If a person abuses alcoholic drinks taking large doses ethyl alcohol, then severe intoxication of his body occurs. Its consequence may be the development of coma - a pathological condition in which the central nervous system is depressed. nervous system leading to loss of consciousness by the patient and lack of response to external and internal stimuli.

Causes

The ingestion of a toxic dose of ethyl alcohol into the blood is the main cause of the development of a life-threatening condition. Even a small amount of drunk vodka or cognac negatively affects the body of some people, poisoning occurs when the ethanol content in the red liquid reaches 0.2‰ (ppm). Alcoholic coma, which has code T51 according to ICD 10 (International Classification of Diseases), develops at a blood alcohol concentration of 0.3 to 7.0 ppm, and death occurs above 7.0-7.5‰.

The following factors influence the occurrence of a pathological condition:

1. The strength of the drink (the more degrees in it, the more toxic it is).
2. Weight of a person (thin people get drunk faster than full ones).
3. Age (teenagers and older people are more difficult to perceive alcohol).
4. Drinking alcohol on an empty stomach, without snacks (in the absence of food in the stomach, intoxication occurs faster).

In some cases, a coma can develop in people who have drunk a little vodka and become drunk (this is typical for those who are not used to drinking strong drinks, chronic alcoholics and those who have an individual intolerance to alcohol).

The effect of ethanol on the brain

Ethanol has the ability to be rapidly absorbed into the intestines (95%) and into the blood (5%). Its small amount, getting into the red liquid, dilutes it, accelerating the movement of red blood cells. With an increase in the dose, the reverse process occurs: dehydration and thickening of the liquid due to the fact that ethyl alcohol dissolves the membranes of erythrocytes and they stick together with each other, forming clots.

Clumped blood cells clog the capillaries of the brain and cause oxygen starvation of its tissues (hypoxia). This is manifested by overexcitation, cheerfulness, euphoria in a drinking person. Then ethanol has a neurotoxic effect on brain function, which leads to disturbances in the functioning of the cerebral cortex.

An increased amount of alcohol in nerve cells (neurons) destroys the connections between them and changes their structure. When these changes affect the medulla oblongata, there is a sharp decrease blood pressure and the person loses consciousness, falling into a coma.

hypovolemia

Hypovolemia is a decrease in the volume of circulating blood. It develops due to the fact that ethyl alcohol causes swelling of the brain tissues and the distribution of fluid in them is disturbed. This is manifested in a person by weakness, a decrease in blood pressure and temperature, and convulsions. Hypovolemia can cause loss of consciousness.

hypoglycemia

Hypoglycemia is a drop in glucose levels. Ethyl alcohol in the body is broken down by liver enzymes, but they cannot cope with a large amount of alcohol, so the level of glycogen carbohydrate decreases, which leads to a sharp drop in blood sugar. Due to energy starvation, an overstrain of the nervous system occurs, which causes loss of consciousness and hypoglycemic coma. Low air temperature accelerates the development of the pathological condition, because if a person drinks in the cold (outdoors in winter), then he needs even more glucose for thermoregulation.

stages

There are 3 stages of a coma:

1. Superficial 1 degree or resorption.
2. Superficial 2 degrees.
3. Deep.

Each phase of the pathology differs from the others in its characteristic features.

Superficial 1 degree

Initially, severe intoxication is manifested in the victim by contraction or muscle spasms, there is an increase in blood pressure and an increase in heart rate. The person feels sick or has a lot of saliva coming out of their mouth. Although the patient is still conscious, he no longer controls his actions. His breathing becomes hoarse, facial expressions and coordination of movements are disturbed, involuntary urination may occur.

The face acquires a purple hue, the pupils narrow, but still react poorly to bright light. If a person in this state is allowed to smell ammonia, then the reaction to the medicine will be positive. Resorption lasts from 4 to 6-7 hours. In this state, the concentration of alcohol in the blood does not exceed 4 ppm, and thanks to ammonia, the patient comes to his senses.

Superficial 2 degree

The duration of this phase is from 10 to 12 hours. It differs from resorption by a decrease in excitation. Everything “freezes” in the victim:

1. Breathing is reduced.
2. The muscles relax.
3. The rapid pulse is barely palpable.
4. Breathing slows down.
5. The pupils stop responding to light.

With a superficial coma of the 2nd degree, a person can still feel severe pain (if he fell and hit the ground), but he involuntarily has defecation and deurination. If the victim loses consciousness, then ammonia no longer helps him. The concentration of ethanol in the blood at this stage reaches 6-6.5 ppm.

Deep

With a deep alcoholic pathology, a person's condition worsens even more. He sweats a lot, although the body temperature drops to +35°C. Blood pressure drops, the pulse weakens and is almost not palpable. No reaction to light or pain. There is a violation of the respiratory system, and the victim cannot take a deep breath. Due to oxygen starvation, the face turns blue, and then turns white.

This state can last up to 24 hours. If you do not help the patient, he dies, because his blood already contains 7 or more ppm of alcohol. High concentration ethanol leads to the development of cardiac and kidney failure, a person stops breathing or chokes on vomit, suffocates with a sunken tongue.

Symptoms

The main signs of intoxication in the victim are: profuse salivation, problems with speech and breathing (wheezing, shortness of breath, inability to say anything), blueness of the skin of the face, absence or weak reaction to pain, convulsions, loss of consciousness. If there are sober people near the victim, having noticed the signs described above, they should give him first aid and call a doctor.

Diagnostics

When diagnosing, doctors pay attention to the external symptoms of a coma and determine the neurological status of the victim (convulsions, reflexes, pupillary response to light, consciousness and sensitivity to pain). Alcoholic pathological condition should be distinguished from other types of coma:

1. Neurological, occurring with head injuries and cerebrovascular accident.
2. Somatic, arising from diabetes and hepatitis.
3. Toxic, due to the intake of alcoholic beverages with drugs or medications.

To conduct a differentiated diagnosis, instrumental methods for examining organs and tissues are used: radiography, CT, ultrasound. To identify the pathological process in the brain, an echoencephaloscopy is prescribed to the patient.

Of great importance in the diagnosis is the data of urine and blood tests for the level of amylase and glucose. To determine the depth of the lesion, an analysis is prescribed for the amount of alcohol in the red liquid.

First aid

The patient should receive emergency first aid as soon as possible. It consists in doing the following:

1. Bring the victim, who is outside, into a warm room and cover him with a blanket or outerwear.
2. Put the patient on his stomach and turn his head to one side so that it hangs down a little. This position will reduce the risk of choking and choking with vomit.
3. Clear the nose and mouth of a person from mucus and food debris.
4. Apply a cold compress to the head.
5. Bring a cloth or cotton wool moistened with ammonia to the nose of the victim.
6. If the patient wakes up, give him a drink of warm, sweet water or weakly brewed tea with sugar to increase the level of glucose in the blood.

If a person cannot be brought to his senses, you need to make him artificial respiration or chest compressions. All other actions can only be performed by an ambulance doctor.

Treatment

Treatment of deep and superficial coma of the 2nd degree is carried out after the patient is hospitalized and the diagnosis is established. To restore the functioning of various body systems, intensive therapy is prescribed.

With superficial

If a person has difficulty breathing, it is necessary to ensure the patency of the bronchi, clearing them of mucus, and supplying oxygen. Then, as soon as possible, the absorption of ethanol into the blood and intestines should be prevented, so the victim is washed with a stomach with clean water using a probe.

To remove alcohol from the body, the patient is given a dropper and an intravenous injection of a solution of glucose and insulin, and saline to replenish fluid losses.

To support the work of the heart and blood vessels, ascorbic acid and preparations containing caffeine are administered intravenously.

To reduce mucus in the lungs and salivation, Atropine is injected under the skin.

To restore the work of the central nervous system, patients are prescribed a large amount of vitamins (C, PP, B1, B6).

In order to prevent oxygen starvation of the brain, catheterization is carried out with diuretic drugs.

With severe

With a deep coma, the patient is placed in intensive care. If the victim is unconscious, tracheal intubation is performed and the device is connected artificial ventilation lungs. Then the gastric lavage is repeated. The patient is shown the above-described means of intensive care.

Additionally, antishock therapy is used: plasma substitutes (Reopoliglyukin, Hemodez) are administered. To prevent disturbances in the functioning of the kidneys, a bilateral lumbar blockade with Novocaine is performed. If muscle protein breakdown (myoglobinuria) is suspected, the hemosorption method (extrarenal blood purification from toxins) is used. If blood pressure is greatly reduced, Prednisolone is administered for several days.

