Despite the tremendous advances in the treatment of diabetes associated with the discovery of insulin, free provision of it and hypoglycemic drugs for all patients, still ketoacidotic coma develops in 1-6% of cases.

IN common cause mortality it takes 2-4%, sometimes the frequency of deaths in the case of a coma is significant and ranges from 5 to 30%.

The reasons that lead to the development of ketoacidotic coma:

Untimely treatment of a patient with beginning insulin-dependent diabetes mellitus (IDDM) to a doctor and delayed diagnosis.

Ketoacidotic coma becomes the debut of IDDM in 1/3 of cases of newly diagnosed disease, especially in children and adolescents;

Errors in the appointment of insulin therapy (incorrect selection and unjustified dose reduction, replacement of one type of insulin with another, to which the patient is insensitive);

The patient is not trained in self-control methods (breaks the diet, drinks alcohol, does not know how to change the doses of antihyperglycemic drugs, does not dose physical activity);

Acute intercurrent diseases (especially purulent infections);

Acute vascular diseases (stroke, myocardial infarction);

Physical and mental trauma;

Pregnancy and childbirth;

Surgical interventions;

Stressful situations.

All these factors significantly increase the need for insulin, which leads to the development of severe insular insufficiency with the subsequent occurrence of metabolic syndrome.

Pathogenesis of ketoacidosis and coma:

As a result of insulin deficiency, the activity of contrainsular hormones (glucagon, ACTH, STH, cortisol, catecholamines) increases sharply, which contribute to an increase in glycemia due to neoglycogenesis.

An excess of counterinsular hormones leads to an increase in the supply of amino acids to the liver, which are formed during the increased breakdown of proteins and fats. They become sources of increased glucose production under the influence of liver enzymes. In this case, the release of glucose by the liver can increase 2-4 times, that is, it can be synthesized up to 1000 g per day.

Hyperglycemia is pronounced, but the peripheral tissues, due to the lack of insulin, do not absorb glucose, which further increases glycemia.

The accumulation of unused glucose in the blood has a number of negative consequences:

Hyperglycemia significantly increases plasma osmolarity. Due to this, the intracellular fluid begins to move into the vascular bed, which ultimately leads to severe cellular dehydration and a decrease in the intracellular content of electrolytes, primarily potassium ions;

As soon as glycemia exceeds the renal permeability threshold for glucose, glucosuria immediately appears. The so-called osmotic diuresis develops.

Due to the high osmolarity of the provisional urine, the renal tubules cease to reabsorb water and electrolytes released with it (sodium, potassium, chlorine, magnesium, calcium, and others).

These disorders lead to dehydration, hypovolemia with significant thickening of the blood, an increase in its viscosity and the ability to thrombus, blood pressure.

The second direction of metabolic disorders is associated with excessive accumulation of ketone bodies, that is, ketosis, and then ketoacidosis.

In parallel with the increase in blood sugar levels, lipid metabolism disorders are progressing, which is due to the excessive content of counterinsular hormones.

Due to disinhibition of tissue lipase, normally inhibited by insulin, intense lipolysis begins.

In the blood, the content of total lipids, triglycerides, cholesterol, phosphhalipids, and NEFA increases sharply. Lipids enter the liver, where ketone bodies are synthesized from them.

The oxidation of fat cells increases with the formation of acetyl coenzyme "A", from which ketone bodies (acetone, β-hydroxybutyric and acetoacetic acids) are actively synthesized in the liver. There is a synthesis of ketone bodies from amino acids. With the decompensation of diabetes, the amount of ketone bodies increases 8-10 times compared with the norm.

Lack of insulin reduces the ability of muscle tissue to utilize ketone bodies, this is the most pronounced indicator of insulin deficiency than the hyperproduction of ketone bodies. Ketone bodies, possessing the properties of moderately strong acids, lead to the accumulation of hydrogen ions in the body, reduce the concentration of sodium bicarbonate, which entails the development of metabolic acidosis (ketoacidosis) with a decrease in blood pH to 7.2-7.0 and below.

Hyperketonemia, among other things, aggravates insulin deficiency, suppressing the residual secretory activity of the beta cells of the islet apparatus.

The entire group of ketone bodies is toxic, with a pronounced toxic effect on the central nervous system. This leads to the development of toxic encephalopathy, impaired hemodynamics with a drop in peripheral vascular tone and impaired microcirculation.

With insular insufficiency, patients with diabetes in a state of ketoacidosis have hypokalemia, which is especially pronounced 3-4 hours after the administration of insulin, which "sends" potassium to the cell, stores it in the liver, potassium continues to be excreted in the urine, if there is no acute renal failure... Against the background of hypokalemia, the following develops:

Hypotension of smooth and striated muscles, which leads to a decrease in vascular tone and a drop in blood pressure;

Various disturbances of rhythm and conduction, ectopic cardiac arrhythmias;

Atony of the gastrointestinal tract with paresis of the stomach and the development of intestinal obstruction;

Hypotension of the respiratory muscles with the development of acute respiratory failure;

Adynamia, general and muscle weakness, flaccid paresis of the muscles of the limbs.

With ketoacidosis and coma, severe hypoxia develops. In patients with diabetes, several types of hypoxia are distinguished:

Transport hypoxia, which is due to high level glycosylated hemoglobin, it loses the ability to give oxygen to tissues;

Alveolar hypoxia is caused by a restriction of the respiratory excursion of the lungs, due to hypokalemia, the function of the neuromuscular synapses is disrupted and the weakness of the respiratory muscles develops due to an increase in the liver, swelling of the gastrointestinal tract, the mobility of the diaphragm is sharply limited;

Circulatory hypoxia is caused by a decrease in blood pressure and impaired microcirculation;

Disruption of tissue respiration is aggravated by acidosis, which makes it difficult for oxygen to pass from blood to cells.

Under conditions of hypoxia, anaerobic glycolysis is activated, as a result of which the level of lactic acid increases with the development of lactic acidosis.

In the presence of lactic acid, the sensitivity of adrenergic receptors to catecholamines is sharply reduced, and irreversible shock develops.

Metabolic coagulopathy appears, manifested by disseminated intravascular coagulation syndrome, peripheral thrombosis, thromboembolism (myocardial infarction, stroke).

Thus, in diabetic ketoacidosis, a sharp deficiency of insulin and excessive secretion of counterinsular hormones leads to severe metabolic disorders, mainly to metabolic acidosis, hypoxia, hyperosmolarity, cellular and general dehydration with the loss of potassium, sodium, phosphorus, magnesium, calcium, bicarbonate ions. This, with a certain severity, and causes a coma with a drop in blood pressure and the development of acute renal failure.

Clinical symptoms

Diabetic coma develops slowly, gradually. From the first signs of ketoacidosis to loss of consciousness, it usually takes from several hours to several days. When acute infections, disorders of cerebral and coronary circulation, ketoacidosis can develop very quickly.

In diabetic ketoacidosis, there are 3 periods:

Beginning ketoacidosis.

Precoma stage.

Coma stage.

Incipient ketoacidosis is characterized by dry mouth, thirst, polyuria, polydipsia, and sometimes itching.

Already in this period, there are signs of intoxication in the form of general weakness, increased fatigue, headache, nausea, vomiting. The smell of acetone appears, which many patients feel themselves.

If treatment is not started, then the dyspeptic syndrome is further aggravated, repeated vomiting appears, which does not relieve the patient's condition, which aggravates the water-electrolyte disorder. Abdominal pain of varying intensity, diarrhea or constipation appear. Lethargy, drowsiness, lethargy grow, patients become indifferent to their surroundings, disoriented in time and space, confused consciousness. Stupor and stupor give way to coma.

When examining a patient in a state of ketoacidotic coma, the following signs draw attention to themselves:

The skin is dry, cold, flaky, with traces of scratching and boils, the turgor is reduced;

Dry lips covered with caked crusts;

Tongue and oral mucosa are dry. Tongue covered with a dirty brown coating, with teeth marks at the edges;

The facial features are pointed, the eyes are deeply sunken. The eyeballs are soft due to dehydration;

Skeletal muscle tone is reduced;

On the face, diabetic rubeosis, as a sign of a decrease in vascular tone and a high level of glycosylated hemoglobin;

Breathing deep, noisy - Kussmaul, in the exhaled air the smell of acetone;

Pulse is small, frequent, weak filling and tension. Sinus heart rhythm, tachycardia, sometimes single extrasystoles, there may be atrial fibrillation, blood pressure is lowered;

In the lungs, usually hard breathing is heard, there may be a pleural friction noise, possibly due to aseptic dry pleurisy, which occurs due to severe dehydration. Recently, acute respiratory failure is often found, which is often the cause of death of patients with diabetes;

The abdomen is soft in most cases, it is often possible to palpate an enlarged liver;

In a coma, patients have completely lost consciousness, sensitivity, reflexes are reduced. Ketoacidotic coma may be atypical with predominant signs of damage of cardio-vascular system; digestive organs; kidney and brain. This introduces certain difficulties in the diagnosis of coma.

Gastrointestinal ketoacidosis.

Almost no case of diabetic ketoacidosis is complete without gastric dyspepsia. Repeated vomiting aggravates the imbalance in water and electrolyte balance. In some patients in the precoma stage, intense abdominal pain appears, as a rule, without clear localization, increasing, with muscle tension of the anterior abdominal wall and symptoms of peritoneal irritation (diabetic false acute abdomen).

At the same time, dyspeptic syndrome of varying severity is observed: from infrequent vomiting of mucus and bile to indomitable vomiting with a large amount of coffee-colored liquid, which is perceived as gastric bleeding. ...

Symptoms of "acute abdomen" and neutrophilic leukocytosis, which is observed at this time, clear signs of intoxication make one think of acute surgical pathology: acute appendicitis, cholecystitis, perforated stomach ulcer, paralytic intestinal obstruction, thrombosis of mesenteric vessels, acute pancreatitis etc.

With suspected acute surgical pathology of organs abdominal patients sometimes operate and make their condition worse.

Correctly prescribed treatment of ketoacidosis eliminates the "diabetic belly" in 4-5 hours.

Cardiovascular form of ketoacidosis.

The cardiovascular form of ketoacidosis is more common in elderly patients. The leading clinical manifestation is severe collapse with a significant decrease in both arterial and venous pressure, tachycardia, threadlike pulse, various rhythm disturbances, cyanosis and cold extremities.

In the pathogenesis of this form, hypovolemia plays a leading role with a significant decrease in the volume of circulating blood, a decrease in myocardial contractility due to atherosclerosis of the coronary vessels and acute metabolic cardiopathy, as well as paresis of peripheral vessels, a decrease in their sensitivity to the vasoconstrictor effect of pressor amines.

There is a deep circulatory disorder at the microcirculatory level with disseminated intravascular microthrombus formation. With this form of ketoacidotic coma, thrombosis of the coronary and pulmonary vessels, as well as blood vessels, is especially common. lower limbs.

