Hyperglycaemic coma

гипергликемическая кома Hyperglycemic coma is the most common complication, mainly of diabetes, caused by a lack of insulin in the body. Hyperglycemic coma can be attributed to the final stage of disturbed metabolic processes against the background of diabetes mellitus. To date, it is observed in almost 30% of patients.

For the first time, a hyperglycemic coma in the form of a manifest symptom may occur during the childhood or adolescent period. A lethal outcome is more often observed among the elderly, who have the presence of SSI pathologies, broncho-pulmonary anomalies, infectious pathologies, after the trauma, as a result of surgical operations.

Sometimes a hyperglycemic coma occurs much earlier than diabetes mellitus can reveal how the disease is self-flowing, and also when various infections join this pathology. In addition, hyperglycemic coma can cause decompensation in diabetes mellitus after discontinuation of insulin treatment or its insufficient amount in the injection.

Hyperglycemic Coma Causes

The main cause of such a condition as hyperglycemic coma is a deficiency in the body of a patient with diabetes insulin. In hyperglycemic coma, immunoreactive insulin falls very sharply. As a result, glucose consumption by tissues is impaired, gluconeogenesis in the liver increases, signs of glucosuria, hyperglycemia, acidosis, deep depression of the CNS activity are associated with reduced glucose uptake by brain cells and cellular nutrition of neurocytes.

Hyperglycemic or diabetic coma is characterized by a significant amount of sugar in the blood, but at the same time disrupted its absorption processes due to insulin deficiency, which distinguishes it from hypoglycemic coma.

The reasons that contribute to the development of hyperglycemic coma include: the presence of inflammatory processes in the body and viral diseases; consuming a large amount of sweet when you administer a regular dose of insulin; ineffective work of stimulants, which help the pancreas to produce insulin; non-compliance with the schedule of insulin therapy.

Hyperglycemic coma has several options. First, it is a hyperketonemic acidotic coma, which is accompanied by the appearance of acidosis. Secondly, it is a hyperosmolar coma, which is characterized by a sharp disruption in the processes of hydration, blood supply and formation of cations in the brain cells in the presence of high diuresis and loss of salts. Thirdly, it is a hyperlactacidemic coma that is formed as a result of severe infections, insufficient kidney and liver function, and after using biguanides. All this provokes a disturbance of the lactate system and pyruvate, the formation of glycolysis and the formation of a powerful metabolic acidosis and damage to the cerebral cortex.

Hyperglycaemic coma symptoms

Symptomatic manifestations of hyperglycemic coma are associated with the poisoning of the organism primarily by the central nervous system with ketones, dehydration, and a shift in acid and alkaline balance to acidosis. As a rule, the toxic signs develop gradually and the hyperglycemic coma is preceded by the precomatous state. Sometimes during the day, dehydration symptoms intensify, characterized by a strong thirst, polyuria, a decrease in working capacity and body weight, anorexia with weakness. In the future, manifestations of acidosis and ketosis are added in the form of irritability, abdominal pain, vomiting, often diarrhea and loss of appetite, as well as impairment of consciousness in varying degrees of severity.

At a physical examination, all signs of hypovolemia and dehydration are noted. This is characterized by dry skin and mucous membranes, a decrease in the turgor of eyeballs and skin, arterial hypotension, tachycardia. In addition, patients with hyperglycemic coma have a decreased muscle tone, when breathing out air, you can feel the acetone smell or the smell of rotting apples. Against the background of pronounced acidosis, Kussmaul's breathing is audible in the form of frequent, deep and noisy.

Almost half of patients with hyperglycemic coma have all the symptoms of pseudo-peritonitis: tense and painful abdominal wall, abdominal pain, decreased peristalsis. When conducting an abdominal examination, sometimes an acute paresis of the stomach is diagnosed as a result of such a sign as hypokalemia. The symptomatology of the false abdomen of the acute form is formed as a result of the action of ketone bodies on the gastric and intestinal tracts, and also as a consequence of the dehydration of the peritoneum.