Recovery period

If the victim was treated in a timely manner, he can come out of a coma in a few hours. After that he has to long period recovery, the purpose of which is to reduce the consequences of a pathological condition.

During the time prescribed by the doctor, the patient will need to take vitamin and mineral complexes and medicines to improve the functioning of the liver, kidneys, and cerebral circulation. It will take more than one day to restore the water-salt balance in the body. The patient will need to adhere to the prescribed diet, do special exercises. The entire period of rehabilitation is prohibited from drinking alcohol.

Consequences

The consequences of the pathological condition are acute renal failure and pneumonia, with untimely assistance - death.

If a person has been in a deep coma from 24 hours to several weeks or months, a number of negative changes can occur in his body.

Upon regaining consciousness, the victim may lose the ability to speak and walk. Violation of the state of his health will be evidenced by: strong headache, swelling in the muscles and their subsequent atrophy, bleeding from mucous membranes, frequent pneumonia. These conditions will disturb a person for several years.

First Aid: Alcoholic Coma

Alcohol intoxication. emergency assistance for alcohol intoxication.

Due to brain damage, the patient's memory worsens, aggression, tearfulness or lethargy may appear. A terrible consequence is the development of dementia, the degradation of the individual.

Coma- an unconscious state due to a violation of the function of the brain stem.

Code according to the international classification of diseases ICD-10:

• R40.2

Causes

Etiology: cranial - brain injury, stroke, infection, status epilepticus, brain tumors, exogenous intoxications, disorders of systemic metabolism (diabetes mellitus, hypoglycemia, uremia, eclampsia, thyrotoxicosis), etc. A decisive role in the development of coma is played by damage to the ascending activating systems of the brain stem and interstitial brain.

Symptoms, course. Depending on the severity of violations of vital functions, who are divided into several degrees. With a mild degree of coma, patients respond to painful stimuli; preserved reflexes from the nasal mucosa, corneal and pupillary; sometimes tendon reflexes persist and Babinsky's symptom is caused. Severe degree of coma: reaction only to intense pain stimuli, swallowing is disturbed, however, when food enters the Airways there is a reflex cough; wheezing, often of the Cheyne-Stokes type. Deep coma: areflexia, atony, mydriasis, severe respiratory and circulatory disorders. Transcendental (terminal) coma: the vital activity of the patient is preserved only due to artificial ventilation of the lungs and stimulation of the heart.

Treatment

Treatment. When establishing the nature of the coma - pathogenetic therapy. At all stages of a coma - resuscitation.

Forecast depends on the cause of the coma and the severity of the brainstem injury. With a deep coma, the prognosis is often unfavorable; absolutely unfavorable prognosis for transcendental coma.

Diagnosis code according to ICD-10. R40.2

• Diabetic:
  • coma with or without ketoacidosis (ketoacidotic)
  • hypermolar coma
  • hypoglycemic coma
• Hyperglycemic coma NOS

1 With ketoacidosis

• acidosis without mention of coma
• ketoacidosis without mention of coma

2† With kidney damage

• Diabetic nephropathy (N08.3*)
• Intracapillary glomerulonephrosis (N08.3*)
• Kimmelstiel-Wilson syndrome (N08.3*)

3† With ocular lesions

4† With neurological complications

5 With peripheral circulatory disorders

6 With other specified complications

7 With multiple complications

8 With unspecified complications

9 No complications

Includes: diabetes (diabetes):

• labile
• with onset at a young age
• prone to ketosis

Excluded:

• diabetes:
  • neonates (P70.2)
• glycosuria:
  • NOS (R81)
  • renal (E74.8)

Included:

• diabetes (diabetes) (non-obese) (obese):
  • with onset in adulthood
  • with onset in adulthood
  • not prone to ketosis
  • stable
• juvenile non-insulin-dependent diabetes mellitus

Excluded:

• diabetes:
  • associated with malnutrition (E12.-)
  • neonates (P70.2)
  • during pregnancy, childbirth and the puerperium (O24.-)
• glycosuria:
  • NOS (R81)
  • renal (E74.8)
• impaired glucose tolerance (R73.0)
• postoperative hypoinsulinemia (E89.1)

[cm. above subheadings]

Includes: diabetes mellitus associated with malnutrition:

• type I
• type II

Excluded:

• diabetes mellitus during pregnancy, childbirth and the puerperium (O24.-)
• glycosuria:
  • NOS (R81)
  • renal (E74.8)
• impaired glucose tolerance (R73.0)
• neonatal diabetes mellitus (P70.2)
• postoperative hypoinsulinemia (E89.1)

[cm. above subheadings]

Excluded:

• diabetes:
  • associated with malnutrition (E12.-)
  • neonatal (P70.2)
  • during pregnancy, childbirth and the puerperium (O24.-)
  • type I (E10.-)
  • type II (E11.-)
• glycosuria:
  • NOS (R81)
  • renal (E74.8)
• impaired glucose tolerance (R73.0)
• postoperative hypoinsulinemia (E89.1)

[cm. above subheadings]

Includes: diabetes NOS

Excluded:

• diabetes:
  • associated with malnutrition (E12.-)
  • neonates (P70.2)
  • during pregnancy, childbirth and the puerperium (O24.-)
  • type I (E10.-)
  • type II (E11.-)
• glycosuria:
  • NOS (R81)
  • renal (E74.8)
• impaired glucose tolerance (R73.0)
• postoperative hypoinsulinemia (E89.1)

In Russia, the International Classification of Diseases of the 10th revision (ICD-10) is adopted as a single regulatory document for accounting for morbidity, reasons for the population to contact medical institutions of all departments, and causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170

The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.

With amendments and additions by WHO.

Processing and translation of changes © mkb-10.com

Emergency care and symptoms in hypoglycemic coma

Hypoglycemic coma is a critical condition endocrine system arising from a sharp drop in blood sugar levels. Coma develops acutely. Sometimes the short-term period of precursors is so small that a coma begins almost suddenly - within a few minutes there is a loss of consciousness and even paralysis of vital centers medulla oblongata.

blood glucose

Glucose is the main source of energy for the brain. The level of glucose in the blood is an important indicator of a person's health. A decrease in blood sugar levels, as well as its increase, triggers pathological processes in the body that can harm health, even death. normal level glucose is considered to range between 3.9 and 5 mol/l.

Unlike other organs that can receive energy from other sources, for the brain, glucose is the only way to feed. With a sharp decrease in sugar concentration, brain cells begin to starve, and as its deficiency increases, their function is impaired, and tissues undergo swelling, partial destruction, and even death.

Hypoglycemic coma (code E-15 according to ICD-10) refers to a life-threatening human condition and is caused by a sharp decrease in blood glucose to less than 3 mm / l or its sudden changes, followed by the development of acute starvation of the brain.

In most cases, adults and children with diabetes mellitus receiving insulin treatment are at risk of developing hypoglycemic coma. However, in rare cases, hypoglycemic coma is possible and in healthy people with a low-carb diet and severe stress.

Reasons for the development of hypoglycemic coma

The main reasons for the development of hypoglycemic coma are usually associated with a violation in the regimen of insulin use in diabetes mellitus:

1. Giving too much insulin. A sharp and excessive decrease in glucose concentration can occur, followed by hypoglycemia and coma.
2. Eating disorders after insulin administration. An important rule after the introduction of insulin is the timely intake of food containing carbohydrates - this prevents the decrease in blood sugar to too low a level under the influence of the administered dose.
3. Incorrect administration of insulin. Insulin is administered subcutaneously, it gradually penetrates from the subcutaneous fat into the blood. If administered incorrectly intramuscularly, the effect of the drug is accelerated and intensified.
4. Incorrect calculation of the dose of insulin. With increased physical activity or the absence of a sufficient amount of carbohydrates in the diet, a dose adjustment of the drug is necessary.
5. Drinking alcohol when it enters the body blocks glucose, as a result of which it stops being delivered to the brain. That is why the treatment of diabetes involves a complete rejection of alcohol.

The above causes of hypoglycemic coma can lead to both the sudden development of this condition and the gradual development of hypoglycemia.

Condition symptoms

The development of hypoglycemic coma is always preceded by certain signs.

Main clinical symptoms hypoglycemia:

• feeling of strong hunger;
• nausea;
• pallor of the skin, accompanied by sweating;
• trembling in the limbs and all over the body;
• change in behavior and mood: anxiety, fear, aggression;
• impaired concentration and coordination of movements.

