Ketoacidotic coma causes. Hyperglycemic ketoacidotic coma (acute care, treatment and clinical manifestations)

diabetic coma

A dangerous complication of diabetes is diabetic coma. In about 1/3 of cases, it is the first manifestation of unrecognized insulin-dependent diabetes mellitus.

There are the following variants of diabetic coma: ketoacidotic, hyperosmolar and hyperlactacidemic. At diabetes most often there is a hypoglycemic coma.

KETOACIDOTIC COMA

Ketoacidotic coma is a complication of diabetes mellitus caused by poisoning of the body and primarily the central nervous system with ketone bodies, dehydration and a shift in the acid-base state towards acidosis. The concepts of "ketoacidosis" and "ketoacidotic state" should also be distinguished. Ketoacidosis is characterized only by biochemical changes, and the ketoacidotic state is characterized by clinical (primarily neuropsychiatric) disorders [Prikhozhan V. M, 1973, 1981]. Ketoacidotic coma is observed in 1-6% of patients hospitalized for diabetes mellitus.

Etiology. The causes of diabetic coma, in particular ketoacidotic coma, can be: a) late diagnosis of diabetes mellitus, poorly organized medical examination, lack of awareness of medical personnel about diabetes, incorrect diagnosis, late treatment(cancellation of insulin therapy or insufficient administration of insulin, etc.), mistakes of the patient’s relatives, especially parents who are entrusted with monitoring children with diabetes, patient’s indiscipline (gross violation of the diet, cancellation or insufficient administration of insulin, etc.). ), self-treatment, formal, superficial analysis of the causes of coma and their outcomes, insufficient and unsatisfactory promotion of elementary knowledge on diabetes mellitus among the population, ignorance of the patient and the people around him about the symptoms of diabetes mellitus, the first signs of a coma, elements of first aid, late referral to doctor; b) physical injury (surgery, etc.), burns, frostbite, food or other poisoning, mental trauma; accession to diabetes mellitus of other diseases that contribute to the deterioration of compensation for diabetes mellitus (flu, pneumonia, myocardial infarction, etc.).

Pathogenesis. The pathogenesis of ketoacidosis and ketoacidotic coma is due to the increasing deficiency of insulin in the body. R. Assan (1973) and E. Balasse (1976) showed that in diabetic coma the content of immunoreactive insulin in the blood is sharply reduced. In parallel with the increase in insulin deficiency, there is also a decrease in the number of receptors and their sensitivity to insulin in peripheral tissues (muscle, fat, liver, etc.).

A sharp deficiency of insulin in the body leads to a decrease in the permeability of the cell membrane for glucose in muscle and adipose tissue, inhibition of the process of glucose phosphorylation (decreased activity of the hexokinase enzyme) and its oxidation, slowing down the processes of lipogenesis of excess glucose production in the liver (increased neoglucogenesis from protein and fat), their increased excretion from the liver (increased activity of the enzyme glucose-6-phosphatase). This causes significant hyperglycemia and glucosuria (Scheme 2). Hyperglycemia is caused not only by a deficiency of insulin in the body, but also by excessive secretion of glucagon, the main hormonal antagonist of insulin. The latter stimulates glycogenolysis and neoglucogenesis and serves main reason accelerated production of glucose.

Due to hyperglycemia, the osmotic pressure in the extracellular fluid increases and the process of intracellular dehydration develops, since water and cellular

electrolytes (potassium, phosphorus, etc.) come from cells into intercellular spaces. As a result of tissue dehydration, thirst (polydipsia) occurs, normal cellular metabolism is disrupted, and diuresis (polyuria) increases. An increase in the osmotic pressure of urine also leads to polyuria. The latter is explained, on the one hand, by glucosuria, and on the other hand, by the excretion of protein and lipid metabolism products (ketone bodies, etc.), as well as sodium ions, with urine. As a result of severe polyuria and increasing hyperglycemia, the brightness of the blood increases to an even greater extent, resulting in a decrease in the volume of circulating blood and the onset of collapse.

Inhibition of the oxidation of glucose-6-monophosphate causes a deficiency of reduced nicotinamide adenine dinucleotide (NADP H 2) (pentose carbohydrate conversion cycle), which entails difficulty in the synthesis of higher fatty acids from acetyl coenzyme A. Violation of the glycolytic pathway of glucose breakdown also leads to a decrease in the formation alpha-glycerolphosphoric acid, necessary for the synthesis of triglycerides. As a result, inhibition of lipogenesis and resynthesis of triglycerides in adipose tissue, liver and lung tissue occurs, followed by the predominance of its lipolytic activity and increased lipolysis.

Violation of glucose utilization by body cells leads to a compensatory increase in the activity of the hypothalamic-pituitary-adrenal system, resulting in an increase in the secretion of hormones that have a fat-mobilizing effect - growth hormone, ACTH, catechol amines, which in turn enhances ketoacidosis.

Glucagon also contributes to the strengthening of lipolysis in ketoacidosis and ketoacidotic coma. A decrease in the content of glycogen in the liver also causes an increase in the mobilization of fat from the depot in the form of non-esterified fatty acids (NEFA) and triglycerides, followed by its entry into the liver and the development of fatty infiltration in it. An increase in the content of NEFA in the blood in decompensated diabetes mellitus is a compensatory reaction that allows the use of NEFA as energy substances [Leites SM, 1968].

The intake of fat in the liver when it is depleted of glycogen is an expression of adaptation processes in energy metabolism: when one of the energy sources in the liver (glycogen) is depleted, another is formed from fat in it

easily recyclable material - ketone bodies (S. M. Leites). Ketone bodies are normal intermediate products of NEFA metabolism (normal content is 0.9-1.7 mmol / l, or 5-10 mg%, as determined by the method of Leites and Odinov). With excessive accumulation in the blood, ketone bodies have a narcotic effect. Ketone bodies include beta-hydroxy-butyric and acetoacetic acids, acetone. About 65% of ketone bodies are beta-hydroxybutyric acid, the remaining 35% are acetoacetic acid and acetone.

With a sharp deficiency of insulin, fatty liver occurs due to a simultaneous increase in the flow of fat into the liver from fat depots in the form of NEFA and triglycerides, as well as a violation of the oxidation and release of fat from the liver. The development of fatty infiltration of the liver is facilitated by depletion of the liver with glycogen, deficiency of lipotropic nutritional factors, excessive production of somatotropic pituitary hormone (STH), fatty diet, anemia, infection, and intoxication. Fatty infiltration of the liver leads to one of the severe disorders of lipid metabolism - ketosis. The immediate causes of ketosis are increased breakdown of NEFA in the liver, impaired resynthesis of acetoacetic acid into higher fatty acids, insufficient oxidation of acetoacetic acid formed during the breakdown of higher fatty acids in the Krebs cycle. The main role in the development of ketosis is played by the increased formation of acetoacetic acid in the liver.

Hyperketonemia is often accompanied by hypercholesterolemia. This is due to the fact that acetoacetic acid and acetylcoenzyme A, which are the raw materials for the formation of cholesterol, which are formed in an increased amount, are intensively converted into cholesterol due to a violation of their resynthesis into higher fatty acids and oxidation in the di- and tri-carboxylic acid cycle (Krebs cycle). ). Normally, acetyl coenzyme A enters the Krebs cycle with the participation of insulin and undergoes final oxidation to CO 2 and H 2 O. In ketoacidosis, due to a sharp deficiency of insulin, the oxidation of acetyl coenzyme A in the Krebs cycle decreases.

The consequence of hyperketonemia and ketonuria is a violation of water-salt metabolism - a decrease in the content of sodium, phosphorus and chlorides in the blood. The level of potassium in the blood is initially elevated, and later lowered, due to its increased excretion in the urine [Knyazev Yu. A., 1974]. The initial relative predominance of potassium over sodium in the blood is due to the fact that sodium is found mainly in the extracellular fluid, and potassium in the intracellular fluid. In this regard, initially sodium is excreted in the urine more than potassium. Increased excretion of sodium in the urine leads to dehydration and increased polyuria. Violation of the electrolyte balance causes a shift in the acid-base state towards acidosis.

An increase in the level of ketone bodies in the blood leads to a decrease in the pH below 7.35. This, in turn, leads to an increase in the partial pressure of CO 2 and the accumulation of hydrogen ions, which play a major role in the development of acidosis. Metabolic acidosis occurs, which, in addition to excessive accumulation of hydrogen ions in the blood, is characterized by a decrease in the concentration of bicarbonate in the blood plasma due to its consumption to compensate for the acid reaction and excretion from the body with exhaled air and kidneys. Accumulation of excess carbon dioxide in the blood ( respiratory acidosis) irritates the respiratory center, resulting in deep Kussmaul breathing, aimed at removing carbon dioxide to compensate for acidosis. The excretion of hydrogen ions by the kidneys occurs as part of ammonium chloride, excretion of keto acids in the urine (in the form of sodium and potassium salts, as well as in free form), increased excretion of one-"basic phosphates.

The volume of extracellular fluid decreases, resulting in a collapse with a drop in blood pressure in the vessels of the kidneys and brain. Loss of fluid by the body in a coma can reach 10 ° / about body weight, i.e. approximately 6-7 liters. Renal blood flow and glomerular filtration are reduced. The release of nitrogenous metabolic products is disrupted, in connection with which the excretion of hydrogen ions decreases and decompensated acidosis develops. Sharp ketosis leads to inhibition of the enzyme systems of the brain, resulting in reduced utilization of glucose by brain cells. This leads to oxygen starvation of the brain. A high concentration of ketone bodies in the blood also inhibits the function of the reticulohistiocytic system, which reduces the protective properties of the body.

Due to the increased conversion of protein into carbohydrates, ammonia, urea and other decay products are formed in an increased amount, which leads to hyperazotemia, hyperazothuria. The latter is due to the increased formation of ammonia both in the liver and in the kidneys from glutamine.

