Causes and treatment of ketoacidotic coma. Diabetic ketoacidotic coma

Ketoacidotic coma is a serious and extremely dangerous consequence of diabetes mellitus. It occurs due to a lack of insulin in the blood, which develops against the background of incorrectly selected insulin therapy. If a person is not provided with timely and qualified medical care, he may die.

Statistics show that ketoacidotic coma occurs in 0.4% of cases of diabetes. Almost always this condition can be stopped. Greatest danger this phenomenon presents in the elderly and children.

Causes

Ketoacidotic coma is caused by improper insulin therapy in diabetes mellitus.

This may be explained by:

• Excessive consumption of alcoholic beverages during treatment;
• Violation of the drug administration technique;
• Incorrect or irregular use of sugar-lowering drugs;
• Insufficient dose of insulin or skipping its administration;
• Availability bad habits, changing insulin production;
• Aggravation of diabetes mellitus by other diseases;
• Taking a number of medications;
• Lack of control over metabolism.

Modern experts argue that ketoacidotic coma usually haunts patients with type 1 diabetes.

If you manage to identify it exact reason, the doctor will be able to take appropriate measures to exclude serious complications.

Symptoms

Symptoms of ketoacidotic coma depend on the type of condition. There are several clinical courses that require completely different effects on the problem. Experts adhere to the following classification:

• Gastrointestinal ketoacidotic coma - manifested by severe pain in the abdominal area, increased body temperature, dry mouth followed by loss of consciousness.
• Renal ketoacidotic coma - it can be recognized by proteinuria, nephroangiopathy, changes in the qualitative composition of urinary sediment.
• Cardiovascular ketoacidotic coma - manifests itself in serious damage to the cardiovascular system, collapse may occur.
• Encephalopathic ketoacidotic coma - it can be recognized by asymmetry of reflexes, hemiparesis, and damage to the blood vessels of the brain. The person experiences severe headaches and fogginess.

Stages

The stages of ketoacidotic coma are distinguished by their gradualness. On average, several days pass from the initial signs of this phenomenon to the onset of coma. It all starts with an acid-base disorder. Experts distinguish the following stages:

• Beginning ketoacidosis manifests itself as symptoms of decompensated diabetes mellitus. A person begins to suffer from constant thirst, a feeling of dry mouth, headache, nausea and vomiting. He also appears Strong smell acetone from the mouth. This condition can be clinically determined by a sharp increase in blood glucose levels.
• Precoma - occurs only if no urgent measures have been taken. It is characterized by constant vomiting, diarrhea or constipation. Many patients complain of strong painful sensations in the abdominal area, drowsiness, disorientation and apathy.
• Coma is a serious complication that requires immediate medical attention. The person loses consciousness and experiences deep and noisy breathing. All internal processes begin to proceed in a special way.

Urgent Care

Diabetes mellitus is a serious disease that all close relatives and people of the patient should be aware of.

If necessary, they must understand what is required of them.

The algorithm for the onset of ketoacidotic coma is as follows:

1. When the first signs of deterioration of the patient’s condition appear: loss of consciousness, rare breathing, - it is necessary to call an ambulance;
2. Before the doctor arrives, you must check your blood pressure and heart rate every 5 minutes;
3. Try to ask the patient questions so that he remains conscious;
4. Pat his face and rub his earlobes for the same purpose.

When the ambulance arrives, doctors will have to take the following measures:

• Inject a small dose of insulin subcutaneously;
• Enter saline solution to facilitate dehydration of the body.

After this, the patient is immediately hospitalized and taken to the hospital. Typically, such patients are sent to the intensive care unit. All necessary therapeutic measures are carried out there.

Diagnostics

To diagnose ketoacidotic coma, a detailed examination of the patient is performed. If he is conscious, the doctor asks clarifying questions and asks about the characteristics of his condition. After this, the patient is sent for a series of laboratory tests, which allow a final conclusion to be made. Diagnosis of this condition includes the following:

• The glucose level as a result of a general blood test ranges from 16-38 mmol/liter.
• Also as a result of this study, you can notice an increased level of hematocrit and hemoglobin, which indicates severe dehydration.
• Ketone bodies in TAM will be significantly increased.
• The level of sodium in the blood will be increased, and potassium will be increased. This can be found out from the results of a biochemical blood test. The growth of urea is also assessed there.
• An acid-base blood test can identify metabolic disorders. It is characterized by an increase in osmolarity to 300 mOsmol/L.
• Blood pressure drops and heart rate increases.

Features of treatment

Treatment of patients with symptoms of ketoacidotic coma or its acute form requires immediate hospitalization. Such people are sent to the intensive care unit, where they are under constant supervision of the attending physicians. After this is carried out differential diagnosis. To distinguish ancestor from coma, the patient is injected with 10-20 cc of insulin. Other therapeutic measures are prescribed only after an accurate diagnosis has been established.

Treatment of diabetic coma requires immediate insulin replacement. This will help normalize blood sugar levels, resulting in an overall improvement in well-being. After this, the patient is given a sodium solution to help get rid of dehydration.

After the doctor confirms ketoacidotic coma, he prescribes insulin injections to the patient. They are administered by jet or intramuscularly at a rate of 10-20 units per hour.

After this, the specialist checks the blood glucose level every hour, after which he makes the appropriate prescriptions.

As the condition improves, the insulin dose is gradually reduced.

To eliminate the manifestations of general dehydration of the body, during a diabetic coma, the patient begins to inject a large amount of liquids into a vein. Initially, a sodium chloride solution is used for this purpose. It should be taken into account that depending on the duration of therapy, the rate of drug administration changes. When the patient's consciousness returns to normal, infusion therapy is stopped.

Special positive result gives energy treatment started at the very beginning of the coma. It helps prevent the development of serious complications in the future.

Treatment errors

Treatment of ketoacidotic coma requires high qualifications from the attending physician. This condition, if treated incorrectly, can lead not only to serious consequences, but even to death. Studies have shown that the most common errors in treatment are:

1. Inadequate insulin therapy, which often leads to a sharp decrease in blood sugar;
2. Insufficient rate of rehydration can lead to hypovolemic shock;
3. Insufficient control over blood glucose levels, due to which the body does not receive the correct treatment;
4. Too fast a rate of decrease in blood sugar, which causes cerebral lining;
5. Insufficient rate of potassium replenishment, which causes the cardiovascular system to suffer.

Monitoring the patient

When the patient is in a ketoacidotic coma, they are constantly monitored. The doctor needs to know how his body works in order to make timely adjustments to the treatment regimen. Control is carried out as follows:

1. Every hour - pulse, blood pressure level, respiratory rate, blood sugar level, state of consciousness, fluid balance, concentration of gases in arterial blood;
2. Every 2-4 hours - the concentration of ketones and mineral components in the serum;
3. Every 8 hours – level of temperature and body weight;
4. After each urination, the level of glucose and ketones in the urine.

Such serious monitoring of the patient is explained by the fact that the patient may experience complications at any time. The most undesirable consequences of ketoacidotic coma, complicating its treatment, are:

• Hyperglycemia or hypoglycemia;
• Hyperchloremia;
• Thromboembolic formations;
• Kidney failure;
• Oxygen starvation, which causes tissue death;
• Metabolic disease.

