What is a ketoacidotic coma. Complications of diabetes: Ketoacidotic coma ketoacidotic coma emergency

Ketoacidotic coma is a life-threatening complication of diabetes mellitus, in which metabolic disorders peculiar to this disease reaches a critical degree and are accompanied by deep impairment of homeostasis and disorder of the function of organs and systems. Ketoacidotic coma is observed in 1-6% of patients hospitalized with diabetes mellitus, and more than 16% of patients suffering from insulin-dependent diabetes dying precisely from ketoacidosis or ketoacidotic coma. At the heart of the pathogenesis of the coma - increasing insulin deficiency. It is preceded by diabetic ketoacidosis. This condition can be caused by several factors:

¨ Intercurrent diseases - acute inflammatory processes, exacerbations of chronic diseases, infectious diseases

¨ Surgical interventions and injuries

¨ Treatment Mode Violations: Insufficient Introduction, Drug Change, Disruption In Insulin Injection Technique

¨ Emotional Stress Situations

¨ Pregnancy

¨ violation of the diet, in particular, abuse of fatty food

¨ termination of insulin administration with suicidal purposes

In the development of diabetic ketoacidosis, three stages are distinguished, the latter of which is ketoacidotic coma.

The first stage or ketoacidosis of the first degree. The leading role in the pathogenesis, as already noted, has absolute insulin deficiency, which leads to a decrease in glucose disposal by insulin-dependent tissues. Hyperglycemia develops in the blood, and in the tissues - heavy energy "hunger". This contributes to a sharp increase in the level of all the counterinsulin hormones in the blood (glucagon, cortisol, catecholamines, STS, ACTH), activation of lipolysis, glycolysis and proteolysis, which leads to the formation of substrates for gychonogenesis in the liver and kidneys. Glukegenesis in combination with a violation of glucose disposal tissues is the most important cause of rapidly increasing hyperglycemia, increasing the osmolarity of plasma, intracellular dehydration and osmotic diurea. Another mandatory pathogenesis factor is the activation of the formation of ketone bodies. Insulin deficiency and excess hormones leads to intensive lipolysis and an increase in the content of free fatty acids, which are a ketogenic substrate. In addition, the synthesis of ketone bodies comes from "ketogenic" amino acids (isoleucine, leucine and valine), which accumulate as a result of excess proteolysis. The accumulation of acetyl-coa, acetoacetate and B-oxybutirate leads to the depletion of alkaline blood reserves and the development of metabolic acidosis. The process is aggravated by the fact that the peripheral utilization and the excretion of ketone bodies with urine decreases due to dehydration and oliginia, replacing the polyuria.

Second stage or precomath state. The catabolism of the protein is enhanced by nitrate balance and azotemia develops. Cell dehydration is replaced first extracellular, and then the total dehydration of the body. The tissue and renal blood flow decreases, the electrolyte deficit is observed - Na +, K +, Cl -. Dehydration leads to hypovolemia, which is the cause of reducing brain, renal and peripheral blood flow. It enhances the already existing CNS hypoxia and peripheral tissues. Hypoxia peripheral tissues contributes to the activation of anaerobic glycolysis and the accumulation of lactic acid, which can cause lactatacidosis. Thus, the severity of the patient's condition is caused by a sharp dehydration of the body, decompensated by metabolic acidosis, a deficit of electrolytes, hypoxia, hyperosmolarity.

In general, the scheme of the pathogenesis of the ketoacidotic coma can be depicted as follows:

Clinically, the first stage is characterized by increased dryness of mucous membranes and skin, headache, drowsiness. Polyuria is replaced by oligo and anuria, the mass of the body decreases, the smell of acetone appears in exhaled air. In the second stage, these signs are exacerbated. Dizziness appear, nausea, vomiting, which soon becomes indomitable. Pumping masses acquire a blood-brown tint. The irritation of the respiratory center protons leads to the appearance of a characteristic noisy and sharp breathing (Kussmouuly's breathing). In addition, as a result of the progressive stimulation of lipolyase in the blood, the CZP, cholesterol, triglycerides are accumulated, which increases blood viscosity, disrupts its rheological properties and impairs microcirculation. During this period, the so-called "abdominal syndrome" of ketoacidase, manifested in the clinical picture of the "acute abdomen", is distinguished. Due to hypokalemia, an intestine atony is observed, which stretches and occurs pain, accompanied by leukocytosis and indoorable vomiting. Depending on the prevalence in the clinic of certain symptoms, the following variants of the precompetusive state are distinguished:

1. Cardiovascular (collaptoid) form.

2. Gastrointestinal (abdominal) form.

3. Renal form.

4. Encephalopathic shape.

Against this background, CNS is constantly oppressed. Developing in the second stage The state of stupidity is characterized by a decrease in the level of wakefulness, slowing conscious reactions to stimuli and an increase in sleep periods. Stunning is replaced by a stupor. The final stage of braking CNS is a coma.

Third stage or ketoacidotic coma. Its pathogenesis includes hypovolemia (leads to circulatory hypoxia), violation of brain and renal blood flow, insufficiency of electrolytes (its result - myopathy, weakness of respiratory muscles and alveolar hypoxia), an increase in the content of glycosylated hemoglobin (it is worse than its function). All listed factors contribute to the development of cardiovascular insufficiency and metabolic coagulopathy, which is manifested by disseminated intravascular coagulation (DVS syndrome), peripheral thrombosis and thromboembolism. The state is aggravated by the edema of the lungs, asphyxia due to the aspiration of the gastric contents, violation of the kidney perfusion.

Clinically ketoacidotic coma is characterized by loss of consciousness, breathing type Kussmouul, sharp smell of acetone; Leather and mucous membranes are dry, the tone of smooth muscles and eyeballs are reduced, reflexes are absent, the pulse is threaded, the arterial hypertension is expressed, a dense enlarged liver is determined during palpation. Blood biochemical indicators - the following: glucose content is 19-33 mmol / l, ketone bodies - 17 mmol / l, lactate - 10 mmol / l, plasma pH less than 7.3.

Treatment Patients in a state of ketoacidotic coma should begin immediately. The main objectives of therapy are the struggle against dehydration and hypovolemic shock, the restoration of the normal acid-base state, the normalization of the electrolyte balance, the elimination of intoxication and the concomitant disease. The diagram of therapeutic measures is as follows:

Hospitalization in the resuscitation department

Washing the stomach solution of sodium bicarbonate

Introduction of urinary catheter

Infusion therapy with warm solutions: to restore insulin levels - its introduction by the method of "small doses", for rehydration - the introduction of isotonic saline solutions for the correction of the electrolyte balance - the introduction of potassium chloride, for the correction of the CB - the introduction of sodium bicarbonate solution (in limited quantities)

Measurement of the pulse, CH, Hell, ECG removal and radiographs

Control over the content of hemoglobin, leukocytes, hematocrit, ESP, indicators of the resulting blood system. At the same time, heparin is introduced to prevent DVS, and for the correction of cardiovascular disorders - cardiac glycosides, Meston, Cordiamin.

Success in treatment is determined by the timeliness of assistance, the state of the CSS, the kidneys, the age of the patient and the cause of ketoacidosis. Prognostically unfavorable features are arterial hypotension, left ventricle, hemorrhagic syndrome, hypokalemia, increasing the content of lactic acid in the blood. At the same time, it should be noted that as a result of improving the effectiveness of measures to exit the ketoacidotic coma, the mortality from it has recently decreased more than three times.

Literature:

1. Demidov I. Yu. Ketoacidosis and ketoacidotic coma. Clinical laboratory diagnostics. 1997 №9, p. 25-32.

2. Potemkin V. V. "Diabetic (hyperketonemic) coma." Russian medical journal. 1996 №3, p. 28-32.

3. Kholodova E. A., Shochort E. V. «ketoacidosis and ketoacidotic coma in patients with diabetes mellitus." Health care of Belarus. 1987 №4, p. 38-41.

4. ADO A. D. "Pathological Physiology". Moscow, 2000

One of the most common diseases of the endocrine system is diabetes, the decompensation of which can manifest itself four types of comatose states:

The ketoacidotic coma is the most common comatose condition in diabetes mellitus, the percentage of mortality at ketoacidotic coma is 2-4%.

Possible causes leading to decompensation of diabetes:

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

As a result of insulin deficiency, when the discrepancy between the production of endogenous insulin or the delivery of exogenous insulin and the needs of the body is developing, the energy starvation of the body is developing in excessive concentration in the blood and extracellular liquid glucose, which is the source of energy.

Reyptized glucose, gradually accumulating, leads to an increase in plasma osmolarity, as a result of which part of an interstitial, and later intracellular fluid, together with the microelements contained in it, is moving into a vascular channel, causing serious cell dehydration and reduction of intracellular electrolyte content, and, above all , potassium. When the concentration of glucose increases so much that the renal threshold of permeability exceeds, glucosuria is developing with the formation of a general heavy dehydration. Blood is thickened, its rheological properties are disturbed, thrombosis is increased, the volume of renal perfusion is reduced.

The described pathological cascade caused by the high blood sugar concentration can be considered the first polyogenesis in the decompensation of diabetes.

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

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

Symptoms of ketoacidotic diabetic coma

From the first signs of ketoacidosis to loss of consciousness passes several days. Three stages of diabetic ketoacidase distinguish:

1. Moderately pronounced (starting) ketoacidosis.
2. Pronounced ketoacidosis (prema).
3. Ketoacidotic coma.

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

• the gastrointestinal version is characterized by pain in the stomach, and is observed with angiopathies with localization in the gravy and the tract walls;
• the renal option is manifested by proteinuria, a change in blade (hematuria, cylinders), and is observed against the background of diabetic nephroangiopathy;
• the cardiovascular version - manifests itself a heavy collapse, and is observed with angiopathies with the damage to the cardiovascular system;
• the encephalopathic option is manifested by hemiparem, asymmetry of reflexes, the appearance of one-sided pyramidal signs, and is observed against the background of angiopathies with the lesion of the brain vessels.

