Coma

Coma is a deep loss of consciousness. A coma is not a diagnosis, but just like a shock, an indication of a critical condition of the body caused by a certain pathology.

Some types of coma are combined with each other and shock. 

[1]

Symptoms of the coma

The development of a coma can be sudden - within a few minutes, often without precursors, against the background of relative well-being, rapid - within 0.5-1 hours in the presence of precursors; gradual for several hours or more. Rapid and sudden development is possible with any coma, but more often observed with brain damage, anaphylaxis.

A coma of a fast type is characterized by a sudden loss of consciousness. Develops a breathing disorder (arrhythmic or stotorous) of the central type of disturbance of regulation. There is a violation of central hemodynamics with the development of hypodynamia, tachycardia, arrhythmia, hypervolemic syndrome with polyfunctional deficiency of the homeostasis system.

Slow development includes a period of precomatric states with a gradual depression of consciousness: first a stupor that can have periods of excitement, then a stopper, and finally the process passes into a coma.

With the slow development of coma, 3 stages are formed (the first two correspond to precoma), which are clinically manifested:

1. mental anxiety, drowsiness during the day and excitation at night, a violation of the coordination of conscious movements, ataxia;
2. drowsiness with a sharp inhibition of reactions to external stimuli, including pain and light; increase, and, then, a decrease in tendon reflexes.
3. patients do not come into contact, however, pain sensitivity is preserved; muscular dystonia, spastic contraction of some muscles, mostly small ones; urination and defecation are involuntary, i.e. The coma of three degrees described above is described with the transition to the agonal state.

[2]

Forms

[3], [4], [5], [6]

Apoplexic coma

The main pathogenetic moment is a disorder of cerebral circulation, with the development of circulatory hypoxia of the brain. It can be of three types: hemorrhagic stroke with hemorrhage and blood imbibition in the brain tissue or trunk; ischemic thrombotic stroke; ischemic embolic stroke. Hemorrhagic stroke: the onset of sudden, may be associated with a craniocerebral trauma (concussion, brain contusion, intracranial or intracerebral hematoma) or in diseases (atherosclerosis of the cerebral vessels, hypertension, in which the vessel ruptures, more often in the afternoon, with physical stress or , stressful situations, mainly develops in the elderly, but may be in boys with an aneurysm of cerebral vascular aneurysms, more often in physical education classes. Often preceded by: dizziness, headaches, sight and hearing disorders, ringing in the ears, high hypertension, orthostatic collapse.

Meningeal syndrome is clearly expressed, with the formation of hemiparesis, violation of craniocerebral innervation, the presence of pathological symptoms. Cramps are possible.

In the laboratory examination of blood and urine, no specific changes are detected. Liqvor comes under increased pressure, xanthochromic, with an admixture of blood. According to indications, which are determined by a neurologist or a neurosurgeon, perform instrumental, functional brain studies (all depends on the capabilities of the hospital), while revealing pronounced changes in the echoencephalogram, rheogram, dopplerogram, computer brain study.

Ischemic thrombotic stroke develops gradually, more often in the morning, dizziness, syncope, stunning, orthostatic collapse, transient motor or sensory disorders, dysarthria serve as harbingers. The basis is the gradual development of atherosclerotic occlusion, less often a tumor.

The main manifestations are: pallor of the face, narrowing of the pupils, lowering of arterial pressure, bradycardia before the development of cardiovascular insufficiency. Meningeal syndrome manifests itself in the formation of mono- or hemiparesis, pathological symptoms are smoothed.

In laboratory studies, hypercoagulation of blood serves as a characteristic feature, other analyzes, including cerebrospinal fluid, are unchanged (unless there is another concomitant pathology). In instrumental studies, clear signs of thrombosis, especially when carrying out angiography of cerebral vessels.

Ischemic embolic stroke develops suddenly with rapid loss of consciousness and coma deepening, more often in young people with chronic diseases of the cardiovascular system, mostly in the pathology of the veins and the presence of varicosities, thrombophlebitis, phlebothrombosis, in which the clot breaks and clogs the brain vessels.

The main manifestations are absence of precursors, pallor of the face, moderate dilatation of the pupils, hyperthermia, various signs of cardiac and respiratory insufficiency. Meningeal syndrome manifests itself mono-, less often hemiparesis.