Renal form.

The renal form of coma usually develops in patients with long-standing diabetes mellitus and diabetic nephropathy. Ketoacidosis is accompanied by proteinuria, hematuria, cylindruria.

These changes in urine, combined with azotemia, neutrophilic leukocytosis, sometimes make it necessary to differentiate ketoacidotic coma from uremic coma.

It is logical to talk about the renal variant of diabetic coma when a drop in blood pressure and renal blood flow leads to anuria, and the entire further course of the disease is determined by acute renal failure. This is usually the case with significantly pronounced diabetic glomerulosclerosis.

Encephalopathic form.

This form is observed in elderly people suffering from cerebral atherosclerosis. With ketoacidosis due to hypovolemia, acidosis, microcirculation disorder, decompensation of chronic cerebrovascular insufficiency occurs. This is manifested by symptoms of brain damage: asymmetry of reflexes, hemiparesis, the appearance of unilateral pyramidal signs.

In this situation, it is very difficult to decide: a coma caused focal cerebral symptoms or a stroke caused ketoacidosis.

Treatment of ketoacidosis leads to an improvement in cerebral circulation and a smoothing of cerebral symptoms.

Laboratory data:

Blood glucose - 25-40 mmol

Ketone bodies up to 500μmol

Acetone in urine is sharply positive.

blood pH 7.0-7.35

Complete blood count - leukocytosis with neutrophilic shift to the left, accelerated ESR.

A patient in a state of ketosis, and even more so in a precomatose and comatose state, should be immediately hospitalized for emergency measures:

Insulin therapy;

Elimination of dehydration;

Normalization of electrolyte disturbances;

Fight ketoacidosis;

Infusion therapy in a state of ketoacidosis is often carried out for several days, so it is necessary to immediately insert a catheter into the subclavian vein. An urgent task is to remove the patient from a coma in the first 6 hours from the moment of admission to the hospital, since later changes occur that are incompatible with life.

IN last years proved the feasibility of introducing adequate doses of simple insulin constantly intravenously under hourly glycemic control.

Insulin therapy:

You can use two methods to inject insulin:

Method 1: in intensive care units using

syringe lineomat or other injection dispensers medicinal substances.

A 20 ml syringe-lineomat is filled with 40 units of short insulin "(insulrap, actrapid MS, actropid, actropid NM, maxirapid) and saline. 1 ml of the mixture contains 2 units of insulin, adjusting the rate, the required dose is administered.

Method 2: the required dose of insulin is calculated by the number of drops per minute. A mixture is prepared containing 400 ml of saline and 40 units of simple insulin. By varying the rate of drops per minute, you can calculate the insulin dose per hour.,

With a glycemia of 30 mmol / l and above, it is recommended to inject 400 ml of saline solution + 10 units of simple insulin into an intravenous stream, then determine the blood sugar level and set up a dropper for continuous intravenous administration of insulin in saline. Insulin dose is determined by blood sugar. It is obligatory to determine blood glucose every hour, the rate of glycemic decrease should not exceed 2-3 mmol / hour. Insulin is injected intravenously until the blood glucose level is 13-14 mmol / l, and against this background, a 5% glucose solution is connected in parallel.

Recovery of water-electrolyte metabolism

The fluid deficiency in ketoacidosis reaches 10% of body weight, that is, 5-7 liters. It is impossible to replenish such an amount quickly because of the danger of acute left ventricular failure and cerebral edema.

To combat dehydration, it is recommended to introduce 1 liter of liquid within 1 hour, the 2nd liter in the next 2 hours, the 3rd liter at 3 hours, that is, 50% of the liquid is injected in the first 6 hours, then in the next 6 hours. 25%, and in the next 12 hours - also 25% of the required daily fluid requirement.

In order to prevent hypoklycemia and to eliminate ketoacidosis with a decrease in blood glucose of 13 mmol / l and below, it is necessary to inject 5% glucose solution intravenously, the daily amount of which may be 1.5-2 liters.

To normalize electrolyte metabolism, the patient needs the introduction of potassium chloride. The daily amount of potassium chloride is 8-12 grams, that is, 200-300 ml. 4% solution.

Restoration of acid-base balance.

The introduction of sodium bicarbonate without determining the pH of the blood is dangerous to the patient's life, as it promotes hypernatremia, hypokalemia, a sharp "gross" change in plasma osmolarity and cerebral edema.

Only if the blood pH is below 6.0 (clinically noisy breathing of Kussmaul) You can enter sodium bicarbonate 2% solution of 200-300 ml within 2 hours, but the patient must first receive at least 40 ml - 4% solution of potassium chloride.

In all other cases, soda is used to wash the stomach and intestines.

In addition to the drugs listed above, patients need antibiotics (maximum permissible doses) in order to prevent infectious and inflammatory diseases. It is necessary to introduce B vitamins, ascorbic acid, cocarboxylase, riboxin, essential. With atony of the gastrointestinal tract, proserin, cerucal is administered. In order to prevent thrombosis - heparin 20,000 units per day. Patients need the introduction of cardiac glycosides, nootropics and other symptomatic therapy.

An integral part of the treatment of ketoacidotic coma is patient care (treatment of the oral cavity, skin, prevention of pressure ulcers).

Ketoacidotic (diabetic) coma is an acute complication of diabetes mellitus in the stage of decompensation, caused by excessive formation of ketone bodies in the body, which have a toxic effect on body systems, in particular the brain, and is also characterized by the development of dehydration, metabolic acidosis and hyperosmolarity of blood plasma. Diabetic coma is recorded in 1-6% of patients with diabetes mellitus.

There are two types diabetes mellitus (Table 3).

Table 3. Types of diabetes

Prevalence
Age		After 35 years
Start		Gradual
Body mass	Normal or decreased	Increased
Clinical symptoms	Expressed
Ketoacidosis	Expressed	Is absent
Vascular damage	Small vessels	Trunk vessels
Insulin sensitivity	Expressed	Not expressed
Number of insulin receptors	Within normal limits
Antibodies

Etiology:

untreated diabetes mellitus;

violations of the treatment regimen (cessation of insulin administration, unreasonable dose reduction)

non-compliance with the diet;

alcohol or food intoxication.

Risk factors: obesity, acromegaly, stress, pancreatitis, liver cirrhosis, the use of glucocorticoids, diuretics, contraceptives, pregnancy, burdened heredity.

Pathogenesis. The main pathogenetic factor of ketoacidotic coma is insulin deficiency, which leads to: a decrease in glucose utilization by peripheral tissues, incomplete oxidation of fats with the accumulation of ketone bodies; hyperglycemia with increased osmotic pressure in the intercellular fluid, cellular dehydration with the loss of potassium and phosphorus ions by cells; glucosuria, increased urine output, dehydration, acidosis.

The clinical manifestations of coma develop slowly - over several hours or even days; coma occurs faster in children than in adults.

Stages of a ketoacidotic coma:

Stage I - compensated ketoacidosis;

Stage II - decompensated ketoacidosis (precoma);

Stage III - ketoacidotic coma.

Typical signs of stage I: general weakness, increased fatigue, headache, decreased appetite, thirst, nausea, polyuria.

In stage II, apathy, drowsiness, shortness of breath (Kussmaul breathing) increase, thirst increases, vomiting and abdominal pain appear. Tongue dry, coated; skin turgor is reduced, polyuria is expressed, in the exhaled air - the smell of acetone.

Stage III is characterized by: severe disorders of consciousness (stupor or deep coma), pupils are constricted, facial features are sharpened; tone eyeballs, muscles, tendon reflexes are sharply reduced; signs of impaired peripheral circulation (arterial hypotension, tachycardia, cold extremities). Despite pronounced dehydration, increased urine output remains. Breathing is deep, loud (breathing of Kussmaul), in the exhaled air - the smell of acetone.

Clinical forms of ketoacidotic coma:

abdominal, or pseudoperitoneal (pain syndrome, positive symptoms of peritoneal irritation, intestinal paresis);

cardiovascular (hemodynamic disturbances are expressed);

renal (olig- or anuria);

encephalopathic (resembles a stroke).

Differential diagnosis of ketoacidotic coma should be carried out with apoplexy, alcoholic, hyperosmolar, lactic acidotic, hypoglycemic, hepatic, uremic, hypochloremic coma and various poisonings (see Table 2). The phenomena of ketoacidosis are characteristic of the state after prolonged fasting, alcohol intoxication, diseases of the stomach, intestines, and liver.

Alcoholic ketoacidosis develops after excessive alcohol consumption in people with chronic alcoholism. With normal or low glycemic levels in combination with ketonemia and metabolic acidosis, the development of alcoholic ketoacidosis is most likely.

The development of lactic acidosis is possible at a blood lactate level of about 5 mmol / l. Lactic acidosis can be associated with diabetic ketoacidosis. If lactic acidosis is suspected, blood lactate levels should be tested.

With intoxication with salicylates, metabolic acidosis develops, but primary respiratory alkalosis may develop, while the level of glycemia is normal or reduced. A study of the level of salicylates in the blood is necessary.

The level of ketones in case of methanol poisoning is slightly increased. Characterized by visual impairment, pain in the abdominal cavity. The glycemic level is normal or elevated. Methanol level research is needed.

With CRF, moderate acidosis is found, while the level of ketones is within normal limits. An increase in the content of creatinine in the blood is characteristic.

Treatment start with the introduction of isotonic sodium chloride solution after determining the level of glucose in the blood. Immediately intravenous insulin is injected (10 U, or 0.15 U / kg, after 2 hours - intravenous drip b U / h). In the absence of effect, the rate of administration is doubled. With a decrease in the level of glycemia to 13 mmol / l, they switch to intravenous administration of a 5-10% glucose solution with insulin. With a decrease in blood glucose less than 14 mmol / l, a 5% glucose solution is infused (1000 ml during the first hour, 500 ml / h - within the next two hours, from the 4th hour - 300 ml / h).

With hypokalemia (less than 3 mmol / l) and preserved diuresis, potassium preparations are prescribed. Correction of violations of CBS with sodium bicarbonate solution is carried out if the pH is less than 7.1.

Lecture course on resuscitation and intensive care Vladimir Vladimirovich Spas

Decompensated ketoacidosis and ketoacidotic coma in patients with diabetes mellitus

Despite the fact that currently there are great opportunities and successes in the treatment of diabetes mellitus, the clinical course of this disease in 1-6% of cases is complicated by the development coma... These serious complications pose an immediate threat to the patient's life and require emergency assistance in the conditions of an intensive care hospital.

These critical conditions include:

1.ketoacidosis and its extreme state - ketoacidotic diabetic coma;

2. hyperosmolar coma;

3. hyperlacticidemic coma;

4.hypoglycemic coma (resulting from an overdose of glucose-lowering medicines, primarily insulin).

