coma

Coma is an extreme inhibition of the central nervous system caused by the influence of factors that have a depressing effect on it.

Among these factors are:

1) traumatic, primary damage to the brain tissue by foreign objects, fragments of the bones of the skull, massive cerebral hemorrhage, compression of the brain by an intracranial hematoma with the development of intracranial hypertension;

2) exotoxic: poisons, medicines in toxic dosages;

3) endotoxic: in severe infectious diseases, at endocrine diseases(diabetic, hypoglycemic coma), lactacidemic (in cancer, patients with cardiovascular diseases in the terminal state), with renal, hepatic, respiratory failure.

Thus, the following types of com are distinguished:

1) cerebral (apoplexy);

2) diabetic (hyperglycemic: hyperosmolar, ketoacidotic);

3) hypoglycemic;

4) hyperlactacidemic;

5) uremic;

6) hepatic;

There is a number of coma (alcoholic, barbiturate, opiate, salicylate, unknown etiology), etc.

A common sign of coma is the lack of consciousness in the patient, the lack of speech, the eyes are closed. There are three degrees of com:

1) hemodynamic parameters are stable, there are reflexes;

2) hemodynamics is stable, deep inhibition of reflexes;

3) sharply reduced blood pressure, abnormal breathing, complete absence of reflexes, terminal state.

To determine the severity of coma, the Glasgow scale is used:

a) the eyes open spontaneously, to a call, with pain irritation, there is no reaction, respectively, 4, 3, 2 and 1 points;

b) speech is distinct, confused, incoherent words, illegible sounds, no reaction, respectively, 5, 4, 3, 2, 1 point;

c) movements: executes commands, indicates a sore spot, withdraws the limb in response to pain, flexion in response to pain, extension in response to pain, no reaction (6, 5, 4, 3, 2 and 1 points). Coma 1 if scored 8 points, coma 2 if 5-7 points, coma 3 corresponds to 3-4 points on the Glasgow scale.

There are also differences in the clinical manifestations of coma, which affect the tactics of managing patients. All patients in a coma, except for hypoglycemic patients, undergo tracheal intubation.

brain coma.

Leading clinical manifestations cerebral coma is focal symptoms: anisocoria, nystagmus (eyeballs turned towards the brain lesion), stiff neck, asymmetry of reflexes, if any, intracranial hypertension syndrome (repeated vomiting, scleral injection). There may be regurgitation of gastric contents into the respiratory tract, which can often be observed in other types of coma. Convulsive syndrome is also characteristic of cerebral coma. Hyperthermic syndrome as a late complication occurs the next day after the injury.

Management of patients in the prehospital stage:

1) removal of foreign objects from the oral cavity;

2) tracheal intubation;

3) suction of aspiration masses from respiratory tract;

4) artificial ventilation of the lungs is carried out in the mode of moderate hyperventilation within two hours in order to reduce the inflow and improve the outflow of blood from the cranial cavity, thereby reducing intracranial hypertension and cerebral edema;

5) oxygen therapy with air-oxygen mixture 5050;

6) intravenously mexidol 5% -4 ml, magnesia sulfate 25% -10 ml.

7) control of ECG, blood sugar;

8) transportation on a stretcher, delivery to the intensive care unit of a specialized hospital.

This is a life-threatening resuscitation condition, because, in addition to loss of consciousness, in coma, violations of the functions of vital organs (respiration and cardiac activity) are observed.

Being in a state of coma, a person is not aware of either the world around him or himself.

Coma is always a complication of any disease or pathological condition (poisoning, injury). All comas have a number of common signs, regardless of the cause of their occurrence. However, there are also differences in clinical symptoms different types com. Treatment of coma should be carried out in the intensive care unit. It is aimed at maintaining the vital functions of the body 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 for the treatment of coma.

What is the basis of coma?

Coma is based on two mechanisms:

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

Primary damage to the brain stem is possible in conditions such as stroke, traumatic brain injury, tumor process. Secondary disorders occur with 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 violations, normal transmission becomes impossible. nerve impulses between brain cells. At the same time, coordination and coordinated activities of all structures are lost, they switch to an autonomous mode. The brain loses its managerial functions over the whole organism.

com classification

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

When divided according to the causal factor, conditionally all coma is classified into coma with primary neurological disorders (when the process in the nervous system itself served as the basis for the development of coma) and secondary neurological disorders (when brain damage occurred indirectly during any pathological process outside the nervous system). Knowing the cause of 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 cranial brain injury);
• cerebrovascular (with acute vascular circulatory disorders in the brain);
• epileptic (the result of epileptic seizures);
• meningoencephalitic (the result of inflammatory diseases of the brain and its membranes);
• hypertension (due to a tumor in the brain and skull).

• endocrine (diabetic with diabetes(there are several types), hypothyroid and thyrotoxic in diseases thyroid gland, hypocorticoid in acute adrenal insufficiency, hypopituitaric in total deficiency of pituitary hormones);
• toxic (with renal or hepatic insufficiency, with poisoning by any substances (alcohol, drugs, carbon monoxide, and so on), with cholera, with an overdose of drugs);
• hypoxic (with severe heart failure, obstructive pulmonary disease, 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, the most common cause of coma is a stroke, drug overdose is in second place, and complications of diabetes mellitus are in third place.

The need for the existence of the second classification is due to the fact that the causative 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, anterior-stem, "hyperactive");
• III degree (deep, rear-stem, "sluggish");
• IV degree (exorbitant, terminal).

