Emergency care for diabetic coma. Coma with diabetes mellitus

What is diabetic coma

Coma (from the Greek Coma - deep sleep) is a state on the verge of life and death, which is characterized by a complete lack of reactions to external stimuli, loss of consciousness and weakening of body functions.

Diabetic coma develops in people diagnosed with diabetes mellitus and this condition is considered an acute and serious complication of this disease. When a coma develops against the background of diabetes mellitus, dangerous changes occur in the body, in particular, the following occurs:

• disruption of internal organs;
• loss of consciousness;
• dysfunction of the brain.

Symptoms of hypoglycemic coma, first aid for hypoglycemic coma

Hypoglycemic conditions are characteristic, for the most part, of type 1 diabetes , although they also occur in patients who take medications in tablets. As a rule, the development of the condition is preceded by a sharp increase in the amount of insulin in the blood . The danger of hypoglycemic coma is damage (irreversible) to the nervous system and brain.

Types of diabetic coma

Diabetic comas can be of two types:

1. Hyperglycemic.
2. Hypoglycemic.

The first type of coma can be caused by a sharp rise in blood glucose levels, usually from 30-35 mmol/liter. In the second case, coma can occur when the blood glucose level drops sharply to 3-3.5 mmol/liter.

Expert opinion

Victoria Khromova

Neurologist, 32 years of experience

It is important that each person with diabetes may have a different dangerous glucose level.

Hyperglycemic coma

There are three subtypes of this comatose state:

• ketoacidotic;
• hypersmolar;
• lactic acidotic.

Ketoacidotic coma develops against the background of diabetic ketoacidosis. To explain it in very simple words, the algorithm for the formation of ketoacidosis is as follows: the human body, with a lack of insulin, is not able to provide cells with glucose and there is a lot of it in the body. The brain begins to “seek resources” to feed the cells from internal sources, which ultimately leads to the production of an increased amount of ketone bodies (ketones) or, simply put, “garbage”. Since the body is sick, ketone bodies cannot be processed quickly, as they do in a healthy body. Naturally, the algorithm for forming such a state is not described in detail, but for a general understanding of what is happening inside, it is enough.

Hypersmolar coma is characterized by the absence of ketoacidosis, and therefore its second name is non-ketoacidotic. It also occurs due to a lack of insulin in the body and, in simple terms, dehydration. In addition, with this type of coma, the level of blood acidity increases.

Lactic acidotic coma (hyperlactic acidemic) - occurs, like the previous two, due to a lack of insulin, but the main factor causing loss of consciousness and other processes accompanying coma is the accumulation of a large amount of lactic acid in the blood, which causes acidosis and loss of consciousness.

Hypoglycemic coma

This type of coma, as mentioned earlier, can occur due to a sharp decrease in the level of glucose in the patient’s blood, which provokes a lack of energy in brain cells and leads to impaired consciousness.

Develops as a result of an overdose of insulin or an excess of counter-insular hormones (taken orally). In the first case we are talking about neuroglycopenia, and in the second case hypercatecholaminemia. In both cases, the external signs of the onset of a diabetic coma are the same, but the precomatose state differs.

Causes and risk factors

The main reason for the development of diabetic coma is a deficiency of insulin in the body of patients suffering from diabetes. This leads not only to an increase in the concentration of glucose in the blood, but also to energy deficiency in peripheral tissues, which are unable to absorb glucose without insulin.

Increasing hyperglycemia leads to an increase in osmotic pressure in the extracellular fluid and intracellular dehydration. As a result, blood osmolarity increases, the severity of hypoglycemia increases, which causes the development of a shock state.

Diabetic coma is a serious pathology that can lead to life-threatening complications.

Insulin deficiency promotes the mobilization of fatty acids from adipose tissue, which causes the formation of ketone bodies (beta-hydroxybutyric acid, acetoacetate, acetone) in liver cells. Excessive production of ketone bodies, which have an acidic reaction, leads to a decrease in the concentration of bicarbonate and, accordingly, the pH level of the blood, that is, metabolic acidosis is formed.

The main cause of diabetic coma is a lack of insulin in the body.

With a rapid increase in hyperglycemia, a rapid increase in the level of blood osmolarity occurs, which leads to a violation of the excretory (excretory) function of the kidneys. As a result, patients develop hypernatremia, further increasing hyperosmolarity. Moreover, the level of bicarbonates and pH remain within normal limits, since there is no ketoacidosis.

