diabetic ketoacidosis This is a very life-threatening complication that occurs in patients with diabetes mellitus.

This complication is characterized by a lack of a specialized hormone insulin (it is responsible for the breakdown of glucose in human blood), and the level of acidity of the body also increases; the appearance of acetone in the urine of the patient is possible.

This disease is quite common among diabetics, especially among those who are ill. Among patients with type 1, this complication can serve as the first symptom of the disease, most often it develops due to untimely diagnosis of the disease. The complication proceeds most often brightly, up to ketoacidotic coma.

Ketoacidosis may develop as a result of trauma, such as surgery. In patients with type 2 diabetes, the complication develops much less frequently, occurs as a result of various infectious diseases of the genitourinary system, heart attacks and strokes.

It can also be provoked by diseases of the endocrine system, such as thyrotoxicosis. The disease usually proceeds not as intensively as in the first type, since it is usually detected on time.

Let's figure out what ketoacidosis is and how to identify the first signs of complications.

Causes of complications

The causes of keotacidosis are not so many. The most common cause of the disease is delayed diagnosis.(in the case of type 1 diabetes), the same reasons can be infectious diseases, various injuries, problems with the cardiovascular system (myocardial infarction).

Another reason for the onset of the disease can be an incorrectly selected dosage of insulin-containing drugs.

Stages of development of the disease

1 stage
This stage characterized by mild symptoms such as thirst, frequent going to the toilet, headaches. If a person diagnosed with diabetes has at least some of the symptoms, this is a reason to suspect something is amiss.

2 stage
This stage of the development of the disease is also called intermediate. Pathogenesis is characterized by an increase in the previously described symptoms. Vomiting is added to them, tachycardia appears (the heart rate increases), the speed of reactions decreases, the pupils begin to react worse to bright light, it may decrease arterial pressure, the skin of the diseased becomes dry and unpleasant to the touch. The smell of acetone, if it was not there before, appears from the mouth, if the smell was present, then it intensifies and becomes more noticeable.

3 stage
The most difficult stage of all. Characterized by loss of consciousness total absence reactions to external stimuli (bright light does not irritate the pupils, which are always in a constricted state). The smell of acetone is so strong that it is felt at a decent distance, you can see noisy and rare breathing (the so-called "Kussmaul's breath"). On the this stage The patient falls into a ketoacidotic coma.

Diagnosis of ketoacidosis

In the laboratory, this complication is diagnosed by analyzing the content of ketones and acetone in the urine. Also, by analyzing the blood, they find out the content of potassium, glucose and ketone bodies. But tests can be done on your own; at the pharmacy you can buy special test strips to check the content of acetone in the urine.

Important!

If the result is high, you should immediately consult a doctor!

Treatment and emergency care

With the acute development of a severe stage of the disease, it is necessary to take a number of measures to maintain normal life before the arrival of doctors and the start of therapy in intensive care.

In case of respiratory arrest, it is necessary to ensure the flow of air to the lungs, for this it is necessary to carry out their ventilation by artificial respiration.

It is advisable to monitor the patient's performance before the arrival of the ambulance in order to inform the specialists of the latest data.

Treatment is necessary to restore large volumes of fluid lost during the course of the disease, insulin therapy is carried out, the level of acetone in the patient's urine and the level of ketone bodies in the blood are checked every hour. The pathological condition of the patient is eliminated, his indicators are monitored.

Ketoacidosis in children

Most often, the signs of complications appear suddenly and in an acute form.

This is due to early undiagnosed type 1 diabetes. The symptoms of the disease in children are identical to those in adults, only in not fully formed organisms, the course of ketoacidosis accelerates several times.

The reasons may be the wrong dosage of insulin-containing drugs or their irregular administration, stressful situations can also harm the child. If this disease is suspected, it is necessary to test for the content of acetone in the urine and show the child to a specialist as soon as possible.

