Diabetic hyperosmolar coma. Hyperosmolar coma in diabetes mellitus: emergency care, preventive measures and the first signs of approaching danger Possible complications of the disease

Uncompensated diabetes mellitus, especially untreated and uncontrolled for a long time, causes a lot of complications that can cause the death of a diabetic.

The two main reasons as a result of which any person can lose consciousness and fall into a coma are both a lack of blood sugar () and its excess ().

In diabetes, both options are possible, the only difference is that with type 1, glucose deficiency occurs more often due to the fact that diabetics better control the sweet disease, trying to keep glycemia as close to normal as possible.

All types of hyperglycemic diabetic coma often develop in type 2 diabetes at an advanced stage of the sweet disease, or if the diet is not followed, improperly adapted hypoglycemic therapy.

Hyperglycemia can cause a special condition called hyperosmolar coma, which is somewhat different from other hyperglycemic coma in that its development is not accompanied by ketoacidosis, therefore, the threshold of ketone bodies will not be exceeded, but is combined with blood hyperosmolarity and dehydration (dehydration).

These two comas are very similar in their symptoms, signs, and causes, however, they are easy to distinguish. With hyperosmolar coma, a diabetic will not smell acetone from the mouth.

This is a complication of diabetes mellitus, when glycemia rises (above 38.9 mmol / l), blood hyperosmolarity is diagnosed (more than 350 mosm / kg), dehydration that develops without transition to ketoacidosis.

This state corresponds to the ICD code - 10:

E10 - E14 .0 - diabetic hyperglycemic hyperosmolar coma
E 87.0 - hyperosmolarity with hypernatremia

This type of coma is much less common than ketoacidosis and is more common in people who already suffer from chronic renal failure (CRF).

Kidney failure in diabetes develops for a long time. It is preceded by, which at the initial stage is easily treatable, but its symptoms are almost imperceptible by a diabetic, therefore, treatment is often delayed, which leads to its launch.

With a decrease in the glomerular filtration rate (the main criterion used in the diagnosis of renal complications), the kidneys can no longer qualitatively purify the blood from metabolic "waste". As a result, a large number of various substances accumulate in the blood.

The more of them in the blood, the higher its osmolarity, i.e. density.

It is much more difficult for the heart to move very thick blood around the body, which affects its actual work, and the pressure drops significantly.

A similar development of events is typical for older people who have lived with a sweet illness for decades.

Hyperosmolar coma develops in approximately the same way in people over 50 years old, but it can also appear in children under two years of age, whose mothers already had type 2 diabetes before pregnancy, or during pregnancy they were diagnosed with a type of diabetes, which sometimes give a complication on fruit in the form

Children under two years of age are extremely vulnerable, especially those who have been diagnosed with a severe diagnosis - Down's syndrome or there have been delays in the development of another genesis. Such babies more often than others suffer from impaired carbohydrate metabolism and are prone to hyperosmolar complications. The older they get, the stronger their body becomes. Gradually, the metabolism comes to a relative norm.

In addition, another reason for the development of this coma in children can be:

undiagnosed diabetes mellitus type 1, type 2 or their severe form without a tendency to ketoacidosis,
improper treatment, glucocorticoids and other drugs

However, the latter also applies to adults.

Other reasons include:

severe dehydration caused, for example, by diarrhea, vomiting, or diuretic abuse
insulin deficiency (incorrect, absent or lack of endogenous, natural insulin, independently produced by the pancreas, this is possible when it is: damaged, surgically removed as a result of a cancerous lesion)
infectious diseases, as a result of which the need for cells in glucose and, accordingly, in insulin increases (pneumonia, infections of the genitourinary system, etc.)
excessive administration of aqueous glucose solutions
gross violation of the diet
taking hormones - insulin antagonists (hormone therapy that suppresses insulin production), etc.

No less dangerous are diuretics!

Medicines of this type can provoke a hyperosmolar coma in relatively healthy people.

Uncontrolled intake of diuretics (diuretics) is extremely detrimental to carbohydrate metabolism.

In people with a hereditary predisposition to diabetes mellitus, when taking large doses of diuretics, a marked deterioration in carbohydrate metabolism occurs, which causes a strong diabetogenic effect. This affects the increase in fasting glycemia and, as well as worsening glucose tolerance.

In some cases, after taking such drugs in a person with a predisposition to the sweet disease, clinical symptoms of diabetes and non-ketonemic hyperosmolar coma may appear.

The higher the initial level of glycemia, the more it rises against the background of the use of thiazide diuretics.

Of course, this indicator is also largely influenced by the age of the person, the diseases he has, and the duration of taking thiazide diuretics. For example, in young people under 25 years of age, such problems can occur after 5 years of continuous use of diuretics, and in older people (over 65 years old) after 1 to 2 years.

As for the diabetics themselves, their situation is even worse. Their glycemic indicators worsen a few days after the start of the intake. In addition, diuretics also adversely affect lipid metabolism, increasing the concentration of total and triglycerides in the blood.

It is extremely dangerous to use diuretics in diabetes! If the doctor has prescribed this class of drugs, then do not violate their intake and dosage!

Pathogenesis

Scientists are still not completely sure how exactly the process of the onset of this diabetic complication proceeds. Only one thing is clear that a hyperosmolar coma occurs as a result of the accumulation of glucose in the blood due to the suppression of, say, insulin synthesis.

If there is little insulin in the blood or insulin resistance progresses, then the cells do not receive proper nutrition. In response to cellular starvation, gluconeogenesis and glycogenolysis are triggered, which provide additional glucose stores by metabolizing sugar from the body's reserves. This leads to an even greater increase in glycemia and increases the osmolarity of the blood.