As a result of insulin deficiency in diabetes mellitus, the activity of pyruvate dehydrogenase, the enzyme responsible for the conversion of pyruvic acid into acetyl coenzyme A, decreases. This causes the accumulation of pyruvate and its conversion to lactate. Significant accumulation of lactic acid in the body leads to acidosis, which blocks adrenergic receptors of the heart and blood vessels, reducing the contractile function of the myocardium. As a result, severe dysmetabolic and cardiogenic shock develops.

The following factors can lead to diabetic coma:

• gross dietary errors (inclusion of a significant amount of carbohydrates in the diet, especially easily digestible ones);
• violations of the insulin therapy regimen or taking sugar-lowering drugs;
• inadequately selected insulin therapy;
• severe nervous shock;
• infectious diseases;
• surgical interventions;
• pregnancy and childbirth.

Causes of coma in diabetes

Based on the above classification, the causes of coma differ, including:

Ketoacidotic:

• late diagnosis;
• insufficient dose of insulin or discontinuation of the drug;
• the use of low-quality insulin (occurs as a result of improper storage of the medicine or its expiration date);
• violation of the diet prescribed by the doctor (intake of alcohol, fats or easily absorbed fats);
• starvation;
• suicide attempt.

Patients with diabetes mellitus who are in one of the following statuses are at risk:

• pregnant women;
• patients with infectious diseases who accidentally joined a person;
• patients taking diuretics or glucocorticoids for a long time;
• athletes and people with increased nervous tension;
• patients who have undergone injury or surgery.

Hypersmolar:

• Any dehydration (diarrhea, increased urination while taking diuretic medications);
• a large amount of carbohydrates entered into the body with food or an overdose of glucose;
• heavy bleeding;
• concomitant disease (diabetes insipidus);
• hemodialysis.

At risk are patients with diabetes mellitus who are in a state that increases insulin deficiency, including:

• any associated disease;
• injury;
• surgical intervention;
• chronic therapy with insulin antagonists.

Lactic acidotic:

• the presence of an infection in the body or an inflammatory process;
• the formation of hypoxemia (usually due to cardiac or respiratory failure);
• chronic liver or kidney diseases with chronic failure of these organs;
• previous myocardial infarction;
• heavy bleeding;
• taking biguanides (such drugs should be administered to a patient with diabetes mellitus only on the recommendation of a specialist);
• alcoholism in the chronic stage.

Hypoglycemic:

• overdose of insulin or hypoglycemic drugs;
• eating low-carbohydrate foods after an insulin injection, as well as abstaining from eating completely after an injection;
• intense physical activity;
• treatment with glucose-lowering drugs;
• taking salicylates.

These reasons are not the only ones, but the most common.

Types of disease

Depending on the characteristics of metabolic disorders, the following types of diabetic coma are distinguished:

1. Ketoacidotic coma is caused by poisoning of the body and primarily the central nervous system with ketone bodies, as well as increasing disturbances in water-electrolyte balance and acid-base balance.
2. Hyperosmolar hyperglycemic non-ketone coma is a complication of type II diabetes mellitus, characterized by pronounced intracellular dehydration and the absence of ketoacidosis.
3. Hyperlactic acidemic coma. Diabetes mellitus itself rarely leads to the accumulation of lactic acid in the body of patients - as a rule, the cause of lactic acidosis is an overdose of biguanides (hypoglycemic drugs).

Mortality in ketoacidotic coma reaches 10%. With hyperosmolar hyperglycemic non-ketone coma, the mortality rate is about 60%, with hyperlactic acidemic coma – up to 80%.

Signs

Symptoms of coma must be considered differentiated, as is the case with the causes. Just before loss of consciousness there is a stage called precoma. What happens to the human body at the precoma stage in one case or another, we will consider below.

Ketoacidotic:

It develops slowly over 1.5-2 days, but if there is an acute infectious disease in the body or a heart attack, the development will be much faster.

Signs of an approaching coma with this type of disease are as follows:

• general weakness;
• dry mouth;
• thirst;
• weight loss;
• urge to urinate;
• complete loss of appetite;
• dry skin and mucous membranes;
• headache;
• nausea and vomiting.