Laboratory changes are not indicative, including the investigation of cerebrospinal fluid. From instrumental studies the most informative angiography of cerebral vessels, magnetic resonance imaging.

[7], [8], [9], [10]

Hemolytic coma

Occurs during the crisis in patients with hemolytic disease. In the pathogenesis of this coma, the leading moments are the hemic hypoxia of the brain due to the violation of oxygen transport and cerebral circulation in connection with neurocirculatory dystonia and thrombus formation in the microcirculatory bed, which leads to gross metabolic disturbances in the brain, up to softening and necrosis with a disorder of central regulation of functions organism.

The development of coma is preceded by progressively increasing hemolytic jaundice, headache, high fever ("hemoglobinuria fever"), shortness of breath, muscle pains, collapse. Against this background, loss of consciousness develops suddenly, with a pronounced meningeal syndrome and seizures. Differential signs - the presence of hemolytic jaundice, confirmed by laboratory indicators.

Hyperthermic coma

At the heart of pathogenesis is the external overheating of the body or the violation of the body's thermoregulation, leading to water-electrolyte and circulatory disorders, the development of perivascular and pericellular edema with small hemorrhages, including in the brain. Can develop against the background of meningeal pathology.

It develops gradually, with the formation of precursors in the form of lethargy, sweating, headaches, dizziness, noise in the ears, feelings of stunning, down to fainting, nausea and vomiting, shortness of breath, palpitations. The body temperature rises.

The main clinical manifestations are: hyperthermia, hyperemia of the face, mydriasis, total hypo- or areflexia; tachypnea, sometimes with the development of Cheyne-Stokes respiration; tachycardia, hypotension, decreased diuresis, hypo- or areflexia.

Laboratory indicators are not typical.

Hypocorticoid (adrenal) coma

The causes of the development of this coma are: hypokorticism (crisis) with a sharp decrease in gluco- and mineralocorticoids (more often in young men or boys - they are obese, with loose body, on the stomach, have striae); acute damage to the adrenal glands; Waterhouse-Frideriksen syndrome; Addison's disease; rapid abolition of steroid therapy. In pathogenesis, the main is the violation of electrolyte metabolism with loss of water and sodium, leading to secondary disorders of vascular tone and cardiac activity.

Develops: gradually (with Addison's disease quickly), more often after stressful situations, infections, surgeries, painful manipulation and trauma. Accompanied by: weakness, rapid fatigue, anorexia, nausea, diarrhea, hypotension, orthostatic collapse and fainting;

At external examination, in such patients the characteristic signs are revealed: in patients with Addison's disease the shade of the skin looks like a bronze tan, while in another pathology there is a hyperpigmentation of the skin folds of the brushes and inguinal area from bronze to black. On the skin can be noted hemorrhages, characterized by hypothermia: Pupils dilated, turgor of eyeballs preserved. Muscles are rigid, areflexia. Breathing is superficial, often of the Kussmaul type. From the cardiovascular system: hypotension, tachycardia, pulsation is mild. Characteristic vomiting without harbingers and relief, involuntary diarrhea. When the shock threshold of irritation is reached, and it is very low in these patients, respiratory and cardiac arrest is possible, which requires the resuscitation aid.

Laboratory indicators: hyponatremia, hyperkalemia, hypoglycemia (it is differentially important not to be confused with acidosis of another genesis); possible - azotemia, lymphocytosis, monocytosis, eosinophilia. With a special study - a decrease in blood ketosteroid (17-KS and 17-ACS) and urine. In the following - a progressive drop in potassium ions.

Hypopituitary (pituitary) coma

The pathogenesis is based on: pituitary damage or tumor compression, long-term radiation therapy, massive corticosteroid therapy, Shikhen's syndrome with loss of hormonal function. This leads to a disruption in the function of the central nervous system and the defeat of central regulation of the activity of all organs and systems through the neurohumoral system. Complex functional changes are formed in the systems: central nervous system, respiration, cardiovascular, metabolism and homeostasis, renal and hepatic function. This kind of coma is the most difficult for differential diagnosis.

The onset is gradual, most often after trauma, infectious diseases, especially viral etiology. Progressive weakness, drowsiness, adynamia are noted. Characteristic: edema of the trunk, dry mouth, dry skin and peeling, bradycardia, lowering blood pressure, often convulsive syndrome.

With the already developed coma, the main differential signs are: hypothermia (below 35 degrees); the skin is pale, rough, sometimes with an icteric shade, dry, cold to the touch. The face is puffy, the eyelids are edematous.