Prevention of complications

If you have already been diagnosed with diabetes mellitus, then in order to avoid the development of the disease, you must be careful in eating and injecting medicines at home.

When deciding to lose weight, you need to do it carefully., do not lose extra pounds abruptly, you need to gradually reduce weight to the desired level. For patients with type 1 diabetes, there are no strict food restrictions, it is enough to follow the advice of the attending physician on the dosage of insulin.

For patients with the second type, you need to follow strict diet to avoid recurrence.

Useful video

This video will show you how to prevent a large number acetone in the body

Ketoacidosis is a very dangerous and insidious enemy that must be fought. By international classification diseases (ICD code 10) ketoacidosis was assigned a code - E10-E14.

If symptoms of the disease are detected in yourself or someone close, it is urgently necessary to carry out all the necessary manipulations and consult a doctor.

diabetic ketoacidosis (ketosis, ketoacidosis) - a variant of metabolic acidosisassociated with impaired carbohydrate metabolism due to insulin deficiency: a high concentration of glucose and ketone bodies in the blood (significantly exceeding physiological values), formed as a result of impaired fatty acid metabolism (lipolysis) and deamination of amino acids. If carbohydrate metabolism disorders are not stopped in a timely manner, diabetic ketoacidotic coma develops.

Non-diabetic ketoacidosis (acetonemic syndrome in children, cyclic acetonemic vomiting syndrome, acetonemic vomiting) - a set of symptoms caused by an increase in the concentration of ketone bodies in the blood plasma - a pathological condition that occurs mainly in childhood, manifested by stereotypical repeated episodes of vomiting, alternating periods of complete well-being. It develops as a result of errors in the diet (long hungry pauses or excessive consumption of fats), as well as against the background of somatic, infectious, endocrine diseases and CNS damage. There are primary (idiopathic) - occurs in 4 ... 6% of children aged 1 to 12 ... 13 years and secondary (against the background of diseases) acetonemic syndrome.

Normally, in the human body, as a result of the main metabolism, ketone bodies are constantly formed and utilized by tissues (muscles, kidneys):

• acetoacetic acid (acetoacetate);
• beta-hydroxybutyric acid (β-hydroxybutyrate);
• acetone (propanone).

As a result of dynamic balance, their concentration in the blood plasma is normally scanty.

Prevalence

Diabetic ketoacidosis ranks first among acute complications of endocrine diseases, mortality reaches 6-10%. It is the most common cause of death in children with insulin-dependent diabetes mellitus. All cases of this condition can be divided into two groups:

• diabetic ketosis - a condition characterized by an increase in the level of ketone bodies in the blood and tissues without a pronounced toxic effect and dehydration phenomena;
• diabetic ketoacidosis - in cases where the lack of insulin is not compensated in time by exogenous administration or the causes that contribute to increased lipolysis and ketogenesis are not eliminated, the pathological process progresses and leads to the development of clinically pronounced ketoacidosis.

Thus, the pathophysiological differences between these conditions are reduced to the degree of metabolic disturbance.

Etiology

The most common cause of severe ketoacidosis is type 1 diabetes. Diabetic ketoacidosis occurs due to an absolute or relative deficiency of insulin that develops over hours or days.

Pathogenesis

In conditions of lack of energy, the human body uses glycogen and stored lipids. The reserves of glycogen in the body are relatively small - about 500 ... 700 g, as a result of its breakdown, glucose is synthesized. It should be noted that the brain, being a lipid structure in structure, receives energy mainly by utilizing glucose, and acetone is a toxic substance for the brain. In connection with this feature, the direct breakdown of fats cannot provide energy to the brain. Since glycogen stores are relatively small and depleted within a few days, the body can provide energy to the brain either through gluconeogenesis (endogenous glucose synthesis) or by increasing the concentration of ketone bodies in the circulating blood to switch other tissues and organs to an alternative energy source. Normally, with a deficiency of carbohydrate foods, the liver synthesizes ketone bodies from acetyl-CoA - ketosis occurs, which does not cause electrolyte disturbances (it is a variant of the norm). However, in some cases, decompensation and the development of acidosis (acetonemic syndrome) are also possible.