Hypersmolar coma develops in the same way as the previous one, but much more slowly, over 10-15 days. In addition to the symptoms described, the patient may experience convulsions, paresis, aphasia and nystagmus. There is no smell of acetone from the mouth (in the first case it is present).

Lactic acidotic coma develops faster than its predecessors and can occur within a few hours. It is characterized by the following harbingers:

• muscle pain;
• angina pectoris (sometimes rapid breathing occurs);
• diarrhea;
• nausea;
• vomit;
• drowsiness;
• confusion.

With neuroglypokenia (a subtype of hypoglycemic coma), a person begins to feel hungry, mental and physical activity decreases, and inappropriate behavior may occur. Mood swings and changes in the visual system are possible, which are expressed either in deterioration or improvement of vision.

With hypercatecholaminemia (the second subtype of hypoglycemic coma), a person may develop tremors of the limbs, tachycardia appears, the skin turns pale, blood pressure rises, sweating increases, a feeling of anxiety appears, and nightmares are possible.

Thus, diabetic coma, as well as its symptoms, are very different and must be considered in each specific case separately.

Hypersmolar coma

This type of coma, although it occurs 6-10 times less frequently than DKA, leads to the death of the patient in 50% of cases. Hypersmolar coma is a diabetic coma in which an increase in blood sugar is not accompanied by the production of ketone bodies and acetone, and the coma is caused by sudden and severe dehydration.

During hypersmolar syndrome, the content of electrolytes in the blood increases, osmolarity increases, the glucose content increases sharply - above 30, usually from 40 to 50 (limit) mmol/l, but the blood pH remains normal.

Elderly diabetics with a “long history” of type 2 diabetes mellitus are most often hospitalized with signs of hypersmolar syndrome. However, all non-insulin-dependent diabetics need to be on their guard - in 10% of cases, diabetic coma of the hypersmolar type ends in ketoacidosis coma.

Hypersmolar coma develops over several days or even weeks. The first days are characterized by frequent urination, which is practically absent by the time of hospitalization. Symptoms and signs of this form:

• general malaise,
• dehydration, extreme thirst,
• convulsions, paralysis,
• nystagmus - convulsive frequent movements of the eyeballs,
• speech disorder,
• decrease in the amount of urine.

Diagnostic methods

To make it easier to distinguish one subspecies from another, we recommend using our summary table. When using it, it will be easy to understand what type of coma may occur or has already occurred in the patient.

Hyperglycemic coma

The most dangerous complication of diabetes is hyperglycemic coma. This is a condition in which there is an increase in insulin deficiency in the body and a global decrease in glucose utilization. Coma can develop with any type of diabetes, however, cases of its occurrence with type 2 diabetes are extremely rare. Most often, diabetic coma is a consequence of type 1 diabetes - insulin-dependent.

Causes

There are several reasons for the development of coma:

• undetected diabetes mellitus;
• improper treatment;
• untimely administration of a dose of insulin or administration of an insufficient dose;
• diet violation;
• taking certain medications, such as prednisolone or diuretics.

In addition, several external factors can be identified that can trigger the mechanism of coma - various infections suffered by patients with diabetes, surgical interventions, stress, mental trauma. This is due to the fact that during inflammatory processes in the body or an increase in mental stress, insulin consumption increases sharply, which is not always taken into account when calculating the required dose of insulin.

Expert opinion

Guseva Yulia Alexandrova

Specialized endocrinologist

Even switching from one type of insulin to another can provoke a hyperglycemic coma, so it is better to replace it under supervision and closely monitor the body’s condition for some time. And under no circumstances should you use frozen or expired insulin!

Pregnancy and childbirth are also factors that can provoke such a crisis. If a pregnant woman has a latent form of diabetes, which even she herself is not aware of, coma can cause the death of both mother and child. If the diagnosis of “diabetes mellitus” was made before pregnancy, you must carefully monitor your condition, report any symptoms to your gynecologist and monitor your blood sugar levels.

For patients with type 2 diabetes mellitus, a complication, hyperglycemic coma, can be triggered by diseases associated with the functioning of the pancreas, for example, pancreatic necrosis. This leads to the fact that insulin, already produced in insufficient quantities, becomes even less - as a result, a crisis may develop.

Risk group

Crisis is the most formidable, but not always developing complication. Risk groups include patients with chronic diseases, those who have undergone surgery, and pregnant women.