Beginning ketoacidosis manifests itself with dry mouth, thirst, half-seine, skin itch, signs of intoxication. The salty of the patient appears the smell of acetone, the blood sugar level rises above 16.5 mmol / l, high glucosuria is noted, acetone is found in the urine.

If adequate treatment is not started on time, the pathology progresses, develops dyspeptic syndrome, accompanied by multiple vomiting that does not bring relief, which can take the nature of indomitable. The appearance of nonspecific stomach pain is possible, a false picture of "acute abdomen" is formed. Signs of consciousness disorder appear - patients become sluggish, apathetic, disorient in time and space, they have a dream.

If at this stage of the disease is not adequate treatment, it develops a comatose state.

Emergency care for ketoacidotic coma

The patient with this pathology is hospitalized in the department of intensive therapy, where he is provided for medical assistance.

• rehydration of cells and extracellular space;
• replacement therapy by simple insulin;
• normalization of the indicators of the KSHC and the level of electrolytes;
• warning insulin overdose;
• treatment of infectious and inflammatory diseases if available;
• treatment of other pathologies that caused to whom;
• symptomatic therapy.

With a ketoacidotic coma, the greatest danger of the patient's life is the total dehydration of its body, especially the cells of the brain. That is why the first help with a ketoacidotic coma should be infusion of saline solutions.

Already at the stage of ambulance after the construction of signs of acute cardiovascular failure and acute respiratory failure, pathogenetic treatment in the form of intravenous infusions 400-500 ml of isotonic solution with a speed of at least 15 ml / min should be launched, 10 in the first fluctuation of the solution is added 10 -16 eg simple insulin. Infusion continues throughout the evacuation phase, it is not recommended at this stage to introduce large doses of insulin subcutaneously.

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

Insulinotherapy

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

In case the patient's blood sugar content does not exceed 33.3 mmol / l, constant insulin intravenous insulin infusion at a rate of 6-10 units / hour. If the initial glycemia exceeds 33.3 mmol / l, then insulin is introduced at a speed of 12-16 units / hour.

Working dose Insulin is customary called the dose of insulin, which is introduced within 1 hour.

There are 3 stages of ketoacidosis treatment:

• Prior to lower blood sugar levels of 16.7 mmol / l.
• Before improving the condition and possibility of oral meal by the patient.
• Prior to the transition of the patient to the usual state.

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

In the event that in the first 3-4 hours of insulin therapy, the glucose concentration in the blood did not fall by 30% compared to the initial value, the initial working dose of insulin is doubled. When the level of sugar drops to 16.7 mmol / l, the working dose of insulin decreases to 2-4 units / hour. When the level of sugar drops to 11-13 mmol / l, they run on the subcutaneous administration of 4-6 units of insulin every 2-4 hours, reducing the level of sugar in the blood, but at least 10-12 mmol / l so that the patient does not develop hypoglycemia.

If there are no special vehicles in the medical institution, resort to method of fractional introduction of small doses insulinwhich lies in the fact that the working doses of insulin are introduced intravenously inkjet every hour.

TO the method of fractional introduction of large doses of insulin (Multiple introduction of large doses of insulin) are currently not resorted, due to the high probability of the development of hypoglycemia, brain edema, hypokalemia, which caused a high level of mortality.

Infusion therapy

Depending on the state of the patient, the treatment tactics of infusion therapy is divided into 3 stages.

Stage 1. Infusion therapy begins with intravenous impact of the saline - in the first hour, 1 liter is introduced in the first hour, then 2, 3, 4 hours - 0.5 liters; In the future, as the signs of dehydration eliminate, the introduction rate is reduced. The physical is introduced until the patient's blood sugar level decreases to 16.7 mmol / l.

In case there is an initial hypokalemia of plasma, its correction is beginning not earlier than in 2-2.5 hours from the beginning of infusion therapy.

Non-specific normalization of the acid-alkaline state begins immediately from the first steps of treatment, thanks to infusion therapy in combination with insulin therapy.

Stage 2. It begins after the blood sugar level is reduced to 16.7 mmol / l. As a rule, by this time the patient comes into consciousness. To prevent the development of hypoglycemia, the 5% glucose solution is transmitted to intravenous administration with a speed of 200 ml / hour with the addition of 4 units for each glucose administered 1 g (not to confuse this insulin insulin entered into the subcutaneously!). Sweet tea gives the patient.

Stage 3. It is carried out in the profile hospital separation, includes subcutaneous insulin injections 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 terminated, the fluid is administered orally. The patient is shown diet No. 9, except for the fatty food for the period of acetionalia, and within 10 days after it.

After the coma of the patient during the week, bedding is shown.

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Citation:Demidova I.Yu. Ketoacidosis and ketoacidotic coma // RMG. 1998. №12. P. 8.

Diagnosis of diabetic ketoacidosis with diabetes mellitus installed does not cause difficulties. Special attention requires cases when diabetes is manifest in the ketoacidosis state. Presented recommendations for the treatment of this state and its complications.

To Diagnose Diabetic Ketoacidosis in Documentd Diabetes Mellitus Presents No DiffiCulties. Emphasis Should be Laid On the Cases in Which Diabetes Mellitus Is Manifestative in The Presentation of Ketoacidosis. Recommendations for Treatment of this Condition and ITS Complications Are Given.

I.Yu. Demidov - Department of Endocrinology MMA. THEM. Sechenov (Head. - Acad. Ramna Prof. I.I. Santov)

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

TO etoacidosis and ketoacidotic coma are one of the main causes of death with diabetes patients (SD) under 20 years. More than 16% of patients suffering from insulin-dependent diabetes (ECD) die from ketoacidosis or ketoacidotic coma. The risk of death of ketoacidosis is especially increasing in cases where the factor provoking the occurrence of this acute complication of the SD is a severe intercurrent disease.
The identification of ECDs in the early stages reduced the incidence of cases of manifestation of this disease in a state of ketoacidosis to 20%. Training of patients suffering from SD, the principles of self-control and tactics of behavior in emergency conditions made it possible to significantly reduce the risk of ketoacidosis - to 0, 5-2% of cases per year.
Study of nuances of ketoacidose pathogenesis and creation the optimal patterns of therapy of this state led to a decrease in the frequency of death, however, the death rate from the ketoacidotic coma is 7 - 19%, and in non-specialized medical institutions, this indicator is higher.

Pathogenesis

The most frequent provoking factors for decompensation of SD and the development of ketoacidosis are any intercurrent diseases (acute inflammatory processes, aggravation of chronic diseases, infectious diseases), surgical interventions, injuries, treatment of treatment (introduction of overdue or incorrectly stored insulin, errors in the appointment or administration of the drug, Malfunction in insulin administration systems, emotional stressful situations, pregnancy and termination of insulin administration with suicidal purposes.
Leading role in the pathogenesis of ketoacidosis Absolute insulin deficiency plays, leading to a decrease in glucose disposal by insulin-dependent tissues and, respectively, hyperglycemia, and severe energy hunger in them. The latter circumstance is the reason for a sharp increase in blood levels of all the counterinsulain hormones (glucagon, cortisol, catecholamines, ACTH, STG), stimulation of glycogenolysis processes, proteolysis and lipolysis supplying substrates for glukegenesis in the liver and to a lesser extent in the kidneys. Gloundogenesis combined with a direct disruption of glucose utilization by tissues due to absolute insulin deficiency is the most important cause of rapidly increasing hyperglycemia, increasing the osmolarity of plasma, intracellular dehydration and osmotic diurea.
The listed factors lead to severe extracellular dehydration, hypovolemic shock and significant electrolyte violations. Dehydration and hypovolemia are the cause of a decrease in cerebral, renal and peripheral blood flow, which, in turn, enhances the existing Hypoxia CNS and peripheral tissues and leads to the development of Oliguria and Anururia. Hypoxia peripheral tissues contributes to the activation of the processes of anaerobic glycolysis and gradual increase in the level of lactate. The relative deficiency of lactate dehydrogenase with insulin deficiency and the impossibility of fully utilization of lactate in the measles cycle are the cause of lactacidosis during decompensation of ECD. Insulin deficiency and a sharp increase in the concentration of all the counterinsulin hormones are the cause of the activation of lipolysis and mobilization of free fatty acids (SZhK), which contributes to the active products of ketone bodies. The enhanced formation of acetyl-economy, the precursor of acetoacetate (and acetone during decarboxylation), and the B-hydroxybutyrate is ensured in these conditions the active admission of the SZhK into the liver due to their mobilization from peripheral tissues and the predominance of lipolyase processes over lipogenesis in the liver cell itself.
The rapid increase in the concentration of ketone bodies during the decomptionation of the SD is due not only to their reinforced products, but also by a decrease in their peripheral disposal and excretion with urine due to dehydration and oliginia, replacing polyuria. The dissociation of ketone bodies is accompanied by equimolar products of hydrogen ions. In conditions of decompensation of the SD, the products of ketone bodies and, therefore, the formation of hydrogen ions exceed the buffer capacity of the tissues and body fluids, which leads to the development of severe metabolic acidosis.
The severity of the state with ketoacidosis is caused by a sharp dehydration of the body, decompensated by metabolic acidosis, a pronounced electrolyte deficiency (potassium, sodium, phosphorus, magnesium, etc.), hypoxia, hyperosmolarness (in most cases) and often accompanying intercurrent disease.