Strengthening the breakdown of tissue proteins and disruption of their resynthesis from amino acids exacerbate intoxication of the body and create conditions of oxygen starvation (hypoxia) for brain tissues. This leads to respiratory distress, collapse, decreased muscle tone, impaired higher nervous activity. Loss of consciousness in ketoacidotic coma is due to a decrease in the utilization of glucose by the brain tissue in combination with intracellular dehydration, acidosis and oxygen starvation of the brain.

Classification. R.Williams and D.Porte (1974), P.Cryer (1976), K. Alberti and M. Nattras (1977) offer the following classification of ketoacidosis, hyperosmolar syndrome and lactic acidosis.

Clinic. Ketoacidotic coma, as a rule, develops gradually - in the period from 12-24 hours to several days. There are four stages of the ketoacidotic cycle. In stage I (mild ketoacidotic state), weakness, lethargy, increased drowsiness and fatigue, apathy, nausea, and sometimes vomiting are noted. headache pulsating, bursting nature, pain in the limbs and torso (neuromyalgia), increased polydipsia and polyuria, the appearance of the smell of acetone in the exhaled air. Drowsiness and stunning is characterized by stage II (pronounced ketoacidotic state). In stage III (severe ketoacidotic state), sopor is observed. With stupor, the patient can be awakened only with the help of strong stimuli. Pain sensitivity, as well as swallowing, pupillary and corneal reflexes are preserved. Tendon reflexes are still high.

In the period preceding the coma, there may be acute abdominal pain that mimics acute surgical diseases abdominal organs. Cause false acute abdomen not definitively established. Some authors [Teplitsky B. I., Kaminsky P. M., 1970] associate the occurrence of acute pain in the abdomen with irritation of the solar plexus by products of diabetic acidosis, others with the loss of cellular potassium, resulting in paralysis and expansion of the stomach. G. B. Isaev (1982) believes that the most likely causes of acute abdominal pain in the ketoacidotic state are the loss of water and electrolytes, intracellular acidosis and ketosis. The occurrence of acute abdominal pain in the ketoacidotic state is also explained by pyloric spasm and spastic contraction of the intestine.

To differentiate a false acute abdomen from a true one, G. B. Isaev (1982) proposes to conduct clinical observation of a patient in a ketoacidotic state for 4-6 hours, carrying out intensive therapy aimed at eliminating ketoacidosis. If, after the specified time, acute pain in the abdomen does not subside, they should be regarded as true.

We present our own observation.

Presented Observation once again emphasizes that in some cases the differentiation of a false acute abdomen from the true one is quite difficult. This led to the misdiagnosis of perforated gastric ulcer by an experienced surgeon. At the same time, this case indicates that the terms recommended by G. B. Isaev (1982) for the differential diagnosis of a false and true acute abdomen are very conditional.

Stage IV of the ketoacidotic cycle is characterized by the development of coma, which can be superficial, severe, deep and terminal. With a coma, there is a complete loss of consciousness. Breathing is noisy, with long inhalation and short exhalation. Each breath is preceded by a long pause (Kussmaul breath). There is a sharp smell of acetone in the exhaled air (the smell of pickled apples). The face is pale, without cyanosis. The skin is dry, cold, inelastic. Tone eyeballs and muscle is drastically reduced. The pupils are constricted. There is convergent or divergent strabismus. The muscles are sluggish, relaxed. Loss of tendon, periosteal and skin reflexes. Body temperature is below normal. The tongue is dry, hyperemic. Pulse small, frequent. Blood pressure drops. There is oliguria and even anuria. In some cases, there may be gastrointestinal bleeding.

With ketoacidotic coma, flutter and atrial fibrillation, extrasystole can be observed. The ECG shows a decrease in the tooth T and elongation of the complex QRST as a result of impaired conduction of the heart muscle (hypokalemia).

It is not uncommon for a ketoacidotic state to mimic other types of pathology. Depending on the predominance of certain symptoms, the following variants of the ketoacidotic state are distinguished: 1) cardiovascular (cardiac or vascular insufficiency prevails - collapse); 2) gastrointestinal (clinical picture of an acute abdomen, cholera); 3) renal (dysuria, hyperazotemia, proteinuria, cvdshndruria, etc. come to the fore, and acetonuria and glucosuria are absent due to a sharp decrease in glomerular filtration); 4) encephalopathic (clinical picture of violation cerebral circulation).

Laboratory data. Crucial in the diagnosis of ketoacidotic coma are the determination of blood sugar and ketone bodies. During the precoma period, the blood sugar level usually exceeds 16.6 mmol/l (300 mg%). Glycosuria increases sharply. intensifies

ketosis. With an increase in the content of ketone bodies in the blood to 2.6-3.4 mmol / l (15-20 mg%), acetonuria appears.

With ketoacidotic coma, the blood sugar content sometimes reaches 55.5 mmol / l (1000 mg%) and even 111 mmol / l (2000 mg%). Ketosis sharply increases, reaching in some cases 172.2 mmol / l (1000 mg%) or more, blood pH decreases to 7.2 and below (the norm is 7.35-7.45 for arterial and capillary blood). There is a sharp decrease in the alkaline reserve of the blood up to 5% by volume (at a rate of 55-75% by volume). The level of standard bicarbonate (SB) drops sharply (norm 20-27 mmol/l). Normal performance acid-base state are presented in table: 3. With ketoacidotic coma, neutrophilic leukocytosis is always in the blood. Often elevated ESR. The amount of hemoglobin and the number of red blood cells are usually increased. Sometimes due to intoxication there may be anemia. The osmolarity of the blood is increased. There is an increase in blood levels of NEZhK, cholesterol triglycerides, residual nitrogen, and urea.

The level of potassium in the blood before treatment is either normal or slightly elevated. Hypokalemia usually develops 4-6 hours after the start of insulin therapy (late hypokalemia). It is caused by an increase in the intake of potassium into cells as a result of improved carbohydrate and protein metabolism, an increase in the permeability of cell membranes, as well as parenteral administration of potassium-poor solutions. The development of late hypokalemia is also facilitated by an improvement in kidney function, which leads to increased excretion of potassium in the urine. In some cases, early hypokalemia may occur, which is associated with massive destruction of cells, their loss of potassium, and the inability of cells to retain potassium with simultaneous kaliyuria.

With hypokalemia (potassium content in the blood below 3.5 mmol / l - 4 mg%), pallor, muscle and general weakness, hyporeflexia up to areflexia appear. Sometimes (with severe and prolonged hypokalemia) a lethargic state is observed. Changes in the cardiovascular system are manifested in the form of cyanosis, tachycardia, intracardiac conduction disturbances - the supraventricular form of paroxysmal tachycardia, other rhythm disturbances up to ventricular fibrillation, characteristic changes in the ECG (decrease or flattening of the wave T, segment decline S-T, interval lengthening R- Q, the appearance of high and pointed teeth R, as well as pathological tooth C /). As a result of paresis of the respiratory

asphyxia occurs in the body muscles. With hypokalemia due to atony of the smooth muscles of the stomach and intestines, there is a violation of intestinal motility up to its paralytic ileus, flatulence, vomiting, expansion of the stomach and intestines. There is paresis Bladder. There is a decrease in mental and mental activity (absent-mindedness, apathy). It should be remembered that with hypokalemia there is an increased sensitivity to digitalis preparations. Electrolyte imbalances are also expressed in the development of severe hyponatremia and hypochloremia. The relative density of urine is high, the reaction is acidic, there are sharp acetonuria and glucosuria, often proteinuria, cylindruria, microhematuria.

diagnostic tests. For express diagnostics, the content of sugar and ketone bodies in the blood, as well as sugar and acetone in the urine are established.

The level of sugar in the blood is determined by methods based on the reducing properties of glucose (methods of Hagedorn - Jensen, Somoji - Nelson) or on its color reactions with certain reagents (orthotoluidine method of Fried and Hoflmayer, etc.). Determining the content of sugar in the blood according to the Hagedorn-Jensen method, along with glucose in the blood, the content of other reducing substances (glutathione, creatinine, uric acid, ergothionine, vitamin C, etc.) is also determined. When using this method, the sugar content in capillary blood in healthy people on an empty stomach ranges from 4.4 to 6.7 mmol / l (80-120 mg%). The sugar content in capillary blood, detected by the Somoji-Nelson method, is 3.3-5.6 mmol / l (60-100 mg%). More accurate glucose oxidase method Natelson (normal blood sugar 2.8-5.3 mmol / l, or 50-96 mg%, orthotoluidine method (normal 3.3-5.5 mmol / l, or 60-100 mg% ) In venous blood, the normal sugar content is 0.3-0.83 mmol / l (5-15 mg%) less than in arterial and capillary blood.

When determining the content of sugar in the blood, it is preferable to use enzymatic methods (hexokinase and glucose dehydrogenase), since they are specific for glucose. Usage chemical methods(orthotoluidine, ferricyanide) blood sugar determinations are less desirable as inflated results may be obtained. This may be due to the accumulation of reduced substrates in the blood. carbohydrate metabolism(for diseases of the liver, kidneys, etc.) or with the introduction of solutions containing dextran to the patient [Petrides P. et al., 1980].

Determination of ketone bodies in the blood. To determine the ketone bodies in the blood (acetone, acetoacetic and beta-hydroxybutyric acids), iodometric and colorimetric methods are often used.

The iodometric method (the Engfeld-Pinkussen method modified by Leites and Odinov) is based on the reaction of acetone with iodine (the concentration of which is precisely known) with the formation of iodoform in an alkaline medium and the subsequent determination of the amount of absorbed iodine by titration with a hyposulfite solution. In healthy people, the concentration of ketone bodies ranges from 0.9 to 1.7 mmol / l (5-10 mg%). When determining ketone bodies by the colorimetric method using salicylic aldehyde (Natelson method) in healthy people, the concentration of ketone bodies does not exceed 0.3-0.4 mmol / l (2-2.5 mg%).

Determination of sugar in urine. Set the content in the daily amount of urine. In the urine of healthy people, glucose is either absent or completely reabsorbed in the tubules. For the qualitative determination of sugar in urine, the methods of Benedict, Nylander, and others are used, based on the reducing properties of sugar. Nylander's test? Included in the following. To 2-3 ml of filtered urine, add the same volume of reagent, consisting of 2 g of bismuth nitrate, 4 g of Rochelle salt and 100 ml of 10% sodium hydroxide solution. The resulting mixture is boiled for 2 minutes. In the presence of sugar, the entire liquid turns black.