Such a sign of hyperglycemic coma, like hypokalemia, develops after the treatment started. At the same time, the heart rhythm is broken in patients, muscle cramps and peristalsis paresis occur. In addition, there is a wavy change in temperature with a possible increase or decrease, which may be the cause of infection.

Symptoms of impaired consciousness also develop gradually. Initially, a drowsy condition and a peculiar deafness appear, then a sopor is noted and a hyperglycemic coma sets in, for which the decrease or loss of all reflexes is characteristic, in the future it leads to collapse and oligoanuria. In urine analysis, a significant amount of sugar is detected with the appearance of ketone bodies.

Hyperglycemic coma (hyperosmolar) is a condition in which the blood osmolarity rises as a result of increased glucose with dehydration and hypovolaemia. This hyperglycemic coma is caused not by ketoacidosis, but by the presence of extra-cellular hyperosmolarity, which develops as a consequence of dehydration at the cellular level and hyperglycemia. In children, it practically does not occur.

As a rule, the development of hyperglycemic coma (hyperosmolar) is affected by: a significant intake of foods rich in carbohydrates; various circulatory disorders, such as coronary and cerebral disorders; surgical operations; infection; injuries; dehydration, etc. Such a hyperglycemic coma can develop for two weeks.

The symptomatology of hyperglycemic coma (hyperosmolar) is characterized by a gradual onset and may subsequently cause hypovolemic shock. Patients are assessed dry skin , decreased its turgor, rapid breathing, high blood pressure and temperature, soft eyeballs, muscle tone in tension, epileptiform cramps, oliguria, hemiparesis with Babinsky's pathological reflex and symptoms of meningeal etiology. The acetone odor is not determined and the Kussmaul symptom is not observed.

In addition, for this type of hyperglycemic coma is characterized by high dehydration, osmolarity and glycemia. Symptoms of thirst, polyuria and polydipsia are also characteristic of this type of hyperglycemic coma. But oliguria with azotemia develop much faster than before, unlike ketoacidosis. Later the child becomes astenic, drowsy, hallucinations appear. At the time of hospitalization, some patients experience fever and shock.

In addition, very early symptoms of a deep neuropsychiatric disorder appear, which can lead to an erroneous diagnosis. All these neurological signs in the form of convulsions, meningism, pathological reflexes can change quickly in the interval of several hours.

Hyperglycemic coma (laktatatsidemicheskaya) is typical for patients in the elderly who have concomitant diseases of the lungs, kidneys, liver, heart and chronic alcoholism.

There are several types of hyperglycemic coma (lactatacidemic), namely the first type develops due to hypoxia of tissues. For the second, the pathology of organs and systems is characteristic. The third type is affected by drugs and toxins. The formation of the fourth type of hyperglycemic coma involves violations at the genetic level.

Signs of hyperglycemic coma are associated with the appearance in the body tissues of a patient with lactic acid. As a rule, the symptoms of S.S.N.

Hyperglycemic coma begins quite sharply with the appearance of delirium, phenomena of dyspeptic nature, pain in the heart, resembling angina. Also, there are pains in the muscles and abdomen, imitating surgical pathology. Then the labored breathing with the symptom of Kussmaul grows, collapse, hypothermia and oliguria are noted. The turgor of skin covers decreases with the appearance of a marble-cyanotic shade. At the same time, the skin is cold to the touch, the eyeballs become soft and it is impossible to detect acetonuria. The content of glucose in the blood is insignificant, about 15 mmol / l. As a rule, this form of hyperglycemic coma has an unfavorable prognosis, since it is difficult to diagnose it, therefore it is also problematic to prescribe an adequate treatment.

Hyperglycaemic coma in children

In childhood, hyperglycemic coma is caused by a slow rise in glucose in the blood to almost 13 mmol / l.

Etiological factor of hyperglycemic coma development is mainly considered diabetes mellitus, and untimely treatment and late diagnosis of the disease. According to some experts, in the formation of this pathology, there are violations in the regulation of the neuro-hormonal nature. Other sources argue that the causes of hyperglycaemic coma development in children can be: erroneous prescribing of insulin therapy, that is, an incorrectly prescribed dose of the drug or its replacement by another species to which the child does not have sensitivity; malnutrition; acute forms of intercurrent diseases, especially this refers to purulent infections; pathology of SSS; surgical interventions; shocks of a nervous nature; use in significant doses of corticosteroid drugs. Thus, these factors contribute to increasing the body's need for insulin, and this causes the development of such a pronounced form as insular insufficiency and metabolic syndrome.