Hyperosmolarity of blood plasma is able to suppress the "release" of fatty acids from adipose tissue, which inhibits lipolysis and ketogenesis. In other words, the production of additional glucose from fat is minimized. If this process is slowed down, then there will be very few ketone bodies obtained as a result of the conversion of fat into glucose.

It is the presence or absence of ketone bodies in the blood that makes it possible to diagnose one of these two types of complications in diabetes - ketoacidotic uremic and hyperosmolar non-ketoacidotic coma.

In addition, hyperosmolarity leads to an increase in the production of aldosterone and cortisol in the event that there is a lack of moisture in the body and, as a result, hypovolemia (decrease in circulating blood volume). As a result, hypernatremia gradually develops.

Violation of the water and electrolyte balance in cells leads to the development of neurological symptoms, since in such a case brain cells also suffer, which contributes to swelling of the brain tissues and, as a result, a coma is brewing.

Blood osmolarity rises much faster against the background of untreated diabetes mellitus and existing renal complications. If you do not control the disease, it will lead to severe consequences!

Symptoms

For the most part, many of the signs of a pre-comatose state caused as a result of hyperglycemia are very similar to each other. They resemble diabetics:

intense thirst
profuse urination (polyuria)
dry skin (body feels hot to the touch)
dry mouth
a sharp decline in strength (adynamia)
general weakness
weight loss
frequent shallow breathing

Severe dehydration that accompanies hyperosmolar coma leads to:

decrease in body temperature (in infectious diseases, body temperature is usually high)
severe drop in blood pressure
to further progress
cardiac arrhythmias and cardiac activity
decrease in the tone of the eyeballs (with a high tone, they are dense and do not spring)
decrease in skin turgor (skin is less firm, dense and elastic)
decreased muscle activity
seizures (less than 35% of patients)
impaired consciousness

In a coma, it is noted: sometimes hypertonicity of the muscles, narrowed or normal pupils that stop responding to light, dysphagia, meningeal signs, there are no tendon reflexes, there may be hemiparesis. replaced by anuria.

The harmfulness of this phenomenon is quite large, therefore, possible complications include:

venous thrombosis (due to the strong density, blood can accumulate in the vessels in those places that were devoid of elasticity, which will lead to their blockage)
pancreatitis (inflammation of the pancreas)
kidney problems (hyperosmolar coma often provokes the development of kidney failure)
cardiovascular complications
etc.

Diagnostics

Unfortunately, as such, contact with a patient in a coma is, of course, impossible. Doctors have to rely on the confused testimony of the one who called the ambulance. Therefore, it is good if a diabetic always has some kind of reminder with him that he is ill with one or another type of diabetes mellitus. For example, on his arm he will wear a bracelet with the inscription "diabetes mellitus type 1 or 2" with a tendency to hypo- or hyperglycemia.

In many cases, such a hint has saved quite a few lives, since with actual hyperglycemia that caused a hyperosmolar attack, the ambulance doctors first inject an aqueous glucose solution in order to stop possible hypoglycemia, since death as a result of a drop in blood sugar occurs much faster, than when it is raised. They do not know what caused the patient's coma, so they choose the lesser of two evils.

But in order to make a really correct diagnosis, it is necessary first of all to take a blood and urine test.

To correct their further actions, the ambulance team always has several test strips that allow you to assess the patient's condition on the way to the hospital. But either everything is left to chance with us, or the budget is too small, but often such express tests are simply impossible for lack of strips. As a result, the correct diagnosis is made to the patient only in the hospital, which complicates both the treatment and further rehabilitation of the diabetic.

In stationary conditions, the following tests will be carried out as soon as possible:

(it is important to check the presence or absence of ketones, glucose, protein)
(potassium, sodium, total cholesterol, triglycerides, etc.)
blood sugar test

Then, after some normalization of the patient's condition, ultrasound, x-ray of the pancreas and other studies will be prescribed in order to stop possible complications.

Treatment

Any patient in a coma, even before hospitalization, ambulance doctors are obliged to help in advance and carry out several mandatory actions:

Restore or maintain in adequate condition all vital signs of the patient

Of course, doctors will monitor breathing, apply artificial ventilation if necessary, and also monitor blood circulation and blood pressure. If blood pressure drops, then put a dropper with a volume of 1000 - 2000 ml with 0.9% sodium chloride solution, 5% glucose solution or 400 - 500 ml of dextran 70, or 500 ml of refortan with the possible combined use of dopamine or norepinephrine.

If the patient has arterial hypertension, then doctors try to normalize the pressure to values exceeding the usual 10-20 mm. rt. Art. (up to 150 - 160/80 - 90 mm Hg). To do this, they use 1250 - 2500 mg of magnesium sulfate, which is administered as a bolus for 7 - 10 minutes or put on a drip. If the blood pressure is not so significantly increased, then aminophylline is administered no more than 10 ml of a 2.4% solution.

With arrhythmia, normal heart rhythm is restored.

Carry out quick diagnostics

Very often, emergency doctors are faced with the fact that they do not know what caused the patient's coma. Even his relatives, who witnessed the incident, cannot give a complete and objective assessment. From the experience, they may even forget to say that the patient is a diabetic.

Therefore, in order not to harm even more in the ambulance, a series of simple tests will be carried out on the way to the hospital. For this, test strips are used, for example: Glucochrome D, Russian-made Biopribor, Glukostiks or Bayer, made in Germany.

Test strips are used to check blood, but they can also be used to make a preliminary diagnosis based on urine results. To do this, a small amount of urine is dripped onto a strip, which can be used to judge glucosuria (glucose in the urine), ketonuria (the presence of ketone bodies in it).

Normalize glycemia

In the fight against hyperglycemia, the main cause of any hyperglycemic diabetic coma (ketoacidotic, hyperosmolar, lactic acidotic), insulin therapy is used. But it is unacceptable to use the hormone at the prehospital stage. Hormone therapy is already carried out directly in the hospital.