A sharp division of the degrees of coma is rather difficult, since the transition from one stage to another can be very fast. This classification is based on clinical symptoms corresponding to a certain stage.

Signs of a coma

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 such 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 lowing, the publication of various sounds out of touch with what is happening from the outside;
• the absence of a normal reaction to a painful stimulus (that is, the reaction is weak and very slow, for example, when a patient pricks the arm with a needle, it does not immediately pull it away, but only weakly bends or unbends some time after applying painful irritation);
• spontaneous active movements are practically absent. Sometimes sucking, chewing, swallowing movements may 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;
• possible pathological hand and foot symptoms (Babinsky, Zhukovsky and others);
• the reaction of the pupils to light is preserved (narrowing), strabismus, spontaneous movements can be observed eyeballs;
• lack of control over the activity of the pelvic organs;
• usually spontaneous breathing is preserved;
• on the part of cardiac activity, an increase in heart rate (tachycardia) is observed.

Coma II degree

At this stage, the activity of subcortical formations is inhibited. Violations descend to the anterior sections of the brain stem. This stage is characterized by:

• the appearance of tonic convulsions or periodic shudders;
• lack of speech activity, verbal contact is impossible;
• a sharp weakening of the reaction to pain (slight movement of the limb during injection);
• oppression of all reflexes (both superficial and deep);
• narrowing of the pupils and their weak reaction to light;
• an increase in body temperature;
• increased sweating;
• sharp fluctuations blood pressure;
• severe tachycardia;
• respiratory failure (with pauses, with stops, noisy, with different depth 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 his limb in response to an injection);
• surface reflexes are absent (in particular, corneal);
• there is a sharp decrease in muscle tone and tendon reflexes;
• pupils are dilated and do not react to light;
• breathing becomes superficial and arrhythmic, unproductive. Additional muscles (muscles of the shoulder girdle) are involved in the act of breathing, which is not normally observed;
• blood pressure decreases;
• occasional seizures are possible.

Coma IV degree

At this stage, there are no signs of brain activity. This manifests itself:

• the absence of all reflexes;
• the maximum possible expansion of the pupils;
• muscle atony;
• lack of spontaneous breathing (only artificial ventilation of the lungs supports the provision of the body with oxygen);
• 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 various stages of coma may differ depending on the cause of the coma. In addition, certain varieties of comatose states have additional signs, in some cases being diagnostic.

Clinical features of some types of com

Cerebrovascular coma

It always becomes the result of a global vascular catastrophe (ischemic or hemorrhagic stroke, aneurysm rupture), therefore it develops suddenly, without precursors. Usually consciousness is lost almost instantly. At the same time, the patient has a red face, hoarse breathing, high blood pressure, and a tense pulse. In addition to the neurological symptoms characteristic of a coma, there are focal neurological symptoms (for example, facial distortion, puffing out of 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, symptoms of Kernig, Brudzinsky).

Traumatic coma

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

epileptic coma

It is usually the result of recurring one after one epileptic seizures. With this coma, the patient's face acquires a bluish tint (if the attack was quite recent), the pupils become wide and do not respond to light, there may be traces of a bite of the tongue, foam on the lips. When the seizures stop, the pupils still remain wide, muscle tone decreases, and reflexes are not evoked. Tachycardia and rapid breathing occur.

Meningoencephalitic coma

Occurs against the background of existing inflammatory disease the brain or its membranes, so it is rarely sudden. There is always an increase in body temperature, varying degrees severity of meningeal symptoms. Possible rash on the body. 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

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

Hepatic coma

It develops gradually against the background of hepatitis or cirrhosis of the liver. A specific hepatic odor emanates from the patient (smell " raw meat"). The skin is yellow, with petechial hemorrhages, scratching places. Tendon reflexes are increased, convulsions 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, the "head of a jellyfish" - the expansion and tortuosity of the saphenous veins of the abdomen).

renal coma

It also develops gradually. The patient smells of urine (ammonia). The skin is dry, pale gray (as if dirty), with traces of scratching. There are swelling in the lumbar region and lower extremities, puffiness of the face. Blood pressure is low, tendon reflexes are high, pupils are narrow. Possible involuntary muscle twitches individual groups muscles.

Alcoholic coma

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

Coma due to carbon monoxide poisoning

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

Coma due to poisoning with sleeping pills (barbiturates)

Coma develops gradually, being a continuation of sleep. Characterized by bradycardia (low heart rate) and low blood pressure. 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, tendon reflexes are not evoked (or they are sharply weakened). Increased salivation.

Coma with drug overdose

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

diabetic coma

It would be more correct to say not a coma, but a coma. Because there can be several of them in diabetes mellitus. These are ketoacidotic (with the accumulation of fat metabolism products in the blood and an increase in glucose levels), hypoglycemic (with a drop in glucose levels and an excess of 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 ketoacidotic coma, there is a smell of acetone from the patient, the skin is pale and dry, the pupils are constricted. With a hypoglycemic coma, foreign odors from the patient are not felt, the skin is pale and moist, and the pupils are dilated. Of course, when determining the type of diabetic coma, the main role is played by additional methods studies (the amount of glucose in the blood, in the urine, the presence of acetone in the urine, and so on).

Principles of treatment for com

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

Measures that ensure the vital functions of the body include:

• breathing support. If necessary, sanitation of the respiratory tract is carried out to restore their patency (foreign bodies are removed, a sunken tongue is straightened), an air duct, an oxygen mask are installed, artificial ventilation of the lungs is carried out;
• support of the circulatory system (the use of agents that increase blood pressure in hypotension, and reduce it in hypertension; agents that normalize heart rhythm; normalization of circulating blood volume).