The risk of developing hyperglycemic coma is significantly increased in those who are prone to violating the prescribed diet or unreasonably underestimating the dose of administered insulin. Drinking alcohol can also trigger the development of coma.

It has been noted that hyperglycemic coma rarely develops in elderly patients, as well as in those who are overweight. Most often, this complication manifests itself in children (usually due to a gross violation of the diet, which often even parents are not aware of) or in patients at a young age and with a short duration of the disease. Almost 30% of diabetic patients experience symptoms of precoma.

Symptoms of an incipient coma

Hyperglycemic coma develops over several hours, and sometimes even days. Signs of an oncoming coma gradually increase. The first symptoms are:

• unbearable thirst, dry mouth;
• polyuria;
• nausea, vomiting;
• skin itching;
• general signs of intoxication of the body are weakness, increasing headache, fatigue.

If you have at least one sign, immediately check your blood sugar level. In a state close to coma, it can reach 33 mmol/l and higher. The worst thing about this condition is to confuse it with ordinary food poisoning, without in any way connecting it with hyperglycemia. This leads to the fact that the time necessary to take measures to prevent the development of coma is lost and the crisis develops.

If no measures are taken to introduce an additional dose of insulin, the symptoms change somewhat, precoma begins: instead of polyuria - anuria, vomiting intensifies, becomes repeated, but does not bring relief. The smell of acetone appears from the mouth. Pain in the abdomen can be of varying degrees of intensity - from acute pain to aching. Either diarrhea or constipation develops and the patient will need help.

The last stage before coma is characterized by confusion, the skin becomes dry and cold, flaky, and body temperature is below normal. The tone of the eyeballs decreases - when pressed, they feel soft, skin turgor is reduced. Tachycardia is present, blood pressure drops.

Kussmaul's noisy breathing is characterized by rhythmic, rare respiratory cycles with noisy deep inhalation and sharp, intense exhalation. Smell of acetone on breath. The tongue is dry, covered with a brown coating. After this, a true coma sets in - the person loses consciousness and does not respond to external stimuli.

The rate of development of hyperglycemic coma is always individual. Typically, precoma lasts 2–3 days. If the necessary medical care is not provided in a hospital setting, death occurs within 24 hours after the onset of coma.

Diabetic crisis - mechanisms

The main point in the development of coma is a violation of cellular metabolism as a result of excess glucose levels in the blood plasma.

High levels of glucose combined with a lack of insulin lead to the fact that the body's cells cannot use the energy of breaking down glucose and experience “energy” starvation. To prevent this, the cell's metabolism changes - from glucose it switches to a glucose-free method of energy production, or, more precisely, the breakdown of proteins and fats into glucose begins. This contributes to the accumulation of a large number of breakdown products, one of which is ketone bodies. They are quite toxic and at the precoma stage their presence causes a feeling akin to euphoria, and with their further accumulation - poisoning of the body, depression of the central nervous system and brain. The higher the level of hyperglycemia and the more ketone bodies, the stronger their effect on the body and the consequences of the coma itself.

Modern pharmacies offer test strips for determining ketone bodies in urine. It makes sense to use them if the blood glucose level exceeds 13–15 mmol/l, as well as for diseases that can provoke the onset of coma. Some blood glucose meters also have a ketone detection feature.

Emergency care for diabetic coma

If there are signs of an approaching coma, it is necessary to administer short-acting insulin subcutaneously - every 2-3 hours, depending on the level of glucose in the blood, monitoring the sugar level every 2 hours. Carbohydrate intake should be strictly limited. Be sure to take potassium and magnesium supplements and drink alkaline mineral waters - this will prevent hyperacidosis.

If, after a double injection of insulin, the symptoms do not go away, and the condition does not stabilize or worsen, it is necessary to urgently seek medical help. Seeing a doctor is necessary even if a pen insulin syringe was used and this allowed the situation to stabilize. A specialist will help you understand the reasons that provoked the complication and prescribe adequate treatment.

If the patient’s condition is serious and close to fainting, emergency assistance is needed. It is possible to bring a patient out of a comatose state with minimal consequences for the body only in a clinical setting.