After the patient is admitted to the intensive care unit (intensive care unit), the patient will immediately take a blood test and send it to the laboratory. After the first 15 to 20 minutes, the results should be obtained.

In stationary conditions, the diabetic will continue to be monitored and monitored: pressure, respiration, heart rate, body temperature, water-electrolyte balance, heart rate, an ECG will be required, etc.

After receiving the results of the blood test and, if possible, urine, depending on the patient's condition, doctors will adjust his vital signs.

Elimination of dehydration

Salt solutions are used for these purposes, because salt has the ability to retain moisture in the body. Sodium chloride is used in its 0.9% aqueous solution with a volume of 1000 - 1500 ml and a dropper is placed for the first hour. Then, during the second and 3 hours, 500 - 1000 ml are also injected intravenously, and the next hours of monitoring the patient 300 - 500 ml of the solution.

To know exactly how much sodium to inject, its level in blood plasma is monitored (its use is shown at Na + 145 - 165 mEq / liter and less).

Therefore, a biochemical blood test is taken several times a day:

determination of sodium and potassium from 3 to 4 times,
glucose test 1 time per hour,
on ketone bodies 2 times / day,
acid-base state from 2 to 3 times / day until the pH of the blood normalizes,
general blood test 1 time in 2 - 3 days.

If the sodium concentration exceeds 165 mEq / l, then it is forbidden to administer its aqueous solutions. In this case, a glucose solution is administered to stop dehydration.

They also put a dropper with a 5% dextrose solution with a volume of 1000 - 1500 ml during the first hour, then reduce the volume to 500 - 1000 ml also within 2 and 3 hours and to 300 - 500 ml in the following hours.

All these solutions, of course, have their own osmolality, which should be taken into account when prescribing these substances:

0.9 Na + 308 mosm/kg
5% dextrose 250 mosm/kg

If rehydration is carried out correctly, this will also have a positive effect not only on the water and electrolyte balance, but will also allow you to quickly reduce glycemia.

The use of insulin therapy

This is one of the most important steps in addition to the above. In the fight against hyperglycemia, short-acting human genetically engineered or semi-synthetic insulins are used. The former are more preferable.

When using insulin, it is worth remembering the half-life of assimilation of simple insulin. With intravenous administration, this time is from 4 to 5 minutes with a duration of action up to 60 minutes. When administered intravenously, its action is prolonged up to 2 hours, and when administered subcutaneously, up to 4 hours.

Therefore, it is best to administer it intramuscularly, and not subcutaneously! If the blood sugar level drops too quickly, it will provoke an attack of hypoglycemia, even with relatively normal levels.

To bring a person out of a hyperosmolar coma, insulin is dissolved together with sodium or dextrose and is administered gradually at a rate of 0.5-0.1 U / kg / hour.

Do not inject large amounts of insulin at once. Therefore, when using an infusion solution, 6-8-12 units of simple insulin per hour are used in an electrolyte solution with the addition of human albumin 0.1-0.2 g to prevent adsorption of the hormone.

After that, the level of glucose in the blood is constantly monitored in order to check how its concentration decreases. It must not be allowed to fall by more than 10 mosm/kg/h. If the concentration of sugar in the blood decreases rapidly, then the osmolality of the blood will also quickly begin to fall, which can lead to a serious complication of treatment - cerebral edema. Young children are the most vulnerable in this regard.

It is also difficult to predict the further well-being of elderly patients, even if adequately performed resuscitation before hospitalization and after treatment in a hospital. Diabetics with advanced diabetic complications often find that recovery from a coma and further therapy depresses cardiac activity and can lead to pulmonary edema. It is especially difficult for older people with heart failure and CRF (chronic renal failure).

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Hyperosmolar coma is a special type of diabetic coma, which is not less than five and not more than 10% of the total number of hyperglycemic coma. Mortality in the present case reaches approximately 30-50%. The presented form of a coma is formed, as a rule, in elderly people with type 2 diabetes mellitus due to dehydration. Also, the use of diuretics, steroids and the pathology of the vessels of the brain, as well as the kidneys, can have a decisive influence on this. In accordance with the statistical data, in almost 50% of patients who developed a hyperosmolar coma, diabetes mellitus was not previously identified.

Clinical picture

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Reasons for the development of the condition

The leading factor in the development of hyperosmolar coma in a diabetic should be considered dehydration against the background of increasing relative insulin deficiency, which leads to an increase in glycemia. In general, the development of the presented condition will be influenced by the addition of intercurrent (accidentally joined, complicating other ailments) diseases, infectious pathologies. Also, burns and even injuries, progressive destabilization of the cerebral and coronary type of blood circulation may well affect this. Another significant development factor should be considered gastroenteritis and pancreatitis, which are traditionally associated with vomiting and diarrhea.

The formation of the presented syndrome will be facilitated by blood loss of various origins, for example, due to surgical intervention. In some cases, the presented type of diabetic coma is formed due to:

therapy with diuretics, glucocorticoids, immunosuppressants;
the introduction of significant volumes of saline, hypertonic solutions, as well as mannitol;
hemodialysis and peritoneal dialysis.

The situation will be exacerbated by the use of glucose and excessive use of carbohydrates.

Talking about what a hyperosmolar coma is, one cannot ignore its main symptoms.

Symptoms of the development of coma

The coma is formed gradually. In the medical history of the vast majority of patients, the course of diabetes immediately before coma was mild and optimally compensated. For this purpose, oral sugar-lowering drugs, as well as dietary nutrition, were used. A few days before the formation of a coma, patients experience increasing thirst, polyuria, and even weakness. The patient's condition with diabetes will constantly worsen, there is a progressive development of such a condition as dehydration. Certain disturbances appear within the framework of consciousness, for example, the addition of drowsiness or lethargy, which gradually turns into a coma.