Swelling of the trunk and extremities - loose, easily pushed. Breathing is rare, superficial, like Kussmaul. From the cardiovascular system: hypotension, bradycardia, hypovolemia. Oligoury is characteristic. From the side of the central nervous system: hypo- or areflexia.

At laboratory researches are revealed: anemia, acceleration of an ESR, a dysproteinemia, a hypercholesterolemia, a hyponotriemia, a hypochloremia. Due to pathogenesis, signs of respiratory acidosis.

Hungry (alimentary-dystrophic) coma

The basis is insufficient or inadequate nutrition with violation of energy exchange processes, accompanied by dystrophy and functional failure of all organs and the system, before the whole brain. Clinically and functionally reminiscent of hypoglycemic coma, often develops in cancer patients or in patients with severe intoxication. But in recent years it has also been found in clinically healthy people (dietary starvation, unbalanced nutrition, etc.).

The onset of coma development is rapid. It is accompanied by a feeling of hunger, excitement, a feverish flush on the cheeks; eyes shining, pupils dilated. There is a rapid transition from syncope to coma.

With the development of coma, clinical manifestations are different, depend on etiology. With onkokakeksii and prolonged starvation: the skin is dry, pale gray / color, cold to the touch, muscles atrophic, reflexes in them are reduced. Rarely formed meningeal syndrome. With alimentary disorders: the skin is pale, cold to the touch, due to vegetative-vascular dystonia, the pupils are wide, the reaction to light is reduced. Common are: hypotension, weak pulse, tachycardia, hyporeflexia, sometimes painful cramps.

Laboratory indicators are not characteristic for differential diagnosis (clinical data and anamnesis play a big role): leukopenia, hypoproteinemia, hypocalcemia, hyperkalemia are revealed, which is more indicative of the development of metabolic acidosis.

Diabetic coma

[11], [12], [13], [14], [15],

Hypoglycemic coma

The main pathogenetic factor is hypoglycemia and a decrease in the utilization of glucose by brain cells. It can be accompanied by disorders of cerebral circulation in the form of a form of apoplectic coma. In the anamnesis in these patients there is a presence of diabetes mellitus with the use of antidiabetic drugs or insulin. If the patient is unconscious, there is usually a note and an "insulin kit" in the pockets.

Develops quickly, less often there is a slow development. Accompanied by: hunger, fear, weakness, sweating, palpitation, trembling in the whole body, psychomotor agitation and inappropriate behavior, shaky walk (resembles the behavior of a person in a state of intoxication - be careful when conducting differential diagnosis).

With the development of the comatose state itself, the distinctive features are pallor and moisture of the skin, the presence of clonic and tonic convulsions, hypertension of the muscles, alternating with hypotension. Sometimes there is a violation of the act of swallowing, but breathing is saved. Pupils are wide, the turgor of eyeballs is not broken. From the cardiovascular system are characterized by: hypotension, tachycardia, arrhythmias. There is no smell of acetone in the exhaled air.

Laboratory indicators: hypoglycemia is detected with a decrease in the sugar level of less than 2.2 mmol / l.

Hyperglycemic coma

The basis of the development of hyperglycemic coma is insulin deficiency in diabetes mellitus, which leads to a decrease in glucose uptake by tissues, its accumulation in the blood with glycemia and hyperosmia of the plasma, disruption of tissue metabolism with ketosis, acidosis, deep depression of CNS function due to reduced glucose uptake by brain cells and disturbance of trophism of neurocytes. Hyperglycemic coma is the opposite of hypoglycemic coma. In contrast to it, there is a lot of sugar in the blood, but it is not digested because of a lack of insulin. The reasons are: abundant reception of sweet food at usual dosage to insulin patients; non-compliance with insulin administration, error in dosage, development of viral and inflammatory diseases in the patient, ineffectiveness of stimulants of natural insulin production by the pancreas (such as bucarban, etc.). There are three variants of hyperglycemic coma:

1. hyperketonemic acidotic coma, is accompanied by the development of metabolic acidosis due to decreased utilization of ketone bodies with excessive ketogenesis in the liver, a sharp decrease in alkaline reserves in tissues, a violation of the cationic composition of cells about excessive excretion of potassium by the kidneys;
2. hyperosmolar coma, caused by abrupt violations of blood supply, hydration and cationic composition of brain cells with high diuresis with loss of salts; accompanied by the development of hypovolemia, hypotension and other disorders of microcirculation, which leads to a decrease in renal filtration and secondary delay in plasma of highly dispersed proteins and salt osmoids;
3. hyperlactacidemic coma, develops in patients with diabetes mellitus in conditions of hypoxia caused by severe infection, renal and hepatic insufficiency, and administration of biguanides. At the same time, anaerobic, glycolysis is increased, the lactate / pyruvate system is disrupted and a powerful metabolic acidosis with damage to the cerebral cortex is formed.

