Ketoacidosis First aid. Emergency care for diabetic coma

Diabetic ketoacidotic coma is a state at which a threat arises for the life of the patient. It is a complication of diabetes. The insulin content becomes excessively small due to incorrectly selected treatment, which leads to dangerous violations in the functioning of the body.

Ketoacidosis is a state characterized by insulin insufficiency, an increased level of sugar and an excess of ketone bodies in the blood and urine of the patient. If you cannot immediately help a person, his state will deteriorate rapidly. Often ends with a fatal outcome.

The reasons

The reason may be errors in treatment. A person can introduce an incorrect dose of the drug, make an injection to a non-time, skip the reception of the drug or forget to introduce insulin. It is possible to develop due to insufficiently careful control of glucose levels.

Complication often occurs when diet violations. To avoid the development of a comatose state, it is necessary to abandon the use of products containing a large number of easily friendly carbohydrates. Another reason for complications is the abuse of alcoholic beverages.

Perhaps development in the presence of a disease complicating the course of diabetes. Such pathologies include stroke, myocardial infarction, inflammatory processes, malignant and benign tumors and others.

It is often noted in the presence of endocrine pathologies, in which the reinforced production of hormones increases, increasing blood sugar levels. Such effect is possible and due to the reception of drugs that increase the concentration of glucose.

Promotes the appearance of a complication of protracted stress, constant nervous overvoltage, recently transferred surgical interventions, injuries.

Signs of ketoacidotic coma

For the pathogenesis of this state, development is characterized within a few days. Occasionally coma may occur during the day, develop quickly. Clinical signs depend on what stage of development pathology is.

At the beginning there is a decrease in the amount of insulin. In addition, the synthesis of conjunral hormones is enhanced. At this stage, the frequent urination is characterized by urinary. The patient is experiencing severe thirst, not passing even after the use of a large amount of liquid. There is a decrease in glucose entering the tissues and organs, due to which sufficient disposal of this substance does not occur, the rapidly increasing hyperglycemia develops. Glikoliz in the liver is suppressed.

Then there is hypovolemia. Electrolytes of potassium, sodium, phosphates leave the body. Dehydration arises. Signs of dehydration are added: dry skin, headache, reducing the turgora.

Noted general symptoms intoxication. Nausea arises, vomiting, weakness. Man quickly tired. Characterized by a general asthenic state. Disrupted appetite. It is observed pain in the limbs. Breathing is expensive, becomes shallow. The rhythm of heart abbreviations is violated due to the decreasing volume of circulating blood in the body. At the same time, the amount of urination at this stage is much reduced, sometimes there is a complete absence of urin.

If the help was not provided timely, a pronounced oppression of consciousness is observed. First there is a confusion, inhibition, a decrease in cognitive functions. If the measures to save the patient will not accept, a person will lose consciousness and will die after a while.

Chassisilate Kussmaul's breath: Frequent surface breathing after a while becomes noisy and rare. Feels the smell of acetone.

Diagnosis of complications

In the early stages, to suspect the developing ketoacidotic who can characteristic symptoms. The doctor survey the patient will find out how long symptoms have appeared. It will also be necessary to provide information on the latest events: missed drug intake, disruptions of diet discovered by pathologies. In addition, laboratory research will be conducted. The level of ketone bodies, glucose is determined. For analysis, samples of urin are taken to determine the presence of ketone bodies in them.

It is necessary to determine the presence of electrolytes, creatinine, urea, bicarbonate, chlorides, lactate levels. The gas composition of the blood is revealed, the acidity of this biological fluid.

How to give first aid for coma

With this state, urgent help is important. It is necessary to immediately call doctors: heal the patient will succeed only in conditions of the hospital. Then check the heart rate and respiration, arterial pressure. Periodically, it is necessary to re-produce measurements to provide information to the doctors when they arrive. To assess the patient's condition, you should ask about something to answer. It is also recommended to rub the uches of the ears, periodically patted the patient in the face so as not to give it to losing consciousness.

Before the arrival of experts, you can independently introduce a solution of sodium chloride (0.9%). Such an injection will help restore part of lost electrolytes. In addition, insulin is introduced, pre-measuring the sugar level with a glucometer. It is necessary to use 8-16 units. It is impossible to leave the patient alone: \u200b\u200bit is necessary to track its condition so that if necessary, take the required measures.

