Symptoms and signs of diabetic coma: consequences of pathology

Diabetes mellitus is a serious disease in which almost all metabolic processes in the body are disrupted, which leads to malfunctions of various organs and systems.

One of the most serious complications of diabetes can be diabetic coma. The consequences of coma due to diabetes mellitus can be fatal for the victim if urgent medical assistance is not provided in time.

Types of diabetic coma

There are several types of comas in diabetes, this is due to the fact that the hormonal imbalance that occurs as a result of this disease affects many processes in the body and, depending on the preponderance of compensatory mechanisms in one direction or another, a diabetic may experience a coma:

• Ketoacidotic;
• Hyperosmolar;
• Lactacidemic;
• Hypoglycemic.

Such a variety of types of comas characterizes the severity of diabetes mellitus, in the absence or incomplete treatment of it. All of the above comas are acute complications of diabetes mellitus, but some of them require a fairly long time interval to develop. Let's take a closer look at each condition and its consequences for the patient's body.

Early symptoms of diabetic coma can be suspected by testing blood sugar

Therapy methods

A person in a state of hypoglycemic coma needs urgent hospitalization and must remain in hospital until his health condition is stabilized. Assistance for hypoglycemic coma should be carried out by an experienced specialist! Treatment consists of a series of measures related to intensive care. First of all, blood hypoglycemia is stopped, then the patient is given special auxiliary measures aimed at maintaining the cardiovascular and respiratory systems. Metabolic disorders are corrected. Only after all of the above measures can the development of hypoglycemic coma be eliminated.

Ketoacidotic

This type of coma, despite the severity of the condition, develops quite slowly and is associated with decompensation of metabolic processes in the diabetic’s body. A ketoacidotic state can occur with relative or absolute insulin deficiency. What is ketoacidosis?

The term diabetic ketoacidosis refers to a metabolic disorder that results in excessive accumulation of glucose and ketone bodies in the blood plasma. This occurs due to an insufficient amount of insulin in the blood, which is a kind of key for the penetration of glucose into the body's cells.

Mechanism of development of ketoacidotic coma

As a result of a violation of carbohydrate metabolism, cells begin to experience an energy deficit (sugar is all in the blood), due to which the process of lipolysis is activated - the breakdown of fats. The metabolism of fatty acids accelerates, which leads to the formation of an increased number of metabolic products of lipid metabolism - ketone bodies. Normally, ketone bodies are excreted from the body through the urinary system with urine, but the rapid increase in the concentration of ketone bodies in the blood cannot be compensated by the work of the kidneys, which leads to the development of ketoacidotic coma.

There are 3 successive stages of development of ketoacidotic coma:

• Moderate ketoacidosis may last several weeks. Symptoms are mild.
• Decompensation of ketoacidosis, symptoms of ketoacidosis begin to increase.
• Actually a coma.

Symptoms and consequences

Ketoacidotic state is a consequence of long-term decompensation of diabetes mellitus. The clinical picture during the development of such a coma is of a peculiar nature and consists in the development of symptoms such as:

• Severe weakness and exhaustion.
• Strong thirst and large volume of urine excreted.
• Drowsiness, loss of appetite, nausea.
• Smell of acetone on breath.
• Blush on the cheeks.

Patients have a high level of glycemia in their blood – more than 16 mmol/l; ketonemia more than 0.7 mmol/l; up to 50 g of sugar is detected in the urine.

Ketoacidotic coma requires immediate treatment, otherwise it can lead to permanent loss of all types of reflex activity and deep damage to the central nervous system.

Possible complications

The development of hypoglycemic coma can lead to severe dysmetabolic disorders that can damage most organs and systems. With the development of hypoglycemic coma, the removal of acetone from the body is impaired. The accumulation of acetone in the blood leads to intoxication of the body. The most serious complications are associated with inhibition of the vasomotor and respiratory centers of the medulla oblongata. With the development of deep coma, death is possible due to cardiovascular and respiratory failure.

Hyperosmolar

Hyperosmolar coma, or otherwise called hyperglycemic coma, is the result of a significant increase in the concentration of glucose in the patient’s blood. Hyperosmolar coma is an extreme degree of disturbance of carbohydrate metabolism, in which there is an increase in osmotic pressure in the liquid part of the blood - plasma, which leads to a disruption of the rheological (physical and chemical) properties of the blood and the activity of all organs. In hyperglycemic coma, there may be an increase in blood sugar of more than 30 mmol/l when the norm is no more than 6 mmol/l.