Clinical picture

Ketoacidosis is developing gradually within a few days. In the presence of a severe concomitant infection, the clinical picture of ketoacidosis unfolds in a more compressed duration.
Early clinical symptoms Ketoacidase are typical signs of SD decompensation, such as increasing dryness of mucous and skin, thirst, polyuria, subsequently replacing Oligira and Anuria, weakness, headache, drowsiness, decreased appetite, body weight loss, appearance of light acetone in exhaled air. In the case of unwise of timely assistance, metabolic disorders are exacerbated, and the clinical signs described above are complemented by non-specific symptoms of intoxication and acidosis, such as headache, dizziness, nausea and vomiting, which is soon exploring and becomes indispensable. Right masses with ketoacidosis often have a blood-brownish tint and doctors mistakenly take it for vomiting "coffee grounds". As the ketoacidosis increases the smell of acetone in the exhaled air is amplified, and the breath becomes frequent, noisy and deep (respiratory compensation, breathing of Kussmouul).
Deserves special attention to the symptom observed by more than half of the patients - the so-called " abdominal syndrome "ketoacidase, manifested by a clinic" acute abdomen ". Often, the combination of pain in the abdomen, vomiting and the leukocytosis observed in ketoacidosis leads to diagnostic errors and unacceptable surgical interventions in this state, often endingly ending. The risk of such errors is especially great in the case of the manifestation of the CD in the ketoacidosis state.
With objective inspection, pronounced signs of dehydration are noted (in severe cases, patients are losing up to 10 to 12% of body weight). Tour tissues decrease sharply. Eyeballs become soft, and skin covers and visible mucous membranes are dry. The language is covered with a thick brown raid. Muscle tone, tendon reflexes, body temperature and blood pressure reduced. The frequent pulse of weak filling and voltage is determined. The liver, as a rule, significantly protrudes from under the edge of the edge arc and painful when palpation. Kussmouul's breathing is accompanied by a sharp smell of acetone in exhaled air.
When examining patients in a state of ketoacidosis, it is necessary to clarify the reason for the reason for the decompensation of the SD as soon as possible. In the presence of a concomitant intercurrent disease, it should be immediately proceeded for its treatment.
From the first signs of decompensation of SD in patients, signs are noted first of the lung, and then more and more pronounced oppression of the CNS. So, first, patients complain of headaches, become irritable, and then - sluggish, apathetic, sleepy. The developing state of stunning is characterized by a decrease in the level of wakefulness, slowing conscious reactions to stimuli and an increase in sleep periods. As the metabolic disorders exacerbate the state of stupor, a frequently referred tortose state, a clinically manifested deep-by-sleep or similar to it on behavioral reactions. The final stage of the growing oppression of the CNS is a coma characterized by a complete absence of consciousness.
In the study of blood, hyperglycemia is determined, hyperketonemia, an increase in the level of nitrogen of urea, creatinine and in some cases - lactate. Plasma sodium level is usually reduced. Despite the considerable loss of potassium with osmotic diurea, vomit masses and a chair, leading to a pronounced shortage of this electrolyte in the body, its plasma concentration may be normal or even slightly elevated under Anururia. In the study of urine, glucosuria, ketonuria and proteinuria are determined. The acid-base state (COS) reflects decompensated metabolic acidosis, and in severe cases, blood pH is lowered below 7.0. The ECG may be signs of hypoxia myocardium and conduction disorders.
In that case, if it is known about the presence of a patient, the diagnosis of ketoacidosis and the ketoacidotic coma does not represent complexity. The diagnosis is confirmed by the clinical picture described above, laboratory indicators (primarily hyperglycemia, the presence of glucose and ketone bodies in the urine) and KPS indicating the presence of decompensated metabolic acidosis. In the case of the manifestation of the CD immediately in a state of ketoacidosis or coma, first of all, it is necessary to focus on the presence of pronounced dehydration, signs of acidosis (breathing of Kussmouul) and a significant loss of body weight in a short period of time. In this case, the research of the CPS excludes respiratory alkalosis as the cause of hyperventilation and confirms the presence of a patient with metabolic acidosis. In addition, the smell of acetone in exhaled air should bring a doctor to the idea of \u200b\u200bthe presence of ketoacidosis in the patient. Lactat-acidosis, uremia, alcoholic ketoacidosis, acid poisoning, methanol, ethylene glycol, paramiageide, salicylate (other causes of metabolic acidosis) are not accompanied by so pronounced dehydration and significant loss of body weight, and also manifests them typical clinical picture. The presence of hyperglycemia and ketonuria confirms the diagnosis of SD and ketoacidosis.

Treatment

Treatment of patients in the state of decompensation of SD, and even more so in a state of ketoacidosis or ketoacidotic coma, should begin immediately. Patients are hospitalized into a specialized branch, and in the state of the coma - in the resuscitation department.
The main objectives of the treatment of ketoacidosis are the fight against dehydration and hypovolemic shock, the restoration of physiological Kos, the normalization of the electrolyte balance, the liquidation of intoxication and the treatment of related diseases.
Immediately before starting therapy, the patient was washed with a stomach solution of sodium bicarbonate. To control the functions of the kidneys and accounting, diuresis is administered by a blade catheter. In order to improve the oxygenation of tissues, the inhalation of oxygen is settled. Given the hypothermia, the patient is necessary to heat heat, and the solutions should be entered with fittings.
To control the effectiveness of the therapy before the start of treatment, control the glycemia, pH of blood, RSO 2, level K, Na, lactate and ketone bodies in blood, glucosuria and kettonuria, blood pressure, ECG, hemoglobin level, hematocrit, respiratory rate (CH), pulse . Subsequently, it is necessary to control the glycemia, blood pH, RSO 2 , Hell, ECG, CH, Pulse. You can evaluate other indicators every 2 - 3 hours.
Important prognostic value (especially in a coma) has an assessment of the reaction of pupils into light. A weak reaction or its complete absence indicates the developed structural changes in the brain barrel and the low probability of a favorable disease.
Rehydatutation It is very important in the treatment of diabetic ketoacidase due to the large role of dehydration in the chain of metabolic disorders at this state. The volume of the lost fluid is replenished with physiological (or hypotonic under hyperosmolarness) and 5 - 10% glucose solutions. The termination of infusion therapy is possible only with the complete restoration of consciousness, the absence of nausea, vomiting and the possibility of receiving fluid with PER OS patients. During the first hour, 1 l 0.9% of the NaCl solution is injected intravenously. In the presence of hyperosmolarity, the saline solution can be replaced by a hypotonic 0.45% NaCl solution.
Effective osmolarity is calculated according to the following formula:
Osmolarity \u003d 2 + blood glucose (MOS) (mmol / l), normal value \u003d 297 ± 2 mos / l
Over the next two hours from the beginning of therapy, 500 ml of 0.9% NaCl solution is introduced. In the following hours, the liquid administration rate usually should not exceed 300 ml/ h. After a decrease in the level of glycemia below 14 mmol / l, the saline solution is replaced by a 5 - 10% glucose solution and administered at the rate indicated above. The purpose of glucose at this stage is dictated by a number of reasons, among which the main is maintained opelolarity of blood. A rapid decrease in the level of glycemia and the concentration of other high-grade blood components against the background of infusion therapy often becomes the reason for the undesirable rapid decrease in plasma osmolarity.
Insulinotherapy Start immediately after the diagnosis of ketoacidosis. In the treatment of ketoacidosis, as well as any other urgent state at SD, insulin is used only by a short action (MS actrapide, an ATTRADID NM, HUMULIN R, Insun Rapid, etc.). Prior to normalization of the brass and reducing the level of glycemia below 14.0 mmol / l, insulin is administered only intravenously drip or intramuscularly into the direct muscle muscle. Upon reaching the caulary level of glycemia and the normalization of KIA, the patient is transferred to the subcutaneous introduction of a short action insulin.
Insulin's dose in the first hour of treatment is 10 units of intravenously inkjet or 20 union intramuscularly. In the case of a concomitant severe purulent infection, the first dose of insulin can be enlarged twice.
Subsequently, an average of 6 units of a short action intramuscularly or with a physiological solution of NaCl intravenously drip. For this, a separate container with a 0.9% NaCl solution is added 10 units for every 100 ml of saline. The resulting mixture is thoroughly shaken. In order to adsorption of insulin on the walls of the system through it, 50 ml of the mixture of inkjno is passed. Application For the same purpose, previously used albumin solutions are currently considered optional. It is hourly 60 ml of the specified mixture is injected intravenously. In the event that during the first 2 - 3 hours from the beginning of therapy, the level of glycemia is not reduced, the insulin dose is recommended to double the insulin.
Upon reaching the level of glycemia, 12-14 mmol / l dose of inserted insulin is reduced by 2 times - up to 3 products is hourly (30 ml of insulin mixture and saline). At this stage of therapy, the patient is translated into intramuscular injections of insulin, however, it should be borne in mind that the insulin syringes used and various individual systems for the introduction of the hormone are equipped with needles only for subcutaneous insulin administration.
It should not strive to reduce the level of glycemia below 10 mmol / l, since the risk of not only hypoglycemia increases, but also above all - hyposmolarity. Nevertheless, if the level of glycemia is reduced below 10 mmol / l with the preserving acidosis, it is recommended to still enter insulin it is hourly, and reduce to 2 - 3 units / h. With the normalization of the CBC (light ketonuria, it can be preserved) should be transferred to the patient to the subcutaneous injection of insulin by 6 pieces every 2 hours, and then every 4 hours in the same dose.
In the absence of ketoacidosis on the 2nd - 3 days of treatment, the patient can be translated by 5 to 6 one-time introduction of a short action insulin, and in the future - to conventional combined insulin therapy.
Restoration of electrolyte balance First of all, potassium deficiency is an important component of the complex treatment of ketoacidosis. Usually, the introduction of the CCL begin 2 hours from the start of infusion therapy. However, before the start of treatment, there are already eg- or laboratory signs confirming hypokalemia with the obligatory absence of Anuria, the introduction of potassium can be started immediately, since the introduction of liquid and insulin contributes to the rapid decrease in the level of potassium in the blood due to the dilution of its concentration and normalization of potassium transport to the cage .
The dose of the KCL solution introduced intravenously drip depends on the concentration of potassium in the plasma. So, at the potassium level below 3 mmol / l, it is necessary to introduce 3 g / h (dry matter), at 3-4 mmol / l - 2 g / h, at 4 - 5 mmol / l - 1.5 g / h, at 5 - 6 mmol / l - 0.5 g / h. Upon reaching the level of potassium in a plasma 6 mmol / l, the introduction of the KCL solution should be stopped.
As a rule, patients do not need additional hypophosphatemia correction. The question of the need to introduce potassium phosphate only in the event that the level of phosphorus in the plasma decreases below 1 mg%.
Restoration of KG. It begins literally from the first minutes of treatment of ketoacidosis, due to the purpose of the liquid and the introduction of insulin. Restoration of the volume of fluid launches physiological buffer systems, in particular, the ability of kidney reabsorbing bicarbonates is restored. The assignment of insulin suppresses ketogenesis and thereby reduces the concentration of hydrogen ions in the blood. However, in some cases, the question arises of the need to appoint sodium bicarbonate in order to correct the COP. Above it was noted that even significant peripheral metabolic acidosis is far from always accompanied by an equally pronounced acidosis of the CNS, due to the presence of a number of protective-adaptive mechanisms. According to J. Ohman et al. J. Posner and F. Plum, in patients with diabetic ketoacidosis before the start of pH therapy, the spinal fluid is usually within the normal range. Attempts to correct plasma acidosis using intravenous administration of sodium bicarbonate can lead to a rapid development of the CNS acidosis and a sharp deterioration in the state of the patient's consciousness. Given the described side effects, with the introduction of soda, very rigid criteria for the purpose of the sodium bicarbonate during diabetic ketoacidosis have been developed. Considering the question of the feasibility of introducing soda only at the level of blood pH below 7.0. It is necessary to emphasize that at the same time it is very important to continuously monitor the changes of the COP, and when the pH is reached, the value of 7.0, the introduction of the bicarbonate should be stopped. A 4% sodium bicarbonate solution is used at the rate of 2.5 ml per 1 kg of actual body weight intravenously drip very slowly. With the introduction of sodium bicarbonate, the KCl solution is additionally injected in addition to 1.5 - 2 g of KCL dry matter intravenously.
In order to treatment or prevention of inflammatory diseases Antibiotics of a wide range of action are prescribed.
For improve the rheological properties of blood And preventing disseminated intravascular coagulation twice in the first day of treatment, 5000 units of heparin intravenously under the control of the coagulogram are introduced.
In order to normalize the oxidative processes, 150-12 ml of caocarboxylase and 5 ml of a 5% solution of ascorbic acid are added.
With low blood pressure and other symptoms of shock, they conduct therapy aimed at raising and maintaining blood pressure and cardiac activity.
After removing the patient from the state of ketoacidosis, a gentle diet rich in carbohydrates, proteins, potassium is prescribed. Fats from the diet of nutrition exclude at least a week.

