Acetonemic vomiting in a child

Acetonemic vomiting is one of the accepted names for a particular type of metabolic disorder. In addition, synonyms are: acetonemic syndrome, nondiabetic ketoacidosis, a syndrome of cyclic vomiting.

There is no disease in the last International Classification precisely because of the ambiguous attitude of scientists from different countries to the mechanism of education and the connection of symptoms with endocrine disorders.

Acetonemic vomiting in children is considered as a primary process or referred to as idiopathic, like any pathology with an unknown cause. It is precisely established that a characteristic syndrome causes paroxysmal growth in the blood of substances left from incomplete oxidation of fatty acids.

"Adult" cases are rare, and they are associated with any chronic diseases, brain tumors, are considered secondary.

Morbidity

In pediatric practice, the incidence of ketoacidosis is 4-6% in children under 12 years of age, in girls slightly more frequently than in boys. The first manifestations of symptoms are noticed after the age of five. Pathology has a crisis current. In 90% of cases it is accompanied by indomitable vomiting.

Classification

It is common to divide the cases of ketoacidosis with vomiting in children for primary and secondary. The manifestations of the child with a special type of development( constitution) are referred to as the primary manifestation, which in old fashion is called "neuro-arthritic" or "neuro-arthritic diathesis".

This term was introduced in 1901.It was noted that children suffering from excitability, eating disorders, predisposition to obesity, early exchange arthritis are more likely to suffer. Modern data allow us to relate pathology to enzymes - disorders caused by a deficiency of enzymes involved in metabolism.

Secondary acetonemic syndrome - occurs against a background of various diseases. Most often, vomiting accompanies the pathology of the digestive tract, if there are severe symptoms of intoxication, delayed bile secretion, liver damage, imbalance of intestinal microflora.

It is possible and development in the postoperative period against the background of removal of palatine tonsils, at high temperature. The clinic in such cases depends on the main disease, acetonemic vomiting stratifies and makes the condition worse.

Secondary disorders may accompany:

• endocrine pathology;
• trauma to the skull and brain;
• infectious diseases with toxicosis;
• brain formation;
• hemolytic anemia;
• state of leukemia;
• fasting.

Which children have a tendency for primary nondiabetic ketoacidosis?

Children who differ in their behavior by increased nervous excitability suffer from acetoneemic vomiting, and they develop a foci of congestive arousal at the level of the hypothalamic-pituitary system.

The body shows a significant deficiency of hepatic enzymes, oxalic, lactic and uric acids. The consequence of changes in regulation is disrupted carbohydrate and fat metabolism.

Such a child is emotionally unstable, tearfulness gives way to a good mood. In physical development may lag behind peers, sleeps poorly, fearsome, suffers from aerophagia( ingestion of air).

Although lagging behind the increase in body weight, mentally even outstrips the skills of his age: he starts talking early, has a good memory, easily learns at school, is interested in various problems.

By 2-3 years the child may have unstable pains in the joints, attacks of colic in the abdomen( due to spasm of the pyloric zone of the stomach, bile ducts).Less common are complaints of headaches associated with intolerance to smells. In urine tests, urate salts are found.

Stimulating the development of ketoacidosis with vomiting are factors that, against a background of high excitability of the nervous system, are a great stress:

• any physical or psychoemotional overexertion;
• long stay in the sun;
• disorders in eating( using a significant amount of fat or, conversely, hunger).

Causes of acetonemic vomiting in children

The basis of nondiabetic ketoacidosis with vomiting in children is a genetic predisposition, expressed in the deficiency of the necessary enzymes for the cleavage of amino acids and fatty compounds in the process of energy production. This predisposing factor in conditions of nervous system overstrain triggers as a trigger and causes a complex chain of disturbances.

Which biochemical processes in the body give energy?

To clarify the mechanism of disorders in acetone-induced vomiting, it is necessary to touch upon the normal process of obtaining calories for the activity of the body's cellular systems.

All protein, fat and carbohydrate components of food eventually decompose to acids, glucose, biologically active substances that enter the Krebs cycle. This is the name of the biochemical process which results in the formation of kilocalories. It requires both starting materials and enzymes + coenzymes( activators of enzymes).

Carbohydrates are transformed into pyruvate, which supports the course of the Krebs cycle. Proteins are exposed to proteases, cleaved to amino acids( asparagine, alanine, serine, cysteine), too, are converted into pyruvate.

A leucine, phenylalanine and tyrosine are sources of the enzyme acetyl-coenzyme A( acetyl-CoA).Fats are affected by lipases, cleavage occurs before the formation of acetyl-CoA.