Symptoms

The victim experiences severe dehydration, up to dehydration shock. Often, before the development of hyperosmolar coma, the patient does not know at all that he has diabetes. This type of coma most often develops in people over 50 years of age against the background of latent type 2 diabetes mellitus, i.e. insulin-resistant. It develops hyperglycemic gradually, and accordingly, the symptoms increase slowly. Main symptoms:

• General weakness;
• Dry mucous membranes and thirst;
• Drowsiness;
• Increased urination;
• Decreased elasticity of the skin;
• Dyspnea.

Symptoms may not be noticed immediately, especially in men who tend to hide their problems.

Consequences

If hyperglycemic coma is not corrected in a timely manner, brain damage may occur with the addition of persistent functional disorders of any organs. Mortality in hyperosmolar coma reaches 50% and depends on the promptness of identifying this condition and the initiation of treatment measures.

Causes

The likelihood of developing a coma due to progressive ketoacidosis increases in the following cases:

• Errors in insulin therapy.
• Increased need for insulin in pregnant women, during surgical operations, the prescription of certain drugs (glucocorticosteroids, diuretics, etc.), physical activity, and stressful situations.
• Excessive intake of easily digestible carbohydrates and fats from food in case of severe dietary violations [4, 7].

Lactacidemic

Lactic acid coma is also called lactic acid coma and develops more often than other types of emergency conditions in diabetes. Lactic acid coma is the most dangerous acute condition, with mortality reaching 75%. This condition can develop against the background of provoking conditions:

• Massive bleeding;
• Myocardial infarction;
• Generalized infectious process;
• Heavy physical activity;
• Kidney or liver failure.

As a result of lactic acidemia, ketone bodies and pyruvic acid are broken down in the blood with the formation of an increase in the concentration of lactate and a decrease in pyruvate - chemicals that shift the acid-base balance of the blood to the acidic side. In 30% of victims, hyperosmolar coma is initially noted.

Clinical picture

The condition of patients is rapidly deteriorating, and negative dynamics are observed. The onset is usually sudden, with severe development of symptoms. Diabetics note:

• Severe muscle pain and weakness;
• Drowsiness or, conversely, insomnia;
• Severe shortness of breath;
• Abdominal pain with vomiting.

With further deterioration of the condition, convulsions or areflexia associated with muscle paresis may occur. These symptoms arise as a result of brain damage due to energy deficiency and disturbances in the ionic composition of the plasma. Even with proper and timely treatment, the prognosis for a victim of lactic acidemia coma is unfavorable.

Clinical picture and symptoms

The symptoms of hypoglycemic coma are well studied and include a number of characteristic features. Knowing the symptoms of hypoglycemic coma can save the life of the victim. It is worth noting. That symptoms develop in proportion to the depression of brain functions as a result of trophic insufficiency. Its characteristic symptoms include:

• Trembling of arms and hands. Subsequently, trembling of the lower extremities and the whole body occurs.
• Rapidly increasing feeling of hunger.
• A person is worried about fever, sweating of the extremities increases. And then the whole body.
• General weakness increases.
• The number of heart contractions increases, the patient is bothered by palpitations.

In the absence of help, the victim’s condition begins to deteriorate, and the above symptoms begin to change. More serious violations occur:

• Paleness of the skin.
• Cramps.
• Bradycardia is a decrease in the number of heartbeats and hypotension is a decrease in blood pressure.
• Hypothermia.
• Depression of consciousness.

Symptoms develop sequentially, as described above, and can often be used to determine the severity of the pathological condition.

Hypoglycemic

The most common type of coma that occurs as a result of a sharp decrease in blood glucose. Hypoglycemic coma develops quickly and more often affects patients with type 1 diabetes mellitus when the insulin dosage is incorrect or when physical activity is too high.

A decrease in blood sugar occurs when there is an inadequate concentration of insulin in the blood, which leads to the transfer of all glucose from the plasma into the cells. First of all, the nervous tissue of the brain begins to suffer from a lack of glucose, which characterizes the clinic of this condition.

Symptoms

Hypoglycemic coma is accompanied by a sequential development of symptoms:

• A sudden feeling of hunger;
• Rapid increase in weakness and drowsiness;
• Numbness of the limbs;
• The appearance of trembling and cold, sticky sweat;
• Loss of consciousness.
• Rare breathing.