It is noteworthy that neurological and neuropsychiatric conditions are characteristic. For example, we can talk about hallucinations, hemiparesis, slurred speech. In some cases, a coma may be accompanied by convulsions, areflexia, and an increase in muscle tone. Also, a likely symptom is the appearance of such a high temperature, which will be held for a long time. Of course, given the criticality of such a condition as hyperosmolar coma, it should be subjected to a correct and complete diagnosis in order to subsequently begin a recovery course.

Diagnostic measures

Diagnosis is most often complicated by the fact that it must be carried out extremely quickly in order to start treating a diabetic as soon as possible. That is why factors such as the addition of sinus tachycardia and arterial hypotension are taken into account. It should be taken into account that:

in a certain part of patients, local edema due to vein thrombosis is identified, therefore, the determination of blood hyperosmolarity is required;
characteristic is the obvious hyperglycemia, reduced diuresis, reaching even anuria, severe glucosuria without the addition of ketonuria.
differentiation with diabetic ketonemic coma is based on the absence of signs of ketoacidosis in diabetic non-ketonemic gynerosmolar coma.

Also, one should not forget about severe dehydration, increased rates of hyperglycemia. A very high level of glycemia and osmolarity is identified in the blood, while ketone bodies are not identified.

Treatment for the development of coma

When providing such support to the patient, it is strongly recommended to eliminate dehydration and hypovolemia. It may also be necessary to restore optimal plasma osmolarity. Infusion procedures, if a hyperosmolar coma has been identified, are carried out in a certain order

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Speaking of this, it is strongly recommended to pay attention to the fact that during the first hours from the moment of hospitalization, the patient will need an intravenous injection of two to three liters of a 0.45% composition based on sodium chloride. A more accurate amount should be determined solely by a specialist, depending on the characteristics of the state of health. After this, a transition to the infusion of isotonic saline will be required. Such treatment of hyperosmolar coma continues in parallel with the use of a hormonal component until the glucose levels decrease to 12-14 mmol per liter.

After that, in order to exclude recurrent coma, a 5% glucose solution is introduced intravenously. Further, the appointment of a hormonal component in order to utilize glucose should be considered an obligatory step. Speaking of the treatment presented, it should be borne in mind that it should be carried out with a proportion: four units of insulin per gram of glucose. In addition, treatment may include:

in order to stop dehydration in such patients, it often becomes necessary to use significant volumes of fluid. In some cases, the figures presented reach 20 liters within 24 hours;
electrolyte indicators are adjusted;
in the vast majority of cases, coma is formed in diabetics with mild or moderate severity of the pathological condition, and therefore their body reacts quite normally to the use of the hormonal component.

In this regard, experts insist that very large dosages of the drug should not be used. An appropriate technique is the introduction of relatively small doses, namely 10 units for 60 minutes. Of course, such indicators may change in connection with the recommendations of a specialist and the individual characteristics of the condition.

Features of emergency care for diabetics

Help with a condition such as hyperosmolar coma is aimed at eliminating metabolic disorders. It will be equally important to eliminate acidosis itself and all its symptoms, as well as take care of qualified treatment of cardiovascular pathologies. When the patient is in intensive care, the first step is to perform a rapid blood glucose test every 60 minutes if glucose was administered intravenously. If its use was carried out subcutaneously, then we will talk about once every three hours.

This is especially necessary if there is a need to identify ketone bodies in the urine.

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Prevention and prognosis

There are no specific measures for the prevention of hyperosmolar coma. It is strongly recommended to maintain optimal sugar levels, monitor other vital criteria for a diabetic. A very important point is proper and nutritious nutrition, the exclusion of bad habits.

Speaking about the prognosis for hyperosmolar coma, it is strongly recommended to pay attention to its ambiguity. The fact is that about 50% of patients die as a result of an unexpected development of the condition. That is why the prognosis can be positive only with the early detection of a coma or mild and moderate severity of the pathology.

Thus, hyperosmolar coma is a severe condition, the diagnosis and treatment of which should be carried out as early as possible. It is very important to provide such interventions that are associated with emergency care for diabetes. It is in this case that it will be possible to talk about the preservation of the patient's life and the maximum degree of activity.

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(more than 38.9 mmol / l), blood hyperosmolarity (more than 350 mosm / kg), pronounced, no.
Epidemiology of hyperosmolar coma
Hyperosmolar coma is 6-10 times less common than ketoacidotic coma. In most cases, it occurs in patients with type 2 diabetes, more often in the elderly. In 90% of cases, it develops against the background.

Causes of hyperosmolar coma:

Hyperosmolar coma can develop due to:
- severe dehydration (with vomiting, diarrhea, burns, long-term treatment with diuretics);
- insufficiency or absence of endogenous and / or exogenous insulin (for example, due to inadequate insulin therapy or in its absence);
- increased need for insulin (with a gross violation of the diet or the introduction of concentrated glucose solutions, as well as with infectious diseases, especially pneumonia and urinary tract infections, other severe concomitant diseases, injuries and operations, long-term therapy with drugs that have the properties of insulin antagonists, - glucocorticosteroids , preparations of sex hormones, etc.).