Prevention

To prevent serious consequences, you must always remember to prevent ketoacidotic coma. Activities include:

• Check blood glucose once a week;
• Following a special diet;
• Taking medications that lower glucose levels;
• Constant monitoring of the body’s condition;
• Rejection of bad habits;
• Timely treatment of all emerging diseases;
• Regular visits to your doctor;
• Maintaining a healthy lifestyle;
• Active and mobile lifestyle.

The patient can recognize the first signs of ketoacidotic coma on his own. It is very important that the treating specialist tells you in advance what to look for. In this case, the person will be able to independently seek medical help to prevent the development of serious complications. Regular monitoring of blood sugar levels will help control the body and also prevent ketoacidotic coma.

Possible complications

Ketoacidotic coma is a serious consequence of diabetes mellitus. In case of incorrect or untimely provision medical care the patient may experience serious complications. The greatest danger is cerebral edema. This phenomenon in the vast majority of cases ends in death. Recognize possible appearance swelling in the brain can be determined by the absence of favorable changes in the patient, despite all the therapeutic measures taken. In this case, the doctor diagnoses a significant improvement in the metabolism of carbohydrates and fats.

Cerebral edema can be recognized by decreased or absent pupillary response to light, papilledema, or ophthalmoplegia.

To confirm this diagnosis, the specialist sends the patient for a computed tomography and ultrasound encephalography.

EEC and REC are also performed to assess the processes occurring in the brain. With their help, you can promptly identify any complications and prescribe appropriate treatment.

Also, complications of ketoacidotic coma may include pulmonary edema, decreased coagulability within blood vessels, metabolic alkalosis, cardiovascular failure, and asphyxia of gastric tract contents.

To prevent such serious consequences of this disease, a specialist must regularly send the patient for a blood test. It is necessary to determine the amount of electrolytes in the blood, hemostasis and hemodynamics. Timely diagnosis any deviations will help to quickly eliminate them, due to which the risk of any complications will be minimal.

Ketoacidotic (diabetic) coma is an acute complication of diabetes mellitus in the decompensation stage, 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 registered in 1-6% of patients with diabetes mellitus.

There are two types of diabetes mellitus (Table 3).

Table 3. Types of diabetes mellitus

Etiology:

untreated diabetes mellitus;

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

non-compliance with diet;

alcohol or food intoxication.

Risk factors: obesity, acromegaly, stress, pancreatitis, liver cirrhosis, use of glucocorticoids, diuretics, contraceptives, pregnancy, family history.

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

Clinical manifestations of coma develop slowly - over several hours or even days; Coma occurs more quickly in children than in adults.

Stages of ketoacidotic coma:

Stage I - compensated ketoacidosis;

Stage II - decompensated ketoacidosis (precoma);

Stage III - ketoacidotic coma.

Characteristic 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 intensifies, vomiting and abdominal pain appear. The tongue is dry, coated; Skin turgor is reduced, polyuria is pronounced, and the exhaled air smells of acetone.

Stage III is characterized by: severe disturbances of consciousness (stupor or deep coma), pupils are constricted, facial features are sharpened; the tone of the eyeballs, muscles, tendon reflexes is sharply reduced; signs of peripheral circulatory disorders (arterial hypotension, tachycardia, cold extremities). Despite severe dehydration, increased diuresis persists. The breathing is deep, loud (Kussmaul breathing), the exhaled air smells of acetone.

Clinical forms of ketoacidotic coma:

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

cardiovascular (hemodynamic disturbances are pronounced);

renal (oligo- or anuria);

encephalopathic (resembles a stroke).

Differential diagnosis of ketoacidotic coma must 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 condition after prolonged fasting, alcohol intoxication, diseases of the stomach, intestines, and liver.

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

The development of lactic acidosis is possible when the level of lactate in the blood is about 5 mmol/l. Lactic acidosis can be combined with diabetic ketoacidosis. If lactic acidosis is suspected, a study of lactate levels in the blood is necessary.

When intoxicated with salicylates, metabolic acidosis develops, but primary respiratory alkalosis may develop, while the glycemic level is normal or reduced. It is necessary to study the level of salicylates in the blood.

The level of ketones in methanol poisoning is slightly increased. Characterized by visual disturbances and abdominal pain. Glycemia level is normal or elevated. A study of methanol levels is necessary.

In chronic renal failure, moderate acidosis is detected, while the level of ketones is within normal limits. An increase in creatinine levels in the blood is typical.

Treatment begin with the administration of an isotonic sodium chloride solution after determining the level of glucose in the blood. Insulin is immediately administered intravenously (10 units, or 0.15 units/kg, after 2 hours - intravenous drip 6 units/hour). If there is no effect, the rate of administration is doubled. When the glycemic level decreases to 13 mmol/l, switch to intravenous administration 5-10% glucose solution with insulin. When the blood glucose level decreases to less than 14 mmol/l, an infusion of 5% glucose solution is performed (1000 ml during the first hour, 500 ml/h over the next two hours, from the 4th hour - 300 ml/h).

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

Diabetic coma

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

There are the following types of diabetic coma: ketoacidotic, hyperosmolar and hyperlactic acidemic. In diabetes mellitus, hypoglycemic coma most often occurs.

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 neuropsychic) ​​disorders [Prikhozhan V. M, 1973, 1981]. Ketoacidotic coma occurs 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 clinical examination, insufficient awareness of medical personnel about diabetes mellitus, incorrect diagnosis, ignoring the need for laboratory monitoring, incorrect or 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, indiscipline of the patient (gross violation of diet, cancellation or insufficient administration of insulin, etc.). ), self-medication, formal, superficial analysis of the causes of comas and their outcomes, insufficient and unsatisfactory promotion of basic knowledge on diabetes among the population, lack of awareness of the patient and people around him about the symptoms of diabetes, the first signs of a coma, elements of first aid, late appeal to doctor; b) physical trauma (surgery, etc.), burns, frostbite, food or other poisoning, mental trauma; addition to diabetes mellitus of other diseases that contribute to the deterioration of diabetes mellitus compensation (influenza, pneumonia, myocardial infarction, etc.).

Pathogenesis. The pathogenesis of ketoacidosis and ketoacidotic coma is caused by an 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 to glucose in muscle and adipose tissue, inhibition of the process of glucose phosphorylation (decreased activity of the hexokinase enzyme) and its oxidation, slowdown of lipogenesis processes of excess glucose production in the liver (increased neoglucogenesis from protein and fat), increased secretion from the liver (increased activity of the enzyme glucose-6-phosphatase). This causes significant hyperglycemia and glycosuria (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 glucose production.

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 the intercellular spaces. As a result of tissue dehydration, thirst occurs (polydipsia), normal cellular metabolism is disrupted and diuresis increases (polyuria). Polyuria is also caused by increased osmotic pressure urine. The latter is explained, on the one hand, by glucosuria, and on the other, by the excretion in the urine of products of protein and lipid metabolism (ketone bodies, etc.), as well as sodium ions. 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 cycle of carbohydrate conversion), which entails difficulty in the synthesis of higher fatty acids from acetyl coenzyme A. Disruption of the glycolytic pathway of glucose breakdown also leads to a decrease in the formation alpha-glycerol phosphoric acid, necessary for the synthesis of triglycerides. As a result, lipogenesis and resynthesis of triglycerides in adipose tissue, liver and lung tissue are inhibited, followed by a predominance of its lipolytic activity and increased lipolysis.