The development of diabetic ketoacidosis (KA) is typical for both insulin-dependent and non-insulin-dependent diabetes (under conditions of intercurrent diseases and stress, leading to decompensation of diabetes mellitus).

Among the circumstances leading to the decompensation of diabetes mellitus with the development of ketoacidosis and coma, in the first place, can be named:

1.nontimely diagnosed diabetes mellitus, as a result of which a significant part of patients for the first time enter the intensive care unit already in a precoma or coma;

2. insufficient administration of insulin to a patient with diabetes mellitus (incorrect calculation of the daily dose or its uneven distribution during the day);

3. replacement of one drug with another, to which the patient was insensitive;

4. violation of the technique of insulin administration (injections into the area of \u200b\u200blipodystrophy or into an inflammatory infiltrate);

5. the wrong attitude of the patient to his disease (violation of the diet, unsystematic administration of insulin or a change in its dose by the patient himself, the termination of insulin therapy);

6.increase in the patient's need for insulin (acute intercurrent diseases, pregnancy, surgical interventions, physical and mental trauma).

The primary triggering factor for the development of CA is progressive insulin deficiency. In the absence of insulin, the penetration of glucose into the cells and the production of energy are blocked, as a result of which the cell experiences energy starvation. Intracellular decrease in glucose "turns on" the mechanisms by which a compensatory increase in glucose in the blood is carried out. These processes are stimulated by contrainsular hormones (glucagon, catecholamines, glucocorticoids).

The process of gluconeogenesis (under the influence of counterinsular hormones) is carried out in two ways:

1. the breakdown of glycogen with a simultaneous suppression of glycogenesis in the liver;

2. activation of enzymes that carry out the processes of glucose formation from non-carbohydrates.

Increased production of liver glucose, on the one hand, and a decrease in its utilization (due to insulin deficiency), on the other, lead to the development of high hyperglycemia. Hyperglycemia is accompanied by an increase in the osmotic pressure of blood plasma, cell dehydration, and glucosuria (glucose begins to be excreted in the urine at a glycemic level of 10-11 mmol / l). Glucosuria increases the osmotic pressure of primary urine, which prevents its reabsorption, polyuria occurs, while the loss of fluid in the urine can reach 3-6 liters per day.

Due to the fact that during glycogenolysis without insulin, the energy deficit of cells continues ("hunger among abundance"), reserve mechanisms for the formation of glucose from non-carbohydrates are activated, the main of which is myolysis.

Under the influence of counterinsular hormones and activation of tissue lipase (normally inhibited by insulin), intense lipolysis begins. In the blood, the content of total lipids, triglycerides, cholesterol, phospholipids, and non-esterified fatty acids increases sharply. With their increased intake into the liver, an excess of acetyl-Coa, beta-hydroxybutyric and acetoacetic acids is formed, the latter of which is converted into acetone. These three compounds (beta-hydroxybutyric acid, acetoacetic acid and acetone) are called ketone bodies and form the state of ketoacidosis in the body during acute insulin deficiency. It should be noted that non-esterified fatty acids are partly used by the liver for the synthesis of triglycerides, which cause its fatty infiltration.

Hyperlipidemia is not the only factor in increasing liver ketogenic activity. Another source of ketogenic substrates is gluconeogenesis through enhanced protein breakdown, stimulated, on the one hand, by insulin deficiency, and, on the other, by high levels of counterinsular hormones. At the same time, there is an increased protein catabolism with an increase in the concentration of ketogenic amino acids in the blood (leucine, isoleucine, valine), while the level of glucogenic amino acids (glycine, alanine, glutamine) decreases. Protein catabolism is accompanied by increased formation of acetyl-CoA, which is a key substrate for carbohydrate, fat, and protein metabolism. Further combustion of acetyl-CoA occurs in the Krebs cycle, however, the ability of the latter to utilize such an amount of acetyl-CoA in insulin-deficient states is significantly limited. Under these conditions, the liver retains the ability, through a series of transformations, to form ketone bodies from acetyl-CoA (acetoacetic, 7b 0-hydroxybutyric acids and acetone), the concentration of which exceeds the norm by 10 or more times.

Ketone bodies, possessing the properties of moderately strong acids, lead to the accumulation of hydrogen ions in the body, reduce the concentration of hydrogen carbonate No. Metabolic acidosis (ketoacidosis) develops with a decrease in blood pH to 7.2-7.0 and below.

In parallel with ketoacidosis, with decompensation of diabetes mellitus, another unfavorable pathological process develops - a violation of water-electrolyte metabolism. The starting point for such disorders is hyperglycemia, accompanied by an increase in osmotic pressure in the vascular bed. To maintain the isoosmolarity of the media, compensatory movement of fluid from cells and extracellular space into the vascular bed begins together with the main ions K 5+ 0 and Na 5+ 0. Due to the fact that hyperglycemia has exceeded the renal threshold at the same time, glucosuria develops and, as a consequence, polyuria ... This so-called osmotic diuresis leads to a massive loss of not only water, but also the main ions K and Na. As a result, high hyperglycemia and glucosuria lead, first, to severe cellular dehydration and loss of potassium ions, and then to general dehydration, that is, hypovolemia with a decrease in tissue and renal perfusion. Due to a sharp thickening of the blood (an increase in the number of erythrocytes, Hb, W), the viscosity of the blood noticeably increases, the rheological properties of the blood, transcapillary exchange are significantly impaired, circulatory and tissue hypoxia develops. Transport hypoxia in hyperglycemia can also be due to the increased formation of glycosylated (glucose-bound) HB, which loses its ability to bind and give oxygen to tissues. Considering that the concentration of glycosylated Hb in hyperglycemia with ketoacidosis reaches 30%, the oxygen transport function of the blood may decrease by one third in these patients.

Violation of tissue respiration is aggravated by acidosis, which complicates the dissociation of oxyhemoglobin and the transfer of oxygen from the blood to the tissue. Tissue hypoxia, in addition, leads to increased formation and accumulation of lactic acid, which is associated with the activation of anaerobic glycolysis and the subsequent development of metabolic acidosis.

Thus, in diabetic ketoacidosis, profound disturbances of carbohydrate, lipid, protein, water-electrolyte metabolism, acid-base state occur and, as a result of these shifts, decompensated ketoacidosis occurs. Accumulating in the body, keto acids and substrates of metabolic acidosis have a toxic effect on tissues, especially on the cells of the central nervous system. In this regard, the developing oxygen starvation, increasing the narcotic effect of keto acids, causes apathy, darkening of consciousness, stupor, and then loss of consciousness - a diabetic ketoacidotic coma develops.

Clinical picture

Ketoacidotic diabetic coma develops slowly, gradually. It takes about two days from the appearance of the first signs of ketoacidosis to the development of coma, and only in cases of acute purulent infection and acute disorders of cerebral or coronary circulation, a coma can develop within a day.

From a clinical point of view, 3 successively developing and replacing each other can be distinguished, depending on the beginning of the provision of resuscitation care, the stage of diabetic coma:

1. stage of moderate ketoacidosis;

2. stage of ketoacidotic precoma;

3. stage of ketoacidotic coma.

At the stage of the onset of moderate ketoacidosis, the clinical picture is accompanied by symptoms of acute and rapidly progressing decompensation of diabetes mellitus: dry mouth, thirst, frequent urination, polyuria appear. Already during this period, signs of intoxication are noted: general weakness, drowsiness, fatigue, loss of appetite, nausea, and the urge to vomit. Usually patients are conscious, correctly oriented in their surroundings. Skin the patient is dry, pronounced dryness of the tongue, mucous membrane of the lips and oral cavity is determined. Already at this stage, the smell of acetone is determined in the exhaled air, and experienced patients who have repeatedly experienced a state of decompensation are able to feel this smell themselves. On examination, an enlarged and painful liver, rapid pulse, muffled heart sounds, arrhythmia can be palpated.

Laboratory data: hyperglycemia up to 18–20 mmol / l; glucosuria, ketonemia up to 5.2 mmol / l. The acid-base state does not change significantly, but the content of hydrocarbonates decreases to 20–19 mmol / l. Water and electrolyte balance at this stage, it is characterized by a slight increase in potassium in the blood plasma, and a decrease in cellular K 5+ 0 is confirmed by ECG data - a decrease in the S-T interval, a biphasic T wave, which may be negative.

Treatment of patients at the stage of moderate ketoacidosis should be carried out in the conditions of the endocrinology department.

First of all, adjustments are made to the patient's diet: easily digestible carbohydrates, fruit juices are prescribed. The total amount of carbohydrates in the diet to suppress ketogenesis should be at least 60–70% of the daily diet (instead of 50%). In the diet, along with fruit juices, oat broths, cereals, jelly are introduced. If the patient has violated the treatment regimen, then it is necessary to conduct an explanatory conversation with him, in which the doctor must make sure that the patient has realized what serious consequences non-adherence to the diet, self-termination of insulin administration, and a change in the prescribed doses of antidiabetic drugs can lead to.

Correction of hyperglycemia is carried out with insulin preparations short acting (actramide, insulran, homorap, humulin R) fractional, at least 5-6 times a day intramuscularly or subcutaneously, based on a daily dose of at least 0.7 units / kg of actual weight under the control of blood glucose.

To eliminate acidosis, the patient is prescribed soda drink (2-3 liters per day), alkaline mineral waters (Borjomi). Sometimes, in cases of dehydration, it is necessary to inject an isotonic (0.9%) solution of sodium chloride under the control of hemoconcentration parameters.

The listed measures are usually sufficient to remove the patient from a state of moderate ketoacidosis. It is imperative to eliminate the cause that caused ketoacidosis, first of all, to identify and thoroughly treat the infection. Such measures help to prevent the transition of moderate ketoacidosis to ketoacidotic precoma.

If a patient with moderate ketoacidosis is not promptly started treatment, then metabolic disorders progress and the stage of ketoacidotic precoma sets in.

Clinically, this is manifested by the onset of a disorder of consciousness, which is preserved in patients, but they are sluggish, inhibited, drowsy, all questions are answered correctly, but in monosyllables, not immediately. the voice is monotonous, quiet, indistinct. Patients complain of severe weakness, dry mouth, thirst, nausea, frequent vomiting (sometimes "coffee grounds"), complete lack of appetite, headache, decreased visual acuity, frequent urge to urinate.

On examination, attention is drawn to deep, noisy breathing (breathing of Kusmaul) with a pungent smell of acetone in the exhaled air, a face with pointed features, sunken eyes, a pronounced diabetic blush on the cheeks, the lips of such patients are dry, with "stuck" in the corners mouth, tongue dry and coated with a brown coating.

