Emergencies in diabetes mellitus. Ketoacidotic coma

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

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

Table 3. Types of diabetes mellitus


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

Etiology:

untreated diabetes mellitus;

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

non-compliance with the diet;

alcohol or food intoxication.

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

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

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

Stages of a ketoacidotic coma:

Stage I - compensated ketoacidosis;

Stage II - decompensated ketoacidosis (precoma);

Stage III - ketoacidotic coma.

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. Tongue dry, coated; skin turgor is reduced, polyuria is expressed, in the exhaled air - the smell of acetone.

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

Clinical forms of ketoacidotic coma:

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

cardiovascular (hemodynamic disturbances are expressed);

renal (olig- or anuria);

encephalopathic (resembles a stroke).

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

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

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

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

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

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

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

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

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

Statistics show that ketoacidotic coma occurs in 0.4% of diabetes cases. Almost always, this condition can be stopped. This phenomenon is most dangerous in the elderly and children.

Causes

Ketoacidotic coma is caused by inappropriate insulin therapy for diabetes mellitus.

This can be explained by:

Excessive consumption of alcoholic beverages during treatment;
Violation of the technique of drug administration;
Incorrect or irregular intake of sugar-reducing drugs;
Insufficient insulin dose or skipping insulin administration;
The presence of bad habits that alter the production of insulin;
Aggravation of diabetes mellitus with other diseases;
Taking a number of medications;
Lack of control over metabolism.

Modern experts say that ketoacidotic coma usually haunts patients diabetes mellitus the first type.

If you can determine the exact cause, your doctor will be able to take appropriate measures to rule out serious complications.

Symptoms

The symptoms of a 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 abdomen, fever, 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 a serious lesion of cardio-vascular system collapse may occur.
Encephalopathic ketoacidotic coma - it can be recognized by the asymmetry of reflexes, hemiparesis, vascular lesions of the naked brain. A person has severe headaches, fogginess.

Stages

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

Beginning ketoacidosis - manifests itself as symptoms of decompensated diabetes mellitus. The person begins to suffer from constant thirst, a feeling of dry mouth, headache, nausea and vomiting. He also has a pungent smell of acetone from his mouth. Clinically, this condition can be determined by a sharp increase in blood glucose levels.
Predcoma - arises only if there are no urgent action was not accepted. It is characterized by persistent vomiting, diarrhea, or constipation. Many patients complain of severe abdominal pain, drowsiness, disorientation, and apathy.
Coma is a serious complication that requires immediate medical attention. A person loses consciousness, he has 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 should understand what is required of them.

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

When the first signs of deterioration of the patient's condition appear: loss of consciousness, infrequent breathing, it is necessary to call an ambulance;
Before the arrival of the doctor, it is necessary to check the level every 5 minutes blood pressure and heart rate;
Try to ask the patient questions so that he remains conscious;
Slap his face and rub his earlobes for the same purpose.

When the ambulance arrives, doctors will have to carry out the following activities:

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

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

Diagnostics

To diagnose a ketoacidotic coma, a detailed examination of the patient is carried out. If he is conscious, the doctor asks clarifying questions and asks about the features of his condition. After that, the patient is sent for a series of laboratory tests, which make it possible to make a final conclusion. Diagnosis of this condition includes the following:

Glucose levels as a result general analysis blood ranges from 16-38 mmol / liter.
Also, as a result of this study, you can see elevated level hematocrit and hemoglobin, indicating severe dehydration.
Ketone bodies in OAM will be significantly increased.
The sodium level in the blood will be increased, and the potassium level will be increased. This can be seen from the results biochemical analysis blood. The growth of urea is also assessed there.
An acid-base blood test can reveal metabolic disorders. It is characterized by an increase in osmolarity up to 300 mosmol / l.
Blood pressure drops, and heart rate increases.

Treatment features

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

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

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

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

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

To eliminate the manifestations of general dehydration of the body, in case of a diabetic coma, a large amount of fluids are injected into a vein to the patient. Initially, a sodium chloride solution is used for this purpose. It should be borne in mind that, depending on the duration of therapy, the rate of administration of the drug changes. When the patient's consciousness returns to normal, infusion therapy is discontinued.