Consequences

With the rapid provision of emergency assistance, which involves the administration of a 40% glucose solution intravenously, the hypoglycemic coma is quickly stopped, and the victim’s condition returns to normal. If there is no one near the victim and hypoglycemia develops, then the victim may develop severe disturbances in the functioning of the central nervous system, including dementia and loss of some functions.

Based on the information received, the conclusion suggests itself - you should not risk your health by neglecting the treatment of diabetes. The consequences of a diabetic coma can be very diverse, from mild temporary disability. To the point of severe disability and death. So be careful about your health, get examined on time and follow the recommendations of your doctor.

Acute complications of diabetes mellitus in the practice of an emergency physician

Acute complications of diabetes mellitus are life-threatening conditions caused by significant changes in blood sugar levels and associated metabolic disorders.

Acute complications of diabetes mellitus:

• hyperglycemic comas - ketoacidotic, hyperosmolar;
• hypoglycemic coma.

Diabetic ketoacidosis and non-ketonic hyperosmolar coma are characterized by varying degrees of insulin deficiency, excess production of counter-insulin hormones and dehydration. In some cases, signs of diabetic ketoacidosis and hyperosmolar coma may develop simultaneously.

Hypoglycemia is caused by an imbalance between the medicine used to treat diabetes (insulin or blood glucose-lowering tablets) and food intake or exercise.

The speed and timeliness of providing care to comatose patients largely determine the prognosis. Therefore, proper management of patients at the prehospital stage is very important.

In the structure of comas at the prehospital stage, hypoglycemic coma ranks third (5.4%), and diabetic coma (3%) ranks fifth (data from the NNPOSMP).

Diabetic ketoacidotic coma (DKA)

DKA is a very serious complication of diabetes mellitus, characterized by metabolic acidosis (pH less than 7.35 or bicarbonate concentration less than 15 mmol/L), increased anion gap, hyperglycemia above 14 mmol/L, and ketonemia. More often develops in type 1 diabetes. DKA accounts for 5 to 20 cases per 1000 patients per year (2/100). The mortality rate is 5-15%, for patients over 60 years old - 20%. More than 16% of patients with type 1 diabetes die from ketoacidotic coma. The cause of the development of DKA is an absolute or pronounced relative deficiency of insulin due to inadequate insulin therapy or an increased need for insulin.

Provoking factors: insufficient dose of insulin or skipping an insulin injection (or taking tableted glucose-lowering drugs), unauthorized cancellation of glucose-lowering therapy, violation of insulin administration technique, addition of other diseases (infections, trauma, surgery, pregnancy, myocardial infarction, stroke, stress, etc.) , dietary disorders (too many carbohydrates), physical activity with high glycemia, alcohol abuse, insufficient self-monitoring of metabolism, taking certain medications (corticosteroids, calcitonin, saluretics, acetazolamide, β-blockers, diltiazem, isoniazid, diphenin, etc. ).

Often the etiology of DKA remains unknown. It should be remembered that in approximately 25% of cases, DKA occurs in patients with newly diagnosed diabetes mellitus.

There are three stages of diabetic ketoacidosis: moderate ketoacidosis, precoma, or decompensated ketoacidosis, coma.

Complications of ketoacidotic coma include deep vein thrombosis, pulmonary embolism, arterial thrombosis (myocardial infarction, cerebral infarction, necrosis), aspiration pneumonia, cerebral edema, pulmonary edema, infections, rarely - gastrointestinal tract and ischemic colitis, erosive gastritis, late hypoglycemia. Severe respiratory failure, oliguria and renal failure are noted. Complications of therapy include cerebral and pulmonary edema, hypoglycemia, hypokalemia, hyponatremia, hypophosphatemia.

Diagnostic criteria for DKA

• The peculiarity of DKA is its gradual development, usually over several days.
• The presence of symptoms of ketoacidosis (the smell of acetone in the exhaled air, Kussmaul breathing, nausea, vomiting, anorexia, abdominal pain).
• The presence of symptoms of dehydration (decreased tissue turgor, tone of the eyeballs, muscle tone, tendon reflexes, body temperature and blood pressure).