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

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

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

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%, when determined by the Leites and Odinov method). When excessively accumulated in the blood, ketone bodies have a narcotic effect. Ketone bodies include beta-hydroxy-butyric acid, acetoacetic acid, and 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 liver infiltration is promoted by depletion of the liver in glycogen, insufficiency of lipotropic nutritional factors, excessive production of pituitary somatotropic hormone (GH), a 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, and 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 acetyl coenzyme A, which are the raw materials for the formation of cholesterol, are formed in increased quantities, and 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. With 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 water-salt metabolism- decrease in the content of sodium, phosphorus and chlorides in the blood. The level of potassium in the blood is initially increased, and then decreased, which is 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 contained mainly in the extracellular fluid, and potassium in the intracellular fluid. In this regard, initially more sodium is excreted in the urine than potassium. Increased urinary sodium excretion leads to dehydration and increased polyuria. Electrolyte imbalance 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 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. Arises metabolic acidosis, 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 removal from the body with exhaled air and kidneys.. The accumulation of excess carbon dioxide in the blood (respiratory acidosis) irritates the respiratory center, in As a result, deep Kussmaul breathing occurs, 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), and increased excretion of mono-basic phosphates.

The volume of extracellular fluid decreases, resulting in collapse with a drop in blood pressure in the vessels of the kidneys and brain. Loss of body fluid during coma can reach 10°/about body weight, i.e. approximately 6-7 liters. Renal blood flow and glomerular filtration decrease. The release of nitrogenous metabolic products is disrupted, and therefore the excretion of hydrogen ions decreases and decompensated acidosis develops. Severe ketosis leads to inhibition of brain enzyme systems, resulting in reduced glucose utilization 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 breakdown products are formed in increased quantities, which leads to hyperazotemia, hyperazoturia. The latter is due to increased formation of ammonia both in the liver and in the kidneys from glutamine.

Increased breakdown of tissue proteins and disruption of their resynthesis from amino acids aggravate the intoxication of the body and create conditions of oxygen starvation (hypoxia) for brain tissue. This leads to respiratory distress, collapse, decreased muscle tone, and disruption of higher nervous activity. Loss of consciousness during ketoacidotic coma is caused by a decrease in glucose utilization by 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 - over a period of 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, sometimes vomiting, headache of a pulsating, bursting nature, pain in the limbs and trunk (neuromyalgia), increased polydipsia and polyuria, the appearance of the smell of acetone in the exhaled air. Stage II (severe ketoacidotic state) is characterized by drowsiness and stupor. In stage III (severe ketoacidotic state), stupor is observed. In case of stupor, the patient can be awakened only with the help of strong irritants. Pain sensitivity, as well as swallowing, pupillary and corneal reflexes are preserved. Tendon reflexes are still high.

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

To differentiate a false acute abdomen from a true one, G. B. Isaev (1982) suggests conducting 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 abdominal pain does not subside, it should be regarded as true.

Here is our own observation.

The presented observation once again emphasizes that in some cases, differentiating a false acute abdomen from a true one is quite difficult. This led to an erroneous diagnosis of a 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 false and true acute abdomen are very arbitrary.

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

In ketoacidotic coma, atrial flutter and fibrillation and extrasystole may be observed. The ECG shows a decrease in the wave T and lengthening 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 (heart or vascular insufficiency prevails - collapse); 2) gastrointestinal (clinical picture of acute abdomen, cholera); 3) renal (dysuric phenomena, hyperazotemia, proteinuria, tsvdshdruria, etc. come to the fore, and acetonuria and glucosuria are absent due to sharp decline glomerular filtration); 4) encephalopathic (clinical picture of cerebrovascular accident).

Laboratory data. Determination of the level of sugar and ketone bodies in the blood is of decisive importance in the diagnosis of ketoacidotic coma. During the precoma period, blood sugar usually exceeds 16.6 mmol/l (300 mg%). Glucosuria increases sharply. Intensifying

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

In ketoacidotic coma, blood sugar sometimes reaches 55.5 mmol/l (1000 mg%) and even 111 mmol/l (2000 mg%). Ketosis increases sharply, reaching in some cases 172.2 mmol/l (1000 mg%) or more, blood pH decreases to 7.2 and lower (the norm is 7.35-7.45 for arterial and capillary blood). There is a sharp decrease in the alkaline reserve of the blood down to 5% by volume (with a norm of 55-75% by volume). The level of standard bicarbonate (SB) drops sharply (normal 20-27 mmol/l). Normal indicators The acid-base state is presented in table: 3. In ketoacidotic coma, there is always neutrophilic leukocytosis in the blood. ESR is often elevated. The amount of hemoglobin and the number of red blood cells are usually increased. Sometimes due to intoxication there may be anemia. Blood osmolarity is increased. There is an increase in the blood levels of NEFA, 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 supply of potassium into cells as a result of improved carbohydrate and protein metabolism, increased permeability of cell membranes, as well as parenteral administration of potassium-poor solutions. The development of late hypokalemia is also facilitated by improved renal function, which leads to increased excretion of potassium in the urine. In some cases, early hypokalemia may occur, which is associated with massive cell destruction, loss of potassium, and the inability of cells to retain potassium with simultaneous kaliuria.

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) observed lethargic state. Changes in the cardiovascular system manifest themselves in the form of cyanosis, tachycardia, intracardiac conduction disturbances - supraventricular form of paroxysmal tachycardia, other rhythm disturbances up to ventricular fibrillation, characteristic changes on the ECG (decrease or flattening of the wave T, segment decline S-T, interval extension R- Q, appearance of tall and pointed teeth R, as well as pathological wave C/). As a result of respiratory paresis,

Asphyxia occurs in the body muscles. With hypokalemia due to atony of the smooth muscles of the stomach and intestines, impaired intestinal motility occurs, including paralytic obstruction, flatulence, vomiting, and dilatation of the stomach and intestines. Paresis is observed 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, severe acetonuria and glucosuria are observed, often proteinuria, cylindruria, and 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, is determined.

Blood sugar levels are determined by methods based on the reducing properties of glucose (Hagedorn-Jensen, Somogyi-Nelson methods) or on its color reactions with certain reagents (orthotoluidine method of Fried and Hoflmeier, etc.). By determining the blood sugar content using the Hagedorn-Jensen method, along with glucose in the blood, the content of other reducing substances (glutathione, creatinine, uric acid, ergothioneine, vitamin C, etc.). 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, determined by the Somogyi-Nelson method, is 3.3-5.6 mmol/l (60-100 mg%). Natelson's glucose oxidase method is more accurate (normal blood sugar is 2.8-5.3 mmol/l, or 50-96 mg%, orthotoluidine method (normal blood sugar is 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 the arterial and capillary.

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

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

The iodometric method (Engfeld-Pincussin 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's 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. The content of the daily amount of urine is determined. In the urine of healthy people, glucose is absent or is completely reabsorbed in the tubules. For the qualitative determination of sugar in urine, the methods of Benedict, Nylander and others, based on the reducing properties of sugar, are used. Nylander's test is as follows. 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 (Biofan G, Klinistix, etc.) impregnated with glucose oxidase and peroxidase. In the presence of glucose in the urine, the 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).