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

Errors in treatment

Treatment of a ketoacidotic coma requires high qualifications from the attending physician. Such a condition, with improperly selected therapy, can lead not only to serious consequences, but even to death. Studies have shown that the following errors are most common in treatment:

Inadequate insulin therapy, which often leads to a sharp drop in blood sugar;
An insufficient rate of rehydration can lead to hypovolemic shock;
Insufficient control over blood glucose levels, due to which the body does not receive the right treatment;
Too fast a rate of decrease in blood sugar, which causes the meninges in the brain;
Insufficient rate of potassium replenishment, due to which the cardiovascular system suffers.

Patient control

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:

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

Such a serious control over the patient is explained by the fact that the patient may experience complications at any time. The most undesirable consequences of a ketoacidotic coma that complicate its treatment are:

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

Prophylaxis

To avoid serious consequences, you must always remember about the prevention of ketoacidotic coma. Activities include:

Checking blood glucose once a week;
Compliance with a special diet;
Taking drugs that lower glucose levels;
Constant monitoring of the state of the body;
Rejection of bad habits;
Timely treatment of all emerging diseases;
Regular visits to your doctor;
Maintaining healthy way life;
Active and mobile lifestyle.

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

Possible complications

Ketoacidotic coma is a serious consequence of diabetes mellitus. In case of improper or untimely medical care, the patient may experience serious complications. The greatest danger is cerebral edema. This phenomenon in the overwhelming majority of cases is fatal. It is possible to recognize the possible appearance of puffiness in the brain 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 a decreased response of the pupils to light, or by its absence at all, swelling of the optic nerve, or ophthalmoplegia.

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

EEC and REC are also carried out, which make it possible to assess the processes occurring in the brain. With their help, you can promptly identify any complications and prescribe the appropriate treatment.

Also, complications of ketoacidotic coma can include pulmonary edema, decreased clotting inside the vessels, metabolic alkalosis, cardiovascular failure, asphyxiation of the contents of the gastric tract.

In order to prevent such serious consequences of this disease, the 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 of any deviations will help to quickly eliminate them, so that the risk of any complications will be minimal.

One of the most common diseases of the endocrine system is diabetes mellitus, the decompensation of which can manifest itself in four types of coma:

Ketoacidotic coma is the most common coma in diabetes mellitus; the mortality rate in ketoacidotic coma is 2-4%.

Possible causes leading to decompensation of diabetes mellitus:

late appeal (diagnosis) of the patient to the doctor, with the development of insulin-dependent diabetes mellitus;
insulin therapy errors;
improper behavior of the patient: errors in diet, alcohol abuse, incorrect dosage of insulin);
acute diseases, especially purulent infections;
physical or mental trauma;
pregnancy;
surgical interventions.

As a result of insulin deficiency, when there is a mismatch between the production of endogenous insulin or the delivery of exogenous insulin and the body's needs for it, energy starvation of the body develops with an excessive concentration of glucose in the blood and extracellular fluid, which is a source of energy.

Unutilized glucose, gradually accumulating, leads to an increase in plasma osmolarity, as a result of which part of the interstitial and later intracellular fluid, together with the microelements contained in it, passes into the vascular bed, causing serious cellular dehydration and a decrease in the intracellular electrolyte content, and, above all , potassium. When the glucose concentration increases so much that it exceeds the renal permeability threshold, glucosuria develops with the formation of general severe dehydration. The blood thickens, its rheological properties are disturbed, thrombus formation increases, and the volume of renal perfusion decreases.

The described pathological cascade, caused by a high concentration of sugar in the blood, can be conditionally considered the first link in the pathogenesis of diabetes mellitus decompensation.

The second conditional link in the decompensation of diabetes mellitus is ketosis (excessive accumulation of ketone bodies in the blood), which turns into ketoacidosis. Ketone bodies, which have the properties of weak acids, cause the accumulation of hydrogen ions in the body, and a decrease in the amount of sodium bicarbonate ions - metabolic acidosis develops.

Diabetic ketoacidosis, accompanied by insulin deficiency and excessive secretion of counterinsular hormones, causes severe metabolic disorders, developing coma. Currently, it is believed that the cause of death in ketoacidotic coma is dehydration of brain neurons, which occurs against the background of plasma hyperosmolarity.

Symptoms of a ketoacidotic diabetic coma

It takes several days from the first signs of ketoacidosis to loss of consciousness. There are three stages of diabetic ketoacidosis:

Moderate (beginning) ketoacidosis.
Severe ketoacidosis (precoma).
Ketoacidotic coma.