Before the ambulance arrives, you can provide first aid:

• put the patient on his side to prevent choking on vomit and tongue sticking;
• cover warmly or cover with heating pads;
• control pulse and breathing;
• if breathing or heartbeat stops, begin resuscitation measures - artificial respiration or cardiac massage.

Three categorical “DON’Ts” when providing first aid!

Expert opinion

Guseva Yulia Alexandrova

Specialized endocrinologist

1. The patient should not be left alone.
2. You cannot prevent him from administering insulin, regarding this as inappropriate actions.
3. You cannot refuse to call an ambulance, even if your condition has stabilized.

Prevention of hyperglycemic coma

In order not to bring the body to such severe conditions as coma, you must adhere to simple rules: always follow a diet, constantly monitor blood glucose levels, and administer insulin in a timely manner.

Expert opinion

Guseva Yulia Alexandrova

Specialized endocrinologist

Be sure to pay attention to the expiration date of insulin. You cannot use expired ones!

It is better to avoid stress and heavy physical activity. Treat any infectious disease.

Parents of children diagnosed with type 1 diabetes need to pay great attention to monitoring their diet. Quite often, a child breaks his diet secretly from his parents - it is better to explain in advance all the consequences of such behavior.

Healthy people need to periodically check their blood sugar levels; if they deviate from the norm, be sure to contact an endocrinologist.

Rehabilitation after coma or precoma

After such severe complications as comatose states, great attention must be paid to the rehabilitation period. When the patient leaves the hospital ward, all conditions must be created for his full recovery.

First, follow all doctor's instructions. This applies to nutrition and lifestyle. If necessary, give up bad habits.

Secondly, to compensate for the lack of vitamins, micro- and macroelements lost during complications. Take vitamin complexes, pay attention not only to the quantity, but also to the quality of food.

And lastly, don’t give up, don’t give up and try to enjoy every day. After all, diabetes is not a death sentence, it’s just a way of life.

Source: diabeteshelp.org

Urgent Care

In order to correctly provide the necessary first aid, the first rule is to assess the situation that led to a loss of consciousness in a person or to the onset of a precomatose state, so as not to begin providing first aid for hypoglycemia to a patient who has fallen into a ketoacidotic coma.

Once you have determined what kind of coma (precoma) the patient has, you can proceed to action. Regardless of the type of coma, the first thing you need to do is call an ambulance and explain to them in detail what happened and clarify about diabetes.

Ketoacidotic:

1. Laying the patient on his side will prevent vomit from entering the respiratory tract if vomiting begins.
2. Monitor your heart rate and blood pressure to inform the emergency team of your observations.
3. If the patient has acetone odor from the mouth, 5 units of short-acting insulin can be administered once.

For hyperosmolar coma, the algorithm of actions is the same as for the previous one, plus we recommend wrapping the patient up. In addition, it is necessary to measure your blood sugar level and, if it is too high, inject short-acting insulin. In addition, in the case when loved ones are able to put a drip on the patient, it is recommended to administer saline solution into the body at a rate of one drop per minute.

For hyperlactic acidemic coma, the algorithm of actions is the same as for the previous two.

First aid for hypoglycemic coma differs from the previous ones in that the patient must be given a piece of sugar to dissolve or fed with food containing easily digestible carbohydrates (cookies, white bread).

If the patient is in a faint or near-fainting state, it is necessary to give him warm sweet tea or water. Lay him on his side and, if possible, inject 1 ml of glucagon intramuscularly.

Expert opinion

Sergey Velichko

Neurologist, 21 years of experience

It is important that if the patient has already lost consciousness, do not force liquid into him, he may choke.

Ketoacidotic coma - first aid

First of all, you should call an ambulance and check all the patient’s vital functions - breathing, blood pressure, heartbeat, consciousness. The main task is to maintain heartbeat and breathing until the ambulance arrives. assess whether a person is conscious in a simple way: ask him a question, lightly hit him on the cheeks and rub his earlobes. If there is no reaction, the person is in serious danger. Therefore, you cannot hesitate to call an ambulance.

Coma in childhood

A child, like an elderly person, can fall into a diabetic coma and the worst thing in this situation is that in most cases this happens due to an incorrect diagnosis and receiving the wrong treatment that is required.

Thus, a precomatose state in a child is often mistaken for signs of an infectious disease or meningitis, and therefore the baby is treated for these diseases.