Laboratory and functional research

In the general analysis of blood - neutrophilic leukocytosis with a shift to the left, accelerated ESR, In biochemical - hyperglycemia reaches values \u200b\u200bof 2-30 mmol / l and more, plasma osmolarity reaches 320 mosm / l, a significant disorder of electrolyte metabolism, which is manifested by hyponatremia (below 120 mmol / l), hypokalemia (less than 3.5 mmol / l). Protein catabolism, due to gluconeogenesis, is accompanied by an increase in blood urea and creatinine. Violation of acid base balance is manifested by the development of metabolic acidosis - blood pH ranges from 7.35 to 7.1.

In the urine - glucosuria, albuminuria, cylindruria, microhematuria, a large number of ketone bodies.

The pulse in such patients is frequent, low filling, often arrhythmic, blood pressure is reduced, heart sounds are deaf, arrhythmic.

It is very important to remember that, depending on the predominance of certain symptoms in the clinic, the ketoacedotic precoma, the following clinical variants are distinguished:

1. Abdominal variant - nausea, vomiting of "coffee grounds", intense pain in the abdomen with tension of the muscles of the anterior abdominal wall with symptoms of peritonism come to the fore. Along with leukocytosis, neutrophilia and a shift of the formula to the left, a similar picture can simulate the clinic of an "acute abdomen", for which sometimes surgical intervention, which sharply worsens the condition of patients. Sometimes, against the background of intestinal colic, diarrhea (sometimes mixed with blood), the diagnosis of acute gastroenterocolitis, food poisoning is mistakenly made.

2. Cardiovascular or collaptoid variant: symptoms of cardiovascular insufficiency predominate - cyanosis, shortness of breath, tachycardia, extrasystole or atrial fibrillation, decrease in blood pressure. Along with the ECG data - a decrease in the voltage of the teeth and interval S-Tthe listed phenomena can mimic the picture acute heart attack myocardium or thromboembolism of small branches of the pulmonary artery.

3. Renal option - characterized by dysuric phenomena with pronounced urinary syndrome - hypoisostenuria, proteinuria, hematuria, cylindruria. In connection with a decrease in glomerular filtration (a similar course is most often found in patients with diabetic nephropathy), mild glucosuria and ketonuria are noted, but azotemia, anuria and acute renal failure may develop.

4. Encephalopathic variant - the clinic resembles a picture of acute cerebrovascular accident and is caused by insufficient blood supply to the brain, hypoxia with asymmetry of reflexes and small-point hemorrhages in the fundus. Such symptomatology most often dominates in elderly people with cerebral atherosclerosis, and the diagnosis of hyperketonemic precoma is presented out of time.

If in a precomatose state the patient does not receive timely assistance, then a ketoacidotic coma develops within 1–2 hours.

Coma is the most severe degree of diabetic ketoacidosis, characterized primarily by complete loss of consciousness and areflexia. Breathing noisy Kussmaul, with a pungent smell of acetone in the exhaled air and in the room where the patient is. The tissue turgor is sharply reduced, the skin is dry and cold to the touch.

The pulse is quickened, threadlike, arrhythmic. Heart sounds are deaf, blood pressure is sharply reduced, in advanced cases it is not determined.

In laboratory data, glycemia usually exceeds 30 mmol / l, the content of urea and creatinine is sharply increased, hyperketonemia, hypokalemia, hyponatremia. There is marked metabolic acidosis, and a decrease in pH below 7.0 indicates a poor prognosis. In the urine - pronounced glucosuria, ketonuria.

Treatment of patients in a precomatose state and coma should be carried out in the intensive care unit (ICU).

Upon admission to the ICU ward, the patient undergoes puncture and catheterization of the main vein, since the administration of all infusion and pharmacological agents during decompensation of blood circulation should be carried out under the control of central venous pressure (CVP) and hourly urine output. Every 2 hours, it is necessary to determine blood glucose, urine glucose and ketone bodies, as well as hemoconcentration indicators - the number of erythrocytes in 1 mm 53 0, hemoglobin, hematocrit; every 4 hours - indicators of potassium, sodium, chlorides, urea, creatinine, acid-base state. When carrying out rehydration, it is necessary to determine the osmolality of the blood according to the formula:

2 (K 5+ 0+ Na 5+ 0 mmol / l) \u003d mosm / l

Usually, this figure does not exceed 300 mosm / l.

The treatment program for IT precomatose and coma consists of the following activities:

1. Elimination of insulin deficiency and normalization of carbohydrate metabolism.

2. Intensive rehydration of the body.

3. Restoration of electrolyte metabolism.

4. Correction of acid-base balance.

5. Normalization of the function of the cardiovascular system.

6. Elimination of the factors that caused the ketoacedotic coma.

Insulin therapy is carried out by administering short-acting insulin preparations (actrapid, monosuinsulin, humulin-R). Currently, an insulin therapy technique has been adopted, which is called the "low dose regimen". The prerequisite for the use of "low doses" was studies that proved that the blood insulin concentration of 10–20 μU / ml is sufficient to suppress lipolysis, gluconeogenesis and glycogenolysis, and the maximum transport of glucose and K into the cell and suppression of ketogenesis are achieved when the insulin content in the blood is 120 –200 μU / l. Therefore, the introduction of insulin at a dose of 6-10 U per hour creates the level in the blood necessary to suppress ketogenesis.

The insulin dose is determined depending on the initial level of glycemia (if the glycemia is above 30 mmol / l - insulin therapy should be started with a dose of 14-16 U / h, with a glycemia of 20-30 mmol / L - with a dose of 12-14 U / h, and with glycemia below 20 mmol / l - from 8-12 U / hour).

In practice, this is done as follows: in a bottle of 400 ml. isotonic NaCl solution is injected with a syringe with 40 units of simple insulin. To eliminate the adsorption of insulin by the elements of the system used for intravenous administration, add 10 ml of 10% albumin solution to the vial. After that, the working solution is placed in the "Infuzomat" drug dispenser and the required infusion rate is set, remembering that every 100 ml of the infused solution contains 10 units. insulin. The optimal rate of glycemic reduction is considered to be 3, -6.0 mmol / hour, depending on the initial level. After reaching a glycemic level of 16.8 mmol / l, when the diffusion of drugs into the cell begins, in parallel with the administration of insulin, it is necessary to use a 5% glucose solution, which helps to suppress ketogenesis. In addition, K 5+ 0, which participates in cellular reactions of oxidative phosphorylation, more easily penetrates into the cell with a glucose solution. To avoid hypoglycemia, when the blood glucose level reaches 11 mmol / L, intravenous insulin is stopped and insulin is prescribed subcutaneously, 4–6 units every 3-4 hours under glycemic control. The glycemic level is maintained within the range of 8-10 mmol / l.

This method of insulin therapy is considered the most effective and safe. The introduction of intravenous insulin at the beginning of treatment ensures its supply and circulation in conditions of dehydration, and small doses prevent a sharp decrease in the level of glycemia, which aggravates hypokalemia and the development of cerebral edema.

Rehydration

In ketoacidotic coma, the deficit of intra- and extracellular fluid is 10-15% of the body weight, or about 6-8 liters. If such a fluid deficit in the body is eliminated within 6–8 hours, then, as a rule, patients develop acute left ventricular failure, pulmonary edema, a rapid increase in hypoglycemia and cerebral edema. Against the background of such clinical picture patients may die. Therefore, it must be remembered that rehydration should be started simultaneously with insulin therapy, and the amount of isotonic solution injected in the first hour should be no more than 1.5 liters, during the second hour - 1 liter, during the 3rd and 4th hours - 0.5 liters each. Infusion therapy is mandatory under the control of hourly urine output, which should be at least 40-50 ml / hour. And only with oliguria (diuresis less than 30 ml / hour) and a high specific gravity (above 1030), an infusion of 500 ml can be added in the second hour. liquids, but with the mandatory appointment of saluretics (lasix). Thus, with a deficit of fluid in the body of 6–8 liters, rehydration is extended for 12–14 hours of the patient's stay in the intensive care unit.

If the patient's plasma osmolality is higher than 340 mosm / l, then the patient should be rehydrated with a 0.45% (hypotonic) solution of sodium chloride.

With persisting low hemodynamic parameters (BP), as well as with a decrease in the level of protein and its fractions during rehydration, it is advisable to pour 250-300 ml intravenously. 10% albumin solution.

An important component of the treatment of ketoacidosis and coma is the correction of electrolyte disturbances and, especially, potassium deficiency. The decrease in potassium in these conditions is more than 300 mmol. Hypokalemia is very dangerous, since, on the one hand, it causes a disturbance in the rhythm of the heart, a deficit of energy, and on the other, atony of the stomach and intestines up to paralytic ileus. It should be noted that with severe dehydration, the serum K content is sharply reduced, therefore hypokalemia is judged by a sharp decrease in it in the cell (erythrocytes - the normal K level in them is 79–96 mmol / l).

Rehydration therapy and a decrease in blood glucose usually promotes the return of potassium to the cell, and in the course of further treatment we always encounter plasma hypokalemia, which must be compensated and maintained at a level of 4-5 mmol / L.

That is why K compensation is carried out at a blood glucose level of 16.5–16.8 mmol / l, ie, when diffusion into the cell begins. But if, upon admission to the hospital, the K level is reduced (below 3.5 mmol / l), its compensation begins immediately, along with insulin therapy and rehydration. The rate of K administration is determined by the initial serum K level.

1. below 3.0 mmol / l - the initial dose of K administered by intravenous drip should be 39–40 mmol / hour;

2. 3.0–4.0 mmol / l - the amount of K injected at the beginning should be up to 26 mmol / hour;

3. 5.0–5.5 mmol / l - IV administration of K is started later only if it decreases during treatment;

4. at 6.0 mmol / l and more - infusion of K is not performed, because patients with diabetic nephropathy and renal failure are extremely sensitive to hyperkalemia. Contraindication to the administration of potassium is olgoanuria and anuria.

When preparing a working solution of chloride K, it should be remembered that 1.0 g of dry matter KC1 contains 13.4 mmol K. The patient should be injected intravenously with no more than 2% solution (i.e., 100 ml of 2% KC1 should contain 26 , 8 mmol K) in order to prevent aseptic phlebitis and sharp pain along the veins.

Recovery of acid base balance begins literally from the first minutes of treatment for a precomatose state and coma, thanks to the ongoing insulin therapy and rehydration. The restoration of fluid volume triggers physiological buffer systems, in particular, the ability of the kidneys to reabsorb bicarbonates is restored. Insulin suppresses ketogenesis and thus decreases the concentration of hydrogen ions in the blood. However, in some cases, when the blood pH drops below 7.0, the question arises of correcting the acid base balance by introducing sodium bicarbonate.

It must be remembered that even significantly pronounced phenomena of acidosis in the periphery are not accompanied by pronounced acidosis in cerebrospinal fluid and the central nervous system, due to the protective and adaptive mechanisms, attempts to correct plasma acidosis with a solution of sodium bicarbonate lead to the rapid development of central nervous system acidosis and a sharp deterioration in the patient's condition.

