Coma treatment. Primary cerebral coma

Coma is a state of complete lack of consciousness when a person does not react to anything. In a comatose state, no stimulus (neither external nor internal) is able to bring a person to life. This is a life-threatening resuscitation state, because, in addition to loss of consciousness, with a coma, violations of the functions of vital important organs (respiration and cardiac activity).

Being in a coma, a person is not aware of any the worldnor yourself.

Coma is always a complication of any disease or pathological condition (poisoning, injury). All comas have a number of common features, regardless of the cause of their occurrence. But there are differences in clinical symptoms for different types of coma. Coma treatment should be carried out in the intensive care unit. It is aimed at maintaining vital body functions and preventing the death of brain tissue. From this article you will learn about what coma are, how they are characterized, and what are the basic principles of treating coma.

What is the root of a coma?

Coma is based on two mechanisms:

• bilateral diffuse lesion of the cerebral cortex;
• primary or secondary lesion of the brain stem with the reticular formation located in it. The reticular formation maintains the tone and active state of the cerebral cortex. When "off" reticular formation deep inhibition develops in the cerebral cortex.

Primary damage to the brainstem is possible in conditions such as a tumor process. Secondary disorders occur during metabolic changes (with poisoning, endocrine diseases, etc.).

A combination of both mechanisms of coma development is possible, which is most often observed.

As a result of these disorders, it becomes impossible for the normal transmission of nerve impulses between the cells of the brain. At the same time, the coordination and coordinated activity of all structures is lost, they go to an autonomous mode. The brain loses its administrative functions over the whole organism.

Com classification

Comatose states are usually divided according to various criteria. The most optimal are two classifications: by the causal factor and by the degree of depression of consciousness (depth of coma).

When dividing by the causal factor, conventionally all comas are classified into comas with primary neurological disorders (when a process in the nervous system itself served as the basis for the development of coma) and secondary neurological disorders (when brain damage occurred indirectly in the course of some pathological process outside the nervous system). Knowing the cause of the coma allows you to correctly determine the tactics of treating the patient.

So, depending on the cause that led to the development of coma, there are such types of coma: neurological (primary) and secondary genesis.

Neurological (primary) genesis:

• traumatic (with traumatic brain injury);
• cerebrovascular (with acute vascular circulatory disorders in the brain);
• epileptic (result);
• meningoencephalitic (the result of inflammatory diseases of the brain and its membranes);
• hypertensive (due to a tumor in the brain and skull).

Secondary genesis:

• endocrine (diabetic in diabetes mellitus (there are several types of them), hypothyroid and thyrotoxic in diseases thyroid gland, hypocorticoid with acute failure adrenal glands, hypopituitary with a total deficiency of pituitary hormones);
• toxic (with renal or hepatic failure, with poisoning by any substances (alcohol, drugs, carbon monoxide, etc.), with cholera, with drug overdose);
• hypoxic (with severe heart failure, obstructive pulmonary disease, with anemia);
• coma when exposed to physical factors (thermal when overheating or hypothermia, with electric shock);
• coma with a significant deficiency of water, electrolytes and food (hungry, with indomitable vomiting and diarrhea).

According to statistics, most common reason the development of a coma is a stroke, in second place is drug overdose, in third - complications of diabetes mellitus.

The need for the existence of a second classification is due to the fact that the causal factor itself does not reflect the severity of the patient's condition in a coma.

Depending on the severity of the condition (the depth of oppression of consciousness), it is customary to distinguish the following types of coma:

• I degree (light, subcortical);
• II degree (moderate, forestem, "hyperactive");
• III degree (deep, rear-stemmed, "sluggish");
• IV degree (transcendental, terminal).

Distinguishing degrees of coma is difficult because the transition from one stage to another can be very rapid. This classification is based on different clinical symptomscorresponding to a certain stage.

Coma signs

Coma I degree

It is called subcortical, because at this stage the activity of the cerebral cortex is inhibited and the deeper parts of the brain, called subcortical formations, are disinhibited. It is characterized by the following manifestations:

• feeling that the patient is in a dream;
• complete disorientation of the patient in place, time, personality (it is impossible to stir up the patient);
• lack of answers to the questions asked. Perhaps inarticulate mooing, making various sounds out of connection with what is happening from the outside;
• the absence of a normal reaction to a pain stimulus (that is, the reaction is weak and very slow, for example, when a needle is pricked by a needle, the patient does not pull it away immediately, but only weakly bends or unbends some time after applying pain irritation);
• spontaneous active movements are practically absent. Sometimes sucking, chewing, and swallowing movements can occur as a manifestation of brain reflexes, which are normally suppressed by the cerebral cortex;
• muscle tone is increased;
• deep reflexes (knee, Achilles and others) increase, and superficial (corneal, plantar and others) are inhibited;
• pathological hand and foot symptoms are possible (Babinsky, Zhukovsky and others);
• the reaction of the pupils to light is preserved (narrowing), squint, spontaneous movements of the eyeballs can be observed;
• lack of control over the activity of the pelvic organs;
• usually spontaneous breathing is preserved;
• from the side of cardiac activity there is an increase in the heart rate (tachycardia).

Coma II degree

At this stage, the activity of the subcortical formations is inhibited. Disturbances descend to the anterior parts of the brainstem. This stage is characterized by:

• the appearance of tonic convulsions or periodic flinching;
• lack of speech activity, verbal contact is impossible;
• a sharp weakening of the reaction to pain (slight movement of the limb when the injection is applied);
• oppression of all reflexes (both superficial and deep);
• constriction of the pupils and their weak reaction to light;
• an increase in body temperature;
• increased sweating;
• sharp fluctuations blood pressure;
• severe tachycardia;
• breathing disorder (with pauses, with stops, noisy, with different depths of breaths).

Coma III degree

Pathological processes reach the medulla oblongata. The risk to life increases, and the prognosis for recovery worsens. The stage is characterized by the following clinical signs:

• protective reactions in response to a painful stimulus are completely lost (the patient does not even move a limb in response to an injection);
• superficial reflexes are absent (in particular, corneal);
• there is a sharp decrease in muscle tone and tendon reflexes;
• pupils are dilated and do not respond to light;
• breathing becomes shallow and arrhythmic, little productive. Additional muscles (muscles of the shoulder girdle) are involved in the act of breathing, which is not normally observed;
• blood pressure decreases;
• periodic convulsions are possible.

Coma IV degree

At this stage, there are no signs of brain activity. This is manifested:

• lack of all reflexes;
• the maximum possible dilation of the pupils;
• muscle atony;
• lack of spontaneous breathing (only artificial ventilation of the lungs supports the supply of oxygen to the body);
• blood pressure drops to zero without medication;
• drop in body temperature.