A characteristic feature of diagnosing abnormalities in infants is due to the fact that there are no ketane bodies in their urine, which causes certain difficulties. All other manifestations are the same as in adults.

Prevention of coma in diabetes

Complications of diabetes, coma in particular, can be very dangerous. That is why it is better to monitor your own condition and follow some precautionary rules:

• you need to follow the diet prescribed by your doctor and follow a diet;
• the patient is obliged to regularly go to the doctor for examinations and undergo tests;
• Self-control and compliance with safety rules are important (the patient must have a glucometer with him and regularly measure blood sugar levels);
• An active lifestyle, frequent walks in the fresh air, and feasible physical activity are recommended;
• it is very important to follow precise recommendations and observe the dosages of insulin and other medications;
• Under no circumstances should you self-medicate or use any traditional medicine without first consulting your treating endocrinologist.

Compliance with such simple rules in most cases helps prevent the development of complications, including the onset of coma. If any alarming changes occur, you should immediately consult a doctor.

Prognosis and prevention

Of course, a diabetic patient must adhere to the recommendations that the doctor gave him and we are sure that this phrase has already set the teeth on edge in such patients, but the rules given below will help prevent severe diabetes and for whom:

1. Stick to the diet that your doctor has chosen for you.
2. Do not lead a sedentary lifestyle, but also do not overwork - physical activity should be in moderation.
3. Drink at least 1.5 liters of water, not counting tea, juices and other liquids.
4. Control your weight.
5. Avoid starvation; the body must be well-fed (frequent meals in small portions).
6. Monitor your blood glucose levels throughout the day.
7. Do not skip insulin injections or change the dosage under any circumstances.
8. Be attentive to your health and treat all emerging diseases.

So, diabetic coma is a serious and dangerous condition of a diabetic patient, which can lead to irreversible consequences in the body and even death. Do not neglect your doctor's recommendations. Take care of yourself!

Diagnostics

The clinical picture of diabetic coma is not always clear. Laboratory testing is of decisive importance in its diagnosis, determining:

• glycemic level;
• the presence of ketone bodies in blood plasma;
• arterial blood pH;
• concentration of electrolytes in plasma, primarily sodium and potassium;
• plasma osmolarity value;
• fatty acid levels;
• the presence or absence of acetone in the urine;
• concentration of lactic acid in blood serum.

The main reason for the development of diabetic coma is a deficiency of insulin in the body of patients suffering from diabetes.

Hyperlactic acidemic coma

This acute complication is caused by a sharp increase in lactic acid levels in the blood. Contribute to the development of lactic acidosis:

• infectious and inflammatory diseases;
• massive bleeding;
• acute myocardial infarction;
• chronic alcoholism;
• severe physical injuries;
• chronic liver diseases;
• insufficiency of kidney function.

A special place among the etiological factors is occupied by the intake of biguanides. It should be emphasized that with liver or kidney damage, even a minimal dose of biguanides can cause lactic acidosis as a result of accumulation of the drug in the body.

Pathogenesis

The pathogenesis of lactic acidosis is based on hypoxia. Under conditions of oxygen deficiency, the anaerobic pathway of glycolysis is activated, which is accompanied by the accumulation of excess lactic acid. Its mechanism is as follows: insulin deficiency leads to the fact that pyruvic acid does not turn into acetyl-coenzyme-A, as it should be, but into lactate; under hypoxic conditions, the resynthesis of lactate into glycogen is inhibited.

The pathogenesis of hyperlactic acidemia during treatment with biguanides is associated with disruption of the passage of pyruvic acid through mitochondrial membranes and acceleration of the conversion of pyruvate to lactate. As a result of anaerobic glycolysis, a lot of lactic acid is formed in the tissues, which enters the blood. From the blood, lactic acid penetrates into the liver, where glycogen is formed from it. But the formation of lactic acid exceeds the ability of the liver to use it for glycogen synthesis.

Clinical signs

Clinical signs are caused by a violation of acid-base balance. The leading syndrome is progressive cardiovascular failure.

The development of coma is very rapid, but the precursors can be digestive disorders, muscle pain, and angina pain. As acidosis increases, abdominal pain increases, simulating surgical diseases. Shortness of breath increases, collapse develops, and Kussmaul breathing occurs. Consciousness is impaired (stupor and coma) due to hypotension and brain hypoxia.