This paradoxical phenomenon is explained by the fact that the introduction of Na bicarbonate is accompanied by an increase in the blood plasma of HCO3-, which diffuses with difficulty through the blood-brain barrier into the extracellular space of the brain, while CO2 molecules penetrate there very easily, increasing the content of H2CO3 in the cerebrospinal fluid. As a result of these phenomena, there is a rapid decrease in the pH of the cerebrospinal and extracellular fluid of the brain, inhibition of the functions of the central nervous system in connection with the development of cerebral edema.

Taking into account the side effects of acidosis therapy with sodium bicarbonate, strict criteria for its use in these conditions have been developed. It should be noted that when controlling acid-base balance, it is necessary to pay attention not only to pH indicators, but also to pCO2, pO2, SpO2, BE.

РСО 2 - partial pressure of carbon dioxide in blood;

PO 2 is the partial pressure of oxygen in the blood;

SрО 2 - saturation of hemoglobin with oxygen;

BE - deficiency of bases.

Only after the correction of hypoxia and hypercapnia with humidified oxygen and a decrease in the pH value below 7.0 against this background, it is possible to introduce 4% Na bicarbonate at the rate of 2.5 ml per 1 kg of body weight intravenously drip, slowly with an additional simultaneous increase in K at the rate of 0 , 2 g of dry matter KC1 per 1 kg of mass in 1 liter of liquid once.

Trisamine has been successfully used to correct acid base balance in coma. When administered intravenously, it reduces the concentration of hydrogen ions, increases the alkaline reserve of the blood, eliminating acidosis, but, unlike Na bicarbonate, does not increase the content of CO2 in the blood and has a hypoglycemic effect. Prescribe it intravenously drip at a rate of 20 drops per minute, 500 ml during the day.

Correction of cardiovascular disorders begins from the moment of rehydration and restoration of fluid loss in the body. In case of persistent hypotension, it is recommended to administer dopamine intravenously in a drip dose of 60.0–80.0 mg in isotonic NaCl solution.

Taking into account the pronounced tendency of patients in a precomatose state and in a coma to hypercoagulation and the development of DIC, it is recommended to administer 5000 IU of heparin intravenously after 6 hours under the control of a coagulogram.

In some cases, the elimination of the etiological factors that caused the ketoacidotic coma contributes to its fastest relief. it antibacterial therapy in the presence of infectious and inflammatory diseases, treatment of hypovolemic shock, acute left ventricular failure; oxygen therapy and mechanical ventilation for severe acute respiratory failure.

It should be noted that prognostically unfavorable signs during a ketoacidotic coma can be:

1. arterial hypotension, not amenable to correction with adequate rehydration and IT disorders of the cardiovascular and respiratory systems;

2. a decrease in urine output to 30 ml / h and below, despite its stimulation;

3. increasing cerebral edema, despite the ongoing dosed dehydration with solution of aminophylline, furosemide.

At the same time, it should be emphasized that over the past 10 years, as a result of the introduction into practice of insulin therapy with "small doses", adequate rehydration and correction of hypokalemia and acid base balance, limitation of indications for intravenous infusion of sodium bicarbonate, intensive therapy of hemodynamic and respiratory disorders, mortality from ketoacidotic coma decreased by more than 3 times.

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From the book An irreplaceable book for a diabetic. Everything you need to know about diabetes author Irina Stanislavovna Pigulevskaya

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5944 0

It is now generally accepted that the life expectancy of patients diabetes mellitus (SD) determine, first of all, late vascular complications of the disease. At the same time a serious threat for their life are acute complications of the disease - hyperglycemic (ketoacidotic, hyperosmolar, hyperlactacidemic) and hypoglycemic coma.

So, today, mortality from diabetic ketoacidotic coma is 5-14%, hyperosmolar coma - 40-60%, lactacidemic coma - 30-90%, hypoglycemic coma - 3-4%. And this despite the fact that advances in the treatment of diabetes, its timely diagnosis, education of patients, and the introduction of self-control principles into practice have led to a decrease in the incidence of coma and mortality from them. Especially the risk of death increases in elderly patients and in the presence of severe intercurrent diseases, which act as factors provoking these complications.

Reduce the incidence of death during development acute complications Diabetes mellitus to a large extent allows timely diagnosis and adequate urgent Care... In this regard, a doctor of any specialty should be familiar with the peculiarities of the development of acute complications of diabetes mellitus, their clinic, diagnostics, modern therapeutic tactics, because in practice one often has to deal with manifestations of diabetes decompensation, including acute diabetes.

Of the acute complications of diabetes, the most common are hypoglycemic conditions and coma. These are life-threatening conditions that develop when blood glucose levels drop rapidly. About 5-10% of people with diabetes mellitus have at least one severe hypoglycemia per year.

Hyperglycemic (diabetic) coma can develop in 3 variants:

1. Ketoacidotic coma.
2. Hyperosmolar coma.
3. Hyperlactacidemic (lactic acid) coma.

Besides the fact that these comas have their own clinical features, they differ in laboratory signs: the degree of hyperglycemia, the presence or absence of hyperketonemia, hyperlactacidemia, the depth of violations of the water-electrolyte balance and acid-base balance. In the formation of a particular type of diabetic coma, a significant role is assigned to the provoking factor, the age of patients, intercurrent diseases, but the type of diabetes mellitus, more precisely, the presence of absolute or relative insulin deficiency, is of decisive importance in this.

Ketoacidotic coma, the most common variant among diabetic coma, is more likely to complicate the course type 1 diabetes mellitus (SD-1), although it can be diagnosed with type 2 diabetes mellitus (SD-2)... Thus, in Russia, the incidence of diabetic ketoacidosis and ketoacidotic coma with T1DM is 0.2-0.26, and with T2DM - 0.07 cases per patient per year. Up to 20-30% of patients with DM-1 are admitted to hospitals in a state of diabetic ketoacidosis or coma at the onset of the disease.

Other types of diabetic coma (hyperosmolar, hyperlactacidemic) are about 10 times less common compared to ketoacidotic coma, but even with correct treatment accompanied by a high frequency of deaths. They develop mainly in people over 50 years old with diabetes mellitus-2.

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) - acute metabolic decompensation threatening the life of patients with diabetes, caused by progressive insulin deficiency, manifested by a sharp increase in glucose levels and the concentration of ketone bodies in the blood, the development of metabolic acidosis.

The pathophysiological essence of it is progressive insulin deficiency, which causes severe disturbances in all types of metabolism, the combination of which determines the severity general condition, the appearance and progression of functional and structural changes in the cardiovascular system, kidneys, liver, central nervous system (CNS) with the suppression of consciousness until its complete loss - coma, which may be incompatible with life. Thus, more than 16% of patients with type 1 diabetes mellitus die precisely from ketoacidosis or ketoacidotic coma.

Metabolic disorders underlying diabetic decompensation with an outcome in ketoacidosis can have varying degrees of severity, and this is determined, first of all, by the stage at which the patient seeks medical help.

The first stage of metabolic disorders, when the content of glucose in the blood and urine increases significantly and the patient develops clinical symptoms hyperglycemia and glucosuria, is defined as the stage of metabolic decompensation.

Then, with the progression of decompensation of diabetes mellitus, the development of the so-called ketoacidotic cycle occurs. The first stage of this cycle - ketosis (compensated ketoacidosis), when, with the progression of metabolic disorders, the concentration of acetone bodies in the blood increases and acetonuria appears. Signs of intoxication at this stage are usually absent or minimal.

Stage two - ketoacidosis (decompensated acidosis), when metabolic disorders increase so much that symptoms of severe intoxication appear with depression of consciousness in the form of stupidity or confusion and a characteristic clinical picture with pronounced laboratory changes: a sharply positive reaction to acetone in urine, high blood glucose, etc. ...

Third stage - precoma (severe ketoacidosis), which differs from the previous stage in more pronounced depression of consciousness (stupor), more severe clinical and laboratory disorders, more severe intoxication.

Fourth stage - the coma itself - completes the ketoacidotic cycle. This stage is characterized by an extreme degree of disorders of all types of exchange with loss of consciousness and a threat to life.

In practice, it is often difficult to distinguish between the stages of the ketoacidotic cycle, especially the last two stages, and therefore in the literature sometimes pronounced acute metabolic disorders with high glycemia, ketonuria, acidosis, regardless of the degree of impairment of consciousness, are combined with the term: "diabetic ketoacidosis".

Etiology and pathogenesis

The most common cause of ketoacidosis in diabetic patients is a violation of the treatment regimen: skipping or unauthorized cancellation of insulin injections. Especially often, patients make this mistake in the absence of appetite, the appearance of nausea, vomiting, and an increase in body temperature.

In patients with type 2 diabetes mellitus, it is often found out that there are many months and even many years of interruption in taking tableted sugar-lowering drugs. The second most common cause of ketoacidosis is acute inflammatory diseases or exacerbation of chronic as well as infectious diseases. There is often a combination of both of these reasons.

One of the common causes of ketoacidosis is an untimely visit to a doctor with the manifestation of CD-1. In 20% of patients at the onset of type 1 diabetes, there is a picture of ketoacidosis. Among the common causes of diabetic decompensation are diet disorders, alcohol abuse, mistakes in administering a dose of insulin.

In principle, any diseases and conditions accompanied by a sharp increase in the concentration of counterinsulin hormones can lead to decompensation of diabetes mellitus and the development of ketoacidosis. Among them, it should be noted operations, injuries, the 2nd half of pregnancy, vascular accidents (myocardial infarction, stroke), the use of insulin antagonist drugs (glucocorticoids, diuretics, sex hormones) and others - these are less common causes of ketoacidosis.

In the pathogenesis of ketoacidosis (Fig. 16.1), the leading role is played by a sharp insulin deficiency, leading to a decrease in glucose utilization by insulin-dependent tissues and, as a result, to hyperglycemia. Energy "hunger" in these tissues is the reason for a sharp increase in the blood of all counterinsulin hormones (glucagon, cortisol, adrenaline, adrenocorticotropic hormone -ACTH, growth hormone - STG), under the influence of which gluconeogenesis, glycogenolysis, proteolysis and lipolysis are stimulated. The activation of gluconeogenesis as a result of insulin deficiency leads to overproduction of glucose by the liver and an increased supply of it into the blood.

Figure 16.1. Pathogenesis of ketoacidotic coma

Thus, gluconeogenesis and impaired glucose utilization by tissues are the most important causes of rapidly increasing hyperglycemia. At the same time, the accumulation of glucose in the blood has a number of negative consequences. First, hyperglycemia significantly increases plasma osmolarity. Due to this, the intracellular fluid begins to move into the vascular bed, which ultimately leads to severe cellular dehydration and a decrease in the content of electrolytes in the cell, primarily potassium ions.