The patient should be put on the side. So the language will not create difficulties for breathing. Tight, close clothes need to unzip or remove. It is necessary that a person has free air access.

What treatment is needed

Help is required in the hospital. It is necessary to pre-determine the level of violations of the functioning of vital organism systems. Then there are measures for their correction. In addition, it is necessary to reduce intoxication. Doctors try to determine the cause that caused to: This will help to organize treatment more efficiently. Restoration of physiological buffer systems at home is impossible.

Water balance

Due to pronounced dehydration, the symptoms of intoxication is enhanced. To normalize the patient's condition, it is necessary to normalize urine removal, fill the loss of fluid.

To restore the water balance, the patient first need to weigh. The indicator is necessary for calculating the required amount of solution. The liquid is administered intravenously with a dropper. On each kg of weight, it is necessary to introduce 10 ml of sodium chloride solution. If the loss of the liquid is too large, the dosage is increased by 2 times. With an increase in the volume of circulating blood, sugar decreases. When urine begins to stand out, ketone bodies are displayed with it, the dosage is reduced. Per day is allowed to introduce no more than 8 liters.

Restoration of electrolyte balance

To restore the level of electrolytes, special preparations are introduced. The most dangerous deficit of potassium. Enter this trace element starts even with normal indicatorSince, when breeding the blood, the concentration decreases with the incoming solution. Preparations are introduced intravenously.

Restoration of acid alkaline state

To normalize the acidity of biological fluid, the introduction of sodium bicarbonate is used. The drug is used if the indicator decreases to 7.0. It can be used with a decrease of up to 7.1 if a violation of the rhythm of heart abbreviations is noted, a decrease in blood pressure, a deep coma.

It should be borne in mind that the recovery of the indicator begins already using insulin and restoration of the water balance. In this case, ketogenesis is suppressed, the concentration of hydrogen ions in the blood is reduced, the ability of the kidney to reabsorption of bicarbonates is restored.

The use of sodium bicarbonate can cause complications, so without special readings from its use it is better to refuse. Otherwise, metabolic alkalosis is often developing.

Insulinotherapy

Insert insulin with a strong increase in glucose levels must be immediately. If the values \u200b\u200bof the indicator are not too large, there is a strong dehydration, this measure is applied after some time after the start of the normalization of the water balance.

Used short insulin. In some cases, 16-20 units intramuscularly administered immediately. If such a measure is not required, the dosage is selected individually. On average, an hour is introduced to 6 units. So that the substance falls immediately to Vienna, a special device is used - infusomat.

When a person returns the ability to eat independently, hormone is beginning to enter subcutaneously. Long time The person who does not fall into consciousness prescribe simultaneous administration of insulin and glucose: it helps to restore the shortage of energy.

Food after removing from ketoacidotic coma

After coma, it is necessary to comply with a special diet. For a week, all sources of fats will have to exclude from the diet. In some cases, the prohibition is preserved for a longer time.

Power should be enriched with potassium. Alkaline mineral water consumption is allowed.

Protein limit for 3 days. In this case, the menu add easily driving carbohydrates. Sugar is prohibited. It should be replaced with xylitol or sorbitol, preventing an increase in the concentration of ketone bodies.

Need a gentle diet. On the first day after leaving the coma, if the patient retains the ability to independently welcome food, honey, jam, manna porridge can be included in its diet, mousse. Drinking alkaline mineral waters are allowed. The abundant use of fluid is shown.

On the second day, the diet is resolved with a mashed potatoes from apples or potatoes, oatmeal, kefir, bread, prostruck, low fatty cottage cheese.

Meat broth, puree from low-fat meat add on the third day.

Over the next week there is a gradual transition to the previous power system.

It is important to strictly follow the dietary menu. Violation of the Doctor's recommendations can lead to a re-emergence of complications.

Errors in treatment

With incorrect insulin therapy, the blood sugar level may decline too much.

If the rate of rehydration is not fast enough, hypovolemic shock develops.

If the blood sugar level is not controlled enough, the therapy may be incorrect. Because of this, it is possible to deteriorate the patient's condition.

Possible complications

In the absence of treatment, the fatal outcome occurs. Without the help of specialists, coma will not cure.