Insulin deficiency

• decrease in glucose utilization by tissues, due not only to insulin deficiency, but also due to insulin resistance;
• a decrease in the volume of extracellular fluid (a consequence of osmodiuresis), leads to a decrease in renal blood flow and to the retention of glucose in the body.

The role of contra-insulin hormones

Clinic

Ketoacidosis is a consequence of persistently decompensated diabetes mellitus and develops with a severe, labile course against the background of:

• accession of intercurrent diseases,
• trauma and surgery,
• incorrect and untimely correction of the dose of insulin,
• untimely diagnosis of newly diagnosed diabetes.

The clinical picture is characterized by symptoms of severe decompensation of the disease:

Diabetic ketoacidosis - emergency requiring hospitalization of the patient. With untimely and inadequate therapy, diabetic ketoacidotic coma develops.

Diagnostics

Ketone bodies are acids and their rate of absorption and synthesis can vary considerably; situations may arise when, due to the high concentration of keto acids in the blood, the acid-base balance is shifted, metabolic acidosis develops. It is necessary to distinguish between ketosis and ketoacidosis, with ketosis there are no electrolyte changes in the blood, and this is a physiological state. Ketoacidosis is a pathological condition, the laboratory criteria of which are a decrease in blood pH below 7.35 and a concentration of standard blood serum bicarbonate less than 21 mmol / l.

Treatment

Ketosis

Therapeutic tactics boil down to eliminating the causes that provoked ketosis, limiting fats in the diet, prescribing alkaline drinks (alkaline mineral waters, soda solutions, rehydron). It is recommended to take methionine, essentiale, enterosorbents, enterodesis (dissolve 5 g in 100 ml of boiled water, drink 1-2 times). If after the above measures ketosis is not eliminated, an additional injection of short-acting insulin is prescribed (on the recommendation of a doctor!). If the patient used insulin in one injection per day, it is advisable to switch to the regimen of intensified insulin therapy. Recommend cocarboxylase (intramuscularly), splenin (intramuscularly) in a course of 7 ... 10 days. it is advisable to prescribe alkaline cleansing enemas. If ketosis does not cause any particular inconvenience, hospitalization is not necessary - if possible, the listed activities are carried out at home under the supervision of specialists.

Ketoacidosis

With severe ketosis and symptoms of progressive decompensation of diabetes mellitus, the patient needs inpatient treatment. Along with the above measures, the dose of insulin is adjusted in accordance with the level of glycemia, they switch to the introduction of only short-acting insulin (4 ... 6 injections per day) subcutaneously or intramuscularly. intravenous drip infusions of isotonic sodium chloride solution (saline) are carried out, taking into account the age and condition of the patient.

Patients with severe forms of diabetic ketoacidosis, stages of precoma are treated according to the principle of diabetic coma.

Forecast

With timely correction of biochemical disorders - favorable. With untimely and inadequate therapy, ketoacidosis passes through a short stage of precoma into a diabetic coma.

Prevention

• Serious attitude to their condition, compliance with medical recommendations.
• Insulin injection technique, proper storage of insulin preparations, correct dosing of preparations, careful mixing of NPH insulin preparations or ex tempore mixtures of short and NPH insulin before injection. Refusal to use expired insulin preparations (besides, they can cause allergic reactions!).
• Timely application for medical care in case of failure of independent attempts to normalize the state.

see also

• Hyperosmolar coma

Notes

Links

• Ketosis and ketoacidosis. Pathobiochemical and clinical aspect. V. S. Lukyanchikov

Categories:

• Diseases alphabetically
• Endocrinology
• Diabetology
• Diabetes
• Urgent states
• insulin therapy
• metabolic diseases

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Pediatric ketoacidosis- a heterogeneous group of conditions accompanied by the appearance of ketone bodies in the blood and urine. Ketone bodies are the main carriers of energy from the liver to other tissues and the main source of energy received by the brain tissue from lipids. Main reasons ketoacidosis in newborns - diabetes, type I glycogenosis (232200), glycinemia (232000, 232050), methylmalonic aciduria (251000), lactic acidosis, deficiency of succinyl-CoA-acetoacetate transferase.