Secondly, hyperglycemia, as soon as the renal threshold of permeability for glucose is exceeded, causes glucosuria, and the latter - the so-called osmotic diuresis, when, due to the high osmolarity of primary urine, the renal tubules cease to reabsorb water and electrolytes released with it. These disorders, lasting for hours and days, eventually cause severe general dehydration with electrolyte disturbances, hypovolemia with significant thickening of the blood, an increase in its viscosity and the ability to thrombus. Dehydration and hypovolemia are the cause of a decrease in cerebral, renal, peripheral blood flow and, thus, severe hypoxia of all tissues.

A decrease in renal perfusion and, consequently, glomerular filtration leads to the development of oligo- and anuria, causing a terminal rapid rise in blood glucose concentration. Hypoxia of peripheral tissues promotes the activation of the processes of anaerobic glycolysis in them and a gradual increase in the level of lactate. The relative deficiency of lactate dehydrogenase with insulin deficiency and the impossibility of complete utilization of lactate in the measles cycle are the cause of lactic acidosis in the case of decompensation of type 1 diabetes mellitus.

The second direction of metabolic disorders caused by insulin deficiency is associated with excessive accumulation of ketone bodies in the blood. The activation of lipolysis in adipose tissue under the influence of counterinsulin hormones leads to a sharp increase in the concentration free fatty acids (FFA) in the blood and their increased supply to the liver. An increase in the oxidation of FFA as the main source of energy in conditions of insulin deficiency is the reason for the accumulation of by-products of their decay - "ketone bodies" (acetone, acetoacetic and B-hydroxybutyric acids).

The rapid increase in the concentration of ketone bodies in the blood is due not only to their increased production, but also to a decrease in their peripheral utilization and urinary excretion due to oliguria developing against the background of dehydration. Acetoacetic and B-hydroxybutyric acids dissociate to form free hydrogen ions. Under conditions of decompensation of diabetes mellitus, the production of ketone bodies and the formation of hydrogen ions exceed the buffering capacity of tissues and body fluids, which causes the development of severe metabolic acidosis, clinically manifested by toxic Kussmaul respiration due to irritation of the respiratory center with acidic products, abdominal syndrome.

Thus, hyperglycemia with a complex of 82% electrolyte disorders and ketoacidosis are the leading metabolic syndromes that underlie the pathogenesis of ketoacidotic coma. On the basis of these syndromes, many secondary metabolic, organ and systemic disorders develop, which determine the severity of the condition and the prognosis of the patient. An important component of metabolic disorders in diabetic ketoacidosis is hypokalemia, which causes cardiac (tachycardia, decreased myocardial contractility, decreased or negative T wave on the ECG), gastrointestinal (decreased peristalsis, spastic contraction of smooth muscles) and other disorders, as well as contributing to edema of the substance brain.

In addition to potassiumuria, intracellular hypokalemia in ketoacidosis is caused by a decrease in the activity of K-ATPase, as well as acidosis, in which potassium ions are exchanged for hydrogen ions inside the cell. At the same time, the initial values \u200b\u200bof potassium in conditions of thickening of blood and impaired renal excretion in oliguria can be normal and even increased. However, already after 2-3 hours from the start of therapy against the background of insulin administration, rehydration, a reduced potassium content in the blood plasma is revealed.

It is most sensitive to the listed numerous severe metabolic disorders of the central nervous system. The disturbance in ketoacidosis of consciousness progresses as metabolic disorders increase and has a multi-causal nature. Hyperosmolarity and the associated dehydration of brain cells are of great importance in suppressing consciousness. In addition, severe cerebral hypoxia, caused by a decrease in cerebral blood flow, an increase in glycosylated hemoglobin, a decrease in 2,3 diphosphoglycerate in erythrocytes, as well as intoxication, hypokalemia, and disseminated intravascular coagulation, play an important role in this.

Metabolic acidosis also contributes to the process of depression of consciousness, however, it is the direct cause of the development of coma only if acidosis occurs in the central nervous system. The fact is that physiological mechanisms such as respiratory hyperventilation, a decrease in cerebral blood flow, and the buffering properties of nerve cells can ensure the stability of the cerebral acid-base balance for a long time even with a significant decrease in blood plasma pH. Thus, the violation of the acid-base balance in the central nervous system occurs last, with a strong decrease in blood pH, after the depletion of such compensatory mechanisms as hyperventilation and the buffering properties of cerebrospinal fluid and neurons.

Clinic

Ketoacidotic coma - this is the final stage of the so-called ketoacidotic cycle, the development of which is preceded by the stages of ketosis, ketoacidosis, precoma. Each of the subsequent stages differs from the previous one by the aggravation of metabolic disorders, an increase in the severity of clinical manifestations, the degree of depression of consciousness and, thus, the severity of the general condition of the patient.

A ketoacidotic coma develops gradually, usually within a few days, however, in the presence of a severe concomitant infection, the timing for its development may be shorter - 12-24 hours.

Early signs of the onset of DM decompensation that characterize the state of ketosis are clinical symptoms such as increasing dryness of the mucous membranes and skin, thirst, polyuria, weakness, decreased appetite, weight loss, headache, drowsiness, slight acetone odor in exhaled air. Sometimes diabetic patients may not have pronounced changes in general well-being (even with moderate signs of hyperglycemia), and the basis for establishing ketosis in this case may be a positive reaction to acetone in urine (ketonuria).

In the absence medical care In such patients, metabolic disorders will progress, the clinical signs described above are complemented by symptoms of intoxication and acidosis, which is defined as the stage of ketoacidosis.

Symptoms of general dehydration expressed at this stage are manifested by dryness of the mucous membranes, tongue, skin, decreased muscle tone and skin turgor, a tendency to arterial hypotension, tachycardia, oliguria, signs of blood thickening (increased hematocrit, leukocytosis, erythremia). The growing intoxication caused by ketoacidosis leads to nausea and vomiting in most patients; the latter becomes more frequent with every hour, acquires an indomitable character, aggravating the general dehydration. Vomit in ketoacidosis often has a bloody brown tint, which is incorrectly regarded by doctors as vomit of "coffee grounds".

As ketoacidosis grows, breathing becomes frequent, noisy and deep (Kussmaul breathing), while the smell of acetone in the exhaled air becomes distinct. Characterized by the appearance at this stage of a diabetic blush on the face due to paretic expansion of the capillaries. In most patients, already at this stage, abdominal disorders are noted, resembling a picture of an "acute abdomen": abdominal pain of varying intensity, more often of a diffuse nature, muscle tension of the abdominal wall (pseudoperitonitis).

The origin of these symptoms is associated with irritation of the peritoneum, "solar" plexus with ketone bodies, dehydration, electrolyte disturbances, intestinal paresis and small punctate hemorrhages in the peritoneum. Abdominal pain and muscle defense in combination with nausea, vomiting, changes in the general blood count (leukocytosis) in ketoacidosis can be mistaken for an acute surgical pathology and cause (with a threat to the patient's life) medical error.

Oppression of consciousness at the stage of ketoacidosis is characterized by stunnedness, rapid exhaustion, indifference to the environment, confusion of consciousness.

Precoma differs from the previous stage in a more pronounced depression of consciousness, as well as in more striking symptoms of dehydration and intoxication. Under the influence of increasing metabolic disturbances, stupor is replaced by stupor. Clinically, stupor is manifested by deep sleep or unresponsiveness. The final stage of the increasing depression of the central nervous system is a coma, characterized by a complete absence of consciousness. An objective examination reveals deep, frequent and noisy breathing with a pungent smell of acetone in the exhaled air. The face is usually pale, with a blush on the cheeks (rubeosis). Signs of dehydration are expressed (in severe cases, due to dehydration, patients lose up to 10-12% of body weight).

The skin and visible mucous membranes are dry, the tongue is dry, coated with a brown coating. Turgor of tissues and tone of eyeballs and muscles are sharply reduced. Frequent, weakly filling pulse, decreased blood pressure, oliguria or anuria. Sensitivity and reflexes, depending on the depth of the coma, are reduced or drop out. The pupils are usually evenly constricted. The liver, as a rule, protrudes significantly from under the edge of the costal arch.

Depending on the predominance of any of the following systems in the clinical picture of the lesion: cardiovascular, digestive, kidney, central nervous system - four clinical forms ketoacidotic coma:

1. Cardiovascular, when the leading clinical manifestation is severe collapse with a significant decrease in arterial and venous pressure. Especially often with this type of coma, thrombosis of the coronary (with the development of myocardial infarction), pulmonary vessels, vessels of the lower extremities and other organs develops.
2. Gastrointestinal, when repeated vomiting, intense abdominal pain with muscle tension of the anterior abdominal wall and symptoms of peritoneal irritation, along with neutrophilic leukocytosis, mimic a wide variety of acute surgical gastrointestinal pathologies: acute appendicitis, cholecystitis, pancreatitis, intestinal obstruction, thrombosis of mesenteric vessels.
3. Renal, characterized by a symptom complex of acute renal failure. At the same time, hyperazotemia, changes in the general analysis of urine (proteinuria, cylindruria, etc.) are expressed, and there is also anuria.
4. Encephalopathic, usually observed in elderly people suffering from cerebral atherosclerosis.

Chronic cerebrovascular insufficiency is aggravated by dehydration, impaired microcirculation, acidosis. This is manifested not only by general cerebral symptoms, but also by symptoms of focal brain damage: hemiparesis, asymmetry of reflexes, and the appearance of pyramidal symptoms. In this situation, it can be very difficult to explain unequivocally whether the coma caused the development of focal cerebral symptoms or the stroke caused ketoacidosis.

Diagnosis and differential diagnosis

The diagnosis of ketoacidosis and ketoacidotic coma can be established already at the prehospital stage on the basis of the clinical picture, information about the gradual deterioration of the patient's condition, and the identification of the causative factor. In the event that it is known that a patient has diabetes mellitus, the diagnosis of ketoacidosis and ketoacidotic coma is not difficult. In the case of manifestation of diabetes immediately in a state of ketoacidosis or coma, first of all, one should focus on the presence of severe dehydration, signs of acidosis (Kussmaul breathing) and significant loss of body weight within a short period of time.

In addition, the smell of acetone in the exhaled air should lead the doctor to think that the patient has precisely ketoacidosis as the cause of the existing metabolic acidosis. Metabolic acidosis can cause lactic acidosis, uremia, alcohol intoxication, poisoning with acids, methanol, ethylene glycol, paraldehyde, salicylates, but these conditions are not accompanied by such pronounced dehydration and significant loss of body weight.

A patient with a diagnosis of ketoacidosis or ketoacidotic coma is subject to immediate transportation to the endocrinological, therapeutic, and intensive care unit. Verification of the diagnosis of hyperglycemic coma and differential diagnosis of its individual pathogenetic forms are possible only on the basis of laboratory research followed by a comparative analysis of the data obtained and clinical symptoms.