Qualitative methods for detecting sugar in urine include a glucose oxidase test using indicator papers (byofan G, clinics, etc.) impregnated with glucose oxidase and peroxidase. In the presence of glucose in the urine, a piece of paper (glucotest, produced by the domestic industry) turns blue, and in its absence remains yellow. This method is very sensitive (about 0.1%) and specific (no reaction with other sugars or reducing substances occurs).

The quantitative determination of sugar in the urine is carried out using a polarimeter. The polarimetric method is based on the property of sugar to rotate the plane of polarization of light to the right. The force of rotation increases with the amount of sugar in the urine.

Determination of acetone in urine. For the qualitative determination of ketone bodies in urine, the Lange test or its modifications are used, as well as indicator tablets that change color when 1-2 drops of urine containing an increased amount of ketone bodies are applied to them. The Lange test is based on the properties of acetone and acetoacetic acid to give a violet color with sodium nitroprusside in an alkaline medium. In the USSR, tablets for the determination of acetone in urine are used for the express diagnosis of acetonuria.

You can also use the following method for the rapid determination of acetone in urine. A few drops of freshly prepared sodium nitroprusside solution and 0.5 ml of concentrated acetic acid are added to a test tube to 8-10 ml of urine, and then several milliliters of concentrated ammonia solution are carefully layered along the test tube wall. In the presence of acetone, a purple ring appears at the interface between the two liquids within 3 minutes. In addition to decompensated diabetes mellitus, acetone can be detected in the urine in severe febrile conditions, indomitable vomiting, prolonged fasting and intoxication.

Diagnostics and differential diagnosis. The diagnosis of ketoacidotic coma is established on the basis of anamnesis (diabetes mellitus) and a characteristic clinical picture (Kussmaul's breathing, a strong smell of acetone in exhaled air, severe tissue dehydration, prolapse of tendon, periosteal and skin reflexes, hypotension, high hyperglycemia, pronounced ketoacidosis, severe acetonuria and glycosuria, etc.).

Ketoacidotic coma should be differentiated from hypoglycemic, hyperosmolar, hyperlactacidemic, hepatic, uremic, apoplexy, hypochloremic, as well as drug and salicylate poisoning. Differential diagnostic signs of coma are presented in table. 4, 5.

The state of ketoacidosis is not an obligatory harbinger of ketoacidotic coma, as it can be observed with prolonged vomiting, massive corticosteroid therapy, alcohol intoxication, deficiency of fibroblastic coenzyme A-transferase, gastrointestinal and infectious diseases, monotonous protein or fatty diet (heart failure, peptic ulcer, liver disease), severe diseases

vaniyah, accompanied by cachexia. Ketosis and ketonuria can also be observed in healthy people with carbohydrate or general starvation. In connection with the foregoing, the doctor's task is to carefully immediately determine the cause of ketoacidosis in order to eliminate it as soon as possible.

Forecast. In ketoacidotic coma, the prognosis is determined by the timeliness of diagnosis and treatment. It is most favorable if the coma does not exceed 6 hours. Without treatment, ketoacidotic coma is fatal. With a combination of diabetic coma with myocardial infarction, cerebrovascular accident, the prognosis is poor.

Prevention. The main measures for the prevention of diabetic coma include early diagnosis of diabetes mellitus, adequate insulin therapy, constant medical supervision with the study of sugar in the blood and urine 1 time in 10-14 days, careful compensation of disturbed metabolic processes (primarily carbohydrate metabolism), strict adherence by patients prescribed diet. With intercurrent infection, injuries, the dose of insulin is increased depending on the indicators of the glycemic profile. To avoid ketoacidosis, fats are excluded from the diet. Required

Treatment. If a patient develops ketoacidosis, precoma or coma, immediate hospitalization is necessary for emergency medical care. The latter is aimed at eliminating metabolic disorders (primarily carbohydrate and lipid metabolism), combating acidosis, dehydration, cardiovascular insufficiency, restoring the alkaline reserve and electrolyte balance, treating concomitant diseases and complications, both post-coma and those that provoked ketoacidotic to whom. Institute of Experimental Endocrinology

dima thorough rehabilitation of even a minor inflammatory focus.

In the Institute of Chemistry and Chemistry of Hormones, the Academy of Medical Sciences of the USSR developed an observation sheet for a patient with diabetes mellitus in a state of ketoacidosis and diabetic coma, which is given with minor changes and additions.

The observation sheet makes it possible to judge not only the dynamics of the indicators of a patient with diabetes mellitus in a state of ketoacidosis and diabetic coma, but also the effectiveness of the prescribed treatment.

1. An effective pathogenetic treatment for ketoacidotic coma is the use of simple fast-acting insulin. The initial (first) dose of insulin depends on the age of the patient, the duration of the coma, the severity of ketoacidosis, the level of hyperglycemia, the magnitude of the previous dose and the presence of concomitant diseases.

With ketoacidotic coma, both incipient and developed, it is necessary to immediately inject 100-200 units of insulin, of which 50 units are intravenous drip, and the rest (50 units) is intramuscularly. Insulin is administered intravenously by drip in isotonic sodium chloride solution at a rate not exceeding 50 U/30 min. In severe ketoacidotic state, accompanied by stupor, or superficial coma, 100 IU of insulin is administered once, with severe coma - 120-160 IU, with deep coma - 200 IU.

Elderly people suffering from atherosclerosis or other cardiovascular diseases (myocardial infarction, cerebrovascular accident, etc.) are administered an initial dose of insulin not exceeding 80-100 units, due to the risk of acute coronary insufficiency or aggravation of other vascular disorders with a sharp decrease in the level of glycemia.

If during the first 3-4 hours from the moment the patient is removed from the coma, the blood sugar level does not decrease and the condition does not improve, repeat intravenous and intramuscular injection half dose of insulin (50-100 IU) every 2 hours. To bring the patient out of a coma, especially in the early stages, insulin should be administered intramuscularly rather than subcutaneously, because the level of blood flow in the muscles is more constant. As a result, under conditions of severe rehydration, insulin is absorbed evenly. With subcutaneous administration, firstly, it is difficult to predict the rate of insulin absorption from subcutaneous adipose tissue, and secondly, insulin can be deposited in subcutaneous adipose tissue with the development of hypoglycemia in the future.

In acute vascular disorders, it is more rational to use the method of insulin therapy proposed by J. Sheldon and D. Hand (1968). In accordance with this technique, the initial dose of insulin is 10% of the glycemic value. In this case, half the dose of insulin is administered intravenously, and half intramuscularly. If 2 hours after the first injection of insulin, glycemia decreases by 25% or more, the administration of insulin is stopped or the dose is reduced adequately to the indicators of glycemia and the patient's condition. In these cases, a constant (1 time per hour) determination of glycemia is necessary. It should be remembered that the introduction of very large doses of insulin is dangerous due to the possible development of hypoglycemia, hypokalemia and cerebral edema.

In order to avoid hypoglycemia in children, a single dose of insulin in coma should not exceed 30 IU (0.7-1 IU / kg). With a complete (deep) coma, half of the first dose of insulin can be administered intravenously, and half intramuscularly. After the introduction of the first dose, insulin is prescribed for the first 2 days, 6-8 units intramuscularly after 2-3 hours under the control of glycemia and glucosuria,

Removal from a diabetic coma during pregnancy is carried out according to general principles treatment of coma, taking into account the risk of hypoglycemia to the same extent for the mother and fetus. In this regard, slightly lower initial doses of insulin (50-80 IU) are used.

In recent years, small doses of insulin have also been used to bring a patient out of a coma, which has a number of advantages over the administration of insulin by the traditional method. With the introduction of large doses of insulin, there is a risk of developing late hypoglycemia, hypoosmolarity, cerebral edema and hyperlactacidemia. In the blood, an insulin concentration is created that is much higher than the physiological one (500-3000 μU / ml). This stimulates the lipolytic action of adrenaline, resulting in a decrease in the biological effect of insulin. With the introduction of small doses of insulin, the level of glycemia decreases more slowly, which significantly reduces the risk of late hypoglycemia, hypoosmolarity and cerebral edema. Frequent (every hour) intramuscular injection of insulin compared with subcutaneous insulin provides faster AND uniform absorption of insulin. A high and stable level of insulin in the blood is reached faster. Reduces the possibility of late hypokalemia. It has been established that when the insulin content in the blood is 10-20 mcU/ml, glycogenolysis, gluconeogenesis and lipolysis are suppressed, and when the insulin concentration in the blood is G20-200 mcU/ml, ketogenesis is suppressed and the maximum transport of glucose and potassium occurs. When insulin is administered at a dose of 1 unit /h in the blood, its concentration is reached, corresponding to 20 μU / ml. Thus, the administration of exogenous insulin at a dose of 6-10 IU creates such a concentration in the blood that is necessary to suppress ketogenesis. With insulin therapy in small doses, depending on the severity of the coma, the drug is administered at a dose of 15-20 to 50 U / h or intravenously for a long time (for 4-8 hours), or periodically intramuscularly (one injection per hour) under the control of glycemia.

M. Page et al. (1974) and others recommend to administer insulin intravenously continuously, starting z doses b U / h. In the future, depending on the effect, the dose of insulin can be doubled every hour. S. A. Birch (1976) considers intramuscular administration of insulin acceptable, taking doses of 10-20 U / h (depending on the severity of the condition), and then 5-10 U / h. To avoid hypoglycemia when blood sugar drops to 16.7-11.1 mmol / l

(300-200 mg%) the dose of injected insulin is reduced to 2-4 U / h. Simultaneously administered intravenously 5,5% glucose solution, to which insulin is added at the rate of 1 unit per 5 g of glucose. According to Y. A. Vasyukova and G. S. Zefirova (1982), in the “low dose regimen”, 16-20 units of insulin are initially prescribed intramuscularly, and then 6-10 units / hour are administered intramuscularly or intravenously. If after 2 hours from the start of insulin therapy the blood sugar level does not decrease, the authors recommend increasing the dose of insulin to 12 U/h.