One of the most dangerous complications is the brain swelling. Developed within 6-48 hours. In cases where the patient does not come into consciousness, it is not always possible to detect this pathological process. Most often detected due to the lack of signs of improving the state. Confirm with help ultrasonic research or computed tomography of the brain. The probability of death increases by 2 times. It is possible to develop pathologies in the field of neurology, psychiatry.

Ketoacidosis diabetic with diabetes: symptoms, treatment

Diabetic ketoacidosis, ketoacidotic coma

The diet must be compliance. Even small deviations can lead to dangerous consequences. For this reason, it is necessary to abandon the use of sweets and alcoholic beverages.

Preparations should be taken in accordance with the scheduled prescribed physician. Passing injections are also unacceptable. The shelf life of the drugs is important to check regularly. Reception of an overdue medication can lead to a deterioration in the state. In addition, it is important to comply with the storage rules. Otherwise, medicines can be spoiled, become ineffective.

Diabetic ketoacidotic coma- a specific acute complication of the disease caused by an absolute or sharply expressed relative deficiency of insulin due to inadequate insulin therapy or an increase in needs. The occurrence of this coma is about 40 cases per 1 thousand patients, and mortality reaches 5-15%, in patients over 60 years old - 20% even in specialized centers.

What provokes a diabetic ketoacidotic coma:

Factors provoking development Diabetic ketoacidotic

Insufficient dose or passing insulin injection (or taking tableted sugar-based tablet)
Unauthorized cancellation of sugar therapy
Violation of insulin administration
Accession of other diseases (infections, injuries, operations, pregnancy, myocardial infarction, stroke, stress, etc.)
Alcohol abuse
Insufficient conduct of self-monitoring of metabolism
Reception of some drugs

It is necessary to emphasize that up to 25% of cases of DCA is noted in patients with newly detected diabetes, and it is more often evolving with 1-type diabetes.

Pathogenesis (what happens?) During the diabetic ketoacidotic coma:

The following pathogenetic mechanisms are based on the development of DCA: insulin deficiency (both as a result of insulted income and as a result of enhancing the insulin need against the background of patients with 1-th type of absolute insulin insuls), as well as excessive products of contrincing hormones (first of all , glucagon, as well as cortisol, catecholamines, growth hormone), which leads to a decrease in glucose utilization by peripheral tissues, stimulating gluconeogenesis as a result of the reinforced breakdown of protein and glycogenolysis, suppressing glycolysis in the liver and, ultimately, to the development of pronounced hyperglycemia. The absolute and expressed relative disadvantage of insulin leads to a significant increase in glucagon's blood concentration - insulin antagonist hormone. Since insulin no longer restrains the processes that glucagagon stimulates in the liver, glucose products of the liver (the total result of the decay of glycogen and the gluconeogenesis process) is sharply enhanced. At the same time, the utilization of glucose liver, muscles and a fatty tissue in the absence of insulin is sharply reduced. The consequence of these processes is pronounced hyperglycemia, which is also growing due to the increase in serum concentrations of other conjunral hormones - cortisol, adrenaline and growth hormone.

With insulin lack, the catabolism of the organism proteins is enhanced, and the resulting amino acids are also included in the glukegenesis in the liver, exacerbating hyperglycemia. The massive decay of lipids in adipose tissue, also caused by insulin deficiency, leads to a sharp increase in the concentration of free fatty acids (SZhK) in the blood. In the insulin deficiency of 80% of the energy, the body receives by oxidation of the SFC, which leads to the accumulation of by-products of their decay - ketone bodies (acetone, acetoxus and beta hydroximaceous acids). The speed of their formation is much higher than the rate of their disposal and renal excretion, as a result of which the concentration of ketone bodies in the blood increases. After the buffer reserve reserve, the acid-alkaline equilibrium is broken, metabolic acidosis occurs.

Thus, gluconeogenesis and its consequence is hyperglycemia, as well as ketogenesis and its consequence - ketoacidosis, are the results of glucagon in the liver under conditions of insulin deficiency. In other words, the initial cause of the formation of ketone bodies with DCA is the lack of insulin that causes the enhanced fat disintegration in its own fatty depot. Excess glucose, stimulating osmotic diuresis, leads to life-threatening dehydration. If the patient can no longer drink the appropriate amount of fluid, the water loss by the body can be up to 12 liters (about 10-15% body weight, or 20-25% of the total amount of water in the body), which leads to intracellular (there are two thirds) on it) and extracellular (one-third) dehydration and hypovolemic insufficiency of blood circulation. As a compensatory reaction aimed at maintaining the volume of circulating plasma, the secretion of catecholamines and aldosterone increases, which leads to sodium delay and helps to enhance the release of potassium with urine. Hypokalemia is an important component of metabolic disorders with DCA, which causes the corresponding clinical manifestations. Ultimately, when the insufficiency of blood circulation leads to a disruption of renal perfusion, urine formation is reduced, causing a terminal rapid rise of glucose concentration and ketone bodies in the blood.