Complications ketoacidase

Among the complications arising against the background of ketoacidosis therapy, the greatest danger represents the edema of the brain, which in 70% of cases ends with letters (R. Couch et al., 1991; A. Glasgow, 1991). The most common cause of brain edema is a rapid decrease in plasma osmolarity and the level of glycemia against the background of infusion therapy and insulin administration. In the case of sodium bicarbonate, additional prerequisites are created for the correction of acidosis for the occurrence of this formidable complication. The imbalance between the pH of peripheral blood and liquor contributes to increasing the pressure of the latter and facilitates the transport of water from the intercellular space into the brain cells, the osmolarity of which is increased. Usually the brain edema is developing after 4 to 6 hours from the start of therapy for diabetic ketoacidosis. In the case when the patient's consciousness is saved, the signs of the beginning of the brain edema are deterioration of well-being, severe headache and dizziness, nausea, vomiting, vision disorders, as well as the stress of eyeballs, instability of hemodynamic indicators, increasing fever. As a rule, the listed clinical symptoms appear after the "light" period of improving well-being against the background of the obvious positive dynamics of laboratory indicators.
It is much more difficult to suspect the beginning of the brain edema in patients in a state of ketoacidotic coma. A faithful sign of this complication at the initial stage is the lack of positive dynamics in the state of the patient's consciousness against the background of an objective improvement of carbohydrate metabolism. The above-described clinical signs of brain edema are accompanied by a decrease or absence of pupils for light, ophthalmoplegia and swelling nerve. Ultrasound encephalography and computed tomography confirm the diagnosis.
The treatment of brain edema represents significantly important difficulties than the diagnosis of this state. Upon confirmation of the presence of brain swelling, osmotic diuretics is prescribed - intravenous drip administration of mannitol solution at the rate of 1 - 2 g / kg. Following this, 80 ± 120 mg of Lazix and 10 ml of hypertensive sodium chloride sodium hypertonic sodium solution are injected intravenously. The question of the feasibility of the purpose of glucocorticoids (preference is given exclusively dexamethane due to its minimum mineralocorticoid properties) is not allowed to end. It is believed that the greatest effect of the purpose of these hormones is observed during the edema of the brain against the background of injury or tumor. However, given the ability of glucocorticoids to reduce the pathologically increased permeability of the vessels and the hemat and hemat and hemat and a membrane, normalize the ion transport through the cell membrane and inhibit the activity of the lysosomal brain cell enzymes, the question of the advisability of their purpose during the edema of the brain with ketoacidosis should be solved individually. Anti-therapeutic measures are added to the brain hypothermia and active hyperventilation of the lungs in order to reduce intracranial pressure due to vasoconstriction arising from this. In some cases, consider the creation of a skull.
Among other complications of ketoacidosis and its therapy should be allocated disseminated intravascular coagulation, pulmonary edema, acute cardiovascular failure, hypokalemia, metabolic alkalosis, asphyxia due to the aspiration of gastric content.
Strict control of hemodynamic, hemostasis, the content of electrolytes, changes in osmolarity and neurological symptoms makes it possible to suspect the complications listed above in the early stages and immediately take effective measures aimed at eliminating them.

Literature:

1. Krane E. Diabetic Ketoacidosis. Ped Clinics N Amer 1987; 34: 935-60.
2. Flame F., Posner J.B. Diagnostics of stupuses and coma. Per.s English: Medicine, 1986. - 544 p. ill.
3. Beaser R. Diabetic Emergencies. Joslin Diabetes Center. Lecture Notes. October 1992: 12.
4. Diabetic Ketoacidosis - A Scheme for Management. In: Diabetes in the Young. ISGD. OFFICIAL BULLETIN 1990; 23: 13-5.

Ketoacidotic coma is an acute complication of diabetes mellitus, resulting from insulin deficiency due to inadequately selected insulin therapy. Such a state is dangerous to human life and can lead to a fatal outcome. According to statistics, this is a complication. occurs in 40 patients out of 1000 patients.

In 85-95% of cases, coma ends favorably, and in 5-15% of cases ends with death for the patient. The most vulnerable people over 60 years old. For the elderly, it is especially important to clarify the correctness of insulin therapy and compliance with the dosage of the drug.

Ethiology of origin

The reasons for which such a serious complication arises. All of them develop due to non-compliance with the therapy, violations of recommendations prescribed by the doctor, as well as the accession of secondary infection. If you disassemble the reasons in more detail, the following factors can be distinguished, provoking the development of such alert as a ketoacidotic coma:

• alcohol consumption in large quantities;
• cancellation of sugar-reducing drugs without permission of a doctor;
• self-altitude transition to the tablet form of treatment in insulin-dependent diabetes;
• missed insulin injection;
• violation of the technical rules for the introduction of insulin;
• creating adverse conditions for metabolic disorders;
• attachment of infectious and inflammatory diseases;
• injuries, operational interventions, pregnancy;
• stress;
• stroke, myocardial infarction;
• reception of drugs that do not combine in a complex with insulin therapy.

The emergence of complications in all of the above cases is due to a decrease in the sensitivity of tissue cells to insulin or amplification of the secretory function of the conjunral hormones (cortisol, adrenaline, norepinephrine, STG, glucagon). Approximately 25% of the development of the ketoacidotic coma fails to recognize the cause of its occurrence.

Pathogenesis of ketoacidotic coma

After the start of the action of some provoking factors for the development of sugar diabetes, a chain of pathological processes begins in the body, which lead to the development of symptoms of complications, as well as possible consequences. How does the ketoacidotic coma and its symptoms develop?

First, the body appears in the body insulin deficiency, as well as production in the excess number of conjunral hormones. Such a violation leads to insufficient provision of tissues and glucose cells and a decrease in its disposal. In this case, the glycolysis is suppressed in the liver and a hyperglycemic state is developing.

Secondly, hypovolemia arises under the influence of hyperglycemia (reduction of the BCC), loss of electrolytes in the form of potassium, sodium, phosphates and other substances, as well as dehydration (dehydration).

Third, due to the reduction of circulating blood (BCC) begins enhanced production of catecholaminesthat become the cause of even greater deterioration of the functional action of insulin in the liver. And with this condition, when an excess of catecholamines and disadvantage of insulin are observed in this organ, the mobilization of fatty acids from adipose tissue begins.