When removing from a ketoacidotic coma, children are prescribed insulin at the rate of 0.1 U / kg once, and then 0.1 U / (kg "h) intramuscularly or intravenously.

When choosing a "mode of large or small doses" of insulin, E. A. Vasyukova and G. S. Zefirova (1982) recommend using small doses of insulin with an initial level of glycemia of not more than 35 mmol / l (630 mg%). However, we have successfully brought patients out of coma by using a "low dose regimen" and at much higher blood sugar levels - up to 50 mmol/l (900 mg%). When choosing a "mode of high and low doses" of insulin, we are guided not so much by the initial level of sugar in the blood, but by the effectiveness of insulin therapy in the first 2-3 hours. If treatment with small doses of insulin is ineffective during this period, then we switch to the "high dose regime". Treatment with only simple insulin using the "high and low dose regimen" is continued until a stable decrease in the level of glycemia to 14-11.1 mmol / l (250-200 mg%) is achieved.

Very promising is the use of artificial pancreas "Biostator" manufactured by Miles (USA-FRG) in decompensated diabetes mellitus and diabetic coma [Yudaev N. A. et al., 1979; Spesivtseva V. G. et al., 1980, etc.]. "Biostator" consists of an automatic glucose analyzer, a pump, a computer and a recording device. It reproduces the work of a normal pancreas and provides intravenous metered administration of insulin and glucose as needed.

2. To combat dehydration and intoxication with normal blood osmolarity, Ringer's solution or isotonic sodium chloride solution in a volume of 200-500 ml / h is intravenously administered simultaneously with the start of insulin therapy until dehydration symptoms decrease. It is more expedient to use Ringer's solution, since

electrolyte composition (in particular, the content of chlorides), it is close to the extracellular fluid, as a result of which it quickly restores the water-salt balance. Isotonic sodium chloride solution contains an excessive concentration of chlorides, which, when large amounts of isotonic sodium chloride solution are administered parenterally, can contribute to increased acidosis. With a decrease in the symptoms of dehydration, 200-300 ml of liquid per hour is administered parenterally under the control of blood osmolarity. When the osmol of blood brightness is more than 300 mole / l or the sodium content in the blood serum is more than 155 mmol / l, a hypotonic (0.45%) solution of sodium chloride is injected intravenously in the volumes indicated above. In diabetic coma, blood osmolarity is increased in 30-50% of patients. Normal plasma osmolarity is 285-295 mos-mol/L.

Blood osmolarity is calculated by the formula: osmo
plasma brightness (mosmol/l) = 2-(K + +Ha +) (mmol/l) +
+ Glycemia (mmol/l) + Urea (mmol/l) +
Proteins (g/l) x 0.243
8 "

With the normalization of blood osmolarity, they switch to parenteral administration of Ringer's solution or isotonic sodium chloride solution. To replenish the intra- and extracellular fluid deficit, which is approximately 10% of body weight, from 4 to 8 liters of fluid are injected parenterally on the 1st day.

At cardiovascular pathology, edema and for patients older than 60 years, the total volume of fluid administered is reduced to 1.5-3 liters. In the first 6 hours of removing the patient from a coma, 50% is usually injected, in the next 6 hours - 25%, in the next 12 hours - 25% of the total amount of fluid. Faster rehydration can lead to overload of the left ventricle of the heart and cerebral edema. Drip intravenous fluid is continued until the patient regains consciousness. The absence of diuresis during rehydration is an indication for hemodialysis.

In order to avoid hypoglycemia, after 3-4 hours from the start of insulin treatment, drip intravenous administration of a 5% glucose solution in isotonic sodium chloride solution is started (approximately 1 liter of each solution).

Intravenous drip infusion of 5% glucose solution can be prescribed in more early dates. This can be after 2-3 hours from the start of insulin therapy with a pronounced decrease in blood sugar, for example, with

33.3 mmol/l (600 mg%) to 16.55 mmol/l (300 mg%). With the phenomena of hypoglycemia (trembling, convulsions, sweating, collapse, etc.), 20-40 ml is administered intravenously 40% glucose solution.

3. To eliminate hypokalemia under constant monitoring of the level of potassium in the blood, kaliyuria and ECG (4-6 hours after the start of insulin and fluid administration), intravenous administration of potassium chloride is started. The indication for its use is the level of potassium in the blood below 4.5 mmol / l (18 mg%) and diuresis of at least 50 ml / h. Potassium chloride is contraindicated in oliguria and anuria due to possible development hyperkalemia due to violation of the filtration function of the kidneys. With hyperkalemia, the ECG shows an increase in the interval S - T, high pointed tooth T and lowered prong R. If, with oliguria and anuria, the potassium content in the blood is below 3.5 mmol / l (14 mg%), it can still be administered in small amounts (1-1.5 g per liter of fluid administered). Indications for the appointment of potassium preparations after withdrawal from a coma are muscle paresis and characteristic changes in the ECG (prolongation of the interval P - Q, segment decline S - T, expansion and flattening of the tooth T, pronounced pathological tooth U).

Prior to the removal of the patient from a diabetic coma, kaliyuria is not accompanied by hypokalemia. During insulin therapy, the level of potassium in the blood falls in proportion to the amount of insulin administered. So, with the "high dose regime" of insulin, the body's need for potassium increases and amounts to 225-343 mmol / day (225-343 meq / day), and with the "low dose regime" it is much less - 100-200 mmol / day (100- 200 meq/day).

To eliminate hypokalemia, intravenous potassium chloride is administered at the rate of 2-3 g per liter of injected fluid at a rate of 500-1000 ml over 3-5 hours. In case of normo-or hypokalemia at the very beginning of coma, potassium preparations are administered simultaneously with the start of insulin therapy and rehydration . In this case, potassium preparations are administered at a rate of at least 80-100 mmol / h (80-100 meq / h).

With the development of a hypokalemic crisis, potassium chloride is administered intravenously at a dose of 2 g (27 mmol, or 27 meq) in 5% glucose solution for 15 minutes under ECG control.

To avoid the development of hypokalemia, potassium chloride is injected intravenously at a dose of 8-14 mmol / h (8-14 meq / h) during the day. If the level of potassium in the blood serum is above 5 mmol / l, potassium chloride is administered intravenously at a dose of 8 mmol / l (6 ml of a 10% solution in tea), and at a level below 5 mmol / l - at a dose of 13-20 mmol / h ( 13-20 meq / h, i.e. 10-15 ml of a 10% solution per hour). If the patient can drink, to prevent hypokalemia, he is given potassium-rich juices (lemon, apple, apricot, orange, carrot).

(20 mmol/l, or blood
20 meq/l

2pgZ

intravenously at a dose of 8 mmol / l (6 ml of a 10% solution in tea), and at a level below 5 mmol / l - at a dose of 13-20 mmol / h (13-20 meq / h, i.e. 10-15 ml 10% solution per hour). If the patient can drink, to prevent hypokalemia, he is given potassium-rich juices (lemon, apple, apricot, orange, carrot).

4. To combat acidosis, sodium bicarbonate is used. With its introduction, cerebral edema, severe hypokalemia and hypernatremia, a decrease in the pH of the cerebrospinal fluid, and a violation of the dissociation of oxyhemoglobin may occur. In this regard, an isotonic (2.5%) solution of sodium bicarbonate is administered and only when the pH arterial blood less than 7.0. When the blood pH is more than 7.0, the introduction of this solution is stopped. The required dose of sodium bicarbonate can be calculated using the formula: NaHCO 3 (mmol) = body weight (kg) X 0.3 X BE (base deficiency). In this formula, it is recommended to use a coefficient of 0.15 and to administer no more than half of the calculated dose at a time. Another formula can be used to calculate the dose of sodium bicarbonate:

Normal level nat - The existing level of "riya bicarbonate in the blood - bicarbonate

(20 mmol/l, or blood
20 meq/l

X The volume of extracellular fluid (15-20 l).

When calculating the amount of sodium bicarbonate by this method, no more than half of the calculated dose is administered simultaneously. The calculation of sodium bicarbonate using this formula is less accurate.

Isotonic (2.5%) freshly prepared sodium bicarbonate solution is injected intravenously in a dose of 100 mmol/h (336 ml/h) under the control of blood pH. For every 100 mmol (100 meq) of sodium bicarbonate, 13-20 mmol (13-20 meq, i.e. 10-15 ml of a 10% solution) of potassium chloride should be administered. If necessary, intravenous drip administration of 2.5% sodium bicarbonate solution can be repeated 2pgZ times a day with an interval of 2 hours. To reduce acidosis, this solution (100-150 ml 3 times with an interval of 2 hours) is administered in an enema or the stomach is washed with it. If the patient can drink, he is given 1-1.5 liters of 2% sodium bicarbonate solution or alkaline mineral water(Borjomi, etc.). To combat acidosis and neutralize ammonia, glutamic acid is prescribed (1.5-3 g per day).

5. To improve the course of oxidative processes

100 mg of cocarboxylase, 5 ml of a 5% solution of ascorbic acid, 200 μg of vitamin B 12, 1 ml of a 5% solution of vitamin B 6 are injected intravenously drip.

6. In case of indomitable vomiting, 200-300 ml of plasma is administered 4-6 hours after the start of treatment to compensate for the protein deficiency and fight starvation. In order to avoid a hypochloremic state, 10-20 ml of a 10% sodium chloride solution is injected intravenously.

7. To prevent cardiovascular insufficiency or to eliminate it, immediately after the diagnosis of ketoacidotic coma is established, subcutaneous administration of cordiamine 2 ml or 20% caffeine-benzoate sodium solution, 1-2 ml every 3-4 hours. Treatment is carried out under constant monitoring of pulse and blood pressure. The use of these drugs requires certain caution, since they excite not only the vasomotor, but also the respiratory center. When the respiratory center is excited (ketoacidotic coma), its overexcitation may occur up to prohibitive inhibition. With persistently low blood pressure, intravenous plasma, dextran, whole blood, intramuscularly 1-2 ml of a 0.5% solution of deoxycorticosterone acetate (DOXA) are prescribed. With severe tachycardia, 0.25-0.5 ml of a 0.05% solution of strophanthin or 1 ml of a 0.06% solution of corglycon in isotonic sodium chloride solution is injected intravenously.