When diagnosing DKA at the prehospital stage, it is necessary to find out whether the patient suffers from diabetes mellitus, whether there is a history of DKA, whether the patient is receiving glucose-lowering therapy, and if so, what kind, when was the last drug taken, the time of the last meal, whether excessive physical activity or alcohol intake, what recent diseases preceded the coma, whether there was polyuria, polydipsia and weakness.

Prehospital treatment of DKA (see Table 1) requires special attention to avoid errors.

Possible errors in therapy and diagnosis at the prehospital stage

• Prehospital insulin therapy without glycemic control.
• The emphasis in treatment is on intensive insulin therapy in the absence of effective rehydration.
• Insufficient volume of fluids administered.
• Administration of hypotonic solutions, especially at the beginning of treatment.
• Use of forced diuresis instead of rehydration. The use of diuretics simultaneously with the administration of fluids will only slow down the restoration of water balance, and in hyperosmolar coma, the use of diuretics is strictly contraindicated.
• Initiating therapy with sodium bicarbonate may be fatal. It has been proven that adequate insulin therapy in most cases helps eliminate acidosis. Correction of acidosis with sodium bicarbonate carries an exceptionally high risk of complications. The introduction of alkalis increases hypokalemia and disrupts the dissociation of oxyhemoglobin; carbon dioxide formed when sodium bicarbonate is administered increases intracellular acidosis (although the blood pH may increase); paradoxical acidosis is also observed in the cerebrospinal fluid, which can contribute to cerebral edema; the development of “rebound” alkalosis cannot be ruled out. Rapid administration of sodium bicarbonate (boost) can cause death due to the rapid development of hypokalemia.
• Administration of sodium bicarbonate solution without additional administration of potassium preparations.
• Withholding or not prescribing insulin for DKA in a patient who is unable to eat.
• Intravenous bolus injection of insulin. Only during the first 15-20 minutes is its concentration in the blood maintained at a sufficient level, so this route of administration is ineffective.
• Three to four times of subcutaneous short-acting insulin (RAI). ICD is effective for 4-5 hours, especially in conditions of ketoacidosis, so it should be prescribed at least five to six times a day without an overnight break.
• The use of sympathotonic drugs to combat collapse, which, firstly, are counter-insulin hormones, and, secondly, in diabetic patients their stimulating effect on glucagon secretion is much more pronounced than in healthy individuals.
• Incorrect diagnosis of DKA. With DKA, the so-called “diabetic pseudoperitonitis” often occurs, which simulates the symptoms of an “acute abdomen” - tension and pain in the abdominal wall, a decrease or disappearance of peristaltic noises, and sometimes an increase in serum amylase. Simultaneous detection of leukocytosis can lead to an error in diagnosis, as a result of which the patient ends up in the infectious (“intestinal infection”) or surgical (“acute abdomen”) department. In all cases of “acute abdomen” or dyspeptic symptoms in a patient with diabetes, it is necessary to determine glycemia and ketotonuria.
• Failure to measure glycemia in any patient who is unconscious, which often leads to erroneous diagnoses - “cerebrovascular accident”, “coma of unknown etiology”, while the patient has acute diabetic metabolic decompensation.

Hyperosmolar nonketoacidotic coma

Hyperosmolar non-ketoacidotic coma is characterized by severe dehydration, significant hyperglycemia (often above 33 mmol/l), hyperosmolarity (more than 340 mOsm/l), hypernatremia above 150 mmol/l, absence of ketoacidosis (maximum ketonuria (+)). It develops more often in elderly patients with type 2 diabetes. It is 10 times less common than DKA. Characterized by a higher mortality rate (15-60%). The reasons for the development of hyperosmolar coma are a relative deficiency of insulin and factors that provoke the occurrence of dehydration.

Provoking factors: insufficient dose of insulin or skipping an insulin injection (or taking tableted glucose-lowering drugs), unauthorized cancellation of glucose-lowering therapy, violation of insulin administration technique, addition of other diseases (infections, acute pancreatitis, trauma, surgery, pregnancy, myocardial infarction, stroke, stress and etc.), dietary disorders (too many carbohydrates), taking certain medications (diuretics, corticosteroids, beta blockers, etc.), cooling, inability to quench thirst, burns, vomiting or diarrhea, hemodialysis or peritoneal dialysis.

It should be remembered that a third of patients with hyperosmolar coma do not have a previous diagnosis of diabetes mellitus.