Hyperketonemic coma

The onset is gradual: polydipsia, polyuria, weakness, severe abdominal pain, nausea, loss of appetite, drowsiness. Clinical manifestations: the face is hyperemic, eyeballs are sunken, their tone is lowered, the pupils are narrowed. The skin is dry, often pale, its turgor is reduced. The limbs are cold to the touch, the muscles are relaxed, flabby. It is characteristic of a rare deep breathing, such as Kussmaul with the smell of acetone from the mouth. The tongue is dry, often covered with a brown coating. Tachycardia is moderate, blood pressure is lowered, heart sounds are not changed, but there can be a rhythm of the pendulum.

Laboratory tests: hyperglycemia over 20 mmol / l; hyperosmolarity of plasma (norm 285-295 mosmol / kg), hyperketonemia, decrease in blood pH to acid side, increase of residual urea nitrogen, creatinine, increase in hematocrit, hemoglobin, neutrophilic leukocytosis. In urine, sugar and acetone.

Hyperosmolar diabetic coma

Hyperosmolar coma can develop not only in diabetes mellitus, but also in other pathologies. In this case, diabetes mellitus is an aggravating factor, since the mortality in this form of coma is more than 50%. It is caused by a massive loss of fluid due to: vomiting, diarrhea, taking diuretics, etc.

The beginning is gradual. Accompanying: increasing weakness, polyuria, diarrhea, mental disorders, orthostatic collapse, hemodynamic disorders, up to hypovolemic shock. Clinical manifestations: hyperthermia, dry skin and mucous membranes; tonic eye removal and their hypotension, nystagmus; breathing fast, deep, without the smell of acetone; BP low, tachycardia, arrhythmia, impaired pulse. Maybe anuria. Because of a breach of cerebral microcirculation possible: hemiparesis, myoclonic or epileptiform convulsions, meningeal, symptoms.

Laboratory indicators: lack of ketonemia, severe hyperglycemia, increased hematocrit, urea, plasma osmolarity, leukocytosis. Proteinuria is possible, but acetone in the urine is never determined.

Hyperlactacidemic diabetic coma

It develops slowly. Characteristic: muscle pains, pain in the chest, rapid breathing, drowsiness, gradual depression of consciousness. Clinical manifestations: skin is dry / pale, amy, mydriasis, areflexia, meningeal symptoms, changes in depth and rhythm of breathing, such as Kussmaul, tachycardia and hypotension, concomitant purulent intoxication clinic, which provokes the development of this coma.

Coma in meningitis

The basis is meningitis of various etiologies, often purulent with a defeat of the cerebral membrane, accompanied by liquor and microcirculatory disorders in the brain with venous congestion, edema of perivascular spaces, swelling and dystrophy of nerve cells and fibers, and increased intracranial pressure. The basic in the clinic is accompanied by the manifestations of the main pathology that caused the penetration of the infection to the brain - craniocerebral trauma, mastoiditis and other diseases of the ENT organs, purulent processes of the face, pneumonia.

It develops quickly, against a background of general malaise, hyperthermia, hyperesthesia, headache, vomiting. Clinical manifestations of coma: hyperthermia is very high, meningeal syndrome, hemorrhagic skin rashes, convulsive seizures and convulsive syndrome, bradycardia and arrhythmia are more common, breathing is frequent and arrhythmic, asymmetry of tendon reflexes and loss of function of cranial nerves. Likvornoe pressure is significantly increased, comes in jet.

Laboratory indicators: from the side of blood - typical changes typical for purulent inflammation; cerebrospinal fluid with high leukocytosis - with purulent meningitis neutrophilic, with serous - the lymphocytic protein in it is elevated moderately.

