Comas: classification, signs, principles of treatment. What is cerebral coma and its causes? Principles of treatment for coma

Director of LLC "Clinic of the Brain Institute", Doctor of Medical Sciences, Professor of the Departments of Nervous Diseases and Anesthesiology-Reanimatology of the Ural State Medical Academy, Chairman of the Supervisory Board of the ANO "Clinical Institute of the Brain".

Deputy chief physician for medical work, kmn, neurologist

Head of the neurological department, neurologist

Cerebral coma is a condition in which the central nervous system is inhibited. The main symptom of central nervous system depression is loss of consciousness and involuntary reflexes. When a comatose state occurs, the vital functions of the body remain functioning, i.e. breathing and cardiac activity remain functioning. There are a large number of varieties of cerebral coma, but in any form the main one is deep damage to the nervous tissue of the brain.

Clinical picture and symptoms

Depending on the underlying disease or condition that led to the development of cerebral coma, symptoms will vary. The immediate main symptom of coma is the consistent shutdown of brain structures from the body’s vital functions. The most sensitive areas of the central nervous system are the neurocytes of the cerebral cortex, which are damaged first, 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.

Brain coma: causes

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

Cerebral coma of the 1st degree is characterized by lethargy. Difficulty in contacting the victim. Cerebral coma of the 2nd degree is characterized by stupor, while contact is completely impossible. The victim's pupils are constricted, unconditioned reflexes are preserved. Cerebral coma of the 3rd degree is considered deep, in which blood pressure is reduced, the pulse is thready, and breathing is shallow and rare. Muscle tone is significantly reduced. Coma 4th degree is characterized by a complete absence of reflexes and muscle tone, the pupils are dilated, there are severe disturbances in breathing and cardiovascular activity.

Treatment

Treatment for cerebral coma should be started immediately. The tactics of the treatment measures carried out largely depend on the cause that caused it. In most cases, coma develops as a result of an acute vascular accident. Cerebral coma during a stroke is a serious condition. Treatment carried out in an intensive care unit. The Clinical Brain Institute has all the facilities necessary to treat cerebral coma. The Center employs high-level specialists who can cope with even the most difficult cases.

Brain coma: complications

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

First aid

If you suspect the initial signs of a cerebral coma, you should urgently call an ambulance. The victim needs to take a horizontal position, allow access to fresh air and remove clothes that are constricting the chest. It is imperative to calm the victim. Do not leave the patient until specialists arrive!

This is a life-threatening resuscitation condition, because, in addition to loss of consciousness, during coma there are dysfunctions of vital organs (respiration and cardiac activity).

While in a coma, a person is unaware of 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 symptoms, regardless of the cause of their occurrence. But there are also differences in clinical symptoms for different types of coma. Treatment of coma should be carried out in an 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 types of comas there are, how they are characterized and what the basic principles of treatment of comatose states are.

What causes coma?

Coma is based on two mechanisms:

bilateral diffuse damage to 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 the reticular formation is “switched off,” deep inhibition develops in the cerebral cortex.

Primary damage to the brain stem is possible in conditions such as stroke, traumatic brain injury, or tumor process. Secondary disorders occur due to metabolic changes (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, the normal transmission of nerve impulses between brain cells becomes impossible. 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 entire body.

Classification com

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

When dividing by causative factor, all comas are conditionally classified into comas with primary neurological disorders (when the basis for the development of coma was a process in the nervous system itself) and secondary neurological disorders (when brain damage occurred indirectly during some pathological process outside the nervous system). Knowing the cause of coma allows you to correctly determine the treatment strategy for the patient.

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

Neurological (primary) genesis:

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

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

According to statistics, the most common cause of coma development is stroke, drug overdose comes in second, and complications of diabetes mellitus come in third.

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 condition of the patient in a coma.

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

I degree (mild, subcortical);
II degree (moderate, anterior trunk, “hyperactive”);
III degree (deep, posterior trunk, “flaccid”);
IV degree (extraordinary, terminal).