Achieving a grade IV coma has a high risk of death, approaching 100%.

It should be noted that some of the symptoms of the different stages of coma may differ depending on the cause of the coma. In addition, certain types of coma have additional signs, which in some cases are diagnostic.

Clinical features of some types of com

Cerebrovascular coma

It always becomes the result of a global vascular catastrophe (ischemic or ruptured aneurysm), therefore it develops suddenly, without precursors. Usually, consciousness is lost almost instantly. Moreover, the patient has a red face, hoarse breathing, high blood pressure, tense pulse. In addition to the neurological symptoms characteristic of a coma, there are focal neurological symptoms (for example, a skewed face, puffing out one cheek when breathing). The first stage of coma may be accompanied by psychomotor agitation. If a subarachnoid hemorrhage occurs, then positive meningeal symptoms are determined (stiff neck muscles, Kernig's, Brudzinsky's symptoms).

Traumatic coma

Since it usually develops as a result of severe traumatic brain injury, damage to the skin can be found on the patient's head. Possible bleeding from the nose, ear (sometimes leakage of cerebrospinal fluid), bruising around the eyes (symptom of "glasses"). Quite often, the pupils have different sizes on the right and left (anisocoria). Also, as with cerebrovascular coma, there are focal neurological signs.

Epileptic coma

It is usually the result of repetitive seizures one by one. With this coma, the patient's face acquires a bluish tint (if the attack was very recent), the pupils become wide and do not respond to light, traces of a tongue bite, foam on the lips are possible. When the seizures stop, the pupils are still wide, the muscle tone is reduced, and reflexes are not triggered. Tachycardia and rapid breathing occur.

Meningoencephalitic coma

It occurs against the background of an existing inflammatory disease of the brain or its membranes, therefore it is rarely sudden. There is always an increase in body temperature, of varying severity. A rash on the body is possible. In the blood, there is a significant increase in the content of leukocytes and ESR, and in the cerebrospinal fluid - an increase in the amount of protein and leukocytes.

Hypertensive coma

It occurs as a result of a significant increase in intracranial pressure in the presence of additional education in the cranial cavity. Coma develops due to compression of some parts of the brain and its infringement in the notch of the cerebellar tentorium or the foramen magnum. This coma is accompanied by bradycardia (slowing down of heart rate), decreased respiratory rate, and vomiting.

Hepatic coma

It develops gradually against the background of hepatitis or liver cirrhosis. A specific hepatic odor emanates from the patient (the smell of "raw meat"). The skin is yellow, with punctate hemorrhages, in places of scratching. Tendon reflexes are increased, and seizures may occur. Blood pressure and heart rate are low. The pupils are dilated. The patient's liver is enlarged. There may be signs of portal hypertension (for example, "jellyfish's head" - expansion and tortuosity of the saphenous veins of the abdomen).

Renal coma

It also develops gradually. The smell of urine (ammonia) emanates from the patient. The skin is dry, pale gray (as if dirty), with traces of scratching. There are edema in the lumbar region and lower extremities, puffiness of the face. Blood pressure is low, tendon reflexes are high, pupils are narrow. Involuntary muscle twitching in certain muscle groups is possible.

Alcoholic coma

It develops gradually with alcohol abuse and taking too much of a dose. Naturally, the smell of alcohol is felt (however, it should be borne in mind that in the presence of this sign, the coma may be different, for example, traumatic. It's just that the person could have consumed alcohol before the injury). The heart rate rises and the blood pressure falls. The skin is red, wet with sweat. Muscle tone and reflexes are low. The pupils are narrow.

Coma with carbon monoxide poisoning

This coma is accompanied by tachycardia with low blood pressure, shallow breathing (respiratory paralysis is possible). Wide pupils with no reaction to light are characteristic. A very specific symptom is the color of the face and mucous membranes: cherry red (this color is given by carboxyhemoglobin), while the limbs can be cyanotic.

Coma with hypnotics (barbiturates) poisoning

Coma develops gradually as a continuation of sleep. Bradycardia (low heart rate) and low blood pressure are common. Breathing becomes shallow and rare. The skin is pale. The reflex activity of the nervous system is so inhibited that there is no reaction to pain at all, tendon reflexes are not triggered (or they are sharply weakened). Salivation increased.

Coma in case of drug overdose

It is characterized by a drop in blood pressure, decreased heart rate, weak pulse, and shallow breathing. The lips and fingertips are bluish and the skin is dry. Muscle tone is sharply weakened. The so-called "pinpoint" pupils are characteristic, they are so narrowed. There may be injection marks (although this is not necessary, since the route of drug use may, for example, be intranasal).

Diabetic coma

It would be more correct to say not a coma, but coma. Because there may be several of them in diabetes mellitus. This is ketoacidotic (with the accumulation of metabolic products of fat in the blood and an increase in glucose levels), hypoglycemic (with a drop in glucose levels and excess insulin), hyperosmolar (with severe dehydration) and lactacidemic (with an excess of lactic acid in the blood). Each of these varieties has its own clinical signs... So, for example, with a ketoacidotic coma, there is the smell of acetone from the patient, the skin is pale and dry, the pupils are narrowed. With a hypoglycemic coma, odors from the patient are not felt, the skin is pale and moist, and the pupils are dilated. Of course, in determining the type of diabetic coma, additional research methods play a major role (the amount of glucose in the blood, in the urine, the presence of acetone in the urine, and so on).

Lump treatment principles

Coma is a condition, first of all, requiring urgent measures to maintain the vital functions of the body. These measures are taken regardless of what reason caused whom. The main thing is not to let the patient die and to preserve the brain cells from damage as much as possible.

The measures that ensure the vital functions of the body include:

• breathing support. If necessary, the airways are sanitized to restore their patency (removed foreign bodies, the sunken tongue is straightened), an air duct, an oxygen mask is installed, artificial lung ventilation is carried out;
• support of the circulatory system (the use of drugs that increase blood pressure with hypotension, and reduce with hypertension; drugs that normalize the heart rate; normalization of the volume of circulating blood).

Symptomatic measures are also used to remove existing violations:

• large doses of vitamin B 1 with suspected alcohol poisoning;
• in the presence of seizures;
• antiemetic drugs;
• sedatives when agitated;
• glucose is injected intravenously (even if the cause of the coma is not known, because the risk of brain damage from low blood glucose is higher than from high blood glucose. Injecting some glucose with high blood glucose will not do much harm);
• gastric lavage if you suspect poisoning with drugs or poor-quality food (including mushrooms);
• drugs to lower body temperature;
• in the presence of signs of an infectious process, the use of antibiotics is indicated.

At the slightest suspicion of injury cervical the spine (or if it is impossible to exclude it), stabilization of this area is necessary. Usually a collar splint is used for this purpose.