Symptomatic measures are also used to remove existing violations:

• large doses of vitamin B 1 for suspected alcohol poisoning;
• anticonvulsants in the presence of seizures;
• antiemetic drugs;
• sedatives for arousal;
• intravenous glucose is given (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. Giving some glucose at high blood levels will not do much harm);
• gastric lavage in case of suspected poisoning with drugs or low-quality food (including mushrooms);
• drugs to reduce body temperature;
• in the presence of signs of an infectious process, the use of antibiotics is indicated.

At the slightest suspicion of an injury to the cervical spine (or in the absence of the possibility of excluding it), stabilization of this area is necessary. Usually, a collar-shaped splint is used for this purpose.

After establishing the cause that caused the coma, the underlying disease is treated. Then a specific therapy is already prescribed, directed against a specific ailment. This may be hemodialysis for renal failure, the introduction of Naloxone for drug overdose, and even surgical intervention(for example, with a hematoma of the brain). The type and extent of therapeutic 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. Treatment of coma is carried out in the intensive care unit and is aimed at saving the life of the patient. At the same time, all measures should ensure the preservation of brain cells.

brain coma

Cerebral coma is a condition in which the central nervous system is depressed. The main symptom of CNS depression is loss of consciousness and involuntary reflexes. When a coma occurs, the vital functions of the body remain functioning, i.e. breathing and heart activity remain functioning. There are a large number of varieties of cerebral coma, however, in any form, the main one is a deep lesion of the nervous tissue of the brain.

Clinical picture and symptoms

Depending on the underlying disease or condition that led to the development of a cerebral coma, the symptoms will change. The immediate main symptom of coma is the sequential shutdown of brain structures from the vital activity of the body. The most sensitive areas of the central nervous system are the neurocytes of the cerebral cortex, the defeat of which occurs in the first place, which is manifested by depression of consciousness. Then voluntary and involuntary reflexes disappear, which is associated with damage to the deeper diencephalic structures of the brain.

Cerebral coma: causes

There are several forms and degrees of cerebral coma. The metabolic form occurs as a result of an acute violation of the metabolism and trophism of brain neurons. The epileptic form is characterized by the occurrence of compression of the brain by an abscess, a neoplasm, or as a result of an infectious process. Cerebrovascular form - occurs as a result of acute cerebrovascular accident in hemorrhagic or ischemic strokes. According to the severity of the disease, the degrees of cerebral coma can be distinguished:

Cerebral coma of the 1st degree is characterized by inhibition. Difficulty in contact with the victim. A cerebral coma of the 2nd degree is characterized by stupor, while contact is completely impossible. The pupils of the victim are narrowed, unconditioned reflexes are preserved. A grade 3 cerebral coma is considered deep, with low blood pressure, a thready pulse, and shallow and rare breathing. Muscle tone is significantly reduced. Coma of the 4th degree is characterized by a complete absence of reflexes and muscle tone, the pupils are dilated, there are gross violations of breathing and cardiovascular activity.

Treatment

Treatment of cerebral coma should be started immediately. The tactics of the ongoing therapeutic measures largely depend on the cause of its cause. In most cases, coma develops as a result of an acute vascular accident. A cerebral coma in a stroke is a serious condition. Treatment, which is carried out in the intensive care unit. The Clinical Institute of the Brain has all the facilities necessary for the treatment of cerebral coma. The Center employs specialists high level capable of handling even the most difficult cases.

Cerebral coma: complications

Cerebral coma is a complication of the underlying disease that led to its occurrence. However, in the absence of proper therapy for this condition, the rate of death is extremely high.

First aid

If you suspect the initial signs of a cerebral coma, you must urgently call an ambulance. The victim must take horizontal position, allow access to fresh air and remove constricting chest clothes Be sure to reassure the victim. Do not leave the patient before the arrival of specialists!

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PRIMARY CEREBRAL COMA. Primary cerebral, or neurological (cerebral) coma is a group of comatose conditions, which are based on depression. - presentation

Presentation on theme: "PRIMARY CEREBRAL COMA. Primary cerebral, or neurological (cerebral) coma is a group of comatose conditions, which are based on oppression. - Transcript:

1 PRIMARY CEREBRAL COMA

2 Primary cerebral, or neurological (cerebral) coma - a group of coma, which are based on depression of the central nervous system due to primary brain damage, This group includes: apoplectic coma, epileptic coma, traumatic coma, coma with encephalitis, meningitis, brain tumors and its shells

3 Apoplexy coma Causes: Hemorrhage in the brain. Acute local ischemia of the brain with an outcome in a heart attack (with thrombosis or embolism major artery brain). Risk factors: Arterial hypertension (especially periods hypertensive crises). Atherosclerotic changes in the walls of cerebral vessels. People aged 45-60 are most susceptible

4 The leading pathogenetic factors of apoplexy coma are: ischemia and hypoxia of the brain (as a result of local or extensive circulatory disorders in it); a significant increase in the permeability of the walls of microvessels; rapidly growing edema of the substance of the brain. stroke is characterized by secondary circulatory disorders around the ischemic zone of the brain with rapidly increasing signs of loss of sensation and movement.

5 Manifestations of apoplexy coma - the patient suddenly loses consciousness; - his face (in typical cases) is purple; - visible vessels are dilated and noticeably pulsate; - pupils do not react to light; - tendon reflexes are reduced or absent (hyporeflexia), pathological reflexes are observed (Babinsky and others); - due to damage and irritation of the brain substance, respiratory disorders are intensively growing (it is noisy, hoarse); - impaired swallowing; - hypertensive reactions and bradycardia are noted.