Code according to the international classification of diseases ICD-10:

• E88. eight - Other specified metabolic disorders

Deficiency of succinyl-CoA-acetoacetate transferase (#245050, EC 2. 8. 3. 5, 5p13, SCOT gene defect, r) - an enzyme of the mitochondrial matrix that catalyzes the first step in the breakdown of ketone bodies.

Clinically

Laboratory

Richards-Randle syndrome (*245100, r) — ketoaciduria with mental insufficiency and other symptoms.

Clinically

Laboratory

Lactic acidosis - several types caused by mutations in various enzymes of lactic acid metabolism:. deficiency of lipoyl transacetylase E2 (245348, r, A); . insufficiency of the component of the pyruvate dehydrogenase complex containing X-lipoyl (*245349, 11p13, PDX1 gene, r); . congenital infantile form of lactic acidosis (*245400, r); . lactic acidosis with the release of D - lactic acid (245450, r). Common symptoms are lactic acidosis, psychomotor retardation, and muscle hypotension. Some forms have specific manifestations, such as microcephaly, muscle twitching, baldness, necrotizing encephalopathy, etc.

Ketoadipic aciduria (245130, r).

Clinically

Laboratory

ICD-10. E88. 8 Other specified metabolic disorders.

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diabetic ketoacidosis(DKA) is a medical emergency that develops as a result of an absolute (usually) or relative (rarely) deficiency of insulin, characterized by hyperglycemia, metabolic acidosis, and electrolyte disturbances. The extreme manifestation of diabetic ketoacidosis is ketoacidotic coma. Statistical data. 46 cases per 10,000 patients with diabetes. The predominant age is up to 30 years.

Code according to the international classification of diseases ICD-10:

The reasons

Risk factors. Late diagnosis of DM. inadequate insulin therapy. Related acute diseases and injury. previous dehydration. Pregnancy complicated by early toxicosis.

Etiopathogenesis

Hyperglycemia. The lack of insulin reduces the utilization of glucose in the periphery and, along with an excess of glucagon, causes an increased formation of glucose in the liver by stimulating gluconeogenesis, glycogenolysis, and inhibiting glycolysis. Protein breakdown in peripheral tissues provides an influx of amino acids to the liver (a substrate for gluconeogenesis).

As a result, osmotic diuresis, hypovolemia, dehydration and excessive excretion of sodium, potassium, phosphate and other substances in the urine develop. A decrease in BCC leads to the release of catecholamines, which interfere with the action of insulin and stimulate lipolysis.

Ketogenesis. Lipolysis, resulting from a lack of insulin and an excess of catecholamines, mobilizes free fatty acids from depots in adipose tissue. Instead of reesterification of incoming free fatty acids into triglycerides, the liver switches their metabolism to the formation of ketone bodies. Glucagon increases the level of carnitine in the liver, which ensures that fatty acids enter the mitochondria, where they undergo b-oxidation with the formation of ketone bodies. Glucagon reduces the content of malonyl in the liver. - CoA, an inhibitor of fatty acid oxidation.

Acidosis. Increased formation in the liver of ketone bodies (acetoacetate and b - hydroxybutyrate) exceeds the body's ability to metabolize or excrete them. Hydrogen ions of ketone bodies combine with bicarbonate (buffer), which leads to a drop in serum bicarbonate and a decrease in pH.. Compensatory hyperventilation leads to decrease in p a CO 2 .. Due to elevated plasma levels of acetoacetate and b-hydroxybutyrate, the anion gap increases. The result is metabolic acidosis with an increased anion gap.