On the developmental mechanism, hyperglycemic coma in children is hyperglycemic ketoacidotic, hyperglycemic hyperosmolar without ketoacidosis and lactatacidemic.

For hyperglycemic coma of a ketoacidotic nature, which is the most frequent complication of diabetes mellitus, there is a pronounced insulin deficiency arising from inadequate treatment of the underlying disease or increased insulin requirements as a result of infections, injuries, surgeries, stresses, etc. Almost one third of cases of this form develop in children as a consequence of unrecognized diabetes.

Hyperglycemic coma (ketoacidotic) develops very slowly, for several days. With insufficient amount of insulin in the body, the child's glucose utilization processes are disrupted. And this causes hyperglycemia and glucosuria, which contributes to the formation of ketosis.

Symptomatically, three consecutive stages of hyperglycemic coma are distinguished: mild ketoacidosis, precomatosis and coma.

Sick children with mild ketoacidosis experience symptoms of general weakness, they are listless, quickly tired, constantly want to sleep. Some complain about the appearance of noise in the ears, they are sick and they constantly want to drink, but the appetite is significantly reduced. Sometimes such children experience abdominal pain and frequent urination. From such patients there is a smell of acetone in conversation. In the urine there is a moderate glucosoria and ketone bodies. In the blood - hyperglycemia, ketonemia and a slight decrease in pH.

In the absence of appropriate treatment, mild ketoacidosis passes into a hyperglycemic premo. Thus, the sick child begins to vomit with attacks of frequent vomiting. He is absolutely indifferent to everything around him. Then abdominal pain intensifies and pains in the heart. The child also feels thirsty, often urinates and still remains conscious, but his reaction is a little inhibited. Questions can be answered monosyllabically and indistinctly. Skin covers dry, rough and cold to the touch. On the lips, a cyanotic shade, cracks and crusts appear, and the tongue has a crimson color and a dirty-brown plaque with prints at the edges of the teeth. All tendon reflexes are weakened, and hyperglycemia reaches almost 25 mmol / l. Such a state of prekoma can last as several hours, and several days. But without the provision of medical measures, the coma stage begins.

This stage is characterized by loss of consciousness, a decrease in temperature, dryness and flabbiness of the skin, muscle hypotension, low tone of the eyes, disappearance of reflexes. At the same time the child begins to breathe deeply, rapidly and noisily. There is an extended inhalation and a short exhalation with a sharp smell of acetone or wet apples. This smell will be present in the room of a sick child. In addition, a frequent, small filling of the pulse is felt, AD decreases, especially diastolic, which can lead to collapse. In this situation, when the palpation of the stomach is tense, a little involved and almost does not take part in breathing. Laboratory diagnostics reveals hyperglycemia almost 50 mmol / l, acetonuria and glucosuria. In the blood, ketone bodies, creatine, urea, and sodium, on the contrary, are greatly increased. A leukocytosis with a neutrophil shift is also observed.

Hyperglycemic coma may contribute to the appearance of insufficient kidney function, therefore, ketonuria and glucosuria decrease or completely cease.

Hyperglycemic coma (ketoacidotic) according to A.A. Martynov has four kinds of such stages of precoma, as abdominal, cardiac, renal and encephalopathic.

The clinic of the abdominal form is characterized by the domination of phenomena of a dyspeptic character, abdominal pains and strained abdominal muscles in front. Sometimes there is vomiting of coffee grounds, there is atony of the intestine, all this imitates the "sharp stomach".

For the cardiac form, the symptoms of vessel collapse and heart failure are in the form of cyanosis , tachycardia, inspiratory dyspnea, and heart rhythm disturbances.

Prekomatoznoe state of the kidney form is diagnosed in children diagnosed with diabetic nephropathy, which manifests itself as dysuric phenomena. In rare cases, anuria and arthritis are observed.