6 In apoplexy coma as a result of ischemic stroke, the following are usually observed: - repeated episodes of rapidly passing dizziness; - unsteady gait; - speech disorders; - sensitivity disorders; - often fainting (these disorders are the result of transient circulatory disorders in the vessels of various regions of the brain with the development of its transient ischemia); - disorders of consciousness, up to its loss;

7 - arterial hypotension; - bradycardia; - cardiac arrhythmias; - rare shallow breathing; - pale and cold skin and mucous membranes; - with prolonged ischemia (depending on the affected area of ​​the brain), the following are detected: - hyporeflexia, - movement disorders, - sensitivity disorders.

8 Sequelae of cerebral hemorrhage or ischemic stroke. Depend on: the scale and topography of damage, the degree of hypoxia and cerebral edema, the number of lesions, severity arterial hypertension, severity of atherosclerosis, age of the patient. Apoplexy coma is one of the most unfavorable flowing coma, fraught with death or disability of the patient.

9 First Aid Action: Call " ambulance” or a doctor (if the incident occurred in a hospital). Provide the patient with rest and bed rest. Release the patient from outer clothing. Provide fresh air to the room. Free the patient's mouth from vomit (for repeated vomiting, turn your head to one side and remove the vomit from your mouth). For apoplexy coma, place an ice pack on the head or cold water. When convulsing, gently hold the head and limbs.

10 Epileptic coma Usually develops in patients with genuine and symptomatic epilepsy in status epilepticus. In the pathogenesis of coma, hemodynamic, liquorodynamic and metabolic disorders in the brain play an important role. Manifestations: Onset is usually sudden In the interictal period, consciousness is not restored Body temperature rises to 39 degrees

11 Respiratory rhythm and cardiac activity are disturbed, vomiting of the color of coffee grounds appears Muscle hypotension increases, the severity and duration of convulsions decrease, breathing becomes shallow, and then periodic according to the Cheyne-Stokes type Convulsions stop, muscle atony is observed, acidosis increases, cerebral edema Respiratory arrest occurs and death.

12 First aid actions Call an ambulance Before the emergency team arrives, lay the patient in a stable position Free the airways from vomiting, mucus, foreign objects Prevent tongue retraction Free the patient from tight clothing Avoid possible injuries

13 Traumatic coma (TBI) Causes: concussion contusion of the brain compression of the brain against the background of its contusion and compression of the brain without concomitant injury closed and open TBI

14 Manifestations: A) Concussion Loss of consciousness lasting from several minutes to several hours Vomiting shortly after injury After regaining consciousness, the patient complains of dizziness, tinnitus, headache, nausea, weakness, sleep disturbance, pain when moving the eyeballs retrograde and anterograde amnesia If a concussion is not diagnosed in a timely manner, or if it is not diagnosed, the condition worsens and may develop into a coma.

15 B) Contusion of the GM and TBI, loss of consciousness can last from several minutes (in mild cases) to several days or weeks mild degree: loss of consciousness does not exceed one hour, moderately pronounced headache, dizziness, nausea, repeated vomiting is possible. As a rule, there is also amnesia. Body temperature usually remains within normal limits, respiratory function is not impaired. However, even with a mild degree of brain contusion, fractures of the bones of the skull and an admixture of blood in the cerebrospinal fluid are possible. Data from special studies revealed signs of cerebral edema and petechial hemorrhages in the substance of the brain. moderate: The duration of loss of consciousness is an average of 46 hours.

16 Symptoms of a bruise are pronounced: there is a severe headache, repeated vomiting, pronounced changes in the heart rate (both slowing down and speeding up are possible), significant shortness of breath, fever. Possible mental disorders. Neurological symptoms are clearly manifested, pupil reactions, eyeball movements are disturbed, sensitivity and speech disorders are expressed. Along with fractures of the bones of the skull, hemorrhages under the lining of the brain are also often noted. Computed tomography with these bruises reveals hemorrhages in the substance of the brain of a small-focal nature or moderate soaking of the brain area in the bruised area with blood. severe degree: the duration of turning off consciousness can range from several hours to several weeks.

17 Severe brain damage corresponds to severe clinical manifestations that threaten vital functions: a sharp slowdown or a sharp increase in heart rate, a significant increase in blood pressure, pronounced disturbances in the rhythm and frequency of breathing, motor excitation is often noted, body temperature is significantly increased, floating movements of the eyeballs are noted, bilateral dilation or constriction of the pupils, swallowing disorders, changes in muscle tone, inhibition of tendon reflexes. Paralysis may be present, rarely seen seizures. As a rule, there are fractures of the vault and base of the skull and massive hemorrhages under the lining of the brain.

18 First aid actions: Immediately call the rescue team Remove tight clothing, clear the upper respiratory tract If a skull fracture is suspected, it is better to fix the victim in the state in which he is Prevent tongue retraction If possible, apply cold to the head Stop bleeding, treat wound follow up appearance and breathing, pulse, blood pressure Limit the movement of the victim as much as possible

19 First aid: As with all emergency conditions, and with coma, the following situations are possible: - there is an anamnesis, previous diseases are known internal organs, in which a coma can develop; objective examination reveals characteristic symptoms this or that pathology: foci in strokes, traces of trauma, jaundice, etc. In these cases, the diagnosis of the cause of a coma usually does not cause difficulties; - a clinical situation in which there is no anamnesis, history of the disease, but they have characteristic clinical symptoms or laboratory and instrumental data of a particular disease.