The final stage of the complication mechanism is strengthening the production of ketone bodies (acetone, acetoacetate, beta-hydroxyma salted acid). Because of such a pathological condition, the body is not able to metabolize and remove ketone bodies, which bind to the accumulating hydrogen ions, resulting in a decrease in blood pH level and the content of bicarbonate and the formation of metabolic acidosis. The organism compensatory response occurs in the form of hyperventilation and reducing the partial pressure of carbon dioxide. The ketoacidotic coma under the influence of such pathogenesis begins to show symptoms.

Symptoms of manifestation of complications

Symptoms of complications are developing gradually and occupy from several hours to several days of time. At the very beginning of the ketoacidotic coma, the patient notes dry mouth, thirst and polyuria. All these symptoms are talking about diabetes decompensation. Next, the clinical picture is complemented skin itch due to dryness of skin, impact of appetite, weakness, adamas, pains in limbs and headaches.

Because of the violation of the appetite and the loss of electrolytes, pain in the abdomen, nausea and vomiting "coffee grounds" begin. Abdominal pain sometimes can wear such a keen character that at first there is a suspicion of pancreatitis, ulcers or peritonitis. Rising dehydration enhances the body intoxication, which can lead to irreversible consequences. The toxic influence on the CNS was not fully studied by scientists, but the main assumptions of death are the dehydration of the neurons of the brain, which occurs as a result of plasma hyperosmolarity.

The main clinical picture with a ketoacidotic coma is typical symptoms for this complication, expressed in ragged, but deep breathing (Kussmouul's breath) with the smell of acetone in exhalation. Patients are reduced by the turgor (elasticity) of the skin, and the skin itself and the mucous membranes are dry. Due to the reduction of the BCC in the patient, an orthostatic hypotension may be observed, accompanied by a confusion of consciousness, gradually turning into a state of coma. It is very important to notice the presence of the presented symptoms in time to provide timely help.

Emergency care for ketoacidotic coma

Probably, it is not necessary to remind that sick diabetes itself, as well as the surrounding close and relatives should know everything about this disease, including emergency care. Nevertheless, it is possible to repeat the algorithm of actions in the event of a ketoacedsis:

1. If there is a deterioration in the state of the patient, and even more so the violation of consciousness, up to the transition to a comatose state, the first to know the "ambulance" brigade.
2. Then it is worth checking the heart rate, ChDD and hell and repeat these events until the arrival of physicians.
3. It is possible to estimate the condition of the patient with the help of questions that the answer should follow or resort to the rubbing of the ears and non-silent polishes in the face.

In addition, it is possible to distinguish a doggypal assistance that turns out to be in the "ambulance" carriage and includes the following actions:

1. The introduction of saline solutions in the form of an isotonic solution in a volume of 400-500 ml in / c at a speed of 15 ml / min. It is carried out to facilitate the symptoms of the body's dehydration.
2. Introduction subcutaneously small doses of insulin.

After arrival in the patient's hospital, it is determined in the separation of intensive therapy, where the treatment of a patient in a state of ketoacidothic coma continues.

Inpatient treatment of the patient implies the fight against hypovolemic shock and dehydration, normalization of the electrolyte balance, the elimination of intoxication, the restoration of the physiological functions of the body and the treatment of related diseases.

Principles of assistance and treatment with a ketoacenedical coma:

1. Rehydration. Important link in the chain elimination of complications. With ketoacidosis, the organism dehydration occurs and physiological fluids are introduced to replenish the lost liquid in the form of 5-10% glucose and 0.9% sodium solution of chloride. Glucose is prescribed to restore and maintain blood osmolarity.
2. Insulinotherapy. A similar method of treatment begins immediately after the diagnosis of the ketoacidonic coma. In this case, as, however, in other urgent states in diabetes, a short-acting insulin is used (Insun Rapid, ACTRADID Nm, ACTRADID MS, Humulin P). Initially, it is injected intramuscularly into the straight muscle of the abdomen or intravenously drip. After the glucose level reaches an indicator of 14 mmol / l, the patient begins the introduction of a short action insulin subcutaneously. Once, the level of glycemia will be fixed in the indicators of 12-13 mmol / l dose of inserted insulin decrease by half. It is impossible to reduce the glycemic indicator below 10 mmol / l. Such actions can provoke the beginning of the development of the hypoglycemic state and hyposmolarity of blood. As soon as all the symptoms of the manifestation of the ketoacedomic coma of the patient are transferred to 5-6 one-time introduction of insulin of a short term, and with a stabilizing dynamics, combined insulin therapy is carried out.
3. Restoration of electrolyte balance and hemostasis. Such events are an important component of the therapy. With the introduction of the necessary drugs, calcium deficiency and the acid-base state of blood is restored, thereby ensuring the normalization of the kidney functions to reabsorb the bicarbonates.
4. Improving the rheological properties of blood. And also to prevent intravascular coagulation can be assigned heparin intravenously under the control of the coagulogram.
5. Treatment of secondary infections. If the patient has the attachment of a secondary infection, as well as for the prevention of their occurrence, antibiotics of a wide range of action can be prescribed.
6. Symptomatic therapy. To restore blood pressure and eliminate the effects of shock, therapeutic measures are carried out aimed at improving cardiac activity. In addition, after the coma, the patient is prescribed a gentle diet rich in potassium, carbohydrates and proteins. Fats from the diet are excluded at least 7 days.

Prevention of ketoaced coma

Nothing is better than just not to hurt. If there is such a moment in life that a chronic disease requires increased attention, it is worth a special responsibility to this circumstance.

First, it is necessary with special care treats all recommendations prescribed by the doctor. Secondly, you need to follow the shelf life of insulin, comply with the technique of administration, dosage and time of injection. Keep the drug you need to store all the rules. In the event that the patient feels the unreason and deterioration of its condition, with whom he cannot cope with himself, should immediately consult a doctor, where he will be provided for emergency care.

Complications of coma

The ketoacenedotic coma with a proper diagnosis and timely correction of biochemical disorders carry a favorable outcome and does not cause severe consequences. The most dangerous complication of this state may be a brain swelling, which in 70% of cases ends with a fatal outcome.

5944 0

Currently, it is generally recognized that the life expectancy of patients diabetes mellitus (Sd) First of all, the late vascular complications of the disease are determined. At the same time, a serious threat to their lifetime is sharp complications of the disease - hyperglycemic (ketoacidotic, hyperosmolar, hyperlactacidemic) and hypoglycemic coma.

So, in our days, mortality from the diabetic ketoacidotic coma is 5-14%, the hyperosmolar coma is 40-60%, the lactacide coma - 30-90%, the hypoglycemic coma - 3-4%. And this is despite the fact that achievements in the field of CD therapy, the timely diagnosis, training of patients, the implementation of the principles of self-controls led to a decrease in the incidence of occurrence of com and mortality from them. Especially the risk of death increases in senior patients and in the presence of severe intercurrent diseases acting as provoking these complications of factors.

Reduce the frequency of death in the development of acute complications of the SD largely allow timely diagnostics and adequate emergency care. In this regard, the doctor of any specialty should be familiar with the peculiarities of developing sharp complications of diabetes, their clinic, diagnosis, modern therapeutic tactics, for in practice it is often necessary to deal with manifestations of decompensation of SD, including acutely arising.

Of the sharp complications of the SD, hypoglycemic states and coma are most frequent. This is a life-threatening state, developing with a rapid decrease in blood glucose concentration. Approximately 5-10% of patients with diabetes are at least one heavy hypoglycemia for the year.

The hyperglycemic (diabetic) coma can develop in 3 versions:

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

In addition, these coma have their clinical features, they differ in laboratory signs: The degree of hyperglycemia, the presence or absence of hyperketonemia, hyperlactacidemia, depth of disorders of the water-election balance and acid-alkaline equilibrium. In the formation of one or another variant of the diabetic coma, a significant role is allocated to the provoking factor, the age of patients, intercurrent diseases, but the type of CD is crucial in this, or rather the presence of absolute or relative insulin deficiency.

Ketoacidotic coma, the most common option among the diabetic com, more often complicates the flow type of type 1 diabetes (SD-1), although it can be diagnosed and type of type 2 diabetesSD-2). Thus, in Russia, the frequency of diabetic ketoacidase and the ketoacidotic coma at SD-1 is 0.2-0.26, with SD-2 - 0.07 cases per patient per year. Up to 20-30% of patients with SD-1 are delivered to hospitals in a state of diabetic ketoacidosis or coma in the debut of the disease.

Other variants of the diabetic coma (hyperosmolar, hyperlactacidemic) occur about 10 times less frequently compared with the ketoacidotic coma, but even with proper treatment are accompanied by a high frequency of lethal outcomes. They are developing mainly in persons over 50 years of suffering from SD-2.

Diabetic ketoacidosis

Diabetic ketoacidosis (DCA) - the threatening life of patients with SD acute decompensation of metabolism due to progressive insulin insufficiency, manifested by a sharp increase in the level of glucose and the concentration of ketone bodies in the blood, the development of metabolic acidosis.

Its pathophysiological essence is a progressive insulin deficiency, which causes the abundant violation of all types of metabolism, which determines the severity of the general condition, the emergence and progression of functional and structural changes from the cardiovascular system, kidneys, liver, central nervous system (CNS) With the oppression of consciousness to its full loss - coma, which may be incompatible with life. Thus, more than 16% of patients suffering from type 1 diabetes die precisely from ketoacidosis or ketoacidotic coma.

The exchange disorders underlying diabetic decompensation with an outcome in ketoacidosis may have a different degree of severity, and this is determined, first of all, at what stage the patient is accessed for medical help.

