Comas: classification, signs, principles of treatment

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A coma is a state of total absence of consciousness, when a person does not react to anything. In a coma, no stimulus (neither external nor internal) is able to bring a person to life. This is a life-threatening resuscitation, because, in addition to losing consciousness, coma has abnormalities in the functions of vital organs (breathing and cardiac activity).

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

Coma is always a complication of any disease or pathological condition (poisoning, trauma). All comas have a number of common signs, regardless of the cause of their occurrence. But there are also differences in clinical symptoms in different types of com. The treatment of coma should be carried out in conditions of resuscitation department. 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 are coma, what they are characterized and what are the basic principles of treating coma.

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Content

  • 1What is the basis of coma?
  • 2Classification com
  • 3Symptoms of coma
    • 3.1Coma I degree
    • 3.2Coma II degree
    • 3.3Coma III degree
    • 3.4Coma IV degree
  • 4Clinical features of some species of coma
    • 4.1Cerebrovascular coma
    • 4.2Traumatic coma
    • 4.3Epileptic coma
    • 4.4Meningoencephalitic coma
    • 4.5Hypertensive coma
    • 4.6Hepatic coma
    • 4.7Renal coma
    • 4.8Alcoholic coma
    • 4.9Coma in carbon monoxide poisoning
    • 4.10Coma for poisoning with sleeping pills (barbiturates)
    • 4.11Coma with an overdose of drugs
    • 4.12Diabetic coma
  • 5Principles of treatment of coma

What is the basis of coma?

At the base of the coma lie two mechanisms:

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

Primary lesion of the brain stem is possible under conditions such as stroke, craniocerebral trauma, and tumor process. Secondary disorders occur during metabolic changes (for 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, normal transmission of nerve impulses between the brain cells becomes impossible. At the same time, coordination and coordinated activity of all structures are lost, they are transferred to the autonomous regime. The brain is losing its management functions over the whole organism.


Classification com

Comatose states are usually divided into different characters. The most optimal are two classifications: the causal factor and the degree of oppression of consciousness (depth of coma).

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

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

Neurological (primary) genesis:

  • traumatic (with craniocerebral trauma);
  • cerebrovascular (with acute vascular disorders of blood circulation in the brain);
  • epileptic (the result of epi-seizures);
  • meningoencephalitic (the result of inflammatory diseases of the brain and its membranes);
  • hypertensive (due to a tumor in the brain and skull).

Secondary genesis:

  • endocrine (diabetic in diabetes mellitus (several of them), hypothyroid and thyrotoxic in diseases of the thyroid gland, hypokorticoid with acute adrenal insufficiency, hypopituitary with total deficiency of pituitary hormones);
  • toxic (in renal or hepatic insufficiency, when poisoning with 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 under the influence of physical factors (thermal overheating or overcooling, electric shock);
  • coma with a significant deficit of water, electrolytes and food (hungry, with indomitable vomiting and diarrhea).

According to statistical data, the most common cause of development of coma is stroke, followed by drug overdose, the third - complications of diabetes.

The necessity of the second classification is due to the fact that the causal factor in itself does not reflect the severity of the condition of the patient in a coma.

Depending on the severity of the state (depth of oppression of consciousness) it is customary to distinguish the following types of com:

  • I degree (mild, subcortical);
  • II degree (moderate, anterolateral, "hyperactive");
  • III degree (deep, posterolateral, "flaccid");
  • IV degree (transcendental, terminal).

A sharp separation of the degrees of coma is rather difficult, since the transition from one stage to another can be very rapid. This classification is based on various clinical symptoms that correspond to a certain stage.