20 Health care: 1. Mandatory immediate hospitalization in the intensive care unit, and in case of traumatic brain injury or subarachnoid hemorrhage - in the neurosurgical unit. Despite the mandatory hospitalization, emergency treatment for comas in all cases should be started immediately. 2. Restoration (or maintenance) of an adequate state of vital functions: a) breathing

21 - 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 at a dose of 0.5 ml (with the exception of poisoning with anticholinergic drugs); b) blood circulation - with a drop in blood pressure - drip injection of ml of 0.9% sodium chloride solution, 5% glucose solution or 70 ml of dextran or ml of refortan with addition in case of inefficiency

22 infusion therapy of pressor amines - dopamine, norepinephrine, - in case of coma on the background of arterial hypertension - correction of high blood pressure to values ​​exceeding the "working" ones by mm Hg (in the absence of anamnestic information - not lower than / mm Hg): a) by lowering intracranial pressure b) administering mg magnesium sulfate as a bolus for 7-10 minutes or drip) c) with contraindications to magnesium, administering mg bendazol (3-4 ml bolus 1% or 6-8 ml 0.5% solution), g ) with a slight increase in blood pressure, aminophylline is sufficient (10 ml of a 2.4% solution), - with arrhythmias - restoration of an adequate heart rhythm.

23 3. Immobilization of the cervical spine in case of any suspicion of injury. 4. Providing the necessary conditions for treatment and control. Rule of three catheters (peripheral vein catheterization, Bladder and the installation of a gastric, better than a nasogastric, tube) when managing a coma at the prehospital stage is not so categorical: in a coma, drugs are administered only parenterally (the risk of aspiration is high when taken orally) and preferably intravenously; obligatory installation of a catheter in a peripheral vein; infusions are carried out through it, and with stable hemodynamics and no need for detoxification

24 an indifferent solution is slowly dripped in, which provides a constant opportunity to inject medications; bladder catheterization should be carried out according to strict indications, since in the conditions of prehospital care this manipulation is associated with the risk of septic complications, and during transportation it is difficult to provide the necessary degree of fixation; the introduction of a gastric tube with a preserved gag reflex without prior intubation of the trachea and its sealing with an inflated cuff is fraught with a coma with the possible development of aspiration of gastric contents (a potentially lethal complication, to prevent which a probe is installed).

25 5. Combating intracranial hypertension, edema and swelling of the brain and meninges: side effects, especially in the absence of adequate control, at the prehospital stage, it can be used only for health reasons; b) in the absence of high blood osmolarity (available, for example, with hyperglycemia or hyperthermia) and in the absence of a threat of development or intensification of bleeding (observed, for example, with trauma, it is impossible to exclude the hemorrhagic nature of a stroke), dehydration is achieved by introducing an osmotic diuretic - mannitol in an amount 500 ml of 20% solution over minutes (1-2 g/kg);

26 to prevent a subsequent increase in intracranial pressure and an increase in cerebral edema (rebound syndrome), up to 40 mg of furosemide is administered after the completion of the mannitol infusion; c) the use of glucocorticoid hormones, which reduce vascular permeability and tissue edema around the brain lesion, is based on their proven effect in cases with the presence of perifocal inflammation; glucocorticoids are used with minimal concomitant mineralocorticoid activity, and therefore do not retain sodium and water; methylprednisolone has the greatest efficacy and safety, a valid alternative to which can be dexamethasone (dose - 8 mg).

27 6. Symptomatic therapy: a) normalization of body temperature - in case of hypothermia - warming the patient without the use of heating pads (burns are possible in the absence of consciousness) and intravenous administration heated solutions, - with high hyperthermia - hypothermia by physical methods (cold compresses on the head and large vessels, wiping with cold water or solutions of ethyl alcohol and table vinegar in water) and pharmacological means(drugs from the group of analgesics - antipyretics); b) relief of seizures - the introduction of diazepam at a dose of 10 mg;

28 c) relief of vomiting - the introduction of metoclopramide at a dose of 10 mg intravenously or intramuscularly. 7. For all comas, an ECG registration is required.

Fractures of the spine Trauma of the skull The initial examination of the victim is a complex of consecutive medical measures aimed at determining.

Tyamina II 301. Occurs with blood loss, various cardiovascular and other diseases, as well as in healthy people e.g. when you are very tired,

The term "anaphylaxis" (from the Greek. ana - reverse and phylaxis - protection) was introduced in 1902 to refer to the unusual reaction of dogs to repeated administration.

Brain contusion, traumatic brain injury

State educational institution of secondary vocational education of the Health Committee of the Administration of the Volgograd Region “Medical.

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TICKET №__________

QUESTION: Anaphylactic shock. Forms. Urgent Care.

STANDARD ANSWER

Anaphylactic shock

In the complex process observed in anaphylactic shock, one can distinguish three stages:

The first stage is immunological. It covers all changes in immune system arising from the moment the allergen enters the body; the formation of antibodies and / or sensitized lymphocytes and their combination with an allergen that has repeatedly entered or persists in the body;

The second stage is pathochemical, or the stage of formation of mediators. The stimulus for the emergence of the latter is the combination of the allergen with antibodies or sensitized lymphocytes at the end of the immunological stage;

The third stage is pathophysiological, or the stage of clinical manifestations. It is characterized by the pathogenic action of the formed mediators on the cells, organs and tissues of the body.