The development of hypoglycemia can be fulminant, possibly sharp deterioration state and development of symptoms of hypoglycemic coma in a matter of minutes.

With signs of hypoglycemic coma in initial stage there is an increase and intensification of all symptoms of hypoglycemia and, in the absence of help, the development of its final stages:

• loss of consciousness;
• convulsions;
• gradual decrease in pressure and heart rate;
• death.

If a hyperglycemic coma occurs, first aid should be provided immediately by any person who is near the victim. For its provision, the most important task is to distinguish this condition from hypoglycemic, in which medical measures completely opposite.

The difference between hypoglycemic coma and hyperglycemic coma

1. With hyperglycemia, the skin is dry, cracking of the lips of the victim is characteristic, while with hypoglycemia, extremely profuse sweating is observed.
2. With hyperglycemia, shortness of breath occurs, breathing is heavy, squeezed. In hypoglycemic coma, breathing is often weakened or not changed at all.

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Emergency care for coma

It is important to understand that hypoglycemic coma always requires emergency medical attention. If possible, it is advisable to call other people and ask them to call ambulance.

Emergency care for hypoglycemic coma is to ensure the entry of glucose into the blood. If the patient is still conscious, you need to offer him a candy or water with sugar dissolved in it. If the consciousness is confused and the victim does not understand your words, it is necessary to gently, opening the patient's mouth, in small portions, try to pour sweet water under the tongue.

In the case when there are signs of seizures, it is necessary:

• lay the patient on his side, preferably on the floor;
• put a pillow or folded clothes under your head;
• if the jaws are not closed, it is advisable to place a soft object between the teeth;
• protect the patient from sharp and hard objects in order to avoid injury to them during convulsions.

Emergency care for hypoglycemic coma requires constant monitoring of the patient's condition before the arrival of doctors.

Upon arrival of the ambulance, medical assistance begins immediately. After measuring the level of sugar in the blood, doctors produce an intravenous infusion of glucose and other drugs to normalize the patient's condition. After stabilization of the situation, hospitalization of the patient is mandatory for further observation and treatment. possible consequences hypoglycemic coma.

Disease prevention

Based on the main causes of the development of an acute hypoglycemic state, prevention primarily includes timely treatment diabetes, as well as patient compliance with all the recommendations of the attending physician and the ability to quickly cope with the symptoms of hypoglycemia.

Hypoglycemic coma in children with diabetes develops for the same reasons as in adults. Therefore, it is important to pay special attention to teaching young patients and their teachers the signs of the onset of a hypoglycemic state and the rules for dealing with them.

Usually, doctors recommend that you always carry sweets with you to consume them at the first sign of low blood sugar. Also, in many countries, patients with diabetes wear special cards or bracelets with the inscription "Diabetes" in order to inform others about them in case of loss of consciousness. possible reasons the emerging state.

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hypoglycemia

Hypoglycemia: Brief Description

Hypoglycemia - a decrease in blood glucose less than 3.33 mmol / l. Hypoglycemia can occur in healthy individuals after a few days of fasting or a few hours after a glucose load, resulting in an increase in insulin levels and a decrease in glucose levels in the absence of symptoms of hypoglycemia. Clinically, hypoglycemia manifests itself when the glucose level drops below 2.4–3.0 mmol/l. The key to diagnosis is Whipple's triad: neuropsychic manifestations during fasting; blood glucose less than 2.78 mmol/l; relief of an attack by oral or intravenous administration of r-ra dextrose. The extreme manifestation of hypoglycemia is hypoglycemic coma.

Hypoglycemia: Causes

Risk factors

Genetic Aspects

Etiology and pathogenesis

Hypoglycemia on an empty stomach Insulinoma Artificial hypoglycemia caused by the use of insulin or oral hypoglycemic drugs (less often due to the intake of salicylates, b-blockers or quinine) Extrapancreatic tumors can cause hypoglycemia. Usually these are large, located in abdominal cavity tumors, most often of mesenchymal origin (eg, fibrosarcoma), although liver carcinomas and other tumors are observed. The mechanism of hypoglycemia is poorly understood; report extensive glucose uptake by some tumors with the formation of insulin-like substances Ethanol-induced hypoglycemia - in individuals with a significant reduction in glycogen stores due to alcoholism, usually 12-24 hours after binge. Mortality is more than 10%, therefore, rapid diagnosis and the introduction of p-ra dextrose are necessary (when ethanol is oxidized to acetaldehyde and acetate, NADP accumulates and the availability of NAD, which is necessary for gluconeogenesis, decreases). Impairment of glycogenolysis and gluconeogenesis, necessary for the formation of glucose in the liver during fasting, leads to hypoglycemia. Liver diseases lead to a deterioration in glycogenolysis and gluconeogenesis, sufficient to cause hypoglycemia on an empty stomach. Similar states are observed during lightning viral hepatitis or acute toxic liver injury, but not in less severe cases of cirrhosis or hepatitis Other causes of fasting hypoglycemia: deficiency of cortisol and / or growth hormone (for example, with adrenal insufficiency or hypopituitarism). Renal and heart failure are sometimes accompanied by hypoglycemia, but the causes of its occurrence are poorly understood.

Reactive hypoglycemia occurs several hours after ingestion of carbohydrates Alimentary hypoglycemia occurs in patients after gastrectomy or other surgical intervention, leading to pathologically rapid intake of food in small intestine. The rapid absorption of carbohydrates stimulates excess secretion of insulin, causing hypoglycemia some time after eating. Reactive hypoglycemia in diabetes. In some cases, patients with early stages DM occurs at a later but excessive release of insulin. After a meal, the plasma glucose concentration rises after 2 hours, but then decreases to the level of hypoglycemia (3–5 hours after a meal) Functional hypoglycemia is diagnosed in patients with neuropsychiatric disorders (for example, with the syndrome chronic fatigue).

Hypoglycemia: Signs, Symptoms

Clinical picture

Neurological symptoms predominate with a gradual decrease in glucose levels Dizziness Headache Confusion Visual disturbances (eg diplopia) Paresthesia Convulsions Hypoglycemic coma (often develops suddenly).

Adrenergic symptoms predominate in acute hypoglycemia Hyperhidrosis Anxiety Tremor of the extremities Tachycardia and a feeling of interruption in the heart Increased blood pressure Angina attacks.

Age features

Pregnancy

Hypoglycemia: Diagnosis

Laboratory research

Influence of drugs. Sulfonylurea stimulates the production of endogenous insulin and C-peptide, therefore, to exclude artificial hypoglycemia, a blood or urine test is performed for sulfonylurea preparations.

Special Studies

Differential Diagnosis

Hypoglycemia: Treatment Methods

Treatment

Tactics of conducting

Drugs of choice

urgent health care If oral glucose is not available, 40–60 ml of 40% r-ra dextrose IV over 3–5 minutes, followed by a continuous infusion of 5 or 10% r-ra dextrose In children with neurological symptoms, treatment is started with an infusion of 10% r-ra dextrose at a rate of 3–5 mg/kg/min or higher For hypoglycemia caused by oral hypoglycemia drugs (eg, sulfonylurea derivatives), continued infusion of dextrose and observation of the patient for 24 to 48 hours is necessary due to the likelihood of recurrence of coma.

It is possible to administer intramuscularly or s / c glucagon to the upper third of the shoulder or thigh (rarely used in our country). Glucagon usually eliminates neurological manifestations hypoglycemia within 10-25 minutes; in the absence of effect, repeated injections are not recommended. Doses of glucagon: children under 5 years old - 0.25-0.50 mg, children from 5 to 10 years old - 0.5-1 mg, children over 10 years old and adults - 1 mg.

Complications

ICD-10 E15 Non-diabetic hypoglycemic coma E16 Other pancreatic endocrine disorders P70 Transient disorders carbohydrate metabolism specific to the fetus and newborn T38. 3 Poisoning by insulin and oral hypoglycemic [antidiabetic] drugs

Notes

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Hypoglycemia: classification, clinical picture and ICD-10 code

Hypoglycemia is a state of the body in which there is a greatly reduced (compared to the norm) concentration of glucose in the blood.

Pathology is diagnosed if the level of this monosaccharide is below 3.5 mmol per liter.

How is this pathology manifested and why is it dangerous? What is the ICD code for hypoglycemia and how is it treated? Let's take a closer look.