A sharp division of degrees of coma is quite difficult, since the transition from one stage to another can be very rapid. This classification is based on different 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 the following manifestations:

the feeling that the patient is in a dream;
complete disorientation of the patient in place, time, personality (it is impossible to rouse the patient);
lack of answers to questions asked. Possible inarticulate mooing, making various sounds out of connection with what is happening outside;
the absence of a normal reaction to a painful stimulus (that is, the reaction is weak and very slow, for example, when a needle pricks the patient’s arm, the patient does not withdraw it immediately, but only weakly bends or straightens it some time after the painful stimulus is applied);
spontaneous active movements are practically absent. Sometimes sucking, chewing, and swallowing movements may occur as a manifestation of brain reflexes, which are normally suppressed by the cerebral cortex;
increased muscle tone;
deep reflexes (knee, Achilles and others) are increased, and superficial (corneal, plantar and others) are suppressed;
pathological hand and foot symptoms are possible (Babinsky, Zhukovsky and others);
the reaction of the pupils to light is preserved (constriction), strabismus and spontaneous movements of the eyeballs may be observed;
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. The disturbances extend down to the anterior parts of the brainstem. 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 when applying an injection);
inhibition of all reflexes (both superficial and deep);
constriction of the pupils and their weak reaction to light;
increased body temperature;
increased sweating;
sharp fluctuations in blood pressure;
severe tachycardia;
breathing disorders (with pauses, with stops, noisy, with different depths of inspiration).

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:

defensive reactions in response to a painful stimulus are completely lost (the patient does not even move the limb in response to the injection);
there are no superficial reflexes (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, less 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 shows up:

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

Reaching stage IV coma has a high risk of death, approaching 100%.

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

Clinical features of some types of coma

Cerebrovascular coma

It always becomes the result of a global vascular catastrophe (ischemic or hemorrhagic stroke, rupture of an aneurysm), and therefore develops suddenly, without warning. Usually consciousness is lost almost instantly. In this case, the patient has a red face, hoarse breathing, high blood pressure, and a tense pulse. In addition to the neurological symptoms characteristic of the comatose state, focal neurological symptoms are observed (for example, facial distortion, swelling of one cheek when breathing). The first stage of coma may be accompanied by psychomotor agitation. If subarachnoid hemorrhage occurs, then positive meningeal symptoms are determined (stiffness of the neck muscles, Kernig's, Brudzinski'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. Bleeding from the nose, ear (sometimes leakage of cerebrospinal fluid), bruising around the eyes (symptom of “glasses”) are possible. 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

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

Meningoencephalitic coma

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

Hypertensive coma

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

Hepatic coma

Develops gradually against the background of hepatitis or cirrhosis of the liver. The patient emits a specific liver odor (the smell of “raw meat”). The skin is yellow, with pinpoint hemorrhages and scratches in places. Tendon reflexes are increased and convulsions may occur. Blood pressure and heart rate are low. The pupils are dilated. The patient's liver is enlarged in size. There may be signs of portal hypertension (for example, “head of the jellyfish” - dilation 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 is swelling in the lumbar area and lower extremities, and puffiness of the face. Blood pressure is low, tendon reflexes are high, pupils are narrow. Involuntary muscle twitching in certain muscle groups is possible.

Alcohol coma

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, the coma may be another, for example, traumatic. The person could simply drink alcohol before the injury). The heart rate increases and blood pressure decreases. 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 (this color is given by carboxyhemoglobin), the limbs may be bluish.

Coma due to poisoning with sleeping pills (barbiturates)

Coma develops gradually, being 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 suppressed that the reaction to pain is completely absent, tendon reflexes are not evoked (or they are sharply weakened). Increased salivation.

Coma due to 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 “pinpoint” pupils are characteristic, they are so narrowed. There may be traces of injections (although this is not necessary, since the method of drug use may be, for example, intranasal).

Diabetic coma

It would be more correct to say not coma, but comas. 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 excess insulin), hyperosmolar (with severe dehydration) and lactic acidemic (with excess lactic acid in the blood). Each of these varieties has its own clinical signs. For example, in a ketoacidotic coma, the patient smells of acetone, the skin is pale and dry, and the pupils are constricted. In a hypoglycemic coma, the patient does not feel any foreign odors, the skin is pale and moist, and the pupils are dilated. Of course, when 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).

Principles of treatment for coma

Coma is a condition that primarily requires urgent measures to maintain the vital functions of the body. These measures are taken regardless of what caused the coma. The main thing is to prevent the patient from dying and to preserve the brain cells from damage as much as possible.

Measures that ensure vital functions of the body include:

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

Symptomatic measures are also used to relieve existing disorders:

large doses of vitamin B1 for suspected alcohol poisoning;
anticonvulsants for seizures;
antiemetics;
sedatives for agitation;
Glucose is given 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 when the blood glucose is high will not cause much harm);
gastric lavage if poisoning with drugs or poor-quality food (including mushrooms) is suspected;
drugs to reduce body temperature;
if there are signs of an infectious process, the use of antibiotics is indicated.