Symptoms of diabetic ketoacidotic coma:

Clinically DCA is usually developing gradually, from several hours to several days. Patients impose complaints against severe dryness in the mouth, thirst, polyuria, testifying to the increase in the decompensation of the SD. Loss of body weight can be recorded, also caused by the noncompensated course of the disease throughout a certain time. As ketoacidosis progresses, such symptoms appear as nausea and vomiting, which in the patient with the SD dictate the need for a mandatory study of the content of acetone in the urine. Patients may complain about strong pain In the abdomen, including accompanied by symptoms of peritonean irritation (data of manifestations can lead to erroneous diagnosis acute belly and carrying out surgical interference, worsening the patient's condition). A typical clinical symptom of a developing DCA is a frequent deep breath (Kussmouul's breathing), often with the smell of acetone in exhaled air. When examining patients, severe dehydration is observed, manifested dry skin and mucous membranes, a decrease in the leather turgora. Due to the reduction of circulating blood (BCC), orthostatic hypotension may develop. Often, patients have a confusion and criminalization of consciousness, approximately 10% of cases, patients enter the hospital in a state of coma. The most typical laboratory manifestation of DCA is hyperglycemia, usually reaching 28-30 mmol / l (or 500 mg / dl), although the blood glucose content in some cases can be increased slightly. The level of the kidney function also affects the level of glycemia. If the excretion of glucose with urine is violated as a result of a decrease in the BCC or deterioration of the kidney function, hyperglycemia can achieve a very high level, and hyperco-attemmia can also be marked. In determining the acid-alkaline state, metabolic acidosis is detected, characterized by a low blood pH (usually in the limits of 6.8-7.3, depending on the severity of ketoacidosis) and a decrease in the content of bicarbonate in the blood plasma (< 10 мэкв/л). Уровни гипергликемии и метаболического ацидоза могут не коррелировать между собой, типичны также глюкозурия и кетонурия, позволяющие быстро установить диагноз ДКА. Возможны изменения уровней электролитов в крови. Содержание калия в плазме может вначале повышаться в результате перехода его ионов из клетки во внеклеточное пространство вследствие инсулиновой недостаточности и метаболического ацидоза, несмотря на дефицит в организме. Позднее оно снижается как в связи с усиленной потерей электролитов с мочой, так и в результате терапевтической коррекции ацидоза. Осмолярность плазмы повышена (обычно > 300 MOS / kg). Despite the decline in the total content of sodium, chlorine, phosphorus and magnesium in the body, the levels of these blood serum electrolytes may not reflect this reduction. The growth of urea and creatinine content in the blood arises as a result of a decrease in the BCC. It is often noted by leukocytosis, hyperitriglyceridemia and hyperlipoproteinemia, sometimes hyperamilasemia is revealed, which sometimes makes doctors think about a possible diagnosis of acute pancreatitis, especially in combination with abdominal pain. However, the detected amylase is produced mainly in salivary glands and is not a diagnostic criterion of pancreatitis. The plasma sodium concentration is reduced due to the effect of breeding, since the osmotic effect of hyperglycemia leads to an increase in the number of extracellular fluid. The reduction in sodium in the blood correlates with the level of hyperglycemia - for each 100 mg / dl (5.6 mmol / l) its level is reduced by 1.6 mmol / l. If the normal sodium content in the blood is detected, this may indicate a pronounced liquid deficiency due to dehydration.

Diagnosis of diabetic ketoacidotic coma:

Basic diagnostic DCA criteria

Gradual development, usually within a few days
Symptoms of ketoacidosis (the smell of acetone in exhaled air, breathing Kussmouul, nausea, vomiting, anorexia, abdominal pain)
Symptoms of dehydration (decreased tissue turgora, tone eye apples, muscle tone A, tendon reflexes, body temperature and blood pressure)

Treatment of diabetic ketoacidotic coma:

In DCA therapy, four directions are distinguished:

insulinatherapy;
restoration of lost fluid;
correction of mineral and electrolyte metabolism;
treatment provoking for some diseases and complications of ketoacidosis.