Classification of pathology

It has a hypoglycemia code according to the ICD 10 - 16.0. But this pathology has several classes:

• hypoglycemia, unspecified - E2;
• hypoglycemic coma in the absence of diabetes - E15;
• 4 - disorders of gastrin synthesis;
• 8 - other violations that were clarified during the study of the patient;
• other forms - E1.

Other forms of hypoglycemia according to the ICD include hyperinsulinism and encephalopathy, which develops after a coma caused by an insufficient amount of sugar in the blood.

Despite the fact that, according to the ICD classification, hypoglycemia has exactly the listed codes, when selecting medicines for its relief and therapy, physicians should also be guided by codes external causes(class XX).

What is unspecified hypoglycemia?

ICD 10 describes unspecified hypoglycemia as a class 4 disease that can be caused by metabolic and/or endocrine disorders, as well as poor nutritional quality.

Severity classification

There are three degrees of severity of hypoglycemia:

• light. When it occurs, the patient's consciousness is not clouded, and he is able to personally correct his own condition: call an ambulance or, if this is not the first episode, take the necessary medication;
• heavy. When it occurs, a person is conscious, but cannot independently stop the manifestations of pathology due to his severe depression and / or physiological disorders;
• hypoglycemic coma. It is characterized by loss of consciousness and its failure to return for a long time. Without outside help, a person in this condition can suffer serious damage - even death.

Reasons for development

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You just need to apply.

Hypoglycemia can occur due to many factors, both exogenous (external) and endogenous (internal). Most often it develops:

• due to malnutrition (in particular, with the regular use of large amounts of carbohydrates);
• in women during menstruation;
• with insufficient fluid intake;
• in the absence of sufficient physical activity;
• against the background of infectious diseases;
• as a result of the appearance of neoplasms;
• as a response to diabetes therapy;
• due to diseases of the cardiovascular system;
• due to weakness of the body (in newborns);
• in view of the abuse of alcohol-containing drinks and some other types of drugs;
• with hepatic, renal, cardiac and other types of insufficiency;
• with intravenous administration of a physical solution.

The listed reasons are considered risk factors. What exactly can serve as a catalyst for the development of hypoglycemic syndrome is determined by the individual characteristics of the organism: genetic determinism, trauma, etc. Also, this condition may be the result of a sharp change in plasma glucose concentration from high to normal. Such glycemia is no less dangerous and can lead to disability or death of the patient.

A number of studies show that most often the pathological condition under consideration appears in people suffering from alcoholism. This is due to the fact that due to the regular intake of ethyl alcohol, the body begins to use NAD abnormally quickly. Also, the process of gluconeogenesis begins to slow down in the liver.

Alcoholic hypoglycemia can occur not only against the background of frequent alcohol abuse, but also with a single use of large doses.

Doctors also diagnose cases when abnormal low sugar in the blood is found in people who have previously taken small doses of alcohol. The highest risk of developing this pathology after the use of ethanol is present in children.

Symptoms

Hypoglycemia is characterized by a complex of symptoms. With a drop in sugar in the body, the patient most often experiences mental arousal, as a result of which he may show aggressiveness and / or anxiety, anxiety and fear.

In addition, he may partially lose the ability to navigate in space and feel a headache. This condition is also characterized by striking physiological disorders.

The patient almost always begins to sweat profusely, his skin turns pale, and his limbs begin to tremble. In parallel with this, he experiences a strong feeling of hunger, which, however, may (but not always) be accompanied by nausea. The clinical picture is complemented by general weakness.

Less frequent manifestations this condition: visual impairment, impaired consciousness up to fainting, from which a person can plunge into a coma, epileptiform seizures, noticeable behavioral disorders.

Hypoglycemic coma

The ICD code for hypoglycemic coma is E15. This is an acute condition that, with a sharp decrease in blood sugar, occurs extremely rapidly.

Its initial manifestation is loss of consciousness. But, unlike ordinary fainting, the patient does not come out of it after a few seconds / minutes, but remains in it at least until the correct medical care is provided to him.

Often the period between the first symptoms of hypoglycemia and the syncope itself is very short. Neither the patient nor those around him notice the harbingers of the onset of coma, and it seems to them sudden. Hypoglycemic coma is the extreme degree of this pathological condition.

Although clinical manifestations, preceding coma, often go unnoticed, they are present and are expressed in the following: severe sweating, vasospasm, change heart rate, feeling of tension, etc.

Hypoglycemic coma is a reaction of the central nervous system to a sharp change in the direction of a decrease in the concentration of glycemia in blood vessels brain.

With its development, disturbances first occur in the neocortex, then in the cerebellum, after which the problem affects the subcortical structures, and, in the end, reaches the medulla oblongata.

Most often, coma occurs as a result of the introduction of the wrong dosage of insulin into the body (if the patient has diabetes). If a person does not suffer from this pathology, then it can also develop as a result of eating or sulfa drugs.

Useful video

Most effective ways treatment and prevention of hypoglycemia:

• Eliminates the causes of pressure violations
• Normalizes blood pressure within 10 minutes after taking

Causes and help with hypoglycemic coma

Hypoglycemic coma is a pathology of the nervous system, which is caused by a severe lack of glucose in the human body. Without it, most organs weaken and gradually lose their capacity. If you do not start a course of therapy in a timely manner, everything can end in death. Competent first aid for hypoglycemic coma is what will save a person's life. Hypoglycemic coma has ICD code 10.

Causes of the condition

The causes of the disease are:

• inability to block this condition in the development of diabetes mellitus;
• excessive alcohol consumption;
• overdose of medication;
• stress: lack of sleep, malnutrition, worries, nervous breakdowns and other;
• problems with the liver and pancreas (its tumor), liver failure;
• overdose of insulin.

The latter happens not only because of a mistake or ignorance. When introducing a substance, it is important to correctly calculate its combination with physical activity and ingested carbohydrates. People sometimes have false information on the rules of the procedure:

• insulin is administered intravenously, not intramuscularly;
• after taking it is necessary to take food saturated with carbohydrates;
• excessive physical activity is prohibited. They are set by the doctor because any unplanned activity must be accompanied by professional adjustments in insulin dosage and a dietary carbohydrate intake program for the day.

Symptoms

Hypoglycemia is a chronic disease, pathogenesis. Without treatment, the person will be susceptible to complications. The first signs are mild, and the patient rarely pays attention to them. Among them: lethargy, fatigue and headaches, which cannot be removed with the help of conventional tonic and painkillers.

The classification of symptoms is as follows:

• 1) Autonomic / parasympathetic / adrenergic. These include: constant nervous tension, breakdowns, stress; excessive aggressiveness, anger, rage and a feeling of anxiety, anxiety, excitement; profuse sweating; convulsions, constant trembling in the limbs; high blood pressure; palpitations; pallor; constant sensation nausea and hunger; lethargy, drowsiness, fatigue.
• 2) Neuroglycopenic. Symptoms of this group: poor concentration, loss of attention; dizziness, glare before the eyes, severe headache; drowsiness, developing chronic fatigue syndrome, lethargy of the body; split image; disorientation in space; hallucinations; paranoia; frequent amnesia; circulatory disorders; respiratory failure, shortness of breath; disruptions and inappropriate behavior; fainting or the condition preceding them.

Precomatose state is calculated by clonic or tonic convulsions and epileptiform seizure. These signs are impossible to predict, they occur spontaneously, which puts a person's life at risk.

In a child, these manifestations progress twice as fast as in an adult. The set of symptoms is identical. Fatal outcome occurs with greater probability and surprise.

Complications

The first stage of the disease is determined by a decrease in blood sugar levels. Glucose is the main source of energy for the functioning of brain cells. It ceases to receive substances for stable functioning. After the cells begin to develop the necessary force from reserve substances that are not designed for such work. This self-regulation is supported by glucagon, a pancreatic hormone. The body is gradually depleted, in children it stops developing. Due to a sharp shortage of trace elements, the brain ceases to receive a standard dose of oxygen.

If emergency care is not provided in a timely manner, the disease will lead to cerebral edema and impaired functioning of the central nervous system (CNS). Such deviations are already irreversible. An adult is faced with a complete change in personality and individual habits, regimen, behavior, character and perception of the world around. The child suffers from a sharp drop in the level of intelligence down to the lowest possible threshold. The elderly are at increased risk if they have coronary disease brain or heart and cardiovascular diseases. Here complications are myocardial infarction, stroke.