The first stage of exchange disorders, when the content of blood glucose and urine is significantly increased and the patient has clinical symptoms of hyperglycemia and glucose, is defined as a stage of decompensation of metabolic processes.

Then, during the progression of decompensation of diabetes mellitus, the so-called ketoacidotic cycle is developed. The first stage of this cycle - ketosis (compensated ketoacidosis), when, as the metabolic disorders progress, the concentration of acetone bodies in the blood increases and acetionaluria appears. Signs of intoxication at this stage are usually no or they are minimal.

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

Third stage - Prema (severe ketoacidosis), differing from the previous stage with a more pronounced oppression of consciousness (to stupor), heavier clinical and laboratory disorders, heavier intoxication.

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

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

Etiology and pathogenesis

The most common cause of the development of ketoacidosis in patients with SD is a violation of the treatment regimen: Pass or unauthorized cancellation of insulin injections. Especially often this error patients are committed in the absence of appetite, the appearance of nausea, vomiting, increasing body temperature.

In patients with diabetes mellitus of the 2nd type, the multi-month and even a long-term break in the reception of tableted sugar-based drugs is often found. On the 2nd frequency of the place among provoking ketoacidosis, there are sharp inflammatory diseases or aggravation of chronic, as well as infectious diseases. Often there is a combination of both these reasons.

One of the frequent causes of ketoacidosis is the late appeal to the doctor under the manifestation of SD-1. In 20% of patients in the debut of SD-1 type there is a pattern of ketoacidosis. Among the frequent causes of diabetic decompensation are called diet disorders, alcohol abuse, error in the administration of insulin dose.

In principle, any diseases and conditions accompanied by a sharp increase in the concentration of counterinsulin hormones can lead to the decompensation of the SD and the development of ketoacidosis. Among them should be noted operations, injuries, 2nd pregnancy, vascular disasters (myocardial infarction, stroke), the use of insulin antagonists (glucocorticoids, diuretics, genital hormones) and others are less common causes of ketoacidosis.

In the pathogenesis of ketoacidosis (Fig. 16.1), the leading role is played by a sharp deficiency of insulin, leading to a decrease in glucose disposal by insulin-dependent tissues and, as a result, to hyperglycemia. Energy "Hunger" in these tissues is the cause of a sharp increase in the blood of all the counterinsulan hormones (glucagon, cortisol, adrenaline, adrenocorticotropic hormone -ACTH, somatotropic hormone -STG), under the influence of which glukegenesis, glycogenolysis, proteolysis and lipolysis are stimulated. The activation of gluconeogenesis as a result of insulin deficiency leads to hyperproduction of glucose liver and increased flow in blood.

Figure 16.1. Pathogenesis of ketoacidotic coma

Thus, gluconeogenesis and disturbed glucose utilization with tissues are the most important causes of rapid increasing hyperglycemia. At the same time, glucose accumulation has a number of negative consequences. First, hyperglycemia significantly increases plasma osmolarity. By virtually this, intracellular fluid begins to move to the vascular channel, which ultimately leads to severe cell dehydration and decrease the content of electrolytes in the cell, primarily potassium ions.

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

Reducing the renal perfusion and, consequently, glomerular filtration leads to the development of oligo- and anourcing, causing a terminal rapid rise of glucose concentration in the blood. Hypoxia peripheral tissues contributes to the activation of the processes of anaerobic glycolysis and gradual increase in the level of lactate. The relative deficiency of lactate dehydrogenase with insulin deficiency and the inability to complete lactate utilization in the measles cycle is the cause of lactacidosis during the decomptionation of the type 1 diabetes mellitus.

The second direction of metabolic disorders caused by insulin deficiency is associated with excess accumulation in the blood of ketone bodies. Activation of lipolyase in adipose tissue under the action of counterinsulin hormones leads to a sharp increase in concentration free fatty acids (szhk) In the blood and enlarged their entry into the liver. Strengthening the oxidation of the SFC as the main source of energy in conditions of insulin deficiency and is the cause of the accumulation of by-products of their decomposition - "ketone bodies" (acetone, acetoxus and B-hydoxymacal acids).

The rapid increase in the concentration of ketone bodies in the blood is due not only to their reinforced products, but also with a decrease in their peripheral recycling and excretion with urine due to the dehydration-based dehydration. Acetoidsus and B-hydroxyma acids are dissociated with the formation of free hydrogen ions. In conditions of decompensation of diabetes mellitus, the products of ketone bodies and the formation of hydrogen ions exceed the buffer capacity of tissues and body fluids, which causes the development of severe metabolic acidosis, clinically manifested toxic breathing of Kussmouul due to irritation of the respiratory center with acidic products, abdominal syndrome.

Thus, hyperglycemia with a complex of 82ol82-electrolyte disorders and ketoacidosis are the leading metabolic syndromes that underlie the pathogenesis of the ketoacidotic coma. On the basis of these syndromes, many secondary exchange, organ and systemic disorders are developing, which determine the severity of the state and the patient's forecast. An important component of metabolic disorders in diabetic ketoacidosis - hypokalemia, causing cardiac (tachycardia, reduction of myocardial reduction ability, reduced or negative TEV to ECG), gastrointestinal (decreased peristaltics, spastic reduction of smooth muscles) and other disorders, as well as contributing to edema brain.

In addition to Kaliyuria, intracellular hypocalemia with ketoacidosis is due to a decrease in the activity of K-ATP-Ase, as well as acidosis, in which the exchange of potassium ions to hydrogen ions inside the cell. At the same time, the initial values \u200b\u200bof potassium in conditions of thickening blood and impaired renal excretion in oliguraury can be normal and even elevated. However, after 2-3 hours from the beginning of therapy, on the background of the introduction of insulin, the rehydration is revealed to the reduced content of potassium in the blood plasma.

The most sensitive to the listed numerous heavy metabolic disorders of the CNS. The violation of the ketoacidosis of consciousness is progressing as metabolic disorders increase and has a multi-doc. Hyperosmolarity and associated dehydration of brain cells have important in the oppression of consciousness. In addition, the heavy hypoxium of the brain is played a large role, due to a decrease in cerebral blood flow, an increase in glycosylated hemoglobin, a decrease in 2.3 dyphosphoglycerat in red blood cells, as well as intoxication, hypokalemia, disseminated intravascular coagulation.

Metabolic acidosis also contributes to the process of oppression of consciousness, but it is directly caused by the development of the coma only if the acidosis occurs in the central nervous system. The fact is that physiological mechanisms as respiratory hyperventilation, a decrease in cerebral blood flow, the buffer properties of nerve cells can provide for a long time the stability of cerebral acid-alkaline balance even with a significant decrease in blood plasma pH. Thus, the disorder of the acid-alkaline balance in the central nervous system occurs lastly, with a strong decrease in blood pH, after the depletion of such compensatory mechanisms as hyperventilation and buffer properties of liquor and neurons.

Clinic

Ketoacidotic coma - This is the final stage of the so-called ketoacidotic cycle, the development of which is preceded by the stage of ketosis, ketoacidase, precomes. Each of the subsequent stages differs from the previous aggravation of metabolic disorders, the increase in the severity of clinical manifestations, the degree of oppression of consciousness and, thus, the severity of the overall state of the patient.

The ketoacidotic coma is developing gradually, usually for several days, however, if there is a severe concomitant infection, the deadlines may be more compressed for its development - 12-24 hours.

Early signs of the beginning decompression of SD, characterizing the state of ketosis, are such clinical symptoms as increasing dryness of mucous membranes, thirst, polyuria, weakness, decline in appetite, body weight loss, headache, drowsiness, lightweight acetone in exhaled air. Sometimes patients with CD may not be pronounced changes in general well-being (even with the existing moderate signs of hyperglycemia), and the basis for establishing ketosis in this case can be a positive reaction to acetone in the urine (ketonuria).

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

The symptoms of general dehydration expressed at this stage appear dryness of mucous membranes, language, skin, a decrease in muscle tone and leather turgora, a tendency to arterial hypotension, tachycardia, oligoran, signs of blood thickening (increase of hematocrit, leukocytosis, eritremia). Increasing inxication due to ketoacidosis leads to most patients to the appearance of nausea, vomiting; The latter with each hour is expensive, acquires an indomitable nature, exacerbating overall dehydration. Robed masses with ketoacidosis often have a blood-brown tint, incorrectly regarded by doctors as vomiting "coffee grounds".

As the ketoacidosis increases, the breathing becomes frequent, noisy and deep (Kussmaul's breathing), while the smell of acetone in exhaled air becomes distinct. It is characteristic of the appearance at this stage of a diabetic blush on his face due to the paretic expansion of capillaries. Most patients already have abdominal disorders, resembling a picture of the "acute abdomen": pain in the stomach of various intensity, more often than spilled nature, the tension of the abdominal muscles (pseudoperitonite).

The origin of these symptoms is associated with the irritation of the peritoneum, the "solar" weaving by ketone bodies, dehydration, electrolyte disorders, intestinal paresis and fine-point hemorrhages in the peritoneum. Abdominal pain and muscle defans in combination with nausea, vomiting, changes in the general blood test (leukocytosis) with ketoacidosis can be taken for acute surgical pathology and cause (with the threat to the patient's life) of the medical error.

The oppression of consciousness at the ketoacidosis stage is characterized by stupidity, rapidly degradability, indifference to the surrounding, confusion of consciousness.