Replacement insulin therapy is the only form of etiological treatment of DCA. Only this hormone with anabolic properties can stop severe generalized catabolic processes caused by its lack. To achieve an optimally active level of insulin in serum, its continuous infusion is required by 4-12 units / h. Such a concentration of insulin in the blood inhibits the disintegration of fats and ketogenesis, contributes to the synthesis of glycogen and inhibits the products of glucose liver, thereby eliminating the two most important Pathogenesis of DCA. Insulin therapy mode using such dosages is called "Small Dose Mode". Previously applied much higher doses of insulin. However, it has been proven that insulin therapy in small doses is accompanied by a significantly smaller risk of complications than in large doses.

large doses of insulin (≥ 20 units. However) may too sharply reduce the level of glucose in the blood, which may be accompanied by hypoglycemia, brain swelling and a number of other complications;
a sharp decrease in glucose concentration is accompanied by an equally rapid drop in serum potassium concentration, therefore, when using large doses of insulin, the danger of hypokalemia increases sharply.

It should be emphasized that under the treatment of the patient in a state of DCA, only short-acting insulins should be used, while insulins of medium and long-term action are contraindicated before the patient is removed from the ketoacidosis state. Human insulins are most effective, however, in the treatment of patients in a comatose or precancetous state, a determining factor that dictates the need to introduce any type of insulin is precisely the duration of its action, not the form. The introduction of insulin in a dose of 10-16 units is recommended. intravenously inkjet or intramuscularly, then intravenously drip 0.1 units / kg / h or 5-10 units / h. Usually, glycemia is reduced at a speed of 4.2-5.6 mmol / l / h. If within 2-4 hours the level of hyperglycemia does not decrease, the dose of inserted insulin increases; When the glycemia is reduced to 14 mmol / l, the speed of its administration decreases to 1-4 units / h. Determining in the selection of the velocity and dose of insulin administration is constant control of blood glucose content. It is desirable to conduct blood test every 30-60 minutes using glucose express analyzers. However, it should be remembered that today many glucose express analyzers used for self-control analyzers can show incorrect glycemia numbers at a high level of blood sugar. After restoring the consciousness of the patient within a few days, infusion therapy should not be carried out. As soon as the patient's condition has improved, and the glycemia is consistently held at the level of ≤ 11-12 mmol / l, he must start eating food again, necessarily rich in carbohydrates (potato mashed potatoes, liquid porridge, bread), and the sooner it can be translated into subcutaneous insulin therapy , all the better. The short-acting insulin is first prescribed fractionally, 10-14 units. Every 4 hours, adjusting the dose depending on the level of glycemia, and then go to the use of simple insulin in combination with such an extended action. Acetonuria can persist for some time and with good carbohydrate exchange. For its complete elimination, it is sometimes required for another 2-3 days, and to enter into a similar purpose of large doses of insulin or give extra carbohydrates.

The condition of the DCA is characterized by a pronounced resistance of peripheral target tissues to insulin, in connection with this, its dose required to remove the patient from the comatose state may be high, significantly exceeding the dose necessary to the patient before or after ketoacidosis. Only after full correction The hyperglycemia and the relief of the DCA patient can be prescribed insulins of the average duration of the action subcutaneously as the so-called basic therapy. Immediately after removing the patient from the ketoacidosis state, the sensitivity of tissues to insulin increases sharply, so control and correction of its dose is necessary in order to prevent hypoglycemic reactions.

Given the characteristic dehydration due to the osmotic diurea, due to hyperglycemia, the necessary element of the treatment of patients with DCA is the restoration of the volume of the fluid. Typically, patients have a liquid shortage of 3-5 liters, which should be completely replaced. For this purpose, the introduction of 2-3 l 0.9% of the physiological solution is recommended during the first 1-3 hours, or at the rate of 5-10 ml / kg / h. Then (usually, with an increase in sodium concentration in plasma\u003e 150 mmol / l), an intravenous administration of 0.45% sodium solution at a speed of 150-300 ml / h is prescribed with a target of hyperchloremia. In order to avoid excessively fast rehydration, the volume of the physiological solution introduced in an hour, with initially sharply pronounced dehydration, should not exceed the hourly diurez by more than 500, a maximum of 1,000 ml. You can also use the rule: the total amount of fluid introduced in the first 12 hours of therapy should not exceed 10% body weight. In systolic hell< 80 мм рт. ст. для предотвращения недостаточности кровообращения в дополнение к изотоническому раствору хлорида натрия показано переливание плазмы или плазмозаменителей.