Pathogenesis:

The pathogenesis of hyperosmolar coma is not completely understood. Severe hyperglycemia occurs as a result of excessive glucose intake in the body, increased production of glucose by the liver, glucose toxicity, suppression of insulin secretion and glucose utilization by peripheral tissues, and also due to dehydration of the body. It was believed that the presence of endogenous insulin interferes with lipolysis and ketogenesis, but it is not enough to suppress the formation of glucose by the liver. Thus, gluconeogenesis and glycogenolysis leads to severe hyperglycemia. However, the concentration of insulin in the blood in diabetic ketoacidosis and hyperosmolar coma is almost the same.
In accordance with another theory, in hyperosmolar coma, the concentration of growth hormone and cortisol is less than in diabetic ketoacidosis; in addition, the insulin/glucagon ratio is higher in hyperosmolar coma than in diabetic ketoacidosis. Plasma hyperosmolarity leads to suppression of the release of FFA from adipose tissue and inhibits lipolysis and ketogenesis.
The mechanism of plasma hyperosmolarity includes increased production of aldosterone and cortisol in response to dehydration hypovolemia; develops as a result. High hyperglycemia and hypernatremia leads to plasma hyperosmolarity, which in turn causes pronounced intracellular dehydration. At the same time, the sodium content also increases in the cerebrospinal fluid. Violation of the water and electrolyte balance in the brain cells leads to the development of neurological symptoms, cerebral edema and coma.

Symptoms of hyperosmolar coma:

Hyperosmolar coma develops over several days or weeks.
The patient develops symptoms of decompensated diabetes mellitus, including:
- ;
- thirst;
- and mucous membranes;
- weight loss;
- weakness, adynamia.
In addition, symptoms of dehydration are noted:
- decrease in skin turgor;
- decreased tone of the eyeballs;
- lowering blood pressure and body temperature.
Typical neurological symptoms:
- hemiparesis;
- hyperreflexia or areflexia;
- ;
- (in 5% of patients).
In a severe, uncorrected hyperosmolar state, stupor and coma develop. The most common complications of hyperosmolar coma include:
- epileptic seizures;
- deep veins;
- ;
- renal failure.

Diagnostics:

The diagnosis of hyperosmolar coma is made on the basis of a history of diabetes mellitus, usually type 2 diabetes (however, it should be remembered that hyperosmolar coma can develop in people with previously undiagnosed diabetes mellitus, in 30% of cases hyperosmolar coma is the first manifestation of diabetes mellitus), characteristic clinical manifestation of laboratory diagnostic data (primarily severe hyperglycemia, hypernatremia and plasma hyperosmolarity in the absence of acidosis and ketone bodies. Similarly to diabetic ketoacidosis, the ECG reveals signs and heart rhythm disturbances.

Laboratory manifestations of a hyperosmolar condition include:
- hyperglycemia and glucosuria (glycemia is usually 30-110 mmol / l);
- a sharply increased plasma osmolarity (usually > 350 mosm / kg with a normal 280-296 mosm / kg); osmolality can be calculated using the formula: 2 x ((Na) (K)) + blood glucose / 18 blood urea nitrogen / 2.8.
- hypernatremia (a reduced or normal concentration of sodium in the blood is also possible due to the release of water from the intracellular space to the extracellular space);
- absence of acidosis and ketone bodies in the blood and urine;
- other changes (possible up to 15,000-20,000 / μl, not necessarily associated with infection, increased hemoglobin and hematocrit levels, a moderate increase in the concentration of urea nitrogen in the blood).

Differential diagnosis of hyperosmolar coma.
Hyperosmolar coma is differentiated from other possible causes of impaired consciousness.
Given the advanced age of patients, most often the differential diagnosis is carried out with impaired cerebral circulation and subdural hematoma.
An extremely important task is the differential diagnosis of hyperosmolar coma with diabetic ketoacidotic and especially hyperglycemic coma.

Treatment of hyperosmolar coma:

Patients with hyperosmolar coma should be admitted to the intensive care unit/intensive care unit. After establishing the diagnosis and initiating therapy, patients need constant monitoring of their condition, including monitoring of the main indicators of hemodynamics, body temperature and laboratory parameters. If necessary, patients undergo mechanical ventilation, bladder catheterization, installation of a central venous catheter,. In the intensive care unit / intensive care unit, the following is carried out:
- express analysis of blood glucose 1 time per hour with intravenous administration of glucose or 1 time 3 hours when switching to subcutaneous administration;
- determination of ketone bodies in serum in the blood 2 times a day (if not possible - determination of ketone bodies in urine 2 r / day);
- determination of the level of K, Na in the blood 3-4 times a day;
- study of the acid-base state 2-3 times a day until stable pH normalization;
- hourly control of diuresis until dehydration is eliminated;
- ECG monitoring,
- control of blood pressure, heart rate, body temperature every 2 hours;
- radiography of the lungs,
- General analysis of blood, urine 1 time in 2-3 days.
As with diabetic ketoacidosis, the main directions of treatment for patients with hyperosmolar coma are rehydration, insulin therapy (to reduce glycemia and plasma hyperosmolarity), correction of electrolyte disorders and disorders of the acid-base state).

Rehydration.
Enter:
Sodium chloride, 0.45 or 0.9% solution, intravenous drip 1-1.5 l during the 1st hour of infusion, 0.5-1 l during the 2nd and 3rd, 300-500 ml in subsequent hours. The concentration of sodium chloride solution is determined by the level of sodium in the blood. At a Na+ level of 145-165 meq/l, sodium chloride solution is injected at a concentration of 0.45%; at a Na+ level of 165 meq/l, the administration of saline solutions is contraindicated; in such patients, a glucose solution is used for rehydration.
Dextrose, 5% solution, intravenously drip 1-1.5 l during the 1st hour of infusion, 0.5-1 l during the 2nd and 3rd, 300-500 ml - in the following hours. Osmolality of infusion solutions:
0.9% sodium chloride - 308 mosm / kg;
0.45% sodium chloride - 154 mosm / kg,
5% dextrose - 250 mosm/kg.
Adequate rehydration helps to reduce.

insulin therapy.
Short-acting drugs are used:
Soluble insulin (human genetically engineered or semi-synthetic) intravenously drip in sodium chloride / dextrose solution at a rate of 00.5-0.1 U / kg / h (in this case, the blood glucose level should decrease by no more than 10 mosm / kg / h) .
In the case of a combination of ketoacidosis and hyperosmolar syndrome, treatment is carried out in accordance with the general principles for the treatment of diabetic ketoacidosis.