Clinical picture

Severe thirst, polyuria, severe dehydration, arterial hypotension, tachycardia, focal or generalized convulsions increasing over several days or weeks. If, with DKA, disorders of the central nervous system and peripheral nervous system occur according to the type of gradual loss of consciousness and inhibition of tendon reflexes, then hyperosmolar coma is accompanied by a variety of mental and neurological disorders. In addition to the soporous state, which is also often observed in hyperosmolar coma, mental disorders often occur as delirium, acute hallucinatory psychosis, and catotonic syndrome. Neurological disorders are manifested by focal neurological symptoms (aphasia, hemiparesis, tetraparesis, polymorphic sensory disorders, pathological tendon reflexes, etc.).

Diagnostic criteria

• Hyperosmolar non-ketoacidotic coma develops more slowly (within 5-14 days) than DKA. Dehydration is more pronounced (decreased tissue turgor, tone of the eyeballs, muscle tone, tendon reflexes, body temperature and blood pressure) with neurological symptoms, there is no ketoacidosis, ketonuria, anuria and azotemia occur more often in elderly and senile age.

Among possible errors in therapy (see Table 2) and diagnosis, it is customary to highlight the administration of hypotonic solutions at the prehospital stage, long-term administration of hypotonic solutions.

Hypoglycemic coma

Hypoglycemic coma develops due to a sharp decrease in blood glucose levels (below 3-3.5 mmol/l) and severe energy deficiency in the brain.

Provoking factors: overdose of insulin and TCC, skipping or inadequate meals, increased physical activity, excessive alcohol intake, taking medications (β-blockers, salicylates, sulfonamides, etc.).

Clinical picture

Symptoms of hypoglycemia are divided into early (cold sweat, especially on the forehead, pale skin, severe paroxysmal hunger, trembling hands, irritability, weakness, headache, dizziness, numbness of lips), intermediate (inappropriate behavior, aggressiveness, palpitations, poor coordination of movements, double vision, confusion) and late (loss of consciousness, convulsions).

Diagnostic criteria

• Sudden onset of symptoms, usually over a period of several minutes, less often hours.
• The presence of characteristic symptoms of hypoglycemia.
• Glycemia is below 3-3.5 mmol/l.

At the prehospital stage, it is necessary to find out: how long the patient has been suffering from diabetes mellitus, whether the patient receives hypoglycemic therapy, and if so, what kind, when was the last drug taken, whether there have been any dietary violations, whether there have been any episodes of hypoglycemia in the past, whether excessive physical activity and alcohol intoxication were allowed.

Therapy for hypoglycemic coma at the prehospital stage (see Table 3) includes the use of thiamine, prednisolone, glucose, adrenaline solution, magnesium sulfate.

After removing the patient from a hypoglycemic coma, it is recommended to use drugs that improve microcirculation and metabolism in brain cells (glutamic acid, aminolon, stugeron, cavinton) for three to six weeks.

Repeated hypoglycemia can lead to brain damage.

Possible diagnostic and therapeutic errors

• An attempt to introduce carbohydrate-containing products (sugar, etc.) into the oral cavity of an unconscious patient. This often leads to aspiration and asphyxia.
• Use of unsuitable foods (bread, chocolate, etc.) to relieve hypoglycemia. These foods do not have a sufficient sugar-raising effect or raise blood sugar levels too slowly.
• Incorrect diagnosis of hypoglycemia. Some symptoms of hypoglycemia may be mistakenly regarded as an epileptic seizure, stroke, “vegetative crisis,” etc. In a patient receiving hypoglycemic therapy, if there is a reasonable suspicion of hypoglycemia, its relief should begin immediately, even before receiving a response from the laboratory.
• Once a patient has been brought out of severe hypoglycemia, the risk of relapse is often not taken into account.

In patients in a comatose state of unknown origin, it is always necessary to assume the presence of glycemia. If it is reliably known that the patient has diabetes mellitus and at the same time it is difficult to differentiate the hypo- or hyperglycemic genesis of the coma, intravenous jet administration of glucose is recommended in a dose of 20–40–60 ml of 40% solution for the purpose of differential diagnosis and emergency assistance for hypoglycemic coma In the case of hypoglycemia, this significantly reduces the severity of symptoms and thus allows differentiation between the two conditions. In hyperglycemic coma, such an amount of glucose will have virtually no effect on the patient’s condition.

In all cases where it is not possible to measure blood glucose immediately, highly concentrated glucose should be administered empirically. If hypoglycemia is not treated urgently, it can be fatal.