If there is the slightest suspicion of injury to the cervical spine (or if it cannot be ruled out), stabilization of this area is necessary. Typically a collar-shaped splint is used for this purpose.

After establishing the cause of the coma, the underlying disease is treated. Then specific therapy is prescribed, directed against a specific ailment. This may include hemodialysis for renal failure, administration of Naloxone for drug overdose, and even surgery (for example, for a cerebral hematoma). The type and volume of treatment measures depends on the established 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 types of comas due to the large number of pathological conditions that can be complicated by them. Treatment of coma is carried out in an intensive care unit and is aimed at saving the patient’s life. At the same time, all measures must ensure the preservation of brain cells.

Brain coma

Clinical picture and symptoms

Brain coma: causes

Treatment

Brain coma: complications

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

First aid

Programs:

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

Presentation on the topic: » PRIMARY CEREBRAL COMA. Primary cerebral, or neurological (brain) coma is a group of comatose states based on depression.” - Transcript:

1 PRIMARY CEREBRAL COMA

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

3 Apoplectic coma Causes: Cerebral hemorrhage. Acute local cerebral ischemia resulting 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 years 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 disorder in it); a significant increase in the permeability of microvascular walls; rapidly increasing swelling of the brain. Stroke is characterized by secondary circulatory disorders around the area of cerebral ischemia with rapidly increasing signs of loss of sensitivity and movement.

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

6 In apoplectic coma as a result of an 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 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, - sensory disturbances.

8 Consequences of cerebral hemorrhage or ischemic stroke. They depend on: the scale and topography of the damage, the degree of hypoxia and cerebral edema, the number of lesions, the severity of arterial hypertension, the severity of atherosclerosis, and the patient’s age. Apoplectic coma is one of the most unfavorable comatose states, fraught with death or disability of the patient.

9 First aid actions: Call an ambulance or a doctor (if the incident occurred in a hospital). Provide the patient with rest and bed rest. Free the patient from outer clothing. Provide a flow of fresh air into the room. Free the patient's mouth from vomit (if vomiting occurs repeatedly, turn your head to the side and remove vomit from the mouth). For apoplectic coma, place an ice pack or cold water on your head. During cramps, gently support your head and limbs.

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

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

12 Actions to provide first aid Call an ambulance Before the ambulance team arrives, place the patient in a stable position Clear the airways of vomit, mucus, and foreign objects Do not allow the tongue to retract Free the patient from constricting clothing Eliminate possible injuries

13 Traumatic coma (In case of TBI) Causes: concussion, brain contusion, compression of the brain due to its contusion and compression of the brain without accompanying contusion, closed and open TBI

14 Manifestations: A) Concussion, loss of consciousness lasting from several minutes to several hours, vomiting soon after the 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 in its absence, the condition worsens and can develop into a coma.

15 B) Brain contusion 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; moderate headache, dizziness, nausea are noted, and 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 skull bones and blood in the cerebrospinal fluid are possible. Data from special studies reveal signs of cerebral edema and pinpoint hemorrhages in the brain substance. moderate degree: The duration of loss of consciousness averages 46 hours.

16 Symptoms of a bruise are pronounced: there is a severe headache, repeated vomiting, pronounced changes in heart rate (both slowing down and speeding up are possible), significant shortness of breath, and increased body temperature. Mental disorders are possible. Neurological symptoms are clearly manifested, pupillary reactions and eyeball movements are impaired, sensitivity and speech disorders are pronounced. Along with fractures of the skull bones, hemorrhages under the lining of the brain are also often observed. Computed tomography for these bruises reveals small-focal hemorrhages in the brain substance or moderate blood saturation of the brain area in the area of the bruise. severe: the duration of loss of consciousness can range from several hours to several weeks.

17 Severe brain damage corresponds to pronounced clinical manifestations that threaten impairment of vital functions: a sharp slowdown or sharp increase in heart rate, a significant increase in blood pressure, pronounced disturbances in the rhythm and frequency of breathing, motor agitation is often noted, body temperature is significantly increased, floating movements of the eyeballs are noted, bilateral dilatation or constriction of the pupils, swallowing disorders, changes in muscle tone, inhibition of tendon reflexes. Paralysis may be detected, and 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.