Diagnostics

Making a diagnosis of lactic acidotic coma is very difficult. Acute onset, dysleptic disorders, pain in the heart area in a patient with diabetes mellitus with liver and kidney damage can serve as an auxiliary test in diagnosing this life-threatening condition.

Laboratory diagnostic criteria include:

• increase in lactic acid content in the blood (more than 1.5 mmol/l);
• decrease in blood bicarbonates (below 2 mmol/l);
• reduction of reserve alkalinity (below 50%);
• moderate hyperglycemia (12-14-16 mmol/l) or normoglycemia;
• absence of acetonuria;
• the degree of glucosuria depends on the functional state of the kidneys.

Urgent Care

Emergency care is aimed primarily at eliminating acidosis and combating hypoxia.

Prevention of hyperlactic acidemic coma consists of preventing hypoxia and an individual approach in prescribing biguanides to patients with diabetes mellitus.

Source happydoctor.ru

Hypoglycemic coma

Hypoglycemic coma is an acutely occurring pathological condition, manifested by the reaction of the nervous system in a certain sequence (cerebral cortex → cerebellum → subcortical-diencephalic structures → vital centers of the medulla oblongata), associated with a fall or sharp change in the level of glycemia (carbohydrate concentration in the blood plasma). Coma develops acutely. Sometimes the short-term period of precursors is so small that the coma begins almost suddenly - within a few minutes, loss of consciousness occurs and even paralysis of the vital centers of the medulla oblongata.

Thus, hypoglycemic coma is an extreme degree of hypoglycemia that develops with a rapid decrease in the concentration of glucose in the blood plasma and a sharp drop in glucose utilization by the brain (most often the result of a mismatch in the dose of administered insulin or, much less frequently, sulfonamide drugs and incoming food). The symptoms of hypoglycemia, which precedes the stage of hypoglycemic coma, are very diverse and are caused by two main mechanisms:

* decrease in glucose content in the brain (neuroglycopenia) - characterized by various behavioral disorders, neurological manifestations, impairment and loss of consciousness, convulsions and, finally, coma; * reactions associated with excitation of the sympathetic-adrenal system - characterized by a variety of autonomic disorders, tachycardia, vasospasm, pilomotor reaction, sweating, a feeling of tension, anxiety, fear.

Symptoms of Hypoglycemic Coma:

As a rule, it develops suddenly. With mild initial hypoglycemia, the patient experiences a feeling of heat, trembling of the hands and the whole body, sometimes headache, hunger, increased sweating, a feeling of palpitations, and general weakness. The initial symptoms of hypoglycemia are usually easily eliminated by timely intake of carbohydrates - all persons receiving insulin therapy should carry glucose tablets (sugar cubes, candy, juice) with them in case of hypoglycemia and use them promptly.

When treated with long-acting insulin preparations (peak action is in the evening and night hours), hypoglycemic reactions are possible in the afternoon and at night. If severe hypoglycemia develops at night, during sleep, it can go unnoticed for a long time. Sleep becomes superficial, anxious, and nightmares are frequent. During sleep, children cry and scream, and upon awakening, confusion and retrograde amnesia are noted. After such nights, patients remain lethargic, moody, irritable, gloomy and apathetic throughout the day. In the morning, patients complain of fatigue, some of them complain of nightmares. Glycemia in the morning on an empty stomach may be high (“reactive” glycemia to an overnight drop in blood sugar).

A patient in a hypoglycemic coma is pale, the skin is moist, tachycardia is noted, breathing is smooth, the turgor of the eyeballs is normal, the tongue is moist, there is no smell of acetone, and muscle tone is increased. If help is not provided, as the hypoglycemic coma deepens, breathing becomes shallow, blood pressure decreases, bradycardia, hypothermia are noted, muscle atonia, hypo- and areflexia develop. There is no reaction of the pupils to light and no corneal reflexes.

If the initial period of hypoglycemia remains unrecognized, the patient’s condition sharply worsens - convulsions of various muscle groups appear, trismus, general agitation, vomiting, depression of consciousness develops and hypoglycemic coma develops. Glucose in urine is usually not determined; the reaction of urine to acetone can be positive or negative, depending on the previous degree of compensation of carbohydrate metabolism.