Evaluation of the effectiveness of treatment.
Signs of effective therapy for hyperosmolar coma are the restoration of consciousness, the elimination of clinical manifestations of hyperglycemia, the achievement of target blood glucose levels and normal plasma osmolality, the disappearance of acidosis and electrolyte disorders.

Mistakes and unreasonable appointments.
Rapid rehydration and a sharp decrease in blood glucose levels can lead to a rapid decrease in plasma osmolarity and the development of cerebral edema (especially in children).
Given the advanced age of patients and the presence of concomitant diseases, even adequately performed rehydration can often lead to decompensation and pulmonary edema.
A rapid decrease in blood glucose levels can cause extracellular fluid to pass into cells and exacerbate arterial hypotension and oliguria.
The use of potassium, even with moderate hypokalemia in individuals with oligo- or anuria, can lead to life-threatening.
The appointment of phosphate in renal insufficiency is contraindicated.

Forecast.
The prognosis of hyperosmolar coma depends on the effectiveness of treatment and the development of complications. Mortality in hyperosmolar coma reaches 50-60% and is determined primarily by severe concomitant pathology.

A complication of diabetes mellitus, the pathogenesis of which is based on hyperosmolarity of the blood, pronounced intracellular dehydration and the absence of ketoacidosis.

Hyperosmolar coma is much less common than ketoacidotic coma. In most cases, it occurs in patients over 50 years of age with non-insulin-dependent type of diabetes mellitus, often combined with obesity, usually on a diet or receiving oral sugar-reducing drugs. Rarely, hyperosmolar coma occurs in childhood and adolescence.

Etiology of hyperosmolar coma

In half of the cases, hyperosmolar coma develops in individuals with previously unrecognized or poorly treated diabetes mellitus. Hyperosmolar coma can develop as a result of severe dehydration of the body due to vomiting, diarrhea, burns, frostbite, blood loss, and profuse urination. Factors contributing to the development of hyperosmolar coma can be excessive administration of carbohydrates, surgical interventions, intercurrent infections, pancreatitis, gastroenteritis. The cause of hyperosmolar coma can also be long-term treatment with diuretics and steroid drugs (glucocorticoids) [Voyer M., 1967; Spenney J. et al., 1969], immunosuppressants. In some cases, hyperosmolar coma occurs after hemodialysis, peritoneal dialysis, resuscitation, and overload with carbohydrate and saline solutions.

Pathogenesis hyperosmolar coma

Hyperglycemia plays a leading role in the pathogenesis of hyperosmolar coma. The rapid increase in hyperglycemia, which reaches a very high level in hyperosmolar coma, is facilitated by the worsening of the course of concomitant diseases in the elderly, as well as various kinds of systemic and organ disorders caused by diabetes mellitus. In addition, a sharp decrease in renal excretory function in coma does not make it possible to sufficiently reduce hyperglycemia by glucosuria. Due to a decrease in the excretion of sodium in the urine, an increase in the secretion of cortisol, aldosterone (a reaction to dehydration hypovolemia), and a decrease in renal blood flow, hypernatremia occurs. Due to the absence of ketoacidosis, bicarbonate levels and blood pH are normal. Very high hyperglycemia (55.5-111 and even 199.8 mmol / l, or 1000-2000 and even 3600 mg%) and hypernatremia, osmotic diuresis lead to a sharp blood hyperosmolarity (normal 285-295 mosmol / l), exceeding 330 mosmol / l and often reaching 500 mosmol / l or more - one of the leading symptoms of coma. The development of blood hyperosmolarity is also facilitated by the high content of chlorine, urea and residual nitrogen in the blood. Hyperosmolarity of blood leads to pronounced intracellular dehydration. Violation of water and electrolyte balance in the brain cells entails severe neurological symptoms and loss of consciousness.

The occurrence of dehydration along with glucosuria equally contributes to the release of salts. As a result of high osmotic diuresis, there is a rapid development of hypovolemia, intracellular and intercellular dehydration. This in turn causes collapse with reduced blood flow to the organs. As a result of dehydration, blood thickens (increase in hematocrit, hemoglobin concentration, leukocytosis), the concentration of its coagulation factors increases, multiple thrombosis and thromboembolism of blood vessels occur, the minute volume of blood decreases, and the filtration capacity of the kidneys is impaired. Oliguria and anuria develop. Chlorides, urea, residual nitrogen accumulate in the blood.

Due to an increase in the osmotic pressure of the blood, dehydration of the brain occurs, as well as a decrease in cerebrospinal fluid pressure. The content of glutamic acid in the brain is reduced. This enhances hypoxia and may be one of the reasons for the development of coma and cerebral edema. There are intracerebral and subdural hemorrhages. Small-point hemorrhages in the substance of the brain are also possible due to hypernatremia. There is another point of view on the pathogenesis of hyperosmolar coma, according to which the leading place in the development of coma should be given not to hyperglycemia, but to dehydration as a result of changes in the incretion of antidiuretic hormone.

A characteristic feature of hyperosmolar coma is the absence of ketoacidosis in it. Some authors try to explain this by the pronounced anti-lipolytic effect of insulin, which is 10 times greater than its effect on the utilization of glucose by cells. In this regard, the presence in this coma of even small amounts of endogenous insulin, which are unable to prevent the development of high hyperglycemia, prevents lipolysis and ketosis. However, glucose itself is an inhibitor of ketogenesis. In addition, in elderly people with mild diabetes mellitus, lipolysis and subsequent ketosis are also prevented by the presence of glycogen stores in the liver.