18 Actions to provide first aid: Immediately call the rescue team Remove tight clothing, free the upper respiratory tract If a fracture of the skull bones is suspected, it is better to fix the victim in the condition in which he is Prevent tongue retraction If possible, apply cold to the head Stop bleeding, treat wound Monitor appearance and breathing, pulse, blood pressure Limit the victim’s movements as much as possible

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

20 Medical care: 1. Mandatory immediate hospitalization in the intensive care unit, and in case of traumatic brain injury or subarachnoid hemorrhage - in the neurosurgical department. Despite mandatory hospitalization, emergency treatment for comas should be started immediately in all cases. 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 using 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); In all cases, tracheal intubation should be preceded by premedication with a 0.1% atropine solution in a dose of 0.5 ml (with the exception of poisoning with anticholinergic drugs); b) blood circulation - if blood pressure drops - drip administration of ml of 0.9% sodium chloride solution, 5% glucose solution or ml of dextran 70 or ml of refortan with addition if ineffective

22 infusion therapy of pressor amines - dopamine, norepinephrine, - in case of coma due to arterial hypertension - correction of high blood pressure to values exceeding “working” values 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 over 7-10 minutes or by drip) c) in case of contraindications to magnesium, by administering mg of bendazole (bolus of 3-4 ml of 1% or 6-8 ml of 0.5% solution), d ) with a slight increase in blood pressure, aminophylline (10 ml of 2.4% solution) is sufficient; - for 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. The rule of three catheters (catheterization of a peripheral vein, bladder and installation of a gastric, preferably a nasogastric, tube) when managing comas at the prehospital stage is not so categorical: in a comatose state, drugs are administered only parenterally (with oral administration there is a high risk of aspiration) and, preferably, intravenously; installation of a catheter in a peripheral vein is mandatory; infusions are carried out through it, and with stable hemodynamics and no need for detoxification

24 an indifferent solution is slowly introduced dropwise, which ensures a constant opportunity to administer medications; Bladder catheterization should be carried out according to strict indications, since in prehospital care this manipulation is associated with the danger of septic complications, and during transportation it is difficult to ensure the required degree of fixation; the introduction of a gastric tube with a preserved gag reflex without preliminary intubation of the trachea and its sealing with an inflated cuff is fraught with the possible development of aspiration of gastric contents in a coma (a potentially fatal complication, to prevent which a tube is installed).

25 5. Combating 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 be used at the prehospital stage 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 increased bleeding (observed, for example, with trauma, the hemorrhagic nature of a stroke cannot be excluded), dehydration is achieved by administering 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 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 with minimal concomitant mineralocorticoid activity are used, and therefore do not retain sodium and water; Methylprednisol has the greatest effectiveness and safety, a permissible alternative to which is dexamethasone (dose - 8 mg).

27 6. Symptomatic therapy: a) normalization of body temperature - in case of hypothermia - warming the patient without using heating pads (in the absence of consciousness, burns are possible) and intravenous administration of heated solutions, - in case of 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 agents (drugs from the group of analgesics - antipyretics); b) relief of seizures - administration of diazepam at a dose of 10 mg;

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First aid for traumatic brain injuries and spinal injuries

is a life-threatening state of impaired consciousness caused by damage to special structures of the brain and characterized by a complete lack of contact between the patient and the outside world. The causes of its occurrence can be divided into metabolic (poisoning by metabolic products or chemical compounds) and organic (in which destruction of parts of the brain occurs). The main symptoms are unconsciousness and lack of eye opening reactions even to strong stimuli. CT and MRI, as well as laboratory blood tests, play an important role in the diagnosis of coma. 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) according to the level of depression of consciousness. Depending on the causes, comas are divided into the following types:

traumatic (for traumatic brain injuries)
epileptic (complication of status epilepticus)
apoplexy (the result of a cerebral stroke), meningeal (develops as a consequence of meningitis)
tumor (space-occupying formations of the brain and skull)
endocrine (with decreased thyroid function, diabetes mellitus)
toxic (with renal and liver failure).

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

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

precom
coma I (in Russian medical literature called stupor)
coma II (stupor)
coma III (atonic)
coma IV (extreme).

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. Other clinical manifestations will vary depending on the cause of the brain damage.

Body temperature. Coma caused by overheating is characterized by high body temperature 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 during coma from hypothyroidism (low levels of thyroid hormones), poisoning from sleeping pills or drugs from the morphine group. Deep breathing movements are characteristic of a coma due to bacterial intoxication in severe pneumonia, as well as for brain tumors and acidosis caused by uncontrolled diabetes mellitus or renal failure.

Blood pressure and heart rate. Bradycardia (decrease in the number of heart beats per minute) indicates a coma caused by acute heart pathology, 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 from carbon monoxide poisoning. Blue discoloration of the fingertips and nasolabial triangle indicates low oxygen levels in the blood (for example, due to suffocation). Bruising, bleeding from the ears and nose, and spectacle-shaped bruises around the eyes are characteristic of a coma that has developed as a result of a traumatic brain injury. Pronounced pale skin indicates a comatose state due to massive blood loss.