Symptoms of coma

Coma I degree

It is called subcortical, because at this stage, the activity of the cerebral cortex is inhibited and disinhibition of the deeper lying parts of the brain, called subcortical formations. 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 disinhibite the patient);
  • lack of answers to the questions asked. Perhaps inarticulate mooing, the publication of various sounds outside of communication with what is happening from the outside;
  • the lack of a normal reaction to a pain stimulus (that is, a weak and very slow reaction, for example, with a needle stab the patient does not withdraw it at once, but weakly flexes or unbends after some time after applying painful irritation);
  • spontaneous active movements are practically absent. Sometimes, sucking, chewing, swallowing movements may occur as a manifestation of cerebral reflexes, which are normally suppressed by the bark of the cerebral hemispheres;
  • muscular tonus elevated;
  • deep reflexes (knee, Achilles and others) increase, and superficial (corneal, plantar and others) are depressed;
  • possible pathological carpal and foot symptoms (Babinsky, Zhukovsky and others);
  • the pupils' reaction to light is preserved (constriction), strabismus, spontaneous movements of the eyeballs can be observed;
  • lack of control over pelvic organs;
  • usually self-contained breathing is preserved;
  • from the side of cardiac activity there is an increase in heart rate (tachycardia).

Coma II degree

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

  • the appearance of tonic convulsions or periodic shudders;
  • absence of speech activity, verbal contact is impossible;
  • a sharp weakening of the reaction to pain (slight wiggling of the limb when applying a prick);
  • oppression of all reflexes (both superficial and deep);
  • narrowing of pupils and their weak reaction to light;
  • increased body temperature;
  • increased sweating;
  • sharp fluctuations in blood pressure;
  • marked tachycardia;
  • violation of breathing (with pauses, with stops, noisy, with different depths of breaths).

Coma III degree

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

  • Protective reactions in response to the pain stimulus are lost completely (the patient does not even move a limb in response to the injection);
  • there are no superficial reflexes (in particular, corneal reflexes);
  • a sharp decrease in muscle tone and tendon reflexes;
  • pupils are dilated and do not respond to light;
  • breathing becomes superficial and arrhythmic, not very productive. In the act of breathing, additional musculature (muscles of the shoulder girdle) is involved, which is not normally observed;
  • blood pressure is reduced;
  • periodic cramps are possible.

Coma IV degree

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

  • absence of all reflexes;
  • the widest possible enlargement of the pupils;
  • muscle atony;
  • lack of independent breathing (only artificial ventilation supports the body's oxygen supply);
  • the blood pressure drops to zero without medications;
  • a drop in body temperature.

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

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


Clinical features of some species of coma

Cerebrovascular coma

It always becomes the result of a global vascular catastrophe (ischemic or hemorrhagic stroke, rupture of an aneurysm), so 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, a strained pulse. In addition to neurological symptoms, peculiar to the coma, there are focal neurological symptoms (for example, a skewed face, inflation of one cheek during breathing). The first stage of coma may be accompanied by psychomotor agitation. If subarachnoid hemorrhage occurred, positive meningeal symptoms (stiff neck muscles, symptoms of Kernig, Brudzinsky) are determined.

Traumatic coma

Since it usually develops as a result of severe head injury, it is possible to detect damage to the skin on the patient's head. There may be bleeding from the nose, ear (sometimes leakage of cerebrospinal fluid), bruising around the eyes (a symptom of "glasses"). Quite often pupils have a different size 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 one after one epimetails. With this coma, the patient's face acquires a cyanotic shade (if the attack was very recently), the pupils become wide and do not respond to light, there may be traces of the bite of the tongue, foam on the lips. When the attacks stop, the pupils are still wide, the muscle tone decreases, the reflexes are not called. There are tachycardia and rapid breathing.

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, of varying degrees of meningeal symptoms. A rash on the body is possible. In the blood there is a significant increase in the content of leukocytes and ESR, and in the cerebrospinal fluid there is an increase in the amount of protein and leukocytes.

Hypertensive coma

It occurs as a result of a significant increase in intracranial pressure in the presence of additional education in the cranial cavity. The coma develops due to the compression of certain parts of the brain and its infringement in the clavicle of a cerebellar nerve or a large occipital opening. This coma is accompanied by bradycardia (slowing heart rate), decreasing breathing rate, vomiting.

Hepatic coma

It develops gradually against the background of hepatitis or cirrhosis of the liver. From the patient comes a specific liver odor (the smell of "raw meat"). Skin covers are yellow, with pinpoint hemorrhages, and places of scratching. Tendon reflexes are increased, there may be convulsions. Arterial 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, "jellyfish head" - expansion and tortuosity of the subcutaneous veins of the abdomen).