Quantitative determination of sugar in 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 increased amount ketone bodies. The Lange test is based on the properties of acetone and acetoacetic acid to give a violet color with sodium nitroprusside in an alkaline environment. In the USSR, tablets for determining acetone in urine are used for rapid diagnosis of acetonuria.

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

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

Ketoacidotic coma should be differentiated from hypoglycemic, hyperosmolar, hyperlactic acidemic, hepatic, uremic, apoplectic, hypochloremic, as well as poisoning with drugs and salicylates. Differential diagnostic signs of comatose states are presented in table. 4, 5.

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

diseases accompanied by cachexia. Ketosis and ketonuria can also be observed in healthy people during carbohydrate or general starvation. In connection with the above, 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. When diabetic coma is combined with myocardial infarction and cerebrovascular accident, the prognosis is poor.

Prevention. The main measures to prevent diabetic coma include early diagnosis diabetes mellitus, adequate insulin therapy, constant medical supervision with the study of sugar in the blood and urine once every 10-14 days, careful compensation of impaired metabolic processes (primarily carbohydrate metabolism), strict adherence by patients to the prescribed diet. In case of intercurrent infection or injury, the dose of insulin is increased depending on the glycemic profile. To avoid ketoacidosis, eliminate fats from the diet. Required

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

Dima thorough sanitation of even a minor inflammatory focus.

The Science and Chemistry of Hormones of the USSR Academy of Medical Sciences has 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 method of 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 size of the previous dose and the presence of concomitant diseases.

In case of ketoacidotic coma, both beginning and developing, it is necessary to immediately administer 100-200 units of insulin, of which 50 units intravenously, and the remaining part (50 units) intramuscularly. Insulin is administered intravenously in an isotonic sodium chloride solution at a rate not exceeding 50 units/30 min. In severe ketoacidosis, accompanied by stupor, or superficial coma, a single dose of 100 IU of insulin is administered, in severe coma - 120-160 IU, in deep coma - 200 IU.

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

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

In case of acute vascular disorders, it is more rational to use the method of insulin therapy proposed by J. Sheldon and D. Rucke (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, insulin administration is stopped or the dose is reduced according to the glycemia indicators and the patient’s condition. In these cases, constant (once per hour) determination of glycemia is necessary. It should be remembered that the administration of very large doses of insulin is dangerous due to the possible development of hypoglycemia, hypokalemia and cerebral edema.

To avoid hypoglycemia in children, a single dose of insulin during coma should not exceed 30 units (0.7-1 unit/kg). In case of complete (deep) coma, half of the first dose of insulin can be administered intravenously and half intramuscularly. After administering the first dose, insulin is prescribed during the first 2 days, 6-8 units intramuscularly every 2-3 hours under the control of glycemia and glucosuria,

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

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 administering insulin using the traditional method. When large doses of insulin are administered, there is a risk of developing late hypoglycemia, hypoosmolarity, cerebral edema and hyperlactic acidemia. A concentration of insulin is created in the blood that is much higher than physiological (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 glycemic level decreases more slowly, which significantly reduces the risk of late hypoglycemia, hypoosmolarity and cerebral edema. Frequent (every hour) intramuscular injection of insulin, compared to subcutaneous administration, ensures faster and more uniform absorption of insulin. A high and stable level of insulin in the blood is achieved faster. The possibility of late hypokalemia decreases. It has been established that when the insulin content in the blood is 10-20 µU/ml, glycogenolysis, gluconeogenesis and lipolysis are suppressed, and when the insulin concentration in the blood is 20-200 µU/ml, ketogenesis is suppressed and maximum transport of glucose and potassium occurs. When insulin is administered at a dose of 1 IU /h in the blood its concentration is reached, corresponding to 20 μU/ml. Thus, the introduction of exogenous insulin in a dose of 6-10 IU creates such a concentration in the blood that is necessary to suppress ketogenesis. For insulin therapy in small doses, depending on the severity of the coma, the drug is administered in a dose of 15-20 to 50 U/hour either intravenously for a long time (over 4-8 hours), or periodically intramuscularly (one injection per hour) under the control of glycemic levels.

M. Page et al. (1974) and others recommend administering 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, starting at a dose of 10-20 U/h (depending on the severity of the condition), and then 5-10 U/h. To avoid hypoglycemia when blood sugar levels drop to 16.7-11.1 mmol/l

(300-200 mg%) the dose of administered insulin is reduced to 2-4 U/hour. 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), with the “small dose regimen”, 16-20 IU of insulin are initially prescribed intramuscularly, and then 6-10 IU/hour are administered intramuscularly or intravenously. If, after 2 hours from the start of insulin therapy, blood sugar does not decrease, the authors recommend increasing the insulin dose to 12 U/hour.

When children are being brought out of a ketoacidotic coma, insulin is prescribed at a rate of 0.1 U/kg once, and then 0.1 U/(kg/h) intramuscularly or intravenously.

When choosing a “regime of large or small doses” of insulin, E. A. Vasyukova and G. S. Zefirova (1982) recommend using small doses of insulin with an initial glycemic level of no more than 35 mmol/l (630 mg%). However, we successfully brought patients out of coma by using a “small dose regimen” and at a much higher blood sugar level - up to 50 mmol/l (900 mg%). When choosing a “regime of large and small 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 during this period treatment with small doses of insulin is ineffective, then we switch to the “regime of large doses.” We continue treatment only with simple insulin using the “high and low dose regimen” until a stable decrease in glycemic levels to 14-11.1 mmol/l (250-200 mg%) is achieved.

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

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

its electrolyte composition (in particular, chloride content) is close to that of 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 administered parenterally in large quantities of isotonic sodium chloride solution, can increase acidosis. When the symptoms of dehydration decrease, 200-300 ml of fluid per hour is administered parenterally under the control of blood osmolarity. When the blood brightness osmol is more than 300 momol/l or the sodium content in the blood serum is more than 155 mmol/l, a hypotonic (0.45%) sodium chloride solution is infused 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 using the formula: osmo
plasma polarity (mosmol/l) = 2-(K + +Na +) (mmol/l) +
+ Glycemia (mmol/l) + Urea (mmol/l) +
Proteins (g/l) x 0.243
8 "

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

At cardiovascular pathology, edema and for patients over 60 years of age, the total volume of administered fluid is reduced to 1.5-3 liters. In the first 6 hours of bringing the patient out of coma, 50% is usually administered, in the next 6 hours - 25%, in the next 12 hours - 25% of the total amount of liquid. Rapid rehydration can lead to left ventricular overload and cerebral edema. Drip intravenous fluid administration is continued until the patient regains consciousness. Lack of diuresis during rehydration is an indication for hemodialysis.

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

Intravenous drip infusion of 5% glucose solution can be prescribed in more early dates. This may occur 2-3 hours after 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%). For symptoms of hypoglycemia (tremors, 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, kaliuria 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 a potassium level 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 impaired renal filtration function. With hyperkalemia, an increase in the interval is noted on the ECG S - T, tall pointed prong T and reduced 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 quantities (1-1.5 g per liter of fluid administered). Indications for prescribing potassium supplements after recovery from coma are muscle paresis and characteristic ECG changes (extension of the interval P - Q, segment decline S - T, expansion and flattening of the tooth T, pronounced pathological tooth U).