Hypoglycemia can also develop against the background of decompensated labile diabetes mellitus with ketoacidosis. In response to hypoglycemia, the release of counterinsular hormones compensatory increases, which contributes to the occurrence of ketoacidosis, decompensation of diabetes mellitus, impaired vascular tone (pressor effect of catecholamines), and the development of thromboembolic complications.

In long-term ill people with chronic hyperglycemia, symptoms of hypoglycemia can be observed at normal glycemic levels, in the absence of an absolute decrease in glucose levels (at 3.3...6.6 mmol/l, and sometimes higher). Such conditions often occur with significant, rapid changes in glycemic levels (for example, a rapid decrease from 18...19 mmol/l to 7...8 mmol/l).

Causes of hypoglycemic coma:

Hypoglycemic coma develops in patients with diabetes mellitus, in most cases, when there is a mismatch between the dose of administered insulin or sulfonylurea drugs and the incoming food, especially carbohydrates. In diabetes mellitus, hypoglycemic coma develops much more often than ketoacidotic coma.

Typically, hypoglycemia and hypoglycemic comas occur in patients with severe, extremely labile forms of insulin-dependent diabetes mellitus, in which it is impossible to determine the external cause of the sudden increase in insulin sensitivity. In other cases, provoking moments are long breaks between meals, increased physical activity, vomiting, diarrhea and other pathological conditions. Impairments in the function of the liver, intestines, endocrine status that accompany diabetes mellitus, and the development of renal failure can lead to severe hypoglycemia. More often, hypoglycemic coma develops with excessive administration of insulin, which can occur in the following cases:

* dosage error (concentration of the insulin drug, for example, with U100 syringes instead of U40, that is, 2.5 times more than prescribed, or an incorrect dose of insulin in the syringe), * error in administering the drug (not under the skin, but intramuscularly) - a long needle, or deliberate intramuscular injection in order to accelerate and enhance the effect of the hormone, * failure to take carbohydrates after administering a dose of short-acting insulin (“forgot to have a snack” - second breakfast, afternoon snack or second dinner at the peak of the action of the short-acting insulin drug), * “unscheduled” physical activity due to lack of additional intake of carbohydrates: injected insulin → “forgot” to eat (did not eat additional carbohydrates to ensure unusual physical activity) → went on a bike ride [skiing, playing football, swimming pool, skating rink, etc.] → hypoglycemia → coma, * massaging the injection site insulin (intentional - in order to speed up the action of a short-acting insulin drug or accidental - while cycling, an injection of insulin made into the thigh), * release of a large amount of active hormone when the insulin-antibody complex is broken, * against the background of alcohol intake, * in the presence fatty liver, * against the background of chronic renal failure, * in early pregnancy, * suicidal actions, * insulin shocks in psychiatric practice, and so on.

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In people with diabetes mellitus, hypoglycemic coma can result from an overdose of insulin, in particular when the patient is brought out of a state of ketoacidosis.

The development of a severe hypoglycemic reaction is possible against the background of alcohol intake, the hypoglycemic effect of which is practically ignored, taking into account only the carbohydrates in the composition of alcoholic beverages when preparing a diet). Alcohol inhibits the synthesis of glucose from non-carbohydrate raw materials in the liver, thereby increasing the frequency of hypoglycemia in patients on insulin therapy. The more alcohol you drink, the longer the inhibition of gluconeogenesis, so hypoglycemia can occur even several hours after drinking alcohol.

A low blood glucose concentration is recorded if:

* glucose is eliminated from the blood at a faster rate than it is absorbed in the intestines or synthesized by the liver, * the breakdown of glycogen and/or the synthesis of glucose from non-carbohydrate raw materials in the liver cannot compensate for the rate of glucose elimination, * the above factors are combined.

Often, the onset of compensation for diabetes mellitus increases the sensitivity of peripheral tissues to insulin, which requires a timely reduction in the dose of externally administered hormone.

Sulfonamide drugs can extremely rarely cause hypoglycemic reactions; they can mainly occur in elderly patients with a combination of diabetes mellitus with kidney disease, liver disease or heart failure, as well as during fasting or malnutrition. The use of certain medications in combination with sulfonamides can provoke the development of a coma. For example, acetylsalicylic acid and other salicylates, by reducing the binding of sulfonamides to plasma proteins and reducing their excretion in the urine, create conditions for the development of a hypoglycemic reaction.