8. At all stages of removing the patient from a coma, oxygen therapy is used. Humidified oxygen is administered through nasal catheters at a rate of not more than 5-8 l/min.

9. Nutrition of the patient depends on the severity of his condition. With ketoacidosis or precoma, easily digestible carbohydrates (honey) are added to the diet while eliminating fats for 7-10 days and limiting proteins. In the future, when ketoacidosis is eliminated, a low-fat diet is prescribed for at least 10 more days. If food intake is not possible, parenteral fluids and 5% glucose solution are administered. As the condition improves, they include full-fledged easily digestible carbohydrates (honey, jam, fruit drink, mousse, semolina porridge), plenty of liquid (up to 1.5-3 liters per day), alkaline mineral waters (borzhom, etc.). On the 2nd day, the diet is expanded. The menu includes potatoes, applesauce, oatmeal, bread, milk and dairy products - low-fat cottage cheese, kefir, yogurt. On the 1-3rd day after the coma, it is advisable to limit animal proteins. This is due to the fact that during the breakdown of proteins, ketogenic amino acids are formed, which exacerbate ketoacidosis. On the 3rd day, in addition to oatmeal and mashed potatoes, meat broth, pureed meat are introduced into the patient's diet. In the future, within a week, the patient is gradually transferred to his usual diet with a slight restriction of fat until compensation is achieved.

10. Particular attention should be paid to the treatment of concomitant diseases and complications that provoked ketoacidotic coma (pneumonia, furuncle, carbuncle, trauma, etc.).

It is necessary to remember about creating optimal hygienic conditions for the patient in order to prevent infections (aspiration pneumonia, skin infection): observe the hygiene of the oral cavity, skin, and prevent tongue retraction. Heating pads, concentrated solutions of iodine, manganese, intramuscular injection of oily solutions, magnesium sulfate are contraindicated.

11. With symptoms of cerebral edema, dehydration therapy (furosemide, etc.) is indicated.

As a result of an untreated disease. Diabetic ketoacidotic coma is the most common and life threatening. A pathological condition develops due to a lack of insulin, which can occur suddenly. Often, the ketoacidotic type of coma is diagnosed in the case of improper treatment diabetes mellitus.

Deviation Features

According to statistics, 5% of patients die from ketoacidotic coma in diabetes mellitus.

This type of coma develops as a complication of diabetes mellitus. Doctors refer to ketoacidotic coma as a variety. Such a pathological condition develops more slowly than. A coma appears in diabetics with a pronounced lack of insulin. A high concentration of glucose in the body can also affect the development of ketoacidotic coma. Before the patient falls into a coma, he is diagnosed with ketoacidosis. Development is influenced by the following factors:

infectious lesions;
significant organ damage;
injury during surgery.

Causes and pathogenesis

A ketoacidotic type of coma can appear in type 1 and type 2 diabetics. It is not uncommon for a patient with type 1 diabetes to become aware of their disease only when they go into a coma. There are the following reasons for the development of ketoacidotic coma:

Factors that cause ketoacidosis can also lead to coma.

prolonged course of diabetes mellitus, which is not treated properly;
lack of insulin treatment or its incorrect use;
non-compliance diet food prescribed by an endocrinologist or nutritionist;
violation of medication intake;
an overdose of narcotic substances, especially cocaine;
prolonged fasting, due to which glucose is produced from adipose tissue;
infectious lesions;
intercurrent diseases of acute manifestation:
- heart attack;
- stroke due to impaired blood supply to the central or peripheral system.

The pathogenesis of ketoacidotic coma is quite complex and goes through several stages. First, the patient experiences an energy hunger caused by an imbalance in the production of endogenous insulin and the delivery of exogenous insulin. Soon, glucose that has not been processed accumulates and provokes an increase in plasma osmolarity. When glucose becomes highly concentrated, the renal permeability threshold rises, resulting in general severe dehydration, in which the blood thickens and blood clots form. In the second stage, the patient develops ketosis, which is characterized by a significant accumulation of ketone bodies. Soon, the pathology turns into ketoacidosis, in which there is a lack of insulin and an excess secretion of contrainsular hormones.

Main symptoms

Ketoacidotic coma is not characterized by rapid development, the pathology manifests itself gradually. Before a person enters a coma, several hours or days pass.
Ketoacidosis can develop as a result of rapid weight loss.
If a patient has diabetes mellitus for a long time, then his body is more adapted to the level of insulin above the norm, so a coma may not occur for a long time. The general condition of the patient, age and other individual characteristics can affect ketoacidotic coma. If ketoacidosis coma manifested itself due to rapid weight loss, then the patient will show the following symptoms:
general malaise and weakening of the body;
sensation of thirst, followed by polydipsia;
itching of the skin.

Harbingers of the development of ketoacidotic coma are:
pathological weight loss;
constant feeling of nausea;
pain in the abdomen and head;
pain in the throat or esophagus.

If a diabetic has a coma associated with acute intercurrent diseases, then the pathology can proceed without any special manifestations. Ketoacidotic coma in diabetes mellitus is manifested by the following symptoms:
severe dehydration of the body;
drying of the skin and mucous membranes;
a decrease in the tension of the eyeballs and skin;
a gradual decrease in the filling of the bladder with urine;
general pallor;
local hyperemia of the cheekbones, chin and forehead;
cooling of the skin;
muscle hypotension;
arterial hypotension;
noisy and heavy breathing;
smell of acetone oral cavity upon exit;
clouding of consciousness, after which a coma occurs.

Features in children

The symptomatic picture of the condition in children is very similar to its manifestations in adults.
In children, ketoacidosis leading to ketoacidotic coma occurs frequently. Especially often the pathology is noted in healthy children at the age of 6. Due to the fact that the child is overly active, and there are no liver reserves, the energy in his body is consumed with increased speed. If at the same time the child's diet is not balanced, then pathological processes are possible, leading to ketoacidosis and coma. The symptoms of a coma in babies are the same as in adults. Parents are forbidden to take any actions to eliminate the pathological condition on their own, insofar as the development of an acetone attack is possible.
Urgent care
When a person with diabetes develops a coma, you should know the algorithm of actions that will help him eliminate pathological manifestations. Emergency care for diabetic coma consists of the following steps:
Call for an ambulance. While waiting for it, the patient is placed in a horizontal position, preferably on the side, since vomiting is possible.
Tracking the heart rate, pulse and blood pressure of the patient.
Check for the presence of the smell of acetone from the oral cavity.
The introduction of insulin in the amount of a single dose - 5 units.

Intravenous saline is the first priority for the patient.
When doctors hospitalize a patient, he is given first aid, which consists in rehydrating the cells and the space outside them. He normalizes the indicators of the acid-base state and restores the electrolyte balance. In intensive care, the pathological conditions that provoked ketoacidotic coma are eliminated. The greatest threat to the life of the patient is dehydration of the body, especially brain cells, therefore, first of all, saline solutions are administered to the patient.

Ketoacidotic coma is a consequence of the causes leading to decompensation of diabetes mellitus (late diagnosis of diabetes mellitus, improperly selected insulin therapy, acute infectious diseases, injuries, stress, pregnancy).

The pathogenesis of ketoacidotic coma

The pathogenesis of ketoacidotic coma is based on insulin deficiency and activation of contrainsular hormones. A paradoxical situation arises - cellular starvation combined with a high level of glucose in the blood. High blood glucose leads to an increase in plasma osmolarity. This causes the transition of interstitial and intracellular fluid into the vascular bed, which is accompanied by the development of cellular dehydration and a decrease in the intracellular electrolyte content. The renal permeability threshold for glucose rises and glucosuria occurs. Under conditions of forming osmotic diuresis, dehydration is aggravated, the balance of electrolytes is disturbed, hypovolemia increases, which leads to thickening of the blood and increased thrombus formation.

The mechanism described above underlies the decompensation of diabetes mellitus. The second mechanism, which will be described below, relates directly to the development of ketoacidotic coma.

Since glucose cannot be utilized, and cellular starvation increases, a compensatory way of obtaining energy through the oxidation of free fatty acids is turned on. end product oxidation is acetyl-CoA, which is necessary for the production of ATP in the tricarboxylic acid cycle. However, the entry of acetyl-CoA into the Krebs cycle blocks the breakdown products of free fatty acids. As a result, the level of unclaimed acetyl-CoA in the blood rises.

Acetyl-CoA enters the liver, where ketone bodies are formed from it - acetoacetic acid, beta-hydroxybutyrate and acetone. Being weak acids, ketone bodies increase the accumulation of hydrogen ions in the body and reduce the concentration of sodium bicarbonate ions. This is how ketoacidosis develops.

Clinic of ketoacidotic coma

The development of ketoacidotic coma is gradual - from the first signs of an acid-base disorder to loss of consciousness, it usually takes several days.

There are three stages in the development of ketoacidotic coma:

beginning ketoacidosis;
precoma;
coma.

Beginning ketoacidosis occurs with symptoms of decompensated diabetes mellitus - with a feeling of dry mouth, thirst, polyuria and symptoms of intoxication - headache, nausea. In such patients, the smell of acetone from the mouth appears. The level of glucose in the blood during this period can reach 16.5 mmol / l.

Lack of treatment leads to the development of dyspeptic syndrome, which consists in repeated vomiting that does not bring relief, diarrhea or constipation. Some patients complain of abdominal pain, which may give a false picture of an "acute" abdomen.

From the side nervous system develops drowsiness, apathy, disorientation in space. Lack of adequate treatment leads to the development of coma.

With a severe form of ketoacidosis, the patient develops frequent, noisy and deep breathing.