With a decrease in blood glucose levels up to 15-16 mmol / l (250 mg / dl), infusion is needed 5% glucose solution to prevent hypoglycemia and providing glucose delivery to tissues, along with 0.45% sodium chloride solution at a rate of 100-200 ml / h . It should be remembered that the achievement of a rack of normoglycemia is not the immediate target of therapy of patients in the state of the DCA in the first stage. If, with a decrease in the level of glycemia, the patient retains dehydration, glucose is injected in parallel with saline. The substitution of the volume of the liquid, along with the stabilizing hemodynamic effect, helps to reduce the glycemia (even without the introduction of insulin) by reducing the content of catecholamines and cortisol in the blood plasma, which occurs in response to a decrease in the BCC.

Correction of the content of minerals and electrolytes lost due to osmotic diuresis is necessary. The correction of the content in the blood plasma of potassium is also important, the reserves of which in the body is small. During the treatment of DCA, as the glycemia decreases, potassium in large quantities will flow into the cage, and also continue to be removed from the urine. Therefore, if the initial level of potassium was within the normal range, in the process of therapy (usually 3-4 hours after its start), it is possible to expect its significant drop. With the saved diuresis, from the very beginning of insulin therapy, even when normal level Serum potassium, begins its continuous infusion, trying to maintain Caliamia in the range of 4-5 mmol / l. Simplified recommendations for its introduction without blood pH look like this: at the level of potassium serum< 3 ммоль/л - хлорид калия по 3 г/ч, при уровне 3-4 ммоль/л - по 2 г/ч, при уровне 4-5 ммоль/л - 1,5 г/ч, при уровне 5-5,9 ммоль/л - 1 г/ч; при уровне ≥ 6 ммоль/л введение прекращают. После выведения из ДКА препараты калия назначают в течение 5-7 дней перорально. Также возможно назначение фосфата калия в зависимости от содержания в плазме крови кальция и фосфора, - слишком интенсивное введение фосфата калия может вызвать гипокальциемию. Следует корригировать содержание фосфатов в плазме крови, вводя 10-20 ммоль/ч фосфата калия, максимально до 40-60 ммоль.

With the correction of the acidosis, it should be remembered that the metabolic (diabetic) acidosis develops due to the enhanced intake of ketone bodies in the blood due to insulin deficiency, therefore, the etiological treatment of this type of acidosis is substitution insulin therapy, which in most cases helps to eliminate it. The introduction of sodium bicarbonate, such a widely used previously used, is associated with an extremely high risk of complications:

hypokalemia;
intracellular acidosis (although blood pH can increase);
paradoxical acidosis of a liquor, which can contribute to a brain edema.

That is why, recently, the testimony for the use of sodium bicarbonate with DCA is significantly narrowed, and its routine use is not categorically recommended. Sodium bicarbonate can be administered only at blood pH< 7,0 или уровне стандартного бикарбоната < 5 ммоль/л. Если же определить эти показатели не представляется возможным, то риск введения щелочей «вслепую» намного превышает потенциальную пользу. В последнее время раствор питьевой соды больным не назначают ни перорально, ни ректально, что довольно широко практиковалось ранее.

Important trends in DCA's therapy - identification and treatment of related diseases that could cause the development of ketoacidosis, as well as worsening its flow. So, it is necessary to carefully examine the patient for the purpose of diagnosis and treatment infectious diseases, especially urinary tract infections. In the case of suspicion of the presence of an infection, it is advisable to prescribe a wide range of action antibiotics. Given the characteristic disturbances of consciousness in patients, a certain complexity may be diagnosed with meningitis, stroke, myocardial infarction. When the blood pressure fall, despite the injection of the fluid, it is possible to transfusion of solid blood or plasma-substituting solutions.