[16], [17], [18],

Coma in encephalitis

It develops with reactive inflammation of the brain substance, accompanied by its swelling and swelling. Echoencephalography reveals signs of an increase; intracranial pressure and expansion of the third ventricle of the brain. Liquor pressure is increased, xanthochromic or hemorrhagic. The development of coma is preceded by: general malaise, hyperthermia, dizziness, vomiting; clinic of a virus infection.

The coma develops rapidly, accompanied by: high hyperthermia, convulsions, paralysis and paresis, loss of cranial nerves, strabismus, ptosis, paralysis of the eye. Laboratory indicators of cerebrospinal fluid are an increase in protein and sugar 10. 

[19], [20], [21], [22], [23],

Coma for acute poisoning 

Below are described only the poisoning, most common in everyday life. It is important to remember that vomit, washing water, blood and urine - must be sent to a toxic center or an ATC laboratory (by order of the investigator) for analysis of the toxic agent.

Poisoning with barbiturates, drugs, clonidine. They have the same picture and are often combined. They develop slowly, except for poisoning with clonidine in combination with alcohol. Accompanying: increasing drowsiness, disorientation, ataxia, vomiting. Muscles are hypotonic, reflexes, lowered, the skin moist, covered with a sticky sweat. The pressure is reduced, the pulse is frequent, small filling. Breathing rare, intermittent, such as Cheyne-Stokes. Eyeballs floating, pupils narrowed. It is possible to stop the heart and breathing, which requires a resuscitation complex. Laboratory indicators do not have specific features.

Poisoning with ethyl alcohol and surrogates of alcohol. When taking pure methyl alcohol, even a small amount, a coma develops within a few minutes, its forerunner is an acute visual impairment. There is a smell of formalin from his mouth. There is a stop of the heart and breathing; Resuscitation, as a rule, does not give an effect. Poisoning with ethyl alcohol (can develop already with the intake of over 700 ml of vodka) and surrogates develops slowly, from the usual alcohol intoxication to coma. It is accompanied by vomiting, sometimes with regurgitation, which has the smell of alcohol, and also the smell of alcohol from the mouth. The face is cyanotic, the skin moist, covered with cold sticky sweat. The pupils are wide, the eyeballs are floating. Muscles atonic, flabby, reflexes reduced. Breathing shallow, may be of the Cheyne-Stokes type. Arterial pressure is reduced, pulse is frequent, small filling.

[24], [25], [26], [27]

Hepatic coma

It is formed in severe form of hepatic insufficiency. Conditionally, since they can be combined, three forms are distinguished:

1. endogenous - caused by a sharp decrease in hepatocytes in cirrhosis, tumors, intoxications, acute violations of microcirculation in it - "shock liver";
2. exogenous - caused by external factors, for example, purulent intoxication, portal shunting, certain types of poisoning, gross violations of diet;
3. electrolytic-hepatic - "false" - is associated with a disturbance of the water-electrolyte balance, especially hypokalemia, the use of saluretics, the formation of ascites, hypoxic syndrome.

It develops gradually, rarely quickly, against the background of apparent improvement. The most severe is the endogenous form, accompanied by high lethality. Development of a coma is preceded by: a growing weakness, drowsiness, a period of psychomotor agitation, an increase in jaundice, dyspeptic and hemorrhagic disorders. The onset of coma is characterized by: an increase in the frequency and depth of breathing, its arrhythmia; there are muscle twitches (convulsions), a clonus of the feet, muscle tone builds up, mydriasis, nystagmus, pathological symptoms are formed. From the mouth the smell of raw meat. There may be bradycardia and hypotension. Laboratory indicators: bilirubinemia, azotemia, a decrease in the prothrombin index, cholesterol, blood sugar. Sedimentary liver samples are increased. In the urine: bilirubin, leucine, tyrosine.

Respiratory coma

It develops with severe respiratory failure, which leads to the development of brain hypoxia. There are two forms: peripheral - with lung diseases and chest trauma, and central - with the defeat of the respiratory center after surgery or with brain trauma. The onset is rapid: headache, dyspnea, breathing arrhythmia, convulsions, convulsions; cardiovascular insufficiency progresses. With the development of coma, there is a sharp, "cast-iron", cyanosis of the face, as the hypercapnia develops, the skin color changes to crimson, and then, to a cyanotic pink color, the cervical veins are swollen, auxiliary muscles participate in the breath, the face is puffy, the extremities are cold, peripheral edema and ascites can be determined. Breathing is superficial, arrhythmic; percussion - boxed or "mosaic" sound; auscultatory - cacophony or "dumb" lung. Arterial pressure progressively decreases, tachycardia, weak pulse. On the ECG - signs of an overload of the right heart:

Laboratory indicators: in the blood - leukocytosis, polycythemia, eosinophilia; in the study of KHS - pronounced and progressive manifestations of metabolic acidosis.