Before the patient begins to recover from a diabetic coma, kaliuria is not accompanied by hypokalemia. During insulin therapy, the level of potassium in the blood drops in proportion to the amount of insulin administered. Thus, with the “high-dose regimen” 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 regimen” it is significantly less - 100-200 mmol/day (100- 200 mEq/day).

To eliminate hypokalemia, potassium chloride is administered intravenously 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).

When a hypokalemic crisis develops, potassium chloride is administered intravenously at a dose of 2 g (27 mmol, or 27 mEq) in a 5% glucose solution over 15 minutes under ECG monitoring.

To avoid the development of hypokalemia, potassium chloride is administered intravenously at a dose of 8-14 mmol/h (8-14 mEq/h) throughout 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 if the level is below 5 mmol/l - at a dose of 13-20 mmol/h ( 13-20 meq/hour, i.e. 10-15 ml of 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. Sodium bicarbonate is used to combat acidosis. When administered, cerebral edema, severe hypokalemia and hypernatremia, a decrease in the pH of the cerebrospinal fluid, and impaired oxyhemoglobin dissociation may occur. In this regard, an isotonic (2.5%) sodium bicarbonate solution is administered only when the arterial blood pH is less than 7.0. When the blood pH is more than 7.0, the administration 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 administer no more than half of the calculated dose at a time. To calculate the dose of sodium bicarbonate, you can use another formula:

Normal level of sodium - Available level of bicarbonate in the blood - bicarbonate

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

X Volume of extracellular fluid (15-20 l).

When calculating the amount of sodium bicarbonate using this method, no more than half of the calculated dose is also administered at a time. Calculation of sodium bicarbonate using this formula is less accurate.

An isotonic (2.5%) freshly prepared sodium bicarbonate solution is administered intravenously at a dose of 100 mmol/h (336 ml/h) under blood pH control. 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 once 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 as 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 waters (Borjomi, etc.). To combat acidosis and neutralize ammonia, glutamic acid (1.5-3 g per day) is prescribed.

5. To improve the course of oxidative processes

100 mg of cocarboxylase, 5 ml of a 5% solution of ascorbic acid, 200 mcg of vitamin B12, 1 ml of a 5% solution of vitamin B6 are administered intravenously.

6. In case of indomitable vomiting, 200-300 ml of plasma is administered 4-6 hours from the start of treatment to replenish protein deficiency and combat starvation. To avoid a hypochloremic state, 10-20 ml of 10% sodium chloride solution is infused intravenously.

7. To prevent cardiovascular failure or to eliminate it, immediately after the diagnosis of ketoacidotic coma is established, subcutaneous administration of cordiamine 2 ml or 20% sodium caffeine benzoate 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 a certain amount of caution, since they stimulate not only the vasomotor center, but also the respiratory center. When the respiratory center is excited (ketoacidotic coma), it may become overexcited to the point of extreme inhibition. For persistently low blood pressure, plasma, dextran, whole blood, and 1-2 ml of a 0.5% solution of deoxy-corticosterone acetate (DOXA) are prescribed intravenously. In case of severe tachycardia, 0.25-0.5 ml of a 0.05% solution of strophanthin or 1 ml of a 0.06% solution of corglycone in isotonic sodium chloride solution is administered intravenously.

8. Oxygen therapy is used at all stages of removing a patient from a comatose state. Humidified oxygen is administered through nasal catheters at a rate of no more than 5-8 l/min.

9. The patient’s nutrition depends on the severity of his condition. In case of ketoacidosis or precoma, easily digestible carbohydrates (honey) are added to the diet while simultaneously 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 another 10 days. If it is impossible to eat, liquids and a 5% glucose solution are administered parenterally. As the condition improves, food includes complete, easily digestible carbohydrates (honey, jam, fruit juice, mousse, semolina), plenty of liquid (up to 1.5-3 liters per day), alkaline mineral waters (Borjom, 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 1st-3rd day after a coma, it is advisable to limit animal proteins. This is due to the fact that the breakdown of proteins produces ketogenic amino acids, which aggravate ketoacidosis. On the 3rd day, the patient’s diet includes, in addition to oatmeal and puree, meat broth, pureed meat. Subsequently, over the course of a week, the patient is gradually transferred to his usual diet with a slight restriction of fats until compensation is achieved.

10. Special attention treatment of concomitant diseases and complications that provoked ketoacidotic coma (pneumonia, boil, carbuncle, trauma, etc.) should be addressed.

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

11. In cases of cerebral edema, dehydration therapy (furosemide, etc.) is indicated.

Despite the enormous successes in the treatment of diabetes associated with the discovery of insulin, the free provision of insulin and glucose-lowering drugs to all patients, ketoacidotic coma still develops in 1-6% of cases.

IN common reason Mortality rate is 2-4%; sometimes the frequency of deaths during coma is significant and ranges from 5 to 30%.

Reasons that lead to the development of ketoacidotic coma:

Untimely referral of a patient with incipient insulin-dependent diabetes mellitus (IDDM) to a doctor and late diagnosis.

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

Errors in prescribing 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 (violates the diet, drinks alcohol, does not know how to change the dose of glucose-lowering 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 insulin insufficiency with the subsequent occurrence of metabolic syndrome.

Pathogenesis of ketoacidosis and coma:

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

An excess of counter-insular hormones leads to an increase in the flow of amino acids into 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. 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 peripheral tissues, due to the lack of insulin, do not absorb glucose, which further increases glycemia.

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

Hyperglycemia significantly increases plasma osmolarity. Because of this, 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 threshold of renal permeability for glucose, glycosuria immediately appears. The so-called osmotic diuresis develops.

Due to the high osmolarity of provisional urine renal tubules they stop reabsorbing water and the 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 form blood clots, and a decrease in 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 progress, which is caused by the excess content of counter-insular hormones.

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

The content of total lipids, triglycerides, cholesterol, phosphalipids, and NEFAs increases sharply in the blood. 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 the active synthesis of ketone bodies (acetone, β-hydroxybutyric and acetoacetic acids) occurs in the liver. The synthesis of ketone bodies from amino acids occurs. With decompensation of diabetes, the number of ketone bodies increases 8-10 times compared to 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 overproduction of ketone bodies. Ketone bodies, having 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, in addition, aggravates insulin deficiency by suppressing the residual secretory activity of the beta cells of the islet apparatus.

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

With insular insufficiency in patients with diabetes in a state of ketoacidosis, there is hypokalemia, especially pronounced 3-4 hours after the administration of insulin, which “sends” potassium to the cell, deposits 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:

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

Various rhythm and conduction disorders, ectopic cardiac arrhythmias;

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

Hypotonia 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, there are several types of hypoxia:

Transport hypoxia, which is caused by a high level of glycosylated hemoglobin, it loses its ability to deliver oxygen to tissues;

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

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

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

Under hypoxic conditions, anaerobic glycolysis is activated, resulting in an increase in the level of lactic acid with the development of lactic acidosis.

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

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

Thus, in diabetic ketoacidosis, a sharp deficiency of insulin and excessive secretion of contrainsular hormones leads to severe metabolic disorders, mainly metabolic acidosis, hypoxia, hyperosmolarity, cellular and general dehydration with loss of potassium, sodium, phosphorus, magnesium, calcium, and bicarbonate ions. This, with a certain severity, 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 appearance of the first signs of ketoacidosis to loss of consciousness usually takes from several hours to several days. In acute infections, cerebral and coronary circulation disorders, ketoacidosis can develop very quickly.

