Coma in diabetes mellitus

Coma in diabetes mellitus – varieties, signs, treatment measures, prevention

Diabetes mellitus is one of the most widespread diseases of the endocrine system, characterized by absolute or relative insufficiency of insulin in the blood. Despite many years of experience in studying the causes and methods of treatment of this pathology, diabetes mellitus remains among the diseases, the complications of which pose a threat to the patient’s life. Despite the indisputable fact that the body of a person with diabetes mellitus over time adapts to small fluctuations in blood glucose levels, a rapid decrease or increase in this indicator often contributes to the development of conditions that require urgent intensive care.

These are the so-called acute complications of diabetes mellitus – coma, which, depending on the mechanism of development and clinical signs, are divided into several types:

– ketoacidotic coma;

– lactacidemic coma;

– hyperosmolar coma

– hypoglycemic coma;

Diabetic ketoacidotic coma – causes and mechanism of development, signs

This type of complication develops with absolute or relative insufficiency of insulin in the body, as well as with impaired utilization of glucose by tissues, which develops in patients with severe insulin-dependent diabetes mellitus. The ketoacidotic state develops unexpectedly, but usually it is preceded by a number of provoking stress factors, such as an incorrectly selected dose of insulin, a change in the drug, cessation of insulin administration for any reason, a gross violation of the diet, alcohol abuse, violation of the technique of insulin administration, an increase in insulin requirements due to the peculiarities of the state of the body (pregnancy, poisoning, surgery, infections, etc.).

The development of ketoacidosis is due to the fact that with a lack of insulin in the body, the process of penetration of glucose into cells is disrupted, which in turn leads to energy depletion of tissues, which contributes to organ dysfunction. Despite compensatory hyperglycemia, which develops due to an increase in the production of adrenocorticotropic, growth hormone and other hormones, as well as an increase in the production of glucose in the liver, due to the lack of a sufficient amount of insulin, glucose cannot penetrate the cellular barrier. In this regard, for compensatory purposes to maintain homeostasis, the body begins to receive the missing energy through the active breakdown of fats – lipolysis, and as a result of this biochemical process, ketone bodies (acetone) are formed, an excess amount of which has a depressing effect on the central nervous system, as a result of which a ketoacidotic coma.

The concentration of ketone bodies in the blood of healthy people is in the range of up to 100 μmol / L, while only traces of acetone can be found in the urine. If the course of diabetes mellitus passes into the stage of decompensation, a large number of ketone bodies are formed in the liver due to metabolic changes (up to 1000 mmol / L per day). This amount of ketone bodies cannot be removed from the body by the muscles and kidneys, so their accumulation leads to ketoacidosis. The condition is aggravated by the formation of a vicious circle, when, as a result of the development of ketoacidosis in the blood, a decrease in the level of immunoreactive insulin is noted, the relative or absolute insufficiency of insulin only increases.

The development of a ketoacidotic coma is usually slow – from several days to several weeks. If the process develops against the background of acute infectious diseases or severe intoxication, a diabetic coma can develop in a few hours. As a rule, clinically diabetic ketoacidosis goes through three stages, which, in the absence of timely correction, follow one after the other.

1. Stage of moderate ketoacidosis – the patient may complain of general weakness, increased fatigue, tinnitus, lethargy, decreased appetite, thirst, nausea, acute abdominal pain, increased urine output. Exhaled air and urine smell like acetone. An increase in sugar levels is found in the blood and urine.

2. Stage of precoma or decompensated ketoacidosis – the patient’s appetite disappears altogether, in addition to nausea, vomiting is noted, which increases general weakness. The patient is indifferent to what is happening around him, his vision deteriorates, shortness of breath appears, pain in the heart and abdomen. Against the background of an indomitable feeling of thirst, there is an increase in the urge to urinate, which is explained by a violation of the water-electrolyte balance and excessive excretion of electrolytes from the body – potassium, sodium ions, etc. Consciousness of patients is preserved, as well as orientation in space and time, but lethargy is noted when trying to answer questions. The skin is dry, rough, cold. The cheeks are slightly flushed, and the tongue is covered with a brown coating, and teeth imprints may be visible on it. This stage can last from several hours to several days. In the absence of timely correction of such a condition, there is a deterioration in the reaction of patients and the transition of the process to the final stage.