Urgent Care

Adrenaline 0.5 mg intramuscularly

Pulse oximetry

oxygen inhalation

With little effect

Sodium chloride 0.9% - 500 ml intravenously drip

STANDARD ANSWERS FOR COMPREHENSIVE EXAM

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

MDK 03.01 Fundamentals of resuscitation

MDC 03.02 Disaster medicine

TICKET №__________

QUESTION: Anaphylactic shock. Flow types. Urgent Care.

STANDARD ANSWER

Anaphylactic shock is an immune response immediate type, which develops when the allergen is repeatedly introduced into the body and is accompanied by damage to its own tissues.

There are 5 types of flow

- With predominant lesion of the cardiovascular system.

The patient suddenly collapses, often with loss of consciousness. At the same time, other manifestations of an allergic reaction (skin rashes, bronchospasm) may be absent;

- With a predominant lesion of the respiratory system in the form of acute bronchospasm (asphyxic or asthmatic variant). This option is often combined with sneezing, coughing, a feeling of heat throughout the body, reddening of the skin, hives, and heavy sweat. Be sure to join the vascular component (decrease in blood pressure, tachycardia).

- With predominant damage to the skin and mucous membranes. The patient experiences severe itching followed by the development of urticaria or allergic edema Quincke type. At the same time, symptoms of bronchospasm or vascular insufficiency may occur. Of particular danger is the angioedema of the larynx, which is manifested first by stridor breathing, and then by the development of asphyxia.

- with a predominant lesion of the central nervous system (cerebral variant). Neurological symptoms come to the fore - psychomotor agitation, fear, severe headache, loss of consciousness and convulsions, reminiscent of status epilepticus or cerebrovascular accident.

- With predominant organ damage abdominal cavity(abdominal). In these cases, the symptoms acute abdomen» ( sharp pains in the epigastric region, signs of peritoneal irritation), leading to the misdiagnosis of ulcer perforation or intestinal obstruction.

Urgent Care

Stopping contact with the allergen

Give a position with a raised foot end

Adrenaline 0.5 mg intramuscularly

Pulse oximetry

oxygen inhalation

Vein catheterization or intraosseous access

Prednisolone 120 mg or Dexamethasone 16 mg IV

Sodium chloride 0.9% - 500 ml intravenously drip

With little effect

Epinephrine 0.5 mg intravenously or diluted with sodium chloride

0.9% - 250 ml intravenously drip 10 - 20 drops. in min. (after

placement of a second intravenous catheter)

Sodium chloride 0.9% - 500 ml intravenously drip

STANDARD ANSWERS FOR COMPREHENSIVE EXAM

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

MDK 03.01 Fundamentals of resuscitation

MDC 03.02 Disaster medicine

TICKET №__________

QUESTION: cerebral coma. Urgent Care.

STANDARD ANSWER

Coma- a pathological condition with an extreme degree of inhibition of brain activity, which is accompanied by loss of consciousness, lack of response to any external stimuli and disorders of various vital functions (impaired thermoregulation, respiration, slowing of the pulse, decreased vascular tone).

Causes of cerebral coma

The causes of this condition are primary or secondary toxic and traumatic factors. To the most common reasons relate:

Head and brain injuries

Strokes

· infectious lesions brain;

Brain damage due to lack of oxygen

Toxic damage caused by toxic substances, some drugs, drugs;

alcohol poisoning;

Symptoms of a cerebral coma

In the initial stages of a coma, a person seems to be just asleep, his eyes are closed, and the minimum possibility of movement remains. The victim can move in his sleep, swallow saliva, some reflexes are preserved. In addition, it is considered that initial stage a cerebral coma person may feel pain. At deeper stages of coma, there is an increasingly strong depression of the central nervous system and respiration, muscle atony, and cardiac dysfunction.

Primary cerebral, or neurological (cerebral) coma is a group of comatose conditions, which are based on depression of the central nervous system due to primary brain damage, This group includes: apoplectic coma, epileptic coma, traumatic coma, coma with encephalitis, meningitis, brain tumors and its shells

Apoplexy coma Causes: Hemorrhage in the brain. Acute local ischemia of the brain with an outcome in a heart attack (with thrombosis or embolism of a large cerebral artery). Risk factors: Arterial hypertension (especially periods of hypertensive crises). Atherosclerotic changes in the walls of cerebral vessels. People aged 45-60 are most susceptible

The leading pathogenetic factors of apoplexy coma are: ischemia and hypoxia of the brain (as a result of local or extensive circulatory disorders in it); a significant increase in the permeability of the walls of microvessels; rapidly growing edema of the substance of the brain. stroke is characterized by secondary circulatory disorders around the ischemic zone of the brain with rapidly increasing signs of loss of sensation and movement.

Manifestations of apoplexy coma - the patient suddenly loses consciousness; - his face (in typical cases) is purple; - visible vessels are dilated and noticeably pulsate; - pupils do not react to light; - tendon reflexes are reduced or absent (hyporeflexia), pathological reflexes are observed (Babinsky and others); - due to damage and irritation of the brain substance, respiratory disorders are intensively growing (it is noisy, hoarse); - impaired swallowing; - hypertensive reactions and bradycardia are noted.

With apoplexy coma as a result of ischemic stroke, the following are usually observed: - repeated episodes of rapidly passing dizziness; - unsteady gait; - speech disorders; - sensitivity disorders; - often fainting (these disorders are the result of transient circulatory disorders in the vessels of various regions of the brain with the development of its transient ischemia); - disorders of consciousness, up to its loss;

arterial hypotension; - bradycardia; - cardiac arrhythmias; - rare shallow breathing; - pale and cold skin and mucous membranes; - with prolonged ischemia (depending on the affected area of ​​the brain), the following are detected: - hyporeflexia, - movement disorders, - sensitivity disorders.