Complications of DCA: deep veins thrombosis, pulmonary embolism, arterial thrombosis (myocardial infarction, stroke), aspiration pneumonia, brain swelling, edema, infection, rarely - gastrointestinal bleeding and ischemic colitis, erosive gastritis, late hypoglycemia. There is severe respiratory failure, oliguria and renal failure. Complications of therapy: brain swelling, pulmonary edema, hypoglycemia, hypokalemia, hyponatremia, hypophosphatemia.

In conclusion, it should be noted that DCA is by no means an integral sign of the flow of SD. Subject to the training of patients suffering from SD, the use of intensified insulin therapy, daily self-determining of metabolism and self-adaptation of the insulin dose of the DCA can be reduced to almost zero.

Etiology.Causes of decompensation of diabetes:

1. Incoming treatment of a patient with beginning insulin-dependent diabetes mellitus to a doctor or late diagnosis (thirst, polyuria, weight loss).

2. Errors in insulin therapy.

3. Incorrect behavior and attitude of the patient to its disease (violation of the diet, alcohol intake, unauthorized change in the dose of insulin, etc.).

4. Acute diseases (especially purulent infections).

5. Physical and mental injuries, pregnancy, operations.

Pathogenesisit is determined by insulin deficiency, i.e., the inconsistency between the production of endogenous or delivery of exogenous insulin and the need for a body in it, and the sharp activation of the contrincing hormonal influences. A phenomenon is formed - energy starvation with excessive content in the blood and extracellular fluid of the energy source - glucose. Excessive accumulation of dense glucose increases plasma osmolarity, as a result of this, part of the interstitial, and then intracellular fluid and microelements contained in it are transferred to the vascular channel, it causes the development of cell dehydration and a decrease in the intracellular content of electrolytes (primarily potassium). Upon exceeding the renal threshold of permeability for glucose, glucose develops, osmotic diuresis is developing, and general heavy dehydration is formed, disipethyremia, hypovolemia, blood thickening occurs, a violation of its rheology, a thrombosis is observed. The volume of renal perfusion is reduced. This pathological cascade associated with a high blood glucose level can be called the first polyogenesis in the decompensation of diabetes mellitus.

The second conditional link is associated with excessive accumulation of ketone bodies, i.e. with ketosis, and then ketoacidosis. As mentioned earlier, an excess glucose accumulates in the body against the background of insulin lack. In response to energy starvation, the body corresponds to an increase in the oxidation of free fatty acids (SZhK) and an increase in the formation of the final product of lipid oxidation - acetyl-soa, which under normal conditions should normalize the production of ATP in the cycle of tricarboxylic acids (Crek-Ca cycle), however semist And the excess of the acetyl-soa is violated its arrival in the Krebs cycle, which blocks energy production. In the blood accumulates a large number of unclaimed acetyl-soa.

In the liver, by simple chemical transformations from acetyl-soa, ketone bodies begin to form, which include acetoacetate (acetoacetic acid), beta-oxybutirate (beta-oxy-oil acid) and acetone. They are normally formed and disposed of anaerobic glycolisis in muscles, which gives approximately 1-2% of the total energy produced in the body, but if they are excess (ketone) and the absence of insulin, the muscles cannot fully utilize the ketone bodies. Cetosis occurs. Ketone bodies, possessing the properties of weak acids, lead to the accumulation of hydrogen ions and a decrease in the concentration of sodium bicarbonate ions, as a result of which metabolic acidosis develops (with pronounced ketoacidosis, blood plasma decreases to 7.2-7.0).

Thus, in diabetic ketoacidosis, insulin deficiency and excessive secretion of cross-rigging hormones lead to severe metabolic disorders, mainly to acidosis, plasma hyperosmolarity, to cellular and general dehydration with loss of potassium ions, sodium, phosphorus, magnesium, calcium and bicarbonates. These violations and cause the development of a comatose state.

Clinic.Ketoacidotic diabetic coma develops slowly, gradually. From the first signs of ketoacidosis to loss of consciousness usually passes several days.

During the diabetic ketoacidosis distinguish 3 periods (stages):

1. Beginning (moderately pronounced) ketoacidosis.

2. Pronounced ketacidosis (prema).

3. Ketoacidotic coma.

Beginning ketoacidosis is accompanied by symptomatics of rapidly progressive decompensation of diabetes: dry mouth, thirst, polyuria, urination is rapidly, the skin sebum and signs of intoxication (total fatigue, headache, nausea, vomiting, are joined). The smell of acetone appears. The blood plasma increases hyperglycemia (the glucose level increases to 16.5 mmol / l and more), urine reaction to acetone becomes positive, high glucose is noted.