Thyrotoxic coma

It develops with decompensated thyrotoxicosis with its characteristic manifestations: the presence of goiter; exophthalmos. The onset is gradual: severe weakness, sweating, anorexia, nausea, diarrhea, palpitation, sudden arousal, insomnia, impaired swallowing, diazartria. With the development of coma: hyperthermia, the skin is initially moist, then dry due to dehydration, tachypnea, tachycardia, atrial fibrillation, high blood pressure is replaced by hypotension, exophthalmos, mydriasis are pronounced, muscle tone is elevated, bulbar disorders are possible,

Laboratory tests: in the blood - reduction of cholesterol, phospholipids, triglycerides, increase in the level of thyroid hormones - thyroxine, triiodothyronine, thyrotropin, protein-bound iodine, KHS - development of metabolic acidosis. In the analysis of urine: a decrease in specific gravity, protein, increased excretion of 17-ACS.

Uremic coma

It develops at the terminal stage of renal failure due to poisoning of the body with blood and metabolic waste, excreted by the kidneys.

Development is gradual, preceded by: headaches, blurred vision, itching, nausea, vomiting, convulsions, drowsiness with gradual depression of consciousness. With the development of coma: the skin is pale, dry, with a gray bloom, often swelling of the face and limbs, pinpoint hemorrhages on the skin; there is muscular fibrillation, mydriasis, Cheyne-Stokes respiration, less often Kussmaul with an ammonia odor; hypertensive syndrome.

Laboratory indicators: anemia, leukocytosis, acceleration of ESR, significant increase in blood slus, indications, metabolic acidosis, hypocalcemia in the urine, if any, high protein, blood.

Chloridropenic coma

It develops due to dehydration and loss of acid ions with: vomiting, eclampsia and toxicosis of pregnant women, use of diuretics, and toxic infections with profuse diarrhea. Development is gradual, accompanied by progressive weakness, anorexia, thirst, headaches, repeated fainting, apathy with a gradual fading of consciousness. Attention is drawn to the sharp depletion and dehydration, chewing of the cheeks, dry skin and mucous membranes, a decrease in skin turgor. In the case of a developed coma: hypothermia, wide pupils, superficial breathing, hypotension and tachycardia, decreased reflexes, minor twitching of the muscles of the face and limbs, there may be meningeal symptoms.

Laboratory indicators: polyglobulose, azotemia, hypochloraemia, hypocalcemia, in the study of KHS - a picture of metabolic alkalosis.

Diagnostics of the coma

A full examination of the patient and the implementation of a complex of medical measures is the competence of the resuscitator, therefore such patients in most cases should be hospitalized or transferred to intensive care units.

General clinical examination is carried out according to the general scheme, but the anamnesis is collected from relatives or accompanying persons. When entering such a hospital, it is optimal to examine the integral team of doctors: an intensive care unit, a neurosurgeon, a traumatologist, a thoracic surgeon and other specialists of a "narrow" profile. The main thing is the time when the diagnosis was made not by the coma itself, but by the reasons for it, and by taking measures to provide assistance. Be as a diagnostician "seven sprouds in the forehead," one with a coma syndrome can not cope!

Laboratory examination includes mandatory blood analysis, urinalysis, blood and urine tests for sugar or glucose, determination of blood slus, research of the coagulation system, electrolytes, plasma osmolarity. Laboratory tests during the first day are repeated every 6 hours, in the following days - twice a day. Vomit, urine, feces should be sent to the toxicology laboratory.

[28], [29], [30],

Treatment of the coma

The possibilities for diagnosis and care depend on circumstances: at home or outside the medical institution, they are limited to establishing the fact of a coma, perhaps its appearance and calling a special emergency brigade, in the polyclinic and a non-specialized department, the possibility is wider - connecting a dropper with glucose or saline solution for hemodelusion, glycosides, cordiamine, euphyllin and ganglioblocator, analgin, despite the unconscious state (drugs are contraindicated), if possible, steroid hormones.