Consequences of cerebral hemorrhage or ischemic stroke. Depend on: the scale and topography of damage, the degree of hypoxia and cerebral edema, the number of lesions, the severity of arterial hypertension, the severity of atherosclerosis, the age of the patient. Apoplexy coma is one of the most unfavorable flowing coma, fraught with death or disability of the patient.

First aid actions: Call an ambulance or a doctor (if the incident occurred in a hospital). Provide the patient with rest and bed rest. Release the patient from outer clothing. Provide fresh air to the room. Free the patient's mouth from vomit (for repeated vomiting, turn your head to one side and remove the vomit from your mouth). For apoplexy coma, place an ice pack or cold water on the head. When convulsing, gently hold the head and limbs.

Epileptic coma Usually develops in patients with genuinous and symptomatic epilepsy in status epilepticus. In the pathogenesis of coma, hemodynamic, liquorodynamic and metabolic disorders in the brain play an important role. Manifestations: Onset is usually sudden In the interictal period, consciousness is not restored Body temperature rises to 39 degrees

The rhythm of respiration and cardiac activity are disturbed, vomiting of the color of coffee grounds appears Muscle hypotension increases, the severity and duration of convulsions decrease, breathing becomes shallow, and then periodic according to the Cheyne-Stokes type Convulsions stop, muscle atony is observed, acidosis increases, swelling of the brain death.

First aid actions Call an ambulance Before the emergency team arrives, lay the patient in a stable position Free the airways from vomit, mucus, foreign objects Do not let the tongue fall Free the patient from tight clothing Avoid possible injuries

Manifestations: A) Concussion loss of consciousness lasting from several minutes to several hours vomiting shortly after injury after recovery of consciousness the patient complains of dizziness, tinnitus, headache, nausea, weakness, sleep disturbance, pain when moving the eyeballs retrograde and anterograde amnesia With untimely diagnosis of a concussion or in its absence, the condition worsens and may develop into a coma.

B) Contusion of the GM and TBI, turning off consciousness can last from several minutes (in mild cases) to several days or weeks mild degree: loss of consciousness does not exceed one hour, moderately severe headache, dizziness, nausea are noted, repeated vomiting is possible. As a rule, there is also amnesia. Body temperature usually remains within normal limits, respiratory function is not impaired. However, even with a mild degree of brain contusion, fractures of the bones of the skull and an admixture of blood in the cerebrospinal fluid are possible. Data from special studies revealed signs of cerebral edema and petechial hemorrhages in the substance of the brain. moderate: The duration of loss of consciousness is an average of 46 hours.

The symptoms of a bruise are pronounced: there is a severe headache, repeated vomiting, pronounced changes in the heart rate (both slowing down and speeding up are possible), significant shortness of breath, fever. Possible mental disorders. Neurological symptoms are clearly manifested, pupil reactions, eyeball movements are disturbed, sensitivity and speech disorders are expressed. Along with fractures of the bones of the skull, hemorrhages under the lining of the brain are also often noted. Computed tomography with these bruises reveals hemorrhages in the substance of the brain of a small-focal nature or moderate soaking of the brain area in the bruised area with blood. severe degree: the duration of turning off consciousness can range from several hours to several weeks.

Severe brain damage corresponds to severe clinical manifestations that threaten vital functions: a sharp slowdown or a sharp increase in heart rate, a significant increase in blood pressure, pronounced disturbances in the rhythm and frequency of breathing, motor excitation is often noted, body temperature is significantly increased, floating movements of the eyeballs are noted, bilateral dilation or constriction of the pupils, swallowing disorders, changes in muscle tone, inhibition of tendon reflexes. Paralysis can be detected, convulsive seizures are less common. As a rule, there are fractures of the vault and base of the skull and massive hemorrhages under the lining of the brain.

First aid actions: Immediately call the rescue team Remove tight clothing, clear the upper respiratory tract If a skull fracture is suspected, it is better to fix the victim in the state in which he is Prevent tongue retraction If possible, apply cold to the head Stop bleeding, treat the wound Monitor the appearance and breathing, pulse, blood pressure Limit the movements of the victim as much as possible

First aid: As with all emergency conditions, the following situations are also possible with coma: - there is an anamnesis, previous diseases of the internal organs are known, in which a coma can develop; with an objective examination, there are characteristic symptoms of a particular pathology: foci in strokes, traces of trauma, jaundice, etc. In these cases, the diagnosis of the cause of a coma usually does not cause difficulties; - a clinical situation in which there is no anamnesis, history of the disease, but they have characteristic clinical symptoms or laboratory and instrumental data of a particular disease.