Severe hyperglycemia (20-35 mmol / L or more), hyperketonemia (from 3.4 to 100 mmol / L or more) and its indirect confirmation - acetonuria are of major importance in the diagnosis of ketoacidotic coma.

The diagnosis of ketoacidotic coma is confirmed by a decrease in blood pH to 7.2 and below (normally 7.34-7.36), a sharp decrease in the alkaline blood reserve (up to 5% by volume), the level of standard bicarbonate, a moderate increase in plasma osmolarity, often increased content blood urea. As a rule, neutrophilic leukocytosis, an increase in the number of erythrocytes and hemoglobin due to blood clots are detected. Hypokalemia is usually recorded several hours after the start of infusion therapy.

Table 16.1. Differential diagnosis of coma in patients with diabetes

Differential diagnostic criteria different types hyperglycemic coma and hypoglycemic coma are presented in table. 16.1.

Algorithm of examination for ketoacidotic coma:

• glycemia on admission and in dynamics;
• acid-base state (KSC)
• the content of lactate, ketone bodies;
• electrolytes (K, Na);
• creatinine, urea nitrogen;
• indicators of the blood coagulation system;
• glucosuria, ketonuria;
• general analysis of blood and urine;
• R-graphy of the lungs;
• effective plasma osmolarity \u003d 2 (Na + K (mol / l)) + blood glucose (mol / l) - normal value \u003d 297 + 2 mOsm / l;
• central venous pressure (CVP)

The dynamics are controlled by:

• blood glucose - hourly as glycemia reaches 13-14 mmol / l, and then once every 3 hours;
• potassium, sodium in plasma - 2 times a day;
• hematocrit, gas analysis and blood pH 1-2 times a day until acid base balance normalizes;
• urine analysis for acetone 2 times a day in the first two days, then 1 time a day;
• general analysis of blood and urine 1 time in 2-3 days;
• ECG at least 1 time per day;
• CVP every 2 hours, with stabilization of the state - every 3 hours

Treatment

Ketoacidosis, especially ketoacidotic coma, is an indication for urgent hospitalization in the intensive care unit or in the intensive care unit. At the prehospital stage, they are usually limited to symptomatic agents that provide an increase in cardiac and vascular tone.

1. Insulin therapy.
2. Rehydration
3. Correction of electrolyte disorders.
4. Elimination of acidosis.
5. Treatment of concomitant diseases.

Insulin therapy - pathogenetic type of treatment aimed at interrupting severe catabolic processes caused by insulin deficiency. When withdrawing from ketoacidosis and ketoacidotic coma, only short-acting insulins are used. It has been proven that continuous infusion of 4-10 units. insulin per hour (on average 6 units) allows you to maintain its optimal level in the blood serum of 50-100 mcU / ml, thereby creating conditions for the restoration of disturbed metabolism. Insulin therapy using these dosages is called a "low dose" regimen.

Insulin in diabetic ketoacidosis and coma is recommended to be administered intravenously as a long-term infusion, and the most optimal method of such administration is infusion using a perfuser (infusion pump) at a rate of 4-8 units. in hour. The initial dose is 10-14 units. injected intravenously. The mixture for infusion with a perfuser is prepared as follows: for 50 units. short-acting insulin is added 2 ml of a 20% solution of albumin (to prevent the adsorption of insulin on plastic) and the total volume is brought to 50 ml of a 0.9% sodium chloride solution. In the absence of a perfuser, insulin can be injected with a syringe every hour into the "rubber band" of the infusion system. The sugar-lowering effect of this way of injected insulin lasts up to 1 hour.

Another method of intravenous administration of insulin can be used:a mixture of 10 units. insulin for every 100 ml of 0.9% sodium chloride solution (without albumin) is administered at a rate of 60 ml per hour, however, it is believed that with this approach it is difficult to control the administered dose of insulin due to its adsorption on the tubes of the infusion system.

Correction of the intravenously administered dose of insulin is carried out in accordance with the dynamics of glycemia, which should be investigated hourly as its level decreases to 13-14 mmol / l, and then once every 3 hours. If in the first 2-3 hours glycemia does not decrease, then the next dose of insulin is doubled. The glycemic level should not be reduced faster than 5.5 mmol / L per hour (the average rate of glycemic decline is 3-5 mmol / L per hour). A more rapid drop in glycemia threatens the development of cerebral edema. On the first day, it is not recommended to lower blood glucose below 13-14 mmol / l. When this level is reached, it is necessary to prescribe an intravenous infusion of 5-10% glucose solution, reduce the dose of insulin by half - to 3-4 units. intravenously in a "rubber band" for every 20 g of injected glucose (200.0 10% solution).

The introduction of glucose is carried out with the aim of preventing hypoglycemia, maintaining plasma osmolarity, as well as inhibiting ketogenesis. As the acid base balance normalizes (mild ketonuria can persist for several days) and the recovery of consciousness, the patient should be transferred to the subcutaneous administration of 4-6 units of insulin. every 2 hours, and then 6-8 units. every 4 hours. In the absence of ketoacidosis on the 2-3rd day of treatment, the patient can be transferred to a 5-6-time administration of short-acting insulin, and later on to conventional combination therapy.

Rehydration plays an exceptional role in the treatment of diabetic ketoacidosis and coma, given the important role of dehydration in the chain of metabolic disorders. Fluid deficiency in this condition reaches 10-12% of body weight.

The volume of lost fluid is replenished with 0.9% sodium chloride solution and 5-10% glucose solution. With an increase in the content of sodium in the blood serum (150 meq / l or more), indicating hyperosmolarity of the plasma, it is recommended to start rehydration with a hypotonic 0.45% sodium chloride solution in a volume of 500 ml. Termination of infusion therapy is possible only when full recovery consciousness, lack of nausea, vomiting and self-intake of fluid by the patient.

So, the drug of choice for initial rehydration is 0.9% sodium chloride solution. The rehydration rate is: In the 1st hour - 1 liter. At the 2nd and 3rd hour - 500 ml. In subsequent hours - no more than 300 ml.

The rate of rehydration is adjusted depending on the central venous pressure (CVP):

• with CVP less than 4 cm of water. Art. - 1 liter per hour;
• with CVP from 5 to 12 cm of water. Art. - 0.5 l per hour;
• with CVP more than 12 cm of water. Art. - 250-300 ml per hour

.
If CVP is not controlled, fluid overload can lead to pulmonary edema. The volume of liquid injected for 1 hour at the initial pronounced dehydration should not exceed the level of 500-1000 ml of the volume of an hour's diuresis.

As blood glucose decreases to 13-14 mmol / L, saline sodium chloride solution is replaced with 5-10% glucose solution at the rate of administration described above. The appointment of glucose at this stage is dictated by a number of reasons, among which the main one is the maintenance of blood osmolarity. A rapid decrease in glycemia and other highly osmolar blood components against the background of rehydration often causes a rapid decrease in plasma osmolarity. In this case, the osmolarity of the cerebrospinal fluid is higher than that of the plasma, since the exchange between these fluids is rather slow. In this regard, fluid from the bloodstream rushes into the cerebrospinal fluid and is the cause of the development of cerebral edema.

In addition, the administration of glucose together with insulin leads to a gradual restoration of glycogen stores in the liver, a decrease in the activity of gluconeogenesis and ketogenesis.

Restoring electrolyte balance

A wide variety of electrolyte metabolism disorders are caused by acute decompensation of diabetes, however, the most dangerous of them is a deficiency in the body of potassium, sometimes reaching 25-75 g. Even with an initially normal value of potassium in the blood, it should be expected to decrease due to dilution of the blood concentration and normalization of transport into the cell. against the background of insulin therapy and rehydration. That is why, provided that diuresis is maintained, from the very beginning of insulin therapy, even with normal potassium, a continuous infusion of potassium chloride is started, trying to maintain its serum level in the range from 4 to 5 mmol / l (Table 15).

• less than 3 mmol / l - 3 g (dry matter) KC1 per hour;
• 3 - 4 mmol / l - 2 g of KC1 per hour;
• 4 - 5 mmol / l - 1.5 g KC1 per hour;
• 6 mmol / l or more - potassium administration is stopped.

After excretion from a ketoacidotic coma, potassium preparations should be administered orally for 5-7 days.

Table 15. The rate of potassium administration depending on the initial level of K + and blood pH

In addition to disorders of potassium metabolism, disturbances in the metabolism of phosphorus and magnesium are also noted during the development of ketoacidotic coma, but the need for additional correction of these electrolyte disorders remains controversial.

Recovery of acid-base state

The most important link in metabolic disorders in ketoacidotic coma - metabolic acidosis, which develops as a result of enhanced ketogenesis in the liver in conditions of insulin deficiency. It should be noted that the severity of acidosis in ketoacidotic coma in different tissues of the body is not the same. So, due to the peculiarities of the buffer mechanisms of the central nervous system, the pH of the cerebrospinal fluid remains normal for a long time even with pronounced acidosis in the blood. Based on this, it is currently strongly recommended to change the approaches to the correction of acidosis when removing from a ketoacidotic coma and especially to limit the indications for the use of sodium bicarbonate due to the risk of complications associated with the introduction of this drug.

It has been proven that the elimination of acidosis and the restoration of blood acid base balance begins already during the administration of insulin and rehydration. The restoration of fluid volume triggers physiological buffer systems, namely, the ability of the kidneys to reabsorb bicarbonates is restored. In turn, the use of insulin suppresses ketogenesis and thereby reduces the concentration of hydrogen ions in the blood.

The introduction of sodium bicarbonate is associated with the risk of complications, among which it is necessary to highlight the development of peripheral alkalosis, aggravation of the existing hypokalemia, and increased peripheral and central hypoxia. This is due to the fact that the rapid restoration of pH suppresses the synthesis and activity of 2,3-diphosphoglycerate of erythrocytes, the concentration of which is already reduced against the background of ketoacidosis. The result of a decrease in 2,3-diphosphoglycerate is a violation of the dissociation of oxyhemoglobin and an aggravation of hypoxia.

In addition, the correction of acidosis with the help of intravenous sodium bicarbonate can lead to the development of "paradoxical" acidosis in the central nervous system, and subsequently, cerebral edema. This paradoxical phenomenon is explained by the fact that the introduction of sodium bicarbonate is accompanied not only by an increase in the content of HCO 3 ions in the plasma, but also by an increase in p CO 2. CO 2 penetrates the blood-brain barrier more easily than bicarbonate, leading to an increase in H 2 CO 3 in the cerebrospinal fluid, dissociation of the latter with the formation of hydrogen ions and, thus, to a decrease in the pH of the cerebrospinal and extracellular fluid of the brain, which is an additional factor in the suppression of the central nervous system.