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

Grimaces and reflexive withdrawal of the hand in response to pain are characteristic of a mild coma.

Diagnosis of coma

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

Interviewing the patient's relatives or random witnesses helps to find out the reasons for the patient's falling into a coma. At the same time, it is clarified whether the patient had previous complaints, chronic diseases of the heart, blood vessels, or endocrine organs. Witnesses are questioned about whether the patient used medications and whether empty blisters or jars of medications were found near him.

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

The examination helps determine the probable cause of the coma. The level of blood pressure, pulse rate, respiratory movements, characteristic bruises, bad breath, traces of injections, body temperature - these are the signs that help the doctor make the correct diagnosis.

Particular attention should be paid to the patient's position. A thrown back head with increased tone of the neck muscles indicates irritation of the membranes of the brain, which occurs with hemorrhages and meningitis. Convulsions of the whole body or individual muscles may occur if the cause of the coma is status epilepticus or eclampsia (in pregnant women). Flaccid paralysis of the limbs indicates a cerebral stroke, and a 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 voluntary 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 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), which do not react to light, are characteristic of alcohol and drug poisoning. Different pupil diameters in the left and right eyes indicate an increase in intracranial pressure. Wide pupils are a sign of damage to the midbrain. The dilation of the diameter of the pupils of both eyes, combined with the complete lack of their reaction to light, is characteristic of an extreme coma and is an extremely unfavorable sign, indicating imminent brain death.

Modern technologies in medicine have made instrumental diagnosis of the causes of coma one of the very first procedures upon admission of any patient with impaired consciousness. Performing a computed tomography (CT scan of the brain) or MRI (magnetic resonance imaging) can determine structural changes in the brain, the presence of space-occupying lesions, and signs of increased intracranial pressure. Based on the images, a decision is made on treatment methods: conservative or emergency surgery.

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

A biochemical blood test helps confirm or refute the metabolic (metabolic failure) nature of the coma. Blood glucose, urea, and ammonia levels are urgently determined. The ratio of blood gases and basic electrolytes (potassium, sodium, chlorine ions) is also determined.

If the results of CT and MRI indicate that there are no reasons from the central nervous system that can put the patient into a coma, a blood test is performed for hormones (insulin, adrenal hormones, thyroid hormones), toxic substances (narcotics, sleeping pills, antidepressants), bacterial blood culture . The most important test 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.

Treatment of coma

Treatment of coma should be carried out in 2 areas: 1) maintaining the patient’s vital functions and preventing brain death; 2) combating the main cause that caused the development of this condition.

Support of vital functions begins already in the ambulance on the way to the hospital and is carried out for all patients in a coma even before receiving the results of the examination. It includes maintaining airway patency (straightening a sunken tongue, clearing the mouth and nasal cavity of vomit, oxygen mask, inserting a breathing tube), normal blood circulation (administration of antiarrhythmic drugs, blood pressure-normalizing drugs, closed heart massage). 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), and gastric lavage if drug poisoning is suspected.

The second stage of treatment is carried out after a detailed examination, and further medical tactics depend on the main cause of the coma. If it is a trauma, brain tumor, intracranial hematoma, then urgent surgery is performed. When a diabetic coma is detected, sugar and insulin levels are taken under control. If the cause is kidney failure, hemodialysis is prescribed.

Forecast

The prognosis for coma depends entirely on the degree of damage to brain structures and the causes that caused it. In the medical literature, the patient’s chances of emerging from a comatose state are assessed as: in case of precoma, coma I - favorable, complete recovery without residual effects is possible; coma II and III – doubtful, that is, there is both a likelihood of recovery and death; coma IV - unfavorable, in most cases ends in the death of the patient.

Preventive measures come down to early diagnosis of the pathological process, prescribing the correct treatment methods and timely correction of conditions that may cause the development of coma.

19049 0

All cases of cerebral coma can be classified as follows.

1. Apoplectic coma:

as a result of parenchymal or subarachnoid hemorrhage;
due to encephalomalacia (ischemic stroke, cerebral infarction).