Encephalopathic form refers to the most severe in hyperglycemic coma (ketoacidotic), which is characterized by symptoms associated with acute circulatory disturbances in the brain.

Hyperglycemic coma treatment

At the very beginning of treatment of hyperglycemic coma, one of the most important measures is therapy with the use of large doses of simple insulin and the introduction of the necessary amount of NaCl solution and 2.5% of sodium bicarbonate solution.

First of all, a patient in a state of precommission or hyperglycemic coma urgently needs to be delivered to the IT department (intensive care).

The basis of the principles of treatment are such actions as carrying out the processes of cellular rehydration and other spaces; Performing substitution therapy with the introduction of simple insulin; normalization of the main indicators of the acid-base state and the level of electrolytes; prevention of iatrogenic hypoglycemia. And in the presence of diseases of infectious and viral etiology it is necessary to conduct appropriate treatment, to identify and treat other pathologies that contributed to the development of hyperglycemic coma and then prescribe symptomatic treatment.

Tactical methods of treating hyperglycemic coma can be conditionally divided into two fragments. Firstly, it is insulin therapy, and secondly, it is infusion therapy. Typically, three regimens of insulin therapy are used to treat hyperglycemic coma. The first regimen is characterized by a method of continuous intravenous administration in small doses of insulin. For the second mode, a method is typical in which the usual introduction of insulin in small amounts is used. And the third regimen is a method where significant doses of this drug are administered, using fractional administration.

In the first mode, syringes are used for intravenous insulin infusions. To date, this method is universally recognized around the world and its essence is as follows: with a quantitative glucose content of up to 33.3 mmol / L, therapy is started with a continuous intravenous insulin injection, where its rate is 6-10 units per hour, and for large values from this indicator - 12-16 units per hour.

Treatment of hyperglycemic coma is divided into three stages. In the first case, it is necessary to reduce the glucose level to sixteen millimoles per liter. Then they begin to improve the condition of the patient with the ability to take their own food. And the third stage of treatment of hyperglycemic coma is the transition of the patient to the habitual way of life for him.

Insulin therapy is carried out with constant monitoring of the amount of blood glucose at the beginning of treatment every hour, and then after two hours, applying adequate infusion therapy. Provided that the level of glucose within three to four hours does not decrease by thirty percent, then the working dose, applied initially, tries to increase almost twofold. Having reached a glucose content of sixteen millimoles per liter, the insulin dose is reduced to two to four units per hour. And with glycemia at eleven to thirteen millimoles per liter, the drug is administered subcutaneously for four to six units in two to four hours. Subsequently, with glucose values ​​of ten to twelve millimoles per liter, it is not recommended to continue the introduction of insulin to avoid the occurrence of a hypoglycemic condition.

The tactics of infusion therapy for hyperglycemic coma are also divided into three stages. In the first stage of treatment begin to inject intravenously fiz. rr. During the first hour of therapy, an intravenous jet of one liter of this drug is produced and then switched to a half dose. In the future, when the dehydration signs are gradually eliminated, fiz. r-p is introduced already slower, until the glucose level reaches a value of sixteen millimoles per liter.

And in the presence of hypokalemia, they begin to correct it not earlier than two hours from the beginning of treatment with the use of solutions. For this, a solution of potassium chloride is injected intravenously. And for the normalization of KHS, intravenous administration of the sodium bicarbonate solution in the presence of acidosis and pH below seven is indicated. All infusion therapy is controlled by central venous pressure and hourly diuresis.

At the second stage of treatment of hyperglycemic coma, when the patient regains consciousness in order to prevent a possible sharp drop in sugar, proceed to intravenous injection of 5% of Glucose's 200 ml per hour with the addition of insulin (4 units). After that, the patient can drink sweet tea or eat a piece of sugar.