With frequent bouts of coma, encephalopathy is predicted. This is a type of organic brain abnormality that has been caused by a non-inflammatory pathway. It is accompanied by a severe degree of oxygen starvation and pathology in the process of blood supply. As a result, there is a local degradation of the personality and deviations in the work of the central nervous system.

A lack of insulin can also trigger insulin shock, a clinical condition characterized by a sudden loss of consciousness due to a perceptible drop in blood sugar. The second threat is hypoglycemic shock - a sudden severe drop in glucose levels, followed by coma. Diabetic ketoacidotic coma is also provoked by a sharp lack of insulin.

It is impossible to avoid death in 40% of cases after hypoglycemic coma.

Emergency care for hypoglycemic coma

Emergency care for hypoglycemic coma can save a person's life and prevent the occurrence and development of pathologies caused by the condition.

Signs of coma are a reaction to stress in the medulla oblongata. Observed:

• absolute loss of consciousness;
• dilated pupils;
• sharp blanching;
• clammy cool sweat on face;
• weakened breathing;
• increased or standard blood pressure, heartbeat, pulse;
• reflexes in the area of ​​the elbows and knees are more pronounced.

The main thing at the same time is to return a person to consciousness and bring the main indicators of the body back to normal.

The stories of eyewitnesses of the event will help to distinguish hypoglycemic coma from any other. Passers-by can easily point out signs of defeat. Only then can you confidently proceed to action.

The first stage of care for hypoglycemic coma:

• You need to raise your blood sugar levels. To do this, carry out the irritation procedure: create sharp pain sensations through pinching or blows to the cheeks. This will provoke the release of catecholamines into the blood and bring the person to his senses, after which he must be taken to the nearest hospital or make an emergency call to the ambulance team and contact the patient's relatives if he is unable to do this on his own.
• This method is acceptable and effective only in the mild stage of coma. Otherwise, you will not be able to get the victim out of this state - only a doctor will help. But the introduction of glucose is still necessary: ​​this will help to avoid serious damage to the brain, central nervous system and disruption of their functioning. An injection of insulin is given intravenously. This will save a person's life. As a rule, patients with diabetes always have a first-aid kit on hand, where you will find all the means for carrying out the “operation”. Then you need resuscitation.

Treatment

It is interesting to know that hypoglycemic and hyperglycemic (with hyperosmolar syndrome) coma are used in psychiatry as a method of shock therapy for existing abnormalities. For example, it slows down the progressive development of schizophrenia. Such procedures are carried out exclusively in a hospital under the supervision of specialists with preliminary patient preparation procedures.

In the treatment of coma, the most important thing is to correctly diagnose. Out of ignorance, an injection with a glucose solution will easily provoke the death of the patient.

The treatment algorithm in the early stages can be observed at home. The mechanism is simple: just take a specific dose of fast carbohydrates. They are found in white bread, cakes, honey, corn flakes. Drink a sugar solution: mix three teaspoons with a glass of warm water. With a protracted attack, it is necessary to consume sugar at regular intervals (every minute) with the same dosage.

In severe cases of damage to a person, they are sent to the clinic, where he will be examined. He is prescribed inpatient treatment for hypoglycemic coma. Inkjet is being carried out intravenous administration forty percent glucose solution in the amount of up to one hundred milliliters. Therapy starts with subcutaneous injection epinephrine along with glucagon or hydrocortisone. If after a couple of hours the patient does not come to his senses, glucose is administered by drip 4 times a day and intramuscularly every hour and a half. To avoid dehydration, water intoxication, a glucose solution is introduced in sodium chloride. With a prolonged coma, mannitol is used.

The main treatment is aimed at restoring glucose metabolism. Intramuscularly, the nurse injects 100 ml of carboxylase and 5 ml of 5% ascorbic acid. Humidified oxygen tones up the work of the brain and heart, improves the functioning of blood vessels.

Prevention

Any disease is much easier to prevent than to cure.

Principles and methods of pre-medical prophylaxis:

• compliance with the established daily routine;
• giving up bad habits (alcohol and smoking);
• proper nutrition;
• adherence to recommendations for controlling the content of carbohydrates in food consumed.

A diabetic should use hypoglycemic drugs, control glucose levels. He should know the glucose index in various products, the consequences of exceeding it. There is an international table of diabetic foods that are acceptable for eating. It is important to know the etiology: symptoms and signs of hypoglycemia, pathophysiology, methods of prevention.

If the course of treatment includes anti-diabetic drugs and tablets such as anticoagulants, beta-blockers, salicylates, tetracyclines, anti-tuberculosis drugs, drugs, then blood sugar control should be especially careful.

Needs to be done every 2-3 months laboratory diagnostics undergo an ECG for hypoglycemia. A medical examination through a test will identify possible abnormalities, conduct an examination and tell you what your glucose level is.

Thus, hypoglycemic coma is a condition whose symptoms are difficult to confuse with anything. Treatment should be urgent, and prevention involves lifestyle control and therapy for the underlying disease.

The information on the site is provided for informational purposes only, does not claim to be reference and medical accuracy, and is not a guide to action. Do not self-medicate. Consult with your physician.

Hypoglycemic coma (signs, emergency management algorithm and consequences)

The consequences of diabetes mellitus are mostly delayed, the patient usually has enough time to notice the symptoms, consult a doctor, and adjust therapy. Hypoglycemic coma, unlike other complications, is not always possible to prevent and stop in time, as it develops rapidly and quickly deprives a person of the opportunity to think rationally.

In this state, the patient can only rely on the help of others who do not always have information about diabetes and can confuse a coma with ordinary alcohol intoxication. To maintain health, and even life, a diabetic needs to learn how to avoid a strong drop in sugar, reduce the dose of drugs in time, when there is a high probability of provoking coma, and determine hypoglycemia by the first signs. It would be useful to learn the rules of emergency care for coma and familiarize loved ones with them.

Hypoglycemic coma - what is it?

Hypoglycemic coma is a severe, acute condition, dangerous with severe starvation of body cells, damage to the cerebral cortex and death. Its pathogenesis is based on the cessation of glucose supply to brain cells. Coma is a consequence of severe hypoglycemia, in which blood sugar levels drop significantly below the critical level - usually less than 2.6 mmol / l at a rate of 4.1.

Most often, coma occurs against the background of diabetes mellitus, especially in patients who are prescribed insulin preparations. Severe hypoglycemia may also develop in elderly diabetics who take drugs that enhance the synthesis of their own insulin for a long time. Usually, a coma is prevented on its own or eliminated in a medical facility if the patient was delivered there in a timely manner. Hypoglycemic coma is the cause of death of 3% of diabetics.

This condition may also be a consequence of other diseases in which an excess of insulin is produced or glucose ceases to flow into the blood.

• E0 - coma in type 1 diabetes,
• E11.0 - 2 types,
• E15 - hypoglycemic coma, not associated with diabetes mellitus.

Reasons for violation

Hypoglycemic coma is provoked by prolonged habitual hypoglycemia or a sharp drop in sugar. They can be caused by the following factors:

1. Disorders in the use or administration of insulin preparations:

• dose increase short insulin due to incorrect calculations;
• usage modern drug insulin with a concentration of U100 with an outdated syringe designed for a more diluted solution - U40;
• after the introduction of insulin there was no food intake;
• replacement of the drug without dose adjustment if the previous one was weaker, for example, due to improper storage or expired shelf life;
• inserting the syringe needle deeper than required;
• increased action of insulin due to massage or heating of the injection site.

1. Reception of hypoglycemic agents related to sulfonylurea derivatives. Medicines with active ingredients glibenclamide, gliclazide, and glimepiride are slowly excreted from the body and may accumulate in the body with long-term use, especially with kidney problems. An overdose of these drugs can also provoke a hypoglycemic coma.
2. Essential exercise stress, not supported by the intake of carbohydrates, with insulin-dependent diabetes.
3. The use of alcohol in diabetes mellitus in significant quantities (more than 40 g in terms of alcohol) negatively affects the liver and inhibits the synthesis of glucose in it. Most often, hypoglycemic coma in this case develops in a dream, in the pre-morning hours.
4. Insulinoma is a neoplasm that can independently synthesize insulin. Large tumors producing insulin-like factors.
5. Violations in the work of enzymes, often hereditary.
6. Liver and kidney failure as a consequence fatty hepatosis or cirrhosis of the liver, diabetic nephropathy.
7. Diseases of the gastrointestinal tract that prevent the absorption of glucose.