2. Meningeal coma.

3. Coma as a result of damage to brain tissue (tumor or brain abscess, encephalitis, etc.).

4. Post-traumatic coma.

At apoplectic coma Usually, severe focal neurological symptoms are detected, including paralysis of half the body (hemiplegia). Hemiplegia is manifested not only by paralysis of the limbs, but also by paralysis of the muscles of the face and tongue. The muscles of the face located below the palpebral fissure, the muscles of the tongue and the trapezius muscle suffer. The function of other facial muscles is usually not impaired because they receive bilateral cortical innervation. Due to the anatomical features of the pathways, the muscles of the face are paralyzed on the side where the affected hemisphere of the brain is located, and the muscles of the limbs are paralyzed on the opposite side.

On the paralyzed side of the body, pathological symptoms appear, for example, Babinsky's symptom: when the outer edge of the plantar surface of the foot is irritated by strokes, the first toe rises upward, and the rest bend towards the plantar side and fan out. On the paralyzed side of the body, the raised limb falls quickly and heavily (like a whip) onto the bed, while the raised unaffected limb returns to its original position more slowly and more gently (this is due to the preservation of its muscle tone). Paralysis of the facial muscles leads to asymmetry of the nasolabial folds, the patient’s mouth is distorted, and during breathing movements the cheek on the affected side fluctuates (“parusitis”).

The clinical picture of apoplexy coma as a result of hemorrhage and encephalomalacia has its own characteristics. At cerebral hemorrhage deterioration of the patient's condition usually occurs suddenly, the age of patients is often between 40-60 years, its development is preceded by physical or emotional stress against the background of severe, poorly controlled arterial hypertension. In the acute period, severe general cerebral symptoms are observed (headache, dizziness, nausea, vomiting, impaired consciousness), which can mask focal neurological symptoms.

The patient quickly falls into a comatose state, stops responding to external stimuli, and there are no active movements. In addition to hemiplegia, pronounced autonomic disorders are observed. The patient's face is purplish-red or very pale, there is often vomiting, and Cheyne-Stokes-type breathing problems. Already in the first or second day, body temperature rises to febrile levels, sometimes reaching 40-41°C (fever of central origin). As a result of swelling of the brain and its membranes, meningeal signs may appear (stiff neck, Kernig's, Brudzinski's symptoms). In the blood, leukocytosis is detected in the range of 10-20.10 in 9 degrees / l and relative lymphopenia.

As a result of severe stress, blood sugar levels may increase to 9-10 mmol/l, as well as the appearance of glucosuria. During a lumbar puncture, cerebrospinal fluid flows out under increased pressure; a few hours after hemorrhage, red blood cells, increased protein content, and pleocytosis appear in it. Echoencephalography reveals a displacement of the median echo by 6-7 mm in the direction opposite to the localization of the hemorrhagic focus.

If the hemorrhage is accompanied by a breakthrough of blood into the ventricles of the brain, the general condition of the patient is especially severe, the symptoms of meningism (headaches, stiff neck) are more pronounced, and hemiplegia may not appear clearly. Babinski's symptom in this case can be positive on both sides; hormetonic syndrome often occurs (periodically repeated, spontaneous or strong tonic muscle spasms of paralyzed limbs arising under the influence of external stimuli). Hemiplegia in such patients is often combined with automated gestures of non-paralytic limbs. At the same time, movements in these limbs may give the impression of being expedient (patients brush away flies, pull a blanket over themselves, etc.). The detection of a significant admixture of blood in the cerebrospinal fluid confirms this diagnosis.

Encephalomalacia(ischemic stroke, cerebral infarction) most often develops in patients over the age of 60 against the background of severe systemic and cerebral atherosclerosis. Its cause is thrombosis or embolism of cerebral vessels; non-thrombotic cerebral infarction is also possible. Blood pressure in such patients can be anything.

The development of thrombotic and non-thrombotic cerebral infarction occurs less rapidly; many patients experience precursor symptoms in the form of paresthesia, short-term paresis, visual and speech disorders. Since slowing cerebral blood flow increases cerebral ischemia, many patients develop these symptoms during rest or sleep. The increase in symptoms occurs gradually and can last for several hours or even days. The coma is shallow, often the disturbance of consciousness is limited by the development of stupor. The nature of focal neurological symptoms indicates the presence of an extensive lesion in the brain; in addition to hemiplegia, speech impairment (dysarthria, aphasia) is often observed.

Other causes of encephalomalacia are observed relatively rarely. The likelihood of cerebral vessel embolism increases with prolonged septic endocarditis, heart valve defects (primarily rheumatic etiology), and atrial fibrillation. Gas embolism is possible as a result of the development of decompression sickness, for example, when a diver rises too quickly (emergency) while working at depth for several hours. When working at depth, a diver breathes air under increased pressure. Under these conditions, nitrogen dissolves in the blood much more intensively than at normal atmospheric pressure. Rapid ascent to the surface results in decompression, which reduces the solubility of nitrogen in the blood.