Diagnosis of ketoacidotic coma

According to laboratory tests, an increase in ketoacidosis can be judged if hyperglycemia, glucosuria is detected, the level of ketone bodies exceeds the norm (177.2 μmol / l), plasma osmolarity increases to 350 or more mosmol / l. Metabolic acidosis is indicated by a pH in the range of 7.2-7.0. Toxic irritation of the bone marrow leads to neutrophilic leukocytosis, erythrocytosis is a consequence of blood clotting. Plasma sodium is reduced to 120 mmol/L.

Treatment of ketoacidotic coma

Already on prehospital stage it is recommended to start intravenous administration of isotonic saline to eliminate dehydration. In this case, 10-16 units of insulin can be added to the solution. From the introduction of large doses of insulin subcutaneously should be avoided.

All patients with extreme ketoacidosis should be admitted to the intensive care unit.

With hyperglycemia up to 33.3 mmol / l, it is recommended to prescribe a constant intravenous infusion of insulin at a rate of 6-10 U / h. If the initial glucose level exceeds 33.3 mmol / l, a constant intravenous infusion of insulin should be carried out at a rate of 12-16 units / hour.

Every 2-3 hours, blood glucose levels are monitored. If after 4 hours the amount of sugar in the blood has not decreased by 30% of the initial level, the initial dose of insulin is doubled.

In addition to insulin therapy, an important aspect of the treatment of ketoacidotic coma is infusion therapy, which is carried out by intravenous administration of a solution of sodium chloride with the addition of potassium chloride to it (in conditions of potassium deficiency).

Decompensated metabolic acidosis should be corrected with 4% sodium bicarbonate solution at a rate of 2.5 ml/kg.

When the glucose level is restored at around 16.7 mmol / l, they switch to intravenous administration of a 5% glucose solution with the addition of 4 units of insulin to it for each gram of glucose administered.

Ketoacidotic coma- the most formidable complication of diabetes mellitus, is a manifestation of absolute or relative insulin deficiency and a sharp decrease in glucose utilization by body tissues. More often it develops in patients suffering from insulin-dependent diabetes, characterized by a severe labile course. Lack of insulin in the body, which can be caused by a decrease in the supply of exogenous insulin (bad syringe, dose reduction, cancellation of insulin administration, etc.) or an increase in the need for insulin (pregnancy, intercurrent infectious diseases, trauma, surgery, etc.). ), is the cause of the development of coma.

clinical picture. A diabetic coma usually develops slowly over several days or weeks. At acute diseases or intoxications, ketoacidosis can occur much faster, within a few hours. From a clinical point of view, three sequentially developing and successive (without treatment) stages of diabetic ketoacidosis can be distinguished: 1) the stage of moderate ketoacidosis; 2) the stage of precoma, or decompensated ketoacidosis, and 3) the stage of coma. A patient in the stage of moderate ketoacidosis is concerned about general weakness, fatigue, lethargy, drowsiness, tinnitus, loss of appetite, nausea, vague abdominal pain, thirst and frequent diuresis. In the exhaled air, the smell of acetone is determined.

With decompensated ketoacidosis, or diabetic precoma, appetite is completely lost, constant nausea is accompanied by vomiting, general weakness and indifference to the environment increase, vision deteriorates, shortness of breath appears, discomfort or pain in the heart and abdomen, frequent urge to urinate, thirst becomes indomitable . The precomatose state can last from several hours to several days. At the same time, consciousness is preserved, the patient is correctly oriented in time and space, however, he answers questions late, in monosyllables, monotonously, in an indistinct voice. The skin is dry, rough, cold to the touch. Lips dry, chapped, crusted, sometimes cyanotic. The tongue is crimson in color, with imprints of teeth remaining along the edges, dry, lined with a dirty brown coating.

If urgent appropriate therapeutic measures are not taken, the patient becomes more and more indifferent to the environment, answers questions with increasing delay or does not react at all and gradually sinks into a deep coma, in which consciousness is completely absent. Clinical manifestations in a patient in a diabetic coma are the same as in precoma, only more pronounced. There is deep, noisy and rare breathing (of the Kussmaul type), a sharp smell of acetone in the exhaled air, severe hypotension (especially diastolic), frequent, small filling and tension (usually rhythmic) pulse, urinary retention, tense, somewhat drawn in and limited participation in the act of breathing the belly. The previously weakened tendon reflexes gradually completely disappear (pupillary and swallowing reflexes remain for some time). Body temperature is most often lowered; even with severe concomitant infectious diseases, it is slightly increased.

It should be noted that ketoacidotic coma can occur in the form of a gastrointestinal (abdominal), cardiovascular (collaptoid), renal (nephrotic), pseudocerebral (encephalopathic) or dehydration form. This or that syndrome rarely prevails, since, having begun with one syndrome (most often gastrointestinal), diabetic ketoacidosis often manifests itself in the future with another usually dehydrated and (or) collaptoid syndrome.

Urgent care. In diabetic ketoacidosis, not only insulin is used, but other measures are required to combat dehydration and restore metabolic disorders that develop due to the lack of insulin, restore and maintain the functions of others. internal organs(heart, lungs, kidneys, etc.).

The traditional, or classical, method of insulin therapy consists of repeated injections of large doses of simple (soluble, crystalline) insulin. The initial dose is 50-100 IU intravenously and the same amount subcutaneously or intramuscularly. The interval between injections is 1-2-3 hours and depends on the initial level and dynamics of glycemia. Blood sugar levels and acetonuria are monitored every 1-2 hours. If 1 hour after the first dose of insulin, hyperglycemia does not decrease, and even more so if it increases, it is recommended to re-administer (intravenously 4-subcutaneously or intramuscularly) insulin in the same or higher dose. If, after 1 hour after the first injection of insulin, there is a tendency to reduce glycemia, then the second dose is halved. Usually, 3-4 hours after the first injection of insulin (its maximum effect), the patient's consciousness is restored. From this point on, they switch only to subcutaneous administration of the drug after 3 hours under continued control of glycemia, glucosuria and acetonuria. When glycemia drops to 11-13 mmol / l (200-250 mg%), the insulin dose is reduced to 5-20 IU every 3 hours, since it is during this period that hypoglycemia often develops. The total dose of insulin required to bring the patient out of a coma using this method is from 200 to 1000 IU.

Already at the prehospital stage in diabetic coma, it is necessary to provide for measures to eliminate dehydration, hypovolemia, and hemocirculation disorders. Infusion therapy should be intravenous and vigorous enough. It is recommended to inject no more than 1 liter of liquid during the first hour, another 1 liter during the next two hours, and the third liter within three hours. In ketoacidotic coma, 0.9% sodium chloride solution is usually used for rehydration.

With a sharp decrease in blood pressure (below 80 mm Hg), an immediate transfusion of blood substitutes is recommended, and then an infusion of 0.9% sodium chloride solution is carried out at a rate of 1 liter in the first 30 minutes and another 1 liter in the next hour.

To combat collapse in diabetic coma, catecholamines and other sympathotonic drugs should not be used. They are contraindicated not only because catecholamines are contrainsular hormones, but also because in diabetic patients their stimulating effect on glucagon secretion is much more pronounced than in healthy ones.

Along with vigorous infusion therapy at the prehospital stage, other anti-shock measures are carried out: adequate pain relief (drugs, inhalation anesthetics, local anesthesia), immobilization of fractures, warming the patient, oxygen therapy, and, if necessary, mechanical ventilation, etc. Although diabetic coma is usually a mixed (including cardiogenic) hypocirculatory syndrome develops, the introduction of cardiotonic drugs of the digitalis series is undesirable, since they, contributing to an increase in the existing severe potassium deficiency in the myocardium, can worsen cardiac activity. There are also relative contraindications to the use of caffeine, cordiamine, corazol and other analeptics with a pronounced stimulating effect on the respiratory center, which is overexcited in ketoacidosis. Additional stimulation of the respiratory center under such conditions can cause its prohibitive inhibition and respiratory paralysis.

Correction of acid-base balance is carried out by intravenous infusion of sodium bicarbonate solution: in the first hour, 400 ml of a 2% solution (about 90 mmol) is poured. The need to correct electrolyte disturbances (mainly potassium deficiency) occurs 3-4 hours after the start of rehydration and insulin therapy and is carried out in a hospital. For this purpose, a 20% solution of potassium chloride is administered intravenously at a rate of 15-20 mmol / h. If, with such therapy, the blood potassium level drops below 4 mmol / l, then the infusion rate is increased to 40-50 mmol / h. With infusion insulin therapy in small doses, subject to the timely start of potassium replacement therapy at a rate of 15-20 mmol / l, diabetic coma is almost never accompanied by the development of hypokalemia, and on the first day there is rarely a need to replace more than 200 mmol of potassium.

Ambulance health care, ed. B. D. Komarova, 1985

For citation: Demidova I.Yu. KETOACIDOSIS AND KETOACIDOTIC COMA // BC. 1998. No. 12. S. 8

Diagnosis of diabetic ketoacidosis in established diabetes mellitus is not difficult. Cases when diabetes mellitus manifests in a state of ketoacidosis require special attention. Recommendations for the treatment of this condition and its complications are presented.

To diagnose diabetic ketoacidosis in documented diabetes mellitus presents no difficulties. Emphasis should be laid on the cases in which diabetes mellitus is manifestative in the presence of ketoacidosis. Recommendations for treatment of this condition and its complications are given.

I.Yu. Demidov - Department of Endocrinology, MMA named after. THEM. Sechenov (Head - Academician of the Russian Academy of Medical Sciences Prof. I.I. Dedov)

I.Yu. Demidova – Department of Endocrinology (Head Prof. I.I.Dedov, Academician of the Russian Academy of Medical Sciences, I.M.Sechenov Moscow Medical Academy

TO etoacidosis and ketoacidotic coma are one of the main causes of death in patients with diabetes mellitus (DM) under the age of 20 years. More than 16% of patients suffering from insulin-dependent DM (IDDM) die from ketoacidosis or ketoacidotic coma. The risk of a fatal outcome of ketoacidosis increases especially in cases where the factor provoking the occurrence of this acute complication of diabetes is a severe intercurrent disease.
Identification of IDDM on early stages reduced the incidence of manifestations this disease in a state of ketoacidosis up to 20%. Teaching patients with diabetes the principles of self-control and tactics of behavior in emergency conditions has significantly reduced the risk of ketoacidosis - up to 0.5-2% of cases per year.
Studying the nuances of the pathogenesis of ketoacidosis and creating optimal treatment regimens for this condition have led to a decrease in the frequency deaths, however, the mortality rate from ketoacidotic coma is 7 - 19%, and in non-specialized medical institutions this figure is higher.