Normally, most of this enzyme reacts with oxaloacetate and is subsequently included in the Krebs cycle. A small part of acetyl-CoA is necessary to restore free fatty acids and further synthesis of cholesterol. The minimum goes to the synthesis of ketone bodies in the liver.

The group of ketone bodies includes:

• acetone;
• acetoacetic acid;
• β-hydroxybutyric acid.

Their concentration is very small.

It is believed that ketone bodies play an important role in supporting the energy balance. It is their growth that provides feedback to the centers of the brain when determining energy requirements, preventing excessive splitting of fat stores.

It is important that the liver is able to synthesize substances from a group of ketone bodies, but it can not spend it on covering energy needs, since it lacks the necessary enzymes.

Derivation of excess ketone bodies is carried out by their oxidation in skeletal muscles, brain, myocardium to carbon dioxide and water. Another way is through the kidneys, lung tissue and intestines without the processes of transformation.

Mechanism of development of ketoacidosis and vomiting

When the intake of carbohydrate food( starvation, excessive feeding of fatty and protein foods) is limited, changes in the liver are activated to obtain energy from the fat depot( lipolysis).As a result, a significant amount of acetyl-CoA accumulates.

At the same time, its entry into the Krebs cycle is limited. The process involves a reduced amount of oxaloacetate, a decreased activity of enzymes that stimulate the resynthesis of free fatty acids and cholesterol.

The only way to utilize acetyl-CoA is to convert to ketone bodies( ketogenesis).In this case, the rate of their accumulation should exceed the process of disposal( removal from the body).

Excess ketone bodies cause pathological abnormalities in the body. Metabolic acidosis - a shift in the acid-base balance towards increased acidity. The body tries to compensate for it by increased ventilation of the lungs, which promotes alkalization of the environment. But the process leads to a loss of carbon dioxide with a reflex narrowing of the vessels, mainly the brain.

The action on the central nervous system resembles narcotic, ketone bodies can cause inhibition up to coma. Acetone has the properties of an organic solvent, its accumulation leads to damage to the cell's lipid membrane.

Adverse effects are maintained by the loss of water and electrolytes due to vomiting, the accumulation of lactic acid. To ensure the utilization of ketone bodies, the body needs additional oxygen. Its deficiency contributes to hypoxia in the tissues, increases the severity of the symptoms.

Symptoms of

Acetonemic syndrome with vomiting varies, often symptomatic is affected by "triggering" disease( influenza and other acute infections, gastroenteritis, pneumonia).The manifestations of toxicosis and disturbance of water balance are mandatory.

In the development of acetonemic vomiting, the role of ketosis is more significant:

• , the child develops nausea, followed by repeated prolonged vomiting;
• the kid refuses food and drink;
• in the air breathes with smell of apple;
• in the abdomen - cramping pain.

is detected. Symptomatic symptoms increase in 3-5 days. There are signs of dehydration - dry skin and mucous membranes, lethargy of the turgor, sunken eyes. The nervous system reacts with increased irritability, then with retardation.

Breathing becomes deep and noisy. The palpitations become more frequent, attacks of an arrhythmia are possible or probable. The daily diuresis decreases.

Diagnostic criteria

To confirm the diagnosis, vomiting is not enough as a single sign. Criteria have been developed that combine the clinic with ketoacidosis. These include:

• repeated persistent, rather than a single vomiting for several hours or days;
• availability of interstitial periods with normal state;
• absence of such signs in confirming the cause of vomiting, as pathologies of the stomach and intestines;
• the same clinic of seizures;
• the possibility of spontaneous cessation of vomiting( without treatment);
• presence of concomitant symptoms of dehydration, fever, diarrhea, pallor of the skin;
• content in the emetic mass of bile, mucus, in 1/3 of the cases, possibly the appearance of blood.

Severe vomiting contributes to the inverse retraction of the cardiac zone of the stomach in the gastroesophageal sphincter( propulsive gastropathy).The enlargement of the liver lasts up to 7 days after the attack.

Methods for laboratory diagnosis of

Clinical blood and urine tests usually reflect pathological changes in diseases that act as metabolic pathway activators, often show moderate leukocytosis, increased ESR.

The method of reaction with nitroprusside in the urine reveals ketonuria from one to four pluses. As a rule, it is accompanied by glucosuria. Biochemical methods determine the increased concentration of ketone bodies, cholesterol, β-lipoproteins.