Symptoms (signs)

Clinical picture ketoacidotic coma is determined by its stage.

Stage I (ketoacidotic precoma) .. Consciousness is not disturbed .. Polydipsia and polyuria .. Moderate dehydration (dryness skin and mucous membranes) without hemodynamic disturbances. General weakness and weight loss. Loss of appetite, drowsiness.

Stage II (beginning ketoacidotic coma) .. Sopor .. Kussmaul-type breathing with the smell of acetone in the exhaled air .. Severe dehydration with hemodynamic disturbances (arterial hypotension and tachycardia) .. Abdominal syndrome (pseudoperitonitis) ... Tension of the muscles of the anterior abdominal wall. .. Symptoms of peritoneal irritation... Repeated vomiting in the form of "coffee grounds" is caused by diapedetic hemorrhages and paretic condition of the vessels of the gastric mucosa.

Stage III (complete ketoacidotic coma) .. Consciousness is absent .. Hypo - or areflexia .. Severe dehydration with collapse.

Diagnostics

Laboratory research. Increasing the concentration of glucose in the blood to 17-40 mmol / l. An increase in the content of ketone bodies in the blood and urine (nitroprusside, which reacts with acetoacetate, is usually used to determine the content of ketone bodies). Glucosuria. Hyponatremia. Hyperamylasemia. Hypercholesterolemia. An increase in the content of urea in the blood. Serum bicarbonate<10 мЭкв/л, рH крови снижен. Гипокалиемия (на начальном этапе возможна гиперкалиемия) . Уменьшение р a СО 2 . Повышение осмолярности плазмы (>300 mosm/kg) . An increase in the anion gap.

Diseases affecting results. With concomitant lactic acidosis, a lot of b-hydroxybutyrate is formed, so the content of acetoacetate is not so high. In this case, the reaction with nitroprusside, which determines only the concentration of acetoacetate, may be slightly positive even with severe acidosis.

Special studies. ECG (especially if MI is suspected). As a rule, sinus tachycardia is detected. Chest X-ray to rule out respiratory tract infection.

Differential diagnosis. Hyperosmolar non-ketoacidotic coma. Coma lactic acid diabetic. Hypoglycemic coma. Uremia.

Treatment

TREATMENT

Mode. Hospitalization in the intensive care unit. Bed rest. The goals of intensive therapy are to accelerate the utilization of glucose by insulin-dependent tissues, to stop ketonemia and acidosis, and to correct water and electrolyte imbalance.

Diet. parenteral nutrition.

Drug therapy. Soluble insulin (human genetically engineered) IV at an initial dose of 0.1 U/kg followed by an infusion of 0.1 U/kg/h (approximately 5-10 U/h). Correction of dehydration.. 1000 ml of 0.9% solution of sodium chloride for 30 minutes IV, then - r sodium chloride at a rate of 500 ml / h (approximately 7 ml / kg / h) for 4 h (or until dehydration stops), then continue infusion at a rate of 250 ml / h (3.5 ml / kg / h) , controlling the content of glucose in the blood .. When the concentration of glucose drops to 14.65 mmol / l - 400-800 ml of 5% r - ra glucose at 0.45% r - re sodium chloride during the day. Compensation for losses of minerals and electrolytes .. With a concentration of potassium in the blood serum<5,5 ммоль/л — препараты калия (например, калия хлорид со скоростью 20 ммоль/ч) .. При рН артериальной крови ниже 7,1 — натрия гидрокарбонат 3-4 мл/кг массы тела.. Фосфаты — 40-60 ммоль со скоростью 10-20 ммоль/ч.

observation. Monitoring the mental state, vital functions, diuresis every 30-60 minutes until the condition improves, then every 2-4 hours during the day. The content of glucose in the blood is determined every hour until a concentration of 14.65 mmol / l is reached, then every 2-6 hours. The level of K +, HCO 3 -, Na +, base deficiency - every 2 hours. The content of phosphates, Ca 2 +, Mg 2+ - every 4-6 hours.