After the cause of the coma is established, the underlying disease is treated. Then a specific therapy is already prescribed, directed against a specific ailment. This can be hemodialysis for renal failure, the introduction of Naloxone in case of drug overdose, and even surgical intervention (for example, with a hematoma of the brain). Type and volume treatment measures depends on the diagnosis.

Coma is a life-threatening complication of a number of pathological conditions. It requires immediate medical attention as it can be fatal. There are a great many varieties of coma due to the large number of pathological conditions that can be complicated by them. Coma treatment is carried out in the intensive care unit and is aimed at saving the patient's life. Moreover, all measures must ensure the preservation of brain cells.

Definition

"Coma" from ancient Greek is translated as deep sleep. According to the classical definition, this term denotes the most significant degree of pathological inhibition of the central nervous system (CNS), characterized by profound loss of consciousness, lack of reflexes to external stimuli and dysregulation of vital body functions.

However, it is more expedient to define whom as a state of cerebral insufficiency, characterized by a violation of the coordinating activity of the central nervous system, the separation of the organism into separate, autonomously functioning systems that lose the ability to self-regulate and maintain homeostasis at the level of the whole organism.

Clinically, coma is manifested by loss of consciousness, impaired motor, sensory and somatic functions, including vital ones.

The main causes and pathogenesis

Comatose states develop for various reasons, which can be grouped into four groups:

• intracranial processes (vascular, inflammatory, volumetric, etc.);
• hypoxic conditions:
  • with somatic pathology;
  • in violation of tissue respiration (tissue hypoxia);
  • with a drop in oxygen tension in the inhaled air;
• metabolic disorders;
• intoxication.

Classification

Depending on the causative factors, primary and secondary comas are distinguished ().

To assess the prognosis and the choice of treatment tactics, it is very important to determine what led to the development of a coma: focal brain damage with a mass effect, damage to the brain stem, or diffuse damage to the cortex and brain stem. In this case, the first two options are characteristic of primary, and the latter is found almost exclusively in secondary coma.

Turning off consciousness - stunning - can have a different depth, depending on what it is divided into:

• obnibulation - fogging, darkening, "cloudiness of consciousness", stunning;
• somnolence - drowsiness;
• sopor - unconsciousness, insensitivity, pathological hibernation, deep stunning;
• to whom - the most profound degree of cerebral insufficiency.

As a rule, the diagnosis of “precoma” is made instead of the first three options. However, there is no pathogenetically substantiated distinction between four degrees of stunning, and therefore, regardless of the degree of loss of consciousness, it is permissible to use the term "coma", the depth of which can be assessed using a simple but informative clinical scale of the depth of coma.

Possible complications

Among the complications of coma that are important at the prehospital stage, one can conditionally distinguish:

• conditions and syndromes directly related to brain damage and edema;
• pathological conditions and reactions caused by a violation of the regulatory function of the central nervous system.
• the first are such formidable complications as:
• various breathing disorders up to and including stopping it;
• hemodynamic disorders, manifested by both arterial hyper- and hypotension, pulmonary edema, and cardiac arrest;
• central hyperthermia.

The latter, although they are "peripheral" in nature, can also be fatal:

• vomiting with aspiration of vomit into the respiratory tract and the development of asphyxia or Mendelssohn's syndrome (acute respiratory failure due to bronchial obstruction, subsequent toxic pulmonary edema when acidic gastric contents enter the respiratory system);
• acute urinary retention ("neurogenic bladder") with rupture bladder;
• eCG changes, which, in contrast to the "heart attack-stroke" syndrome, are in the nature of myocardial dystrophy.

Call structure "03"

According to our data, obtained from the analysis of the work of the SSiNMP in Moscow, the frequency of coma at the prehospital stage is 5.8 per 1000 calls. Quite often, the cause of coma at the prehospital stage remained not only unexplained, but even unsuspected (coma of unknown origin) - 11.9%. At the same time, prehospital mortality reaches 4.4%.

Diagnostic criteria

The diagnosis of coma is based on the identification of:

Differential diagnosis is carried out with pseudocomatous states (isolation syndrome, psychogenic unresponsiveness, abulic status, non-convulsive status epilepticus).

Clinical picture

In addition to specific signs in the clinical picture of coma, signs of depression of consciousness and weakening of reflexes (tendon, periosteal, cutaneous and cranial nerves) play an essential, and sometimes leading role, and progress to complete extinction as the coma deepens. The youngest reflexes are the first to fade, and the oldest reflexes last. In the absence of focal lesions of the brain, the deepening of the coma is accompanied by the appearance, and in the future - the loss of bilateral pathological signs (Babinsky's reflex); focal lesions are characterized by their one-sidedness. Meningeal signs - stiffness of the occipital muscles, Kernig's and Brudzinsky's symptoms, characteristic of the lesion meninges - meningitis, meningoencephalitis, also appear with cerebral edema and irritation of the meninges. The progression of cerebral insufficiency with the extinction of functions leads to various respiratory disorders with hypo- or hyperventilation and corresponding respiratory changes in the acid-base state. Gross hemodynamic disturbances are usually associated with the terminal state.

Questions that an ambulance doctor should get answers to

The list of questions and the interpretation of the answers are given in.

UNDIFFERENTIATED AND DIFFERENTIATED THERAPY

Treatment of coma consists of differentiated therapy of individual coma and general, universal measures that do not depend on the causes, pathogenesis and clinical manifestations.

Undifferentiated therapy for coma

First aid measures for a patient in a coma have several goals, and the main measures must be carried out simultaneously:

• Mandatory immediate hospitalization in the intensive care unit, and in case of traumatic brain injury or subarachnoid hemorrhage - in the neurosurgical department.

Despite the mandatory hospitalization, emergency treatment for coma in all cases should be started immediately.

• Restoration (or maintenance) of an adequate state of vital functions:

• breathing:
  - sanitation of the airways to restore their patency, installation of an air duct or fixation of the tongue, artificial ventilation of the lungs with a mask or through an endotracheal tube, in rare cases - tracheo- or conicotomy; oxygen therapy (4-6 l / min through a nasal catheter or 60% through a mask, endotracheal tube); tracheal intubation in all cases should be preceded by premedication with a 0.1% solution of atropine in a dose of 0.5-1.0 ml (except for poisoning with anticholinergic drugs);
• circulation:
  - with arterial hypertension, the introduction of 5-10 ml of a 25% solution of magnesium sulfate (IV bolus for 7-10 minutes or drip), bolus administration of 3-4 ml of a 1% solution (6-8 ml 0.5 % solution) of dibazol, and with a slight increase in blood pressure, a bolus injection of 5-10 ml of a 2.4% solution of aminophylline (within 3-5 minutes) is sufficient;
• the fight against arterial hypotension is carried out in three stages:
  - slow intravenous administration of dexamethasone at a dose of 8-20 mg or mazipredon (prednisolone) at a dose of 60-150 mg;
  - in case of ineffectiveness - dextran 70 (polyglucin) at a dose of 50-100 ml i.v. jet, then i.v. drip in a volume of up to 400-500 ml; coma against the background of intoxication, exicosis and hemoconcentration serve as an indication for the infusion of 1000-2000 ml of 0.9% sodium chloride solution or 5% glucose solution;
  - if ineffective - drip dopamine at a dose of 5-15 mcg / kg / min or norepinephrine;
• with arrhythmias - restoration of an adequate heart rate.