Pathogenesis

The most common provoking factors for decompensation of diabetes and the development of ketoacidosis are any intercurrent diseases (acute inflammatory processes, exacerbations of chronic diseases, infectious diseases), surgical interventions, injuries, violations of the treatment regimen (administration of expired or improperly stored insulin, errors in prescribing or administering the dose of the drug, malfunction in insulin administration systems, emotional stressful situations, pregnancy, and stopping insulin administration for suicidal intent.
Leading role in the pathogenesis of ketoacidosis absolute insulin deficiency plays a role, leading to a decrease in glucose utilization by insulin-dependent tissues and, accordingly, hyperglycemia, and severe energy hunger in them. The latter circumstance causes a sharp increase in the blood level of all counter-insulin hormones (glucagon, cortisol, catecholamines, ACTH, growth hormone), stimulation of glycogenolysis, proteolysis and lipolysis, supplying substrates for gluconeogenesis in the liver and, to a lesser extent, in the kidneys. Gluconeogenesis in combination with direct impairment of glucose utilization by tissues due to absolute insulin deficiency is the most important cause of rapidly increasing hyperglycemia, increased plasma osmolarity, intracellular dehydration and osmotic diuresis.
These factors lead to severe extracellular dehydration, hypovolemic shock, and significant electrolyte disturbances. Dehydration and hypovolemia cause a decrease in cerebral, renal and peripheral blood flow, which, in turn, enhances the existing hypoxia of the central nervous system and peripheral tissues and leads to the development of oliguria and anuria. Hypoxia of peripheral tissues contributes to the activation of anaerobic glycolysis processes in them and a gradual increase in the level of lactate. The relative deficiency of lactate dehydrogenase in insulin deficiency and the impossibility of complete utilization of lactate in the Cori cycle are the cause of lactic acidosis in decompensated IDDM. Insulin deficiency and a sharp increase in the concentration of all counter-insulin hormones are the cause of the activation of lipolysis and the mobilization of free fatty acids (FFA), which contributes to the active production of ketone bodies. Enhanced formation of acetyl-CoA, a precursor of acetoacetate (and acetone during its decarboxylation), and B-hydroxybutyrate is provided under these conditions by the active intake of FFAs into the liver due to their mobilization from peripheral tissues and the predominance of lipolysis processes over lipogenesis in the liver cell itself.
The rapid increase in the concentration of ketone bodies during decompensation of DM is due not only to their increased production, but also to a decrease in their peripheral utilization and excretion in the urine due to dehydration and oliguria, which replaced polyuria. The dissociation of ketone bodies is accompanied by an equimolar production of hydrogen ions. Under conditions of decompensated diabetes, the production of ketone bodies and, consequently, the formation of hydrogen ions exceed the buffering capacity of body tissues and fluids, which leads to the development of severe metabolic acidosis.
The severity of the condition in ketoacidosis is due to a sharp dehydration of the body, decompensated metabolic acidosis, a pronounced deficiency of electrolytes (potassium, sodium, phosphorus, magnesium, etc.), hypoxia, hyperosmolarity (in most cases) and often concomitant intercurrent disease.

Clinical picture

Ketoacidosis develops gradually over several days. In the presence of severe concomitant infection, the clinical picture of ketoacidosis unfolds in a shorter time.
Early clinical symptoms ketoacidosis are typical signs of DM decompensation, such as increasing dryness of the mucous membranes and skin, thirst, polyuria, subsequently replaced by oliguria and anuria, weakness, headache, drowsiness, loss of appetite, weight loss, the appearance of a slight smell of acetone in the exhaled air. In case of failure to provide timely assistance, metabolic disorders are aggravated, and the above-described Clinical signs supplemented by nonspecific symptoms of intoxication and acidosis, such as headache, dizziness, nausea and vomiting, which soon becomes more frequent and becomes indomitable. The vomit in ketoacidosis is often bloody-brown in color and doctors mistake it for vomiting.” coffee grounds". As ketoacidosis increases, the smell of acetone in the exhaled air increases, and breathing becomes frequent, noisy and deep (respiratory compensation, Kussmaul breathing).
A symptom that is observed in more than half of patients deserves special attention - the so-called “ abdominal syndrome" ketoacidosis, manifested by the clinic "acute abdomen". Often, the combination of abdominal pain, vomiting, and leukocytosis observed in ketoacidosis leads to diagnostic errors and surgical interventions that are unacceptable in this state, often ending in death. The risk of such errors is especially high in the case of manifestation of diabetes in a state of ketoacidosis.
An objective examination shows pronounced signs of dehydration (in severe cases, patients lose up to 10-12% of body weight). Tissue turgor is sharply reduced. The eyeballs become soft and skin and visible mucous membranes are dry. Tongue coated with thick brown coating. Muscle tone, tendon reflexes, body temperature and arterial pressure reduced. A frequent pulse of weak filling and tension is determined. The liver, as a rule, protrudes significantly from under the edge of the costal arch and is painful on palpation. Kussmaul's breath is accompanied by a pungent odor of acetone in the exhaled air.
When examining patients in a state of ketoacidosis, it is necessary to clarify the cause that provoked decompensation of diabetes as soon as possible. If there is a concomitant intercurrent disease, treatment should be started immediately.
From the first signs of DM decompensation, patients show signs of first mild, and then more and more pronounced CNS depression. So, at first, patients complain of a headache, become irritable, and then lethargic, lethargic, drowsy. The developing state of stunnedness is characterized by a decrease in the level of wakefulness, a slowdown in conscious reactions to stimuli, and an increase in periods of sleep. As metabolic disorders worsen, a state of stupor, often called a precomatous state, is clinically manifested by deep sleep or unresponsiveness similar to it in behavioral reactions. The final stage of increasing CNS depression is coma, characterized by total absence consciousness.
In a blood test, hyperglycemia, hyperketonemia, an increase in the level of urea nitrogen, creatinine and, in some cases, lactate are determined. Plasma sodium levels are usually low. Despite a significant loss of potassium with osmotic diuresis, vomit and stool, leading to a pronounced deficiency of this electrolyte in the body, its plasma concentration may be normal or even slightly elevated in anuria. In the study of urine, glucosuria, ketonuria and proteinuria are determined. The acid-base state (ACS) reflects decompensated metabolic acidosis, with blood pH dropping below 7.0 in severe cases. The ECG may show signs of myocardial hypoxia and conduction disturbances.
In the event that it is known that the patient has diabetes, the diagnosis of ketoacidosis and ketoacidotic coma is not difficult. The diagnosis is confirmed by the above clinical picture, laboratory parameters (primarily hyperglycemia, the presence of glucose and ketone bodies in the urine) and CBS, indicating the presence of decompensated metabolic acidosis. In the case of manifestation of diabetes immediately in a state of ketoacidosis or coma, one should first of all focus on the presence of severe dehydration, signs of acidosis (Kussmaul respiration) and significant weight loss in a short period of time. At the same time, the CBS study excludes respiratory alkalosis as the cause of hyperventilation and confirms the presence of metabolic acidosis in the patient. In addition, the smell of acetone in the exhaled air should lead the doctor to the idea that the patient has ketoacidosis. Lactate acidosis, uremia, alcoholic ketoacidosis, poisoning with acids, methanol, ethylene glycol, paraldehyde, salicylates (other causes of metabolic acidosis) are not accompanied by such pronounced dehydration and significant weight loss, and also manifest a typical clinical picture for them. The presence of hyperglycemia and ketonuria confirms the diagnosis of DM and ketoacidosis.