The basic drugs for patients in a coma, in the absence of the possibility of clarifying the diagnosis and immediate hospitalization, are considered to be thiamine 100 mg IV, glucose 40% 60 ml and naloxone 0.4-2 mg IV. The effectiveness and safety of this combination have been repeatedly confirmed in practice.

Kh. M. Torshkhoeva, Candidate of Medical Sciences A. L. Vertkin, Doctor of Medical Sciences, Professor V. V. Gorodetsky, Candidate of Medical Sciences, Associate Professor of NNPO Emergency Medical Care, MGMSU

Consequences and prognosis

Due to the fact that in a comatose state the brain and central nervous system are affected, the consequences of a coma can be the most severe. Life-threatening are cerebral edema, heart attack, pulmonary edema, thromboembolism (blockage) of the pulmonary artery. Such complications often lead to the patient not waking up from a coma and dying. The mortality rate is higher in hyperglycemic coma:

• ketoacidosis – from 5 to 15%;
• lactic acidosis – up to 45–50%;
• hyperosmolar type – from 50 to 90%.

With timely emergency care and a favorable course, the post-coma state can be regulated, however, the complication does not go away without a trace. As a rule, patients experience ataxia (impaired coordination of movements), speech and memory disorders, and the development of renal failure. Partial or complete impairment of motor functions (paralysis) is possible.

Prevention

Severe complications of diabetes can only be avoided if you strictly follow medical recommendations for controlling the disease: strict adherence to a diabetic diet, rational physical activity, timely treatment of infectious diseases, avoidance of alcoholic beverages and nicotine, and regular visits to an endocrinologist. It is strictly forbidden to independently change the regimen and dosage of prescribed medications. You should not delay visiting your doctor if you experience symptoms of illness. The development of further events can be dangerous for health and life.

Laboratory diagnostics

When diagnosing, in addition to the obvious symptoms, it is necessary to differentiate the type of diabetic complication. To do this, a number of rapid blood tests are performed:

• for sugar;
• for the presence of acetone bodies (ketones);
• arterial pH;
• on lactate concentration;
• for sodium and potassium content.

Water homeostasis (blood plasma osmolarity), the level of fatty acids, and the presence of acetone in the urine are determined. Glucose levels in the patient's precomatous and comatose state always exceed 30 mmol/liter. The presence of sugar in the urine is detected. With ketoacidosis, acetone bodies are detected in the blood. Hyperosmolar coma is characterized by a significant increase in plasma osmolarity. In lactic acidosis, excessively high levels of lactate are detected.

Causes

Most often, hyperosmolar non-acidotic coma develops in elderly people living with type 2 diabetes [3]. Provoking factors include any diseases and conditions in which the body actively loses fluid:

• irrational use of diuretics;
• diseases accompanied by recurring diarrhea and vomiting;
• staying in conditions that cause active sweating (working in a hot shop, moving to a country with a hot climate, etc.).

Also, this type of diabetic coma can develop with myocardial infarction, massive bleeding, and in patients on hemo- or peritoneal dialysis [7].

First aid measures

Decompensation of diabetes mellitus

In case of primary symptoms, first of all, you need to call an ambulance. Emergency assistance before the arrival of the brigade is provided as follows:

• Place the diabetic on his side to prevent him from choking on vomit. If necessary, manually clean the mouth and airways.
• Cover the patient with a blanket to reduce heat transfer.
• Open a window to provide fresh air.
• Measure your sugar level (every diabetic has a portable glucometer).

If the patient is conscious, he should be given sweet water to drink. In case of hypoglycemia, this measure will allow you to hold out stably until the ambulance arrives. In case of hyperglycemia, it will not do much harm. Solid sweets are not suitable, since in a precomatous state, swallowing disorders (dysphagia) and chewing function develop. A person may choke. If the patient is unconscious, it is necessary to monitor the breathing rate and pulse. It is advisable to record the data. This information may be useful to the emergency doctor. If medical skills are available, resuscitation measures should begin once the person returns to consciousness.

First aid at home should be carried out with extreme caution. You cannot shake the patient, hit him on the cheeks, or pour water on him in order to bring him to his senses. A diabetic should not be given insulin until the ambulance arrives. Especially with alcohol intoxication. In most cases, a diabetic with coma symptoms is hospitalized. The hospital carries out measures for primary diagnosis and provision of resuscitation care.