There are 3 periods in diabetic ketoacidosis:

Beginning ketoacidosis.

Precoma stage.

Coma stage.

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

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

If treatment is not started, then the dyspeptic syndrome further worsens, repeated vomiting appears, which does not alleviate the patient’s condition, which aggravates the fluid and electrolyte disorder. Abdominal pain appears varying intensity, diarrhea or constipation. Lethargy, drowsiness, lethargy increase, patients become indifferent to their surroundings, disoriented in time and space, and their consciousness is confused. Stupor and stupor give way to coma.

When examining a patient in a state of ketoacidotic coma, the following signs attract attention:

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

Dry lips covered with caked crusts;

The tongue and oral mucosa are dry. The tongue is covered with a dirty brown coating, with teeth marks along the edges;

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

Skeletal muscle tone is reduced;

Diabetic rubeosis on the face, as a sign of decreased vascular tone and high levels of glycosylated hemoglobin;

Breathing is deep, noisy - Kussmaul, the exhaled air smells of acetone;

The pulse is small, frequent, weak filling and tension. The heart rhythm is sinus, tachycardia, sometimes single extrasystoles, there may be atrial fibrillation, blood pressure is reduced;

Hard breathing is usually heard in the lungs; there may be a pleural friction noise; perhaps it is caused by aseptic dry pleurisy, which occurs due to severe dehydration. Recently, acute respiratory failure, which is often the cause of death in patients with diabetes;

The abdomen is soft in most cases, and an enlarged liver can often be palpated;

In a coma, patients completely lose consciousness, sensitivity, and reduced reflexes. Ketoacidotic coma can proceed atypically with a predominance of signs of damage to the cardiovascular system; digestive organs; kidneys and brain. This introduces certain difficulties in diagnosing coma.

Gastrointestinal form of ketoacidosis.

Almost no case of diabetic ketoacidosis occurs without gastric dyspepsia. Repeated vomiting aggravates water-electrolyte imbalance. Some patients in the precoma stage experience intense abdominal pain, usually without clear localization, increasing, with tension in the muscles of the anterior abdominal wall and symptoms of peritoneal irritation (diabetic false acute abdomen).

In this case, dyspeptic syndrome of varying severity is observed: from infrequent vomiting of mucus and bile to uncontrollable vomiting of large amounts of coffee-colored liquid, which is perceived as gastric bleeding. .

The symptoms of an “acute abdomen” and neutrophilic leukocytosis, which is observed at this time, clear signs of intoxication make one think about acute surgical pathology: acute appendicitis, cholecystitis, perforated gastric ulcer, paralytic intestinal obstruction, thrombosis of mesenteric vessels, acute pancreatitis, etc.

With suspicion of acute surgical pathology of the abdominal organs, patients are sometimes operated on and their condition is aggravated.

Properly prescribed treatment for ketoacidosis eliminates the “diabetic stomach” within 4-5 hours.

Cardiovascular form of ketoacidosis.

The cardiovascular form of ketoacidosis is more common in elderly patients. Leading clinical manifestation is a severe collapse with a significant decrease in both arterial and venous pressure, tachycardia, thready pulse various disorders rhythm, cyanosis and coldness of the extremities.

In the pathogenesis of this form, the leading role is played by hypovolemia with a significant decrease in circulating blood volume, 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.

A deep circulatory disorder occurs at the microcirculatory level with disseminated intravascular microthrombosis. With this form of ketoacidotic coma, thrombosis of the coronary and pulmonary vessels, as well as the vessels of the lower extremities, especially often develops.

Kidney form.

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

These changes in urine in combination with azotemia and 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 usually happens with significantly severe diabetic glomerulosclerosis.

Encephalopathic form.

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

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

Treatment of ketoacidosis leads to improved cerebral circulation and smoothing of cerebral symptoms.

Laboratory data:

Blood glucose - 25-40 mmol

Ketone bodies up to 500 µmol

Acetone in urine is sharply positive.

Blood pH 7.0-7.35

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

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

Insulin therapy;

Elimination of dehydration;

Normalization of electrolyte disturbances;

Fighting ketoacidosis;

Infusion therapy In a state of ketoacidosis, it often lasts 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 comatose state in the first 6 hours from the moment of admission to the hospital, since subsequently changes occur that are incompatible with life.

In recent years, the feasibility of administering adequate doses of simple insulin continuously intravenously under hourly glycemic control has been proven.

Insulin therapy:

Two methods can be used to administer insulin:

Method 1: in intensive care units using

lineomat syringe or other dispensers for administering medicinal substances.

A syringe lineomat with a capacity of 20 ml is filled with 40 units of short-acting insulin (insulrap, actrapid MS, actropid, actropid NM, maxirapid) and physiological solution. 1 ml of the mixture contains 2 units of insulin; by adjusting the speed, 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 solution and 40 units of simple insulin. By changing the drop rate per minute, you can calculate the insulin dose per hour.

For glycemia of 30 mmol/l and above, it is recommended to administer 400 ml of saline solution + 10 units of simple insulin intravenously, then determine the blood sugar level and set up a drip for continuous intravenous administration of insulin in saline solution. The insulin dose is determined by the blood sugar level. It is necessary to measure blood glucose every hour; the rate of decrease in glycemia should not exceed 2-3 mmol/hour. Insulin is administered intravenously until the blood glucose level is 13-14 mmol/l, and against this background a 5% glucose solution is added in parallel.

Restoration of water-electrolyte metabolism

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

To combat dehydration, it is recommended to administer 1 liter of fluid within 1 hour, the 2nd liter in the next 2 hours, the 3rd liter at 3 hours, that is, 50% of the fluid is administered 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 hypoglycemia and to eliminate ketoacidosis when blood glucose decreases to 13 mmol/l and below, it is necessary to administer intravenously a 5% glucose solution, the daily amount of which can 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 g, that is, 200-300 ml. 4% solution.

Restoration of acid-base balance.

The administration of sodium bicarbonate without determining the pH of the blood is life-threatening for the patient, as it contributes to hypernatremia, hypokalemia, a sharp “gross” change in plasma osmolarity and cerebral edema.

Only if the blood pH is determined below 6.0 (clinically noisy Kussmaul breathing). Sodium bicarbonate 2% solution 200-300 ml can be administered for 2 hours, but the patient must first receive at least 40 ml - 4% potassium chloride solution.

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

In addition to the drugs listed above, patients require antibiotics (maximum permissible doses) for the purpose of preventing infectious and inflammatory diseases. It is necessary to introduce B vitamins, ascorbic acid, cocarboxylase, riboxin, essentiale. For atony of the gastrointestinal tract, prozerin and cerucal are administered. To prevent thrombosis - heparin 20,000 units per day. Patients require the administration 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 bedsores).

Course of lectures on resuscitation and intensive care Vladimir Vladimirovich Spas

Decompensated ketoacidosis and ketoacidotic coma in patients with diabetes mellitus

Despite the fact that there are currently enormous 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 of comatose states. These severe complications pose an immediate threat to the patient’s life and require emergency assistance in an intensive care hospital.

Such critical conditions include:

1. ketoacidosis and its extreme condition – ketoacidotic diabetic coma;

2. hyperosmolar coma;

3. hyperlactic acidemic coma;

4. hypoglycemic coma (arising as a result of an overdose of hypoglycemic drugs, primarily insulin).