This is why the indications for the use of baking soda are now significantly narrowed. Its intravenous administration is permissible under the control of blood gas composition, potassium and sodium levels, and only at blood pH below 7.0 and / or standard bicarbonate level below 5 mmol / l. A 4% sodium bicarbonate solution is used at the rate of 2.5 ml per 1 kg of body weight intravenously slowly at a rate of no more than 4 g per hour. With the introduction of sodium bicarbonate, a solution of potassium chloride is additionally injected intravenously at the rate of 1.5 - 2 g of dry matter.

If it is not possible to determine blood acid base balance, then the introduction of alkaline solutions "blindly" can be more harmful than potential benefit.

There is no need to prescribe to patients a solution of baking soda by mouth, through an enema or in the exclusive use of alkaline mineral water, which was widely practiced earlier. If the patient is able to drink, then ordinary water, unsweetened tea, etc. are recommended.

Non-specific therapeutic measures when withdrawing from diabetic ketoacidosis and coma include:

1. Purpose antibacterial drugs (AB) wide range actions that do not have a nephrotoxic effect for the treatment or prevention of inflammatory diseases.
2. The use of small doses of heparin (5000 IU intravenously 2 times a day on the first day) for the prevention of thrombosis, mainly in patients old age, with a deep coma, with severe hyperosmolarity - more than 380 mosmol / l.
3. With low blood pressure and other symptoms of shock, the use of cardiotonic, adrenomimetic drugs.
4. Oxygen therapy in case of insufficient respiratory function - pO 2 below 11 kPA (80 mm Hg).
5. Installation in the absence of consciousness of the gastric tube for constant aspiration of the contents.
6. Placement of urinary catheter for accurate hourly assessment of water balance.

Nutrition after excretion from a ketoacidotic coma

After the restoration of consciousness and the ability to swallow in the absence of nausea and vomiting, the patient should be prescribed a sparing diet with a sufficient amount of carbohydrates, a moderate amount of protein, rich in potassium and the exclusion of fats (cereals, mashed potatoes, bread, broth, omelet, diluted fruit juices without sugar). 1-2 days after the start of a meal in the absence of an exacerbation of gastrointestinal diseases, the patient can be transferred to a regular diet.

Complications of ketoacidosis therapy

Among the complications arising during the therapy of ketoacidosis, the greatest danger is cerebral edema, which in 90% of cases is fatal. In the study of the brain tissue of patients who died from cerebral edema when removed from a ketoacidotic coma, the presence of the so-called cellular or cytotoxic variant of cerebral edema was established, which is characterized by swelling of all cellular elements of the brain (neurons, glia) with a corresponding decrease in extracellular fluid.

Optimization of treatment methods when removing from a ketoacidotic coma has significantly reduced the incidence of this dangerous complication, but often cerebral edema occurs in cases of ideally conducted therapy. There are isolated reports of the development of cerebral edema even before the start of therapy. It is assumed that cerebral edema is associated with an increase in the production of sorbitol and fructose in brain cells due to the activation of the sorbitol pathway of glucose metabolism, as well as cerebral hypoxia, which reduces the activity of sodium-potassium ATPase in the cells of the central nervous system with the subsequent accumulation of sodium ions in them.

However, most common reason the occurrence of cerebral edema is considered a rapid decrease in plasma osmolarity and glycemic level against the background of the introduction of insulin and fluids. The introduction of sodium bicarbonate creates additional opportunities for the development of this complication. An imbalance between the pH of peripheral blood and cerebrospinal fluid increases the pressure of the latter and facilitates the transport of water from the intercellular space to brain cells, the osmolarity of which is increased.

Typically, cerebral edema develops within 4-6 hours from the start of therapy for ketoacidotic coma. With the patient's consciousness preserved, signs of incipient cerebral edema are deterioration of well-being, severe headache, dizziness, nausea, vomiting, visual disturbances, eyeball tension, instability of hemodynamic parameters, and increasing fever. As a rule, the listed symptoms appear after a period of improvement in well-being against the background of positive dynamics of laboratory parameters.

It is more difficult to suspect the onset of cerebral edema in unconscious patients. The absence of positive dynamics in the patient's consciousness with an improvement in glycemic values \u200b\u200bmay give reason to suspect cerebral edema, which will be clinically confirmed by a decrease or absence of pupil response to light, ophthalmoplegia and edema. optic nerve... Ultrasound encephalography and cT scan confirm this diagnosis.

For the treatment of cerebral edema, osmotic diuretics are prescribed in the form of an intravenous drip of mannitol solution at the rate of 1-2 g / kg. Following this, 80-120 mg of lasix and 10 ml of hypertonic sodium chloride solution are injected intravenously. The question of the use of glucocorticoids should be decided individually, giving preference to dexamethasone, taking into account its minimal mineralocorticoid properties. Cerebral hypothermia and active hyperventilation of the lungs are added to the ongoing therapeutic measures in order to reduce intracranial pressure due to the resulting vasoconstriction.

Other complications of ketoacidotic coma and its therapy include disseminated intravascular coagulation, pulmonary edema, acute cardiovascular failure, metabolic alkalosis, asphyxia due to aspiration of gastric contents.

Strict control over the parameters of hemodynamics, hemostasis, electrolytes, changes in osmolarity and neurological symptoms allows you to suspect the listed complications on early stages and take measures to eliminate them.

Subject table of contents "Thyrotoxic crisis. Acute adrenal insufficiency (adrenal crisis). Ketoacidotic coma.":
1. Thyrotoxic crisis. Causes (etiology) of thyrotoxic crisis. Pathogenesis of thyrotoxic crisis. Clinic (signs) of a thyrotoxic crisis.
2. Treatment of thyrotoxic crisis. Emergency aid (first aid) for thyrotoxic crisis.
3. Acute adrenal insufficiency (adrenal crisis). Causes (etiology) of adrenal insufficiency. Pathogenesis of adrenal crisis.
4. Clinic (signs) of adrenal insufficiency (adrenal crisis). Emergency aid (first aid) for adrenal insufficiency (adrenal crisis).
5. Emergencies in diabetes mellitus. Ketoacidotic coma. Causes (etiology) of ketoacidotic coma. Pathogenesis of ketoacidotic coma.
6. Clinic (signs) of a ketoacidotic diabetic coma.
7. Diagnosis of ketoacidotic diabetic coma. Emergency aid (first aid) for ketoacidotic coma.
8. Principles of treatment of ketoacidotic diabetic coma. Treatment tactics for ketoacidotic coma. Insulin therapy. Method of constant intravenous infusion of small doses of insulin.
9. Infusion therapy of ketoacidotic diabetic coma. Method of fractional administration of small doses of insulin in ketoacidotic coma. The method of fractional administration of large doses of insulin in ketoacidotic coma.

Emergencies in diabetes mellitus. Ketoacidotic coma. Causes (etiology) of ketoacidotic coma. Pathogenesis of ketoacidotic coma.

Diabetes is one of the most common diseases endocrine system. Decompensation this disease can manifest itself as the development four types of coma.
1. Ketoacidosis and its extreme expression - ketoacidotic (ketoacidemic) diabetic coma.
2. Hyperosmolar coma.
3. Lactacidemic (lactic acid) coma.
4. Hypoglycemic coma.

The most common of the above coma conditions occurs ketoacidotic coma... The mortality rate for this pathology is 2-4%.

Ketoacidotic coma

Etiology of ketoacidotic coma... Reasons for decompensation of diabetes mellitus:
1. Untimely treatment of a patient with incipient insulin-dependent diabetes mellitus to a doctor or delayed diagnosis (thirst, polyuria, weight loss).
2. Errors in insulin therapy.
3. Wrong behavior and attitude of the patient to his illness (violation of diet, alcohol intake, unauthorized change in the dose of insulin, etc.).
4. Acute diseases (especially purulent infections).
5. Physical and mental trauma, pregnancy, surgery.

Pathogenesis of ketoacidotic comais determined by insulin deficiency, that is, the discrepancy between the production of endogenous or the delivery of exogenous insulin and the body's need for it, and the sharp activation of counterinsular hormonal influences. A phenomenon is formed - energy starvation with an excess content in the blood and extracellular fluid of the energy source - glucose. Excessive accumulation of unused glucose increases the osmolarity of the plasma, as a result of which part of the interstitial, and then the intracellular fluid and the microelements contained in it pass into the vascular bed, this causes the development of cellular dehydration and a decrease in the intracellular content of electrolytes (primarily potassium). When the renal threshold of permeability for glucose is exceeded, glucosuria develops, osmotic diuresis occurs, and as a result, general severe dehydration, diselectrolitaemia, hypovolemia are formed, blood thickens, its rheology is disturbed, and thrombus formation is increased. The volume of renal perfusion decreases. This pathological cascade, associated with high blood glucose levels, can be conditionally called the first link in the pathogenesis of diabetes mellitus decompensation.

The second conditional link is associated with excess accumulation of ketone bodies, i.e., with ketosis, and then ketoacidosis. As mentioned earlier, excess glucose accumulates in the body against the background of a lack of insulin. In response to energy starvation, the body responds with an increase in the oxidation of free fatty acids (FFA) and an increase in the formation of the final product of lipid oxidation - acetyl-CoA, which under normal conditions should normalize the production of ATP in the tricarboxylic acid cycle (Krebs cycle), however, the half-life products of FFA and an excess of acetyl-CoA itself disrupts its entry into the Krebs cycle, which blocks energy production. A large amount of unclaimed acetyl-CoA accumulates in the blood.

In the liver, through simple chemical transformations from acetyl-CoA, they begin to form ketone bodies, which include acetoacetate (acetoacetic acid), beta-hydroxybutyrate (beta-hydroxy-butyric acid) and acetone. They are normally formed and utilized by anaerobic glycolysis in the muscles, which gives about 1-2% of the total energy produced in the body, but with their excess (ketone bodies) and the absence of insulin, muscles cannot completely utilize ketone bodies. Ketosis occurs. Ketone bodies, possessing the properties of weak acids, lead to the accumulation of hydrogen ions in the body and a decrease in the concentration of sodium bicarbonate ions, as a result of which metabolic acidosis develops (with pronounced ketoacidosis, blood plasma pH decreases to 7.2-7.0).

Thus, for diabetic ketoacidosis insulin deficiency and excessive secretion of contrainsular hormones lead to severe metabolic disorders, mainly to acidosis, plasma hyperosmolarity, cellular and general dehydration with loss of potassium, sodium, phosphorus, magnesium, calcium and bicarbonate ions. These violations also cause the development of a coma.

Causes of dysfunction of the central nervous system with ketoacidotic coma are not fully understood. The assumptions about the toxic effect of acid base balance disorders on the central nervous system did not come true. It is currently believed that the direct cause of death in ketoacidosis is dehydration of brain neurons, which occurs against the background of plasma hyperosmolarity.