Medical assistance: 1. Mandatory immediate hospitalization in the intensive care unit, and in case of traumatic brain injury or subarachnoid hemorrhage - in the neurosurgical unit. Despite the mandatory hospitalization, emergency treatment for comas in all cases should be started immediately. 2. Restoration (or maintenance) of an adequate state of vital functions: a) 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 at a dose of 0.5 ml (with the exception of poisoning with anticholinergic drugs); b) blood circulation - with a drop in blood pressure - drip injection of ml of 0.9% sodium chloride solution, 5% glucose solution or 70 ml of dextran or ml of refortan with addition in case of inefficiency

Infusion therapy pressor amines - dopamine, norepinephrine, - in case of coma on the background of arterial hypertension - correction of high blood pressure to values ​​exceeding the "working" ones by mm Hg (in the absence of anamnestic information - not lower than / mm Hg): a) by reducing intracranial pressure b) by administering mg of magnesium sulfate as a bolus for 7-10 minutes or drip) c) with contraindications to magnesium, by administering mg of bendazol (bolus 3-4 ml of 1% or 6-8 ml of 0.5% solution), d) with a slight an increase in blood pressure is sufficient aminophylline (10 ml of a 2.4% solution), - with arrhythmias - the restoration of an adequate heart rate.

3. Immobilization of the cervical spine for any suspicion of injury. 4. Providing the necessary conditions for treatment and control. The rule of three catheters (catheterization of a peripheral vein, bladder and installation of a gastric, preferably nasogastric, tube) when managing a coma at the prehospital stage is not so categorical: in a coma, drugs are administered only parenterally (the risk of aspiration is high when taken orally) and preferably intravenously; obligatory installation of a catheter in a peripheral vein; infusions are carried out through it, and with stable hemodynamics and no need for detoxification

An indifferent solution is slowly dripped in, which provides a constant opportunity to administer drugs; bladder catheterization should be carried out according to strict indications, since in the conditions of prehospital care this manipulation is associated with the risk of septic complications, and during transportation it is difficult to provide the necessary degree of fixation; the introduction of a gastric tube with a preserved gag reflex without prior intubation of the trachea and its sealing with an inflated cuff is fraught with a coma with the possible development of aspiration of gastric contents (a potentially lethal complication, to prevent which a probe is installed).

5. The fight against intracranial hypertension, edema and swelling of the brain and meninges: a) the most effective and universal method is mechanical ventilation in hyperventilation mode, however, due to many severe side effects, especially in the absence of adequate control, it can only be used at the prehospital stage according to vital indications; b) in the absence of high blood osmolarity (available, for example, with hyperglycemia or hyperthermia) and in the absence of a threat of development or intensification of bleeding (observed, for example, with trauma, it is impossible to exclude the hemorrhagic nature of a stroke), dehydration is achieved by introducing an osmotic diuretic - mannitol in an amount 500 ml of 20% solution over 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 after the completion of the mannitol infusion; c) the use of glucocorticoid hormones, which reduce vascular permeability and tissue edema around the brain lesion, is based on their proven effect in cases with the presence of perifocal inflammation; glucocorticoids are used with minimal concomitant mineralocorticoid activity, and therefore do not retain sodium and water; methylprednisolone has the greatest efficacy and safety, a valid alternative to which can be dexamethasone (dose - 8 mg).

6. Symptomatic therapy: a) normalization of body temperature - in case of hypothermia - warming the patient without the use of heating pads (in the absence of consciousness, burns are possible) and intravenous administration of heated solutions, - with high hyperthermia - hypothermia by physical methods (cold compresses on the head and large vessels, wiping cold water or solutions of ethyl alcohol and table vinegar in water) and pharmacological agents (drugs from the group of analgesics - antipyretics); b) relief of seizures - the introduction of diazepam at a dose of 10 mg;

Cerebral coma was previously known as apoplexy coma, and its main cause is primary or secondary brain damage as a result of impaired blood supply to the brain tissue.

Causes

The cause of cerebral coma is extensive brain damage under the influence of toxic and, less often, traumatic factors. Among the toxic factors in the first place are alcohol and drug intoxication, coma on the background of carbon monoxide poisoning. Closed traumatic brain injury is the leading traumatic etiology of cerebral coma. Despite the general similarity of pathogenetic processes, disorders that occur in the main parts of the brain differ with various types coma.

However, with any kind and type of coma, there are lesions at the level of the cerebral cortex, the reticular formation, the basal nuclei and the limbic system. It is the vastness of such disorders (transient or chronic) that leads to the fact that the body loses the ability to coordinate activities, which leads to disorders of almost all functions.

Symptoms

Cerebral coma, first of all, is manifested by loss of consciousness with the preservation of basic reflexes, which indicates the preserved viability of the brain. The second group of symptoms - lack of response to stimuli - tactile primarily. The victim seems to be asleep, especially since the cerebral coma is accompanied by a dream-like state - the eyes are closed, the person literally "fell" into sleep.

In the first stages of a cerebral coma, the patient retains at least a minimal amount of movement - he is able to change the position of the body, swallows saliva. The deeper the brain damage, the more pronounced the clinic of depression of consciousness, up to the shutdown of spontaneous breathing. Convulsions, vomiting, fever are also signs of a cerebral coma.

Diagnosis and treatment

The diagnosis of cerebral coma cannot be established by examination alone, although typical signs coma and may indicate its development. A thorough neurological examination is required, using special rating scales. Electroencephalogram, CT scan are also necessary for the diagnosis of cerebral coma.

Treatment depends on the cause of the coma, that is, if the cerebral coma is toxic, then the cause that caused it is eliminated, and detoxification therapy is performed. Tracheal intubation, dynamic assessment and maintenance of basic vital functions, meticulous care - all this requires hospitalization in the intensive care unit.

Forecast

The prognosis depends entirely on the etiological cause of coma. Some coma leads to a slow fading of brain functions, which is almost impossible to stop, and the person goes into a vegetative existence. A cerebral coma of toxic origin is easier to treat. The overall average mortality in the case of cerebral coma can reach 35%. It should be remembered that not a single coma passes without a trace for the body.