Clinic hyperosmolar coma

Coma usually develops within a few days, less often in a shorter time. Polydipsia and polyuria are observed. Rapid dehydration followed by polyuria is very characteristic. There is drowsiness, a soporous state or a deep coma occurs. There is a sharp dryness of the skin and visible mucous membranes. The tone of the eyeballs is reduced. The pupils are constricted, sluggishly react to light. Tachycardia, arrhythmia, arterial hypotension are observed. Breathing shallow, rapid (tachypnea). Exhaled air without the smell of acetone. In connection with hypokalemia, which usually occurs after 3-6 hours from the start of treatment and very rarely before treatment, changes in the gastrointestinal tract occur (vomiting, flatulence, abdominal pain, impaired intestinal motility up to paralytic ileus), but usually they less pronounced than in ketoacidotic coma. There is oliguria up to anuria. Unlike ketoacidotic coma, oliguria develops more often and earlier. Focal functional neurological symptoms are noted, which are much brighter and appear earlier than in ketoacidotic coma. Bilateral spontaneous nystagmus and muscle hypertonicity are especially characteristic. Aphasia, hemiparesis, paralysis, Babinsky's pathological symptom, central hyperthermia, hemianopsia may occur. Vestibular disorders, hallucinatory psychoses, epileptoid seizures develop. Tendon reflexes are absent. Often there are thromboses of arteries and veins [Vasyukova EA, Zefirova GS, 1982].

Laboratory data. Changes in the biochemical composition of the blood are characterized by pronounced hyperglycemia (55.5-111.1 and even 200 mmol / l, or 1000-2000 and even 3636 mg%), an increase in blood osmotic pressure up to 500 mosmol / l (normal 285-295 mosmol / l), hyperchloremia, hypernatremia (sometimes the sodium level in the blood is normal), an increase in the content of total serum protein, residual nitrogen (up to 16 mmol / l, or 22.4 mg%) in the absence of ketoacidosis, an increase in urea. The level of potassium in the blood before treatment is usually normal or slightly elevated. In the future, against the background of insulin therapy and a decrease in blood sugar, severe hypokalemia may occur. There is a high content of hemoglobin, hematocrit, leukocytes. Bicarbonate levels and blood pH are normal. Glucosuria and hyponatriuria are expressed.

Diagnosis and differential diagnosis of hyperosmolar coma

Diagnosis of hyperosmolar coma is based on the absence of the smell of acetone in the exhaled air and ketoacidosis, pronounced hyperglycemia and blood osmolarity, the presence of neurological symptoms (pathological symptom of Babinsky, muscle hypertonicity, bilateral nystagmus, etc.). In addition to diabetes mellitus, hyperosmolar syndrome can also be observed when thiazide diuretics are prescribed for hepatic and renal insufficiency (differential diagnosis, see tables 4 and 5).

The prognosis of hyperosmolar coma is uncertain. Lethality reaches 50%. The most common causes of death are hypovolemic shock, severe comorbidities and complications (pancreatic necrosis, renal failure, multiple vascular thrombosis and thromboembolism, myocardial infarction, cerebral edema).

Prevention. See section Ketoacidotic Coma.

Treatment of hyperosmolar coma

When removing patients from hyperosmolar coma, the main attention should be paid to the elimination of dehydration by the introduction of large amounts of fluid and the reduction of hyperglycemia by the administration of insulin.

1. To combat dehydration, a hypotonic solution (0.45%) of sodium chloride is injected intravenously in an amount of 6 to 10 liters or more per day. Within 2 hours, 2 liters of a 0.45% sodium chloride solution are injected intravenously g, further intravenous drip administration of a hypotonic sodium chloride solution at a dose of 1 l / h is continued until the blood osmolarity and venous pressure normalize. Rehydration is carried out until the patient's clear consciousness is restored.

2. To reduce hyperglycemia, under strict control of blood sugar, insulin is administered intramuscularly and intravenously in a single dose of 50 units (half the dose intravenously and half intramuscularly). With hypotension, insulin is recommended to be used only intravenously. Subsequently, insulin is administered every hour at 25 IU intravenously and 25 IU intramuscularly until the level of glycemia drops to 14 mmol / l (250 mg%).

In order to reduce hyperglycemia, insulin can also be administered in small doses. In this case, 20 IU of insulin is first administered intramuscularly, and then 5-8 IU every hour intramuscularly or intravenously until the level of glycemia decreases. After removing the patient from a coma, if necessary, they are transferred to treatment with long-acting insulin preparations.

3. When the blood sugar level drops to 13.88 mmol / l (250 mg%), instead of a hypotonic sodium chloride solution, the introduction of a 2.5% glucose solution is started intravenously (up to 1 liter).

4. In case of hypokalemia under the control of potassium content in the blood and ECG, intravenous potassium chloride is used at a dose of 4-12 g / day (for details, see the section "Ketoacidotic coma").

5. To combat hypoxia and prevent cerebral edema, intravenous administration of 50 ml of a 1% solution of glutamine vdslota is carried out with oxygen therapy.

6. For the prevention of thrombosis, if necessary, heparin is prescribed at 5000-6000 IU 4 times a day under the control of the blood coagulation system.

7. In order to avoid the development of cardiovascular insufficiency or to eliminate it, cordiamin, strophanthin or corglicon are used. With persistently low blood pressure, 1-2 ml of a 0.5% DOX solution is prescribed intramuscularly. Plasma, gemodez (500 ml), human albumin, whole blood are administered intravenously.

Potemkin V.V. Emergency conditions in the clinic of endocrine diseases, 1984

Diabetes is a disease of the 21st century. More and more people are becoming aware of the presence of this terrible disease. However, a person can live well with this disease, the main thing is to follow all the prescriptions of doctors.