In the absence of treatment arises disps syndrome, manifesting multiple, not bringing relief to vomiting, sometimes taking the nature of the indomitable. Diarrhea joins, however, there may be constipation. In some patients, there may be nonspecific stomach pain, which forms a false picture of the "acute" abdomen (gastrointestinal version of Ke-Gaacidotic coma). At this stage of the disease, signs of consciousness disorder begin to appear: drowsiness, apathy increases, patients become indifferent to surrounding, disoriented in time and space, and in the absence of treatment there may be a comatose state. Characteristic clinical signs of severe metabolic acidosis, developing with this pathology, is the appearance of compensatory frequent, noisy and deep breathing in a patient . Auscultation in the lungs listened to hard breathing, blood pressure, as a rule, is below the norm, compensatory tachycardia develops. Characteristic signs of hypertensive dehydration are observed. .

Depending on the complications of the underlying disease (diabetes) and related pathologies, various options for the clinical pattern of ketoacidase are possible:

Gastrointestinal and intestinal (characteristic of abdominal pain; observed with angiopathies, with predominant localization in the mesentery and the walls of the tract);

Cardiovascular (characterized by severe collapse; is observed in angiopathies with a predominant lesion of the CSS);

Kidney (arises against the background of diabetic nephrohangiopathy, manifests itself with proteinuria and a change in blade (hematuria, cylinders);

Encephalopathic (against angiopathy with preferably lesions of brain vessels, in combination with their atherosclerosis; it is clinically manifested by hemiparem, asymmetry of reflexes, the appearance of one-sided pyramidal signs). With this embodiment, the complication of the main disease is very often difficult to decide which primary - coma or stroke.

Differential diagnosisthe ketoacidotic coma is carried out with the apoplexic form of OIM, uremic, chlorohydropenic, hyperosmolarnya, lactacidemic and hypoglycemic komami.

Laboratory research.For ketoacidosis, the following laboratory data is most characteristic:

Hyperglycemia;

Glucosuria;

High ketonemia and cotonoria concomitant. Plasma's ketone bodies increase many times compared with the norm (norm of 177.2 μmol / l);

Ascending plasma osmolarity up to 350 or more mosmol / l (norm 285-295 mosmol / l);

PH offset to 7.2-7.0 and below;

Neutrophilic leukocytosis with a shift to the left and secondary errit-rococytosis. Leukocytosis is associated with toxic irritation of bone marrow, red blood cells - with blood concentration;

Hyperlipidemia, an increase in free fatty acids and beta lipoproteins;

Plasma hyponatremia - 120 mmol / l (norm 130-145 mmol / l).

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 secretor function Confinylular hormones (cortisol, adrenaline, norepinephrine, hardware, 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:

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.
Then it is worth checking the heart rate, ChDD and hell and repeat these events until the arrival of physicians.
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:

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.
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:

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.
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.
Restoration of electrolyte balance and hemostasis. Such events are an important component of the therapy. With the help of administration required drugs Calcium deficiency and acid-base blood condition is restored, thereby ensuring the normalization of the kidney functions to reabsorb the bicarbonates.
Improving the rheological properties of blood. And also to prevent intravascular coagulation can be assigned heparin intravenously under the control of the coagulogram.
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.
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 a point in life that a chronic disease requires increased attentionIt 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 drug Treatment Need to 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. Most hazardous complication This state may be a brain swelling, which in 70% of cases ends with a fatal outcome.

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, exacerbations. chronic diseases, infectious diseases), surgical interventions, injuries, treatment disorders (introduction of overdue or incorrectly stored insulin, errors in prescribing or administering the dose 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 CD 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 The smell of 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 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 described above. clinical picture, laboratory indicators (primarily hyperglycemia, the presence of glucose and ketone bodies in the urine) and KS, 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 a developed structural changes In the brain barrel and the low probability of a favorable outcome of the 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. Termination infusion therapy It is possible only with the complete restoration of consciousness, the absence of nausea, vomiting and the possibility of receiving fluid to 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 used insulin syringes and various individual systems for the introduction of 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 spinal fluid 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). Most frequent cause The occurrence of brain edema is fast decline Plasma osmolarity and 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.