As a result, nitrogen appears in the vascular bed in the form of gas bubbles that can cause gas embolism. Gas embolism during decompression sickness is characterized by severe headaches, attacks of dizziness, paresis of the limbs and loss of consciousness. After massive bone fractures, fat contained in the bone marrow may enter the bloodstream. Therefore, severe injuries with multiple fractures can lead to the development of fat embolism. Unlike thrombotic and non-thrombotic cerebral infarction, embolic stroke occurs suddenly, but the coma is not as long and deep as with a cerebral hemorrhage.

Meningeal coma can develop in patients with severe forms of meningitis; its clinical manifestations largely depend on the nature of the pathogen. In its typical form, this coma is observed with meningococcal infection. In this case, against the background of severe general intoxication and headaches, signs of damage to the meninges are observed: meningeal symptoms. These symptoms include stiff neck, positive Kernig's signs (inability to passively bend the straightened leg at the hip joint to an angle of 90°; during the test, the leg involuntarily bends at the knee joint) and Brudzinski's (bending the legs at the knees in response to a passive tilt of the head forward) . The patient often takes a forced position - the “pointing dog position”.

Meningococcal meningitis is characterized by a star-shaped hemorrhagic rash of varying diameters with areas of necrosis in the center of the rash. The rash can also spread to the mucous membranes. Possible hemorrhages in internal organs, incl. - into the adrenal glands. In this case, an adrenal hypoadrenal crisis develops, manifested by severe persistent collapse. Characteristic clinical and laboratory signs of a severe infectious process are observed: high body temperature, leukocytosis with a shift in the leukocyte formula to the left, an increase in ESR. The presence of meningitis is confirmed by increased cerebral liquor pressure, the cerebrospinal fluid is turbid, and laboratory testing reveals inflammatory changes (increased protein content, pleocytosis, etc.).

Cerebral coma can be caused by a brain tumor. The disease in this case usually begins with nonspecific cerebral symptoms: gradually increasing headaches, which can be constant or periodic, vomiting appears, often multiple times, does not bring relief to the patient and is not associated with food intake. The development of coma is often preceded by gradually progressive focal neurological symptoms (like an “oil stain”). Bulbar and (or) peduncular dislocation syndromes are characteristic. Body temperature is usually normal, there are no changes in general blood and urine tests.

When examining the fundus of the eye, in 75-90% of cases, congestive optic discs are detected: the boundaries of the discs are unclear, the discs themselves seem enlarged, and a thin radial striation appears on the periphery of the discs, extending to the retina. The veins are dilated, the arteries are narrowed, the physiological excavation is smoothed. An X-ray examination of the skull (craniography) can reveal indirect signs of tumor formation: an increase in the size of the sella turcica, destruction of its walls, etc. With severe liquor hypertension, specific changes in the bones of the cranial vault may appear. However, craniography often does not reveal signs of a tumor lesion, and the diagnosis of a brain tumor as the cause of a coma can only be confirmed or rejected using computed tomography or magnetic resonance imaging.

Protein-cell dissociation is detected in the cerebrospinal fluid, but it should be remembered that the localization of the tumor in the posterior cranial fossa is an absolute contraindication to lumbar puncture. With such a localization of the tumor, this manipulation leads to dislocation of the cerebellum, its herniation into the foramen magnum, compression of the brain stem and death of the patient from respiratory arrest as a result of paralysis of the respiratory center.

Clinical picture brain abscess in general resembles that of brain tumors; its development is usually preceded by otitis media, sinusitis, traumatic brain injury, sepsis and severe purulent-inflammatory diseases of other localization (lung abscesses, etc.). Due to the faster progression of the process than with tumors, stagnant changes in the fundus are detected less frequently. Due to more pronounced intoxication, increased body temperature, leukocytosis and other nonspecific signs of the purulent-inflammatory process are more noticeable. However, with pronounced encapsulation of the abscess, general signs of a purulent-inflammatory process may be absent. Thrombosis of the cerebral sinus and non-purulent encephalitis can also lead to loss of consciousness.

If cerebral coma is suspected, an urgent consultation with a neurologist is indicated, and if it is impossible to exclude a neuroinfection, an examination by an infectious disease specialist is indicated.