Prema differs from the previous stage with a more pronounced oppression of consciousness, as well as brighter symptoms of dehydration and intoxication. Under the influence of increasing metabolic disorders, stupor is replaced by a stupor. Clinically stupor is manifested by deep sleep or ashautility. The final stage of the growing oppression of the CNS is a coma characterized by a complete absence of consciousness. With objective inspection, there is a deep, frequent and noisy breathing with a sharp smell of acetone in exhaled air. The face is usually pale, with a blush on the cheeks (Rubes). Signs of dehydration are expressed (in severe cases, due to dehydration, patients are losing up to 10-12% of body weight).

Skin surfaces and visible mucous dry, dry tongue, is covered with brown raid. Sharply reduced tours of fabrics and the tone of eyeballs and muscles. Frequent, weak pulse filling, decrease in blood pressure, oliguraury or anouria. Sensitivity and reflexes depending on the coma depths are reduced or falling out. Pupils are usually evenly narrowed. The liver is usually significantly protruding from under the edge of the edge arc.

Depending on the prevalence in the clinical picture of the defeat of any of the listed systems: Cardiovascular, digestive, kidney organs, CNS - four clinical forms of ketoacidotic coma:

1. Cardiovascular, when a leading clinical manifestation is a heavy collapse with a significant decrease in arterial and venous pressure. Especially often, at this embodiment, the coma are developing vehicle thrombosis (with the development of myocardial infarction), pulmonary vessels, vessels of the lower extremities and other organs.
2. Gastrointestinal, when repeated vomiting, intense abdominal pain with the muscle tension of the front abdominal wall and the symptoms of peritoneal irritation along with neutrophilic leukocytosis, imitate the most varying acute surgical gastrointestinal pathology: acute appendicitis, cholecystitis, pancreatitis, intestinal obstruction, mesenteric thrombosis vessels.
3. Renal, characterized by symptom complex of acute renal failure. At the same time, hyperazotemia are expressed, changes in the general analysis of urine (proteinuria, cylindruria, etc.), and there is an anury.
4. Encephalopathic, observed usually in elderly people suffering from atherosclerosis of the brain vessels.

Chronic cerebrovascular insufficiency is aggravated due to dehydration, microcirculation disruption, acidosis. This is manifested not only by the overall symptoms, but also the symptoms of focal brain damage: hemiparem, asymmetry of reflexes, the appearance of pyramidal symptoms. In this situation, it is very difficult to explain unambiguously, whether the development of focal brain symptoms or stroke caused ketoacidosis.

Diagnosis and Differential Diagnosis

The diagnosis of ketoacidosis and ketoacidotic coma can already be installed already in the pre-hospital stage on the basis of a clinical picture, information about the gradual deterioration of the state of the patient, identify the causal factor. In the event that it is known about the presence of sugar diabetes, the diagnosis of ketoacidosis and the ketoacidotic coma is not difficult. In the case of the manifestation of the SD immediately in a state of ketoacidosis or coma, first of all, it is necessary to focus on the presence of a pronounced dehydration, signs of acidosis (Kussmouul breathing) and a significant loss of body weight for a short period of time.

In addition, the smell of acetone in the exhaled air should bring a doctor to the idea of \u200b\u200bthe presence of ketoacidase in the patient as the causes of the available metabolic acidosis. Metabolic acidosis can cause lactacidosis, uremia, alcohol intoxication, acid poisoning, methanol, ethylene glycol, paramedia, salicylate, but these states are not accompanied by such a pronounced dehydration and significant loss of body weight.

The patient with a diagnosis of ketoacidosis or ketoacidotic coma is subject to immediate transportation to the endocrinological, therapeutic, resuscitation department. Verification of the diagnosis of hyperglycemic coma and the differential diagnosis of individual pathogenetic forms are possible only on the basis of laboratory studies with subsequent comparable analysis of the data and clinical symptoms.

Pronounced hyperglycemia (20-35 mmol / l or more) (20-35 mmol / l and more), hyperketonemium (from 3.4 to 100 mmol / l or more) and the indirect confirmation is acetionalura, have a major importance in the diagnosis of ketoacidotic coma.

Confirm the diagnosis of ketoacidotic coma decreased pH of blood to 7.2 and lower (normally 7.34-7.36), a sharp decrease in the alkaline reserve of blood (up to 5% by volume), standard bicarbonate level, moderate increase in plasma osmolarity, often increased content Urea blood. As a rule, neutrophilic leukocytosis is detected, an increase in the number of erythrocytes and hemoglobin due to blood thickening. Hypokalemia is usually registered in a few hours from the start of infusion therapy.

Table 16.1. Differential diagnosis of comatose states in patients

Differential-diagnostic criteria for various types of hyperglycemic coma and hypoglycemic coma are presented in Table. 16.1.

Algorithm of surveys with a ketoacidotic coma:

• glycemia when admission and in dynamics;
• acid-alkaline state (Ksp)
• lactate content, ketone bodies;
• electrolytes (K, Na);
• creatine, urea nitrogen;
• indicators of the coagulation system of blood;
• glucosuria, ketonuria;
• general analysis of blood and urine;
• R-graphic lungs;
• effective plasma osmolarity \u003d 2 (Na + K (mol / l)) + blood glucose (mol / l) - normal value \u003d 297 + 2 mos / l;
• central venous pressure (FVD)

The dynamics are controlled:

• glucose shelter is hourly as glycemia achieves 13-14 mmol / l, and subsequently 1 time at 3 o'clock;
• potassium, sodium in plasma - 2 times a day;
• hematocrit, gas analysis and blood pH 1-2 times a day before the normalization of the KSHC;
• urine analysis on acetone 2 times a day in the first two days, then 1 time per day;
• general blood test and urine 1 time in 2-3 days;
• ECG at least 1 time per day;
• FLOV every 2 hours, when stabilizing the state - every 3 hours

Treatment

Ketoacidosis, especially ketoacidotic coma, are an indication for urgent hospitalization into the separation of intensive therapy or in the resuscitation department. At the pre-hospital stage, it is also limited to symptomatic means that ensure an increase in cardiac and vascular tone.

1. Insulinotherapy.
2. REGRATATATION
3. Correction of electrolyte disorders.
4. Elimination of acidosis.
5. Treatment of related diseases.

Insulinotherapy - pathogenetic type of treatment, aimed at the interruption of severe catabolic processes caused by insulin deficiency. When removing from ketoacidosis and ketoacidotic coma, insulins are used only short action. It has been proven that continuous infusion is 4-10 units. Insulin per hour (on average 6 units) allows you to maintain its optimal level in blood serum 50-100 μED / ml, thereby creating conditions for the restoration of impaired metabolism. Insulin therapy with the use of such dosages is called "Small Dose" regime.

Insulin in diabetic ketoacidosis and coma is recommended to introduce intravenously in the form of a long-term infusion and the most optimal method of such an introduction is infusion using perfusion (infusomate) at a rate of 4-8 units. at one o'clock. Initial dose 10-14 units. Intravenously introduced. The mixture for infusion perfusor is prepared as: to 50 units. Insulin of a short action is added 2 ml of a 20% albumin solution (to prevent insulin adsorption on plastic) and the total volume of up to 50 ml of 0.9% sodium chloride solution is brought. In the absence of perfusor, the inkjet introduction of insulin by a syringe is allowed every hour to the "gum" of the infusion system. The sublease effects in such a means of inserted insulin continues up to 1 hour.

You can use another method of intravenous insulin administration:mix of 10 units. Insulin per 100 ml of a 0.9% sodium chloride solution (without albumin) is administered at a rate of 60 ml per hour, however, it is considered that with this approach, it is difficult to control the insulin administered dose due to its adsorption on the infusion system tubes.

The correction of the intravenously administered dose of insulin is carried out in accordance with the dynamics of glycemia, which should be examined hourly as its level decreases to 13-14 mmol / l, and then 1 time at 3 o'clock. If in the first 2-3 hours glycemia is not reduced, then the next dose of insulin is doubled. The level of glycemia should not be reduced faster than 5.5 mmol / l per hour (the average rate of reduction of glycemia is 3-5 mmol / l per hour). A faster drop in glycemia threatens the development of brain edema. In the first day it is not recommended to reduce blood glucose below 13-14 mmol / l. Upon reaching this level, an intravenous infusion of 5-10% glucose solution is needed, reduce insulin dose to 3-4 units. Intravenously in the "rubber band" for every 20 g of injected glucose (200.0 10% solution).

The introduction of glucose is carried out in order to prevent hypoglycemia, maintaining plasma osmolarity, as well as braking ketogenesis. As the KSHC is normalized (light ketonuria can be maintained for several days) and the recovery of consciousness should be transferred to the patient to the subcutaneous introduction of insulin of 4-6 units. Every 2 hours, and then 6-8 units. Every 4 hours. In the absence of ketoacidosis, on the 2-3 days of treatment, the patient can be translated into a 5-6 one-time introduction of the insulin of a short action, and in the future - on conventional combined therapy.

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

The volume of the lost fluid is replenished with a 0.9% solution of sodium chloride and 5-10% glucose solution. With an increase in the content of sodium serum (150 MEKV / L or more), indicating the hyperosmolarity of plasma, to start rehydration is recommended by a hypotonic 0.45% solution of sodium chloride in a volume of 500 ml. The termination of infusion therapy is possible only with the complete restoration of consciousness, the absence of nausea, vomiting and self-taking fluid to the patient.

So, the drug selection for initial rehydration is 0.9% sodium chloride solution. The speed of rehydration is: in the 1st hour - 1 liters. 2- and 3 hours - 500 ml. In subsequent hours - no more than 300 ml.

