrations of acetone in the body may include:

weakness, lethargy, depressed state;
lack of appetite, refusal to eat;
characteristic odor of acetone from the mouth and when urinating;
vomiting with a characteristic odor.

A high temperature may be due to respiratory illness or inflammation and may cause elevated ketone levels, but this is not necessarily a symptom.

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What not to eat with acetonomia

To prevent a deterioration in the general condition and not provoke a re-increase in acetone levels, the following should be excluded from the diet:

Fatty broths made from bones or meat (including poultry or fish)
Fatty meats
By-products (liver, kidneys, etc.)
Smoking
Crayfish and some types of fish
Fat cottage cheese and sour cream
Some types of vegetables

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How to detect acetonemia?

In the vast majority of cases, acetonemia is detected using the parent's sense of smell. If a child has acetone, the smell on his breath is quite pungent and difficult to confuse with something else.

If ketone bodies are detected, in the future, you can buy special tests at the pharmacy that will help determine acetone in the urine of children. The principle is quite simple, the child must go to a clean container for minor needs, and then a test strip is placed in the urine, which will give a positive result in the presence of acetone, and also shows the approximate quantitative concentration of acetone in the body.

If there is bad breath, no tests are needed, the conclusion is already clear - there is acetone and its amount in the body is increasing, measures need to be taken.

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What to do?

Do not panic! Responsibility for the condition of the child lies only with you!

So, the child is nervous, hungry, and has a smell of acetone on his breath - give him a sweet drink, give him some sweets. Coca-Cola is best, because this drink has a lot of sugar and the child will drink it with great pleasure. This category also includes various sweet lemonades and sodas.

Do not put your child on a diet, especially a hungry one, especially one without sweets. This can make the situation worse. Don't limit your child's sweets! It is necessary to ensure that the distance between meals for the child is at least 4 hours.

It is also important to remember that stress in a state of acetonymia is contraindicated, just like a sharp increase in physical activity. You should always carry 40% glucose and candy with you.

If you doubt that your child has acetone, buy special test strips to determine it in urine. These are paper strips with a reagent that changes color depending on the acetone content in the urine.

If the child’s condition is more severe, then it is necessary to start giving him a sweet drink; in this case, saline solutions will only help against dehydration, but will not affect his well-being. But you can give a saline solution in parallel with sweets.

Sometimes it happens that if there is severe vomiting, it is impossible to give the child a sweet drink. In this case, glucose is administered intravenously or an injection of an antiemetic is given, and while it is working, this is about 2-3 hours, you need to let the child drink as much sweet liquid as possible.

If the condition does not improve, vomiting does not stop, and signs of dehydration appear, call an ambulance, as in this case infusion therapy is needed. As soon as the acetone crisis has passed, you just need to forget about it. Do not torment your child with diets, do not look for reasons, but simply live and do not forbid your child sweets, because in 100% of cases children outgrow this condition.

The main thing is to know how to provide first aid and not to scare the child with hospitalization. Of course, there are situations when a hospital cannot be avoided, for example, when intoxication and dehydration of the body are too severe, then the introduction of glucose through a vein is inevitable, but such conditions are very rare and most often we can cope at home ourselves.

It is worth remembering that this condition can develop in an absolutely healthy child, and acetone syndrome without other signs most often does not mean the presence of diabetes. But if acetone appears in a child often for no reason and is accompanied by sudden weight loss, the child often urinates and is constantly thirsty, then it is worth checking for type 1 diabetes.

Preparing a saline solution for dehydration

A treatment method aimed at introducing fluid into the body is called rehydration therapy. Rehydration is, in fact, the replenishment of fluid losses. There are two main methods of rehydration - intravenous, when the necessary solutions are injected into a vein through a dropper, and oral - when a person receives the necessary solutions through the mouth.

What it is? Sometimes it is a ready-made solution, but usually it is a powder, or tablet, or granules, which contain the sodium, potassium, chlorine and other substances necessary for the body in specially selected combinations and concentrations equivalent to pathological losses. Let me explain: sweating is a loss of not only fluid, but also sodium and chlorine (after all, sweat is salty, and everyone probably remembers the school formula NaCl). If you replenish fluid losses, but do not replenish salt losses, this is fraught with serious problems. How much salt do you still need? So smart scientists calculated the optimal amount of salts for a certain volume of water.

The formulas for rehydrating agents are based on these calculations. In addition to salts, the preparations often contain glucose; sometimes extracts of medicinal plants (chamomile extract, for example), and decoctions of cereals (rice, wheat, etc.) are added.

Oral rehydrating agents are an ideal option for quickly and effectively replenishing physiological and pathological fluid losses.

This is why oral rehydration products are over-the-counter medications.

That is why oral rehydration products should be an essential component of a home first aid kit.

Risk group

Children aged 1 to 7 years are most susceptible to acetonemia. If you have smelled acetone from your child at least once in your life, this may happen again in the future. As a rule, in the vast majority of cases this goes away after 7 years. If there are problems with acetone after 7, a medical examination is necessary.

In rare cases, acetone can be a symptom of diabetes if not treated correctly.

There is no specific risk group for children, except for the age category, it all depends on the physiological characteristics of each organism. One child may have a high content of acetone, but it is quickly excreted in the urine and does not have time to accumulate in critical concentrations. For another child, the moment from the onset of the smell to vomiting may be very short, which is dangerous.