• Immobilization of the cervical spine for any suspicion of injury.

• Providing the necessary conditions for treatment and control.

The requirement to comply with the "rule of three catheters" (catheterization of the peripheral vein, bladder and the installation of a gastric, preferably nasogastric, probe) when managing a coma at the prehospital stage is not so categorical:

• in a coma medicines administered only parenterally and preferably intravenously; installation of a catheter in a peripheral vein is required;
• bladder catheterization should be carried out according to strict indications;
• introduction in a coma of a gastric tube with a preserved vomiting reflex without prior intubation of the trachea and its sealing with a swollen cuff is fraught with the possible development of aspiration of gastric contents.

• Diagnostics of carbohydrate metabolism disorders and ketoacidosis:

• determination of the concentration of glucose in capillary blood using visual test strips; at the same time, in patients with diabetes mellitus accustomed to hyperglycemia due to inadequate treatment, it is necessary to take into account the possibility of developing hypoglycemic coma even at normal glucose levels;
• determination of ketone bodies in urine using visual test strips; this manipulation is impracticable in case of anuria, and if ketonuria is detected, it requires differential diagnosis of all conditions in which ketoacidosis is possible.

• Differential diagnosis and fight against hypoglycemia, which is a pathogenetic link in a number of coma.

Bolus injection of 40% glucose solution in the amount of 20.0-40.0; when the effect is achieved, but its intensity is insufficient, the dose is increased (see below).

• Prevention of a potentially fatal complication - acute Wernicke encephalopathy.

This syndrome is the result of a deficiency of vitamin B1, which is most pronounced with alcohol intoxication and prolonged fasting and is aggravated by the intake of large doses of glucose. In this regard, the introduction of a 40% glucose solution in the absence of intolerance in all cases should be preceded by a bolus injection of 100 mg of thiamine (2 ml of vitamin B1 in the form of a 5% solution of thiamine chloride).

• Therapeutic and diagnostic use of antidotes:

• opiate receptor antagonist:
  - the diagnostic administration of naloxone should be treated with caution, since a positive reaction (albeit incomplete and short-term) is possible with other types of coma, for example, with alcohol;
  - indications for the introduction of naloxone are:
  breathing rate< 10 в мин;
  pinpoint pupils; suspicion of drug intoxication;
  - the initial dose of naloxone (IV or endotracheal) can range from 0.4-1.2 to 2 mg with possible additional administration after 20-30 minutes with repeated deterioration, to prolong the effect, it is possible to combine IV administration with subcutaneous administration;
• benzodiazepine receptor antagonist:
  - in case of poisoning or suspicion of poisoning with drugs of the benzodiazepine series, flumazenil is indicated (0.2 mg intravenously for 15 seconds, followed by the introduction, if necessary, of 0.1 mg every minute to a total dose of 1 mg);
  - the danger of using flumazenil is the risk of developing convulsive syndrome in case of mixed poisoning with benzodiazepines and tricyclic antidepressants.

• Combating intracranial hypertension, edema and swelling of the brain and meninges:

• the most effective and universal method - Ventilation in hyperventilation mode, providing the required result within an hour. However, at the prehospital stage, this method can only be used for health reasons;
• in the absence of high blood osmolarity (for example, with hyperglycemia or hyperthermia), and also if there is no threat of development or increased bleeding, dehydration is achieved by the introduction of an osmotic diuretic - mannitol - in an amount of 500 ml of a 20% solution for 10-20 minutes (1-2 g / kg); to prevent a subsequent increase in intracranial pressure and an increase in cerebral edema ("rebound" syndrome), up to 40 mg of furosemide is administered at the end of the mannitol infusion;
• the traditional use of glucocorticoid hormones is based on their proven effect in the case of a brain tumor; Dexamethasone (8 mg) has the greatest efficacy and safety;
• restriction of the introduction of hypotonic solutions, as well as 5% glucose solution and 0.9% sodium chloride solution (no more than 1 l / m2 / day), which does not apply to coma occurring against the background of hemoconcentration (hyperglycemic, hyperthermic, hypocorticoid, alcoholic).

• Neuroprotection and increased wakefulness:

• when focal symptoms prevail over cerebral symptoms, piracetam is effective (drip infusion at a dose of 6-12 g);
• in case of impaired consciousness to the level of superficial coma, the following are shown:
  - sublingual (or cheek) administration of glycine at a dose of 1 g;
  - intravenous administration antioxidant mexidol at a dose of 200 mg (6 ml of a 0.5% solution) bolus for 5-7 minutes;
• with deep coma, Semax is administered intranasally at a dose of 3 mg (3 drops of a 1% solution in each nasal passage).

• Measures to stop the intake of toxin in the body in case of suspected poisoning:

• gastric lavage through a tube with the introduction of a sorbent (when the poison enters the mouth);
• washing the skin and mucous membranes with water (when the poison enters through the integumentary tissues).

• Symptomatic therapy:

• normalization of body temperature:
  - with hypothermia - warming the patient without using heating pads and intravenous administration of heated solutions;
  - with high hyperthermia - hypothermia by physical methods and pharmacological agents (drugs from the group of analgesics-antipyretics);
• relief of seizures:
  - the introduction of diazepam (relanium) at a dose of 10 mg;
• stopping vomiting:
  - introduction of metoclopramide (cerucal, raglan) at a dose of 10 mg i / v or i / m.

• For all comas, ECG registration is required.