The development of diabetic ketoacidosis (KA) is characteristic of 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 decompensation of diabetes mellitus with the development of ketoacidosis and coma, first of all, the following can be named:

1. untimely diagnosis of diabetes mellitus, as a result of which a significant proportion of patients are first admitted to the intensive care unit already in a precoma or comatose state;

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

3. replacing one drug with another, to which the patient turned out to be insensitive;

4. violation of the insulin administration technique (injections into the area of ​​lipodystrophy or into the inflammatory infiltrate);

5. the patient’s incorrect attitude towards his disease (diet violation, unsystematic administration of insulin or changing its dose by the patient himself, cessation of insulin therapy);

6. increasing the patient’s body’s need for insulin (acute intercurrent diseases, pregnancy, surgical interventions, physical and mental trauma).

The primary trigger for the development of CA is progressive insulin deficiency. In the absence of insulin, the penetration of glucose into cells and the production of energy is blocked, resulting in the cell experiencing energy starvation. An intracellular decrease in glucose “switches on” the mechanisms through which a compensatory increase in glucose is achieved in the blood. These processes are stimulated by counterinsular hormones (glucagon, catecholamines, glucocorticoids).

The process of gluconeogenesis (under the influence of contrainsular hormones) occurs in two ways:

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

2. activation of enzymes that carry out the processes of formation of glucose 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 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 osmotic pressure primary urine, which prevents its reabsorption, polyuria occurs, while fluid loss 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 counter-insular 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 a state of ketoacidosis in the body during acute insulin deficiency. It should be noted that non-esterified fatty acids are partially used by the liver for the synthesis of triglycerides, which cause its fatty infiltration.

Hyperlipidemia is not the only factor in increasing the ketogenic activity of the liver. 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 contrainsular hormones. In this case, increased protein catabolism is observed with an increase in the concentration of ketogenic amino acids (leucine, isoleucine, valine) in the blood while simultaneously decreasing the level of glucogenic amino acids (glycine, alanine, glutamine). Protein catabolism is accompanied by increased formation of acetyl-CoA, which is a key substrate of carbohydrate, fat and protein metabolism. Further combustion of acetyl-CoA occurs in the Krebs cycle, but the latter’s ability 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 (acetoacetic, 7 b 0-hydroxybutyric acid and acetone) from acetyl-CoA, the concentration of which exceeds the norm by 10 or more times.

Ketone bodies, having the properties of moderately strong acids, lead to the accumulation of hydrogen ions in the body and reduce the concentration of bicarbonate 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 trigger point for such disorders is hyperglycemia, accompanied by an increase in osmotic pressure in the vascular bed. To maintain isosmolarity of the media, a compensatory movement of fluid from the cells and extracellular space into the vascular bed begins, along with the main ions K 5+ 0 and Na 5+ 0. Due to the fact that hyperglycemia exceeded the renal threshold at the same time, glycosuria 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 glycosuria lead first to severe cellular dehydration and loss of potassium ions, and then to general dehydration, that is, to hypovolemia with decreased tissue and renal perfusion. Due to a sharp thickening of the blood (increase in the number of red blood cells, Hb, Sh), the viscosity of the blood increases noticeably, the rheological properties of the blood and transcapillary exchange are significantly impaired, and circulatory and tissue hypoxia develops. Transport hypoxia during hyperglycemia can also be caused by increased formation of glycosylated (glucose-bound) HB, which loses its ability to bind and release oxygen to tissues. Considering that the concentration of glycosylated HB in hyperglycemia with ketoacidosis reaches 30%, the oxygen transport function of the blood can decrease by one third in these patients.

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

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

Clinical picture

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

From a clinical point of view, we can distinguish 3 sequentially developing and replacing each other, depending on the beginning of the provision of resuscitation care, stages of diabetic coma:

1. stage of moderate ketoacidosis;

2. stage of ketoacidotic precoma;

3. stage of ketoacidotic coma.

In the stage of incipient moderate ketoacidosis, the clinical picture is accompanied by symptoms of acute and rapidly progressing decompensation of diabetes mellitus: dry mouth, thirst, frequent urination, and polyuria. Already during this period, signs of intoxication are noted: general weakness, drowsiness, fast fatiguability, loss of appetite, nausea, vomiting. Usually patients are conscious and correctly oriented in their surroundings. The patient's skin is dry, with pronounced dryness of the tongue, mucous membranes of the lips and oral cavity. Already at this stage, the smell of acetone is detected in the exhaled air, and experienced patients who have experienced a state of decompensation more than once are able to smell this smell themselves. During the examination, an enlarged and painful liver, rapid pulse, muffled heart sounds, and arrhythmia may 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 bicarbonates decreases to 20–19 mmol/l. The water-electrolyte balance at this stage 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 can be negative.

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

First of all, adjustments are made to the patient’s diet: easily digestible carbohydrates and 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%). The diet, along with fruit juices, includes oatmeal infusions, porridges, and jelly. 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 understands what severe consequences may result from non-compliance with the diet, self-cessation of insulin administration, or changes in prescribed doses of hypoglycemic agents.

Correction of hyperglycemia is carried out with insulin preparations short acting(Actramid, Insulran, Homorap, Humulin R) in fractional doses, 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 glycemia.

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

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

If treatment is not started in a timely manner for a patient with moderate ketoacidosis, then metabolic disorders progress and the stage of ketoacidotic precoma occurs.

Clinically, this is manifested by the onset of a disorder of consciousness, which is preserved in patients, but they are lethargic, inhibited, drowsy, and answer all questions 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 for urination.

Upon examination, attention is drawn to deep, noisy breathing (Kusmaul breathing) with a pungent odor 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 “jams” in the corners mouth, tongue is dry and covered with a brown coating.

Laboratory and functional studies

IN general analysis blood – neutrophilic leukocytosis with a shift to the left, accelerated ESR, In biochemical – hyperglycemia reaches values ​​of 2–30 mmol/l or 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. A 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, ketone bodies in large quantities.

The pulse in such patients is frequent, small in filling, often arrhythmic, blood pressure is reduced, heart sounds are muffled and arrhythmic.

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

1. Abdominal option– Nausea, vomiting “coffee grounds”, intense abdominal pain with muscle tension in 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, such a picture can imitate the clinic of an “acute abdomen”, for which surgical interventions, which sharply worsens the condition of patients. Sometimes in the background intestinal colic, diarrhea (sometimes mixed with blood) is misdiagnosed acute gastroenterocolitis, food poisoning.

2. Cardiovascular or collaptoid variant: symptoms of cardiovascular failure predominate - cyanosis, shortness of breath, tachycardia, extrasystole or atrial fibrillation, decreased blood pressure. Along with ECG data - a decrease in wave voltage and S-T interval, the listed phenomena can simulate the picture of acute myocardial infarction or thromboembolism of small branches of the pulmonary artery.

3. Renal option– characterized by dysuric phenomena with pronounced urinary syndrome– hypoisosthenuria, proteinuria, hematuria, cylindruria. Due to a decrease in glomerular filtration (a similar course is most often found in patients with diabetic nephropathy), mild glucosuria and ketonuria are noted, but the development of azotemia, anuria and acute renal failure is possible.