With diabetic neuropathy and alcohol intoxication, the first manifestations of hypoglycemia are difficult to feel, so you can skip a small decrease in sugar and bring your condition to a coma. Also, the erasure of symptoms is observed in patients with frequent mild hypoglycemia. They begin to feel trouble in the body when the sugar drops below 2 mmol / l, so they have less time for emergency care. Conversely, diabetics with constantly high sugar signs of hypoglycemia begin to be felt when sugar becomes normal.

What is typical for GC

Symptoms of hypoglycemia do not depend on the cause that caused it. In all cases, the clinical picture of the development of coma is the same.

Normally, constant blood sugar is maintained even with a lack of carbohydrates due to the breakdown of glycogen stores and the formation of glucose in the liver from non-carbohydrate compounds. When sugar drops to 3.8, the autonomic nervous system activates in the body, processes begin to prevent hypoglycemic coma, insulin antagonist hormones are produced: first glucagon, then adrenaline, and lastly growth hormone and cortisol. Symptoms of hypoglycemia at this time are a reflection of the pathogenesis of such changes, they are called "vegetative". In diabetics with experience, the secretion of glucagon gradually decreases, and then adrenaline, while the initial signs of the disease decrease, and the risk of hypoglycemic coma increases.

With a decrease in glucose to 2.7, the brain begins to starve, neurogenic symptoms are added to the autonomic symptoms. Their appearance means the beginning of damage to the central nervous system. With a sharp drop in sugar, both groups of signs occur almost simultaneously.

It becomes difficult for the patient to concentrate, navigate the area, thoughtfully answer questions. He begins to have a headache, dizziness is possible. There is a feeling of numbness and tingling, most often in the nasolabial triangle. Doubling of objects, convulsions are possible.

With a serious lesion of the central nervous system, partial paralysis, speech impairment, and memory loss are added. At first, the patient behaves inappropriately, then he develops severe drowsiness, he loses consciousness and falls into a coma. When in a coma without medical care blood circulation, respiration are disturbed, organs begin to fail, the brain swells.

First aid algorithm

Vegetative symptoms are easily eliminated by taking a serving of fast carbohydrates. In terms of glucose, usually enough grams. It is not recommended to exceed this dose, since an overdose can cause the opposite condition - hyperglycemia. To raise blood glucose and improve the patient's condition, a couple of sweets or pieces of sugar, half a glass of juice or sweet soda are enough. Diabetics usually carry fast carbohydrates with them in order to start treatment on time.

Note! If the patient is prescribed acarbose or miglitol, sugar will not be able to stop hypoglycemia, since these drugs block the breakdown of sucrose. First aid for hypoglycemic coma in this case can be provided with pure glucose in tablets or solution.

When a diabetic is still conscious, but can no longer help himself on his own, he is given any medication to stop hypoglycemia. sweet drink making sure he doesn't choke. Dry foods at this time are dangerous with the risk of aspiration.

If there is a loss of consciousness, you need to call an ambulance, lay the patient on his side, check whether the airways are free and whether the patient is breathing. If necessary, begin to do artificial respiration.

Hypoglycemic coma can be completely eliminated even before the arrival of doctors; this requires a first aid kit. It includes the drug glucagon and a syringe for its administration. Ideally, every diabetic should carry this kit with him, and his relatives should be able to use it. This tool is able to quickly stimulate the production of glucose in the liver, so the consciousness returns to the patient within 10 minutes after the injection.

Exceptions are coma due to alcohol intoxication and multiple excess doses of insulin or glibenclamide. In the first case, the liver is busy cleansing the body of alcohol breakdown products, in the second case, the glycogen stores in the liver will not be enough to neutralize insulin.

Diagnostics

Signs of hypoglycemic coma are not specific. This means that they can be attributed to other conditions associated with diabetes. For example, diabetics with persistently high blood sugar may feel hungry due to severe insulin resistance, and diabetic neuropathy may cause palpitations and sweating. Convulsions before the onset of a coma are easily mistaken for epilepsy, and panic attacks have the same autonomic symptoms as hypoglycemia.

The only reliable way to confirm hypoglycemia is with a laboratory test that measures plasma glucose levels.

The diagnosis is made under the following conditions:

1. Glucose is less than 2.8, while there are signs of hypoglycemic coma.
2. Glucose is less than 2.2 if there are no such signs.

A diagnostic test is also used - 40 ml of glucose solution (40%) is injected into a vein. If blood sugar has dropped due to a lack of carbohydrates or an overdose of drugs in diabetes, the symptoms immediately subside.

Part of the blood plasma taken upon admission to the hospital is frozen. If, after the elimination of the coma, its causes are not identified, this plasma is sent for a detailed analysis.

Hospital treatment

With a mild coma, consciousness is restored immediately after a diagnostic test. In the future, a diabetic will only need an examination to identify the cause of hypoglycemic disorders and correction of the previously prescribed treatment for diabetes mellitus. If the patient does not regain consciousness, a severe coma is diagnosed. In this case, the amount of intravenously administered 40% glucose solution is increased to 100 ml. Then they switch to continuous administration with a dropper or infusion pump of a 10% solution until blood sugar reaches mmol / l.

If it turned out that the coma arose due to an overdose of hypoglycemic agents, they do a gastric lavage and give enterosorbents. If a severe overdose of insulin is likely and less than 2 hours have passed since the injection, soft tissue excision is made at the injection site.

Simultaneously with the elimination of hypoglycemia, its complications are treated:

1. Diuretics for suspected cerebral edema - mannitol (15% solution at the rate of 1 g per kg of body weight), then lasix (mg).
2. Nootropic Piracetam improves blood flow in the brain and helps maintain cognitive abilities (10-20 ml of a 20% solution).
3. Insulin, potassium preparations, ascorbic acid, when there is already enough sugar in the blood and it is necessary to improve its penetration into tissues.
4. Thiamine for suspected alcoholic hypoglycemic coma or exhaustion.

Complications of hypoglycemic coma

With the onset of severe hypoglycemic conditions, the body tries to prevent Negative consequences for the nervous system - accelerates the release of hormones, increases cerebral blood flow several times to increase the flow of oxygen and glucose. Unfortunately, compensatory reserves are able to prevent damage in the brain for a fairly short time.

If the treatment does not give results for more than half an hour, it is highly likely that complications have arisen. If the coma does not stop for more than 4 hours, there is a high chance of severe irreversible neurological pathologies. Due to prolonged starvation, cerebral edema develops, necrosis of individual areas. Due to the excess of catecholamines, the tone of the vessels decreases, the blood in them begins to stagnate, thrombosis and small hemorrhages occur.

In elderly diabetics, hypoglycemic coma can be complicated by heart attacks and strokes, mental damage. Long-term consequences are also possible - early dementia, epilepsy, Parkinson's disease, encephalopathy.

We will publish information shortly.

Diseases of this organ can provoke serious condition- hepatic coma. It has several stages, can be caused by various reasons and lead to serious consequences, even death. Our article will tell you more about this disease.

Definition and code according to ICD-10

Regulatory document defining international classification medical diagnoses ICD - 10 regulates the following diseases liver.

ICD code - 10:

• K 72 - not classified elsewhere.
• K 72.0 - acute and subacute liver failure.
• K 72.1 - chronic liver failure.
• K 72.9 - liver failure unaccounted for.

The disease develops against the background of general intoxication of the body. The body accumulates phenol, ammonia, sulfur-containing amino acids and low molecular weight fatty acids. They have a toxic effect on the brain, which increases with a violation of the water - electrolyte balance.

Forms

Liver dysfunction can be varied. In total, three variants of hepatic coma have been identified, which can lead to serious consequences.

What types of coma are:

• Endogenous, in which disorders can be caused by viral forms of hepatitis, dystrophic and destructive processes in the organ during cirrhosis, as well as the replacement of healthy liver tissues with a tumor or scars. It proceeds very painfully and progresses rapidly, with pain in the area of ​​the affected organ, hemorrhoidal disorders, jaundice and itching of the skin and severe "liver" breath odor occur. Psychosomatic disorders are often manifested, periods of increased activity alternate with a complete breakdown, depression and excessive fatigue.
• Exogenous hepatic coma is more common with chronic disorders organ function, cirrhosis and chronic renal failure. In this form of diseases, there is no characteristic smell and psychosomatic signs. The disease proceeds relatively painlessly and without pronounced symptoms. You can identify the problem by identifying hypertension of the portal veins.
• Mixed forms are characterized by symptoms of endogenous and exogenous forms of hepatic coma. At the same time, along with necrotic processes in the tissues of the organ, problems of the hematopoietic function are diagnosed, and the symptoms may include various manifestations of previous forms of the disease.