Differentiated therapy of individual coma

• Hypoglycemic coma. Bolus injection of 40% glucose solution (with preliminary introduction of 100 mg of thiamine) at a dose of 20-40-60 ml, but due to the threat of cerebral edema, no more than 120 ml; if necessary, its further introduction - infusion of glucose in a decreasing concentration (20-10-5%) with the introduction of dexamethasone at a dose of 4-8 mg to prevent cerebral edema and as a counter-insular factor; with the introduction of large doses of glucose and the absence of contraindications, subcutaneous administration of up to 0.5-1 ml of a 0.1% solution of adrenaline is permissible; with a prolonged coma (more than a few hours), intravenous administration of up to 2500 mg of magnesium sulfate (10 ml of a 25% solution) is indicated.
• Hyperglycemic ketoacidotic and hyperosmolar non-ketoacidotic coma. Infusion of 0.9% sodium chloride solution in a volume of 1 liter and 1.5 liters, respectively, in the first hour. With hyperosmolar coma and a long course of ketoacidotic coma, heparin therapy is indicated - up to 10 thousand units intravenously.
• Hungry (alimentary-dystrophic) coma. Warming the patient, infusion of 0.9% sodium chloride solution (with the addition of 40% glucose solution at the rate of 60 ml per 500 ml of solution) at an initial rate of 200 ml per 10 minutes under the control of respiratory rate, heart rate, blood pressure and auscultatory picture lungs, fractional administration of vitamins - thiamine (100 mg), pyridoxine (100 mg), cyanocobalamin (up to 200 μg), ascorbic acid (500 mg); hydrocortisone - 125 mg; with hemodynamic ineffectiveness adequate infusion therapy and the appearance of signs of stagnation of pressor amines - dopamine, norepinephrine.
• Alcoholic coma. For the suppression of bronchorrhea and as a premedication before tracheal intubation, the bolus administration of 0.5-1 ml of a 0.1% solution of atropine. Within 4 hours after taking alcohol, gastric lavage through a tube (after tracheal intubation) to clean washings and the introduction of enterosorbent, warming, infusion of 0.9% sodium chloride solution with an initial rate of 200 ml for 10 minutes under the control of the respiratory rate are shown, Heart rate, blood pressure and auscultatory picture of the lungs with a possible subsequent transition to Ringer's solution, bolus or drip administration of up to 120 ml of a 40% glucose solution, fractional administration of vitamins - thiamine (100 mg), pyridoxine (100 mg), cyanocobalamin (up to 200 μg ), ascorbic acid (500 mg); with hemodynamic ineffectiveness of adequate infusion therapy, pressor amines - dopamine, norepinephrine.
• Opiate coma. Administration of naloxone (see above); if tracheal intubation is necessary, premedication of 0.5-1.0 ml of 0.1% atropine solution is required.
• Cerebrovascular coma (coma in stroke). Since at the prehospital stage of care, the differential diagnosis of ischemic and hemorrhagic strokes is absolutely impossible, only undifferentiated treatment is carried out here (see above):
  • in severe cases, to reduce capillary permeability, improve microcirculation and hemostasis - bolus administration of 250 mg of ethamsylate, to suppress proteolytic activity - drip introduction of aprotinin (gordox, contrikal, trasilol) at a dose of 300 thousand KIE (30 thousand ATre);
  • stroke is the main indication for the use of glycine, semax, mexidol, piracetam.
• Eclampsic coma. Bolus administration of 3750 mg of magnesium sulfate for 15 minutes, while maintaining convulsive syndrome - diazepam bolus of 5 mg until its relief; drip injection of Ringer's solution at a rate of 125-150 ml / h, dextran 40 (rheopolyglucin) - 100 ml / h.
• Hyperthermic coma (heatstroke). Cooling, normalization external respiration, infusion of 0.9% sodium chloride solution at an initial rate of 1-1.5 l / h, hydrocortisone - up to 125 mg.
• Hypocorticoid (adrenal) coma. Bolus administration of 40% glucose and thiamine solution, hydrocortisone - 125 mg, infusion of 0.9% sodium chloride solution (with the addition of 40% glucose solution at the rate of 60 ml per 500 ml of solution, taking into account the amount already administered by the bolus) with an initial speed of 1-1.5 l / h under the control of respiratory rate, heart rate, blood pressure and auscultatory picture of the lungs.

Measures unacceptable in coma

In any coma, regardless of the depth of cerebral insufficiency, the use of drugs that depress the central nervous system (narcotic analgesics, neuroleptics, tranquilizers) is fraught with aggravation of the severity of the condition; the exception is coma with convulsive syndrome, in which diazepam is indicated.

Coma is a contraindication to the use of drugs that have a stimulating effect (psychostimulants, respiratory analeptics); the exception is the respiratory analeptic bemegrid, which is indicated as a specific antidote for barbiturate poisoning.

Nootropic drugs (piracetam) are contraindicated for impaired consciousness deeper than superficial stupor. At the prehospital stage, insulin therapy is prohibited.

Indications for hospitalization

Coma serves absolute indication to hospitalization, the refusal of which is possible only with the diagnosis of an agonal state.

Common mistakes

Most frequent mistakes at the prehospital stage in general and in coma in particular are associated with the correction of arterial hypertension. As a rule, it is carried out by intramuscular (!) Injection of magnesium sulfate, less often - dibazol, which is always combined with papaverine, which is not shown in these cases; dangerous clonidine and pentamine are used, and often in combination with other antihypertensive drugs, which often leads to an excessive decrease in blood pressure.

The most commonly used solution for infusion therapy is isotonic sodium chloride solution, less often 5% glucose solution, which is at the expense of colloidal solutions.

It is extremely rare that diagnostic administration of a 40% glucose solution is carried out, which is mandatory when providing assistance to comatose patients; however, in no case was the administration of concentrated glucose preceded by the administration of thiamine.

Due to the lack of opportunity at the pre-hospital stage, the determination of glycemia and ketonuria is not carried out, flumazenil and mexidol, which are absent in the packing, are not used. Only in a few cases is a catheter inserted into a peripheral vein, which does not allow taking seriously the possibility of "infusion therapy". Before tracheal intubation, atropine premedication is not performed. Oxygen therapy is extremely rare.

Doses of a number of drugs are limited and for naloxone rarely exceed 0.4 mg, and for piracetam - 2 g. Moreover, the latter was administered in patients with the most pronounced cerebral symptoms, that is, when it is contraindicated. In the treatment of cerebral edema, furosemide is used too actively and osmotic diuretics are almost never used. Quite often, glucocorticoids are used to treat and prevent cerebral edema, but prednisone is preferred over the drug of choice - dexamethasone.

Often, drugs are used that are contraindicated in coma.

An insufficiently thorough examination of patients should be considered a significant mistake: it is impossible to carry out a full-fledged differential diagnosis, to assess the severity of the condition, the prognosis and to determine the tactics of treatment without information on the respiratory rate, heart rate or blood pressure. ECG is not recorded very often. A gross mistake, which, however, is observed too often, is the refusal to hospitalize comatose patients.

If treatment begins before the arrival of the ambulance team, then most often drugs are used that are contraindicated for patients in a coma: respiratory analeptics and psychostimulants (sulfocamfocaine, cordiamine, caffeine), clonidine, droperidol and cardiac glycosides.