Depending on the complications of diabetes mellitus and concomitant pathology, various options for the clinical picture of ketoacidosis are possible:

the gastrointestinal variant is characterized by abdominal pain, and is observed in angiopathies with localization in the birch and the walls of the gastrointestinal tract;
renal variant - manifested by proteinuria, changes in urinary sediment (hematuria, casts), and is observed against the background of diabetic nephroangiopathy;
cardiovascular variant - manifested by severe collapse, and is observed in angiopathies with damage to the cardiovascular system;
encephalopathic variant - manifested by hemiparesis, asymmetry of reflexes, the appearance of one-sided pyramidal signs, and is observed against the background of angiopathies with damage to the cerebral vessels.

Beginning ketoacidosis manifests itself as dry mouth, thirst, semi-iria, itchy skin, signs of intoxication. A smell of acetone appears from the patient's mouth, the blood sugar level rises above 16.5 mmol / l, there is a high glucosuria, acetone is found in the urine.

If adequate treatment is not started on time, then the pathology progresses, dyspeptic syndrome develops, accompanied by repeated vomiting, which does not bring relief, which can take on an indomitable character. The appearance of nonspecific pain in the abdomen is possible, a false picture is formed " sharp abdomen". Signs of a disorder of consciousness appear - patients become lethargic, apathetic, disoriented in time and space, their sleep is disturbed.

If at this stage of the disease adequate treatment is not performed, a coma develops.

Emergency care for ketoacidotic coma

A patient with this pathology is hospitalized in the intensive care unit, where he is provided with medical assistance.

rehydration of cells and extracellular space;
replacement therapy with simple insulin;
normalization of acid base balance and electrolyte levels;
prevention of insulin overdose;
treatment of infectious and inflammatory diseases if available;
treatment of other pathologies that caused coma;
symptomatic therapy.

With a ketoacidotic coma, the greatest danger to the patient's life is the general dehydration of his body, especially of the brain cells. That is why the first aid for ketoacidotic coma should be the infusion of saline solutions.

Already at the stage of ambulance, after relief of signs of acute cardiovascular failure and acute respiratory failure, if any, pathogenetic treatment should be started in the form of intravenous infusions of 400-500 ml of isotonic solution at a rate of at least 15 ml / min, 10 -16 IU of simple insulin. Infusions are continued throughout the entire evacuation stage; it is not recommended at this stage to inject large doses of insulin subcutaneously.

The mainstay of treatment for ketoacidotic coma is insulin therapy and infusion therapy.

Insulin therapy

Currently, the generally accepted method of insulin therapy is continuous intravenous infusion of small doses of insulin, which is carried out using special automatic syringes. The essence of insulin therapy is as follows.

If the patient's blood sugar does not exceed 33.3 mmol / L, continuous intravenous infusion of insulin is started at a rate of 6-10 U / hour. If the initial glycemia exceeds 33.3 mmol / L, then insulin is administered at a rate of 12-16 U / hour.

Working dose insulin is usually called the dose of insulin that is administered within 1 hour.

There are 3 stages of treatment for ketoacidosis:

Until the blood sugar level drops to 16.7 mmol / l.
Until the condition and the possibility of oral intake of food by the patient improve.
Until the transition of the patient to a normal state.

Insulin therapy is carried out with constant monitoring of the patient's blood sugar level every 1-2 hours against the background of infusion therapy.

In the event that in the first 3-4 hours of insulin therapy, the blood glucose concentration did not fall by 30% compared to the initial value, the initial working dose of insulin is doubled. When the sugar level drops to 16.7 mmol / L, the working dose of insulin drops to 2-4 U / hour. When the sugar level drops to 11-13 mmol / l, 4-6 units of insulin are administered subcutaneously every 2-4 hours, gradually lowering the blood sugar level, but not less than 10-12 mmol / l, so that the patient does not develop hypoglycemia.

If there are no special automatic syringes in a medical institution, they resort to the method of fractional administration of small doses of insulin, which consists in the fact that working doses of insulin are injected intravenously every hour.

TO method of fractional administration of large doses of insulin(repeated administration of large doses of insulin) is not currently used, due to the high likelihood of hypoglycemia, cerebral edema, hypokalemia, which became the cause of a high mortality rate.

Infusion therapy

Depending on the patient's condition, treatment tactics infusion therapy divided into 3 stages.

Stage 1. Infusion therapy begins with intravenous administration of saline - 1 liter is injected in the first hour, then 2, 3, 4 hours - 0.5 liters each; further, as the signs of dehydration are eliminated, the rate of administration is reduced. Saline is administered until the patient's blood sugar drops to 16.7 mmol / L.