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Calendar of events:

19Nov
All-Russian conference “Life with diabetes from 0 to 100” ending date: November 20, 2021 Venue: Online
Read also: It’s very difficult for me to live
30November
Integration summit “World-class scientific centers (NCMC) in the field of healthcare” end date: November 30, 2021 Venue: Moscow, congress center of the First Moscow State Medical University named after. THEM. Sechenov, st. Trubetskaya 8
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Third annual conference “What’s happening in the dietary supplement market?” End date: November 30, 2021 Venue: Moscow, Hilton Moscow Leningradskaya/online
02Dec
Congress on Molecular Immunology and Allergology IMAC 2021 closing date: November 03, 2021 Venue: Moscow/online

Why is acetone dangerous for a child?

It is important to prevent the appearance of ketones (acetone) in high concentrations! If ketone bodies accumulate in the body in a critical concentration, they begin to act on the vomiting center and appetite center in the brain, the child refuses to eat, and when trying to take liquid, vomiting immediately occurs.

Children's acetone does not pose a direct threat to health and life, but the consequences, such as dehydration with constant vomiting and the inability to take liquids orally, are deadly for the body

If it is impossible to give the child water to drink and there is continuous vomiting, a hospital and IV drips are required.

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The smell of acetone as a symptom of disease

It happens that acetonemic pathology occurs suddenly, and may indicate a serious illness.

How to treat acetone in children: basic principles

Treatment of acetone in children does not

in its neutralization, but in eliminating the cause of intensive formation of ketone bodies!
The child needs to be given glucose (sweets, glucose-containing drinks)
. This will restore the normal process of obtaining energy from glucose, thereby stopping the breakdown of fats and the formation of new acetone molecules.

If the body refuses to accept sweets and drinks, it is necessary to put in a glucose drip to replenish normal metabolism and fluid.

The basic principle - sweets at the right time - cures acetone in a child!

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Causes of acetone in the blood

Due to the development, primary and secondary acetonemic syndrome are distinguished. Primary often develops in children with a genetic metabolic disorder predisposed to impaired purine metabolism. The provoking factor for the development of primary AS is a violation of the diet. According to Medscape recommendations, the most common trigger foods are:

Chocolate
Yellow cheese
Food additive monosodium glutamate (E 621)

Secondary acetone syndrome occurs against the background of various diseases:

viral and bacterial infections
as the temperature rises
against the background of other vomiting
in the postoperative period and after injuries
after suffering stress
with excessive physical activity
against the background of fasting (which can also be attributed to a violation of the diet and diet)

How to reduce acetone in a child at home

What to do with acetone at home? All the mechanisms for this are in the body; there is no need to invent anything. It is necessary to give the child glucose to restore normal metabolism and drink plenty of fluids to quickly remove acetone bodies from the body.

Theoretically, alkaline water can neutralize acetone on a chemical level, but it has not been medically proven to be an effective treatment for acetonemia. Sweet compotes, sweet tea, water with honey or sugar and drinks with a high glucose content (Coca-cola, Pepsi, Fanta, etc.) will be much more effective.

What should you feed your child?

Doctor Komarovsky - what should you give a child with acetonemia?

If acetone has already shown itself, then you shouldn’t even think about feeding the child by force. To digest food, the body requires energy, which means fats will be broken down and acetone bodies will be formed in even larger quantities. The child first needs to be given drinks, sweet water, or ideally a concentrated glucose solution, which can be bought at any pharmacy.

If you manage to give a glucose-containing liquid, that’s good, after a while you can start giving fruit. Ideal - raisins, fresh grapes, dried apricots, prunes, peaches, bananas, apples, sweets - sweets, chocolate, jam, etc. If there are improvements - porridge and any foods high in carbohydrates. This is the acetone diet for children.

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Risk factors

Risk factors for the appearance of an acetone odor are noted, such as infectious diseases with a significant increase in temperature, persistent infections, helminthic infestation, and stress conditions. At a young age, a risk factor is also poor nutrition in children with a lack of the required amount of carbohydrates. Ketosis can be triggered by consuming large amounts of fat, as well as physical overload. It should be borne in mind that the trigger for the development of autoimmune diabetes mellitus in children can be the frequent use of corticosteroids (negatively affecting the adrenal cortex) and antiviral agents containing recombinant interferon alpha-2b. [5], [6], [7]

About prevention

A child has stress - sweet, active games - sweet, physical activity - sweet, cold - sweet, high temperature - sweet. It is important not to feed with sweets, which can lead to obesity, namely, not to allow all glucose and very small volumes of glycogen to be consumed; if this happens, the process of synthesis of acetone bodies (acetone production) will inevitably start.

If the first manifestation of acetone in a child occurred after the age of 4 years or periodically continues after 7 years, this is a reason for an in-depth medical examination; it should not be like this!

Diagnosis of the syndrome

To make a correct diagnosis, anamnesis data, patient complaints, clinical manifestations and the results of additional examination are important.

Laboratory tests include a biochemical blood test and a general urine test. Please note that the amount of acetone in children who do not suffer from this disease does not exceed 0.01 grams.

Instrumental diagnostics is echocardioscopy, with which you can see indicators of central hemodynamics. Acetone syndrome is characterized by a decrease in the diastolic volume of the left ventricle and a decrease in venous pressure. Against this background, the cardiac index is increased due to tachycardia.

Recently, you can even test your urine for acetone at home. For this purpose, special indicator test strips are used.

On our website you can familiarize yourself with the qualifications of specialists advising on this issue and learn how to check the level of acetone in children.