A. L. Vertkin, Doctor of Medical Sciences, Professor
V.V. Gorodetsky, Candidate of Medical Sciences

- This is a life-threatening state of impaired consciousness, caused by damage to special structures of the brain and characterized by a complete absence of patient contact with the outside world. The causes of its occurrence can be divided into metabolic (poisoning by metabolic products or chemical compounds) and organic (in which the destruction of parts of the brain occurs). The main symptoms are unconsciousness and lack of response to opening the eyes, even to strong stimuli. In the diagnosis of coma, CT and MRI, as well as laboratory blood tests, play an important role. Treatment primarily involves combating the main cause of the development of the pathological process.

ICD-10

R40.2 Coma, unspecified

General information

Classification

Who can be classified according to 2 groups of criteria: 1) depending on the reason that caused it; 2) by the level of oppression of consciousness. Comas are classified into the following types, depending on the cause:

• traumatic (with craniocerebral trauma)
• epileptic (complication of status epilepticus)
• apoplexy (the result of a cerebral stroke), meningeal (develops as a consequence of meningitis)
• tumor (volumetric formations of the brain and skull)
• endocrine (with a decrease in thyroid function, diabetes mellitus)
• toxic (with renal and hepatic failure).

However, such a division is not often used in neurology, since it does not reflect the true state of the patient. The classification of coma by the severity of impairment of consciousness - the Glazko scale - has become more widespread. On its basis, it is easy to determine the severity of the patient's condition, build a scheme of urgent medical measures and predict the outcome of the disease. The Glazko scale is based on the cumulative assessment of the patient's three indicators: speech, presence of movements, eye opening. Points are given depending on the degree of their violation. According to their sum, the patient's level of consciousness is assessed: 15 - clear consciousness; 14-13 - moderate stun; 12-10 - deep stun; 9-8 - stupor; 7 or less - coma.

According to another classification, which is used mainly by resuscitators, coma is divided into 5 degrees:

• precom
• coma I (in the domestic medical literature they call stupor)
• coma II (stupor)
• coma III (atonic)
• coma IV (transcendental).

Coma symptoms

As already noted, the most important symptoms of coma, which are characteristic of any type of coma, are: complete lack of contact of the patient with the outside world and lack of mental activity. The rest of the clinical manifestations will differ depending on the cause of the brain damage.

Body temperature. Coma caused by overheating is characterized by high temperature body up to 42-43 C⁰ and dry skin. Poisoning with alcohol and sleeping pills, on the contrary, is accompanied by hypothermia (body temperature 32-34 C⁰).

Breathing rate.Slow breathing occurs when coma from hypothyroidism (low levels of thyroid hormones), poisoning with sleeping pills or drugs from the morphine group. Deep breathing is characteristic of a coma against the background of bacterial intoxication in severe pneumonia, as well as for brain tumors and acidosis caused by uncontrolled diabetes mellitus or renal failure.

Pressure and heart rate. Bradycardia (a decrease in the number of heartbeats per minute) indicates a coma that has arisen against the background acute pathology heart, and the combination of tachycardia (increased heart rate) with high blood pressure indicates an increase in intracranial pressure.

Skin color. Cherry red skin color develops with carbon monoxide poisoning. Blue tips of the fingers and nasolabial triangle indicate a low oxygen content in the blood (for example, when suffocating). Bruising, bleeding from the ears and nose, bruises in the form of glasses around the eyes are characteristic of a coma that develops against the background of a traumatic brain injury. Pronounced pale skin indicates a coma due to massive blood loss.

Contact with others. With stupor and mild coma, involuntary vocalizations are possible - the issuing of various sounds by patients, this serves as a favorable prognostic sign. As the coma deepens, the ability to pronounce sounds disappears.

Grimaces, reflex withdrawal of the hand in response to pain are characteristic of mild coma.

Coma diagnostics

When diagnosing a coma, a neurologist simultaneously solves 2 problems: 1) finding out the reason that led to a coma; 2) direct diagnosis of coma and its differentiation from other similar conditions.

Interviewing the patient's relatives or bystanders helps to find out the reasons for the patient's falling into a coma. At the same time, it is specified whether the patient had previous complaints, chronic diseases heart, blood vessels, endocrine organs. Witnesses inquire about whether the patient used drugs, whether empty blisters or drug jars were found next to him.

The speed of development of symptoms and the age of the patient are important. A coma that occurs in young people against the background of complete health, most often indicates poisoning with drugs, sleeping pills. And in elderly patients with concomitant diseases of the heart and blood vessels, there is a high probability of developing a coma against the background of a stroke or heart attack.

The examination helps to establish the suspected cause of the coma. The level of blood pressure, pulse rate, respiratory movements, characteristic bruising, bad breath, injection marks, body temperature - these are the signs that help the doctor establish the correct diagnosis.

Particular attention should be paid to the position of the patient. A thrown back head with an increased tone of the neck muscles indicates irritation of the membranes of the brain, which occurs with hemorrhages, meningitis. Cramps of the whole body or individual muscles can occur if the cause of the coma was status epilepticus, eclampsia (in pregnant women). Flaccid paralysis of the extremities indicates a cerebral stroke, and the complete absence of reflexes indicates deep damage to the large surface of the cortex and spinal cord.

The most important thing in the differential diagnosis of coma from other states of impaired consciousness is the study of the patient's ability to open his eyes to sound and pain stimulation. If the reaction to sound and pain manifests itself in the form of an arbitrary opening of the eyes, then this is not a coma. If the patient, despite all the efforts of the doctors, does not open his eyes, then the condition is considered as comatose.

The reaction of the pupils to light is carefully studied. Its features not only help to establish the expected location of the lesion in the brain, but also indirectly indicate the cause of the coma. In addition, the pupillary reflex serves as a reliable prognostic sign.

Narrow pupils (pupils-points) that do not respond to light are characteristic of alcohol poisoning and narcotic substances... The different diameters of the pupils in the left and right eyes indicate an increase in intracranial pressure. Wide pupils are a sign of damage to the midbrain. The expansion of the diameter of the pupils of both eyes, together with the complete absence of their reaction to light, is characteristic of an outrageous coma and is an extremely unfavorable sign indicating imminent brain death.

Modern technologies in medicine have made instrumental diagnostics of the causes of coma one of the very first procedures for admission of any patient with impaired consciousness. Computed tomography (CT of the brain) or MRI (magnetic resonance imaging) can determine structural changes in the brain, the presence of masses, signs of increased intracranial pressure. Based on the images, a decision is made on the methods of treatment: conservative or urgent surgery.

If it is not possible to perform CT or MRI, the patient should undergo radiography of the skull and spinal column in several projections.