Complications. Brain edema. Pulmonary edema. Venous thrombosis. Hypokalemia. THEM. late hypoglycemia. Erosive gastritis. Infections. Respiratory distress syndrome. Hypophosphatemia.

Current and forecast. Ketoacidotic coma is the cause of 14% of hospital admissions in patients with diabetes and 16% of deaths in diabetes. Mortality is 5-15%.

Age features. Children. Often there are serious mental disorders.. Treatment - intravenous bolus administration of mannitol 1 g / kg in the form of 20% r - ra .. In the absence of effect - hyperventilation up to r a CO 2 2-28 mm Hg. Elderly. Particular attention should be paid to the condition of the kidneys, chronic heart failure is possible.

Pregnancy. The risk of fetal death in ketoacidotic coma during pregnancy is about 50%.

Prevention. Determination of the concentration of glucose in the blood under any stress. Regular administration of insulin.
Abbreviations. DKA is diabetic ketoacidosis.

ICD-10. E10.1 Insulin-dependent diabetes mellitus with ketoacidosis. E11.1 Non-insulin-dependent diabetes mellitus with ketoacidosis. E12.1 Diabetes mellitus associated with malnutrition with ketoacidosis. E13.1 Other specified forms of diabetes mellitus with ketoacidosis. E14.1 Diabetes mellitus, unspecified with ketoacidosis.

Note. Anion difference- the difference between the sum of the measured cations and anions in plasma or serum, calculated by the formula: (Na + + K +) - (Cl- + HCO 3 -) = 20 mmol / l. May be increased in diabetic acidosis or lactic acidosis; not changed or reduced in metabolic acidosis with loss of bicarbonate "cation - anion difference.

Acetonemic syndrome is a complex of symptoms that occurs due to metabolic disorders in the body. As a result, the accumulation of ketone bodies occurs. This is a pathological condition, which is accompanied by an increase in the blood of acetone, acetoacetic acid.

The disease occurs mainly in childhood. Manifested by stereotypical and regularly recurring episodes that alternate with periods of complete well-being.

The primary form occurs in 4-6% of children aged 1 to 13 years. More girls are subject to it. The mean age of onset of vomiting is 5.2. Half of all patients require symptomatic relief by intravenous fluids.

The secondary form develops in the presence of concomitant diseases and after operations. It needs a clear trigger.

ICD-10 code

According to ICD-10, the syndrome is not distinguished as a separate nosological unit. But in pediatrics, doctors often encounter various metabolic disorders, which are accompanied by the described pathological condition.

According to the classification, it is classified as acetonuria (code R82.4). With this disease, an increased content of acetone in the urine is detected.

Reasons for development

The main reason is the absolute or relative lack of carbohydrates in the child's diet or the predominance of fatty and ketogenic acids.

A prerequisite for acetonemic syndrome is that they must take an active part in oxidative processes.

When there is a lack of carbohydrates in the body, energy needs begin to be compensated by lipolysis. This leads to the formation of a large amount of fatty acids.

A large number of ketone bodies leads to imbalances in the acid sphere and water-electrolyte. This has a toxic effect on the nervous system, gastrointestinal tract. Provoking factors can be:

• stress;
• SARS;
• pneumonia;
• neuroinfections.

Sometimes the prerequisite is starvation or overeating. When exposed to several adverse factors, ketosis is formed.

With a significant increase in the level of keto acids, metabolic acidosis occurs. An excess of ketone bodies has such a strong effect on the central nervous system that there are risks of developing a coma.

Symptoms of acetone syndrome in children

The manifestation of a classic attack can last from a day to a week. Always accompanied by seizures. Its frequency and duration depends on the initial level of health and diet.