If there is an initial plasma hypokalemia, its correction begins no earlier than 2-2.5 hours after the start of infusion therapy.

Nonspecific normalization of the acid-base state begins immediately from the first stages of treatment, thanks to infusion therapy in combination with insulin therapy.

Stage 2. Begins after the blood sugar level is lowered to 16.7 mmol / L. As a rule, by this time the patient regains consciousness. To prevent the development of hypoglycemia, they switch to intravenous administration of a 5% glucose solution at a rate of 200 ml / hour with the addition of 4 units of insulin for each 1 g of glucose injected (do not confuse this insulin with insulin injected subcutaneously!). The patient is given sweet tea.

Stage 3. It is carried out in the specialized department of the hospital, includes subcutaneous injections of insulin every 4-6 hours under the control of glucose levels. After each injection, the patient receives a portion of food containing 50 g of carbohydrates. Infusion therapy is discontinued and fluid is administered orally. The patient is shown diet No. 9, excluding fatty foods for the period of acetonuria, and within 10 days after it.

After a coma, the patient is shown bed rest for a week.

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

Pathogenesis of ketoacidotic coma

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

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

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

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

Clinic of ketoacidotic coma

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

There are three stages in the development of a ketoacidotic coma:

incipient ketoacidosis;
precom;
coma.

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

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

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

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

Diagnostics of the ketoacidotic coma

According to laboratory tests, an increase in ketoacidosis can be judged if hyperglycemia, glucosuria are detected, the level of ketone bodies exceeds the norm (177, 2 μmol / l), and plasma osmolarity rises to 350 or more mosmol / l. Metabolic acidosis is indicated by a pH in the range of 7.2-7.0. Toxic irritation bone marrow leads to neutrophilic leukocytosis, erythrocytosis is a consequence of blood thickening. The amount of sodium plaza is reduced to 120 mmol / L.

Ketoacidotic coma treatment

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

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

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

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

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

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

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

Ketoacidotic coma- the most formidable complication of diabetes mellitus, is a manifestation of absolute or relative insulin deficiency and a sharp decrease in glucose utilization by body tissues. It develops more often in patients with insulin-dependent diabetes, characterized by a severe labile course. Lack of insulin in the body, which can be caused by a decrease in the introduction of exogenous insulin (bad syringe, dose reduction, cancellation of insulin administration, etc.) or an increase in insulin requirements (pregnancy, intercurrent infectious diseases, trauma, surgical operations etc.), causes the development of a coma.

The clinical picture. Diabetic coma usually develops slowly, gradually, over several days or weeks. At acute diseases or intoxicated ketoacidosis can occur much faster, within a few hours. From a clinical point of view, three successively developing and replacing each other (without treatment) stages of diabetic ketoacidosis can be distinguished: 1) the stage of moderate ketoacidosis; 2) the stage of precoma, or decompensated ketoacidosis, and 3) the stage of coma. A patient in the stage of moderate ketoacidosis is worried about general weakness, increased fatigue, lethargy, drowsiness, tinnitus, decreased appetite, nausea, vague abdominal pain, thirst, and increased urine output. In the exhaled air, the smell of acetone is determined.

With decompensated ketoacidosis, or diabetic precoma, appetite is completely lost, constant nausea is accompanied by vomiting, general weakness, indifference to the environment intensifies, vision deteriorates, shortness of breath appears, discomfort or pain in the heart and abdomen, frequent urge to urinate, becomes indomitable ... The precomatose state can last from several hours to several days. At the same time, consciousness is preserved, the patient is correctly oriented in time and space, however, answers questions with a delay, monosyllabic, monotonous, inaudible voice. The skin is dry, rough, cold to the touch. Lips dry, cracked, covered with caked crusts, sometimes cyanotic. The tongue is crimson, with teeth imprints remaining at the edges, dry, coated with a dirty brown coating.

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

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

Urgent care. In diabetic ketoacidosis, not only insulin is used, but it is imperative to carry out other measures aimed at combating dehydration and restoring metabolic disorders that develop due to the lack of insulin, restoring and maintaining the functions of others internal organs(heart, lungs, kidneys, etc.).

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

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

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

Catecholamines and other sympatotonic drugs should not be used to combat collapse in diabetic coma. They are contraindicated not only because catecholamines are counter-insular hormones, but also because in diabetic patients their stimulating effect on glucagon secretion is much stronger than in healthy ones.

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

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

Ambulance, ed. B.D.Komarova, 1985