Renal coma

It also develops gradually. The patient emits a smell of urine (ammonia). Skin covers are dry, pale gray (as if dirty), with traces of scratching. There are swelling in the zone of the lower back and lower extremities, the puffiness of the face. Arterial pressure is low, tendon reflexes are high, pupils are narrow. There may be involuntary muscular twitching in separate muscle groups.

Alcoholic coma

It develops gradually when you abuse alcohol and take too much. Naturally, there is a smell of alcohol (but you should bear in mind that if there is this symptom of a coma, there may be another, for example, traumatic. Just a person could drink alcohol before the injury). The heart rate increases, and blood pressure decreases. Skin covers are red, wet with sweat. Muscle tone and reflexes are low. The pupils are narrow.

Coma in carbon monoxide poisoning

This coma is accompanied by a tachycardia with low arterial pressure, shallow breathing (possible respiratory paralysis). Characterized by wide pupils with no response to light. A very specific symptom is the complexion and mucous membranes: cherry red (this color gives carboxyhemoglobin), the limbs can be bluish at the same time.

Coma for poisoning with sleeping pills (barbiturates)

Coma develops gradually, being a continuation of sleep. Typical bradycardia (low heart rate) and low blood pressure. Breathing becomes superficial and rare. The skin is pale. Reflex activity of the nervous system is so oppressed that there is no reaction to pain, tendon reflexes are not called (or they are sharply weakened). Increased salivation.

Coma with an overdose of drugs

It is characterized by a drop in blood pressure, a decrease in the heart rate, a weak pulse, and shallow breathing. Lips and fingertips have a cyanotic color, the skin is dry. Muscle tone is sharply weakened. Characterized by the so-called "point" pupils, so narrowed. There may be traces from injections (although this is not necessary, since the way of drug use can be, for example, intranasal).

Diabetic coma

It is more correct to say not coma, but coma. Because they can be several with diabetes. This ketoacidotic (with the accumulation of products of metabolism of fats in the blood and increase in glucose levels), hypoglycemic (with a drop in the level glucose and excess insulin), hyperosmolar (with severe dehydration) and lactacidemic (with excess lactic acid in the blood). Each of these species 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 narrowed. With hypoglycemic coma, no foreign smells from the patient are felt, the skin is pale and damp, and the pupils are dilated. Of course, in determining the type of diabetic coma, the main role is played by additional methods of investigation (the amount of glucose in the blood, in the urine, the presence of acetone in the urine, and so on).

Principles of treatment of coma

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

Measures that provide vital functions of the body include:

  • support breathing. If necessary, sanitation of the respiratory tract is done to restore their patency (foreign bodies are removed, straightened sunken tongue), air duct, oxygen mask is installed, artificial ventilation is performed;
  • support of the circulatory system (use of drugs that increase blood pressure in hypotension, and reducing with hypertension; means that normalize the heart rhythm; normalization of the volume of circulating blood).

Symptomatic measures are also used to remove the existing violations:

  • large doses of vitamin B1 for suspected alcohol poisoning;
  • anticonvulsants in the presence of seizures;
  • antiemetics;
  • sedatives during excitation;
  • intravenously injected glucose (even if the cause of coma is not known, because the risk of brain damage from low blood glucose is higher than from high. The introduction of a certain amount of glucose at a high content of it in the blood will not do much harm);
  • gastric lavage in case of suspected poisoning with drugs or poor-quality food (including fungi);
  • drugs to reduce body temperature;
  • if there are signs of an infectious process, the use of antibiotics is indicated.

At the slightest suspicion of trauma to the cervical spine (or if it is not possible to exclude it), stabilization of this area is necessary. Usually for this purpose a tire is used in the form of a collar.

Comas classification signs principles of treatmentAfter determining the cause, which caused someone, they treat the underlying disease. Then a specific therapy directed against a particular ailment is already prescribed. This can be hemodialysis in renal failure, the administration of Naloxone in overdose of drugs and even surgical intervention (for example, with brain hematoma). The type and amount of treatment 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 lead to death. There is a great variety of species due to the large number of pathological conditions that can complicate them. The treatment of coma is carried out in the conditions of 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.


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