3. Stage of coma – the patient is absolutely indifferent, may fall into a deep sleep. Examination reveals deep, noisy breathing with a pungent smell of acetone in the exhaled air, a decrease in blood pressure, and a rapid rhythmic pulse. Tendon reflexes gradually fade away. There is a decrease in body temperature.

If you suspect the development of a ketoacidotic coma, the patient should be immediately hospitalized in order to carry out the necessary complex of resuscitation measures.

Lactic acidosis coma – development mechanism and symptoms

This type of diabetic coma is less common than other types, but is one of the most severe complications of diabetes mellitus. This type of coma develops as a result of a complex biochemical reaction – anaerobic glycolysis, which is one of the alternative methods of obtaining energy, the residual product of which is lactic acid. If in a healthy body the level of lactic acid is in the range of 0.5 – 1.4 mmol / l, then with lactic acidotic coma, this figure reaches 2 mmol / l when the blood pH level drops below 7.3. In addition, there is a change in the lactate-pyruvate balance towards an increase in the concentration of lactate.

Lactic acidotic coma often develops against the background of shock, intoxication, sepsis, extensive blood loss, cardiovascular and renal failure. Despite the fact that the liver is normally capable of processing more than 3 thousand mmol of lactic acid, due to the state of tissue hypoxia that accompanies the above pathological processes, the ability to process lactic acid becomes much less lactate formed. If the patient is given intravenous administration of solutions containing xylitol, sorbitol, fructose and other sugars, this is also a provoking moment for the development of lactic acidotic coma.

The onset of this type of coma is usually sudden, characterized by signs of depression of consciousness (apathy, drowsiness, delirium), as well as a rapid loss of appetite, nausea, vomiting, muscle pain. On examination, the patient’s skin is pale, cold. The effect of lactic acid on the cardiovascular system is manifested by a rapid pulse, a decrease in blood pressure, impaired excitability and contractility of the myocardium, paresis of peripheral vessels, and collapse.

Patients with the first signs of coma require prompt hospitalization. Confirmation of the diagnosis of lactic acidotic coma is carried out based on laboratory data, namely, a high concentration of lactic acid and pyruvate in the blood, as well as a violation of the acid-base balance towards acidification.

Hyperosmolar coma – prerequisites for development, clinical manifestations

Hyperosmolar coma usually develops in patients with non-insulin dependent diabetes mellitus of mild to moderate severity, as therapeutic measures in which diet therapy and taking medications that lower blood sugar levels are carried out. This complication often develops in elderly patients, limited in movement, as well as in such concomitant pathological processes as burns, hypothermia, infectious diseases of the kidneys and urinary tract, lungs, pancreas, myocardial infarction, etc., which aggravate the process of impaired blood supply. With a high concentration of sugar in the blood, there is an increase in the excretion of urine from the body by the kidneys, as a result of which dehydration develops, leading in turn to thickening of the blood and difficulty in its movement through small vessels. The consequence of such microcirculatory disorders is a deficiency of cerebral blood supply.

The development of a hyperosmolar coma is extended over time. The first signs are a constant feeling of thirst, an increase in the volume of urine, and general weakness. The increase in dehydration leads to lethargy and clouding of consciousness, hallucinations, convulsions, paresis of the arms and legs. At the first signs of an impending complication, patients should be hospitalized in order to immediately restore water-salt metabolism through the introduction of infusion solutions.

Hypoglycemic coma – causes, symptoms

This complication of diabetes mellitus develops due to a rapid decrease in blood glucose levels, which can be caused by an overdose of insulin or other drugs that lower sugar levels, or excessive physical exertion, leading to a sharp consumption of glucose. If the patient does not eat after the insulin injection, this can also cause hypoglycemia.

The development of a hypoglycemic coma is always sudden. The harbingers of an impending coma are increased anxiety, trembling, sweating, flashing “flies” before the eyes, a feeling of numbness of the tongue and lips, a sharp feeling of hunger. In the absence of a correction of the condition at this stage, the patient has the appearance of seizures, agitation, and an increase in blood pressure. In the future, you can observe depression of consciousness, increased sweating, slowing of breathing and the gradual disappearance of reflexes.