Stages of the disease

Depending on the severity of the patient's condition, there are three stages of this disease. In this case, the central nervous system is affected, the functions of brain activity are disturbed, concomitant symptoms are observed.

The disease has the following stages:

1. The phase of precursors or ancestor. The patient is emotionally unstable, mood changes are very abrupt and do not depend on external influences. Aggression, sleep disturbances (drowsiness during the day, insomnia at night) may occur. It is difficult to concentrate on any issue, consciousness is clouded, mental activity is inhibited. Common symptoms: tremor of the limbs, severe headache, nausea, vomiting, hiccups, excessive sweating, dizziness.
2. Excitation phase or threatening coma. Strong emotional upsurge, aggressiveness, anxiety. Mental activity is practically absent, movements are mechanical and without a specific goal. Often there is disorientation in time and environment. Pain blunted, reactions only to external stimuli.
3. Complete or deep coma. Complete absence of consciousness, emotions and reactions to stimuli. The respiratory rate may change (up to a complete stop), blood circulation slows down. The level of arterial pressure is reduced, paralysis of sphincters occurs, corneal reflexes go out.

Causes

Hepatic coma develops against the background of already existing chronic diseases and pathologies of the liver, as well as with toxic effects.

The main reasons are:

• Viral hepatitis of groups A, B, C, D, E, G.
• Viral liver diseases, including herpes, Infectious mononucleosis, Coxsackie's disease, measles,.
• Vasiliev-Weil disease (icteric leptospirosis).
• Liver damage by fungal or microplasma infection.
• Severe intoxication with toxic substances.

Threatening factors include the use of alcohol and psychotropic substances, the inclusion in the diet of an excessive amount of protein foods, as well as wild mushrooms.

Pathogenesis

The processes of pathogenesis are not fully understood. It is known that in this state, the work of neurotransmitter systems is disrupted, and an excess of decay products (nitrogen compounds, fatty acids and neurotransmitters), negatively affects the functioning of the brain and central nervous system.

Symptoms

Depending on the causes and severity of the disorders, the symptoms of the disease may vary. It is also worth considering the individual characteristics of the patient, on which the severity of the lesion and the prognosis of treatment also depend.

The main symptoms can be called:

1. Feelings of anxiety, thought disorders.
2. Sleep problems at night, daytime sleepiness.
3. Muscle cramps and increased tone.
4. Yellowing of the skin.
5. Accumulation of fluid in the abdomen (ascites).
6. Bleeding, the appearance of hematomas.
7. Pain in the region of the liver.
8. Increased body temperature, chills and fever.
9. Tachycardia, lowering blood pressure.
10. Tremor of limbs, usually fingers.

In various stages, increased mental arousal, aggression and sudden changes in mood can be observed. In addition, evidence of problems in the liver may be a strong bad smell from the mouth, digestive disorders (prolonged vomiting, constipation or diarrhea), sphincter paralysis.

Complications

Progressive liver failure affects general state patient, threatening his life. As such, this disease has no complications, because hepatic coma itself is a very serious condition, leading to irreversible processes in the body.

Diagnostics

Determine the disease by.

These include bilirubinemia (increased concentration of bile pigment), azotemia (excess normal indicators nitrogenous products), a decrease in the level of prothrombin, cholesterol and glucose.

Urine acquires a rich yellow color, bile acids and urobilin can be found in it, feces become discolored.

Urgent Care

If a sharp deterioration in health occurred outside the walls medical institution, the patient must be laid on his side, providing a normal flow of air and urgently call an ambulance.

Until the arrival of doctors, you can not change position, shake and carry the patient. Such conditions require immediate hospitalization, and already in the hospital an active struggle for the patient's life begins.

What can be done in the hospital:

• Introduce a glucose solution with panangin to improve brain activity.
• A complex of saline and insulin in severe catatonic conditions.
• On the first day, an increased dose of prednisolone is prescribed to relieve the toxic effects on the organ.
• Stimulation of liver activity is carried out using an intravenous or intramuscular solution. nicotinic acid, riboflavin, thiamine chloride and pyridoxine.

First aid is to reduce the symptoms of intoxication, stabilize the respiratory function, water - electrolyte balance and protein metabolism. Until stabilization of the condition and in order to prevent deep coma, the patient is in the intensive care unit.

Treatment

Measures for further treatment are agreed with the attending physician. The prognosis and chances of recovery depend on many factors, including the presence of comorbidities, age, and the extent of organ damage.

The following methods are commonly used:

1. Diet and protein restriction.
2. Taking antibacterial agents that reduce the activity of the intestinal flora and the formation of waste products.
3. Maintenance therapy consists of the use of glucose solution, saline, and glucocorticoids.
4. To reduce the level of ammonia, you need to take glutamic acid and arginine.
5. Excessive psychosomatic symptoms are corrected with special antipsychotics.
6. In case of dysfunction of the respiratory system, the patient is connected to an oxygen mask.

In the case of a diagnosis of "toxic poisoning", all measures should be aimed at detoxifying the body. The doctor may suggest a blood transfusion, as well as hemodialysis, if kidney failure has been added to the main symptoms.

How long does hepatic coma last?

Even the most highly qualified doctor will not be able to give accurate predictions. A patient in a state of complete coma will be extremely difficult to get out of it, so it is best to seek help in the early stages of the disease.

The percentage of recovery is significantly affected by accurate diagnosis and elimination of the cause, but in more than 15% of cases it cannot be determined.

Forecast and prevention

The chances of recovery in patients who have had a hepatic coma are extremely low.

Basically, this is no more than 20% of survivors in the ancestral stage, less than 10% in the threatening phase and about 1% in a deep coma. Even such disappointing forecasts are far from always possible, and even then with timely and competent treatment.

Irreversible processes that occur in the body under the influence of decay products, as well as with inhibition of functions or complete failure of the organ, affect the activity of the central nervous system and brain.

It is extremely difficult to bring a person out of a state of deep coma, and the most successful treatment at the moment is a donor liver transplant and long-term drug therapy.

There are no preventive measures against this disease. To maintain the health of this organ, it is necessary to follow general recommendations: refuse, and take, observe moderation in nutrition, and also regularly expose the body to feasible physical exertion.

All problems and identified diseases must be cured in time and regularly examined if possible. Hepatic coma, regardless of the forms and stages, causes irreparable harm to health and significantly reduces the quality and life expectancy, so its symptoms should never be ignored.

ICD 10. CLASS XVIII. SYMPTOMS, SIGNS AND ABNORMALITIES DETECTED IN CLINICAL AND LABORATORY STUDIES, NOT OTHERWISE CLASSIFIED (R20-R49)

SYMPTOMS AND SIGNS RELATED TO THE SKIN AND SUBCUTANEOUS FIBRE (R20-R23)

R20 Disturbance of skin sensation

Excludes: dissociative anesthesia and sensory loss
perception ( F44.6)
psychogenic disorders ( F45.8)

R20.0 Skin anesthesia
R20.1 Skin hypoesthesia
R20.2 Skin paresthesia. "Crawling" sensation. Sensation of "tingling with pins and needles"
Excludes: acroparesthesia ( I73.8)
R20.3 Hyperesthesia
R20.8 Other and unspecified skin sensory disorders

R21 Rash and other non-specific skin eruptions

R22 Localized bulge, thickening or swelling of the skin and subcutaneous tissue

Includes: subcutaneous nodules (localized) (superficial)
Excludes: abnormalities detected upon receipt
diagnostic image ( R90-R93)
enlarged The lymph nodes (R59. -)
localized fat deposition ( E65)
thickening or swelling:
mammary gland ( N63)
intra-abdominal or pelvic R19.0)
edema ( R60. -)
bulging intra-abdominal or pelvic ( R19.0)
joint swelling ( M25.4)

R22.0 Localized bulge, hardness, or swelling in the scalp
R22.1 Localized bulge, hardness, or swelling in the neck
R22.2 Localized bulge, hardness, or swelling in the trunk
R22.3 Localized bulge, induration, or swelling of the upper upper limb
R22.4 Localized bulge, induration, or swelling in the lower extremity
R22.7 Localized bulging, hardening, or swelling in multiple areas of the body
R22.9 Localized bulge, induration or swelling, unspecified