Confirm or refute the metabolic (metabolic failure) nature of the coma helps biochemical analysis blood. An urgent determination of the level of glucose, urea, blood ammonia is carried out. And also the ratio of blood gases and basic electrolytes (potassium, sodium, chlorine ions) is determined.

If the results of CT and MRI indicate that there are no reasons on the part of the central nervous system that can enter the patient into a coma, a blood test is performed for hormones (insulin, adrenal hormones, thyroid gland), toxic substances (drugs, sleeping pills, antidepressants), bacterial blood culture. The most important study that helps differentiate the types of comas is electroencephalography (EEG). When it is carried out, the electrical potentials of the brain are recorded, the assessment of which makes it possible to distinguish a coma caused by a brain tumor, hemorrhage, or poisoning.

Coma treatment

Coma treatment should be carried out in 2 directions: 1) maintenance of vital functions of the patient and prevention of brain death; 2) the fight against the main cause that caused the development of this condition.

Life support begins in the ambulance on the way to the hospital and is performed for all comatose patients before the test results are received. It includes maintaining airway patency (straightening the sunken tongue, cleansing the mouth and nasal cavity from vomit, oxygen mask, inserting a breathing tube), normal blood circulation (introduction antiarrhythmic drugs, drugs that normalize blood pressure, indoor massage hearts). In the intensive care unit, if necessary, the patient is connected to a ventilator.

The administration of anticonvulsants in the presence of seizures, mandatory intravenous infusion of glucose, normalization of the patient's body temperature (covering and covering with heating pads for hypothermia or fighting fever), gastric lavage if drug poisoning is suspected.

The second stage of treatment is carried out after a detailed examination, and further medical tactics depends on the main reason that caused the coma. If it is an injury, brain tumor, intracranial hematoma, then urgent surgery is performed. When diabetic coma is detected, sugar and insulin levels are monitored. If the cause is renal failure, then hemodialysis is prescribed.

Forecast

The prognosis for coma depends entirely on the degree of damage to the structures of the brain and the reasons that caused it. In the medical literature, the patient's chances of getting out of a coma are regarded as: with a precoma, coma I - favorable, complete recovery is possible without residual effects; coma II and III - doubtful, that is, there is both the likelihood of recovery and death; coma IV - unfavorable, in most cases ends with the death of the patient.

Preventive measures are reduced to early diagnosis pathological process, the appointment of the correct methods of treatment and the timely correction of conditions that can cause the development of coma.

- the most common cause of damage to the structures of the central nervous system. If a severe violation of cerebral tissue occurs, a coma may occur, which is fraught with disability or death.

Impairment of consciousness: the mechanism of occurrence

After damage to the central nervous system due to traumatic brain injury, a person loses the ability to respond to any external stimulus. The psycho-emotional state is completely disturbed, the victim cannot contact with people around him. Coma sets in.

Coma with TBI is characterized by a person's immersion in a specific state, which is associated with the oppression of certain zones. The victim does not react to pain syndrome, bright light and loud sound, he has no reflexes.

Consciousness is impaired when certain parts of the brain are damaged, which are responsible for speech, thinking, wakefulness, reasoning. Based on the degree of damage, loss of consciousness can have a different duration:

• mild traumatic brain injury (for example, contusion): impairment of consciousness does not occur or lasts no more than 5 seconds;
• injury moderate (for example, open head injury): duration of impaired consciousness - 2 hours-2 days;
• severe trauma: deep coma and vegetative states occur.

Coma after TBI is not a separate disease, but only a consequence of damage to the central nervous system. If a serious general condition is observed that threatens a person's life, it can be immersed in. This condition allows you to cause a controlled decrease in the activity of reflexes and vital functions.

An artificial coma is the introduction of special medications into the body. In this case, the respiratory function is carried out by a ventilator.

Typical symptoms

Coma after traumatic brain injury is primarily characterized by impaired consciousness. All symptoms of this condition can be divided according to its severity:

1. Superficial disturbance of consciousness. The person falls into a deep sleep. When trying to talk to the victim, he can open his eyes, and sometimes - start a conversation. Speech - with punctuation. The patient can carry out light movements of the limbs.
2. Normal coma. The patient is able to make sounds, inadvertently open his eyes and make sudden movements with his hands. The doctor can fix the victim's limbs with special devices to avoid physical injury.
3. Deep coma. Reflexes and mobility, respiratory function are completely absent. There is no reaction to pain syndrome, just like to the light of the pupils.

Treatment during a coma

After a diagnosis of coma due to traumatic brain injury has been made, appropriate treatment is started. First of all, measures are taken to increase blood flow to the brain. Emergency treatment begins in the ambulance.

They use artificial ventilation of the lungs, inject drugs into the body that help to normalize blood pressure. It requires the introduction of drugs that improve the functioning of organs such as the liver and kidneys.

In case of respiratory arrest, the ambulance doctor inserts a special tube into the tracheal cavity, which is a conductor of oxygen air emanating from the breathing apparatus.

Since, being in a coma, a person cannot eat on his own, the introduction nutrients produced by the probe method. To prevent secondary infection of the urinary tract and lungs, powerful antibacterial drugs are prescribed.

Rehabilitation period

Not all cases of impaired consciousness require prolonged rehabilitation period... According to statistics, recovery from a coma caused by diabetes, taking a high dose of drugs or alcohol does not last long. In such cases, impairment of consciousness is present before the toxic substance is removed from the body.

Coming out of a coma of grade 3 after TBI or grade 1 equally requires rehabilitation measures. First of all, measures are taken to restore the functioning of the brain. Amnesia does not develop in every case, but memory and attention deterioration is observed.

How do you get out of a coma after TBI? During this period, the ability to sit, walk without assistance and improvised means is lost. Confusion of consciousness is observed, the person loses orientation in space. Such specialists help to correct such violations caused by prolonged disturbance of consciousness:

• neurologist (helps to restore speech);
• psychologist (normalizes the psycho-emotional state);
• occupational therapist (helps to improve motor skills);
• neurologist, physiotherapist, etc.

When coming out of a coma after TBI, it is not necessary to expose the patient to physical and mental stress immediately on the first day. Rehabilitation should take place gradually. How many months or years it will take to fully restore the activity of the central nervous system, and what the prognosis will be, depends on the severity of the traumatic brain injury.

Rehabilitation after a coma consists in helping the patient in all everyday activities: eating, going to the toilet and showering. It is required to conduct educational games that contribute to the restoration of motor skills, memory, speech. It is important to normalize the diet so that it includes all the useful vitamins and minerals.

To restore muscle tone, massage procedures are prescribed, which are carried out in a specialist's office and in the future - at home. During the massage, you can use any essential oil... The procedure also improves blood circulation. The main condition is the continuity of therapy, even if the first positive changes are visible.