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

• with a FED, less than 4 cm waters. Art. - 1 l per hour;
• with CVD from 5 to 12 cm of water. Art. - 0.5 l per hour;
• with CVD, more than 12 cm waters. Art. - 250-300 ml per hour

.
In the absence of control over the FED overload, the fluid may lead to the development of pulmonary edema. The volume of liquid administered in 1 hour during the initial sharply pronounced dehydration should not exceed the level of 500-1000 ml on the volume of the hourly diurea.

As blood glucose decreases to 13-14 mmol / l, the sodium chloride saline solution is replaced by a 5-10% glucose solution at the rate of administration described above. The purpose of glucose at this stage is dictated by a number of reasons, among which the main thing is to maintain blood osmolarity. Fast reduction in glycemia and other high-grade blood components against the background of rehydration often causes a rapid decrease in plasma osmolarity. In this case, the osmolarity of the spinal fluid turns out to be higher than plasma, since the exchange between these liquids proceeds quite slowly. In this regard, the fluid from the bloodstream rushes to the lyingvore and is the cause of the development of brain edema.

In addition, the purpose of glucose together with insulin leads to a gradual reduction of glycogen reserves in the liver, a decrease in gluconeogenesis and ketogenesis.

Restoration of electrolyte balance

The most distinguished violations of the electrolyte metabolism causes an acute decompensation of SD, but the most dangerous of them is the deficiency in potassium organism, reaching sometimes 25-75 g. Even with the initially normal value of potassium in the blood, it should be expected to decline due to the breeding of blood concentration and the normalization of transport to the cell Against the background of insulin therapy and rehydration. That is why, provided that the diuresis is preserved, from the very beginning of insulin therapy, even with normal Caliamia, the continuous infusion of potassium chloride is beginning to maintain its serum level ranging from 4 to 5 mmol / l (tab. 15).

• less than 3 mmol / l - 3 g (dry matter) ks1 per hour;
• 3 - 4 mmol / l - 2 g KS1 per hour;
• 4 - 5 mmol / l - 1.5 g KS1 per hour;
• 6 mmol / l and more - the introduction of potassium is stopped.

After removing from the ketoacidotic coma preparations of potassium should be prescribed inwards for 5-7 days.

Table 15. Potassium administration rate depending on the initial level to + and blood pH

In addition to the disorders of potassium metabolism, there are also violations of the exchange of phosphorus, magnesium in the development of a ketoacidotic coma, but the need for additional correction of these electrolyte disorders remains controversial.

Restoration of acid alkaline state

The most important link of exchange disorders with a ketoacidotic coma - Metabolic acidosis, developing as a result of enhanced ketogenesis in the liver under insulin deficiency. It should be noted that the severity of acidosis with a ketoacidotic coma in various tissues of the body is not the same. Thus, due to the peculiarities of the buffer mechanisms of the central nervous system, the pH of the spinal fluid is long preserved normal even with pronounced acidosis in the blood. Based on this, currently it is highly recommended to change the approaches to the adjustment of the acidosis in the elimination of the ketoacidotic coma and especially limit the indications for the use of sodium bicarbonate due to the risk of complications associated with the introduction of this drug.

It has been proven that the elimination of acidosis and the restoration of the KSHC of the blood begins along the introduction of insulin and rehydration. The recovery of the volume of the fluid launches physiological buffer systems, namely, the rebeling ability to reabsorb the bicarbonates is restored. In turn, the use of insulin suppresses ketogenesis and thereby reduces the concentration of hydrogen ions in the blood.

The introduction of sodium bicarbonate is associated with the risk of complications, among which it is necessary to allocate the development of peripheral alkalosis, aggravation of existing hypokalemia, enhancing peripheral and central hypoxia. This is due to the fact that during the rapid reduction of pH, the synthesis and activity of the 2,3-diphosphoglycerat of erythrocytes are suppressed, the concentration of which against the background of ketoacidosis is already reduced. The result of a reduction of 2,3-diphosphoglycerate is a violation of the dissociation of oxygemoglobin and the aggravation of hypoxia.

In addition, the correction of acidosis using intravenous administration of sodium bicarbonate can lead to the development of a "paradoxical" acidosis in the central nervous system, and in the subsequent and edema of the brain. This paradoxical phenomenon explains that the introduction of sodium bicarbonate is accompanied not only by an increase in the plasma of NSO 3 ions, but also an increase in p from 2. CO 2 penetrates the hematostephalic barrier easier than bicarbonate, leading to an increase in H 2 CO 3 in the liquor, the dissociation of the latter to the formation of hydrogen ions and, thus, to a decrease in the pH of the spinal and extracellular brain fluid, which is an additional factor in the oppression of the CNS.

That is why testimony for the use of soda is currently significantly narrowed. Its intravenous administration is permissible under the control of blood gas composition, potassium and sodium levels and only at blood pH below 7.0 and / or standard bicarbonate level of less than 5 mmol / l. A 4% sodium bicarbonate solution was used at the rate of 2.5 ml per 1 kg of body weight intravenously slowly at a speed of not more than 4 g per hour. With the introduction of sodium bicarbonate, the solution of potassium chloride at the rate of 1.5 - 2 g of dry substance is additionally injected intravenously.

If there is no possibility to determine the KCHC of the blood, the introduction of alkaline solutions "blindly" can have greater harm than potential benefits.

There is no need to appoint a patient with a solution of drinking soda inside, through the enema or in the exclusive use of alkaline mineral water, which is quite widely practiced earlier. If the patient is able to drink, then ordinary water, unsweetened tea, etc. are recommended.

Nonspecific medical measures when removing from diabetic ketoacidosis and coma include:

1. Purpose antibacterial drugs (Ab) A wide range of action that does not possess nephrotoxic effects in order to treat or prevent inflammatory diseases.
2. The use of small doses of heparin (5000 units 2 times a day in the first day) in order to prevent thrombosis mainly in patients of senile age, with a deep coma, with severe hyperosmolarness - more than 380 mosmol / l.
3. With low blood pressure and other shock symptoms, the use of cardiotonic, adrenomimetic drugs.
4. Oxygen therapy with insufficient respiratory function - PO 2 below 11 kPa (80 mm Hg).
5. Installation in the absence of the consciousness of the gastric probe for constant aspiration of content.
6. Installation of the blade for accurate hourly assessment of the water balance.

Food after removing from ketoacidotic coma

After the restoration of consciousness and the ability to swallow in the absence of nausea and vomiting the patient should be prescribed gentle nutrition with a sufficient amount of carbohydrates, a moderate amount of protein, rich in potassium and the exception of fats (porridge, potato, bread, broth, omelet, diluted fruit juices without sugar). After 1-2 day after the start of food intake, in the absence of exacerbation of diseases of the patient, the patient can be translated into normal nutrition.

Complications of ketoacidase therapy

Among the complications arising against the background of ketoacidosis therapy, the greatest danger represents the edema of the brain, which in 90% of cases ends fadingly. In the study of the cerebral tissue of patients who died from brain edema when removing from the ketoacidotic coma, the presence of a so-called cellular or cytotoxic version of the brain edema, which is characterized by swelling of all cellular elements of the brain (neurons, glill) with a corresponding decrease in extracellular fluid.

Optimization of methods of treatment in the elimination of the ketoacidotic coma made it possible to significantly reduce the incidence of this dangerous complication, but often the brain edema occurs in cases of ideally conducted therapy. There are isolated reports on the development of brain edema even before the start of therapy. It is assumed that the brain swelling is associated with an increase in sorbitol and fructose products in brain cells due to the activation of the sorbitol glucose metabolic path, as well as cerebral hypoxia, which reduces the activity of sodium-potassium ATP-Ase in the cells of the central nervous system, followed by the accumulation of sodium ions in them.

However, the most common cause of brain edema is considered to be a rapid decrease in plasma osmolarity and the level of glycemia against the background of the introduction of insulin and liquids. The introduction of sodium bicarbonate creates additional opportunities for the development of this complication. The imbalance between the pH of peripheral blood and liquor contributes to increasing the pressure of the latter and facilitates the transport of water from the intercellular space into the brain cells, the osmolarity of which is increased.

Usually, the brain edema is developing 4-6 hours from the beginning of the therapy of the ketoacidotic coma. With the stored consciousness, the patient with signs of the beginning of the beginning of the brain edema is deterioration of well-being, pronounced headache, dizziness, nausea, vomiting, vision disorder, the stress of the eyeballs, the instability of hemodynamic indicators, increasing fever. As a rule, listed symptoms appear after a period of improving well-being against the background of the positive dynamics of laboratory indicators.

It is more difficult to suspect the beginning of the brain edema in patients who are unconscious. The lack of positive dynamics in the consciousness of the patient with the improvement of glycemia values \u200b\u200bcan give reason to suspect the brain swelling, the clinical confirmation of which will be a decrease or absence of the reaction of pupils into light, ophthalmoplegia and swelling nerve. Ultrasound encephalography and computed tomography confirm this diagnosis.

Osmotic diuretics are prescribed for the treatment of brain edema in the form of intravenous drip administration of mannitol solution at the rate of 1-2 g / kg. Following this, 80-120 mg of lazix and 10 ml of hypertensive sodium chloride solution are injected intravenously. The question of the use of glucocorticoids should be solved individually, giving preference to dexamethane, taking into account its minimum mineralocorticoid properties. Anti-therapeutic measures are added to the brain hypothermia and active hyperventilation of the lungs in order to reduce intracranial pressure due to vasoconstriction arising from this.

Among other complications of the ketoacidotic coma and its therapy, the DVS syndrome, the edema of the lungs, the acute cardiovascular insufficiency, metabolic alkalosis, asphyxia due to the aspiration of gastric contents is noted.

Strict monitoring of hemodynamics, hemostasis, electrolytes, changes in osmolarity and neurological symptoms makes it possible to suspect listed complications in the early stages and take measures to eliminate them.