Treatment

Treatment of patients in a state of decompensated diabetes, and even more so in a state of ketoacidosis or ketoacidotic coma, should begin immediately. Patients are hospitalized in a specialized department, and in a state of coma - in the intensive care unit.
The main goals of ketoacidosis therapy are to combat dehydration and hypovolemic shock, restore physiological acid-base balance, normalize electrolyte balance, eliminate intoxication, and treat comorbidities.
Immediately before the start of therapy, the patient's stomach is washed with a solution of sodium bicarbonate. A urinary catheter is inserted to monitor kidney function and account for diuresis. In order to improve tissue oxygenation, oxygen inhalation is established. Considering hypothermia, the patient must be warmly covered, and the solutions should be administered warm.
To monitor the effectiveness of ongoing therapy before treatment, control glycemia, blood pH, pCO 2, the level of K, Na, lactate and ketone bodies in the blood, glucosuria and ketonuria, blood pressure, ECG, hemoglobin levels, hematocrit, respiratory rate (RR), pulse . Subsequently, it is necessary to hourly monitor glycemia, blood pH, pCO 2 , blood pressure, ECG, respiratory rate, pulse. You can evaluate other indicators every 2-3 hours.
An important prognostic value (especially in a state of coma) is the assessment of the reaction of pupils to light. A weak reaction or its complete absence indicates the development of structural changes in the brain stem and a low probability of a favorable outcome of the disease.
Rehydration is very important in the treatment of diabetic ketoacidosis due to the large role of dehydration in the chain of metabolic disorders in this condition. The volume of lost fluid is replenished with physiological (or hypotonic with hyperosmolarity) and 5-10% glucose solutions. Termination of infusion therapy is possible only with a full recovery of consciousness, the absence of nausea, vomiting and the possibility of fluid intake by the patient per os. During the first hour, 1 liter of 0.9% NaCl solution is injected intravenously. In the presence of hyperosmolarity, saline may be replaced with a hypotonic 0.45% NaCl solution.
The effective osmolarity is calculated using the following formula:
Osmolarity = 2 + blood glucose (mOsm) (mmol/l), normal value = 297 ± 2 mOsm/l
Over the next two hours from the start of therapy, 500 ml of a 0.9% NaCl solution are injected hourly. In the following hours, the rate of fluid administration should usually not exceed 300 ml./h After reducing the level of glycemia below 14 mmol / l, the physiological solution is replaced with a 5 - 10% glucose solution and administered at the rate indicated above. The appointment of glucose at this stage is dictated by a number of reasons, among which the main one is maintaining the necessary osmolarity of the blood. A rapid decrease in the level of glycemia and the concentration of other high-osmolar blood components during infusion therapy often causes an undesirable rapid decrease in plasma osmolarity.
insulin therapy begin immediately after the diagnosis of ketoacidosis. In the treatment of ketoacidosis, as well as any other urgent condition in diabetes, only short-acting insulin is used (Actrapid MS, Actrapid NM, Humulin R, Insuman Rapid, etc.). Before the normalization of CBS and the decrease in the level of glycemia below 14.0 mmol / l, insulin is administered only intravenously by drip or intramuscularly into the rectus abdominis muscle. Upon reaching the indicated level of glycemia and normalization of the CBS, the patient is transferred to the subcutaneous injection of short-acting insulin.
The dose of insulin in the first hour of treatment is 10 units intravenously by bolus or 20 units intramuscularly. In the case of concomitant severe purulent infection, the first dose of insulin can be doubled.
Subsequently, an average of 6 IU of short-acting insulin is administered hourly intramuscularly or together with physiological NaCl solution intravenously. To do this, 10 IU of insulin for every 100 ml of physiological saline is added to a separate container with a 0.9% NaCl solution. The resulting mixture is thoroughly shaken. In order to adsorb insulin on the walls of the system, 50 ml of the mixture is passed through it in a jet. The use of previously used albumin solutions for the same purpose is now considered optional. 60 ml of this mixture is injected intravenously every hour. In the event that during the first 2-3 hours from the start of therapy the level of glycemia does not decrease, it is recommended to double the dose of insulin in the next hour.
Upon reaching the level of glycemia 12 - 14 mmol / l, the dose of insulin administered is reduced by 2 times - up to 3 units hourly (30 ml of a mixture of insulin and saline). At this stage of therapy, it is possible to transfer the patient to intramuscular injections of insulin, however, it should be borne in mind that the insulin syringes used and the various individual systems for administering the hormone are equipped with needles only for subcutaneous insulin injection.
One should not strive to reduce the level of glycemia below 10 mmol / l, since this increases the risk of not only hypoglycemia, but, above all, hyposmolarity. However, if glycemia falls below 10 mmol/l with persistent acidosis, it is recommended that insulin be continued hourly and the dose reduced to 2 to 3 U/h. With the normalization of CBS (mild ketonuria may persist), the patient should be transferred to subcutaneous insulin, 6 IU every 2 hours, and then every 4 hours at the same dose.
In the absence of ketoacidosis on the 2nd - 3rd day of treatment, the patient can be transferred to 5 - 6 single injections of short-acting insulin, and later on to conventional combined insulin therapy.
Restoration of electrolyte balance , primarily potassium deficiency, is an important component complex treatment ketoacidosis. Usually, the introduction of KCl is started 2 hours after the start of infusion therapy. However, if before the start of treatment there are already ECG or laboratory signs confirming hypokalemia in the absence of anuria, potassium administration can be started immediately, since the administration of liquid and insulin contributes to a rapid decrease in the level of potassium in the blood by diluting its concentration and normalizing the transport of potassium into the cell .
The dose of KCL solution administered by intravenous drip depends on the concentration of potassium in the plasma. So, at a potassium level below 3 mmol / l, it is necessary to inject 3 g / h (dry matter), at 3 - 4 mmol / l - 2 g / h, at 4 - 5 mmol / l - 1.5 g / h, at 5 - 6 mmol / l - 0.5 g / h. Upon reaching a plasma potassium level of 6 mmol / l, the administration of the KCl solution should be discontinued.
As a rule, patients do not need additional correction of hypophosphatemia. The question of the need for the introduction of potassium phosphate arises only if the level of phosphorus in plasma decreases below 1 mg%.
Restoration of KOS begins literally from the first minutes of the treatment of ketoacidosis, thanks to the appointment of liquid and the introduction of insulin. The restoration of fluid volume triggers physiological buffer systems, in particular, the ability of the kidneys to reabsorb bicarbonates is restored. The administration of insulin suppresses ketogenesis and thereby reduces the concentration of hydrogen ions in the blood. However, in some cases, the question arises of the need to prescribe sodium bicarbonate in order to correct the CBS. It was noted above that even a significant peripheral metabolic acidosis is not always accompanied by an equally pronounced CNS acidosis, due to the presence of a number of protective and adaptive mechanisms. According to J. Ohman et al. J. Posner and F. Plum, in patients with diabetic ketoacidosis before therapy, the pH of the cerebrospinal fluid is usually within the normal range. Attempts to correct plasma acidosis with intravenous administration of sodium bicarbonate can lead to the rapid development of CNS acidosis and a sharp deterioration in the patient's state of consciousness. Taking into account the described side effects with the introduction of soda, very stringent criteria for the appointment of sodium bicarbonate in diabetic ketoacidosis have been developed. The question of the advisability of introducing soda should be considered only at a blood pH level below 7.0. It should be emphasized that in this case it is very important to constantly monitor changes in acid-base balance, and when a pH value of 7.0 is reached, the introduction of bicarbonate should be stopped. Use a 4% solution of sodium bicarbonate at the rate of 2.5 ml per 1 kg of actual body weight intravenously drip very slowly. With the introduction of sodium bicarbonate, a KCl solution is additionally injected intravenously at the rate of 1.5-2 g of KCl of dry matter.
In order to treatment or prevention inflammatory diseases broad-spectrum antibiotics are prescribed.
For improve the rheological properties of blood and prevention of disseminated intravascular coagulation, twice on the first day of treatment, 5000 units of heparin are administered intravenously under the control of a coagulogram.
In order to normalize oxidative processes, 150 - 200 ml of cocarboxylase and 5 ml of a 5% solution of ascorbic acid are added.
With low blood pressure and other symptoms of shock, therapy is carried out aimed at increasing and maintaining blood pressure and cardiac activity.
After removing the patient from the state of ketoacidosis, a sparing diet rich in carbohydrates, proteins, and potassium is prescribed. Fats are excluded from the diet for at least a week.

Complications of ketoacidosis

Among the complications arising from the treatment of ketoacidosis, the greatest danger is cerebral edema, which ends in death in 70% of cases (R. Couch et al., 1991; A. Glasgow, 1991). The most common cause of cerebral edema is a rapid decrease in plasma osmolarity and glycemia levels during infusion therapy and insulin administration. In the case of the use of sodium bicarbonate in order to correct acidosis, additional prerequisites are created for the occurrence of this formidable complication. An imbalance between the pH of peripheral blood and cerebrospinal fluid contributes to an increase in the pressure of the latter and facilitates the transport of water from the intercellular space to brain cells, the osmolarity of which is increased. Usually cerebral edema develops after 4-6 hours from the start of therapy for diabetic ketoacidosis. In the event that the patient's consciousness is preserved, the signs of the onset of cerebral edema are deterioration in well-being, severe headache and dizziness, nausea, vomiting, visual disturbances, as well as tension of the eyeballs, instability of hemodynamic parameters, increasing fever. Typically listed clinical symptoms appear after a “bright” period of improvement in well-being against the background of an obvious positive dynamics of laboratory parameters.
It is much more difficult to suspect the onset of cerebral edema in patients in a state of ketoacidotic coma. A sure sign of this complication at the initial stage is the absence of positive dynamics in the state of consciousness of the patient against the background of an objective improvement in carbohydrate metabolism. The clinical signs of cerebral edema described above are accompanied by a decrease or absence of pupillary response to light, ophthalmoplegia, and edema of the optic nerve. Ultrasound encephalography and CT scan confirm the diagnosis.
Treatment of cerebral edema is much more difficult than the diagnosis of this condition. When confirming the presence of cerebral edema in a patient, osmotic diuretics are prescribed - intravenous drip of a mannitol solution at the rate of 1 - 2 g / kg. This is followed by intravenous injection of 80-120 mg of lasix and 10 ml of hypertonic sodium chloride solution. The question of the advisability of prescribing glucocorticoids (preference is given exclusively to dexamethasone due to its minimal mineralocorticoid properties) has not been fully resolved. It is believed that the greatest effect from the appointment of these hormones is observed with cerebral edema on the background of an injury or tumor. However, given the ability of glucocorticoids to reduce pathologically increased vascular permeability and the blood-brain barrier, normalize ion transport through the cell membrane and inhibit the activity of lysosomal enzymes of brain cells, the question of the advisability of their appointment for cerebral edema in ketoacidosis should be decided individually. To ongoing therapeutic measures are added brain hypothermia and active hyperventilation of the lungs in order to reduce intracranial pressure due to the resulting vasoconstriction. In some cases, a craniotomy should be considered.
Among other complications of ketoacidosis and its therapy, one should highlight disseminated intravascular coagulation, pulmonary edema, acute cardiovascular insufficiency, hypokalemia, metabolic alkalosis, asphyxia due to aspiration of gastric contents.
Strict monitoring of hemodynamic parameters, hemostasis, electrolytes, changes in osmolarity and neurological symptoms makes it possible to suspect the above complications in the early stages and immediately take effective measures aimed at their elimination.

Literature:

1. Krane E. Diabetic Ketoacidosis. Ped Clinics N Amer 1987;34:935-60.
2. Plum F., Posner J.B. Diagnosis of stupor and coma. Translated from English: Medicine, 1986. - 544 p. ill.
3. Beaser R. Diabetic emergencies. Joslin Diabetes Center. lecture notes. October, 1992:12.
4. Diabetic ketoacidosis - A Scheme for management. In: Diabetes in the Young. ISGD. Official Bulletin 1990;23:13-5.