Unfortunately, in severe cases, a person with diabetes can experience a hyperosmolar coma.

What's this?

Hyperosmolar coma is a complication of diabetes mellitus, in which there is a serious metabolic disorder. This condition is characterized by the following:

hyperglycemia - a sharp and strong increase in blood glucose levels;
hypernatremia - an increase in the level of sodium in the blood plasma;
hyperosmolarity - an increase in the osmolarity of blood plasma, i.e. the sum of the concentrations of all active particles per 1 liter. blood greatly exceeds the normal value (from 330 to 500 mosmol / l at a rate of 280-300 mosmol / l);
dehydration - dehydration of cells, which occurs as a result of the fact that the liquid tends to the intercellular space to reduce the level of sodium and glucose. It occurs throughout the body, even in the brain;
the absence of ketoacidosis - the acidity of the blood does not increase.

Hyperosmolar coma most often occurs in people over 50 years of age and accounts for approximately 10% of all types of coma in diabetes mellitus. If you do not provide emergency care to a person in such a state, then this can lead to death.

The reasons

There are a number of reasons that can lead to this type of coma. Here is some of them:

Dehydration of the patient's body. This can be vomiting, diarrhea, decreased fluid intake, long-term use of diuretics. Burns of a large surface of the body, disturbances in the functioning of the kidneys;
Lack or at all lack of adequate insulin;
Unrecognized diabetes. Sometimes a person does not even suspect the presence of this disease in himself, so he is not treated and does not follow a certain diet. As a result, the body cannot cope and coma may occur;
Increased need for insulin, for example, when a person violates the diet by eating foods containing a large amount of carbohydrates. Also, this need may occur with colds, diseases of the genitourinary system of an infectious nature, with prolonged use of glucocorticosteroids or drugs that replace sex hormones;
Taking antidepressants;
Diseases arising as complications after the underlying disease;
Surgical interventions;
Acute infectious diseases.

Symptoms

Hyperosmolar coma, like any disease, has its own signs by which it can be recognized. In addition, this condition develops gradually. Therefore, some symptoms predict the occurrence of hyperosmolar coma in advance. The signs are the following:

A few days before the coma, a person has a sharp thirst, constant dryness in the mouth;
The skin becomes dry. The same applies to the mucous membranes;
The tone of soft tissues decreases;
A person constantly has weakness, lethargy. Constantly want to sleep, which leads to a coma;
The pressure drops sharply, tachycardia may occur;
The development of polyuria increased urine production;
There may be speech problems, hallucinations;
Muscle tone may increase, convulsions or paralysis may occur, but the tone of the eyeballs, on the contrary, may fall;
Very rarely, epileptic seizures can occur.

Diagnostics

In blood tests, a specialist determines elevated levels of glucose and osmolarity. In this case, ketone bodies are absent.

Diagnosis is also based on visible symptoms. In addition, the age of the patient and the course of his disease are taken into account.

For this the patient must take tests to determine glucose, sodium and potassium in the blood. Urine is also given to determine the level of glucose in it. In addition, doctors may prescribe ultrasound and X-ray of the pancreas and its endocrine part and electrocardiography.

Treatment

Emergency care for hyperosmolar coma is, first of all, to eliminate dehydration of the body. Then it is necessary to restore the osmolarity of the blood and bring the glucose level back to normal.

A patient who develops a hyperosmolar coma urgently need to be taken to the intensive care unit or intensive care unit. After the diagnosis is made and treatment is started, the condition of such a patient is under constant control:

Once an hour, an express blood test must be done;
Twice a day, ketone bodies are determined in the blood;
Several times a day, an analysis is made to determine the level of potassium and sodium;
A couple of times a day check the acid-base state;
The amount of urine that is formed in a certain time is constantly monitored until dehydration is eliminated;
ECG and blood pressure control;
Every two days, a general analysis of urine and blood is carried out;
They can take x-rays of the lungs.

Sodium chloride is used for rehydration. It is administered intravenously using a dropper in certain amounts. The concentration is selected depending on how much sodium is contained in the blood. If the level is high enough, then a glucose solution is used.

In addition, a dextrose solution is used, which is also imported intravenously.

In addition, a patient in a state of hyperosmolar coma is given insulin therapy. Short-acting insulin is used, which is administered intravenously.

Emergency First Aid

But what about a person if his loved one has a hyperosmolar coma completely unexpectedly (this happens when a person does not pay attention to the symptoms).

You need to act as follows:

Be sure to ask someone to call a doctor;
The patient should be well covered or overlaid with heating pads. This is done in order to reduce heat loss;
It is necessary to control body temperature, the state of breathing;
It is necessary to check the condition of the eyeballs, skin tone;
Control glucose levels;
If you have experience then you can put a dropper with saline solution. 60 drops should pass per minute. The volume of the solution is 500 ml.

Complications

Hyperosmolar coma often occurs in people over 50 years of age. Therefore, some complications can sometimes arise. For example:

With rapid rehydration and a decrease in glucose cerebral edema may occur;
Due to the fact that this condition often occurs in older people, the development of heart problems and the occurrence of pulmonary edema are likely;
If the glucose level drops very quickly, then a sharp drop in blood pressure is possible;
The use of potassium can lead to its high content in the body, which can be a threat to human life.

Forecast

Hyperosmolar coma is considered a serious complication of diabetes mellitus. Death occurs in about 50% of cases of this condition. After all, most often it appears at an age when, in addition to diabetes, a person can have many other diseases. And they can be the cause of a difficult recovery.

With timely assistance, the prognosis is favorable, the most important thing is that after leaving this state, the patient follows all the doctor's instructions and adheres to a healthy diet and lifestyle in general. And his close people need to know the rules of emergency care in order to provide it in time if necessary.