Post-traumatic coma. Traumatic brain injury, both with and without fractures of the skull bones, can lead to prolonged (hours, days) loss of consciousness. Unconsciousness can occur either as a result of a concussion or contusion of the brain, or as a result of hemorrhage provoked by trauma (epidural and subdural hematomas). In patients with diabetes, a traumatic brain injury can be caused by a fall as a result of severe hypoglycemia or other causes not related to diabetes (road traffic accident, etc.).

On examination, such patients often exhibit scalp injuries. Fractures of the bones of the base of the skull are accompanied by bleeding and discharge of cerebrospinal fluid from the ears and nose. Massive bruises appear in the area of the eye sockets (symptom of “glasses”). Craniograms can reveal cracks and fractures of the vault and base of the skull.

In case of post-traumatic loss of consciousness, you should always remember the possibility of developing a subdural hematoma. Diagnosis of this condition is necessary for timely neurosurgical intervention to save the patient’s life. Deterioration of the condition with a subdural hematoma often occurs after a “clear interval”, the duration of which reaches several hours or even days. It is for this reason that patients who have suffered a concussion are hospitalized in the neurosurgical department and forced to comply with a medical and protective regime for 1.5-2 weeks.

But even during the “light interval”, patients are often bothered by headaches and intolerance to bright light. The deterioration of the condition occurs suddenly and is manifested by loss of consciousness against the background of paralysis, convulsive seizures, increased blood pressure and body temperature. Dilation of the pupils on the affected side is typical, and terminal Cheyne-Stokes respiration often occurs. In some cases, focal neurological symptoms may be mild and include changes in reflexes and mild unilateral paresis. The xanthochromic nature of the cerebrospinal fluid confirms the diagnosis of subdural hematoma, however, in some cases, the cerebrospinal fluid may be completely transparent or, conversely, contain a significant admixture of blood.

Zhukova L.A., Sumin S.A., Lebedev T.Yu.

Emergency endocrinology

Cerebral coma was formerly known as apoplexy coma, and its main cause is primary or secondary damage to the brain 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 commonly, traumatic factors. Among the toxic factors in the first place are alcohol and drug intoxication, coma due to carbon monoxide poisoning. Closed craniocerebral injuries are 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 in different types of comas.

However, with any type and type of coma, there are lesions at the level of the cerebral cortex, reticular formation, basal ganglia and limbic system. It is the extent of such disorders (transient or chronic) that lead to the body losing 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 preservation of basic reflexes, which indicates preserved vitality of the brain. The second group of symptoms is lack of response to stimuli, primarily tactile. The victim seems to have fallen asleep, especially since cerebral coma is accompanied by a sleep-like state - the eyes are closed, the person literally “fell” into sleep.

In the first stages of cerebral coma, the patient retains at least a minimal range of movements - he is able to change body position and swallows saliva. The deeper the brain damage, the more pronounced the clinical manifestations of depression of consciousness, up to the shutdown of spontaneous breathing. Convulsions, vomiting, increased body temperature are also signs of cerebral coma.

Diagnosis and treatment

The diagnosis of cerebral coma cannot be established through examination alone, although typical signs of coma may indicate its development. A thorough neurological examination is required, using special rating scales. An electroencephalogram and computed tomography are also necessary to diagnose 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 carried out. Tracheal intubation, dynamic assessment and maintenance of vital signs, and careful nursing all require admission to the intensive care unit.

Forecast

The prognosis depends entirely on the etiological cause of the coma. Some comas lead to a slow decline of brain function, which is almost impossible to stop and the person switches to a vegetative existence. Brain coma of toxic origin is easier to treat. The overall average mortality rate in the case of cerebral coma can reach 35%. It should be remembered that not a single coma passes without leaving a trace on the body.

Comas: classification, signs, principles of treatment. What is cerebral coma and its causes? Principles of treatment for coma

Clinical picture and symptoms

Brain coma: causes

Treatment

Brain coma: complications

First aid

What causes coma?

Classification com

Signs of a coma

Coma I degree

Coma II degree

Coma III degree

Coma IV degree

Clinical features of some types of coma

Cerebrovascular coma

Traumatic coma

Epileptic coma

Meningoencephalitic coma

Hypertensive coma

Hepatic coma

Renal coma

Alcohol coma

Coma due to carbon monoxide poisoning

Coma due to poisoning with sleeping pills (barbiturates)

Coma due to drug overdose

Diabetic coma

Principles of treatment for coma

Brain coma

Clinical picture and symptoms

Brain coma: causes

Treatment

Brain coma: complications

First aid

Programs:

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ICD-10

General information

Classification

Coma symptoms

Diagnosis of coma

Treatment of coma

Forecast

Causes

Symptoms

Diagnosis and treatment

Forecast