Therapeutic measures aimed at the prevention and elimination of coma in patients with diabetes mellitus

The treatment regimen for diabetic coma consists mainly of a number of key principles:

1.Elimination of insulin deficiency and normalization of carbohydrate metabolism;

2. the fastest possible recovery of fluid reserves in the body;

3. restoration of the balance of electrolytes inside cells and in the intercellular environment and acid-base homeostasis;

4. normalization of glucose levels and its reserves in the body;

5. correction of pathological conditions and diseases that provoked the development of diabetic coma;

6. restorative treatment measures aimed at maintaining the functioning of all vital organs.

A number of the above measures should be started at the first signs of an impending coma before hospitalization of the patient. These include the elimination of dehydration and the normalization of hemodynamics by intravenous administration of isotonic sodium chloride solution, as well as insulin therapy for ketoacidotic coma, which involves the introduction of physiological doses of insulin that suppress the processes of lipolysis, glucose formation in an alternative way, and the formation of ketone bodies.

The introduction of insulin in such a situation is possible in two ways:

1. Introduce to the patient 20 U of insulin intramuscularly in the shoulder area (deltoid muscle), and after every hour, 5-10 U under the control of the level of glucose and ketone bodies in the blood and urine. When the sugar level drops to 11-13 mmol / l, the administration of insulin is continued subcutaneously. If, within two hours from the start of intramuscular administration of insulin, the glucose level does not decrease, they switch to intravenous administration of insulin, and drip administration is more expedient, since it allows simultaneously injecting fluids that restore electrolyte balance.

2. After a single-stage intravenous administration of 10 U of insulin, a continuous intravenous drip infusion of insulin diluted in saline at a dosage of 0.05-0.1 U / kg of the patient’s weight at a rate of 5-10 U / hour is switched. The rate of infusion solution is determined depending on the dynamics of changes in blood glucose levels. A decrease in the level by 4 – 5.5 mmol / h is considered optimal. If, during the first hour of insulin administration, the blood glucose content decreases by less than 10% from the initial figures, the simultaneous administration of 10-15 U of insulin should be repeated.

Regardless of which of the above methods of insulin therapy was used to prevent the development of coma, after lowering the blood glucose level to 11-13 mmol / L, the physiological solution for infusion is replaced with a 5% glucose solution in order to restore glycogen stores and prevent a condition characterized by a decrease blood glucose levels are below normal. When the patient begins to take liquid and food on his own, the required dose of insulin is administered fractionally, and after a few days, if the cause of the development of diabetic coma is eliminated, the patient is injected with the usual doses of insulin.

The main advantage of infusional administration of insulin in small doses, undoubtedly, is the absence of the process of its accumulation in tissues, which significantly reduces the likelihood of an overdose in conditions of constant monitoring of blood sugar levels.

The restoration of fluid and electrolyte deficiencies is an important step in the treatment regimen in the fight against diabetic coma. Depending on the type of coma, measures to regulate acid-base balance can vary significantly in terms of volumes, composition of solutions, and rate of administration. So, for example, if in a ketoacidotic coma due to a lack of intra- and extracellular fluid, patients lose up to 15% of body weight, then in a hyperosmolar coma these figures reach 25%. It is not possible to restore such a volume of fluid quickly without consequences in the form of pulmonary and cerebral edema, the development of heart failure, therefore, a specific scheme for the administration of fluids has been developed, which involves the introduction of the first liter of fluid within an hour, the next – within two hours, etc. If the patient has a sharp drop in blood pressure below 80 mm Hg. an early blood (plasma) transfusion is required, followed by the infusion of two liters of saline over one and a half to two hours.

In case of hyperosmolar coma, the infusion of a hypotonic sodium chloride solution (0.45%) is recommended, since it is required to restore a greater fluid deficit in a short period of time and at the same time avoid complications in the form of cerebral edema. Large volumes of solution, even less saturated with sodium salts, are also impractical to inject, since this can provoke another complication – intravascular hemolysis.

The restoration of electrolyte balance also depends on the urgent elimination of the deficiency of potassium ions, since a lack of potassium entails the development of such serious complications as heart block, paralysis of intercostal muscles with the development of suffocation, atony of the gastrointestinal tract with intestinal obstruction. It should be remembered that even with a slight lack of potassium, to replace it, it is required to pour a potassium-containing solution, the potassium content of which will be twice as high as the deficit, since more than half of it is lost in the first day with urine.