The hematocrit indicator increases with dehydration, indicating uncompensated fluid loss. In the blood, the concentration of urea increases considerably, the potassium in the serum first increases, then falls.

Differential diagnosis of

Treatment of a child requires differentiation of vomiting with ketoacidosis caused by diabetes mellitus. Here, one should take into account the absence of high glucose values ​​in the blood, much less severity of the patient's condition and anamnestic data.

Disturbances from the central nervous system require additional examination to exclude congenital pathology, brain tumor. Symptoms of abdominal pain with vomiting must be distinguished from acute surgical pathology.

With repeated vomiting, the doctor can not immediately exclude an infectious disease, so the child is often hospitalized in the boxed ward of the infectious disease department. In diagnosis, children need to think about vomiting:

• in case of kidney pathology( hydronephrosis), pancreatitis;
• possible side effects of medications;
• household poisoning;
• epilepsy;
• of adrenal insufficiency;
• other enzymes.

True acetone crises can occur suddenly, after preliminary manifestations of aura( harbingers) in the form of loss of appetite, excitation or inhibition, a headache resembling a migraine, nausea, pain around the navel, light stool, the smell of apples from the mouth.

Treatment of

The modern concept of therapeutic measures for acetone-induced vomiting is based on the allocation in the clinical course of successive phases:

• the onset of an attack( aura, the period of precursors);
• maximum changes in metabolism or the attack itself;
• recovery;
• inter-offense period.

When the auras appear close, the older child understands that the attack is approaching. If it lasts from several minutes to several hours, there is time for taking the medicine through the mouth.

Some patients are treated with a non-steroidal anti-inflammatory drug Ibuprofen, a proton pump inhibitor. If a harbinger is a headache, then sumatriptan is considered effective.

has not yet appeared. For acetylmitic vomiting, the following are used:

• every 15 minutes drinking alkaline mineral water without gas, sweet tea with lemon, special solutions for rehydration;
• cleansing enema with a weak solution of soda;
• infusion intravenous therapy to compensate for fluid loss;
• Ondansetron - for blocking serotonin receptors in the brain.

Infusion therapy aims to normalize the volume and composition of blood, interstitial fluid, the removal of intoxication, parenteral nutrition of the child. Scheme rehydration therapy for vomiting should include a control determination of the degree of dehydration, loss of electrolytes, age standards, the state of the cardiovascular system.

Current data on the pathophysiological mechanism of acetonemic vomiting makes it critical to approach previously recognized methods of treatment:

• accumulated ketone bodies are able to block the transport of glucose molecules through cell membranes( as in diabetes mellitus), this raises questions about the effectiveness of intravenous glucose solution;
• hyperglycemia with increased glucose introduction promotes its transition into urine and further electrolyte removal, which increases dehydration;
• alkalinizing solutions increase the concentration of bicarbonates in the plasma, affect metabolic acidosis, but do not stop the accumulation of ketone bodies.

Therefore, promising drugs for severe, frequent repeated vomiting are intravenous use of metoclopramide, which blocks dopamine receptors in the central region of the brain causing vomiting. And also a serotonin blocker - Ondansetron.

. Other medications include:

• prokinetics( Metoclopramide, Motilium);
• enzymatic agents and co-factors of carbohydrate metabolism( vitamins B1 and B6).

Some authors prove the expediency of introducing glucose solutions of alcohol( Sorbitol or Xylitol) to eliminate ketosis and vomiting. These substances are independent of insulin regulation.

The main directions of treatment in the inter-attack period

After vomiting, treatment is limited to diet and vitamin therapy. It is necessary to observe the following rules:

• to "unload" the Krebs cycle from the menu, all fats, extractives, sharp sauces, excluding vegetable oils, fish oils( they are absorbed from the intestine more easily than animals) are excluded;
• it is necessary to maintain a sufficient volume of liquid;
• , in order to ensure an alkaline urine reaction, it is necessary to limit the food to acidic fruits;
• products rich in potassium slow down the elimination of keto acids, so in the diet you should avoid bananas, apricots, baked potatoes;
• to restore peristalsis of the intestine, it is required to limit products with increased properties of gassing( black bread, legumes, cabbage, radish), as well as irritating mucous membranes( onions, garlic).

In the recovery period, the child's activity and appetite gradually increase.

Children with cyclical vomiting syndrome are considered for the endocrinologist at risk for diabetes. Therefore, urine and blood should be checked more often for glucose than others.

As a teenager, crises cease. Perhaps this is due to hormonal changes in the body. Prior to this period, parents have to carefully monitor the child, his behavior and nutrition.