The last stage of this treatment is already being done in a specialized department. Thus put subcutaneous injections of insulin in four hours or six, with the obligatory control of glucose. After each introduction of insulin, the patient should consume food with 50 grams of carbohydrates. Then, the administration of solutions is canceled, and the patient begins to take the food orally. Diet No. 9 is prescribed, in which the intake of fatty foods for the period of the existing acetonuria and after its disappearance is excluded, for another ten days. In addition, for the purpose of preventive measures after removal from the hyperglycemic coma, the patient is assigned a bed rest for seven days.

In some situations, when there are no automatic syringes, proceed to such a method as fractional insulin administration in small doses. All working doses of the drug are similar to the first method of therapy, but here only intravenous jet injection is used every hour.

But for the third method of treatment of hyperglycemic coma is characterized by the introduction of insulin in significant doses, however, to date it is practically not applied. Its essence consists in the introduction of a single dose of insulin 40-60 ED without attention to infusion therapy, so this very often became the cause of lactic acidosis, edema of the brain, a sharp decrease in glucose, which led to a lethal outcome.

Therapeutic treatments for various infectious and inflammatory diseases include the use of a wide range of antibiotics. If in the process of treatment there is a surgical pathology, for example, gangrene of the foot, then an emergency surgical intervention is prescribed. But before the operation, the patient should be taken out of the decompensation state. All identified other diseases that provoked hyperglycemic coma are subject to symptomatic treatment.

Hyperglycemic coma emergency care

Hyperglycemic coma is characterized by slow development for several days. In this case, the increasing amount of glucose in the patient's blood becomes the cause of accumulation of toxic harmful substances in the body, which are formed from the processing of carbohydrates. As a rule, a patient with a diagnosis, for example, diabetes mellitus knows about such a condition as a hyperglycemic coma and can almost always monitor the situation with increasing symptoms. To do this, he excludes from his diet products containing carbohydrates, normalizes the intake of tableted or injected insulin, begins to drink a large amount of liquid.

But in some cases, a hyperglycemic coma may be caused by other causes, for example, after getting an injury, as a consequence of an infectious disease, drinking, during pregnancy or after a stressful situation. In this case, the victim needs emergency care before the arrival of doctors.

First, you need to make sure that this is really a state of hyperglycemic coma, and not signs of another pathology. First of all it is necessary to know that at the beginning of the attack, when the patient is still conscious, he has a weakness, a feeling of sleepiness, he is thirsty, he completely refuses to eat, has lost his appetite, complains of frequent urination and pain in the head, and also breathes heavily. In this case, the patient needs to find out if he takes insulin and, with a positive response, help the victim to enter the necessary dose of the drug, and if possible give the patient a significant amount of fluid to drink. Lay it horizontally and ensure the arrival of fresh air, and after that call for qualified medical care.

With a loss of consciousness, decreased sensitivity of the skin, the appearance of the first signs of convulsions in the form of twitching of the limbs, the fall of blood pressure and a strong odor of acetone from the patient, it is necessary to urgently enter 50-100 units of insulin subcutaneously and as much intravenously. If the victim has stopped breathing or heartbeat is not listened to, then they begin to perform resuscitation measures in the form of indirect heart massage and artificial respiration before the arrival of doctors. It is also necessary to monitor the pulse in order to prevent the death of the patient.

In cases where the victim is found unconscious, quite often there are some difficulties in diagnosing and providing emergency care. In this case, first of all, it is necessary to examine the patient and find out the causes of loss of consciousness. Whether there are hematomas as a result of stroke, wounds, traces from injection injections of preparations, whether there is a smell of acetone, if palpation is determined whether eyeballs are in reduced tone, etc. With the available characteristic signs indicating hyperglycemic coma, it is important to provide first aid. In this case, it is required to provide the patient with a horizontal position with a turn of the head, to prevent the tongue from falling, and also to provide access to the intake of air for free inhalation.

Further emergency care for hyperglycemic coma will already be in the ambulance. In this case, for rehydration intravenously, 0.9% NaCl solution is injected dropwise to one liter, Ringer's solution up to a liter with vitamins B, C. Also inject Co-carboxylase, cardiac glycosides and conduct oxygen therapy. To eliminate acidosis, 4% of hydrochloric acid Na is administered at 300 ml per hour, and also intravenously - 20 ml of Panangin or 10% of KCl solution.