Complications

If the central nervous system is affected at the time of the traumatic brain injury, complications are likely to arise. Coma is one of those. In severe TBI, the consequences can be so serious that the patient will no longer be able to take care of himself, get up, or sit. In such cases, outside help and special medical equipment will be required.

A coma is not always accompanied by such serious consequences. In some cases, a person quickly recovers from trauma and impaired consciousness, the basic functions and reflexes return to normal.

The most common consequences of a coma include amnesia or incomplete memory loss, impaired concentration, loss of the ability to self-service (eating, taking water treatments and etc.).

While in a supine position long time, a person may begin to suffer from pressure ulcers, which require a different specific therapy with the use of drugs.

Other consequences of TBI

The consequences of traumatic brain injury include not only someone. These depend on the severity of the injury. Complications do not always occur in the first weeks or months after injury. Sometimes negative consequences develop after a long time, which is more typical for children. In old age, TBI is often fatal.

The consequences of traumatic brain injury include:

• external manifestations: hematoma, tissue edema, pain, febrile syndrome, general malaise, etc.;
• paralysis of the legs and / or arms of a partial or complete nature;
• loss of sensitivity of the skin in the lower and / or upper limbs;
• pain syndrome in the head, which is chronic;
• loss of visual, auditory, speech function, memory;
• violation of respiratory function, swallowing;
• inability to control urination and defecation;
• post-traumatic epileptic syndrome with the development of seizures, impaired consciousness;
• upper and lower limbs;
• violation of concentration of attention;
• increased irritability.

Despite such a large list of negative consequences, this does not mean that a person will have all of them. The type of consequences depends on the exact location of the head and brain injury, as well as its severity.

Some clinical picture occurs only in the early post-traumatic period. These include paralysis of the legs and arms, impaired respiratory function, which disappear after taking rehabilitation measures. Headaches can begin to disturb a person long after the injury.

An important advice given by specialists is the continuity of treatment during the recovery period after TBI and coma. The rehabilitation course must be completed completely. This is the only way to hope for a favorable prognosis and maximum recovery of the body.

In a coma, only specialists can help. If there is a suspicion that the person has fallen into a coma, you must immediately call ambulance... The only thing that can be done before the doctors arrive is to ensure that the victim can breathe. Since in a coma there is a relaxation of muscles, a decrease in the swallowing and respiratory reflex, the victim must check the pulse, turn him over on his stomach and, if possible, clear the airways

MDK 03.02 Disaster Medicine

TICKET No. __________

QUESTION: Hyperglycemic coma. Causes. The clinical picture. Urgent Care.

THE STANDARD OF ANSWER

As a rule, it complicates the course of mild or moderate diabetes mellitus, when the administration of insulin is stopped, its dose is insufficient, when diabetes mellitus is not recognized, against the background of physical and mental trauma, with gross violations of the diet.

Characterized by: a slow onset of a coma (the patient falls into a coma for several hours) against the background of pain in the muscles and heart (like angina pectoris), the pulse is fast, weak, blood pressure is low, dyspepsia, abdominal pain. Shortness of breath increases, which is joined by Kussmaul's breathing, the exhaled air smells like acetone, collapse, oliguria, hypothermia develop. The skin becomes dry and cold, its marble-cyanotic tug is reduced. The tongue is coated eyeballs sunken, narrowed pupils, decreased muscle tone.

2. Urgently call a doctor, laboratory assistant.

3. Give a stable lateral position.

4. Control of blood pressure, pulse, NPV.

5. Determination of blood sugar from a fingertip portable
glucometer.

As prescribed by a doctor:

Glucometry

Vein catheterization

Sodium chloride 0.9% - 1000 ml intravenously in a stream during the first hour, then 500 ml per hour

Before intubation:

Atropine 0.5-1 mg IV

Midazolam 5 mg or Diazepam 10 mg IV - for coma

\u003e 6 points on the GLASGOW coma scale

Rehabilitation of the upper respiratory tract

Tracheal intubation or laryngeal ventilation / IVL

STANDARD OF ANSWERS FOR A COMPREHENSIVE EXAM

PM.03. Providing medical care in case of emergency and extreme conditions

MDK 03.01 Fundamentals of resuscitation

MDK 03.02 Disaster Medicine

TICKET No. __________

QUESTION: Hypoglycemic coma. The clinical picture. Urgent Causes help.

THE STANDARD OF ANSWER

Most often occurs with an overdose of insulin, untimely food intake, great physical exertion, fasting.

It is characterized by: an acute onset (within a few minutes), the patient before this is worried about a feeling of severe hunger, increasing weakness, sweating, trembling of the limb, sometimes a severe headache, double vision. Usually there is a mild impairment of consciousness, which quickly stops with the start of therapy. In the case of persisting hypoglycemia, general motor excitement appears, turning into stupor and coma.

With a superficial coma, blood pressure is normal or slightly increased, breathing is normal, there is no smell of acetone from the mouth. The skin is pale and damp.

With the deepening of the hypoglycemic coma, skin moisture disappears, breathing becomes more frequent and becomes superficial, tachycardia can turn into bradycardia, cardiac arrhythmias occur, and blood pressure decreases. Vomiting and hyperemia are noted.

The sugar level can drop to 2.2 - 1 mmol / l, there is no glucosuria and ketonuria.

Actions nurse to provide assistance:

1. Record the time of the onset of coma development.

2. Call a doctor and laboratory assistant.

3. Give the patient a stable lateral position.

4. Conduct an examination of the oral cavity.

According to the doctor's prescription, inject 20-40-50 ml of 40% glucose solution into / in drip.

STANDARD OF ANSWERS FOR A COMPREHENSIVE EXAM

PM.03. Providing medical care in case of emergency and extreme conditions

MDK 03.01 Fundamentals of resuscitation

MDK 03.02 Disaster Medicine

TICKET No. __________

QUESTION: Renal coma. Causes. The clinical picture. Urgent Care.

THE STANDARD OF ANSWER

Uremic coma Is a complication of chronic renal failure (CRF - uremia). CRF is the terminal (end) stage of progressive kidney disease. Chronic renal failure is complicated by chronic glomerulonephritis, pyelonephritis, diabetic nephropathy, rheumatoid arthritis, gout - renal causes, long-standing obstruction (blockage) urinary tract - post-renal, renal artery stenosis - prerenal.

Clinic.The coma develops gradually. There are 3 stages of coma development.

First stage - initial manifestations: poor appetite, nausea, vomiting, epigastric pain, odor of ammonia from the mouth, weakness, fatigue, chilliness, itchy skin, insomnia, apathy.

Second stage - precom. Patients are at first lethargic, sleepy, and then fall into stupor.

Third stage: coma. Miosis, Cheyne-Stokes or Kussmaul breathing are observed. Reflexes are reduced.