4. Encephalopathic variant– the clinical picture resembles a picture of acute cerebrovascular accident and is caused by insufficient blood supply to the brain, hypoxia with asymmetry of reflexes and pinpoint hemorrhages in the fundus. Such symptoms most often dominate in elderly people with cerebral atherosclerosis and the diagnosis of hyperketonemic precoma is not made in a timely manner.

If a patient in a precomatous state 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. Noisy Kussmaul breathing, with a pungent odor of acetone in the exhaled air and in the room where the patient is. Tissue turgor is sharply reduced, the skin is dry and cold to the touch.

The pulse is rapid, thread-like, arrhythmic. Heart sounds are muffled, blood pressure is sharply reduced, and in advanced cases it is not detectable.

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

Treatment of patients in a precomatous 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 introduction of all infusion and pharmacological agents in case of circulatory decompensation, it should be carried out under the control of central venous pressure (CVP) and hourly diuresis. Every 2 hours it is necessary to determine blood glycemia, the content of glucose and ketone bodies in the urine, as well as hemoconcentration indicators - the number of red blood cells in 1 mm 53 0, hemoglobin, hematocrit; every 4 hours - indicators of potassium, sodium, chlorides, urea, creatinine, acid-base status. When performing rehydration, it is necessary to determine blood osmolality using the formula:

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

Typically, this figure normally does not exceed 300 mOsm/l.

The treatment program for IT precomatosis 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 factors that caused ketoacedotic coma.

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

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

In practice, this is done as follows: into a bottle with 400 ml. 40 units of simple insulin are injected into an isotonic NaCI solution with a syringe. To eliminate insulin adsorption by elements of the system used for intravenous administration, 10 ml of 10% albumin solution should be added to the bottle. After this, the working solution is placed in the Infusomat drug dispenser and the required infusion rate is set, remembering that every 100 ml of infused solution contains 10 units. insulin. The optimal rate of reduction in glycemia 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 suppress ketogenesis. In addition, K 5+ 0, which participates in cellular oxidative phosphorylation reactions, penetrates into the cell more easily with a glucose solution. To avoid hypoglycemia, when blood glucose levels reach 11 mmol/L, intravenous insulin is stopped and insulin is administered subcutaneously at 4-6 units every 3-4 hours under glycemic control. The glycemic level is maintained within 8–10 mmol/l.

This method of insulin therapy is considered the most effective and safe. Intravenous administration of insulin at the beginning of treatment ensures its supply and circulation in conditions of dehydration, and small doses protect against a sharp decrease in glycemic levels, aggravating hypokalemia and the development of cerebral edema.

Rehydration

In ketoacidotic coma, the deficiency of intra- and extracellular fluid is 10–15% of body weight, or about 6–8 liters. If such a deficiency of fluid 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 a clinical picture, patients may die. Therefore, we must remember that rehydration should begin simultaneously with insulin therapy, and the amount of isotonic solution administered 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 l each. Infusion therapy must be carried out under the control of hourly diuresis, which should be at least 40–50 ml/hour. And only with oliguria (diuresis less than 30 ml/hour) and high specific gravity(above 1030) you can add a 500 ml infusion in the second hour. liquids, but with the obligatory prescription of saluretics (Lasix). Thus, with a fluid deficit of 6–8 liters in the body, rehydration is extended over 12–14 hours of the patient’s stay in the intensive care unit.

If the patient's plasma osmolality is above 340 mOsm/L, then rehydration of the patient should begin with a 0.45% (hypotonic) sodium chloride solution.

If low hemodynamic parameters (BP) persist, as well as when the level of protein and its fractions decreases during rehydration, it is advisable to transfuse 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 cardiac arrhythmia, energy deficiency, and on the other, atony of the stomach and intestines up to paralytic ileus. It should be noted that with severe dehydration, the K content in the blood serum is sharply reduced, therefore hypokalemia is judged by a sharp decrease in it in the cell (erythrocytes - the normal level of K in them is 79–96 mmol/l).

Rehydration therapy and a decrease in blood glycemia usually promotes the return of potassium to the cell and, in the process, further treatment we are always faced with plasma hypokalemia, which must be compensated and maintained at a level of 4–5 mmol/l.

That is why compensation for K occurs at a blood glycemic level of 16.5–16.8 mmol/l, i.e., 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 intravenously should be 39–40 mmol/hour;

2. 3.0–4.0 mmol/l – the amount of K administered initially should be up to 26 mmol/hour;

3. 5.0–5.5 mmol/l – intravenous administration of K begins later only when it decreases during treatment;

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

When preparing a working solution of chloride K, it should be remembered that 1.0 g of dry substance KS1 contains 13.4 mmol K. No more than 2% solution should be administered to the patient intravenously (i.e., 100 ml of 2% KS1 should contain 26 .8 mmol K) for the purpose of preventing aseptic phlebitis and sharp pain along the veins.

The restoration of acid-base balance begins literally from the first minutes of treatment of the precomatose state and coma, thanks to insulin therapy and rehydration. Restoring fluid volume triggers physiological buffer systems, in particular, the ability of the kidneys to reabsorb bicarbonates is restored. Insulin suppresses ketogenesis and thereby reduces the concentration of hydrogen ions in the blood. However, in a number of cases, when the blood pH decreases below 7.0, the question arises of correcting 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 the cerebrospinal fluid and the central nervous system; thanks to protective-adaptive mechanisms, attempts to correct plasma acidosis with a solution of sodium bicarbonate lead to the rapid development of acidosis of the central nervous system and a sharp deterioration in the patient’s condition.

This paradoxical phenomenon is explained by the fact that the administration of Na bicarbonate is accompanied by an increase in HCO3- in the blood plasma, 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 H2CO3 content 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, depression of the functions of the central nervous system due to 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 monitoring acid base, it is necessary to pay attention not only to pH indicators, but also to pCO2, pO2, 8pO2, BE.

PCO 2 – partial pressure of carbon dioxide in the blood;

PO 2 – partial pressure of oxygen in the blood;

SрО 2 – saturation of hemoglobin with oxygen;

BE – base deficiency.

Only after correction of hypoxia and hypercapnia with humidified oxygen and a decrease in the pH value below 7.0 against this background is it possible to administer 4% Na bicarbonate at the rate of 2.5 ml per 1 kg of body weight intravenously, slowly, with an additional simultaneous increase in K at the rate of 0 .2 g of dry substance KS1 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 CO2 content of the blood and has a hypoglycemic effect. It is prescribed intravenously 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. For persistent hypotension, it is recommended to administer dopamine intravenously at a dose of 60.0–80.0 mg in an isotonic NaCl solution.

Considering the pronounced tendency of patients in a precomatous state and in a coma to hypercoagulation and development DIC syndrome, it is recommended to administer 5000 units of heparin intravenously every 6 hours under the control of a coagulogram.

In some cases, eliminating etiological factors, which caused ketoacidotic coma, contributes to its rapid relief. This is 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 ketoacidotic coma may be:

1. arterial hypotension that cannot be corrected with adequate rehydration and IT disorders of the cardiovascular and respiratory systems;

2. decrease in diuresis to 30 ml/h or lower, despite its stimulation;

3. increasing cerebral edema, despite dosed dehydration with aminophylline solution and furosemide.

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

Contraindications for patients with diabetes Since the severity and nature of diabetes can be different, the contraindications are very relative. If a person has been sick with diabetes for more than one year, but has managed to adapt to his illness, he feels great,