Sometimes there are single episodes of vomiting, but more often it is repetitive. It is also caused by an attempt to drink ordinary water. Because of this, signs of intoxication occur and form.

The child turns pale, but a bright, unhealthy blush may appear on the cheeks. Gradually there is a decrease in the activity of the child associated with muscle weakness. It becomes difficult for the baby to raise his arms, get out of bed.

The attack is characterized by staging of neurological and clinical manifestations. At low doses of acetone, excitation occurs. The baby begins to scream, cry, show sharp anxiety.

With the accumulation of toxic products, excitement is replaced by drowsiness, impotence. With a sharp progression of the disease, seizures and loss of consciousness may occur.

Video about acetonemic syndrome in children of Dr. Komarovsky's school:

Diagnostics

Usually parents call an ambulance because of incessant vomiting. In a hospital, a urine and blood test is taken. It is revealed that the amount of acetone in biological fluids is very high.

In the future, test strips can be used at home to determine the level of acetone in the urine to adjust therapeutic and preventive measures.

The brighter the color of the strip after immersion in urine, the higher the level of ketone bodies. This technique is not absolutely accurate, therefore, it allows only an approximate assessment of the severity.

In hospitals, the amount of acetone is measured in units or mol/l. When deciphering into a form, pluses become. With one or two treatments are carried out at home. If there are 3-4 pluses, then treatment in the hospital is prescribed, since a life-threatening condition occurs.

Treatment

Treatment is carried out in 3 stages:

• The first. In the initial stages or when precursors appear, the intestines are cleansed with a 1-2% solution of sodium bicarbonate. The child should be watered every 10 minutes, sweet tea or compote. There is no need to starve, but diet becomes the main method of treatment. If necessary, antispasmodics are prescribed. Enterobrents are used to remove ketones.
• Second. When repeated vomiting appears, the intestines are cleansed and infusion therapy is carried out. For the latter, solutions with the lowest concentration of glucose are used. If the child is willing to drink, parenteral administration can be replaced by oral hydration. With indomitable vomiting, metoclopramide and antispasmodics are prescribed. With excessive excitement, tranquilizers are prescribed.
• Third. It is aimed at normalizing metabolism and preventing relapses. To do this, you need to follow a diet. You will have to follow it for the rest of your life.

Cerucal

This is a common one used for acetonemic syndrome. It is a dopamine receptor blocker and acts as an antiemetic drug. Available in ampoules for injection.

Diet

In a crisis, you need to drink sweet tea, eat watermelons or melons. It is possible to use mineral water. The latter cannot be used if frequent rises of acetone are observed.

At the stage of precursors (lethargy, headache, smell of acetone from the mouth), the child should not starve. When vomiting appears, it will not work to feed the child.

Give preference to foods that contain easily digestible carbohydrates. It can be bananas, vegetable purees, kefir, liquid semolina. In minimal quantities, you can eat buckwheat, oatmeal, corn porridge, baked apples of sweet varieties, biscuit cookies.

When the general condition improves, vegetable soup is introduced. Completely have to exclude marinades, smoked meats. All products should be steamed or boiled. The baby should be fed every 2-3 hours.

The main principle of nutrition is the exclusion from the diet of foods that contain purine compounds and fats in large quantities. The emphasis should be placed during periods of remission on dairy products, vegetables, fruits.

Forecast and prevention

Children with the syndrome should be registered with an endocrinologist, undergo an annual glucose test, and. The prognosis is generally favorable.

As you grow older, the occurrence of acetone crisis ceases. Most often this happens during adolescence. With timely medical care received and with competent treatment tactics, ketoacidosis is stopped.

When diagnosing recurrent acetonemic conditions, it is necessary to follow a high-carbohydrate and high-protein diet, regularly check the presence of acetone in the urine using test strips. It is important to avoid long breaks between meals.