R23 Other skin changes

R23.0 Cyanosis
Excludes: acrocyanosis ( I73.8)
an attack of cyanosis in a newborn ( P28.2)
R23.1 Pallor. Cold, damp skin
R23.2 Hyperemia. Excessive redness
Excludes: associated with menopause and climacteric conditions in women ( N95.1)
R23.3 Spontaneous ecchymosis. petechiae
Excludes: ecchymosis in fetus and newborn ( P54.5)
purpura ( D69. -)
R23.4 Changes in the structure of the skin
peeling)
Seal ) skin
scaly)
Excludes: epidermal thickening NOS ( L85.9)
R23.8 Other and unspecified skin changes

SYMPTOMS AND SIGNS RELATED TO THE NERVOUS AND MUSCLE-SKELETAL SYSTEMS (R25-R29)

R25 Abnormal involuntary movements

Excludes: specific movement disorders ( G20-G26)
stereotypic movement disorders F98.4)
ticks ( F95. -)

R25.0 Abnormal head movements
R25.1 Tremor, unspecified
Excludes: chorea NOS ( G25.5)
tremor:
essential ( G25.0)
dissociative ( F44.4)
intentional ( G25.2)
R25.2 Cramp and spasm
Excludes: carpopedal spasm ( R29.0)
baby spasms ( G40.4)
R25.3 Fasciculation. Jerking NOS
R25.8 Other and unspecified abnormal involuntary movements

R26 Gait and mobility disorders

Excludes: ataxia:
NOS ( R27.0)
hereditary ( G11. -)
motor (syphilitic) ( A52.1)
immobility syndrome (paraplegic) ( M62.3)

R26.0 Ataxic gait. staggering gait
R26.1 Paralytic gait. Spasmodic gait
R26.2 Difficulty walking, not elsewhere classified
R26.8 Other and unspecified disorders of gait and mobility. Unsteady walking NOS

R27 Other incoordination

Excludes: ataxic gait ( R26.0)
hereditary ataxia ( G11. -)
dizziness NOS ( R42)

R27.0 Ataxia, unspecified
R27.8 Other and unspecified incoordination

R29 Other symptoms and signs relating to the nervous and musculoskeletal systems

R29.0 Tetany. Carpopedal spasm
Excludes: tetany:
dissociative ( F44.5)
newborn ( P71.3)
parathyroid ( E20.9)
after removal thyroid gland (E89.2)
R29.1 Meningism
R29.2 abnormal reflex
Excludes: abnormal pupillary reflex ( H57.0)
increased gag reflex J39.2)
vasovagal reaction, or fainting ( R55)
R29.3 Abnormal body position
R29.4 Snapping hip
Excludes: congenital deformity of the hip ( Q65. -)
R29.8 Other and unspecified symptoms and signs relating to the nervous and musculoskeletal systems

SYMPTOMS AND SIGNS RELATED TO THE URINARY SYSTEM (R30-R39)

R30 Pain associated with urination

Excludes: psychogenic pain ( F45.3)

R30.0 Dysuria. Difficulty urinating [stranguria]
R30.1 Tenesmus of the bladder
R30.9 Painful urination, unspecified. Painful urination NOS

R31 Nonspecific hematuria

Excludes: recurrent or persistent hematuria ( N02. -)

R32 Urinary incontinence, unspecified

Enuresis NOS
Excludes: enuresis of inorganic nature ( F98.0)
stress incontinence and more
specified urinary incontinence ( N39.3-N39.4)

R33 Urinary retention

R34 Anuria and oliguria

Excluded: cases complicating:
abortion, ectopic or molar pregnancy ( O00 -O07 , O08.4 )
pregnancy, childbirth and postpartum period (O26.8, O90.4)

R35 Polyuria

Frequent urination
Nocturnal polyuria [nocturia]
Excludes: psychogenic polyuria ( F45.3)

R36 Discharge from urethra

Discharge from the male penis

R39 Other symptoms and signs relating to the urinary system

R39.0 Extravasation of urine
R39.1 Other difficulties associated with urination. Intermittent urination. Weak urine stream
Split urine stream
R39.2 extrarenal uremia. Prerenal uremia
R39.8 Other and unspecified symptoms and signs relating to the urinary system

SYMPTOMS AND SIGNS RELATED TO COGNITIVITY,
PERCEPTION, EMOTIONAL STATE AND BEHAVIOR (R40-R46)

Excludes: symptoms and signs that are part of clinical picture mental disorder (F00-F99)

R40 Somnolence, stupor and coma

Excludes: coma:
diabetic ( E10-E14 with a common fourth sign.0)
hepatic ( K72. -)
hypoglycemic (non-diabetic) ( E15)
newborn ( P91.5)
uremic ( N19)

R40.0 Somnolence [hypersomnia]. Drowsiness
R40.1 Stupor. Precoma
Excludes: stupor:
catatonic ( F20.2)
depressive ( F31-F33)
dissociative ( F44.2)
manic ( F30.2)
R40.2 Coma unspecified. Unconsciousness NOS

R41 Other symptoms and signs relating to cognition and awareness

Excludes: dissociative [conversion] disorders ( F44. -)

R41.0 Disorientation, unspecified. Confusion NOS
Excludes: psychogenic disorientation ( F44.8)
R41.1 Anterograde amnesia
R41.2 retrograde amnesia
R41.3 Other amnesias. Amnesia NOS
Excludes: amnesic syndrome:
caused by the use of psychoactive
funds ( F10-F19 with a common fourth character.6)
organic ( F04)
transient total amnesia ( G45.4)
R41.8 Other and unspecified symptoms and signs relating to cognition and awareness

R42 Dizziness and impaired stability

Lightness of the head
Dizziness NOS
Excludes: syndromes related to vertigo ( H81. -)

R43 Disorders of smell and taste

R43.0 Anosmia
R43.1 Parosmia
R43.2 Parageusia
R43.8 Other and unspecified disorders of smell and taste. Combined impairment of smell and taste

R44 Other symptoms and signs relating to general sensations and perceptions

Excludes: disturbances of skin sensitivity ( R20. -)

R44.0 auditory hallucinations
R44.1 visual hallucinations
R44.2 Other hallucinations
R44.3 Hallucinations, unspecified
R44.8 Other and unspecified symptoms and signs related to sensations and perceptions

R45 Symptoms and signs relating to emotional state

R45.0 Nervousness. nervous tension
R45.1 Anxiety and agitation
R45.2 A state of anxiety in connection with failures and misfortunes. Alarm condition NOS
R45.3 Demoralization and apathy
R45.4 Irritability and anger
R45.5 Hostility
R45.6 Physical aggressiveness
R45.7 State of emotional shock and stress, unspecified
R45.8 Other symptoms and signs related to the emotional state

R46 Symptoms and signs relating to appearance and behavior

R46.0 Very low level personal hygiene
R46.1 Quirky appearance
R46.2 Strange and unexplained behavior
R46.3 Excessive activity
R46.4 Lethargy and delayed reaction
Excluded: stupor ( R40.1)
R46.5 Suspicion and obvious evasiveness
R46.6 Excessive interest and increased attention to stressful events
R46.7 Verbosity and unnecessary details that make unclear reason contact
R46.8 Other symptoms and signs related to appearance and behavior

SYMPTOMS AND SIGNS RELATED TO SPEECH AND VOICE (R47-R49)

R47 Speech disorders, not elsewhere classified

Excludes: autism ( F84.0-F84.1)
fluent speech ( F98.6)
specific developmental disorders of speech and language ( F80. -)
stammering [stammering] ( F98.5)

R47.0 Dysphasia and aphasia
Excludes: progressive isolated aphasia ( G31.0)
R47.1 Dysarthria and anartria
R47.8 Other and unspecified speech disorders

R48 Dyslexia and other disorders of recognition and understanding of symbols and signs, not elsewhere classified

Excludes: specific developmental disorders of learning skills ( F81. -)

R48.0 Dyslexia and alexia
R48.1 agnosia
R48.2 Apraxia
R48.8 Other and unspecified disorders of recognition and understanding of symbols and signs. Acalculia. Agraphia

R49 Voice disorders

R49.0 Dysphonia. Hoarseness
R49.1 Aphonia. loss of voice
R49.2 Open nasal and closed nasal
R49.8 Other and unspecified voice disorders. Voice change NOS