The need for potassium administration may not arise immediately, but several hours after the start of rehydration, therefore, the level of potassium in the patient’s blood should be kept under constant control. Experts believe that even in the case of a normal or slightly reduced level of potassium in the blood of a patient admitted to the hospital, the administration of potassium chloride should be included along with the start of insulin therapy and therapy to restore the volume of fluid, since both processes contribute to the development of hypokalemia. Part of the potassium deficiency can be replenished through potassium-containing foods (meat broths, fruit juices).

If an adequate drug correction of ketoacidosis is carried out, the increase in the formation of ketone bodies stops, and the production of hydrocarbonate ions by the kidneys replaces the lack of bases and eliminates acidosis. But in cases when the pH of the blood drops below 7.0, and the concentration of bicarbonate becomes less than 10 mmol / l, an intravenous infusion of sodium bicarbonate solution should be carried out, and it should not be administered by jet, since this is fraught with death due to a sharp decrease in the level of potassium in the blood, but drip. Another way to prevent the development of hypokalemia is the introduction of 13-20 mmol of potassium for every 100 mmol of sodium bicarbonate.

Among other things, diabetic coma is characterized by a decrease in the level of organic and inorganic phosphorus compounds in the blood, which is aggravated by the administration of insulin. The restoration of phosphorus reserves is one of the urgent measures in the correction of diabetic coma, since phosphorus ions perform such important functions as glucose utilization, oxygen delivery to tissues, and establishment of high-energy bonds. As replacement therapy, the introduction of a complex preparation of potassium mono- or biphosphate is used, combining the process of eliminating phosphorus deficiency with potassium therapy.

The restoration of glucose reserves in the body is the final stage in the treatment of diabetic coma. To do this, after lowering the blood sugar level to 11-14 mmol / l, along with a decrease in the dose of injected insulin, an intravenous infusion of 5% glucose solution is started at a rate of 500 ml for 4-6 hours. a stable blood glucose level (9-10 mmol / l) can be maintained for a long time. In diabetic ketoacidosis, it is recommended to replace the isotonic glucose solution with Buttler’s solution, which contains many salts necessary to restore the electrolyte balance.

Along with the fact that the principles of correction of hyperosmolar coma are similar to those in ketoacidotic coma, there are a number of differences, including the absence of the need for the introduction of alkaline solutions, an increase in the total amount of intravenous fluid administered. In addition, the administration of solutions must be accompanied by constant monitoring of venous pressure. Since the insulin sensitivity in hyperosomolar coma is greater than that in ketoacidotic coma, the amount of insulin administered to the patient will be less. Despite the development and implementation of optimal treatment regimens for hyperosomolar coma, the number of deaths is quite high (20-60%), so the prognosis in this case is worse than in ketoacidosis.

Elimination of lactic acidosis is possible only when diagnosing the condition in the early stages and eliminating the causes that contribute to its development. So, in case of type A lactic acidosis coma, which developed as a result of tissue hypoxia due to shock, anemia, left ventricular failure, the primary task is to carry out oxygen therapy, restore the volume of circulating fluid using injections of electrolytes, colloidal solutions, plasma and blood components. in order to expand the walls of the vascular bed, patients are prescribed izadrin, euspiran and other vasodilators. The use of vasoconstrictor agents is undesirable, since it can provoke an increase in lactic acidosis and lead to a deterioration in the patient’s condition.

With type B lactic acidosis, which, along with diabetes mellitus, leads to renal or hepatic failure, alcohol abuse and congenital disorders of carbohydrate metabolism, corrective measures should be aimed at eliminating the cause of the pathological condition, for which prolonged administration of sodium bicarbonate solution is carried out under ECG control, indicators of central venous pressure, levels of potassium, calcium and blood gases. If a lactic acidotic coma develops against the background of cardiovascular failure or myocardial infarction, in which the use of sodium bicarbonate solutions is contraindicated, trisamine or triolamine is used for correction, which increases the alkaline blood reserve by reducing the concentration of hydrogen ions.

The mortality rate in lactic acid coma is the highest (70-80%), therefore, timely diagnosis of diabetes mellitus is important, which implies the implementation of therapeutic measures that provide stable compensation for carbohydrate metabolism.